Female Urology 3rd Edition

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FEMALE UROLOGY Copyright © 2008, 1996, 1983 by Saunders, an imprint of Elsevier Inc.

ISBN: 978-1-4160-2339-5

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Library of Congress Cataloging-in-Publication Data (in PHL) Female urology / [edited by] Shlomo Raz, Larissa V. Rodriguez.—3rd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4160-2339-5 1. Urogynecology. I. Raz, Shlomo, 1938- II. Rodríguez, Larissa V. [DNLM: 1. Genital Diseases, Female. 2. Urologic Diseases. WJ 190 F329 2008] RG484.F46 2008 616.60082—dc22 2007042440

Acquisitions Editor: Scott Scheidt Developmental Editor: Elizabeth Hart Publishing Services Manager: Frank Polizzano Senior Project Manager: Peter Faber Design Direction: Steven Stave

Working together to grow libraries in developing countries Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

www.elsevier.com | www.bookaid.org | www.sabre.org

I dedicate this book to my wife Sylvia and our children Alan, Yael, Daniela, and Karyn for their support and sacrifice during this year. Shlomo Raz To my sons Marcelo and Andre, because you are the strength of my life, my love, and my inspiration. Thank you for the sacrifices you make to help me fulfill my dreams. Larissa Rodríguez

CONTRIBUTORS

Paul Abrams, MD, FRCS Professor, Bristol Urological Institute, Southmead Hospital, Bristol, United Kingdom 17: Clinical Diagnosis of Overactive Bladder Ilana Beth Addis, MD, MPH Assistant Professor, University of Arizona College of Medicine, Associate Director, Female Pelvic Medicine and Reconstructive Surgery, University Physicians Healthcare, Tucson, Arizona 6: Social Impact of Urinary Incontinence and Pelvic Floor Dysfunction Danita Harrison Akingba, MD Fellow, Department of Gynecology, Female Urology, and Pelvic Surgery, Greater Baltimore Medical Center, Baltimore, Maryland 62: Transabdominal Paravaginal Cystocele Repair Michael E. Albo, MD Associate Clinical Professor of Surgery and Urology, University of California–San Diego, San Diego, California; Co-Director of Women’s Pelvic Medical Center, University of California–San Diego Hospital, San Diego, California 29: Selecting the Best Surgical Option for the Treatment of Stress Urinary Incontinence Samih Al-Hayek, MD, MRCS, LMSSA, LRCP, LRCS Research Registrar, Bristol Urological Institute, Southmead Hospital, Bristol, United Kingdom 17: Clinical Diagnosis of Overactive Bladder

Walter Artibani, MD Full Professor of Urology, University of Padova Medical School, Department of Urology, University of Padova Medical School, Padova, Italy 82: Abdominal Approach for the Treatment of Vesicovaginal Fistula Anthony Atala, MD Chair, Department of Urology, Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina 98: Tissue Engineering for Reconstruction of the Urinary Tract and Treatment of Stress Urinary Incontinence Richard C. Bennett, MD Resident, Department of Urology, William Beaumont Hospital, Royal Oak, Michigan 24: Pudendal Nerve Stimulation Alfred Bent, MD Chairman, Department of Gynecology, Female Urology, and Pelvic Surgery, Greater Baltimore Medical Center, Baltimore, Maryland 62: Transabdominal Paravaginal Cystocele Repair Jerry G. Blaivas, MD Clinical Professor of Urology, Weill-Cornell Medical College, New York, New York; Attending Surgeon, New York Presbyterian Hospital, New York, New York; Attending Surgeon, Lenox Hill Hospital, New York, New York 7: Clinical Evaluation of Lower Urinary Tract Dysfunction; 80: Reconstruction of the Absent or Damaged Urethra

Cindy Amundsen, MD Associate Professor of Obstetrics and Gynecology, Duke University School of Medicine, Durham, North Carolina; Director, Fellowship in Urogynecology and Pelvic Reconstructive Surgery, Department of Obstetrics and Gynecology, Duke University School of Medicine, Durham, North Carolina 77: Complications of Vaginal Surgery

David A. Bloom, MD Jack Lapides Professor of Urology, Department of Pediatric Urology, University of Michigan, Ann Arbor, Michigan 1: Developmental Anatomy and Urogenital Abnormalities

Rodney U. Anderson, MD Professor of Urology, Stanford University, Stanford, California 91: Focal Neuromuscular Therapies for Chronic Pelvic Pain Syndromes in Women

Sylvia M. Botros, MD Assistant Professor, Evanston Northwestern Healthcare, Northwestern University, Feinberg School of Medicine, Evanston, Illinois 67: Sacrospinous Ligament Suspension for Vaginal Vault Prolapse

Karl-Erik Andersson, MD, PhD Wake Forest Institute of Regenerative Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina 4: Pharmacologic Basis of Bladder and Urethral Function and Dysfunction

Alain Bourcier, PT Tenon Hospital, Department of Urology, University of Paris, Paris, France; Director, Pelvic Floor Rehabilitation Services, Clinique International Monceau, Paris, France 19: Behavior Modification and Conservative Management of Overactive Bladder; 28: Pathophysiology of Stress Incontinence

Rodney A. Appell, MD, FACS Professor and Chief, Division of Voiding Dysfunction and Female Urology, Baylor College of Medicine, Houston, Texas; Medical Director, Baylor Continence Center, Baylor College of Medicine, Houston, Texas 33: Vaginal Wall Sling

Timothy Bolton Boone, MD, PhD Professor and Chairman, Scott Department of Urology, Baylor College of Medicine, Houston, Texas 11: Urodynamic Evaluation

Lousine Boyadzhyan, MD Resident Physician, Department of Radiology, David Geffen School of Medicine at UCLA, Los Angeles, California 8: Imaging of the Female Genitourinary Tract; 55: Imaging in the Diagnosis of Pelvic Organ Prolapse v

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CONTRIBUTORS

C. A. Tony Buffington, DVM, PhD, DACVN Professor, Department of Veterinary Clinical Sciences, Ohio State University College of Veterinary Medicine, Columbus, Ohio 90: Neuroendocrine Role in Interstitial Cystitis and Chronic Pelvic Pain in Women

Firouz Daneshgari, MD Assistant Professor of Surgery, Department of Urology, Case Western Reserve University, Cleveland, Ohio; Director, Center for Female Pelvic Medicine and Reconstructive Surgery, Cleveland Clinic, Cleveland, Ohio 51: Epidemiology of Pelvic Organ Prolapse

Linda Cardozo, MD Professor of Urogynaecology, Department of Urogynaecology, King’s College Hospital, London, United Kingdom 5: Hormonal Influences on the Female Genital and Lower Urinary Tract

William de Groat, PhD Professor, Department of Pharmacology, University of Pittsburgh. Pittsburgh, Pennsylvania 3: Neuroanatomy and Neurophysiology: Innervation of the Lower Urinary Tract

Mauro Cervigni, MD Professor, Catholic University, Rome, Italy; Chief of Urogynecology, San Carlo-IDI Hospital, Rome, Italy 66: Tension-Free Cystocele Repair Using Prolene Mesh

John O. L. DeLancey, MD Department of Obstetrics and Gynecology, University of Michigan, Women’s Hospital, Ann Arbor, Michigan 53: Functional Anatomy and Pathophysiology of Pelvic Organ Prolapse

R. Duane Cespedes, MD Associate Professor, Department of Urology, University of Texas Health Sciences Center, San Antonio, Texas; Director of Female Urology and Urodynamics, Wilford Hall Medical Center, Lackland AFB, Texas 97: Transvaginal Closure of the Bladder Neck in the Treatment of Urinary Incontinence Christopher R. Chapple, BSc, MD, FRCS, FEBU Visiting Professor, Sheffield Hallam University, Sheffield, South Yorkshire, United Kingdom; Consultant Urological Surgeon, Royal Hallamshire Hospital, Sheffield Teaching Hospitals National Health Service Foundation Trust, Sheffield, South Yorkshire, United Kingdom 27: Pathophysiology of Stress Incontinence Chi Chiung Grace Chen, MD Fellow, Female Pelvic Medicine/Reconstructive Pelvic Surgery and Minimally Invasive Surgery, Department of Obstetrics and Gynecology, Cleveland Clinic, Cleveland, Ohio 54: Pelvic Organ Prolapse: Clinical Diagnosis and Presentation; 73: Open Abdominal Sacral Colpopexy Emily E. Cole, MD Department of Urology, Vanderbilt University Medical Center, Nashville, Tennessee 46: Radiofrequency for the Management of Genuine Stress Urinary Incontinence Craig V. Comiter, MD Associate Professor, Stanford University, Stanford, California 56: Dynamic Magnetic Resonance Imaging in the Diagnosis of Pelvic Organ Prolapse Matthew Cooperberg, MD Chief Resident, Department of Urology, University of California–San Francisco, San Francisco, California 23: Posterior Tibial Nerve Stimulation for Pelvic Floor Dysfunction Jaques Corcos, MD Professor of Urology, Director of the Urology Department, McGill University, Montreal, Quebec, Canada; Director of the Urology Department, Jewish General Hospital, McGill University, Montreal, Quebec, Canada 31: Urethral Injectables in the Management of Stress Urinary Incontinence

Donna Y. Deng, MD Assistant Professor of Urology, Division of Pelvic Reconstruction, Incontinence, and Neurourology, Department of Urology, University of California–San Francisco, San Francisco, California 64: Transvaginal Paravaginal Repair of High-Grade Cystocele; 68: Repair of Vaginal Vault Prolapse Using Soft Prolene Mesh; 83: Rectovaginal Fistula Hans Peter Dietz, MD, PhD Associate Professor, Department of Obstetrics and Gynaecology, Western Clinical School, University of Sydney, Nepean Hospital, Penrith, NSW, Australia 9: Pelvic Floor Ultrasound Connie DiMarco, MD Urogynecology Department, Sacred Heart Medical Center, McKenzie Willamette Medical Center, Springfield, Ohio 60: Managing the Urethra in Vaginal Prolapse Ananias Diokno, MD Department of Urology, William Beaumont Hospital, Royal Oak, Michigan 93: Epidemiology of Incontinence and Voiding Dysfunction in the Elderly Roger Roman Dmochowski, MD Professor, Department of Urologic Surgery, Vanderbilt University Medical Center, Nashville, Tennessee 46: Radiofrequency for the Management of Genuine Stress Urinary Incontinence Neil T. Dwyer, MD Fellow, Department of Urology, University of Iowa, Iowa City, Iowa 38: Fascia Lata Sling Daniel Eberli, MD Wake Forest Institute for Regenerative Medicine, WinstonSalem, North Carolina 98: Tissue Engineering for Reconstruction of the Urinary Tract and Treatment of Stress Urinary Incontinence Karyn Schlunt Eilber, MD Director, Comprehensive Center for Continence and Pelvic Reconstruction, Los Angeles, California 88: Benign Cystic Lesions of the Vagina and Vulva

CONTRIBUTORS

Ahmad Elbadawi, MD Departments of Pathology and Urology, State University of New York, Syracuse, New York 2: Structural Basis of Voiding Dysfunction Ahmad Elbadawi, MD Lecturer in Urology, Alazhar University, Cairo, Egypt; Urology Fellow, Jewish General Hospital, McGill University, Montreal, Quebec, Canada 31: Urethral Injectables in the Management of Stress Urinary Incontinence Raymond T. Foster, Sr., MD, MS, MHSc Assistant Professor of Obstetrics and Gynecology, University of Missouri–Columbia, School of Medicine, Columbia, Missouri; Director, Missouri Center for Female Continence and Advanced Pelvic Surgery, Department of Obstetrics, Gynecology, and Women’s Health, University of Missouri– Columbia, Columbia Missouri 70: Transvaginal Repair of Apical Prolapse: The Uterosacral Vault Suspension; 77: Complications of Vaginal Surgery Clare J. Fowler, MBBS, MSc, FRCP Professor of Neurophysiology, Department of Uro-Neurology, National Hospital of Neurology and Neurosurgery, London, United Kingdom 10: Electrophysiological Evaluation of the Pelvic Floor Joel Funk, MD Chief Resident, University of Arizona, Tucson, Arizona 56: Dynamic Magnetic Resonance Imaging in the Diagnosis of Pelvic Organ Prolapse Michelle M. Germain, MD Clinical Instructor, Department of Gynecology, Female Urology, and Pelvic Surgery, Greater Baltimore Medical Center, Baltimore, Maryland 62: Transabdominal Paravaginal Cystocele Repair Jason P. Gilleran, MD Assistant Professor, Department of Urology, The Ohio State University College of Medicine, Columbus, Ohio 79: Urethrovaginal Fistula David Alan Ginsberg, MD Assistant Professor of Clinical Urology, Keck School of Medicine of the University of Southern California, Los Angeles, California; Chief of Urology, Rancho Los Amigos National Rehabilitation Center, Downey, California 84: Ureterovaginal Fistula

Angelo E. Gousse, MD Associate Professor of Urology, Chief of Female Urology and Voiding Dysfunction, University of Miami, Miller School of Medicine, Miami, Florida; Attending Urologist, Jackson Memorial Hospital, Miami, Florida 15: Effect of Pelvic Surgery on Voiding Dysfunction Fred E. Govier, MD Clinical Professor of Urology, University of Washington Medical Center, Seattle, Washington; Chief of Surgery, Virginia Mason Medical Center, Seattle, Washington 59: Use of Synthetics and Biomaterials in Vaginal Reconstructive Surgery Asnat Groutz, MD Senior Lecturer, The Sackler Faculty of Medicine, Tel Aviv University Tel Aviv, Israel; Urogynecology Unit, Lis Maternity Hospital, Tel Aviv Medical Center, Tel Aviv, Israel 52: Pregnancy, Childbirth, and Pelvic Floor Injury Sender Herschorn, MD, FRCSC Professor and Chair, Division of Urology, University of Toronto, Martin Barkin Chair in Urological Research, University of Toronto, Toronto, Ontario, Canada; Attending Urologist, Sunnybrook Health Science Center, Toronto, Ontario, Canada 57: Urodynamics Evaluation of the Prolapse Patient Ken Hsiao, BS, MD Assistant Professor of Urology, Indiana School of Medicine, Indianapolis, Indiana; Staff Urologist, John Muir Medical Center, NorCal Urology, Walnut Creek, California 59: Use of Synthetics and Biomaterials in Vaginal Reconstructive Surgery Yvonne Hsu, MD Lecturer, University of Michigan, Ann Arbor, Michigan 53: Functional Anatomy and Pathophysiology of Pelvic Organ Prolapse Chad Huckabay, MD North Shore Long Island Jewish Health System, Smith Institute of Urology, New Hyde Park, New York 49: Complications of Incontinence Procedures in Women Tracy Hull, MD Staff Colorectal Surgeon, Cleveland Clinic Foundation, Cleveland, Ohio 78: Pathophysiology, Diagnosis, and Treatment of Defecatory Dysfunction

Roger P. Goldberg, MD, MPH Assistant Professor, Northwestern University, Feinberg School of Medicine, Evanston, Illinois 67: Sacrospinous Ligament Suspension for Vaginal Vault Prolapse

Nancy Itano, MD Assistant Professor and Senior Associate Consultant, Department of Urology, Mayo Clinic, Scottsdale, Arizona 60: Managing the Urethra in Vaginal Prolapse

Irwin Goldstein, MD Director, Sexual Medicine, Alvarado Hospital; Clinical Professor of Surgery, University of California, San Diego, California 50: Female Sexual Function and Dysfunction

Theodore M. Johnson, II, MD Associate Professor of Medicine, Emory University, Atlanta, Georgia; Atlanta Site Director, Atlanta VA GRECC, Atlanta VA Medical Center, Decatur, Georgia 94: Lower Urinary Tract Disorders in the Elderly Female

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CONTRIBUTORS

Mickey M. Karram, MD Volunteer Professor of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio; Director of Urogynecology and Reconstructive Pelvic Surgery, Department of Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, Ohio 71: Vaginal Hysterectomy in the Treatment of Vaginal Prolapse Kathleen Kieran, MD Resident, Department of Urology, University of Michigan Health System, Ann Arbor, Michigan 1: Developmental Anatomy and Urogenital Abnormalities Adam P. Klausner, MD Assistant Professor, Department of Urology, University of Virginia School of Medicine, Charlottesville, Virginia; Assistant Professor, Department of Surgery, Virginia Commonwealth University, Richmond, Virginia 18: Pathophysiology of Overactive Bladder Carl George Klutke, MD Division of Urologic Surgery, Washington University School of Medicine, St. Louis, Missouri 39: Tension-Free Vaginal Tape; 44: Transobturator Approach to Midurethral Sling John J. Klutke, MD Assistant Professor of Clinical Gynecology, Department of Obstetrics and Gynecology, Keck School of Medicine, University of Southern California, Los Angeles, California 39: Tension-Free Vaginal Tape; 44: Transobturator Approach to Midurethral Sling Kathleen C. Kobashi, MD Clinical Associate Professor, Urology, University of Washington, Seattle, Washington; Co-Director, Clinical Fellowship for Voiding Dysfunction and Pelvic Floor Reconstruction, Continence Center at Virginia Mason, Seattle, Washington 59: Use of Synthetics and Biomaterials in Vaginal Reconstructive Surgery Karl J. Kreder, MD, FACS Professor of Urology, University of Iowa, Iowa City, Iowa 38: Fascia Lata Sling Henry Lai, MD Fellow, Female Urology and Neurourology, Scott Department of Urology, Baylor College of Medicine, Houston, Texas 11: Urodynamic Evaluation Jerilyn M. Latini, MD Assistant Professor of Urology, University of Michigan Health System, Ann Arbor, Michigan 1: Developmental Anatomy and Urogenital Abnormalities

Gary E. Lemack, MD Associate Professor of Urology and Neurology, University of Texas Southwestern Medical Center, Dallas, Texas 14: Voiding Dysfunction and Neurological Disorders Malcolm A. Lesavoy, MD Department of Plastic Surgery, University of California–Los Angeles, Encino, California 99: Reconstruction of Congenital Female Genital Defects Amanda M. Macejko, MD Urology Fellow, Northwestern University School of Medicine, Chicago, Illinois 86: Urinary Tract Infections in Women Mary Grey Maher, MD Urology Center, Yale Medical Center, New Haven, Connecticut 41: Distal Urethral Polypropylene Sling; 47: Surgery for Refractory Urinary Incontinence: Spiral Sling Francesca Manassero, MD Doctoral Training, Department of Urology, University of Pisa, Pisa, Italy 27: Pathophysiology of Stress Incontinence Mariangela Mancini, MD Affiliate Professor, Residency in Urology Program, Department of Urology, University of Padova Medical School, Padova, Italy 82: Abdominal Approach for the Treatment of Vesicovaginal Fistula Edward J. McGuire, MD Professor, Department of Urology, University of Michigan, Ann Arbor, Michigan 25: Detrusor Myomectomy; 26: Bladder Augmentation; 36: Autologous Fascial Slings; 48: Mixed Urinary Incontinence Sarah E. Moeller, MS University of Minnesota, Minneapolis, Minnesota 22: Sacral Neuromodulation Interstim for the Treatment of Overactive Bladder Courtenay K. Moore, MD Assistant Professor, Department of Surgery, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio; Staff, Female Pelvic Medicine and Reconstructive Surgery, Glickman Urological and Kidney Institute, Cleveland Ohio 51: Epidemiology of Pelvic Organ Prolapse

Gary E. Leach, MD Director, Tower Urology Institute for Incontinence, Los Angeles, California 45: Cadaveric Fascia Using Bone Anchors; 61: Cadaveric Fascial Repair of Cystocele; 75: Posterior Repair Using Cadaveric Fascia

Arthur Mourtzinos, MD Assistant Professor of Urology, Tufts University Medical School, Boston, Massachusetts; Senior Staff Physician, Institute of Urology, Continence Center, Lahey Clinic Medical Center, Burlington, Massachusetts 47: Surgery for Refractory Urinary Incontinence: Spiral Sling

Monica Lee, MD David Geffen School of Medicine at the University of California–Los Angeles, Los Angeles, California 87: Vulvar and Vaginal Pain, Dyspareunia, and Abnormal Vaginal Discharge

M. Louis Moy, MD Assistant Professor, Division of Urology, University of Pennsylvania Health System, Philadelphia, Pennsylvania 13: Categorization of Voiding Dysfunction; 20: Drug Treatment of Urinary Incontinence in Women

CONTRIBUTORS

Tristi W. Muir, MD Assistant Professor, Uniformed Services University of the Health Sciences; Assistant Chief, Female Pelvic Medicine and Reconstructive Pelvic Medicine, Department of Obstetrics and Gynecology, Brooke Army Hospital, Fort Sam Houston, Texas 63: Anterior Colporrhaphy for Cystocele Repair; 74: Posterior Repair and Pelvic Floor Repair: Segmental Defect Repair

Virgilio G. Petero, Jr., MD Urology Research Fellow, William Beaumont Hospital, Royal Oak, Michigan; Clinical Fellow, Division of Immunology and Organ Transplantation, University of Texas, Medical School at Houston, Houston, Texas 93: Epidemiology of Incontinence and Voiding Dysfunction in the Elderly

Franca Natale, MD San Carlo–IDI Hospital, Rome, Italy 66: Tension-Free Cystocele Repair Using Prolene Mesh

Kenneth M. Peters, MD Chairman, Department of Urology, Peter and Florine Ministrelli Distinguished Chair in Urology, William Beaumont Hospital, Royal Oak, Michigan 24: Pudendal Nerve Stimulation

Linda Ng, MD Assistant Professor of Urology, Boston University School of Medicine, Boston, Massachusetts 25: Detrusor Myomectomy; 26: Bladder Augmentation; 36: Autologous Fascial Slings Victor Nitti, MD Associate Professor and Vice Chairman, Department of Urology, New York University School of Medicine, New York, New York 49: Complications of Incontinence Procedures in Women Peggy A. Norton, MD Professor, Department of Obstetrics and Gynecology, and Chief of Urogynecology and Reconstructive Pelvic Surgery, University of Utah School of Medicine, Salt Lake City, Utah 58: Nonsurgical Treatment of Vaginal Prolapse: Devices for Prolapse and Incontinence Pat D. O’Donnell, MD Professor and Chairman, Department of Urology, University of Arkansas for Medical Sciences, Little Rod, Arkansas 95: Urodynamics Evaluation in the Elderly Joseph G. Ouslander, MD Director, Division of Geriatrics and Gerontology, Wesley Woods Geriatric Hospital, Atlanta, Georgia 94: Lower Urinary Tract Disorders in the Elderly Female Priya Padmanabhan, MD Resident, Department of Urology, New York University School of Medicine, New York, New York 16: Idiopathic Urinary Retention in the Female Maria Fidel Paraiso, MD Staff Physician, Department of Obstetrics and Gynecology and the Glickman Urological Institute, Cleveland Clinic, Cleveland, Ohio; Head, Center of Urogynecology and Reconstructive Pelvic Surgery, Cleveland, Ohio; Co-Director, Program of Female Pelvic Medicine and Reconstructive Surgery, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio 72: Laparoscopic Sacral Colpopexy; 73: Open Abdominal Sacral Colpopexy Christopher Kennerly Payne, MD Associate Professor of Urology, Director, Female Urology and Neurourology, Stanford University Medical Center, Stanford, California 92: Painful Bladder Syndrome and Interstitial Cystitis

Peter E. Petros, MBBS, PhD, DS, MD, FRCOG, FRANZCOG CU Adjunct Professor, Department of Gynaecology, University of Western Australia, Perth, Australia; Consultant Emeritus, Royal Perth Hospital, Perth, Australia 40: Midurethral to Distal Urethral Slings; 69: Use of IVS Device for Vaginal Vault Prolapse Simon Podnar, MD, DSc Associate Professor of Neurology, University of Ljubljana Medical School, Ljubljana, Slovenia; Staff Neurologist and Clinical Neurophysiologist, Institute of Clinical Neurophysiology, University Medical Center, Ljubljana, Slovenia 10: Electrophysiologic Evaluation of the Pelvic Floor Dimitri U. Pushkar, MD, PhD Professor and Head, Department of Urology, Moscow State Medical Stomatological University, Moscow, Russia 34: Free Vaginal Wall Sling Raymond Robert Rackley, MD Co-Head, Section of Voiding Dysfunction and Female Urology; Director, Urothelial Biology Laboratory, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 21: Pharmacologic Neuromodulation; 43: Percutaneous Vaginal Tape Sling Procedure Steven S. Raman, MD Associate Professor, Division of Abdominal Imaging and Cross Sectional Interventional Radiology, Department of Radiology, David Geffen School of Medicine at UCLA, Los Angeles, California 8: Imaging of the Female Genitourinary Tract; 55: Imaging in the Diagnosis of Pelvic Organ Prolapse Andrea J. Rapkin, MD Professor, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, California 87: Vulvar and Vaginal Disorders: Chronic Pain and Abnormal Discharge Shlomo Raz, MD Professor of Urology, Chief of Female Urology, Urodynamics, and Reconstruction, University of California–Los Angeles, School of Medicine, Los Angeles, California 47: Surgery for Refractory Urinary Incontinence: Spiral Sling; 64: Transvaginal Paravaginal Repair of High-Grade Cystocele; 68: Repair of Vaginal Vault Prolapse Using Soft Prolene Mesh; 81: Vesicovaginal Fistula: Vaginal Approach; 83: Rectovaginal Fistula

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CONTRIBUTORS

Dudley Robinson, MRCOG Consultant Urogynaecologist, Department of Urogynaecology, King’s College Hospital, London, United Kingdom 5: Hormonal Influences on the Female Genital and Lower Urinary Tract Larissa V. Rodríguez, MD Associate Professor of Urology, Division of Female Urology; Co-Director, Division of Pelvic Medicine and Female Urology; Director of Female Urology Research, University of California– Los Angeles, Los Angeles, California 41: Distal Urethral Polypropylene Sling; 47: Surgery for Refractory Urinary Incontinence: Spiral Sling; 64: Transvaginal Paravaginal Repair of High-Grade Cystocele; 68: Repair of Vaginal Vault Prolapse Using Soft Prolene Mesh; 81: Vesicovaginal Fistula: Vaginal Approach; 83: Rectovaginal Fistula Christopher M. Rooney, MD Instructor, Urogynecology and Pelvic Reconstruction, Department of Obstetrics and Gynecology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 71: Vaginal Hysterectomy in the Treatment of Vaginal Prolapse Nirit Rosenblum, MD Assistant Professor of Urology, New York University School of Medicine, New York, New York 16: Idiopathic Urinary Retention in the Female; 76: Perineal Hernia and Perineocele Eric Scott Rovner, MD Associate Professor of Urology, Department of Urology, Medical University of South Carolina, Charleston, South Carolina 85: Urethral Diverticula Sarah A. Rueff, MD Staff Urologist, Director of the Continence Center, Billings Clinic, Billings, Montana 45: Cadaveric Fascia Using Bone Anchors; 61: Cadaveric Fascial Repair of Cystocele; 75: Posterior Repair Using Cadaveric Fascia Matthew P. Rutman, MD Assistant Professor, Department of Urology, Columbia University Medical Center, New York, New York 64: Transvaginal Paravaginal Repair of High-Grade Cystocele; 68: Repair of Vaginal Vault Prolapse Using Soft Prolene Mesh; 81: Vesicovaginal Fistula: Vaginal Approach; 83: Rectovaginal Fistula Peter K. Sand, MD Professor, Northwestern University, Feinberg School of Medicine, Evanston, Illinois; Evanston Northwestern Healthcare, Evanston, Illinois 67: Sacrospinous Ligament Suspension for Vaginal Vault Prolapse Jaspreet S. Sandhu, MD Urology Fellow, Department of Voiding Dysfunction, Neurourology, and Pelvic Reconstructive Surgery, New York Presbyterian Hospital, Weill-Cornell Medical Center, New York, New York 7: Clinical Evaluation of Lower Urinary Tract Infection; 80: Reconstruction of the Absent or Damaged Urethra

Anthony J. Schaeffer, MD Herman L. Kretschmer Professor and Chairman, Department of Urology, Feinberg School of Medicine, Northwestern University; Chairman, Department of Urology, Northeastern Medical Hospital, Chicago, Illinois 86: Urinary Tract Infections in Women Patrick J. Shenot, MD Assistant Professor, Department of Urology, Thomas Jefferson University, Jefferson Medical College, Philadelphia, Pennsylvania 21: Pharmacologic Neuromodulation Neil D. Sherman, MD Assistant Professor, Division of Urology, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 37: Use of Cadaveric Fascia for Pubovaginal Slings; 65: Cystocele Repair Using Biological Material Steven W. Siegel, MD Associate Clinical Professor, Department of Urology, University of Minnesota Medical School, St. Paul, Minnesota; Director, Center for Continence Care, Metropolitan Urologic Specialists, St. Paul, Minnesota 22: Sacral Neuromodulation Interstim for the Treatment of Overactive Bladder Larry Thomas Sirls, MD, FACS Director, Urodynamic Laboratory, William Beaumont Hospital, Royal Oak, Michigan 12: The Measurement of Urinary Symptoms, Health related Quality of Life and Outcomes of Treatment for Urinary Incontinence Christopher P. Smith, MD Assistant Professor, Division of Female Urology and Voiding Dysfunction, Scott Department of Urology, Baylor College of Medicine, Houston, Texas 11: Urodynamic Evaluation Karen E. Smith, MD Kanephe, Hawaii 48: Mixed Urinary Incontinence David Staskin, MD Associate Professor of Urology, Weill-Cornell Medical College, New York, New York; Director, Female Urology and Voiding Dysfunction, New York Presbyterian Hospital, New York, New York 42: The SPARC Sling System William Donald Steers, MD Hovey Dabney Professor and Chair, Department of Urology, University of Virginia School of Medicine, Charlottesville, Virginia 18: Pathophysiology of Overactive Bladder Marshall L. Stoller, MD Professor and Vice-Chair, Department of Urology, University of California–San Francisco, San Francisco, California 23: Posterior Tibial Nerve Stimulation for Pelvic Floor Dysfunction

CONTRIBUTORS

Lynn Stothers, MD, MHSc, FRCSC Assistant Professor of Surgery and Urology and Associate Member of the Department of Health Care and Epidemiology and Department of Pharmacology, University of British Columbia, Vancouver, British Columbia; Director, Bladder Care Center, University Hospital, British Columbia, Canada 30: Outcome Measures for Pelvic Organ Prolapse Elizabeth B. Takacs, MD Assistant Professor, University of Iowa, Carver College of Medicine, Iowa City, Iowa 32: Role of Needle Suspensions Emil Tanagho, MD Professor of Urology, Department of Urology, University of California–San Francisco, San Francisco, California 35: Colpocystourethropexy Joachim W. Thüroff, MD Chairman, Department of Urology, Johannes Gutenberg University Medical School, Mainz, Germany 96: Use of Bowel in Lower Urinary Tract Reconstruction in Women Hari Siva Gurunadha Rao Tunuguntla, MD Resident, Department of Urology, University of Miami, Miller School of Medicine, Miami, Florida; Resident Physician in Urology, Jackson Memorial Hospital, Miami, Florida 15: Effect of Pelvic Surgery on Voiding Dysfunction Christian Twiss, MD Resident, Department of Urology, New York University School of Medicine, New York, New York 76: Perineocele Renuka Tyagi, MD Assistant Professor of Urology, Assistant Professor of Obstetrics and Gynecology, Weill-Cornell Medical Center, New York Presbyterian Hospitals, New York, New York 42: The SPARC Sling System Sandip P. Vasavada, MD Associate Professor of Surgery/Urology, Cleveland Clinic Lerner College of Medicine, Cleveland, Ohio; Center for Female Pelvic Medicine and Reconstructive Surgery, Glickman Urological and Kidney Institute, Cleveland, Ohio 43: Percutaneous Vaginal Tape Sling Procedure

Mark Walters, MD Professor of Surgery, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, Ohio; Professor and Vice-Chair of Gynecology, Center of Urogynecology and Reconstructive Pelvic Surgery, Department of obstetrics and Gynecology, Cleveland Clinic, Cleveland, Ohio 54: Pelvic Organ Prolapse: Clinical Diagnosis and Presentation George D. Webster, MB, FRCS Professor of Surgery, Duke University Medical Center, Durham, North Carolina; Chief, Section of Urodynamics and Reconstructive Urology, Division of Urology, Department of Surgery, Duke University Medical Center, Durham, North Carolina 37: Use of Cadaveric Fascia for Pubovaginal Slings; 65: Cystocele Repair Using Biological Material; 70: Transvaginal Repair of Apical Prolapse: The Uterosacral Vault Suspension; 77: Complications of Vaginal Surgery Alan J. Wein, MD Division of Urology, University of Pennsylvania Health System, Philadelphia, Pennsylvania 13: Categorization of Voiding Dysfunction; 20: Drug Treatment of Urinary Incontinence in Women Ursula Wesselmann, MD Associate Professor of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 89: Pathophysiology of Pelvic Pain Christoph Wiesner, MD Department of Urology, Johannes Gutenberg University Medical School, Mainz, Germany 96: Use of Bowel in Lower Urinary Tract Reconstruction in Women Nasim Zabihi, MD Resident, University of California–Los Angeles, Los Angeles, California 41: Distal Urethral Polypropylene Sling Philippe Zimmern, MD Professor, University of Texas Southwestern Medical Center, Dallas, Texas 32: Role of Needle Suspensions; 79: Urethrovaginal Fistula Massarat Zutshi, MD Associate Staff Surgeon, Cleveland Clinic Foundation, Cleveland, Ohio 78: Pathophysiology, Diagnosis, and Treatment of Defecatory Dysfunction

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PREFACE

The mere formulation of a problem is far more essential than its solution, which may be merely a matter of mathematical or experimental skills. To raise new questions, new possibilities, to regard old problems from a new angle requires creative imagination and marks real advances in science. Imagination is more important than knowledge. The important thing is not to stop questioning. Albert Einstein During the past 30 years, thanks to the efforts of leading urologists, gynecologists, basic scientists, pharmacologists, neurophysiologists, and geriatricians, we have made unprecedented achievements in female pelvic medicine and reconstruction. These people have worked hard and deserve all the respect and honor they receive. They have done remarkably well in applying new ideas and technologic advances to the field. Intellectual capital is knowledge, information, and experience that can used to create better medicine. This collective brainpower it is hard to identify and harder still to deploy effectively, but once found and exploited, success is at hand. In this book, we have used this intellectual brainpower of all our collaborators to address simple and complex clinical conditions, with a focus on many medical and surgical specialties.

We have resisted the temptation to offer easy formulas and checklists because the fields of female pelvic medicine and reconstructive surgery are new and continuing to evolve. Although some of the chapters written today may be outdated at the time of publication, we have done our best to provide the most current information available. The principal contribution of this book is the array of chapters written by leaders in the field that describe the challenges of female pelvic medicine and reconstruction and that offer a framework on which health care professionals can build useful and valuable strategies for treating patients. Although the authors have expressed their own opinions, they also have incorporated the most current scientific and clinical information into accessible formats. They have researched the best evidence for clinical application and have critically appraised that evidence for its validity and usefulness. We thank them all for their great efforts. We will count this book a success if it inspires many readers to generate ideas far beyond any we have included or we could imagine. Shlomo Raz and Larissa Rodríguez

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DEVELOPMENTAL ANATOMY AND UROGENITAL ABNORMALITIES Kathleen Kieran, Jerilyn M. Latini, and David A. Bloom Knowledge of the prenatal development of the genitourinary system is essential to understand congenital disorders and normal urinary tract function and anatomy. This chapter summarizes the key milestones in genitourinary tract development at the organ and cellular levels. Many genes appear to play key roles in the molecular signals for development and differentiation of components of the genitourinary system. These genes are temporally and locally expressed during development, and without them, normal development fails.1 The kidney development database2 (http://www.ana.ed.ac.uk/anatomy/database/kidbase) provides a list of these genes, and updated or revised designations can be found in the international database (http://www.gene.ucl.ac.uk/ nomenclature).

absorbed into the urogenital sinus, providing an island of mesoderm in the otherwise endoderm-based urogenital sinus (Fig. 1-2). This mesodermal island expands laterally to become the trigone of the bladder. The location of the ureteric bud relative to the urogenital sinus determines whether the ureteral

DEVELOPMENT OF THE GENITOURINARY SYSTEM The genitourinary system begins to take form from intermediate mesoderm in the third week of gestation. At this point, the embryo is a bilaminar disk composed of external ectoderm and internal endoderm. The longitudinal growth of the embryo begins to exceed its transverse growth, such that the resulting tension induces folding of the cranial and caudal ends toward one another around the umbilical stalk. This folding brings the cloacal membrane (a bilaminar membrane in the caudal portion of the embryo, distal to the allantois) ventrally. The endodermlined yolk sac dilates, and the cloaca forms. The cloaca ultimately is divided into the anterior urogenital sinus and the posterior rectum (Fig. 1-1), although the mechanism is debated. It was once believed that urorectal folds on either side of the midline grew caudomedially to fuse with the cloacal membrane and divide the cloacal membrane into the urogenital sinus and the dorsal rectum by week 7. Subsequent regression of the tail then rotated the urogenital sinus and rectum dorsally. Some investigators3,4 have suggested that the urorectal septum may not exist or may not fuse with the cloacal membrane. The development of the urinary tracts and portions of the genital system is induced by the mesonephric and paramesonephric (müllerian) ducts. Both ductal systems grow toward the urogenital sinus; the mesonephric ducts grow medially, whereas the müllerian ducts have already fused into a single midline structure. Fusion of the wolffian ducts with the cloaca occurs by the middle of the fourth week (day 24). The junction of the müllerian ducts and the urogenital sinus is a central embryologic location called Müller’s tubercle. The mesonephric ducts bend laterally; at this bend, a ureteric bud forms. The portion of the mesonephric duct between the urogenital sinus and the ureteric bud is called the common nephric duct, and by day 33, it is

Figure 1-1 Development of the lower urinary tract. At 4 weeks, the cloaca is divided by a septum into an anterior urogenital sinus and posterior rectum. The mesonephric duct already joins the anterior portion of the cloaca, and the ureteral bud has started to develop at the bend of the mesonephric duct as it turns forward and medially to join the urogenital sinus. At 6 weeks, the urorectal septum progressively separates the urogenital sinus anteriorly from the rectum posteriorly. By week 7, the separation is complete, and the ureter and the mesonephric duct acquire separate openings in the urogenital sinus. After the 12th week, the ureter starts its upward and lateral movement as the mesonephric duct moves downward and medially. Tissue absorbed in between forms the trigone.

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tion between intramural muscle fibers. Intramural muscle fibers form as perivesical splanchnic mesoderm matures after induction by epithelial-mesenchymal interactions. Compliance of the fetal bladder increases over time in human fetuses and in animal models.6,7 Koo and colleagues7 showed a decreasing ratio of type 3 to type 1 collagen in the fetal bovine bladder; the changing ratios of perivesical collagen and muscle likely account for at least a portion of this evolution.

Normal Development single ureter Urogenital sinus Mesonephric duct

4 wks

Trigone precursor: normal length

6 wks

Ureter Vas deferens 7 wks

Trigone

8 wks

Normal orifices

Over 12 wks

Figure 1-2 The lower end of the mesonephric duct as it joins the anterior division of the cloaca. Notice that the common nephric duct is progressively absorbed into the urogenital sinus. By week 7, the ureter and the mesonephric duct have separate openings, and rotation takes place. The ureter moves upward and laterally, and the mesonephric duct moves downward and medially, expanding the absorbed tissue to form the trigonal structure.

orifices will be orthotopic; a ureteric bud that originates on a short, common nephric duct will be incorporated sooner into the bladder, with resultant lateral displacement of the ureteral orifices. The intramural ureteral tunnel predisposes to vesicoureteral reflux. Conversely, ureteric buds that are located a great distance from the urogenital sinus will be incorporated into the urogenital sinus later and may be associated with ectopic drainage into surrounding structures. The ureteric bud continues to grow craniolaterally while the mesonephric duct (distal to the bifurcation of the common nephric duct into the mesonephric duct and ureteric bud) grows caudomedially. The ureter undergoes a process of obstruction during the sixth week (37 to 40 days) and then is recanalized from the central portion to the cranial and caudal limits. Incomplete recanalization at either end may account for obstruction at the ureteropelvic junction or at the ureterovesical junction, where a thin transient membrane (i.e., Chwalla’s membrane) may fail to dissolve. The cuboidal epithelium of the immature ureter evolves to a lining of transitional cells by 14 weeks.5 The urogenital sinus expands caudally to form the bladder and gives rise to the posterior urethra in males or the entire urethra and distal third of the vagina in females. The cranial portion of the urogenital sinus tapers during the third month of gestation so that the allantois forms the urachus and the saccular bladder remains in place. The intramural bladder wall develops throughout the remainder of gestation, with collagen formation beginning in the lamina propria and with subsequent intercala-

Renal and Ureteral Development The renal excretory unit is the result of a complex developmental process influenced by reciprocal induction of mesenchyme and the ureteric bud and by many molecular events. The kidney develops in three stages. The first is the pronephros, which arises late in the third week in the cranial portion of the embryo. Pronephric tubules develop cranially and extend caudally, but they degenerate quickly, and the pronephros is obliterated by the start of the fifth week. By day 24, mesonephric ducts are present at the ninth and tenth somites. These ducts grow caudally to the cloacal membrane by day 28, fuse in the midline, and eventually form the bladder. Caudal canalization and then cranial canalization follows. The mesonephros, unlike its predecessor, is able to accomplish limited excretory function for the growing embryo. Mesonephric tubules along the medial nephrogenic cords form and dissolve, sequentially disappearing by the fourth month of development to leave only remnants. Some tubules develop lumens and vesicles and twist into an S shape, in which the lateral portion becomes the mesonephric duct and the medial portion surrounds capillaries originating in the aorta and forms a primitive renal corpuscle. Cranially, the tubules form efferent ductules. The mesonephric ducts give rise to the epididymis and vas deferens, and in females, remnants persist as the paroöphoron and epoöphoron, which are vestigial mesosalpingeal structures. The metanephros gives rise to the fetal kidney. It forms in the sacral region as the ureteric buds arise from the mesonephric ducts. As the ureteric buds grow cranially, they encounter metanephric mesenchyme on about day 28. After the ureteric bud contacts the mesenchyme, release of many factors culminates in reciprocal induction of growth factors governing the development of the metanephric system. The ureteric bud divides repeatedly between weeks 6 and 32 of development, ultimately giving rise to the collecting system: the collecting ducts, calyces, renal pelvis, and ureter. The metanephric mesenchyme gives rise to the parenchymal portions of the kidney that perform filtration and clearance: the glomeruli, proximal and distal tubules, and loop of Henle. Because of the lengthy period during which branching of the ureteral bud occurs, the growth of the metanephric mesenchyme that will give rise to renal parenchyma is not uniform; nephrons at the juxtamedullary region are formed earlier and mature sooner than nephrons in more peripheral locations. Nephrons undergo four defined stages of development in the human. Stage I occurs when the metanephric mesenchyme is fully discrete from the ureteral bud. Stage II begins when the Sshaped nephron connects with the ureteral bud. In stage III, an ovoid structure emerges, and in stage IV, a round glomerulus is seen. Most nephrons in humans are stage IV at birth, although maturation is completed fully in the early postnatal period.5 As the kidneys grow, their location in the embryo becomes progressively more cranial; this is likely caused by active growth of the kidney parenchyma and by increased differential growth of the caudal portion of the embryo. As a result, the kidneys

Chapter 1 DEVELOPMENTAL ANATOMY AND UROGENITAL ABNORMALITIES

ascend from their initial pelvic location to the upper retroperitoneum. As renal ascent proceeds, new blood vessels are generated cranially, and the more caudal blood vessels break down. In postnatal patients with renal ectopia, the renal blood supply is typically anomalous because angiogenesis is arrested when renal ascent ceases. The possibility of an aberrant blood supply should be considered in any patient with renal ectopia. Formation of the Urogenital Sinus and External Genitalia With dissolution of the tail and further development of the lower abdominal wall, the cloaca returns to a more dorsal position, and mesodermal proliferation in the fifth week forms genital tubercles. These tubercles ultimately fuse in the midline to form the phallus or clitoris. The urogenital sinus remains at the base of the tubercles; the folds of the urogenital sinus ultimately fuse in the male to form the penile urethra and widen in the female to form the vaginal vestibule and the discrete labia minora. The endodermally derived urethral groove develops from the urogenital sinus in the sixth week, and the urethral plate (a deepening of this groove) forms shortly thereafter. Male and female embryos remain morphologically identical until approximately 12 weeks’ gestation. Abnormalities of the Urogenital Sinus Bladder exstrophy occurs in approximately 1 of 30,000 births and is seven times more likely in children conceived through in vitro fertilization.8 This disorder is characterized by early rupture of the cloacal membrane, which is sometimes related to an intrinsic defect in the membrane. It is more common in males than in females by a ratio of approximately 2:1 to 6:1,9 and it is related to epispadias and to cloacal exstrophy. The latter condition is also associated with early rupture of the cloacal membrane, although it occurs much less commonly (1 in 200,000 to 400,000 births10). Although no genes associated with either condition have been definitively identified, the risk of bladder exstrophy is substantially greater with an affected relative (1 in 275) or an affected parent (1 in 70).9 Mesenchymal ingrowth between the ectodermal and endodermal layers of the cloacal membrane ultimately results in formation of the lower anterior abdominal wall and division of the cloaca into the anterior urogenital sinus and posterior rectum. Both disorders are associated with malformations of other organ systems, including the limbs, lower anterior abdominal wall, pelvic girdle, and in the case of cloacal exstrophy, the hindgut. Management of these conditions remains challenging. Gonadal Development Development of the testes and ovaries is initiated in the fifth week of gestation, when germ cells from the yolk sac migrate to the posterior body wall, inducing formation of the urogenital ridge medial to the mesonephros (Fig. 1-3). Invasion of the adjacent mesenchyme in the sixth week creates a primitive gonad with epithelium and blastema; the latter is formed from loosened epithelial cells. Persistent growth of the germinal epithelium into the adjacent mesenchyme forms cords that ultimately branch many times and form seminiferous tubules. Initially, all embryos have the potential to become male or female; the development of internal or external genitalia is an event influenced by genetic, endocrine, and paracrine factors.

SRY, a gene on the short arm of the Y chromosome, induces formation of the Sertoli and Leydig cells. It also induces secretion of anti-müllerian hormone (AMH), formerly called müllerianinhibiting substance (MIS), which induces regression of the müllerian system between 8 and 10 weeks’ gestation.5 Remnants of the müllerian system in the male include the prostatic utricle and the appendix testis. AMH has unilateral paracrine activity, and expression is required locally and bilaterally to achieve eradication of müllerian structures. Failure of testicular secretion of AMH or lack of receptive tissue results in persistence of the müllerian structures ipsilaterally as a miniature uterus and fallopian tube, typically associated with an inguinal hernia (i.e., hernia uteri inguinale). In the absence of SRY protein and AMH, ovarian follicles form from the maturing cortex at 3 to 4 months. Testosterone, which is secreted by the Leydig cells, and dihydrotestosterone, which is a derivative of testosterone arising from the action of 5α-reductase, play key roles in the development of the male ductal anatomy and external genitalia. Testosterone induces formation of the vasa deferentia and efferent ductules. Cranially, the mesonephric ducts degenerate, leaving the epididymis and its appendix. The distal mesonephric ducts give rise to the seminal vesicles. Testosterone stimulation and local conversion to dihydrotestosterone induce development of the prostate. Dihydrotestosterone also is locally responsible for fusion of the labioscrotal folds and the phenotypic development of the male external genitalia. Figure 1-4 illustrates the developmental and phenotypic correlates of male and female external genitalia. Descent of the fetal gonad is a two-step process. During the third month, the embryonic gonad is retroperitoneal and descends caudally so that by the seventh month, it is at the internal inguinal ring. The gubernaculum forms in the seventh week, and the processus vaginalis develops as a peritoneal outpouching. The second phase of scrotal descent occurs during the eighth and ninth months. The exact mechanism by which the testicle descends into the scrotum is unknown. Theories include contraction of the cremasteric fibers with resultant shortening of the gubernaculum, swelling of the tissue surrounding the inguinal canal such that the canal is widened sufficiently for passage of the testis, and increased intra-abdominal pressure with subsequent passage of the testis through the inguinal canal.5 The ovarian gubernaculum attaches to the müllerian ducts in the seventh week when fusion of the paramesonephric structures creates the broad ligament from folds of peritoneum. The gubernaculum then divides into two portions. Superiorly, the ovarian ligament connects the uterus and ovary, and inferiorly, the round ligament connects the ovary and the labioscrotal folds. Abnormalities in Development of Internal and External Genitalia Abnormalities in the development of the internal and external genitalia can be divided into those in which only the external genitalia are affected and those in which the internal and external genitalia are affected. Disorders in which the external genitalia are affected are considered ambiguous genitalia (“hermaphroditism”) and occur in approximately 1 of 30,000 live births. Male pseudohermaphrodites are genetically 46,XY, with preserved wolffian duct structures and internal testicular tissue but feminized external genitalia.11,12 Female pseudohermaphrodites (60% to 70% of hermaphrodites) are genetically 46,XX, with preserved müllerian structures and internal ovarian tissue but virilized

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Genital tubercle Urethral folds Urogenital slit Labioscrotal swelling Anal pit Tail 16.8 mm

Glans Genital tubercle Urogenital slit Urethral folds Labioscrotal swelling Anus

49.0 mm

45.0 mm

Figure 1-3 The undifferentiated sexual structures early in embryonic life (eighth week) grow and differentiate into female or male forms. The representative segments and their future course (depending on sexual differentiation) are illustrated. (From Tanagho EA: Embryology of the genitourinary system. In Tanagho EA, McAninch JW [eds]: General Urology, 14th ed. Norwalk, CT, Appleton & Lange, 1995.)

Glans penis Clitoris Urethral meatus

Labia minora

Scrotum

Vaginal orifice Labia majora

Raphe

Anus

external genitalia. True hermaphrodites are rare and have both ovarian and testicular tissue, typically with a 46,XX genotype11; there is no consistent appearance of the external genitalia, but about 75% of patients have male external genitalia with hypospadias and variable gonadal descent.12 Female pseudohermaphrodites are most commonly the result of 21-hydroxylase deficiency,11 an autosomal recessive disorder in which insufficiency of this enzyme leads to incomplete synthesis of all products in the steroidogenic pathway in the adrenal gland. The lack of production of the final product yields lack of feedback on the precursors, and intermediate products (many of them androgenic at high doses) accumulate. Less commonly, other enzymes in the steroidogenic pathway are affected; 3β-

hydroxylase deficiency is rare, whereas 11-hydroxylase deficiency is associated with salt retention and hypertension rather than the salt wasting observed with 21-hydroxylase deficiency. The end result is virilization of the external genitalia while the normal female internal genitalia are preserved. Less frequently, extrinsic exposure to androgens can be the cause. In either case, management of the affected patient includes correction of the electrolyte abnormalities and reconstruction of functional phenotypic anomalies. Male pseudohermaphrodites arise through defects in androgen synthesis or recognition in the developing embryo. Androgen resistance is an X-linked abnormality seen in approximately 1 of 60,000 newborns, in which the testes form and function normally

Chapter 1 DEVELOPMENTAL ANATOMY AND UROGENITAL ABNORMALITIES

Figure 1-4 Development of the male and female external genitalia. Notice that the genital tubercles that develop on the undersurface of the cloacal membrane progressively enlarge and fuse to form the body of the penis in the male and to form the clitoris in the female. Fusion of the urethral folds completes the urethral formation in the male, whereas the folds remain as the labia in the female. The post-tubercle segment of the urogenital sinus opens to become the vaginal vestibule of the female, whereas in the male, it forms part of the urethra, which is completed by the urethral fold fusion.

but the target tissues have a receptor defect that renders them insensitive to androgens.11,13 AMH is still secreted by the normal testes, and the müllerian ducts degenerate. Wolffian structures are preserved. Many of these patients present at puberty, but patients who are identified soon after birth can be given testosterone or human chorionic gonadotropin to stimulate phallic

growth and determine whether male gender assignment is feasible.11 Testes should be closely monitored or removed because of the risk of dysgerminoma. True hermaphroditism is associated with the presence of ovarian and testicular tissue. Lateral hermaphroditism is associated with the presence of an ovary on one side and a testis on the

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other. Unilateral hermaphroditism is associated with an ovotestis on one side and a normal gonad on the other. Bilateral hermaphroditism is associated with bilateral ovotestes. Like male pseudohermaphroditism, true hermaphroditism is associated with an increased risk of neoplastic conversion in the testis.11 Less common abnormalities of gonadal development include mixed gonadal dysgenesis and pure gonadal dysgenesis. In the former, karyotypes are typically 45,X/46,XY, and patients have a single testis accompanied by a streak ovary. These patients are at increased risk for dysgerminoma. In pure gonadal dysgenesis, ambiguous genitalia are not present; these patients are at increased risk for gonadoblastoma.11,12 Because formation of the female reproductive system from the müllerian ducts relies on fusion of primitive structures, abnormalities of fusion are not uncommon. Normal development of the müllerian system relies on elongation of the epithelial tubes lateral to the wolffian ducts, fusion of these ducts after reaching Muller’s tubercle, independent recanalization of each side, and resorption of the residual septum in a caudad-to-cephalad fashion. Failure at any of these steps may result in disorders such as unicornuate uterus, persistent vaginal septum with resultant septate vagina, or Mayer-Rokitansky-Küster-Hauser syndrome (1 in 5000).14 In the latter syndrome, failure of müllerian duct fusion gives rise to vaginal agenesis, although the ovaries and fallopian tubes develop normally. Concomitant renal and genitourinary (15% to 40%) or skeletal (12% to 50%) abnormalities occur.11,15

MOLECULAR CAUSES OF ABNORMAL DEVELOPMENT During the past decade, significant advances have been made in the identification of the genes and their proteins involved in the normal and abnormal development of the genitourinary tract. Knowledge of the precise molecular events involved in embryogenesis is evolving rapidly, and key genes and proteins crucial to certain steps in genitourinary development are discussed in the following sections. FGF10 Fibroblast growth factor 10 (FGF10) is expressed in the mesenchyme of the genital tubercle; FGF8 is expressed by urethral tissues. Interactions between these structures likely induce growth of the male phallus. The lack of FGF10 expression is theorized to account for the hypospadiac morphology with failure of fusion of the distal urethral plate, although the plate itself appears to develop normally because of the presence of FGF-8.16,17 GDNF Glial cell–derived neurotrophic factor (GDNF) is a mesenchymederived signaling factor that is a member of the transforming growth factor-β (TGF-β) family. It acts as the ligand for the RET receptor and induces growth of the ureteral bud during its interaction with the metanephric mesenchyme. In GDNF-knockout animals, development of the pronephros and mesonephros proceeds normally, but metanephric development is stunted by the lack of reciprocal interactions between the mesenchyme and the ureteral bud.18 Similar defects are seen in WT1 mutants19 and

RET-deficient mutants, although the latter may have primitive, poorly developed kidneys.1,19 WNT4 WNT4 (i.e., wingless-type mouse mammary tumor virus [MMTV] integration site family member 4 protein) is expressed in the mesenchyme adjacent to the mesonephric ducts and in the metanephric mesenchyme. WNT4 mutants have abnormally small, dysplastic kidneys and arrest of development at the level of formation of the renal tubules and renal epithelium from the mesenchyme.1 It is theorized that WNT4 signals enable organization of the epithelial cells into tubular structures.19 AMH Behringer and colleagues20 found that in AMH knockouts, testes were bilaterally descended, but the female reproductive organs remained intact, although they were often hypoplastic. Testes had Leydig cell hyperplasia, but spermatogenesis and semen analyses were normal in the affected animals. In contrast, mice that did not produce AMH but who also had a defect in the androgen receptor had absent wolffian structures and bilaterally undescended testes with maturational arrest in spermatogenesis. AMH is thought to exert its effects through paracrine actions, and it must be present before week 8 of gestation to induce müllerian regression.18 Bartlett and coworkers21 evaluated mice heterozygous for the AMH gene. These heterozygotes had poor development of the cremaster-gubernacular complex; the gubernaculums did develop but remained fibrotic and had poor cremaster development. Testes descended normally in these mice. The investigators concluded that AMH was not the determinant of gubernacular development or testicular descent but that it did play a key role in cremaster development. Defects in the type II anti-müllerian hormone receptor gene (AMHR2) (formerly referred to as the MIS type II receptor gene) have also been associated with persistent presence of paramesonephric structures. Persistent müllerian duct syndrome (PMDS) is a subtype of male pseudohermaphroditism in which the external genitalia are virilized and are morphologically normal, but paramesonephric structures persist. Hoshiya and associates22 reported a novel mutation in the AMHR2 gene caused by abnormal splicing; prior research identified additional abnormalities in the gene caused by base pair mutation in an intron and by deletion of genetic material from an exon. AMH is a hormone associated with the TGF-β family that is expressed in neonates, with a peak level occurring in male infants and in prepubertal girls. In addition to effects on degeneration of the müllerian system, its exact hormonal effects are unknown. However, it was shown to decrease testosterone production by the Leydig cells by a cytochrome P450–dependent mechanism in one study.23 Testosterone levels were increased in normal controls compared with hypospadiacs, and AMH protein levels were inversely correlated, suggesting that AMH may influence external genital development and induce the hypospadiac phenotype. AMH expression has been a useful means of differentiating between patients with extrinsic and those with intrinsic virilization. Because AMH is synthesized by the Sertoli cells, elevated AMH levels in male infants with undescended testes suggest the presence of normal or malignant testicular tissue, whereas the absence of AMH is associated with residual ovarian tissue.24

Chapter 1 DEVELOPMENTAL ANATOMY AND UROGENITAL ABNORMALITIES

KSP-Cadherin KSP-cadherin, also designated CHD16 or cadherin 16, is a celladhesion molecule expressed solely in the tubular epithelial cells of the kidney and genitourinary tract during prenatal development. Using protein linkage and immunoassays, expression of KSP-cadherin has been localized to the embryonic ureteric bud, wolffian duct, müllerian ducts, and mesonephric and metanephric structures. In adults, expression is limited to the thick ascending loop of Henle, proximal renal tubules, and Bowman’s capsules. Shao and colleagues25 demonstrated that tissue-specific expression of this protein could be established through linkage to a promoter and that a small segment of DNA adjacent to the promoter was adequate for tissue-specific expression. Although the exact function of KSP-cadherin has not been elucidated, its tissue-specific expression during development suggests that it may be involved with organogenesis of the genitourinary system.25

PAX2 PAX genes have been linked in previous research to abnormal prenatal development of the renal and visual systems, including Waardenburg’s syndrome, aniridia, and alveolar rhabdomyosarcoma. PAX2 (i.e., paired box gene 2) is localized to chromosome 10. It is expressed in the mesonephric ducts, ureteral bud, and the periureteral mesenchyme, and it is absent in mature nephrons. Animals heterozygous for the PAX2 gene had diminished kidney size and disorganized structure, with a thin cortex, decreased number of cortical structures, increased cystic components, and immaturity of mesenchyme-derived tissue.18 Homozygous PAX2-knockout animals manifested renal agenesis associated with failure of wolffian duct formation.26 These abnormalities are referable to failed branching of the ureteral bud, lack of appropriate differentiation of the metanephric mesenchyme, or failure of reciprocal induction of the mesenchyme and ureteral bud.26 Sanyanusin and coworkers27 found similar ultrastructural abnormalities in heterozygotes in a family cohort with a known PAX2 mutation who were affected by optic nerve colobomas and genitourinary abnormalities, including vesicoureteral reflux and anomalous renal development. Animal models homozygous for PAX2 mutations failed to develop genitourinary tracts; development of the external genitalia was also abnormal because of limited growth of the mesonephric duct and subsequent failure of the subdivision of the cloaca.1

WT1 Wilms’ tumor 1 gene (WT1) is one of the most well-known genes in renal development. Located on chromosome 11p, its linkage to the appropriate receptor results in blockage of transcription, and abnormal linkage is associated with development of Wilms’ tumors. Clarkson and associates28 demonstrated that mutations in the WT1 gene were associated with nephric anomalies and genital anomalies, although the latter were not observed independently of the former. Expression of the WT1 protein has been localized to the mesonephric tubules and metanephric mesenchyme, and prenatal lack of expression is associated with failure of metanephric development; WT1-knockout mice fail to develop caudal mesonephric tubules, which ultimately give rise to renal structures.18 The local events surrounding WT1 expression appear

to include suppression of insulin-like growth factor 2 (IGF2) expression in the local mesenchyme, because IGF2 is expressed before WT1 activity, and IGF2 expression declines in the presence of WT1.19 WT1 has been associated with prenatal expression of PAX2 and AMH. WT1-knockout mice fail to express PAX2, and WT1 is thought to exert effects on AMH expression in the developing embryo. Activity of the AMH promoter is known to be under the influence of many substances, including WT1, GATA-binding protein 4 (GATA4), SRY-box 9 (SOX9), and splicing factor 1 (SF1). WT1 expression in the developing embryo parallels that of AMH expression while müllerian regression takes place, and WT1 binds to a specific region of the AMH promoter.29 Abnormalities in the WT1 gene are associated with development of Wilms’ tumor and with less common syndromes such as the Denys-Drash syndrome (i.e., ambiguous genitalia, rudimentary gonads, nephrotic syndrome, and Wilms’ tumor) and Frasier syndrome,29 which is characterized by dysgenetic gonads and renal anomalies with development of the nephrotic syndrome.30 Abnormalities in sex differentiation of WT1 mutants are linked to preservation of a triplet of amino acids (KTS: lysine, threonine, and serine); without KTS preservation, there is decreased synthesis of AMH and SRY. Genetic males with a 46,XY karyotype will be phenotypic females with preservation of müllerian structures.30

HOXA Homeobox genes have been identified in multiple organisms, from mammals to insects and lower organisms, and they appear to affect structural symmetry during organogenesis. Research has identified homeobox genes as important for the normal development of the genitourinary tract. Cohn31 reviewed the research that found that homeobox genes were needed for the normal growth and differentiation of the urethral plate and distal genital tubercle. Development of the genital tubercle parallels that of development of the limb buds in the embryo; without HOXA genes, growth of the distal genital tubercle remains rudimentary. Mutations in the homeobox genes have also been associated with abnormal development of the external genitalia, often in the setting of a syndrome of developmental abnormalities. One such novel syndrome is X-linked lissencephaly with abnormal genitalia (XLAG), in which patients have frameshift or point mutations in the Aristaless-related homeobox gene (ARX).32 Affected patients present with neural malformations, including agenesis of the corpus callosum, abnormalities of midline structures in the brain, disorganized and incomplete development of the cerebral cortex, and micropenis with bilateral undescended testicles. Some patients also have associated renal phosphate wasting.33 The importance of the homeobox genes in regulating normal organogenesis is underscored by duplication of function. HOXA and HOXD genes have been found to have compensatory activity for mild mutations such that affected embryos may develop without significant congenital abnormalities. However, more severe or extensive mutations in either gene cannot be compensated by the remaining normal gene.34 Work by Utsch and colleagues34 found that novel mutations in the homeobox genes associated with the hand-foot-genital syndrome may reflect the limitations of duplicated function in compensatory genes.

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Androgen Receptor Androgen resistance is associated with decreased growth of the glans and corpora cavernosal structures, but the corpus spongiosum develops normally and may be hypertrophied. This pattern of development suggests that although growth of the corpora cavernosa may be induced by androgens, growth of the corpus spongiosum is androgen independent.17 Shapiro and coworkers35 evaluated an animal model of congenital adrenal hyperplasia by exposing embryos to androgens for different periods. They found that virilization resulting from congenital adrenal hyperplasia could be induced through exogenous androgen exposure between 8 and 13 weeks’ gestation. However, even within this time frame, morphologic changes observed after early androgen exposure differed from those induced by later exposure. Exposure to androgens earlier in the critical period was associated with increased virilization, including complete fusion of the labioscrotal folds and clitoromegaly.

Clitoromegaly alone was observed with later exposure to androgens. Shapiro’s group theorized that somatic growth of the embryo and genital structures later than 13 weeks’ gestation was independent of the influence of testosterone and other androgens.

CONCLUSIONS Development of the genitourinary tract is a complex series of events and interactions over time and space. Common and uncommon errors in these events and interactions result in anomalies and may set the stage for dysfunctions later in life. Understanding the prenatal events involved in the development of the genitourinary tract facilitates comprehension of normal and aberrant postnatal anatomy and informs management of urologic disorders.

References 1. Lipschutz JH: Molecular development of the kidney: A review of the results of gene disruption studies. Am J Kidney Dis 331:383-397, 1998. 2. Davies JA, Brandli A: Kidney development database. Available at http://www.ana.ed.ac.uk/anatomy/database/kidbase 3. Kluth D, Hillen M, Lambrecht W: The principles of normal and abnormal hindgut development. J Pediatr Surg 30:1143-1147, 1995. 4. Nievelstein RA, van der Werff JF, Verbeck FJ, et al: Normal and abnormal development of the anorectum in human embryos. Teratology 57:70-78, 1998. 5. Park JM: Normal and anomalous development of the urogenital system. In Walsh PC, Retik AB, Vaughn ED Jr, Wein WJ (eds): Campbell’s Urology, 8th ed. Philadelphia, WB Saunders, 2002, pp 1737-1764. 6. Kim KM, Kogan BA, Massad CA, Huang Y: Collagen and elastin in the normal fetal bladder. J Urol 146:524-527, 1991. 7. Koo HP, Howard PS, Chang SL, et al: Developmental expression of interstitial collagen genes in fetal bladders. J Urol 158:954-961, 1997. 8. Wood HM, Trock BJ, Gearhart JP: In vitro fertilization and the cloacal-bladder exstrophy-epispadias complex: Is there an association? J Urol 69:1512-1515, 2003. 9. Shapiro E, Lepor H, Jeffs RD: The inheritance of the exstrophyepispadias complex. J Urol 132:308-310, 1984. 10. Casale P, Grady RW, Waldehausen JHT, et al: Cloacal exstrophy variants: Can blighted conjoined twinning play a role? J Urol 172:1103-1107, 2004. 11. Breech LL, Laufer MR: Developmental abnormalities of the female reproductive tract. Curr Opin Obstet Gynecol 11:441-450, 1999. 12. Duckett J, Baskin L: Genitoplasty for intersex anomalies. Eur J Pediatr 152(Suppl 2):S80-S84, 1993. 13. Schweiken HU: The androgen resistance syndromes: Clinical and biochemical aspects. Eur J Pediatr 152(Suppl 2):S50-S57, 1993. 14. Edmonds DK: Vaginal and uterine anomalies in the paediatric and adolescent patient. Curr Opin Obstet Gynecol 13:463-467, 2001. 15. Spevak MR, Cohen HL: Ultrasonography of the Adolescent Female Pelvis. Ultrasound Q 18:275-288, 2002. 16. Haraguchi R, Suzuki K, Murakami R, et al: Molecular analysis of external genitalia formation: The role of fibroblast growth factor (FGF) genes during genital tubercle formation. Development 127:2471-2379, 2000. 17. Yucel S, Liu W, Cordero D, et al: Anatomical studies of the fibroblast growth factor-10 mutant, Sonic Hedge Hog mutant and androgen

18. 19. 20. 21. 22.

23. 24.

25.

26. 27.

28. 29. 30. 31.

receptor mutant mouse genital tubercle. Adv Exp Med Biol 545:123148, 2004. Coplen DE: Molecular aspects of genitourinary development. AUA Update Series 23:13, 2004. Glassberg KI: Normal and abnormal development of the kidney: A clinician’s interpretation of current knowledge. J Urol 167:23392351, 2002. Behringer RR, Finegold MJ, Cate RL: Mullerian-inhibiting substance function during mammalian sexual development. Cell 79:415-425, 1994. Bartlett JE, Lee SM, Mishina Y, et al: Gubernacular development in mullerian inhibiting substance receptor-deficient mice. BJU Int 89:113-118, 2002. Hoshiya M, Christian BP, Cromie WJ, et al: Persistent Mullerian duct syndrome caused by both a 27-bp deletion and a novel splice mutation in the MIS type II receptor gene. Birth Defects Res 67:868874, 2003. Austin PF, Siow Y, Fallat ME, et al: The relationship between mullerian inhibiting substance and androgens in boys with hypospadias. J Urol 168:1784-1788, 2002. Misra M, MacLaughlin DT, Donahoe PK, Lee MM: The role of müllerian inhibiting substance in the evaluation of phenotypic female patients with mild degrees of virilization. J Clin Endocrinol Metab 88:787-792, 2003. Shao X, Johnson JE, Richardson JA, et al: A minimal KSP-cadherin promoter linked to a green fluorescent protein reporter gene exhibits tissue-specific expression in the developing kidney and genitourinary tract. J Am Soc Nephrol 13:1824-1836, 2002. Piscione TD, Rosenblum ND: The malformed kidney: Disruption of glomerular and tubular development. Clin Genet 56:341-356, 1999. Sanyanusin P, Schimmenti LA, McNue LA, et al: Mutation of the PAX2 gene in a family with optic nerve colobomas, renal anomalies, and vesicoureteral reflux. Nat Genet 9:358-364, 1995. Clarkson PA, Davies HR, Williams DM, et al: Mutational screening of the Wilms’ tumour gene, WT1, in males with genital abnormalities. J Med Genet 30:767-772, 1993. Hossain A, Saunders GF: Role of Wilms tumor 1 (WT1) in the transcriptional regulation of the Mullerian-inhibiting substance promoter. Biol Reprod 69:1808-1814, 2003. MacLaughlin DT, Donahoe PK: Sex determination and differentiation. N Engl J Med 350:367-378, 2004. Cohn MJ: Developmental genetics of the external genitalia. Adv Exp Med Biol 545:149-157, 2004.

Chapter 1 DEVELOPMENTAL ANATOMY AND UROGENITAL ABNORMALITIES

32. Hartmann H, Uyanik G, Gross C, et al: Agenesis of the corpus callosum, abnormal genitalia and intractable epilepsy due to a novel familial mutation in the Aristaless-related homeobox gene. Neuropediatrics 35:157-160, 2004. 33. Hahn A, Gross C, Uyanik G, et al: X-linked lissencephaly with abnormal genitalia associated with renal phosphate wasting. Neuropediatrics 35:202-205, 2004.

34. Utsch B, Becker K, Brock D, et al: A novel stable polyalanine [poly(A)] expansion in the HOXA13 gene associated with handfoot-genital syndrome: Proper function of poly(A)-harbouring transcription factors depends on a critical repeat length? Hum Genet 110:488-494, 2002. 35. Shapiro E, Huang H, Wu, XR: New concepts on the development of the vagina. Adv Exp Med Biol 545:173-185, 2004.

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STRUCTURAL BASIS OF VOIDING DYSFUNCTION Ahmad Elbadawi Functional behavior of the urinary bladder has been investigated for more than a century, but several aspects of the mechanism of voiding and the way it is altered in vesical dysfunction remain unresolved. This can largely be attributed to the complexity of structural organization of the bladder and its outlet and the matching complexity of their functions.1-7 The storage (i.e., filling) and expulsion (i.e., voiding) phases of micturition involve essentially opposite functions of the bladder and urethra.8 The bladder acts as a reservoir for urine during filling and as a pump for expelling its stored urine during voiding. The urethra during bladder filling is closed, sealed, and noncompliant, acting as a sphincter to maintain continence, but it opens, dilates, and becomes compliant during voiding, acting as a conduit for the urinary stream. Efficient urine storage requires a compliant and stable detrusor together with a continent bladder outlet.5,9 Compliance of the detrusor allows distention of the bladder to capacity, and its stability ensures absence of untimely contractions that could involuntarily force some urine past the closed outlet, resulting in incontinence. Complete emptying of the full bladder9 depends on optimal contractility of the detrusor so that it can mount a strong, speedy, sustained, and unitary voiding contraction; coordinated opening of the bladder outlet; and maintenance of the opened outlet as a free conduit for an uninterrupted and strong urinary stream. The anatomy and structure of the bladder and urethra must be optimally suited to the complex dynamic events in the micturition cycle.6 Important elements in this regard are the inherent physical and biomechanical properties of the tissue components of the vesical and urethral walls and their bearing on organ distensibility and contractility.8,10-12 Two crucial elements are the topographic and microstructural organization of the musculature of the bladder wall and urethra and the elaborate system of vesicourethral innervation, with complex central cephalospinal control and intricate peripheral pathways.1-6,13,14 Various disciplines have contributed through experimental and clinical investigation to our knowledge of bladder function and dysfunction. Gross anatomy was the natural start during the previous century, and it prevailed for many decades. It resulted in some fundamental concepts that have been expanded and refined in the current century as the result of improved methods of dissection, neuroanatomic tracing techniques, and microscopic staining procedures. After the initial era of anatomic investigation, the principal approach to studies on voiding has been the characterization of physiologic and muscular responses of the lower urinary tract, mainly the bladder. It is undeniable that definition and measurement of these responses are important for understanding the overall nature of neuromuscular function of the bladder and urethra. Nonetheless, such an approach cannot define the factors that determine function of the effector 12

organ (i.e., smooth muscle of detrusor and urethral wall) in regard to the exact mechanism and balance of their contractility, distensibility, and stability during the filling and expulsion phases of micturition. Attempts to define these factors based purely on physiopharmacologic studies are largely inferential and have generated some misconceptions. One such misconception is the idea that the sympathetic autonomic nervous system has little or no role in vesical or urethral function.15,16 This dogma prevailed through the mid-1960s, until it was invalidated by microscopic proof of sympathetic innervation of the vesicourethral muscularis, which was subsequently confirmed by innumerable physiopharmacologic observations.1,4,5,7 Landmarks in our knowledge of muscular anatomy of the lower urinary tract3,6,17,18 include continuation of the muscularis of the terminal ureters as the vesical “trigone” and beyond into the dorsal wall of the urethra; the nonlayered, interwoven organization of muscle bundles of the detrusor13; identification of a vesical sheath around the terminal ureters,19 which was eventually refined as the concept of dual ureteral sheath20,21; and the concept of the rhabdosphincter as an integral striated muscle component of urethral muscularis.1,3,6,22 Milestones in our knowledge of the innervation and neural control of the bladder and urethra include1-5 definition in the spinal cord of a sacral parasympathetic and a lumbar sympathetic nucleus for subcephalic bladder control, as well as a sacral cord nucleus supplying peripheral somatomotor innervation of the volitional urinary sphincter23-26; multilevel localization of centers of bladder control in the brain, their interconnections, and their spinal neurotract projections27-30; description of the topographic organization of peripheral sympathetic and parasympathetic outflows, respectively, through the hypogastric and pelvic nerve or plexus pathways and their differences in different species23,31,32; recognition of dual sympathetic and parasympathetic innervation of the bladder and urethra and introduction of the functional concept of bladder body versus bladder base33,34; localization of the origin of intrinsic vesicourethral innervation in peripheral ganglia close to and within the organs, including the concept of sympathetic and parasympathetic effector short neurons35,36; concepts of infraspinal interaction of sympathetic and parasympathetic pathways within peripheral ganglia (through collaterals and interneurons)34-39 and the vesicourethral muscularis (through axoaxonal synapses at the effector cell level)40-42; recognition of auxiliary autonomic innervation of the rhabdosphincter in animals and humans22,43-45; and recognition of neuropeptides as a class of putative neurotransmitters or modulatory cotransmitters in peripheral vesicourethral innervation.5-7,46,47 Full knowledge of the structure of an organ is key to the understanding of how it functions. A corollary of this axiom is that alteration of the structure of an organ is reflected in altera-

Chapter 2 STRUCTURAL BASIS OF VOIDING DYSFUNCTION

tion of its function. The axiom and its corollary should be fundamental premises in studies of the bladder in view of its unique function and intimate anatomic relationship to two other organs of different but closely integrated function—the ureter supplying it with urine and the urethra serving as the conduit for its expulsion. Tacit awareness of these premises stimulated research at the biochemical and molecular levels during the past few decades. This research has yielded important information on the biomechanics, energetics, and neuroreceptor attributes of the bladder and urethra. Not unexpectedly, such information has not fully clarified the basis of normal or abnormal smooth muscle function of either organ. Microscopic study of the vesicourethral muscularis has yet to attain its full potential for determining the true basis of normal and abnormal voiding. Routine tissue histology and histochemistry have provided only limited information about tissue topography and general organization of this system. The notoriously tedious nature of electron microscopy has in part been responsible for its lagging use in investigation of bladder function and dysfunction until recently. Another major stumbling block has been the lack of clear guidelines and precisely defined criteria for such ultrastructural approaches. In this chapter, the microstructure of the vesicourethral muscularis and its functional correlates are reviewed. Observations on microstructural defects in various forms of voiding dysfunction are presented, and their bearing on the pathophysiology and management of such disorders is discussed. The information presented is derived largely from overlapping studies on bladder ultrastructure in normal experimental animals, experimental voiding dysfunction, and various clinical disorders of micturition. ULTRASTRUCTURE OF THE VESICOURETHRAL MUSCULARIS Until the previous decade, the urinary bladder had received little attention by students of tissue ultrastructure, unlike organs such as the intestine. The rather simplistic ideas about bladder function and its neural control that prevailed until the mid-1960s probably thwarted interest in serious electron microscopic investigation, or perhaps no one suspected that bladder structure and function were sufficiently complex to justify such investigation. The few reports on vesical ultrastructure available before the 1980s presented general, vague, or imprecise information and therefore were largely noncontributory. A notable exception was a study on the distribution of intrinsic afferent (sensory) nerves in the cat bladder, including the relative contributions of sympathetic and parasympathetic pathways.48,49 The observations reported in this study confirmed and supplemented earlier accounts of the cholinergic and adrenergic suburothelial nerves demonstrated histochemically in the cat bladder.33 The existence of nerve terminals within the urothelium is ultrastructurally indisputable in animals and humans.1 A proposal for distinguishing suburothelial sensory nerves by electron microscopic counting of axonal synaptic vesicles50 remains unfulfilled. Studies on the detrusor and “internal sphincter”51-53 have provided detailed information about their intrinsic innervation and have shown that their muscle cells have the ultrastructural features of smooth muscle in general.54-56 Definitions of the various terms and structural parameters have been provided in other reports.51,56-58

Figure 2-1 Muscle cells of a normal detrusor. The sarcolemma (i.e., cell membrane) has alternating thick, dense bands and interposed thin zones with caveolae, with outlying basal laminae (arrowheads). Cells are adjoined by intermediate junctions (thick arrows) and separated by narrow spaces. The nucleus is capped on one side by endoplasmic reticulum and mitochondria (thin arrows). The sarcoplasm is packed with myofilaments and with evenly distributed, cigar-shaped dense bodies and scattered mitochondria (magnification ×13,890). (From Elbadawi A: Functional pathology of urinary bladder muscularis: The new frontier in diagnostic uropathology. Semin Diagn Pathol 10:319, 1993.)

Muscle Cells Ultrastructurally, each of the grossly recognizable bundles of vesicourethral muscularis in various animals and in humans is composed of incompletely separated and imperfectly outlined compact groups (fascicles) of muscle cells.51,56,58 The muscle cell profile (Fig. 2-1) has a smooth contour and a polygonal to cylindrical configuration, depending on the plane of sectioning relative to its long axis. Nuclei of typical appearance are centrally located and rarely have nucleoli. Mitoses are ordinarily absent in muscle cells of the adult bladder.59 The perimeter of each cell profile is delineated by a continuous cell membrane (i.e., sarcolemma) that displays alternating thick, electron-dense and thinner, less dense zones, with an outlying basal lamina of even thickness and moderate electron density. The thick sarcolemmal zones (i.e., dense bands) are composed of sarcolemma plus subjacent highly dense material in sarcoplasm. The interposed thinner zones consist only of sarcolemma, with strings of caveolae that appear as rows of flask-shaped surface vesicles of uniform size.

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The sarcoplasm is packed with evenly distributed myofilaments of uniform orientation and alignment, with evenly dispersed dense bodies of uniform cigar-shaped appearance in cylindrical cell profiles of longitudinally sectioned cells. The myofilaments are slanted at an approximately 10-degree angle from the long cell axis and are anchored to dense bands of sarcolemma. Organelles of typical structure, mainly mitochondria and endoplasmic reticulum, are aggregated in a conical zone capping each nuclear pole (in cylindrical profiles); some mitochondria, cisternae of reticulum, and clusters of ribosomes are also scattered in sarcoplasm, particularly beneath sarcolemmal caveolae. Individual cells within muscle fascicles are separated by spaces of uniform width (usually 7 MHz) usually lead to improved spatial resolution at the expense of depth of imaging, whereas lower frequencies (2 to 5 MHz) enable imaging of deeper tissues with lower spatial resolution. The chief advantages of sonography are its lack of ionizing radiation, its real-time imaging capability, its 2D and 3D imaging capability, and its ability to depict flow direction and velocity in blood vessels and tissues.4 Disadvantages of sonography are its operator dependence and its inability to image through hollow viscera or bone. In urology, ultrasound is the initial test of choice for adult and pediatric renal and bladder imaging. A wide variety of pathologies, such as congenital anomalies, hydronephrosis, and vascular disorders, may be diagnosed. In bladder applications, it may be used to determine residual postvoid urine volume and to delineate the urethrovesical anatomy (Figs. 8-6 and 8-7).5 Sonography is integral to diagnosis in obstetrics and gynecology (Figs. 8-8 and 8-9; see Fig. 8-1). The reproductive organs may be evaluated by means of transabdominal, transvaginal, or transrectal approaches, as appropriate. Transvaginal and transrectal sonography enable high-resolution imaging of the uterus, adnexa, bladder, and pelvic side wall. For endometrial abnormalities,

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Figure 8-6 Transverse views of the bladder on ultrasound show prevoid (A) and postvoid (B) bladder volume of urine.

Figure 8-7 Color doppler ultrasound of the bladder shows the urinary jet, which indicating urine flow from the right ureter in the blatter.

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especially in the setting of vaginal bleeding, saline infusion hysterosonography, which involves catheterizing the endometrium and infusing saline during imaging, has become the initial test of choice in the evaluation of endometrial and subendometrial disorders such as polyps, fibroids, and cancer (see Fig. 8-9).6,7 Endoanal ultrasonography enables high-resolution visualization of the anal sphincter muscles in patients with incontinence, as well as delineation of fistulas, abscesses, and anal malignancies.5 Computed Tomography Introduction of CT revolutionalized evaluation of the retroperitoneum and disorders of the upper urinary tract, essentially replacing most indications for the intravenous urogram (see Figs. 8-2 to 8-5). Although many systems have been devised, on most CT scanners, a thin narrowly collimated beam of x-rays from a

B Figure 8-8 Sagittal views of the uterus in a female patient with menometrorrhagia were obtained from transabdominal (A) and transvaginal (B) approaches. In B, notice some endometrial displacement, which led to additional studies in this patient (see Fig. 8-9).

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Figure 8-9 Series of transvaginal studies in a female patient presenting for a gynecologic evaluation of menometrorrhagia. Color (A) and power Doppler (B) images show a displaced endometrium with a heterogeneous structure demarcated (C), which has Doppler flow to it. After infusion of saline (D), an intracavitary solid mass can be seen protruding into the endometrial cavity. The mass was shown to be a submucosal myoma during surgery.

generator rotates around a patient’s body on a ring in a continuous circular arc. A panel of electronic x-ray detectors lies directly opposite the x-ray tube on the ring and converts the x-ray beams exiting the patient’s body into electronic signals, which are converted by a computer to display the density of each point (i.e., voxel) of the region being scanned, eventually generating a crosssectional image. Helical multidetector CT (MDCT) scanners are configured to scan a volume of the body continuously. With MDCT, the principal advantages compared with conventional “step and shoot” CT are rapid, near-isotropic voxel (x = y = z) data acquisition with greater radiation dose efficiency. With isotropic voxels and sophisticated software, multiplanar and 3D imaging has become routine. Many postprocessing techniques exist, and two of the most useful are known as multiplanar reformation (MPR) and volume rendering (VR). These display techniques that are especially important for determining renal vascular anatomy, determining the relation of tumors to collecting system and vessels, and detecting fine filling defects on excretory CT urography. In the realm of female uroradiology, CT has become a well-established imaging modality for conditions such as congenital anomalies, tumors, acute and chronic inflammatory diseases, and abscesses.

Magnetic Resonance Imaging MRI provides unparalleled tissue contrast and multiplanar, highresolution imaging of urologic and pelvic floor structures without ionizing radiation. With MRI, a variety of tissues, such as muscle, fat, fluid, blood, blood vessels, and bone marrow, may be delineated with exceptional clarity (Figs. 8-10 to 8-12).8 In MRI, the water protons in the human body are magnetized by a main magnetic field ranging between 1 and 3 Tesla. Using a variety of supplemental magnetic fields, a region of interest may be selected, and based on subtle magnetic field perturbations of water protons and their various relaxation times, diagnostic images are obtained. Tissues such as fat and fluid are differentiated based on their different relaxation properties by a variety of excitation algorithms known as MR sequences. One of the most useful in urology and pelvic floor imaging is the half-Fourier acquisition turbo spin-echo (HASTE) or single-shot fast spin-echo (SSFSE) T2-weighted sequence. This is a rapid, cost-effective, and noninvasive sequence that allows a multiplanar survey of the entire abdomen and pelvis within less than 1 minute. It may also be used to provide a dynamic study of the pelvic floor during relaxation and straining, providing superb anatomic detail survey of

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A Figure 8-10 Sagittal magnetic resonance image shows the detailed anatomy of a post-hysterectomy patient.

B Figure 8-12 Magnetic resonance imaging used in staging cervical cancer. The tumor is shown to protrude into the vaginal fornix (A, arrows) with its walls clearly intact (B, arrowheads). Figure 8-11 Vaginal coil magnetic resonance imaging provides a detailed view of the urethral mucosa.

the extent of suspected pelvic floor relaxation and pelvic organ prolapse. It is very likely that it will replace ultrasound for evaluating women, even those with pelvic pain.9 Like CT, MRI may be performed with the use of contrast agents; gadolinium-diethylenetriamine penta-acetic acid (GdDTPA), which is a water-soluble, inert agent excreted primarily through the kidneys. Advantages compared with iodinated agents include a much lower incidence of dose-related and idiosyncratic reactions. T1-weighted, gradient-echo MR sequences in combination with a small dose of gadolinium contrast enables a comprehensive evaluation of the kidneys and ureters, similar to CT and CT urography, without ionizing radiation or iodinated contrast risk. T2-weighted sequences enable differentiation of cysts, tumors, and normal tissue parenchyma.

In patients with hydronephrosis, use of the HASTE T2weighted sequence enables acquisition of the collecting system, including the calyces, pelvis, and ureters. MRI with T1- and T2weighted sequences can be used for urinary tract disorders in pregnant patients without any radiation exposure risk to the fetus.10 Endoanal MRI is an invaluable method for assessing the integrity of the anal sphincter components in patients with incontinence. CLINICAL APPLICATIONS Bladder Imaging MDCT and MRI have enabled more sophisticated, noninvasive bladder imaging primarily because of their unparalleled resolution and multiplanar display (Figs. 8-13 to 8-15). Both methods

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Figure 8-13 Coronal virtually rendered images of bilateral, simple ureteroceles obtained with multidetector computed tomography show bilateral, mild intramural dilation at the opening into the urinary bladder filled with contrast medium (A). Radiolucent layers of adjacent mucosa and contrast-filled surrounding bladder resemble a cobra head (B).

Figure 8-15 A sagittal magnetic resonance image shows cervical carcinoma in the lower third of the vagina invading the bladder (arrows).

Figure 8-14 A coronal virtually rendered image obtained with multidetector computed tomography shows a double collecting system on the right.

can easily detect bladder filling defects, demonstrate bladderrelated fistulas, and determine the extent of extravesicular tumor invasion. Based on the isotropic MR or CT 3D data sets, a virtual cystogram, similar to more clinically accepted virtual colonoscopy techniques, can be performed. Using 2D and 3D methods, CT and MRI have shown very high correlation with conventional cystoscopy in the detection of bladder lesions that are 0.5 cm or larger. Although CT and MRI are limited in detecting small and intramuscular lesions of the muscle layer of the bladder, contrastenhanced techniques may help improve this approach. However, in cases of invasive neoplasms, MRI has been shown to be superior to transvesical ultrasound, clinical staging, and CT.11,12

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Although intraluminal ultrasound has been reported as an imaging technique for staging of bladder neoplasms, this application is limited to a handful of medical centers in the country and has not gained widespread acceptance.4 MRI can be used for dynamic imaging studies of the pelvic floor, enabling assessment of pelvic floor musculature and organs during relaxation phases and Valsalva maneuvers. MRI produces superb soft tissue detail without radiation or contrast exposure to help triage patients with a range of difficult-to-manage problems such as pelvic floor disorders and urinary and rectal incontinence. In the daily practice of uroradiology, ultrasonography has remained a rather useful modality in the determination of the postvoid residual urine volume and for characterizing the size and location of bladder diverticula, neoplasms, and radiolucent calculi.4 Urethral Imaging: Urethral Diverticula Traditionally, VCUG has been the imaging study of choice for urethral diverticula. However, some investigators have shown

Figure 8-16 An inflamed cystic periurethral cyst led to a urethral diverticulum (arrows), which is depicted on magnetic resonance imaging (A and B) and ultrasound (C).

that high-resolution, fast spin-echo MRI has a higher sensitivity for detecting such diverticula and a higher negative predictive rate than double-balloon urethrography. Other experts in the field believe that a combination of VCUG and MRI leads to a more accurate diagnosis and localization of the lesion (Fig. 8-16).13 Vaginal Imaging: Benign Cystic Lesions Benign cystic lesions of the vagina are a relatively common finding in female urologic practice and represent a spectrum of abnormalities ranging from an asymptomatic small finding to a cyst large enough to cause incontinence or urinary obstruction. They can originate in the vagina or the urethra and the surrounding tissues. Some of the more common examples of vaginal lesions are müllerian cysts, epidermal inclusion cysts, Gartner’s duct cysts, Bartholin’s gland cysts, and endometriotic-type cysts (Figs. 8-17 and 8-18).14 In addition to a careful physical examination, an imaging study is warranted to characterize lesions. Overall, the most

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the past few years, MRI has emerged as the definitive imaging modality for evaluation of uterine disorders. MRI enables evaluation of the uterine zonal anatomy with clear T2-weighted signal differences between endometrium (i.e., bright), junctional zone (i.e., dark), and myometrium (i.e., intermediate). If the appropriate views are acquired, a variety of congenital fusion anomalies, such as septate uterus and bicornuate uterus with obstructed horns, can be demonstrated.18 Associated anomalies of the kidneys are also easily demonstrated. MRI is considered to be the best noninvasive method of assessment for women with symptoms related to uterine leiomyomas and adenomyosis (Fig. 8-19 and Fig. 8-20). MRI is the best modality to determine the vascular supply of pelvic vascular malformations and has been shown to be highly accurate in local staging of endometrial and cervical cancer. MR angiography is performed with MRI to assess the arterial supply and venous drainage to the uterus. It is especially useful in delineating the collateral supply through the gonadal arterial branches. Endometriosis Imaging

B Figure 8-17 A Gartner’s duct is depicted on ultrasound (A, arrows) and magnetic resonance (MR) imaging (B, arrow). Notice the usual anterolateral paravaginal location, with the cyst typically bright on T1-weighted and dark on T2-weighted MR sequences.

useful imaging modalities are sonography and MRI, although CT and VCUG may be useful on occasion.15 For instance, when evaluating a Skene duct cyst, it must be differentiated from a urethral diverticulum to assist in proper surgical planning, potentially preventing complications such as urethrovaginal fistulas. Pelvic MRI is useful for this purpose, because it enables the clinician to determine whether there is a communication between the lesion and the urethra, leading to the correct diagnosis.15 Ultrasound, CT, or MRI can be used to detect a Bartholin duct cyst. Uterine Imaging Transvaginal and transabdominal sonography are the most widely used imaging modalities for the detection and characterization of a wide variety of uterine anomalies and pathologies. Common indications include evaluation of congenital uterine anomalies; assessment of uterine leiomyomas in women with related symptoms such as pelvic pain, pressure, or heavy bleeding; and assessment of the endometrium. Hysterosonography, which involves instilling saline during continuous endovaginal sonographic uterine imaging, is particularly useful for detecting endometrial polyps, tumors, and leiomyomas.16,17 However, over

Laparoscopy has traditionally been the gold standard for diagnosis of endometriosis, which most commonly manifests as small implants with or without related adhesions on the parametrial surfaces, uterosacral ligament, ovaries, serosal surface of the uterus, and the cul-de-sac. Because laparoscopy is an invasive technique and visual inspection of the pelvis has limitations, especially in the diagnosis of retroperitoneal implants, major efforts are being made in the field of female urogynecology to improve the diagnostic utility of current noninvasive imaging modalities. Transvaginal ultrasonography and contrast-enhanced MRI have been used for noninvasive diagnosis and clinical follow-up of patients with endometriosis (Fig. 8-21; see Fig. 8-1). They allow imaging of the retroperitoneal space for determining the presence and characterization of deep pelvic endometriosis and bowel involvement.19,20 Although patients with endometriosis more commonly present to their gynecologists, these ectopic endometrial implants can create urinary symptoms due to direct bladder involvement or deep pelvic involvement causing ureteral obstruction. These patients therefore often present to urologists for clinical and radiographic evaluation. Bladder endometriosis, which is not easily palpable on vaginal examination, may mimic interstitial cystitis and interfere with bladder function.21,22 In experienced hands, transvaginal ultrasonography performed on a slightly filled bladder can detect solid nodules (>0.5 cm) within the posterior bladder wall that cause urinary symptoms in these patients with dysmenorrhea. The presence of low to moderate vascularity demonstrated by color Doppler signal within these nodules and focal pain precipitated by mild pressure applied with the vaginal probe in the involved area helps confirm the diagnosis when suspected.19,20 Nodules in the cul-de-sac may be biopsied transvaginally or percutaneously for confirmation. A high-resolution, contrast-enhanced MR scan of the pelvis at a field strength of 1.5 or 3 Tesla may help diagnose large, focal implants or confluent, small implants on the peritoneal surfaces by the findings of a concomitant thickened peritoneum and enhancement. Adnexal Imaging A comprehensive examination of the female pelvis mandates evaluation of the adnexa for determining the ovarian volume,

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Figure 8-18 An inclusion cyst is shown first on a magnetic resonance image (A) and then in the operating room (B).

Figure 8-20 Focal adenomyoma (arrowheads) and leiomyoma (arrow) are present on the same sagittal T2 Haste magnetic resonance image.

Figure 8-19 Leiomyomas are appreciated on a sagittal magnetic resonance image.

assessing blood flow, and detecting and characterizing masses, especially in any evaluation of pelvic pain and other genitourinary symptoms. Functional ovarian disorders such as polycystic ovary syndrome also may be detected with limited sensitivity. In premenopausal women, ovarian ultrasonography has been the primary imaging modality for benign and pathologic adnexal

entities. However, MRI has become an invaluable addition in this field because of its superb soft tissue characterization, contrast resolution, and multiplanar capabilities. MRI enables the imager to determine with certainty whether a given mass is ovarian or extraovarian, which is an important distinction in evaluating the malignant potential of a tumor. It also plays an essential role in characterizing benign adnexal diseases such as mature teratomas, endometriomas, and ovarian fibromas because of their specific MR features (Fig. 8-22). For instance, MRI can delineate the internal architecture of cystic masses, such as thick internal septations and enhancing mural nodularity, especially after administration of Gd-DTPA-based contrast.8 Pelvic Inflammatory Disease Imaging Most ovarian infections in the Western world result from pelvic inflammatory disease of bacterial origin. They classically manifest

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Figure 8-21 Endometriosis is appreciated on ultrasound (A and B, arrow), which classically manifests as a cystic mass with diffuse, low-level echoes. Notice the septations, fluid-fluid levels, unilocularity or multilocularity, and an echogenic retracting clot.

A

B

Figure 8-22 Endometrioma is appreciated on magnetic resonance imaging with T1-weighted (A) and T2-weighted (B) sequences. Notice characteristic high T1 and low T2 appearances, caused by high protein and iron content from recurrent bleeding and grading within the lesion.

with abdominal pain, fever, and an elevated white blood cell count. Some patients may present with vaginal discharge and urinary complaints. Involvement of the ovaries in this process usually results from salpingitis. In cases of delayed diagnosis and inadequate treatment, disease can progress to cause a tuboovarian abscess (TOA) (Fig. 8-23). In up to 20% of cases of infection that result in TOAs, the patients are afebrile and have normal white blood cell counts.23 The gold standard for the diagnosis of pelvic inflammatory disease is laparoscopy and tubal culture; the sensitivity and specificity of transvaginal ultrasound has not been reported in the literature.23 Sonography is relied on heavily in the initial evaluation of a patient, because it can show pelvic and endometrial fluid in addition to other characteristic findings. Pyosalpinx and hydrosalpinx appear as cystic structures, with internal echoes resulting

in adnexal distortion.24 A TOA usually appears as a well-defined, thick-walled, tubular structure, containing fluid-debris levels within the abscess. Most clinicians advocate a follow-up CT scan of the abdomen and pelvis to fully characterize any other intraabdominal collections to prepare for a subsequent drainage procedure, especially when the abscesses do not respond to an antimicrobial treatment.25 When the clinical and ultrasonographic findings are questionable, MRI can play an important role (see Fig. 8-23). Pyosalpinx typically appears as a fluid-filled, tortuous, and dilated structure, and the signal intensity of the fluid depends on its viscosity and protein concentration. It is usually appreciated as a hypointense area on T2-weighted sequences in the peripheral area of a hyperintense, pus-filled cavity. The adjacent inflamed structures usually have low signal intensity

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A

B

Figure 8-23 A tubo-ovarian abscess is appreciated on sagittal (A) and axial (B) magnetic resonance images in a patient who presented with fever and chills after a uterine artery embolization procedure.

on T1-weighted sequences and intermediate to high signal intensity on T2-weighted MR images. Wall enhancement and thickening usually have greater signal intensity than those observed with hydrosalpinx. The TOA is usually a thick-walled, fluid-filled mass in an adnexal location with significant wall

enhancement and adjacent soft tissue inflammation characterized by similarly intense enhancement.8 The most specific sign of an abscess is the presence of internal gas bubbles, best appreciated on T2-weighted sequences due to differences in magnetic susceptibility.26

References 1. Dunnick MR, Sandler CM, Newhouse JH, Amis ES: Textbook of Uroradiology, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2001. 2. Goldman SM, Sandler CM: Genitourinary imaging: The past 40 years. Radiology 215:313-324, 2000. 3. Novelline RA: Squire’s Fundamentals of Radiology, 6th ed. Cambridge, MA, Harvard University Press, 2004. 4. Marinkovic SP, Badlani GH: Imaging of the lower urinary tract in adults. J Endourol 15:75-86, 2001. 5. Weidner AC, Low VHS: Imaging studies of the pelvic floor. Obstet Gynecol Clin North Am 25:825-848, 1998. 6. Berridge DL, Winter TC: Saline infusion sonohysterography. J Ultrasound Med 23:97-112, 2004. 7. Laifer-Narin S, Ragavendra N, Parmenter EK, Grant EG: Falsenormal appearance of the endometrium on conventional transvaginal sonography: Comparison with saline hysterosonography. AJR Am J Roentgenol 178:129-133, 2002. 8. Sala EJS, Atri M: Magnetic resonance imaging of benign adnexal disease. Top Magn Reson Imaging 14:305-328, 2003. 9. Gousse AE, Barbaric ZL, Safir MH, et al: Dynamic half-Fourier acquisition single shot turbo spin-echo magnetic resonance imaging for evaluating the female pelvis. J Urol 164:1606-1613, 2000. 10. Nolte-Ernsting CCA, Staatz G, Tacke J, Gunther RW: MR urography today. Abdom Imaging 28:191-209, 2003. 11. Bernhardt TM, Rapp-Bernhardt U: Virtual cystoscopy of the bladder based on CT and MRI data. Abdom Imaging 26:325-332, 2001.

12. Lawler LP, Fishman EK: Bladder imaging using multidetector row computed tomography, volume rendering, and magnetic resonance imaging. J Comput Assist Tomogr 27:553-563, 2003. 13. Neitlich JD, Foster HE Jr, Glickman MG, Smith RC: Detection of urethral diverticula in women: Comparison of a high resolution fast spin echo technique with double balloon urethrography. J Urol 159:408-410, 1998. 14. Pradhan S, Tobon H: Vaginal cysts: A clinicopathological study of 41 cases. Int J Gynecol Pathol 5:35-46, 1986. 15. Eilber KS, Raz S: Benign cystic lesions of the vagina: A literature review. J Urol 170:717-722, 2003. 16. Farquhar C, Ekeroma A, Furness S, Arroll B: A systematic review of transvaginal ultrasonography, sonohysterography and hysteroscopy for the investigation of abnormal uterine bleeding in premenopausal women. Acta Obstet Gynecol Scand 82:493-504, 2003. 17. Fleischer AC: Color Doppler sonography of uterine disorders. Ultrasound Q 19:179-189, 2003. 18. Togashi K, Nakai A, Sugimura K: Anatomy and physiology of the female pelvis: MR imaging revisited. J Magn Reson Imaging 13:842849, 2001. 19. Brosens I, Puttemans P, Campo R, et al: Non-invasive methods of diagnosis of endometriosis. Curr Opin Obstet Gynecol 15:519-522, 2003. 20. Brosens J, Timmerman D, Starzinski-Powitz A, Brosens I: Noninvasive diagnosis of endometriosis: The role of imaging and markers. Obstet Gynecol Clin North Am 30:95-114, 2003.

Chapter 8 IMAGING OF THE FEMALE GENITOURINARY TRACT

21. Siegelman ES, Outwater E, Wang T, Mitchell DG: Solid pelvic masses caused by endometriosis: MR imaging features. AJR Am J Roentgenol 163:357-361, 1994. 22. Sircus SI, Sant GR, Ucci AA Jr: Bladder detrusor endometriosis mimicking interstitial cystitis. Urology 32:339-342, 1988. 23. Cartwright PS: Pelvic inflammatory disease. In Beck JS (ed): Novak’s Textbook of Gynecology, 11th ed. Baltimore, Williams & Wilkins, 1988. 24. Bulas DI, Ahlstrom PA, Sivit CJ, et al: Pelvic inflammatory disease in the adolescent: Comparison of transabdominal and transvaginal sonographic evaluation. Radiology 183:435-439, 1992.

25. Varghese JC, O’Neill MJ, Gervais DA, et al: Transvaginal catheter drainage of tubo-ovarian abscess using the trocar method: Technique and literature review. AJR Am J Roentgenol 177:139-144, 2001. 26. Dohke M, Watanabe Y, Okumura A, et al: Comprehensive MR imaging of acute gynecologic diseases. Radiographics 20:1551-1566, 2000.

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Chapter 9

PELVIC FLOOR ULTRASOUND Hans Peter Dietz The increasing availability of ultrasound and magnetic resonance imaging (MRI) equipment has triggered a renewed interest in diagnostic imaging in female urology and urogynecology, after radiologic methods, developed since the 1920s,1-6 had largely fallen into disuse. Because of cost and access problems, MRI has had limited clinical use in the evaluation of pelvic floor disorders, and until recently, slow acquisition speeds have precluded dynamic imaging. In contrast, ultrasound is almost universally available and provides real-time observation of diagnostic maneuvers. Beginning in the 1980s, transabdominal,7,8 perineal,9,10 transrectal,11 and transvaginal ultrasound12 have been investigated for use in women with urinary incontinence and pelvic organ prolapse. Because of its noninvasive nature, ready availability, and the absence of distortion, perineal or translabial ultrasound has become the most widely used method. The development of three-dimensional (3D) ultrasound13,14 has opened up new diagnostic possibilities. The first attempts at producing 3D-capable systems were made in the 1970s, when processing a single volume of data required 24 hours of computer time on a system that filled a small room.15 Such data processing is now possible on a laptop computer and is achieved in real time. Transvaginal, transrectal, and translabial 3D ultrasound techniques have been reported, and significant development in this field is likely to occur in the next few years. TWO-DIMENSIONAL PELVIC FLOOR ULTRASOUND

racy and sometimes necessitates a repeat assessment after bowel emptying. Parting of the labia can improve image quality, which is optimal in pregnancy and poorest in menopausal women with marked atrophy, most likely due to various levels of tissue hydration. The transducer usually can be placed quite firmly against the symphysis pubis without causing significant discomfort, unless there is marked atrophy. The resulting image includes the symphysis pubis (specifically, the interpubic disk) anteriorly, the urethra and bladder neck, the vagina, cervix, rectum, and anal canal (see Fig. 9-1) with the internal and external anal sphincter. Posterior to the anorectal junction, a hyperechogenic area indicates the central portion of the levator plate, the puborectalispubococcygeus (or pubovisceral) muscle. The cul-de-sac may also be seen as filled with a small amount of fluid, echogenic fat, or peristalsing small bowel. Parasagittal or transverse views may yield additional information, such as enabling assessment of the puborectalis muscle and its insertion on the on the pelvic sidewall and imaging of transobturator implants. There has been disagreement regarding image orientation in the midsagittal plane. Some clinicians prefer orientation as in the standing patient facing right,16 which requires image inversion on the ultrasound system, a facility that is not universally available. Others (including me) prefer an orientation as on conventional transvaginal ultrasound (i.e., cranioventral aspects to the left, dorsocaudal to the right). The latter orientation seems more convenient when using 3D or 4D systems because it automatically results in rendered volumes that are oriented as on conventional MRI of the pelvic floor (discussed later). Because

Basic Methodology Because translabial ultrasound is the most commonly used modality for pelvic floor evaluation, it is the focus of this chapter. A modification of the translabial or transperineal technique is introital imaging, which typically uses high-frequency endocavitary transducers placed in the introitus. This results in higher resolution of urethra and paraurethral tissues or of the anal sphincter complex, but it does not allow simultaneous imaging of all three compartments and may complicate quantification of findings because the symphysis pubis may not be included in the field of vision. Distortion of tissues is also more likely. However, most of the following discussion also applies to this technique. A midsagittal view is obtained by placing a transducer (usually a curved array with frequencies between 3.5 and 9 MHz) on the perineum (Fig. 9-1) after covering the transducer with a glove or thin plastic wrap for hygienic reasons. Powdered gloves can markedly impair imaging quality because of reverberations and should be avoided. Imaging can be performed with the patient in the dorsal lithotomy position, with the hips flexed and slightly abducted, or in the standing position. Bladder filling should be specified; for some applications, prior voiding is preferable, and a full bladder can prevent complete development of a prolapse. The presence of a full rectum may also impair diagnostic accu100

Urethra

Vagina Anal canal

Symphysis

Bladder

Ampulla recti Uterus

Cul-de-sac Cranial

Figure 9-1 Drawing of the field of vision for translabial or perineal ultrasound in the midsagittal plane. Image adapted from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-2 Lateral urethrocystogram with a bead chain outlining the urethra. The images are rotated by 180 degrees to allow comparison with standard translabial ultrasound views. The image on the left was obtained with the patient at rest; the image on the right was obtained during a Valsalva maneuver. Reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

any image reproduced in one of these orientations can be converted to the other by rotation through 180 degrees, formal standardization may be unnecessary. Orientations that require mirroring for conversion should be avoided. Translabial ultrasound of the lower urinary tract, even if limited to B-mode imaging in the midsagittal plane, yields information equivalent or superior to the lateral urethrocystogram (Fig. 9-2, shown rotated by 180 degrees for comparison) or fluoroscopic imaging. Comparative studies have mostly shown good correlation between radiologic and ultrasound data.11,17-22 The one remaining advantage of x-ray fluoroscopy may be the ease with which the voiding phase can be observed, although some investigators have used specially constructed equipment to document voiding with ultrasound.23 Bladder Neck Position and Mobility Bladder neck position and mobility can be assessed with a high degree of reliability. Points of reference are the central axis of the symphysis pubis24 or its inferoposterior margin.17 The former may be more accurate because measurements are independent of transducer position or movement; however, because of calcification of the interpubic disk, the central axis is often difficult to obtain in older women, reducing reliability. Imaging can be undertaken with the patient supine or erect and with a full or empty bladder. The full bladder is less mobile25 and may prevent complete development of pelvic organ prolapse. In the standing position, the bladder is situated lower at rest but descends about as far as in the supine patient during a Valsalva maneuver.26 Either way, it is essential to not exert undue pressure on the perineum to allow full development of pelvic organ descent, although this may be difficult in women with severe prolapse, such as vaginal eversion or procidentia. Measurements of bladder neck position are generally performed at rest and during maximal Valsalva maneuver. The dif-

ference yields a numeric value for bladder neck descent. During a Valsalva maneuver, the proximal urethra may rotate in a posteroinferior direction. The extent of rotation can be measured by comparing the angle of inclination between the proximal urethra and any other fixed axis (Fig. 9-3). Some investigators measure the retrovesical (or posterior urethrovesical) angle between proximal urethra and trigone (see Fig. 9-3).27 Others determine the angle γ between the central axis of the symphysis pubis and a line from the inferior symphyseal margin to the bladder neck.28,29 Of all the ultrasound parameters of hypermobility, bladder neck descent may have the strongest association with urodynamic stress incontinence.30 The reproducibility of this dynamic measurement has been assessed,31 with a percent variation or coefficient of variation of 0.16 between multiple effective Valsalva maneuvers, 0.21 for interobserver variability, and 0.219 for a test-retest series at an average interval of 46 days. Intraclass correlations were between 0.75 and 0.98, indicating excellent agreement.31 There is no definition of normal for bladder neck descent, although cutoffs of 20 and 25 mm have been proposed to define hypermobility. Average measurements in stress-incontinent women are consistently around 30 mm (HP Dietz, unpublished data). Figure 9-4 shows a relatively immobile bladder neck before a first delivery and a marked increase in bladder neck mobility after childbirth. Figure 9-5 demonstrates typical ultrasound findings in a stress-incontinent patient with a first-degree cystourethrocele, 25.5 mm of bladder neck descent, and funneling. Bladder filling, patient position, and catheterization influence measurements,25,26,32,33 and it sometimes is difficult to obtain an effective Valsalva maneuver, especially in nulliparous women. Perhaps not surprisingly, publications have presented widely different reference measurements in nulliparous women. Although two series documented mean or median bladder neck descent of only 5.1 mm34 and 5.3 mm35 in continent, nulliparous women, another study of 39 continent, nulliparous volunteers measured

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A

B Figure 9-3 The ultrasound image (A) and line drawing (B) illustrate some of the parameters measured to quantify bladder and urethral mobility: the location of the bladder neck relative to the symphysis pubis (coordinates x-r, y-r, x-s, y-s), urethral rotation and retrovesical angle (RVA). This figure is reproduced from Br J Obstet Gynecol 2005; 112:334-339, with permission.

Figure 9-4 Immobile bladder neck (bladder neck distance [BND] = 6 mm) before childbirth (left pair of images) and a marked increase in bladder neck mobility (BND = 38.1 mm) after vaginal delivery (right pair of images). The figure is reproduced from Obstet Gynecol 2003; 102:223-228, with permission.

an average bladder neck descent of 15 mm.36 The author has obtained bladder neck descent measurements of 1.2 to 40.2 mm (mean, 17.3 mm) in a group of 106 stress-continent, nulligravid women between the ages of 18 and 23 years.37 It is likely that methodologic differences, such as patient position, bladder filling, and quality of the Valsalva maneuver (i.e., controlling for confounders such as concomitant levator activation), account for the measurement discrepancies, with all known confounders tending to reduce descent. Attempts at standardizing Valsalva maneuvers38,39 have not found widespread application because this requires intra-abdominal pressure measurement (i.e., use of a rectal balloon catheter). Other methods, such as the use of a spirometer, are likely to lead to suboptimal Valsalva maneuvers; the pressures used in the one study describing the use of such a

device38 were clearly insufficient to achieve maximal or even near-maximal descent.39 The cause of increased bladder neck descent is likely to be multifactorial. The wide range of values obtained in young, nulliparous women suggests a congenital component, and a twin study has confirmed a high degree of heritability for anterior vaginal wall mobility.44 Vaginal childbirth45-47 is probably the most significant environmental factor (see Fig. 9-4), with a long second stage of labor and vaginal operative delivery associated with increased postpartum descent of the bladder neck.47 This association between increased bladder descent and vaginal parity is also evident in older women with symptoms of pelvic floor dysfunction.48 While the pelvic floor is undoubtedly affected by labor and delivery, it has been speculated that progress in labor

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-5 Typical findings in a patient with stress incontinence and mild anterior vaginal wall descent (i.e., cystourethrocele grade 1): posteroinferior rotation of the urethra, opening of the retrovesical angle, and funneling of the proximal urethra (arrow). Figure reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

may not be independent of pelvic floor biomechanics.49 Anterior vaginal wall mobility during a Valsalva maneuver was found to be a potential predictor of progress in labor in two independent studies.50,51

this hypothesis is lacking. Marked urethral kinking in these patients may protect against stress incontinence but can lead to voiding dysfunction and urinary retention. Occult stress incontinence may be unmasked once a successful prolapse repair prevents urethral kinking.

Funneling In patients with stress incontinence and in asymptomatic women,40 funneling of the internal urethral meatus may be observed during a Valsalva maneuver (see Fig. 9-5) and sometimes even at rest. Funneling is often associated with leakage. Other indirect signs of urine leakage on B-mode real-time imaging are weak gray-scale echoes (i.e., streaming) and the appearance of two linear echoes defining the lumen of a fluidfilled urethra. However, funneling may also be observed in patients with urge incontinence, and it cannot be used to prove urodynamic stress incontinence. Its anatomic basis is unclear, but marked funneling is associated with poor urethral closure pressures.41,42 Classifications developed for the evaluation of radiologic imaging43 can be modified for ultrasound; however, this approach is not generally accepted. The most common finding in cases of bladder neck hypermobility is a so-called rotational descent of the internal meatus (i.e., proximal urethra and trigone rotate around the symphysis pubis in a posteroinferior direction). In these cases, the retrovesical angle opens to up to 160 to 180 degrees from a normal value of 90 to 120 degrees, and the change in the retrovesical angle usually is associated with funneling. Often, there seems to be increased mobility of the entire urethra. A cystocele with intact retrovesical angle (90 to 120 degrees) is frequently seen in continent patients with prolapse (Fig. 9-6), and distal and central urethral fixation to the pubic rami usually seems to be relatively normal, resulting in urethral kinking. It has been surmised that this configuration distinguishes a central from a lateral defect of the endopelvic fascia,16 although proof for

Color Doppler Color Doppler ultrasound has been used to demonstrate urine leakage through the urethra during a Valsalva maneuver or coughing.58 Agreement between color Doppler and fluoroscopy results was high in a controlled group with indwelling catheters and identical bladder volumes.59 Color Doppler ultrasound velocity (Fig. 9-7) and energy mapping (Color Doppler or power Doppler) (Fig. 9-8) were able to document leakage. Color Doppler ultrasound velocity was slightly more likely to show a positive result, probably because of its better motion discrimination. This results in less flash artifact and better orientation, particularly on coughing, although imaging quality depends on the systems used and selected color Doppler settings. As a result, routine sonographic documentation of stress incontinence during urodynamic testing has become feasible. Color Doppler imaging may also facilitate documentation of leak point pressures.60 Whether this is desired depends on the clinician’s preferences, because it may be argued that urine leakage and leak point pressures can be determined more easily with other methods. Bladder Wall Thickness There has been considerable interest in the quantification of bladder wall thickness by transvaginal or translabial ultrasound.61,62 Measurements are obtained after bladder emptying, and they are acquired perpendicular to the mucosa (Fig. 9-9). In the original description, three sites were assessed—anterior wall, trigone, and dome of the bladder—and the mean of all three was

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Figure 9-6 A cystocele with an intact retrovesical angle. Notice the absence of funneling. The bladder neck and proximal urethra are virtually inverted compared with their position at rest. Reproduced from Textbook of Female Urology and Urogynecology, Abingdon UK, 2006.

Figure 9-7 Color Doppler velocity (CDV) demonstrates urine leakage (arrowhead) through the urethra during a Valsalva maneuver. Reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

calculated. A bladder wall thickness of more than 5 mm seems to be associated with detrusor instability,61,63 although this has been disputed.64 Increased bladder wall thickness is likely caused by hypertrophy of the detrusor muscle,64 which is most evident at the dome; this may be the cause of symptoms or the effect of an underlying abnormality. Although bladder wall thickness on its own seems only moderately predictive of detrusor instability and is not in itself a useful diagnostic test, the method may be of value when combined with symptoms of the overactive bladder.65 It remains to be seen whether determination of this parameter can contribute to the workup of a patient with pelvic floor and

Figure 9-8 Color Doppler energy mapping (CDE) of stress urinary incontinence. The Doppler signal outlines most of the proximal urethra (arrowhead). Reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

bladder dysfunction, such as serving as a predictor of postoperative voiding function or de novo or worsened detrusor overactivity. Levator Activity Perineal ultrasound has been used for the quantification of pelvic floor muscle function in women with stress incontinence and in continent controls66 before and after childbirth.67,68 A cranioventral shift of pelvic organs imaged in a sagittal midline orientation is taken as evidence of a levator contraction. The resulting dis-

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-9 Measurement of bladder wall thickness at the dome in four women with nonneuropathic bladder dysfunction. In all cases, the residual urine volume is well below 50 mL.

Figure 9-10 Quantification of levator contraction. Cranioventral displacement of the bladder neck is measured relative to the inferoposterior symphyseal margin. The measurements indicate 4.5 (range, 31.9 minus 27.4) mm of cranial displacement and 16.2 (range, 17.9 minus 1.7) mm of ventral displacement of the bladder neck. Figure reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

placement of the internal urethral meatus is measured relative to the inferoposterior symphyseal margin (Fig. 9-10). In this way, pelvic floor activity is assessed at the bladder neck, where its effect as part of the continence mechanism is most likely to be relevant.69 Another means of quantifying levator activity is to measure reduction of the levator hiatus in the midsagittal

plane or to determine the changing angle of the hiatal plane relative to the symphyseal axis. The method can also be used for pelvic floor muscle exercise teaching by providing visual biofeedback.70 The technique has helped validate the concept of the knack, a reflex levator contraction immediately before increases in intra-abdominal pressure, such as those resulting

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Cystocele

Rectocele

Symphysis

Enterocele Uterine prolapse

Cranial

Figure 9-11 Line drawing demonstrating the ultrasound quantification of uterovaginal prolapse. The inferior margin of the symphysis pubis serves as a line of reference against which the maximal descent of the bladder, uterus, cul-de-sac, and rectal ampulla on Valsalva maneuver can be measured. Figure reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

from coughing.71 Good correlations have been found between cranioventral shift of the bladder neck and palpation or perineometry.72 Prolapse Quantification Translabial ultrasound can demonstrate uterovaginal prolapse.73,74 The inferior margin of the symphysis pubis serves as a convenient (if arbitrary) line of reference against which the maximal descent of the bladder, uterus, cul-de-sac, and rectal ampulla during a Valsalva maneuver can be measured (Fig. 911). On Valsalva the transducer is withdrawn to allow full development of the prolapse, while retaining contact with the insonated tissues. Angling of the transducer should be avoided in order to prevent changes in the relative position of transducer and symphysea axes. Figure 9-12 shows a three-compartment prolapse, with the uterus leading. Findings have been compared with clinical staging and the results of a standardized assessment according to criteria developed by the International Continence Society,75 with good correlations shown for the anterior and central compartments.76 Although there may be poorer correlation between posterior compartment clinical assessment and ultrasound, not the least due to variable rectal filling, it is possible to distinguish between true rectocele (i.e., defect of the rectovaginal septum) (Fig. 9-13A) and perineal hypermobility without fascial defects (see Fig. 9-13B). True rectoceles may be present in young, nulliparous women but are more common in parous women. In some instances, they arise in childbirth.77 From imaging experience, fascial defects seem to almost always be found in the same area (i.e., very close to the anorectal junction), and they most commonly are transverse. Many are asymptomatic. Routine posterior repair often results in reduction or distortion of such defects without effecting closure. The ability to differentiate different forms of posterior compartment descent should allow better surgical management in the future, especially because enterocele (Fig. 9-14) can easily be

Figure 9-12 Three-compartment prolapse on translabial ultrasound. The line of reference is placed through the inferior margin of the symphysis pubis. Measurements indicate descent of the bladder to 6.8 mm below the symphysis pubis, of the uterus to 11.3 mm, and of the rectal ampulla to 3.9 mm below. Arrows indicate the leading edges of those organs. The clinical examination showed a seconddegree uterine prolapse and first-degree anterior and posterior compartment descent.

distinguished from rectocele. It appears that colorectal surgeons are starting to use the technique to complement or replace defecography,78 and perineal ultrasound can also be used for exoanal imaging of the anal sphincter.79,80 Disadvantages of the method include incomplete imaging of bladder neck, cervix, and vault with large rectoceles and possible underestimation of severe prolapse due to transducer pressure. Occasionally, apparent anterior vaginal wall prolapse turns out to be caused by a urethral diverticulum81,82 (Fig. 9-15) or a paravaginal cyst. The main use of this technique may prove to be in outcome assessment after prolapse and incontinence surgery for clinical and research applications. Elevation and distortion of the bladder neck arising from a colposuspension is easily documented.83,84 Fascial and synthetic slings are visible posterior to the trigone or the urethra (Figs. 9-16 and 9-17). Bulking agents such as Macroplastique (Fig. 9-18) show up anterior, lateral, and posterior to the proximal urethra. It has been demonstrated that overelevation of the bladder neck on colposuspension is unnecessary for cure of urodynamic stress incontinence, and elevation may also have a bearing on postoperative symptoms of voiding dysfunction and de novo detrusor instability.83,84 Implants Ultrasound has contributed significantly to the investigation of new surgical procedures, such as wide-weave suburethral Prolene slings, showing that they act by urethral kinking or dynamic compression against the posterior surface of the symphysis pubis.85 Available synthetic slings are easily visualized posterior to the urethra86-93 (see Fig. 9-16). Wide-weave monofilament mesh such as tension-free vaginal tape (e.g., Gynecare TVT), SPARC sling, and Monarc Subfascial Hammock or transobturator (TOT) sling are more echogenic than more tightly woven multifilament implants, such as the IVS (i.e., polypropylene mesh) (see Fig.

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-13 A, The top pair of images shows a first-degree rectocele. The anal canal is seen to the right of both images, with a small rectocele (deep 2 cm) clearly visible during a Valsalva maneuver (right). B, The lower pair of images demonstrates descent of the rectal ampulla without herniation of rectal contents into the vagina, a condition that may mimic rectocele and that has been called perineal hypermobility or pseudorectocele. Figure reproduced from Textbook of Female Urology and Urogynecology, Abingdon UK, 2006.

A

B

Figure 9-14 Rectocele after Burch colposuspension with the patient at rest (left) and during a Valsalva maneuver (right). Usually, enteroceles (filled by peristalsing small bowel, epiploic fat, or omentum) appear more homogeneous and nearly isoechoic, whereas the rectocele is filled by a stool bolus and/or air, resulting in hyperechogenicity with distal shadowing. Figure reproduced from Ultrasound Obstet Gynecol 2005; 26:73-77, with permission.

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Figure 9-15 Urethral diverticulum (arrow), herniating downward and clinically simulating a cystourethrocele during a Valsalva maneuver. The neck of the diverticulum is close to the bladder neck. Reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

Figure 9-16 Synthetic implants such as the tension-free vaginal tape or SPARC are easily visualized as highly echogenic structures posterior to the urethra. The images illustrate tape position relative to the symphysis pubis and urethra with the patient at rest (left) and during a Valsalva maneuver (right). Reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

9-17), but virtually all can be identified and followed in their course from the pubic rami laterally to the urethra centrally. The difference between transobturator tapes (e.g., Monarc, TOT) and tapes placed through the space of Retzius (e.g., TVT, SPARC, IVS) is evident when following the tapes in the parasagittal or axial planes. In the parasagittal plane, transobturator tapes often

can be seen to perforate the obturator fascia and muscle close to the insertion of the pubovisceral muscle; sometimes, they traverse the most inferomedial component of the levator before exiting the pelvis.93 Wide-weave mesh implants used in procedures, such as the Perigee, Apogee or Prolift implants, are very echogenic and easily identified,94 and their transobturator or

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-17 A comparison of tension-free vaginal tape (TVT), SPARC mesh, and IVS mesh (left to right) on midsagittal imaging. The TVT often appears slightly curled, signifying a greater degree of tension compared with the SPARC material, which often is under less tension because of a central suture that avoids pretensioning of the tape on removal of plastic sheaths during surgery. Reproduced from Ultrasound Obstet Gynecol 2005; 26:175-179, with permission.

Figure 9-18 Macroplastique (silicone macroparticles), an injectable used in USI surgery, is very echogenic and can be located ventral, dorsal and lateral to the proximal and mid-urethra. Figure reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

pararectal extensions can be followed for some distance, although 3D or 4D imaging allows much more comprehensive evaluation. Ultrasound has demonstrated the wide margin of safety and efficacy of suburethral tapes in regard to placement (which helps explain their extraordinary success) and allayed concerns regarding tape shrinkage and tightening due to scar formation.90,91 The assessment of bladder neck mobility before implantation of a suburethral sling may predict success or failure,95 an observation that makes perfect sense considering that dynamic compression relies on relative movement of implant and native tissues. Paravaginal Defect Imaging Transabdominal ultrasound has been used to demonstrate lateral defects of the endopelvic fascia, also called paravaginal defects. However, this method has not been fully validated, and a prospective study showed poor correlation with clinically observed defects.96 Several factors may limit the predictive value of transabdominal ultrasound in the identification of paravaginal defects:

Figure 9-19 A Gartner duct cyst is shown close to the bladder neck (arrow). Reproduced from Ultrasound Obstet Gynecol 2004; 23:80-92, with permission.

the poor definition of an optimal scanning plane, the influence of uterine prolapse or a full rectum, and the inability to observe the effect of a Valsalva maneuver (which would dislodge the transducer) by transabdominal imaging. It is likely that levator trauma (see below) is frequently misinterpreted as a “paravaginal defect.” Fascial trauma is highly likely in patients with a full avulsion, but it is conceivable that fascial defects may occur in women with intact muscle. Much work remains to be done in this field. Other Findings A range of other abnormalities, incidental or expected, may sometimes be detected on translabial ultrasound, although a full pelvic ultrasound assessment does require a transvaginal approach. Urethral diverticula (see Fig. 9-15),78,97 labial cysts, Gartner’s duct cysts (Fig. 9-19), or bladder tumors (Fig. 9-20) may be identified, and intravesical stents and bladder diverticula also can be visualized.16 Postoperative hematomas may be visible after vaginal surgery or TVT placement and sometimes explain clinical symptoms such as voiding dysfunction or persistent pain (Fig. 9-21).

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Most recently, it has become clear that rectal intussusception and rectal prolapse can be diagnosed on pelvic floor ultrasound in the midsagittal plane. The pathognomonic feature of intussusception is splaying of the anal canal and inversion of the anterior rectal wall into the anal canal (see Figure 9-21). The intussuscipiens is propelled by small bowel or sigmoid colon, resulting in inversion of the rectal wall: an enterocele that does not develop into the vagina, but down the anal canal. Mucosal prolapse, on the other hand, is much more discrete as it does not involve the full thickness of the rectal wall, and seems limited to the area immediately proximal to the anal canal. The usefulness of translabial ultrasound in patients with symptoms of obstructed defecation, in particular as compared to defecation proctography, is not yet clear however. Several comparative studies are in progress in urogynaecological and colorectal units at the time of writing. THREE-DIMENSIONAL PELVIC FLOOR IMAGING Technical Overview Two main engineering solutions have been developed to allow integration of two-dimensional (2D) sectional images into 3D

Figure 9-20 A transitional cell carcinoma (arrow) of the bladder is seen on parasagittal translabial ultrasound. Reproduced from Ultrasound Ostet Gynecol 2004; 23:80-92, with permission.

volume data: motorized acquisition and external electromagnetic position sensors. A simplified technique is the freehand acquisition of volumes without any reference to transducer position. In essence, this means that a cine loop of images is collated to form a volume data set; because the system has no information on transducer position relative to the insonated tissues, measurements on volume data are impossible. Nevertheless, qualitative information may be obtained, and such systems have been used for clinical research in urogynecology.98 Quantitative evaluation of volumes requires information on transducer position at the time of acquisition. If probe movement is achieved with the help of a motor, its characteristics will determine imaging data coordinates. Motorized acquisition may take the shape of automatic withdrawal of an endocavitary probe, motorized rotation of such a probe, or motor action within the transducer itself. The first such motorized probe was developed in 1974, and by 1987, transducers for clinical use were developed that allowed motorized acquisition of imaging data.99 The first commercially available platform, the Kretz Voluson system, was developed around such a “fan scan” probe. Endocavitary probes make a freehand acquisition technique impractical, which is why the company did not develop this alternative approach further99 and instead concentrated on a technology reminiscent of (otherwise obsolete) mechanical sector transducers. The results have been the abdominal and endovaginal probes used in systems such as the GE Kretz Voluson 530, 730, 730 expert, E8 and Volusoni System. The widespread acceptance of 3D ultrasound in obstetrics and gynecology was helped considerably by this development because these transducers do not require any movement relative to the investigated tissue during acquisition. Most of the major suppliers of ultrasound equipment have developed their own transducers along such lines, although it is widely recognized that this technology will probably be replaced by matrix array transducers within the next 5 to 10 years. Such transducers are already available for echocardiography.100 With current mechanical 3D transducers, automatic image acquisition is achieved by rapid oscillation of a group of elements within the transducer. This allows the registration of multiple sectional planes that can be integrated into a volume as the location of a given voxel (i.e., a pixel that has a defined location in space) is determined by transducer and insonation characteristics. Fortuitously, transducer characteristics on available systems for transabdominal use have been highly suitable for pelvic floor imaging. A single volume obtained at rest with an acquisition angle of 70 degrees or higher includes the entire levator hiatus

Figure 9-21 Retroperitoneal hematoma and subcutaneous vaginal hematoma after mesh sacrocolpopexy and posterior repair. Reproduced from ASUM Bulletin 2007; 10:17-23, with permission.

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-22 The usual acquisition or evaluation screen on Voluson-type systems shows the three orthogonal planes: sagittal (top left), coronal (top right), and axial (bottom left). It also shows a rendered volume (bottom right), which is a semitransparent representation of all gray-scale data in the region of interest (arrows).

with the symphysis pubis, urethra, paravaginal tissues, the vagina, anorectum, and pubovisceral (i.e., puborectalis or pubococcygeus part of the levator ani) muscle from the pelvic side wall in the area of the arcus tendineus of the levator ani (ATLA) to the posterior aspect of the anorectal junction (Fig. 9-22). Depending on the anteroposterior dimensions of the pubovisceral muscle, it may also include the anal canal and the external anal sphincter. This also holds true for volumes acquired on levator contraction. A Valsalva maneuver may result in lateral or posterior parts of the puborectalis being pushed outside the field of vision, especially in women with significant prolapse (discussed later). The abdominal 8-4-MHz volume transducer for Voluson systems allows acquisition angles of up to 85 degrees, ensuring that the levator hiatus can be imaged in its entirety, even in women with significant enlargement (i.e., ballooning) of the hiatus during a Valsalva maneuver. Display Modes Figure 9-22 demonstrates the two basic display modes used on 3D ultrasound systems. The multiplanar or orthogonal display mode shows cross-sectional planes through the volume in question. For pelvic floor imaging, this most conveniently means the midsagittal, the coronal, and the axial or transverse plane. One of the main advantages of volume ultrasound for pelvic floor imaging is that the method gives access to the axial plane. Until recently, pelvic floor ultrasound was limited to the midsagittal plane.9,101,102 Parasagittal and coronal plane imaging have not been reported, perhaps because there are no obvious points of reference, unlike the convenient reference point of the sym-

physis pubis on midsagittal views. The axial plane was accessible only on MRI; Figure 9-23 provides an axial view of the levator hiatus on MRI and 3D ultrasound.103 Pelvic floor MRI is an established investigational method, at least for research applications, with a multitude of papers published over the past 10 years.104-113 Imaging planes on 3D ultrasound can be varied in a completely arbitrary fashion to enhance the visibility of a given anatomical structure at the time of acquisition or offline at a later time. The levator ani, for example, usually requires an axial plane that is slightly tilted in a cranioventral to dorsocaudal direction. The three orthogonal images are complemented by a rendered image, which is a semitransparent representation of all voxels in an arbitrarily definable box, termed the Region of Interest (ROI). Figure 9-22 (bottom right image) shows a standard rendered volume of the levator hiatus, with the rendering direction set caudally to cranially, which seems to be most convenient for pelvic floor imaging. The possibilities for postprocessing are restricted only by the software used for this purpose; programs such as GE Kretz 4D View (GE Medical Systems Kretztechnik, Zipf, Austria) allow extensive manipulation of image characteristics and output of stills, cine loops, and rotational volumes in bitmap and AVI formats. FOUR-DIMENSIONAL IMAGING The use of 4D imaging implies the real-time acquisition of volume ultrasound data, which can then be represented in orthogonal planes or rendered volumes. It has become possible

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Figure 9-23 The axial plane on magnetic resonance imaging (MRI) and ultrasound (rendered volume) in a young nulliparous volunteer. (MRI courtesy of J Kruger, Auckland.) Reproduced from Obstet Gynecol 2005; 106:707-712, with permission.

to save cine loops of volumes, which is important in pelvic floor imaging because it allows enhanced documentation of functional anatomy. Even on 2D, single-plane imaging, a static assessment at rest gives little information compared with the evaluation of maneuvers such as a levator contraction and Valsalva. Observation enables better assessment of levator function and improved delineation of levator or fascial trauma. Avulsion of the pubovisceral muscle from the arcus tendineus of the levator ani is often more evident on levator contraction, and most significant pelvic organ prolapse is not visible with the patient at rest in the supine position. Fascial defects such as those defining a true rectocele often only become visible during a Valsalva maneuver. The ability to perform a real-time 3D (or 4D) assessment of pelvic floor structures makes the technology clearly superior to MRI. Prolapse assessment by MRI requires ultrafast acquisition,107,109 which is of limited availability and does not allow optimal resolutions. Alternatively, some systems allow imaging of the sitting or erect patient,108 but accessibility will remain limited for the foreseeable future. The sheer physical characteristics of MRI systems make it much harder for the operator to ensure efficient maneuvers because more than 50% of women do not perform a proper pelvic floor contraction when asked114 and a Valsalva maneuver is often confounded by concomitant levator activation.115 Without real-time imaging, it is impossible to control for these confounders. Ultrasound therefore has major potential advantages when it comes to describing prolapse, especially when it is associated with fascial or muscular defects, and for defining functional anatomy. Offline analysis packages such as the GE Kretz 4D View or Philips QL AB software allow distance, area, and volume measurements in any user-defined plane (e.g., oblique, orthogonal), which is superior to what is possible with Digital Imaging and Communications in Medicine (DICOM) viewer software on a standard set of single-plane MRI images. DICOM is a standard for distributing and viewing any kind of medical image, regardless of the origin. Speckle Reduction Techniques Technical developments such as volume-contrast imaging (VCI) and speckle-reduction imaging (SRI) employ rendering algo-

rithms as a means of improving resolutions in the coronal plane. As a result, speckle artifact is markedly reduced.116 Measuring in the axial or C plane has been limited to raw data without significant postprocessing. Consequently, resolutions were much poorer than in the sagittal plane, reducing the accuracy of measurements and our ability to identify structural changes. By using VCI on slices 1 to 3 mm thick, resolutions of about 1 mm can be reached on axial or oblique axial slices that allow distance and area measurements on the ultrasound system and offline on a computer. Figure 9-24 shows normal C-plane imaging and VCI in the axial plane in a patient with major bilateral levator trauma after rotational forceps delivery. Another technique using rendering algorithms to enhance single plane resolutions, Speckle Reduction Imaging or “SRI,” results in improved tissue discrimination, which should help to improve detection of morphologic abnormalities. Figure 9-22 provides an example of image quality using SRI for orthogonal planes and rendered volumes. Tomographic Ultrasound Imaging During or after acquisition of volumes, it is possible to process imaging information into slices of predetermined number and spacing, reminiscent of computed tomography (CT) or nuclear MRI. This technique has been called multislice imaging or tomographic ultrasound imaging (TUI) by manufacturers. Unlike CT or MRI, the location, number, depth, and tilt of slices can be adjusted at will after volume acquisition. The combination of true 4D (volume cine loop) capability and TUI or multislice imaging allows simultaneous observation of the effect of maneuvers at many different levels. The pelvic floor easily lends itself to such techniques, and I suggest using the plane of minimal dimensions as plane of reference: an oblique axial plane that is defined in the midsagittal plane by the shortest line between the posterior symphyseal margin and the levator ani immediately posterior to the anorectal angle (Fig. 9-25). For the sake of convenience, I use 8 × 2.5-mm steps recorded from 5 mm below this plane to 12.5 mm above, which should encompass the entire puborectalis muscle. Figure 9-26 shows the standard TUI format most appropriate to pelvic floor imaging, with the coronal plane for reference

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-24 Axial plane translabial imaging with the patient at rest, illustrating a severe case of delivery-related pelvic floor trauma. A bilateral avulsion and complete loss of tenting bilaterally is shown on conventional axial-plane, 3D ultrasound (left). The same plane in the same volume data set (right) is shown using volume-contrast imaging (VCI). This patient has severe stress incontinence and prolapse 3 years after a rotational forceps delivery.

Figure 9-25 Determination of the plane of minimal hiatal dimensions. The minimal distance between the posterior symphyseal margin and the levator ani immediately posterior to the anorectal angle (left, midsagittal plane) identifies the correct axial plane (right), which in this case was obtained by volume-contrast C-plane imaging.

in the top left corner and eight axial-plane slices at a distance of 2.5 mm each, in a nulliparous patient with normal pelvic floor function and anatomy. The presence and extent of injuries is evident at a glance from one printout or film, without requiring any further manipulation of data, as is familiar from radiologic cross-sectional techniques. It is likely that such techniques will help with the standardization of assessment methods and allow more accurate classification and quantification of morphologic abnormalities.117 PRACTICAL CONSIDERATIONS Pelvic floor ultrasound is highly operator dependent, as is true for all real-time ultrasound procedures. The 3D systems have the potential to reduce this operator dependence because volume acquisition is easily taught and should be within the capabilities of every sonographer or sonologist after a day’s training. Although

the method does require postprocessing (and the skills involved in this are more significant), static volume data typically of 1 to 6 MB can be de-identified and transmitted electronically so that evaluation may be obtained by e-mail, and this opens up new possibilities for local and international cooperation. Unfortunately, the de facto software standard of 3D image files provided by licensing of original technology has been lost, with many companies developing their own standards, which are incompatible with the others. A DICOM standard for 3D imaging data would be the solution, but standardization does not appear to be imminent. Consequently, increasing numbers of clinicians and researchers are frustrated by the inability to exchange volume data. Users need to exert significant pressure on manufacturers, who may not be inclined to cooperate with competitors on this issue. Most publications on 3D ultrasound in obstetrics and gynecology deal with obstetric applications.15 The visualization of fetal structures such as extremities, skeleton, and face has to a large

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Figure 9-26 Normal pelvic floor. Tomographic ultrasound imaging provides cross-sectional imaging at user-definable depths and intervals and at arbitrarily definable angles or tilts within the acquired volume. A cine loop of volumes allows observation of the effect of maneuvers in multiple cross sections at any time.

extent driven the research, development, and marketing of these systems. Although well-selected 3D data may enhance the understanding of certain conditions or abnormalities for patients and caregivers,15 some critics contend that 3D ultrasound has been a technology searching for an application. Pelvic floor imaging is a minor niche within the field of ultrasound diagnostics, but it may provide one of the first true indications for 3D and 4D volume ultrasound imaging. Pelvic floor 3D ultrasound has been used for the evaluation of the urethra and its structures, for imaging of the more inferior aspects of the levator ani complex (i.e., pubococcygeus and puborectalis), for the visualization of paravaginal supports, and for prolapse and implant imaging. Three-Dimensional Imaging of the Urethra Technically, 3D pelvic floor ultrasound imaging became feasible in 1989 with the advent of the Kretz Voluson 530 system. However, there are no records of the early use of such systems; the first publication on 3D ultrasound in urogynecology was in 1994,118 when Khullar et al demonstrated that this technique could be employed to assess the urethra.118 They used transvaginal probes with motorized withdrawal to allow the use of calipers in all three planes. Subsequently, it was shown that urethral volumetric data correlated with urethral pressure profilometry118 and that urethral volume decreased with parity. This technique has been used to assess delivery-related changes,119 and 3D ultrasound with intracavitary transducers may also aid in identifying paraurethral support structures such as the pubourethral ligaments. Probes designed for prostatic imaging have also been

employed for the assessment of the urethra and paraurethral structures by the transrectal route.120 Three-Dimensional Imaging of the Levator Ani Complex The inferior aspects of the levator ani were identified on early studies using transvaginal techniques14 and translabial freehand volume acquisition,98 as well as on translabial ultrasound using a Voluson system,13 but the focus of these reports was on the urethra and paraurethral tissues. With translabial acquisition, the whole levator hiatus and surrounding muscle (i.e., pubococcygeus and puborectalis) can be visualized, provided acquisition angles are at or above 70 degrees. Similar to MRI, it is impossible to distinguish the different components of the pubovisceral or puborectalis-pubococcygeus complex. In a series of 52 young, nulligravid women, no significant asymmetry of the levator was observed, supporting the hypothesis that morphologic abnormalities of the levator are likely to be evidence of delivery- related trauma.121 Contrary to MRI data,112 there was no significant side difference in thickness or area. A number of biometric parameters of the puborectalispubococcygeus complex itself and of the levator hiatus have been defined.121 Results agreed with MRI data obtained in small numbers of nulliparous women for the dimensions of the levator hiatus112 and levator thickness.110 Hiatal depth, width, and area measurements seem highly reproducible (intraclass correlation coefficients of 0.70 to 0.82) and correlate strongly with pelvic organ descent at rest and during a Valsalva maneuver.121 This study was replicated in a Chinese population, with very similar results for repeatability measures and intriguing differences in

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-27 Hiatal appearance in a patient during a Valsalva maneuver. At 36 weeks, the hiatus measured 25 cm2, and this had increased to 32 cm2 4 months after a normal vaginal delivery.

the shape of the hiatus.122 Other investigators have confirmed good repeatability of this technique123-125, and a comparison with measures obtained on magnetic resonance imaging showed high levels of agreement.126 Although it is not surprising that the hiatal area during a Valsalva maneuver correlates with descent (because downward displacement of organs may displace the levator laterally), it is much more interesting that hiatal area at rest seems associated with pelvic organ descent during a Valsalva maneuver. These data constitute the first real evidence for the hypothesis that the state of the levator ani is important for pelvic organ support,127 even in the absence of levator trauma. Relative enlargement of the hiatus during Valsalva maneuvers, or rather distention or elongation of its muscular component, may be a measure of compliance or elasticity and seems to correlate with resting tone as determined by palpation.128 The population distribution for hiatal area enlargement during Valsalva maneuvers in nulligravid white women seems to be remarkably wide, with measurements from 6 to 36 cm2 in one study.121 The 95th percentile of the distribution seems to lie at about 25 cm2, and based on this and receiver operator characteristics,129 the author considers hiatal enlargement in excess of this cutoff to be ballooning of the hiatus, indicating abnormal biomechanical properties. Figure 9-27 shows a case of de novo ballooning of the hiatus after vaginal childbirth. It is not clear whether such changes are due to myopathy, neuropathy or microtrauma to connective tissue structures. Pelvic floor compliance or distensibility deserves further study because it may be important for the progress of labor and in the diagnosis and treatment of pelvic organ prolapse. In fact, it is likely that surgical reduction of the levator hiatus, now feasible as a minimally invasive technique, will become an entirely new concept in pelvic reconstructive surgery.

The most common form of levator trauma, a unilateral avulsion of the pubococcygeus muscle off the pelvic side wall, is related to childbirth (Figs. 9-28 to 9-30; see Fig. 9-24) and is generally palpable as an asymmetric loss of substance in the inferomedial portion of the muscle at the site of its insertion on the pelvic side wall. It is usually occult but may occasionally be observed directly in women after major vaginal tears (see Fig. 9-28). Bilateral defects (see Figs. 9-24 and 9-30) are more difficult to palpate because of the lack of asymmetry and are much less common, probably in the order of 1% to 4% of the vaginally parous population. In one study,129 the investigators found that more than one third of women delivering vaginally suffered avulsion injuries, an incidence that is unexpectedly high compared with observations in older, symptomatic women.130 The clinical significance of such defects is being studied. Our data130,131 and evidence from MR studies132,133 suggest that levator avulsion is common (affecting about 15% to 20% of vaginally parous women) and that it is associated with maternal age at first delivery, which is a concern in view of the continuing trend toward delayed childbearing in Western societies. It seems that the likelihood of major levator trauma at vaginal delivery triples during the reproductive years, from 15% at about 18 years of age to 45% at 40 years. Forceps seem to double the risk.131 Taken together with the increasing likelihood of cesarean section, it seems that the likelihood of a successful vaginal delivery without levator trauma decreases from more than 80% at age 20 to less than 30% at age 40 (our unpublished data). Levator avulsion is associated with anterior and central compartment prolapses,117,129,130 and it likely represents the missing link between childbirth and prolapse, but the relationship with bladder dysfunction is not as obvious.130 The larger a defect

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Figure 9-28 A comparison of intrapartum appearances (left), 4D pelvic floor ultrasound findings (middle) and magnetic resonance (right) imaging in the axial plane after a normal vaginal delivery that resulted in a right-sided levator avulsion *. (MRI courtesy of Dr. Lennox Hoyte, Boston, MA.)

Figure 9-29 Small, left-sided, unilateral levator avulsion. Normal antepartum findings are shown on the left, and the postpartum state is demonstrated on the right.

(width and depth), the more likely are symptoms and signs of prolapse.117 However, cross-sectional studies of levator anatomy in asymptomatic and symptomatic older women are needed to determine whether such abnormalities are associated with clinical symptoms or conditions in the general population. Another interesting question is whether major morphologic abnormalities of the levator ani affect surgical outcomes. A study using MRI

demonstrated that recurrence after anterior colporrhaphy was much more likely in women with levator trauma.135 From our experience, it appears that major levator trauma (i.e., avulsion of the puborectalis or pubococcygeus from the pelvic side wall) is associated with early presentation and recurrent prolapse after surgical repair. If this is the case, we should create in vitro models for such trauma and start thinking about surgical intervention.

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-30 Major bilateral levator avulsion. Normal antepartum findings are shown on the left, and the postpartum state is demonstrated on the right.

The presence of levator avulsion may indicate the need for something other than conventional surgical management. Three-Dimensional Imaging of Paravaginal Supports It has been assumed that anterior vaginal wall prolapse and stress urinary incontinence are at least partly caused by disruption of paravaginal and paraurethral support structures (i.e., endopelvic fascia and pubourethral ligaments) at the time of vaginal delivery. In a pilot study using the now-obsolete technology of freehand acquisition of 3D volumes, alterations in paravaginal supports were observed in 5 of 21 women seen before and after delivery, and the interobserver variability of the qualitative assessment of paravaginal supports was shown to be good.98 In light of current knowledge, the loss of tenting documented in this study was probably at least partly caused by levator avulsion. Paravaginal tissues also can be assessed by transrectal or transvaginal 3D ultrasound using probes designed for pelvic or prostatic imaging.14 One study using transrectal, high-frequency, 3D ultrasound suggested that defects of the subvesical or paravaginal fascia might be similar in appearance to striae gravidarum, making direct surgical repair impractical.136 Three-Dimensional Imaging of Prolapse The downward displacement of pelvic organs during a Valsalva maneuver in itself does not require MRI or ultrasound 3D imaging technology. Descent of the urethra, bladder, cervix, cul-de-sac, and rectum is easily documented in the midsagittal plane.76 However, rendered volumes may allow a complete 3D visualization of a cystocele or rectocele (Figs. 9-31 to 9-33) and help with operative planning. When processed into rotational volumes,

hyperechoic structures such as a rectocele become particularly evident (see Fig. 9-33). The ease with which preoperative and postoperative data can be compared with the help of stored imaging volumes can be especially useful in audit activities. Three-Dimensional Imaging of Synthetic Implant Materials The imaging of synthetic implants may prove to be a major factor in the uptake of this new investigational technique into clinical practice. Suburethral slings such as the TVT, SPARC, IVS, Monarc, and TOT have become very popular during the past 10 years137-139 and have become the primary anti-incontinence procedure in many developed countries. These slings are not without their problems, even if biocompatibility is markedly better than for previously used synthetic slings, and they differ in some important aspects. Imaging may be indicated in research to determine the location and function of such slings and possibly for assessing in vivo biomechanical characteristics. Clinically, complications such as sling failure, voiding dysfunction, erosion, and postoperative symptoms of the irritable bladder may benefit from imaging assessment. Often, patients do not remember the exact nature of an incontinence or prolapse procedure, and implants may be identified in women who are not aware of their presence or type. Most modern synthetic implant materials are highly echogenic; TVT Sparc, TVT-O, Monarc and TOT are usually more visible than the IVS sling. Implants can be located with 3D ultrasound, usually over most of thier intrapelvic course.140 (Fig 9-34). Variations in placement, such as asymmetry, varying width, the effect of tape division, and tape twisting, can be visualized. The difference between transobturator tapes and the TVT-type

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Figure 9-31 A large cystocele (arrow) is seen in the three standard planes (sagittal, top left; coronal, top right; axial, bottom left) and in a rendered image (axial, caudocranial rendering), showing a view through the cystocele onto the bladder roof. Reproduced from Textbook of Female Urology and Urogynecology, Chapter 26; Informa Healthcare, Abingdon UK, 2006.

Figure 9-32 Second-degree true rectocele imaged in the three orthogonal planes and a rendered volume (bottom right). Stars indicate the rectocele, showing it to be symmetrical, arising from the anorectal junction, and filling most of the hiatus.

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-33 A rectocele is shown in a rendered volume of the levator hiatus during a Valsalva maneuver. Reproduced from Textbook of Female Urology and Urogynecology, Chapter 26, Informa Healthcare, Abingdon UK, 2006.

Figure 9-34 The tension-free vaginal tape (TVT) sling is imaged on an oblique rendered volume of the levator hiatus. The mesh structure of the tape is clearly visible. There is also a very unusual local abnormality of the levator on the patient’s right side (i.e., left side of the image, arrow). Reproduced from Obstet Gynecol 2004; 23:615-625, with permission.

Figure 9-35 Monarc sling (left) compared with tension-free vaginal tape (TVT) sling in rendered volumes of the levator hiatus. Notice the difference in placement. The Monarc sling is inserted through the obturator foramen, and the TVT sling is inserted through the space of Retzius. As a result, the TVT sling arms are situated much more medially. Reproduced from Obstet Gynecol 2004; 23:615-625, with permission.

implants, which is difficult to distinguish on 2D imaging, is readily apparent in the axial plane (Fig. 9-35). It is therefore likely that 3D imaging will turn out to be very helpful in the assessment of patients with suburethral slings. The same holds true for mesh implants used in prolapse surgery. There is a worldwide trend toward mesh implantation, especially for recurrent prolapse, and complications such as failure and mesh erosion are not uncommon.141,142 Polypropylene meshes such as the Perigee, Prolift, and Apogee are highly echogenic, and their visibility is limited only by persistent prolapse and transducer distance. Translabial 3D ultrasound has demonstrated that the implanted mesh often does not remain as flat as it was on implantation (Fig. 9-36).143 Surgical technique seems to

play some role, because fixation of mesh to underlying tissues results in a flatter, more even appearance (Fig. 9-37). The position, extent, and mobility of anterior vaginal wall mesh can be determined and may sometimes uncover complications such as dislodgment of anchoring arms.94 Translabial 4D ultrasound can be useful in determining functional outcome and the location of implants, and it can help in optimizing implant design and surgical technique. Although it is not much more than an afterthought in this age of minimally invasive slings, most of the injectables used in anti-incontinence surgery are highly echogenic and can be visualized as a hyperechoic donut shape surrounding the urethra (Fig. 9-38).

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Figure 9-36 A Perigee transobturator mesh implant is imaged in the midsagittal plane (left) and as an oblique axial rendered volume (right). Reproduced from ASUM Bulletin 2007; 10:17-23, with permission.

Figure 9-37 Perigee and Apogee mesh implants are seen in a patient with massive levator ballooning, and despite this, prolapse repair was successful. Both implants appear flat and smooth, and both are functional, blocking a large part of the hiatus during a Valsalva maneuver.

CONCLUSIONS Ultrasound imaging, particularly translabial or transperineal ultrasound, is becoming the new diagnostic standard in urogynecology. Several factors have contributed to its acceptance, but the most important is the availability of suitable equipment. Developments such as the assessment of levator activity and prolapse and the use of color Doppler to document urine leakage enhance the clinical usefulness of the method. Increasing standardization of parameters should make it easier for clinicians and researchers to compare data.

The convenience with which pretreatment and posttreatment imaging data is obtained can simplify outcome studies after prolapse and incontinence surgery. Ultrasound imaging may be able to significantly enhance our understanding of the different mechanisms by which conservative and surgical methods achieve—or fail to achieve—continence. It may even be possible to identify distinct fascial defects, such as defects of the rectovaginal septum in true rectoceles, which should generate new surgical possibilities. Regardless of which methodology is used to determine descent of pelvic organs, it is evident that there is a wide variation in

Chapter 9 PELVIC FLOOR ULTRASOUND

Figure 9-38 Macroplastique as demonstrated in a rendered axial volume, axial plane, surrounding the uretha in a donut shape. Figure reproduced from Obstet Gynecol 2004; 23:615-625, with permission.

pelvic organ mobility, even in young, nulliparous women. This variation is likely to be at least partly genetic in origin. Ultrasound imaging allows quantification of the phenotype of pelvic organ prolapse, which will facilitate molecular and population genetic approaches to evaluate the cause of pelvic floor and bladder dysfunction. Childbirth causes significant alterations of pelvic organ support and levator structure and function, and there is some relationship between the prior state of pelvic organ supports and labor outcome. Pelvic floor ultrasound can help us in identify women

at high risk of emergency operative delivery,144 and in the future we will be able to predict significant pelvic floor trauma. It remains to be seen, however, whether such information can have a positive effect on clinical outcomes in what is no doubt a highly politicized environment. The use of 3D volume ultrasound adds several dimensions to pelvic floor imaging, particularly in its most recent incarnations using automatic volume acquisition, 4D cine volume ultrasound, SRI techniques, and TUI. Spatial resolutions now equal or exceed those obtained on static MRI, and temporal resolutions are far superior, although most clinicians working in this field are largely unaware of recent developments because of a traditional lack of access to imaging techniques. The technology opens up new possibilities for observing functional anatomy and examining muscular and fascial structures of the pelvic floor. Data acquisition can be simplified and research capabilities enhanced, and surgical audits in this field are likely to undergo a significant change. Modern imaging will allow us to optimize current surgical techniques and to develop new ones. There is no evidence to prove that modern imaging techniques can improve outcomes in pelvic floor medicine for patients. However, this limitation is true for many diagnostic modalities in clinical medicine. Because of methodologic problems, the situation is unlikely to improve soon. In the meantime, it must be recognized that any diagnostic method is only as good as the operator behind the machine, and diagnostic ultrasound is well known for its operator-dependent nature. Training is essential to ensure that imaging techniques are used appropriately and effectively. Acknowledgments This chapter is based on three review articles published in Ultrasound in Obstetrics and Gynecology, John Wiley & Sons, 2004.

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Chapter 9 PELVIC FLOOR ULTRASOUND

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127. DeLancey JO: Anatomy. In Cardozo L, Staskin D (eds): Textbook of Female Urology and Urogynaecology. London, Isis Medical Media, 2001, pp 112-124. 128. Thyer I, Dietz HP, Shek KL: Clinical validation of a new imaging method for assessing pelvic floor biomechanics [abstract]. Paper presented at the ISUOG International Meeting, Hong Kong, 2007. 129. De Leon J, Shek KL, Dietz HP: Ballooning: can we define pathological distensibility of the levator hiatus? Int Urogynecol J 18(S1): S102, 2007. 130. Dietz HP, Steensma A: The prevalence and clinical significance of major morphological abnormalities of the levator ani. BJOG 113:225-230, 2006. 131. Dietz HP: Does delayed childbearing increase the risk of levator injury in labour? Neurourol Urodyn (in press). 132. DeLancey JO, Kearney R, Chou Q, et al: The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 101:46-53, 2003. 133. Kearney R, Miller JM, Ashton-Miller JA, Delancey JO: Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol 107:144-149, 2006. 134. Adekanmi B, Freeman R, Puckett M, Jackson S: Cystocele: Does anterior repair fail because we fail to correct the fascial defects? A clinical and radiological study. Int Urogynecol J 16(Suppl 2):S73, 2005. 135. Reisinger E, Stummvoll W. Visualization of the endopelvic fascia by transrectal three-dimensional ultrasound. Int Urogynecol J 17:165-169, 2006. 136. Ulmsten U, Falconer C, Johnson P, et al: A multicenter study of tension-free vaginal tape (TVT) for surgical treatment of stress urinary incontinence. Int Urogynecol J 9:210-213, 1998. 137. Nilsson CG: The tension-free vaginal tape procedure (TVT) for treatment of female urinary incontinence. A minimal invasive surgical procedure. Acta Obstet Gynecol Scand Suppl 168:34-37, 1998. 138. Ward KL, Hilton P, for United Kingdom and Ireland Tension-free Vaginal Tape Trial Group: Prospective multicentre randomised trial of tension-free vaginal tape and colposuspension as primary treatment for stress incontinence. Br Med J 325:67, 2002. 139. Dietz HP, Wilson PD: The Iris effect: How 2D and 3D volume ultrasound can help us understand anti-incontinence procedures. Ultrasound Obstet Gynecol 22:999, 2004. 140. Iglesia CB, Fenner DE, Brubaker L: The use of mesh in gynecologic surgery. Int Urogynecol J 8:105-115, 1997. 141. Fenner DE: New surgical mesh. Clin Obstet Gynecol 43:650-658, 2000. 142. Tunn R, Picot A, Marschke J, Gauruder-Burmester A: Sonomorphological evaluation of polypropylene mesh implants after vaginal mesh repair in women with recurrent prolapse. Ultrasound Obstet Gynecol 29:449-452, 2007. 143. Shek KL, Dietz HP, Rane A: Transobturator mesh anchoring for the repair of large or recurrent cystocele. Neurourol Urodyn (in press). 144. Dietz HP, Lanzarone V, Simpson JM: Predicting Operative Delivery. Ultrasound Obstet Gynecol 27:419-415, 2006.

Chapter 10

ELECTROPHYSIOLOGIC EVALUATION OF THE PELVIC FLOOR Simon Podnar and Clare J. Fowler Clinical neurophysiologic tests have been proposed for research applications in patients with sacral dysfunction, but the emphasis in this chapter is on describing investigations with established diagnostic value. The roles of electrodiagnostic tests in various clinical conditions are described first, and brief descriptions of these investigative procedures are given at the end of the chapter. CLINICAL APPLICATION OF SACRAL ELECTRODIAGNOSTIC TESTS Electrodiagnostic tests are an extension of the clinical neurologic examination, and they are helpful in evaluating patients in whom a neurologic lesion is suspected. An international consensus statement proposes that sacral electrodiagnostic studies are most useful in patients with focal peripheral sacral lesions (i.e., conus medullaris, cauda equina, sacral plexus, and pudendal nerve lesions), in patients with multiple system atrophy, and in women with urinary retention.1 They can document the severity of a clinically diagnosed lesion and provide data on the integrity of various neurologic structures. However, these tests have limitations. They require trained personnel to be properly performed, they are not useful for screening, and they are uncomfortable for the patient. The results do not correlate well with clinical bladder, anorectal, or sexual dysfunction. Neurogenic sacral organ dysfunction can be caused by a variety of neurologic disorders, but the value of sacral electrodiagnostic studies in such patients may be minor. In patients with brain and spinal cord disease, who may have pronounced pelvic organ complaints, imaging studies—magnetic resonance imaging (MRI) in particular—are more useful for establishing the underlying neurologic diagnosis. In this context, neurophysiologic testing outside the pelvic region may provide information about relevant abnormal spinal conduction, and somatosensory evoked potentials (SEPs) elicited by stimulation of the tibial nerve are more useful in these circumstances than pudendal SEPs.2,3 Similarly, in patients with sacral dysfunction due to a generalized peripheral neuropathy such as diabetes, nerve conduction studies in the lower limbs are a more sensitive adjunct to clinical examination than are sacral electrodiagnostic studies.4 ASSESSMENT OF PATIENTS BEFORE ELECTRODIAGNOSTIC TESTING Clinical and laboratory evaluation of a woman with pelvic organ dysfunction is necessary before electrodiagnostic investigations can be considered. This order is followed so that there can be

proper formulation of the questions for those in the clinical neurophysiology laboratory carrying out the tests. Examples of such questions are listed in Box 10-1. Necessary preliminary investigations may include urodynamics, anorectal manometry, cine defecography, or colonic transit studies. Imaging studies such as ultrasound, computed tomography (CT), and MRI of the anorectum and the lower urinary and genital tracts may aid the diagnosis because they can exclude structural abnormalities (e.g., anal sphincter tears, abnormal position of the bladder neck, vaginal wall prolapse) that can cause or contribute to sacral organ dysfunction. ELECTRODIAGNOSTIC TESTING IN WOMEN WITH SACRAL COMPLAINTS Incontinence after Childbirth Research studies have used needle electromyography to examine the extent of nerve damage contributing to urinary stress incontinence after childbirth. The first studies using single-fiber electromyography (SFEMG) to look at fiber density showed partial reinnervation changes in the external anal sphincter (EAS)5 and pubococcygeus muscles in women with stress incontinence and genital prolapse.6 Needle electromyographic examination of the pubococcygeus muscle revealed a significant increase in motor unit potential (MUP) duration (i.e., an indication of reinnervation) after vaginal delivery, which was most marked in women with urinary incontinence 8 weeks after delivery, a prolonged second stage, and heavier babies.7 However, an electromyographic study, using less biased methods of automated MUPs and interference pattern analysis, questioned the widely held notion that significant damage to the innervation of the EAS occurs even during uncomplicated deliveries. Although vaginal delivery was related to minor electromyographic abnormalities, there was no indication that this correlated with loss of sphincter function.8 A

Box 10-1 Questions to Consider before Requesting Electrodiagnostic Testing Is there a neurogenic component to this patient’s complaint? How severe is the neurologic damage? Are there signs of acute denervation or chronic reinnervation? Is there abnormal sphincter electromyographic activity suggesting a cause for obstructed voiding or urinary retention? 125

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histomorphologic study supported these data by failing to demonstrate significant neuropathic changes in pelvic floor muscles.9 In the urethral sphincter, in contrast, electromyography and muscle biopsy showed more neuropathic changes in women with stress incontinence than in controls.10 Even uncomplicated delivery may cause some distal pudendal nerve damage. Significant neurogenic damage proximal to the EAS muscle innervation probably occurs only rarely,11 and it is mainly caused by compression of the sacral plexus by fetal head.12 The prevalence and relevance of minor proximal injuries is unknown. Kinesiologic electromyography performed using hook electrodes so that a prolonged recording could be made without causing discomfort showed some loss of coordination between the two sides of the pubococcygeus muscle in women with stress incontinence, implying an abnormal primary role of the central nervous system or a neurologic response to muscle or tendon damage.13 In addition to age-related neurogenic changes, the interference pattern changes consistent with motor unit loss, and failure of central activation has been found in the levator ani and EAS muscles of women with stress incontinence.14 Sufficient research data exist for us to know that the changes of denervation in pelvic floor in stress incontinence do occur, but they are quite subtle. Sphincter electromyography does not have an important role in the routine investigation in stress incontinence. Although extensively used in the past,15,16 the pudendal nerve terminal motor latency test is probably of no clinical use in women with urinary stress incontinence.11 Nerve latencies evaluate only the fastest nerve fibers and are therefore not sensitive to axonal loss, which is the major type of damage causing muscle denervation. Detrusor Overactivity Detrusor overactivity may result from neurologic disease or occur in an otherwise healthy individual, in which case the condition is called idiopathic detrusor overactivity. Clinical neurologic examination is the most useful means of differentiating these two entities. In addition to the clinical examination, imaging studies and electrodiagnostic tests of central nervous system conduction (i.e., motor evoked potentials [MEPs] and SEPs) may reveal underlying spinal cord disease, such as multiple sclerosis. In this respect, tibial SEPs are the most useful investigation.2,3 Extensive neurophysiologic investigations (e.g., electromyography of the EAS, bulbocavernosus reflex after dorsal clitoral nerve stimulation, tibial and pudendal SEPs, MEPs on cortical magnetic stimulation, recording from the EAS and abductor hallucis brevis muscles) in women with idiopathic detrusor overactivity failed to reveal any abnormality.17 No significant differences were reported in comparing this group with a group of 13 agematched, healthy control women, thereby excluding even an occult neurologic abnormality. This result supports the view that idiopathic detrusor overactivity is caused by intrinsic bladder defects (i.e., neurogenic or myogenic). The role of electrodiagnostic investigations in detrusor overactivity is limited to establishing or excluding an underlying neurologic disease. Urinary Retention Isolated urinary retention in young women was formerly considered to be psychogenic or the first symptom of multiple sclerosis. However, needle electromyography of the urethral sphincter

Figure 10-1 Profuse pathologic spontaneous activity (i.e., complex repetitive discharges) in the urethral sphincter muscle of a 26-yearold, otherwise healthy woman with an 8-year history of difficult emptying of the bladder. Her sister has similar problems and electromyographic abnormalities of the urethral sphincter muscle. Activity was provoked by movement of the concentric needle electrode or by voluntary muscle contraction.

muscle has demonstrated that many such patients have profuse, complex, repetitive discharges and decelerating burst activity (Fig. 10-1).18 The cause of this activity is unknown, but an association with polycystic ovaries was described in a syndrome by Fowler and colleagues.19 The explanation probably lies with some unidentified hormonal susceptibility of the female striated urethral sphincter muscle that causes a loss of stability of the muscle membrane and permits direct muscle fiber to muscle fiber (ephaptic) transmission to develop, which manifests as complex, repetitive discharges. The current hypothesis is that the sustained contraction of the urethral sphincter has an inhibitory effect on the detrusor, resulting in urinary retention. When recording from the striated urethral sphincter in this condition, only complex repetitive discharges (which sound like helicopters) may be heard, and the distinction between these and reinnervated motor units can be problematic, but if decelerating bursts (which sound like underwater recordings of whales) are also present, it is easier to be certain that the characteristic electromyographic activity has been recorded. Although electromyography may indicate the presence of an abnormality, it is inevitably only a very limited sample of the muscle activity in the immediate vicinity, and it is difficult to know whether the abnormality is sufficient to account for the clinical finding of complete or partial urinary retention. The investigations that have proved to be useful adjuncts are measurement of the urethral pressure profile and volume of the urethral sphincter muscle estimated with ultrasound.20 Young women with urinary retention due to the urethral sphincter abnormality often have urethral pressure profiles in excess of 100 cm H2O. The typical clinical presentation of Fowler’s syndrome is of a young woman with spontaneous onset of urinary retention or retention after some sort of operative intervention. The mean age of a series of women with this problem was 27 years, and a spontaneous onset appears to be more common in women younger than 30 years.21 The woman may present with a bladder capacity in excess of 1 L, and although this may cause painful distention, she lacks any of the expected sensations of urinary urgency. There may or may not be a history of infrequent voiding before the onset of urinary retention. These women are taught to do clean, intermittent self-catheterization and commonly experience difficulties with the technique, particularly pain and difficulty in

Chapter 10 ELECTROPHYSIOLOGIC EVALUATION OF THE PELVIC FLOOR

removing the catheter. A retrospective study of 248 women presenting with urinary retention over a 5-year period showed that this was by far the most common cause for urinary retention in young women.22 Patients with Fowler’s syndrome seem to respond particularly well to sacral neuromodulation.23 Although the mechanism of its action is still the subject of research using functional brain imaging methods,24 stimulation does not appear to lower the urethral pressure profile or cause a cessation of the abnormal electromyographic activity.25 The same type of abnormal spontaneous electromyographic activity may also occur in women with obstructed voiding. The electromyographic abnormality may persist during attempts at micturition,26 leading to interrupted flow, high detrusor pressure, low flow, and incomplete bladder emptying. It is thought that in this condition, the overactive urethral sphincter, although it produces obstruction, does not have the same inhibitory effect on the detrusor muscle as it does in women who become unable to void and develop urinary retention. Because needle electromyography of the urethral sphincter detects changes related to denervation and reinnervation, as well as this peculiar abnormal, spontaneous activity, it has been proposed that needle electromyography of the urethral sphincter muscle should always be undertaken in women with unexplained urinary retention.1,18 Anal Incontinence Needle electromyography of the EAS was thought to be useful in patients with anal incontinence.27 However, there is no consensus regarding the utility of electrophysiologic testing in neurologically normal patients with isolated anal incontinence. In a series evaluated by Podnar and coworkers,28 patients with isolated anal incontinence rarely had neuropathic electromyographic changes in sacral segments. In a subgroup of patients in whom no cause of anal incontinence could be established (i.e., idiopathic anal incontinence), the only electrophysiologic abnormality found was a diminished number (absence) of continuously firing, lowthreshold motor units during relaxation.28 In patients with fecal incontinence and an increased fiber density on SFEMG, lower anal squeeze pressures and diminished rectal sensation have been demonstrated. If marked changes of denervation and reinnervation are found in the EAS in the appropriate clinical setting, a more generalized disorder, such as multiple system atrophy or a cauda equina or conus medullaris lesion, should be considered. If performed, it is probably better that needle electromyography follows an anal ultrasound examination that excludes structural lesions of the sphincter mechanism.29 Chronic Constipation Constipation occurs for a variety of reasons. Its prevalence depends on the diagnostic criteria applied. Radiographic methods can demonstrate prolonged colonic transit (using radiopaque markers) and abnormal pelvic floor movement during defecation (using cine defecography), which are the main mechanisms.30 Electromyography can be used to demonstrate continuous puborectalis muscle contraction characteristic of a subtype of obstructed defecation (i.e., nonrelaxing puborectalis syndrome),31 but this would be considered only if other investigations suggested that particular pathophysiology. Chronic constipation with repetitive straining was thought to be the main cause of advancing pudendal neuropathy and

increased fiber density identified on SFEMG in patients with urinary and anal incontinence.32 Semiquantitative or quantitative MUP changes on conventional electromyography of the EAS muscles of severely constipated subjects have been reported by some investigators. In a study using advanced MUP and interference pattern analysis, no abnormalities were demonstrated in the EAS muscles of patients with mild chronic constipation. This finding is important for the interpretation of electromyographic findings in patients with other conditions, a significant proportion of whom also suffer from chronic constipation.33 Sexual Dysfunction Neurophysiologic techniques have been applied extensively in the research of male erectile dysfunction, but much less research has gone into female sexual dysfunction. Pudendal SEP recordings have been employed in women with sexual dysfunction due to spinal cord lesions, multiple sclerosis, and diabetes,34 but in a placebo-controlled trial of the effect of sildenafil citrate in women with sexual dysfunction and multiple sclerosis, the pudendal SEP was not found to be contributory.35 Pudendal SEPs usually have been found to be of no greater value than clinical examination in detecting relevant spinal cord disease.3

ELECTRODIAGNOSTIC TESTING IN WOMEN WITH ESTABLISHED NEUROLOGIC DISEASE Cauda Equina and Conus Medullaris Lesions Lesions of the cauda equina or conus medullaris may cause severe bladder, bowel, and sexual dysfunction. The sacral roots that innervate pelvic organs may be compressed within the spinal canal by intervertebral disk herniation, spinal fractures, hematomas, and tumors or may be a result of lumbar disk surgery. After detailed clinical examination of the lumbosacral segments (with particular emphasis on perianal sensation), neurophysiologic testing can assess the severity of the lesion and clarify the diagnosis. In our series, approximately 10% of patients with cauda equina lesions reported normal perianal sensation. Bilateral needle electromyography of the EAS muscle (Fig. 10-2) and sometimes of the bulbocavernosus muscle and electrophysiologic evaluation of the bulbocavernosus reflex (Fig. 10-3) are the electrodiagnostic tests that should be considered. Most of these lesions cause partial denervation. Three weeks to several months after injury, spontaneous denervation activity and later reinnervation MUP changes can be demonstrated by needle electromyography (Fig. 10-4). The bulbocavernosus reflex complements electromyography and increases sensitivity of electrodiagnostic studies in patients with cauda equina or conus medullaris lesions. Sacral Plexus and Pudendal Nerve Lesions After uncomplicated deliveries, electromyographic changes in the EAS are minor,8 but they may be more pronounced in the urethral sphincter muscle.10 It is commonly assumed that these lesions may be contributory to some degree in the pathogenesis of urinary stress incontinence and pelvic organ prolapse in women.11 However, electrodiagnostic testing in these women is recommended only when a proximal peripheral sacral neurogenic lesion is a possibility.1

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Other lesions of the sacral plexus and pudendal nerves are less common than are cauda equina or conus medullaris lesions. They can be caused by pelvic fractures, hip surgery, complicated deliveries,12 malignant infiltration, local radiotherapy, and use of orthopedic traction tables. They are usually unilateral. There are no validated techniques for differentiating cauda equina lesions from more distal lesions. Parkinsonism and Multiple System Atrophy Multiple system atrophy is a progressive neurodegenerative disease of unknown origin that is often mistaken for Parkinson’s disease in its early stages. It is characterized at onset by an akinetic, rigid parkinsonian syndrome; cerebellar ataxia; or auto-

Figure 10-2 Motor unit potential (MUP) analysis of the external anal sphincter (EAS) muscles of a 53-year-old woman 8 years after a traumatic fracture of the L4 vertebra. She continues to have back pain radiating to the right leg, right leg weakness with paresthesia, and moderate bladder, bowel, and sexual dysfunction. MUPs were within normal limits in the left EAS muscle and definitely abnormal in the right EAS muscle. Quantitative sphincter electromyography findings were compatible with a lesion of the right half of the cauda equina.

nomic failure, usually accompanied by severe incontinence. In the advanced stages of the disease (formerly called Shy-Drager syndrome), all these features may be present. The severe and early incontinence probably results from neuronal atrophy in the brainstem, which causes detrusor overactivity, and in the sacral spinal cord, where degeneration of the parasympathetic intermediolateral cell columns causes incomplete emptying and degeneration of the somatic anterior horn cells forming Onuf’s nucleus causes incontinence. Using needle electromyography of the sphincter muscles prolonged duration of MUPs has been described as the main electrodiagnostic marker for degeneration of Onuf’s nucleus.36-38 Changes consistent with chronic reinnervation can also be demonstrated as an increase in fiber density on SFEMG. Sphincter electromyography may not be sensitive in the early phase of the disease, and it is not specific after 5 years of parkinsonism. The changes of chronic reinnervation may also be found in another parkinsonian syndrome, progressive supranuclear palsy,39 a disease in which neuronal loss in Onuf’s nucleus has been demonstrated histologically.40 Unilateral needle electromyography, including observation of denervation activity and quantitative MUP analysis, is indicated in patients with suspected multisystem atrophy, particularly in its early stages if the diagnosis is unclear.38,41 If the test result is normal, but suspicion of the diagnosis persists, it may be of value to repeat the test later. Kinesiologic electromyography performed during urodynamics can also help to document detrusorsphincter dyssynergia in patients with Parkinson’s disease or multiple system atrophy.42 Primary Muscle Diseases There are no reports of a myopathy manifesting or remaining confined to the pelvic floor or sphincter muscles. Even in patients with a generalized myopathy, normal and abnormal muscle biopsy and needle electromyographic findings and abnormal histology with normal electromyographic findings have been reported.

Figure 10-3 Bulbocavernosus reflex (BCR) on electrical stimulation in a 42-year-old woman with a sudden onset of urinary frequency, urgency, and incontinence 4 years earlier. On clinical examination, she reported normal sensation of touch and abnormal sensation of temperature and pinprick (i.e., dissociated sensory loss) in sacral segments on the right. Notice a very prolonged latency of the BCR on the right (56 ms) and a normal latency response on the left (34 ms). On concentric needle electromyography, definite motor unit potential abnormalities were found in the right and normal results in the left external anal sphincter muscle. She had an episode of right-sided retrobulbar neuritis 6 years before the onset of transient urinary dysfunction. Brain magnetic resonance imaging revealed several lesions in the white substance of the brain consistent with demyelinization. Based on these data, the diagnosis of multiple sclerosis was made.

Chapter 10 ELECTROPHYSIOLOGIC EVALUATION OF THE PELVIC FLOOR

tapers and then branches to innervate muscle fibers constituting an individual motor unit. In health, muscle fibers that belong to the same motor unit do not lie adjacent to one another (i.e., checkerboard pattern of muscle innervation).

Figure 10-4 Spontaneous denervation electromyographic (EMG) activity is seen during relaxation (top), and a single, extremely polyphasic motor unit potential (MUP) is recruited on maximal voluntary contraction (bottom). The former is a sign of muscle fiber denervation, and the latter is a sign of collateral reinnervation. Both signals were recorded by a concentric EMG needle in the left subcutaneous external anal sphincter muscle of a 50-year-old woman 3 months after surgery for a large, centrally herniated intervertebral disk (between L5 and S1).

Exclusion of a Neurologic Lesion Occasionally, it may be necessary to exclude a neurologic basis for bladder dysfunction. A normal EAS muscle electromyographic pattern indicates integrity of the sacral lower motor neuron, a normal bulbocavernosus reflex indicates preservation of the sacral reflex arc (including conus medullaris with parasympathetic sacral center), a normal sympathetic skin response indicates preservation of the sympathetic lumbosacral center, and a normal pudendal SEP correlates with preserved spinal somatosensory pathways.43 ELECTRODIAGNOSTIC TESTS Electromyography Electromyography relies on the extracellular recording of spontaneous and reflexively or voluntarily provoked bioelectrical activity generated by muscle fibers. Bioelectrical activity consisting of action potentials is generated by depolarization of muscle fibers. Motor neurons that innervate striated pelvic floor and sphincter muscle lie in the anterior horn of the sacral spinal cord (i.e., conus medullaris). Within the muscle, the motor axon

Concentric Needle Electromyography The needle electrode most commonly used in electromyography is the single-use, disposable, concentric needle electrode. It can provide information on insertion activity, spontaneous activity, MUPs, and interference patterns.41 In healthy skeletal muscle, initial placement of the needle elicits a short burst of insertion activity due to mechanical stimulation of excitable membranes. Absence of insertion activity with an appropriately placed needle electrode (if all technical causes have been excluded) may mean complete denervation of the muscle being examined. In contrast to most other skeletal muscles, the sphincter muscles exhibit continuous firing of lowthreshold motor units. This activity can be quantified most easily and reproducibly by template-operated MUP sampling techniques (e.g., multi-MUP analysis), which provides information on excitability and loss of motor units.28 An abnormal, spontaneously active type of activity may be recorded from the urethral sphincter muscle in some young women with retention or obstructed voiding, so-called decelerating bursts and complex repetitive discharges (see Fig. 10-1).18,21 Between 10 and 20 days after an acute denervating injury, the abnormal, spontaneous activity appears: fibrillation potentials and positive sharp waves (Fig. 10-4). This type of activity originates from denervated, single muscle fibers. In partially denervated sphincter muscle, this activity is mingled with continuously firing MUPs, and examination of the bulbocavernosus muscle, which in contrast to sphincter muscles lacks on-going MUP firing during relaxation, is particularly useful.41 Examination of MUPs recorded by a needle electrode has proved to be the most valuable process in the neurophysiologic assessment of the pelvic floor. A MUP is generated by summation of action potentials of all muscle fibers constituting individual motor unit, and MUP morphology is determined by the bioelectrical characteristics of muscle fibers constituting the motor unit and by their spatial distribution. In partially denervated muscle, collateral reinnervation tends to take place, and surviving motor nerves sprout and grow out to reinnervate muscle fibers that have lost their nerve supply. This results in a change in the arrangement of muscle fibers within the motor unit and in a consequent change in MUP shape (see Figs. 10-2 and 10-4), which can be quantitatively described by several MUP parameters (Fig. 10-5). For diagnosis of neuropathic changes in the EAS muscle, an optimal set of MUP parameters (i.e., area, duration, and number of turns) was identified.44 In addition to duration, MUP amplitude and number of phases traditionally were used. MUPs are identified by their repetitive appearance in a prolonged recording of electromyographic activity (i.e., manualMUP analysis), using a trigger and delay line (i.e., single-MUP analysis) or using the template-based multi-MUP analysis. The multi-MUP analysis is an automated computer operated analysis, and is fast (5 to 10 minutes per muscle), easy to apply, and minimizes examiner’s bias.45 A representative sample of 20 MUPs (i.e., standard number in limb muscles) must be analyzed for the test to be valid (see Fig. 10-2). The EAS muscle is regarded as the best indicator muscle for proximal neuropathic sacral lesion, and bilateral examination of only the subcutaneous EAS muscle usually suffices.46 Normative

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Conduction Studies Conduction studies examine the capacity of a nerve (or a nervous pathway) to transmit a test volley of depolarization along its length. If the tested nerve contains motor fibers, its responsiveness can be recorded from the muscle as a compound muscle action potential (CMAP).48 The time taken from stimulation to muscle response (i.e., latency) and the amplitude of the muscle response can be measured. The latency reflects the conduction speed of only the fastest motor fibers and is therefore a poor guide to the overall function of the nerve. The amplitude of the CMAP reflects the number of intact motor units and gives a somewhat better guide to the severity of a neuropathic lesion. However, in anatomically complex muscles of the pelvis, recording of a well-formed CMAP is difficult.49 Figure 10-5 Motor unit potential (MUP) parameters. Amplitude is the voltage difference (μV) between the most positive and most negative point of the MUP trace. The MUP duration is the time (ms) between the first deflection and the point when MUP waveform finally returns to the baseline. The number of MUP phases (circles) is defined by the number of MUP areas alternately below and above the baseline and can be counted as the number of baseline crossings plus one. Turns (asterisks) are defined as changes in direction of the MUP trace that are larger than the specified amplitude (50 μV). MUP area measures the integrated surface of the MUP waveform (shaded area).

data for the EAS muscle have been published and show no significant changes with age, gender, number of uncomplicated vaginal deliveries,8 and mild, chronic constipation.33 Similar in-depth analysis of normative data from standardized technique for other pelvic floor and perineal muscles is not available. At increased levels of voluntary and reflex activation, a more dense interference pattern can be seen. This can be quantitatively assessed, but its sensitivity for detecting neuropathic EAS muscles is only about one half of that for MUP analysis techniques.45 Qualitative assessment of the interference pattern has been recommended for sphincter and pelvic floor muscles to assess motor unit loss.41 Kinesiologic Electromyography The aim of kinesiologic electromyography is to assess patterns of individual muscle activity during physiologic maneuvers (e.g., electromyographic activity patterns of pelvic floor muscle during bladder filling and voiding). Various types of surface or intramuscular (needle or hook wire) electrodes can be used for recording kinesiologic electromyography, but there are often technical problems to overcome, such as electrical artifacts and contamination with electromyographic signals from other muscles. Large pelvic floor muscles are not adequately represented by the signal measured with intramuscular electrodes. Little is known about the normal activity patterns of different pelvic floor and sphincter muscles. It is assumed that they all act in a coordinated fashion, which is frequently lost in abnormal conditions.26 On voiding, disappearance of all electromyographic activity in the urethral sphincter precedes detrusor contraction. In central nervous system disorders, however, detrusor contractions may be associated with an increase of sphincter electromyographic activity (i.e., detrusor-sphincter dyssynergia),47 which can be most easily demonstrated by kinesiologic electromyography performed during cystometry.

Pudendal Nerve Terminal Motor Latency Terminal motor latency of the pudendal nerve can be measured by recording with a concentric needle electrode from the bulbocavernosus, EAS, or urethral sphincter muscles in response to bipolar stimulation placed on the perianal or perineal surface. The latencies of MEPs obtained by this means are between 4.7 and 5.1 ms.50 The more widely employed technique of obtaining the pudendal terminal motor latency relies on a bipolar stimulating electrode fixed to the tip of the gloved index finger, with the recording electrode pair placed 8 cm proximally on the base of the finger (i.e., St. Mark’s stimulator).51 The finger is inserted into the rectum or vagina, and stimulation is performed close to the ischial spine. Using this stimulator, the terminal motor latency for the EAS CMAP is typically about 2 ms.51 If a catheter-mounted electrode is used, responses from the urethral sphincter can also be obtained. The difference in latencies obtained by the perineal and transrectal methods has not yet been explained. Unfortunately, amplitudes of the pudendal CMAP have not proved contributory because of their large variability.1 Electrical and Magnetic Stimulation of Sacral Roots With development of special electrical and magnetic stimulators, transcutaneous stimulation of deeply situated nervous tissue became possible. When applied over the spine, the roots at the exit from the vertebral canal mainly are stimulated.49 Recording of MEPs with magnetic stimulation has been less successful, at least with standard coils, than with electrical stimulation, and there is often a large stimulus artifact. Positioning of the ground electrode between the recording electrodes and the stimulating coil should decrease the artifact.49,52 Sacral Reflexes Sacral reflexes refer to electrophysiologically recordable responses of perineal or pelvic floor muscles to electrical stimulation in the urinary-genital-anal region. Two reflexes, the anal and the bulbocavernosus reflex, are commonly clinically elicited in the lower sacral segments. Both have the afferent and efferent limb of their reflex arc in the pudendal nerve, and both are centrally integrated at the S2 to S4 cord levels.49,53 In women, the bulbocavernosus reflex is clinically elicited by squeezing or taping of the clitoris and observing movement of the perineum or anal sphincter. It is, however, much less reliable than in men,53,54 and in our opinion, is not useful. The anal reflex is elicited by a pinprick of the perianal skin, producing an anal wink.

Chapter 10 ELECTROPHYSIOLOGIC EVALUATION OF THE PELVIC FLOOR

Electrophysiologic correlates of these reflexes have been described using electrical, mechanical, and magnetic stimulation. Whereas the latter two modalities have been applied only to the clitoris, electrical stimulation can be applied to other sites, such as the dorsal clitoral nerve and perianal area. Responses are usually detected by needle electrode inserted into the EAS or bulbocavernosus muscle. The bulbocavernosus detection site is preferred because traces do not contain continuously firing, low-threshold MUPs. The bladder neck or proximal urethra can be stimulated using a catheter-mounted ring electrode, and reflex responses can be obtained from perineal muscles. With visceral denervation, such as after radical hysterectomy, these reflexes may be lost while the sacral reflex mediated by pudendal nerve is preserved. Loss of vesicourethral reflex with preservation of vesicoanal reflex has been described for patients with urethral afferent injury after recurrent urethral operations. Reports of sacral reflexes obtained after electrical stimulation of the clitoral nerve give consistent mean latencies of between 31 and 39 ms (see Fig. 10-3). Sacral reflex responses obtained on perianal, bladder neck, or proximal urethra stimulation have latencies between 50 and 65 ms.49 This more prolonged response is thought to be caused by the afferent limb of the reflex being conveyed by thinner myelinated pelvic nerves with slower conduction velocities than the thicker myelinated pudendal afferents. The longer-latency anal reflex, the contraction of the EAS on stimulation of the perianal region, may also have thinner myelinated fibers in its afferent limb because it is produced by a nociceptive stimulus.49 Sympathetic Skin Response The sympathetic skin response is a reflex served by myelinated sensory fibers (i.e., afferent limb), a complex central integrative mechanism, and sympathetic postganglionic nonmyelinated C fibers (i.e., efferent limb).55 The responses can be recorded from the perineum with some difficulty. The stimulus used in clinical practice typically is an electrical pulse delivered to a peripheral nerve in the limbs, but the genital organs also can be stimulated. Only an absent sympathetic skin response can be considered abnormal. The response is reportedly useful in the assessment of patients with neuropathies involving unmyelinated nerve fibers56 and patients with spinal cord injury. In the latter group, it may serve as an indicator of the preserved sympathetic lumbosacral center, which is particularly important for bladder neck competence.57

Cerebral Somatosensory Evoked Potentials The pudendal evoked response is easily recorded after electrical stimulation of the dorsal clitoral nerves. The first positive peak at 41 ± 2.3 ms (called P1 or P40) is usually clearly defined in healthy subjects. This SEP is of the highest amplitude (0.5 to 12 μV) at a site central over the sensory cortex and is highly reproducible. Later negative (at about 55 ms) and then additional positive waves are quite variable in amplitude and expression and have little known clinical relevance.49 Cerebral SEPs can be obtained on stimulation of the bladder urothelium. These cerebral SEPs have low amplitudes (≤1 μV), have variable configurations, and may be difficult to identify in some control subjects. The typical latency of the most prominent negative potential (N1) is about 100 ms. The responses are of more relevance to neurogenic bladder dysfunction than the pudendal SEP, because the Aδ sensory afferents from bladder and proximal urethra accompany the autonomic fibers in the pelvic nerves. Another stimulation site is the anal canal; after stimulation, cerebral SEPs with a slightly longer latency than those obtained after stimulation of the clitoris have been reported. However, because it is not possible to record this response from all control subjects, these tests have not proved clinically useful. The rectum and sigmoid colon have also been stimulated, and cerebral SEPs of two types have been recorded. One was similar in shape and latency to the pudendal SEP, and the other was similar to the SEP recorded on stimulation of bladder and posterior urethra.

CONCLUSIONS Several electrodiagnostic tests have been proposed for evaluation of the sacral nervous system in women with bladder, bowel, and sexual dysfunction. Although all of the tests discussed here are of research interest, concentric needle electromyography is of greatest value in the diagnostic evaluation of selected groups of patients with pelvic floor dysfunction: those with traumatic lesions and those with atypical parkinsonism. Bulbocavernosus reflex and pudendal SEP studies are useful in the evaluation of selected patients with suspected peripheral or central neurogenic sacral lesions. Probably the only patients in whom sacral dysfunction in itself should be considered an indication for electromyography of the urethral sphincter are young women with unexplained urinary retention.

References 1. Fowler CJ, Benson JT, Craggs MD, et al: Clinical neurophysiology. In Abrams P, Cardozo L, Khoury S (eds): Incontinence. The Second International Consultation on Incontinence, 2001 July 1-3, Paris. Plymouth, UK, Health Publication, 2002, p 389. 2. Rodi Z, Vodusek DB, Denislic M: Clinical uro-neurophysiological investigation in multiple sclerosis. Eur J Neurol 3:574, 1996. 3. Delodovici ML, Fowler CJ: Clinical value of the pudendal somatosensory evoked potential. Electroencephalogr Clin Neurophysiol 96:509, 1995. 4. Hecht MJ, Neundorfer B, Kiesewetter F, et al: Neuropathy is a major contributing factor to diabetic erectile dysfunction. Neurol Res 23:651, 2001. 5. Anderson RS: A neurogenic element to urinary genuine stress incontinence. Br J Obstet Gynaecol 91:41, 1984.

6. Smith AR, Hosker GL, Warrell DW: The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine. A neurophysiological study. Br J Obstet Gynaecol 96:24, 1989. 7. Allen RE, Hosker GL, Smith AR, et al: Pelvic floor damage and childbirth: A neurophysiological study. Br J Obstet Gynaecol 97:770, 1990. 8. Podnar S, Lukanovic A, Vodusek DB: Anal sphincter electromyography after vaginal delivery: Neuropathic insufficiency or normal wear and tear? Neurourol Urodyn 19:249, 2000. 9. Jundt K, Kiening M, Fischer P, et al: Is the histomorphological concept of the female pelvic floor and its changes due to age and vaginal delivery correct? Neurourol Urodyn 24:44, 2005. 10. Hale DS, Benson JT, Brubaker L, et al: Histologic analysis of needle biopsy of urethral sphincter from women with normal and stress

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11. 12. 13.

14.

15. 16. 17. 18. 19.

20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.

incontinence with comparison of electromyographic findings. Am J Obstet Gynecol 180:342, 1999. Vodusek DB: The role of electrophysiology in the evaluation of incontinence and prolapse. Curr Opin Obstet Gynecol 14:509, 2002. Feasby TE, Burton SR, Hahn AF: Obstetrical lumbosacral plexus injury. Muscle Nerve 15:937, 1992. Deindl FM, Vodusek DB, Hesse U, et al: Pelvic floor activity patterns: Comparison of nulliparous continent and parous urinary stress incontinent women. A kinesiological EMG study. Br J Urol 73:413, 1994. Weidner AC, Barber MD, Visco AG, et al: Pelvic muscle electromyography of levator ani and external anal sphincter in nulliparous women and women with pelvic floor dysfunction. Am J Obstet Gynecol 183:1390, 2000. Snooks SJ, Setchell M, Swash M, et al: Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 2:546, 1984. Smith AR, Hosker GL, Warrell DW: The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 96:29, 1989. Del Carro U, Riva D, Comi GC, et al: Neurophysiological evaluation in detrusor instability. Neurourol Urodyn 12:455, 1993. Fowler CJ, Kirby RS: Electromyography of urethral sphincter in women with urinary retention. Lancet 1:1455, 1986. Fowler CJ, Christmas TJ, Chapple CR, et al: Abnormal electromyographic activity of the urethral sphincter, voiding dysfunction, and polycystic ovaries: A new syndrome? Br Med J 297:1436, 1988. Wiseman OJ, Swinn MJ, Brady CM, et al: Maximum urethral closure pressure and sphincter volume in women with urinary retention. J Urol 167:1348, 2002. Swinn MJ, Wiseman OJ, Lowe E, et al: The cause and natural history of isolated urinary retention in young women. J Urol 167:151, 2002. Kavia R, Datta S, DasGupta R, et al: Urinary retention in women: Its causes and its management. BJU Int 97:281, 2006. Swinn MJ, Kitchen ND, Goodwin RJ, et al: Sacral neuromodulation for women with Fowler’s syndrome. Eur Urol 38:439, 2000. DasGupta R, Critchley HD, Dolan RJ, Fowler CJ: Changes in brain activity following sacral neuromodulation for urinary retention. J Urol 174:2268, 2005. DasGupta R, Fowler CJ: Urodynamic study of women in urinary retention treated with sacral neuromodulation. J Urol 171:1161, 2004. Deindl FM, Vodusek DB, Bischoff C, et al: Dysfunctional voiding in women: Which muscles are responsible? Br J Urol 82:814, 1998. Aanestad O, Flink R: Interference pattern in perineal muscles. A quantitative electromyographic study in patients with faecal incontinence. Eur J Surg 160:111, 1994. Podnar S, Mrkaic M, Vodusek DB: Standardization of anal sphincter electromyography: quantification of continuous activity during relaxation. Neurourol Urodyn 21:540, 2002. Sultan AH, Kamm MA, Hudson CN, et al: Anal-sphincter disruption during vaginal delivery. N Engl J Med 329:1905, 1993. Snape WJ Jr: Role of colonic motility in guiding therapy in patients with constipation. Dig Dis 15(Suppl 1):104, 1997. Jorge JM, Wexner SD, Ger GC, et al: Cinedefecography and electromyography in the diagnosis of nonrelaxing puborectalis syndrome. Dis Colon Rectum 36:668, 1993. Snooks SJ, Barnes PR, Swash M, et al: Damage to the innervation of the pelvic floor musculature in chronic constipation. Gastroenterology 89:977, 1985. Podnar S, Vodusek DB: Standardization of anal sphincter electromyography: Effect of chronic constipation. Muscle Nerve 23:1748, 2000.

34. Yang CC, Bowen JR, Kraft GH: Cortical evoked potentials of the dorsal nerve of the clitoris and female sexual dysfunction in multiple sclerosis. J Urol 164:2010, 2000. 35. DasGupta R, Wiseman OJ, Kanabar G, et al: Efficacy of sildenafil in the treatment of female sexual dysfunction due to multiple sclerosis. J Urol 171:1189, 2004. 36. Palace J, Chandiramani VA, Fowler CJ: Value of sphincter electromyography in the diagnosis of multiple system atrophy. Muscle Nerve 20:1396, 1997. 37. Libelius R, Johansson F: Quantitative electromyography of the external anal sphincter in Parkinson’s disease and multiple system atrophy. Muscle Nerve 23:1250, 2000. 38. Vodusek DB: Sphincter EMG and differential diagnosis of multiple system atrophy. Mov Disord 16:600, 2001. 39. Valldeoriola F, Valls-Sole J, Tolosa ES, et al: Striated anal sphincter denervation in patients with progressive supranuclear palsy. Mov Disord 10:550, 1995. 40. Scaravilli T, Pramstaller PP, Salerno A, et al: Neuronal loss in Onuf’s nucleus in three patients with progressive supranuclear palsy. Ann Neurol 48:97, 2000. 41. Podnar S, Vodusek DB: Protocol for clinical neurophysiologic examination of the pelvic floor. Neurourol Urodyn 20:669, 2001. 42. Sakakibara R, Hattori T, Uchiyama T, et al: Urinary dysfunction and orthostatic hypotension in multiple system atrophy: Which is the more common and earlier manifestation? J Neurol Neurosurg Psychiatry 68:25, 2000. 43. Schmid DM, Curt A, Hauri D, et al: Clinical value of combined electrophysiological and urodynamic recordings to assess sexual disorders in spinal cord injured men. Neurourol Urodyn 22:314, 2003. 44. Podnar S, Mrkaic M: Predictive power of motor unit potential parameters in anal sphincter electromyography. Muscle Nerve 26:389, 2002. 45. Podnar S, Vodusek DB, Stalberg E: Comparison of quantitative techniques in anal sphincter electromyography. Muscle Nerve 25:83, 2002. 46. Podnar S: Electromyography of the anal sphincter: Which muscle to examine? Muscle Nerve 28:377, 2003. 47. Chancellor MB, Kaplan SA, Blaivas JG: Detrusor-external sphincter dyssynergia. Ciba Found Symp 151:195, 1990. 48. AAEE glossary of terms in clinical electromyography. Muscle Nerve 10:G1, 1987. 49. Vodusek DB: Evoked potential testing. Urol Clin North Am 23:427, 1996. 50. Vodusek DB, Janko M, Lokar J: Direct and reflex responses in perineal muscles on electrical stimulation. J Neurol Neurosurg Psychiatry 46:67, 1983. 51. Kiff ES, Swash M: Normal proximal and delayed distal conduction in the pudendal nerves of patients with idiopathic (neurogenic) faecal incontinence. J Neurol Neurosurg Psychiatry 47:820, 1984. 52. Lefaucheur JP: Intrarectal ground electrode improves the reliability of motor evoked potentials recorded in the anal sphincter. Muscle Nerve 32:110, 2005. 53. Blaivas JG, Zayed AA, Labib KB: The bulbocavernosus reflex in urology: A prospective study of 299 patients. J Urol 126:197, 1981. 54. Wester C, FitzGerald MP, Brubaker L, et al: Validation of the clinical bulbocavernosus reflex. Neurourol Urodyn 22:589, 2003. 55. Arunodaya GR, Taly AB: Sympathetic skin response: A decade later. J Neurol Sci 129:81, 1995. 56. Ertekin C, Ertekin N, Mutlu S, et al: Skin potentials (SP) recorded from the extremities and genital regions in normal and impotent subjects. Acta Neurol Scand 76:28, 1987. 57. Rodic B, Curt A, Dietz V, et al: Bladder neck incompetence in patients with spinal cord injury: Significance of sympathetic skin response. J Urol 163:1223, 2000.

Chapter 11

URODYNAMICS H. Henry Lai, Christopher P. Smith, and Timothy B. Boone

The term urodynamics was first coined by Davis1 in 1953 to define the study of the storage and emptying phases of the lower urinary tract. Patients with voiding and storage symptoms cannot be reliably diagnosed by history and physical examination alone.2,3 Urodynamic studies offer objective measurements of bladder and urethral functions and dysfunctions while reproducing the patient’s presenting symptoms. REPRODUCTION OF SYMPTOMS FOR URODYNAMIC EVALUATION The urodynamic armamentarium is extensive, including bedside eyeball urodynamics, noninvasive uroflowmetry, and multichannel fluoroscopic studies (Table 11-1). A “reflex hammer” approach to urodynamic testing is condemned. Before any urodynamic evaluation, the clinician must formulate specific questions about the case, and a working diagnosis must be in place. The most accurate and least invasive study tailored to answer specific questions and to confirm the diagnosis is performed. It is crucial that urodynamic tests reproduce the patient’s presenting symptoms. A study that does not duplicate the patient’s symptoms is not diagnostic.4 For instance, if a patient states that she loses urine only in an upright position, little is gained by a supine cystometrogram.5 Failure to record an abnormality on urodynamic assessment does not rule out its clinical existence.4 Conversely, not all abnormalities detected on urodynamic tests are clinically significant.4 If urodynamic testing reveals information that is totally unexpected, the history and working diagnosis should be re-evaluated. Urodynamic testing should be done in a quiet, private, and orderly suite with as little distraction and as few observers as possible so that patients can relax to replicate their usual voiding habits. Patients must be told what to expect, how the tests are done, and what information the clinician is seeking. For example, in evaluating incontinence, patients need to understand that the goal of the study is to demonstrate leakage characteristic of their experience, so that they do not voluntarily and mistakenly contract the external sphincter to avoid the embarrassment of incontinence and falsely elevate the abdominal leak point pressure (ALPP). In evaluating outlet obstruction, patients are encouraged to void as close to their normal pattern as possible so that they does not strain excessively nor involuntarily tighten the pelvic floor out of anxiety. Accurate interpretation of urodynamic studies is an art. It relies on patient cooperation and open communication between the patient and the clinician during the procedure, allowing urodynamic events to be correlated with the patient’s symptoms in real time.

INDICATIONS, CONTRAINDICATIONS, AND PATIENT PREPARATION Urodynamic assessment is indicated if the diagnosis is uncertain, empirical treatment has failed, or an invasive procedure or surgery is contemplated. Urodynamic testing is deferred during an active urinary tract infection or after recent instrumentation. When possible, patients with a chronically indwelling catheter should be started on intermittent catheterization before the study because bladder sensation, capacity, and compliance may be altered by a chronic Foley catheter. Routine antibiotic prophylaxis is unnecessary unless the patient is at high risk for urinary infection, endocarditis, or prosthetic infection.6 Patients with a history of or at risk for autonomic dysreflexia (i.e., T6 or above spinal cord injury) should be pretreated with oral nifedipine or α-blockers and have their blood pressures monitored during urodynamic studies.7,8 If sweating, headache, flushing, severe hypertension, and reflex bradycardia do not respond to bladder drainage, oral nifedipine or intravenous hydralazine, or both, should be administrated immediately. Pharmacologic agents may alter bladder and sphincter functions. Whether these medications should be stopped before the study depends on the goal of the study. If the goal is to evaluate the response to medications (e.g., response of bladder compliance to anticholinergics), the medications should be taken. If the goal is to uncover the cause of urge symptoms, the medications should be stopped before the study.

Table 11-1 The Urodynamic Armamentarium Phase

Study of Bladder Functions

Storage

Eyeball urodynamics Cystometrogram Video urodynamics

Voiding

Uroflowmetry Pressure-flow study Video urodynamics

Study of Urethral Functions Detrusor leak point pressure Abdominal leak point pressure Resting urethral pressure profilometry Stress urethral pressure profilometry Video urodynamics Uroflowmetry Pressure-flow study Micturitional urethral pressure profilometry Video urodynamics Electromyography

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Urodynamic Evaluation for Stress Urinary Incontinence The indications for urodynamic evaluation of stress urinary incontinence (SUI) are controversial and deserve special consideration. Many investigators argued that patients with classic SUI symptoms and obvious urethral hypermobility without associated irritative symptoms (e.g., urge, urge continence, nocturia), voiding dysfunction (e.g., weak stream, high postvoid residual volume), pelvic organ prolapse, neurologic disease, or history of incontinence surgery or radical pelvic surgery require no invasive urodynamic testing if they choose nonoperative treatments. Urodynamic tests are indicated when empirical therapy is ineffective and surgery is planned; patients complain of a confusing mix of urge and stress incontinence symptoms or significant emptying symptoms; or patients have equivocal urethral hypermobility, large prolapse, neurologic disease, or a history of failed incontinence surgery or pelvic surgery. Classically, preoperative urodynamic assessments help to define the exact cause of incontinence and therefore guide the SUI surgical approach; evaluate detrusor function (e.g., capacity, instability, poor contractility) and identify patients at risk for voiding dysfunction (i.e., instability, retention) after SUI surgery; predict the impact of prolapse and its correction on storage and voiding functions; and identify urodynamic factors (e.g., high detrusor leak point pressure) that place the upper tract at risk postoperatively.9 In the modern era of minimally invasive pubovaginal and mid-urethral slings, the roles of preoperative urodynamics become more controversial. Although few would argue that additional information could be gleaned from preoperative testing (albeit with a finite risk of urinary infection), it remains unclear whether urodynamics can improve SUI surgical success or alter the surgical approach.10,11 Pubovaginal and mid-urethral slings appear to have reasonable success for any type and severity of SUI.12-15 Patients without preoperative urodynamic evaluation before mid-urethral synthetic slings appear to do as well as those who underwent preoperative urodynamics routinely.16 Nevertheless, urodynamics may identify subpopulation of patients at risk for postoperative failure or voiding complications (e.g., urge, retention).17-19

thral hypermobility, and pelvic organ prolapse are assessed in the lithotomy and upright positions. Pure SUI and stress-induced detrusor instability may be distinguished by the characteristics of the incontinence; the former is associated with a few drops of leakage, and the latter is associated with urge and continuous, uncontrollable voiding after the stress maneuver. Cystometrography A cystometrogram measures the intravesical pressure (Pves) during bladder filling. The bladder is filled physiologically (i.e., diuresis) or through a catheter using room-temperature saline, water, or contrast (for video urodynamic studies [VUDS]). Fluid infusion is preferred over gas (CO2) infusion because the fluid is less irritative to the bladder than CO2, fluid is noncompressible and can detect smaller detrusor contractions than CO2, fluid leakage (i.e., incontinence) can be easily demonstrated, and leak point pressures, pressure-flow studies (PFSs), and anatomic studies can be performed using fluid but not a gaseous medium. Pressure is transmitted through an intravenous line to an external strain gauge transducer, or it is measured directly on a cathetermounted, solid-state microtip transducer or fiberoptic transducer.20 In the single-channel cystometrogram, only Pves is monitored, whereas in the multichannel cystometrogram, the Pves and intraabdominal pressure (Pabd) are measured. A rectal balloon catheter is advanced well past the anal sphincter to measure Pabd to avoid interference with rectal contractions.21 In patients with no anus (e.g., after abdominoperineal resection), Pabd can be monitored inside a colostomy, ileostomy, or vagina. Detrusor pressure (Pdet) is calculated by subtracting intra-abdominal pressure from intravesical pressure (Pdet = Pves − Pabd) (Fig. 11-1). Pdet is a computergenerated number and is subject to error if negative abdominal pressures are recorded. Having both Pves and Pabd monitored simultaneously allows the examiner to differentiate bladder

Normal saline

EVALUATION OF STORAGE FUNCTION Eyeball Urodynamics The so-called bedside eyeball urodynamics is the simplest of all tests. It enables detection of bladder sensation, overactivity, and capacity without sophisticated instruments. It requires only a catheter, filling syringe, normal saline, and careful observation. After voiding, a red rubber catheter is inserted, and the postvoid residual (PVR) volume is measured. A 60-mL syringe (with its barrel removed) is then used to fill the bladder under gravity. Intravesical pressure is estimated by the height of the saline column above the pubic symphysis. Changes in intravesical pressure are detected as slowing of the rate of fall or a rise in the fluid meniscus. Rising intravesical pressure may result from involuntary detrusor contraction (i.e., associated with a sudden urge to void and possibly leakage around the catheter), abdominal straining (i.e., the abdomen can be palpated or inspected to confirm a Valsalva response), or poor bladder compliance. The bladder is filled until the patient is comfortably full. The catheter is removed, and the patient is asked to cough and perform a Valsalva maneuver with increasing abdominal force. Stress incontinence, ure-

Bladder

Vagina

Rectum

Pves

Pabd

Pdet⫽Pves⫺Pabd

Figure 11-1 Intravesical pressure (Pves) and intra-abdominal pressure (Pabd) are measured independently during multichannel cystometrography. Detrusor pressure (Pdet ) is calculated by subtracting Pabd from Pves.

contractions from abdominal straining. This is particularly useful in the evaluation of SUI to differentiate stress-induced detrusor overactivity from genuine SUI during cystometrography; in the evaluation of obstruction to distinguish bladder hypocontraction or straining from high-pressure detrusor contraction during PFSs; and to monitor bladder behavior during leak point pressure determinations and VUDS. The rate of bladder filling (slow: 100 mL/min; physiologic: ≤ body weight [kg]/4 [mL/min]; nonphysiologic) and the size of urethral catheter must be specified. Most patients are filled at medium rate initially. Filling is slowed if poor compliance, neurogenic bladder, decreased capacity, or excessive detrusor overactivity is encountered. Filling is increased during provocative maneuvers. Because large catheters may cause obstruction, smaller catheters (100 mL/min), filling with cold saline, coughing, heel bouncing, squatting, and hand washing may unmask the

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Leakage occurs

40 cm H2O “Danger zone”

Pressure (Pves)

DLPP Pressure (Pdet)

136

ALPP

Valsalva Leakage starts occurs Volume (v)

Figure 11-3 Detrusor leak point pressure (DLPP) measurement in the absence of straining or detrusor contraction. The shaded area represents the “danger zone,” with the DLPP and filling pressure higher than 40 cm H2O.

abnormalities. Up to 40% of patients with urge incontinence fail to demonstrate detrusor overactivity on conventional cystometrography.26 The absence of documented detrusor overactivity on cystometrography does not rule out its existence. Conversely, patients with detrusor overactivity may not have any symptoms, and its documentation on cystometrography may have no clinical significance.27 Even though patients with irritative symptoms and stressinduced detrusor overactivity often improve after bladder neck suspension surgery,28 presumably as a result of eliminating the entrance of urine into the proximal urethra,29 patients with mixed incontinence as a group appear to fare worse than those with pure SUI after tension-free tape surgery (69% versus 97% cure).16 There is no consensus about whether the finding of detrusor overactivity in addition to SUI on preoperative cystometrography alters the outcome after surgery.30 Detrusor Leak Point Pressure A concept first introduced by McGuire and associates31 in 1981 in the evaluation of myelodysplasia patients, detrusor leak point pressure (DLPP) is defined as the lowest detrusor pressure (Pdet) at which leakage occurs in the absence of detrusor contraction or increased abdominal pressure (Fig. 11-3).25 The bladder is filled until overflow incontinence occurs, and the instantaneous Pdet at which leakage occurs (i.e., DLPP) reflects the resistance of the urethra against the expulsive force of bladder storage pressure. When outlet resistance is high, high bladder pressure is needed to overcome this resistance and cause leakage. Bladder pressure higher than 40 cm H2O impedes ureteral peristalsis, causes hydroureters, and damages the upper tracts. In the classic study of McGuire and colleagues,31 81% and 68% of myelodysplasia patients with DLPP greater than 40 cm H2O developed hydronephrosis and vesicoureteral reflux, respectively. In long-term follow-up, 100% of patients with DLPP greater than 40 cm H2O exhibited upper tract deterioration or reflux, or both.32 A DLPP higher than 40 cm H2O is a prognostic marker for upper tract damage.

Volume (v)

Figure 11-4 Abdominal leak point pressure (ALPP) measurement in the presence of straining but without detrusor contraction.

Patients with low bladder compliance and a low DLPP may be floridly incontinent, but their upper tracts are safe because the low-resistance urethra functions as a pop-off mechanism to relieve the high detrusor pressure. Patients with low bladder compliance and a DLPP higher than 40 cm H2O risk upper tract damage unless the outlet resistance is reduced or compliance is improved with medication or surgery. Correction of outlet resistance in patients with detrusor–external sphincter dyssynergia (DESD) by sphincter dilation results in an immediate decrease in DLPP and a gradual but significant improvement of bladder compliance over time.33 Failure to reduce DLPP to below 40 cm H2O after sphincterotomy predicts surgical failure, persistent DESD, and upper tract deterioration.34 The use of intermittent catheterization, anticholinergics, and vesicostomy are effective in protecting the upper tracts of neonates with myelodysplasia.35 Plotting the danger zone on a filling cystometrogram is an effective method to establish a storage baseline for patients with neurogenic dysfunction and subsequently track effective management by reducing the danger zone. Abdominal Leak Point Pressure The idea of ALPP emerged from McGuire’s group a decade after the description of DLPP.36 Originally designed to categorize women with SUI into two groups—urethral hypermobility and intrinsic sphincter deficiency (ISD)—ALPP measurement and Q-tip examination became indispensable tools in the diagnosis of SUI. The International Continence Society defined ALPP as the intravesical pressure (Pves) at which urine leakage occurs due to increased abdominal pressure in the absence of a detrusor contraction.25 The bladder is half-filled to an arbitrary volume of 200 to 250 mL. The patient is then asked to perform a Valsalva maneuver or cough until leakage occurs. If no leakage is observed, the bladder is filled in 50-mL increments. The smallest recorded Pves associated with urodynamic demonstration of SUI is the ALPP (Fig. 11-4). ALPP (leakage) usually occurs on the upward slope of the curve and not at the peak pressure generated unless the peak pressure represents the exact ALPP (i.e., exact moment of incontinence).

Chapter 11 URODYNAMICS

Abdominal Leak Point Pressure versus Detrusor Leak Point Pressure Unlike DLPP, which is a static reflection of urethral resistance to bladder intrinsic storage pressure, ALPP measures the dynamic urethral resistance to brief increases in abdominal pressure. Abdominal pressure (ALPP) and detrusor pressure (DLPP) are different expulsive forces with respect to the urethra. Whereas detrusor pressure tends to open the bladder neck, abdominal pressure tends to close the internal sphincter shut. Normally, the internal sphincter does not leak or open, regardless of how much abdominal pressure is exerted. For instance, during blunt trauma to a full bladder, the bladder will rupture before the bladder neck is forced open. If SUI occurs as a result of an increase in abdominal pressure, the proximal urethra and bladder neck are rotated and descended away from its resting intra-abdominal position during a Valsalva maneuver (i.e., urethral hypermobility), or there is an intrinsic malfunction of the internal urethral sphincter (i.e., ISD).37 All women with urethral hypermobility and SUI are considered to have some degree of ISD, because the normal internal sphincter should remain closed no matter how much stress and rotational descent it experiences.23 ISD is a spectrum of urethral dysfunction. Abdominal Leak Point Pressure, Urethral Hypermobility, and Internal Urethral Sphincter SUI patients with urethral hypermobility leak at considerably higher abdominal pressures than those with pure ISD. Leakage at an ALPP less than 60 cm H2O is characteristic of ISD. Eightyone percent of patients with an ALPP less than 60 cm H2O reported a history of severe incontinence, and 76% of patients with an ALPP less than 60 cm H2O demonstrated type III SUI on fluoroscopic studies (i.e., no urethral hypermobility). Leakage at an ALPP greater than 90 cm H2O is indicative of urethral hypermobility. These patients reported lesser degrees of incontinence and exhibited type I or type II SUI on VUDS (i.e., minimal to gross hypermobility).36 Patients with an ALPP between 60 and 90 cm H2O have type II or type III SUI. Patients with an ALPP less than 60 cm H2O classically failed to respond to suspension operations designed for the hypermobile urethra. They should be treated with pubovaginal slings, periurethral bulking agents (if there is no associated hypermobility), or artificial sphincters. Subdividing patients into hypermobility or ISD groups based on ALPP measurement and Q-tip test results on physical examination may become less important because pubovaginal slings and mid-urethral slings have been shown to be effective for anatomic incontinence.12-15 Abdominal Leak Point Pressure and Pelvic Organ Prolapse ALPP measurements are more difficult to interpret in the presence of pelvic organ prolapse. Anterior vaginal wall prolapse may falsely elevate the ALPP because the prolapse functions as a sink to dissipate and absorb the effect of abdominal pressure on the proximal urethra.38 The urethra may be kinked or compressed by the prolapsed organ, causing partial obstruction and elevating the ALPP. This is why patients with high-grade cystoceles rarely complain of clinical SUI. When the prolapse is reduced, up to 60% of patients with grade 1 to 2 cystocele and 91% of patients with grade 3 to 4 cystocele who do not complain of incontinence demonstrate SUI on urodynamic evaluations.39 If the cystocele is repaired without addressing the urethra, occult stress incontinence may be unmasked postoperatively. It is unclear what per-

centage of patients with no symptoms of SUI will be symptomatic after a prolapse repair. It is also unclear whether performing ALPP with a pessary helps to predict that population. Whether prophylactic sling should be placed at the time of concomitant prolapse surgery and what roles preoperative ALPP plays in that decision remain controversial. Nevertheless, all patients undergoing ALPP measurements should have a pelvic examination in supine and upright positions to determine whether prolapse exists. If significant prolapse is found, upright ALPP measurements should be repeated with the prolapse reduced.40 Abdominal Leak Point Pressure Measurement The technique for ALPP determination has not been standardized. ALPP decreases significantly as the bladder volume increases.41 There is no consensus about whether ALPP should be measured at an absolute volume (e.g., 150 mL),36 one-half the functional bladder capacity,42 or near capacity.43 Most expects agree that testing should be done at a “moderate filling volume” that is sufficient to provide a urine bolus for abdominal pressure to act on but not full enough to induce a detrusor contraction, which opens the bladder neck and gives a false impression of ISD.38 Cough leak point pressure is significantly higher and more variable than Valsalva leak point pressure,44 possibly due to reflex contraction of the pelvic floor during cough.45 The size and necessity of bladder catheters have not been standardized. Larger catheters correlate with higher ALPP values, presumably due to partial obstruction.45 Patients with a history of SUI who do not leak with a urethral catheter in place should have ALPP measurements repeated with the catheter removed.46 Some investigators recommended measuring ALPP using a rectal catheter alone to measure Pabd.46,47 Others argued that Pdet should be monitored to ensure that that the detrusor is stable during a Valsalva maneuver. It is unclear whether the absolute pressure value48 or the subtracted pressure value from baseline pressure49 should be used. It is recommended that the location of pressure sensors, type of catheters, position of patient, status of prolapse (reduced or not), methods in which the bladder is filled (e.g., diuresis, catheter fill), types of ALPP (e.g., cough, Valsalva maneuver), and volume at which measurements are made should be specified. ALPP measurement is inaccurate if the patient cannot generate adequate abdominal pressure. Resting Urethral Pressure Profilometry Urethral pressure profilometry (UPP) is a topographic curve that plots the urethral closure pressure (UCP) along the length of the urethra. Intravesical pressure (Pves) and intraluminal urethral pressure (Pure) are measured simultaneously while a mechanical puller withdraws the pressure transducer from the urethra at a set rate (1 to 2 mm/sec). The difference between these two pressures is defined as UCP (UCP = Pure − Pves), and it is plotted on the y-axis. The urethral length is plotted on the x-axis. UPP attempts to quantify the contributions of urinary sphincters and periurethral structures to urethral closure at rest (i.e., resting UPP), during periods of straining (i.e., stress UPP), and during voiding (i.e., micturitional UPP). Resting UPP measures the static urethral pressure along its length in a resting patient with a full bladder (i.e., no Valsalva maneuver and no voiding). It is measured using the technique of Brown and Wickham.50 A urethral catheter with radially drilled side holes is slowly withdrawn from the urethra while being

137

138

Section 2 EVALUATION AND DIAGNOSIS

UCP

Normal saline

Point of maximal Pure

MUCP

Pves

Catheter is withdrawn Side-hole measures Pure

End-hole measures Pves

0 Bladder neck

Percent urethral length

100 Meatus

UCP ⫽ Pure ⫺ Pves

Figure 11-5 Schematic diagram of the resting urethral pressure profile (UPP) shows the calculated urethral closure pressure (UCP), which is equal to the urethral pressure minus the intravesical pressure (Pure − Pves) along the length of the urethra.

infused. The intraluminal urethral pressure that is recorded corresponds to the pressure needed to lift the urethral wall off the catheter side holes, and it is presumed that this reflects the radial stress at the urethral surface.51 The intravesical pressure is simultaneously measured with the end holes of the same catheter. The maximal urethral closure pressure (MUCP), the highest point along the UCP curve, corresponds anatomically to the area of mid-urethra where the striated and smooth muscle sphincters overlap (Fig. 11-5). Resting UPP has no role in the evaluation of the patient with SUI.52,53 MUCP lacks the sensitivity and specificity to diagnose and classify incontinence.54 MUCP cannot be used to distinguish continent from incontinent patients. A low MUCP (30 days) after radical hysterectomy is associated with worse long-term PVR and total bladder capacity. Fortunately, this voiding dysfunction becomes permanent in less than 5% of patients. 30 In a prospective study of 18 patients who underwent modified radical hysterectomy (involving restricted dissection of the anterior parts of the cardinal ligament and preservation of the posterior cardinal ligament), Chuang and coworkers31 demonstrated only temporary (1 month); one required urethrolysis. Enterocele Repair and Voiding Dysfunction Enterocele was consistently found to be associated with reduced maximum and average uroflow rate centiles.70. Winters and colleagues71 reported the outcomes for 20 women between 45 and 82 years old (mean age, 67.9 years) with complex pelvic floor prolapse (all patients had cystocele, enterocele, and vaginal vault

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Section 3 PATHOPHYSIOLOGY OF VOIDING DYSFUNCTION

prolapse) managed by abdominal sacral colpopexy and abdominal enterocele repair. Three patients developed SUI postoperatively, two despite having a Burch suspension and one after a pubovaginal sling. Two patients were successfully managed by collagen injection. No complications involving the mesh have been encountered. Sacrospinous Ligament Fixation and Voiding Dysfunction Cespedes72 reported outcomes of treating total vault prolapse using bilateral sacrospinous ligament fixation through an anterior vaginal approach in 28 patients. All patients had grade 3 or 4 vault prolapse, and all patients had associated enteroceles, cystoceles, and rectoceles. At a mean follow-up of 17 months (range, 5 to 35 months), SUI had been cured in all patients; however, two patients continued to have mild urge incontinence requiring less than 1 pad per day. One patient had elevated PVR volumes requiring intermittent catheterization for 2 months. Orthotopic Neobladders and Voiding Function In a multicenter study of orthotopic neobladders, Carrion and coworkers73 did not show any difference in outcomes after ileal neobladder versus colonic neobladder. Even a moderate degree of nocturnal incontinence is a significant problem for these patients. The incidences of diurnal incontinence, nocturnal incontinence, and intermittent catheterization were 7%, 31%, and 14% of patients undergoing ileal neobladder, respectively. The corresponding figures for those that underwent colonic neobladder are 12%, 30%, and 11%, respectively. Fujisawa and colleagues74 have shown that the location of the neobladder and avoidance of angulation (>90 degrees) of the

outlet are important for obtaining normal voiding after neobladder reconstruction in women. These investigators showed that intrareservoir pressure is less critical for normal voiding function. Although an increased intrareservoir pressure (contributed mostly by abdominal straining) was associated with increased frequency, it did not correlate with the peak urinary flow rate (Table 15-2). CONCLUSIONS Female bladder outlet obstruction after pelvic surgery is a multifaceted topic because of the lack of defined criteria for the evaluation. The long-term outcome is often not as good as expected. Short-term and long-term bladder dysfunction remains a common side effect after radical hysterectomy, with bladder atony reported in as many as 42% of patients. Bladder outlet obstruction can occur after a Marshall-Marchetti-Krantz procedure, Burch colposuspension, and pubovaginal sling procedure. Although the vaginal TVT is placed without tension at the midurethra, studies have shown that it may still be associated with voiding dysfunction in 4.9% to 10% of patients. Urethral erosion may occasionally manifest with obstructive or irritative voiding symptoms. Most patients with advanced pelvic organ prolapse and elevated PVR volumes had normalization of PVR volumes after surgical correction of the pelvic organ prolapse. De novo urge incontinence occurs in 11% of patients after high-grade cystocele repair. Postoperative urinary retention after sacrospinous ligament fixation is less affected by the vault suspension than by the preoperative and postoperative management and

Table 15-2 Incidence of Voiding Dysfunction after Pelvic Surgery Type of Surgery

Incidence of Voiding Dysfunction (%)

Study

Radical hysterectomy Hysterectomy for benign causes

42 0.1 (abdominal) 0.05 (vaginal) 2.5-24

Artman et al27 Diels et al32

Slings for urinary incontinence

Marshall-Marchetti-Krantz colposuspension Burch colposuspension

5-20 4-7 21.4

Tension-free vaginal tape (TVT)

4.9-10

Anterior plus posterior compartment pelvic organ prolapse repair Cystocele repair

16* 4.7† 11.7‡ 7 (diurnal incontinence) 31 (nocturnal incontinence) 14 (clean catheterization) 12 (diurnal incontinence) 30 (nocturnal incontinence) 11 (clean catheterization)

Ileal neobladder

Colonic neobladder

*Incidence of persistent urge incontinence. † Incidence of urinary retention. ‡ Incidence of de novo urge incontinence.

Dorflinger et al40 Morgan et al53 Chaiken et al55 Klutke et al55 Zimmern et al46 Akpinalr et al47 Ward et al48 Bombieri et al59 Dorflinger et al51 Karram et al52 Milani et al64 Leboeuf et al68 Carrion et al73

Carrion et al73

Chapter 15 VOIDING DYSFUNCTION AFTER PELVIC SURGERY

concurrent pelvic surgical procedures (e.g., cystocele repair). Postoperative stress incontinence may occur in 10% of patients when the bladder neck and urethra are not adequately supported. Guidelines on postoperative outcome measures offer a more effective way to manage this problem. Quality-of-life scores,

including the 7-item Incontinence Impact Questionnaire (IIQ7), 6-item Urogenital Distress Inventory (UDI-6), and American Urological Association (AUA) symptom scores may be used to gain more information on the quality-of-life changes that may be induced with management of bladder outlet obstruction in these patients.

References 1. Gosling J: The structure of the bladder and urethra in relation to function. Urol Clin North Am 6:31-38, 1979. 2. American College of Obstetricians and Gynecologists: Chronic pelvic pain. ACOG technical bulletin no. 223. Int J Gynecol Obstet 54:59-68, 1996. 3. Havenga K, DeRuiter MC, Enker WE, Welvaart K: Anatomical basis of autonomic nerve-preserving total mesorectal excision for rectal cancer. Br J Surg 83:384-388, 1996. 4. Woodside JR, Crawford ED: Urodynamic features of pelvic plexus injury. J Urol 124:657-658, 1980. 5. Blaivas JG, Barbalias GA: Characteristics of neural injury after abdomino-perineal resection. J Urol 129:84-87, 1983. 6. Pavlkis AJ: Cauda equine and pelvic plexus injury. In Krane RJ, Siroky ME (eds): Clinical Neuro-Urology, 2nd ed. Boston, Little, Brown, 1991, pp 333-344. 7. Gomelsky A, Nitti VW, Dmochowski RR: Management of obstructive voiding dysfunction after incontinence surgery: Lessons learned. Urology 62:391-399, 2003. 8. Harrison SC, Hunnam GR, Farman P, et al: Bladder instability and denervation in patients with bladder outflow obstruction. Br J Urol 60:519-522, 1987. 9. Speakman MJ, Brading AF, Guilpin CJ, et al: Bladder outflow obstruction: A cause of denervation supersensitivity. J Urol 138:14611466, 1987. 10. Cardozo LD, Stanton SL, Williams JE: Detrusor instability following surgery for genuine stress incontinence. Br J Urol 51:204-207, 1979. 11. Miller EA, Amundsen CL, Toh KL, et al: Preoperative urodynamic evaluation may predict voiding dysfunction in women undergoing pubovaginal sling. J Urol 169:2234-2237, 2003. 12. Mutone N, Brizendine E, Hale D: Factors that influence voiding function after the tension-free vaginal tape procedure for stress urinary incontinence. Am J Obstet Gynecol 188:1477-1481, 2003. 13. Wang AC, Chen MC: Comparison of tension-free vaginal taping versus modified Burch colposuspension on urethral obstruction: A randomized controlled trial. Neurourol Urodyn 22:185-190, 2003. 14. Iglesia CB, Shott S, Fenner DE, et al: Effect of preoperative voiding mechanism on success rate of autologous rectus fascia suburethral sling procedure. Obstet Gynecol 91:577-581, 1998. 15. Sze EH, Miklos JR, Karram MM: Voiding after Burch colposuspension and effects of concomitant pelvic surgery: Correlation with preoperative voiding mechanism. Obstet Gynecol 88:564-567, 1996. 16. McLennan MT, Melick CF, Bent AE: Clinical and urodynamic predictors of delayed voiding after fascia lata suburethral sling. Obstet Gynecol 92:608-612, 1998. 17. Vasavada SP: Evaluation and management of postoperative bladder outlet obstruction in women. Issues Incontinence Fall:1, 5-7, 2002. 18. Petrou SP, Nitti VW: Urethrolysis. Lession 22. AUA Update Series 20:169-176, 2001. 19. McGuire EJ, Letson W, Wang S: Transvaginal urethrolysis after obstructive urethral suspension procedures. J Urol 142:1037-1039, 1989. 20. Nitti VW, Raz S: Obstruction following anti-incontinence procedures: Diagnosis and treatment with transvaginal urethrolysis. J Urol 152:93-98, 1994.

21. Cross CA, Cespedes RD, English SF, et al: Transvaginal urethrolysis for urethral obstruction after anti-incontinence surgery. J Urol 159:1199-1201, 1998. 22. Chassagne S, Bernier PA, Haab F, et al: Proposed cutoff values to determine bladder outlet obstruction in females. Urology 51:408411, 1998. 23. Blaivas JG, Groutz A: Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn 19:553-564, 2000. 24. Nitti VW, Tu LM, Gitlin J: Diagnosing bladder outlet obstruction in women. J Urol 161:1535-1540, 1999. 25. Klutke C, Siegel S, Carlin B, et al: Urinary retention after tensionfree vaginal tape procedure: Incidence and treatment. Urology 58:697-701, 2001. 26. Abouassally R, Steinberg JR, Corcos J: Complications of tension-free vaginal tape surgery: A multi-institutional review of 242 cases [abstract 416]. J Urol 167(Suppl):104, 2002. 27. Artman LE, Hoskins WJ, Bibro MC, et al: Radical hysterectomy and pelvic lymphadenectomy for stage 1B carcinoma of the cervix: 21 year experience. Gynecol Oncol 28:8-13, 1987. 28. Mundy AR: An anatomical explanation for bladder dysfunction following rectal and uterine surgery. Br J Urol 54:501-504, 1982. 29. Buchsbaum HJ, Plaxe SC: The urinary tract and radical hysterectomy. In Buchsbaum HJ, Schmidt JD (eds): Gynecologic and Obstetric Urology. Philadelphia, WB Saunders, 1993. 30. Bandy LC, Clarke-Pearson DL, Soper JT, et al: Long-term effects on bladder function following radical hysterectomy with and without postoperative radiation. Gynecol Oncol 26:160-168, 1987. 31. Chuang TY, Yu KJ, Penn IW, et al: Neurourological changes before and after radical hysterectomy in patients with cervical cancer. Acta Obstet Gynecol Scand 82:954-959, 2003. 32. Diels J, Cluyse L, Gaussin C, Mertens R: Hysterectomy in Belgium. Thematic files. Leuven, Christelijk Ziekenfonds, 1999. 33. Weber AM, Walters MD, Schover LR, et al: Functional outcomes and satisfaction after abdominal hysterectomy. Am J Obstet Gynecol 181:530-535, 1999. 34. Roovers JP, van der Brom JG, Huub van der Vaart C, et al: Does mode of hysterectomy influence micturition and defecation? Acta Obstet Gynecol Scand 80:945-951, 2001. 35. Everaert K, De Muynck M, Rimbaut S, Weyers S: Urinary retention after hysterectomy benign disease: Extended diagnostic evaluation and treatment with sacral nerve stimulation. BJU Int 91:497-501, 2003. 36. Wyndaele JJ: Is abnormal electrosensitivity in the lower urinary tract a sign of neuropathy? Br J Urol 72:575-579, 1993. 37. Long C, Hsu SC, Wu TP, et al: Effect of laparoscopic hysterectomy on bladder neck and urinary symptoms. Aust N Z J Obstet Gynaecol 43:65-69, 2004. 38. Long CY, Jang MY, Chen SC, et al: Changes in vesicourethral function following laparoscopic hysterectomy versus abdominal hysterectomy. Aust N Z J Obstet Gynaecol 42:259-263, 2002. 39. Virtanen H, Makinen J, Tenho T, et al: Effects of abdominal hysterectomy on urinary and sexual symptoms. Br J Urol 72:868-872, 1993. 40. Dorflinger A, Monga A: Voiding dysfunction. Curr Opin Obstet Gynecol 13:507-512, 2001. 41. Wang AC: Burch colposuspension vs. Stamey bladder neck suspension: A comparison of complications with special emphasis on

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42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58.

59.

detrusor instability and voiding dysfunction. J Reprod Med 41:529533, 1996. Gomelsky A, Nitti VW, Dmochowski RR: Management of obstructive voiding dysfunction after incontinence surgery: Lessons learned. Urology 62:391-399, 2003. Mundy AR: A trial comparing the Stamey bladder neck suspension with colposuspension for the treatment of stress incontinence. Br J Urol 55:687-690, 1983. Juma S, Sdrales L: Etiology of urinary retention after bladder neck suspension [abstract]. J Urol 149:400A, 1993. Carr LK, Webster GD: Voiding dysfunction following incontinence surgery: Diagnosis and treatment with retropubic or vaginal urethrolysis. J Urol 157:821-823, 1997. Zimmern PE, Hadley HR, Leach GE, Raz S: Female urethral obstruction after Marshall-Marchetti-Krantz operation. J Urol 138:517-520, 1987. Akpinalr H, Cetinel B, Demirkesen O: Long-term results in Burch colposuspension. Int J Urol 7:119-125, 2000. Ward KL, Hilton P, Browning J: A randomized trial of colposuspension and tension free vaginal tape for primary stress incontinence. Neurourol Urodyn 19:386-388, 2000. Holschneider CH, Solh S, Lebhertz TB, Montz FJ: The modified Pereyra procedure in recurrent stress urinary incontinence: A 15 year review. Obstet Gynecol 83:573-578, 1994. Horbach NS: Suburethral sling procedures. In Ostergard D, Bent AE (eds): Urogynecology and Urodynamics Theory and Practice, 3rd ed. Baltimore, Williams & Wilkins, 1991, pp 413-421. Dorflinger A, Monga A: Voiding dysfunction. Curr Opinion Obstet Gynecol 13:507-512, 2001. Karram MM, Segal JL, Vassallo BJ, Kleeman SD: Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 101:929-932, 2003. Morgan TO, Westney OL, McGuire EJ: Pubovaginal sling: 4-year outcome analysis and quality of life assessment. J Urol 163:16451648, 2000. Chaiken DC, Rosenthal J, Blaivas JG: Pubovaginal fascial sling for all types of stress urinary incontinence: Long-term analysis. J Urol 160:1312-1316, 1998. Klutke C, Siegel S, Carlin B, et al: Urinary retention after tensionfree vaginal tape procedure: Incidence and treatment. Urology 58:697-701, 2001. Kobashi KC, Dmochowski R, Mee SL, et al: Erosion of woven polyester pubovaginal sling. J Urol 162:2070-2072, 1999. Leng WW, Davies BJ, Tarin T, et al: Delayed treatment of bladder outlet obstruction after sling surgery: Association with irreversible bladder dysfunction. J Urol 172(Pt 1):1379-1381, 2004. Wang AC: Burch colposuspension vs. Stamey bladder neck suspension. A comparison of complications with special emphasis on detrusor overactivity and voiding dysfunction. J Reprod Med 41:529533, 1996. Bombieri L, Freeman RM, Perkins EP, et al: Why do women have voiding dysfunction and de novo detrusor instability after colposuspension? Br J Obstet Gynaecol 109:402-412, 2002.

60. Bump RC, Fantl JA, Hurt WG: Dynamic urethral pressure profilometry. Pressure transmission ratio determinations after continence surgery: Understanding the mechanism of success, failure and complications. Obstet Gynecol 72:870-874, 1988. 61. Hudson CN: Female genital prolapse and pelvic floor deficiency. Int J Colorectal Dis 3:181-185, 1988. 62. Roovers JPWR, van der Vaart CH, van der Bom JG, et al: A randomised controlled trial comparing abdominal and vaginal prolapse surgery: effects on urogenital function. BJOG 111:50-56, 2004. 63. Rosenzweig BA, Pushkin S, Blumenfeld D, Bhatia NN: Prevalence of abnormal urodynamic test results in continent women with severe genitourinary prolapse. Obstet Gynecol 79:539-542, 1992. 64. Milani R, Salvatore S, Soligo M, et al: Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with prolene mesh. BJOG 111:1-5, 2004. 65. Theofrastous JP, Addison WA, Timmons MC: Voiding function following prolapse surgery. Impact of estrogen replacement. J Reprod Med 41:881-884, 1996. 66. FitzGerald MP, Kulkarni N, Fenner D: Postoperative resolution of urinary retention in patients with advanced pelvic organ prolapse. Am J Obstet Gynecol 183:1361-1364, 2000. 67. Safir MH, Gousse AE, Rovner ES, et al: 4-Defect repair of grade 4 cystocele. J Urol 161:587-594, 1999. 68. Leboeuf L, Miles RA, Kim SS, Gousse AE: Grade 4 cystocele repair using four-defect repair and porcine xenograft acellular matrix (Pelvicol): Outcome measures using SEAPI. Urology 64:282-286, 2004. 69. Frederick RW, Leach GE: Cadaveric prolapse repair with sling: Intermediate outcomes with 6 months to 5 years of follow-up. J Urol 173:1229-1233, 2005. 70. Dietz HP, Haylen BT, Vancaillie TG: Female pelvic organ prolapse and voiding function. Int Urogynecol J 13:284-288, 2002. 71. Winters JC, Cespedes RD, Vanlangendonck R: Abdominal sacral colpopexy and abdominal enterocele repair in the management of vaginal vault prolapse. Urology 56:55-63, 2000. 72. Cespedes RD: Anterior approach bilateral sacrospinous ligament fixation for vaginal vault prolapse. Urology 56:70-75, 2000. 73. Carrion R, Arap S, Corcione G, et al, for the Confederation of American Urology: A multi-institutional study of orthotopic neobladders: Functional results in men and women. BJU Int 93:803-806, 2004. 74. Fujisawa M, Isotani S, Gotoh A, et al: Voiding dysfunction of sigmoid neobladder in women: a comparative study with men. Eur Urol 40:191-195, 2001. 75. Petrou SP, Broderick GA: Valsalva leak point pressure changes after successful suburethral sling. Int Urogynecol J Pelvic Floor Dysfuct 13:299-302, 2002. 76. Foster HE, McGuire EJ: Management of urethral obstruction with transvaginal urethrolysis. J Urol 150(5 pt 1):1448-1451, 1993. 77. Goldman HB, Rackley PR, Appell RA: The efficacy of urethrolysis without resuspension for iatrogenic urethral obstruction. J Urol 161(1):196-198; discussion 198-199, 1999.

Chapter 16

IDIOPATHIC URINARY RETENTION IN THE FEMALE Priya Padmanabhan and Nirit Rosenblum

Urinary retention describes the inability to void voluntarily with a bladder volume exceeding the expected bladder capacity. More attention has been placed on male urinary retention caused by benign prostatic hypertrophy than urinary retention in women. Causes of incomplete bladder emptying in women are as variable and numerous as in men, but the presumed infrequency and difficulty in diagnosis accounts for less focus on them.1 The largest body of medical literature on causes of female urinary retention, even in the past decade, assumes a psychogenic or hysterical basis to the problem.2 The exact incidence of female urinary retention is unknown, but proper workup ensures that psychogenic retention is a diagnosis of exclusion and not an assumption. Excellent reviews of causes, workup, and management of urinary retention in females were published by Nitti and Raz1 and Smith and coworkers.3 Classically cited causes of urinary retention include neurologic, pharmacologic, anatomic, myopathic, functional, and psychogenic origins. There are no quantitative definitions for bladder volumes associated with urinary retention. Instead, it is the effects of the urinary retention on the female patient that is of clinical concern. Diagnosis and management are not directed at addressing a specific volume or postvoid residual (PVR) volume; instead, the focus is on treating the effects of urinary retention. The symptomatic female patient may present with abdominal discomfort, irritative voiding symptoms, recurrent urinary tract infections, and incontinence and may eventually suffer from the sequelae of long-term retention, upper tract deterioration. Instead of describing all of the causes of urinary retention in women, we focus on the area of idiopathic urinary retention, a group of causes that was previously gathered under the term psychogenic retention. The following sections provide an overview of common causes of urinary retention, discuss the history and basis of idiopathic retention, and describe the diagnostic tools and treatment options for the management of pseudomyotonia, a term coined by Fowler in 1986.

ETIOLOGY AND PATHOPHYSIOLOGY OF URINARY RETENTION Reviews have classified urinary retention as transient or established (i.e., requiring a more comprehensive workup). Transient causes include immobility (especially postoperative), constipation or fecal impaction, medications, urinary tract infections, delirium, endocrine abnormalities, and psychological problems. After the underlying cause is treated or the offending agent is removed, there is usually a return to normal voiding.1,3 Common causes of established urinary retention are listed in Box 16-1.

Neurogenic Causes Disruption in neural pathways and non-neurogenic causes can cause bladder outlet obstruction and decreased bladder contractility, leading to urinary retention. Normal voiding requires the coordinated contraction by the detrusor of adequate magnitude and concomitant lowering of resistance at the smooth and striated sphincters, with an absence of obstruction.4 The pontine micturition center controls voiding by stimulating parasympathetic fibers at S2 to S4, causing a detrusor contraction and inhibiting sympathetic fibers (T11 to L2) and somatic fibers of the pudendal nerve (S2 to S4). This causes relaxation of the bladder neck and proximal urethra and the external urethral sphincter, respectively.3 Detrusor–external sphincter dyssynergia (DESD) is a neurogenic cause of bladder outlet obstruction resulting from a suprasacral spinal cord lesion. DESD is associated with myelitis, spinal cord injury (i.e., upper motor neuron), and multiple sclerosis. Video urodynamics studies (VUDS) demonstrate detrusor hyperreflexia, high detrusor pressures, an increase in external sphincter activity, and small voided volumes. The ideal treatment for DESD is anticholinergics with clean intermittent catheterization (CIC).1,5 Multiple sclerosis is a focal demyelinating disease with a predilection for women between the ages of 20 and 50 years. Multiple sclerosis is associated with upper motor neuron and lower motor neuron lesions and therefore causes bladder outlet obstruction and decreased bladder contractility. Between 50% and 90% of patients with multiple sclerosis complain of voiding symptoms, usually urinary retention.6 Detrusor hyperreflexia is the most common findings on VUDS, with areflexia identified in up to 40% and DESD in up to 66%.7 The most important factors predisposing a multiple sclerosis patient to complications are high detrusor filling pressure (>40 cm H2O) and an indwelling Foley catheter.8 Management includes anticholinergics with or without CIC and behavioral therapy.9 Cauda equina syndrome is caused by distal spinal cord injury, intervertebral disk protrusion, myelodysplasia, neoplasms, and vascular malformations, leading to decreased bladder contractility. It is associated with a complex of lower back pain, sciatica, saddle anesthesia, lower extremity weakness, sexual dysfunction, and bowel or bladder dysfunction. Urinary retention and straining are the most common urologic presentation. Diagnosis is made by computed tomography, magnetic resonance imaging (MRI), or myelography.1,3 VUDS indicate an areflexic bladder, variable detrusor pressures, and sphincter denervation on electromyography.10 The extent of sensory deficit in the perineal or saddle area is the most significant negative predictor of bladder function recovery.11 Recovery of bladder function occurs 187

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Box 16-1 Causes of Urinary Retention in Females I.

Neurogenic causes A. Obstruction 1. Detrusor-sphincter dyssynergia a. Suprasacral spinal cord injury b. Myelitis c. Multiple sclerosis 2. Parkinson’s disease B. Decreased bladder contractility 1. Lower motor neuron lesion a. Cauda equina injury (e.g., distal spinal cord, intervertebral disk protrusion, myelodysplasia, primary and metastatic neoplasms, vascular malformations) b. Pelvic plexus injury c. Peripheral neuropathy (e.g., diabetes mellitus, pernicious anemia, alcoholic neuropathy, tabes dorsalis, herpes zoster, Guilland-Barré syndrome, Shy-Drager syndrome) 2. Multiple sclerosis II. Non-neurogenic causes A. Obstruction 1. Anatomic causes a. Primary bladder neck obstruction b. Inflammatory processes (e.g., bladder neck fibrosis, urethral stricture, meatal stenosis, urethral caruncle, Skene’s gland cyst or abscess, urethral diverticulum) c. Pelvic prolapse d. Neoplasm (e.g., urethral carcinoma) e. Gynecologic, extrinsic compression (e.g., retroverted uterus, vaginal carcinoma, cervical carcinoma, ovarian mass) f. Iatrogenic obstruction (e.g., anti-incontinence procedures, multiple urethral dilations, urethral excision or reconstruction) g. Miscellaneous causes (e.g., urethral valves, ectopic ureterocele, bladder calculi, atrophic vaginitis, reconstruction) 2. Functional causes a. Dysfunctional voiding b. External sphincter spasticity B. Decreased bladder contractility 1. Hypotonia or atony a. Chronic obstruction b. Radiation cystitis c. Tuberculosis 2. Detrusor hyperactivity with impaired contractility 3. Psychogenic retention 4. Infrequent voider’s syndrome III. Idiopathic causes (e.g., Fowler’s syndrome)

over 3 to 4 years in 25% of patients with prompt surgical intervention.3 Pelvic plexus injury is most common during abdominoperineal resection, radical hysterectomy, proctocolectomy, and low anterior resection after injury or malignant extension to pelvic, hypogastric, and pudendal nerves. Findings of VUDS are similar

to those for cauda equina syndrome. Urinary retention usually resolves within months, with one third of patients having permanent voiding dysfunction. Urodynamically, permanent voiding dysfunction is characterized by fixed, residual, striated sphincter tone and an open, nonfunctional smooth sphincter. CIC is the management of choice until normal voiding returns.1,12 Multiple infectious, endocrine, and nutritional abnormalities cause peripheral neuropathy and decreased bladder contractility, leading to urinary retention. The classic example is diabetic cystopathy, but others include pernicious anemia, alcoholic neuropathy, tabes dorsalis, herpes zoster infection, Guillain-Barré syndrome, and Shy-Drager syndrome. Diabetic cystopathy often has insidious loss or impairment of bladder sensation, with progressive increase in bladder volumes and hypocontractility.13-16 Management combines behavioral modification (e.g., timed voiding, Credé voiding) and CIC to facilitate emptying.1 Non-neurogenic Causes There are many non-neurogenic causes of bladder outlet obstruction and decreased bladder contractility that lead to urinary retention in the female patient (see Box 16-1). Most obstruction is classified as anatomic and functional. Anatomic obstruction includes primary bladder neck obstruction, inflammatory processes, prolapse, neoplasm, gynecologic, iatrogenic, and other causes. Functional obstruction is usually described in terms of dysfunctional voiding and external sphincter spasticity. Primary bladder neck obstruction was introduced in 1933 by Marion17 as a diagnosis of exclusion. Typically, these women present with irritative voiding symptoms and are given a trial of anticholinergics or antispasmodics; the course is eventual progression to periodic urinary retention or high PVR urine volumes. The exact cause is unknown, but the advent of video urodynamic testing has made diagnosis more accurate. The hallmark of primary bladder neck obstruction is incomplete opening or funneling of the bladder neck in the setting of sustained detrusor contraction of normal or high amplitude. There is resultant poor or nonexistent flow but a synergic external urethral sphincter. Management is medical and surgical. Terazosin has been used with improvement in flow rate and reduction of PVR volumes. Surgical options include transurethral incision of the bladder neck and Y-V-plasty of the bladder neck. Care is taken to avoid injury to the external sphincter, which can lead to stress urinary incontinence.1,3,18-20 Inflammatory processes, such as bladder neck fibrosis, urethral stricture, meatal stenosis, urethral caruncle, Skene’s gland cyst or abscess, and urethral diverticulum, are associated with anatomic obstruction. Management usually involves treatment of the offending infection and surgical excision of obstructing lesions. Patients with pelvic prolapse (e.g., uterine, cystocele, enterocele, rectocele) usually present with incomplete emptying, lower urinary tract symptoms, and recurrent urinary tract infections with or without stress urinary incontinence. They may describe positional changes or the need to reduce the prolapse to void. Bladder outlet obstruction is caused by kinking or compression of the urethra during voiding. VUDS are useful in making the diagnosis. After the initial diagnosis, a pessary or packing should be used to reduce the prolapse and confirm the diagnosis. This helps predict the outcome of prolapse repair. Treatment of symptomatic prolapse is usually surgical.1,21 In cases of significant morbidity or age, a pessary alone may be used.

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There are multiple neoplastic, obstetric, and gynecologic causes of bladder outlet obstruction in women. Urethral carcinoma is the only urologic malignancy more frequent in women (0.2%), although it remains rare. Patients present with bleeding and develop irritative and obstructive symptoms. Treatment ranges from local excision to anterior exenteration with complementary radiation therapy.22 Gynecologic neoplasms and masses usually cause urinary retention by external compression or direct invasion. A retroverted, impacted uterus that occurs in the first trimester of pregnancy is associated with urinary retention. Gravid females are usually managed with manual dislodging of the uterus or a pessary until voiding resumes.1 The most common iatrogenic cause of urinary retention is surgical correction of stress urinary incontinence. The published incidence ranges from 2.5% to 24%, which may be underestimated. The irritative or obstructive voiding symptoms and recurrent urinary tract infections that result may be overlooked if the patient demonstrates normal emptying. The placement of sutures is the key factor determining a procedure’s likelihood of causing obstruction. For example, sutures placed too medially cause urethral deviation or periurethral scarring; those placed too distally can cause kinking, leading to stress urinary incontinence; and tying sutures too tightly leads to hypersuspension, closing the bladder neck.1 Newer mid-urethral slings can cause bladder outlet obstruction if the urethra is injured or the tape is placed under tension. The diagnosis is made by a patient’s history before the procedure, physical examination, VUDS, endoscopy, and imaging. Urethrolysis is the treatment of choice. However, several studies have not correlated urodynamics and successful voiding after urethrolysis.23-25 Other iatrogenic causes of bladder outlet obstruction include a history of recurrent urethral dilation and postoperative urethral strictures. Urethral dilation leads to postdilatation bleeding or urine extravasation into periurethral tissue, causing scarring of the urethral wall and periurethral fibrosis.26 This is diagnosed with VUDS and managed with transurethral resection or incision. Urethral strictures are rare in women, but they are seen endoscopically after urethral surgery and prior instrumentation. They are usually managed with periodic selfcatheterization, permanent CIC, transurethral incision, or urethral reconstruction.1 Dysfunctional voiding and external sphincter spasticity are non-neurogenic functional causes of bladder outlet obstruction. Both conditions have been associated with inappropriate electromyographic activity during micturition with decreased urinary flow27 and with high pressure increases in the urethral pressure profile. Dysfunctional voiding is referred to as pseudodyssynergia (which mimics DESD), because it is a learned behavior that can be treated and cured. Treatment combines timed voiding, biofeedback, and anticholinergics.1 External sphincter spasticity, characterized by “spasticity of the external sphincter and pelvic floor”28 results from introital or vaginal infections, Skene’s gland abscesses, adnexal disease, or cystitis. Pudendal nerve block improves voiding. VUDS reveal a bladder with intact sensation without the ability to contract due to cortical inhibition from the spastic pelvic floor.21 After managing painful or inflammatory lesions, treatment involves pharmacologic agents, including muscle relaxants and α-blockers. α-Blockers relax the bladder neck and urethra and enhance pelvic ganglionic transmission, which improves detrusor contraction. α-Blockers also treat the urinary retention that develops from transient spasticity.1,26,28

Non-neurogenic bladder hypocontractility is associated with radiation cystitis, chronic obstruction, and tuberculosis. Irradiation causes fibrosis of the lamina propria and muscular layers, leading to muscle cell death. The enlarged intercellular gaps in circular and longitudinal muscle fibers cause spasms and poorly coordinated detrusor contractions, with eventual hypocontractility or areflexia.29-31 In chronic obstruction, the detrusor develops smooth muscle hypertrophy, a reduction in myofilaments, and damaged mitochondria within detrusor smooth muscle cells. This leads to a progressive decrease in detrusor contractility.32 In all of these cases, complete VUDS are required for diagnosis and treatment of the urinary retention. Decreased bladder contractility occurs in the detrusor hyperactivity with impaired contractility syndrome. This was discovered in a nursing home population; the women had opposite bladder reflex and contractile functions. Uninhibited contractions emptied less than one half of the bladder. Impaired neuromuscular transmission at the detrusor or myopathic processes (e.g., cellular degeneration) are proposed causes of the decreased contractility.33,34 VUDS are essential for diagnosis, with the addition of fluoroscopically monitored synchronous cystosphincterometry to rule out other conditions. CIC is the mainstay of therapy.33 When urinary retention occurs with no organic disease but with centrally mediated, subconscious inhibition of detrusor contraction or sphincter relaxation, it is referred to as psychogenic retention. Psychological trauma (e.g., sexual) is one cause. Findings of VUDS are normal except for delayed sensation and a large-capacity bladder. It is usually temporary and responds well to supportive management. Treatment includes psychiatric support and CIC until normal voiding returns. With severe detrusor degeneration, some patients become dependent on CIC.35 IDIOPATHIC URINARY RETENTION: FOWLER’S SYNDROME Pathogenesis Historically, women with chronic, painless bladder distention were labeled as having a psychological problem. In 1986, Fowler and Kirby36 identified a group of 19 young women with longstanding urinary retention who had distinctive electromyographic activity and impaired urethral relaxation. Electromyography with a concentric-needle electrode was used to study the striated muscle of the urethral sphincters in these patients. Concentric needle electromyography is useful in testing the integrity of the motor innervation arising from the S2 to S4 spinal levels and the activity associated with urethral sphincter striated muscle impairment. The impairment identified by Fowler and Kirby36 was referred to as decelerating bursts and complex repetitive discharges (CRDs). CRDs are caused by direct spread of electrical activity form one muscle fiber to another, producing a low “jitter” sound on the audio output of the electromyographic machine. The decelerating bursts produce a sound similar to whales singing in the ocean, and laboratory research describes patients in retention with these findings as “whale noise, positive or negative.”37-39 The bursts of depolarizing activity in the semicircular urethral sphincter muscle impair normal relaxation of the muscle. This impedes normal bladder emptying, causing an insidious increase in residual volumes and bladder distention. The investigators noticed the similarity of this electromyographic activity and the bizarre, high-frequency discharges associated with reinnervation.36 However, reinnervation was thought unlikely, because

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abnormal burst discharges are infrequent in patients with cauda equina lesions or Shy-Drager syndrome.40,41 Fowler and colleagues42 further associated these electromyographic abnormalities with endocrine dysfunction and polycystic ovarian disease (PCOD). Thirty-three of 57 women with urinary retention or voiding dysfunction had abnormal electromyographic activity. Sixty-four percent of this group had polycystic ovaries, seen on pelvic ultrasound. The other women in the group also demonstrated ovarian disturbances (e.g., single or bilateral oophorectomy, premature ovarian failure). High concentrations of circulating androgens and estrogens and low levels of progesterone are seen in women with PCOD. Progesterone stabilizes membranes. Progesterone deficiency in PCOD was hypothesized to reduce urethral sphincter muscle membrane stability, enabling the establishment of a circuitous excitatory pathway between muscle fibers.42 Concentric needle electromyographic measurements of the external urethral sphincter during micturition in women with voiding dysfunction and proximal urethral dilation (on VUDS) by Deindl and coworkers43 confirmed the correlation between abnormal bursts of CRD and poor urinary stream. This provided support for the association between sphincter electromyographic overactivity and impaired relaxation.44 A significant number of women with voiding dysfunction also have symptoms of fecal incontinence. Webb and colleagues45 described the dysfunction of the urethral sphincter in idiopathic urinary retention as part of a more widespread disorder of the entire pelvic floor. All of the women studied had undergone urethral dilation in the past and were performing CIC. Similar abnormalities in the urethral and anal sphincters were seen, including polyphasic and abnormally long duration of potentials and CRD.45 Anatomically, the striated sphincter muscle of the urethra and the anal sphincter receive their nerve supply through the pudendal nerve from the sacral plexus, explaining the correlation in electromyographic abnormalities.46 Clinical Presentation Using a survey questionnaire, Swinn and associates2 described the typical profile of a woman with idiopathic urinary retention. Of 91 women who completed the survey, the mean age at retention onset was 27.7 years (range, 10 to 50 years), with a mean maximal bladder capacity of 1208 mL at the initial episode of retention. Thirty-five percent of these women developed retention spontaneously, 43% developed retention after a surgical procedure (usually gynecologic), and in 15%, childbirth was the preceding event. Eighty-six (94%) of the 91 women performed CIC, with 69% complaining of difficulty passing the catheter because of “something gripping” it. Fifty percent of the study group had PCOD. Voiding spontaneously returned in 38 patients. Sacral neuromodulation was the only therapy that restored function in the other 53 patients.2

tion.47-51 Based on the criteria used to evaluate bladder outlet obstruction, women with idiopathic retention are within the mildly obstructed range. VUDS in these patients typically show a prolonged filling phase and large bladder capacity, with reduced sensations of filling and limited detrusor pressure rise during the voiding phase. However, there are no definite urodynamic criteria to diagnose idiopathic retention in women. The basis for diagnosis remains a typical history and the abnormalities of the sphincter electromyographic activity as described earlier.52,53 Other ancillary indicators used in the diagnosis of idiopathic retention include urethral pressures and urethral sphincter volumes. Urethral pressure measurements have been used for almost a century to assess urethral closure function,54 representing the urethra’s ability to leak. Urethral pressures are criticized for not being a “real physical pressure” in a fluid, based on Griffiths’ definition of urethral pressure as the fluid pressure needed to open a closed (collapsed) tube.55,56 Measurement of urethral pressure (UPM) requires introduction of a Foley catheter, which introduces a nonzero cross-sectional area (zero cross-sectional area when urethra collapses) and changes the shape of the urethral lumen.57 Historically, these measurements have not been standardized and fluctuate based on catheter type, cross section of the probe, patient position, and bladder filling pressures. The standard parameters do not discriminate between voiding dysfunctions, identify underlying pathophysiology, return to normal after surgery (as seen after incontinence procedures), or provide a reliable indicator of surgical success. UPM is useful in identifying strictures or diverticula and targeting interventions (e.g., low-pressure urethra).55 In 2002, The Standardisation Sub-committee of the International Continence Society attempted to define UPM and recommend standards for measurement.57 The abnormal, myotonia-like electromyographic activity seen in women with idiopathic retention is theoretically expected to increase the bulk of urethral sphincter muscle by work-induced hypertrophy. Transvaginal or transrectal ultrasound (TRUS) has been used to image bladder outlet obstruction and identify pelvic pathology.58,59 Later, MRI was used for the diagnosis of female urethral pathology.60 Noble and associates61. used TRUS to compare urethral sphincter volumes in women with obstructed voiding with age-matched controls. The volume of the urethral sphincter in obstructed women was more than 2 cm3 greater (P < .001) than in the control group. TRUS was unable to visualize the three layers of the urethral sphincter, which is elucidated better with MRI.61 Wiseman and colleagues.62 evaluated urethral closure pressure and sphincter volume transvaginally in women with electromyographic abnormalities and idiopathic urinary retention. The maximum urethral closure pressure and ultrasound volume were significantly higher in the group with electromyographic abnormalities.62 These studies support the concept of sphincter electromyographic overactivity producing sphincteric hypertrophy. These assessments may be improved with the use of MRI instead of ultrasound for volume measurement.53

Diagnosis There are no universally accepted criteria for diagnosing bladder outlet obstruction in women. Many investigators47-51 have proposed urodynamic criteria for classification of bladder outlet obstruction, attempting to identify cutoffs for maximal flow rate, maximal detrusor pressure, and PVR volumes. Consistently, the absolute values were not as dramatic as seen in men, and diagnosis relied on imaging of the bladder outlet during micturi-

Treatment All management strategies are directed at successful bladder emptying. Successful treatment abolishes the myotonia-like electromyographic activity and improves urethral relaxation. CIC, rather than indwelling or suprapubic cystotomy, is traditionally the option given to many women with idiopathic retention. Other medical and surgical options, such as oral agents, urethral

Chapter 16 IDIOPATHIC URINARY RETENTION IN THE FEMALE

botulinum toxin, sacral neuromodulation, and biofeedback, have been used. The only treatment that has conclusively restored voiding is sacral neuromodulation.53 Oral Agents There are limited data on the use of oral agents, such as αblockers or β-agonists, in the treatment of functional bladder neck obstruction. In a study of 24 women with retention treated with α-blockers and initial CIC, only 50% had a significantly sustained improvement in PVR and peak flow. The group that failed α-blocker treatment returned to CIC or had a bladder neck incision.63 The effects of tamsulosin on urethral pressures in healthy women were studied at rest and after sacral magnetic stimulation. Tamsulosin did significantly reduce the mean and maximal urethral pressures acquired in all three segments (i.e., proximal, middle and distal) of the urethra. The amplitude of urethral contractions after sacral magnetic stimulation was unchanged after tamsulosin. These results may support tamsulosin’s use in female retention from an overactive or nonrelaxing urethra.64 Bethanechol has been used as treatment for retention caused by detrusor acontractility, but it has not been used in women with sphincteric overactivity.65 Its treatment value is therefore unknown. Botulinum A Toxin There has been mixed success with the use of botulinum toxin in treating chronic urinary retention in women. Botulinum A toxin is an inhibitor of acetylcholine release at the presynaptic neuromuscular junction, which decreases regional muscle contractility and causes muscle atrophy at the site of injection.66,67 Fowler and coworkers68 evaluated six women with a characteristic pattern of electromyographic activity by injecting botulinum toxin into each of their striated urethral sphincters. Three of the six women experienced stress incontinence for 10 days, and three had no change. Although the botulinum toxin did not have a beneficial effect, the result of stress incontinence did ensure that sufficient botulinum was given to weaken the striated sphincter muscle. This supported the hypothesis that abnormal sphincteric activity results from an “ephaptic transmission of impulses between muscle fibers” and not repetitive firing of reinnervated motor units.68 Phelan and colleagues66 were the first to report successful outcomes with botulinum A injections in women and in nonneurogenic voiding dysfunction. They studied 21 patients (13 women) with impaired bladder emptying who were dependent on catheterization. All except one were able to void spontaneously after an injection of 80 to 100 units of botulinum toxin.66 This denervation by botulinum is reversible because new axons sprout in 3 to 6 months.69 Patients had repeat injections at intervals consistent with this regrowth. In some cases, the injection had clinical efficacy beyond 6 months, suggesting neural plasticity or altered neuromuscular junction dynamics.66 Kuo and associates70 repeated this study in 20 patients with urinary retention or dysuria due to detrusor hypocontractility and nonrelaxing urethral sphincter who were refractory to conservative therapy. This study clearly showed that botulinum toxin is effective in decreasing urethral sphincter resistance and improving voiding efficiency in patients with various type of lower urinary tract dysfunction.70 Botulinum A toxin injections do have therapeutic value in urethral spasticity, but larger, controlled trials are necessary to establish their role.71

Tanagho and Schmidt72 are responsible for the first implantable sacral nerve stimulators (SNSs). The effects of SNSs depend on the electrical stimulation of somatic afferent axons in spinal roots, which modulate voiding and continence reflex pathways in the central nervous system. In urinary retention, SNSs are responsible for turning off excitatory outflow to the urethral outlet, which promotes bladder emptying.73 Traditionally, a test percutaneous nerve evaluation is performed under local anesthesia by inserting a stimulating electrode through the S3 foramen. This lead is left in place for 4 to 7 days, during which a voiding diary is kept. If the patient has a more than 50% improvement in voiding function, the implant is considered effective, and a permanent implantable pulse generator (IPG) is placed. Recognized complications of neuromodulation include lead migration, pain at the IPG box site or ipsilateral leg, infection, and lack of efficacy.53 To improve the efficacy of chronic sacral neuromodulation, the placement of bilateral SNSs has been proposed. Scheepens and colleagues74 compared unilateral with bilateral SNSs in a series of women with urinary retention and found no significant differences, except for two patients with complete obstruction, who voided only with bilateral stimulation. Sacral Neuromodulation Sacral neuromodulation has been shown in many studies to restore voiding function in women with urinary retention. The results of peripheral nerve evaluation testing in 34 patients with Fowler’s syndrome revealed an overall success rate of 68%. This compares favorably with a reported success rate of 30% to 50% for the period of trial stimulation of all lower urinary tract dysfunctions.75 Shaker and Hassouna76 treated 20 patients (19 women) with idiopathic, nonobstructing, chronic urinary retention dependent on CIC who had at least a 50% improvement on percutaneous nerve evaluation screening. These patients were followed for a mean of 15.2 months and had significant improvement in voiding function, pelvic pain, and sensation of emptiness after voiding. The study authors emphasize that the lack of change in cystometrography after SNS implantation indicates that the cause of the problem is not the bladder but the pelvic floor musculature.76 Investigators have reported good results after SNS when there are pelvic floor electromyographic activity abnormalities. Their explanation is that patients with chronic urinary retention fail to identify their pelvic floor muscles and are incapable of relaxing the pelvic floor to initiate the voiding reflex. The permanent contraction of the pelvic floor is thought responsible for detrusor inhibition. Neuromodulation provides increased awareness of the pelvic floor and allows relaxation of the hypertonic pelvic floor musculature. The mechanism involves sacral stimulation of presynaptic inhibition of afferents to the spastic muscle motor neurons at the level of the dorsal column.77-80 A prospective, randomized, multicenter trial enrolled 177 patients with urinary retention (74% were female), with a followup of 18 months. Sixty-eight of these women qualified for an IPG and were divided into treatment and control groups. At 6 months, 83% of the implant groups had successful results, compared with 9% of the controls. Temporary inactivation of the SNS resulted in a significant increase in the PVR volume. This supports the idea that the SNS does not cure the underlying mechanism of urinary retention, but instead controls aberrant dysfunctional reflexes causing voiding dysfunction.77,81

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Dasgupta and colleagues82 provided long-term results of SNSs in women with Fowler’s syndrome. This retrospective study included 26 women who were followed for more than 6 years. Seventy-seven percent were voiding successfully more than 5 years postoperatively; 54% required revision surgery. The longevity of an IPG battery is 7 to 10 years. This study supported the effectiveness of SNSs for at least 5 years after implantation.82 Behavioral Treatment and Biofeedback Behavioral and biofeedback treatments are safe, noninvasive, and effective interventions that are useful in the management of idiopathic urinary retention. Behavioral changes enlighten patients about their fluid intake and voiding behavior. Biofeedback involves surface or internal (vaginal or rectal) electrodes that transduce muscle potentials into auditory or visual signals. This helps the patient learn to increase or decrease voluntary muscle activity.83

CONCLUSIONS There are many neurogenic and non-neurogenic causes of urinary retention in the female patient. Idiopathic urinary retention and Fowler’s syndrome should be considered in any young female with insidious, painless retention and urethral sphincter overactivity identified on electromyography. The diagnosis combines a thorough history with abnormal electromyographic and urodynamic findings. Sacral neuromodulation offers the best option in restoring voiding function. Although the exact mechanism of action of sacral stimulation is not established, evidence supports action through the afferent pathways. Other accessory treatment options, such as botulinum and tamsulosin, have some therapeutic merits, but they require larger, long-term, case-controlled studies in women with urethral overactivity. Behavioral modification and biofeedback are safe and effective and should be considered as first-line treatment for voiding dysfunction.

References 1. Nitti VW, Raz S: Urinary Retention in Female Urology, 2nd ed. Philadelphia, WB Saunders, 1996, pp 197-213. 2. Swinn MJ, Wiseman OJ, Lowe E, Folwer CJ: The causes of and natural history of isolated urinary retention in young women. J Urol 167:151-156, 2002. 3. Smith CP, Kraus SR, Boone TB: Urinary retention in the young female. AUA Update Series 18:145-152, 1999. 4. Wein AJ, Levin RM, Barrett DM: Voiding function and dysfunction. Voiding function relevant to anatomy, physiology and pharmacology. In Gillenwater JY, Grayhack JT, Howards SS, Duckett JW (eds): Adult and Pediatric Urology, 2nd ed, vol I. St. Louis, Mosby–Year Book, 1991, p 933. 5. O’Donnell PD: Electromyography. In Nitti VW (ed): Practical Urodynamics. Philadelphia, WB Saunders, 1998, p 70. 6. Litwiller SE, Frohman EM, Zimmern PE: Multiple sclerosis and the urologist. J Urol 61:743-757, 1999. 7. Hinson JL, Boone TB: Urodynamics and multiple sclerosis. Urol Clin North Am 12:475-481, 1996. 8. Chancellor MB, Blaivas JG: Multiple sclerosis. Probl Urol 7:15-33, 1993. 9. Sirls LT, Zimmern PE, Leach GE: Role of limited evaluation and aggressive medical management in multiple sclerosis: A review of 113 patients. J Urol 151:946-950, 1994. 10. Watanabe T, Chancellor MB, Rivas DA: Neurogenic voiding dysfunction. In Nitti VW (ed): Practical Urodynamics. Philadelphia, WB Saunders, 1998, p 148. 11. Kostuik JP, Harrington I, Alexander D, et al: Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am 68:386391, 1986. 12. Wein AJ: Neuromuscular dysfunction of the lower urinary tract and its management. In Walsh PC, Retik AB, Vaughan ED, Wein AJ (eds): Campbell’s Urology, 8th ed, vol II. Philadelphia, Saunders, 2002, p 955. 13. Frimodt-Moller C, Mortensen S: Diabetic cystopathy: Epidemiology and related disorders. Ann Intern Med 92:327-328, 1980. 14. Ellenberg M: Development of urinary bladder dysfunction in diabetes mellitus. Ann Intern Med 92(Pt 2):321-323, 1980. 15. Bradley WE: Diagnosis of urinary bladder dysfunction in diabetes mellitus. Ann Intern Med 92(Pt 2):323-326, 1980. 16. Frimodt-Moller C, Mortensen S: Treatment of diabetic cystopathy. Ann Intern Med 92(Pt 2):327-328, 1980. 17. Marion G: Surgery of the neck of the bladder. Br J Urol 5:351, 1933. 18. Axelrod SL, Blaivas JG: Bladder neck obstruction in women. J Urol 137:497-499, 1987.

19. Gronbaek K, Struckmann JR, Frimodt-Moller C: The treatment of female bladder neck dysfunction. Scand J Urol Nephrol 26:113-118, 1992. 20. Diokno AC, Hollander JB, Bennett CJ: Bladder neck obstruction in women: A real entity. J Urol 132:294-298, 1984. 21. Nitti VW: Bladder outlet obstruction in women. In Nitti VW (ed): Practical Urodynamics. Philadelphia, WB Saunders, 1998, pp 207-209. 22. Sardosky MF: Urethral carcinoma. AUA Update Series 6:13, 1987. 23. Nitti VW, Raz S: Obstruction following anti-incontinence procedures: Diagnosis and treatment with transvaginal urethrolysis. J Urol 152:93-98, 1994. 24. Foster HE, McGuire EJ: Management of urethral obstruction with transvaginal urethrolysis. J Urol 150:1448-1451, 1993. 25. Webster GD, Kreder KJ: Voiding dysfunction following cystourethropexy: Its evaluation and management. J Urol 144:670-673, 1990. 26. Bass JS, Leach GE: Bladder outlet obstruction in women. Probl Urol 5:141, 1991. 27. Kaplan W, Firlit CF, Schoenber HW: The female urethral syndrome: External sphincter spasm as etiology. J Urol 124:48-49, 1980. 28. Raz S, Smith RB: External sphincter spasticity syndrome in female patients. J Urol 115:443-446, 1976. 29. Antonakopoulous GN, Hicks RM, Berry RJ: The subcellular basis of damage to the human urinary bladder induced by radiation. J Pathol 143:103-116, 1984. 30. Mikhailov MCH, Elsaber E, Welscher UE: Immediate mechanical reactions of isolated human detrusor muscle on x-irradiation. Strahlentherapie 155:284-286, 1979. 31. Zoubek J, McGuire EJ, Noll F, et al: The late occurrence of urinary tract damage in patients successfully treated by radiotherapy for cervical carcinoma. J Urol 141:1347-1349, 1989. 32. Gosling JA, Kung LS, Dixon JS, et al: Correlation between the structure and function of the rabbit urinary bladder following partial outlet obstruction. J Urol 163:1349-1356, 2000. 33. Resnick NM, Yalla SV: Detrusor hyperactivity with impaired contractile function—An unrecognized but common cause of incontinence in elderly patients. JAMA 257:3076-3081, 1987. 34. Elbadawi A, Yalla SV, Resnick NM: Structural basis of geriatric voiding dysfunction. III. Detrusor overactivity. J Urol 150:16681680, 1993. 35. Barrett DM: Evaluation of psychogenic urinary retention. J Urol 120:191-192, 1978. 36. Fowler CJ, Kirby RS: Electromyography of urethral sphincter in women with urinary retention. Lancet 1:1455-1456, 1986.

Chapter 16 IDIOPATHIC URINARY RETENTION IN THE FEMALE

37. Butler WJ: Pseudomyotonia of the periurethral sphincter in women with urinary incontinence. J Urol 122:838-840, 1979. 38. Fowler CJ, Kirby RS, Harrison MJG: Decelerating bursts and complex repetitive discharges in the striated muscle of the urethral sphincter associated with urinary retention in women. J Neurol Neurosurg Psychiatry 48:1004-1009, 1985. 39. Trontelj J, Stolberg E: Bizarre repetitive discharges recorded with single fibre EMG. J Neurol Neurosurg Psychiatry 46:310-316, 1983. 40. Fowler CJ, Kirby RS, Harrison MJG et al: Individual motor unit analysis in the diagnosis of disorders of urethral sphincter innervation. J Neurol Neurosurg Psychiatry 47:637-641, 1984. 41. Kirby R, Fowler C, Gosling J, Bannister R: Urethro-vesical dysfunction in progressive autonomic failure with multiple system atrophy. J Neurol Neurosurg Psychiatry 49:554-562, 1986. 42. Fowler CJ, Christmas TJ, Chapple CR, et al: Abnormal electromyographic activity of the urethral sphincter, voiding dysfunction, and polycystic ovaries: A new syndrome? BMJ 297:1436-1438, 1988. 43. Deindl FM, Vodusek DB, Bischoff C, et al: Dysfunctional voiding in women: Which muscles are responsible? Br J Urol 82:814-819, 1998. 44. DasGupta R, Fowler CJ: The management of female voiding dysfunction: Fowler’s syndrome—A contemporary update. Curr Opin Urol 13:293-299, 2003. 45. Webb RJ, Fawcett PRW, Neal DE: Electromyographic abnormalities in the urethral and anal sphincters of women with idiopathic retention of urine. 70:22-25, 1992. 46. Brooks JD: Anatomy of the lower urinary tract and male genitalia. In Walsh PC, Retik AB, Vaughan ED, Wein AJ (eds): Campbell’s Urology, 8th ed, vol 1. Philadelphia, WB Saunders, 2002, pp 5455. 47. Farrar DJ, Osborne JL, Stephenson TP, et al: A urodynamic view of bladder outflow obstruction in the female: Factors influencing the results of treatment. Br J Urol 47:815-822, 1976. 48. Axelrod SL, Blaivas JG: Bladder neck obstruction in women. J Urol 137:497-499, 1987. 49. Massey JA, Abrams PH: Obstructed voiding in the female. Br J Urol 61:36-39, 1988. 50. Nitti VN, TU LM, Gitlin J: Diagnosing bladder outlet obstruction in women. J Urol 161:1535-1540, 1999. 51. Blaivas JG, Groutz A: Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn 19:553-564, 2000. 52. DasGupta R, Fowler CJ: Urodynamic study of women in urinary retention treated with sacral neuromodulation. 171:1161-1164, 2004. 53. DasGupta R, Fowler CJ: The management of female voiding dysfunction: Fowler’s syndrome—A contemporary update. Curr Opin Urol 13:293-299, 2003. 54. Bonney V: On diurnal incontinence of urine in women. J Obstet Gynaecol Br Emp 30:358-365, 1923. 55. Lose G: Urethral pressure measurement—Problems and clinical value. Scand J Urol Nephrol 207(Suppl):61-66, 2001. 56. Griffiths D: The pressure within a collapsible tube with special reference to urethral pressure. Phys Med Biol 9;951-961, 1985. 57. Lose G, Griffiths D, Hosker G, et al: Standardisation of urethral pressure measurement: Report from the Standardisation SubCommittee of the International Continence Society. 21:258-260, 2002. 58. Hennigan HW, DuBose TJ: Sonography of the normal female urethra. AJR Am J Roentgenol 145:839-841, 1985. 59. Leonor de Gonzalez E, Cosgrove DO, Joseph AE, et al: The appearances on ultrasound of the female urethral sphincter. Br J Radiol 61:687-690, 1988. 60. Klutke C, Golomb J, Barbaric Z, Raz S: The anatomy of stress incontinence: Magnetic resonance imaging of the female bladder neck and urethra. J Urol 143:563-566, 1990.

61. Noble JG, Dixon PJ, Rickards D, et al: Urethral sphincter volumes in women with obstructed voiding and abnormal sphincter electromyographic activity. Br J Urol 76:741-746, 1995. 62. Wiseman OJ, Swinn MJ, Brady C, et al: Maximum urethral closure pressure and sphincter volume in women with urinary retention. J Urol 167:1348-1352, 2002. 63. Kumar A, Mandhani A, Gogoi S, et al: Management of functional bladder neck obstruction in women: Use of α-blockers and pediatric resectoscope for bladder neck incision. J Urol 162:2061-2065, 1999. 64. Reitz A, Haferkamp A, Kyburz T, et al: The effect of tamsulosin on the resting tone and the contractile behaviour of the female urethra: A functional urodynamic study in healthy women. Eur Urol 46:235240, 2004. 65. Riedl CR, Stephen RL, Daha LK, et al: Electromotive administration of intravesical bethanechol and the clinical impact on acontractile detrusor management: Introduction of a new test. J Urol 164:21082111, 2000. 66. Phelan MW, Franks M, Somogyi GT, et al: Botulinum toxin urethral sphincter injection to restore bladder emptying in men and women with voiding dysfunction. J Urol 165:1107-1110, 2001. 67. Duchen LW: Changes in motor innervation and cholinesterase localization induced by botulinum toxin in skeletal muscle of mouse: Differences between fast and slow muscles. J Neurol Neurosurg Psychiatry 33:40-54, 1970. 68. Fowler CJ, Betts CD, Swash CM, et al: Botulinum toxin in the treatment of chronic urinary retention in women. Br J Urol 70:387-389, 1992. 69. Borodic GE, Joseph M, Fay L, et al: Botulinum A toxin for the treatment of spasmodic torticollis—Dysphagia and regional toxin spread. Head Neck 12:392-399, 1990. 70. Kuo H-C: Botulinum A toxin urethral injection for the treatment of lower urinary tract dysfunction. J Urol 170:1908-1912, 2003. 71. Leippold T, Reitz A, Schurch B: Botulinum toxin as a new therapy option for voiding disorders: Current state of the art. Eur Urol 44:165-174, 2003. 72. Tanagho E, Schmidt R: Electrical stimulation in the clinical management of the neurogenic bladder. J Urol 140:1331-1339, 1988. 73. Leng WW, Chancellor MB: How sacral nerve stimulation neuromodulation works. Urol Clin North Am 32:11-18, 2005. 74. Scheepens WA, de Bie RA, Weil EH, et al: Unilateral versus bilateral sacral neuromodulation in patients with chronic voiding dysfunction. J Urol 168:2046-2050, 2002. 75. Swinn MJ, Kitchen ND, Goodwin RJ, et al: Sacral neuromodulation for women with Fowler's syndrome. Eur Urol 38:439-443, 2000. 76. Shaker H, Hassouna M: Sacral root neuromodulation in idiopathic nonobstructive chronic urinary retention. J Urol 159:1476-1478, 1998. 77. Schultz-Lampel D, Jiang C, Lindstrom S, et al: Experimental results on mechanism of action of electrical neuromodulation in chronic urinary retention. World J Urol 16:301-304, 1998. 78. De Ridder D, Van Poppel H, Baert L: Sacral nerve stimulation is a successful treatment for Fowler syndrome. Neurourol Urodyn 15:120, 1996. 79. Everaert K, Plancke H, Oosterlinck W: Urodynamic evaluation of neuromodulation (subchronic) in patients with voiding dysfunctions. Neurourol Urodyn 14:114, 1996. 80. Schmidt RA, Vapnek J, Tanagho EA: Restoration of voiding in chronic retention states. Neurourol Urodyn 15:365, 1996. 81. Jonas U, Fowler CJ, Chancellor MB, et al: Efficacy of sacral nerve stimulation for urinary retention: Results 18 months after implantation. J Urol 165:15-19, 2001. 82. Dasgupta R, Wiseman OJ, Kitchen N, et al: Long-term result of sacral neuromodulation for women with urinary retention. BJU Int 94:335-337, 2004. 83. Doggweiler-Wiygul R, Sellhorn E: Role of behavioral changes and biofeedback in urology. World J Urol 20:302-305, 2002.

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CLINICAL DIAGNOSIS OF OVERACTIVE BLADDER Samih Al-Hayek and Paul Abrams TERMINOLOGY Overactive bladder (OAB) is a newly described condition. It was probably first alluded to by Dudley in 1905 when he distinguished between active and passive incontinence due to sphincter weakness.1 In 1917, Taylor and Watt reported the importance of urgency, as a symptom, during history taking, to distinguish incontinence with and without urgency.2 Bates and colleagues introduced the term unstable bladder in 1970 when they used cinecysturethrography to investigate urge incontinence.3 The International Continence Society (ICS) established a committee for the standardization of terminology of lower urinary tract function to facilitate comparison of results and enable effective communication by investigators. Since 1976, a large number of standardization reports have been published, the latest in 2002.4-19 In 2002, the ICS subcommittee restated the principle of describing any lower urinary tract dysfunction from four aspects: as a symptom (taken by detailed history), a sign (physical examination and bedside tests), a condition, and a urodynamic observation in addition to the terminology related to therapies.1 The lower urinary tract is composed of the bladder and the urethra. When reference is made to the whole anatomic organ, “vesica urinaria,” the correct term is bladder. When the smooth muscle structure known as the “m. detrusor urinae” is being discussed, the correct term is detrusor. OAB was defined by the ICS in 2002 as urgency, with or without urge incontinence, usually with frequency and nocturia, in the absence of local pathologic or endocrine factors. The OAB term was introduced for use in a consensus conference in 1996, as an alternative to “unstable bladder.” It was believed that the term “overactive bladder” would facilitate communication between patients and health care staff. OAB symptoms are part of the storage symptoms that are experienced during the storage phase of the bladder and include the following: ■ ■

■

Urgency is the complaint of a sudden compelling desire to pass urine that is difficult to defer. Increased daytime frequency is the complaint by the patient who considers that she voids too often by day. This term is equivalent to “pollakisuria,” a term used in many countries. Nocturia is the complaint that the patient has to wake at night one or more times to void. The term nighttime frequency differs from nocturia, because it includes voids that occur after the patient has gone to bed but before he or she has gone to sleep, as well as voids that occur in the early morning and prevent the patient from getting back to sleep as he or she wishes. These voids before and after sleep may

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need to be considered in research studies (e.g., nocturnal polyuria). If this definition were used, then an adapted definition of daytime frequency would need to be used with it. Urinary incontinence (UI) is the complaint of any involuntary leakage of urine. In each specific circumstance, UI should be further described by specifying relevant factors such as type, frequency, severity, precipitating factors, social impact, effect on hygiene and quality of life, measures used to contain the leakage, and whether the patient seeks or desires help because of UI. Urinary leakage may need to be distinguished from sweating or vaginal discharge. Urgency urinary incontinence (UUI) is the complaint of involuntary leakage accompanied by or immediately preceded by urgency. UUI can manifest in various symptomatic forms; for example, as frequent small losses between micturitions or as a catastrophic leak with complete bladder emptying.

These symptom combinations of OAB are suggestive of detrusor overactivity (DO), a urodynamic diagnosis, which is characterized by involuntary detrusor contractions during bladder filling; it may be spontaneous or provoked. Figure 17-1 represents the relationships among OAB, UUI, and DO.

EPIDEMIOLOGY Until recently, most studies have looked at the prevalence of UI; as a result, prevalence data on OAB are lacking. The other difficulty in estimating the scale of the problem is the variation among studies in definitions used, methods of collecting data, and populations studied. Almost all surveys on UI concluded that stress urinary incontinence (SUI) is the most common type of UI in women. In the large Epidemiology of Incontinence in the County of NordTrondelag (EPINCONT) study, 50% of the incontinent women had SUI, 36% had mixed urinary incontinence (MUI), and 11% had UUI.20 The recent literature review by Minassian and colleagues reported similar prevalence rates for the various types of UI.21 The survey carried out by Diokno and associates22 showed that symptoms of MUI were most frequently reported; however, this study differed from the others in that only elderly people were assessed. The results of these studies were based on symptoms only; if urodynamics had been used to confirm the diagnosis, the results might have been different. In one study with 863 women, most of the subjects with symptoms of MUI were diagnosed to have pure SUI (42%) during urodynamic testing.23 Weidner and 197

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Figure 17-1 The relationships among symptoms of overactive bladder (OAB), urgency urinary incontinence (UUI), and detrusor overactivity (DO).

Sanvik and their colleagues showed similar results.24,25 This reinforces the fact that SUI is the major type of UI in women. A large population-based survey that was conducted in France, Germany, Italy, Spain, Sweden, and the United Kingdom defined OAB as the presence of chronic frequency, urgency, and urge incontinence (either alone or in any combination). This definition is somewhat different from the new ICS definition, which uses urgency as the cornerstone of the diagnosis. The authors reported that the overall prevalence of OAB symptoms in subjects aged 40 years or older was 16.6%. Frequency (85%) was the most commonly reported symptom, followed by urgency (54%) and urge incontinence (36%). The prevalence of OAB symptoms increased with advancing age. Overall, 60% of respondents with symptoms had consulted a doctor, but only 27% were currently receiving treatment.26 The National Overactive Bladder Evaluation (NOBLE) Program that was undertaken in the United States used the new ICS definition from 2002 in a clinically validated interview and a follow-up nested study. A sample of 5204 adults aged 18 years or older was studied. The overall prevalence of OAB was similar between men (16.0%) and women (16.9%), but sex-specific prevalence differed substantially by severity of symptoms: 55% of the women with OAB symptoms had OAB associated with urge incontinence (“wet OAB”), and the rest had OAB without incontinence (“dry OAB”). In women, prevalence of urge incontinence increased with age, from 2.0% among those 18 to 24 years of age to 19% among those 65 to 74 years of age, with a marked increase after 44 years of age. However, the dry OAB tended to have gradual increase before 44 years of age and reached a plateau at that point. The prevalence of urge incontinence increased in relation to increased body mass index across all age groups. Dry OAB was more common in men than in women. The NOBLE study does not support the commonly held notion that women are considerably more likely than men to have urgency-related symptoms. However, sex-specific anatomic differences may increase the probability that OAB is expressed as urge incontinence among women compared with men.27 The

prevalence of OAB among women in this study was higher than what was reported by Milsom26 but similar to the prevalence of UI reported by Simeonova28 and by Samuelsson (20- to 59-year-olds).29 Not all studies distinguish wet from dry OAB. On average, urgency without UI appears to be as common as urgency with UI (Table 17-1). EVALUATION History Because OAB is a symptomatic diagnosis, history plays an important part in assessing the patient. The purpose of the clinical history is to have an empiric diagnosis, to exclude other causes for the patient’s symptoms, and to assess the effects of the problem on the patient’s daily activities that would help in deciding the treatment strategy. Excluding secondary causes is important; these include diabetes, congestive heart failure, bladder cancer, urinary tract infection (UTI), medications, and pregnancy or recent birth. Questions should include details of the following: ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■

Nature and duration of symptoms Which symptoms are most bothersome Current management, including pad usage Previous medical or surgical treatment for the condition History of radiation exposure Environmental issues Patient mobility Mental status Other disease status, especially neurologic conditions (stoke, trauma) Patient medication Sexual function Bowel function, bearing in mind that irritable bowel syndrome may be associated with OAB35

Chapter 17 CLINICAL DIAGNOSIS OF OVERACTIVE BLADDER

Table 17-1 Prevalence of Urgency and Urgency Urinary Incontinence (UUI) in Community-Dwelling Women* First Author and Ref. No.

Year

Age (yr)

Sample size

Swithinbank30 Lapitan31 Milsom26 Van Der Vaart32 Chen33

1999 2001 2001 2002 2003

19+ 18+ 40+ 20-45 20+

2,075 5,502 16,776 1,393 1,253

Definition of urgency or UUI Any Any Current Any Any

Prevalence of urgency (%)

Prevalence of UUI (%)

61 35 54 45 13

46 11 36 15 9

Ratio† 1.3 3.2 1.5 3.0 1.4

*There are few data on the incidence of new cases of overactive bladder (OAB), the incidence of new cases of detrusor overactivity (DO), or the natural history of established cases of OAB or DO (or the combination of both). † Overall median: 2.1. From Hunskaar H, Burgio K, Diakno AC, et al: Epidemiology and natural history of urinary incontinence. In Abrams P, Cardozo L, Khoury S, Wein A (eds): Incontinence. Plymouth, UK, Health Publication Ltd., 2002, pp 515-551.

■ ■ ■ ■ ■

Gynecologic and obstetric history, especially pelvic organ prolapse The effect of the condition on daily activity (social restriction, reduced physical activities) Patient’s goals or expectations of treatment Patient’s fitness for possible surgical procedures For a complicated history, other symptoms, such as the presence of pain or hematuria

Quantification of Symptoms Questionnaires Taking a detailed history from the patient depends to a great deal on the physician’s skills. The questions, and the aspects tackled, are different for each clinician. Another issue is the embarrassment of the patient, which can lead her to avoid talking about some or all of her symptoms. In addition, clinicians tend to rate the patient’s quality of life lower than the patients themselves do.36 For all of these reasons, patient-completed questionnaires were developed. They provide details regarding the presence of symptoms, their frequency, their severity, and the bother caused to the patient. Questionnaires also assess quality of life in general and in relation to the symptoms. In theory, validated questionnaires can be used for making the diagnosis, as a tool in prevalence studies, and to measure the outcome of treatment. Several questionnaires have been developed to assess UI. The modular International Consultation on Incontinence Questionnaire (ICIQ) has been validated and includes modules for lower urinary tract symptoms (LUTS) as well as OAB.37 ICIQ-OAB is a short form based on the Bristol Female Lower Urinary Tract Symptoms Questionnaire (BFLUTS) and should be a helpful tool in assessing these patients (Box 17-1).38,39 The full list of ICI questionnaires may be found by visiting the web site, www.iciq.net. Fluid Input/Output Charts Asking the patient to record each micturition for a period of days provides valuable information. For some women, it may be therapeutic, because it provides them with insight into their bladder behavior. Micturition events can be recorded in three main forms: ■

Micturition time chart: records only the times of micturitions, day and night, for at least 24 hours.

Box 17-1 Questions Included in the International Consultation on Incontinence Modular Questionnaire on Overactive Bladder Do you have to rush to the toilet to urinate? Does urine leak before you can get to the toilet? How often do you pass urine during the day? During the night, on average, how many times do you have to get up to urinate? Do you have a sudden need to rush to the toilet to urinate? Does urine leak after you feel a sudden need to go to the toilet?

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■

Frequency-volume chart (FVC): records the volumes voided as well as the time of each micturition, day and night, for at least 24 hours. Bladder diary: records the times of micturitions and voided volumes, incontinence episodes, pad usage, and other information such as fluid intake, degree of urgency, and degree of incontinence.

It is useful to ask the patient to make an estimate of liquid intake in a 24-hour period. Consumption of significant quantities of water-containing foods (vegetables, fruit, and salads) should be taken into account. The time at which any diuretic therapy is taken should be marked on the chart or diary. The following measurements can be abstracted from FVCs and bladder diaries using the 2002 ICS definitions40: ■

■ ■ ■

Daytime frequency is the number of voids recorded during waking hours and includes the last void before sleep and the first void after waking and rising in the morning. Nocturia is the number of voids recorded during a night’s sleep: each void is preceded and followed by sleep. 24-Hour frequency is the total number of daytime voids and episodes of nocturia during a specified 24-hour period. 24-Hour production is measured by collecting all urine for 24 hours. This is usually commenced after the first void produced after rising in the morning and is completed by including the first void produced after rising the following morning. Polyuria is defined as the measured production of more than 2.8 L of urine in 24 hours in adults. It may be useful to look at output over shorter time frames.41

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Nocturnal urine volume is defined as the total volume of urine passed between the time the patient goes to bed with the intention of sleeping and the time of waking with the intention of rising. Therefore, it excludes the last void before going to bed but includes the first void after rising in the morning. Nocturnal polyuria is present when an increased proportion of the 24-hour output occurs at night (normally during the 8 hours while the patient is in bed). The nighttime urine output excludes the last void before sleep but includes the first void of the morning. The normal range of nocturnal urine production differs with age, and the normal ranges remain to be defined. Therefore, nocturnal polyuria is present when greater than 20% (young adults) to 33% (>65 years) is produced at night. Hence, the precise definition is dependent on age. Maximum voided volume is the largest volume of urine voided during a single micturition and is determined from the FVC or bladder diary. The term “functional bladder capacity” is no longer recommended by the ICS, because “voided volume” is a clearer and less confusing term, particularly if qualified (e.g., “maximum voided volume”). If the term “bladder capacity” is used, in any situation, it implies that this has been measured in some way, if only by abdominal ultrasonography. In adults, voided volumes vary considerably.

In OAB /DO, the patient has reduced variable volumes of urine during the day. The nighttime volumes and the first void on waking in the morning are often larger and of normal quantity.42 In a recent study, the authors correlated the patients’ symptoms of frequency, urgency, nocturia, and urge incontinence with the parameters on the bladder diary. They found that frequency and urgency symptoms were associated with a higher 24-hour frequency, lower maximum volume voided, and lower mean voided volume.43,44 There has been wide variation in the number of days over which the patient is complete a bladder diary, ranging from 1 day to 2 weeks, with 7 days probably being the previous “gold standard.” A recent study by Schick and coworkers indicated that a 4-day chart in women is as reliable as a 7-day chart. They suggested that a 4 day chart optimizes patients’ compliance without compromising the diagnostic value of the FVC.43 It is advised that a simple FVC with the additional recording of incontinent episodes, pad usage, and overall assessment of fluid intake be used for routine clinical use. In a research setting, urinary diaries may add significant additional information, allowing a more complete evaluation of novel therapies.45 Quality of Life Assessment Severe OAB is a disabling condition that may render the patient housebound to avoid the embarrassment of leakage episodes. Assessing the severity and the impact of the symptoms on the patient’s daily activity is an essential part of evaluating these patients. OAB symptoms can have an effect on the psychological, occupational, and sexual function of the patient.46 In the study by Milsolm and colleagues, 67% of women with OAB reported that their symptoms had a deleterious effect on daily living.26 The OABqol is a quality-of-life questionnaire that is specifically designed to assess the effect of OAB on the patients’ life.47

Physical Examination In addition to the general examination, there are a number of other essential components in the examination of patients with OAB: Abdominal examination after voiding in an effort to detect a palpable bladder or abnormal masses. Focused neurologic examination, in particular of the lower limbs, looking for any focal signs that might suggest a neurologic cause for OAB. Patients with a history suggestive of possible neurogenic OAB require a more extensive neurologic examination. Rectal examination to assess anal tone, pelvic floor function, and the consistency of stool as a sign of constipation. External genitalia and perineal examination allows inspection of the skin (e.g., atrophy, excoriation) or any abnormal anatomic features. In addition, the area should be tested for normal sensation Vaginal examination to assess pelvic organ prolapse, with the patient bearing down, and pelvic floor function as described in the ICS report on Pelvic Organ Prolapse.48 Pelvic floor muscle function can be qualitatively defined by the tone at rest and the strength of a voluntary or reflex contraction (strong, weak, or absent) or by a validated grading system (e.g., modified Oxford scale).49 A pelvic muscle contraction may be assessed by visual inspection, palpation, electromyography, or perineometry. Factors to be assessed include strength, duration, displacement, and repeatability. Changes due to lack of estrogen should also be noted Simple Investigations Urinalysis Because UTI is a readily detected and easily treatable cause of LUTS, urine testing is highly recommended. Patients with UTI often suffer from frequency and have urgency to pass urine, with nocturia and sometimes urge incontinence that mimics OAB. Therefore, all patients with OAB should have their urine tested to exclude UTI. Testing may range from examination of urine in a clear glass container, to dipstick testing, to urine microscopy. Estimation of Postvoid Residual Urine In patients with suspected voiding dysfunction, the postvoid residual urine (PVR) estimation is part of the initial assessment. The result is likely to influence management; for example, in patients with neurologic disorders. PVR can be estimated by noninvasive methods such as the standard ultrasound scan or hand-held bladder scan, or invasively with the use of a urethral catheter; the latter method has the advantage of taking a clean specimen of urine for microbiologic testing. Urinary Tract Imaging Routine imaging of the urinary tract in patients with OAB symptoms is not recommended. However, if the history or the initial assessment indicate a complex problem or is suspicious for an associated pathology, then imaging could be used to exclude it. To start with, an ultrasound scan or plain radiographic study should be used. Imaging of the lower urinary tract is recommended in those women with suspected lower tract or pelvic pathology (e.g., bladder stone, pelvic mass).

Chapter 17 CLINICAL DIAGNOSIS OF OVERACTIVE BLADDER

Imaging of the upper urinary tract is recommended only in specific situations, including ■ ■ ■ ■ ■ ■

Neurogenic UI (e.g., myelodysplasia, spinal cord trauma) Incontinence associated with significant PVR Coexistent loin or kidney pain Severe pelvic organ prolapse, not being treated Suspected extraurethral UI Hematuria

Invasive Investigations Invasive investigations are used only after the initial workup has failed to make the diagnosis. Endoscopy Flexible or rigid cystoscopy has a limited role in patients with pure symptoms of OAB unless other pathology is suspected. Hence, endoscopy is recommended in the following situations: ■ ■

When initial testing suggests other pathologies, such as microscopic hematuria (possibility of bladder tumor) When pain or discomfort occurs in a patient with OAB (suggesting a possible intravesical lesion)

Urodynamics There is some controversy in regard to the use of urodynamic testing in patients with LUTS, particularly those with OAB, based on several issues: ■ ■ ■

Urodynamics is an invasive test with possible side effects, mainly UTI. The test is uncomfortable and could be embarrassing for the patient. The test has a considerable false-negative rate.

DO incontinence is incontinence caused by an involuntary detrusor contraction. In a patient with normal sensation, urgency is likely to be experienced just before the leakage episode. ICS recommends that the terms “motor urge incontinence” and “reflex incontinence” should no longer be used, because they have no intuitive meaning and are often misused. In everyday life, the patient attempts to inhibit detrusor activity until he or she is in a position to void. Normally, after the aims of the filling study have been achieved and the patient has a desire to void, the “permission to void” is given. That moment is indicated on the urodynamic trace, and all detrusor activity before this point of “permission” is defined as “involuntary detrusor activity.”40 Normal detrusor function allows bladder filling with little or no change in pressure. No involuntary phasic contractions occur despite provocation. There is no lower limit for the amplitude of an involuntary detrusor contraction, but confident interpretation of low-pressure waves (amplitude 5 hr/wk) were investigated. The investigators reported that urine loss in group I was related to sneezing or coughing in 87% of the women; in group II, urine loss was related to running or tennis in 38% and aerobics in 35%. The purpose of the study by Larsen and Yavorek54 was to determine the prevalence of UI and to assess the stages of pelvic support in a population of nulliparous, physically active college students at the United States Military Academy. This was an observational study of 143 female cadets. Cadets in the freshman and sophomore classes were asked to participate in an ongoing study comparing UI and pelvic organ support before and after attending military jump school. The results were as follows. Overall, the group of women were found to be very physically active, with 69.2% (99/143) exercising four or more times per week and 91.6% (131/143) working out three or more times. Additionally, 49.7% (60/131) of those exercising spent 60 minutes or more per session. Running was the most common form of exercise, with 77.6% (111/143) running for at least part of their workout. Of the women examined, 50.3% (72/143) were found to be at pelvic prolapse stage 0 and 49.7% (71/143) at stage I. A total of 18.8% (27/143) women who reported recurrent incontinence, with the largest percentage (44%) being SUI by history. The conclusion of the authors was that 50% of nulliparous cadets had stage I prolapse on standardized pelvic support examination, primarily in the anterior compartment. A small percentage admitted to incontinence at the time of examination. This study indicates that trauma from physical activity might cause pelvic support defects that could predispose women to incontinence problems later in life. Because the percentage of women who exercise and participate in sports is increasing, it is important to determine what effect this increase has on pelvic support. Jorgensen and coworkers55 reported that Danish nursing assistants, who are exposed to frequent heavy lifting, were 1.6-fold more likely to undergo surgery for pelvic organ prolapse or UI than women in the general population. Fitzgerald and colleagues17 surveyed women who worked for a large academic center. Of the 1113 women surveyed, 21% (n = 232) reported UI at least monthly. Incontinent women were significantly older and had a higher BMI than continent women. Women in this study used self-care practices such as using absorbent products or limiting fluids. Several studies have reported on the relationship between UI and military training and activities. Women in the military have physically demanding roles, and the presence of UI can interfere with lifestyle as well as ability to perform assigned duties. Sherman and associates56 found that 27% (N = 450) of U.S. female army soldiers (average age, 28.5 years) experienced problematic UI, with 19.9% saying they leaked significantly during training tests. However, only 5.3% felt that urine leakage had a significant impact on their regular duties. This may due to the fact that 30.7% women stated that they took precautions such as voiding before training, wearing “extra-thick” pads, and limiting fluid intake. A very disturbing finding in this study was that 13.3% of women restricted fluid intake while participating in strenuous

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field training. A third study57 looked at women flying in highperformance combat aircraft. Aircrews who fly in high-gravity aircraft perform an M-1 maneuver, which is a modified Valsalva with an isometric contraction of the lower extremities. This movement may place women pilots at risk for urine loss due to increased intra-abdominal pressure and increased gravity load. Results of a questionnaire of aircrew (N = 274) indicated that 26.3% had experienced urine loss at some time. However, pilots did not have higher UI rates than women in other positions (e.g., navigators, weapon systems operators). In this study, as in others, crew position, history of vaginal delivery, and age were found to be significant risk factors.3 The data from these studies demonstrate that UI is not rare among young women. We think that young incontinent women need an appropriate treatment to prevent the possible worsening of symptoms, and it seems logical to develop strategies for screening those with high risk factors.58 We assume that UI is a female disease with much higher prevalence than medical literature has demonstrated and with a surprisingly high prevalence in groups of physically active women.48,53 Based on our current knowledge of the effect of pelvic floor muscle training (PFMT), we recommend that specific training pelvic programs be proposed as the first choice of treatment. The perineal blockage technique and the Knack technique appear to be effective adjunctive modalities for pelvic floor rehabilitation and can be proposed for active women.48,53 The impact of carefully instructed pelvic floor exercises on sports incontinence has not been as beneficial as that in a normal female population. BLADDER RETRAINING AND PELVIC FLOOR MUSCLE EXERCISES Bladder Retraining No single treatment modality should be considered the first choice of treatment in the management of either the unstable bladder or the urge syndrome. Bladder retraining, sometimes termed bladder drill, is a noninvasive treatment modality that has been used not only for these two conditions but also for mixed incontinence and even SUI.59 It has been widely studied over the last 20 to 25 years, although little scientific work has been published recently. An excellent review of the subject is available in the Cochrane Library.60 Bladder retraining is a form of behavioral therapy in which a patient with an intact nervous system “relearns” to inhibit a detrusor contraction or a sensation of urgency. Such behavioral therapies include biofeedback, hypnotherapy, and acupuncture. There are good reasons why behavioral methods or therapies may be of value in idiopathic urge syndromes. Although these have been a subject of review,59,61 they can be summarized as follows: ■ ■

■ ■ ■

A strong emotive event in a patient' life may be the initial trigger for urinary symptoms. Patients with detrusor instability have a higher neuroticism score on formal testing than do patients with genuine SUI. There is relationship between detrusor instability and hysterical personality trait. Patients with detrusor instability are more likely to have psychosexual problems than patients with genuine SUI. Other behavioral forms of therapy, such as hypnosis, are effective methods of treatment.

■

Treatment is itself associated with a strong placebo effect, which has been estimated at between 4% and 47% in clinical trials.

A frequently used treatment regimen59 can be broken into the following components: ■ ■ ■ ■

■

■ ■

■

Exclude pathology. Explain the condition to the patient. Explain the treatment and its rationale to the patient. Instruct the patient to void at set times during the day, for instance, every hour. The patient must not void between these times; she must wait or be incontinent. The voiding interval is increased by increments (of perhaps 30 minutes) after the initial goal is achieved, and the process is then repeated. The patient should have a normal fluid intake. The patient should keep her own input and output chart. The increasing volumes of urinary output at increasing intervals act as a reinforcement reward. The patient should receive praise and encouragement on reaching her daily targets.

Typical results note that up to 90% of patients become continent, although there is a relapse rate up to 40% within 3 years of treatment. Such relapses could be treated by reinstitution of a retraining program. Most patients with a urodynamically demonstrable unstable bladder who were rendered symptom free also became stable on urodynamic assessment.59 Several studies have compared bladder retraining regimens with pharmacologic treatment. Further studies have addressed the issue of supplementing bladder retraining with drug treatment. Although the data from such studies are currently limited, there is no evidence so far that supplemental drug therapy is superior to bladder retraining alone.59,61 Therefore, bladder retraining appears to be equal or superior to drug treatment and may have greater long-term benefits. There are numerous areas for future study. There is a lack of consistency in bladder retraining programs. There is a need not only to evaluate an optimal program but also, most importantly, to identify the optimal increment in both the voiding interval and the rate at which the voiding interval is iterated after attainment of each stage of the regimen. A shorter initial voiding interval, for instance, may be necessary for women with more intense frequency or with less confidence. There is clearly a popular benefit from widespread treatment in a community as opposed to treatment of a small number of patients in hospital, but there is a need to determine the optimal supervision in the community. There is a need for comparison between bladder retraining and other physical interventions. There are limited data, for instance, comparing bladder retraining with PFMT, estrogen replacement, and electrical stimulation. Bladder retraining is an effective treatment for women with urge, stress, or mixed UI. It is not yet clear whether the urodynamic diagnosis specifically affects the likelihood of success. There is a lack of consistency in bladder retraining programs, and an optimal regimen needs to be identified. However, it is possible that regimens will need to be tailored to the individual patient.59 Bladder retraining appears to have benefits similar to those of drug treatment; it does not appear to be benefited by supplementary drug treatment; and it may have greater long-term benefits than drug therapy. Bladder retraining appears to be largely free of adverse effects and is acceptable to patients.59

Chapter 19 CONSERVATIVE MANAGEMENT OF OVERACTIVE BLADDER

Figure 19-1 Pelvic floor muscle strength is important to the control of urge incontinence. Patients are taught “urge strategies” to prevent loss of urine. The goal is to challenge the urgency by using pelvic floor muscles to inhibit the involuntary detrusor contraction; this is accomplished by rapidly contracting the pelvic floor muscles and taking a deep breath. Pabd: Intra-abdominal pressure; Pdet: Detrusor pressure; Pves: Intra vesical pessure; SSUE: Externam Striated Urethral Sphincter; PFM: Pelvic Floor Muscles.

Pelvic Floor Muscle Exercises The role of the PFMs in urge incontinence is less clear. Therapy is usually based on improving PFM function—in particular, the ability to sustain a contraction—and then using the improved muscle function in a bladder retraining program. Reflex inhibition of a detrusor contraction may be possible by producing a voluntary contraction of the striated muscles of the pelvic floor and activating the perineodetrusor inhibitory reflex, as described by Mahony and colleagues.62 PFM exercises are also used for the treatment of OAB. The rationale behind the use of PFMT to treat urge incontinence is the observation that electrical stimulation of the pelvic floor inhibits detrusor contractions. The aims of this approach are to inhibit detrusor muscle contraction by voluntary contraction of the PFMs when the patient has the urge to void and to counteract the fall in urethral pressure or urethral relaxation that occurs with an involuntary detrusor contraction.63 It has been suggested that reflex inhibition of detrusor contractions may accompany repeated voluntary PFM contraction or maximum contractions (Fig. 19-1). Clinical Results: Bladder Retraining and Pelvic Floor Muscle Exercises Berghmans and associates64 recently reviewed the literature concerning the effectiveness of pelvic floor exercises for the treatment of OAB and concluded that, although bladder retraining seems to yield some benefit, the available data are insufficient to fully evaluate the efficacy of this strategy. Conservative treatment

of women with UI, specifically PFMT and bladder retraining, is recognized as effective therapy.65 Only three published reports of a single-session group education were identified, but none assessed improvement of pelvic floor contraction strength, an expected outcome of PFMT, or lengthening of intervoid interval, an expected outcome of bladder retraining.66-68 Frequency-volume charts (FVCs) are an important tool in the investigation of patients with lower urinary tract dysfunction, because they provide the ability to study lower urinary tract function during normal daily activities. The information obtained by FVCs is currently limited to the number of voidings, the voided volumes, the distribution of voidings between daytime and nighttime, the registration of episodes of urgency and leakage, and the number of incontinence pads used. Little research has been done to incorporate a sensory evaluation into these charts. However adequate sensation of bladder filling is important for proper bladder function. Currently, sensory information related to bladder filling is mainly deducted from cystometric studies in which the patient is catheterized and, in case of conventional cystometry, the bladder is artificially filled. To what extent these factors confound the sensory evaluation remains unknown. De Wachter and Wyndaele69 studied whether FVCs can be used as a noninvasive tool for sensory evaluation. Furthermore, they studied the agreement between sensory data derived from these charts and data obtained during conventional cystometry. Fifteen healthy female, nulliparous students, without urologic history, between 18 and 24 years old, were asked to fill out a 3-day FVC during normal daily activities. They noted the time and volume of each micturition and scored the grade of perception of bladder fullness according to predefined grades before each micturition. All volunteers also underwent a conventional cystometric bladder filling at 30 mL/min and were asked to describe all sensations related to bladder filling. They also correlated these sensations to the same predefined grades of perception of bladder fullness that were used on the FVCs. Data from this pilot study showed that the information obtained from FVCs can be extended beyond just recording “classic” parameters such as voided volumes: these charts can be used as a noninvasive, inexpensive tool to evaluate sensations of bladder filling during normal daily activities. Moreover, sensory data deducted from FVCs show good agreement with sensory data from cystometric bladder filling. Because the largest proportion of the micturitions was made without a desire to void in the healthy female population we studied, the distribution of sensation-related micturitions may provide a new parameter to study bladder behavior. Including a sensory evaluation into FVCs and evaluating the distribution between sensationrelated and non–sensation-related micturitions may improve the power of these charts to discriminate among different pathologies. The use of these “sensation-related FVCs” is currently being investigated in groups of incontinent patients.64 In a randomized controlled trial, Sampselle and colleagues70 examined changes in pelvic floor contraction strength and intervoid interval at 12 months after intervention in women who attended a single group teaching session followed up with a single brief individual visit. They further examined the treatment group’s knowledge of PFMT and bladder training as well as technique and adherence. Volunteers who qualified from telephone screening were randomly assigned to a control (no treatment) group or to a treatment group that received the behavioral modification program. Both groups underwent clinical baseline screening and evaluation of pelvic floor contraction strength (measured by palpation of pressure and displacement), as well as

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documentation of intervoid interval (measured by a 3-day voiding diary). The treatment group received a 2-hour classroom presentation of the anatomy and physiology of continence, with an explanation of the rationale and verbal instruction in PFMT and bladder training. This was followed in 2 to 4 weeks with an individualized evaluation to test knowledge (measured by response to eight multiple-choice items), technique (measured by palpation), and adherence (measured by report of practice). Brief additional instruction in PFMT and bladder training was provided as needed. Follow-up was by phone and mail every 3 months except at the 12th month, when all participants underwent a final clinical examination. A total of 195 control and 164 treated participants completed the study.70 In the treatment group, mean knowledge at 2 to 4 weeks after instruction was 87% for PFMT and 89% for bladder training. Palpation of PFMT technique revealed that 65% of participants needed no further instruction, and 32% required brief individual instruction (approximately 5 minutes); 3% were unable to demonstrate effective PFM contraction techniques after individual instruction and were excluded from the study. With respect to adherence, participants in the behavioral modification program were encouraged to practice PFMT every day throughout the 12-month postinstruction period. At the 3month data point, 82% of participants reported practicing PFMT two to three or more times per week. At 12 months, the treatment group demonstrated significant increases in pelvic floor contraction pressure (P = .0008) and displacement (P < .0001), compared with controls. Intervoid interval also was significantly lengthened for those in the treatment group compared with the control group (P < .0001). A regression model that adjusted for UI level at baseline and other covariants, including race, age, and education, revealed a treatment group effect that was significant at P < .0001 for each of the three outcomes (i.e., pelvic floor contraction pressure, displacement, and intervoid interval). The authors concluded70 that this randomized controlled trial of the effectiveness of group teaching of behavioral therapies followed by brief individual instruction as needed demonstrated positive effects on knowledge, technique, and adherence. The significant 12-month outcome differences between treatment and control groups provided evidence that this was an effective method to teach these behavioral therapies. Clearly, the necessary knowledge and skills were imparted to enable women to perform PFMT and bladder training at levels that resulted in significant differences in pelvic floor contraction strength and lengthened intervoid interval. The greater efficiency of instruction when provided to groups rather than individually warrants further study to document cost-effectiveness outcomes. BIOFEEDBACK THERAPY Biofeedback can be defined as the use of monitoring equipment to measure internal physiologic events, or various body conditions of which the person is usually unaware, to develop conscious control of body processes. Biofeedback uses instruments to detect, measure, and amplify internal physiologic responses to provide the patient with feedback concerning those responses.71,72 The most common modalities of biofeedback involve electromyography (EMG), manometry, thermal measurement, electroencephalography (EEG), electrodermal feedback, and respiration

rate. The instruments include sensors (EMG, pressure sensors) for detecting and measuring the activity of anal or urinary sphincters and PFMs, and techniques also have been developed to measure activity of the detrusor muscle for treatment of UI. A major reason for high interest in biofeedback is that the patient is actively involved in treatment. Biofeedback has now gained several potential applications for urologic conditions, having been successfully used for patients with urologic disorders such as detrusor instability. Biofeedback is a very specific treatment that can restore bladder control by teaching patients to modulate the mechanisms of continence. Also, behavioral therapy can be used in combination with pharmacologic therapy to provide an excellent response with minimal side effects.73 For biofeedback to be useful, several conditions must be met. There must be a readily detectable and measurable response (e.g., bladder pressure, PFM activity), and there must be a perceptible cue (e.g., the sensation of urgency) that indicates to the patient when control should be performed. Of particular importance is the patient’s ability to modify bladder function through operant conditioning. In the application of biofeedback to the treatment of UI, the concepts of neurophysiology of voiding and learning and conditioning are combined to accomplish the clinical objective of voluntary control of bladder function.74,75 Cystometric Biofeedback During cystometry, bladder pressure readings are available to the patients and may provide a mechanism for feedback that allows them to acquire better control. An overactive detrusor contraction with imperative urge should be inhibited before it escalates. Cystometric biofeedback is used to teach the patient how to recognize and inhibit detrusor contractions. Other authors have described similar methods.76 The original technique for biofeedback in the management of idiopathic detrusor instability was described by Cardozo and colleagues.77 After an initial explanation, the patient’s detrusor pressure was measured cystometrically and recorded on a chart recorder. A voltage-to-frequency converter was connected to the detrusor pressure strain-gauge amplifier. This emitted an auditory signal rather like a siren. Alternatively, for patients who exhibited confusing rectal contractions during the treatment sessions, the auditory feedback could be transferred to the intravesical-pressure strain gauge. The gain and frequency range were adjusted to suit the individual patient, but once a baseline tone was decided upon, the note emitted through the loudspeaker increased in pitch as the detrusor pressure rose and decreased as it fell. A mirror was positioned in such a way that the patient could observe the detrusor (or intravesical) pressure tracing. Female patients attended four to eight 1-hour sessions, during which the bladder was filled two or three times with 0.9% saline prewarmed to body temperature. When detrusor contractions occurred, they could be heard and seen, and these signals were associated with the symptoms of urgency and urge incontinence. The women were instructed to attempt to control the pitch of the auditory signal by deep breathing, general relaxation, tightening certain muscle groups, or any other means they found helpful. As patients learned to control their detrusor pressure during supine cystometry, provocative maneuvers such as erect cystometry, laughing, coughing, and running the water taps were employed.78 Burgio and colleagues79 used a similar technique of bladder biofeedback in a behavioral training program for older

Chapter 19 CONSERVATIVE MANAGEMENT OF OVERACTIVE BLADDER

Figure 19-2 During cystometric biofeedback, bladder pressure readings are available to the patient and may provide feedback that allows the patient to acquire better control. The rectal catheter measures and subtracts the intra-abdominal pressure. When detrusor contraction occurs, it can be seen on the screen. The patient is requested to produce a voluntary pelvic floor contraction when she feels the strong urge to void. Pabd (top): Intra-abdominal pressure; Pves (middle): Intra-vesical pressure.

men and women with urge incontinence. During training sessions, patients observed bladder pressure during retrograde filling and practiced keeping bladder pressure low. Cystometric biofeedback requires the use of a transurethral bladder catheter and a rectal pressure monitor for suppression of the uninhibited contractions (Fig. 19-2). The bladder catheter measures increases in intravesical pressure indicative of uninhibited contractions. The rectal catheter measures and subtracts the intra-abdominal pressure. Artificial filling of the bladder is necessary for this technique of biofeedback and represents more accurately the conditions under which continence must be achieved during regular daily activities. Although this concept appears to be clinically relevant, filling of the bladder requires catheterization, with its associated discomfort and a small degree of risk. Such therapy could be proposed using urodynamics equipment with the biofeedback included. Pelvic Floor Muscle Biofeedback The three common signal sources (bladder pressure, anal sphincter pressure, and vaginal EMG) are significantly altered by increases in intra-abdominal pressure. Simultaneous measurement of abdominal activity should be done with all biofeedback therapy techniques. Intra-abdominal pressure can be measured easily using an internal rectal balloon. Electromyographic activity of the rectus abdominis muscles can be determined by surface electrodes. The abdominal muscle activity is displayed via two active electrodes placed 3 cm apart just below the umbilicus. A ground electrode is placed on a convenient bony prominence, such as the iliac crest.73,80,81 Myographic biofeedback training has a twofold purpose: to increase the activity of weak muscle groups and to promote relaxation of spastic or tense muscles. Biofeed-

back equipment has become sophisticated, and there are two basic types designed to suit the setting in which biofeedback is implemented: the outpatient clinic, where the patient is trained using a comprehensive clinic system, and the individual’s home, where a smaller unit is used, generally on a more frequent basis. Abdominal muscle activity should be monitored simultaneously with PFMs so that patients can learn to contract the PFMs selectively. These measurements can be accomplished through a twochannel system. Another approach to biofeedback for UI79,82 combines bladder pressure and pelvic floor musculature biofeedback in a procedure that provides simultaneous visual feedback of bladder, external anal sphincter, and intra-abdominal pressures. Using twochannel biofeedback (one with surface electrodes and one using an internal rectal balloon), patients are taught to contract and relax the PFMs selectively without increasing bladder pressure or intra-abdominal pressure. The initial step in treatment is to help the patient identify the PFMs. It is important to test contractility and to know how the patient contracts the PFMs when instructed to squeeze around the examining fingers. Very often, the contraction is performed incorrectly (Fig. 19-3). Instead of lifting up with the muscles, the patient is observed to be bearing down, which is counterproductive because it increases intra-abdominal pressure and therefore bladder pressure.82-84 This response has been referred to as a “reversed perineal command”82,85 or a “paradoxical perineal command.” The frequency of such incorrect contraction is about 22% in women after childbirth, and it decreases to about 10% in women in the perimenopausal period. Bump and colleagues86 reported that 50% of women were unable to perform a voluntary PFM contraction after brief verbal instruction, and as many as 25% mistakenly performed a Valsalva maneuver. This type of

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A

B

Figure 19-3 Recording of electromyographic (EMG) surface activity of pelvic floor muscles (bottom), urethral pressure (middle), and vesical pressure (top) during a hold maneuver. The graphs demonstrate abnormal voluntary perineal contractions. A, Paradoxical Perineal Command: Instead of lifting up the anus and vagina in drawing up, the patient is observed to be bearing down or pushing, which is counterproductive because it increases intra-abdominal pressure and therefore bladder pressure. From bottom to top, four tracings: Surface EMG of Pelvic floor muscles activity (bottom); Urethral pressure Profile (second); Vesical Pressure (third); Differential pressure: Urethral Pressure minus Vesical Pressure (top). B, Co-contraction of abdominal muscles. Some patients use antagonist muscles when contracting the pelvic floor From bottom to top, four tracings: Surface EMG of Pelvic floor muscles activity (bottom); Urethral Pressure Profile (second); Vesical pressure (third); Differential pressure: Urethral Pressure minus Vesical Pressure (top).

improper PFM activity needs to be identified and eliminated as soon as possible. It seems clear that patients who bear down in this way must be identified before being asked to practice Kegel exercises at home, or the efforts will be futile. In addition, such maneuvers might increase vaginal wall descent or worsen UI by increasing intra-abdominal pressure. Except for the group of patients who are unable to perform a proper voluntary pelvic floor contraction, it seems very rare to perform a voluntary pelvic floor contraction without a co-contraction of the abdominal muscles. Research suggests that it is not possible to maximally contract the PFM without co-contraction of transverse abdominal muscle (transversus abdominis). Contraction of this muscle can be observed as a pulling in of the abdominal wall with no movement of the pelvis. During the initial biofeedback session, it is also common to observe patients perform pelvic muscle contractions accompanied by contraction of synergistic muscles such as adductors (pressing the knees), or gluteal muscles (squeezing the buttocks). This natural substitution of the stronger muscles for the weakened or minimally perceived motor response can also have negative consequences. An instrumentation system allows multiple measurements and modalities to be displayed on a monitor and stored in a computer database. Feedback must be relevant in order to enhance learning and to focus on agonist (levator ani) and antagonist (abdominal) muscles. Patients should be able to recognize that the proper muscles are being used appropriately. Therapy is

first concentrated on inhibition of the antagonist muscles and decreasing the activity of surrounding muscles while increasing the response of the agonists. Because the aim of performing the contraction is to contract the PFMs correctly, the proprioceptive signals generated by the substituting muscles can easily be misinterpreted as originating from the pelvic floor rather than from the strong antagonist muscles. When the substituting muscles contract, their afferents can mask low-intensity sensory signals that may be generated by the weakened PFMs. This faulty maneuver perpetuates the substitution pattern and delays the development of increased awareness of the isolated PFMs. During the initial session (Fig. 19-4), this pattern occurs quite often as the patient attempts to contract her PFMs by moving the upper part of the abdomen, even rising off the table. When the patient is instructed to relax the abdominal muscles or the surrounding muscles (adductors/gluteal), substitution of the interfering muscles may be detected by the biofeedback equipment. An abdominal substitution pattern used when attempting to “hold back” leads to a false maneuver of pushing down, which causes a rise in intra-abdominal pressure. With such recruitment, the contraction would only maximize a rise of intra-abdominal pressure, resulting in an increase in EMG abdominal signals. To minimize inappropriate tensing, it is helpful to train patients to keep these muscles relaxed when trying to prevent urine loss. For this purpose, patients are instructed to breathe evenly and to relax abdominal muscles. During the training

Chapter 19 CONSERVATIVE MANAGEMENT OF OVERACTIVE BLADDER

Figure 19-4 The initial step in treatment is to help the patient identify the pelvic floor muscles. During the session, the patient needs to be comfortably installed with legs slightly apart and abducted. Patient is instructed to breathe evenly and to relax abdominal muscles.

sessions, the patient is also asked to place one hand on her lower abdomen to palpate the faulty abdominal contraction. Biofeedback therapy provides the patient with better volitional control over skeletal muscles such as levator ani and urinary sphincter, heightened sensory awareness of the pelvic floor area, and decreased muscle antagonist contractions. PFM strength and control are also important to the control of urge incontinence.79,82 Patients with urge incontinence are taught “urge strategies” to prevent loss of urine during detrusor contractions. Patients with urge incontinence typically report that they rush to the toilet when they experience a sensation of urgency to void. Voluntary PFM contraction to control urge has been shown to be effective in the management of urge incontinence.79,82,87,88 Godec and colleagues89 inhibited reflex contraction of the detrusor muscle with an electrically stimulated contraction of the PFM. Reflex inhibition of detrusor contractions may accompany repeated voluntary pelvic floor contractions.90 Patients are taught a more effective pattern of responding to urgency. They are told not to rush to the toilet, because this movement increases abdominal pressure on the bladder, increasing the likelihood of incontinence. Instead, they are encouraged to pause, sit down if possible, practice relaxing, and contract the PFMs maximally several times in an effort to diminish urgency, inhibit detrusor contraction, and prevent urine loss. When urgency subsides, they then proceed at a normal pace to the toilet.79,82,87 Multichannel systems (Figs. 19-5 and 19-6) allow pressure and EMG measurements as well as abdominal measurements, thereby providing the clinician with multiple methods of biofeedback. Clinical Results Many studies have demonstrated that treatment with biofeedback reduces incontinence. The data show clearly that the treatments are safe and effective, and they yield high levels of patient satisfaction. Cardozo and colleagues91 reported a study of 34 women between the ages of 16 and 65 years treated by bladder biofeedback. They were given an average of 5.4 sessions of cystometric biofeedback. Female patients were treated in 4- to 8-hour

sessions at weekly intervals, during which the bladder was filled two to three times using 0.9% saline prewarmed to body temperature. A total of 87% were cured or improved subjectively and 60% objectively. No patient’s condition was worsened by biofeedback. The six patients who failed to improve had severe detrusor instability, with detrusor contractions greater than 60 cm H2O and a cystometric capacity of less than 200 mL. They found it impossible to inhibit detrusor activity. One of them was later found to have multiple sclerosis. Patient follow-up proved difficult, but of 11 women who were initially cured or improved, 4 remained completely cured and 2 had undergone surgery. These long-term results seem disappointing, but all the patients in the group had previously failed drug therapy.92 Millard and Oldenburg93 used bladder training, bladder biofeedback, or a combination of both to treat 59 women with frequency, nocturia, urgency, and urge incontinence. The women underwent urodynamic testing, which revealed detrusor instability alone in 38 women, detrusor instability and sphincter incompetence in 6, sensory urgency in 12, and sensory urgency and sphincter incompetence in 3. All patients were initially hospitalized for 5 to 14 days and then assigned to either a Frewen-type bladder training program or a weekly outpatient biofeedback program. Millard and Oldenburg stated that “biofeedback was undoubtedly the most useful of the techniques.”55 They claimed a 74% rate of cure or major improvement for patients with detrusor instability. None of the patients with detrusor instability and urethral incompetence was cured, although three of them improved, with conversion to stable cystometry. Of the women with sensory urgency, 92% benefited. It is difficult to see how biofeedback could have helped them, because their symptoms could not have been associated with cystometric changes. We think that patients were using their inhibition skills to abort detrusor contractions and give themselves enough time to reach the bathroom; it is difficult to separate components of treatment (bladder retraining, biofeedback). Kjolseth and colleagues94 assessed the outcome of biofeedback therapy (bladder filling with visual stimuli) in 15 children (6 to 12 years of age) and 7 adults (aged 20 to 50 years) with cystometrically proven detrusor instability. Detrusor pressure was visually conveyed to the patient during repeated bladder fillings. Patients were instructed to inhibit detrusor pressure incrementally by tensing the pelvic floor musculature. None of the children was completely cured, but nine showed a marked decrease in the number or extent of symptoms. Two children showed moderate improvement, and for four children the treatment failed. One adult was completely cured, two showed moderate improvement, and four remained the same. None of these patients was converted to stable bladder. In an uncontrolled study, Burgio and colleagues79,82 demonstrated an 88% reduction in incontinence episodes in elderly men with urge incontinence who participated in an average of four 30-minute biofeedback training sessions. O’Donnell and Doyle95 treated 20 male patients (>65 years old) with urge incontinence using 1-hour sessions twice weekly for 5 weeks. The mean number of incontinence episodes was decreased from 5.1 to 2.0 per day after treatment. Burns and colleagues96,97 conducted a randomized clinical trial of vaginal EMG biofeedback in the treatment of SUI or mixed UI.9 As part of this trial, older women (>55 years old) were assigned to 8 weeks of biofeedback-assisted PFMT. A no-treatment control group contained 38 subjects. Biofeedback combined with daily practice resulted in a mean 61% reduction in frequency of urine losses; this was not significantly better than

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Figure 19-5 The unit used by the patient at home could be connected the stationary device. (Courtesy of HMT Inc.)

Figure 19-6 Multichannel system allows pressure and electromyographic measurements as well as abdominal measurements. (Courtesy of Incare Medical Products Inc.).

training without biofeedback, which resulted in a mean 59% reduction of incontinence. Both results were significantly better than the mean 9% increase in incontinence demonstrated by the control group. Because the mechanisms of urge incontinence are in some ways different from the mechanisms for SUI, the role that biofeedback plays in treating these conditions may be different as well. The contribution of biofeedback in the treatment of urge incontinence was examined in a randomized study of 20 older men and women with persistent urge incontinence.98 Patients who were trained without biofeedback responded as well to treatment as those trained with bladder-sphincter biofeedback. Later, a larger randomized controlled trial corroborated this finding. Burgio and colleagues82,88 studied 222 older women with predominantly urge incontinence. Patients were randomly assigned to behavioral training with biofeedback, behavioral training without biofeedback, or behavioral training with a self-help booklet. Instead of biofeedback, training was done with verbal feedback based on vaginal palpation. Patients in the biofeedback group showed a 63% reduction of incontinence, which was not significantly different from the 69% reduction in the verbal feed-

Chapter 19 CONSERVATIVE MANAGEMENT OF OVERACTIVE BLADDER

back group. These findings indicate that careful training with verbal feedback is as effective as biofeedback in the first-line treatment of urge incontinence, and that biofeedback can be reserved for those cases in which women cannot successfully identify their muscles. Stein and colleagues evaluated the long-term effectiveness of transvaginal or transrectal EMG biofeedback in 28 patients with stress and urge incontinence.99 Sixty percent of the patients had detrusor instability, as demonstrated by urodynamics. Biofeedback successfully treated 5 (36%) of 14 patients with SUI and 9 (43%) of 21 with urge incontinence. The treatment response was durable throughout follow-up, from 3 to 36 months, in all of the responding patients. The authors concluded that biofeedback is a moderately effective treatment for stress and urge incontinence and should be offered to patients as a treatment option. PFMT with biofeedback is also effective for treatment of predominantly urge incontinence. Burgio and colleagues82,87 conducted a randomized clinical trial to compare biofeedback-assisted behavioral training with drug therapy (oxybutynin chloride) for treatment of urge incontinence in ambulatory, communitydwelling older women. A volunteer sample of 197 older women (55 to 92 years of age) was evaluated. Subjects were randomized to four sessions (8 weeks) of biofeedback-assisted behavioral treatment, drug treatment, or a placebo control condition. Daily bladder diaries were completed by patients before, during, and after treatment. Behavioral training, which resulted in a mean 80.7% improvement, was significantly more effective than drug treatment (mean, 68.5% improvement; P = .009). Similarly, a larger proportion of subjects in the behavioral group achieved at least 50% and 75% reductions of incontinence (P = .002 and P = .001, respectively). Although the values for full recovery of continence (100%) followed a similar pattern, the differences were not statistically significant (P = .07). Several secondary outcome measures were used to assess the patients’ perceptions of treatment. On every parameter, the behavioral group reported the highest perceived improvement and satisfaction with treatment progress (P < .001). Wyman and colleagues compared the efficacy of bladder training, PFM exercise with biofeedback-assisted instruction, and combination therapy in women with genuine SUI and in those with detrusor instability.100 This was a large randomized clinical trial with three treatment groups. Women with incontinence (N = 204: 145 with SUI and 59 with urge incontinence due to instability) received a 12-week intervention program, including six weekly office visits and six weekly mail or telephone contacts. They were followed up immediately and after 3 months. The combination therapy group had significantly fewer incontinent episodes, better quality of life, and greater treatment satisfaction immediately after the therapy. No differences between groups were observed at the 3-month follow-up. The authors concluded that combination therapy consisting of bladder training and PFMT with biofeedback had the greatest immediate efficacy in the management of female UI.

ELECTRICAL STIMULATION Basic Principles and Mechanism of Action Electrical currents are applied therapeutically to stimulate muscle contraction, usually through activation of nerves that supply muscles. Electrical stimulation was first used in the management

of UI in 1952, when Bors101 described the influence of electrical stimulation on the pudendal nerves, and in 1963, when Caldwell102 developed electrodes that were permanently implanted into the pelvic floor and controlled by radiofrequency. Godec and associates103 first described the use of nonimplanted stimulators specifically for bladder inhibition. Initial work in animals indicated the potential of this therapy, and early clinical experience in Europe supported its likely efficacy. Much confusion surrounds electrical stimulation, and some is the result of inconsistent nomenclature. Commonly used terms include “functional electrical stimulation” and “neuromuscular electrical stimulation.” Further confusion has arisen because of the wide range of stimulators, probes, and applications used. Electrical stimulation is an effective treatment for urge incontinence. This technique uses natural pathways and the micturition reflexes , and its efficacy relies on a preserved reflex arc, with complete or partial integrity of the PFM innervation.104 Based on animal experiments, direct stimulation of afferent or efferent fibers appears to be the most important mechanism to enhance the reflex response. The mechanism of electrical stimulation for urge incontinence is a reflex inhibition of detrusor contraction. Bladder inhibition is accomplished through three mechanisms105,106: 1. Activation of afferent fibers within the pudendal nerve by activation of the hypogastric nerve at low intravesical pressure, corresponding to the filling phase 2. Direct inhibition of the pelvic nerve within the sacral cord at high intravesical pressure 3. Supraspinal inhibition of the detrusor reflex In principle, defective control of the urinary bladder, resulting in urge incontinence, is caused by a central nervous dysfunction that affects central inhibitory control of the micturition reflex. Appropriate electrical stimulation may restore the inhibition effect.107 Threshold intensity varies inversely with fiber diameter. Any pulse configuration can provide nerve activation, and many stimulation waveforms have been used to cause neural excitation.105,107 These include biphasic capacitively coupled pulses, monophasic square pulses, biphasic square pulses, and monophasic capacitively coupled spike pulses. Pulse durations ranged from 0.08 milliseconds up to 100 milliseconds but the most common used pulse duration is 0.2 milliseconds. To minimize electrochemical reactions at the electrode-mucosa interface, biphasic or alternating pulses are recommended.108 The effects of electrical stimulation on detrusor inhibition are optimal with different stimulation parameters: 10 to 20 Hz. The sacral afferent nerves, particularly the autonomic nerves of the pelvic organs, are poorly myelinated (Aδ) or unmyelinated (C) fibers, which conduct current at a slow rate of 5 to 20 Hz. Thus, in the treatment of bladder instability and hyperreflexia, low-frequency stimulation is applied to the pudendal nerve afferents through probes. In both forms of electrical stimulation, the frequencies are chosen based on the clinical diagnosis. In mixed incontinence, two strategies are used. One strategy involves the use of a compromise setting of approximately 20 Hz; the other involves delivering both low-frequency and high-frequency stimuli.109 Low frequencies (1 to 5 Hz) generate twitch contractions, allowing little sustained tension to develop in the muscle. Slow-twitch muscle fibers have a natural firing rate of 10 to 20 Hz, whereas fast-twitch fibers fire at 30 to 60 Hz. Treatment of chronic lower urinary tract dysfunction can be challenging and difficult. Behavioral and medical therapies in

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the sacral micturition center and the nucleus of Onuf). These are most probably the areas where the therapeutic effect of neuromodulation of the bladder through PTNS takes place. PTNS has a clear carry-over effect: 30 minutes of stimulation induces a lasting beneficial effect. In cat experiments, a 5-minute stimulation of afferent nerves resulted in more than 1 hour of bladder inhibition.119 Perhaps some kind of learned behavior is activated by intermittent stimulation such as PTNS. This supposition suggests that higher regions within the cortical central nervous system are also involved. Furthermore, in rats, PTNS exerted its influence on FOS expression, suggesting neuromodulating action.120 In addition, activation of endorphin pathways at sites within the spinal cord could affect detrusor behavior.121 Parallel to the gate control theory for pain, it can be suggested that stimulation of large somatic fibers modulates or inhibits the thinner afferent Aδ or C fibers, thus decreasing the perception of urgency.122 Clinical Practice and Selection of Patients

Figure 19-7 Transcutaneous electrical stimulation of the peripheral nerves may facilitate inhibition of detrusor activity, with specific parameters: intensity of 5 to 8 V, frequency of 10 Hz, and pulse width of 5 to 20 msec. Transcutaneous posterior nerve stimulation is performed with a needle inserted 5 cm cephalad to the medial malleolus.

patients with urge incontinence often result in unsatisfactory outcomes, leaving the patient with refractory incontinence no other option but surgery (e.g., bladder transsection phenolization, clam-ileocystoplasty).110 To sidestep surgery, electrostimulation offers an alternative for therapy-resistant urge incontinence. During the past decades, electrical stimulation of the bladder, sacral roots, and pudendal nerves has been explored with varying success. However, these treatments involve technical problems, high cost, or low patient compliance because of the discomfort associated with treatment procedures.111-113 Transcutaneous electrical nerve stimulation (TENS) of the S3 segment is a useful alternative in patients with detrusor instability.114 Okada and coworkers stimulated thigh muscles and observed clinical improvement for several weeks to months.115 However, TENS therapy can induce skin irritation and allergy at the stimulation site due to chemical and mechanical irritation. Consequently, other stimulation approaches have been explored. Research has focused on the effect of stimulation of afferent nerves in the lower limb. In cat experiments, Lindstrom and Sudsuang demonstrated detrusor inhibition through stimulation of the myelinated afferents of the hip adductor muscles.116 Inspired by acupuncture points over the tibial and peroneal nerves, McGuire and Zhang applied TENS to these nerves to treat bladder overactivity. They reported restoration of bladder control in a small group of patients.117 Stoller proposed percutaneous posterior tibial nerve stimulation (PTNS) for treatment of bladder and pelvic floor dysfunction.118 In this multicenter study, PTNS was used for the treatment of symptoms related to bladder overactivity. The posterior tibial nerve is a mixed nerve, containing motor and sensory nerve fibers. Correct placement of the needle electrode induces a motor and sensory response (Fig. 19-7). Centrally, the posterior tibial nerve projects to the sacral spinal cord in the same area where bladder projections are found (i.e.,

Different types of electrical stimulation (see Figs. 19-4 and 19-5) include office therapy and the home treatment program.123,124 Office therapy is also called the outpatient program or in-clinic treatment. With this approach, a stationary device with a wide range of electrical parameters is used in the office or clinic under the control of the therapist. The system can be modified to suit the needs of each patient. Devices with microcomputers allow the caregiver to change the stimulation parameters (e.g., waveform, pulse width, frequency) based on patient history and urodynamic data. Many probes are available (Fig. 19-8), including a standard two-ring vaginal probe; an intra-anal probe; and a two-channel vaginal and anal insertion probe. Special conditions that affect the choice of probe include the following: ■ ■ ■

Vaginal size (depth of 4 to 12 cm) and shape (e.g., atresia or gaping vagina) Vaginal angle (10 to 45 degrees) and quality of the levator ani (thin or thick fibers) Type and degree of vaginal wall descent

Accurate assessment of individual anatomic differences allows the therapist to select the appropriate electrodes to obtain the most effective results. Low frequencies (10 to 20 Hz) are used for urge incontinence. Some stimulators have controls that are used to adjust frequency, duty cycle, and timing. The stimulus and intensity of the current are also adjustable, and all of these systems allow easy graduation in the intensity of contraction. Therapeutic stimulation is recommended for women with UI who have undergone unsuccessful PFMT as a first-line treatment.125,126 Pelvic floor electrical stimulation is one of the nonsurgical approaches when treating UI. The stimulation decreases detrusor contractions in cases of OAB. Electrical stimulation must be performed in conjunction with a bladder drill and biofeedback. The main contraindications to electrical stimulation are as follows: 1. 2. 3. 4.

Demand heart pacemakers Pregnancy, if the risk of pregnancy exists Postvolume residual (PVR) greater than 100 mL Obstruction of the urethra, a fixed and radiated urethra, or a heavily scarred urethra

Chapter 19 CONSERVATIVE MANAGEMENT OF OVERACTIVE BLADDER

Figure 19-8 Many probes are available with special conditions that affect the choice of probe. A, A probe designed specifically for patients with a wide vaginal hiatus (top left). B, The reference electrode is inserted in the middle of the vaginal probe (top right). C, During a severe relaxation of the pelvic floor or an important defect of levator ani muscles, the “finger” probe is used (bottom left). The patient is in lithotomy position with a one leg well supported while the therapist stimulates one side of the pubococcygeal portion of the levator ani with the “finger probe,” which is a two channel probe. D, An anal probe with the reference electrode inserted in the middle (bottom right).

5. 6. 7. 8.

Bleeding Urinary tract infection or vaginal discharge Complete peripheral denervation of the pelvic floor Severe genital prolapse with complete eversion of the vagina

There are a few strict contraindications,1,2,6,7 and there is general agreement that a patient with pelvic floor disorder associated with other conditions4,5,8 will not respond to treatment. Although patients with severe genital prolapse are poor candidates, mild prolapse is not a significant problem. Many patients will not accept treatment with vaginal or anal probes because of ethical and religious beliefs. These concerns must be taken into account before this therapy is advocated. This issue is especially relevant when home treatment is being considered, because some patients will not agree to insert the device themselves, and some will refuse this type of treatment altogether. Functional, anatomic, and attitudinal barriers are more common in frail elderly people. Cognitively or functionally impaired subjects require a participating caregiver. In the elderly, home care treatment could be performed by a nurse or a physical therapist. Patients with mild to moderate incontinence are the best candidates for this treatment, regardless of age. Because of the slight discomfort and embarrassment that may occur during stimulation, motivated patients of any age are the best candidates for this therapy. For unmotivated patients, another technique may be recommended, such as PTNS or electromagnetic stimulation. In PTNS, the posterior tibial nerve is stimulated. This nerve closely relates to pelvic nerves for bladder and perineal floor; therefore, a retrograde stimulation of S3 roots and of sacral spinal

cord can be obtained. Several studies on the effects of this treatment on OAB syndrome have been published.127,128 TENS of acupuncture points (see Fig. 19-7) may be used to inhibit detrusor activity. Surface electrodes are placed bilaterally over both tibial nerves or both common peroneal nerves.129 Percutaneous stimulation of peripheral S2 and S3 afferents by way of the posterior tibial nerve modulates unstable detrusor activity. PTNS130 is performed with a 34-gauge needle inserted 5 cm cephalad to the medial malleolus TENS of the peripheral nerves may facilitate inhibition of detrusor activity with specific parameters, such as intensity of 5 to 8 V, frequency of 2 to 10 Hz, and pulse width of 5 to 20 msec. Clinical Results One major problem in reviewing the literature on incontinence is the lack of data on the pretreatment status of patients, particularly when noninvasive forms of therapy are studied.131 The interpretation of data may be limited because patients often are not classified urodynamically. Nonimplanted stimulators are effective in treating UI: overall, an improvement or cure rate of approximately 50% is common. No serious morbidity is reported with this type of therapy. Side effects that are common with drug therapy (e.g., anticholinergics, α-adrenergics) do not occur with electrical stimulation. Eriksen and Eik-Nes132 performed a study of chronic stimulation with a dual vaginal-anal electrode in 55 patients. They found an initial response rate of 68%, with 47% of the overall group becoming dry. The objective response was an improved stress

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profile. Kralj133 studied the influence of the type of idiopathic urge incontinence on the efficient outcome of treatment with acute maximal electrical stimulation. Eighty-eight female patients were divided into a motor urge group (n = 40) and a sensory group (n= 48). Both groups underwent vaginal stimulation for 20 minutes. Of the 40 patients in the motor urge group, 55% were cured and 20% showed improvement, whereas 25% showed no change. Of the 48 patients in the sensory group, 87.5% were cured and 12.5% showed improvement. Bent and associates134 conducted a study of 45 patients with genuine SUI (n = 14), detrusor instability (n = 10), or mixed incontinence (n = 21) and assessed the applicability of electrical stimulation and patient response to short-term electrical home therapy. Treatment was administered for 15 minutes twice daily for 6 weeks. Treatment consisted of biphasic stimulation at 20 Hz for urge incontinence and at 50 Hz for genuine SUI. The ratio of the duty cycle was 2 seconds “on” and 4 seconds “off.” Subjective results showed improvement in 71% of patients with genuine SUI, 70% of patients with urge incontinence, and 52% of patients with mixed incontinence. The pressure-transmission ratio improved in four patients, and urethral pressure profiles improved in five patients with genuine SUI. Bladder capacity during cystometry improved in only one patient with detrusor instability. Bourcier and Juras135 conducted a study to establish the effectiveness of two different modalities: home treatment, consisting of treatment for 20 minutes twice daily for a 6-week period, and office therapy, consisting of twice-weekly treatment administered in the clinic for an average of 12 sessions. Of the 95 patients included in the study, 50 received home treatment and 45 received office therapy. Twelve patients had undergone a hysterectomy, and six had previously undergone colposuspension. All were evaluated with urodynamic tests. Patients with urge incontinence received biphasic capacity-coupled pulses with a continuous current of 20 Hz at a pulse width of 0.75 msec. Patients with genuine SUI received biphasic square pulses of 50 Hz at a pulse width of 1 msec. Current intensity was 0 to 90 mA or 0 to 24 V. During the first follow-up period (3 months), 71% of patients in the office therapy group reported subjective improvement, as did 51% of patients in the home treatment group. During the late follow-up period (6 months), 85 patients were studied (7 patients in the home treatment group and 3 in the office therapy group withdrew). Of the patients who participated in late follow-up, 47 were in the office therapy group (28 patients with genuine SUI and 19 with urge incontinence) and 38 were in the home treatment group (23 patients with genuine SUI and 15 with urge incontinence). The cure rate was approximately 50%. This study showed that both office therapy and home treatment are effective forms of treatment for patients with genuine SUI or urge incontinence. In addition, this treatment has no side effects. The results showed a higher degree of improvement with office therapy than with home treatment. The number of patients who did not continue physiotherapy was much higher in the group with urge incontinence (43%) than in the group with genuine SUI (15%). Patients with urge incontinence had less motivation to continue with therapy and also had a higher degree of psychological factors (e.g., chronic depression, psychosomatic disturbances, hysterical personality), which included reluctance to cooperate actively with treatment. Many factors (e.g., age, severity of incontinence) are less crucial than previously thought, but the single factor that is consistently associated with positive outcome is greater motivation

and/or compliance with the intervention.136 Brubaker and colleagues137 compared electrical stimulation with sham electrical stimulation in women with urodynamically proven detrusor instability and found a significant reduction in detrusor overactivity in the electrical stimulation group only. This prospective double-blind, randomized control trial included 121 women who had genuine SUI (n = 60), urge incontinence (n = 28), or mixed incontinence (n = 33). The study had two groups: a treated group (n = 61) and a placebo-controlled group (n = 60) with sham electrical stimulation. Patients underwent 8 weeks of treatment. Electrical stimulation was administered twice daily for 20 minutes with a vaginal probe at 20 Hz, a pulse duration of 0.1 msec, and a duty cycle of 2 seconds “on” and 4 seconds “off.” The output was 0 to 100 mA; in the placebo group, sham electrical stimulation was characterized by no current in patient circuit. Objective cure was reported in 49% of patients in the treatment group who had detrusor instability, but no change was observed in patients with genuine SUI in either group. The authors found no significant change in the number of women who had genuine SUI on urodynamic testing at 2 months. In a prospective multicenter study,138 35 patients with complaints of urge incontinence underwent 12 weekly sessions of PTNS at one of five sites in the Netherlands and one site in Italy. FVCs and I-QoL and SF-36 questionnaires were completed at 0 and 12 weeks. Success was analyzed by using subjective and objective criteria. Overall subjective success was defined as the willingness to continue treatment, whereas objective success was defined as a significant decrease (to 10 voids/day, >2 voids/night, subjective “unchanged”). Significant increases were seen in bladder capacity measurements; maximum flow rate and maximum detrusor pressure decreased somewhat. This study is the only one to date to report cost data. SANS treatment for each patient cost b895 (US$770), compared to b10,290 (US$8849) for implantation of the Medtronic InterStim device.23 Three centers in the Netherlands collectively enrolled 49 patients (34 female, 15 male) over a 5-month period; 37 enrollees had OAB, and 12 had nonobstructive retention (detrusor hypocontractility urodynamically confirmed). Patients were treated

PTNS trials reported as of February 2005 are summarized in Table 23-1. Klingler and coworkers were the first European group to report results, having treated 15 OAB patients (11 women) with 12 weekly SANS sessions. They documented follow-up at a mean of 11 months. All patients enjoyed a reduction in pelvic pain (statistically significant reduction in visual analogue scale from a mean of 7.6 to 3.1). Mean diurnal frequency fell from 16.1 to 4.4 episodes, and nocturnal frequency from 8.3 to 1.4 episodes. Seven patients (47%) were considered to have complete responses (≤8 voids/day, ≤2 voids/night, subjective “cure”); three (20%)

Table 23-1 Trials of Percutaneous Tibial Nerve Stimulation First Author and Ref. No.

Year

Primary Symptoms

N

Criteria

Key Findings

Stoller22

1998

Frequency, incontinence, pelvic pain

98

Decrease in frequency, pain

Klingler23

2000

OAB

15

Urgency, voiding diary, urodynamics, pelvic pain

Govier29

2001

Refractory OAB

53

Van Balken24

2001

OAB, nonobstructive retention

49

>25% reduction in diurnal/nocturnal voiding frequency Frequency, nocturia, voided volumes, HRQOL

Statistically significant improvement in diurnal and nocturnal frequency; 80% of patients had 75% reduction in incontinence >50% reduction in mean pelvic pain score; decrease in mean diurnal and nocturnal frequency from 16 and 4 episodes to 8 and 1 episodes, respectively 71% of patients met success criteria (P < .05)

Vadoninck26

2003

OAB

90

Frequency, incontinence, HRQOL, urodynamics

Vandoninck25

2003

Urge incontinence

35

Incontinence episodes, frequency, nocturia, HRQOL, pad use

Vandoninck27,28

2003

Nonobstructive urinary retention

39

Daily catheterizations, residual volume, voided volume, HRQOL

Van Balken34

2003

Chronic pelvic pain

33

Visual analogue pain scale, HRQOL

Shafik36

2003

Fecal incontinence

32

Congregado Ruiz45

2004

Frequency/urgency, urge incontinence

51

HRQOL questionnaire, rectometric parameters HRQOL, voiding diaries

HRQOL, health-related quality of life; OAB, overactive bladder; QOL, quality of life.

OAB patients: mean 17% reduction in frequency, 38% reduction in nocturia; increased voided volumes; improved HRQOL. Retention patients: modest, nonsignificant improvements in voided volumes and catheterization episodes Decrease in 24-hour frequency from 13 to 10 and in incontinence episodes from 5 to 2 daily; improved bladder capacity but no overall improvement in detrusor instability Median incontinence episodes per day reduced from 5 to 1; 16 patients completely dry; significant decreases in nocturia and pad use and improvements in HRQOL Decrease in mean catheterizations from 2.5 to 2.0 and in residual volume from 241 to 163 mL; improvements in HRQOL, especially incontinencespecific QOL. ≥50% reduction in pain score in 21% of patients, 25%-50% reduction in 18%; improved SF-36 scores Improvement in 78% of patients by fecal incontinence questionnaire Statistically significant improvements in frequency/urgency, HRQOL, and pain

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with 12 weeks of SANS. The results were positive and statistically significant24 but considerably more modest than those reported by Klingler and colleagues.23 Among the OAB cohort, diurnal frequency was reduced by an average of 2.8 episodes, to 16.5 times per day, and nocturnal frequency was reduced by 1 to 2.6 episodes per night. Voided volumes were also increased, and patients reported significant improvements in both general and incontinence-specific health-related QOL. Among the patients with retention, mean voided volumes increased slightly, and number of catheterizations decreased, but these findings were not significant.24 The same group later expanded to five sites in the Netherlands and one in Italy and has published three additional papers, focusing, respectively, on urge incontinence,25 OAB,26 and nonobstructive retention.27 A total of 164 patients were treated. Vandoninck and coworkers reported the largest single cohort of patients treated with PTNS to date, accruing 90 consecutive OAB patients (67 female, 23 male) to 12 weekly stimulation sessions. The 24-hour frequency decreased from a mean of 13 to 10 episodes, leakage episodes decreased from a mean of 5 to 2 daily, and mean voided volume increased from 135 to 191 mL (all statistically significant results). Health-related QOL scores also improved significantly. Among 46 patients undergoing urodynamic profiling both before and after PTNS, mean cystometric bladder capacity increased from 243 to 340 mL. The proportion of patients with detrusor instability (70%) did not change, but the volume at which instability was triggered increased from 133 to 210 mL. Also of note, improvement in urodynamic parameters significantly predicted treatment success in terms of subjective improvement.26 Thirty-five patients (25 women) with documented urge incontinence received the same 12 weeks of PTNS and had, on average, more dramatic responses. The median baseline number of incontinence episodes was 5 per day. After treatment, this median fell to 1 episode per day, and 16 patients had no leakage episodes. Nocturia likewise decreased from a median of 2 to 1 per night, and pad use declined from a median of 3.5 daily to none. Health-related QOL once again improved. Thirty-one percent of these patients decreased their 24-hour voiding frequency to eight episodes or less. There was a trend toward greater likelihood of subjective improvement with increased stimulation intensity in terms of amperage.25 Finally, these authors accrued 39 patients (27 women) with chronic nonobstructive urinary retention to 12 weeks of PTNS. The mean number of catheterizations decreased from 2.5 to 2.0 per day, and the mean catheterized (residual) volume decreased from 241 to 163 mL; the total voided volume increased accordingly. Forty-one percent of patients had a 50% or greater reduction in catheterized volume. Seven patients reduced their catheterization frequency to once daily; two of these patients had no residual urine on frequency-volume charts, but no patient became consistently catheter-free. Once again, both overall and incontinence-specific health-related QOL increased significantly. Contrary to this group’s experience with urge-incontinence patients, however, increased amperage in urinary retention patients decreased the likelihood of positive subjective success.27 In a companion paper focusing on urodynamic findings in this cohort, the authors reported that, on multivariate analysis, four pretreatment urodynamic parameters—maximal detrusor pressure, maximal flow rate, bladder voiding efficacy, and bladder contractility index—predicted subjective success on PTNS, with an area under the curve of 0.73.28

In the United States, only one experience with PTNS has been reported to date. Govier and associates reported their results from a prospective, multicenter trial at five medical centers, including 53 patients (48 women, mean age 57 years) with OAB refractory to all standard treatments, which they treated with weekly bilateral SANS sessions. Eighty-nine percent of patients completed the 12-session study. Seventy-one percent of patients met the study goal of at least a 25% reduction in diurnal and/or nocturnal urinary frequency, with the mean reductions in diurnal, nocturnal, 24-hour, and excess (>10 episodes/day) frequency being 25%, 21%, 22%, and 70%, respectively (all P < .05). On standardized questionnaires administered during the study, study participants reported a mean 35% improvement in urge incontinence episodes, a 30% improvement in pain, and a 20% improvement in incontinence-related QOL (all P < .05). The authors did not report longer-term efficacy results. There were no serious adverse events. One patient each experienced moderate pain at the needle site, moderate right foot pain, and stomach discomfort; all of these symptoms resolved spontaneously.29 None of these studies examined either survey- or urodynamics-based acute effects of PTNS. One paper, however, reported on the acute urodynamic effects of TTNS in 44 patients with OAB. During stimulation, mean first involuntary detrusor contraction occurred at 232 mL of filling, compared with 163 mL at baseline. Maximum cystometric capacity likewise increased, from 221 to 277 mL. Only 50% of these patients had an acute positive response during stimulation in terms of either increased volume at first involuntary detrusor contraction or total cystometric capacity.30 PTNS FOR NONURINARY MANIFESTATIONS OF PELVIC FLOOR DYSFUNCTION To date, PTNS has been studied primarily in patients with OAB, urge incontinence, and detrusor hypocontractility. However, increasing evidence supports the use of this modality for other indications referable to PFD, many of which have been previously validated in studies of central stimulation. Van Balken and coworkers treated 33 patients (22 male) who had chronic pelvic pain with 12 weeks of PTNS. Twenty-one percent of these patients experienced at least 50% improvement in pain as assessed by the visual analogue scale; an additional 18% experienced improvement of 25% to 50%. Among the 14 (42%) subjective responders (i.e., those who requested continued treatment), the mean pain score fell from 5.9 (range, 4.5 to 7.3) to 3.7 (range, 2.7 to 5.2). The authors also reported improvement in several domains of the Medical Outcomes Study Short Form-36 (SF-36), including role physical, physical functioning, pain, change of health, and overall score.31 Andrews and Reynard reported a single case of a patient with detrusor hyperreflexia resulting from a T8 spinal cord injury whose bladder capacity doubled, from 150 to 165 mL at baseline to 310 to 320 mL with PTNS.32 Finally, Shafik and colleagues applied 4 weeks of PTNS treatment using the SANS device every other day to 32 patients (22 women) with fecal incontinence refractory to standard treatments, which was caused either by uninhibited rectal contractions (26 patients) or by anal sphincter relaxation (6 patients). They reported improvement in 78%; after treatment, eight patients relapsed, and six of these responded to repeated PTNS therapy.33 Further tangential evidence for the efficacy of PTNS in the management of nonurinary PFD symptoms can be found in

Chapter 23 POSTERIOR TIBIAL NERVE STIMULATION

small studies of traditional acupuncture and acupressure treatments at the Sp-6 site. Acupuncture at this point has been shown to stimulate labor and to ameliorate labor pains34; acupressure has been used for symptoms of acute cystitis, and it was used successfully to alleviate the pain of primary dysmenorrhea in the majority of a cohort of young women.35 For this latter indication, growing evidence supports the use of transcutaneous neurostimulation at Sp-6 and other sites for greater efficacy.36

Box 23-1 Key Advantages of Percutaneous Tibial Nerve Stimulation • Efficacy is comparable to gold-standard pharmaceutical treatment. • Nerve stimulation has a minimal side effect profile. • The approach is cost-effective. • PTNS does not preclude central neuromodulation or other treatments.

CONCLUSIONS AND FUTURE DIRECTIONS In a recent review of various techniques of neurostimulation, central and peripheral, for bladder dysfunction, Van Balken and colleagues estimated the overall intent-to-treat success of these modalities at 30% to 50%.37 Results achieved to date with PTNS should be considered in relation to anticholinergic medications, which constitute the “gold standard” treatment for many of the symptoms related to PFD. In the largest trial to date of women with OAB, Swift and associates41 reported on 417 women treated with extended-release tolterodine. They found a 53% reduction in incontinence episodes, from a mean of 3.2 to 1.5 per day, and a 16% drop in 24-hour frequency, from 10.8 to 9.0 voids. These results were statistically significantly better than those realized among the 410 women treated with placebo, whose incontinence episodes and 24-hour frequency fell by 30% and 12%, respectively. The results of Vandoninck and colleagues, described earlier, compare favorably, with a 60% reduction in incontinence episodes and a 23% drop in frequency.26 The increase in mean voided volume was likewise higher with PTNS (from 135 to 191 mL, for a 41% increase)26 and with tolterodine (from 141 to 179 mL, for a 26% increase) than with placebo (from 136 to 149 mL, for a 10% increase).41 Although the PTNS studies were less rigorously designed and less powerful statistically than the larger pharmaceutical trials, it should be stressed that PTNS studies universally have been conducted among patients whose PFD symptoms are refractory to standard therapy, including oral anticholinergic medications; the results of PTNS might therefore be better still among unselected, treatment-naïve cohorts, who have et to be treated with neurostimulation in the context of a published study. Side effects of treatment are an important further consideration. Twenty-five percent of patients taking extended-release tolterodine complained of dry mouth, 40% of whom had moderate or severe symptoms. There was also a statistically significant increase in abdominal pain with extended-release tolterodine versus placebo (4.3% vs 1.7%).38 In contrast, no major complications of PTNS have been reported in any of the studies published to date; indeed, even minor complications, such as persistent puncture site bleeding or pain, appear to be consistently rare. Puncture site infection has never been reported. PTNS may also be more cost-effective than chronic oral medication; Klinger reported a cost of $770 for 12 weeks of PTNS and reported sustained improvement in voiding parameters at a mean of 11 months of follow-up.23 By comparison, 11 months of tolterodine treatment would cost about $1030.39 Finally, if percutaneous neuromodulation fails, patients may still potentially benefit from central sacral neuromodulation; in pursuing a trial of PTNS, no bridges have been burned with respect to eligibility for or potential success of central stimulation. The principal advantages of PTNS are summarized in Box 23-1.

An implantable device currently under development, named the Urgent-SQ (Cystomedix, Andover, MN), combines the benefits of chronic, at-home therapy—currently offered only by the InterStim sacral stimulator—with the relatively low cost and minimal invasiveness of peripherally targeted neuromodulation. In an ongoing trial, patients with OAB, urge incontinence, and/or functional bladder retention who demonstrate successful responses to percutaneous neuromodulation will receive the Urgent-SQ implant, which consists of a small (30 minutes), the use of the forceps, high birth weight (>4 kg), and a third-degree perineal tear are important risk factors for pudendal nerve damage.43 After spontaneous and instrumental deliveries, 21% and 34% of women complained of stress urinary incontinence and 5.5% and 4% reported fecal incontinence, respectively. Only 22% of patients incontinent during pregnancy continued to complain about it after delivery.44 Episiotomy, one of the few surgical procedures that does not require the patient’s informed consent, is widely performed during delivery despite its doubtful usefulness. It is becoming increasingly accepted that an episiotomy may be more harmful that useful. Supporters of routine episiotomy maintain that it avoids uncontrolled lacerations and extended relaxation of the pelvic floor; the contrary view is that there is no evidence that first- or second-degree perineal tears cause long-term consequences and that episiotomies do not seem to protect against third- and fourth-degree tears, which are associated with unpleasant sequelae. Midline episiotomies cause significantly higher rates of third- and fourth-degree perineal tears than mediolateral episiotomies; they are not helpful in protecting the pelvic floor during delivery and can heavily prejudice anal continence.45,46 Despite this, midline episiotomy is still widely used, probably because it is believed to improve healing and reduce postpartum pain. Restrictive episiotomy guidelines have many potential advantages, such as less suturing, more minor complications, and less posterior perineal trauma, but they do not result in any difference in pain therapy and the incidence of severe trauma, and they are associated with an increase risk of anterior perineal trauma.47,48 The consequences of episiotomy are independent of maternal age, duration of second stage of labor, possible complications, the use of forceps or vacuum extraction during delivery, and baby birth weight. Regional anesthesia may be used to relieve labor pain, but its correlation with pelvic floor damage remains controversial. Epidural anesthesia, relaxing the pelvic floor, provides a greater control of passage of the fetal head and subsequently reduces perineal lacerations, but a prolonged second stage of labor can enhance the incidence of pudendal nerve damage. Analysis of the relationship between regional anesthesia and pelvic floor injury suggested that the rate of significant damage was higher with epidural anesthesia because of the increase in episiotomies and instrumental deliveries.49 In many women with stress incontinence, pelvic floor muscle exercise has been effective in improving it,50 with no additional benefit accruing from biofeedback.51 The theoretical basis for physical therapy is that facilitation and strengthening of muscles may improve periurethral muscular efficiency and that training of pelvic floor muscles can improve structural support of the pelvic organs. Morkved and Bo,52 after a prospective, matched, controlled study evaluating the long-term effect of an immediate

Chapter 27 PATHOPHYSIOLOGY OF STRESS INCONTINENCE

postpartum pelvic floor training course, concluded that it is helpful in the prevention and treatment of urinary incontinence and that improvement is still present 1 year after delivery. Miller and coworkers, 53 after studying the characteristics of women “responders” compared with “nonresponders” to pelvic floor electrical stimulation, affirmed that a minimum of 14 weeks was needed to see the first objective improvements (i.e., at least 50% reduction in leakage episodes). Pelvic floor exercises are not effective in all women. Patient motivation is essential for long-term success, but the quality of the pelvic floor muscles and their innervation are also important. If the muscle is normally innervated and is sufficiently attached to the endopelvic fascia, by contracting her pelvic muscles before and during the stress, a woman is able to reduce the leakage, and the pelvic floor exercises are likely to be an effective therapy. If the pelvic floor muscle is denervated as a result of significant neural damage, it may not be possible to rehabilitate the muscle adequately to make pelvic muscle exercises an effective strategy. If the muscle is totally disconnected from the fascial tissues, any possible contraction may not be effective in supporting the urethra or maintaining its position under strain.54,55 ROLE OF CONNECTIVE TISSUE The bladder is a complex, distensible organ comprising of an inner urothelium and suburothelial layer, an important smooth muscle component (i.e., detrusor muscle) with neurologically controlled tissue, and an outer serosal layer. Connective tissue, composed of collagen, elastin, smooth muscle, fibroblasts, and blood vessels, is present in all of these layers. It has been suggested that collagen has the primary function of tension transfer in most tissues, and it is reasonable to suppose that it plays an equivalent role in the bladder. Types I and III collagen can be found in the detrusor layer, and type IV collagen is in the basement membrane under the urothelial layer and surrounding individual smooth muscle cells. Although the connective tissue is passive in that it does not require energy to function, it plays a unique structural role in providing the bladder wall tissues with resilience and tensile strength. These physical properties are related to the quantity and types of collagen present and its arrangement. Changes in collagen type and content may affect bladder compliance. Collagen is the main constituent of endopelvic fascia, and abnormalities in the quantity, type, and quality of collagen have been observed in women with stress incontinence and in those with genitourinary prolapse.56-58 Regulation of collagen synthesis depends on intrinsic factors within individual cell types and on extrinsic factors such as cytokines, growth factors, and mechanical forces. Because progressive alteration of the connective tissue of the bladder or in the pelvis may result in structural weakness, it is important to investigate and define the factors that contribute to abnormal pathophysiology. It was suggested by Petros and Ulmsten59 in 1990 in their integral theory that stress and urge incontinence may have a common cause, with the anatomic defects related to a primary abnormality of connective tissue failure. With laxity, the anterior vaginal can be a primary etiologic factor, and this may result in the activation of stretch receptors in the bladder neck and proximal urethra, which triggers an inappropriate micturition reflex. These events may produce detrusor overactivity and cause the filling symptoms of the overactive bladder, including urgency,

frequency, nocturia, and urgency incontinence. The deficient anterior vaginal wall does not efficiently transmit the closure pressure that would otherwise be generated by proper functioning of the pubourethral ligaments, the vaginal hammock, and the pubococcygeus muscles. We need to identify the cells responsible for the synthesis of the proteins that contribute to defective connective tissue and to describe the mechanisms by which these cells acquire the altered synthetic phenotype. In some individuals, the changes in connective tissue, which can be associated with the pathogenesis of incontinence, may be related to age or the hormonal milieu. With increasing age, the ratio of connective tissue to muscle is reduced, and although the formation of collagen cross-links stabilizes the collagen molecules, this also prevents remodeling and flexibility. The hormonal changes during pregnancy can result in abnormal remodeling of collagen, which may be another important factor in the development of incontinence. In every case, the exact cellular mechanisms by which hormones, cytokines, or other peptide factors influence the mechanical properties of connective tissue remain unclear. Connective tissue plays an important role in the overall physiologic function of the lower urinary tract and pelvic floor. The age-related weakening of connective tissues can influence tissue and organ function, and it is likely that the increased focus on connective tissue changes will in the future provide a better understanding of the pathophysiology and lead to more effective management of stress urinary incontinence and vaginal prolapse.

EFFECT OF URETHRAL POSITION AND FUNCTION ON STRESS URINARY INCONTINENCE Urethral Hypermobility The cause of urethral hypermobility (i.e., increased mobility) is thought to be a loss of normal extrinsic support of the urethra because of weakness of the endopelvic fascia and pelvic floor muscles. During stress, the bladder neck and the proximal urethra descend, and there is an incomplete distribution of abdominal pressure to the urethra (i.e., pressure-transmission deficit). The bladder pressure exceeds urethral pressure, and urine leaks. Urethral hypermobility can result from abnormalities of vaginal and pelvic anatomy. It is usually initiated by childbirth, and it is worsened by aging and alterations in hormone levels. Stretching, tearing, and avulsion of the levator muscles result in the urogenital hiatus becoming longer and wider. This change results in chronic anterior displacement of the pelvic organs, with loss of any organ support at rest and especially during straining. Stretching or tearing of the cardinal and uterosacral ligaments may result in anterior displacement of the uterus at rest or during straining, and the resultant stretching of the vaginal wall continues this displacement and causes the loss of the normal superior vaginal sulcus and vaginal folds. The consequence of these forces is a rotational descent of the proximal urethra away from its retropubic position and the eventual development of stress urinary incontinence. On lateral cystourethrograms, the main anatomic change is loss of the posterior urethrovaginal angle, with the urethra and trigone falling into the same plane.60-62 Radiographic studies cannot distinguish between lateral or central defects in vaginal wall support because they appear in the same sagittal plane. It is

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necessary when examining the patient to determine which defect is present and to what extent. Because the proximal urethra rotates out of the focal plane of ultrasonographic probes or magnetic resonance imaging (MRI), coronal images of vaginal relaxation cannot provide adequate anatomic information during leakage. Despite extensive data about anatomic defects, it is difficult to correlate the influence of these defects, the vaginal position, and the urethral closure mechanism. Not all women with stress incontinence had vaginal prolapse, and prolapse repairs do not always cure the stress incontinence. Conversely, women who redevelop stress incontinence after an apparently successful operation do not always have a recurrence of prolapse.63 Vaginal support is important for maintaining urinary continence, but intrinsic sphincter deficiency also must be considered. Intrinsic Sphincter Deficiency In 1988, Olsson and Blaivas64 suggested a new classification of stress incontinence, in which for the first time appeared the concept of intrinsic urethral weakness as a cause for incontinence without a vaginal support defect. They called this type III incontinence to differentiate it from types I and II, both of which were associated with movement. This category is often described by the term intrinsic sphincter deficiency (ISD),65 which emphasizes the importance of the intrinsic components of the sphincter acting under the influence of pudendal innervation and comprises the urethral striated and smooth muscle, mucosa, and submucosal layers. When ISD was proposed as a new type of stress incontinence without vaginal mobility, the diagnostic trend was to evaluate the cause of stress incontinence as a dichotomy caused by hypermobility or ISD. The typical ISD patient was described as having a low urethral closure pressure, a stovepipe (pipe stem) appearance on cystoscopy, and an open or funneled urethra at rest or during minimal effort on radiographic images. Typical causes included ischemia after pelvic or vaginal surgery, multiple previous operations, denervation in neurogenic patients, or radiation damage. These examples of ISD now represent extreme forms and the most severe cases. Another important aspect is urethral denervation after childbirth and its association with urinary and fecal incontinence.66,67 Crushing or traction injuries to the pudendal nerve during labor and delivery are a primary cause of sphincteric incompetence. A causal relationship between pudendal nerve injury and stress incontinence has been established in animal studies.68-70 Because the pudendal nerve innervates the external urethral sphincter, pudendal nerve injury causes denervation and dysfunction of the urethra, resulting in decreased urethral resistance, which is especially evident during stressful physical activities. Stress incontinence is often associated with a decrease in the electrophysiologic function of the pudendal nerve,71 the striated urethral sphincter,72 and the pelvic floor muscles.73,74 Hypermobility and Intrinsic Sphincter Deficiency: From Dichotomy to Continuum In the past few years, there has been a gradual change from a dichotomous classification of stress incontinence as hypermobility or ISD. ISD alone is rare, and urethral hypermobility may occur commonly without significant ISD, but usually there is a combination of both. This evolution in our understanding followed development of the concept of Valsalva leak point pressure

(VLPP), introduced by McGuire in 1995,75,76 and the analysis of long-term results of incontinence surgery. During studies of urethral bulking with collagen, researchers documented that continence improvements were not related to changes in urethral closure pressure, but instead corresponded to the level of abdominal pressure required to produce leakage in the absence of intrinsic detrusor contraction. Despite lacking a specific anatomic or theoretical basis and standardization of recording methods or a consensus on how to deal with an associated prolapse, a low VLPP (65 years) who were matched to a younger cohort for BMI, parity, mode of anesthesia, and whether it was a primary or secondary continence procedure. Exclusion criteria included mixed symptoms and concomitant prolapse surgery. The investigators demonstrated lower satisfaction rates for incontinence outcomes in the elderly group. At a median of 12 months, 15 (45%) older versus 24 (73%) younger women had no urinary symptoms (P = .05).51 Other reports are primarily observational and did not match the patients for other variables. Sevestre and associates52 reported a 70% cure rate for a group of 76 women after a mean of 2 years. Rezapour and colleagues19 demonstrated that women older than 70 years with a low MUCP and no hypermobility had a lower success rates with TVT procedures than women not fitting these criteria. Two studies have suggested no difference for outcomes in the elderly. Lo and coworkers26 performed an observational study of 45 older women who had undergone TVT procedures and reported a 90% cure rate with a low rate of morbidity.42 Carey and associates53 compared women older than 80 years with those younger than 80 and found no difference in outcomes for procedures using the cadaveric fascia sling. Herschorn and colleagues25 reported no difference in outcomes of transurethral collagen injections based on age. In summary, most case-control series of older women demonstrate lower efficacy and higher morbidity, but there is no evidence that this is specific to the type of procedure performed. Age is associated with a higher incidence of other factors affecting the outcome and morbidity of the treatment, and only when a multivariate analysis is performed are we able to determine definitive correlations. If someone is not a candidate for surgical therapy because of comorbidities, it is irrelevant whether a Burch colposuspension is as effective as a TVT procedure. The deciding factor is which procedure the patient can tolerate given her comorbidities. Body Mass Index Some studies suggest that obese patients have worse outcomes and higher complication rates with traditional surgical procedures for stress incontinence,54,55 although others have not found obesity to affect outcomes.56-61 The transobturator procedures are being promoted as less morbid procedures in obese women because the abdomen can be completely avoided. This idea has not been substantiated. Although there is no level 1 evidence comparing procedures in patients with high BMIs, a number of published studies have looked at the safety and efficacy of the mid-urethral sling in this population. Chung and colleagues56 retrospectively compared the efficacy and safety of the TVT and laparoscopic Burch procedures in treating genuine SUI in obese patients. They described 91 consecutive cases of TVT alone or TVT combined with other procedures from April 1999 to March 2000 and 51 consecutive cases of the laparoscopic Burch procedures from January 1998 to February 1999. They found no difference in the outcomes based on BMI.56 Mukherjee and Constantine59 compared the subjective cure rates for TVT procedures at 6 months in three groups of women: BMI of 30 or more (n = 87), BMI of 25 to 29 (n = 98), and BMI less than 25 (n = 58). They reported similar cure rates for all three groups.59 Zivkovic and coworkers61 retrospectively

reviewed the 5-year outcome data from 187 of 291 patients who had undergone various procedures for stress incontinence. Patients were separated into similar groups by BMI: BMI of 30 or more (n = 42), BMI of 25 to 29 (n = 90), and BMI less than 25 (n = 55). They also reported no difference in efficacy among the BMI groups, although they had only 26% power to show a significant difference because of the sample size.61 Rafii and colleagues60 reported a series of 187 patients who had undergone TVT procedures and who were separated into the three groups according to BMI: BMI of 30 or more (n = 86), BMI of 25 to 29 (n = 62), and BMI less than 25 (n = 39). No differences were detected in the persistence of stress incontinence or the complication rate. Statistically significant differences were seen in the rate of urge incontinence between first group (3.4%) and the second group (6.4%) and third group (17.9%).60 The 2000 review of obesity and stress incontinence therapy by Cummings and Rodning58 is still relevant. They concluded that “although intuitively and experimentally such procedures are technically more difficult, outcome data reported to date justifies recommending them as the standard of care.”58 In summary, although patients with higher BMIs may have higher overall risks associated with surgery and although the mid-urethral sling procedures may theoretically reduce these risks with less anesthetic and surgical time, there are no data to support selecting a procedure based only on BMI. Neurogenic Bladder The therapeutic approach to the neurogenic patient must be based on an understanding of how her neurologic disease plays a role in the symptoms and the role it may play afterward. These patients have the potential for higher morbidity after surgical treatment of SUI, including voiding dysfunction, urinary retention, or de novo urge incontinence. The implications of a lower success rate or higher morbidity on the patient’s quality of life are more profound then in the non-neurogenic patient. Preoperative UDS plays a significant role in this group of patients as a plan is developed. They all are at risk for postoperative urinary retention requiring catheterization to empty the bladder. It is therefore important to assess their ability and willingness to do so. Documentation of urodynamic overactivity may make postoperative management of urge symptoms easier.62 There is no specific evidence to suggest one procedure over another based solely on the presence of neurologic disease. The potential need for intermittent catheterization may reduce the efficacy with collagen. Use the artificial urinary sphincter may be considered in this group of patients. History of Pelvic Radiation Therapy Patients who have previously undergone radiation therapy have a number of confounding variables that may affect the outcomes and morbidity of stress incontinence procedures. Irradiated tissue has reduced elasticity and vascularity. The patients are more likely to have an immobile urethra and lower urethral resistance because of atrophy and decrease submucosal vascularity. The use of synthetic material, although not contraindicated, may have a higher rate of complications because of urethral or vaginal wall erosion. The need to add compression to a fixed urethra as describe previously may preclude the use of synthetic material due to the added tension that must be place on the sling. The higher incidence of detrusor overactivity or small-capacity

Chapter 29 SURGICAL OPTIONS FOR STRESS URINARY INCONTINENCE

bladder must be assessed before increasing urethral resistance. There are no studies in the literature specifically looking at this challenging group of patients. Plans for a Future Pregnancy The usually recommendation from most clinicians is that patients should wait until they completed their childbearing years before undergoing a repair procedure for SUI.63,64 The TVT product label states that the desire to have children is a contraindication to placement of the TVT. If they have undergone a procedure, they may be advised to undergo a cesarean section as the mode of delivery. A survey of European urogynecologists asked clinicians what type of procedure they would do for a woman who expressed interest in having more children.63 Seventy-eight percent said they would offer treatment if the patient expressed interest, but 91% would offer cesarean section to women who were continent at the time of delivery. Although most would offer the woman a surgical option, many would not perform a TVT procedure, and most would advise cesarean section as the method of delivery. Urethral injection therapy is also an option in this population. There are few published data to guide the clinician in this area. In all cases, the patient needs to be informed about the potential risks. HOW AND WHEN TO INCLUDE A NEW PROCEDURE New procedures are being developed rapidly in this field, but we should remember that there are procedures with documented efficacy and safety that are considered the gold standards in incontinence surgery. Deviation from these established procedures should be based on clearly outlined advantages in achieving better efficacy or less morbidity and demonstrated with high level of evidence. As clinicians, we must remain committed to studying these procedures before widespread use is accepted When that evidence is lacking but clinical experience suggests a benefit exists for our patients, we must demand that the properly designed studies be performed to assess the procedure or product. We must make sure our patients understand what we know about a new procedure when we counsel them about which procedure is best for them. The fastest-growing procedure for incontinence is the TMUS. Although it addresses an important concern of many clinicians and educators regarding the RMUS—the potential morbidity associated with passing a trocar blindly into the retropubic space—it has not undergone sufficient evaluation to recommend it for widespread use, even in subpopulations of women with SUI. The RMUS sling has produced a significant body of literature over the past 10 years, with more than 250 articles posted on PubMed. It has been compared with one of the gold standards in incontinence surgery, the Burch colposuspension, in a well-

designed trial intreating incontinence surgery and found to be equally as effective.6 Before the TMUS procedure can be considered interchangeable with the RMUS procedure, which has been in use for 8 years and has hundreds of articles published in the international literature on its safety and efficacy, the TMUS procedures must be subjected to a rigorous comparison. This procedure must continue to undergo evaluation in properly designed trials before it can be accepted as a standard option in our surgical armamentarium for the treatment of SUI. The following algorithm for choosing an incontinence procedure is based on the information provided in this chapter. Retropubic mid-urethral sling: for the otherwise healthy woman who is bothered by predominant SUI and desires surgical therapy, exhibits hypermobility on examination (i.e., Q-tip resting or straining angle > 30 degrees), has postvoid residual volume of less than 100 mL, with or without the need for concomitant prolapse surgery, regardless of the following urodynamic study parameters: VLPP, detrusor overactivity, or voiding mechanism Urethral bulking agent: for the poor operative candidate Transobturator mid-urethral sling (after discussing paucity of data with patient): for those at high risk for retropubic scarring or with a history of multiple procedures Autologous pubovaginal sling or urethral bulking agent: for those at high risk for erosion, with a history of radiation therapy, with an immobile urethra, or with acute urethral syndrome Urinary diversion: for a woman with a neurogenic bladder or severely incompetent urethra Burch colposuspension or mid-urethral sling: for those undergoing simultaneous abdominal prolapse repair

CONCLUSIONS Despite having many options for treating SUI, we still have insufficient evidence to recommend which procedure will have the greatest efficacy and least morbidity to specific patient populations. To make more evidence-based decisions on which procedure to perform in which patients, we must randomize similar groups of patients to undergo different procedures. Until we have the results of those trials, we must continue to rely on case report series and theoretical reasons for our decisions. Ultimately, the most important tool we have as clinicians is the individualized assessment of and conversation with each patient. This approach includes a thorough history and physical examination that evaluates the neurologic and anatomic condition of the pelvic floor and the patient’s comorbidities. These data are combined with our understanding of the mechanism by which a given procedure resolves incontinence to guide the choice of procedure.

References 1. Leach GE, Dmochowski RR, Appell RA, et al: Female stress urinary incontinence clinical guidelines panel summary report on surgical management of female stress urinary incontinence. J Urol 158:875880, 1997. 2. Canadian Task Force on the Periodic Health Examination: The periodic health exam. Can Med Assoc J 121:1193-1254, 1979.

3. Meakins JL: Innovation in surgery: The rules of evidence. Am J Surg 183:399-405, 2002. 4. Black NA, Downs SH: The effectiveness of surgery for stress incontinence in women: A systematic review. Br J Urol 78:497-510, 1996. 5. Valpas A, Kivela A, Penttnen J, et al: Tension-free vaginal tape and laparoscopic mesh colposuspension in the treatment of stress urinary

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6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

20. 21. 22. 23. 24. 25. 26. 27. 28.

incontinence: immediate outcome and complications—A randomized clinical trial. Acta Obstet Gynecol Scand 82:665-671, 2003. Ward K, Hilton P: Prospective multi-center randomized trial of tension-free vaginal tape and colposuspension as primary treatment for stress incontinence. Br Med J 325:789-790, 2002. McGuire EJ, Fitzpatrick CC, Wan J: Clinical assessment of urethral sphincter function. J Urol 1993; 150:1452-1454. Swift SE, Ostergard DR: A comparison of stress leak-point pressure and maximal urethral closure pressure in patients with genuine stress incontinence. Obstet Gynecol 85:704-708, 1995. Weber AM: Is urethral pressure profilometry a useful diagnostic test for stress urinary incontinence? Obstet Gynecol Surv 56:720-735, 2001. Weber AM: Leak-point measurement and stress urinary incontinence: A review. Curr Womens Health Rep 1:45-52, 2001. Sand PK, Bowen LW, Panganiban R, Ostergard DR: The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 869:399-402, 1987. Blaivas JG, Jacobs BZ: Pubo-vaginal sling for the treatment of complicated stress urinary incontinence. J Urol 145:1214-1218, 1991. Chaikin DC, Rosenthal J, Blaivas JG: Pubovaginal sling for all types of stress urinary incontinence: Long-term analysis. J Urol 160:13121316, 1998. Morgan TO Jr, Westney OL, McGuire EJ: Pubovaginal sling: 4-year outcome analysis and quality of life assessment. J Urol 163:18451848, 2000. Hassouna ME, Ghoniem GM: Long-term outcome and quality of life after modified pubovaginal sling for intrinsic sphincter deficiency. Urology 53:287-291, 1999. Zaragoza MR: Expanded indications for the pubovaginal sling: Treatment of type 2 or 3 stress incontinence. J Urol 156:1620-1622, 1996. Culligan PJ, Goldberg RP, Sand PK: A randomized controlled trial comparing a modified Burch procedure and a suburethral sling: Long-term follow-up. Int Urogynecol J 14:229-233, 2003. Maher CF, Dwyer PL, Carey MP, Moran PA: Colposuspension or sling for low urethral pressure stress incontinence? In Urogyncol J 10:384-389, 1999. Rezapour M, Falconer C, Ulmsten U: Tension-free vaginal tape (TVT) in stress incontinent women with intrinsic sphincter deficiency (ISD)—A long-term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 12:S12-S14, 2001. Kulseng-Hanssen S: Success rate of TVT operation in patients with low urethral pressure [abstract]. Neururol Urodyn 20:417, 2001. Paick JS, Ku JH, Shin JW, et al: Tension-free vaginal tape procedure for urinary incontinence with low Valsalva leak-point pressure. J Urol 172:1370-1373, 2004. Fritel X, Zabak K, Pigne A, et al: Predictive value of urethral mobility before suburethral tape procedure for urinary stress incontinence in women. J Urol 168:2472-2475, 2002. Rodriguez LV, De Almeida F, Dorey F, Raz S: Does Valsalva leak point pressure predict outcome after distal polypropylene sling? Role of urodynamics in the sling era. J Urol 172:210-214, 2004. Mellier G, Benayed B, Bretones S, Pasquier JC: Suburethral tape via the obturator route: Is the TOT a simplification of the TVT? Int Urogynecol J 15:227-232, 2004. Herschorn S, Steele DJ, Radomski SB: Follow-up of intraurethral collagen injection for female stress urinary incontinence. J Urol 156:1305-1309, 1996. Lo TS, Huang HJ, Chang CL, et al: Use of intravenous anesthesia for tension-free vaginal tape therapy in elderly women with genuine stress urinary incontinence. Urology 59:349-353, 2002. Enzelsberger H, Kurz C, Seifert M, et al: Surgical treatment of recurrent stress incontinence: Burch versus Lyodura sling operation a prospective study. Geburtshilfe Frauenheilkd 53:467-471, 1993. Thakar R, Stanton S, Prodigalidad L, den Boon J: Secondary colposuspension: Results of a prospective study from a tertiary referral centre. Br J Obstet Gynaecol 109:1115-1120, 2002.

29. Nilsson CG, Kuuva N: The tension-free vaginal tape procedure is successful in the majority of women with indications for surgical treatment of urinary stress incontinence. Br J Obstet Gynaecol 108:414-419, 2001. 30. Rardin CR, Kohli N, Rosenblatt PL, et al: Tension-free vaginal tape: Outcomes among women with primary vs. recurrent stress urinary incontinence. Obstet Gynecol 100:893-897, 2002. 31. Tamussino K, Hanzel E, Kolle D, et al: The Austrian tension-free vaginal tape registry. Int Urogynecol J Pelvic Floor Dysfunct 12(Suppl 2):S28-S29, 2001. 32. Haab F, Traxer O, Ciofu C: Tension-free vaginal tape: Why an unusual concept is so successful. Curr Opin Urol 11:293-297, 2001. 33. Rezapour M: Tension-free vaginal tape (TVT) in women with recurrent stress urinary incontinence—A long term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 12:S9-S11, 2001. 34. Gorton E, Stanton SL, Monga A, et al: Periurethral collagen injections long-term follow-up. Br J Urol 84:966-971, 1999. 35. Chou EC, Flisser AJ, Panagopoulos G, Blaivas JG: Effective treatment for mixed urinary incontinence with a pubovaginal sling. J Urol 170:494-497, 2003. 36. Schrepferman CG, Griebling TL, Nygaard IE, Kreder KJ: Resolution of urge symptoms following sling urethropexy. J Urol 164:1628, 2000. 37. Liapis A, Bakas P, Creatsas G: Burch colposuspension and tensionfree vaginal tape in the management of genuine stress incontinence in women. Eur Urol 41:469-473, 2002. 38. Ward K, Hilton P: Prospective multi-center randomized trial of tension-free vaginal tape and colposuspension as primary treatment for stress incontinence: Two-year follow-up. Am J Obstet Gynecol 190:324-331, 2004. 39. Rezapour M, Ulmsten U: Tension-free vaginal tape (TVT) in women with mixed urinary incontinence—A long-term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 12:S15-S18, 2001. 40. Lukacz ES, Luber KM, Nager CW: The effects of the tension-free vaginal tape on voiding function: A prospective evaluation. Into Urogynecol J 15:32-38, 2004. 41. Wall LL, Hewitt JK: Voiding function after Burch colposuspension for stress incontinence. J Reprod Med 41:161-165, 1996. 42. Bhatia NN, Bergman A: Urodynamic predictability of voiding following incontinence surgery. Obstet Gynecol 63:85-91, 1984. 43. Iglesia CB, Shott S, Fenner DE, Brubaker L: Effect of preoperative voiding mechanism on success rate of autologous rectus fascia suburethral sling procedure. Obstet Gynecol 91:577-581, 1998. 44. Kobak W, Walters MD, Piedmont MR: Determinants of urinary retention after three types of incontinence surgery: A multivariable analysis. Obstet Gynecol 97:86-91, 2001. 45. Miller EA, Amundsen CL, Toh KL, et al: Preoperative urodynamic evaluation may predict voiding dysfunction in women undergoing pubovaginal sling. J Urol 169:2234-2237, 2003. 46. Lo TS: Tension-free vaginal tape procedures in women with stress urinary incontinence with and without co-existing genital prolapse. Curr Opin Obstet Gynecol 16:399-404, 2004. 47. Sokol AI, Jelovsek JE, Walters MD, et al: Incidence and predictors of prolonged urinary retention after TVT with and without concurrent prolapse surgery. Am J Obstet Gynecol 192:1537-1543, 2005. 48. Cross CA, Cespedes RD, McGuire EJ: Treatment results using pubovaginal slings in patients with large cystoceles and stress incontinence. J Urol 158:431-434, 1997. 49. Meschia M, Pifarotti P, Bernasconi F, et al: Tension-free vaginal tape: Analysis of outcomes and complications in stress incontinence women. Int Urogynecol J 12(Suppl 2):S24-S27, 2001. 50. Gillon G, Stanton SL: Long-term follow-up of surgery for urinary incontinence in elderly women. Br J Urol 56:478-481, 1984. 51. Karantanis E, Fynes MM, Stanton SL: The tension-free vaginal tape in older women. Br J Obstet Gynaecol 111:837-841, 2004. 52. Sevestre S, Ciofu C, Deval B, et al: Results of the tension-free vaginal tape techniques in the elderly. Eur Urol 44:128-131, 2003.

Chapter 29 SURGICAL OPTIONS FOR STRESS URINARY INCONTINENCE

53. Carey J, Leach G: Transvaginal surgery in the octogenarian using cadaveric fascia for pelvic prolapse and stress incontinence: Minimal one-year results compared to younger patients. Urol 63:665-670, 2004. 54. Dwyer PL, Lee ET, Hay DM: Obesity and urinary incontinence in women. Br J Obstet Gynaecol 95:91-96, 1988. 55. O’Sullivan DC, Chilton CP, Munson KW: Should Stamey colposuspension be our primary surgery for stress incontinence? Br J Urol 75:457-460, 1995. 56. Chung MK, Chung RP: Comparison of laparoscopic Burch and tension-free vaginal tape in treating stress urinary incontinence in obese patients. JSLS 6:17-21, 2002. 57. Cummings JM, Boullier JA, Parra RO: Surgical correction of stress incontinence in morbidly obese women. J Urol 160:754-755, 1998. 58. Cummings JM, Rodning CB: Urinary stress incontinence among obese women: Review of pathophysiology therapy. Int Urogynecol J 11:41-44, 2000. 59. Mukherjee K, Constantine G: Urinary stress incontinence in obese women: Tension-free vaginal tape is the answer. Br J Urol Int 88:881-883, 2001.

60. Rafii A, Darai E, Haab F, et al: Body mass index and outcome of tension-free vaginal tape. Eur Urol 43:288-292, 2003. 61. Zivkovic F, Tamussino K, Pieber D, Haas J: Body mass index and outcome of incontinence surgery. Obstet Gynecol 93:753-756, 1999. 62. Hamid R, Arya M, Patel HRH, Shah PJR: Experience of tension-free vaginal tape for the treatment of stress incontinence in females with neuropathic bladders. Spinal Cord 41:118-121, 2003. 63. Arunkalaivanan A, Barrington J: Questionnaire-based survey on obstetricians’ and gynaecologists’ attitudes towards the surgical management of urinary incontinence in women during their childbearing years. Eur J Obstet Gynecol Reprod Biol 108:85-93, 2003. 64. Davila GW, Ghoniem GM, Kapoor DS, Contreras-Ortiz O: Pelvis floor dysfunction management practice patterns: A survey of members of the International Urogynecological Association. Int Urogynecol J 13:319-325, 2002.

335

Chapter 30

OUTCOME MEASURES FOR PELVIC ORGAN PROLAPSE Lynn Stothers Developers of outcome measures for pelvic organ prolapse are faced with the difficult task of addressing a wide range of symptoms from the bowel, bladder, and uterus. Historically, instruments were developed that addressed a single organ, but they have progressed to validated tools that include information relating to all three organs. The modern tools should be completed as part of the patient’s medical record, along with the physical examination and diagnostic tests. They can be performed before and after medical or surgical treatment. They are an essential part of the clinician’s and researcher’s tools in partnership with diagnostic tests. This chapter describes commonly used validated tools developed specifically for women with pelvic organ prolapse and related symptoms. The instruments can be broadly classified as those that quantify and stage prolapse and those that quantify the range of symptoms associated with prolapse. Some scales, such as the Pelvic Organ Prolapse Questionnaire (POP-Q),1 provide a means of accurately describing the position of the organs relative to one another and the amount of relative descent of each of the organs. Others provide a means of assessing the wide range of urinary tract, bowel, sexual, pain, and quality-of-life symptoms related to prolapse. Some symptom scales are comprehensive measures that try to address all symptoms resulting from bowel, bladder, and uterine prolapse. Others are focused scales that ask detailed questions about a single complex, such as sexual dysfunction. QUANTIFYING AND STAGING PROLAPSE Historically, outcome measures for pelvic organ prolapse were single-organ instruments that required supplementation with diagnostic tests for accuracy and reproducibility. For example, the degrees of a cystocele could be staged using a standing-voiding cystourethrogram. To be accurate over time, these scales required repetition of the diagnostic tests to maintain the accuracy of the staging through the patient’s treatment and follow-up. More commonly, staging is done by physical examination alone, without the benefit of diagnostic tests. When physical examination of the patient with prolapse is done, the clinician can only speculate about which organs may be included in the prolapse in the descent of the anterior or posterior vaginal wall or the top of the vault. In this situation, the terms anterior vaginal wall prolapse and posterior vaginal wall prolapse are more appropriate than the terms cystocele or rectocele. Researchers and clinicians recognized the need for a more comprehensive staging system that included all the pelvic organs. Although some of the older scales, such as the traditional fourstage classification system,2 are still in limited use, the POP-Q is the most widely recognized internationally.3-6 336

Pelvic Organ Prolapse Questionnaire The POP-Q provides a descriptive and quantifying system for the relative position of the organs within the pelvis and enables objective staging of pelvic prolapse. The system, adapted from several classifications by Baden and Walker,7 was developed by the International Continence Society Committee on Standardisation of Terminology, Subcommittee on Pelvic Organ Prolapse and Pelvic Floor Dysfunction, in collaboration with the American Urogynecologic Society and the Society of Gynecologic Surgeons.1 The POP-Q system arose from the efforts of the committee to develop a terminology standardization document. The original document was drafted in 1993 and refined in 1994. In 1994, it underwent a 1-year review and trial, during which time several minor revisions were made. Reproducibility studies for the POP-Q were conducted in six centers in the United States and Europe, documenting interobserver and intraobserver reliability and clinical utility of the system in 240 women.8-12 Interobserver reliability was studied in 48 women with a mean age of 61 ± 14 years, parity of 3 ± 2, and weight of 74 ± 31 kg. Correlations for each of the nine measurements (r = 0.817, 0.895, 0.522, 0.767, 0.746, 0.747, 0.913, 0.514, and 0.488) were highly significant (P = 0.0008 to 0.5). Total scores for each P-QOL domain were significantly different between symptomatic and asymptomatic women (P < 0.0001). Interrater reliability on all items was good (Cronbach’s alpha > 0.80). Test-retest reliability showed a highly significant correlation between the total scores for each domain. Mouritsen and Larsen26 evaluated patients with pelvic organ prolapse using their own validated questionnaire by relating type and severity of symptoms from the bladder, mechanical, sexual, and bowel domains to bother from the symptoms and to type and grade of prolapse measured. The symptoms from all domains were common and had little relation to the POP-Q value. Pain Pain is a recognized symptom related to pelvic organ prolapse. The nature of an individual patient’s pain should be evaluated, including vaginal pressure or heaviness, vaginal or perineal pain, sensation or awareness of tissue protrusion from the vagina, low back pain, abdominal pressure or pain, and observation or palpation of a mass.1 Many standardized tools are available for the evaluation of pain, but none is specific for pelvic organ prolapse. The visual analogue scale (Fig. 30-8) has been shown to be a reliable tool for measuring pain in urogynecologic research.27,28 Bowel Dysfunction There are no isolated scales specifically designed to elicit information about bowel dysfunction associated with pelvic organ prolapse. However, there are useful tools included in more comprehensive scales, including the Pelvic Floor Impact Questionnaire–Long Form (PFIQ-L) (Fig. 30-9) and the PFDI Wexner (Fig. 30-10).24 These scales include questions related to urgency of bowel movements, frequency of bowel incontinence, and behavioral techniques that women adopt to reduce the impact of bowel dysfunction on quality of life. Sexual Dysfunction Pelvic organ prolapse has been strongly associated with sexual complaints in studies of women seeking treatment for pelvic floor disorders. According to a study by Barber and coworkers,29 pelvic floor symptoms and detrusor instability are more commonly cited as reasons for sexual inactivity than other conditions. According to Bump and colleagues,1 some of the sexual function symptoms that should be evaluated include the following areas: ■ ■

Is the patient sexually active? If she is not sexually active, why?

■ ■ ■ ■ ■ ■

Does sexual activity include vaginal coitus? What is the frequency of vaginal intercourse? Does the patient have pain with coitus? Is the patient satisfied with her sexual activity? Has there been any change in orgasmic response? Is any incontinence experienced during sexual activity?

Several instruments have been designed specifically to address sexual dysfunction related to pelvic organ prolapse, including the long and short versions of the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ). Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire The Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ-31) is the long or research form of a conditionspecific, self-administered, valid, and reliable questionnaire designed to evaluate sexual function in patients with incontinence or uterovaginal prolapse. In the original study by Rogers and associates,30 factor analysis identified three domains— Behavioral/Emotive, Physical, and Partner-Related—for the 31 questions. There was a strong correlation between sexual function scores and scores on the Sexual History Form-12 (SHF-12) for the questionnaire (r = −0.74; P < 0.001) and for the Behavioral/Emotive and Partner-Related domains (r = −0.79 and −0.5, respectively; P < 0.001). The Physical domain was correlated with scores on the IIQ-7 (r = −0.63; P < 0.001). The PISQ, along with the IIQ, was used in a study of sexual function after surgery for pelvic organ prolapse and showed a decline in sexual function scores after surgery despite improvement in IIQ scores.21 The questionnaire can be found in the original journal article.30 Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire A shorter version of the PISQ-31, the Pelvic Organ Prolapse/ Urinary Incontinence Sexual Questionnaire (PISQ-12) (Fig. 30-11),31 is less time consuming to complete and therefore more appropriate for clinical use. A data subset from 99 of the original 182 woman surveyed for the PISQ-31 was used, along with data from an additional 46 patients. All subset regression analyses with r greater than 0.92 identified 12 items that predicted PISQ-31 scores. Short-form scores correlated well with longform scores (r = 0.75 to 0.95). Correlations between the shortform score and other tests such as the IIQ-7, SHF-12, and symptom questionnaires scores were similar to correlations between the long-form score and these same tests. Test-retest reliability using data from 20 patients showed moderate to high reliability. A Spanish version of the PISQ-12 also has been validated.32

Chapter 30 OUTCOME MEASURES FOR PELVIC ORGAN PROLAPSE

Instructions: Please answer these questions by putting an X in the appropriate box. If you are unsure about how to answer a question, give the best answer you can. Q1:

In general, would you say your health is: 1  Excellent 2  Very Good 3  Good 4  Fair 5  Poor

Q2:

For each of the items, please indicate how much of the time the issue is a concern of you due to accidental bowel leakage. If it is a concern for you for reasons other than accidental bowel leakage then check the box under Not Apply (N/A).

Q2. Due to accident bowel leakage: a. I am afraid to go out b. I avoid visiting friends c. I avoid staying overnight away from home d. It is difficult for me to get out and do things like going to a movie or to church e. I cut down on how much I eat before I go out f. Whenever I am away from home, I try to stay near a restroom as much as possible g. It is important to plan my schedule (daily activities) around my bowel pattern h. I avoid traveling i. I worry about not being able to get to the toilet in time j. I feel I have no control over my bowels k. I can’t hold my bowel movement long enough to get to the bathroom l. I leak stool without even knowing it m. I try to prevent bowel accidents by staying very near a bathroom Q3:

Most of the Time 1 1 1

Some of The Time 2 2 2

A little of the Time 3 3 3

None of the Time 4 4 4

N/A

1 1

2 2

3 3

4 4

 

1

2

3

4



1 1 1 1 1 1 1

2 2 2 2 2 2 2

3 3 3 3 3 3 3

4 4 4 4 4 4 4

      

  

Due to accidental bowel leakage, indicate the extent to which you AGREE or DISAGREE with each of the following items. (If it is a concern for you for reasons other than accidental bowel leakage then check the box under Not Apply, N/A).

Strongly Somewhat Somewhat Strongly N/A Q3. Due to accidental bowel leakage: Agree Agree Disagree Disagree a. I feel ashamed 1 2 3 4  b. I can not do many of things I want to do 1 2 3 4  c. I worry about bowel accients 1 2 3 4  d. I feel depressed 1 2 3 4  e. I worry about others smelling stool on me 1 2 3 4  f. I feel like I am not a healthy person 1 2 3 4  g. I enjoy life less 1 2 3 4  h. I have sex less often than I would like to 1 2 3 4  i. I feel different from other people 1 2 3 4  j. The possibility of bowel accidents is always on my mind 1 2 3 4  k. I am afraid to have sex 1 2 3 4  l. I avoid traveling by plane or train 1 2 3 4  m. I avoid going out to eat 1 2 3 4  n. Whenever I go someplace new, I specifically locate where the bathrooms are 1 2 3 4  Q4: During the past month, have you felt so sad, discouraged, hopeless, or had so many problems that you wondered if anything was worthwhile? 1  Extremely so – to the point that i have just about given up 2  Very much so 3  Quite a bit 4  Some – enough to bother me 5  A little bit 6  Not at all

Figure 30-9 Pelvic Floor Impact Questionnaire–Long Version, bowel-related items. (Adapted from the University of Southern California Center for Colorectal and Pelvic Floor Disorders. Available at http://www.surgery.usc.edu/divisions/Cr/makeanappointment.html/ Accessed July 11, 2005.)

345

346

Section 5 STRESS INCONTINENCE

Instruction: Please circle the number that describes the status of your fecal incontinence. Incontinence type

Never

Rarely: less than once a month.

Sometimes: less than once a week but more than once a month.

Usually: less than once a day but more than once a week

Always: once a day or more

Solid

0

1

2

3

4

Liquid

0

1

2

3

4

Gas

0

1

2

3

4

Wears pad

0

1

2

3

4

Lifestyle alterations

0

1

2

3

4

Figure 30-10 Pelvic Floor Distress Inventory–Wexner (Adapted from the Cleveland Clinic Foundation, Gynecology. Available at http://www.surgery.usc.edu/divisions/Cr/makeanappointment.html/ Accessed July 11, 2005.) The Pelvic Organ Prolapse/Urinary Incontinence Sexual Function Questionnaire (PISQ-12) Instructions: Following is a list of questions about you and your partner’s sex life. All information is strictly confidential. Your confidential answers will be used only to help doctors understand what is important to patients about their sex lives. Please check the box that best answers the question for you. While answering the questions, consider your sexuality over the past six months. Thank you for your help. Always

Usually

Sometimes

Seldom

Never

1.

How often do you feel sexual desire? This feeling may include wanting to have sex, planning to have sex, feeling frustrated due to lack of sex, etc.











2.

Do you climax (have an orgasm) while having sexual intercourse with your partner?











3.

Do you feel sexually excited (turned on) when having sexual activity with your partner?











4.

How satisfied are you with the variety of sexual activities in your current sex life?











5.

Do you feel pain during sexual intercourse?











6.

Are you incontinent of urine (leak urine) with sexual activity?











7.

Does fear of incontinence (either stool or urine) restrict your sexual activity?











8.

Do you avoid sexual intercourse because of bulging in the vagina (either the bladder, rectum or vagina falling out?)











9.

When you have sex with your partner, do you have negative emotional reactions such as fear, disgust, shame or guilt?











10.

Does your partner have a problem with erections that affects your sexual activity?











11.

Does your partner have a problem with premature ejaculation that affects your sexual activity?











12.

Compared with orgasms you have had in the past, how intense are the orgasms you have had in the past six months?

Much less intense 

Less intense 

Same intensity 

More intense 

Much more intense 

Scoring: Scores are calculated by totaling the scores for each question with 0 = never, 4 = always. Reverse scoring is used for items 1, 2, 3, and 4. The short-form questionnaire can be used with up to two missing responses. To handle missing values, the sum is calculated by multiplying the number of items by the mean of the answered items. If there are more than two missing responses, the short form no longer accurately predicts long-form scores. Short-form scores can only be reported as total or on an item basis. Although the short form reflects the content of the three factors in the long form, it is not possible to analyze the data at the factor level. To compare long- and short-form scores, multiply the short-form score by 2.58 (12/31).

Figure 30-11 Pelvic Organ Prolapse/Urinary Incontinence Sexual Function Questionnaire (PISQ-12). (Adapted from Rogers RG, KammererDoak D, Villarreal A, Coates K, Qualls C: A short form of the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire [PISQ-12)]. Int Urogynecol J 14:164-168, 2003.)

Chapter 30 OUTCOME MEASURES FOR PELVIC ORGAN PROLAPSE

CONCLUSIONS The most comprehensive clinical picture of a patient with pelvic organ prolapse includes an anatomic assessment using the POPQ (descriptive and staging) and a comprehensive symptom index. The clinician may choose to supplement these with an in-depth, symptom-specific index to document the patient’s perception of

the impact of treatment on her symptoms. The benefit of consistent use of a validated, descriptive, and standardized staging index is accurate, ongoing documentation of the success or failure of treatment for the individual patient, regardless of whether management is medical or surgical. It also serves as the foundation for communication among clinicians and researchers.

References 1. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. 2. Tarnay CM, Dorr CH II: Relaxation of pelvic supports. In DeCherney AH, Nathan L (eds): Current Obstetric and Gynecologic Diagnosis and Treatment, 9th ed. New York, Lange Medical Books/ McGraw-Hill, 2003, pp 776-797. 3. Culligan PJ, Blackwell L, Goldsmith LJ, et al: A randomized controlled trial comparing fascia lata and synthetic mesh for sacral colpopexy. Obstet Gynecol 106:29-37, 2005. 4. Digesu GA, Chaliha C, Salvatore S, et al: The relationship of vaginal prolapse severity to symptoms and quality of life. BJOG 112:971976, 2005. 5. Novara G, Artibani W: Surgery for pelvic organ prolapse: Current status and future perspectives. Curr Opin Urol 15:256-262, 2005. 6. Tan JS, Lukacz ES, Menefee SA, et al, for the San Diego Pelvic Floor Consortium: Predictive value of prolapse symptoms: A large database study. Int Urogynecol J Pelvic Floor Dysfunct 16:203-209; discussion 209, 2005. 7. Baden W, Walker T: Surgical repair of vaginal defects. Philadelphia, JB Lippincott, 1992. 8. Anthanasiou S, Hill S, Gleeson C, et al: Validation of the ICS proposed pelvic organ prolapse descriptive system [abstract]. Neurourol Urodyn 14:414-415, 1995. 9. Schussler B, Peschers U: Standardisation of terminology of female genital prolapse according to the new ICS criteria: Interexaminer reproducibility [abstract]. Neurourol Urodyn 14:437-438, 1995. 10. Montella JM, Cater JR: Comparison of measurements obtained in supine and sitting position in the evaluation of pelvic organ prolapse [abstract]. Proceedings of the Annual Meeting of the American Urogynecologic Society, Oct 12-14, 1995. Seattle, WA. Seattle, American Urogynecologic Society, 1995. 11. Kobak WH, Rosenberg K, Walters MD: Interobserver variation in the assessment of pelvic organ prolapse using the draft International Continence Society and Baden grading systems [abstract]. In Proceedings of the Annual Meeting of the American Urogynecologic Society, Oct 12-14, 1995. Seattle, WA. Seattle, American Urogynecologic Society, 1995. 12. Hall AF, Theofrastous JP, Cundiff GW, et al: Interobserver and intraobserver reliability of the proposed International Continence Society, Society of Gynecologic Surgeons, and American Urogynecologic Society pelvic organ prolapse classification system. Am J Obstet Gynecol 175:1467-1470, 1996. 13. Elkadry EA, Kenton SK, FitzGerald MP: Patient-selected goals: A new perspective on surgical outcome. Am J Obstet Gynecol 189:15511558, 2003. 14. Hullfish KL, Bovbjerg VE, Gibson J, Steers WD: Patient-centered goals for pelvic floor dysfunction surgery. What is success, and is it achieved? Am J Obstet Gynecol 187:88-92, 2002. 15. Raz S, Erickson DR: SEAPI-QMM incontinence classification system. Neurourol Urodyn 111:187-192, 1992. 16. Stothers L: Reliability, validity, and gender differences in the quality of life index of the SEAPI-QMM incontinence classification system. Neurourol Urodyn 23:223-228, 2004.

17. Shumaker SA, Wyman JF, Uebersax JS, et al: Health-related quality of life measures for women with urinary incontinence: The Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Qual Life Res 3:291-306, 1994. 18. Uebersax JS, Wyman JF, Shumaker SA, et al: Short forms to assess life quality and symptom distress for urinary incontinence in women. The Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Neurourol Urodyn 14:131-139, 1995. 19. Lubeck DP, Prebil LA, Peebles P, et al: A health related quality of life measure for use in patients with urge urinary incontinence. A validation study. Qual Life Res 8:337-344, 1999. 20. FitzGerald MP, Kenton K, Shott S, Brubaker L: Responsiveness of quality of life measurements to change after reconstructive pelvic surgery. Am J Obstet Gynecol 185:20-24, 2001. 21. Rogers RG, Kammerer-Doak D, Darrow A, et al: Sexual function after surgery for stress urinary incontinence and/or pelvic organ prolapse: A multicenter prospective study. Am J Obstet 191:206-210, 2004. 22. Karram M, Goldwasser S, Kleeman S, et al: High uterosacral vaginal vault suspension with fascial reconstruction for vaginal repair of enterocele and vaginal vault prolapse. Am J Obstet Gynecol 185:13391343, 2001. 23. Pang MW, Chan LW, Yip SK: One-year urodynamic outcome and quality of life in patients with concomitant tension-free vaginal tape during pelvic floor reconstruction surgery for genitourinary prolapse and urodynamic stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 14:256-260, 2003. 24. Barber MD, Kuchibhatla MN, Pieper CF, Bump RC: Psychometric evaluation of 2 comprehensive condition-specific quality of life instruments for women with pelvic floor disorders. Am J Obstet Gynecol 185:1388-1395, 2001. 25. Digesu GA, Khullar V, Cardozo L, et al: P-QOL: A validated questionnaire to assess the symptoms and quality of life of women with urogenital prolapse. Int Urogynecol J Pelvic Floor Dysfunct 16:176181, 2005. 26. Mouritsen L, Larsen JP: Symptoms, bother and POPQ in women referred with pelvic organ prolapse. Int Urogynecol J 14:122-127, 2003. 27. Lukacz ES, Lawrence JM, Burchette RJ, et al: The use of Visual Analog Scale in urogynecologic research: A psychometric evaluation. Am J Obstet Gynecol 191:165-170, 2004. 28. Barber MD, Visco AG, Wyman JF, et al: Sexual function in women with urinary incontinence and pelvic organ prolapse. Am J Obstet Gynecol 99:281-289, 2002. 29. Rogers RG, Kammerer-Doak D, Villarreal A, et al: A new instrument to measure sexual function in women with urinary incontinence and/or pelvic organ prolapse. Am J Obstet Gynecol 184:552-558, 2001. 30. Rogers RG, Kammerer-Doak D, Villarreal A, et al: A short form of the Pelvic organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ-12). Int Urogynecol J 14:164-168, 2003. 31. Romero AA, Hardart A, Kobak W, et al: Validation of a Spanish version of the Pelvic Organ Prolapse Incontinence Sexual Questionnaire. Obstet Gynecol 102:1000-1005, 2003.

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Chapter 31

URETHRAL INJECTABLES IN THE MANAGEMENT OF STRESS URINARY INCONTINENCE Ehab A. Elzayat and Jacques Corcos HISTORICAL BACKGROUND Urethral bulking agents have been used for many years to treat intrinsic sphincter deficiency. They are minimally invasive alternatives to operative procedures such as anterior repairs, suspensions, and urethral slings for the management of stress urinary incontinence (SUI). Urethral injection, which can be delivered under local anesthesia as an outpatient procedure, is relatively safe and has few complications. It is an effective treatment for SUI, with complete patient satisfaction comparable to surgery. Urethral injection is cost-effective with less operating time and a shorter hospital stay compared with more invasive surgery.1,2 The concept of urethral injectables to increase urethral resistance has been known for 70 years. Murless,3 in 1938, was the first to report his experience with injection of the sclerosing agent sodium morrhuate into the anterior vaginal wall in 20 patients to induce an inflammatory reaction that compressed the urethra with sclerosis, leading to destruction of the urethral musculature and decreased the compliance of the urethral wall. Quackels,4 in 1955, injected paraffin wax perineally in two incontinent patients after prostatectomy. Dondren is another sclerosing agent that has been used for urethral injection with some success.5 The injection of sclerosing materials such as sodium morrhuate, paraffin, or Dondren causes unacceptable complications, including sloughing of the urethra, urethral stenosis, and pulmonary embolism.5 Polytetrafluoroethylene (Teflon) was proposed as the first bulking agent by Lopez and colleagues8 in 1964, and it became popular in the 1970s.6,7 Since then, several bulking agents have been developed, and new ones are being studied. Nonautologous substances, such as collagen and hyaluronic acid, and autologous substances, such as fat, chondrocytes, and muscle, have been employed clinically or are still under investigation. This chapter reviews the safety and efficacy of available injectable agents for the treatment of female SUI.

MECHANISM OF ACTION OF BULKING AGENTS The mechanism of continence in urethral injection therapy is uncertain and controversial. Many factors enable normal continence in females, including contraction of the sphincter muscles, musculofascial support of the bladder neck, and a urethra seal mechanism.8 The functional urethral seal mechanism is probably a major contributor to continence because of its ability to increase urethral resistance and urethral opening pressure during coughing and straining. Common causes for loss of the urethral seal 348

mechanism are scarring from previous operations, birth trauma, estrogen deprivation, or pelvic radiotherapy.9 Submucosal urethral injection of bulking materials augments bladder neck length and urethral mucosa coaptation and improves the closure mechanism of the urethral sphincter in response to increased intraabdominal pressure.10 Some investigators suggest an obstructive mechanism for the action of urethral injectables, as witnessed sometimes by a decrease in the maximum flow rate and heightened voiding maximum detrusor pressure after injection.11,12 Several laboratories have reported elevation of Valsalva leak point pressure (VLPP) as a result of an increase in functional urethral length.13-15 Others have found that bulking materials improve the ratio of urethral resistance to abdominal pressure by raising the VLPP but not the detrusor leak point pressure or voiding pressure.16,17 Monga and Stanton18 postulated that prevention of bladder neck opening during stress is the mechanism of action of collagen injection, not obstruction. Cephalad elongation of the urethra caused by bulking agent injection at the bladder neck or proximal urethra probably accounts for increased abdominal pressure transmission in the first quarter of the urethra.18,19 Placement of the injectable material more distally does not increase the functional length of the urethra or prevent bladder neck opening during episodes of stress. It is suggested that the bulking materials should be placed just distal to the urethral–vesical junction and that the position of the injectable is more important than its quantity for a good bulking effect.19,20

INDICATIONS AND CONTRAINDICATIONS Injectable agents are classically indicated in patients with SUI. Several studies have shown good efficacy for bulking agents, even in the presence of bladder neck mobility. There is a trend to admit some degree of intrinsic sphincter deficiency (ISD) in all cases of SUI. Bulking agent indications then become much broader, and physicians are influenced by other parameters, such as patient preferences, cost, the need for concomitant procedures (e.g., for prolapse), and product availability.22-25 An overactive bladder should be treated before undertaking urethral injection. Many physicians believe that untreated bladder instability and low compliance are contraindications to urethral injection; others think that urethral injection can be used to treat the incompetent outlet of an overactive bladder without adverse effects on clinical outcome.26 Contraindications to urethral injections are untreated urinary tract infection and hypersensitivity to the injectable materials

Chapter 31 URETHRAL INJECTABLES

Figure 31-1 Hypersensitive cutaneous reaction after collagen skin testing.

(Fig. 31-1). Extensive scarring of tissue from irradiation or previous surgery or trauma may decrease the retention of injectable material in tissue, leading to a poor outcome.

Figure 31-2 Coaptation of the urethra after injection of bulking agents at the 3- and 9-o’clock positions.

INJECTION TECHNIQUE The goal of injection therapy in SUI patients is restoration of the urethral submucosal “cushion” to improve urethral closure pressure during stress episodes without compromising voiding detrusor pressure. The advantages of injection therapy are its minimal invasiveness and technical simplicity, allowing delivery in an outpatient facility under local anesthesia. Urine culture for all patients should be negative, and if collagen is chosen, a skin test to rule out hypersensitivity to collagen must be performed at least 4 weeks before the treatment (see Fig. 31-1). Perioperative antibiotics (e.g., one dose of extended-release quinolone) are usually recommended. After having emptied her bladder, the patient is installed in the lithotomy position, prepared with antiseptic cleaning solution at the level of the external genitalia and urethral meatus, and then draped as usual. Three injection methods have been proposed: periurethral, transurethral or intraurethral, and antegrade.27 Only the transurethral technique is still in use. Periurethral Technique Injections are usually administered with instillation of transurethral topical anesthetic (i.e., 2% lidocaine jelly) and 3 to 4 mL of 1% lidocaine injected in the periurethral tissues at the 3- and 9-o’clock positions. A 20-gauge needle connected to the syringe of bulking agent is successively inserted slowly at the 3-, 6-, and 9-o’clock positions and advanced into the submucosal tissues (i.e., layer just under the urothelium), approximately 0.5 cm distal to the bladder neck, to raise a urethral bleb. Needle position is controlled by urethroscopy under a 0-degree lens. At each position, the bulking agent should be injected slowly to avoid rupturing the expanding urothelium. The injection is continued until the mucosa appears pale and the lumen is about 30% occluded.24 To ensure success, visualization of complete coapta-

Figure 31-3 Perforation of the mucosa during periurethral injection (arrow points to the needle).

tion (i.e., bilateral kissing lobes) of the urethral mucosa at the end of the procedure is recommended (Fig. 31-2). For some physicians, this technique can also be done under ultrasonic guidance.28 In some cases, positioning of the needle can be difficult, leading to repeated mucosal perforations (Fig. 31-3). Transurethral or Intraurethral Technique Two transurethral techniques are available: the cystoscopically guided technique and the blind technique. In the first one, needle insertion into the submucosal tissue is achieved under cystoscopic vision with different injection devices. It requires a

349

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Section 5 STRESS INCONTINENCE

Figure 31-4 Macroplasty injection device.

cystoscope or a urethrocystoscope with an injection needle (needle size depends on the viscosity of the injectable material) and usually a 0- or 12-degree lens.29 The needle should be inserted into the submucosal space approximately 0.5 to 1.5 cm distal to the bladder neck at the 3-, 6-, and 9-o’clock positions. The bulking agent is injected slowly until it raises a urethral bleb. Because of the high viscosity of some injectable agents, such as Teflon or silicone microparticles, an injection gun may be necessary (Fig. 31-4). After injection, the physician must avoid advancing the cystoscope beyond the injection site to prevent compression and extrusion of the injectable material. Faerber and associates30 compared the intraurethral and periurethral routes and demonstrated significant differences in cure (46% versus 33%) and improvement (50% versus 67%) rates in favor of the intraurethral route. However, Schulz and colleagues31 compared periurethral and intraurethral injection randomly in 40 women and concluded that both routes of injection were equally effective. In Faerber’s report, it was evident that the intraurethral route required much less injectable material (4.7% versus 10.1 mL) for better results. The average number of sessions (1.3) was identical with both approaches. These findings explain why most centers now use only the intra-urethral approach. The blind transurethral technique uses injection devices that do not require cystoscopic guidance. Henalla and coworkers32 were the first to apply Macroplastique implantation system to improve and simplify the injection technique (see Fig. 31-4). With this device, the success rate was 74.3%, and the rate of acceptability by surgeons was 95%. The implantation device was developed to control accurate placement of the bulking agent at predefined sites and depth in the female urethra without the need for cystoscopic guidance.33 The device is advanced into the urethra until urinary drainage is established and then withdrawn 1 cm. The injection needle is inserted into the first deployment site, angling the device in the direction of the injection site to ensure penetration of the mucosa.34 The device enables consistent bolus placement at a predetermined depth and site. Usually, two to three punctures (at the 4-, 8-, and 12-o’clock positions) are needed for material delivery. If injection treatment fails, transvaginal or transurethral ultrasound can be performed to investigate correct Macroplastique placement. A different version of the device has been introduced by Q-Med AB (Uppsala, Sweden) (Fig. 31-5). The Implacer device has been developed for administration of dextranomer/hyaluronic acid (Dx/HA; Zuidex) without the need for cystoscopic guidance. The Implacer uses

Figure 31-5 Implacer device for Zuidex injection.

four syringes (each containing 0.7 mL of Dx/HA) and 23-guage needles. The device unfolds and fixates the urethral wall to ensure symmetric placement of the injectable agent at four evenly spaced locations around the urethra. Antegrade Technique The antegrade technique has been described mainly for incontinence in men after prostatectomy. It is performed through a suprapubic cystostomy and under cystoscopic control. The bulking agent is injected submucosally around the bladder neck until coaptation occurs. The technique can be performed under intravenous sedation, general anesthesia, or spinal anesthesia. It is indicated for patients with a scarred, noncompliant urethra. POSTOPERATIVE CARE Patients are usually discharged to their homes after satisfactory voiding. If urinary retention occurs, a small-caliber catheter (14 Fr or smaller) is inserted to empty the bladder. In rare cases of persistent retention, intermittent catheterization with a smallcaliber catheter is required until normal micturition resumes.24 Mechanical pressure to the perineum (e.g., hard seat covers, hard stools, intravaginal sexual intercourse) should be avoided for 2 weeks. If a second injection is necessary, it should be performed after a few weeks to allow healing of the previous implant.28 ASSESSMENT OF CLINICAL OUTCOMES No validated, reproducible, well-accepted instruments have existed for the assessment of outcomes of treatment of urinary incontinence.35 There is no standard definition of success in studies of anti-incontinence procedures, making it difficult to objectively compare results. Assessment of cure depends on subjective or objective measurements, which are not correlated. In most reported studies, cure is defined as the patient being dry by the end of the follow-up period. Improvement is defined as rare or minimal leakage and patient satisfaction with the result of the injection.36

Chapter 31 URETHRAL INJECTABLES

Table 31-1 Results of Polytetrafluoroethylene Injections Study 43

Politano, 1982 Lim et al,48 1983 Schulman et al,49 1983 Deane et al,50 1985 Osther and Rohl,51 1987 Lockhart et al,44 1988 Vesey et al,52 1988 Kiilholma and Makinen,53 1991 Beckingham et al,45 1992 Lopes et al,54 1993 Harrison et al,46 1993 Herschorn and Glazer,47 2000

No. of Patients

Follow-up (mo)

Mean No. of Injections

Mean Injection Volume (mL)

51 28 56 28 36 20 36 22 26 74 36 46

6 (6-16) 12 3 (3-24) 13 (3-24) 3 NS 9 (3-36) 60 36 31 5.1 yr 12

1.8 1 1.5 NS NS 1.9 1-2 NS 1-3 1.3 1-3 2

10-15 11-12 9 10 12 7 7-14 7.3 9 19 7 2.5

Results 71% (51% dry, 20% improved) 54% (33% improved, 21.4% dry) 86% (16% improved, 70% cured) 29% improved, 32% dry 50% good or moderate results 50% dry, 35% improved 67% (56% dry, 11% improved) 18% (dry or improved) 27% improved, 7% dry 19% improved, 54.3% dry 33% (11% dry, 22% improved) 30.4% dry, 41.3% improved

NS, not stated.

Initial patient assessment should include a symptom evaluation, patient satisfaction score, quality-of-life questionnaire, leakage gravity index (e.g., pad test, visual scale), physical examination, and urodynamic measurement. Follow-up should monitor the same parameters plus the length of time since the last injection, number of injections performed, volume per injection, and cure criteria (e.g., physical examination, pad usage, pad-weighing tests, urodynamics).37 There is a large consensus in favor of a redefinition of outcomes for incontinence treatment. Clinicians and researchers are developing new measures that take into consideration the patient’s goals and expectations. We strongly believe that these new paradigms will in the near future replace classic assessments. INJECTABLE MATERIALS Ideal bulking agents should be biocompatible, biodegradable, nonmigratory (bulking > 80 μm), nonerosive, noncarcinogenic, nonimmunogenic, permanently bulking, and easily injected.25 Unfortunately, none of the available bulking agents entirely meets these requirements. Polytetrafluoroethylene Polytetrafluoroethylene (PTFE; Teflon, Polytef) was described as a bulking agent by Lopez and colleagues in 1964,8 and it was popularized by Berg6 and Politano7 in 1970. It is a paste consisting of colloidal PTFE micropolymeric, various-sized particles (up to 300 μm, with most being < 50 μm).8 It is an inert, stable material with a high molecular weight and high viscosity, and it is nonallergenic. Teflon has several disadvantages that limit its acceptability and prevent it from being approved by the U.S. Food and Drug Administration (FDA) for periurethral injection in the United States. It is difficult to inject because of its density, requiring very high pressure through a large-bore needle. Because of the small size of the particles, PTFE (90% < 40 μm in diameter) can be phagocytosed, resulting in distant migration to the brain, lungs, and lymph nodes.38,39 Among other major inconveniences, PTFE is not biodegradable, and it carries a risk of granuloma formation

at the injection site and at some sites of distant migration.40 PTFE produces an inflammatory reaction that may lead to urethral fibrosis, periurethral abscess, and urethral diverticulum.41 The carcinogenic potential of PTFE injection has been suggested but not proved and never reported clinically.42 Politano and coworkers43 first used Teflon for incontinence in men after prostatectomy and later for stress incontinence in women. Their short-term results were promising, with cure and improvement rates of 57% to 85%. However, long-term data have ranged from 18% to 76%.44-46 The reasons for failure of Teflon injection include the high pressure needed for injection, leading to tissue extrusion, absorption, and migration of Teflon particles, and the inflammatory reactions affecting urethral function.37 Failures in this series were associated with prior incontinence operations and bladder instability. To minimize the risk of migration, Herschorn and Glazer47 evaluated the injection of low-volume Teflon, with a success rate of 71.7% (Table 31-1). Glutaraldehyde Cross-Linked Collagen Bovine glutaraldehyde cross-linked collagen (Contigen) is the most widely studied bulking agent. It is a well-established injectable material that gained FDA approval in 1993.24 Periurethral injection of glutaraldehyde cross-linked collagen was first reported by Shortliffe and associates in 1989.55 Contigen, a highly purified suspension of bovine collagen in normal saline, contains more than 95% type I collagen and less than 5% type III collagen cross-linked with glutaraldehyde. This cross-linking makes collagen more stable and durable, hindering its breakdown by fibroblast-secreted collagenase and enhancing its invasion by fibroblasts and blood vessels with deposition of host collagen, promoting long-term efficacy of the implant.56 The decreased antigenicity of this mixed collagen is obtained by hydrolysis of the antigenic parts of the molecules, the amino-terminal and carboxyl-terminal segments. Cross-linking also reduces hypersensitivity. Collagen injection is an easy procedure. It can be delivered periurethrally or transurethrally through a small needle (22 gauge) under local anesthesia. Each syringe contains approximately 2.5 mL of collagen, and some patients may need repeated injections (e.g., two to five injections). If the collagen is placed

351

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too deeply, it will be quickly reabsorbed. However, the position and volume of injected collagen are not predictive of clinical outcome, as determined by a magnetic resonance study.57,58 The advantages of collagen injection include its durable efficacy and safety, with no proven risk of granuloma formation or migration.59 Considering its price, cost-effectiveness is a concern. Berman and Kreder60 reported that sling cystourethropexy is more cost-effective than collagen injection in women with type III incontinence. The collagen injection is allergenic in up to 5% of patients, requiring skin tests to rule out hypersensitivity 1 month before injection.61 There also is some concern regarding the potential for disease transmission from bovine products.34 Early results have disclosed subjective cure and improvement rates up to 95% and objective cure rates of 61% to 91%.36 Herschorn and colleagues62 reported an early experience with intra-urethral injection of collagen in 31 women, with a mean follow-up of 6 months. The combined cure and improvement rate was 90.3%. Longer-term results of cure and improvement rates vary from 57% to 94% (Table 31-2). In a North American multicenter study, 148 women underwent collagen injection for ISD, with an overall success rate of 78% (45% cured, 33% improved) at 2 years of follow-up.63 Monga and coworkers67 achieved a success rate of 86% at 3 months, 77% at 12 months, and 68% at 24 months after urethral injection of collagen in 60 women with SUI. Swami and associates74 treated 111 patients with periurethral collagen injection for a success rate of 85% at 6 months and 65% at 3 years after injection. There was no difference in maximum urethral closure pressure before and after collagen injection and no predictive factors of success. Some physicians have reported that patients who underwent prior antiincontinence surgery may have better results than those without previous surgery.63,65 These findings may be explained by periurethral tissue support and limited mobility by scarring.63,65 Others have observed no correlation between the degree of urinary incontinence preoperatively and the success rate.70 Some investigators have obtained higher percentages of injection failure in patients with preoperative detrusor instability.70,73 The use of collagen in cases of urethral hypermobility has produced results comparable to those without hypermobility.16,67,69,70,72 Steele and colleagues82 reported a higher success rate for collagen injection in patients with hypermobility than in those without hypermobility. Long-term studies have demonstrated continuing success, with a cure rate of 25% to 45% and an improvement rate between 25% and 50%. Corcos and Fournier78 reported the 4-year followup results for 40 women who underwent collagen injection. The cure rate was 30%, and the improvement rate was 40%. One third of these patients required a top-up injection 18 to 24 months after the initial treatment. Gorton and coworkers79 published their long-term results of collagen injection in 46 women with ISD, showing an overall success rate of 35%. The morbidity associated with collagen injection is minimal and self-limited. The most common complication is transient urinary retention, urinary tract infection, and transient hematuria. In 337 collagen injection cases, Stothers and associates83 documented a complication rate of 20%, including de novo urinary urgency in 12.6% of patients. In many patients, the symptoms were irreversible (21% did not respond to anticholinergics) and included hematuria (5%) and urinary retention (1.9%). Delayed reaction at the skin test site occurred in 0.9% (3) of patients and was associated with arthralgia in two cases. Others identified urinary retention (8%,) urinary tract infection (4%), hematuria (2%), and urinary urgency in less than 1%.84

Rare complications after collagen injection included sterile abscess at the injection site.85,86 Pulmonary embolism, urethral prolapse, and osteitis pubis have been encountered after urethral collagen injection.86-88 Autologous Fat Autologous fat was first used in plastic surgery to augment soft tissue defects. Periurethral fat injection was introduced in 1989 by Gonzales and colleagues89,90 to treat ISD. Fat was harvested from lower abdominal subcutaneous tissue by liposuction using a trocar or aspiration syringe under local or general anesthesia. Between 15 and 20 mL of fat was mixed with Ringer’s solution or insulin before periurethral or transurethral injection. The advantage of autologous fat is that it is readily available, biocompatible, and inexpensive. Its disadvantages are fat resorption and replacement by fibrous tissues, which necessitate repeated injections. Horl and coworkers91 employed magnetic resonance imaging to demonstrate a 55% volume loss at 6 months after fat injection but no further volume decline at 9 and 12 months of follow-up. Approximately 50% to 90% of transferred adipose grafts do not survive.92 Graft survival depends on minimal handling, low suction pressure during liposuction, and large-bore needles for reinjection to minimize injury.93 Periurethral fat injection has a reported success rate that is lower than with other injectables (Table 31-3). Palma and associates97 obtained a success rate of 76% (64% dry and 12% improved) with repeated injections of fat, compared with 69% (31% dry and 38% improved) with a single injection. Haab and associates76 compared the outcome of fat and collagen injection in 67 women with ISD and achieved cure rates of 13% and 24% for the fat and collagen groups, respectively. Lee and colleagues99 published the results of a randomized, double-blind, controlled study of fat and saline injection (as a control) and reported success rates of 22% and 20.7% for the fat and saline groups, respectively. They concluded that periurethral fat injection does not appear to be more effective than placebo for treating stress incontinence. The complications of fat injection include urinary tract infection, urinary retention, hematuria, pain, and hematomas at the site of liposuction. Complications such as urethral pseudolipoma and death due to fat embolism have also been reported.99-101 These data should exclude fat injection for the treatment of SUI.37 Silicone Microimplants Silicone microimplants (e.g., Macroplastique) are soft, flexible, solid-textured, irregularly shaped implants of heat-vulcanized polydimethylsiloxane (i.e., silicone rubber) suspended in a carrier gel (i.e., polyvinylpyrrolidone). The silicone particles are encapsulated in fibrin, and the nonsilicone carrier gel is absorbed by the reticuloendothelial system and excreted in the urine. The injected particles are organized within 6 to 8 weeks into firm nodules with infiltrated collagen and surrounded by a fibrous sheath that is well developed at 9 months.102 Silicone particles are inert, inducing very little local inflammatory reaction. The material is biocompatible, nonbiodegradable, nongenotoxic, noncarcinogenic, and nonteratogenic. The mean particle size ranges from 100 to 300 μm in diameter, limiting the risk of migration, which usually occurs with particles less than 70 μm.103 Macroplastique can be injected transurethrally or periurethrally under cystoscopic vision or transurethrally with a

Chapter 31 URETHRAL INJECTABLES

Table 31-2 Results of Collagen Injections No. of Patients

Study 63

Eckford and Abrams, 1991 Kieswetter et al,64 1992 Stricker and Haylen,65 1993 McGuire and Appell,16 1994

Type of Incontinence

25

NS

16

NS

50

ISD

No. of Injections

Follow-up (mo) 3

NS

1.7

15 (10-22)

8

1

11 (1-21)

1.9

14.4 NS

154

137 ISD 17 HU

>12

NS

44

Longest: 7 mo

1.5

42

42 ISD 2 HU ISD

60

Winters and Appell,68 1995 Moore et al,69 1995

160 10

Nataluk et al,14 1995

12

O’Connell et al,12 1995 Richardson et al,66 1995 Monga et al,67 1995

Herschorn et al,70 1996

187

Mean Collagen Volume (mL)

9.1

46 (10-66)

2

28.3

NS

24

3

19

ISD

24

NS

NS

Type I and III

2

1.5

9.5

Type III

2

1.8

12.3

Homma et al,71 1996

78

124 HU 64 ISD 6 neurogenic GSI and ISD

Faerber,72 1996

12

Type I

10

1.2

2.2

Smith et al,73 1997

94

ISD

14

2.1

11.9

Swami et al,74 1997

111

NS

38 (24-70)

1.7

12.8

Stanton and Monga,75 1997

32

NS

12-24

1.5

17.6

Haab et al,76 1997

22

ISD

1.9

13.5

Khullar et al,191997

26

NS

24

1.7

21.6

Cross et al,77 1998

103

Type III

18

NS

NS

8 type I 20 type II 12 type III GSI

50 (47-55)

2.2

9

>5 yr

1-3

17

24.4

1.9

14.6

12 (1-32)

1-5

3.1

1.9 with HU 1.4 without HU

5.6 with HU 5.3 without HU

Corcos and Fournier,78 1999

40

Gorton et al,79 1999

46

Winters et al,80 2000

58

Groutz et al,81 2000

63

49 ISD 9 GSI (37 HU) NS

Steele et al,82 2000

40

9 HU

22 (4-69)

2.5 (success) 2 (failure)

24

1.9

23.5

Minimum: 12

8.4

9.6 (success) 7.8 (failure)

GSI, genuine stress incontinence; HU, hypermobile urethras; ISD, intrinsic sphincter deficiency; NS, not stated.

Success Rate 80% (64% dry, 16% improved) 83% (44% cured, 39% improved) 82%(42% cured, 40% improved) HU: 64% (47% cured, 17% improved) ISD: 80% (47% cured, 34% improved) 63% (45% dry, 18% improved) 83% (40% cured, 43% improved) 68% (48% cured, 20% improved) 78% cured or improved 80% (20% cured, 60% improved) 33% cured, 67% improved 75% (23% cured, 52% improved) 72% (7% cured, 65% improved) 83% cured, 17% improved 67% (38% dry, 29% improved) 65% (25% cured, 40% improved) Subjective success rate 69%, objective cured rate 54% at 2 yr post-operation) 86% subjective success, 64% objective success 57% (48% cured, 9% improved) 94% (74% cured, 20% improved) 70% (30% cured, 40% improved) 35% subjectively improved 48.3% cured, 31.0% improved, long-term success 60.3% 82% (13% cured, 69% improved) 71% with HU 32% without HU

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Table 31-3 Results of Autologous Fat Injections No. of Patients

Study 89

Follow-up (mo)

Gonzalez de Garibay et al, 1989 Cervigni and Panei,94 1993 Scotti et al,95 1993 Santarosa and Blaivas,96 1994 Trockman and Leach,92 1995 Palma et al,97 1997

14 10 15 32 30

9.7 (3-19) 0.5 12 (1-40) 6 12

Haab et al,76 1997 Su et al,98 1998 Lee et al,99 2001

45 26 35

>7 17.4 (12-30) 3

12

6

No. of Injections

Mean Fat Volume (mL)

1

10-20

100%

NS 1 2.7 1.6 12

21.7 14-20 5-15 21.3 40

86% (57% cured, 29% improved) 60% 58% cured 56% (12% cured, 44% improved) Single injection: 69% Multiple injections: 76% 42% (13% cured, 29% improved) 65% (50% cured, 15% improved) 22% overall success

1.7 1 1-3

20 15 30

Success Rate

NS, not stated.

Dextranomer/Hyaluronic Acid Copolymer

Figure 13-6 Ratchet gun and flexible needle for Macroplastique injection.

special injection system (see Fig. 31-5). The material is viscid, and the needle must be prelubricated with 1 to 2 mL of carrier gel before the vial (2.5 mL) of silicone paste is discharged by means of a high-pressure ratchet gun (Fig. 31-6). Silicone elastomers have been used since the early 1990s as bulking agents for treating SUI, but they are still not approved for application in the United States. The reported cure rate with silicone ISD varies between 14% and 66.7%. Improvement rates range from 46% to 80%. When ISD is associated with urethral hypermobility, the cure and improvement rates are between 0% and 21.4% and between 0% and 58.9%, respectively.104 Sheriff and colleagues105 reported a success rate of 90% at 1 month after injection, with a time-dependent decrease to 48% at 2 years postoperatively. Other long-term results usually show a lower cure rate and are summarized in Table 31-4. Reported complications after silicone injection are minimal and self-limited, such as hematuria, dysuria, urinary tract infection (0.9%), and urinary retention (6.8%).108 There is still concern about small particle migration and granuloma formation, with possible risks of autoimmune reactions associated with silicone injection.103

Dextranomers are well-known polysaccharides that have been used for topical wound cleaning. HA has been applied in eye surgery and for joint injection.116 Dx/HA is a copolymer (Zuidex) in a gel of nonanimal, stabilized HA. A high-molecular-weight polysaccharide, HA works as a carrier gel and is resorbed within 2 weeks after injection. Zuidex is a highly viscous solution, nonimmunogenic and biocompatible, with no risk of allergy or granuloma formation. Dx microspheres, the bulking agent, are 80 to 200 μm in diameter and do not fragment, eliminating the risk of distance migration.117 Dx/HA is biodegraded very slowly by hydrolysis, and it remains at the injected site for up to 4 years. Stenberg and coworkers118 established that the volume of subcutaneously injected Dx/HA implants decreased by 23% over 12 months in rats. Because the implant consists of 50% microspheres and 50% HA, volume reduction soon after injection should be expected. However, endogenous tissue augmentation is caused by ingrowths of collagen and fibroblasts between the microspheres. Dx/HA has been shown to be well tolerated for endoscopic injection in vesicoureteric reflux (VUR) in children, with efficacy persisting for at least 5 years.119 It has been approved by the FDA in the United States for VUR and approved in Europe and Canada for the treatment of VUR and SUI.120 Initial studies of Dx/HA injection in patients with stress incontinence are promising. Stenberg and associates121 attained an initial success rate of 85% (cured or improved) for 20 patients with stress incontinence. Long-term follow-up (up to 6.7 years) of their cohort revealed that 57% were still cured or improved without any adverse effects (Table 31-5).122 Van Kerrebroek and colleagues123 reported a success rate of 71% among 42 women 1 year after Dx/HA injection. The few adverse effects encountered included a sterile abscess (n = 1), urinary tract infection (n = 5), hematuria (n = 4), urethral disorder (n = 3), and decreased urinary flow (n = 3). A case of granuloma after Dx/HA injection has been documented.126 Injection therapy does appear to preclude future surgical interventions, because it does not cause any major tissue changes.127 Carbon-Coated Zirconium Beads Durasphere is a mixture of nonabsorbable, carbon-coated zirconium beads in a water-based carrier gel with β-glucan (i.e., 97%

Chapter 31 URETHRAL INJECTABLES

Table 31-4 Results of Silicone Microimplant Injections No. of Patients

Study 106

Follow-up (mo)

No. of Injections

Injected Volume (mL)

Harriss et al, 1996 Sheriff et al,105 1997

40 34

50 cm H2O) were evaluated with 6 to 48 months of follow-up. Sixteen patients (89%) were dry postoperatively, 3 (17%) developed de novo urgency, and no patients had recurrence of their prolapse. The vaginal wall sling appears to afford a mid-term success rate comparable to that of the fascial pubovaginal sling.52 Two studies, that of Mikhail and colleagues50 with a minimum followup of more than 5 years and that of Kilicarslan and associates32 with a mean follow-up of 4 years, reported dry rates of 83% and 97%, respectively. However, neither study included patients with ISD based on urodynamic criteria. Raz cautioned against performing the procedure in sexually active women with a short vagina due to the risk of shortening.

Chapter 32 ROLE OF NEEDLE SUSPENSIONS

A

B

Figure 32-8 Vaginal wall sling. A, A “Block A” incision is outlined on the anterior vaginal wall. B, Four suspension sutures have been placed with a narrow base anchor. Proximally, a vaginal wall flap has been created and will be advanced over the in situ vaginal sling patch at the end of the procedure. (Adapted from Raz S, Little NA, Juma S. Female Urology. In Walsh PC, Gittes RF, Perlmutter AD, Stamey TA: Compbell’s Urology, 6th ed., chap. 75, pp. 2782-2806; 1992. Philadelphia: WB Saunders.)

In older women with significant atrophic vaginitis, adequate tissue strength may be lacking. Additionally, women with significant scarring of the anterior vaginal wall may not be good candidates. In regard to dyspareunia, Mikhail and coworkers, using a longitudinal closure over the flap, reported no de novo dyspareunia in 49 of 51 sexually active patients.50 Angulo and associates reported a modification using a longitudinal flap placed transversely to avoid the potential of foreshortening the vagina. No sexually active patient had complaints of dyspareunia 6 months postoperatively.53 With the technique of the vaginal wall sling, buried epithelium creates a potential for the development of inclusion cysts in the area of the sling. Mubiayi and colleagues reported a 5% (4/75) rate of vaginal mucocele.49 In the English literature, there have been two further case reports.54,55 Goalpost Technique Raz described his four-defect repair of grade 4 cystocele, a procedure known as the goalpost technique. He used a vaginal wall sling to support the bladder neck and urethra with concomitant reduction of the cystocele by reapproximation of the perivesical fascia and the cardinal ligaments over the midline (Fig. 32-9). Safir and associates reported a 92% (103/112) success rate for cystocele correction and, in patients with preoperative SUI, a cure rate (dry or improved) of 90% (44/49).57 Leboeuf and

colleagues reported a modified procedure wherein Pelvicol mesh was interposed between the reapproximated perivesical fascia and the vaginal wall closure. In this study, 24 patients had the standard four-defect repair, and 19 had Pelvicol interposition. Overall, there was a 93% cure rate of the cystocele. Only 3 of 43 patients had a recurrence, all within the Pelvicol group. For SUI, 22/24 (91.6%) had resolution of their symptoms.58

DEBATE: A FUTURE FOR NEEDLE SUSPENSIONS? [T]he Burch colposuspension was better in controlling stress incontinence but it led to an unacceptable high rate of prolapse recurrence. The anterior colporrhaphy was more effective in restoring vaginal anatomy but it was accompanied by an unacceptable low cure rate of stress incontinence. Neither of the two operations is recommended for women who are suffering from a combination of stress incontinence and advanced cystocele.59 As time has progressed, it has become apparent that prolapse and urethral hypermobility are not independent events. The vagina is a dynamic organ, and redistribution of forces may result in herniation in other parts of the vagina. Therefore prolapse disease can be viewed as a global vaginal phenomenon.60 In recent

369

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Section 5 STRESS INCONTINENCE

A

Periurethral fascia Cystocele Puboocervial fascia

Vaginal flap Cardinal ligaments tied Cardinal ligament

B

C

Figure 32-9 Goalpost technique. A, Goalpost incision is outlined. The arms extend from the mid-urethra to 1 cm proximal to the bladder neck. The transverse crossbar connects the arms. The post extends from the crossbar (which is 1 cm proximal to the bladder neck and extends to the vaginal cuff). B, The vaginal mucosa is dissected off the underlying structures. The mucosa between the arms of the goalpost remains in situ to serve as the vaginal wall sling. C, Final appearance, with vaginal wall sling sutures passed through the retropubic space. Sutures are placed transversely to reapproximate the perivesical fascia for correction of the cystocele.

Chapter 32 ROLE OF NEEDLE SUSPENSIONS

statistics, 18% to 41% of patients undergoing procedures for POP received concomitant anti-incontinence procedures.2,3 The paradigm has shifted with regard to the needle suspension procedures. Pereyra first conceptualized needle suspension for the correction of urethral hypermobility and treatment of incontinence; we now have needle suspension procedures that can concomitantly correct cystoceles and SUI secondary to urethral hypermobility. One of the greatest assets of current needle suspension procedures has been the use of native tissue to provide broad support to the anterior vaginal wall as a single unit. Unlike the anterior colporrhaphy, the anterior vaginal wall suspension and the vaginal wall sling do not rely on weakened muscular or fascial attachments but use the actual vaginal mucosa beneath the bladder neck and bladder base to provide the support mechanism. Careful review of more recent literature indicates that experienced vaginal surgeons can attain a good success rate

in the correction of cystocele and urethral hypermobility with one simple procedure and with minimal perioperative risks (Table 32-3). The concept of using a foreign tissue to reinforce the strength of a defective tissue was first applied in general surgery. However, the use of foreign materials such as synthetics, allografts, and xenografts has both real and theoretical beneficial and adverse implications. In the area of vaginal reconstruction and treatment of SUI, surgeons began using foreign materials for midurethral slings a decade ago, and, with increasing practice, this experience has now been extended to reinforce the vaginal mucosa in cystocele repairs and other vaginal compartments. One can argue for the advantages and disadvantages of every material regarding safety, durability, and effectiveness (Table 32-4). This is beyond the scope of this chapter, but it is fair to state that, for the transvaginal repair of SUI with

Table 32-3 Midterm Incontinence Results of Contemporary Needle Suspension Procedures, Alone and with Associated Anterior Compartment Prolapse First Author and Ref. No. 46

Year

Raz Juma61 Kaplan62

1989 1992 1996

Serels51

1999

Goldman48

2000

Follow-up, Follow-up, Mean Range (mo) (mo) 23.9 21.4

10-28 7-52 6-51 12-48

19

13-28

Kaplan60

2000

39.8

Angulo53

2001

42

12-83

Mikhail50

2003

67

63-98

Kilicarslan32

2003

Raz26 Dmochowski33 Costantini34

1989 1997 2003

43.2 45.6 49 24 37 62

Safir57 Leboeuf58 Lemack39

1999 2004 2000

21 15 25

4-77

6-60 15-80 36-83

6-42 6-48 Minimum 12

N

Procedure

% Cystocele Correction

26 65 43 36 18

VWS VWS PVS VWS VWS + AC No comment 39 VWS Group 1: VLPP >50 Group 2: VLPP 20 cm H2O). Operative Techniques The TVT procedure was carried out according to the technique described by Ulmsten and associates,3 and the PVT was performed according to the technique we described earlier.5 All patients were sent home on the same day without a catheter if a voiding trial was successful. If a patient could not void or the bladder was perforated during the procedure, catheter drainage for 1 to 2 days was required, and a voiding trial was completed on an outpatient basis. Outcome Measures The primary outcome measure was the AISRS.10 Patient responses were classified as cure, good, fair, poor, or failure according to the AISRS. For example, the patient was considered cured if she scored 0—that is, she had no stress or urge urinary incontinence episodes, she considered herself to be cured, and the total weight gain of the pad on her postoperative 24-hour pad test was less than 8 g.10,11 Secondary outcome measures were Global, IIQ-7, and UDI-6. Our sample size was based on testing the noninferiority of PVT to TVT on the primary outcome measure of being cured (score of 0) on the AISRS. We used a noninferiority “delta” of 10%, defined as the smallest true difference in the distribution of the AISRS such that PVT would still be considered noninferior to TVT. Assuming a 90% cure rate for both groups, we needed 226 total patients (113 patients in each group) to have 80% power

to conclude noninferiority of PVT. With our recruited sample size of 191 patients, we had about 75% power to show noninferiority under these assumptions. In our data analysis of the AISRS, we conservatively used a smaller delta of 5% than we had planned for in the AISRS analysis. In regard to the safety analysis, with our sample size of 191 we had little power (31%) to show noninferiority on any of the binary complication outcomes using an equivalency delta of 5%. Nonsignificant results for complications are therefore not interpreted as evidence of no difference between the groups. Sample size calculations were made using the sample size software Unify POW, a macro for the SAS system.12 Statistical Analysis PVT and TVT groups were compared on baseline variables including demographics, medical history, diagnosis, surgical variables, and incontinence questionnaires (IIQ, UDI, and Global), using chi-square tests for binary variables and either t tests or Wilcoxon rank-sum tests for ordinal or continuous variables, as appropriate. We also compared those with and without complete follow-up data for the AISRS, the UDI, and the IIQ on baseline factors to determine whether responders and nonresponders were similar at baseline. One-tailed noninferiority tests of PVT versus TVT were made for the primary and secondary outcomes, using both univariate and multivariate methods, although all conclusions were based on the multivariate results. We adjusted for as many baseline covariates as possible in attempts to negate any assignment bias or baseline differences (due to nonrandomization). The usual tests for superiority of either PVT or TVT were done as well. Tests for superiority of PVT or TVT were also performed. In the univariate case, we used chi-square tests for the AISRS and either two-tailed t tests or Wilcoxon rank-sum tests for ordinal outcomes. In multivariate analysis, we used the usual tests for significance from the logistic regression and cumulative logic regression analyses described earlier. For the change in Global score, we used cumulative logic regression to adjust for the covariates, and we reported the estimated odds ratio for having a higher change in TVT versus PVT. RESULTS A total of 278 women met the study criteria and, with input from their physician, chose to be treated with either TVT or PVT. Seventy-seven patients (27.7%) did not fully complete the questionnaires and were excluded from analysis (51 in the TVT group and 26 in the PVT group); 49 of these 77 patients were not willing to complete the follow-up even when contacted by telephone, and 28 were lost to follow-up because we were not able to contact them. The remaining 191 patients (72.3%) responded and followed our protocol; 99 (51.8%) of them underwent TVT, and 92 (48.2%) underwent the PVT procedure. Of the 191 patients, 107 (56%) were compliant to perform the entire study protocol, including the three domains of the AISRS (questionnaire, 24hour voiding diary, and 24-hour pad test) and the three questionnaires of the secondary outcome measures; 84 patients (44%) refused to perform both the 24-hour pad test and the 24-hour voiding diary, whereas 60 patients (31%) refused to perform the 24-hour pad test only.

Chapter 43 PERCUTANEOUS VAGINAL TAPE SLING PROCEDURE

Table 43-1 Effectiveness of TVT versus PVT Based on AISRS Score* % Cured Analysis Univariate Adjusted for covariates‡

Superiority

Noninferiority

TVT (N = 84)

PVT (N = 85)

Chi-Square P Value

% Cured (95% CI), TVT minus PVT

OR (95% CI), TVT vs PVT (Ref = PVT)

P Value†

33 (39.3%) 33 (38.6%)

48 (56.5%) 48 (55.4)

.025 .060

−17.2 (−29.6 to −4.7) −16.8 (−32.6 to 0.67)§

0.50 (0.27 to 0.92) 0.51 (0.26 to 1.03)

.002 .003§,¶

*Association between AISRS “cured” (yes/no) and procedure (TVT or PVT) while adjusting for all preoperative baseline covariates. “Cured” was defined as a score of 0 on the AISRS. † One-tailed test with noninferiority delta (or buffer) of .05. ‡ Logistic regression adjusting for prolapse (P = .22), previous operation (P = .31), stress incontinence vs mixed incontinence (P = .24), age (OR = 0.68 per 10 yr, P = .008), and follow-up months (P = .08). § Covariate-adjusted CI and noninferiority P value based on 1000 bootstrap resamples. ¶ One-tailed upper limit for CI on difference in predicted percent success was −3.3%, well less than the +5% noninferiority delta (P = .003). AISRS, Anti-Incontinence Surgery Response Score; CI, confidence interval; OR, odds ratio; PVT, percutaneous vaginal tape; TVT, tension-free vaginal tape.

AISRS: Primary Outcome Assessment Multivariate analysis showed the noninferiority of PVT to TVT in the proportion cured (P = .002) after adjusting for baseline covariates and follow-up months, but PVT was not found to be superior to TVT (P = .06). We used a logistic regression model to assess the association between AISRS cured (yes/no) and procedure (TVT or PVT) while adjusting for all preoperative baseline covariates, including associated prolapse, previous operation (yes/no), preoperative diagnosis of stress incontinence versus mixed incontinence, age, and duration of postoperative followup in months (Table 43-1). Of the preoperative covariates assessed, only age was significantly associated with the outcome (P = .008). Higher age was associated with lower odds of success (odds ratio, 0.68; 95% confidence interval [CI], 0.52 to 0.90). The covariate-adjusted noninferiority test, using a delta of 5%, was significant (P = .022), so we concluded that PVT is not inferior to TVT (i.e., at least not 5% worse) on the AISRS cure score. Using bootstrap resampling, we also obtained a one-tailed upper limit estimate for the difference between PVT and TVT on the predicted probability of being cured after adjusting for covariates. This estimated upper limit was −3.3% (PVT 3.3% better), which is 8.3% lower (i.e., better in favor of PVT) than the +5% tolerance we had set. Our naïve (i.e., unadjusted) univariate analysis revealed that PVT had a higher proportion “cured” in the test for superiority (chi-square P = .025), with the 95% CI ranging from 0.05 to 0.30 better than TVT (see Table 43-1). The estimated odds ratio from logistic regression indicated that TVT patients were only about half as likely to be cured as PVT patients. The univariate noninferiority test was then, of course, significant as well (P = .002), meaning that there was evidence to reject the null hypothesis and conclude that PVT is not inferior to TVT based on the AISRS. Secondary Outcome Measures Table 43-2 compares PVT and TVT on change from baseline to last follow-up on the secondary outcome measures. Univariate and multivariate results for superiority and noninferiority tests are given, along with estimated 95% CIs for the difference (TVT minus PVT) in mean or median change. In testing for the superiority of either TVT or PVT, we found no significant differences

between treatment groups (Table 43-3), evidenced by zero being included within the confidence limits for each score and P values greater than .05. In univariate analysis, PVT was shown to be noninferior to TVT for both IIQ and UDI (using three-point and two-point buffers, respectively) in change from baseline, but not for change in global assessment (one-point buffer). In multivariate analysis adjusting for all available covariates, noninferiority of PVT was found only in the change in IIQ score (P = .038). The covariate-adjusted one-tailed upper 95% confidence limit for the change in IIQ was 2.8 (favoring TVT); this is significant because it is lower than the prespecified delta of 3.0. The adjusted one-tailed upper limit for UDI is above the prespecified delta (and therefore nonsignificant). We used cumulative logic regression for the Global assessment, because the data were far from normally distributed and linear regression was not appropriate. The odds of having a higher change score after PVT was an estimated 1.4 (95% CI, 0.69 to 2.7) times higher that for TVT. This method did not allow assessment of noninferiority of the Global assessment, but the odds ratio CI is quite wide and does not suggest noninferiority. For each of IIQ (P = .005), UDI (P < .001), and Global (P = .005) scores, higher or increasing age was significantly associated with less improvement in the score (negative correlation). For both the IIQ and the UDI, patients with stress incontinence patients had significantly more improvement than did patients with mixed incontinence; the adjusted mean (and standard error) for the difference in score between these two groups was 4.7 (1.6) for the IIQ and 3.4 (0.89) for the UDI. None of the other covariates was significant at the .05 level, but they were retained in the multivariate models to improve the inference regarding PVT and TVT. Nine surgeons performed the procedures, but we were not able to make a meaningful adjustment for surgeon because most surgeons did either PVT or TVT surgery exclusively. For example, the PVT procedures were done by one of two surgeons who respectively performed 68% and 26% of the PVTs (together, 94.5%) but only 13% of the TVT procedures. Likewise, 77% of the TVT procedures were done by one of three surgeons, and two of them performed only one PVT surgery each. Analysis of domain no. 2 of the UDI-6 (Do you experience urinary leakage related to the feeling of urgency? If yes, how much

449

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Section 5 STRESS INCONTINENCE

Table 43-2 Effectiveness of TVT versus PVT Based on Secondary Outcomes* Superiority

Outcome

TVT

PVT

P Value

Difference between TVT-PVT (95% CI)

Noninferiority

Buffer

IIQ-7 Sum Preop Sum Postop Change Adjusting for covariates

17.8 (6.6) 5.1 (6.5) 12.7 (8.6)† —

16.1 (7.7) 3.6 (6.6) 12.5 (10.2) —

.91‡ .88¶

0.18 (−3.0, 3.4) −0.20 (−3.8, 3.3)

UDI-6 Sum Preop Sum Postop Change Adjusting for covariates

11.3 (3.8) 3.6 (3.7) 7.7 (4.7)¶ —

11.6 (3.7) 4.3 (4.5) 7.3 (5.8) —

.66‡ .70§

0.41(−1.4, 2.2) 0.38 (−1.6, 2.3)

¶¶

Global Preop Postop Change Adjusting for covariates

10.0 (8.0, 10.0) 1.0 (0.0, 3.0) 8.0 (5.0, 10.0)** —

10.0 (8.0, 10.0) 1.0 (0.0, 3.0) 7.0 (5.0, 9.0) —

.35†† .37§§

0.26 (−2, 2)‡‡ 1.4 (0.69, 2.7)§§

‡

§ §

¶¶

One-tailed Upper CL

One-tailed P Value

2.9 2.8

.044 .038

1.9 2.01

.044 .10

¶¶

.10 5 N/A

N/A

*Change (mean or median) from baseline to last follow-up on the Incontinence Impact Questionnaire–Short form (IIQ-7), the Urogenital Distress Inventory–Short form (UDI-6), and the Patient Global Subjective Score (Global). † N = 68 TVT, 65 PVT. ‡ Student’s t test, mean (standard deviation). § Multiple linear regression adjusting for prolapse (P = .51), previous operation (P = .57), SI vs MI (P < .001), age (P < .001), and follow-up months (P = .79). ¶¶ Multiple linear regression adjusting for prolapse (P = .67), previous operation (P = .40), SI vs MI (P = .005), age (P = .008), and follow-up months (P = .62). ¶ N = 65 TVT, 63 PVT. **N = 63 TVT, 65 PVT. †† Wilcoxon rank-sum test, median (25th percentile, 75th percentile). ‡‡ Univariate confidence interval for difference in medians and noninferiority P value based on 1000 bootstrap resamples of difference in medians. §§ Odds ratio (95% CI) from cumulative logic regression adjusting for previous operation (P = .21), SI vs MI (P = .10), age (P = .005), and follow-up months (P = .61). Interpretation: odds for higher level of improvement in PVT vs TVT. CI, confidence interval; CL, confidence limit; MI, mixed incontinence; PVT, percutaneous vaginal tape; SI, stress incontinence; TVT, tension-free vaginal tape.

Table 43-3 Comparison of Treatment Groups on Baseline Variables Preoperative Variable Prolapse, n Previous anti-incontinence operation, n Preoperative diagnosis (SI vs MI), n Low ALPP (defined urodynamically as 56.7 min) active second stage of labor (defined as the stage of active pushing) and heavier (>3.41 kg) babies showed the most EMG evidence of nerve damage. The investigators concluded that vaginal delivery causes partial denervation of the pelvic floor in the majority of women delivering their first baby. For most women, the degree of denervation is slight, but in some there is severe damage that may be associated with loss of sphincteric control. Of the original study cohort of 96 women, 77 (80%) were available for 7-year and 65 (68%) for 15-year follow up.22 The motor unit potential durations were found to be increased significantly after delivery, and again at 7 and 15 years; however, no correlation was found between this EMG finding and the symptom of stress incontinence. The investigators concluded that the absence of an adequate marker for pelvic floor denervation makes it difficult to determine the role of denervation/reinnervation after the first delivery in the etiology of stress urinary incontinence.

PATHOPHYSIOLOGY Labor and delivery have long been known to be the major causes of pelvic floor injury. However, it is unknown whether the insult begins during pregnancy, before the active process of labor and delivery, and whether delivery by elective cesarean section, with no trial of labor, provides any protective effect. Major injury mechanisms include partial denervation of the pelvic floor and direct injury to the pelvic soft tissues. Neurologic Damage Electromyography (EMG) and pudendal nerve terminal motor latency (PNTML) measurements are considered to be useful in detecting denervation of the pelvic floor. Prolonged PNTML is obtained when large myelinated nerve axons have been damaged. Snooks and colleagues18,19 used electrophysiologic techniques to study 71 women at 48 to 72 hours after delivery and again, in 70% of these women, 2 months later. An increased PNTML was found in 42% of the women 48 to 72 hours after vaginal delivery, but not in any of those who delivered by cesarean section. Multiparity, forceps delivery, increased duration of the second stage of labor (defined as the interval between full cervical dilatation and the delivery of the newborn), third degree perineal tear and high birth weight were all found to be associated with increased risk of pudendal neuropathy. However, by 2 months postpartum, the PNTML had returned to normal in 60% of the women, implying that the denervation injury is usually reversible. Fourteen multiparas of the original cohort underwent repeated neurophysiologic studies 5 years after delivery.20 Five of these 14 women complained of stress urinary incontinence and were found to have marked pudendal neuropathy. The investigators concluded that childbirth-associated pudendal neuropathy may persist and worsen with time. Allen and colleagues21 studied the innervation of the pelvic floor muscles before and 2 months after delivery in 96 nulliparas. Using motor unit potential duration as a sign of reinnervation in response to denervation injury, they found evidence of partial denervation of the pelvic floor with consequent reinnervation in 80% of the women after vaginal delivery. It was unclear whether the EMG changes were due to stretching of the pudendal nerve or to direct pressure of the fetal head on the nerve branches. Furthermore, evidence of partial denervation was also found in women who had undergone cesarean section during labor. This

Muscular Damage Relative weakness of the pelvic floor muscles after vaginal delivery was confirmed in several clinical studies. Insult may be secondary to nerve damage, local ischemia, muscle distention, or direct tearing of muscle fibers. Peschers and associates23 demonstrated that pelvic muscle strength was significantly reduced 3 to 8 days after vaginal delivery but not after cesarean section. In most women, muscle strength was restored to antepartum values 6 to 10 weeks postpartum. However, Sampselle and coauthors24 reported that recovery of levator ani contractility could take as long as 6 months after delivery. Advanced imaging techniques have enabled visualization of the pelvic floor structures before and after labor and delivery. Sultan and colleagues25 used endosonography to assess antenatal and postnatal anal sphincter anatomy. At 6 to 8 weeks postpartum, 35% of the 79 primiparous women studied had occult disruption of the internal or external anal sphincter. None had such sphincter defects before delivery. Of 48 multiparous women, 40% had a sphincter defect before delivery and 44% thereafter. None of the 23 women who underwent cesarean section had a new sphincter defect after delivery. Further analysis revealed that forceps delivery was significantly associated with anatomic damage. Magnetic resonance imaging (MRI) has been used to detect anatomic and chemical changes, as well as to localize specific injury sites. DeLancey and coworkers26 used MRI to explore the appearance of the levator ani muscle after vaginal delivery. The study population consisted of 80 nulliparous and 160 primiparous women. The primiparas were all examined 9 to 12 months after vaginal delivery. As many as 20% of the primiparas were found to have levator ani defects on MRI. Most defects were identified in the pubovisceral portion of the levator ani (consists of the pubococcygeus, puborectalis, and puboperineus muscles), and some were in the iliococcygeal portion of the muscle. No levator ani muscle defects were identified in nulliparous women. Moreover, stress-incontinent women were twice as likely to have levator ani defects than continent women. More recently, Lien and colleagues27 used MRI to create a three-dimensional computer model of the levator ani muscle. This model was used to quantify levator ani muscle stretch during the second stage of labor. The investigators found that the medialmost pubococcygeus muscle is at greater risk for stretch-related injury than any

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other levator ani muscle during the second stage of labor. Tissue stretch ratios were also proportional to fetal head size. Connective Tissue Damage Normally, the endopelvic fascia and the anterior vaginal wall form a hammock-like layer in which the bladder and vesical neck rest. During increased intra-abdominal pressure, the urethra is compressed against this supporting hammock, and continence is maintained. Simultaneous contraction of the levator ani and the urethral sphincter muscles must also occur to support the vesical neck and to occlude the urethra.28 Indirect evidence of the effects of childbirth on this coordinated support mechanism was obtained by sonogram measurements of the vesical neck position before and after delivery. Both transperineal and transvaginal ultrasound were used to facilitate visualization of the vesical neck at rest; then, with the Valsalva maneuver, the relative descent was measured. Several studies showed lower vesical neck position in women who delivered vaginally, compared with those who underwent elective cesarean section and with nulliparous women. Likewise, mobility of the vesical neck during the Valsalva maneuver was found to increase after vaginal delivery. However, it is less clear whether this increased vesical neck mobility is also associated with long-term pelvic floor disorders.8,10,29-31 OBSTETRIC RISK FACTORS Parity, prolonged labor, instrument-assisted delivery, and increased birth weight have always been considered predisposing factors for pelvic floor injury and subsequent development of long-term pelvic floor dysfunction. However, clear scientific data regarding various obstetric parameters, as well as the possible protective effects of cesarean section, are inconsistent. These conflicting data stress the need for further investigation of the role of pregnancy and delivery in the development of pelvic floor disorders. Parity Several investigators reported a positive correlation between parity and stress urinary incontinence.32-35 However, data concerning a possible linear correlation versus a certain threshold of parity for the development of urinary incontinence are subject to controversy. Foldspang and colleagues36 found the prevalence of urinary incontinence in women aged 30 to 44 years to be correlated with parity. However, in women aged 45 years or older, only three or more deliveries were associated with an increased risk of incontinence. Thomas and associates,37 in a postal questionnaire study of more than 7000 women, reported an increased prevalence of urinary incontinence in women with four or more children. Nulliparous women had a lower prevalence of urinary incontinence than did those who had been delivered of one, two, or three babies, but within the parity range of one to three there were no differences in prevalence. Similarly, Wilson and coworkers38 reported that the odds ratio for postpartum urinary incontinence increased significantly after four deliveries. The association between parity and urinary incontinence was also investigated by two large epidemiologic studies, the Norwegian Epidemiology of Incontinence in the County of NordTrondelag (EPINCONT) study39 and the Nurses’ Health Study.40 The EPINCONT study was a large survey performed in one county in Norway during the years 1995-1997. The association

between parity and urinary incontinence was analyzed in an unselected sample of 27,900 women who answered a detailed questionnaire. Overall, urinary incontinence was reported by 25% of participants. Parity was associated only with stress and mixed types of incontinence, the first delivery being the most significant. The association was strongest in the age group 20 to 34 years, with relative risks of 2.2 and 3.3 for primiparas and grand multiparas, respectively. A weaker association was found in the age group 35 to 64 years (relative risks, 1.4 and 2.0, respectively), and no association was found among women older than 65 years of age. The investigators concluded that all effects of parity seem to disappear in later years. The Nurses’ Health Study comprised 83,168 women aged 50 to 75 years. Overall, urinary incontinence was reported by 34% of participants. Similar to the EPINCONT study results, parity was associated with increased prevalence of urinary incontinence; however, the association was weaker among women aged 60 years or older. Results of these two large epidemiologic studies suggest that additional factors, other than childbirth, become more significant in older women, thereby minimizing the effects of parity per se. Birth Weight The importance of specific labor parameters and their etiologic role in the development of pelvic floor disorders remains controversial. Dimpfl and associates41 found a similar incidence of postpartum stress urinary incontinence among mothers whose neonates weighed 3500 g or more and those with infants weighing less than 3500 g. Viktrup and coworkers42 reported increased birth weights in infants of mothers who developed stress urinary incontinence after delivery, although statistical significance was not reached. Our group34 found that the prevalence of postpartum stress incontinence among grand multiparas who had given birth to at least one baby weighing more than 4000 g was significantly higher than in those who had not (29.4% versus 16.7%, respectively). Similarly, Persson and colleagues35 found that the risk of later surgery for stress incontinence after vaginal delivery correlated with the weight of a woman’s largest infant. The effect of various obstetric parameters and urinary incontinence in later life was also investigated in the Norwegian EPINCONT study.43 The investigators analyzed data from 11,397 women who had delivered vaginally only and who had no more than five children. Nine obstetric parameters were investigated: birth weight, gestational age, head circumference, functional delivery disorders, injuries/tears, breech, forceps, vacuum deliveries, and epidural anesthesia. Statistically significant associations were found between any incontinence and birth weight of 4000 g or more and between stress urinary incontinence and high birth weight; however, odds ratios were relatively weak (1.1 and 1.2, respectively). Dysfunctional Labor Early electrophysiologic studies showed that prolonged second stage of labor can cause partial denervation of the pelvic floor.18,19,21 However, clinical studies have presented conflicting data regarding the association between duration of labor and the later risk of sphincteric incontinence.44-48 The EPINCONT study grouped various disorders, among which were labor duration of more than 24 hours, cervical dystocia, uterine atonia, and attenuation of contraction, into one category entitled “functional delivery disorders.”43 Statistically significant association was observed between this general category and moderate or severe urinary

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incontinence; however, the odds ratio (1.3) was relatively weak. No further analysis was undertaken to examine specific parameters, such as duration of the second stage of labor, within this category. Instrument-Assisted Delivery Results regarding the possible role of instrument-assisted vaginal delivery (i.e., vacuum or forceps) in the development of pelvic floor disorders are also conflicting. Dimpfl and colleagues41 found a higher incidence of incontinence after instrumental-assisted vaginal delivery. However, other studies did not confirm this finding.38,49,50 Sultan and coworkers25 used endosonography to assess antenatal and postnatal anal anatomy. Forceps delivery was found to be significantly associated with anatomic damage: sphincter defects developed in 8 of the 10 primiparas who underwent forceps delivery, but not in any of the 5 who had underwent vacuum extraction. In another study of 43 patients who had undergone an instrumental delivery, Sultan’s group50 reported that 81% of forceps deliveries were associated with sonographic anal sphincter damage, compared with 24% of vacuum deliveries. Several other studies also demonstrated an increased risk of pelvic floor injury after forceps compared with vacuum deliveries.52-55 However, one study reported a higher rate of vacuum rather than forceps deliveries in patients with postpartum fecal incontinence.56 Differences between obstetricians in their primary choice of instrument delivery (vacuum versus forceps), as well as their clinical skills and experience, may explain some of these results. Furthermore, it is possible that the main cause of pelvic floor damage during instrument deliveries is the obstetric indication for such an intervention, namely a prolonged second stage, rather than the type of instrument used per se. Therefore, avoidance of instrumental intervention may facilitate prolonged distention of the vagina by the fetal head, causing greater damage to the pelvic floor.57 This speculation may be supported by the recent EPINCONT findings suggesting a tendency for these procedures to protect against urinary incontinence, particularly for vacuum delivery.43 Cesarean Section Several studies have examined the association between delivery by cesarean section and urinary incontinence. Persson and colleagues,35 in a large population-based study of 1942 women, studied risk factors for stress urinary incontinence as represented by a history of anti-incontinence surgery. No association was found between anti-incontinence surgery and pregnancy per se. Vaginal delivery was found to be associated with increased risk for anti-incontinence surgery, compared with elective cesarean section. Moreover, the odds ratio for anti-incontinence surgery was similarly decreased for nulliparas and for primiparas delivered by elective cesarean section. Wilson and associates38 studied the prevalence of urinary incontinence at 3 months after delivery in a heterogeneous group of 1505 primiparous and multiparous women. They found a significantly lower prevalence of urinary incontinence after cesarean section, in particular among primiparas with no previous history of incontinence, compared to normal vaginal delivery. However, the difference between cesarean sections performed before labor and those performed during labor was nonsignificant. A follow-up study, performed 5 to 7 years later,58 confirmed the lack of difference between elective and emergency cesarean sections; however, no differentiation

was made between the various indications for emergency cesarean section. Farrell and colleagues59 studied the association between the mode of first delivery and prevalence of urinary incontinence at 6 months postpartum. Vaginal delivery was associated with a higher prevalence of urinary incontinence (relative risk, 2.8) compared with cesarean section. No significant difference was found between cesarean sections performed before and during labor. The authors concluded that cesarean section at any stage of labor reduced postpartum urinary incontinence. Rortveit and coworkers60 investigated the association between childbirth and urinary incontinence in a large community-based cohort of 15,307 women who were younger than 65 years of age and were either nulliparous, had undergone only cesarean deliveries, or had had only vaginal deliveries. This analysis was part of the EPINCONT study described earlier. The prevalence of stress urinary incontinence was 4.7% in the nulliparous group, 6.9% in the cesarean section group, and 12.2% in the vaginal delivery group. Further classification of cesarean sections into elective versus nonelective, performed in a subgroup of 239 primiparas, failed to reveal a statistically significant difference. However, as in all other aforementioned studies, nonelective cesarean sections were analyzed as one group, with no further differentiation among cesarean sections for obstructed labor, fetal distress, maternal indications, and other obstetric conditions. Grouping all cesarean section deliveries into one category may be associated with an overestimation bias, because it is possible that, in cases of cesarean section performed for obstructed labor, pelvic floor injury is already too extensive to be prevented by surgical intervention. To investigate this possibility, our group recently studied the prevalence of stress urinary incontinence 1 year postpartum according to the mode of delivery: spontaneous vaginal delivery versus elective cesarean section versus cesarean section performed for obstructed labor.61 Our results showed a similar prevalence of stress urinary incontinence 1 year after delivery among primiparas who underwent spontaneous vaginal delivery and those who had undergone cesarean section for obstructed labor (10.3% and 12%, respectively; P = .7). Conversely, elective cesarean section, with no trial of labor, was associated with a significantly lower prevalence of postpartum stress incontinence (3.4%; P = .02). This low prevalence of stress urinary incontinence among primiparas who had elective cesarean sections was similar to that reported for nulliparous women.34,60 Whether prevention of pelvic floor injury should be an indication for elective cesarean section is controversial62 and involves medical, financial, and ethical aspects. It should be borne in mind that cesarean section may expose women to greater morbidity and mortality. Furthermore, the etiology of stress urinary incontinence is multifactorial. Additional risk factors, other than mode of delivery, include heredity, collagen abnormalities, aging, obesity, and parity. Specific labor plans should therefore be based on overall judgment, taking into consideration personal clinical status and risk factors.

CLINICAL PRESENTATIONS Stress Urinary Incontinence Stress urinary incontinence is an exceedingly common symptom during pregnancy and the puerperium. Viktrup and associates42 interviewed 305 primiparas in regard to stress urinary inconti-

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nence before and during pregnancy and after delivery. Of these, 4% had stress urinary incontinence before pregnancy, 32% during pregnancy, and 7% after delivery. Among those women who reported stress incontinence during pregnancy, fewer than 5% remained symptomatic 12 months after delivery. Of those who developed the condition after delivery, 24% remained symptomatic at 12 months. These observations suggest that pregnancy-associated stress incontinence resolves after delivery in most women. The question of greater interest is whether women with pregnancy-associated stress incontinence are at increased risk for incontinence in later life. Of the original study cohort of 305 primiparous women reported by Viktrup and colleagues,42 278 (91%) were available for a 5-year follow-up.63 The overall prevalence of stress urinary incontinence at 5 years postpartum was 30%. Among those women with pregnancyassociated stress incontinence but full remission at 3 months postpartum, symptoms recurred 5 years later in 42%. Up to 92% of those with stress incontinence at 3 months postpartum developed stress incontinence 5 years later. The investigators concluded that first pregnancy and delivery are important in the development of long-lasting stress incontinence and that the use of vacuum delivery and episiotomy seems to increase the risk. Schytt and colleagues64 studied the prevalence and predictors of stress incontinence 1 year after childbirth. The study cohort comprised 2390 Swedish women who completed questionnaires during pregnancy and again at 2 months and 1 year after delivery. One year postpartum, 22% of the women were stressincontinent, but only 2% considered it a major problem. The strongest predictor for stress incontinence at 1 year, in primiparas as well as multiparas, was urinary incontinence during pregnancy and at 4 to 8 weeks after delivery. Of those who had urinary incontinence during the third trimester, 31% to 41% were stressincontinent 1 year after delivery. Of those who had urinary incontinence 4 to 8 weeks after delivery, 44% to 59% were stress incontinent 1 year postpartum. Other predictors unrelated to parity were obesity and constipation during pregnancy and after delivery. Several other investigators found that, regardless of the mode of first delivery, new onset of stress urinary incontinence during pregnancy is associated with increased risk of long-lasting stress urinary incontinence5,34,35,38,61,65 These observations suggest that the etiology of stress incontinence is more complicated than previously estimated and that the onset of incontinence is also related to the pregnant status, rather than to obstetric trauma per se.

Anal Incontinence The true prevalence of anal incontinence is unknown and most probably has been underestimated. Although anal incontinence is more common among elderly patients, many young female patients are also affected. Previous studies reported that 3% to 7% of women experienced anal incontinence several months after delivery.45,56,66 Pollack and colleagues67 studied the prevalence of anal incontinence in primiparous women 5 years after their first delivery. The study population included 242 women who completed questionnaires before pregnancy and at 5 months, 9 months, and 5 years after delivery. Among women with no visible sphincter tears at their first delivery, 25% reported anal incontinence at 9 months and 32% at 5 years. Among those with sphincter tears, 44% reported anal incontinence at 9 months and 53% at 5 years. The majority of symptomatic women had infre-

quent incontinence to flatus, whereas frank fecal incontinence was rare. Risk factors for anal incontinence at 5 years were age, sphincter tear, and subsequent childbirth. The reported incidence of anal sphincter tears after first delivery and subsequent childbirth varies widely. Moreover, sphincter tears may be overt (third- or fourth- degree tears), diagnosed and repaired immediately after delivery, or occult, identified by endoanal ultrasonography after childbirth. The incidence of overt sphincter injury is estimated to be 0.5% to 3.3% in centers where mediolateral episiotomy is practiced or higher, 11% to 28%, in centers where midline episiotomies are used.68-70 Women with third- and fourth-degree sphincter tears are more likely to develop anal incontinence. Fornell and associates71 compared 51 women with and 31 women without anal sphincter injury and found that as many as 40% of the affected women reported fecal incontinence 6 months after delivery. Twenty-six of the original study group and 6 of the original controls were objectively and subjectively re-examined 10 years later.72 Incontinence to flatus and liquid stool was more severe in the study group than in controls. Subjective and objective anal function after sphincter injury was found to deteriorate over time and with subsequent vaginal deliveries. Moreover, 7 of the original 51 women underwent second repair of the sphincter defect (5 before the follow-up study, and 2 more afterward by referral for secondary repair due to fecal incontinence). The investigators indicated that fecal incontinence must be considered a strong marker for unsatisfactory results of primary repair. In view of the disappointing results obtained with secondary repairs, preventive measures and optimal primary repair are strongly recommended. A relatively high incidence of occult sphincter injury was reported after apparently uneventful vaginal deliveries. Sultan and associates25 used endosonography to assess antenatal and postnatal anal anatomy. No sphincter defects were demonstrated antenatally among 79 primiparous patients studied. However, at 6 to 8 weeks postpartum, 35% had occult disruption of the internal or external anal sphincter. Of the 48 multiparous women, 40% had a sphincter defect prenatally and 44% postnatally. None of the 23 women who underwent cesarean section had a new sphincter defect after delivery. When the women studied 6 weeks after delivery, anal incontinence or fecal urgency was found in 13% of the primiparas and 23% of the multiparas who delivered vaginally. A strong association was observed between sphincter defects and the development of bowel symptoms. In another study of 43 patients who had had instrumental deliveries, Sultan and colleagues51 reported that 81% of forceps deliveries were associated with sonographic anal sphincter damage, compared with 24% of vacuum deliveries. A recent meta-analysis of five studies, with overall 717 women who underwent endoanal ultrasonography after childbirth, revealed a 26.9% incidence of anal sphincter defects in primiparous women and an 8.5% incidence of new sphincter defects in multiparous women. About one third of women with occult anal sphincter defects were symptomatic after delivery.73

Pelvic Organ Prolapse Pelvic organ prolapse is very common and is seen in up to 50% of parous women.74 Hendrix and associates75 studied the prevalence of pelvic organ prolapse among 27,342 women (the Women’s Health Initiative Study). Among the 16,616 women with a uterus, the rate of uterine prolapse was 14.2%; the rate of

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cystocele was 34.3%, and the rate of rectocele was 18.6%. Among the 10,727 women who had undergone hysterectomy, prevalence of cystocele was 32.9% and that of rectocele was 18.3%. In 1997, the rate of pelvic organ prolapse surgery in the United States was 22.7 per 10,000 women, making prolapse one of the most common surgical indications in women.76 Similarly, the lifetime risk of surgery for prolapse by age 80 years was estimated to be 11%.77 Pregnancy and childbirth are major risk factors for pelvic organ prolapse. Both the levator ani muscle and the endopelvic fascia are important in maintaining the pelvic organs in their normal anatomic position. Both may be injured during pregnancy and delivery, thus predisposing to the later development of pelvic organ prolapse. Sze and colleagues78 found that some degree of pelvic organ prolapse existed in their subjects during the third trimester of pregnancy and that the prevalence of prolapse at 6 weeks after delivery was similar in women who underwent vaginal delivery and those who had emergency cesarean section. Similarly, O’Boyle and associates79 found that nulliparous pregnant women were more likely to have pelvic organ prolapse than their nulliparous, nonpregnant controls. These findings imply that the prolapse process begins during pregnancy and early labor. The risk is further increased after vaginal deliveries. Mant and colleagues80 studied a cohort of 17,000 British women. Parity was the strongest variable related to surgery for pelvic organ prolapse. Samuelsson and coworkers81 studied a cohort of 487 Swedish women. The risk for pelvic organ prolapse was found to increase with parity and age. Parity and obesity were also strongly associated with increased risk for pelvic organ prolapse in the large Women’s Health Initiative Study.75 Women who had had at least one child were twice as likely to have pelvic organ prolapse as were nulliparous controls, after adjusting for age, ethnicity, body mass index, and other factors. Richardson and colleagues82 documented breaks in the endopelvic fascia in women with pelvic organ prolapse and stress urinary incontinence. These breaks are considered to be secondary to obstetric trauma. The anatomic injury may be further complicated by childbirth-associated denervation injury. Evidence of such denervation has been detected in up to 50% of women with symptomatic pelvic organ prolapse.83-85 However, one should bear in mind that, as with sphincteric incontinence, the etiology of pelvic organ prolapse is complex and multifactorial. Possible risk factors, other than pregnancy and childbirth, include connective tissue abnormalities, aging, hysterectomy, menopause, and factors associated with chronically raised intraabdominal pressure.86

Voiding Difficulties Data regarding the correlation between obstetric parameters and voiding phase disorders are scarce and controversial. Conceptually, voiding phase dysfunction may be result from bladder and/ or urethral causes. Bladder causes include detrusor contraction of inadequate magnitude and/or duration to effect bladder emptying (detrusor underactivity) and the absence of detrusor contraction (detrusor areflexia). Urethral causes consist of bladder outlet obstruction due to urethral overactivity (functional obstruction) or anatomic pathologies (mechanical obstruction). These mechanisms may all be responsible for abnormal voiding during the puerperium. Mechanical bladder outlet obstruction may develop secondary to local hematoma or edema, functional

obstruction may be secondary to pain, and detrusor underactivity may be the end result of pelvic floor denervation or neglected bladder overdistention. Most previously published studies used postvoid residual urine volume, measured by either ultrasound or transurethral catheterization, to detect postpartum voiding dysfunction. Andolf and colleagues87 investigated residual urinary volumes on the third postpartum day in 539 women who delivered vaginally. Eight women (1.5%) had a residual volume exceeding 150 mL. Retention was more common after instrument delivery or epidural analgesia. Yip and associates88,89 reported a 4.9% incidence of acute, symptomatic postpartum urinary retention among 691 women who delivered vaginally. An additional 9.7% of patients had no urinary symptoms, but their postvoid residual urinary volume on the first postpartum day was 150 mL or greater (up to 1000 mL). A significant correlation was found between the duration of the first and second stages of labor and postpartum residual urinary volume. We recently reported that approximately half of 277 consecutive women complained of significant voiding difficulties in the immediate postpartum period. The main risk factors included prolonged first and second stages of labor, vacuum extraction, and birth weight 3800 g or greater.90 Most cases of early postpartum voiding difficulties resolve spontaneously within few days. Persistent postpartum urinary retention, beyond the early puerperium, is uncommon. In a study of 8402 consecutive, unselected parturients delivered in a university-affiliated maternity hospital over a 1-year period, only 4 patients (0.05%) developed persistent postpartum urinary retention.91 Risk factors for persistent postpartum urinary retention included vaginal delivery after cesarean section, prolonged second stage of labor, epidural analgesia, and delayed diagnosis and intervention. Urodynamic evaluation, performed in two of these patients 1 month after removal of the suprapubic catheter, revealed stress incontinence in one and detrusor overactivity in the other. Similarly, Carley and colleagues92 reported a 0.45% prevalence rate of clinically overt postpartum urinary retention among 11,332 vaginally delivered women. Urinary retention was found to be highly associated with instrument-assisted delivery and epidural analgesia. Most affected women resumed spontaneous voiding within 72 hours, but 13 women (0.1%) developed persistent postpartum urinary retention. These two studies indicate that persistent postpartum urinary retention is rare in modern obstetric practice but may be associated with long-term bladder dysfunction. Early diagnosis of postpartum voiding dysfunction and adequate intervention are therefore required to prevent irreversible bladder damage.

SUMMARY Pregnancy and childbirth are associated with anatomic and neuromuscular injuries of the pelvic floor. These injuries predispose for various pelvic organ disorders that may manifest during pregnancy and after delivery or develop in later years. Cesarean section appears to be protective, especially if undertaken electively, with no trial of labor. Whether the prevention of pelvic floor injury should be an indication for elective cesarean section is controversial. It should be borne in mind that cesarean section may expose women to greater morbidity and mortality, and that the etiology of pelvic organ disorders is multifactorial. Additional risk factors, other than pregnancy and childbirth, include hered-

Chapter 52 PREGNANCY, CHILDBIRTH, AND PELVIC FLOOR INJURY

ity, collagen abnormalities, obesity, and aging. Better understanding of pathophysiologic mechanisms associated with pelvic floor dysfunction may provide the possibility of using appropriate preventive measures other than elective cesarean section. Fur-

thermore, as new therapies emerge, it is likely that different pathophysiologies will be treated differently. Exploring these processes and quantifying subjective and objective findings remains a clinical challenge.

References 1. Dafnis E, Sabatini S: The effect of pregnancy on renal function: physiology and pathophysiology. Am J Med Sci 303:184-205, 1992. 2. Francis WJA: Disturbances of bladder function in relation to pregnancy. J Obstet Gynaecol Br Empire 67:353-366, 1960. 3. Stanton SL, Kerr-Wilson R, Harris GV: The incidence of urological symptoms in normal pregnancy. Br J Obstet Gynaecol 87:897-900, 1980. 4. Cutner A, Carey A, Cardozo LD: Lower urinary tract symptoms in early pregnancy. J Obstet Gynecol 12:75-78, 1992. 5. Thorp JM Jr, Norton PA, Wall LL, et al: Urinary incontinence in pregnancy and the puerperium: A prospective study. Am J Obstet Gynecol 181:266-273, 1999. 6. Hundley JM Jr, Siegel IA, Hachtel FW, Dumler JC: Some physiological and pathological observations on the urinary tract during pregnancy. Sur Gynecol Obstet 66:360-379, 1938. 7. Malpas P, Jeffcoate TNA, Lister UM: The displacement of the bladder and urethra during labor. J Obstet Gynaecol Br Empire 56:949-960, 1949. 8. Peschers U, Schaer G, Anthuber C, et al: Changes in vesical neck mobility following vaginal delivery. Obstet Gynecol 88:1001-1006, 1996. 9. Wijma J, Weis Potters AE, de Wolf BT, et al: Anatomical and functional changes in the lower urinary tract during pregnancy. Br J Obstet Gynaecol 108:726-732, 2001. 10. King JK, Freeman RM: Is antenatal bladder mobility a risk factor for postpartum stress incontinence? Br J Obstet Gynaecol 105:13001307, 1998. 11. Dietz HP, Eldridge A, Grace M, Clarke B: Does pregnancy affect pelvic organ mobility? Aust N Z J Obstet Gynecol 44:517-520, 2004. 12. Lavin JM, Smith ARB, Anderson J, et al: The effect of the first pregnancy on the connective tissue of the rectus sheath. Neurourol Urodyn 16:381-382, 1997. 13. Van Geelen JM, Lemmens WA, Eskes TK, Martin CB Jr: The urethral pressure profile in pregnancy and after delivery in health nulliparous women. Am J Obstet Gynecol 144:636-649, 1982. 14. Chaliha C, Bland JM, Monga A, et al: Pregnancy and delivery: A urodynamic viewpoint. Br J Obstet Gynaecol 107:1354-1359, 2000. 15. Nel JT, Diedericks A, Joubert G, Arndt K: A prospective clinical and urodynamic study of bladder function during and after pregnancy. Int Urogynecol J 12:21-26, 2001. 16. Muellner SR: Physiological bladder changes during pregnancy and the puerperium. J Urol 41:691-695, 1939. 17. Youssef AF: Cystometric studies in gynecology and obstetrics. Obstet Gynecol 8:181-188, 1956. 18. Snooks SJ, Swash M, Setchell M, Henry MM: Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 2:546550, 1984. 19. Snooks SJ, Swash M, Henry MM, Setchell M: Risk factors in childbirth causing damage to the pelvic floor innervation. Int J Colorectal Dis 1:20-24, 1986. 20. Snooks SJ, Swash M, Mathers SE, Henry MM: Effect of vaginal delivery on the pelvic floor: A 5-tear follow-up. Br J Surg 77:13581360, 1990. 21. Allen RE, Hosker GL, Smith ARB, Warrell DW: Pelvic floor damage and childbirth: A neurophysiological study. Br J Obstet Gynaecol 97:770-779, 1990. 22. Dolan LM, Hosker GL, Mallett VT, et al: Stress incontinence and pelvic floor neurophysiology 15 years after the first delivery. Br J Obstet Gynaecol 110:1107-1114, 2003.

23. Peschers UM, Shaer GN, DeLancey JO, Schuessler B: Levator ani function before and after childbirth. Br J Obstet Gynaecol 104:10041008, 1997. 24. Sampselle CM, Miller JM, Mims BL, et al: Pelvic muscle exercise reduces transient incontinence during pregnancy and after birth. Obstet Gynecol 91:406-412, 1998. 25. Sultan AH, Kamm MA, Bartram CI, Hudson CN: Anal-sphincter disruption during vaginal delivery. N Engl J Med 329:1905-1911, 1993. 26. DeLancey JO, Kearney R, Chou Q, et al: The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 101:46-53, 2003. 27. Lien KC, Mooney B, DeLancey JOL, Ashton-Miller JA: Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol 103:31-40, 2004. 28. DeLancey JOL: Stress urinary incontinence: Where are we now, where should we go? Am J Obstet Gynecol 175:311-319, 1996. 29. Wijma J, Weis Potters AE, De Wolf BTHM, et al: Anatomical and functional changes in the lower urinary tract following spontaneous vaginal delivery. Br J Obstet Gynaecol 110:658-663, 2003. 30. Meyer S, Schreyer A, DeGrandi P, Hohlfeld P: The effects of birth on urinary continence mechanisms and other pelvic-floor characteristics. Obstet Gynecol 92:613-618, 1998. 31. Dietz HP, Steensma AB: Which women are most affected by delivery-related changes in pelvic organ mobility? Eur J Obstet Gynecol Reprod Biol 111:15-18, 2003. 32. Jolleys JV: Reported prevalence of urinary incontinence in women in a general practice. BMJ 296:1300-1302, 1988. 33. Milsom I, Ekelund P, Molander U, et al: The influence of age, parity, oral contraception, hysterectomy and menopause on the prevalence of urinary incontinence in women. J Urol 149:1459-1462, 1993. 34. Groutz A, Gordon D, Keidar R, et al: Stress urinary incontinence: Prevalence among nulliparous compared with primiparous and grand mulitiparous premenopausal women. Neurourol Urodyn 18:419-425, 1999. 35. Persson J, Wolner-Hanssen P, Rydhstroem H: Obstetric risk factors for stress urinary incontinence: A population-based study. Obstet Gynecol 96:440-445, 2000. 36. Foldspang A, Mommsen S, Lam GW, Elvin L: Parity as a correlate of adult female urinary incontinence prevalence. J Epidemiol Community Health 46:595-600, 1992. 37. Thomas TM, Plymat KR, Blannin J, Meade TW: Prevalence of urinary incontinence. BMJ 281:1243-1245, 1980. 38. Wilson PD, Herbison RM, Herbison GP: Obstetric practice and the prevalence of urinary incontinence three months after delivery. Br J Obstet Gynaecol 103:154-161, 1996. 39. Rortveit G, Hannestad YS, Daltveit AK, Hunskaar S: Age- and typedependent effects of parity on urinary incontinence: The Norwegian EPINCONT study. Obstet Gynecol 98:1004-1010, 2001. 40. Grodstein F, Fretts R, Lifford K, Curhan G: Association of age, race, and obstetric history with urinary symptoms among women in the Nurses` Health Study. Am J Obstet Gynecol 189:428-434, 2003. 41. Dimpfl T, Hesse U, Schussler B: Incidence and cause of postpartum urinary incontinence. Eur J Obstet Gynecol Reprod Biol 43:23-33, 1992. 42. Viktrup L, Lose G, Rolff M, Barfoed K: The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 79:945-949, 1992.

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43. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S: Vaginal delivery parameters and urinary incontinence: The Norwegian EPINCONT study. Am J Obstet Gynecol 189:1268-1274, 2003. 44. Thom DH, Van den Eeden SK, Brown JS: Evaluation of parturition and other reproductive variables as risk factors for urinary incontinence in later life. Obstet Gynecol 90:983-989, 1997. 45. Groutz A, Fait G, Lessing JB, et al: Incidence and obstetric risk factors of postpartum anal incontinence. Scand J Gastroenterol 34:315-318, 1999. 46. Varma A, Gunn J, Lindow SW, Duthie GS: Do routinely measured delivery variables predict anal sphincter outcome? Dis Colon Restum 42:1261-1264, 1999. 47. Abramowitz L, Sobhani I, Ganansia R, et al: Are sphincter defects the cause of anal incontinence after vaginal delivery? Dis Colon Restum 43:590-596, 2000. 48. Van Kessel K, Reed S, Newton K, et al: The second stage of labor and stress urinary incontinence. Am J Obstet Gynecol 184:15711575, 2001. 49. Foldspang A, Mommsen S, Djurhuus JC: Prevalent urinary incontinence as a correlate of pregnancy, vaginal childbirth, and obstetric techniques. Am J Public Health 89:209-212, 1999. 50. Meyer S, Holfeld P, Achtari C, et al: Birth trauma: Short and long term effects of forceps delivery compared with spontaneous delivery on various pelvic floor parameters. Br J Obstet Gynaecol 107:13601365, 2000. 51. Sultan AH, Kamm MA, Hudson CN, et al: Anal sphincter trauma during instrumental delivery: A comparison between forceps and vacuum extraction. Int J Gynaecol Obstet 43:263-70, 1993. 52. Johanson RB, Rice C, Doyle M, et al: A randomized prospective study comparing the new vacuum extractor policy with forceps delivery. Br J Obstet Gynaecol 100:524-530, 1993. 53. Sultan AH, Kamm MA, Hudson CN, Bartram CI: Third degree obstetric anal sphincter tears: Risk factors and outcome of primary repair. BMJ 308:887-891, 1994. 54. Bofill JA, Rust OA, Schorr SJ, et al: A randomized prospective trial of the obstetric forceps versus the M-cup vacuum extractor. Am J Obstet Gynecol 175:1325-1330, 1996. 55. Arya LA, Jackson ND, Myers DL, Verma A: Risk of new-onset urinary incontinence after forceps and vacuum delivery in primiparous women. Am J Obstet Gynecol 185:1318-1323, 2001. 56. MacArthur C, Bick DE, Keighley MRB: Faecal incontinence after childbirth. Br J Obstet Gynaecol 104:46-50, 1997. 57. DeLancey JOL: Childbirth, continence, and the pelvic floor. N Engl J Med 329:1956-1957, 1993. 58. Wilson PD, Herbison P, Glazener C, et al: Obstetric practice and urinary incontinence 5-7 years after delivery [abstract]. Neurourol Urodyn 21:289-291, 2002. 59. Farrell SA, Allen VM, Baskett TF: Parturition and urinary incontinence in primiparas. Obstet Gynecol 97:350-356, 2001. 60. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S: Urinary incontinence after vaginal delivery or cesarean section. N Engl J Med 348:900-907, 2003. 61. Groutz A, Rimon E, Peled S, et al: Cesarean section: Does it really prevent the development of postpartum stress urinary incontinence? A prospective study of 363 women one year after their first delivery. Neurourol Urodyn 23:2-6, 2004. 62. Bewley S, Cockburn J. Commentary: The unfacts of “request” caesarean section. Br J Obstet Gynaecol 109:597-605, 2002. 63. Viktrup L, Lose G: The risk of stress incontinence 5 years after first delivery. Am J Obstet Gynecol 185:82-87, 2001. 64. Schytt E, Lindmark G, Waldenstrom U: Symptoms of stress incontinence 1 year after childbirth: Prevalence and predictors in a national Swedish sample. Acta Obstet Gynecol Scand 83:928-936, 2004. 65. Pregazzi R, Sartore A, Troiano L, et al: Postpartum urinary symptoms: Prevalence and risk factors. Eur J Obstet Gynecol Reprod Biol 103:179-182, 2002. 66. Sleep S, Grant A: Pelvic floor exercises in postnatal care. Br J Midwifery 3:158-164, 1987.

67. Pollack J, Nordenstam J, Brismar S, et al: Anal incontinence after vaginal delivery: A five-year prospective cohort study. Obstet Gynecol 104:1397-1402, 2004. 68. Coats PM, Chan KK, Wilkins M, Beard RJ: A comparison between midline and mediolateral episiotomies. Br J Obstet Gynaecol 87:408412, 1980. 69. Samuelsson E, Ladfors L, Wennerholm UB, et al: Anal sphincter tears: Prospective study of obstetric risk factors. Br J Obstet Gynaecol 107:926-931, 2000. 70. Fenner DE, Genberg B, Brahma P, et al: Fecal and urinary incontinence after vaginal delivery and sphincter disruption in an obstetrics unit in the United States. Am J Obstet Gynecol 189:1543-1550, 2003. 71. Fornell E, Berg G, Hallbook O, et al: Clinical consequences of anal sphincter rupture during vaginal delicery. J Am Coll Surg 183:553558, 1996. 72. Fornell EU, Matthiesen L, Sjodahl R, Berg G: Obstetric anal sphincter injury ten years after: Subjective and objective long term effects. Br J Obstet Gynaecol 112:312-316, 2005. 73. Oberwalder M, Connor J, Wexner SD: Meta-analysis to detrmine the incidence of obstetric anal sphincter damage. Br J Surg 90:13331337, 2003. 74. Beck RP, McCormick S, Nordstrom L:. A 25-year experience with 519 anterior colporrhaphy procedures. Obstet Gynecol 78:10111018, 1991. 75. Hendrix SL, Clark A, Nygaard I, et al: Pelvic organ prolapse in the Women’s Health Initiative: Gravity and gravidity. Am J Obstet Gynecol 186:1160-1166, 2002. 76. Brown JS, Waetjen LE, Subak LL, et al: Pelvic organ prolapse surgery in the United States, 1997. Am J Obstet Gynecol 186:712-716, 2002. 77. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-505, 1997. 78. Sze EH, Sherard GB, Dolezal JM: Pregnancy, labor, delivery and pelvic organ prolapse. Obstet Gynecol 100:981-986, 2002. 79. O’Boyle AL, Woodman PJ, O’Boyle JD, et al: Pelvic organ support in nulliparous pregnant and non-pregnant women: A case control study. Am J Obstet Gynecol 187:99-102, 2002. 80. Mant J, Painter R, Vessey M: Epidemiology of genital prolapse: Obstervations from the Oxford Family Planning Association study. Br J Obstet Gynaecol 104:579-585, 1997. 81. Samuelsson EC, Victor FTA, Tibblin G, Svardsudd KF: Sings of genital prolapse in a Swedish population of women 20 to 59 years of age and possible related factors. Am J Obstet Gynecol 180:299305, 1999. 82. Richardson AC, Lyon WB, Williams NL: A new look at pelvic relaxation. Am J Obstet Gynecol 126:568-571, 1976. 83. Sharf B, Zilberman A, Sharf M, Mitrani A: Electromyogram of pelvic floor muscles in genital prolapse. Int J Gynaecol Obstet 14:2-4, 1976. 84. Gilpin SA, Gosling JA, Smith ARB, Warrell DW: The pathogenesis of genitourinary prolapse and stress incontinence of urine: A histological and histochemical study. Br J Obstet Gynaecol 96:15-23, 1989. 85. Smith ARB, Hosker GL, Warrell DW: The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: A neurophysiological study. Br J Obstet Gynaecol 96:24-28, 1989. 86. Maher C, Baessler K, Glazener CMA, et al: Surgical management of pelvic organ prolapse in women. Cochrane Database Syst Rev (4): CD004014, 2004. 87. Andolf E, Iosif CS, Jorgensen C, Rydhstorm H: Insidious urinary retention after vaginal delivery: Prevalence and symptoms at followup in a population-based study. Gynecol Obstet Invest 38:51-53, 1994. 88. Yip SK, Brieger G, Hin LY, Chung T: Urinary retention in the postpartum period: The relationship between obstetric factors and the

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post-partum post-void residual bladder volume. Acta Obstet Gynecol Scand 76:667-672, 1997. 89. Yip SK, Hin LY, Chung TKH: Effect of the duration of labor on postpartum postvoid residual bladder volume. Gynecol Obstet Invest 45:177-180, 1998. 90. Groutz A, Hadi E, Wolf Y, et al: Early postpartum voiding dysfunction: Incidence and correlation with obstetric parameters. J Reprod Med 49:960-964, 2004.

91. Groutz A, Gordon D, Wolman I, et al: Persistent postpartum urinary retention: prevalence, obstetric risk factors and management. J Reprod Med 46:44-48, 2000. 92. Carley ME, Carley JM, Vasdev G, et al: Factors that are associated with clinically overt postpartum urinary retention after vaginal delivery. Am J Obstet Gynecol 187:430-433, 2002.

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FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE Yvonne Hsu and John O.L. DeLancey Pelvic floor disorders, including pelvic organ prolapse and urinary incontinence, are debilitating conditions that result in surgery in one of nine women.1 In the United States, the National Center for Health Statistics estimates that 400,000 operations are performed for pelvic floor dysfunction each year, with 300,000 of these occurring in the inpatient setting.2,3 This is six to eight times more operations than radical prostatectomies performed each year. Although there is wide recognition of urinary incontinence, pelvic organ prolapse is responsible for twice as many operations, yet its causes are largely unknown. Prolapse arises because of injuries and deterioration of the muscles, nerves, and connective tissues that support and control normal pelvic function. This chapter addresses the functional anatomy of the pelvic floor in women and specifically focuses on how the pelvic organs are supported by the surrounding muscle and fasciae. It also considers the pathophysiology of pelvic organ prolapse as it relates to changes in these structures. SUPPORT OF THE PELVIC ORGANS: CONCEPTUAL OVERVIEW The pelvic organs rely on their connective tissue attachments to the pelvic walls and on support from the levator ani muscles, which are under neuronal control from the peripheral and central nervous systems. In this chapter, the term pelvic floor is used broadly to include all of the structures that support the pelvic cavity rather than just the levator ani group of muscles. The pelvic floor consists of several components lying between the peritoneum and the vulvar skin. From above downward, these are the peritoneum, pelvic viscera and endopelvic fascia, levator ani muscles, perineal membrane, and superficial genital muscles. The support for all these structures comes from connections to the bony pelvis and its attached muscles. The pelvic organs are often thought of as being supported by the pelvic floor, but they are actually a part of it. The pelvic viscera play an important role in forming the pelvic floor through their connections with structures such as the cardinal and uterosacral ligaments. In 1934, Bonney pointed out that the vagina is in the same relationship to the abdominal cavity as the in-turned finger of a surgical glove is to the rest of the glove (Fig. 53-1).4 If the pressure in the glove is increased, it forces the finger to protrude downwards in the same way that increases in abdominal pressure force the vagina to prolapse. Figure 53-2 provides a schematic illustration of this prolapse phenomenon. In Figure 53-2C, the lower end of the vagina is held closed by the pelvic floor muscles, which 542

prevents prolapse by constricting the base of the invaginated finger. Figure 53-2D shows suspension of the vagina to the pelvic walls. Figure 53-2E demonstrates that spatial relationships are important in the flap-valve closure, in which the suspending fibers hold the vagina in a position against the supporting walls of the pelvis; increases in pressure force the vagina against the wall, thereby pinning it in place. Vaginal support is a combination of constriction, suspension, and structural geometry. The female pelvis can naturally be divided into anterior and posterior compartments (Fig. 53-3). The genital tract (vagina and uterus) divides these two compartments through lateral connections to the pelvic sidewall and suspension at its apex. The levator ani muscles form the bottom of the pelvis. The organs are attached to the levator ani muscles when they pass through the urogenital hiatus and are supported by these connections. Functional Anatomy and Prolapse The pelvic organ support system is multifaceted and includes the endopelvic fascia, the perineal membrane, and the levator ani muscles, which are controlled by the central and peripheral nervous system. The supports of the uterus and vagina are different in different regions (Fig. 53-4).5 The cervix (when present) and the upper third of the vagina (level I) have relatively long suspensory fibers that are vertically oriented in the standing position, whereas the midportion of the vagina (level II) has a more direct attachment laterally to the pelvic wall (Fig. 53-5). In the most caudal region (level III), the vagina is attached directly to the structures that surround it. At this level, the levator ani muscles and the perineal membrane have important supportive functions. In the upper part of the genital tract, a connective tissue complex attaches all the pelvic viscera to the pelvic sidewall. This endopelvic fascia forms a continuous, sheet-like mesentery, extending from the uterine artery at its cephalic margin to the point at which the vagina fuses with the levator ani muscles below. The fascial region that attaches to the uterus is called the parametrium, and that which attaches to the vagina is the paracolpium. Level I is composed of both parametrium and paracolpium. The uterosacral and cardinal ligaments together form the parametrium and support the uterus and upper third of the vagina. The paracolpium portion of level I consists of a relatively long sheet of tissue that suspends the superior aspect of the vagina by attaching it to the pelvic wall. This is true whether or not the cervix is present. The uterosacral ligaments are important components of this support. At level II, the paracolpium changes configuration and forms more direct lateral attachments of the

Chapter 53 FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE

Figure 53-1 Bonney’s analogy of vaginal prolapse. The vagina is in the same relationship to the abdominal cavity as the in-turned finger of a surgical glove is to the rest of the glove (left). The eversion of an intussuscepted surgical glove finger by increasing pressure within the glove is analogous to prolapse of the vagina (right). (© 2002 DeLancey; with permission.)

A

C

B

D

E

Figure 53-2 Diagrammatic display of vaginal support. A, Invaginated area in a surrounding compartment. B, The prolapse opens when the pressure (arrow) is increased. C, Closing the bottom of the vagina prevents prolapse by constriction. D, Ligament suspension. E, With flap-valve closure, suspending fibers hold the vagina in a position against the wall, allowing increases in pressure to pin it in place. (© 2002 DeLancey; with permission.)

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Figure 53-5 Levels of vaginal support after hysterectomy. In level I (suspension), the paracolpium suspends the vagina from the lateral pelvic walls. Fibers of level I extend both vertically and also posteriorly toward the sacrum. In level II (attachment), the vagina is attached to the arcus tendineus fascia pelvis and the superior fascia of levator ani. Sagittal view (inset) shows the three regions of support. (© 2002 DeLancey; with permission.)

Figure 53-3 Compartments of the pelvis. The vagina, connected laterally to the pelvic walls, divides the pelvis into an anterior and posterior compartment. (© 1998 DELANCEY.)

Figure 53-6 Close-up diagram of the lower margin of level II vaginal support system after a wedge of vagina has been removed (inset). Note how the anterior vaginal wall, through its connections to the arcus tendineus fascia pelvis, forms a supportive layer clinically referred to as the pubocervical fascia. (© 2002 DeLancey; with permission.)

Figure 53-4 Attachments of the cervix and vagina to the pelvic walls, demonstrating different regions of support with the uterus in situ. Note that the uterine corpus and the bladder have been removed. (© 2002 DeLancey; with permission.)

midportion of the vagina to the pelvic walls (Fig. 53-6). These lateral attachments have functional significance: they stretch the vagina transversely between the bladder and the rectum. In the distal vagina (level III), the vaginal wall is directly attached to surrounding structures without any intervening paracolpium. The vagina fuses anteriorly with the urethra, posteriorly with the perineal body, and laterally with the levator ani muscles. Damage to level I support can result in uterine or vaginal prolapse of the apical segment. Damage to the level II and III portions of vaginal support results in anterior and posterior vaginal wall prolapse. The varying combinations of these defects

Chapter 53 FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE

Figure 53-7 Uterine prolapse, showing the cervix protruding from the vaginal opening (left) and vaginal prolapse where the puckered scar indicates where the cervix used to be (right). (© 2002 DeLancey; with permission.)

are responsible for the diversity of clinically encountered problems and are discussed in the following sections. Apical Segment In level I, the cardinal and uterosacral ligaments attach the cervix and the upper third of the vagina to the pelvic walls.6,7 Neither is a true ligament in the sense of a skeletal ligament that is composed of dense regular connective tissue similar to knee ligaments. Rather, they are “visceral ligaments” that are similar to bowel mesentery. They are made of blood vessels, nerves, smooth muscle, and adipose tissue intermingled with irregular connective tissue. They have a supportive function in limiting the excursion of the pelvic organs, much as the mesentery of the small bowel limits the movement of the intestine. When these structures are placed on tension, they form condensations that surgeons refer to as ligaments. The uterosacral ligaments are bands of tissue that run under the rectovaginal peritoneum; they are composed of smooth muscle, loose and dense connective tissue, blood vessels, nerves, and lymphatics.6 They originate from the posterolateral aspect of the cervix at the level of the internal cervical os and from the lateral vaginal fornix.6 Although macroscopic investigation showed insertion of the ligament to the levator ani, the coccygeus, and the presacral fascia,8 examination by magnetic resonance imaging (MRI) showed that the uterosacral ligaments overlie the sacrospinous ligament and coccygeus in 82% of the cases and overlie the sacrum in only 7% of the cases.9 The difference between the appearance of these structures on MRI and on dissection may have to do with the tension placed on the structures during dissection and require further research to clarify. The cardinal ligament is a mass of retroperitoneal areolar connective tissue in which blood vessels predominate; it also contains nerves and lymphatic channels.7 It has a configuration similar to

that of “chicken wire” or fishing net in its natural state, but when placed under tension it assumes the appearance of a strong cable as the fibers align along the lines of tension.7 It originates from the pelvic sidewall and inserts on the uterus, cervix, and upper third of the vagina. Both the uterosacral and cardinal tissues are critical components of level I support and provide support for the vaginal apex after hysterectomy (see Figs. 53-5 and 53-6). The cardinal ligaments are oriented in a relatively vertical axis (in the standing posture), whereas the uterosacral ligaments are more dorsal in their orientation. The nature of uterine support (Fig. 53-7) can be understood when the cervix is pulled downward with a tenaculum during dilation and curettage. After a certain amount of descent, the level I supports become tight and arrests further cervical descent. Similarly, downward descent of the vaginal apex after hysterectomy is resisted by the paracolpium. Damage to the upper suspensory fibers of the paracolpium (cardinal and uterosacral ligaments) allows uterine or apical segment prolapse (Fig. 53-8). Although descriptions of uterine support often imply that the uterus is suspended by the cardinal/uterosacral complex, much like a light suspended by a wire from the ceiling, this is not the case. The suspensory ligaments hold the uterus in position over the levator muscles, which in turn reduce the tension on the ligaments and protect them from excessive tension. This concept is discussed later, in the section on interactions between muscles and ligaments. Anterior Compartment Anterior compartment support depends on the connections of the vagina and periurethral tissues to the muscles and fascia of the pelvic wall via the arcus tendineus fascia pelvis (Fig. 53-9). On both sides of the pelvis, the arcus tendineus fascia pelvis is a

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Figure 53-8 Damage to the suspensory ligaments (tears) can lead to eversion of the vaginal apex when subjected to downward forces (arrow). (© 2002 DeLancey; with permission.)

Figure 53-9 Lateral view in the standing position of the pelvic floor structures related to urethral support. The cut is just lateral to the midline. Note that windows have been cut in the levator ani muscles, vagina, and endopelvic fascia so that the urethra and anterior vaginal walls can be seen. (© 2002 DeLancey; with permission; redrawn after © 1994 DeLancey).

Figure 53-10 Left, Attachment of the arcus tendineus pelvis to the pubic bone, the arcus tendineus pelvis (black arrows). Right, A paravaginal defect wherein the cervical fascia has separated from the arcus tendineus (black arrows point to the sides of the split). PS, pubic symphysis. (© 2002 DeLancey; with permission.)

band of connective tissue attached at one end to the lower sixth of the pubic bone, 1 cm lateral to the midline, and at the other end to the ischium, just above the spine. The anterior wall fascial attachments to the arcus tendineus fascia pelvis have been called the paravaginal fascial attachments

by Richardson.10 Lateral detachment of the paravaginal fascial connections from the pelvic wall is associated with stress incontinence and anterior prolapse (Fig. 53-10). Further details of the structural mechanics of anterior wall support are provided later. In addition, the upper portions of the anterior vaginal wall are

Chapter 53 FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE

Figure 53-11 Left, Displacement “cystocele”: the intact anterior vaginal wall has prolapsed downward due to paravaginal defect. Note that the right side of the patient’s vagina and cervix has descended more than the left because of a larger defect on that side. Right, Distention “cystocele”: the anterior vaginal wall fascia has failed, and the bladder is distending the mucosa. (© 2002 DeLancey; with permission.)

affected by the suspensory actions of level I. If the cardinal and uterosacral ligaments fail, the upper vaginal wall prolapses downward while the lower vagina (levels II and III) remains supported. Anterior vaginal wall prolapse can occur either because of lateral detachment of the anterior vaginal wall at the pelvic side wall, referred to as a displacement “cystocele,” or as a central failure of the vaginal wall itself that results in distention “cystocele” (Fig. 53-11). Although various grading schemes have been described for anterior vaginal prolapse, they are often focused on the degree of prolapse rather than the anatomic perturbation that results in descent; therefore, it is important to describe anterior prolapse with regard to the location of the fascial failure (lateral detachment versus central failure). At present, although a number of investigators have described techniques to distinguish central from lateral detachment, validation of these techniques remains elusive. Cystocele caused by defects of the midline fascia is easy to understand, but understanding how lateral detachment results in cystocele is not as obvious. The fact that lateral detachment is associated with cystourethrocele was first established by Richardson and colleagues10 (see Fig. 53-10). A study of 71 women with anterior compartment prolapse showed that paravaginal defect usually results from a detachment of the arcus tendineus fascia pelvis from the ischial spine, and rarely from the pubic bone.11 A visual analogy is that of a swinging trapezoid (Fig. 53-12). The mechanical effect of this detachment allows the trapezoid to rotate downward. When this happens, the anterior vaginal wall protrudes through the introitus. Upward support of the trapezoid is also provided by the cardinal and uterosacral ligaments in level I. For this reason, resuspension of the vaginal apex at the

time of surgery, in addition to paravaginal or anterior colporrhaphy, helps to return the anterior wall to a more normal position. Anatomically, the term endopelvic fascia refers to the areolar connective tissue surrounding the vagina. It continues down the length of the vagina as loose areolar tissue surrounding the pelvic viscera (Fig. 53-13). The term “fascia” is often used by surgeons to refer to the strong tissue that they sew together during anterior repairs. This has led to confusion and misunderstanding of the anatomy. Histologic examination has shown that the vagina is made up of three layers: epithelium, muscularis, and adventitia (Fig. 53-14).12-14 The adventitial layer is loose areolar connective tissue made up of collagen and elastin. These layers form the vaginal tube. The tissue that surgeons plicate during repairs is not what an anatomist would refer to as endopelvic fascia; rather, it is the vaginal muscularis and the adventitial layer of the vaginal tube. Also, many basic science studies that are addressed later in this chapter have used biopsies from the vaginal tube and not from the endopelvic fascia that connects the vaginal wall to the pelvic sidewalls. Perineal Membrane (Urogenital Diaphragm) Spanning the anterior part of the pelvic outlet, below the levator ani muscles, there is a dense triangular membrane called the perineal membrane. The term perineal membrane replaces the old term, urogenital diaphragm, reflecting the fact that this layer is not a single muscle layer with a double layer of fascia (i.e., a “diaphragm”) but rather a set of connective tissues that surround the urethra.15 The orientation consists of a single connective tissue membrane, with muscle lying immediately above. The

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A B

C

D

Figure 53-12 Conceptual diagram showing the mechanical effect of detachment of the arcus tendineus fascia pelvis from the ischial spine. A, Trapezoidal plane of the pubocervical fascia. The attachments to the pubis and the ischial spines are intact. B, The connection to the spine has been lost, allowing the fascial plane to swing downward. C, Normal anterior vaginal wall as seen with a weighted speculum in place. D, The effect of dorsal detachment of the arcus from the ischial spine. (© 2002 DeLancey; with permission.)

perineal membrane lies at the level of the hymen and attaches the urethra, vagina, and perineal body to the ischiopubic rami (Fig. 53-15). The compressor urethrae and urethrovaginal sphincter muscles are associated with the cranial surface of the perineal membrane.

Posterior Compartment and Perineal Membrane The posterior vagina is supported by connections between the vagina, the bony pelvis, and the levator ani muscles.16 The lower third of the vagina is fused with the perineal body (level III), (Fig. 53-16) which connects the perineal membranes on either side. The midposterior vagina (level II) is connected to the inside of the levator ani muscles by sheets of endopelvic fascia (Fig. 53-17). These connections prevent vaginal descent during increases in abdominal pressure. The most medial aspects of these paired sheets are the rectal pillars. In its upper third, the posterior vagina is connected laterally by the paracolpium of level I. Separate

systems for anterior and posterior vaginal support do not exist at level I. The fibers of the perineal membrane connect through the perineal body, thereby providing a layer that resists downward descent of the rectum. If this attachment becomes broken, then the resistance to downward descent is lost (see Fig. 53-16B). This situation is somewhat like an incisional hernia seen after disruption of a vertical incision, in which the bowel protrudes through a defect between the rectus abdominus muscles if the hernia is due to a defect in the rectus sheath. In the same way, protrusion of the rectum between the levator ani muscles can be seen if a disruption of the perineal body and connections of the perineal membrane occurs (Fig. 53-18). Reattachment of the separated structures during perineorrhphy corrects this defect and is a mainstay of reconstructive surgery. Because the levator ani muscles are intimately connected with the cranial surface of the perineal membranes, this reattachment also restores the muscles to a more normal position under the pelvic organs, in a location where they can provide support.

Chapter 53 FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE

Levator Ani Muscles

Figure 53-13 Histiologic cross-section of pelvis at the level of the mid-urethra. (From the collection of Dr. Thomas E Oelrich. © 2005 DeLancey; with permission.)

Figure 53-14 Higher magnification of a section of vaginal wall. Note the lack of a fascial layer. The endopelvic fascia is not seen at this magnification. (© 2005 DeLancey; with permission.)

A

Below and surrounding the pelvic organs are the levator ani muscles (Fig. 53-19).17 When these muscles and their covering fascia are considered together, the combined structures are referred to as the pelvic diaphragm (not to be confused with the so-called urogenital diaphragm, discussed in the previous section). There are three components of the levator ani muscle. The iliococcygeal portion forms a thin, relatively flat, horizontal shelf that spans the potential gap from one pelvic sidewall to the other. The pubovisceral muscle (also known as the pubococcygeus muscle) attaches the pelvic organs to the pubic bone, and the puborectal muscle forms a sling behind the rectum. The origins and insertions of these muscles as well as their characteristic anatomic relations are shown in Table 53-1 and Figure 53-19.18 The opening between the levator ani muscles through which the urethra, vagina, and rectum pass is the levator hiatus. The portion of the levator hiatus that lies ventral to the perineal body

Figure 53-15 Position of the perineal membrane and its associated components of the striated urogenital sphincter, the compressor urethrae, and the urethrovaginal sphincter (© DeLancey; with permission.)

B

Figure 53-16 A, The perineal membrane spans the arch between the ischiopubic rami, with each side attached to the other through their connection in the perineal body. B, Note that separation of the fibers in this area leaves the rectum unsupported and results in a low posterior prolapse. (© 1999 DeLancey; with permission.)

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is referred to as the urogenital hiatus, and it is through this opening that prolapse of the vagina, uterus, urethra, and bladder occurs. The urogenital hiatus is bounded anteriorly by the pubic bones, laterally by levator ani muscles, and posteriorly by the perineal body and external anal sphincter. The baseline tonic activity of the levator ani muscle keeps the hiatus closed by compressing the urethra, vagina, and rectum against the pubic bone, pulling the pelvic floor and organs in a cephalic direction.19 This continuous muscle action closes the lumen of the vagina, much as the anal sphincter closes the anus. This constant action eliminates any opening within the pelvic floor through which prolapse could occur and forms a relatively horizontal shelf on which the pelvic organs are supported.20 Damage to the levators resulting from nerve or connective tissue injury leaves the urogenital hiatus open and results in prolapse.

in abdominal pressure. If the muscles become damaged so that the pelvic floor sags downward, the organs are pushed through the urogenital hiatus. Once they have fallen below the level of the hymenal ring, they are unsupported by the levator ani muscles, and the ligaments must carry the entire load. Although the endopelvic fascia can sustain these loads for short periods, if the pelvic muscles do not close the urogenital hiatus, the connective tissue

Endopelvic Fascia and Levator Ani Interactions The interaction between the levator ani muscles and the endopelvic fascia is one of the most important biomechanical features of pelvic organ support. As long as the muscles maintain their constant tone closing the pelvic floor, the ligaments of the endopelvic fascia have very little tension on them even with increases

Figure 53-17 Lateral view of the pelvis showing the relationships of the puborectalis, iliococcygeus, and pelvic floor structures after removal of the ischium below the spine and sacrospinous ligament (SSL). EAS, external anal sphincter. The bladder and vagina have been cut in the midline, with the rectum left intact. Note how the endopelvic fascial “pillars” hold the vaginal wall dorsally, preventing its downward protrusion. (© 1999 DeLancey; with permission.)

Figure 53-18 Posterior prolapse due to separation of the perineal body. Note the end of the hymenal ring that lies laterally on the side of the vagina, no longer united with its companion on the other side. (© DeLancey; with permission.)

Table 53-1 International Standardized Terminology: Divisions of the Levator Ani Muscles Nomina Terminologica

Origin

Insertion

Pubovisceral muscle (pubococcygeus) Puboperinealis (PPM) Pubovaginalis (PVM) Puboanalis (PAM)

Pubis Pubis Pubis

Puborectalis (PRM) Iliococcygeus (ICM)

Pubis Tendinous arch of the leavtor ani

Perineal body Vaginal wall at the level of the mid-urethra Intersphincteric groove between internal and external anal sphincter to end in the anal skin Forms sling behind the rectum The two sides fuse in the iliococcygeal raphe

Chapter 53 FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE

A

B

Figure 53-19 A, Schematic view of the levator ani muscles from below after the vulvar structures and perineal membrane have been removed, showing the arcus tendinius levator ani (ATLA); external anal sphincter (EAS); puboanal muscle (PAM); perinal body (PB) uniting the two ends of the puboperineal muscle (PPM); iliococcygeal muscle (ICM); and puborectal muscle (PRM). Note that the urethra and vagina have been transected just above the hymenal ring. B, The levator ani muscle seen from above, looking over the sacral promontory (SAC), showing the pubovaginal muscle (PVM). The urethra, vagina, and rectum have been transected just above the pelvic floor. (The internal obturator muscles have been removed to clarify levator muscle origins.) (© 2003 DeLancey; with permission.)

eventually fails, resulting in prolapse. The support of the vagina has been likened to a ship in its berth, floating on the water and attached by ropes on either side to a dock.21 The ship is analogous to the vagina, the ropes to the ligaments, and the water to the supportive layer formed by the pelvic muscles. The ropes’ function to hold the ship (pelvic organs) in the center of its berth as it rests on the water (pelvic muscles). However, if the water level were to fall far enough that the ropes would be required to hold the entire weight of the ship, the ropes would all break. Once the pelvic musculature becomes damaged and no longer holds the organs in place, the ligaments are subjected to excessive forces. These forces may be enough to cause ligament failure over the course of time. A woman who sustains an injury to her pelvic floor muscles when she is young must depend to a greater extent on strength of her ligaments to prevent pelvic organ prolapse over the subsequent years of her life. An woman with injured muscles may have strong connective tissue that compensates and therefore may never develop prolapse, whereas another woman, who has the same degree of muscular damage but was born with weaker connective tissue, may experience prolapse as she ages. In addition, the interaction between the pelvic floor muscles and the endopelvic fascia is responsible for maintaining the flapvalve configuration in the pelvic floor that lessens ligament tension because of the supportive nature of the levator plate (see Fig. 53-2E). The flap-valve requires the dorsal traction of the uterosacral ligaments, and to some extent the cardinal ligaments, to hold the cervix back in the hollow of the sacrum. It also requires the ventral pull of the pubovisceral portions of the levator ani muscle to swing the levator plate more horizontally to close the urogenital hiatus. It is this interaction between the two forces that is so critical in maintaining the normal structural relationships that lessen the tension on ligaments and muscles.

Nerves There are two main nerves that supply the pelvic floor relative to pelvic organ prolapse. One is the pudendal nerve, which supplies the urethral and anal sphincters and perineal muscles, and the other is the nerve to the levator ani, which innervates the major musculature that supports the pelvic floor. These are distinct nerves with differing origins, courses, and insertions. The nerve to the levator originates from S3 to S5 foramina, runs inside the pelvis on the cranial surface of the levator ani muscle, and provides the innervation to all the subdivisions of the muscle.22 The pudendal nerve originates from S2 to S4 foramina and runs through Alcock’s canal, which is caudal to the levator ani muscles. The pudendal nerve has three branches—the clitoral, perineal, and inferior hemorrhoidal—which innervate the clitoris, the perineal musculature and inner perineal skin, and the external anal sphincter, respectively.22 PATHOPHYSIOLOGY The previous section described how different structures work together to provide pelvic organ support; this section explores the current scientific literature regarding possible causes of structural failure leading to prolapse. The discussion has been divided based on the components that are thought to be important in pelvic support: connective tissue supports and vaginal wall, levator ani muscles, and nerves. At the end of each component section, we discuss the challenges and questions that confront future research. In addition to the three components, we also briefly discuss the pathophysiologic effects of vaginal delivery, because of its special importance in the natural history of prolapse. Finally, we have devoted a section to biomechanical research on prolapse, an area of increasing clinical and research interest.

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Connective Tissue Supports and Vaginal Wall The adventitial layer of the vagina, referred to as the endopelvic fascia, is composed of collagen and elastin that separates the muscular wall of the vagina and the paravaginal tissues. Investigators have studied the biology of pelvic connective tissue. Its structural support comes from its composition, which includes collagen and elastin arranged in different fiber orientations and embedded in a dynamic ground substance. Much of the distensibility of collagen and connective tissues comes from rearrangement of the fibers. A collagen fiber by itself is relatively inelastic, able to stretch only 4% longitudinally, whereas an elastin fiber can stretch up to 70%.23 Therefore, if the fibers were arranged longitudinally, the tissue would not be able to stretch much before rupture. Instead, collagen and elastin fibers are arranged in different directions, so that, when placed under strain, they can stretch much more before being subject to rupture. An analogy can be made in comparing a cotton ball to a cotton dress shirt. When you pull on a cotton ball, there is a great deal of stretch that occurs until all the individual fibers become aligned in the same direction. After fiber alignment occurs, there is little stretch before rupture as the mechanical properties of the individual fiber come into play. In a cotton dress shirt, the individual fibers are already in alignment, and not much stretch can occur before rupture. Several studies have explored whether differences in the vaginal tissues of women with prolapse and normal support explain the pathophysiology of prolapse. Researchers have focused on collagen, elastin, smooth muscle, and hormone receptors as the major factors in vaginal support. Collagen Collagen provides much of the tensile strength for the endopelvic fascia and vaginal epithelium. Over the years, collagen studies have yielded varying, and at times conflicting, results. Women with prolapse had just as much if not greater rates of collagen synthesis than women without prolapse in earlier histochemical studies using fibroblast cultures.24 In contrast, Jackson and colleagues found that women with prolapse had a 25% reduction in total collagen compared to controls.25 Types I and III are the most common collagen fibers in vaginal tissues. Type I fibers are the more abundant, and type III contributes more of the elastic properties of the tissue.26 Liapis and associates found a modest reduction in collagen type III in women with prolapse and a more significant decrease in women with stress incontinence, suggesting that an altered ratio could lead to pelvic floor dysfunction.26 However, other researchers found no difference in the collagen ratios.25 Recently, attention has turned toward collagen metabolism and turnover as markers of prolapse. There does seem to be consistent evidence that collagen metabolism is significantly altered in the pelvic tissues of women with prolapse. Collagen fibers are stabilized by intermolecular covalent cross-links. The formation of cross-links and glycation lead to maturation and inhibit turnover. Degradation depends on the activity of proteinases secreted from connective tissue cells.25 Whereas women with prolapse have collagen with more cross-links and other signs of maturation, they also have increased synthesis of new collagen, which is degraded in preference to older material because it has fewer cross-links.25 Chen and cowrkers found increased expression of matrix metalloproteinase messenger RNA, which is

responsible for collagen breakdown, and decreased expression of inhibitors of metalloproteinases in women with stress incontinence and prolapse.27 Elastin Elastin provides much of the elastic properties of the pelvic connective tissue.23 Compared with collagen, fewer studies have examined the role of elastin in the development of prolapse. Jackson and colleagues did not find a difference in elastin content between premenopausal women with prolapse and controls.25 Chen and coworkers examined elastolytic activity in women with both stress incontinence and prolapse compared with controls. They found little difference in elastolyic activity but a decrease in α1-antitrypsin, an inhibitor of elastin turnover, in women with prolapse, suggesting that there may be higher elastin turnover in prolapse.28 Smooth Muscle Smooth muscle is another important aspect of the endopelvic fascia, because it is a major component of the vaginal wall. Smooth muscle analysis of anterior vaginal wall sections from the urethrovesical junction of fresh cadavers showed quantifiable variations in thickness and densities.29 Morphometric analysis of the anterior and posterior vaginal walls showed decreased fraction of smooth muscle in the muscularis of women with pelvic organ prolapse compared with controls.30,31 Other markers suggest that women with prolapse have less smooth muscle contractility and force maintenance.32 Hormone Receptors It has long been assumed that pelvic floor dysfunction is related to changes in menopause and is influenced by hormones. Untangling loss of hormonal action from age-related changes is extremely difficult. In blinded, randomized, placebo-controlled studies, two selective estrogen receptor modulators (SERMs), idoxifene and levormeloxifene, were thought to be associated with an increased incidence of pelvic organ prolapse in postmenopausal women participating in clinical trials of osteoporosis.33 In contrast, neither amoxifen nor toremifene, two clinically available SERMs, was associated with pelvic floor relaxation.34,35 More recently, there has been evidence that raloxifene reduces the likelihood or need for prolapse surgery by 50%.36 Paradoxically, Vardy and coauthors suggested that there was an increase in prolapse in women receiving raloxifene and tamoxifen, but the status of support in the population was not given, and most changes were small (1 cm), with only one individual having a change in prolapse stage.37 This finding might be a result of minor differences in vaginal pliability and might not reflect structural changes, such as connective tissue rupture and muscle damage, that go with actual prolapse. Several studies have looked at the presence or absence of hormone receptors in tissues that are involved in pelvic organ support.38,39 Other studies have examined the effects of estrogen on biologic markers such as collagen.40-42 Estrogen receptors are present throughout the body, and yet there are important differential effects. For example, endometrium is highly sensitive to fluctuations in estrogen, but skin is much less responsive. Any supposition that hormones play a major role in pelvic organ prolapse must be based on human studies that actually prove differences in prolapse occurring in those with and without

Chapter 53 FUNCTIONAL ANATOMY AND PATHOPHYSIOLOGY OF PELVIC ORGAN PROLAPSE

hormonal supplementation or administration of hormonal antagonists. Challenges There has been a significant body of basic science research regarding the components of the vaginal wall (vaginal tube). However, relatively little has been done to investigate the connections of the vagina to the pelvic walls (e.g., endopelvic fascia). Most of the studies reviewed used either partial- or full-thickness vaginal biopsies. It is difficult to make any assumptions about the endopelvic fascia, because it is not included in samples of the vaginal wall (see Fig. 53-13). Therefore, the question of whether it is the connection between the vagina to the pelvic sidewall that fails, as suggested by Richardson,10 or whether it is the vaginal wall itself that is involved in prolapse remains scientifically unresolved. Also, although some of the differences found in women with prolapse suggest that biochemical changes in the connective tissue may play an important role in prolapse, these studies were unable to explain the sequence of prolapse progression. In other words, we are left to wonder whether the alterations in connective tissue led to the prolapse or were a response to the mechanical effects of prolapse. Levator Ani MRI has been established as a technique for examination of the levator ani muscle.43,44 Using MRI, visible levator ani defects are beginning to be linked to the development of prolapse. Up to 20% of primiparous women have a visible defect in the levator ani muscle, probably as a result of birth injury.45 Also, computergenerated birth models using MRI have found that the medial puboviseral muscle is at greatest risk for stretch-induced injury.46 A few investigations have found that the levator ani mucles of women with prolapse have different morphologic characteristics than those of controls.47-49 The changes in morphoglogy are beginning to be quantified. Investigators have found that women with prolapse have smaller overall levator volume,47,48 larger levator symphysis gap, and wider levator hiatus.49 Aside from these MRI findings, histologic evidence of muscle damage has been found as well50 and is associated with operative failure.51 Challenges Quantification of levator ani differences or defects in prolapse have so far been limited to measurements of volume or thickness.47,48,52 The maximal force that a muscle generates depends on the cross-sectional area of the muscle perpendicular to its fiber direction.53 Measurement of this force is challenging because of the complex shape of the levator ani muscles, with different sections having differing fiber directions. Continued advances in imaging may make it possible to relate levator ani appearance to function. Nerves A unifying neurogenic hypothesis has been well established as a contributor to pelvic floor dysfunction. Although there is a significant body of literature regarding neurogenic causes of fecal incontinence and urinary incontinence, there is comparatively little exploring the relation between nerve damage and prolapse. Prospective study of perineal descent on defecography and pudendal nerve terminal motor latency failed to show any rela-

tionship between pudendal nerve damage and increased degree of perineal descent.54 Two studies in which patients with prolapse were included did not show a difference in pudendal nerve terminal motor latencies in patients with prolapse.55,56 However, electromyographic studies of women with pelvic floor dysfunction, including prolapse and incontinence, found changes consistent with motor unit loss or failure of central activation.57 More electromyographic and nerve studies are needed to tie neurogenic injury and pelvic organ prolapse. Vaginal Birth Although it is clear that incontinence and prolapse increase with age,1 there is no time during a woman’s life when these structures are more vulnerable than during childbirth. Vaginal delivery confers a fourfold to 11-fold higher risk of prolapse that increases with parity.58 Increased descent of vaginal wall points after vaginal delivery has been found in studies using a combined method of clinical examination and functional cine-MRI.59 Two studies suggested that pregnancy alone may be a risk factor for worsening prolapse; however, both of these studies used definitions of prolapse that many would consider clinically normal.60,61 Biomechanics Biologic specimens exhibit a mixture of elastic, viscous, and plastic properties. Elasticity is the ability of a tissue to return to its original shape after loading. Viscosity refers to the elongation of the tissue over time. Plasticity is the residual deformation that remains after loading is complete. There is a paucity of biomechanical studies of pelvic organ supports. Previous biomechanical research was performed using constant elongation to induce failure or rupture.62-64 This does not provide accurate information about the physiologic function of the tissue, because it does not account for the viscoelastic and plastic properties of connective tissues. Ettema and colleagues proposed a more accurate way of measuring the elastic properties of vaginal tissue, using a slowrate, linear elongation method.65 This method is able to discriminate small changes in a tissue’s elastic properties at lower stress levels and therefore is functionally more meaningful. Using this method, Goh and coworkers compared the biomechanical properties of premenopausal and postmenopausal women with prolapse and found little difference between the groups.66 CONCLUSION Understanding the functional anatomy of prolapse lays the necessary groundwork for understanding the mechanisms of pelvic organ prolapse. When the components of pelvic support and how they relate to each other have been identified, we will be able to understand how disruptions result in failure. Compared to stress incontinence, prolapse has received relatively little scientific attention. Although basic science research concerning the vaginal connective tissue and levator ani muscles has been performed, little has been done on other vital structures, such as the endopelvic fascia. In addition, investigations into the biomechanical processes of prolapse are lacking. Although this chapter provides an overview of existing knowledge on pelvic organ prolapse, it also looks ahead to the many unanswered scientific questions.

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References 1. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-506, 1997. 2. Boyles SH, Weber AM, Meyn L: Procedures for pelvic organ prolapse in the United States, 1979-1997. Am J Obstet Gynecol 188:108115, 2003. 3. Boyles SH, Weber AM, Meyn L: Procedures for urinary incontinence in the United States, 1979-1997. Am J Obstet Gynecol 189:7075, 2003. 4. Bonney V: The principles that should underlie all operations for prolapse. Obstet Gynaecol Br Empire 41:669, 1934. 5. DeLancey JO: Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 166(6 Pt 1):1717-1724; discussion 17241728, 1992. 6. Campbell RM: The anatomy and histology of the sacrouterine ligaments. Am J Obstet Gynecol 59:1, 1950. 7. Range RL, Woodburne RT: The gross and microscopic anatomy of the transverse cervical ligaments. Am J Obstet Gynecol 90:460, 1964. 8. Blaisdell FE: The anatomy of the sacro-uterine ligaments. Anat Record 12:1-42, 1917. 9. Umek WH, Morgan DM, Ashton-Miller JA, DeLancey JO: Quantitative analysis of uterosacral ligament origin and insertion points by magnetic resonance imaging. Obstet Gynecol 103:447-451, 2004. 10. Richardson AC, Edmonds PB, Williams NL: Treatment of stress urinary incontinence due to paravaginal fascial defect. Obstet Gynecol 57:357, 1981. 11. DeLancey JOL: Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol 187:93-98, 2002. 12. Ricci JV, Thom CH: The myth of a surgically useful fascia in vaginal plastic reconstructions. Q Rev Surg Obstet Gynecol 11:253-261, 1954. 13. Gitsch E, Palmrich AH: Operative Anatomie. Berlin: De Gruyter; 1977. 14. Weber AM, Walters MD: Anterior vaginal prolapse: Review of anatomy and techniques of surgical repair. Obstet Gynecol 89:311317, 1990. 15. Oelrich TM: The striated urogenital sphincter muscle in the female. Anat Rec 205:223, 1983. 16. DeLancey JO: Structural support of the urethra as it relates to stress urinary incontinence: The hammock hypothesis. [Comment.] Am J Obstet Gynecol 170:1713, 1994. 17. Lawson JO: Pelvic anatomy: I. Pelvic floor muscles. Ann R Coll Surg Engl 54:244, 1974. 18. Kearney R, Sawhney R, DeLancey JO: Levator ani muscle anatomy evaluated by origin-insertion pairs. Obstet Gynecol 104:168-173, 2004. 19. Taverner D: An electromyographic study of the normal function of the external anal sphincter and pelvic diaphragm. Dis Colon Rectum 2:153, 1959. 20. Nichols DH, Milley PS, Randall CL: Significance of restoration of normal vaginal depth and axis. Obstet Gynecol 36:251, 1970. 21. Paramore RH: The uterus as a floating organ. In Paramore RH (ed): The Statics of the Female Pelvic Viscera. London: HK Lewis and Company, 1918, p. 12. 22. Barber MD, Bremer RE, Thor KB, et al: Innervation of the female levator ani muscles. Am J Obstet Gynecol 187:64-71, 2002. 23. Goh JT: Biomechanical and biochemical assessments for pelvic organ prolapse. Curr Opin Obstet Gynecol 15:391-394, 2003. 24. Makinen J, Kahari VM, Soderstrom KO, et al: Collagen synthesis in the vaginal connective tissue of patients with and without uterine prolapse. Eur J Obstet Gynecol Reprod Biol 24:319-325, 1987. 25. Jackson SR, Avery NC, Tarlton JF, et al: Changes in metabolism of collagen in genitourinary prolapse. Lancet 347:1658-1661, 1996.

26. Liapis A, Bakas P, Pafiti A, et al: Changes of collagen type III in female patients with genuine stress incontinence and pelvic floor prolapse. Eur J Obstet Gynecol Reprod Biol 97:76-79, 2001. 27. Chen BH, Wen Y, Li H, Polan ML: Collagen metabolism and turnover in women with stress urinary incontinence and pelvic prolapse. Int Urogynecol J Pelvic Floor Dysfunct 13:80-87, 2002. 28. Chen B, Wen Y, Polan ML: Elastolytic activity in women with stress urinary incontinence and pelvic organ prolapse. Neurourol Urodyn 23:119-126, 2004. 29. Morgan DM, Iyengar J, DeLancey JO: A technique to evaluate the thickness and density of nonvascular smooth muscle in the suburethral fibromuscular layer. Am J Obstet Gynecol 188:1183-1185, 2003. 30. Boreham MK, Wai CY, Miller RT, et al: Morphometric analysis of smooth muscle in the anterior vaginal wall of women with pelvic organ prolapse. Am J Obstet Gynecol 187:56-63, 2002. 31. Boreham MK, Wai CY, Miller RT, et al: Morphometric properties of the posterior vaginal wall in women with pelvic organ prolapse. Am J Obstet Gynecol 187:1501-1508; discussion 1508-1509, 2002. 32. Boreham MK, Miller RT, Schaffer JI, Word RA: Smooth muscle myosin heavy chain and caldesmon expression in the anterior vaginal wall of women with and without pelvic organ prolapse. Am J Obstet Gynecol 185:944-952, 2001. 33. Silfen SL, Ciaccia AV, Bryant HU: Selective estrogen receptor modulators: Tissue specificity and differential uterine effects. Climacteric 2:268-283, 1999. 34. Fisher B, Costantino JP, Wickerham DL, et al: Tamoxifen for prevention of breast cancer: Report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst 90:13711388, 1998. 35. Maenpaa JU, Ala-Fossi SL: Toremifene in postmenopausal breast cancer: Efficacy, safety and cost. Drugs Aging 11:261-270, 1997. 36. Goldstein SR, Neven P, Zhou L, et al: Raloxifene effect on frequency of surgery for pelvic floor relaxation. Obstet Gynecol 98:91-96, 2001. 37. Vardy MD, Lindsay R, Scotti RJ, et al: Short-term urogenital effects of raloxifene, tamoxifen, and estrogen. Am J Obstet Gynecol 189:8188, 2003. 38. Fu X, Rezapour M, Wu X, et al: Expression of estrogen receptoralpha and -beta in anterior vaginal walls of genuine stress incontinent women. Int Urogynecol J Pelvic Floor Dysfunct 14:276-281, 2003. 39. Ewies AA, Thompson J, Al-Azzawi F: Changes in gonadal steroid receptors in the cardinal ligaments of prolapsed uteri: immunohistomorphometric data. Hum Reprod 19:1622-1628, 2004. Epub 2004 May 13. 40. Jackson S, James M, Abrams P: The effect of oestradiol on vaginal collagen metabolism in postmenopausal women with genuine stress incontinence. BJOG 109:339-344, 2002. 41. Chen B, Wen Y, Wang H, Polan ML: Differences in estrogen modulation of tissue inhibitor of matrix metalloproteinase-1 and matrix metalloproteinase-1 expression in cultured fibroblasts from continent and incontinent women. Am J Obstet Gynecol 189:59-65, 2003. 42. Moalli PA, Talarico LC, Sung VW, et al: Impact of menopause on collagen subtypes in the arcus tendineous fasciae pelvis. Am J Obstet Gynecol 190:620-627, 2004. 43. Tunn R, DeLancey JO, Quint EE: Visibility of pelvic organ support system structures in magnetic resonance images without an endovaginal coil. Am J Obstet Gynecol 184:1156-1163, 2001. 44. Singh K, Reid WM, Berger LA: Magnetic resonance imaging of normal levator ani anatomy and function. Obstet Gynecol 99:433438, 2002. 45. DeLancey JO, Kearney R, Chou Q, et al: The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 101:46-53, 2003.

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46. Lien KC, Mooney B, DeLancey JO, Ashton-Miller JA: Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol 103:31-40, 2004. 47. Hoyte L, Schierlitz L, Zou K, et al: Two- and 3-dimensional MRI comparison of levator ani structure, volume, and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 185:1119, 2001. 48. Hoyte L, Fielding JR, Versi E, et al: Variations in levator ani volume and geometry in women: the application of MR based 3D reconstruction in evaluating pelvic floor dysfunction. Arch Esp Urol 54:532-539, 2001. 49. Singh K, Jakab M, Reid WM, et al: Three-dimensional magnetic resonance imaging assessment of levator ani morphologic features in different grades of prolapse. Am J Obstet Gynecol 188:910-915, 2003. 50. Koelbl H, Saz V, Doerfler D, et al: Transurethral injection of silicone microimplants for intrinsic urethral sphincter deficiency. Obstet Gynecol 92:332-336, 1998. 51. Hanzal E, Berger E, Koelbl H: Levator ani muscle morphology and recurrent genuine stress incontinence. Obstet Gynecol 81:426, 1993. 52. Hoyte L, Jakab M, Warfield SK, et al: Levator ani thickness variations in symptomatic and asymptomatic women using magnetic resonance-based 3-dimensional color mapping. Am J Obstet Gynecol 191:856-861, 2004. 53. Ikai M, Fukunaga T: Calculation of muscle strength per unit crosssectional area of human muscle by means of ultrasonic measurement. Int Z Angew Physiol 26:26-32, 1968. 54. Jorge JM, Wexner SD, Ehrenpreis ED, et al: Does perineal descent correlate with pudendal neuropathy? Dis Colon Rectum 36:475-483, 1993. 55. Beevors MA, Lubowski DZ, King DW, Carlton MA: Pudendal nerve function in women with symptomatic utero-vaginal prolapse. Int J Colorectal Dis 6:24-28, 1991. 56. Bakas P, Liapis A, Karandreas A, Creatsas G: Pudendal nerve terminal motor latency in women with genuine stress incontinence and prolapse. Gynecol Obstet Invest 51:187-190, 2001.

57. Weidner AC, Barber MD, Visco AG, et al: Pelvic muscle electromyography of levator ani and external anal sphincter in nulliparous women and women with pelvic floor dysfunction. Am J Obstet Gynecol 183:1390-1399; discussion 1399-1401, 2000. 58. Mant J, Painter R, Vessey M: Epidemiology of genital prolapse: Observations from the Oxford Family Planning Association Study. Br J Obstet Gynaecol 104:579-585, 1997. 59. Dannecker C, Lienemann A, Fischer T, Anthuber C: Influence of spontaneous and instrumental vaginal delivery on objective measures of pelvic organ support: Assessment with the pelvic organ prolapse quantification (POPQ) technique and functional cine magnetic resonance imaging. Eur J Obstet Gynecol Reprod Biol 115:3238, 2004. 60. Sze EH, Sherard GB 3rd, Dolezal JM: Pregnancy, labor, delivery, and pelvic organ prolapse. Obstet Gynecol 100(5 Pt 1):981-986, 2002. 61. O’Boyle AL, Woodman PJ, O’Boyle JD, et al: Pelvic organ support in nulliparous pregnant and nonpregnant women: A case control study. Am J Obstet Gynecol 187:99-102, 2002. 62. Kondo A, Narushima M, Yoshikawa Y, Hayashi H: Pelvic fascia strength in women with stress urinary incontinence in comparison with those who are continent. Neurourol Urodyn 13:507-513, 1994. 63. Reay Jones NH, Healy JC, King LJ, et al: Pelvic connective tissue resilience decreases with vaginal delivery, menopause and uterine prolapse. Br J Surg 90:466-472, 2003. 64. Cosson M, Lambaudie E, Boukerrou M, et al: A biomechanical study of the strength of vaginal tissues: Results on 16 post-menopausal patients presenting with genital prolapse. Eur J Obstet Gynecol Reprod Biol 112:201-205, 2004. 65. Ettema GJC, Goh JTW, Forwood MR: A new method to measure elastic properties of plastic-viscoelastic connective tissue. Med Eng Physics 20:308-314, 1998. 66. Goh JT: Biomechanical properties of prolapsed vaginal tissue in pre- and postmenopausal women. Int Urogynecol J 13:76-79, 2002.

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PELVIC ORGAN PROLAPSE: CLINICAL DIAGNOSIS AND PRESENTATION Chi Chiung Grace Chen and Mark D. Walters Pelvic organ prolapse (POP) is a heterogeneous condition in which weaknesses of the pelvic floor musculature and connective tissue result in herniation of pelvic organs into the vaginal lumen. In more severe cases, this herniation can protrude through the vaginal introitus and beyond the hymenal ring. Organs that may potentially herniate into the vaginal canal include the bladder with or without involvement of the urethra, resulting in cystourethroceles and cystoceles, respectively. Patients may have uterine prolapse, or, after hysterectomy, the vaginal cuff may herniate resulting in apical vaginal prolapse. The rectum, small bowel, and sigmoid colon may also herniate, resulting in rectoceles, enteroceles, and sigmoidoceles, respectively. This chapter focuses on the definition, diagnosis, and classification of POP. DEFINITION AND EPIDEMIOLOGY It is estimated that more than 300,000 surgeries are performed to correct POP annually, at a cost of greater than $1 billion.1 Furthermore, the number of patients seeking care for these disorders is expected to increase by 45% in the future.2 Despite this high prevalence, POP is a poorly understood condition, and many of the accepted definitions are based on expert opinion and consensus rather than epidemiologic or clinical data. The American College of Obstetrics and Gynecology (ACOG) defines POP as the protrusion of pelvic organs into the vaginal canal.3 More specifically, in a terminology workshop convened by the National Institutes of Health (NIH) for researchers in female pelvic floor disorders, POP was defined as the descent of vaginal segments to within 1 cm of the hymen or lower.4 POP encompasses anterior and posterior vaginal prolapse as well as apical or uterine prolapse. Terms such as “cystocele” and “rectocele” are intentionally not used because they imply an unrealistic certainty as to the specific organs behind the vaginal wall at the time of physical examination. It is important to note that, although most clinicians can recognize the extremes of normal support versus severe prolapse, most cannot objectively state at what point vaginal laxity becomes pathologic and requires intervention. There are limited data concerning the normal distribution of POP in the population and the correlations between symptoms and physical findings. In a study of 497 women, Swift demonstrated that the distribution of prolapse in a population exhibited a bell-shaped curve, with most women having stage I or II prolapse by the Pelvic Organ Prolapse Quantification (POPQ) classification system (discussed later) and only 3% having stage III prolapse.5 This signifies that, at baseline, most women have some degree of pelvic relaxation. However, these women are typically asymptomatic and develop symptoms only as their prolapse increases in severity.6 Therefore, 556

even if POP is found on physical examination by the definition given, it may not be clinically relevant and may not require intervention if the patient is asymptomatic. HISTORY Although it has been shown previously that patients’ histories cannot be used alone to differentiate or diagnose different types of urinary incontinence,7,8 less is known about the reliability of patients’ symptoms for diagnosing POP. Patients with POP may present with a plethora of symptoms relating to voiding, defecatory, and sexual dysfunction as well as symptoms directly associated with the prolapse, such as vaginal pressure and discomfort. Despite the few studies specifically addressing the association between reported symptoms and POP, the consensus in the literature seems to be that the severity of the prolapse is not necessarily associated with increased visceral symptomatology. Vaginal prolapse in any compartment—anterior, apical, or posterior—can manifest as vaginal fullness, pain, and/or protruding mass. In a recent study by Tan and associates, the feeling of “a bulge or that something is falling outside the vagina” had a positive predictive value of 81% for POP, and the lack of this symptom had a negative predictive value of 76%.9 Not surprisingly, increased degree of prolapse, especially beyond the hymen, is associated with increased pelvic discomfort and visualization of a protrusion.10 Stress urinary incontinence and voiding difficulties can occur in association with anterior and apical vaginal prolapse. However, women with advanced degrees of prolapse may not have overt symptoms of stress incontinence, because the prolapse may cause a mechanical obstruction of the urethra, leading to a higher urethral closure pressure and thereby preventing urinary leakage.11 Instead, these women may require vaginal pressure or manual replacement of the prolapse in order to accomplish voiding. They are therefore at risk for incomplete bladder emptying and recurrent or persistent urinary tract infections, and for the development of de novo stress incontinence after the prolapse is repaired. Patients who require digital assistance to void in general have more advanced degrees of prolapse.12 In addition to difficulty voiding, other urinary symptoms such as urgency, frequency, and urge incontinence, are found in women with POP.13 However, it is not clear whether the severity of prolapse is associated with more irritative voiding symptoms or bladder pain.10,12 POP, especially in the apical and posterior compartments, can be associated with defecatory dysfunction, such as pain with defecation, the need for manual assistance with defecation, and anal incontinence of flatus, liquid or solid stool. These patients

Chapter 54 PELVIC ORGAN PROLAPSE: CLINICAL DIAGNOSIS AND PRESENTATION

often have outlet-type constipation secondary to the trapping of stool within the rectal hernia, necessitating splinting or application of manual pressure in the vagina, rectum, or perineum to reduce the hernia and aid in defecation. Although defecatory dysfunction remains the area that is least understood in patients with POP, clinical and radiographic studies have shown that the severity of prolapse is not strongly correlated with increased symptomatology.9,10,12,14 Although women with isolated posterior prolapse (e.g., rectocele, enterocele, perineal body defect) may also have the sensation of vaginal bulge and pressure, these women are often asymptomatic and the prolapse is recognized only on physical examination. Once a posterior vaginal defect is identified, questions regarding defecatory dysfunction must be elicited. Although the relationship between sexual function and POP is not clearly defined, questions regarding sexual dysfunction must be included in the evaluation of any patient with POP. Patients may report symptoms of dyspareunia, decreased libido and orgasm, and increased embarrassment with altered anatomy that affects body image. Some studies have reported that prolapse adversely affects sexual functioning, with subsequent improvement in sexual function after repair of prolapse.15-17 However, other studies have shown little correlation between the extent of prolapse and sexual dysfunction.12 It is important to note that the evaluation of sexual function may be especially difficult in this patient population because the hindrances to sexual function may include factors other than POP, such as partner limitations and functional deficits. PHYSICAL EXAMINATION The physical examination for POP should be conducted with the patient in dorsal lithotomy position, as for a routine pelvic examination. If physical findings do not correspond to symptoms, or if the maximum extent of the prolapse cannot be confirmed, the woman can be reexamined in the standing position. Initially, the external genitalia are inspected; if no displacement is apparent, the labia are gently spread to expose the vestibule and hymen. The integrity of the perineal body is evaluated, and the extent of all prolapsed parts is assessed. A retractor, a Sims speculum, or the posterior blade of a bivalve speculum may be used to depress the posterior vagina to aid in visualizing the anterior vagina, and vice versa for the posterior vagina. Because most patients with POP are postmenopausal, the vaginal mucosa should be examined for atrophy and thinning, which may affect management. Healthy, estrogenized tissue without significant evidence of prolapse, is well perfused and exhibits rugations and physiologic moisture. Atrophic vaginal tissue appears pale and thin, is without rugation, and can be friable. After the resting vaginal examination, the patient is instructed to perform a Valsalva maneuver or to cough vigorously. During this maneuver, the order of descent of the pelvic organs is noted, as is the relationship of the pelvic organs at the peak of increased intra-abdominal pressure. A rectovaginal examination is also required to fully evaluate prolapse of the posterior vaginal wall and perineal body. Digital assessment of the contents of the rectovaginal septum during straining examination can differentiate between a “traction” enterocele (in which the posterior cul-desac is pulled down by the prolapsing cervix or vaginal cuff but is not distended by intestines) and a “pulsion” enterocele (in which the intestinal contents of the enterocele distend the rectovaginal

septum and produce a protruding mass). Other clinical observations and tests to help delineate POP include cotton swab (Q-tip) testing for the measurement of urethral axis mobility; measurement of perineal descent; measurement of the transverse diameter of the genital hiatus or of the protruding prolapse; measurement of vaginal volume; description and measurement of posterior prolapse; and examination techniques differentiating among various types of defects (e.g., central versus paravaginal defects of the anterior vaginal wall). Inspection should also be made of the anal sphincter because fecal incontinence is often associated with posterior vaginal support defects. Grossly, women with a torn external sphincter may have scarring or a “dovetail” sign on the perineal body. Anterior vaginal wall descent usually represents bladder descent with or without concomitant urethral hypermobility. However, in 1.6% of women with anterior vaginal prolapse, an anterior enterocele can mimic a cystocele on physical examination.18 Furthermore, lateral paravaginal defects, identified as detachment of the lateral vaginal sulci, may be distinguished from central defects, seen as a midline protrusion with preservation of the lateral sulci. This is done with the use of a curved forceps placed in the anterolateral vaginal sulcus and directed toward the ischial spine. Bulging of the anterior vaginal wall in the midline between the forcep blades implies a midline defect; blunting or descent of the vaginal fornices on either side with straining suggests lateral paravaginal defects. However, researchers have shown that the physical examination technique used to detect paravaginal defects is not particularly reliable or accurate. In a study by Barber and colleagues of 117 women with prolapse, the sensitivity of clinical examination to detect paravaginal defects was good (92%), yet the specificity was poor (52%).19 Despite a high prevalence of paravaginal defects, the positive predictive value was only 61%. Fewer than two thirds of the women believed to have a paravaginal defect on physical examination were confirmed to possess the same at surgery. Another study by Whiteside and associates, demonstrated poor reproducibility of clinical examination to detect anterior vaginal wall defects.20 Therefore, the clinical value of determining the location of midline, apical, and lateral paravaginal defects remains unknown. In regard to posterior defects, it has previously been demonstrated that preoperative clinical examinations do not always accurately differentiate between rectoceles and enteroceles.21,22 Some investigators have advocated performing imaging studies to further delineate the exact nature of the posterior wall prolapse. Traditionally, most clinicians believe they are able to detect the presence or absence of these defects without anatomically localizing them. However, little is known regarding the accuracy or utility of clinical examinations in evaluating the anatomic locations of posterior vaginal defects. Burrows and colleagues found that clinical examinations often did not accurately predict the specific location of defects in the rectovaginal septum subsequently found intraoperatively.23 Clinical findings corresponded with intraoperative observations in 59% of patients and differed in 41%; sensitivities and positive predicative values of clinical examinations were less than 40% for all posterior defects. However, what remains unclear is the clinical consequence of not detecting these defects preoperatively. Clinical evaluation for POP also should include a lumbosacral neurologic evaluation consisting of strength, sensory, and reflex examinations. First, the strength of the pelvic floor musculature is assessed by palpating the levator ani muscle complex in the posterior vaginal wall approximately 2 to 4 cm cephalad to the

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hymen. The patient is then asked to squeeze around the examiner’s fingers. Weakness in this muscle can be a result of neurologic deficits or direct trauma during childbirth. Internal and external anal sphincter tone is assessed by placing a finger in the rectum and noting the initial resistance to entry and then the resistance after the patient maximally squeezes her anal sphincter. Sensory function is assessed with the use of pinprick and light-touch of the mons pubis, perineum/perianal area, and labia majora. Cystometry and anal manometry can be used to evaluate the visceral sensation of the bladder and rectum, respectively. Lastly, anal and bulbocavernosus reflexes can be elicited by lightly stroking the perianal skin and observing or palpating the contraction of the anal sphincter, and by lightly tapping the clitoris and observing the contraction of the bulbocavernosus muscle and/or anal sphincter. CLASSIFICATION OF PELVIC ORGAN PROLAPSE Presently, there are two widely accepted classification systems for assessing the severity of POP: the Baden-Walker “half-way” vaginal profile and the POPQ, which was established by the International Continence Society (ICS) in 1996.24 The purpose of any classification system is to facilitate understanding of the etiology and pathophysiology of disease, to establish and standardize treatment and research guidelines, and to aid precision and avoid confusion among practitioners. For many years, POP has been described using criteria modified from the Baden-Walker “half-way” vaginal profile.25-27 This grading system is simple to use; it is widely understood among gynecologic surgeons and has been found to have reasonable inter-examiner reliability for all segments of the vagina and for uterine support.28 The most dependent position of the pelvic organs during maximum straining or standing is used and graded as normal or first-, second-, or third-degree prolapse. First-degree prolapse refers to vaginal segments that descend halfway (but not to) the hymen; second-degree is descent to the hymen; and third-degree is prolapse beyond the hymen. A rectovaginal examination can also be used to better delineate the severity of rectoceles. This classification system, although popular, is slowly being replaced by the more precise and standardized POPQ system. In the POPQ system, the pelvic organ anatomy is described during physical examination of the external genitalia and vaginal canal.24 Segments of the lower reproductive tract replace the terms cystocele, enterocele, rectocele, and urethrovesical junction, because these terms imply an unrealistic certainty as to the structures on the other side of the vaginal bulge, particularly in women who have had previous prolapse surgery. The examiner sees and describes the maximum protrusion noted by the patient during her daily activities. The details of the examination, including criteria for the end point of the examination and full development of the prolapse, should be specified. Suggested criteria for demonstration of maximum prolapse include any or all of the following: any protrusion of the vaginal wall that has become tight during straining by the patient; traction on the prolapse causes no further descent; the subject confirms that the size of the prolapse and the extent of the protrusion seen by the examiner are as extensive as the most severe protrusion she has had (a small hand-held mirror to visualize the protrusion may be helpful); and a standing/straining examination confirms that the full extent of the prolapse was observed in the other positions.

Figure 54-1 Six sites (points Aa, Ba, C, D, Bp, and Ap), genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) are used for pelvic organ support quantitation. (From Bump RC, Mattiasson A, Bø K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10, 1996.)

Details about patient position, types of vaginal specula or retractors, type and intensity of straining used to develop the prolapse maximally, and fullness of the bladder should be stated. This descriptive system contains a series of site-specific measurements of the woman’s pelvic organ support. It can be easily learned and taught by means of a video tutorial.29 Prolapse in each segment is evaluated and measured relative to the hymen (not introitus), which is a fixed anatomic landmark that can be identified consistently and precisely. The anatomic position of the six defined points for measurement should be in centimeters above or proximal to the hymen (negative number) or centimeters below or distal to the hymen (positive number), with the plane of the hymen being defined as zero. For example, a cervix that protrudes 3 cm distal to (beyond) the hymen should be described as +3 cm. Six points (two on the anterior vaginal wall, two in the superior vagina, and two on the posterior vaginal wall) are located with reference to the plane of the hymen (Fig. 54-1). In describing the anterior vaginal wall, the term anterior vaginal wall prolapse is preferable to cystocele or anterior enterocele unless the organs involved are identified by ancillary tests. There are two anterior sites: Point Aa: A point located in the midline of the anterior vaginal wall 3 cm proximal to the external urethral meatus, corresponding to the proximal location of the urethrovesical crease. By definition, the range of position of point Aa relative to the hymen is −3 to +3 cm. Point Ba: A point that represents the most distal (i.e., most dependent) position of any part of the upper anterior vaginal wall from the vaginal cuff or anterior vaginal fornix to point Aa. By definition, point Ba is at −3 cm in the absence of prolapse and would have a positive value equal to the position of the cuff in women with total posthysterectomy vaginal eversion.

Chapter 54 PELVIC ORGAN PROLAPSE: CLINICAL DIAGNOSIS AND PRESENTATION

Two points are on the superior vagina. These points represent the most proximal locations of the normally positioned lower reproductive tract. Point C: A point that represents either the most distal (i.e., most dependent) edge of the cervix or the leading edge of the vaginal cuff (hysterectomy scar) after total hysterectomy. Point D: A point that represents a location of the posterior fornix in a woman who still has a cervix. It represents the level of uterosacral ligament attachment to the proximal posterior cervix. It is included as a point of measurement to differentiate suspensory failure of the uterosacral— cardinal ligament complex from cervical elongation. Point D is omitted in the absence of the cervix. Two points are located on the posterior vaginal wall. Analogous to anterior prolapse, posterior prolapse should be discussed in terms of segments of the vaginal wall rather than the organs that lie behind it. Thus, the term posterior vaginal wall prolapse is preferable to rectocele or enterocele unless the organs involved are identified by ancillary tests. If small bowel appears to be present in the rectovaginal space, the examiner should comment on this fact and clearly describe the basis for this clinical impression (e.g., by observation of peristaltic activity in the distended posterior vagina or palpation of loops of small bowel between an examining finger in the rectum and one in the vagina). Point Ap: A point located in the midline of the posterior vaginal wall 3 cm proximal to the hymen. By definition, the range of position of point Ap relative to the hymen is −3 to +3 cm. Point Bp: A point that represents the most distal (i.e., most dependent) position of any part or the upper posterior vaginal wall from the vaginal cuff or posterior vaginal fornix to point Ap. By definition, point Bp is at −3 cm in the absence of prolapse and would have a positive value equal to the position of the cuff in a woman with total posthysterectomy vaginal eversion. Other landmarks include the genital hiatus, which is measured from the middle of the external urethral meatus to the posterior midline hymen. The perineal body is measured from the posterior margin of the genital hiatus to the midanal opening. The total vaginal length is the greatest depth of the vagina in centimeters when point C or D is reduced to its full normal position. The points and measurements are presented in Figure 54-1. The positions of points Aa, Ba, Ap, Bp, C, and (if applicable) D with reference to the hymen are measured and recorded. Positions are expressed as centimeters proximal to (above) the hymen (negative number) or centimeters distal to (below) the hymen (positive number), with the plane of the hymen defined as zero. Measurements may be recorded as a simple line of numbers (e.g., −3, −3, −7, −9, −3, −3, 9, 2, and 2 for points Aa, Ba, C, D, Bp, Ap, total vaginal length, genital hiatus, and perineal body, respectively). Alternatively, a 3 × 3 grid can be used to concisely organize the measurements, as shown in Figure 54-2, or a line diagram of a configuration can be drawn, as shown in Figures 54-3 and 54-4. Figure 54-3 is a grid and line diagram contrasting measurements that indicate normal support with those of complete posthysterectomy vaginal eversion. Figure 54-4 is a grid and line diagram representing predominant anterior and posterior vaginal wall prolapse with partial apical descent.

Figure 54-2 Three-by-three grid for recording quantitative description of pelvic organ support. (From Bump RC, Mattiasson A, Bø K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10, 1996.)

The profile for quantifying prolapse provides a precise description of anatomy for individual patients. An ordinal staging system of pelvic organ prolapse is suggested using these measurements and can be useful for the description of populations and for research comparisons. Stages are assigned according to the most severe portion of the prolapse when the full extent of the protrusion has been demonstrated. For a stage to be assigned to an individual subject, it is essential that her quantitative description be completed first. The five stages of pelvic organ support (0 through IV) are described in Table 54-1. Because precise characterization of pelvic floor muscle strength and description of functional symptoms are of vital importance, the reader is referred to the ICS committee document for further details.24 Studies have demonstrated excellent interexaminer and intraexaminer reliability for the POPQ system in quantifying POP.28,30 Steele and associates showed that the system can be taught effectively to residents and medical students using a 17minute video.29 Furthermore, the measurements can be obtained quickly by both experienced and nonexperienced clinicians (2.1 and 3.7 minutes, respectively).30 The POPQ system does not take into account lateral defects and perineal body prolapse, but these can be added in descriptive terms. Despite its limitations, the POPQ system is currently the classification system used in most research studies and NIH trials, and it is gaining popularity in clinic practice. DIAGNOSTIC TESTS After a careful history and physical examination, few diagnostic tests are needed to further evaluate patients with POP if there is no concomitant voiding or defecatory dysfunction. For example, hydronephrosis does occur in a small proportion of women with prolapse, but even if it is identified, it usually does not change management in the women for whom surgical repair is planned.

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Figure 54-3 A, Grid and line diagram of complete eversion of vagina. The most distal point of the anterior wall (point Ba), vaginal cuff scar (point C), and the most distal point of the posterior wall (point Bp) are all at same position (+8), and points Aa and Ap are maximally distal (both at +3). Because total vaginal length equals maximum protrusion, this is stage IV prolapse. B, Normal support. Points Aa and Ba and points Ap and Bp are all −3 because there is no anterior or posterior wall descent. The lowest point of the cervix is 8 cm above the hymen (−8), and the posterior fornix is 2 cm above this (−10). The vaginal length is 10 cm, the genital hiatus is 2 cm, and the perineal body measures 3 cm. This represents stage 0 prolapse. (From Bump RC, Mattiasson A, Bø K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10, 1996.)

Table 54-1 Stages of Pelvic Organ Prolapse Stage

Description

0

No prolapse is demonstrated. Points Aa, Ap, Ba, and Bp are all at −3 cm, and either point C or point D is between −TVL cm and −(TVL−2) cm; that is, the quantitation value for point C or D is ≤−[TVL−2] cm. In Fig. 54-3, B represents stage 0. The criteria for stage 0 are not met, but the most distal portion of the prolapse is >1 cm above the level of the hymen (i.e., its quantitation value is 1 cm below (distal to) the plane of the hymen but protrudes no further than 2 cm less than the TVL (i.e., its quantitation value is >+1 cm but 4 cm below H-line Only for cystourethrocele

(no prolapse) (mild, small) (moderate) (severe, large) (procidentia)

Three-dimensional Magnetic Resonance Imaging Three-dimensional MRI represents an advanced method of presentation and interpretation of data obtained during MRI studies (Fig. 55-6). It has been gaining popularity among investigators in the field, because it enables volumetric analysis of the data and demonstrates with remarkable clarity the spatial relationships among the anatomic structures of interest.34 For instance, this method has been applied to better define the levator ani morphology and to demonstrate, not only qualitatively but also quantitatively, the pathologic changes involved in various grades of pelvic prolapse.35-37 Although these findings have not been applied to clinical practice as yet, they could potentially be important in generating treatment plans for patients, predicting the course of progression of prolapse severity, and even predicting the likelihood of recurrence after corrective surgery.34

From Barbaric ZL, Marumoto AK, Raz S: Magnetic resonance imaging of the perineum and pelvic floor. Topics Magn Res Imaging 12:83-92, 2001.

Table 55-2 Proposed Pelvic Floor Descent (Length of the M-Line) Grading System Using Dynamic Magnetic Resonance Imaging Data Grade 0 1 2 3

(normal) (mild) (moderate) (severe)

Pelvic Floor Descent (cm) 0-2 2-4 4-6 >6

From Barbaric ZL, Marumoto AK, Raz S: Magnetic resonance imaging of the perineum and pelvic floor. Topics Magn Res Imaging 12:83-92, 2001.

A

B

Figure 55-6 Image of perineum shown in conventional magnetic resonance imaging (A) and in three-dimensional reconstruction (B).

Chapter 55 IMAGING IN THE DIAGNOSIS OF PELVIC ORGAN PROLAPSE

Computed Tomography Computed tomography (CT) scanning allows multiplanar visualization of anatomy and becomes especially useful for patients who are unable to tolerate MRI due to the presence of medical devices such as pacemakers, general debilitation, or claustrophobia. However, even though CT is a well-established axial imaging modality, it has limited application in the field of female pelvic prolapse simply because of anatomic limitations. The urogenital diaphragm and levator ani are mostly situated in the axial plane, they are best assessed by coronal imaging. However, with traditional CT, one is able to obtain coronal images only by reformatting the axial images, resulting in loss of spatial resolution during the process and inevitable degradation of the image quality.5 Because of these factors, very little attention has been paid in the field of radiology to CT scanning as a possible imaging modality for female pelvic floor dysfunction. A preliminary study using a small number of patients explored the use of CT scanning in the diagnosis of prolapse of female pelvic organs and commented on its potential role in patients intolerant of MRI.38 Despite the fact that the soft tissue contrast on CT if far inferior to that of MRI, it was possible to identify the bladder, uterus, small bowel, peritoneal fat, and rectum, as well as changes in position with straining, if CT was performed adequately. Another possible advantage of CT scanning is its ability to assess the contour of the levator ani muscles and obtain pelvic images in multiple planes. Both modalities image the patient while supine, thus introducing the possibility of suboptimal results in this nonphysiologic position, especially if the patient’s straining is suboptimal.38 With further evolution of CT technology, such as availability of multiple-detector-row CT scanners and lower image acquisition times, it might be possible to obtain dynamic images almost in real time. In addition, the possibility of acquiring thinner slices will potentially lead to decreased artifacts during volume rendering. However, as with fluoroscopy, radiation exposure will always remain a major concern with CT scanning.

CLINICAL APPLICATIONS Cystoceles In an ideal world, imaging studies used in the evaluation of cystoceles should yield information on the presence or absence of urinary retention, ureteral obstruction, urethral hypermobility, and other forms of pelvic floor prolapse, as well as evaluation for stress urinary incontinence, in the least invasive manner to the patient.3 Radiographically, a cystocele usually appears during the maximal straining phase of the imaging study as descent of the normally horizontal bladder base below the inferior margin of the pubic symphysis and as a concave impression on the superior aspect of the vagina.5 Traditionally, a VCUG and videourodynamics with the patient standing in both straining and relaxed states have been performed as part of the workup for cystoceles. Although these studies are helpful in the evaluation of cystocele severity, postvoid residual volume, stress urinary incontinence, and urethral hypermobility, they fail to comment on the presence of related pelvic floor dysfunction.3 Because of this drawback of the technique, fluoroscopic cystocolpoproctography or dynamic contrast roentgenography with pelvic organ opacification have been used to determine the presence of related pelvic floor pro-

lapse. However, these studies fail to detect up to 20 % of enteroceles, are time-consuming, and expose the patient to ionizing radiation.1,11,30-32,39,40 Even though ultrasonography does not have the drawback of radiation exposure to the patient, it fails to provide optimal visualization of soft tissue planes and is extremely operator dependent.41 MRI lacks most of these shortcomings and has numerous advantages previously mentioned.4,19,24 Studies have shown a very high degree of correlation between dynamic MRI and lateral cystourethrography.42 The only possible disadvantage of MRI is the fact that, because it is performed with the patient in the supine position, the physiologic effect of gravity cannot be studied.3 With dynamic MRI, one is able to both quantitate the degree of a cystocele present and diagnose any coexisting pelvic floor descent (Figs. 55-7 and 55-8). Enteroceles Before the introduction of MRI to the study of female pelvic prolapse, defecography was the primary modality in the diagnostic workup of enteroceles (Figs. 55-9 and 55-10). In order to visualize the small bowel loops between the rectum and the vagina, indicative of an enterocele, the patient is asked to strain repeatedly after evacuation. Very often, opacification of the vagina is also necessary to better visualize the pathology.5 In some cases, voiding cystograms were performed to rule out a cystocele. Later, fluoroscopic cystocolpoproctography or dynamic contrast roentgenography gained popularity. These studies involve opacification of the bladder, vagina, small bowel, and rectum in order to visualize pelvic prolapse. Even though triphasic opacification is more time-consuming, it has been shown to improve recognition of enteroceles during the examination. In addition to performing the imaging study with all organs opacified at the same time, one can also choose to opacify each organ individually before each straining phase.1,31,32,39 The diagnosis of an enterocele is made by comparing the images obtained during the straining phase of the study with those recorded during relaxation. Here, an increase in the distance between the vagina and the rectum, which are delineated by the contrast material, is suggestive of an enterocele. Occasionally, physiologic bowel gas bubbles in the contents of this herniated small bowel may be seen to further identify it as such.30 Unfortunately, in addition to being rather time-consuming and invasive, defecography and cystocolpoproctography fail to detect enteroceles in up to 20% of cases.3,11,30,40 Before the introduction of MRI into the field, many considered multiphasic cystocolpoproctography to be the best-suited imaging modality for detection of female organ prolapse (Fig. 55-11). However, many experts now believe that dynamic MRI is a superior radiographic technique in the diagnosis of enteroceles and that the invasiveness of organ opacification is not justified in the light of the very minimal yield of additional information, if any.3,4,30,32 Studies have shown repeatedly that MRI is far more sensitive than physical examination and dynamic cystocolpoproctography in the diagnosis of enteroceles.4,30 The diagnosis of an enterocele on an MRI study is made by measuring the distance between the lowest point of the peritoneal borderline and the H (hiatal) anteroposterior reference line obtained during the dynamic (straining) phases of the study. In fact, magnetic resonance colpocystorectography, which utilizes sonography gel to opacify the vagina and the rectum, is the only method available

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A

B

Figure 55-7 Magnetic resonance images showing a cystocele in resting position (A) and with pelvic floor descent appreciated on straining (B).

A

B

Figure 55-8 Magnetic resonance images in resting (A) and dynamic (B) phases, demonstrating pelvic floor prolapse and severe cystocele in a 52-year-old woman with complaints of vaginal prolapse and frequency.

Chapter 55 IMAGING IN THE DIAGNOSIS OF PELVIC ORGAN PROLAPSE

A

B Figure 55-9 A and B, Enteroceles shown on dynamic evacuation proctography images.

that can precisely visualize the parietal peritoneum, thus allowing one to make the diagnosis of an enterocele with utmost confidence.30 An isolated enterocele can be differentiated from one present as part of a combined organ prolapse, and any other coexisting conditions can be diagnosed as well (Fig. 55-12). More importantly, MRI enables the differentiation of contents of enteroceles, revealing such entities as mesenteric fat, rectosigmoidoceles, and small and large bowel. In fact, by taking into account the axial turbo spin echo sequences, often one is able to differentiate sigmoid colon from small bowel loops. On the contrary, hernias containing mostly fluid and components of the mesenteric tissue give a homogenous intense signal on the T2-

A

B Figure 55-10 A and B, Enterocele with pelvic floor prolapse demonstrated on dynamic defecography study.

weighted images. In addition, this method of visualization of the herniated contents does not require prior additional measures (e.g., small bowel opacification) to be taken. Many urologists find MRI particularly useful in differentiating high rectoceles from enteroceles, which is an important distinction as far as safe and efficient surgical planning is concerned.3-4,30 Because it does not expose patients to ionizing radiation, MRI also has the advantage of no time pressure constraints and gives patients more flexibility and control during repeated phases of straining which often needed to visualize pelvic floor defects. For completeness, comments should be made about the utility of ultrasonography and defecoperitoneography in the diagnosis

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A

B

Figure 55-11 A, Sagittal magnetic resonance image showing an enterocele on dynamic phase. B, Corresponding operating room findings.

of enteroceles. It is possible to indirectly visualize the intestinal loops in the herniated sack as a dorsal attenuation with endovaginal sonography. However, this examination is rather difficult, because it requires a firm and stable contact between the ultrasound probe and the vaginal wall, even during repeated straining phases of the examination.17 Defecoperitoneography is a combination of a small-bowel enteroclysm, evacuation proctography, and intra-abdominal puncture.43,44 Even though magnetic resonance colpocystorectography is comparable to defecoperitoneography in its timeconsuming aspects, the latter is a much more invasive procedure associated with several rather morbid complications (e.g., perforation).45 In addition, defecoperiotoneography misses many cases of enteroceles, because the radiation dose with this technique forbids more than one round of straining, and several rounds of repeated straining and defecation are often required to induce and visualize organ prolapse during a given study.30,46 Therefore, MRI is a superior technique in the diagnosis of enteroceles or peritoneoceles, because it is highly specific, sensitive, versatile, noninvasive, radiation-free, and relatively safe. Figure 55-12 Large cystocele and an enterocele in a patient with chronic frequency, nocturia, urgency, urge incontinence, and history of urine leaks with standing appreciated on a dynamic sagittal magnetic resonance image.

Rectoceles Because physical examination has a wide range of sensitivities for diagnosis of rectoceles and is unreliable in differentiating enteroceles from high rectoceles, imaging modalities are very helpful in the diagnostic workup of suspected rectoceles.3 Defecography has

Chapter 55 IMAGING IN THE DIAGNOSIS OF PELVIC ORGAN PROLAPSE

A

B

C

been traditionally the study of choice for rectoceles (Fig. 55-13). A rectocele usually appears as an anterior bulge in the extrapolated line of the normal rectal wall that appears with evacuation or strain and is measured as the maximum extent of that bulge (Fig. 55-14).10 It should be noted that, because rectoceles quite often appear as transient findings during defecography, many prefer to obtain and review the videotape of the evacuation process.5 To evaluate for other concurrent forms of pelvic prolapse, dynamic contrast roentography or fluoroscopic cystocolpoproctography has been used by various investigators.1,3,31,32,39 However, all of these techniques have the disadvantage of significant radiation exposure and poor visualization of soft tissues in the evaluation of the pelvic floor. MRI eliminates all of these flaws and allows superb visualization of soft tissue structures and concurrent pelvic floor pathology (Fig. 55-15). Studies seem to indicate that rectal opacification should be used to increase the detection rates of rectoceles with MRI. This usually entails the

Figure 55-13 Resting (A), squeezing (B), and straining (C) phases of a defecography study.

introduction of sonographic transmission gel into the rectum, which yields a high signal on T2-weighted MRI sequences. Some radiologists prefer to mix it with diluted gadolinium contrast medium for easier visualization. The only caveat to this method is the fact that it can introduce air bubbles and thus image artifacts.4,25,32 It has been theorized that MRI fails to detect small rectoceles due to collapse of the walls of the empty rectum during the imaging study.3,4 Uterine Prolapse From a surgical perspective, while evaluating high grade uterine prolapse, it is critical to rule out any kind of uterine or ovarian malignancy, in order to decide on the kind of hysterectomy to be performed. MRI is an ideal imaging modality, because it allows evaluation for all forms of pelvic pathology preoperatively (Fig. 55-16).3

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Figure 55-14 A through C, Dynamic phases of defecography in chronological order showing a rectocele in a 54-year-old patient with chronic constipation.

C

A

B

Figure 55-15 Resting phase magnetic resonance image (A) with its counterpart straining phase (B) demonstrating a rectocele.

Chapter 55 IMAGING IN THE DIAGNOSIS OF PELVIC ORGAN PROLAPSE

Figure 55-16 Uterine prolapse appreciated on dynamic magnetic resonance sagittal image.

References 1. Altringer WE, Saclarides TJ, Dominguez JM, et al: Four-contrast defecography: Pelvic “floor-oscopy.” Dis Colon Rectum 38:695-699, 1995. 2. Maglinte DD, Kelvin FM, Fitzgerald K, et al: Association of compartment defects in pelvic floor dysfunction. AJR Am J Roentgenol 172:439-444, 1999. 3. Rodriguez LV, Raz S: Diagnostic imaging of pelvic floor dysfunction. Curr Opin Urol 11:423-428, 2001. 4. Gousse AE, Barbaric ZL, Safir MH, et al: Dynamic half Fourier acquisition single shot turbo spin-echo magnetic resonance imaging for evaluating the female pelvis. J Urol 164:1606-1613, 2000. 5. Weidner AC, Low VHS: Imaging studies of the pelvic floor. Obstet Gynecol Clin North Am 25:825-848, 1998. 6. Halligan S: Evacuation proctography. In Bartram CI, DeLancey JOL (eds): Imaging Pelvic Floor Disorders. Berlin: Springer-Verlag, 2003, pp 45-50. 7. Halligan S, Bartram CI, Park HY, Kamm MA: The proctographic features of anismus. Radiology 197:679-682, 1995. 8. Freimanis MG, Wald A, Caruana B, Bauman DH: Evacuation proctography in normal volunteers. Invest Radiol 26:581-585, 1991. 9. Ott DJ, Donati DL, Kerr RM, Chen MY: Defecography: Results in 55 patients and impact on clinical management. Abdom Imaging 19:349-354, 1994. 10. Shorvon PJ, McHugh S, Diamant NE, et al: Defecography in normal volunteers: Results and implications. Gut 30:1737-1749, 1989. 11. Hock D, Lombard R, Jehaes C, et al: Colpocystodefecography. Dis Colon Rectum 36:1015-1021, 1993. 12. Kelvin FM, Pannu HK: Dynamic cystoproctography: Fluoroscopic and MRI techniques for evaluating pelvic organ prolapse. In Bartram CI, DeLancey JOL (eds): Imaging Pelvic Floor Disorders. Berlin: Springer-Verlag, 2003, pp 51-68. 13. Frudinger A, Bartram CI, Kamm MA: Transvaginal versus anal endosonography for detecting damage to the anal sphincter. AJR Am J Roentgenol 168:1435-1438, 1997. 14. Frudinger A, Bartram CI, Halligan S, Kamm M: Examination techniques for endosonography of the anal canal. Abdom Imaging 23:301-303, 1998. 15. Bartram CI: Ultrasound. In Bartram CI, DeLancey JOL (eds): Imaging Pelvic Floor Disorders. Berlin: Springer-Verlag, 2003, pp 69-79. 16. Quinn MJ, Beynon J, Mortensen NJ, Smith PJ: Transvaginal endosonography: A new method to study the anatomy of the lower urinary tract in urinary stress incontinence. Br J Urol 62:414-418, 1988.

17. Halligan S, Northover J, Bartram CI: Vaginal sonography to diagnose enterocele. Br J Radiol 69:996-999, 1996. 18. Beer-Gabel M, Teshler M, Barzilai N, et al: Dynamic transperineal ultrasound in the diagnosis of pelvic floor disorders: Pilot study. Dis Colon Rectum 45:239-245, 2002. 19. Lienemann A, Anthuber C, Baron A, et al: Dynamic MR colpocystorectography assessing pelvic floor descent. Eur Radiol 7:13091317, 1997. 20. Bump RC, Norton PA: Urogynecology and pelvic floor dysfunction: Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 25:723-746, 1998. 21. Maubon A, Martel-Boncoeur MP, Juhan V, et al: Static and dynamic magnetic resonance imaging of the pelvic floor. J Radiol 81(12 Suppl):1875-1886, 2000. 22. Stoker J, Halligan S, Bartram CI: Pelvic floor imaging. Radiology 218:621-641, 2001. 23. Pannu HK, Kaufman HS, Cundiff GW, et al: Dynamic MR imaging of pelvic organ prolapse: Spectrum of abnormalities. Radiographics 20:1567-1582, 2000. 24. Comiter CV, Vasavada SP, Barbaric ZL, et al: Grading pelvic floor prolapse and pelvic floor relaxation using dynamic magnetic resonance imaging. Urology 54:454-457, 1999. 25. Maubon A, Aubard Y, Berkane V, et al: Magnetic resonance imaging of the pelvic floor. Abdom Imaging 28:217-225, 2003. 26. Schoenenberger AW, Debatin JF, Guldenschuh I, et al: Dynamic MR defecography with a superconducting, open-configuration MR system. Radiology 206:641-646, 1998. 27. Fielding JR, Versi E, Mulkern RV, et al: MR imaging of the female pelvic floor in the supine and upright position. J Magn Reson Imaging 6:961-963, 1996. 28. Yang A, Mostwin JL, Rosenshein NB, Zerhouni EA: Pelvic floor descent in women: Dynamic evaluation with fast MR imaging and cinematic display. Radiology 179:25-33, 1991. 29. Barbaric ZL, Marumoto AK, Raz S: Magnetic resonance imaging of the perineum and pelvic floor. Topics Magn Res Imaging 12:83-92, 2001. 30. Lienemann A, Anthuber C, Baron A, Reuser M: Diagnosing enteroceles using dynamic magnetic resonance imaging. Dis Colon Rectum 43:205-212, 2000. 31. Kelvin FM, Hale DS, Maglinte DD, et al: Female pelvic organ prolapse: diagnostic contribution of dynamic cystoproctography and comparison with physical examination. AJR Am J Roentgenol 173:31-37, 1999. 32. Kelvin FM, Maglinte DDT, Hale DS, Benson JT: Female pelvic organ prolapse: A comparison of triphasic dynamic MR imaging and tri-

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33.

34.

35.

36.

37.

38.

phasic fluoroscopic cystocolpoproctography. AJR Am J Roentgenol 174:81-84, 2000. Rentsch M, Paetzel CH, Lenhart M, et al: Dynamic magnetic resonance imaging defecography: A diagnostic alternative in the assessment of pelvic floor disorders in proctology. Dis Colon Rectum 44:999-1007, 2001. Singh K, Jakab M, Reid WMN, et al: Three-dimensional magnetic resonance imaging assessment of levator ani morphologic features in different grades of prolapse. Am J Obstet Gynecol 188:910-915, 2003. Fielding JR, Dumanli H, Schreyer AG, et al: MR-based threedimensional modeling of the normal pelvic floor in women: quantification of muscle mass. AJR Am J Roentgenol 174:657-660, 2000. Hoyte L, Fielding JR, Versi E, et al: Variations in levator ani volume and geometry in women: The application of MR based 3D reconstruction in evaluating pelvic floor dysfunction. Arch Esp Urol 54:532-539, 2001. Hoyte L, Schierlitz L, Zou K, et al: Two- and 3-dimensional MRI comparison of levator ani structure, volume, and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 185:1119, 2001. Pannu HK, Genadry R, Kaufman HS, Fishman EK: Computed tomography evaluation of pelvic organ prolapse. J Comput Assist Tomogr 27:779-785, 2003.

39. Takano M, Hamada A: Evaluation of pelvic descent disorders by dynamic contrast reontography. Dis Colon Rectum 43:S6-S11, 2000. 40. Brubaker L, Retzky S, Smith C, Saclarides T: Pelvic floor evaluation with dynamic fluoroscopy. Obstet Gynecol 82:863-868, 1993. 41. Mouritsen L: Techniques for imaging bladder support. Acta Obstet Gynecol Scand Suppl 166:48-49, 1997. 42. Gufler H, DeGreforio G, Allman KH, et al: Comparison of cystourethrography and dynamic MRI in bladder neck descent. J Comput Assist Tomogr 24:382-388, 2000. 43. Bremmer S, Ahlback SO, Uden R, Mellgren A: Simultaneous defecography and peritoneography in defecation disorders. Dis Colon Rectum 38:969-973, 1995. 44. Sentovich SM, Rivela LJ, Thorson AG, et al: Simultaneous dynamic proctography and peritoneography for pelvic floor disorders. Dis Colon Rectum 38:912-915, 1995. 45. Ekberg O: Complications after herniography in adults. AJR Am J Roentgenol 140:491-495, 1983. 46. Goei R, Kemerink G: Radiation dose in defecography. Radiology 176:137-139, 1990.

Chapter 56

DYNAMIC MAGNETIC RESONANCE IMAGING IN THE DIAGNOSIS OF PELVIC ORGAN PROLAPSE Craig V. Comiter and Joel T. Funk Weakness and subsequent dysfunction of the pelvic floor is common in parous women of middle or advanced age. Pelvic organ prolapse (POP) and pelvic floor relaxation are caused by anatomic abnormalities, including weakness of the muscles of the pelvic floor and the fascial attachments of the pelvic viscera. The prevalence of POP has been reported to be as high as 16% of women aged 40 to 56 years.1 Approximately 500,000 surgeries for POP are performed in the United States each year.2 Women with POP present not only to the gynecologist but also to the urologist, as up to one third of patients with prolapse also suffer from urinary incontinence. POP is also associated with fecal incontinence, incomplete voiding, and constipation. A detailed knowledge of pelvic anatomy is paramount for the proper evaluation and management of such conditions. Pelvic support defects result from both neurophysiologic and anatomic changes3 and often occur as a constellation of abnormal findings. Symptomatic individuals often have multifocal pelvic floor defects, not always evident on physical examination.4 Even experienced clinicians may be misled by the physical findings, having difficulty differentiating among cystocele, enterocele, and high rectocele by physical examination alone. Depending on the position of the patient, the strength of the Valsalva maneuver, and modesty of the patient, the examiner may be limited in his or her ability to accurately diagnose the various components of pelvic prolapse. Furthermore, with uterine prolapse, the cervix and uterus may fill the entire introitus, making the diagnosis of concomitant anterior or posterior compartmental prolapse even more difficult. Regardless of the etiology of the support defect, the surgeon must identify all aspects of vaginal prolapse and pelvic floor relaxation for proper surgical planning. Incorrect diagnosis of these defects may lead to inadequate surgical treatment.5 Accurate preoperative staging should reduce the risk of recurrent prolapse, which can occur in up to 34% of patients after surgery.6

RADIOGRAPHIC EVALUATION Radiographic evaluation plays an important role in the identification of these defects and should be used as an extension of the physical examination. Various methods have been used to visualize the pelvic structures and lower urinary tract, including fluoroscopy, sonography, computed tomography (CT), and, most recently, magnetic resonance imaging (MRI). Levator Myography Levator myography is an outdated method of visualizing the pubococcygeus and iliococcygeus via direct injection of contrast solution into the levator muscles. Originally described in 1953, this technique allows visualization of the position and supportive role of these muscle groups.7 Widening of the levator hiatus, which often occurs after traumatic childbirth and predisposes to pelvic floor relaxation and to visceral prolapse, can be demonstrated with levator myography. Today, this information may be obtained noninvasively with CT8 and MRI.9,10 Voiding Cystourethrography Voiding cystourethrography (VCUG) is mainly used for demonstrating a cystocele, evaluating bladder neck hypermobility, and demonstrating an open bladder neck at rest (sphincteric incompetence). Dynamic lateral cystography at rest and during straining is an important adjunct to the urodynamic evaluation; it is useful for demonstrating the presence of and degree of urethravesical hypermobility and cystocele formation (Fig. 56-1).11 In additional, dynamic fluoroscopy has been shown to be more accurate than physical examination in demonstrating an enterocele.12,13 Other pathologic conditions detected by VCUG include

Figure 56-1 Lateral cystogram, with patient relaxed (left) and straining (right).

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vesicoureteral reflux, vesicovaginal fistula, and urethral diverticular disease. Dynamic Proctography Dynamic proctography, in the cooperative patient, allows precise identification and quantification of a rectocele, measured as the maximum extent of an anterior rectal bulge beyond the expected line of the rectum.14,15 Limitations of this examination include the cumbersome and potentially painful instillation of rectal barium paste and lack of correlation between the viscosity of the paste and the individual patient’s stool. Modesty makes this a difficult technique for many patients, because they are unable to defecate on command. Colpocystourethrography The colpocystourethrogram was first described in France in 1965 and combines opacification of the bladder, urethra, and vagina.16 Modified and made popular in the mid 1970s, the colpocystourethrogram is a dynamic study of pelvic support and function.17 The anatomic relationships among the bladder, urethra, and vagina may be demonstrated, and, when the study is combined with proctography, it may be even more useful in outlining the anatomy of the normal pelvis and of complex POP. An enterocele, defined as a herniation of the peritoneum and its contents at the level of the vaginal apex, may be appreciated via straining or defecation during colpocystoproctography. This is demonstrated by a widening of the rectovaginal space.18 The accuracy of dynamic colpocystoproctography is even further enhanced by opacification of the small bowel. The patient drinks oral barium 2 hours before the examination. With the vagina, bladder, small intestine, and rectum opacified, the vaginal axis may be measured at rest and with straining, and prolapse of the anterior, middle, and/or posterior vaginal compartment should become evident. Sonography Sonography offers a convenient, painless, and radiation-free technique. As with fluoroscopy, a dynamic component may be added to sonography. In particular, dynamic ultrasound allows identification of an enterocele during straining maneuver, evidenced by widening of the rectovaginal septum, diminution of the peritoneal-anal distance, and herniation of bowel contents into the cul-de-sac.19 Ultrasongraphy using an abdominal, rectal, vaginal, or perineal transducer is also useful for demonstrating vesicourethral anatomy,20-23 So-called contrast sonography uses echogenic material instilled into the bladder or vagina and is able to identify bladder neck funneling with straining24 as well as paravaginal defects.25 Computed Tomography CT pelvimetry is an accurate and reproducible method for measuring pelvic dimensions and the capacity of the maternal birth canal.26,27 However, CT has not been shown to be particularly useful in the evaluation of pelvic visceral prolapse. The components of the levator plate and urogenital diaphragm are better seen in the coronal plane or sagittal view, but CT images are routinely presented in the axial plane. Although CT images can

be reconstructed into a coronal view with the use of cumbersome and expensive computer software, poor image quality and distorted spatial resolution has limited the utility of this presentation technique.8 Magnetic Resonance Imaging Most recently, MRI has emerged as an important diagnostic tool, both for evaluating the functional relationships among the pelvic floor viscera and supporting structures and for assessing pelvic pathology. MRI offers the advantages of being noninvasiveness, lack of exposure of the patient and examiner to ionizing radiation, and superior soft tissue contrast and multiplanar imaging without superimposition of structures. Axial images provide information about the urogenital hiatus and its contents, whereas sagittal images more easily demonstrate visceral prolapse. Because static images alone do not demonstrate relevant pelvic floor changes with activity, dynamic MRI has been used to reveal the structural functional changes that occur during stress maneuvers. Those established criteria for abnormality derived from fluoroscopy (colpocystoproctography) are directly applicable to MRI.28 The development of fast-scanning MRI techniques has greatly improved the ability to describe and quantify anatomic changes that have a causative role in pelvic floor relaxation. Fast-scan Valsalva imaging formatted in a pseudokinematic cine-loop provides a dynamic method to study the anatomic changes that occur with straining. Additionally, MRI offers a noninvasive method to evaluate the female pelvis without exposure to the ionizing radiation that is integral to prior modalities such as CT, colpocystoproctography, and fluoroscopy. MRI also allows evaluation of all three pelvic compartments simultaneously for organ descent. Kelvin’s group used “triphasic” dynamic MRI, consisting of a cystographic, a proctographic, and a post-toilet phase to facilitate the recognition of prolapsed organs that may be obscured by other organs that remain unemptied.29 Fielding showed that MRI is useful for measuring levator muscle thickness,30 demonstrating focal levator ani eventrations (outpouching) not visible with levator myography,31 and measuring urethral length and the thickness and integrity of periurethral muscle ring.9 Hoyte and colleagues48 demonstrated that the anterior portion of the levator (puborectalis) is typically thinner in women with POP and/or stress incontinence compared with asymptomatic controls—possibly due to muscle atrophy caused by denervation from childbirth injuries or muscle wasting secondary to loss of insertion points for the puborectalis. Yang and associates were the first to popularize dynamic fast MRI for the evaluation of POP,9 using T1-weighted gradient recalled acquisition in a steady-state pulse (GRASS) sequence, with acquisition times between 6 and 12 seconds. Since then, other investigators have shown that MRI is more sensitive than physical examination for defining pelvic prolapse.5,10,32 Whereas some advocate the use of contrast opacification of the bladder, vagina, and rectum,29,33 others have shown that the vagina, rectum, bladder, urethra, and peritoneum are adequately visualized without any contrast administration.5 By avoiding instrumentation of the vagina or urethra, iatrogenic alteration of the anatomy is minimized.10 Several years ago, Comiter and coworkers published their experience with dynamic half-Fourier acquisition, single-shot turbo spin-echo (HASTE sequence) T2-weighted MRI using a 1.5-Tesla magnet with phased array coils (Siemens) or single-

Chapter 56 DYNAMIC MAGNETIC RESONANCE IMAGING OF PELVIC ORGAN PROLAPSE

Figure 56-2 Lateral magnetic resonance image denoting normal pelvic structures.

Figure 56-3 The H-line (levator hiatus width) measures the distance from the pubis to the posterior anal canal. The M-line (muscular pelvic floor relaxation) measures the descent of the levator plate from the fixed pubococcygeal line (PCL).

shot fast spin-echo (SSFSE, General Electric) for evaluating the female pelvis.5 Midsagittal and parasagittal resting and straining supine views were obtained for the purpose of identifying the midline and for evaluating the anterior pelvic compartment (anterior vaginal wall, bladder, urethra), posterior compartment (rectum), and middle compartment (uterus, vaginal cuff), as well as the pelvic floor muscles, adnexal organs, and intraperitoneal organs (Fig. 56-2). Images were looped for viewing on a digital station as a cine stack and for measuring the relationship of pelvic organs to fixed anatomic landmarks. The first set of images comprised volumetric sagittal cuts from left to right, used to locate the midsagittal plane and to survey the pelvic anatomy. The second set of images was obtained with four cycles of repeated

relaxation and Valsalva maneuver.5,8 Total image acquisition time was 2.5 minutes, and total room time was 10 minutes per study. This dynamic MRI technique, known as the HMO classification system, has been shown to be useful for grading pelvic visceral prolapse and pelvic floor relaxation in a simple and objective manner.5 The size of the levator hiatus and the degree of muscular pelvic floor relaxation and organ prolapse were measured. The “H-line” (levator hiatus width) measures the distance from the pubis to the posterior anal canal. The “M-line” (muscular pelvic floor relaxation) measures the descent of the levator plate from the fixed pubococcygeal line (PCL). The PCL spans the distance from the pubis to the sacrococcygeal joint (Fig. 56-3). The “O”

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A

C

B

Figure 56-4 Organ prolapse. A, Cystocele. B, Rectocele. C, Enterocele.

classification (organ prolapse) describes the degree of visceral prolapse beyond the H-line. The degrees of cystocele, rectocele, enterocele, and uterine descent are graded as 0, 1, 2, or 3, corresponding to none, mild, moderate, or severe (Fig. 56-4). In a group of women with symptomatic prolapse, the levator hiatus width (H-line) was significantly wider than in a control group (7.5 ± 1.5 cm versus 5.2 ± 1.1 cm; P < .001). Similarly, the levator muscular descent (M-line) was greater in the prolapse group than in the control group (4.1 ± 1.5 cm versus 1.9 ± 1.2 cm; P < .001).5 These objective findings fit well with our knowledge of the pathophysiology of pelvic prolapse. Trauma to the pubococcygeus and iliococcygeus, usually from childbirth, results in widening of the levator hiatus and laxity of the musculofascial

support structures.34 This results in a sloping levator plate, with the more vertically oriented vagina and rectum tending to slide down through the widened hiatus. Therefore, the H and M lines both increase with pelvic floor relaxation. This in turn leads to organ prolapse (O classification). Because of the excellent visualization of fluid-filled viscera and soft tissues, MRI can differentiate among cystocele, enterocele, and high rectocele, which may be difficult by physical examination alone. MRI findings were compared to physical examination and intraoperative findings. HASTE-sequence MRI was more accurate than physical examination in identifying cystocele, enterocele, vault prolapse, and pelvic organ pathology such as uterine fibroids, urethral diverticula, ovarian cysts, and Nabothian and

Chapter 56 DYNAMIC MAGNETIC RESONANCE IMAGING OF PELVIC ORGAN PROLAPSE

Figure 56-5 Magnetic resonance urography demonstrates hydroureteronephrosis secondary to pelvic organ prolapse obstructing the ureters.

Bartholin gland cysts.32 Comiter and colleagues found that, with dynamic MRI, surgical planning was altered in more than 30% of cases, most often because of occult enterocele not appreciated on physical examination.35 In patients with severe prolapse, especially if renal insufficiency is present, the surgeon must rule out obstructive hydroureteronephrosis. This may be accomplished by magnetic resonance urography, which adds only 30 seconds of examination time and no additional morbidity (Fig. 56-5). MRI may also be useful for the radiographic evaluation of stress incontinence. Hypermobility of the proximal urethra and bladder neck descent are important pathophysiologic features in the diagnosis of genuine stress urinary incontinence.36,37 Measurement data on dynamic MRI for the bladder neck position and the extension of cystocele at maximal pelvic strain are comparable with data obtained by lateral cystourethrography (Fig. 56-6).38 Recent urogynecologic and radiologic publications have validated MRI as a reliable alternative to colpocystoproctography.29,38,39 The information obtained via MRI is often superior to that obtained via colpocystoproctography, because the former allows for direct visualization of the pelvic organs and their fluid content, whereas the latter presents a silhouetted view of contrast-filled organs (complete opacification is not usually achieved). Gufler and associates demonstrated that dynamic MRI is helpful in the evaluation of persistent patient complaints after surgery for POP and is, in fact, more sensitive than physical examination.40 Dynamic MRI is particularly sensitive for diagnosing enteroceles and is superior to colpocystoproctography or physical examination.41 A minority of studies have shown that MRI

Figure 56-6 Lateral magnetic resonance image demonstrating stress urinary incontinence secondary to urethral hypermobility.

may not be as accurate for the identification of vaginal vault prolapse or for rectocele as is colpocystoproctography.42 Gousse’s group from the University of Miami postulated that the anterior rectal wall is not well differentiated from the posterior wall on rapid-sequence MRI when the rectum is empty, because the rectal walls are collapsed.32,43 At our institution intravaginal, intravesical, or intrarectal contrast is not instilled, but others have shown that such “triphasic dynamic” studies may even further improve the diagnostic accuracy of MRI.29,34 The disadvantage of MRI is that the study often must be performed with the patient in the supine position, because upright MRI scanners are not yet universally available. Colpocystoproctography is clearly more amenable to performance in a sitting position than is MRI. However, dynamic MRI with relaxing and straining views has been shown to adequately demonstrate POP during straining in the supine position.44 Additionally, in those institutions that have access to an upright MRI scanner, sitting MRI was not shown to be superior to supine MRI for demonstrating POP. Although patients undergoing sitting MR imaging demonstrated a greater degree of visceral descent, supine studies were not inferior for demonstrating clinically relevant prolapse.45 Competition among prolapsing organs filling a finite introital space may also limit MRI, just as it may limit physical examination and dynamic fluoroscopy. This is especially true for identification of a rectocele. Additionally, claustrophobic patients and those with cardiac pacemakers or sacral nerve stimulators cannot enter the enclosed magnet. Despite these limitations, dynamic MRI has become the study of choice at our institution for evaluating POP and pelvic floor relaxation.

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Alternative MRI sequences have recently been demonstrated to be as good or better than the HASTE sequence. Lienemann and colleagues recommended a true fast imaging with steadystate precession (True FISP) sequence, because it may be associated with superior image quality compared to the HASTE sequence.41,45 Gousse’s group from Miami demonstrated the utility of extended-phase conjugate-symmetry rapid spin-echo sequence (EXPRESS) as a novel and very rapid scanning technique; individual images are obtained in 0.8 seconds with the use of half-Fourier reconstruction and fast gradients with sophisticated recently available software.43 Both the True FISP and EXPRESS dynamic MRI examinations were superior to physical examination in accuracy and completeness for the preoperative evaluation of POP. Over the last decade, there has been an increasing interest in use of elective cesarean delivery to reduce maternal birth trauma and decrease long-term morbidity,46,47 but reliable prepartum criteria have not been established to identify those women most likely to develop pelvic floor injuries during childbirth. Fielding’s group at Harvard recently published their experience with MRI pelvimetry as a potentially important research tool.48 Their protocol is easily performed with the patient in the supine position using a pelvic coil, fast spin-echo T2-weighted sequences, 2-mm cuts, and a 1.5-T system. Pelvimetry measurements are obtained from coronal, axial, and midsagittal images. Significant differences in mean pelvimetry measurements were demonstrated between women with and without pelvic visceral prolapse and pelvic floor relaxation. With multivariate analysis, POP patients had a wider transverse inlet diameter, and a trend toward a wider interspinous diameter. Recent CT studies have demonstrated that women with wider transverse inlet diameters have a higher prevalence of prolapse after childbirth,26 and perhaps MRI pelvimetry may contribute to the identification of such risk factors.

SUMMARY Most cases of incontinence and minimal pelvic floor weakness can be treated based on physical examination with or without urodynamic evaluation. On the other hand, in women with complex or recurrent POP and pelvic floor relaxation, radiographic evaluation is recommended as an extension of the physical examination. A detailed working knowledge of normal and abnormal female pelvic anatomy is necessary for the proper evaluation of pelvic visceral prolapse. However, even the most experienced gynecologist or urologist may have difficulty distinguishing among prolapsing organs competing for introital space. Accurate identification of all aspects of vaginal prolapse and pelvic floor relaxation are vital, not only to permit adequate surgical planning but also to reduce the risk of recurrent prolapse. Urography, voiding cystography, dynamic colpocystodefecography, sonography, and MRI are each useful for the evaluation of pelvic prolapse and pelvic floor relaxation. MRI can demonstrate the levator muscles in threedimensional fashion, providing details about herniation during straining, muscle thickness, and asymmetry. MRI allows complete analysis of the anterior, middle, and posterior pelvic compartments in a single procedure without the use of ionizing radiation. Differentiation among soft tissues is excellent, anatomic information is accurate, and no contrast agent is needed. The advent of rapid sequencing with cine stacking has enabled MRI to replace dynamic colpocystoproctography at many institutions, providing not only superb differentiation among fluid-filled, air-filled, and solid pelvic viscera but also a functional demonstration of all three pelvic compartments during relaxation and straining. As dynamic MRI becomes more widespread, standardization of the technique will become more important.

References 1. Hagstad A, Janson PO, Lindstedt G: Gynaecological history, complaints, and examinations in a middle-aged population. Maturitas 7:115-128, 1985. 2. Morren GL, Balasingam AG, Wells JE, et al: Triphasic MRI of pelvic organ descent: Sources of measurement error. Eur J Radiol 54:276283, 2005. 3. Brubaker L, Heit MH: Radiology of the pelvic floor. Clin Obstet Gynecol 36:952-959, 1993. 4. Spence-Jones C, Kamm MA, Henry MM, Hudson CN: Bowel dysfunction: A pathogenic factor in uterovaginal prolapse and urinary stress incontinence. Br J Obstet Gynecol 101:147-152, 1994. 5. Comiter CV, Vasavada SP, Barbaric AL, et al: Grading pelvic prolapse and pelvic floor relaxation using dynamic magnetic resonance imaging. Urology 54:454-458, 1999. 6. Shull BL, Benn SJ, Kuehl TJ: Surgical management of prolapse of the anterior vaginal segment: An analysis of support defects, operative morbidity, and anatomic outcome. Am J Obstetr Gynecol 171:1429-1439, 1994. 7. Berglas B, Rubin IC: Study of the supportive structures of the uterus by levator myography. Surg Gynecol Obstet 97:677-692, 1953. 8. Weidner AC, Low VHS: Imaging studies of the pelvic floor. Obstet Gynecol Clin North Am 25:825-848, 1998. 9. Yang A, Mostwin, JL, Rosenshein NB: Pelvic floor descent in women: Dynamic evaluation with fast MR imaging and cinematic display. Radiology 179:25-33, 1991.

10. Goodrich MA, Webb M.J, King BF: Magnetic resonance imaging of pelvic floor relaxation: Dynamic analysis and evaluation of patients before and after surgical repair. Obstet Gynecol 82:883-891, 1993. 11. Kelvin FM, Maglinte DD, Hale D, Benson JR: Voiding cystourethrography in female stress incontinence. AJR Am J Roentgenol 167:1065-1066, 1996. 12. Kelvin FM, Maglinte DDT, Hornback JA, Benson JT: Pelvic prolapse: Assessment with evacuation proctography (defecography). Radiology 184:547-551, 1992. 13. Altringer WE, Saclarides TJ, Dominguez JM: Four-contrast defecography: Pelvic “flooroscopy.” Dis Colon Rectum 38:695-699, 1995. 14. Kelvin FM, Maglinte DD: Dynamic evaluation of female pelvic organ prolapse by extended proctography. Radiol Clin North Am 41:395-407, 2003. 15. Shorvon PJ, McHugh S, Diamant NE: Defecography in normal volunteers: Results and implications. Gut 30:1737-1740, 1989. 16. Bethoux A, Bory S, Huguier M, Sheao SL: Le colpocystogramme. J Chir (Paris) 8:809-828, 1965. 17. Lazarevski M, Lazarov A, Novak J, Dimcevski D: Colpocystography in cases of genital prolapse and urinary stress incontinence in women. Am J Obstet Gynecol 122:704-716, 1975. 18. Shorvon PJ, Stevenson GW. Defaecography: Setting up a service. Br J Hosp Med 41:460-467, 1989. 19. Karaus M, Neuhaus P, Weidenmann B: Diagnosis of enteroceles by dynamic anorectal endosonography. Dis Colon Rectum 43:16831688, 2000.

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20. Gordon D, Pearce M, Norton P, Stanton SL: Comparison of ultrasound and lateral chain cystourethrography in the determination of bladder neck descent. Am J Obstet Gynecol 160:12-18, 1989. 21. Bergmann A, Ballard CA, Platt LD: Ultrasonic evaluation of urethrovesical junction in women with stress urinary incontinence. J Clin Ultrasound 16:295-300, 1998. 22. Mouritsen L, Rasmussen A: Bladder neck mobility evaluated by vaginal ultrasonography. Br J Urol 71:166-171, 1993. 23. Kohorn E, Scioscia AL, Jeaty P, Hobbins JC: Ultrasound by perineal scanning for the assessment of female stress urinary incontinence. Obstet Gynecol 68:269-272, 1986. 24. Schaer GN, Koechli OR, Schuessler B: Improvement of perineal sonographic bladder neck imaging with ultrasound contrast medium. Obstet Gynecol 86:950-954, 1995. 25. Ostrzenski A, Osborne NG, Ostrzenska K: Method for diagnosing paravaginal defects using contrast ultrasonographic technique. J Ultrasound Med 16:673-677, 1997. 26. Sze EH, Kohli N, Miklos JR, et al: Computed tomography comparison of bony pelvis dimensions between women with and without genital prolapse. Obstet Gynecol 93:229-232, 1999. 27. Federle MP, Cohen HA, Rosenwein MR, et al: Pelvimetry by digital radiography: A low dose examination. Radiology 143:733-735, 1982. 28. Goh V, Halligan S, Kaplan G, et al: Dynamic MR imaging of the pelvic floor in asymptomatic subjects. AJR Am J Roentgenol 174:661666, 2000. 29. Kelvin FM, Maglinte DDT, Hale DS, et al: Female pelvic organ prolapse: A comparison of triphasic dynamic MR imaging and triphasic fluoroscopic cystocolpoproctography. AJR Am J Roentgenol 174:8188, 2000. 30. Fielding JR, Dumanli H, Schreyer AG, et al: MR-based three dimensional modeling of the normal pelvic floor in women: Quantification of muscle mass. AJR Am J Roentgenol 174:657-660, 2000. 31. Pannu KH, Genardry R, Gearhart S, et al: Focal levator ani eventrations: Detection and characterization by magnetic resonance in patients with pelvic floor dysfunction. Int Urogynecol J Pelvic Floor Dysfunct 14:89-93, 2003. 32. Gousse AE, Barbaric ZL, Safir MH, et al: Dynamic half Fourier acquisition, single shot turbo spin-echo magnetic resonance imaging for evaluating the female pelvis. J Urol 164:1606-1613, 2000. 33. Lienemann A, Fischer T: Functional imaging of the pelvic floor. Eur J Radiol 27:117-122, 2003. 34. Babiarz JW, Raz S: Pelvic floor relaxation. In Raz S (ed): Female Urology. Philadelphia: WB Saunders, 1996, pp 445-456.

35. Comiter CV, Vasavada S, Raz S: Pre-operative Evaluation of Pelvic Prolapse Using Dynamic Magnetic Resonance Imaging. Presented at the 29th Annual International Continence Society, Denver, CO, August, 1999. 36. Jeffcoate TN, Roberts H: Observation on stress incontinence of urine. Am J Obstet Gynecol 64:721-738, 1952. 37. Enhorning G: Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand 276(Suppl):1-68, 1956. 38. Gufler H, DeGregorio G, Allman K-H, et al: Comparison of cystourethrography and dynamic MRI in bladder neck descent. J Comput Assist Tomogr 24:382-388, 2000. 39. Deval B, Vulierme MP, Poilpot S, et al: [Imaging pelvic floor prolapse] [French]. Gynecol Obstet Biol Reprod (Paris) 32:22-29, 2003. 40. Gufler H, CeGregorio G, Dohnicht S, et al: Dynamic MRI after surgical repair for pelvic organ prolapse. J Comput Assist Tomogr 26:724-729, 2002. 41. Lienemann A, Anthuber C, Baron A, Reiser M: Diagnosing enteroceles using magnetic resonance imaging. Dis Colon Rectum 43:205212, 2000. 42. Cortes E, Reid WM, Singh K, Berger L: Clinical examination and dynamic magnetic resonance imaging vaginal vault prolapse. Obstet Gynecol 103:41-46, 2004. 43. Kester RR, Leboeuf L, Amendola MA, et al: Value of EXPRESS T2weighted pelvic MRI in the evaluation of severe pelvic floor prolapse: A prospective study. Urology 61:1135-1139, 2000. 44. Lienemann A, Anthuber CJ, Baron A: Dynamic MR colpocystorectogrpahy assessing pelvic floor descent. Eur Radiol 7:1309-1317, 1997. 45. Bertshinger 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 closed-magnet unit. Radiology 223:501-508, 2002. 46. Faridi A, Willis S, Schelzig P, et al: Anal sphincter injury during vaginal delivery: An argument for cesarean section on request? J Perinat Med 30:279-287, 2002. 47. Heit M, Mudd K, Culligan P: Prevention of childbirth injuries to the pelvic floor. Curr Womens Health Rep 1:72-80, 2001. 48. Hoyte L, Schierlitz L, Zou K, et al: Two and 3-dimensional MRI comparison of levator ani structure, volume, and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 185:1119, 2001.

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URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE Sender Herschorn

Symptoms caused by pelvic organ prolapse may or may not be specific to the prolapsing compartment or compartments, and the correlation of many pelvic symptoms with the extent of prolapse is weak.1,2 Many women with pelvic organ prolapse have no symptoms, especially if the prolapse remains inside the vagina.3 Others present with symptoms in addition to the vaginal bulge, as a result of the associated organ dysfunction. It is recommended that symptoms be elucidated in four primary areas: lower urinary tract, bowel, sexual symptoms, and other local symptoms.4 Documentation of symptoms not only serves as a guide to treatment but also permits an accurate assessment of post-treatment results. There is general agreement that the aim of urodynamic testing is to reproduce symptoms of the patient under controlled and measurable conditions. Ideally, this allows diagnosis, helps with informed treatment choice, and improves treatment outcome. Specifically, the testing identifies or excludes contributing factors to incontinence or voiding dysfunction and assesses their relative importance.5 However, the role of urodynamics in the evaluation of symptoms related to prolapse is not yet fully established. A recent Cochrane review attempted to test the hypotheses that urodynamic testing improves the clinical outcome of incontinence management, that it alters clinical decision-making, and that one type of test is better than another in these areas.6 Only two trials were found, but the numbers of patients were too small to determine whether clinical outcomes were affected by the urodynamics. This chapter reviews the various tests that are available and may be helpful in patient evaluation.6 LOWER URINARY TRACT SYMPTOMS Urinary incontinence is one of the most common symptoms associated with prolapse. Blaivas and Groutz7 described the clinical evaluation in detail. However, the specific symptoms and their impact on the patient’s quality of life should be elucidated in each case. Urinary symptoms may include stress incontinence; symptoms of bladder overactivity, such as frequency, nocturia, urgency, and urgency incontinence; and voiding symptoms such as difficulty with bladder emptying. The mechanisms for stress incontinence include hypermobility and intrinsic sphincter deficiency. It is not unusual for patients to present with a combination of urge and stress incontinence.8,9 If both symptoms are present, the patient has mixed incontinence.10 Mixed incontinence is especially common in older women. Often, however, one symptom (urge or stress) is more bothersome to the patient than the other. 586

Identifying the most bothersome symptom is important in targeting diagnostic and therapeutic interventions. Many women with severe prolapse recall that, as the prolapse worsened, their stress incontinence symptoms improved. Reducing the vaginal prolapse with a pessary or a speculum during the examination by the clinician can produce stress incontinence in up to 80% of clinically continent patients with severe prolapse.11-14 This phenomenon has been termed latent, masked, occult, or potential stress incontinence, and it should be elicited when considering therapy. Although the clinical experience reported refers primarily to cystocele, occult incontinence may also be unmasked in a similar manner in patients with severe middle or posterior compartment prolapse. The postulated mechanism for continence may be urethral kinking by the cystocele or external compression of the urethra.15 Other storage symptoms, such as frequency, nocturia, and urgency, have been listed as symptoms of prolapse,16 although the mechanism is unknown and there are frequently other associated factors. Urge incontinence may also be present. However, urge incontinence is a common complaint in patients without organ prolapse, may or may not be the result of detrusor overactivity,17 and becomes more prevalent with aging. Patients with advanced organ prolapse and urge incontinence have also been shown to have detrusor overactivity15 that may resolve after surgical correction of the prolapse.13,18 The mechanism is unclear; however, many of those patients may have outflow obstruction caused by the prolapse that is alleviated after repair. Nguyen and Bhatia reported resolution of urgency incontinence after pelvic prolapse repair in patients who had no obstruction preoperatively.18 A number of tools are now available to aid the clinician in elucidating the symptoms and their impact on quality of life, to gain as accurate a picture as possible. These tools include questionnaires, voiding diaries, and pad tests, which are also used to evaluate treatment outcomes.19 Difficult voiding symptoms are common with severe prolapse and should be elicited. Patients with prolapse may have urethral kinking or external pressure on the urethra that not only prevents incontinence but also may cause difficult voiding.15 They occasionally have to digitally reduce the prolapse to void (splinting) or need to assume unusual positions to initiate or complete micturition.4 Urinary splinting has been reported to be 97% specific for severe anterior prolapse.20 Urodynamic abnormalities with decreased uroflow, increased postvoid residual urine,21 and bladder outlet obstruction have been reported.15,22,23 The degree of obstruction may be related to the severity of the prolapse.15 Acute urinary retention secondary to the prolapse is rarely seen.24

Chapter 57 URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE

INITIAL EVALUATION OF URINARY SYMPTOMS The initial evaluation includes a history, physical examination, urinalysis, and measurement of postvoid residual urine.25 The basic evaluation may be satisfactory for proceeding with treatment, including surgery, for patients with straightforward stress incontinence associated with hypermobility and normal postvoid residual volume.10 However, the International Scientific Committee of the Third International Consultation on Urinary Incontinence advised that urodynamic testing is highly recommended for women who desire interventional treatment,25 although the specific chapter indicates the lack of evidencedbased medicine for this recommendation.5 Furthermore, Diokno and coworkers26 showed that a systematic history, vaginal speculum examination and postvoid residual measurement were 100% accurate in identifying patients who had pure type II stress incontinence on urodynamic studies. Other groups have shown a positive correlation of symptoms and urodynamic findings,27,28 potentially bypassing the need for urodynamic studies in many patients.29,30 Investigators have also shown that symptoms are not always related to the actual dysfunction causing the incontinence demonstrated on urodynamics.31-35 As mentioned previously, the actual role of urodynamics in case selection and in predicting the continence outcome of surgery is still unknown.36 There are many instances in which a basic clinical evaluation is insufficient. The Agency for Health Care Research and Quality (formerly the Agency for Health Care Policy and Research) published guidelines in 1996 that are still relevant.10 Criteria for further evaluation of incontinence include ■ ■ ■

■

■ ■

■ ■ ■ ■ ■

uncertain diagnosis and inability to develop a reasonable treatment plan based on the basic diagnostic evaluation uncertainty in diagnosis when there is lack of correlation between symptoms and clinical findings failure to respond or patient dissatisfaction with an adequate therapeutic trial and patient desire to pursuefurther therapy consideration of surgical intervention, particularly if previous surgery failed or the patient is a high surgical risk hematuria without infection the presence of other comorbid conditions, such as incontinence associated with recurrent symptomatic urinary tract infection persistent symptoms of difficult bladder emptying history of previous anti-incontinence surgery or radical pelvic surgery symptomatic pelvic prolapse beyond the hymen abnormal postvoid residual urine volume a neurologic condition, such as multiple sclerosis or spinal cord lesions or injury.

Additional testing includes urodynamics but may also include cystoscopy and imaging.

Urodynamics in the Patient with Prolapse For good urodynamic practices, the reader is referred to the International Continence Society (ICS) publication that reviews current standards for carrying out uroflowmetry, filling cystometry, and pressure-flow studies.37

Urinary Flow Rate A urinary flow rate is a simple urodynamic test that can provide objective and quantitative measures on both storage and voiding symptoms.37 The curve is either continuous or intermittent. The continuous flow curve is smooth and arc-shaped or a fluctuating (if there are multiple peaks during a period of continuous urine flow). The precise shape of the curve is determined by detrusor contractility, the presence of abdominal straining, and the bladder outlet.38 The parameters of uroflowmetry include the following38: ■ ■ ■ ■

■ ■

■

Flow rate is defined as the volume of fluid expelled via the urethra per unit time (mL/sec). Voided volume is the total volume expelled via the urethra. Maximum flow rate (Qmax) is the maximum measured value of the flow rate after correction for artefacts. Voiding time is the total duration of micturition (i.e., including interruptions). If voiding is completed without interruption, voiding time is equal to flow time. Flow time is the time over which measurable flow actually occurs. Average flow rate (Qave) is voided volume divided by the flow time. The average flow should be interpreted with caution if flow is interrupted or if there is a terminal dribble. Time to maximum flow is the elapsed time from onset of flow to maximum flow.

The Liverpool Nomogram (Fig. 57-1) was created in 1989 by Haylen and colleagues, who plotted voided volume against peak flow (Qmax) in 249 normal women.39 Normal peak flowranges between 12 and 30 mL/sec, depending on the voided volume (Fig. 57-2). Average flow rates vary from 6 to 25 mL/sec, with a substantial overlap between normal and abnormal individuals.40 Voiding time varies, from 10 to 20 seconds for a volume of 100 mL to 25 to 35 seconds for a volume of 400 mL. The first half of the urinary volume is rapidly evacuated in the first one third of the total voiding time, and the rest in the remaining two thirds of the voiding period.41 Arbitrary criteria have been set by a number of authors to diagnose voiding difficulty, including peak flow less than 15 mL/sec and residual urine greater than 50 mL with a minimum total bladder volume of 150 mL before the void (volume voided + residual).15,42 The 10th percentile curve of the Liverpool Nomogram has also been identified as a useful discriminant in the diagnosis of voiding difficulties.43 Bottacini and colleagues44 reported that women with stress incontinence void with a lower flow rate than healthy women; however, other investigators have demonstrated the opposite: women with stress incontinence void with a higher flow rate because of the reduced outlet resistance.44 Uroflowmetry findings (peak flow rate, average flow rate, and voided volume) in prolapse have been described to be significantly lower than in normal controls.29 Cystocoele is significantly more frequent in patients with voiding difficulties and abnormal uroflowmetry.35 Valentini and colleagues26 demonstrated a constrictive effect on outflow in women with varying degrees of cystocele. A poor flow rate and elevated residual urine may be associated with large cystoceles.41 In general, an abnormal pattern is generated in the presence of a weak detrusor, abdominal straining, or bladder outlet obstruction. Although urodynamic catheters have less effect on voiding patterns in females than in males, it is still useful to obtain a urinary flow rate on arrival of the patient, to compare

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Figure 57-3 Commode chair for uroflow measurement.

with flow data generated during the subsequent urodynamic study. After the initial flow is completed, a postvoid residual can also be determined on introduction of the urodynamic catheters.

Figure 57-1 The Liverpool Nomogram showing maximum (Top) and average (Bottom) flow for women.39

Figure 57-2 Normal flow curve for a voided volume of 350 mL with maximum flow (Qmax) of 27 mL/sec. (Modified from Lose G: Urethral pressure measurements. In Cardozo L, Staskin D [eds]: Textbook of Female Urology and Urogynaecology. London: Isis Medical Media, 2001, pp 215-226.)

Urine Flow Meters Flow meters are commonly of one of three types: weight, electronic dipstick, or rotating disc.45 The first measures the weight of the collected urine; the second measures the changes in electrical capacitance of a dipstick mounted in the collecting chamber; and the third measures the power required to keep a disc rotating at a constant speed while the urine, which tends to slow it down, is directed toward it. All three can provide high sensitivity and reproducibility of data. A commode chair with uroflow measuring apparatus is shown in Figure 57-3. Cystometry The first part of the filling study is cystometry, the method by which the pressure-volume relationship of the bladder is measured.38 It is used to assess detrusor sensation, capacity, and activity. The detrusor pressure (Pdet) is calculated by subtraction of the abdominal pressure (Pabd), as measured by a balloon in the rectum, vagina, or bowel stoma, from the total intravesical pressure (Pves), as measured by the intravesical catheter. The resulting detrusor pressure reflects the activity and pressure generated by the detrusor muscle alone. Artifacts in the Pdet may be produced by intrinsic rectal contractions.46 Filling rates in the past were described as slow, medium, or fast. Currently, the filling rate is classified as physiologic or nonphysiologic, and the actual rate should be specified.38 Most studies in non-neurologic patients are done with medium fill rates of 50 to 100 mL/min. Bladder storage function should be noted with bladder sensation (normal; first sensation of filling; first and strong desire to void; increased, reduced, or absent bladder sensation; bladder pain; and urgency), detrusor overactivity, bladder compliance, and capacity.38 The terminology to describe detrusor activity has been standardized by the ICS.38 Detrusor overactivity is characterized by spontaneous or provoked involuntary detrusor contractions during filling. Although an involuntary contraction was originally defined as a minimum pressure rise of 15 cm H2O,47

Chapter 57 URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE

there is presently no lower limit for the amplitude of an involuntary contraction (Fig. 57-4).38 If leakage is detected in association with an involuntary detrusor contraction, it is termed detrusor overactivity incontinence. Detrusor overactivity can be further characterized into idiopathic and neurogenic detrusor overactivity. Idiopathic detrusor overactivity describes involuntary detrusor contractions of unknown etiology and has replaced the term “detrusor instability.” An involunatary detrusor contraction secondary to an underlying neurologic condition is neurogenic detrusor overactivity, which has replaced “detrusor hyperreflexia.”38 Another type of overactive bladder dysfunction is reduced compliance. Bladder compliance is defined as the change in pressure for a given change in volume. It is calculated by dividing the volume change by the change in detrusor pressure during that change in bladder volume, and it is expressed as milliliters per centimeters of water pressure (see Fig. 57-4B).38 Normal bladder compliance is high, and in the laboratory the normal pressure rise is less than 6 to 10 cm H2O.48 Low bladder compliance implies a poorly distensible bladder. The actual numeric values to indicate normal, high, or low compliance have yet to be defined.38 The finding of detrusor overactivity on cystometry is important if it correlates with the clinical condition of the patient. Idiopathic detrusor overactivity has been reported in 30% to 35% of patients with stress incontinence undergoing surgery. It resolves in most such patients after repair and may not have a significant impact on outcome.49,50 Alternatively, if the patient’s symptoms are primarily from bladder overactivity, or other factors predisposing to abnormal bladder behavior are present, the cystometric findings will influence treatment. These predisposing factors include a history of radiation, chronic bladder inflammation, indwelling catheter, chronic infection, chemotherapy, voiding dysfunction after pelvic surgery, and other neurologic conditions.

measurement cannot be determined. The presence of a catheter in the urethra may prevent incontinence.53 Furthermore, a cystocele or other prolapsing segment may produce inferior pressure on an incompetent urethra that prevents incontinence or falsely elevates the VLPP. If a cystocele is present, the VLPP should be repeated with the prolapse reduced by insertion of a vaginal pack or pessary. The detrusor or bladder leak point pressure (DLPP) is the lowest detrusor pressure (Pdet) on cystometry at which urinary leakage occurs during bladder filling in the absence of a detrusor contraction or increased abdominal pressure.38 This parameter is used to investigate and monitor patients with neurogenic and low-compliance bladders. In general, patients with a DLPP greater than approximately 25 to 30 cm H2O are at risk for upper tract deterioration from reflux or obstruction.54,55 In these patients, it is necessary to assess compliance as well. A high DLPP indicates poor compliance with urethral obstruction, whereas a low DLPP is seen in patients with incompetent urethras. In order to demonstrate poor compliance in these patients. filling may be done with a Foley catheter to obstruct the outlet.56

Urethral Function Tests The normal urethral closure mechanism maintains a positive urethral closing pressure during bladder filling, even in the presence of increased abdominal pressure. An incompetent mechanism allows leakage in the absence of a detrusor contraction.38 Two urodynamic tests have been used to depict urethral competence: the Valsalva or abdominal leak point pressure (VLPP or ALPP) and the urethral pressure profile (UPP).

Intraluminal urethral pressure may be measured with the subject at rest, with the bladder at any given volume; during coughing or straining; and during voiding.57 Measurements can be made at one point in the urethra over a period of time (continuous urethral pressure recording) or as a UPP. A mechanical retracting puller that is synchronized with the chart or digital recorder allows measurement of anatomic distances in the profile. Two types of UPP may be measured: Resting UPP (Fig. 57-5A), with the bladder and subject at rest, and stress UPP (see Fig. 57-5B), with a defined applied stress (e.g., cough, strain, Valsalva maneuver). The simultaneous recording of both intra-urethral (Pura) and intravesical (Pves) pressure enables calculation of urethral closure pressure (i.e., Pura − Pves). The three main methods for UPP measurement are perfused catheters with side holes, catheter-tip transducer catheters, and balloon catheters. Recordings of profile parameters must be repeated several times to verify reproducibility.58 An MUCP of less than 20 cm H2O (“low-pressure urethra”) has been reported to be predictive of poor outcome of conventional bladder neck suspension procedures59 and has been called a predictor of ISD.58 However, the MUCP alone does not provide any information about the integrity of the bladder neck or proximal urethra, and it can be highly variable as a result of involuntary contractions of the smooth and striated muscles of the

Leak Point Pressures The VLPP is the intravesical pressure that exceeds the continence mechanism resulting in a leakage of urine in the absence of a detrusor contraction.38 The test is performed by a progressive Valsalva maneuver or cough.51 VLPP tests the strength of the urethra. The study is performed with the patient in the sitting or standing position with at least 150 to 200 mL of fluid in the bladder. Historically, a VLPP of less than 60 cm H2O was evidence of significant intrinsic sphincter deficiency (ISD), between 60 and 90 cm H2O suggested a component of ISD, and greater than 90 cm H2O suggested minimal ISD with leakage mainly due to hypermobility.48 Currently, no prospective studies have shown that VLPP less than 60 cm H2O can accurately diagnose ISD. Although the VLPP may be reproducible,52 it has not yet been standardized.5 There are limitations to a VLPP. If the patient’s Valsalva effort is inadequate, urinary leakage may not be seen, and a VLPP

Urethral Pressure Profile Urethral pressure is defined as the fluid pressure needed to just open a closed urethra. The urethral pressure measurements recorded are38 ■ ■

■ ■

urethral pressure profile (UPP), a graph indicating the intraluminal pressure along the length of the urethra maximum urethral closure pressure (MUCP), the maximum difference between the urethral pressure and the intravesical pressure functionalprofile length, the length of the urethra along which the urethral pressure exceeds intravesical pressure in women pressure transmission ratio, the increment in urethral pressure on stress as a percentage of the simultaneously recorded increase in intravesical pressure

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A

B Figure 57-4 A, Detrusor overactivity. The uninhibited contraction at the end of the filling phase leads to leakage (detrusor overactivity incontinence). EMG, electromyograhic tracing; Pabd, abdominal pressure; Pdet, detrusor pressure; Pves, intravesical pressure. B, Reduced bladder compliance. As the bladder is filled, the detrusor pressure rises by 50 cm H2O (ΔPdet) while the increase in bladder volume (ΔV) is 150 mL. The compliance (ΔV/ΔPdet) is 3 mL/cm H2O, which is much lower than the normal range of at least 30 mL/cm H2O. Griffiths D, Kondo A, Bauer S, et al: Dynamic testing. In Abrams P, Khoury S, Wein A (eds): Incontinence: Third International Consultation. Paris, France: Health Publications, 2005, pp 585-673.

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A

Figure 57-5 A, Resting urethral pressure profile. (Modified from Lose G: Urethral pressure measurements. In Cardozo L, Staskin D [eds]: Textbook of Female Urology and Urogynaecology. London: Isis Medical Media, 2001, pp 215-226.) B, Urethral pressure profile during coughs in a continent woman. The bottom trace shows the bladder response to a series of coughs (Pves). The middle trace shows the corresponding urethral responses (Pura) while the measuring catheter is slowly withdrawn out of the bladder and through the urethra. The top trace shows the difference between the middle and the bottom traces. The pressure transmission ratio (PTR) is the increment in urethral pressure on stress as a percentage of the simultaneously recorded increase in intravesical pressure: (ΔPura/ΔPves × 100%). (Modified from Lose G: Urethral pressure measurements. In Cardozo L, Staskin D [eds]: Textbook of Female Urology and Urogynaecology. London: Isis Medical Media, 2001, pp 215-226.)

10 to 52 cm H2O). However, despite this variability, the mean MUCP was less in stress-incontinent patients than in non–stressincontinent women, sometimes significantly so and sometimes not. Some of the variations are the result of different patient populations, and others are the result of technical errors. A weighted averaging of the mean values suggests that a normal (±SD) MUCP is about 54 ± 25 cm H2O. In stress-incontinent women, the corresponding figure is 39 ± 24 cm H2O. Clearly, there is so much overlap that it has been impossible to define a cutoff level that allows differentation between women with and without stress incontinence.5 Stress profiles show greater variability than static variables do. The within-subject standard deviation for the pressure transmission ratio varies between 13% and 18.5% (95% confidence limits up to ± 37%) in published reports. The coefficient if variation has been estimated to be 20% (95% confidence limits, ± 39%). Maximum urethral pressure (MUP), like MUCP, also declines with aging.60 There clearly are limitations to the test that prevent it from providing reliable pathophysiologic information.5 In summary, although the VLPP under ideal circumstances may indicate the severity of stress urinary incontinence, it is not clear whether it is more useful than clincal grading,5 and, although UPP measurements may be interesting as a research tool, their practical applicability is still to be determined.

B

urethral sphincter, possibly provoked by the catheter itself. Furthermore, the size, stiffness and type of catheter, rate of perfusion, patient position, and bladder volume affect the pressure readings.5 A variety of values of MUCP have been obtained by different authors in normal and abnormal female populations.5 They have several notable features. The first is the intercenter variability in the values reported, with mean MUCP varying from 36 to 101 cm H2O in subjects without stress incontinence. The second is the large intersubject standard deviation in most studies (from

Pressure-Flow Studies Pressure-flow studies are designed to provide dynamic information on the emptying phase of lower urinary tract function. Obstruction is not common in women61 but may be found after surgical correction of stress urinary incontinence or, less commonly, with detrusor sphincter dyssynergia, non-neurogenic voiding dysfunction, and, rarely, stricture disease. Interference with voiding may also be associated with pelvic organ prolapse. There are no established nomograms to depict pressure-flow relationships in women as there are in men (although one has been proposed62), but the pattern of high detrusor pressure and low urinary flow indicates obstruction (Fig. 57-6). Simultaneous cystography can demonstrate the level of obstruction. Detrusor pressure during voiding is characteristically low in women. A preoperative study that demonstrates a low detrusor pressure with a low flow rate may aid in counseling the patient about postoperative urinary retention after stress incontinence surgery. The urodynamic definition of obstruction in women is

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Figure 57-6 A and B, Videourodynamic study of a 62-year-old woman with urgency, frequency, and slow stream after multiple urethral dilatations. The study shows a normal bladder on filling, with no overactivity. Her voiding pressure exceeds 170 cm H2O, and her flow rate is low. There is a urethral stricture visible (arrow in B) with proximal urethral dilatation.

different than in men. A cutoff value of 12 mL/sec or less maximum flow rate and a detrusor pressure at maximum flow of 25 cm H2O or more, in conjunction with high clinical suspicion, provides good predictive value.63 Electromyography Sphincter electromyography (EMG) during videourodynamics is used to examine striated sphincter activity during filling and voiding. These are termed kinesiologic studies, and they can be performed with surface electrodes, vaginal or anal probes, or needles. Normal sphincter EMG activity has characteristic audio quality that may be monitored simultaneously. Its most important role is the identification of abnormal sphincter activity in patients with neurogenic bladder dysfunction and in those with behavioral voiding dysfunction.64 The fluoroscopy component, however, can demonstrate detrusor external sphincter dyssynergia in patients with suprasacral lesions and can show urethral obstruction in patients with dysfunctional voiding. EMG recordings are not usually necessary in routine videourodynamics for incontinence in women who have no neurologic abnormalities. Artifacts can occur secondary to room appliances, fluorescent lights, defective insulation, and patient movement.48 Videourodynamics Videourodynamics is a diagnostic tool that incorporates urodynamics with simultaneous imaging of the lower urinary tract. The incorporation of radiologic visualization of the lower urinary tract during bladder filling and voiding is useful for determining the site of bladder outlet obstruction, the integrity of the sphincter mechanism, and the presence of vesicoureteral reflux, bladder diverticula, fistulas, and trabeculation.40 Urodynamics was first

synchronized with cineradiography in the early 1950s through the pioneering efforts of E. R. Miller.65,66 The initial goal was to minimize the radiation exposure to the patient during cystourethrography. Originally, patient exposure to radiation was high when movies were taken, but with the advent of image intensifiers, video transduction, and, later, videotape recording, the patient exposure was reduced. This permitted bursts of continuous activity to be recorded during critical phases of lower urinary tract activity without overexposing the patient. Today, most studies can be done with less than 1 minute of fluoroscopy time.48 These developments have contributed to the wealth of information about lower urinary tract function and dysfunction. Modern videourodynamic techniques incorporate fluoroscopy, and the urodynamic machine has evolved from a strip chart recorder to a microcomputer. Videourodynamic studies are not necessary in every patient, and simpler studies frequently provide enough information to adequately delineate and treat the dysfunction. Videourodynamic studies are beneficial if simultaneous evaluation of function and anatomy is needed to provide detailed information about the whole or parts of the storage and emptying phases. Common indications well suited for videourodynamic evaluation include complex incontinence, in which the history does not fit with the findings on preliminary investigations; incontinence in women with previous anti-incontinence surgery; and incontinence in the face of a neurologic abnormality. Aside from the minimal radiation exposure to the patient, the only disadvantage of videourodynamics is its cost. This is a result of the time and effort of the personnel required and the expense of the equipment, which may limit its utility to larger centers with larger patient populations. The cost can, however, be justified by the utility of videourodynamics in solving complicated problems.

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helpful but not essential, as these values can be measured manually. The sphincter EMG channel is not necessary for routine clinical practice but can be helpful in patients with neurologic disease; its inclusion introduces another level of complexity and sophistication. For a review of the currently recommended urodynamic technique of pressure measurements the reader is referred to the article of Schaeffer and colleagues describing “Good Urodynamic Practices.”37

Figure 57-7 Diagram of a videourodynamic suite. The patient is in the upright position after the filling catheter has been removed. She will be asked to cough and strain to demonstrate stress incontinence and then to void. The left arrow indicates the multichannel recorder, and the right arrow indicates the transducers.

Figure 57-8 Schematic diagram of videourodynamic setup.

Components of Videourodynamics A typical arrangement for videourodynamic studies includes a multichannel recorder, a flouroscopy unit with a table that can be positioned in the supine and upright positions, and a flow meter (Figs. 57-7 and 57-8). A commode seat attachment facilitates fluoroscopic screening of voiding in the seated position, which is ideal for women. Most modern systems are computer based, which allows for complex analysis to be performed. Multichannel Recorder Because the procedure involves measuring simultaneous pressures during both phases of lower urinary tract function and flow during the voiding phase, a multichannel recorder is necessary. Many systems are available,67 most of which have dispensed with a strip chart output in favor of television monitor display of the procedure. The choice of components of the study is up to the individual clinician. Figure 57-8 illustrates possible inclusions. The channels demonstrating volume of fluid instilled and volume voided are

Fluoroscopy A good-quality fluoroscopy unit with a high-resolution image intensifier and a table that can function in both the supine and the erect position is required. Fluoroscopic images are obtained selectively during the filling and voiding study and are either superimposed on the pressure-flow tracing or displayed on a separate screen. The fluoroscopic images can be stored and reproduced individually or as continuous clips during key parts of the study. A recording of the procedure can be made for subsequent review. Because the contrast medium instilled into bladder is unlikely to be absorbed, we use the less expensive high-osmolality contrast media. A dilute solution of 1 L of Hypaque is prepared by the pharmacy and supplied in sterile intravenous bags. Videourodynamic Technique The patient reports for the study with a full bladder, and a flow rate is obtained. The equipment is zeroed, and the transducer is placed at a height adjacent to the upper edge of the patient’s symphisis pubis. Either a double-lumen catheter or two 8-Fr feeding tubes (one for filling, which is removed before the voiding study, and one for pressure measurements) are inserted into the bladder. Residual urine is measured. The rectal catheter is a 42-cm 14-Fr tube with a balloon over the tip. If desired, EMG recording devices may be applied to the patient. The study is conducted by a urodynamics specialist who is present in the room, communicates with the patient throughout the procedure, and records the findings manually and electronically. A supine or semioblique filling study is carried out, various measurements are taken during the study, and responses to actions such as Credé, cough, and Valsalva maneuvers are recorded. The filling rate is no longer divided into slow, medium, or fast but rather is described as physiologic or nonphysiologic.38 In practice, most clinicians use a medium fill rate of 50 to 75 mL/min.46 A commonly used method is to fill the bladder supine and then stand the patient up for provocative manoeuvres. During the study, recordings are made of bladder images in the filling phase in the supine and/or upright position (see Fig. 57-8). Anteroposterior (AP) and oblique views are obtained. The AP position permits documentation of reflux and its extent, and in the oblique position the course of the urethra can be seen separate from a cystocele. Notation is made of the bladder outline, the appearance of the bladder neck at rest, and its position relative to the inferior margin of the symphysis at rest and with straining and coughing. Leakage of urine with overactivity, decreased compliance, or leakage with various stress maneuvers is recorded. In the upright position, the presence of a cystocele and its relationship to the urethra are also noted. If the patient is able to void in front of the camera, the voiding phase (or parts of it) are recorded, along with the pressures and flow tracings. If the patient is unable to void with the catheters in place, they are removed, and a flow rate and voided volume are measured. Total fluoroscopy time is usually less than 1 minute.

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Table 57-1 Radiologic Type of Stress Incontinence Type

Description

0

Vesical neck and proximal urethra closed at rest and situated at or above the lower end of the symphysis pubis. They descend during stress, but incontinence is not seen. Vesical neck closed at rest and well above the inferior margin of the symphysis. During stress, the vesical neck and proximal urethra are open and descend less than 2 cm. Incontinence is seen. Vesical neck closed at rest and above the inferior margin of the symphysis. During stress, the vesical neck and proximal urethra open and descend more than 2 cm. Incontinence is seen. Vesical neck closed at rest and at or below the inferior margin of the symphysis. During stress, there may or may not be further descent but as the proximal urethra opens incontinence is seen. Vesical neck and proximal urethra are open at rest. The proximal urethra no longer functions as a sphincter. There is obvious urinary leakage with minimal increases in intravesical pressure.

I

IIa

IIb

III

From Blaivas JG, Olsson CA: Stress incontinence: Classification and surgical approach. J Urol 139:727-731, 1988.

The recorded study provides an opportunity for the case to be reviewed and discussed. All of the events of the study are recorded and displayed on the monitor during the study. The urodynamics machine is usually equipped with the capability of compressing the study so that it can be viewed on an ordinary letter-size sheet of paper. Urinary Incontinence The main advantage of fluoroscopic imaging during the urodynamic study is to obtain an anatomic view of the function or dysfunction. The technique is ideally suited to the evaluation of incontinence. A useful anatomic/radiologic classification of female incontinence, devised by Blaivas,68 is described in Table 57-1 and illustrated in Figure 57-9. We use this classification to determine the radiologic abnormality and add to it the information from the VLPP and the position of the urethra in relation to the cystocele to describe the functional problem. Each of the urodynamic tracings in the figures described in the next few paragraphs is shown in full with annotations made during the study. The video recordings depicting parts of the studies were obtained from a video printer connected to the fluoroscopy equipment. Type I abnormalities are illustrated in Figure 57-10; the patient had a VLPP of 62 cm H2O and minimal hypermobility. The patient in Figure 57-11 had a VLPP of more than 120 cm H2O on straining during upright filling. At the end of filling, a cough caused a large leak without much hypermobility and appeared to be accompanied by a small bladder contraction. This indicated that the patient had stress incontinence as well as cough-induced overactivity. Figures 57-12 thru 57-14 demonstrate type IIa abnormalities. The patient in Figure 57-12 has a high VLPP without any appreciable cystocele. In Figure 57-13, the patient has an involuntary detrusor contraction with incontinence in the upright position and a high VLPP. The patient shown in Figure 57-14 has a grade

II cystocele that appears with straining; she probably has mainly a lateral defect. Type IIb abnormalities are shown in Figures 57-15 thru 57-17. The bladder neck in Figure 57-15 is seen well below the lower margin of the symphysis and is associated with a grade II cystocele. Because the bladder neck is above the base of the cystocele but below the lower margin of the symphysis, the patient most likely has a combined central and lateral defect. In Figure 57-16, the large cystocele is not associated with demonstrable stress incontinence, despite coughing and straining pressures greater than 100 cm H2O. It appears to be primarily a central defect. Clinical examination must include reducing the cystocele and checking for stress incontinence. The patient in Figure 57-17 has a combined central and lateral defect. She has marked detrusor overactivity with leakage, but stress incontinence is not demonstrated, most likely because of the compressive effect of the cystocele. Type III incontinence or pure ISD is demonstrated by the patient in Figure 57-18. Her bladder neck is open at rest, no appreciable descent is seen with coughing or straining, and her VLPP is low at 59 cm H2O. Videourodynamic and fluoroscopic studies, in addition to demonstrating incontinence and degree of hypermobility, may also allow characterization of the type of cystocele (see Fig. 57-15). Obstruction Although outflow obstruction is uncommon in females, it is occasionally seen. The patient in Figure 57-6 had an iatrogenic and functionally significant urethral obstruction that was treated with a visual internal urethrotomy and subsequent long-term self-dilation. Pitfalls of Videourodynamics Patient cooperation, comfort, and compliance are necessary to obtain a meaningful and relevant study. Occasionally, an apprehensive patient has a vasovagal reflex and faint when the table is moved from the supine to the upright position, and the study cannot be completed. Moreover, stress incontinence may not be demonstrated in an anxious patient. Of 2259 studies that we reviewed in our laboratory for neurologically normal women whose chief complaint was stress incontinence, we were unable to demonstrate stress incontinence on fluoroscopy in 630 (28%). It is also difficult for many patients to void in front of the camera with catheters in the bladder and rectum and observers watching them. In our series, only 1348 patients (59.7%) were able to void, and some of these did so with abdominal straining. The others were unable to void during the procedure, and the voiding data was obtained from the uroflow measurements. To optimize visibility of the lower urinary tract on fluoroscopy, patient positioning must be correct. However, visibility may be poor or absent with very obese patients. The clinician must also maintain a dialogue with the patient to image crucial events, because the patient must relay changes in sensation during filling and may be the first to sense incontinence. The radiation equipment must be well maintained and undergo regular maintenance and safety inspections. The failure to maintain equipment may lead to inaccurate results. Because fluoroscopy time is short, radiation exposure to the patient is inconsequential; however, the clinician should use radiation protection, including aprons and thyroid shields.

Chapter 57 URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE

A

B

C

D

Figure 57-9 Schematic diagrams of the radiologic images obtained from women with the various types of female stress urinary incontinence. A, Type I. The bladder neck is closed at rest and is well above the inferior margin of the symphysis. During stress, the bladder neck and proximal urethra open and descend less than 2 cm, and incontinence is seen. B, Type IIa. The bladder neck is closed at rest and is above the inferior margin of the symphysis. During stress, the bladder neck and proximal urethra open and descend more than 2 cm. Incontinence is seen. C, Type IIb. The bladder neck is closed at rest and is at or below the inferior margin of the symphysis. During stress, there may or may not be further descent, but as the proximal urethra opens, incontinence is seen. D, Type III. The bladder neck and proximal urethra are open at rest. The proximal urethra no longer functions as a sphincter. There is obvious urinary leakage with minimal increases in intravesical pressure. (From Blaivas JG, Groutz A: Urinary incontinence: Pathophysiology, evaluation, and management overview. In Walsh PC, RetikAB, Vaughan ED Jr, Wein AJ [eds]: Campbell’s Urology, 8th ed. Philadelphia: Saunders, 2000, pp 1027-1052.)

Other pitfalls relate to the urodynamic aspects and are similar to those previously outlined by O’Donnell.69 Standardized terminology to communicate results and concepts should always be used.38 The testing procedures and equipment should be compatible with commonly accepted methodologies. The value and limitations of each measurement must be realized; for example, the VLPP may not be useful in the presence of a large prolapsing cystocele. To confirm reliability within a particular laboratory, it is necessary to have a high test-retest

correlation of studies. The validity of a test refers to its ability to measure what it is supposed to measure. The clinician must always be aware of the how the test in question compares to a “gold standard” test, which in urodynamics may be difficult to establish. The urodynamic studies should correlate with other clinical data. The voiding history, physical examination, endoscopic examination, and videourodynamic evaluation should serve to validate one another and strengthen the clinical assessment.

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Figure 57-10 A through C, Videourodynamic study of a 64-year-old gravida 0, para 0 woman with type I stress incontinence. She had a bladder capacity of more than 300 mL. The bladder neck was slightly open at rest (A). With coughing, there was a small amount of descent and Valsalva leak point pressure was 62 cm H2O. She had no apparent cystocele, and her voiding phase was normal.

Figure 57-11 A through D, Videourodynamic study of a 74-year-old gravida 2, para 2 woman with type I stress incontinence. The bladder neck is slightly open at rest (A). In the upright position (B), leaks occur with straining and a Valsalva leak point pressure of 122 cm H2O is recorded. On coughing (C), leaking is followed by a detrusor contraction (arrow). Voiding is normal (D).

Chapter 57 URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE

Figure 57-12 A and B, Videourodynamic study of a 47-year-old gravida 1, para 1 woman with type IIa stress incontinence. Her bladder neck is open at rest (A). Leakage and hypermobility are seen with coughing (B).

Figure 57-13 A through C, Videourodynamic study of a 52-year-old gravida 2, para 2 woman with a type IIa abnormality who complained of both stress and urgency incontinence. The bladder neck is slightly open at rest (A). She has an involuntary detrusor contraction (arrow) on upright filling that results in incontinence (B). With straining, leaking occurred, with a Valsalva leak point pressure of more than 140 cm H2O (C).

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Figure 57-14 A and B, Videourodynamic study of a 64-year-old gravida 2, para 2 woman with type IIa stress incontinence. Her bladder neck is well supported on upright filling (A). With straining, leaking occurs with a Valsalva leak point pressure of 144 cm H2O, and a cystocele is demonstrated (B). She most likely has mainly a lateral defect.

Figure 57-15 A and B, Videourodynamic study of a 62-year-old gravida 5, para 5 woman with type IIb stress incontinence. Her bladder neck (arrow) on filling (A) is below the lower margin of the inferior symphysis, and a cystocele is seen. She most likely has a combined central and lateral defect. She has leakage with coughing (B) and a Valsalva leak point pressure of 62 cm H2O on straining.

Chapter 57 URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE

Figure 57-16 Videourodynamic study of a 75-year-old gravida 1, para 1 woman with a large cystocele. Although she complained of stress incontinence, it is not visible on this study. The bladder neck (arrow) is at the lower margin of the symphysis. The cystocele appears primarily to be a central defect. Clinical evaluation must include reducing the cystocele and testing for stress incontinence.

Figure 57-17 Videourodynamic study of an 81-year-old gravida 1, para 1 woman with a central and lateral defect. The bladder neck is below the symphysis (arrow on image). She has marked detrusor overactivity on supine and upright filling (arrows on graph). Although she complained of stress incontinence in addition to urge incontinence, it is not demonstrated on this study.

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Figure 57-18 A and B, Videourodynamic study of a 69-year-old gravida 3, para 3 woman with type III abnormality after two previous stress incontinence repairs. Her bladder neck is open at rest (arrow in A). There is almost no urethral movement on straining (B), and her Valsalva leak point pressure is 59 cm H2O.

ROLE OF URODYNAMICS IN PREDICTING OCCULT STRESS INCONTINENCE IN WOMEN DUE TO BE TREATED FOR PROLAPSE The problem of occult stress incontinence in women due to be treated for prolapse was reviewed in the recent Third International Consultation on Urinary Incontinence.5 It has been reported that 11% to 22% of continent women undergoing vaginal repair for large cystocele develop stress incontinence after surgical repair.70,71 Therefore, it would be helpful to have a test that predicts for the occurrence of occult stress incontinence, if stress incontinence has not been present preoperatively, either symptomatically or by reducing the prolapse. According to the literature, advanced age, incontinence before development of pelvic organ prolapse, and extensive dissection at the time of the repair seem to increase the risk of postoperative incontinence. There are a number of studies that report the finding of unmasked stress incontinence on videourodynamic testing in 25% to 83% of patients.72,73 Low-pressure urethras are also seen after prolapse reduction in 20% to 56% of individuals13,73; however, stress profiles are not particularly reliable measures. Urethral hypermobility is correlated with the degree of prolapse,15 as is detrusor overactivity revealed by prolapse reduction. The literature emphasizes the importance of urodynamic assessment with prolapse reduction to assess occult stress incontinence and possibly detrusor overactivity.72,74-76 However, there are no studies assessing reproducibility or testing whether incontinence revealed by prolapse reduction occurs after surgery if no

procedures are done to prevent it. The prophylactic use of the Pereyra or Kelly procedure does not reduce the risk of postoperative incontinence.77-79 In a recently reported randomized, prospective study,80 concomitant Burch colposuspension was shown to significantly reduce the incidence of postoperative stress incontinence after abdominal sacropcolpopexy. Before surgery, about 36% of both groups had occult stress incontinence on urodynamics. Postoperatively, the control group had an incidence of 24.5%, compared with 6.1 in the colposuspension group (P < .0001). In those patients with no leakage detected on urodynamics preoperatively, the Burch procedure reduced the postoperative incidence from 38.2% to 20.8% (P = .0007). Questions remain about the reproducibility and predictability of urodynamics in prolapse. In the randomized controlled trial just described, Burch colposuspension significantly reduced postoperative stress incontinence regardless of the preoperative urodynamic findings.80 Another study concluded that urodynamic testing before prolapse surgery was not cost-effective.76 Therefore, we do not have a consistently reliable test that identifies and determines appropriate management of occult stress urinary incontinence.5 CONCLUSION Detailed clinical assessment of the patient with prolapse is essential in deciding therapy. Urodynamic studies provide additional information about the various symptoms of which the patient may or may not be complaining. Uroflowmetry and postvoid

Chapter 57 URODYNAMIC EVALUATION OF THE PATIENT WITH PROLAPSE

residual urine measurement are good screening tests for voiding dysfunction. More invasive testing may be helpful in many cases, including those involving complex or recurrent symptoms. Although there are benefits of urodynamic studies, in that the

lower urinary tract problem may be more clearly elucidated, overall there still exists a lack of evidence of reproducibility and predictive value in assigning treatments and determining outcomes.

References 1. Mouritsen L, Larsen JP: Symptoms, bother and POPQ in women referred with pelvic organ prolapse. Int Urogynecol J Pelvic Floor Dysfunct 14:122-127, 2003. 2. Burrows LJ, Meyn LA, Walters MD, Weber AM: Pelvic symptoms in women with pelvic organ prolapse. Obstet Gynecol 104(5 Pt 1): 982-988, 2004. 3. Swift SE, Tate SB, Nicholas J: Correlation of symptoms with degree of pelvic organ support in a general population of women: What is pelvic organ prolapse? Am J Obstet Gynecol 189:372-377; discussion 377-379, 2003. 4. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. 5. Griffiths D, Kondo A, Bauer S, et al: Dynamic testing. In Abrams P, Khoury S, Wein A (eds): Incontinence: Third International Consultation. Paris, France: Health Publications, 2005, pp 585-673. 6. Glazener CM, Lapitan MC: Urodynamic investigations for management of urinary incontinence in adults. Cochrane Database Syst Rev 3:CD003195, 2002. 7. Blaivas JG, Groutz A: Urinary incontinence: Pathophysiology, evaluation, and management overview. In Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds): Campbell’s Urology, 8th ed. Philadelphia: Saunders, 2000, pp 1027-1052. 8. McGuire EJ: Bladder instability and stress incontinence. Neurourol Urodyn 7:563-567, 1988. 9. Fantl JA, Wyman JF, McClish DK, Bump RC: Urinary incontinence in community-dwelling women: Clinical, urodynamic, and severity characteristics. Am J Obstet Gynecol 162:946-951; discussion 951942, 1990. 10. Fantl JA, Newman DK, Colling J, et al: Urinary Incontinence in Adults: Acute and Chronic Management. Clinical Practice Guideline No. 2 Update. AHCPR Publication No. 96-0682. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, March 1996. 11. Fianu S, Kjaeldgaard A, Larson B: Preoperative screening for latent stress incontinence in women with cystocele. Neurourol Urodyn 4:3, 1985. 12. Bump RC, Fantl JA, Hurt WG: The mechanism of urinary continence in women with severe uterovaginal prolapse: Results of barrier studies. Obstet Gynecol 72(3 Pt 1):291-295, 1988. 13. Rosenzweig B, Pushkin S, Blumenfeld D, Bhatia N: Prevalence of abnormal urodynamic test results in continent women with severe genitourinary prolapse. Obstet Gynecol 79:539-542, 1992. 14. Romanzi LJ: Management of the urethral outlet in patients with severe prolapse. Curr Opin Urol 12:339-344, 2002. 15. Romanzi LJ, Chaikin DC, Blaivas JG: The effect of genital prolapse on voiding. J Urol 161:581-586, 1999. 16. American College of Obstetricians and Gynecologists: Pelvic organ prolapse. ACOG Technical Bulletin No. 214. Washington, DC: ACOG; 1995. 17. Fantl JA, Wyman JF, McClish DK, et al: Efficacy of bladder training in older women with urinary incontinence. JAMA 265:609-613, 1991. 18. Nguyen JK, Bhatia NN: Resolution of motor urge incontinence after surgical repair of pelvic organ prolapse. J Urol 166:2263-2266, 2001. 19. Donovan J, Bosch R, Gotoh M, et al: Symptom and quality of life assessment. In Abrams P, Cardozo L, Khoury S (eds): Incontinence 3rd International Consultation. Paris: Health Publications, 2005, pp 519-584.

20. Tan JS, Lukacz ES, Menefee SA, et al: Predictive value of prolapse symptoms: A large database study. Int Urogynecol J Pelvic Floor Dysfunct 16:203-209; discussion 209, 2005. 21. Coates KW, Harris RL, Cundiff GW, Bump RC: Uroflowmetry in women with urinary incontinence and pelvic organ prolapse. Br J Urol 80:217-221, 1997. 22. Nitti VW, Tu LM, Gitlin J: Diagnosing bladder outlet obstruction in women. J Urol 161:1535-1540, 1999. 23. Chassagne S, Bernier PA, Haab F, et al: Proposed cutoff values to define bladder outlet obstruction in women. Urology 51:408-411, 1998. 24. Klarskov P, Andersen JT, Asmussen CF, et al: Acute urinary retention in women: A prospective study of 18 consecutive cases. Scand J Urol Nephrol 21:29-31, 1987. 25. Abrams P, Andersson KE, Brubaker L, et al: Recommendations of the International Scientific Committee: Evaluation and treatment of urinary incontinence, pelvic organ prolapse and faecal incontinence. In Abrams P, Cardozo L, Khoury S, Wein A (eds). Third International Consultation on Urinary Incontinence. Paris: Health Publications, 2005, pp 1589-1630. 26. Diokno AC, Dimaculangan RR, Lim EU, Steinert BW: Office based criteria for predicting type II stress incontinence without further evaluation studies. J Urol 161:1263-1267, 1999. 27. Nitti VW, Combs AJ: Correlation of Valsalva leak point pressure with subjective degree of stress urinary incontinence in women. J Urol 155:281-285, 1996. 28. Lemack GE, Zimmern PE: Predictability of urodynamic findings based on the Urogenital Distress Inventory-6 questionnaire. Urology 54:461-466, 1999. 29. Lemack GE, Zimmern PE: Identifying patients who require urodynamic testing before surgery for stress incontinence based on questionnaire information and surgical history. Urology 55:506-511, 2000. 30. Weber AM, Taylor RJ, Wei JT, et al: The cost-effectiveness of preoperative testing (basic office assessment vs. urodynamics) for stress urinary incontinence in women. BJU Int 89:356-363, 2002. 31. Bergman A, Bader K: Reliability of the patient‘s history in the diagnosis of urinary incontinence. Int J Gynaecol Obstet 32:255-259, 1990. 32. Versi E, Cardozo L, Anand D, Cooper D: Symptoms analysis for the diagnosis of genuine stress incontinence. Br J Obstet Gynaecol 98:815-819, 1991. 33. Haeusler G, Hanzal E, Joura E, et al: Differential diagnosis of detrusor instability and stress-incontinence by patient history: The Gaudenz-Incontinence-Questionnaire revisited. Acta Obstet Gynecol Scand 74:635-637, 1995. 34. Amundsen C, Lau M, English SF, McGuire EJ: Do urinary symptoms correlate with urodynamic findings? J Urol 161:1871-1874, 1999. 35. Weidner AC, Myers ER, Visco AG, et al: Which women with stress incontinence require urodynamic evaluation? Am J Obstet Gynecol 184:20-27, 2001. 36. Lemack GE: Urodynamic assessment of patients with stress incontinence: How effective are urethral pressure profilometry and abdominal leak point pressures at case selection and predicting outcome? Curr Opin Urol 14:307-311, 2004. 37. Schafer W, Abrams P, Liao L, et al: Good urodynamic practices: Uroflowmetry, filling cystometry, and pressure-flow studies. Neurourol Urodyn 21:261-274, 2002. 38. Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology of lower urinary tract function: Report from the Standardisation

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39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57.

58. 59. 60.

Sub-committee of the International Continence Society. Neurourol Urodyn 21:167-178, 2002. Haylen BT, Ashby D, Sutherst JR, et al: Maximum and average urine flow rates in normal male and female populations: The Liverpool nomograms. Br J Urol 64:30-38, 1989. Blaivas JG: Techniques of evaluation. In Yalla SV, McGuire EJ, Elbadawi A, Blaivas JG (eds): Neurourology and Urodynamics: Principles and Practice. New York: MacMillan, 1988. Kondo A, Mitsuya H, Torii H: Computer analysis of micturition parameters and accuracy of uroflowmeter. Urol Int 33:337-344, 1978. Costantini E, Mearini E, Pajoncini C, et al: Uroflowmetry in female voiding disturbances. Neurourol Urodyn 22:569-573, 2003. Haylen BT, Law MG, Frazer M, Schulz S: Urine flow rates and residual urine volumes in urogynecology patients. Int Urogynecol J Pelvic Floor Dysfunct 10:378-383, 1999. Lemack GE, Baseman AG, Zimmern PE: Voiding dynamics in women: A comparison of pressure-flow studies between asymptomatic and incontinent women. Urology 59:42-46, 2002. Massey A, Abrams P: Urodynamics of the female lower urinary tract. Urol Clin North Am 12:231-246, 1985. Abrams P, Blaivas JG, Stanton SL, Andersen JT: Standardisation of of lower urinary tract function. Neurourol Urodyn 7:403-427, 1988. Bates P, Bradley WE, Glen E, et al: The standardization of terminology of lower urinary tract function. Eur Urol 2:274-276, 1976. Webster GD, Guralnick MS: The neurourologic evaluation. In Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds). Campbell’s Urology, 8th ed. Philadelphia: WB Saunders, 2002, pp 900-930. Awad SA, Flood HD, Acker KL: The significance of prior antiincontinence surgery in women who present with urinary incontinence. J Urol 140:514-517, 1988. McGuire EJ, Lytton B, Kohorn EI, Pepe V: The value of urodynamic testing in stress urinary incontinence. J Urol 124:256-258, 1980. McGuire EJ, Fitzpatrick CC, Wan J, et al: Clinical assessment of urethral sphincter function. J Urol 150(5 Pt 1):1452-1454, 1993. McGuire EJ, Leng WW: Leak-point pressures. In Cardozo L, Staskin D (eds): Textbook of Female Urology and Urogynaecology. London: Isis Medical Media, 2001, pp 225-237. Maniam P, Goldman HB: Removal of transurethral catheter during urodynamics may unmask stress urinary incontinence. J Urol 167:2080-2082, 2002. McGuire EJ, Woodside JR, Borden TA, Weiss RM: Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 126:205209, 1981. Blaivas JG: Cystometry. In Blaivas JG (ed): Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996, pp 31-47. Woodside JR, McGuire EJ: Technique for detection of detrusor hypertonia in the presence of urethral sphincteric incompetence. J Urol 127:740-743, 1982. Lose G, Griffiths D, Hosker G, et al: Standardisation of urethral pressure measurement: Report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 21:258-260, 2002. Lose G: Urethral pressure measurements. In Cardozo L, Staskin D (eds): Textbook of Female Urology and Urogynaecology. London: Isis Medical Media, 2001, pp 215-226. Sand PK, Bowen LW, Panganiban R, Ostergard DR: The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 69(3 Pt 1):399-402, 1987. Schick E, Tessier J, Bertrand PE, et al: Observations on the function of the female urethra: I. Relation between maximum urethral closure pressure at rest and urethral hypermobility. Neurourol Urodyn 22:643-647, 2003.

61. Farrar D, Warwick RT: Outflow obstruction in the female. Urol Clin North Am 6:217-225, 1979. 62. Groutz A, Blaivas JG, Chaikin DC: Bladder outlet obstruction in women: Definition and characteristics. Neurourol Urodyn 19:213220, 2000. 63. Defreitas GA, Zimmern PE, Lemack GE, Shariat SF: Refining diagnosis of anatomic female bladder outlet obstruction: Comparison of pressure-flow study parameters in clinically obstructed women with those of normal controls. Urology 64:675-679; discussion 679-681, 2004. 64. Fowler C: Electromyography. In Blaivas JG (ed): Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996, pp 60-76. 65. Enhoerning G, Miller ER, Hinman F Jr: Urethral closure studied with cineroentgenography and simultaneous bladder-urethra pressure recording. Surg Gynecol Obstet 118:507-516, 1964. 66. Miller E: The beginnings. Urol Clin North Am 6:7-9, 1979. 67. Blaivas JG: Deciding on the right urodynamic equipment. In Blaivas JG (ed): Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996, pp 19-28. 68. Blaivas JG, Olsson CA: Stress incontinence: Classification and surgical approach. J Urol 139:727-731, 1988. 69. O’Donnell PD: Pitfalls of urodynamic testing. Urol Clin North Am 18:257-268, 1991. 70. Beck RP, McCormick S, Nordstrom L: A 25-year experience with 519 anterior colporrhaphy procedures. Obstet Gynecol 78:10111018, 1991. 71. Borstad E, Rud T: The risk of developing urinary stress-incontinence after vaginal repair in continent women: A clinical and urodynamic follow-up study. Acta Obstet Gynecol Scand 68:545-549, 1989. 72. Versi E, Lyell DJ, Griffiths DJ: Videourodynamic diagnosis of occult genuine stress incontinence in patients with anterior vaginal wall relaxation. J Soc Gynecol Investig 5:327-330, 1998. 73. Veronikis DK, Nichols DH, Wakamatsu MM: The incidence of lowpressure urethra as a function of prolapse-reducing technique in patients with massive pelvic organ prolapse (maximum descent at all vaginal sites). Am J Obstet Gynecol 177:1305-1313; discussion 1313-1304, 1997. 74. Ghoniem GM, Walters F, Lewis V: The value of the vaginal pack test in large cystoceles. J Urol 152:931-934, 1994. 75. Marinkovic SP, Stanton SL: Incontinence and voiding difficulties associated with prolapse. J Urol 171:1021-1028, 2004. 76. Weber AM, Walters MD: Cost-effectiveness of urodynamic testing before surgery for women with pelvic organ prolapse and stress urinary incontinence. Am J Obstet Gynecol 183:1338-1346; discussion 1346-1337, 2000. 77. Gordon D, Groutz A, Wolman I, et al: Development of postoperative urinary stress incontinence in clinically continent patients undergoing prophylactic Kelly plication during genitourinary prolapse repair. Neurourol Urodyn 18:193-197; discussion 197-198, 1999. 78. Colombo M, Maggioni A, Scalambrino S, et al: Surgery for genitourinary prolapse and stress incontinence: A randomized trial of posterior pubourethral ligament plication and Pereyra suspension. Am J Obstet Gynecol 176:337-343, 1997. 79. Bump RC, Hurt WG, Theofrastous JP, et al: Randomized prospective comparison of needle colposuspension versus endopelvic fascia plication for potential stress incontinence prophylaxis in women undergoing vaginal reconstruction for stage III or IV pelvic organ prolapse. The Continence Program for Women Research Group. Am J Obstet Gynecol 175:326-333; discussion 333-325, 1996. 80. Brubaker L, Cundiff GW, Fine P, et al: Abdominal sacrocolpopexy with Burch colposuspension to reduce urinary stress incontinence. N Engl J Med 354:1557-1566, 2006.

Chapter 58

NONSURGICAL TREATMENT OF VAGINAL PROLAPSE: DEVICES FOR PROLAPSE AND INCONTINENCE Peggy A. Norton NONSURGICAL TREATMENT OF VAGINAL PROLAPSE Surgery for pelvic floor disorders such as stress urinary incontinence and pelvic organ prolapse (POP) is aimed at restoring or improving the function of the pelvic organs. By its nature, such functional surgery cannot be guaranteed to restore continence and support to its original state. Up to one third of surgeries for pelvic floor disorders fail.1 Given these facts, many women are interested in nonsurgical options for vaginal prolapse that offer less risk and expense. Once fitted, patients are immediately aware of whether the device is comfortable and whether it is effective in treating the condition. Although use of these devices should not be viewed as a permanent solution for prolapse, many women successfully use them for many years without much bother. Such devices are widely available but require some professional intervention to determine correct use and fit, similar to fitting a contraceptive diaphragm. Little has been published on the use of vaginal devices for prolapse, possibly because there is no industry support for (or profit from) conducting properly controlled clinical trials.

Indications for Pessary Use Indications for a pessary in the management of POP include patient desire for nonsurgical management of the condition. Traditionally, this group of patients has included those few women who are unable to undergo surgical management because of medical problems. But there are many women who might be interested in a pessary, because it manages the prolapse without the need to undergo surgery. In our practice, pessaries are used successfully in women who cannot take time off for surgery, such as mothers with small children at home and women with busy careers outside the home. Willingness to use a vaginal device may be cultural, especially in areas where contraceptive diaphragms are used. Prashar and colleagues2 found that only a fifth of 104 women who presented to a community continence clinic in Australia felt very comfortable about inserting a device into the vagina (and half felt uncomfortable). In our practice at the University of Utah, most women who are believed to be good candidates for a pessary trial are readily fitted and can demonstrate removal and replacement of the device. Clemons and colleagues3 successfully fitted threequarters of patients with POP with a pessary. It has even been suggested that use of a pessary longer than 1 year may have some therapeutic effect, in that a minority of users have an improvement in prolapse stage.4

Patient Selection In addition to a patient’s interest in nonsurgical management, there are physical factors that favor use of a pessary. The best clinical situation is an anterior and/or apical defect (cystocele, uterine prolapse, vaginal vault prolapse) in a woman with adequate vaginal capacity, a narrow pubic arch, and good pelvic floor strength. This is because the ventral edge of a pessary is held behind the pubic rami, and a wide arch would allow extrusion of the device. Likewise, the dorsal edge of the pessary is braced by the pelvic floor muscles. In the absence of these factors, one must consider the use of pessaries that utilize suction or inflation (see later discussion). An isolated posterior wall defect (rectocele) is more difficult to manage with a pessary, because the force vectors act to extrude the pessary. If the vaginal capacity is reduced after surgery, a narrower pessary may be needed (e.g., oval, Hodge, cube). Other reported risk factors for pessary failure include a shortened vagina and a wide levator hiatus.3 Selection of a Pessary Vaginal pessaries have been used for many centuries, but improvements in materials and design have increased the usefulness of these devices for prolapse. Most are made of silicone (latex-free), are flexible to allow easier placement and removal, and should last for several years with proper care. Sources for vaginal pessaries are listed in Table 58-1. Supportive Pessaries Supportive pessaries (which depend on some levator muscle support to stay in place) include the Gehrung, Hodge, and Schatz designs, as well as rings and ovals with support. Although individual practices may vary, flexible ring pessaries and Gelhorn pessaries are used most commonly. Members of the American Urogynecologic Society (AUGS) were surveyed by Cundiff and colleagues,5 and more than three quarters of respondents reported that they tailored the pessary to the defect. A ring pessary was more common for anterior and apical defects, a Gelhorn was more common for large Stage III and IV prolapse, and a donut pessary was used for posterior defects. Twenty-two percent of respondents used the same pessary, usually a ring pessary, for all support defects. One questionnaire study of gynecologists reported that ring and donut pessaries were the types most commonly used.6 In a tertiary referral practice in Texas, Sulak and colleagues7 used a Gelhorn pessary in 96 of 107 women with symptomatic POP. Because many of the women desiring pessary use have stage II prolapse, the pessary we use most at the 603

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Table 58-1 Sources for Vaginal Pessaries Web Site Address

Description

http://www.milexproducts.com/products/pessaries Milex Products Online Catalog?? http://www.urology.coloplast.com/pelvic-organ-prolapse/evacare EvaCare formerly prod. by Mentor, not Coloplast; Mentor bought DesChutes incontinence line in 2000, maybe sold it now?; site has only breast info & press releases re these items. www.urology.coloplast.com/bladder-control/incontinencewomen/index.htm?? http://www.augs.org

Source for many continence devices, including continence dish, rings, other pessaries with knobs, and so on. Patient information source for EvaCare continence devices including continence dish. Source for intravaginal continence devices.

University of Utah is the ring with support in sizes 3 and 4 (size refers to diameter in centimeters.) Supportive pessaries are the easiest pessaries to use because they fold to a smaller dimension for insertion. Many of them, because they are similar to a contraceptive diaphragm, permit coitus while wearing the device. Perhaps because they are easier to manage, supportive pessaries may not be sufficient to support large prolapses. Pessaries are easiest to insert lying down, easiest to remove standing up, and may require digital bracing per vaginum during bowel movements. Some women have difficulty removing the pessary, and in the past some pessaries came with removal strings that became malodorous over time. Instead, we recommend tying a strand of dental floss around the ring, so that the pessary can be pulled out by the floss, and renewing the floss each time. Space-Occupying Pessaries Space-occupying pessaries include the cube, donut, Gelhorn, and inflatoball. These pessaries are more difficult to insert and remove, but they work in situations in which other devices would be extruded: with larger prolapse, poor pelvic floor strength, or wider pubic arch. Of these, we use the donut and the Gelhorn with the most frequency. The donut is simply pushed into the vagina quickly, and it is easiest to use in women without significant atrophy or scarring. The Gelhorn is held by the knob, aligned along an almost vertical axis (but sparing the urethra) and rapidly inserted, then adjusted so that the knob faces the introitus or posterior distal vagina. We have not found that pinching the flexible disk of the Gelhorn makes much difference to the relative discomfort with which this pessary is placed. To remove the Gelhorn, an index finger should be inserted to break the slight suction seal of the disk in the vagina, and the thumb and index finger of the other hand may grasp and pull the knob. Occasionally, we use a ring forceps to grasp the knob and bring it to the introitus. Although insertion and removal of the Gelhorn sounds daunting, it is a highly successful pessary for large prolapses, and with practice this pessary is inserted and removed on a regular basis in many patients. The cube has a relative suction effect and may be effective in cases of lax vaginal walls, but it generates significant discharge and in our experience is more prone to excoriation and ulceration than other pessaries. The inflatoball is

Web site for the American Urogynecologic Society, with sites for members and patients. For bladder diaries and bladder retraining, click on information for women, diagnostic and treatment information on overactive bladder/urge incontinence. Information on pelvic floor muscle training (Kegel exercises) is also available.

pumped up with a small bulb and is similarly prone to excoriation unless care is taken. Care and Long-Term Use of a Vaginal Pessary Postmenopausal women may benefit from vaginal estrogen. This has little systemic absorption, may increase vaginal skin thickness and tolerance of the device, and is best given as a vaginal pill (Vagifem 25 μg, Novo Nordisk, Princeton, NJ) once nightly for 10 nights, then twice weekly thereafter. After an initial follow-up examination to demonstrate efficacy and self-management, women who manage their own pessary without difficulty may be seen annually. Women may need to brace the device digitally during straining for bowel movements to prevent extrusion. A device that is easily dislodged or uncomfortable is not satisfactory and should be removed and replaced. Care of a vaginal pessary depends on the type used. Because it is easy to remove and reinsert, we recommend that women remove the ring pessary at least weekly, wash it with soap and water, leave it out overnight, and then reinsert in the morning. In our experience, women rarely encounter excessive or malodorous vaginal discharge using this approach and therefore have little use for creams other than estrogen. Space-occupying pessaries are sometimes difficult for a woman to remove on her own. In such cases, we try to individualize the intervals between insertions. We may ask a patient with a donut or Gelhorn device to return for reexamination within a few weeks. If discharge is minimal and no erosions are present, we examine next at 4 weeks and then at increased intervals. The appropriate pessary interval is either a maximum of 3 months or the interval at which foul-smelling discharge or early erosions appear. For women who can remove and replace their own pessaries, we schedule a follow-up evaluation within 1 month of placement and then monitor the patient annually, depending on her comfort level. For women who retain the pessary for several months at a time, we believe that a visual inspection of the vagina should occur at least twice yearly. It is important to examine the anterior and posterior vaginal walls during the examination (by turning the speculum 90 degrees), as well as the obvious lateral walls that are visible when the speculum is placed in the usual fashion. This

Chapter 58 NONSURGICAL TREATMENT OF VAGINAL PROLAPSE: DEVICES FOR PROLAPSE AND INCONTINENCE

vaginal inspection is not only important in preventing erosions from the pessary, but it can offset the poor compensation for pessary placement in individual practices. If an area of redness or erosion is seen, the patient is asked to remove the device more often, use vaginal estrogen, and even consider leaving the device out for a week or two. Clinical Outcomes Several series have demonstrated that POP can be managed with pessary use. In one study by Wu and colleagues,8 of the 62 women that used a pessary for more than 1 month, 66% were still using it after 12 months. In Sulak’s series,7 half of women continued to use the pessary at the time of manuscript preparation (average duration of use, 16 months). Clemons and coworkers9 (2004) prospectively evaluated women with symptomatic POP, and 73 of 100 women were satisfied with their pessary at 1 week. At 2 months, only 3% of women endorsed feeling a bulge, compared to 90% at baseline. Other symptoms that improved included pressure, discharge, and splinting. One third of women had urge incontinence at baseline; this improved in 54%. Twenty-three percent had voiding difficulty at baseline, which improved in half. At 2 months, 92% were either very or somewhat satisfied with their pessary. Ring pessaries were used more with stage II and III prolapse (100% and 71%, respectively), whereas Gelhorn pessaries were used more with stage IV prolapse (64%, P < .001). Factors associated with long-term pessary use included older age (76 versus 61 years; P < .001) and poor surgical risk (26% versus 0%; P = .03). Characteristics that were associated with women going on to surgery were sexual activity, the presence of stress incontinence (a coexisting problem that may not be helped by a vaginal pessary for prolapse), and desire for surgery at the first visit. Age 65 years was the best cutoff value for continued pessary use, with a sensitivity of 95% (95% confidence interval [CI], 84% to 99%) and a positive predictive value of 87% (95% CI, 74% to 94%). Logistic regression demonstrated that age greater than or equal to 65 years (P < .001), stage III-IV posterior vaginal wall prolapse (P = .007), and desire for surgery (P = .04) were independent predictors In contrast, other researchers have found that pessary use is acceptable to women who are sexually active. Brincat and colleagues10 reviewed 136 women who initiated pessary treatment for POP or urinary incontinence over a 2-year period. Of the 60% of women who became long-term pessary users, those who were more likely to continue pessary use were those who were using

the pessary for treatment of prolapse and those who were sexually active. Recommendations for Initiating Pessary Use Wu and colleagues8 recommended a simple management strategy in which a flexible ring pessary with support was the first pessary tried, and 70% of patients were successfully fitted with a size 3, 4, or 5 ring. In Utah, many urologists and gynecologists keep a few simple pessaries in their practice for fitting. A number 3 or 4 ring pessary with support can be inserted, and, if appropriate, a prescription can be written and the pessary ordered through a pharmacy. The fitting pessary can then be sterilized for refitting. Alternatively, a few high-volume urogynecologic practices keep large numbers of pessary types and sizes. Once fitted, patients return to their clinician for long-term management. This practice is more feasible for pessaries such as the Gelhorn. If the patient is postmenopausal, a 2- to 3-week course of vaginal estrogen is recommended, and a pessary may be ordered in the interval for placement in the office. NONSURGICAL TREATMENT OF URINARY INCONTINENCE In women, treatment of urge urinary incontinence (overactive bladder) is primarily pharmacologic and behavioral. Although stress urinary incontinence can be treated surgically, many women choose nonsurgical options such as intravaginal devices and new pharmacologic treatments. Both types of urinary incontinence may benefit from lifestyle interventions, physical therapy, biofeedback, bladder retraining, and behavioral modifications. Mixed urge and stress incontinence is sometimes treated as two separate entities, although there is increasing evidence that both components of mixed incontinence may respond to treatments aimed at a single type of incontinence, such as anticholinergics/ antimuscarinics and combination selective serotonin/norepinephrine reuptake inhibitors (SSRI/NERIs). A consensus conference on urinary incontinence was sponsored by the World Health Organization in 2001, and levels of evidence for many of nonsurgical treatments were summarized by Wilson and associates11 (Table 57-2). We consider here the use of devices for stress urinary incontinence. Intravaginal devices work by creating a “backstop” at the level of the bladder neck. Devices that have been studied include a short super tampon inserted just inside the vagina, a Hodge pessary placed backward and upside down, and a variety of

Table 58-2 Device and Pharmacologic Treatments for Urinary Incontinence Device or Treatment

Efficacy

Effort

Evidence

Continence devices Intravaginal (pessary-like) devices Occlusive urethral devices (not currently marketed) Intraurethral devices (not currently marketed)

Moderate to high Moderate High

Low to moderate Low to moderate Moderate

Scant 1-2 Level 3-4 Level 2-3

Pharmacologic treatments Of overactive bladder Of stress urinary incontinence Of mixed urinary incontinence

Moderate Moderate Moderate

Low but expensive Low, no cost estimates Low

Level 1 Level 1 Level 1

Adapted from Wilson D, et al., 2002.

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Section 7 FEMALE ORGAN PROLAPSE

Table 58-3 Studies of Devices for Stress Urinary Incontinence Device and Ref. No. Smith-Hodge pessary

12

RCT of super tampon and Hodge pessary13 Bladder neck support prosthesis15 (no current distributor)

N

Indication

Follow-up

Outcome

30

Stress incontinence

None

18

Exercise-induced stress incontinence Stress and mixed Incontinence

None

Cough pressure profile; 24/30 patients continent 36% of pessary users continent; 58% of tampon users continent On subjective pad test, 29% continent, 51% decreased severity by more than half; 81% had combined subjective/ objective some or maximum benefit 53/70 completed trial; significant improvement on pad tests, diaries; high subjective improvement and quality of life 6/38 continued device use long term; improved scores on pad test, voiding diary 59% continued use long term, with significant reduction in incontinence

77

12 wk

Bladder neck support prosthesis16 (no current distributor)

70

Stress or mixed incontinence

4 wk

Continence ring pessary17

38

Stress incontinence

1 yr

Variable continence pessaries18

100

11 mo

Continance dish14

119

Stress and mixed incontinence, prolapse Stress Incontinence

6 mo

89% successful device fitting; >50% continued use for 6 mo

RCT, randomized controlled trial. Summarized and updated from Wilson et al., 2001.

continence devices manufactured by several companies who also manufacture pessaries for prolapse (Table 57-3). Additionally, there are several disposable intravaginal devices that are not yet available for use in the United States. These devices are easy to use and seem to have moderately good efficacy, especially for the woman with predictable stress incontinence, who may use such devices when exercising or for that week of coughing from a bad cold. Use among urogynecologic and urology practices is variable: some specialists offer these devices to all women with stress incontinence, whereas others do not include intravaginal devices in their practice. The devices have not been well studied. These are low-cost devices sold in modest volumes whose manufacturers do not have research funds, and there are no sham devices for randomized controlled trials. Types of Devices Nonpessary Devices Many women report use of their contraceptive diaphragm as being effective. Its mechanism is probably similar to that of other continence devices: creation of a “backstop” against which the urethra is briefly compressed during increased abdominal pressure. A short menstrual tampon may be inserted just comfortably inside the introitus; patients need to be instructed to use the tampon under dry conditions, which improves the adherence of the tampon. We instruct patients to use this “tampon trick” with a super tampon, and only on an occasional basis. The Conveen Continence Guard is a polyurethane foam cushion that is folded on its long axis and placed in the vagina. When moistened and partially unfolded, it acts as a backstop under the bladder neck. The device is available in three sizes and is worn for up to 18 hours and then discarded. It is not yet available in the United

States. Several studies have documented good tolerance and significant reductions in urine loss with use.19,20 Supportive (Modified Pessary) Devices The majority of continence devices have been modified from vaginal pessaries used for POP, and all recreate the supportive “backstop” effect for the urethra. These include rings with knobs placed at the bladder neck, the Hodge pessary inserted backward and upside down, the incontinence dish with support, the PelvX ring, and the Suarez ring. Nonsupportive Devices Nonsupportive devices include a urethral insert (Rochester Medical, Inc., Rochester, MN) and urethral suction caps (Uromed; not currently available.) Such urethral plugs and caps have been studied with some success but do not seem to be popular in clinical practice. Some women may wear these devices for activities only, whereas others need to wear them on a daily basis. Care of these pessaries is similar to that for supportive pessaries. Clinical Use Although use of a short super tampon may be suggested on a temporary basis, we use the incontinence dish as our main incontinence pessary. Patients can immediately see the advantages (effective, no surgery) and disadvantages (small amount of bother with insertion, need for continued use) associated with these devices. Although most women wear these devices on an asneeded basis, some patients who have daily stress incontinence prefer to wear the device on a continual basis. Once an appropriate candidate for a supportive device has been identified, we prefer to fit the device in a separate session,

Chapter 58 NONSURGICAL TREATMENT OF VAGINAL PROLAPSE: DEVICES FOR PROLAPSE AND INCONTINENCE

often after several weeks of vaginal estrogen in postmenopausal women. It is helpful to demonstrate leakage with a standing cough stress test, then to demonstrate continence after a device is fitted. A comfortable bladder volume does not seem to impair fitting of the device. In supine lithotomy, the capacity of the vagina laterally is assessed; this may be limited in women who have had vaginal surgery. We begin with a continence dish of a similar diameter, squeezing the device to narrow its entry into the vagina. All of these devices are placed with the knob just inside the introitus, creating the support for the urethra. The best fit is that which leaves a fingerbreadth or two between the device and the pubic symphysis, is comfortable, and does not readily extrude with straining. Women with a narrow pubic arch and good pelvic floor strength are the best candidates for a supportive device, because the pessary is more easily retained. For a narrow vagina with limited capacity, a Hodge pessary (placed so that the arch is directed at the bladder neck) or a knobbed device may be preferable. We recommend that women remove the intravaginal supportive device at least weekly, leave it out overnight, and then reinsert it in the morning. The device can be washed with simple soap and water, rinsed, and air-dried. In our experience, women rarely encounter vaginal excoriations or excessive or malodorous vaginal discharge using this approach. Postmenopausal women may benefit from vaginal estrogen. This has little systemic absorption, may increase vaginal skin thickness and tolerance of the device, and is best given as a vaginal pill (Vagifem 25 μg, Novo Nordisk) once nightly for 10 nights, then twice weekly thereafter. After an initial follow-up examination to demonstrate efficacy and self-management, women who manage their own pessary without difficulty can be seen annually. Women may need to brace the device digitally during straining for bowel movements to prevent extrusion. A device that is easily dislodged or uncomfortable is not satisfactory and should be removed and replaced. Most studies evaluating the effectiveness of devices for stress incontinence are small in numbers and short in duration. In a prospective, randomized study by Nygaard,13 6 of 14 women were cured and an additional 2 improved during exercise while wearing a super-sized tampon in the vagina. Nine of 12 women had resolution of stress incontinence while wearing a contraceptive diaphragm during urodynamic testing, and 4 of 10 women wearing a contraceptive diaphragm for 1 week had improved continence.

Of 190 women presenting to a tertiary care center with symptoms of stress or mixed urinary incontinence who were offered pessary management, 63% chose to undergo fitting and 89% achieved a successful fit in the office. Of the 106 women who took a pessary home, follow-up was available on 100. Fifty-five women used the pessary for at least 6 months as their primary method of managing urinary incontinence (median duration, 13 months). Of the remaining 45 women who discontinued use before 6 months, most did so by 1 month.14 Intraurethral devices work through occlusion of the urethra. They are removed for voiding, and most cannot be reinserted. Several trials of several products have been conducted with favorable efficacy and low risk of side effects, but the intraurethral devices are less comfortable than the intravaginal ones. Studies of intraurethral inserts showed that most women who used them (66% to 95%) were dry or improved while the device was in place. It is not surprising that urinary tract infections may occur with these devices; however, the incidence of infection decreases after the first several months of use. These intraurethral devices have failed to gain popularity with patients and physicians. Although few women choose an intraurethral device as a first option, an occasional patient is highly satisfied with long-term use of an intraurethral device. Use of occlusive (extra)urethral devices or patches have been reported with similar results: the devices seem to work in many patients, but acceptance by physicians and patients has been poor, and the devices are not currently marketed in the United States.

CONCLUSION Pessaries and other devices are an important part of the treatment scheme for stress urinary incontinence. Although some patient effort is required for removal and maintenance of the devices, the risk and costs are minimal with moderate efficacy. Further research is needed to determine which women are most likely to respond to the various types of devices, and to evaluate both effectiveness and adverse events associated with these devices compared to surgery. Nevertheless, the risk-benefit ratio seems quite favorable with these devices for stress urinary incontinence.

References 1. Olsen A, Smith V, Bergstrom J, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89(4):501–506, 1997. 2. Prashar S, Simons A, Bryant C, et al: Attitudes to vaginal/urethral touching and device placement in women with urinary incontinence. Int Ungynecol J Pelvic Floor Dysfunct. 11(1):4–8, 2000. 3. Clemons J, Aguilar V, Tillinghast T, et al: Risk factors associated with an unsuccessful pessary fitting trial in women with pelvic organ prolapse. Am J Obstet Gynecol 190:345-350, 2004. 4. Handa VL, Jones M: Do pessaries prevent the progression of pelvic organ prolapse? Int Urogynecol J Pelvic Floor Dysfunct 13:349-351, 2002. 5. Cundiff GW, Weidner AC, Visco AG, et al: A survey of pessary use by members of the American Urogynecologic Society. Obstet Gynecol 95:931-935, 2000. 6. Pott-Grinstein E, Newcomer JR: Gynecologists’ patterns of prescribing pessaries. J Reprod Med 46:205-208, 2001.

7. Sulak PJ, Kuehl TJ, Shull BL: Vaginal pessaries and their use in pelvic relaxation. J Reprod Med 38:919-923, 1993. 8. Wu V, Farrell SA, Baskett TF, Flowerdew G: A simplified protocol for pessary management. Obstet Gynecol 90:990, 1997. 9. Clemons JL, Aguilar VC, Tillinghast TA, et al: Patient satisfaction and changes in prolapse and urinary symptoms in women who were fitted successfully with a pessary for pelvic organ prolapse. Am J Obstet Gynecol 190:1025-1029, 2004. 10. Brincat C, Kenton K, FitzGerald M, Brubaker L: Sexual activity predicts continued pessary use. Am J Obstet Gynecol 191:198-200, 2004. 11. Wilson D, Bø K, Hay-Smith E: Conservative treatment in women. In Incontinence. Ed P Abrams, L Cardozo, S Khoury. Health Publications, Ltd. Plymouth. pp 571-624, 2002. 12. Bhatia N, Bargman A: Pessary test in women with urinary incontinence. Obstet Gynecol 65(2):220-226, 1985.

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13. Nygaard I: Prevention of exercise incontinence with mechanical devices. J Reprod Med 40:89-94, 1995. 14. Donnelly M, Powell S, Olsen A, et al: Vaginal pessaries for the management of stress and mixed urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 15(5):302-307, 2004. 15. Kondo K, Yokoyama E, Koshiba K, et al: Bladder neck support prosthesis: a nonoperative treatment for stress or mixed urinary incontinence. J Urol 157(3):824-827, 1997. 16. Davila G, Neal D, Horbach N, et al: A bladder-neck support prosthesis for women with stress and mixed incontinence. Obstet Gynecol 93(6):938-942, 1999.

17. Robert M, Mainprize T: Long-term assessment of the incontinence ring pessary for the treatment of stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 13(5):326-329, 2002. 18. Jarrell S, Singh B, Aldakhil L: Continence pessaries in the management of urinary incontinence in women. J Obstet Gynecol Can 26(2):113-117, 2004. 19. Hahn I, Milsom I: Treatment of female stress urinary incontinence with a new anatomically shaped vaginal device (Conveen Continence Guard). Br J Urol 77:711-715, 1996. 20. Mouritsen L: Effect of vaginal devices on bladder neck mobility in stress incontinent women. Acta Obstet Gynecol Scand 80:428-431, 2001.

Chapter 59

USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY Fred E. Govier, Kathleen C. Kobashi, and Ken Hsiao The surgical field encompassing vaginal reconstructive surgery and urinary incontinence is extensive and extremely complex. As opposed to many surgical disciplines that focus on a single isolated organ, we are dealing with multiple organs that interact with multiple complex supporting structures that must function as a single unit to be maximally effective. The trauma of childbirth, the ever-present effect of gravity, and the inevitable deterioration of these organs and their supporting structures with age and hormone deficiency continuously stress this intricate system. Deficiency in one or more of these components can lead to urinary incontinence, dyspareunia, pelvic pressure, or any of a multitude of other symptoms associated with pelvic floor descent and/or prolapse. Over the last century, a variety of autologous tissues, absorbable and nonabsorbable synthetic materials, and, more recently, allografts and xenografts have been used in attempts to reconstruct the pelvic floor and its supporting structures. This chapter focuses on the relative strengths and weaknesses of each of these materials, realizing that in 2005 we still lack the perfect material for vaginal reconstructive surgery. We address urethral support, support of the anterior compartment, and support of the vaginal apex as somewhat separate topics, as well as autologous materials, allografts, xenografts, and synthetic mesh products as separate groups. Although this chapter’s focus is on the materials themselves, it must be realized that failure is not limited only to the materials. Surgical technique, points of attachment, and methods of attachment can all play a crucial role in the ultimate success or failure of the operative intervention. Because the use of these materials is relatively new in reconstruction of the anterior compartment and apex, we will use our experience with urethral slings to further highlight the relative strengths and weaknesses of these materials. Even then, teasing out the exact cause of a surgical failure or a complication in this setting is challenging and at the present time there are still many unanswered questions.

PREVALENCE OF URINARY INCONTINENCE AND PELVIC FLOOR RELAXATION Interest in women’s health care issues and public awareness of stress urinary incontinence (SUI) and pelvic floor relaxation have increased substantially over the past several years. In 2000, an estimated 17 million community-dwelling individuals had daily urinary incontinence in the United States, and an additional 34 million had symptoms of overactive bladder. The costs of urinary incontinence in the United States were recently estimated at $19.5 billion, with an additional $12.6 billion for overactive bladder.1

A postal survey regarding urinary incontinence involving 29,500 community-dwelling women aged 18 years or older in France, Germany, Spain, and the United Kingdom was recently reported.2 Of the women responding, 35% reported involuntary loss of urine in the proceeding 30 days, with SUI being the most prevalent type. Only 25% of the women had consulted a physician, and fewer than 5% had undergone surgery for their condition. It is estimated that a woman’s lifetime risk of needing a single prolapse surgery by 80 years of age is 11.1%, and the risk of needing reoperation for recurrent prolapse is 29.2%.3 Undoubtedly, as the population ages, life expectancy increases, and the stigma of incontinence and pelvic prolapse is replaced by education, these numbers and their associated costs will rise.

HISTORY OF THE URINARY SLING WITH AUTOLOGOUS FASCIA In 1907, Van Girodano introduced the concept of the urinary sling for the treatment of urinary incontinence, when he wrapped a gracilis graft around the urethra.4 Credit for the first pubovaginal sling (PVS) goes to Goebell, who, in 1910, rotated the pyramidalis muscles beneath the urethra and joined them in the midline.5 In 1942, Aldridge described the first fascial sling. He used rectus fascia, without muscle, passed through the retropubic space to support the proximal urethra and bladder neck.6 Variations on this procedure over the following decades involved attempts to minimize morbidity and obtain suitable fascia from patients with multiple previous abdominal procedures and/or pelvic radiation. Ridley7 described the use of fascia lata in 1955, followed by reports from Williams and Telinde,8 Moir,9 Morgan,10 and Stanton and associates11 involving the use of synthetic materials with variations on the approach or on anchoring sutures. Using autologous fascia and synthetic materials, these original investigators showed encouraging results, but the outcomes were plagued with urethral obstruction, erosion, fistula formation, and infections. McGuire and Lytton revived the PVS in 1978 with their series showing an 80% success rate for intrinsic sphincter deficiency (ISD) using rectus fascia tensioned loosely around the urethra.12 Blaivas and Jacobs modified the procedure by penetrating the endopelvic fascia, as described by Peyrera,13 and completely detaching the rectus fascia from the abdominal wall.14 They also stressed the importance of minimizing tension on the sling and stated that, “in the majority of patients the sling should be placed under no tension at all.” Subsequent studies showed no difference in histologic or performance characteristics between free and pedicle fascia flaps for sling surgery.15 609

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As the PVS was gaining acceptance, the first reports of poor long-term results from needle suspension procedures were being published. In a landmark study published in 1995, Trockman and Leach’s group monitored 125 patients for a mean of 10 years after a modified Peyrera needle suspension. By questionnaire data, 51% reported that they had SUI, and only 20% reported no incontinence of any kind.16 The American Urological Association guidelines panel for the surgical management of SUI was published in 1997 and concluded, based on cure/dry rates, that retropubic suspensions and slings were the most efficacious procedures for long-term success.17 Since these early reports, many authors have published longterm data that attest to the durability of the autologous fascial sling. Morgan and colleagues observed 247 patients with type II and III SUI for a mean of 51 months after autologous rectus sling placement. They reported an overall continence rate of 88% to 91% for type II and 84% for type III SUI. Among those patients with at least 5 years of follow-up, the continence rate was very durable at 85%.18 Chaiken and coworkers reported on 251 patients with all types of anatomic incontinence treated with an autologous rectus PVS.19 At a median follow-up of 3.1 years, 73% of patients were cured and 19% were improved. Among the 20 patients with a minimum of 10 years’ follow-up, the cure rate was 95%. Brown and Govier, using autologous fascia lata, monitored 46 patients for a mean of 44 months; 90% reported overall cure of their anatomic component, and 73% described no or minimal leakage requiring no pads.20 The two greatest advantages of the autologous PVS were that all types of anatomic incontinence could be addressed and, if a good result were achieved at 1 year, the result would be durable. Because of these attributes, by the late 1990s most authorities agreed that the PVS using autologous fascia was the gold standard for the surgical management of anatomic incontinence. Unfortunately, harvesting this fascia from the abdominal wall or thigh adds operative time and incurs a risk of hematoma formation, wound infection, and/or hernia formation. Only relatively narrow strips of fascia can be harvested, and even then the patient requires several weeks of recovery time to achieve a normal activity level. In an effort to minimize patient morbidity and yet further improve surgical results, a variety of biomaterials (allografts, xenografts) and synthetic products (absorbable and permanent) have been introduced and are currently being used for the construction of urinary slings and vaginal reconstructions.

HISTORY AND CHARACTERISTICS OF BIOMATERIALS IN PELVIC RECONSTRUCTION Allografts Allografts are harvested from a human donor, usually a cadaver, and transplanted into a human recipient. The most common tissues used for pelvic floor reconstruction are fascia lata, dermis, and dura matter. Table 59-1 lists some of the companies supplying these components and their trade names. There are many advantages to the use of allografts or xenografts for pelvic floor reconstruction. Several studies have documented decreased recovery time, length of hospitalization, and postoperative pain using these materials.21-23 Compared with permanent synthetic materials, allografts carry a lower risk of vaginal extrusion, and, if extrusion does occur, in general the graft does not require removal. Finally, larger-sized grafts for pelvic reconstructive procedures can be obtained easily without incurring additional patient morbidity. All cadaveric donor materials in the United States are processed by licensed tissue banks regulated by the Food and Drug Administration.24 Cadaveric donors are carefully screened by review of their medical and social history with the family, partners, and friends. Donors are excluded if the cause of death is unknown or the medical history suggests any of the following: hepatitis, bacterial sepsis, syphilis, intravenous drug abuse, cancer, collagen vascular disease, rabies, Creutzfeld-Jakob’s disease (CJD), or significant risk factors for human immunodeficiency virus (HIV) infection.25 Serologic testing is performed for HIV-1 and HIV-2 antibodies, hepatitis B surface antigen, and hepatitis C antibodies. One of the most significant problems with serologic testing is that false-negative results can occur, because it takes time after the initial infection before the immunologic response is sufficient for serologic detection. The delay can be up to 6 weeks in the case of hepatitis B, and up to 6 months for HIV.26,27 Tissue processing allows for the removal of most of the cellular content, along with the associated antigens, making donor and recipient tissue matching unnecessary. Additionally, tissue sterilization, while preserving the inherent collagen matrix, is required to eliminate infectious complications and ensure satisfactory graft assimilation. Although the American Association of Tissue Banks has made recommendations, no federally mandated

Table 59-1 Allografts and Xenografts Type

Component

Autologous

Rectus fascia Fascia lata Vaginal wall Fascia lata

Allograft

Dermis

Xenograft

Dura mater (no longer used) Porcine small intestine submucosa Porcine dermis Bovine pericardium

Trade Name (Manufacturer)

Tutoplast (Mentor, Santa Barbara, CA) Faslata (Bard, Covington, GA) Repliform (LifeCell Corporation, The Woodlands, TX) Duraderm (CR Bard, Inc., Murray Hill, NJ) Stratasis (Cook, West Lafayette, IN) Pelvicol (Bard, Covington, GA) IneXen (American Medical Systems, Minnetonka, MN) (Braile Biomedical Industria, Brazil)

Chapter 59 USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY

processing techniques for all tissue banks exist. Currently, allografts are prepared using a variety of proprietary processing techniques that vary depending on the vendor. Various mechanisms are used for cellular destruction and include hypertonic solutions that osmotically rupture cells and destroy bacteria and viruses; oxidative destruction with hydrogen peroxide, which oxidatively destroys most proteins; and isopropyl alcohol to destroy cells, bacteria, and viruses by dissolving the lipids in their cell walls.28,29 An additional method used for tissue sterilization is gamma irradiation, which kills bacteria by disrupting nucleic acids but does not guarantee sterilization of viruses or prions, even at the American Association of Tissue Banks recommended level of 1500 Gy (1.5 megarads).27,30 Options for long-term preservation include cryopreservation, freeze-drying (lyophilization), and solvent dehydration. Controversy exists with regards to tissue processing and how it affects tissue strength. Most of the concern regarding processing and storage revolves around two issues. The first is irradiation and how it affects the tensile strength of collagen, and the second is the ice crystal formation that occurs with cryopreservation and the freeze-drying processes and whether they adversely affect the collagen microstructure.28,31,32 Thomas and Gresham found no significant difference in tensile strength among fresh, frozen and freeze-dried fascia lata specimens.33 Sutaria and Staskin found no significant difference in the tensile strength of fascias that were freeze-dried and gamma-irradiated, freeze-dried alone, or solvent-dehydrated and gamma-irradiated.34 In contrast, Hinton and colleagues found solvent-dehydrated, irradiated fascia lata to be significantly stiffer, with a higher tensile strength than freeze-dried fascia.32 Two studies reported that tissue irradiated after dehydration resulted in significant loss of tensile strength, and the investigators recommended that irradiation be performed before dehydration.28,35 In an excellent review, Gallentine and Cespedes concluded that “a number of processing techniques are available that may have different adverse affects on the mechanical properties of allografts, but currently no definitive evidence is available that one technique is superior to another.”25 With current federal regulations in place to obtain, process, and store cadaveric materials, the risk of infectious disease transmission is extremely small. As of 1995, approximately 220,000 soft tissue transplants were being performed annually in the United States, and no cases of a transmitted infectious disease had been reported for processed cadaveric fascia lata (CFL) or dermal grafts.24 The risk of acquiring HIV-infected tissue from a properly screened donor is reported to be between 1 in 1,667,600 and 1 in 8 million from banked cadaveric fascia.36-38 Seroconversion was reported in recipients of solid organs (4 of 4) and unprocessed fresh-frozen bone (3 of 3); however, 0 of 34 patients receiving other tissues, including 3 who received lyophilized tissue, became infected with HIV.26 Still, it is alarming that intact genetic material (DNA segments) was isolated from four commercial sources of processed human cadaveric allografts.39 Prion transmission has gained increasing attention because of the neurodegenerative symptoms that occur in the recipient but not in the host. Prions are proteinaceous pathogens that use a novel mechanism of amino acid transposition to change the protein configuration to a that of a neurotoxic prion protein peptide, leading to cases of neurodegenerative Creutz feld–Jakob Disease. Iatrogenic cases have been reported after many types of procedures, including corneal transplants and dura mater graft-

ing.40 It has been described in 43 patients receiving cadaveric dural grafts after neurosurgical or orthopedic procedures, and, for this reason, dura mater is no longer being used as a biomaterial.41 However, prion transmission has not been described with the use of cadaveric fascia or dermis for anti-incontinence or prolapse procedures. Even though no transmission has been documented in our field, the potential for infectious transmission with these allografts does exist, and all patients need to be informed of the risk before their use. Xenografts The most popular xenograft materials used for sling surgery are derived from porcine and bovine sources (see Table 59-1). Being from an animal source, xenografts are readily available and are devoid of the potential ethical issues associated with use of human tissue. The types most frequently used for pelvic reconstruction are porcine dermis and small intestinal submucosa (SIS) or bovine pericardium. The Food and Drug Administration has strict guidelines controlling all phases of their production.42 Fate of Autologous Tissue and Biomaterials The most significant controversy involving biomaterials is the ultimate fate of the graft material itself, within the host. When autologous rectus fascia or fascia lata is used to construct a urinary sling, the results of these procedures in terms of durability are uniformly excellent.17-20 Three studies in the literature examined the fate of autologous fascia in the host. In 1969, Crawford evaluated autologous and frozen fascia lata in rabbits by attaching strips of each from the flank to the posterior abdominal wall.43 After killing the animals and examining the tissue, he concluded that “fresh fascia is living sutures and cadaveric tissue merely provides a bridge for host fibroblasts.” A more recent paper, in 1997, looked at free versus pedicled fascial flaps again in rabbits.44 Strips of 7 and 15 mm of each were obtained from the abdominal wall and used to create a urethral sling. The rabbits were killed at 3 months, and all slings were found to be viable with the original histology preserved. The authors surmised that the fascia survives in the early postoperative period by diffusion. Later, neovascularization from the loose connective tissue around the flaps provides long-term vascularity. FitzGerald and colleagues evaluated the histologic appearance of autologous rectus fascial slings that were examined at revision at 3, 5, and 8 weeks for urinary retention and at 17 and 208 weeks for persistent SUI.45 They concluded that autologous fascial slings remain viable after implantation. They did note fibroblast proliferation, neovascularization, and some remodeling of the graft, but no evidence of graft degeneration was detected. A linear orientation of the connective tissue and fibroblasts was seen in some areas, whereas other areas had remodeled to form tissue similar to noninflammatory scar. In contrast, cadaveric fascial allografts have been extensively studied in multiple human models in the orthopedic literature as well as animal models.43,46,47 With the use of serial biopsies, it was found that there is an initial donor fibrocyte death, which is followed by neovascularization of the graft. Fibroblast migration into the implant is then followed by remodeling and eventually by maturation of the graft.48,49 The maturation of xenografts is similar to that described for allografts. The processed material serves as an acellular mesh or

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scaffolding, which requires remodeling by the host to end up as a viable graft. It is this need to “remodel” the graft that appears to be the Achilles heel for many or all of the allograft and xenograft products on the market today. As one examines the surgical results with these materials, it is evident that some patients quickly remodel this material to a strong durable structure. In others, it appears that the scaffolding entirely disappears. Authors have theorized that increasing age, poor vascularity, excessive scarring, diabetes, or the use of steroids can adversely affect the remodeling process; however, studies are lacking, and at this time the discrepancies in outcome are largely unexplained.

SURGICAL RESULTS OF BIOMATERIALS FOR URINARY SLINGS Allografts Hanada and associates,50 in 1996, and Labasky and Soper,51 in 1997, were the first to report on the use of cadaveric products for urinary slings. In 1998, Wright and colleagues published the first paper comparing cadaveric allograft fascia lata to autologous rectus fascia.52 This series reported on a group of 92 patients undergoing sling procedures over a 28-month period. Fifty-nine patients received a 13 × 2 cm portion of freeze-dried allograft fascia lata, and 33 patients received autologous rectus fascia. With a mean follow-up of 9.6 months for the allograft and 16 months for the autologous fascia, no differences in surgical outcome were found. Chaikin and Blaivas described an early failure of a freezedried cadaveric fascia sling in which the holding sutures pulled through.53 In 1999, FitzGerald and associates reported 35 patients who underwent PVS placement using freeze-dried irradiated CFL.54 At the time of re-exploration in seven of the failures, “histopathologic analysis revealed areas of disorganized remodeling and graft degeneration, as well as complete absence of the graft in some patients.” In 2000, Brown and Govier compared 121 consecutive patients undergoing slings constructed with fresh-frozen CFL with 46 earlier patients undergoing the same surgical procedure with autologous fascia lata.20 Although the mean follow-up was longer in the autologous group (44 versus 12 months), questionnaire data demonstrated no significant difference in surgical outcomes. Elliott and Boone, in 2001, reported 12-month follow-up using solvent-dehydrated CFL in 26 patients. Ninety-six percent of patients reported improvement.55 In 2001, Carbone and Raz’s group reported on a series of irradiated freeze-dried cadaveric fascial sling procedures with a 40% failure rate and a reoperation rate of 16.9%. At the time of reoperation in 26 patients, they found the allografts to be “fragmented, attenuated or simply absent.”56 On the basis of these findings, they abandoned the use of allografts for sling construction. In 2002, O’Reilly and Govier re-examined a group of 121 patients who had slings constructed with fresh-frozen CFL; these patients had been reported earlier to have similar results to those treated with autologous slings.57 They identified 8 patients who experienced intermediate-term failure at 4 to 13 months after they had initially been dry. This development was not noted in the autologous sling group, and, on the basis of these findings, they too abandoned the use of fresh-frozen CFL for slings. In 2005, the debate over biografts continues, but the pendulum clearly appears to be heading away from the use of biografts

for construction of urinary slings. Crivellaro and colleagues published a prospective series of 253 patients with 18-month followup using human dermal allografts for slings.58 They found that 78% of the patients were improved or cured of their incontinence and were happy with their experience. Owens and Winters also looked at human dermal allografts in slings in 25 patients.59 At a mean follow-up of 6 months, 68% of the patients were dry, but this rate fell to 32% at a mean follow-up of 14.8 months. They concluded that graft degeneration was the most likely cause of the failures. FitzGerald and coworkers looked at a longer-term follow-up in patients from a previously reported group who had undergone abdominal sacrocolpopexies (67) and/or urinary slings (35) with freeze-dried, irradiated fascia lata. They found that 83% of the sacrocolpopexy patients experienced failure at a mean follow-up of 12 months, and, at the time of reoperation in 16 patients, the graft was still present in only 3 patients.60 In 2005, Frederick and Leach reported on 251 patients who had undergone a combined anterior repair/sling procedure for SUI using solvent-dehydrated fascia lata. They found a cure/dry rate of 56% with a cure/improved rate of 76% at a mean follow-up of 24 months. They did note that, of the failures, 56% occurred after 12 months. They concluded the late failures were of concern and are continuing to monitor this group.61 Xenografts The two most commonly used xenografts in reconstructive urology are porcine dermis and porcine small intestinal submucosa (SIS). As with allografts, the results for urinary slings are controversial, and there are even fewer published reports, or fewer publications with shorter follow-up. Porcine SIS gained increased attention after being successfully implanted in a canine model for bladder augmentation without evidence of rejection or shrinkage.62 Histologically, the SISregenerated bladders demonstrated three separate layers, indicating that a regenerative healing process was occurring rather than a simple replacement with fibroblasts. During the manufacturing process, the serosa, tunica muscularis, and mucosa are removed mechanically from porcine jejunum. Intestinal submucosa is transferred into an acellular collagen matrix which, once implanted, induces local host tissue cell infiltration and is subsequently remodeled within 90 to 120 days. The biomatrix in SIS lacks cellular elements; however, collagen and other growth factors with activities similar to those of transforming growth factor-β and fibroblast growth factor 2 are present. These growth factors may act as signals for local epithelial cells to proliferate, thereby colonizing the graft and leading to tissue healing without scarring.63 Several groups have employed porcine SIS with good shortterm results. Palma and colleagues reported that 92% of 50 patients were cured of SUI at a mean follow-up of 13 months without any serious postoperative complications.64 Rutner and associates reported on a series of 152 patients undergoing placement of an SIS sling fixed to the pubic bone without bone anchors. Of those patients, 142 (93.4%) remained dry at a median follow-up of 2.3 years.65 Intermediate-term failures at 9 and 11 months occurred in 2 patients. Histopathologic studies in which porcine SIS grafts were biopsied and removed have suggested variable levels of biocompatibility. Implant site biopsies under the vaginal mucosa were taken in three cases of recurrent SUI after PVS using SIS. In all three cases, exceptional biocompatibility was demonstrated, with

Chapter 59 USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY

minimal foreign body or inflammatory reaction.66 Ho and colleagues were less enthusiastic about the biocompatibility of porcine SIS.67 They noted postoperative inflammatory reactions consisting of erythema and pain in 6 of 10 patients undergoing eight-ply SIS tension-free sling placement. SIS is an attractive material because of its theoretical ability to stimulate local tissue in-growth. Whether this will translate into long-term efficacy and durability remains to be seen. As for porcine dermis, Arunkalaivanan and Barrington reported a prospective randomized trial of tension-free vaginal tape (n = 74) versus porcine dermis (n = 68).68 With a mean follow-up of 12 months (range, 6 to 24 months), they found no difference in success for correcting SUI. In another prospective randomized trial of porcine dermis (n = 34) versus autologous rectus fascia (n = 31), Giri and colleagues demonstrated similar rates of cure and improvement between the two groups but noted significantly less morbidity for the xenograft group.69 In contrast, Gandhi and colleagues performed histopathologic analysis of porcine dermis sling specimens in eight patients with urinary retention and two failures.70 Variable tissue reactions were seen, suggestive of a vigorous foreign body reaction. In cases of retention, the original graft was mostly intact, with minimal remodeling and tissue in-growth. However, surgical failures revealed minimal graft remnants left within the resected suburethral tissue. Encapsulation of porcine dermis slings with poor tissue ingrowth was also observed by Cole and coworkers.71 They found no tissue remodeling or incorporation of porcine dermis into the host tissue at 4 months in a patient operated on for retention. This tendency of porcine dermis to encapsulate might retard host tissue infiltration and, ultimately, graft integration. In a recent attempt to look at time-dependent variations in biomechanical properties of several types of grafts implanted into rabbits, Dora and colleagues found that cadaveric fascia, porcine dermis, and porcine SIS had a reduction in tensile strength of 60% to 89% at 2 to 6 weeks.72 Polypropylene mesh and autologous fascia did not differ in strength from baseline over the same period. Although the use of xenografts is appealing, the variable biocompatibility and tissue responses, combined with unpredictable clinical outcomes observed, clearly require further investigation. HISTORY AND CHARACTERISTICS OF SYNTHETIC MATERIALS Synthetic materials include both absorbable and nonabsorbable (permanent) materials. Other than for historical interest, all of the synthetics discussed here are mesh products, most of which are permanent. Synthetic materials have long been an attractive option for pelvic reconstruction and have many desirable attributes. The permanent mesh products are stronger than native tissue, are available in any size, and are free of any potentially infectious agents. No harvesting is necessary, limiting patient morbidity and enabling outpatient surgery under minimal anesthesia. Drawbacks include difficulty with tissue integration, infection, erosion (vaginal or other structures), and the potential for foreign body reactions. The first use of synthetic material for construction of a female urethral sling was reported by Williams and Te Linde in 1962; they used Mersilene in 12 patients.73 Ridley,74 in 1966, and

Morgan,75 in 1970, reported their results using Mersilene ribbon and Marlex to construct slings. In 1985, Morgan and colleagues reported on 208 consecutive patients who had undergone Marlex sling placement with a minimum 5-year follow-up.76 Although these early investigators showed encouraging results for control of incontinence using synthetic materials, these materials and surgical techniques were plagued with problems of erosion, infection, and fistula formation. Silicone was introduced in 1985 and was thought to be superior to Marlex or Mersilene due to its smooth surface and its ability to promote formation of a fibrous sheath.77 Again, initial success was good, but a high rate of sinus formation and rejection due to foreign body reaction limited its use.78 Ulmsten and associates were first to report the use of a polypropylene mesh around the mid-urethra, in 1996.79 They used a loosely woven mesh placed with vaginal trocars under no tension around the midportion of the urethra. Although this procedure was controversial when first introduced, Ulmsten and many others have confirmed the incidence of infection, erosion, and extrusion of the material itself to be extremely low when used for the construction of a sling.80-86 Cumberland87 and Scales88 delineated a series of ideal properties for a synthetic biocompatible material. This material should be clinically and physically inert, noncarcinogenic, and mechanically strong and should cause no allergic or inflammatory reaction. It should be easily sterilized, must not be physically modified by body tissues, and should be available in a convenient and affordable format for clinical use. None of the synthetic meshes currently in use meet all of these criteria. It appears that three of the most important components for a mesh product used in reconstructive urology are pore size, fiber type, and stiffness.89 Pore size and fiber type have been used to classify the most common synthetic meshes into four types (Table 59-2; Figs. 59-1 through 59-4). Type I meshes, such as soft Prolene (Ethicon, Endosurgery Inc., Summerville, NJ) and Marlex, contain large pores (>75 μg) and are usually constructed from polypropylene. This large pore size allows the admission of macrophages and in-growth of fibroblasts (fibroplasia), blood vessels (angiogenesis), and collagen, which helps prevent infection and forms fibrous connections to the surrounding tissue.90 Type II mesh, such as Gore-Tex (WL Gore & Associates, Inc., Flagstaff, AZ), has a pore size of less than 10 μg in at least one of three dimensions (microporous). Type III meshes, such as Mersilene, are macroporous in nature but have microporous components that often include braided and/or multifilamentous materials. Type IV materials have submicronic pore size and are not used for sling surgery. A second important property is the composition of the fibers. Polypropylene meshes are monofilament materials, whereas many other commonly used meshes are multifilament materials. The monofilament materials have a distinct advantage in terms of pore size. Most of the multifilamentous meshes have interstices less than 10 μg wide, which allows small bacteria to infiltrate and proliferate. Theoretically, these small interstices do not allow the entry of macrophages (16 to 20 μg) or leukocytes (9 to 15 μg) to eliminate the bacteria, resulting in the potential for a higher infection rate. Flexibility, or stiffness, is another important property that appears to be related to pore size. Marlex has a higher flexural rigidity (stiffness) than Mersilene or Teflon. Prolene is composed of knitted filaments of polypropylene, as is Marlex. However, Prolene has a pore size twice as large as Marlex (1500 versus

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Table 59-2 Synthetic Fiber Types and Pore Size Type

Component

Fiber Type

Pore Size

I

Polypropylene Gynemesh PS (Ethicon, Summerville, NJ) Prolene Soft (Ethicon, Johnson & Johnson, Summerville, NJ) Marlex (Bard, Covington, GA) ProLite (Atrium, Hudson, NH) Polypropylene/Polyglactin 910 Vypro (Ethicon) Polyglactin 910 Vicryl (Ethicon) Expanded PTFE Gore-Tex (Gore, Flagstaff, AZ) Polyethylene Mersilene (Ethicon) Polypropylene sheet Cellgard (not used for slings)

Monofilament Mono/multifilament Multifilament

Macro Macro Macro

Multifilament

Micro

Multifilament

Micro/macro

Monofilament

Submicro

II III IV

Macro, >75 μm; Micro, 500 mL; 1.9% pelvic hematoma; 1.0% vaginal erosion 1 bowel injury; 4 transfusions; 0% erosion 91% cured; 3.1% urinary retention; 0% erosion

SUI, stress urinary incontinence; TOT, transobturator tape; TVT, tension-free vaginal tape.

600 μg) and is therefore more flexible.91 Because of this property, Prolene theoretically may have a lower erosion rate through the vagina and adjacent viscera. SURGICAL RESULTS OF SYNTHETIC MATERIALS FOR SLINGS In contrast to biomaterials, whose success appears to rest on the ability of the host to repopulate and remodel an acellular scaffolding, nonabsorbable synthetic mesh products are strong and permanent at the time they are placed. Assuming they are placed in the proper position, under minimal or no tension, and the fixation points are secure, the issues we should focus on are the complications of infection, erosion, and/or extrusion. As discussed earlier, it appears that the specific characteristics of the materials themselves may have a significant impact on the complication rate. Table 59-3 lists surgical success and complication rates for several synthetic materials used to construct slings. The highest rates of erosion/extrusion have been associated with polymeric silicone (Silastic),92,93 silicone mesh,94 polytetrafluoroethylene (Gore-Tex)95 and polyester (ProteGen)96 and range from 12.5% to 71%. Although this has not always been accomplished in the past, authors should either specify the structure through which the material has eroded (vagina, urethra, bladder) or use the terms “erosion” and “extrusion,” with extrusion signifying vaginal exposure. A multifactorial etiology appears to be involved in the development of erosions and extrusions. They may occur because of subclinical or delayed infection that eventually leads to separation of the vaginal incision. Excess sling tension or unrecognized urethral injury at the time of surgery may predispose to urethral erosion. As mentioned earlier, the degree of tissue in-growth and host reaction may vary according to pore size and fiber type. Mesh flexibility may also play a role, with stiffer, smaller pore materials more prone to erode or extrude. The smooth surface

of silicone slings may prevent tissue in-growth, leading to poor integration into the surrounding tissues.94 Ulmsten and colleagues introduced tension-free vaginal tape (TVT)79 in 1996, and it was estimated to have been used in more than 600,000 cases worldwide over the first 8 years.97 TVT uses a large-pore, type I, monofilament, polypropylene sling placed at the mid-urethra in a tension-free manner to reconstitute the continence mechanism. SPARC (American Medical Systems, Minnetonka, MN) represents a modification of the original delivery system by directing the needles antegrade from two suprapubic incisions to the vaginal incision. Transobturator tape (TOT) delivery, the newest method of placement, leaves the mesh in a more transverse, broad-based position under the urethra from one obturator foramen to the other, completely avoiding the retropubic space. Nilsson and associates presented 7-year follow-up data on 90 women undergoing primary TVT placement for SUI (see Table 59-3).98 Of the patients available for evaluation, 81.3% met criteria for objective and subjective cure. No change in continence status was reported between 5- and 7-year follow-up visits in 87.5% of the patients. There was no evidence of tape erosion or tissue reaction indicative of material rejection in any of the patients. Abouassaly and coworkers performed a retrospective review of 241 patients undergoing TVT sling procedures and identified 48 (5.8%) intraoperative bladder perforations, with only 2 patients (1%) having vaginal mesh erosions.99 Early data on the SPARC polypropylene procedure revealed one bowel injury but no mesh erosions in the first 140 patients.82 The earliest data for polypropylene TOT demonstrated little difference in subjective and objective end points compared with TVT.100,101 At 1-year follow-up, no sling-related complications were observed. As shown in Table 59-3, the erosion rates of the newer polypropylene type I mesh slings have fallen dramatically, to between 0% and 1% in these four series. This was also illustrated in a recent review by Bhargava and Chapple, who looked at six centers

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that published data from 2002 to 2004 and found a vaginal erosion rate of only 0.6% in 2709 patients undergoing polypropylene mesh sling placement.102 Management of erosion or extrusion depends on the type of material, the location, and whether the patient has an erosion or an extrusion. Management varies from observation and antibiotics, to partial excision and closure, to complete removal of all synthetic materials.95,96,103-105 The decreased erosion rate seen with modern synthetics is most likely due to a combination of the improved biocompatibility of large-pore, monofilament mesh products; a greater emphasis on surgical technique (specifically tension-free placement); and maintenance of strict aseptic conditions. In 2005, many authorities contend that the type I, monofilament, polypropylene midurethral sling, under minimal to no tension, is the new “gold standard” for the treatment of anatomic urinary incontinence. HISTORY OF BIOMATERIALS AND SYNTHETICS FOR THE ANTERIOR COMPARTMENT Compromise of the structural integrity of the pelvic floor allows herniation or descent of the normally well-contained abdominalpelvic organs. Recognition that the native tissue may no longer assume the position, strength, or functionality to repair the prolapse by simple reapproximation has prompted investigators to evaluate various techniques and materials to overcome the problem. Furthermore, recognition of the complex interplay of components of the pelvic floor has prompted investigators to view any one intervention for pelvic prolapse as a potential risk factor for further pelvic support problems. Consequently, clinicians now view the manifestations of pelvic prolapse, such as a cystocele or apical prolapse, not as an isolated defect but in a more global context and with a better understanding of what surgery a patient may require. Although early techniques to repair anterior vaginal prolapse were theoretically sound, it quickly became clear that the use of a patient’s inherently weak tissue did not provide the durability necessary to prevent recurrence. Recurrence rates after standard anterior colporrhaphy have been reported to range from 20% to 40%.106-108 This high recurrence rate has given rise to consideration of graft reinforcement for prolapse repair. The use of Tantalum mesh in the anterior compartment was reported in 1955 and abandoned after 4 of 10 patients had vaginal extrusion of the mesh.109 In 1996, Julian reported vaginal extrusions in 3 of 12 patients with Marlex mesh and did not recommend its use.110 Nicita, in 1998, reported using polypropylene mesh anchored to the arcus tendineus to correct urinary incontinence and anterior prolapse in 44 patients.111 With a mean follow-up of 14 months, there were no recurrences and only one vaginal extrusion managed by partial excision. Also in 1998, Flood and colleagues reported on 142 patients who had anterior colporrhaphies reinforced with Marlex mesh.112 With a mean follow-up of 3.2 years, no recurrent cystoceles were noted, and only three patients had vaginal extrusions, requiring partial excision of the mesh at 3 months, 4 years, and 7 years. The authors were enthusiastic about the use of Marlex in the anterior compartment. In 2000, Kobashi and associates described the cadaveric prolapse repair with sling (CaPS) technique, a combined cystocele/ sling procedure using a single piece of solvent-dehydrated CFL.113

A 6 × 8 cm fascial graft was cut into a “T” configuration and attached to the vaginal apex superiorly and the levators laterally with the wings of the T, constituting the sling, secured to the pubic bone anteriorly with transvaginal bone anchors. Although this was a technique paper, follow-up at an interval of 1 to 6 months revealed no failures or allograft complications of any kind. Since these early reports, there has been an ever-increasing number of reports of the use of allografts, xenografts, and a variety of permanent and absorbable synthetic mesh products to reinforce the anterior compartment. In addition to a myriad of materials, some authors have advocated this repair for grade 4 relaxation, and others advocate repairs for any grade 2 through 4 relaxation. Some advocate for lateral attachment directly to the arcus tendineus, the obturator fascia, or the levators, whereas others do not attach the graft to any structures at all. There are fixation techniques using absorbable sutures, permanent sutures, and bone anchors. There are centers advocating a concomitant sling in all patients and centers that continue to try to determine preoperatively who requires additional urethral support. There are those performing the combined repair through a single incision and those who advocate two separate incisions. Some authors advocate the sling and anterior repair with two separate portions of material, using separate attachment points, and some use a single piece of material to construct both, with combined attachment points. In most series, the numbers are small and the follow-up is short. As opposed to failure of an incontinence procedure, which often prompts a return visit or can be picked up with questionnaires, mild or moderate recurrent pelvic relaxation is often largely asymptomatic and is often discovered only by repeated physical examination. When all of these variables are combined, it is virtually impossible at this point to determine which material, if any, should be used to resupport the anterior compartment. At best, one can take what has been learned from the sling experience and make some broad generalizations. Tables 59-4 and 59-5 summarize much of the experience to date with biomaterials and synthetics used to reconstruct the anterior compartment. For biomaterials, we would highlight the series by Kobashi and colleagues in 2000113 and 2002114 and by Frederick and Leach in 2005.61 These three series used a combined cystocele/sling repair with a 6 × 8 cm portion of solventdehydrated CFL. The attachment points were described earlier. This is by far the largest group of allograft repairs of the anterior compartment to date and involves two separate institutions with follow-up out to 5 years in the most recent series. In the latest series, it is concerning that, in terms of continence, 56% (33 patients) of failures were initially dry and failed after 1 year. Although there are multiple possible causes, one has to consider that these patients failed to adequately remodel the allograft. On the positive side, the recurrence rate of the anterior compartment was very low, especially for symptomatic relaxation (7% at a mean follow-up of 20 months), and were no complications from the graft material itself. Perhaps even a partial remodeling of the graft supporting the anterior compartment can provide enough additional support in the most of these patients. Among the synthetic series in Table 59-5, we would highlight the series by Sand115 and Weber116 and their colleagues with absorbable Vicryl mesh. If successful, the Vicryl mesh would be much less expensive than biomaterials, would put the recipient at no risk from a transmittable disease, and would have virtually

Chapter 59 USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY

Table 59-4 Anterior Prolapse Repair Using Allograft or Xenograft Techniques Study (Ref. No.)

N

Graft Material and Technique

Follow-up (Mo)

Outcome

*Kobashi et al, 2000 (113)

50

1-6

0% recurrence; 0% extrusion; 72% completely dry; 6% stress urinary incontinence

*Groutz et al, 2001 (120)

21

Combined cystocele/sling using 6 × 8 cm solvent-dehydrated CFL attached anteriorly to the pubis, laterally to the levators, and posteriorly to the vaginal apex Tutoplast CFL reinforcement with 19 concomitant pubovaginal slings

20.1 (range, 12-30)

*Chung et al, 2002 (121)

19

Combined cadaveric dermal allograft sling and prolapse repair. Sling attached “tension free” to rectus fascia with prolene

28

*Kobashi et al, 2002 (114)

172

12.4 (range, 6-28)

Clemons et al, 2003 (127)

33

*Powell et al, 2004 (123)

58

*Gomelsky et al, 2004 (124)

70

Combined cystocele/sling using 6 × 8 cm solvent-dehydrated CFL attached anteriorly to the pubis, laterally to the levators, and posteriorly to the vaginal apex AlloDerm 3 × 7 cm portion attached anteriorly to periurethral tissues, laterally to the arcus tendineus, and posteriorly to the vaginal apex 19 autologous fascia lata with 12 suburethral slings, 39 donor fascia lata with 29 slings; fascia attached at arcus tendineus. Porcine dermis graft with 65 concomitant fascia (autologous or donor) pubovaginal slings

No recurrent cystoceles; 2 patients developed postoperative rectocele/ enterocele; 85% patients with overt SUI cured; 100% of occult SUI cured 1 acute graft infection requiring reoperation and rectus sling; 1 grade 1 cystocele; 1 grade 2 cystocele; 1 patient with persistent SUI; 1 patient with de novo urgency 11% grade 1 cystocele; 1.5% grade 2 cystocele; 9.8% vaginal prolapse; 10.6% SUI

Leboeuf et al, 2004 (125)

19

Porcine xenografts (Pelvicol) attached anteriorly to periurethral fascia, laterally to the arcus tendineus, posteriorly to the vaginal apex Combined cystocele/sling using 6 × 8 cm solvent-dehydrated CFL attached anteriorly to the pubis, laterally to the levators, and posteriorly to the vaginal apex

15

*Frederick and Leach, 2005 (61)

251

18

36% asymptomatic grade 2 cystocele; 3% symptomatic grade 2 cystocele

24.7 (range, 12-57)

23% grade 2 cystocele; 16% grade 2 cystocele (autologous fascia); 27% persistent SUI

24

4 patients with recurrent but improved SUI; 2 patients with SUI similar to preoperative; 6 grade 2 cystocele; 3 grade 3 cystocele; 6 de novo grade 2 rectoceles 6.9% recurrence

24 (range, 6-60)

7% grade 2-4 symptomatic cystocele; 45% completely dry; 76% dry/improved; 56% of sling failures occurred after 1 yr

CFL, cadaveric fascia lata; SUI, stress urinary incontinence. *Indicates combined prolapse and incontinence procedures.

no risk of erosion. Unfortunately, one group found a substantial improvement with the mesh and one group found no difference at all. On review of the abstracts of studies using permanent mesh products, it is clear that most authors have learned from our sling experience and have used a type I, monofilament, polypropylene mesh. Although the use of permanent mesh products clearly seems to provide a durable repair, the most significant concerns are the risk of vaginal extrusion and dyspareunia. Even with relatively short-term follow-up, the vaginal extrusion rate in these

abstracts ranged from 2% to 25%, with several using polypropylene in the midrange at 8%, 8.3%, and 13%.104,117,118 The abstract published by Milani and colleagues in 2005 showed that, in addition to a high erosion rate, 20% of the anterior repairs and 60% of the posterior repairs exhibited an increased incidence of dyspareunia.117 In our institution, 46 patients have undergone mesh reinforcement of the anterior compartment with polypropylene (Prolene Soft) for grade 3 and 4 defects. We are monitoring one patient who has experienced a vaginal extrusion, and we have

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Table 59-5 Anterior Prolapse Repair with Synthetic Mesh Reinforcement N

Study (Ref. No.) Julian, 1996 (110)

12/12

*Nicita, 1998 (111)

44

*Flood et al, 1998 (112)

142

Mage, 1999 (126)

46

Migliari et al, 2000 (127)

12

Sand et al, 2001 (115)

73/70

Weber et al, 2001 (116)

33/24/26

De Tayrac et al, 2002 (118)

48

*De Tayrac et al, 2004 (101)

48/26

Milani et al, 2005 (117)

32/31

Graft Material and Technique

Follow-up (Mo)

Outcome

Randomized study using Marlex (polypropylene) mesh reinforcement for the anterior compartment with other sitespecific repairs

24

Polypropylene mesh attached taut to arcus tendineus

13.9 (range, 9-23)

Marlex (polypropylene) mesh reinforcement extended laterally into retropubic space Polyester mesh attached at vaginal angles Polypropylene mesh attached “tension-free” with absorbable sutures Absorbable polyglactin 910 (Vicryl) mesh placed over plication line versus standard colporrhaphy

38

All patients had 2 or more previous failed anterior repairs. No cystocele recurrences in mesh group; 4 recurrences in control group; 25% vaginal mesh erosions 1 grade 3 rectocele; 2% vaginal mesh erosion; 16% de novo urge incontinence No recurrent cystocele; 2% vaginal mesh erosion; 74% success for SUI treatment No recurrence of cystocele; 2% vaginal mesh erosion 3 patients with asymptomatic grade 1 cystocele

Three-armed trial of standard versus “ultralateral” versus standard plus absorbable polyglactin 910 mesh anchored to lateral limits with absorbable suture

23 (range, 5-44)

Polypropylene mesh placed into retropubic space “tension-free” 48 polypropylene mesh with wings placed into retropubic space “tension-free” and 26 TVT 32 anterior repairs polypropylene mesh attached with Maxon sutures and 31 posterior repairs polypropylene mesh

18 (range, 8-32)

26 20.5 (range, 15-32)

12

30/70 (43%) without mesh and 18/73 (25%) with mesh had grade 2-3 recurrent cystocele— 40% reduced risk; 8/70 (11%) without and 2/73 (3%) with mesh had grade 3 recurrent cystocele; 13 had recurrent rectoceles No significant difference in postoperative prolapse/urinary/ sexual function symptoms between groups; all groups reported significant improvement of symptoms compared to preoperatively 97.9% success rate reported; 8.3% vaginal mesh erosions

20

6.7% SUI in TVT group, 36% in no-TVT group; 6% recurrent cystocele; 8% vaginal erosion

17 (range, 3-48)

32 anterior repairs—dyspareunia increased 20%, 13% vaginal mesh erosion; 31 posterior repairs—dyspareunia increased 63%, 6.5% vaginal erosions, 1 pelvic abscess. Recommended abandoning synthetic mesh for the anterior and posterior compartment.

SUI, stress urinary incontinence; TVT, tension-free vaginal tape. *Indicates combined prolapse and incontinence procedures.

reoperated on two additional patients who failed to re-epithelialize with vaginal estrogens. All three of these patients appeared to be well healed at their 6-week examination, and extrusion occurred at a later date. Based on this early experience, we have stopped using synthetic mesh for the anterior compartment and are continuing to monitor this group.

The question we must ask ourselves as pelvic surgeons, is how much risk are we willing to accept now and for many years down the line as the patients we treat age and experience worsening atrophic vaginitis? All permanent synthetic mesh products are going to carry some risk of extrusion. Staskin and Plzak theorized that use of mesh with a higher cross-sectional area would carry

Chapter 59 USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY

Table 59-6 Synthetic and Biomaterials for Apical Support Study (Ref. No.) Snyder et al, 1991 (137) Kohli, 1998 (133)

Costantini et al, 1998 (138) Culligan et al, 2002 (140)

Brizzolara et al, 2003 (139)

N

Graft Material and Technique

Follow-up (Mo)

Outcome

OASC: 65 Dacron, 78 polytetrafluoroethylene OASC: double-thickness synthetic mesh (?), nonabsorbable braided sutures OASC: Gore-Tex

43 (range, 1-204)

93% success; 2.7% graft erosion

14 (range, 14-24)

12% vaginal erosion (5 mesh, 2 suture); switched to cadaveric fascia lata

31.6 (range, 12-68)

245

OASC: synthetic mesh (unspecified)

13.3 yr

124

OASC: 99 prolene mesh, 25 allograft fascia; 60 concomitant hysterectomy, 64 prior hysterectomy OASC: Marlex mesh

55.5 (range, 0-74)

90% (19/21) success; 2 pulmonary emboli; 0 erosions Follow-up by questionnaire or physical examination; no apical failure; 15.1% failure (most anterior compartment); 2.4% vaginal mesh erosion 1% mesh erosion in patient with previous hysterectomy; felt primary ASC at the time of hysterectomy was no added risk

147 57

21

Hilger et al, 2003 (136)

38

FitzGerald et al, 2004 (60)

54

OASC: freeze-dried donor irradiated fascia lata

17 (range, 3-54)

Latini et al, 2004 (129) Begley et al, 2005 (134)

10

OASC: autologous fascia lata

30.8 (range, 19-42)

92

OASC and LASC: • 33 Gore-Tex • 21 Silicone-coated polyester mesh (AMS Triangle) • 38 Prolene (J&J soft hernia) • 14 Fascia OASC and LASC: polypropylene (J&J mesh)

Elneil et al, 2005 (141)

128

164 (range, 120-204)

Questionnaire data plus physical examination; 10% reoperation rate “prolapse”; 16% “prolapsing tissue”; 2.6% vaginal mesh erosion 83% failure; 16 patients reoperated on with only 19% having viable graft present at 12 mo 30% SUI postoperative by questionnaire; 0% failure; 0% erosion

29.3 15.5

9% erosion rate 19% erosion rate

9.8 18.6 19 (range, 1.5-62)

0% erosion 0% erosion; 1% apical failure rate Mesh not retroperitonealized; 0% bowel complication; 10% apical failure; 2.3% vaginal erosion

ASC, abdominal sacrocolpopexy; LASC, laparoscopic abdominal sacrocolpopexy; OASC, open abdominal sacrocolpopexy; SUI, stress urinary incontinence.

a higher risk of vaginal extrusion, and examination of these series appears to support that supposition.119 Most pelvic surgeons seem to believe that the risk of vaginal extrusion with a narrow piece of a type I monofilament mesh placed around the midurethra under minimal to no tension is acceptable in most patients to prevent urinary incontinence. Whether to use a larger portion of the same mesh, which appears to carry a significantly higher risk of vaginal extrusion, for repair of the anterior compartment in an effort to prevent a recurrence (especially with a grade 2 or 3 defect), which is often minimally symptomatic, is something that pelvic surgeons need to consider very carefully. MATERIALS USED FOR APICAL SUPPORT A variety of surgical repairs have been described to resupport the vaginal apex. With one exception, these reports are primarily transvaginal procedures using the patient’s own tissues for

support and abdominal sacrocolpopexies (open or laparoscopic) that attach the apex of the vagina to the hollow of the sacrum with some type of graft. The exception is the transvaginal approach of Drs. Raz and Rodriguez, in which the arms of a type I polypropylene mesh are attached to the origin of the sacrouterine ligaments. The body of the mesh is carried down to the perineum via the posterior vaginal wall.128 With that notable exception, we will concentrate on the open abdominal sacrocolpopexies (OASC) and laparoscopic abdominal sacrocolpopexies (LASC) for the remainder of this section. As we have seen in the anterior compartment, there are a large number of variations in how one may perform an abdominal sacrocolpopexy (ASC). These variations, along with the reporting methodologies, make it very difficult to compare series and isolate any differences made by the materials themselves. Table 59-6 summarizes several publications looking at a variety of materials used for support. As with slings and in the anterior compartment, most of the more recent series are now using a large pore, type I polypropylene mesh. At least for the more

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recent series, we have to assume that a meticulous vaginal and abdominal preparation and intraoperative antibiotics were used. Most of the synthetic series used a “Y” configuration with the anterior and posterior leaflets attached to the respective portions of the vaginal wall and the main body of the graft attached to the longitudinal ligament of the sacrum or directly to the sacral bone with bone anchors. Where possible, we have tried to report the type of graft material used, whether the sutures used to attach the graft to the vaginal wall were permanent or absorbable, and whether failures occurred at the apex or involved other compartments. The only recent report using autologous products was that of Latini and colleagues, who performed OASC on 10 patients with a mean follow-up of 30.8 months using autologous fascia lata.129 They described harvesting adequate-size grafts through a 3-cm thigh incision and reported no vaginal erosions, apical failures, or graft complications as determined by chart review and questionnaires. There are no published reports for biomaterials using xenografts and only a small number using allografts. The largest series to date is that of FitzGerald and associates, who recently updated their series of OASC using freeze-dried, irradiated CFL.60 Of 54 patients undergoing OASC, 83% had experienced failure at a mean follow-up of 12 months. At the time of exploration in 16 patients, viable graft could be found in only 3 patients. The use of synthetic materials for ASC was first reported in 1970 when Soichet reported the use of Silastic grafts in two patients.130 Feldman and Birnbaum131 reported on the use of Teflon in 1979, and Dewhurst and coworkers132 used Marlex mesh in 1980. Since these early reports, a variety of synthetic products have been used. In addition to the materials themselves, there are several other controversial areas regarding the use of synthetics for ASC. The first is the type of sutures used to attach the graft to the vagina. In the past, many authors have used a permanent braided suture to minimize the risk of failure and to provide a suture that the patient and her partner would not feel. In 1998, Kohli and colleagues reported a 12% vaginal erosion rate using an unspecified type of double-thickness mesh and braided sutures.133 Begley’s group, in 2005, reported a 19% erosion rate in 21 patients using a silicone polyester mesh attached to the vagina with braided permanent suture.134 However, most of the abstracts do not specify the type of suture used. A braided suture that is placed or erodes into the vagina is a theoretical source of infection for the graft. If that graft material has any characteristics that do not allow it to resist infection, this could be a cause of graft failure. A second controversy is the effect of a simultaneous hysterectomy at the time of ASC. This could potentially increase the risk of infection from vaginal microbes, and, with a fresh suture line in the vagina against the graft, it could also theoretically increase the risk of vaginal extrusion. In an excellent review of ASCs published in 2004, Nygaard and coauthors found the data inconclusive but recommended that the mesh should be attached as far from the suture lines in the vaginal apex as possible.135 Addressing the apical failure rate in Table 59-6, one can see that, with the exception of the allograft report by FitzGerald’s group, it is less than or equal to 10%; the anterior compartment appears to be an increasing concern, especially as duration of follow-up increases. As for as longevity, a more recent abstract of a study by Hilger and colleagues using Marlex is significant.136 Thirty-eight patients underwent OASC and had a mean follow-up of 13.7 years. By

questionnaire data and chart review, there was a 26% overall failure rate, including 10% undergoing reoperation for prolapse and 16% who responded that they had “prolapsing” tissue from the vagina. It is not noted how many of these failures were apical and how many involving other compartments. The vaginal erosion rate in this series was 2.6%. Regarding the vaginal extrusion rate, Begley and coworkers examined the use of silicone-coated mesh.134 After noticing several vaginal erosions, with a new commercially available silicone-covered polyester mesh (AMS Triangle), they reviewed a series of 93 patients undergoing OASC or LASC with various materials. Details are shown in Table 59-6, but their vaginal erosion rates with the silicone product, Gore-Tex, polypropylene, and autologous fascia were 19%, 9%, 0%, and 0%, respectively. Among those with the silicone mesh erosions, transvaginal attempts at repair were unsuccessful in all patients, who eventually required open explorations with removal of all mesh. In contrast the Gore-Tex erosions were successfully managed by partial excision of the mesh via a transvaginal approach in most patients. As to the vaginal extrusion rates in Table 59-6, the rates for the specific materials ranged from 0% for autologous grafts and biografts,60,129,134,139 to 19% with the silicone coated polyester,134 to 2.3% and 2.6% with the polypropylene (Prolene and Marlex, respectively).136,141 In the previously mentioned review by Nygaard and associates,135 the following vaginal erosion rates for specific materials were found: cadaveric fascia or dura mater, 0% (0/88); polypropylene (Prolene), , 0.5% (1/211); polyethylene (Mersilene, Johnson & Johnson), 3.1% (25/811); Gore-Tex, 3.4% (12/350); and Teflon (EI Dupont, deMours, and Co.), 5.5% (6/119). In conclusion, it would appear that the risk of vaginal extrusion, from an ASC using a type I polypropylene mesh lies somewhere between that of the sling and that of anterior repair. Because it is a formidable procedure for the patient to undergo, even laparoscopically, we do not believe that most practitioners will accept the high failure rate of biomaterials. Additionally, regardless of the approach, the morbidity from harvesting autologous tissue of these dimensions is concerning. At this time, most surgeons performing this operation appear to believe that the current vaginal extrusion rates with the newer mesh products are acceptable in view of the high success rates in terms of apical support. Theoretically, there is a small risk to using a braided permanent suture to attach this graft material to the vaginal wall, and, in a case of a concomitant hysterectomy, it is prudent to keep the graft as far from the suture line in the vaginal apex as possible.

CONCLUSIONS CONCERNING THE USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY Tissue engineering and/or stem cell research may one day render the controversies discussed in this chapter obsolete. When that day arrives, we will have an unlimited supply of biocompatible, healthy, living fascia to use in pelvic reconstruction. Until then, it remains incumbent on pelvic surgeons to closely follow the literature, to provide informed consent, and to carefully weigh the risks and benefits of the use of these materials in our patients.

Chapter 59 USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY

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73. 74. 75. 76. 77. 78. 79.

80. 81.

82. 83. 84. 85.

86. 87. 88. 89. 90. 91. 92. 93. 94. 95.

and autologous fascia in the rabbit model: implications for sling surgery. J Urol 171:1970-1973, 2004. Williams TJ, Te Linde RW: The sling operation for urinary incontinence using Mersilene ribbon. Obstet Gynecol 19:241-245, 1962. Ridley JH: Appraisal of the Goebell-Frangenheim-Stoeckel sling procedure. Am J Obstet Gynecol 95:714-721, 1966. Morgan JE: A sling operation using Marlex polypropylene mesh for treatment of recurrent stress incontinence. Am J Obstet Gynecol 106:369-377, 1970. Morgan JE, Farrow GA, Stewart FE: The Marlex sling operation for the treatment of recurrent stress urinary incontinence: A 16-year review. Am J Obstet Gynecol 151:224, 1984. Stanton SL, Brindley GS, Holmes DM: Silastic sling for urethral sphincter incompetence in women. Br J Obstet Gynaecol 92:747, 1985. Duckett JRA, Constantine G: Complication of silicone sling insertion for stress urinary incontinence. J Urol 163:1835, 2000. Ulmsten U, Heriksson L, Jonson P, Varhos G: An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 7:81, 1996. Shah DK, Paul EM, Amukele S, et al: Broad based tension-free synthetic sling for stress urinary incontinence: 5-Year outcome. J Urol 170:849-851, 2003. Rodriguez LV, Raz S: Prospective analysis of patient treated with a distal urethral polypropylene sling for symptoms of stress urinary incontinence: Surgical outcome and satisfaction determined by patient driven questionnaires. J Urol 170:857-863, 2003. Kobashi KC, Govier FE: Perioperative complications: The first 140 polypropylene pubovaginal slings. J Urol 170:1918-1921, 2003. Wilson TS, Lemack GE, Zimmerman PE: Management of intrinsic sphincteric deficiency in women. J Urol 169:1662-1669, 2003. Karram MM, Segal JL, Vassallo BJ, Kleeman SD: Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 101(5 Pt 1):929-932, 2003. Levin I, Groutz A, Gold R, et al: Surgical complications and medium-term outcome results of tension free vaginal tape: A prospective study of 313 consecutive patients. Neurourol Urodyn 23:79, 2004. Tsivian A, Kessler O, Mogutin B, et al: Tape related complications of the tension-free vaginal tape procedure. J Urol 171:762-764, 2004. Cumberland VH: A preliminary report on the use of prefabricated nylon weave in the repair of ventral hernia. Med J Aust 1:143-144, 1952. Scales JT: Materials for hernia repair. Proc R Soc Med 46:647-652, 1953. Vervigni M, Natale F: The use of synthetics in the treatment of pelvic organ prolapse. Curr Opin Urol 11:429-435, 2001. White TA: The effect of porosity and biomaterial on the healing and long-term mechanical properties of vascular prostheses. ASAIO J 11:95-100, 1988. Voyles CR, Richardson JD, Bland SM, et al: Emergency abdominal wall reconstruction with polypropylene mesh: Short-term benefits versus long-term complications. Ann Surg 194:219-223, 1981. Chin YK, Stanton SL: A follow up of silastic sling for genuine stress incontinence. Br J Obstet Gynaecol 102:143, 1995. Duckett JR, Constantine G: Complications of silicone sling insertion for stress urinary incontinence. J Urol 163:1835, 2000. Govier FE, Kobashi KC, Committer C, et al: Multi-center prospective study of a transvaginal silicone coated synthetic mesh sling. Urology 66:741-745, 2005. Barbalias G, Liatsikos E, Barbalias D: Use of slings made of indigenous and allogenic material (Gore-Tex) in type III urinary incontinence and comparison between them. Eur Urol 31:394, 1997.

Chapter 59 USE OF SYNTHETICS AND BIOMATERIALS IN VAGINAL RECONSTRUCTIVE SURGERY

96. Kobashi KC, Dmochowski RR, Mee SL, et al: Erosion of woven polyester pubovaginal sling. J Urol 162:2070, 1999. 97. Bhargava S, Chapple CR: Rising awareness of the complications of synthetic slings. Curr Opin Urol 14:317, 2004. 98. Nilsson CG, Falconer C, Rezapour M: Seven-year follow-up of the tension-free vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 104:1259, 2004. 99. Abouassaly R, Steinberg JR, Lemieux M, et al: Complications of tension-free vaginal tape surgery: A multi-institutional review. BJU Int 94:110, 2004. 100. Delorme E, Droupy S, deTayrac R, Delmas V: Transobturator tape (Uratape): A new minimally-invasive procedure to treat female urinary incontinence. Eur Urol 45:203, 2004. 101. De Tayrac R, Deffieux X, Droupy S, et al: A prospective randomized trial comparing tension-free vaginal tape and transobturator suburethral tape for surgical treatment of stress urinary incontinence. Am J Obstet Gynecol 190:602, 2004. 102. Bhargava S, Chapple CR: Rising awareness of the complications of synthetic slings. J Urol 14:317-321, 2004. 103. Volkmer BG, Nesslauer T, Rinnab L, et al: Surgical intervention for complications of tension-free vaginal tape procedure. J Urol 169:570, 2003. 104. Clemens JQ, DeLancey JO, Faerber GJ, et al: Urinary tract erosions after synthetic pubovaginal slings: Diagnosis and management strategy. Urology 56:589, 2000. 105. Kobashi KC, Govier FE: Management of vaginal erosion of polypropylene mesh slings. J Urol 169:2242-2243, 2003. 106. Paraiso MFR, Ballard LA, Walter MD, et al: Pelvic support defects and visceral and sexual function in women treated with sacrospinous ligament suspension and pelvic reconstruction. Am J Obstet Gynecol 175:1423-1431, 1996. 107. Shull BL, Capen CV, Riggs MW, Kuehl TJ: Preoperative and postoperative analysis of site-specific pelvic support defects in 81 women treated with sacrospinous ligament suspension and pelvic reconstruction. Am J Obstet Gynecol 166:1764-1771, 1992. 108. Shull BL, Ben SJ, Kuehl TJ: Surgical management of prolapse of the anterior vaginal segment: An analysis of support defects, operative morbidity, and anatomic outcome. Am J Obstet Gynecol 171:14291439, 1994. 109. Moore J, Armstrong JR, Willis SW: The use of tantalum mesh in cystocele with critical report of ten cases. Am J Obstet Gynecol 69:1127-1135, 1955. 110. Julian TM: The efficacy of Marlex mesh in the repair of severe recurrent vaginal prolapse of the anterior mid vaginal wall. Am J Obstet Gynecol 175:1472-1475, 1996. 111. Nicita G: A new operation for genitourinary prolapse. J Urol 160:741-745, 1998. 112. Flood CG, Drutz HP, Waja L: Anterior colporrhaphy reinforced with Marlex mesh for the treatment of cystoceles. Int Urogynecol J 9:200-204, 1998. 113. Kobashi KC, Mee SL, Leach GE: A new technique for cystocele repair and transvaginal sling: The cadaveric prolapse repair and sling (CaPS). Urology 56(S6A):9-14, 2000. 114. Kobashi KC, Leach GE, Chon J, Govier FE: Continued multicenter followup of the cadaveric prolapse repair with sling. J Urol 168:2063-2068, 2002. 115. Sand PK, Koduri S, Lobel RW, et al: Prospective randomized trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Am J Obstet Gynecol 184:1357-1362, 2001. 116. Weber AM, Walters MD, Piedmonte MR, et al: Anterior colporrhaphy: A randomized trial of three surgical techniques. Am J Obstet Gynecol 185:1299-1304; discussion 1304-1306, 2001. 117. Milani R, Salvatore S, Soligo M, et al: Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with Prolene mesh. BJOG 112:107-111, 2005. 118. De Taryac R, Gervaise A, Fernandez H: [Cystocele repair by the vaginal route with a tension-free sub-bladder prosthesis] [French]. J Gynecol Obstet Biol Reprod 31:597-599, 2002.

119. Staskin DR, Plzak L: Synthetic slings: Pros and cons. Curr Urol Reports, 3:414-417, 2002. 120. Groutz A, Chaikin DC, Theusen E, Blaiva JG: Use of cadaveric solvent-dehydrated fascia lata for cystocele repair: Preliminary results. Urology 58:179-183, 2001. 121. Chung SY, Frank M, Smith CP, et al: Technique of combined pubovaginal sling and cystocele repair using a single piece of cadaveric dermal graft. Urology 59:538-541, 2002. 122. Clemmons JL, Myers DL, Aguilar VC, Arya LA: Vaginal paravaginal repair with an AlloDerm graft. Am J Obstet Gynecol 189:16121619, 2003. 123. Powell CR, Simsiman AJ, Menefee SA: Anterior vaginal wall hammock with fascia lata for the correction of stage 2 or grater anterior vaginal compartment relaxation. J Urol 171:264-267, 2004. 124. Gomelsky A, Rudy DC, Dmochowski RR: Porcine dermis interposition graft for repair of high grade anterior compartment defects with or without concomitant pelvic organ prolapse procedures. J Urol 171:1581-1584, 2004. 125. Leboeuf L, Mile RA, Kim SS, Gousse AE: Grade 4 cystocele repair using four-defect repair and porcine xenograft acellular matrix (Pelicol): Outcome measure using SEAPI. Urology 64:282-286, 2004. 126. Mage P: [Interposition of a synthetic mesh by vaginal approach in the cure of genital prolapse.] [French] J Gynecol Obstet Biol Reprod 28:825-829, 1999. 127. Migliari R, De Angelis M, Madeddu G, Verdacchi T: Tension-fee vaginal mesh repair for anterior vaginal wall prolapse. Eur Urol 38:151-155, 2000. 128. Rutman MP, Deng DY, Rodriquez LV, Raz S: Restoring the strength of the weakened sacrouterine ligaments (SUL) in vaginal vault prolapse and repair of pelvic floor relaxation with the use of polypropolene mesh [abstract 867]. J Urol 173(4):236, 2005. 129. Latini JM, Brown JA, Kreder KJ: Abdominal sacral colpopexy sing autologous fascia lata. J Urol 171:1176, 2004. 130. Soichet S: Surgical correction of total genital prolapse with retention of sexual function. Obstet Gynecol 36:69-75, 1970. 131. Feldman GB, Birnbaum SJ: Sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 53:399-401, 1979. 132. Dewhurst J, Toplis PJ, Shepherd JH: Ivalon sponge hysterosacropexy for genital prolapse in patients with bladder extrophy. Br J Obstet Gynaecol 87:67-69, 1980. 133. Kohli N, Walsh RM, Roat TW, Karram MM: Mesh erosion after abdominal sacrocolpopexy. Obstet Gynecol 92:999-1004, 1998. 134. Begley JS, Kupferman SP, Kuznetsov DD, et al: Incidence and management of abdominal sacrocolpopexy mesh erosions. Am J Obstet Gynecol 192:1956-1962, 2005. 135. Nygaard IE, McCreery R, Brubaker L, et al: Abdominal sacrocolpopexy: A comprehensive review. Am Coll Obstet Gynecol 104:805, 2004. 136. Hilger WS, Poulson M, Norton PA: Long-term results of abdominal sacrocolpopexy. 29th Annual Meeting of the Society of Gynecologic Surgeons, Anaheim, CA, March 5-7, 2003. 137. Snyder TE, Krantz KE: Abdominal-retroperitoneal sacral colpopexy for the correction of vaginal prolapse. Obst Gynecol 77:944949, 1991. 138. Costantini E, Lombi R, Micheli C, et al: Colposacropexy with GoreTex mesh in marked vaginal and uterovaginal prolapse. Eur Urol 34:111-117, 1998. 139. Brizzolara S, Pillai-Allen A: risk of mesh erosion with sacral colpopexy and concurrent hysterectomy. Obstet Gynecol 102:306, 2003. 140. Culligan PJ, Murphy M, Blackwell L, et al: Long-term success of abdominal sacral colpopexy using synthetic mesh. 28th Annual Meeting of the Society of Gynecologic Surgeons, Dallas, TX, March 4-6, 2002. 141. Elneil S, Cutner AS, Remy M, et al: Abdominal sacrocolpopexy for vault prolapse without burial of mesh: A case series. BJOG 112:486489, 2005.

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Part A ANTERIOR VAGINAL WALL PROLAPSE Chapter 60

MANAGEMENT OF THE URETHRA IN VAGINAL PROLAPSE Connie S. DiMarco and Nancy B. Itano One of the greatest challenges to the reconstructive pelvic floor surgeon is the approach to pelvic organ prolapse (POP) in the clinically continent woman. It is controversial whether the urethra should be surgically addressed at the time of vaginal prolapse repair. It has been proposed that a prophylactic antiincontinence procedure be performed concomitantly due to the risk of developing stress urinary incontinence (SUI) once the vaginal axis has been restored. The counterargument suggests that, because only a small percentage of continent women with POP develop SUI postoperatively, many patients would undergo an unnecessary procedure with this approach. Even the most minimally invasive anti-incontinence procedures carry a potential risk of morbidity to the patient.

EFFECT OF PELVIC ORGAN PROLAPSE ON URINARY SYMPTOMS Moderate and severe pelvic floor relaxation can present with a variety of lower urinary tract symptoms. Many urinary symptoms can be attributed to obstructive voiding. These symptoms may include frequency, urgency, nocturia, hesitancy, doublevoiding, sense of inadequate emptying, stranguria, flow intermittency, and suprapubic discomfort. Elevated postvoid residual volumes can also lead to recurrent or persistent urinary tract infections. Hypothetical causes include urethral kinking, urethral compression, bladder neck elongation, and detrusor hypocontractility/dysfunction. When severe prolapse involves the bladder, patients can also present with ureteral obstruction and hydronephrosis.1,2 Patients with POP may be continent or incontinent. Mechanisms for continence in prolapse include urethral obstruction, anatomic urethral kinking with descent of the bladder base, and abdominal pressure dissipation.3 These mechanisms may also contribute to obstructive voiding symptoms. Bergman and colleagues4 proposed that, in prolapse, a large cystocele provides a “cushion effect” that absorbs some of the intraabdominal pressure, effectively lowering the abdominal pressure placed on the continence mechanism (urethral complex). Ghoniem and associates3 proposed that the only fixed portion of the lower urinary tract in large cystoceles is the distal urethra, supported by the pubourethral ligament. They hypothesized that the pubourethral ligament may be the only supporting structure that maintains its 624

strength in the setting of severe prolapse, allowing for urinary continence. There are many theories on the cause of stress urinary incontinence (SUI), which are beyond the scope of this chapter. However, POP is a common coexisting condition, and prolapse reduction (surgical or manual) may reveal an underlying incompetent urethral continence mechanism. Pelvic Organ Prolapse Dietz and coworkers5 reported on 223 vaginal prolapse patients with symptoms of lower urinary tract symptoms presenting in two urogynecology clinics. Urinary symptoms included SUI in 64% (142 patients), urge incontinence in 61% (134), frequency in 38% (84), nocturia in 38% (84), and obstructive symptoms (including stranguria, sense of incomplete emptying, intermittency, and hesitancy) in 56% (124). Cystocele Romanzi and colleagues6 prospectively evaluated 60 women with various degrees of cystocele and found the following urinary complaints (patients could have more than one symptom): frequency/urgency, 35%; urge incontinence, 15%; stress incontinence, 60%; and difficult voiding 23%. Women with higher stages of anterior prolapse had a statistically greater likelihood of obstructive voiding than did those with lower stages of prolapse (70% in grades 3/4 versus 3% in grades 1/2). Obstruction was defined as a maximum detrusor pressure at maximum flow (PdetQmax) of greater than 25 cm H2O and a maximum flow of less than 15 mL/sec. Uterovaginal Prolapse Patients with uterovaginal prolapse may also present with lower urinary tract symptoms. The group at Kaohsiung Medical University7 studied 38 clinically continent and 20 incontinent women with stage III/IV complete uterovaginal prolapse. Incontinent women were more likely to report urinary frequency, urgency, and nocturia. However, the continent women had a higher incidence of voiding hesitancy. Urodynamic parameters between the two groups were compared. The women without stress incontinence had significantly higher (PdetQmax), maximum urethral closure pressures (MUCP), and urethral-abdominal pressure

Chapter 60 MANAGEMENT OF THE URETHRA IN VAGINAL PROLAPSE

Table 60-1 Urodynamic Comparison of Continent and Incontinent Women with Stage III/IV Uterovaginal Prolapse Parameter

Continent Patients (n = 20)

Incontinent Patients (n = 38)

P Value

38 84 1.02

24 63 0.66

.01 .03 .02

PdetQmax (mean, cm H2O) MUCP (mean, cm H2O) Urethral-abdominal pressure transmission ratio

MUCP, maximum urethral closing pressure; PdetQmax, detrusor pressure at maximum flow. From Long CY, Hsu SC, Wu TP, et al: Urodynamic comparison of continent and incontinent women with severe uterovaginal prolapse. J Reprod Med 49:33-37, 2004.

transmission ratios (Table 60-1). The pressure transmission ratio should be 1.0 (ideal) when increases in abdominal pressure are transmitted equally to the abdominal transducer (usually rectal or vaginal) and the urethral transducer. With rotation of the urethra, compressive forces from the abdominal cavity are incompletely transmitted to the urethral complex, creating a ratio of less than 1.0. Posthysterectomy Vault Prolapse and Enterocele Wall and Hewitt8 described urinary characteristics in 19 women with complete posthysterectomy vaginal vault prolapse. Symptoms of urgency was present in 79% (15 patients) and urge incontinence in 63% (12 patients). Occult SUI was demonstrated by prolapse reduction with a single-bladed speculum in 47% (9 patients). Urodynamic parameters included peak flow rate (Qmax) and PdetQmax. The mean Qmax was 11 mL/sec, and PdetQmax was 50 cm H2O, meeting the pressure-flow parameters for female outlet obstruction outlined by Massey and Abrams.9 Rectocele Even patients with isolated posterior wall support defects can have masked SUI. Myers and colleagues10 evaluated 90 patients with isolated posterior compartment prolapse, including 28 with grade III+ rectoceles. Fourteen percent (n = 4/28) demonstrated SUI when their prolapse was reduced with a split Pederson speculum that was not present without prolapse reduction. The mean decrease in MUCP with rectocele reduction was 7.0 cm H2O. The authors theorized that severe posterior wall defects act to compress and support the anterior wall, artificially raising the MUCP, increasing functional length, and masking SUI. Women with POP can present with a myriad of urinary symptoms. A thorough history must include extensive details of voiding habits, including a previous history of incontinence that improved with worsening prolapse. As with staging of prolapse severity, physical examination findings can vary with bladder volume, rectal contents, and position. The Pelvic Floor Disorders Network recently published their findings on technique modifications that can result in intraobserver variability.11 Prolapse was graded as more severe in the standing position compared with the lithotomy supine position. The type of speculum was not standardized. Prolapse severity was consistent using either a split speculum or a manual (two-digit) reduction method. Urinalysis should be performed to rule out urinary tract infection, and a culture with sensitivities can be sent if necessary. A screening postvoid residual volume measurement, either by catheterization or by bladder ultrasound, is a simple means to identify patients with urinary retention.

OCCULT STRESS INCONTINENCE IN PROLAPSE Many patients with significant POP are continent and demonstrate SUI only when their prolapse is reduced. There is no “gold standard” method for determining whether a patient has occult SUI. The incidence of “masked” incontinence varies with the method of prolapse reduction, with rates of 25% to 80% reported in the literature.12-15 The goal of prolapse reduction is to simulate surgical repair and determine whether the patient will be at risk for development of postoperative de novo SUI. Potential pitfalls include obstructing the urethra, which would lower the SUI detection rate, and mechanically widening the levator hiatus, which would falsely elevate the SUI detection rate (Table 60-2). Several methods of prolapse reduction to detect occult SUI have been described. A positive cough stress test (CST) is determined by objective urethral leakage with increased intraabdominal pressure. Bladder volumes vary but are commonly reported between 150 and 250 mL. Urodynamics can be employed to ensure that urinary leakage is not the result of bladder compliance abnormalities or detrusor instability. Fluoroscopy may also contribute additional anatomic information. Pessary The primary objective of a pessary is to reduce symptomatic vaginal prolapse. A pessary can be used temporarily to assess for underlying SUI, as described later. Patient satisfaction is also high when these devices are used for nonoperative management of prolapse. Clemons and associates16 recently studied patient satisfaction and changes in urinary symptoms among women using either a ring or a Gellhorn pessary after 2 months. Of the initial 100 patients, 73% were successfully fitted with a pessary. SUI improved in 45% of the patients who had incontinence symptoms at baseline. Among women without incontinence at baseline, de novo SUI developed in 21%. Pessaries may be employed both in the office setting and in long-term home use to unmask SUI. Placement of a pessary to reduce prolapse requires appropriate sizing. There should be one fingerbreadth of room around the pessary circumferentially, to prevent compression. Similarly, if the pessary is too small, the patient may extrude it when attempting to cough or perform a Valsalva maneuver. Some pessaries are designed to prevent stress incontinence (e.g., a shelf pessary) and should be avoided in this scenario. This requires a health care provider who is facile in pessary fitting and an inventory of pessaries of various shapes and sizes on hand. In one of the earliest studies, Richardson and colleagues13 found that 8 (80%) of 10 continent patients with uterine prolapse were incontinent after reduction with an inflatable pessary.

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Section 7 FEMALE ORGAN PROLAPSE

Table 60-2 Detection Rate of Occult SUI after Anti-incontinence Surgery According to Preoperative Status SUI after Surgery (% [No.]) Study & Ref. No.

Year

Surgery Type

N

Stanton et al Kayano et al22 Chaikin et al23 Gordon et al27 Barnes et al24 Meschia et al26

1982 2002 2000 2001 2002 2004

73 33 24 30 38 25 25

de Tayrac et al25

2004

Anterior plication Kelly-Kennedy PVS TVT PVS TVT Anterior plication TVT No sling

21

Detection of Occult SUI (% [No.])

Incontinent Preoperatively

Occult SUI Preoperatively

69 (20/29)

11 (5/44) 61 (14/23) 14 (2/14) 10 (3/30) 5 (2/38) 4 (1/25) 36 (9/25) 0 (0/11) 13 (1/8)

69 (23/33) 58 (14/24)

40 (19/48)

7 (1/15) 36 (5/14)

Continent Preoperatively (No Occult SUI)*

0 (0/10)

PVS, bladder neck pubovaginal sling; SUI, stress urinary incontinence; TVT, tension-free vaginal tape. *Negative cough stress test for occult SUI.

Bergman and coauthors4 described the use of a Smith-Hodge pessary (size 2 or 3) to reduce prolapse in 67 women without symptoms of SUI. Twenty-four patients had a drop in abdominal pressure transmission to the urethra (30 days), only one of which required urethrolysis. The most common

The CaPS procedure, which uses nonfrozen cadaveric fascia lata for cystocele repair, has several advantages over traditional anterior repair. Both central and lateral defects can be repaired simultaneously, avoiding the use of the patient’s inherently weak tissues. The procedure is performed entirely transvaginally, resulting in minimal morbidity, and avoids the use of synthetic materials in the vagina. Most patients are discharged on postoperative day 1. Sling placement at the time of cystocele repair allows simultaneous treatment of symptomatic SUI, as well as occult SUI demonstrated preoperatively with cystocele reduction, with minimal risk of urinary retention. Results of prolapse repair have been excellent and durable, with a symptomatic cure rate of 94% at long-term follow-up. Continence rates with the cadaveric fascial sling have been less durable, with failure rates approaching 30% at long-term follow-up. In order to improve continence results, we are currently exploring other materials and approaches to sling placement, as mentioned earlier, and continue to use cadaveric fascia lata for cystocele repair given its excellent long-term results.

References 1. Kohli N, Sze EHM, Roat TW: Incidence of recurrent cystocele after anterior colporraphy with and without concomitant bladder neck suspension. Am J Obstet Gynecol 175:1476-1482, 1996. 2. Benson JT, Lucente V, McClellan E: Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: A prospective randomized study with long-term evaluation outcome. Am J Obstet Gynecol 175:1418-1422, 1996. 3. Chopra A, Raz S, Stothers L: Pathogenesis of cystoceles: Anterior colporrhapy. In Raz S (ed): Female Urology. Philadelphia, WB Saunders, 1996. 4. Lemer ML, Chaikin DC, Blaivas JG: Tissue strength analysis of autologous and cadaveric allografts for the pubovaginal sling. Neurourol Urodyn 18:497-503, 1999. 5. Jinnah RH, Johnson C, Warden K, Clarke HJ: A biomechanical analysis of solvent-dehydrated and freeze-dried human fascia lata allografts: A preliminary report. Am J Sports Med 20:607-612, 1992. 6. Gordon D, Groutz A, Wolman I, et al: Development of postoperative stress urinary incontinence in clinically continent patients undergoing prophylactic Kelly plication during genitourinary prolapse repair. Neurourol Urodyn 18:193-198, 1999. 7. Chaikin DC, Groutz A, Blaivas JG: Predicting the need for antiincontinence surgery in continent women undergoing repair of severe urogenital prolapse. J Urol 163:531-534, 2000. 8. Groutz A, Gold R, Pauzner D, et al: Tension-free vaginal tape (TVT) for the treatment of occult stress urinary incon-

9. 10. 11. 12. 13. 14. 15. 16. 17.

tinence in women undergoing prolapse repair: A prospective study of 100 consecutive cases. Neurourol Urodyn 23:632-635, 2004. Kobashi KC, Mee SL, Leach GE: A new technique for cystocele repair and transvaginal sling: The cadaveric prolapse repair and sling (CaPS). Urology 56:9-14, 2000. Kobashi KC, Leach GE, Chon J, Govier FE: Continued multicenter followup of the cadaveric prolapse repair with sling. J Urol 168:20632068, 2002. Frederick RW, Leach GE: Cadaveric prolapse repair with sling: Intermediate outcomes with 6 months to 5 years of followup. J Urol 173:1229-1233, 2005. Raz S, Erickson DR: SEAPI QNM Incontinence classification system. Neurourol Urodyn 11:187-199, 1992. Kobashi KC, Gormley EA, Govier F, et al: Development of a validated quality of life assessment instrument for patients with pelvic prolapse [abstract]. J Urol 163:76, 2000. Baden WF, Walker TA: Surgical Repair of Vaginal Defects. Philadelphia, JB Lippincott, 1992. Leach GE: Urethrolysis. Urol Clin North Am 2:23-27, 1994. Sutaria PM, Staskin DR: A comparison of fascial “pull-through” strength using four different suture fixation techniques [abstract]. J Urol 161:79, 1999. Wein AJ: Transobturator Tape (Uratape): A new minimimallyinvasive procedure to treat female urinary incontinence [abstract]. J Urol 172:1214, 2004.

Chapter 62

TRANSABDOMINAL PARAVAGINAL CYSTOCELE REPAIR Danita Harrison Akingba, Michelle M. Germain, and Alfred E. Bent

HISTORY In 1909, Dr. George White described a novel idea for the etiology of cystoceles based on his work with cadaver dissection.1 He first described the supportive attachments of the vagina. He next illustrated how lateral detachment of the pubocervical fascia from the arcus tendineous fascia pelvis, or white line, results in cystocele. He also outlined the critical steps for the transvaginal paravaginal repair of these types of cystoceles. It is clear after reading the peer review section following his article that his idea was unique at the time and that a fundamental understanding of the threedimensional relationship of female pelvic anatomy was lacking. Three years later, White submitted a treatise in which he reviewed the three theories of that period regarding the etiology of cystocele2: 1. Cystocele is due to thinning out of the anterior vaginal wall and thus a hernia. 2. Ligaments suspend the bladder, like the stomach. 3. The bladder descends because its ligamentous attachments to the uterus and obliterated hypogastric arteries have been stretched or broken during labor. In his paper, White rejected each of these theories based on clinical examination findings, lack of histologic and anatomic evidence to support the theories, and, finally, the fact that not all women having hysterectomy developed cystoceles. White again described his technique for vaginal paravaginal repair for the management of cystocele. He acknowledged that the vaginal approach was more difficult because of limited visibility, but he believed that the surgical approach for treatment of cystocele should remain vaginal because of the then-widespread practice of concurrent perineorrhaphy. He conceded that, “to incise the peritoneum at the side of the bladder, push the bladder aside until the white line comes into view, then by the aid of an assistant’s finger in the vagina, suture the anterior lateral side of the vagina to the white line, and close the peritoneum” may be “the easiest and simplest way to accomplish this.”2 However, he believed that the abdominal approach was seldom indicated, unless the patient suffered from procidentia. In that case, the patient would be best served by concurrent restoration of the broad and uterosacral ligaments. White’s papers were largely forgotten for the next 70 years. Historically, it is not clear why his ideas were not readily accepted. Perhaps it was because the approach was difficult to perform, or because his peers lacked a proficient understanding of the lateral

fascial defects and their role in anterior vaginal wall prolapse. Even more significant was the almost simultaneous publication of Howard Kelly’s treatise on cystocele, its repair, and the treatment of stress incontinence.3 The Kelly plication is straightforward in its conceptualization and technically easier to perform. Failures of the Kelly plication in a large number of cystocele repairs led to a series of “new” techniques for the repair of lateral anterior wall defects, including work by John C. Burch and Cullen Richardson.4,5 In 1961, Burch reported his experience with colposuspension in the treatment of stress incontinence. He attached the paravaginal fascia to the white line of the pelvis in the first seven of his patients. He wrote that the maneuver “produced a most satisfactory restoration of the normal anatomy of the bladder neck . . . and a surprising correction of most of the cystocele . . . overcoming the anterior cystocele involving the neck of the bladder, but also the posterior cystocele involving the base of the bladder.”4 Despite such positive results with correction of both urethral hypermobility and bladder prolapse, Burch believed that the white line held sutures poorly and therefore sought another fixation point. Subsequently, he chose Cooper’s ligament as the point of fixation. In 1976, Richardson, Lyon, and Williams published a “new” look at pelvic relaxation. They outlined the technique for transabdominal paravaginal repair—echoing the descriptions of White and Burch. They also identified the four areas of defects or breaks in the pubocervical fascia, in their order of occurrence5: 1. Lateral (paravaginal), where the pubocervical fascia attaches to the arcus tendineous fascia pelvis or white line 2. Transverse, in front of the cervix, where the pubocervical fascia blends into the pericervical ring of fibromuscular tissue (or at the cuff in a woman who has had a hysterectomy) 3. Central, on anterior vaginal wall between the lateral margins of the vagina 4. Distal, where the urethra perforates the urogenital diaphragm (Fig. 62-1) Sixty-seven percent of their patients had paravaginal defects. Typically, today, no clinical distinction is made between central and distal tears. In addition, no effort is usually made intraoperatively to distinguish among these types of defects, because Kellytype plication procedures have been performed for both for years with good results. However, transverse defects require reapproximating the tears in the fascia. 635

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Distal defect Paravaginal defects Central defect

Levator arcus

Arcus tendoneous fascia pelvis Transverse defect

Figure 62-1 The four locations of breaks in pubocervical fascia: lateral (perivaginal), where the pubocervical fascia attaches to the arcus tendineous fascia pelvis or white line; transverse, in front of the cervix, where the pubocervical fascia blends into the pericervical ring of fibromuscular tissue (or at the cuff in a woman who has had a hysterectomy); central, on the anterior vaginal wall between the lateral margins of the vagina; and distal, where the urethra perforates the urogenital diaphragm. (From Richardson AC: Operative Techniques in Gynecologic Surgery. Philadelphia, WB Saunders, 1996.)

Pubocervical fascia

Rectovaginal fascia

Arus tendoneous fascia pelvis Levator arcus

Figure 62-2 The arcus tendineous fascia pelvis extends from the inferior margin of the pubic symphysis to the ischial spine parallel to the levator arcus. Anteriorly, the bladder has been cut away. A cross-section through the vagina reveals the apposition of the rectovaginal fascia to the rectum and perirectal space. (From Richardson AC: Operative Techniques in Gynecologic Surgery. Philadelphia, WB Saunders, 1996.)

ANATOMY The pubocervical fascia (or endopelvic fascia), a trapezoidshaped, fibromuscular band of tissue, supports the urethra, bladder, and uterus anteriorly (Fig. 62-2). Its lateral border extends from a point just anterior to the ischial spines, along the arcus tendineous fascia pelvis or white line, to the pubic ramus anteriorly. Posteriorly, it reaches the cervix or vaginal cuff at the level of the base of the broad ligament and cardinal-uterosacral ligaments and reaches across toward the ischial spines.

Figure 62-3 The arcus tendineous fascia pelvis has separated entirely off the pelvic sidewall. (From Richardson AC: Operative Techniques in Gynecologic Surgery. Philadelphia, WB Saunders, 1996.)

Anterior vaginal wall prolapse results from herniation of the pelvic organs normally supported by the pubocervical fascia into the vaginal lumen. Many gynecologists believe that identification and repair of defects in this fascia are essential to achieve successful anterior colporrhaphy. However, the existence of fascial tissue between the vagina and bladder or vagina and rectum has never been proven histologically.6-9 To examine the histology of surgical fascia used during anterior colporrhaphy, to compare it to rectovaginal fascia, and to determine the consistency with which this tissue is diagnosed surgically, Farrell and his colleagues examined the fascia of women who were scheduled to undergo a primary surgical correction of pelvic organ prolapse.9 Biopsies taken of surgically identified pubocervical fascia and rectovaginal fascia during colporrhaphy failed to identify a distinct fascial layer. Instead, histologic examinations of tissue identified as fascia intraoperatively showed it to be indistinguishable from deep vaginal wall connective tissue. It is possible to have both central and lateral defects concurrently. Lateral detachment of the pubocervical fascia may occur if the entire arcus pulls away from the pelvic sidewall (Fig. 62-3). Alternatively, the entire arcus may remain attached to the sidewall while the pubocervical fascia pulls away.27 Finally, the arcus could split, with a portion remaining attached to the pubocervical fascia medially and another portion remaining attached to the pelvic sidewall laterally (Fig. 62-4). Most anterior compartment prolapse results from lateral detachment of the pubocervical fascia.5 Although Richardson and colleagues were not the first to publish on the anatomic concept of paravaginal defects, they popularized the concept of discrete isolated fascial defects in the mid-1970s. Based on this work, the overall incidence of paravaginal defects was 67%, with the great majority being right-sided defects. Some years later, Barber and Cundiff conducted a retrospective chart review of 70 patients with a preoperative diagnosis of paravaginal defect.10 Sixty-three percent (44/70) were believed to have unilateral or bilateral paravaginal defects preoperatively, based on clinical examination. The intraoperative findings confirmed the prevalence of paravaginal defects as just 42%.

Chapter 62 TRANSABDOMINAL PARAVAGINAL CYSTOCELE REPAIR

Diagnosis A thorough physical examination in the office is the principal method of diagnosis of paravaginal defects. The patient is examined in the dorsal lithotomy position. With gentle downward traction of the posterior blade of the speculum, the anterior

Arcus tendoneous fascia pelvis

Figure 62-4 The arcus tendineous fascia pelvis has split down the middle, leaving some of its remnants attached to the pubocervical fascia and some still attached to the pelvic sidewall. (From Richardson AC: Operative Techniques in Gynecologic Surgery. Philadelphia, WB Saunders, 1996.)

compartment is examined at rest and with maximum Valsalva maneuver. It is important to restore normal anatomy, so a ring forceps, Baden-Walker defect analyzer, or a wooden tongue blade should be used to gently elevate the lateral vaginal sulci, angling parallel to the white line (Fig. 62-5). Each side is checked separately, and then both together by elevating both sulci while the patient bears down. Bilateral paravaginal defects are corrected with this maneuver; central defects will prolapse around the elevating device. Suspected central defects should be supported with these instruments during Valsalva maneuver. If anterior prolapse is only partially reduced by either maneuver, then the patient is thought to have both paravaginal and central defects. Paravaginal defects can be misdiagnosed. Barber and Cundiff found that the sensitivity of physical examination for the detection of right-sided paravaginal defects was 94% and the specificity was 54%. The positive predictive value of clinical examination was 65%, and negative predictive value was 91%. For left-sided defects, the sensitivity, specificity, positive predictive value, and negative predictive value were 90%, 50%, 57%, and 88%, respectively.10 Ultrasound and magnetic resonance imaging have both been used for the diagnosis of paravaginal defects.11-13 However, given the time and expense of these tests, they are not recommended for routine diagnosis of paravaginal defects in the urogynecologist’s office. The clinical examination remains the standard for diagnosis.

Bulging anterior vaginal wall

A

B

Figure 62-5 A, Cystocele defect seen protruding through the introitus. B, Lateral cystocele defect reduced with ring forceps placed laterally to elevate the pubocervical fascia toward the ischial spines. (From Retzky SS, et al. Urinary incontinence in women. Summit, NJ: Clinical Symposia Ciba-Geigy Corp, 47(3):22, 1995; adapted from Plate 11. Copyright 1995 ICON Learning Systems, LLC, a subsidiary of MediMedia USA Inc.)

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TRANSABDOMINAL REPAIR In 1976, Richardson described the transabdominal paravaginal repair. Although modifications have been described, the standard accepted technique has not been altered significantly from his original description. The patient is placed in low lithotomy position, and a Foley catheter is passed transurethrally. The bladder should be drained for adequate exposure and visualization into the retropubic space. If the patient has a uterus, the hysterectomy is performed first and the peritoneum is closed before proceeding with the paravaginal repair. A Pfannenstiel fascial incision is used most often. The rectus muscles are divided in the midline and held laterally by a self-retaining retractor. As with the Burch procedure, care must be taken to avoid injury to the inferior epigastric vessels. The space of Retzius is entered bluntly and developed cautiously under direct visualization to avoid injuring the large veins in this space. If the patient has had a prior Burch procedure, this space may be difficult to develop atraumatically (Fig. 62-6). Hemoclips are often required to maintain hemostasis. Once the space is fully developed, the retropubic anatomy may be visualized, including the pubic symphysis, the bladder neck in the midline, and the obturator neurovascular bundles and Cooper’s ligament laterally. The obturator fossa can usually be identified first by palpation, because it feels like a vertically positioned buttonhole. Care should be taken while dissecting around this fossa to avoid damaging the obturator nerve, artery, and vein. Finally, the white line is identified along the pelvic sidewall as it travels from the inferior border of the pubic symphysis to the ischial spine. Further, blunt dissection using a sponge on a stick or Kittner may be required to remove adipose tissue adherent to the pubocervical fascia. The surgeon’s fingers are placed inside the vagina to elevate the lateral sulcus and aid in demonstrating the white pubocervi-

cal fascia and the superior extent of the vagina (Figs. 62-7 and 62-8). It is important to plan suture locations before actual placement, to avoid undue lateral tension on the vaginal wall when the sutures are tied. Synthetic, nonabsorbable sutures are used. The first suture is placed laterally, near the apex of the vagina, through the paravesical portion of the pubocervical fascia or the detached white line if it is visible. The needle is then passed through the ipsilateral obturator internus fascia around the arcus tendineus fascia pelvis (white line) at its origin, 1 cm anterior to the ischial spine. Three to five sutures are placed sequentially through the pubocervical fascia, distal to the prior fixation point, and attached to the white line or obturator fascia at a corresponding level from the ischial spine to the lateral pubic symphysis. If the patient has bilateral paravaginal defects, the same technique is used on the opposite side. Sutures are usually tagged and held until cystoscopy is performed with the sutures both relaxed and under tension, to ensure the integrity of the bladder and the normal function of both ureters. Gelfoam may be placed into the space of Retzius for hemostasis and to aid scarification of this space. Finally, the sutures are tied so that the lateral vaginal walls are in direct contact with the obturator fascia and arcus tendineus fascia pelvis. LAPAROSCOPIC REPAIR Laparoscopic pelvic floor repair was described in 1995.14 The laparoscopic paravaginal repair is similar to the laparoscopic Burch procedure. The patient is positioned in low lithotomy position, and a Foley urethral catheter is placed into the bladder. The Foley catheter should be clamped in order to partially distend the bladder and demarcate its boundaries. Some surgeons pass 30 mL of diluted methylene blue or indigo carmine transurethrally and clamp the urethral catheter so that any iatrogenic

Figure 62-6 Visualization of the entire space of Retzius. (From Richardson AC: In Gershenson DM, Aronson MP (eds): Operative Techniques in Gynecologic Surgery. Philadelphia, WB Saunders, 1996, p 71.)

Chapter 62 TRANSABDOMINAL PARAVAGINAL CYSTOCELE REPAIR

Figure 62-7 With one finger inside the vagina elevating the lateral sulcus (insert), a full-thickness bite of the pubocervical fascia is taken. The needle is then passed through the ipsilateral obturator internus fascia around the arcus tendineous fascia pelvis. Sutures are placed from cephalad to caudad.

Figure 62-8 All sutures are held and tied down after cystoscopy confirms the integrity of the bladder. (From Richardson AC: In Gershenson DM, Aronson MP (eds). Operative Techniques in Gynecologic Surgery. Philadelphia, WB Saunders, 1996, p 72.)

cystotomies are recognized immediately by expression of blue into the operative field. Placement of trocar ports is left to the discretion of the surgeon. The space of Retzius is entered by making a transverse incision 2 inches above the pubic symphysis, spanning all three

obliterated umbilical ligaments, cephalad to the dome of the bladder. The bladder is then drained. The space of Retzius is dissected bluntly until the retropubic anatomy is clearly visualized. Some advocate removal of retropubic adipose tissue to aid in scarification.15 The pubic symphysis and bladder neck are noted

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in the midline, and the obturator neurovascular bundle, Cooper’s ligament, and the white line are noted along the pelvic sidewall. The obturator fossa is identified. With the operator’s fingers elevating the superior lateral sulcus of the vagina, the first suture is placed near the apex of the vagina, through the paravesical portion of the pubocervical fascia or the detached white line if it is visible. The needle is then passed through the ipsilateral obturator internus muscle and fascia and the white line at its origin, 1 cm anterior to the ischial spine. The lateral wall suture technique is facilitated by moving the fingers in the vagina medially to open up the sidewall compartment; this readily exposes the ischial spine and white line. The same technique is used in the open procedure. Three to five sutures are placed sequentially through the pubocervical fascia distal to the prior fixation point on each side, but in this case the sutures are tied as they are placed, using an extracorporeal knot-tying technique without a suture bridge. Often, the third and fourth sutures are placed through Cooper’s ligament to support the bladder neck (Burch), and there is usually no room for a fifth suture. Cystoscopy verifies integrity of the bladder and the normal function of both ureters. Laparoscopic paravaginal repair requires great skill, dexterity, and ingenuity. The learning curve for laparoscopic Burch or paravaginal repair is 20 to 30 procedures. There are many modifications to laparoscopic repair, but ideally the laparoscopic method should be exactly the same as the open method to achieve the same result. The laparoscope is a vehicle for performing a repair and should not be a reason to modify a technique. Seman and his colleagues described two modifications to the laparoscopic paravaginal repair16: simultaneous Burch colposuspension and paravaginal repair and the modified paravaginal repair, in which the sutures are placed caudad to cephalad and each one includes a third bite of the ipsilateral iliopectineal (Cooper’s) ligament. The use of mesh as a bridge between Cooper’s ligament and the endopelvic fascia has also been described in the literature.17 However, there is a paucity of good data regarding longterm success and feasibility of this approach. COMPLICATIONS Good surgical technique should be used in gaining exposure to the retropubic space. Damage to the large veins coursing along the detrusor muscle can cause massive hemorrhage. Anatomically, there are few structures along the pelvic sidewall that contribute to complications. The obturator neurovascular bundle lies anterior to the white line, and dissection should be limited to the medial aspect of the neurovascular bundle. Cadaver dissection of the tissues underlying and adjacent to the white line

reveals that there are no neurovascular structures along the white line, obturator fascia, or levators that preclude taking a full bite of tissue.18 Unlike procedures that create a compensatory distortion of normal anatomy, the paravaginal repair typically does not lead to postoperative problems of de novo detrusor instability or long-term urinary retention. Shull and Baden reported the rate de novo detrusor instability in their patients to be 6% in 1989. Published data reporting objective outcomes and complications of the paravaginal repair are scarce. A review of the literature revealed several articles that comment on complications. Postoperative infections, such as cystitis and wound infection, ranged from 0% to 11%; and pneumonia was reported in 4% of patients.5,19-21 Miklos and Kohli reviewed the outcomes for 171 consecutive patients who underwent laparoscopic Burch procedure, paravaginal repair, or both concurrently. Cystotomies were noted in 2.3% of patients.22 C. Y. Liu reported no lower urinary tract injuries, retropubic hematomas, or abscess formation with laparoscopic repair of paravaginal defects.15 OUTCOMES Few studies have examined the long-term anatomic success of abdominal paravaginal repair. Much of the data focuses on correction of stress urinary incontinence rather than resolution of anterior vaginal wall prolapse. Shull and Baden reported that 97% of patients treated with paravaginal repair for lateral anterior defects and stress urinary incontinence had no postoperative complaints of stress incontinence.19 Colombo and his group had more sobering results.23 In 1996, they published the only prospective, randomized, controlled trial comparing Burch colposuspension to paravaginal repair for the treatment of stress urinary incontinence. The objective cure rate was 100% for Burch and 61% for paravaginal repair. Bruce and associates had similar results, with a 72% cure rate for paravaginal repair.24 Paravaginal repair alone should not be offered for the treatment of stress incontinence. The standard of care for the treatment of stress incontinence remains a Burch or a sling procedure. There are no good studies directly comparing abdominal paravaginal repair with laparoscopic or vaginal paravaginal repair for the treatment of anterior vaginal wall prolapse. The recurrence rate for cystocele has been reported to be 5% to 50%. Failure rates for paravaginal repair reported in several retrospective studies range from 5% to 13%.15,20,21,25 De novo enterocele and cuff prolapse developed in 6% of patients who had abdominal paravaginal repair.19 As far as we know, no studies have reviewed long-term major or minor complication rates of laparoscopic paravaginal repair alone.

References 1. White GR: Cystocele: A radical cure by suturing lateral sulky of vaginal to white line of pelvic fascia. JAMA 21:1707-1710, 1909. 2. White GR: An anatomic operation for the cure of cystocele. Am J Obstet Dis Women Child 65:286, 1912. 3. Kelly HA, Dumm WM: Urinary incontinence in women without manifest injury to the bladder. Surg Gynecol Obstet 18:444-450, 1914. 4. Burch JC: Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele, and prolapse. Am J Obstet Gynecol 81:281-290, 1961.

5. Richardson AC, Lyon J, Williams N: A new look at pelvic relaxation. Am J Obstet Gynecol 126:568-573, 1976. 6. Weber A, Walters MD: Anterior vaginal prolapse: Review of anatomy and techniques of surgical repair. Obstet Gynecol 89:311-318, 1997. 7. Ricci JV, Lisa JR, Thom CH, Kron WL: The relationship of the vagina to adjacent organs in reconstructive surgery: A histologic study. Am J Obstet Gynecol 74:387-410, 1947. 8. Goff BH: A histologic study of the perivaginal fascia in a nullipara. Surg Gynecol Obstet 52:32-42, 1931.

Chapter 62 TRANSABDOMINAL PARAVAGINAL CYSTOCELE REPAIR

9. Farrell S, Dempsey T, Geldenhuys L: Histologic examination of “fascia” used in colporrhaphy. Obstet Gynecol 98:794-798, 2001. 10. Barber MD, Cundiff GW: Accuracy of clinical assessment of PV defects in women with anterior vaginal wall prolapse. Am J Obstet Gynecol 181:87-90, 1999. 11. Huddleston HT, Dunnihoo DR, Huddleston PM, Meyers PC: Magnetic resonance imaging of defects in DeLancey’s vaginal support levels I, II, and III. Am J Obstet Gynecol 172:1778-1782, 1995. 12. Martan A, Masata J, Halaska M, et al: Ultrasound imaging of paravaginal defects in women with stress incontinence before and after paravaginal defect repair. Ultrasound Obstet Gynecol 19:496-500, 2002. 13. Nguyen JK, Hall CD, Taber E, Bhatia NN: Sonographic diagnosis of paravaginal defects: A standardization of technique. Int Urogynecol J Pelvic Floor Dysfunct 11:341-345, 2000. 14. Ross JW: Post-hysterectomy Total Vaginal Vault Prolapse Repaired Laparoscopically. Presented at the second world symposium on laparoscopic hysterectomy, American Association of Gynecologic Laparoscopists, New Orleans, April 7-9, 1995. 15. Liu CY: Laparoscopic cystocele repair: Paravaginal suspension. In Liu CY (ed): Laparoscopic Hysterectomy and Pelvic Floor Reconstruction. Oxford, UK, Blackwell Scientific, 1996, pp 330-340. 16. Seman E, Cook J, O’Shea R: Two-year experience with laparoscopic pelvic floor repair. J Am Assoc Gynecologic Laparosc 10:38-45, 2003. 17. Washington J, Somers K: Laparoscopic paravaginal repair: A new technique using staples. J Soc Laparoendoscopic Surgeons 7:301303, 2003. 18. Scotti RJ, Garely AD, Greston WM, Olson TR: Paravaginal repair of lateral vaginal wall defects by fixation to the ischial periosteum and obturator membrane. Am J Obstet Gynecol 179:1436-1445, 1998.

19. Shull B, Baden W: A six-year experience with paravaginal defect repair for stress urinary incontinence. Am J Obstet Gynecol 160:1432-1440, 1989. 20. Shull B, Benn S, Kuehl T: Surgical management of prolapse of the anterior vaginal segment: An analysis of support defects, operative morbidity, and anatomic outcome. Am J Obstet Gynecol 171:14291439, 1994. 21. Ostrzenski A: Genuine stress urinary incontinence in women: New laparoscopic paravaginal reconstruction. J Reprod Med 43:477-482, 1998. 22. Miklos JR, Kohli N: Laparoscopic paravaginal repair plus Burch colposuspension: Review and descriptive technique. Urology 56:6469, 2000. 23. Colombo M, Milani R, Vitobello D, Maggioni A: A randomized comparison of Burch colposuspension and abdominal paravaginal defect repair for female stress urinary incontinence. Am J Obstet Gynecol 175:78-84, 1996. 24. Bruce RG, El-Galley RE, Galloway NT: Paravaginal defect repair in the treatment of female stress urinary incontinence and cystocele. Adult Urol 54:647-651, 1999. 25. Larrieux JR, Noel JW, Vragovic O, Scotti RJ: Persistent site-specific defects after reconstructive pelvic surgery. Int Urogynecol J 12:151155, 2001. 26. Burch JC: Cooper’s ligament urethrovesical suspension for stress incontinence: Nine years’ experience—Results, complications, technique. Am J Obstet Gynecol 100:764-774, 1968. 27. Shull B: How I do abdominal paravaginal repair. J Pelvic Surg 1:43, 1995. 28. Benson JT, Lucente V, McClellan E: Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: A prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 175:1418-1422, 1996.

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ANTERIOR COLPORRHAPHY FOR CYSTOCELE REPAIR Tristi W. Muir Pelvic organ prolapse is common in women. The anterior wall of the vagina primarily provides support for the bladder and urethra. If the support for the bladder sags, a cystocele results. The lifetime risk of undergoing an operation for prolapse or urinary incontinence has been estimated to be 11.1%.1 Of the women undergoing surgery for prolapse with and without urinary incontinence, 48% had an anterior colporrhaphy included in their surgical management. This chapter discusses the anatomy and possible causes of anterior wall prolapse. A discussion of an anterior colporrhaphy for surgical repair of a cystocele is presented. ANATOMY AND PATHOLOGY The anterior vaginal wall is the trapezoid of fibromuscularis and provides support to the bladder and urethra. At the apex, the broad portion of the trapezoid, the anterior vaginal wall has suspensory support provided by the cardinal-uterosacral ligaments. The lateral support is provided by a condensation of connective tissue over the levator ani muscles, the arcus tendineus fascia pelvis. The arcus tendineus fascia pelvis extends from the posterior, inferior aspect of the pubic bone to the ischial spine (Fig. 63-1). Nichols and Randall proposed that a cystocele is an end result of either distention (overstretching of the fibromuscularis of the anterior vaginal wall) or displacement (breaks in the connective tissue).2 In 1976, A. Cullen Richardson popularized the “site-specific” approach to identifying specific breaks in the connective tissue and repairing those defects.3 Apical loss of support of the anterior vaginal wall may occur with an apical, transverse separation of the anterior vaginal fibromuscularis with the cardinal-uterosacral ligaments. As abdominal pressure is placed on the lateral connective tissue attachments, these attachments may fail, allowing the anterior vaginal wall to swing toward the hymen (Fig. 63-2). John DeLancey made surgical observations in 71 women undergoing a retropubic procedure for anterior wall prolapse and stress urinary incontinence.4 He found that 88.7% of these women had a paravaginal defect and that the area of detachment was at the apex near the ischial spine. Detachment from the back of the pubic bone was rare. Although the majority of women with anterior wall prolapse and stress urinary incontinence may have a paravaginal loss of connective tissue support, the support for the anterior wall of the vagina is much more complex than a list of fascial attachments. The support for the pelvic organs is maintained by the interaction of connective tissue attachments and innervated, intact pelvic floor musculature. The levator ani muscles provide the primary support for the pelvic floor. The pelvic organs are supported within the abdominal cavity, and the levator hiatus, through which the urethra, vagina, and rectum pass, is closed. 642

The etiology of pelvic organ prolapse is thought to be multifactorial, including abnormalities of connective tissue, pelvic floor muscles, and/or the innervation to the pelvic floor. Norton5 used the analogy of a boat in a dry dock to describe the interplay of the functioning pelvic floor and connective tissue supports (Fig. 63-3). The pelvic floor muscles (primarily the levator ani muscles) play the supporting role of the water. When the water level is adequate, little stress is placed on the ropes (connective tissue supports) keeping the boat in place. However, if the water level is dropped, the ropes will not be able to hold the boat for long. If the levator ani muscles no longer are able to maintain a closed levator hiatus, the stress of maintaining the pelvic organs is placed on the connective tissue supports. Direct damage to the levator ani muscle or to its innervation may open the hiatus and place the burden of support on the connective tissue of the pelvic organs. Prior damage to the connective tissue support of the anterior vaginal wall may be evident only in light of the loss of levator ani function. DeLancey and Hurd clinically determined that the levator hiatus is larger in women with prolapse than in those without prolapse.6 Magnetic resonance imaging (MRI) confirmed that the size of the levator hiatus and levator symphysis gap increases with increasing stage of prolapse.7 Lennox Hoyte and colleagues evaluated the change in morphology of the levator ani muscles with two- and three-dimensional MRI images.8 They demonstrated

Figure 63-1 Apical and sidewall connective tissue support of the anterior vaginal wall as viewed in the retropubic space. ATFP, arcus tendineus fascia pelvis; IS, ischial spine; USL, uterosacral ligaments.

Chapter 63 ANTERIOR COLPORRHAPHY FOR CYSTOCELE REPAIR

A

B

Figure 63-2 Pelvic floor disorders: the role of fascia and ligaments. The water represents functioning pelvic floor muscles, and the ropes are the connective tissue supports. A, With water in the dock (functioning pelvic floor muscles), the ropes can maintain the position of the boat (connective tissue supports the position of the pelvic organs). B, With loss of the water (loss of function of the pelvic floor muscles), the support of the boat (pelvic organs) is maintained only by the ropes (connective tissue). (From Norton PA: Pelvic floor disorders: The role of fascia and ligaments. Clin Obstet Gynecol 36:926-938, 1993.)

that women with prolapse have significantly more levator ani degradation, laxity, and loss of the integrity of the sling portion of the levator ani compared with asymptomatic controls. This change may be occur as a result of direct muscle damage associated with childbirth or chronic straining or damage to the innervation of the pelvic floor. Abnormalities in the histology of connective tissue have also been described in women with prolapse. Abnormalities of collagen synthesis may derive from an intrinsic abnormality of collagen synthesis (due to abnormal collagen, an imbalance between synthesis and degradation, or an imbalance between collagen types). The environment (e.g., excessive straining) may also contribute to the condition of the connective tissue. Error in the repair of damaged ligaments and fascia or lack of remodeling in mature collagen may occur. Dietz and colleagues examined bladder neck descent in nulliparous twins.9 A significant genetic contribution was proposed to contribute to the phenotype of the bladder neck mobility. SIGNS AND SYMPTOMS A woman with anterior wall prolapse may be asymptomatic, or she may present with symptoms related to a vaginal mass with or without changes in sexual and urinary function. Pelvic pressure, heaviness, or a bulge may occur. Women often feel that their symptoms are more significant as the day progresses and gravity allows the prolapse to fully descend. The bladder follows the anterior vaginal wall as it descends through the genital hiatus in

women with an anterior wall bulge. Because the distal urethra remains fixed under the pubic symphysis, voiding difficulties due to obstruction may arise. Women who have to manually reduce their prolapse to empty their bladder are likely to have more significant prolapse than those who do not.10 This obstructive effect on the urethra may protect a woman from leaking urine with abdominal stress (occult incontinence). Women with anterior wall prolapse extending more than 1 cm beyond the hymen are less likely to describe stress urinary incontinence than those will lesser prolapse.10 Sexual function has also been examined in women with prolapse and appears to be similar to that in women without prolapse.10,11 The goal of the physical examination is to recreate the woman’s symptoms. A validated measure of pelvic organ prolapse is the pelvic organ prolapse quantification (POPQ) method.12 Measurement of the descent of the anterior vaginal wall is made at maximal strain. If a woman describes prolapse more significant than that observed in the supine or sitting positions, a standing examination may be employed. The woman’s position and the degree of bladder distention (empty or full) should be documented. A full bladder may help to recreate the patient’s most prominent symptoms of vaginal bulging. Bob Shull described a method to evaluate the anterior vagina for site-specific defects.13 Curved ring forceps are placed in the vagina, supporting the lateral anterior vaginal wall to the ischial spine. The patient is asked to bear down in a Valsalva maneuver. If the anterior vaginal wall prolapse is reduced, a paravaginal defect is diagnosed. A bilateral and a unilateral paravaginal defect may be differentiated with alternating unilateral paravaginal

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B

A

D C Figure 63-3 Connective tissue support of the anterior vaginal wall. A, Intact connective tissue support. B, Loss of apical and paravaginal support (beginning at the ischial spines) allows the anterior vaginal wall to swing toward the introitus. (From DeLancey JOL: Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol 187:93-98, 2002).

support. If the anterior vaginal wall continues to balloon forward despite paravaginal support, a midline defect is diagnosed. A superior or high transverse defect may be suspected if the prolapse is reduced with apical support. Loss of rugation at one of these sites is also thought to be associated with localization of the defect. Whiteside and colleagues evaluated the inter-examiner and intra-examiner reliability of site-specific defect examination.14 They found that there was poor examiner concordance for the presence of superior, paravaginal, or central defects. Not surprising is that the reliability of the examination increased with stage of prolapse. Evaluation of urinary function is important in women with anterior wall prolapse. A postvoid residual volume may be measured by an in-and-out catheterization, or an ultrasonic determination may be made with a bladder scan.15 A test for hypermobility of the urethra may be performed with a sterile, lubricated cotton swab (Q-tip test). The cotton swab is inserted into the urethra to the level of the bladder neck. Measurement of the resting and straining angles from the horizontal axis may be obtained with a goniometer. Hypermobility of the bladder neck is determined if the difference between the resting and straining angles is more than 30 degrees. For patients with stage 3 or 4 anterior wall prolapse, urodynamic assessment with prolapse reduction has been

suggested to identify those women with occult urinary incontinence. The method of prolapse reduction (pessary, rolled gauze, tampons, ring forceps) has not been standardized, and the reliability of this test has not been established. TECHNIQUE The anterior colporrhaphy involves a plication of the fibromuscularis of the anterior vaginal wall. This procedure serves to “tighten up” the overdistended support of the anterior vaginal wall or repair a midline defect. The patient is in the dorsal lithotomy position with the legs elevated. A single dose of perioperative antibiotics is administered. A weighted speculum is placed in the vagina, and a 16-Fr Foley catheter is inserted into the bladder. The epithelium of the anterior vaginal wall is incised in the midline and dissected away from the underlying fibromuscularis or “pubocervical fascia.” Hydrodissection of the vaginal epithelium away from the underlying fibromuscularis with saline or an anesthetic/vasoconstrictive agent may facilitate the dissection. With traction and countertraction, the dissection is carried laterally to the levator ani muscular sidewall. It is important to continue the dissection to the apex of the anterior vaginal wall. If an

Chapter 63 ANTERIOR COLPORRHAPHY FOR CYSTOCELE REPAIR

Kelly plication suture at bladder neck Kelly stitch Vagina Pubocervical fascia Bladder

A

B

Figure 63-4 Anterior colporrhaphy with Kelly plication.

anti-incontinence procedure is included in the woman’s surgery, the anterior wall dissection typically spares the mid-urethra and distal urethra. This area may be palpated with a Foley catheter in place. If the surgeon wishes to provide improved support underneath the urethra and bladder for treatment of a distal anterior wall prolapse (urethrocele), the dissection is continued distally toward the inferior aspect of the public bone. A plication underneath the urethra and bladder neck (a Kelly plication) may be performed to provide a shelf of support underneath the urethra. The fibromuscularis associated with the inferior portion of the pubic bone, just lateral to the urethra, is grasped bilaterally. Interrupted sutures are placed to reapproximate this tissue underneath the urethra, creating a posterior urethral shelf of support. A separate suture is placed plicating the fibromuscularis underneath the bladder neck. Continuation of the midline plication is performed, reducing the width of the fibromuscular wall of the anterior vagina with interrupted sutures (Fig. 63-4). Attention should be directed to the length of the anterior vaginal wall. In some women with prolapse, an elongated (stretched out) vaginal wall is present. Vertically oriented plication sutures tend to shorten the length of the fibromuscularis.16 However, some women, particularly those with recurrent prolapse, may have a shortened anterior segment. Horizontally oriented plication sutures will preserve the vaginal length of the anterior segment. More than one row of plicating sutures may be required to reduce anterior wall prolapse in women with stage 3 or 4 prolapse. The aggressiveness of the plication and the longevity of the sutures are dependent on the surgeon’s preference. Anne Weber and colleagues described a standard plication and an “ultralateral” plication as two different procedures in a prospective, randomized trial.17 Placement of the plication sutures should be tailored to the prolapse anatomy of the patient. The apex of the plicated fibromuscularis of the anterior vaginal wall must be suspended to the apical support of the vagina. If the woman has a well-supported apex, reattachment of the apical

portion of the repair should be performed. If the woman is undergoing a concomitant apical suspension procedure, the apical portion of the anterior colporrhaphy should be attached to the suspension sutures. Without apical suspension of the fibromuscularis, the anterior vaginal wall will continue to sag down toward the introitus. After plication and suspension of the anterior fibromuscularis, the vaginal epithelium may be trimmed and closed with absorbable suture. The surgeon should be cautious not to overtrim the vaginal epithelium (particularly in the postmenopausal woman with vaginal atrophy). A vaginal pack and Foley catheter are placed for 2 to 24 hours postoperatively. Voiding trials should be performed postoperatively to ensure that the patient is able to void to completion. Hakvoort and colleagues found that removal of the Foley catheter on the morning after surgery, rather than on postoperative day 4, was associated with fewer days requiring catheter drainage and a lower incidence of urinary tract infections.18

SURGICAL OUTCOMES The anterior colporrhaphy has been performed for more than a century, but few studies have reported the efficacy of the procedure for the treatment of anterior wall prolapse. Most studies have addressed the efficacy (or lack thereof) of the anterior colporrhaphy in the management of stress urinary incontinence. The anatomic cure rate of the procedure for treatment of anterior vaginal wall prolapse varies between 30% and 97% (Table 63-1).17,19-22 Clark and colleagues monitored a cohort of women who had undergone anterior colporrhaphy and found that 7% underwent a reoperation by 71 months.23 Risk factors for recurrent anterior wall prolapse include age less than 60 years and preoperative stage 3 or 4 prolapse.24

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Table 63-1 Efficacy of Anterior Colporrhaphy Study (Ref. No.) Goff (19) Stanton et al (20) Porges & Smilen (21) Colombo et al (22) Weber et al (17)

Year 1933 1982 1994 2000 2001

No. Patients 86* 73 486 (388 with follow-up) 33 57†

Mean Follow-up

Anatomic Cure (%)

1-8 yr 3 to 24 mo 31 mo 8-17 yr 23 mo (median)

93 89 97 97 37

*Study included 31 patients who underwent excision of the vaginal wall and 55 patients with overlapping fibromuscularis. † Study included both patients who underwent “standard” plication and patients who underwent an “ultralateral” plication.

COMPLICATIONS Complications of anterior colporrhaphy include injury to the surrounding organs, deterioration of bladder or sexual function, and recurrence of prolapse. The routine risks of surgery inclusive of blood transfusion are uncommon with this procedure (blood transfusion occurred in 3 of 519 women undergoing prolapse surgery that included an anterior colporrhaphy, most often linked to other prolapse procedures).25 Injury to Ureters, Bladder, and Urethra Injury to the lower urinary tract may occur during an anterior colporrhaphy. Kwon and colleagues reported a 2% incidence of ureteral obstruction during 346 anterior colporrhaphies, making this procedure the most common cause of unsuspected intraoperative injury to the lower urinary tract in their pelvic reconstructive procedures.26 The cause was thought to be an aggressive lateral plication of the fibromuscularis, which kinked the ureter at the ureterovesical junction. A case report of bilateral ureteric obstruction after an anterior colporrhaphy has been described.27 Additionally, recurrent postoperative urinary tract infections may occur because of an unrecognized intravesical suture.28 R. Peter Beck reported 2 cases of urethrovaginal fistula among 519 women undergoing anterior colporrhaphy for prolapse with or without urinary incontinence.25 Of note, in an attempt to improve the surgical cure of stress incontinence, Beck’s group modified the bladder neck plication by attempting to be more aggressive in differential support of the urethra (to a higher retropubic position) compared with the bladder base. This more aggressive plication technique may result in ischemia or occult injury to the urethra. These cases suggest a role for universal cystoscopy in patients undergoing anterior colporrhaphy to identify and correct injury to the ureters, bladder, or urethra. De Novo Urinary Symptoms De novo urinary incontinence or voiding dysfunction is a known complication of prolapse and incontinence procedures. The risk of postoperative de novo urinary incontinence for women undergoing an anterior colporrhaphy for anterior wall prolapse is 10% (5% for stress urinary incontinence, 4% for overactive bladder with incontinence, and 1% for mixed urinary incontinence).25 De novo detrusor overactivity may be the result of a number of possible postoperative changes, including outlet obstruction, and changes in detrusor innervation. Most women who undergo an anterior colporrhaphy are able to obtain postvoid residuals of less than 100 mL by 1 week.25

However, urethral obstruction leading to irritative voiding symptoms after an anterior colporrhaphy with Kelly plication has been described.29 Aggressive plication under the urethra is thought to be the culprit. In some cases, a band of constriction may be palpated by vaginal examination. A vaginal approach to release of the area of constriction may be curative. Evaluation of the effect of anterior wall dissection on innervation of the urethral sphincters was performed by measuring the terminal motor latency of the perineal branch of the pudendal nerve. Zivkovic and colleagues found that there was not a significant difference between preoperative and postoperative perineal nerve terminal motor latencies in women undergoing an anterior colporrhaphy without a needle urethropexy.30 Sexual Function Sexual function in women is a complicated issue, one that may be further complicated by the presence of prolapse or incontinence. Many sexually active women with prolapse or incontinence describe preoperative dissatisfaction with their sex lives due to a variety of reasons, inclusive of decreased libido, vaginal prolapse, and fear of urinary incontinence with intercourse. Rogers and colleagues evaluated the sexual and continence functions in women preoperatively and postoperatively.31 They found that sexual function scores declined from their preoperative values at 3 and 6 months after surgery, despite an improvement in incontinence impact scores. Gungor and colleagues also described a deterioration in sexual function, primarily related to dyspareunia, in 8 (18%) of 44 sexually active women who underwent an anterior colporrhaphy coupled with a posterior colpoperineorrhaphy.32 However, they found an improvement in 20 (67%) of 30 sexually active women who preoperatively had dissatisfaction in their sexual life. Sexual function remains a complicated issue in the postoperative period. Patients should be counseled that their sexual function has the potential to improve, remain unchanged, or deteriorate after prolapse surgery. In the operating room, the surgeon should make every effort to maintain vaginal caliber, to reduce the likelihood of postoperative dyspareunia.

ANTERIOR COLPORRHAPHY WITH KELLY PLICATION AS AN INCONTINENCE PROCEDURE Most of the studies evaluating the postoperative results of anterior colporrhaphy with Kelly plication have used cure of stress urinary incontinence as the measure of success. Anterior colporrhaphy with Kelly plication has not been found to be as effective as retropubic urethropexy for the treatment of urinary inconti-

Chapter 63 ANTERIOR COLPORRHAPHY FOR CYSTOCELE REPAIR

nence, and it has largely been abandoned as a method of operative management of urinary incontinence.33-35

CONCLUSIONS Anterior wall prolapse most likely develops after loss of levator ani function (through direct muscle damage or nerve damage) and breaks or attenuation of connective tissue supports. Our surgical approach to repair of prolapse focuses on connective tissue support until a time in the future when muscle and nerve regeneration are feasible. The anterior colporrhaphy has been a part of the surgeon’s armamentarium for more than a century. The key to support of the anterior vaginal wall is apical support. Because the anterior vaginal wall rarely loses distal support at the posterior aspect of the pubic bone, does it matter, if the other

end of the fibromuscularis hammock of support is reestablished at the apex, how the “sag” is taken out (anterior colporrhaphy versus paravaginal repair)? Even those who advocate paravaginal repair often perform a concomitant anterior colporrhaphy.36,37 There are no studies comparing the site-specific approach to repair of the anterior vaginal wall, using a paravaginal defect repair with or without a midline defect repair (colporrhaphy), to an anterior colporrhaphy alone. The addition of graft materials in an attempt to decrease the likelihood of recurrent prolapse has been described. Comparative studies are needed to determine the risks and benefits of this practice. Anterior wall prolapse is often associated with bladder dysfunction. Preoperative evaluation of bladder function may be necessary, especially in patients with stage 3 or 4 anterior wall prolapse. Sexual function is a complex issue. Maintenance of vaginal caliber is important in sexually active women undergoing surgical management.

References 1. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-506, 1997. 2. Nichols DH, Randall CL (eds): Vaginal Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1989, pp 241-244. 3. Richardson AC, Lyon JB, Williams NL: A new look at pelvic relaxation. Am J Obstet Gynecol 126:568-573, 1976. 4. DeLancey JOL: Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol 187:93-98, 2002. 5. Norton PA: Pelvic floor disorders: The role of fascia and ligaments. Clin Obstet Gynecol 36:926-938, 1993. 6. DeLancey JO, Hurd WW: Size of the urogenital hiatus in the levator ani muscles in normal women and women with pelvic organ prolapse. Obstet Gynecol 91:364-368, 1998. 7. Singh K, Jakab M, Reid WM, et al: Three-dimensional magnetic resonance imaging assessment of levator ani morphologic features in different grades of prolapse. Am J Obstet Gynecol 188:910-915, 2003. 8. Hoyte L, Schierlitz L, Zou K, et al: Two- and 3-dimensional MRI comparison of levator ani structure, volume, and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 185:1119, 2001. 9. Dietz HP, Hasell NK, Grace ME, et al: Bladder neck mobility is a heritable trait. BJOG 112:334-339, 2005. 10. Burrows LJ, Meyn LA, Walters MD, Weber AM: Pelvic symptoms in women with pelvic organ prolapse. Obstet Gynecol 104:982-988, 2004. 11. Weber AM, Walters MD, Schover LR, Mitchinson A: Sexual function in women with uterovaginal prolapse and urinary incontinence. Obstet Gynecol 85:483-487, 1995. 12. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. 13. Shull BL: Clinical evaluation of women with pelvic support defects. Clin Obstet Gynecol 36:939-951, 1993. 14. Whiteside JL, Barber MD, Paraiso MF, et al: Clinical evaluation of anterior vaginal wall support defects: Interexaminer and intraexaminer reliability. Am J Obstet Gynecol 191:100-104, 2004. 15. Paltieli Y, Degani S, Aharoni A, et al: Ultrasound assessment of the bladder volume after anterior colporrhaphy. Gynecol Obstet Invest 28:209-211, 1989. 16. Nichols DH: Anterior colporrhaphy technique to shorten a pathologically long anterior vaginal wall. Int Surg 64:69-71, 1979.

17. Weber AM, Walters MD, Peidmonte MR, Ballard LA: Anterior colporrhaphy: A randomized trial of three surgical techniques. Am J Obstet Gynecol 185:1299-1306, 2001. 18. Hakvoort RA, Elberink R, Vollebregt A, et al: How long should urinary bladder catheterization be continued after vaginal prolapse surgery? A randomized controlled trial comparing short term versus long term catheterization after vaginal prolapse surgery. BJOG 111:828-830, 2004. 19. Goff BH: An evaluation of the Bissell operation for uterine prolapse: A follow-up study. Surg Gynecol Obstet 57:763-767, 1933. 20. Stanton SL, Hilton P, Norton C, Cardozo L: Clinical and urodynamic effects of anterior colporrhaphy and vaginal hysterectomy for prolapse with and without incontinence. Br J Obstet Gynecol 89:459463, 1982. 21. Porges RF, Smilen S: Long-term analysis of the surgical management of pelvic support defects. Am J Obstet Gynecol 171:1518-1528, 1994. 22. Colombo M, Vitobello D, Proietti, F, Milani R: Randomised comparison of Burch colposuspension versus anterior colporrhaphy in women with stress urinary incontinence and anterior vaginal wall prolapse. BJOG 107:544-551, 2000. 23. Clark AL, Gregory T, Smith VJ, Edwards R: Epidemiologic evaluation of reoperation for surgically treated pelvic organ prolapse. Am J Obstet Gynecol 189:1261-1267, 2003. 24. Whiteside JL, Weber AM, Meyn LA, Walters MD: Risk factors for prolapse recurrence after vaginal repair. Am J Obstet Gynecol 191:1533-1538, 2004. 25. Beck RP, McCormick S, Nordstrom L: A 25-year experience with 519 anterior colporrhaphy procedures. Obstet Gynecol 78:10111018, 1991. 26. Kwon CH, Goldberg RP, Koduri S, Sand PK: The use of intraoperative cystoscopy in major vaginal and urogynecologic surgeries. Am J Obstet Gynecol 187:1466-1472, 2002. 27. Pang MW, Wong WS, Yip SK, Law LW: An unusual case of bilateral ureteric obstruction after anterior colporrhaphy and vaginal hysterectomy for pelvic organ prolapse. Gynecol Obstet Invest 55:125-126, 2003. 28. Neuman M, Alon H, Langer R, et al: Recurrent urinary tract infections in the presence of intravesical suture material after vaginal hysterectomy and anterior colporrhaphy. Aust N Z J Obstet Gynaecol 30:184-185, 1990. 29. Erickson DR, Olt GJ: Urethral obstruction after anterior colporrhaphy: Correction by simple vaginoplasty. Urology 48:805-808, 1996. 30. Zivkovic F, Tamussino K, Ralph G, et al: Long-term effects of vaginal dissection on the innervation of the striated urethral sphincter. Obstet Gynecol 87:257-260, 1996.

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31. Rogers RG, Kammerer-Doak D, Darrow A, et al: Sexual function after surgery for stress urinary incontinence and/or pelvic organ prolapse: A multicenter prospective study. Am J Obstet Gynecol 191:206-210, 2004. 32. Gungor T, Ekin M, Dogan M, et al: Influence of anterior colporrhaphy with colpoperineoplasty operations for stress incontinence and/or genital descent on sexual life. J Pak Med Assoc 47:248-250, 1997. 33. Van Geelen JM, Theeuwes AG, Eskes TK, Martin CB Jr: The clinical and urodynamic effects of anterior vaginal repair and Burch colposuspension. Am J Obstet Gynecol 159:137-144, 1988.

34. Tamussino KF, Zivkovic F, Pieber D, et al: Five-year results after antiincontinence operations. Am J Obstet Gynecol 181:1347-1352, 1999. 35. Hutchings A, Black NA: Surgery for stress incontinence: A nonrandomised trial of colposuspension, needle suspension, and anterior colporrhaphy. Eur Urol 39:375-382, 2001. 36. Shull BL, Benn S, Kuehl TJ: Surgical management of prolapse of the anterior vaginal segement: An analysis of support defects, operative morbidity, and anatomic outcome. Am J Obstet Gynecol 171:14291439, 1994. 37. Young SB, Daman JJ, Bony LG: Vaginal paravaginal repair: One-year outcomes. Am J Obstet Gynecol 185:1360-1367, 2001.

Chapter 64

TRANSVAGINAL PARAVAGINAL REPAIR OF HIGH-GRADE CYSTOCELE Donna Y. Deng, Matthew P. Rutman, Larissa V. Rodriguez, and Shlomo Raz Anterior compartment defect or cystocele is defined as anterior vaginal wall relaxation or prolapse with or without urethral hypermobility. It represents one of the most common types of genital organ prolapse. Cystoceles have been described by several different classification systems and were previously categorized based on the relative degree of bladder descent and anatomic defect. More recently, the International Continence Society (ICS) has accepted standardization of the terminology for prolapse of the lower urinary tract.1 To ensure consistency, examiners must note the conditions of the examination findings, such as rest, strain, or supine positioning. This chapter concentrates on repair of the high-grade cystocele that has prolapsed past the vaginal introitus—grade 3/4 in the Baden-Walker classification or stage 3/4 in the pelvic organ prolapse quantification (POPQ) terminology. The natural history of a cystocele is a continuous progression from mild to severe prolapse, but the actual risk of progression is unknown. In some patients, the progression is rapid; in others, it can be insidious, taking many years. Most lesser degrees of prolapse (stages 1 and 2) are asymptomatic except when accompanied by urinary incontinence. Pelvic prolapse does not spontaneously regress, nor does it become symptomatic until the descent reaches the introitus.2 Cystoceles with an isolated central defect represent only 5% to 15% of all cystoceles, whereas a lateral paravaginal defect is present in 70% to 80% of patients. Stage 4 cystoceles usually manifest with both defects. Proposed risk factors for the development of a cystocele have included difficult or prolonged vaginal deliveries, elevated body mass index (BMI), parity, menopause, and previous vaginal surgery. Cystocele may occur as an isolated defect. However, it is most commonly associated with prolapse of other genital organs, such as rectocele, enterocele, and uterine descensus. Michael and colleagues3 observed a simultaneous enterocele in 35%, rectocele in 63%, and uterine prolapse in 38% of patients with grade 4 cystoceles. Therefore, in cases of severe anterior compartment prolapse, all of the compartments must be corrected. Treatment must involve a thoughtful and thorough evaluation plus a strong knowledge of pelvic floor anatomy The goals of surgery must be to restore vaginal depth, vaginal axis, the levator hiatus, and bladder and bowel function, while also preserving sexual function. ANATOMY In a well-supported woman in the standing position, the vagina forms an inverted “C” shape with two distinct vaginal angles. This can be demonstrated on a midsagittal pelvic magnetic

resonance image in a patient with normal anatomy. The distal vaginal canal forms a 45-degree angle from the vertical plane, whereas the proximal vagina lies more horizontally over the posterior levator plate, forming an angle of 110 degrees. The upper vagina is held over the levator plate by the cardinal and uterosacral ligaments, and the angle is maintained by a strong levator plate and the anterior traction of the levator sling and prerectal fascia. The bony pelvis is a scaffold from which the pelvic structures draw their support. The pelvis can be divided into posterior and anterior regions by a line traversing the ischial spines. The sacrospinous ligaments are true ligaments in that they span between bony structures, arising from the posterior aspect of the ischial spines and connecting with the anterolateral sacrum and coccyx, providing a broad support for the posterior pelvis. A linear fascial condensation arising from the obturator internus muscle, the arcus tendineus, extends from the ischial spine to the lower portion of the pubic symphysis. The arcus tendineus is also the insertion point for the semilunar-shaped levator muscles, and it provides the musculofascial support for a large portion of the anterior pelvis. The pelvic diaphragm is the superior layer of striated muscle and fascia that provides the inferior support for the pelvic viscera. The levator ani muscle group, composed of the pubococcygeus and iliococcygeus, is a broad muscular structure that originates on each side from the arcus tendineus of the obturator fascia and the inner surface of the pubis anteriorly and sweeps medially to join its contralateral partner in the midline. The levator ani thereby forms a broad hammock upon which the bladder, proximal vagina, and intrapelvic rectum lie. The vagina, rectum, and urethra traverse the pubococcygeus through a funneled hiatus. Pubococcygeal muscle fibers entering this “U”-shaped levator hiatus form the external sphincter of the urethra. Medial fibers of the pubococcygeal portion of the levator, sometimes referred to as the puborectalis, travel posteriorly along the urethra, vagina, and rectum and fuse anterior to the rectum, forming part of the perineal support deep to the perineal body. Reflex and active contraction of the pubococcygeus elevates the urethra, vagina, and rectum, thereby helping to compress the lumens of these structures. Like the pubococcygeus, the iliococcygeus arises from the tendinous arc, but it sweeps more posteriorly and unites with the contralateral iliococcygeus in the median raphe posterior to the rectum. The coccygeus extends from the ischial spine to the lateral aspect of the sacrum and coccyx, overlying the sacrospinous ligament. The coccygeus is a thin muscle that overlies the strong and fibrous sacrospinous ligament. These two structures are identically shaped, and when they are encountered during 649

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surgical procedures, they are approached as a single complex useful for fixation of the vaginal vault. It is important to realize that the pudendal neurovascular bundle runs in the lateral insertion of the sacrospinous ligament, near the ischial spine. The pelvic diaphragm has investing connective tissue that is often referred to as “fascia”; it is, however, less organized and less distinct than traditional fascia (e.g., rectus abdominis fascia). This visceropelvic fascia consists of collagen, smooth muscle, and elastin. Microscopic studies suggest that it may be histologically indistinct from the deep vaginal wall and not a separate “fascia.”4 In our discussion of the musculofascial support, we will continue to refer to this tissue as “fascia” for the sake of accepted nomenclature. The pelvic fasciae have been given a confusing array of appellations by anatomists and surgeons interested in female pelvic organ prolapse. To add to the confusion, the strength of pelvic fasciae can differ significantly among individuals and races, and these differences may predispose some individuals to pelvic prolapse.5 The pelvic fascia consists of two leaves—the endopelvic fascia (abdominal side) and the perivesical fascia (vaginal side). The urethra, bladder, vagina, and uterus are all contained within these two layers of fascia. The two leaves fuse laterally to insert along the arcus tendineus. The pelvic fascia can be divided, distally to proximally, into four specialized areas; these areas play important roles in pelvic support and during surgical reconstruction of the female pelvis. They are not true ligaments; rather, they are condensations or a meshwork of connective tissue and smooth muscle that invests the visceral neurovascular pedicles.1,6 The socalled pubourethral ligaments attach to the lower portion of the pubis and insert on the proximal third of the urethra; they are analogous to the puboprostatic ligaments in the male.2 The urethropelvic ligaments provide support of the proximal urethra to the lateral pelvic sidewall.3 The vesicopelvic fascia is the region of the pelvic fascia that attaches and supports the bladder base to the arcus tendineus. Finally, the vesicopelvic ligaments are all of the structures that support the bladder to the lateral pelvic wall. Weakness in the vesicopelvic fascia results in cystocele formation. Cystoceles are generally classified as being caused by a central defect or a lateral defect. A central defect manifests as a midline weakness. There is good lateral support, but central herniation of the bladder base into the vagina occurs through a separation or attenuation of the vesicopelvic fascia (with separation of the cardinal ligaments). A lateral defect occurs when there is weakness or disruption of the lateral (paravaginal) attachments of the vesicopelvic ligaments to the arcus tendineus fascia pelvis. Highgrade cystoceles tend to involve a combination of lateral and central defects with urethral hypermobility.4 The cardinalsacrouterine ligament complex attaches to the bladder base and cervix (or vaginal vault, if reapproximated during the hysterectomy). PATHOPHYSIOLOGY Pelvic organ prolapse is prevented by several mechanisms. The most important support is from the continuous contraction of the levator ani pelvic muscles. The activity of skeletal muscle is a combination of basic tone, reflex contraction or relaxation, and voluntary contraction or relaxation. The basic tone of the skeletal musculature is similar to that in other areas of the body. Muscles of the pelvic diaphragm contain type I (slow-twitch) fibers, which

provide tonic support to pelvic structures, and type II (fasttwitch) fibers, for sudden increases in intra-abdominal pressure.7 The continuous contraction closes the urogenital hiatus and forms a shelf for the pelvic organs to rest upon. Patients with multiple deliveries exhibit widening and descent of the levator plate. The musculature becomes less important and the “fascial” structures become the more important elements of support as the organs cross the pelvic floor. Innervation of the muscles is primarily derived from the ventral rami of the second, third, and fourth sacral nerve roots. These pelvic somatic efferent nerves travel on the pelvic surface of the levator ani in close association with the rectum and are separated from the pelvic autonomic plexus by the endopelvic fascia. They supply the levator ani and extend anteriorly to the striated urethral sphincter.8,9 Static support is provided by the investing connective tissue layers. Under normal conditions, the levator ani contract, and the ligaments and fasciae are under minimal stress. The fasciae stabilize the pelvic organs. Because of the complexity of pelvic organ support, the cause of vaginal prolapse is likely to be multifactorial, including myopathic or neuropathic disorders, aging, atrophy, chronic increase in abdominal pressures, multiple deliveries, hysterectomy, and hormonal changes. Poor function of the levator ani muscles may result from direct myopathic injury or from an abnormality of innervation. Loss of tonic contraction causes the urogenital hiatus to widen, increasing the risk of organ prolapse. Pelvic relaxation decreases the angulation of the mid-vagina, so the upper vagina does not lie flat against the pelvic floor plate. Instead of an inverted “C” configuration, the vagina becomes vertically oriented and can more easily intussuscept on itself. The reason for neuropathy in a healthy woman is not clear. Childbirth has been suggested as the cause of pelvic denervation, but studies in this area have shown that uncomplicated childbirth creates only transient neurologic damage to the pelvic floor that is restored after two postpartum months.10 The pelvic floor neuropraxia related to vaginal delivery is associated with multiple births, prolonged labor, high birth weight, and traumatic deliveries. Other risk factors for neurologic damage are congenital abnormalities, aging, chronic constipation (abdominal straining), and perineal laxity.11,12 In a study of 50 women with prolapse, Sharf and associates performed electromyography of the levator ani and found evidence of denervation in half of the patients.10 Other studies have also confirmed evidence of neurologic damage to the urogenital muscles in pelvic prolapse.13,14 The connective tissue of the pelvic floor, the endopelvic fascia, can be described as a group of collagen fibers interlaced with elastin, smooth muscle cells, fibroblasts, and vascular structures. These structures may be weakened by pregnancy, parturition, lack of estrogen, aging, diet, chronic straining, and certain connective tissue disorders (e.g., Ehlers-Danlos syndrome, Marfan’s syndrome).15 However, intrinsic collagen abnormalities and other individual predisposing factors, such as genetics, differences in pelvic architecture, inherent quality of the pelvic musculature, and tissue response to injury, might explain why many patients with known risk factors do not develop prolapse and many patients without risk factors do. Correction of a cystocele alone, without addressing the entire pelvic floor laxity and alignment, may further alter the vaginal axis as the bladder and vesicopelvic fascia are brought anteriorly. This may increase the likelihood of uterine prolapse, enterocele, and rectocele formation.

Chapter 64 TRANSVAGINAL PARAVAGINAL REPAIR OF HIGH-GRADE CYSTOCELE

EVALUATION Symptoms Cystoceles are often asymptomatic until pelvic organ prolapse is severe. The most common complaint related to anterior compartment prolapse is vaginal bulging, with or without suprapubic pressure and pain. Other symptoms include urgency, frequency, urge incontinence, recurrent urinary tract infections, back pain, renal failure, staghorn calculi, and urinary retention. Obstructive voiding symptoms are caused by urethral kinking that occurs when the bladder descends beyond the pubic ramus but the urethra remains fixed. This is commonly seen in the setting of previous surgery (bladder neck suspension, urethropexy, sling).3 Patients may describe using unusual positions to void, such as pelvic tilting, squatting, or standing. In contrast, patients with concomitant urethral dysfunction may present with stress urinary incontinence, especially when the cystocele is manually reduced. Clinical Evaluation There are critical points in the evaluation of a cystocele that must be answered before treatment. The degree of cystocele and other concurrent bladder symptoms (e.g., stress incontinence, detrusor overactivity) and ability to empty the bladder to completion should be known. Surgical planning is also affected by the need to preserve sexual function and vaginal depth. The overall health of the patient must be considered, as well as the quality of vaginal tissue, presence of associated prolapse, bowel and bladder function, hormonal status, and presence of urinary tract infection. It is also important to assess the impact of the symptoms on the patient’s quality of life. Physical Examination A thorough physical examination should be done while the patient has a full bladder, at rest and with straining, in both the standing and supine positions. The goal of examination is to determine the degree of prolapse, the specific anatomic defects, and the presence of concomitant organ prolapse. Straining and standing should accentuate the degree of descent. In the supine position, the origin of prolapse should be determined. With a half-speculum blade, the posterior vaginal wall is retracted; the patient is asked to strain while the anterior defect is evaluated. An isolated central defect is identified as bulging in the central region of the vagina (midline) with loss of vaginal rugae. However, in older patients, loss of vaginal rugae alone can be caused by smooth muscle atrophy of the vaginal wall. A lateral defect is identified by loss of the lateral vaginal sulci as the vesicopelvic fascia attenuates from the arcus tendineus fascia pelvis. There will be loss of the “M” vaginal profile (coronal view) and sliding herniation of the bladder into the vagina. After the anatomic defects have been characterized, it is important to reduce the cystocele in order to elicit occult stress urinary incontinence and hypermobility. Similarly, we retract the anterior vaginal wall to determine the presence of any posterior defect. A digital rectal examination assesses rectal tone, presence of impacted stool, attenuation of the prerectal fascia, and perineal laxity. With the use of both blades of speculum, the vaginal vault or cervix can be examined for uterine descent, vault prolapse, and enterocele.

The ICS approved the POPQ validated system for describing pelvic organ support.1 Six points (two on the anterior vaginal wall, two in the superior vagina, and two on the posterior vaginal wall) are located with reference to the plane of the hymen. The system assigns negative numbers (in centimeters) to structures that have not prolapsed beyond the hymen and positive numbers to structures that protrude. With specific reference to the anterior compartment, point Aa is located in the midline of the anterior vaginal wall, 3cm proximal to the external urethral meatus. Point Ba represents the most dependent position of any part of the upper anterior vaginal wall, from the vaginal cuff or fornix to point Aa. Point C represents either the most distal edge of the cervix or the leading edge of the vaginal cuff after total hysterectomy. This system allows objective and reproducible documentation of the degree of prolapse. Imaging Studies In the setting of a large introital bulge, it may be difficult to differentiate between a severe cystocele, an enterocele, and a high rectocele by physical examination only.16 Imaging studies should be done to specifically identify which organs are prolapsing. An ideal imaging study should provide precise information about which structures are prolapsed, the presence of urinary retention and obstruction, urethral hypermobility, and urinary incontinence. Cystourethrography For a cystourethrogram, the patient should be upright with a full bladder. Films should be taken during both rest and strain. This examination provides information about bladder position, bladder neck funneling, urethral mobility, stress incontinence, and postvoid residual volumes. The presence of a rectocele can also be inferred if bowel gas is identified below the pubic symphysis. This examination is static and does not provide information about other pelvic organs or soft tissues of the pelvic floor. Dynamic Fluoroscopy Dynamic fluoroscopy (colpocystodefecography, vaginography) relies on making the organs of interest (bladder, vagina, rectum) radiopaque and studying their positional changes with straining under fluoroscopy. This is a dynamic examination done with the patient upright. Standing recreates the setting in which the patient experiences maximal vaginal bulging. For this procedure, contrast paste must be placed into the vagina and rectum, which can be uncomfortable. Vaginography and defecography are little used now, given the increasing experience and precision of magnetic resonance imaging (MRI). Ultrasonography Ultrasound is an attractive imaging modality because it is easy to perform, is minimally invasive, and avoids radiation exposure. Tubo-ovarian and renal disease can also be assessed during the same examination. There is evidence that ultrasound is useful in evaluating bladder neck hypermobility; however, transvaginal imaging for pelvic prolapse does not provide adequate visualization of the soft tissues.17 Translabial ultrasound can be used to quantify prolapse, although it appears to be better for the anterior compartment and uterine descent than for the posterior compartment.18 This is not an imaging modality often used for prolapse.

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Dynamic Magnetic Resonance Imaging MRI is becoming a standard in the evaluation of pelvic prolapse. It is performed quickly, without contrast or ionizing radiation, and permits visualization of the soft tissues as well as the upper urinary tract. Gousse and colleagues30 showed that, in comparison with findings at surgery, MRI had 100% sensitivity, 83% specificity, and a positive predictive value of 97% in assessing cystoceles. Compared with colpocystodefecography, MRI does not require intravesical catheterization, does not require contrast, is fast, and is noninvasive. The drawback is that MRI may underestimate the extent of cystocele and enterocele, because the examination must be performed with the patient in the supine position, which diminishes the downward forces that can be generated with abdominal straining.19,20 Standing MRI is the ultimate modality in obtaining an even more precise study for prolapse. Videourodynamics A urodynamic study can be done with or without video assistance. Both methods provide information about bladder compliance, capacity, sensation of filling, detrusor instability, and contractility. An advantage in performing videourodynamics is the additional information gained in terms of anatomy by monitoring the position and funneling of the bladder neck during filling and straining. The choice to use fluoroscopy should be based on cost, availability, and familiarity with this method. The importance of documenting the presence of urinary incontinence in patients with large cystoceles is controversial. The incidence of occult stress urinary incontinence is believed to be as high as 22% to 80% among patients with high-stage vaginal vault prolapse.21 Because of the frequent masked urinary incontinence and the high incidence of postoperative de novo stress incontinence, many surgeons routinely perform a concomitant anti-incontinence procedure along with anterior vaginal reconstruction, independent of the continence status. A study by Barnes and colleagues22 retrospectively reviewed the charts of 38 women who had grade 3/4 prolapse without significant symptoms of stress incontinence. None of the patients demonstrated stress incontinence during physical examination or videourodynamics studies until the prolapse was mechanically reduced. All patients subsequently had documented stress incontinence, with a mean abdominal leak point pressure of 86 cm H2O. All patients then underwent surgical repair of the prolapse with placement of a pubovaginal sling. None of the patients developed permanent retention. Recurrent stress incontinence occurred in 5% of the patients. On the other hand, Chaikin and colleagues23 evaluated 24 “continent” women with severe cystocele. They used a pessary to reduce the cystocele during urodynamic studies and documented incontinence in only 58% of patients. The patients with overt incontinence received an anti-incontinence procedure, and the others did not. With a mean follow-up of 47 months, none of the patients treated only by colporrhaphy developed incontinence. The authors recommended concomitant antiincontinence procedures only for patients with overt leakage (after the cystocele is reduced). To improve the sensitivity of the urodynamic test to reveal urinary incontinence, a pessary or vaginal pack can be used to reduce the cystocele.24,25 However, if there is significant pelvic floor relaxation, a pessary may not be able to prevent the prolapse, and it can cause artificial urethral kinking. Additionally, there is no proven correlation between pessary reduction and the reduction obtained with surgery.

Therefore, the results of urodynamic testing with a pessary in place cannot be equated with the urinary symptoms after the surgical repair. Determining the presence of bladder instability is important in preoperative counseling, because it can affect the postoperative result. In most cases (60% to 80%), urgency resolves after surgery.26 However, some patients have no change in urgency or a worsening of their urgency with sling placement and/or bladder neck elevation. Urodynamic studies may also suggest urinary obstruction with elevated voiding pressure, low urinary flow, or radiographic evidence of urethral kinking. Cystourethroscopy Cystourethroscopy is performed to rule out concurrent intraurethral or intravesical pathology such as bladder carcinoma, urethral diverticulum, stones, or foreign bodies (i.e., suture material) from previous surgery. Cystoscopic illumination can also be used to differentiate an enterocele from a cystocele.27 A pelvic examination is performed with the cystoscope in the bladder. The bladder transilluminates through the anterior vaginal wall so that the extent of the bladder prolapse is demarcated. We assess bladder neck competence both at rest and during straining. Cystourethroscopy can also be used as a bedside urodynamic examination, assessing filling sensation, postvoid residual volume, and visual cystometrics for bladder contractions. With a full bladder, a supine Valsalva stress test can be performed, looking for urethral leakage. Upper Urinary Tract Evaluation Patients with a stage 4 cystocele should have upper tract imaging, because there is a 4% to 7% incidence of moderate hydroureteronephrosis among patients with severe vaginal prolapse.28,29 This risk is greater in patients with procidentia than in those with vault prolapse. Ultrasonography, excretory urography, computed tomography, or MRI may be used. An advantage of MRI is the ability to evaluate the upper urinary tract, tubo-ovarian disease, and pelvic organ prolapse simultaneously. Laboratory Evaluations Patients must have sterile urine before proceeding with an operative procedure. In preparation for surgery, we routinely obtain a complete blood count, basic metabolic panel, and coagulation profile in addition to the urine culture.

SURGICAL REPAIR The goal of repair is to restore pelvic anatomic support of the anterior vaginal wall. This is rarely an independent surgery. Often, surgery entails addressing incontinence as well as prolapse of the uterus and posterior compartment. The end result must restore anatomy and function by restoring the normal vaginal axis and depth and preserving urinary, bowel, and sexual function. It must be kept in mind that anatomy does not always correlate with function. Treatment of high-grade or symptomatic cystocele must address all defects of the pelvic floor. In the anterior compartment, we must correct urethral hypermobility as well as weakness of lateral bladder support (paravaginal), perivesical fascia (central), and the cardinal-sacrouterine ligament complex.

Chapter 64 TRANSVAGINAL PARAVAGINAL REPAIR OF HIGH-GRADE CYSTOCELE

Transvaginal Paravaginal Repair This technique simultaneously repairs the four defects present in patients with significant cystocele: support of the hypermobile urethra by a sling procedure, approximation of the cardinal ligaments back to the midline to form the most proximal support of the bladder, repair of the central defect by approximation of the perivesical fascia to the midline, and correction of the lateral defect by support of the bladder neck and bladder base to the obturator fascia using polypropylene mesh. The infralevator obturator “fascia” as it condenses on the pubic bone is the basis of our vaginal paravaginal defect repair; it acts as an immobile structure to secure the mesh. If only the central defect repair is performed, the cystocele may recur (due to the lack of lateral support), and de novo incontinence may ensue because of a poorly supported and hypermobile urethra. On the other hand, if only a bladder neck suspension or plication procedure is performed without correction of the cystocele, the patient may develop aggravation of the prolapse, obstructive symptoms, and urinary retention. As mentioned, a distal urethral sling is always performed concomitantly with a stage 4 cystocele repair. The sling is placed before the cystocele repair, and the details are described in a separate chapter. Here, we concentrate on the steps of the cystocele repair. If total vaginal prolapse was present, the order of repair would be as follows: transvaginal hysterectomy, vault suspension sutures placed, enterocele repair with pursestring sutures, sling, cystocele repair, vault sutures tied, and rectocele repair. 1. Preparation includes creation of a 1 × 10 cm Prolene mesh sling and a 5 × 5 cm round Prolene mesh disc. Labial sutures are placed, and the weighted speculum is inserted. A suprapubic cystostomy tube and urethral catheter are placed. The bladder is emptied. A ring retractor with multiple hooks is used for additional exposure. 2. A vertical incision is made from the bladder neck to the vaginal cuff. The incision should be superficial enough to avoid bladder perforation but deep enough to expose the perivesical fascia. 3. The vaginal wall is dissected to expose the bladder and proximal urethra. The dissection is carried out in the avascular plane between the vaginal wall and the bladder, laterally toward the lateral pelvic wall and obturator fascia and posteriorly to expose the cardinal ligaments. The lateral dissection need only extend so far as make it easy to palpate the inferior ramus. 4. A figure-of-eight 2-0 Vicryl suture is applied to the cardinal ligaments to approximate them to the midline. The sutures are not tied at this time. The needle is left attached to the suture and will be used to anchor the mesh later. Intravenous injection of indigo carmine (5 mL) is given at this time, followed by a bolus of 500 mL saline. 5. Interrupted horizontal mattress sutures of 3-0 Vicryl are applied to plicate the attenuated perivesical and periurethral fascia to the midline (anterior colporrhaphy). The sutures are placed superficially but incorporate a wide segment of the perivesical fascia. Deep placement of the sutures should be avoided, to prevent bladder injury or ureteric obstruction. This is not the strength of the central repair but rather facilitates reduction of the defect.

6. Cystoscopy is performed to confirm that the suprapubic tube is in place, the bladder is free of injury, and the ureters excrete indigo-stained urine. 7. The bladder is retracted laterally, using the back of forceps, to facilitate placement of a 2-0 Vicryl suture (CT 1 needle) in the obturator fascia on each side. The key is to palpate the inferior ramus, then place the suture just over the periosteum, taking a strong bite of the infralevator obturator fascia. A strong tug on the suture ensures secure placement. We have found this to be a reliable, strong, nonmobile anchor. Check to make sure the suture was not placed through the vaginal flap. 8. The circular 5 × 5 cm mesh is now used to cover the perivesical fascia and secure the repair. The already placed obturator fascial sutures are used to fix the mesh laterally. Posteriorly, the mesh is fixed to the cardinal ligaments using the previously placed midline suture. Distally, two simple interrupted sutures of 3-0 Vicryl are used to secure the mesh on each side of the bladder neck, taking strong bites of the perivesical fascia. The mesh is trimmed as needed to ensure taut positioning. 9. The excess vaginal wall is trimmed and closed without tension using multiple runs of 3-0 Vicryl. A vaginal packing soaked in antibiotic cream is inserted. No urethral catheter is placed. Postoperative Care The antibiotic-soaked vaginal pack is kept in place until discharge. Most patients go home after 24 hours of observation. The suprapubic tube is capped and attempts at voiding are instituted before discharge. Patients are instructed in the use of the suprapubic catheter to check postvoid residuals at home. Most patients void within 24 hours, so the placement of a suprapubic tube or urethral catheter (and possible preoperative teaching of intermittent catheterization) is the surgeon’s preference. We do keep the suprapubic catheter in place for at least 1 week to minimize possible urinary extravasation with its removal.

RESULTS Our early series of 94 consecutive patients with stage 4 cystocele repair showed cure or improvement of the anatomic prolapse in 82% of patients. The range of follow-up was 8 to 22 months. The complication rate was 8%. There was transient retention in two patients and de novo urinary incontinence in 4% of the patients. Although no patient developed recurrent high-grade cystocele, two patients developed mild grade 2 cystoceles. No complications related directly to the mesh were seen; specifically, there were no erosions or graft infections. There have been no cases of permanent urinary retention to date.

CONCLUSION Armed with a fundamental grasp of the anatomy and pathophysiology of pelvic support, once can more effectively address patients with deficiencies in pelvic support and appropriately apply the current methods of evaluation and treatment discussed in other chapters of this book.

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References 1. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. 2. Zimmern PE, Leach GE, et al: The urological aspects of vaginal wall prolapse. Part I: Diagnosis and surgical indications. AUA Update Series 1993, 12 (Lesson 25). 3. Michael HS, Gousse AE, Rovner ES, et al: Four-defect repair of grade 4 cystocele. J Urol 161:587-594, 1999. 4. Farrell SA, Dempsey T, Geldenhuys L: Histologic examination of “fascia” used in colporrhaphy. Obstet Gynecol 98:794-798, 2001. 5. Zacharin RF: Pelvic Floor Anatomy and the Surgery of Pulsion Enterocele. New York, Springer-Verlag, 1985. 6. DeCaro R, Aragona F, Herms A, et al: Morphometric analysis of the fibroadipose tissue of the female pelvis. J Urol 160:707-713, 1998. 7. Gosling JA, Dixon JS, Critchley HOD, et al: A comparative study of human external sphincter and periurethral levator ani muscles. Br J Urol 53:35-41, 1981. 8. Lawson JO: Pelvic anatomy. I: Pelvic floor muscles. Ann R Coll Surg Engl 54:244-252, 1974. 9. Zvara P, Carrier S, Kour N-W, et al: The detailed neuroanatomy of the human striated urethral sphincter. Br J Urol 74:182-187, 1994. 10. Sharf B, Zilberman A, Sharf M, Mitrani A: Electromyogram of pelvic floor muscles in genital prolapse. Int J Gynecol Obstet 14:2-4, 1976. 11. Wall LL: The muscles of the pelvic floor. Clin Obstet Gynecol 36:910-925, 1993. 12. Babiarz JW, Raz S: Pelvic floor relaxation. In: Raz S (ed): Female Urology, 2nd ed. Philadelphia, WB Saunders, 1996, pp 445-456. 13. Gilpin SA, Gosling JA, Smith ARB, Warrell DW: The pathogenesis of genitourinary prolapse and stress incontinence of urine: A histological and histochemical study. Br J of Obstet Gynecol 96:15-23, 1999. 14. Smith ARB, Hosker GL, Warrell DW: The role of partial denervation of the pelvic floor in teh etiology of genitourinary prolapse and stress incontinence of urine: A neurophysiological study. Br J Obstet Gynecol 96:24-28, 1989. 15. Norton PA: The role of fascia and ligaments. Clin Obstet Gynecol 36:926-938, 1993. 16. Rodriguez LV, Raz S: Diagnostic imaging of pelvic floor dysfunction. Curr Opin Urol 11:423-428, 2001. 17. Gordon D, Pearce M, Norton PA, Stanton SL: Comparison of ultrasound and lateral chain urethrocystography in the determina-

18. 19.

20. 21. 22.

23. 24. 25. 26. 27. 28. 29. 30.

tion of bladder neck descent. Am J Obstet Gynecol 160:182-184, 1989. Dietz HP, Haylen BT, Broome J: Ultrasound in the quantification of female pelvic organ prolapse. Ultrasound Obstet Gynecol 18:511514, 2001. Kelvin FM, Maglinte DD, Hale DS, Benson JT: Female pelvic organ prolapse: A comparison of triphasic dynamic MR imaging and triphasic fluoroscopic cystocolpoproctography. AJR Am J Roentgenol 174:81-88, 2000. Vandbeckevoort D, Van Hoe L, Oyen R, et al: Comparative study of copocystodefography and dynamic fast MR imaging. J Magnetic Resonance 9:373-377, 1999. Gallentine ML, Cespedes RD: Occult stress urinary incontinence and the effect of vaginal vault prolapse on abdominal leak point pressures. Urology 57:40-44, 2001. Barnes NM, Dmochowski RR, Park R, Nitti VW: Pubovaginal sling and pelvic prolapse repair in women with occult stress urinary incontinence: Effect on postoperative emptying and voiding symptoms. Urology 59:856-860, 2002. Chaikin DC, Groutz A, Blaivas JG: Predicting the need for antiincontinence surgery in continent women undergoing repair of severe urogenital prolapse. J Urol 163:531-534, 2000. Ghoneim GM, Walters F, Lewis V: The value of the vagina pack test in large cystoceles. J Urol 152:931, 1994. Bhatia NN, Bergman A: Pessary test in women with urinary incontinence. Obstet Gynecol 65:220, 1985. Blaivas JG, Jacobs BZ: Pubovaginal fascial sling for the treatment of complicated stress urinary incontinence. J Urol 145:1214, 1991. Vasavada SP, Comiter CV, Raz S: Cystoscopic light test to aid in the differentiation of high-grade pelvic organ prolapse. Urology 54:10851087, 1999. Beverly CM, Walters MD, Weber AM, et al: Prevalence of hydronephrosis in patients undergoing surgery for pelvic organ prolapse. Obstet Gynecol 90:37-41, 1997. Gemer O, Bergman M, Segal S: Prevalence of hydronephrosis in patients with genital prolapse. Eur J Obstet Gynecol Reprod Biol 86:11-13, 1999. Gousse AE, Barberic ZL, Safir MH, et al: Dynamic half Fourier acquisition, single turbo spin-echo magnetic resonance imaging for evaluating the female pelvis. J Urol 164(8):1606-13, 2000.

Chapter 65

CYSTOCELE REPAIR USING BIOLOGIC MATERIAL George D. Webster and Neil D. Sherman A variety of surgical options are available to the reconstructive surgeon for treatment of anterior vaginal wall prolapse. The traditional surgical approach for cystocele repair is anterior colporrhaphy with plication of the pubocervical fascia. Despite an increased knowledge of pelvic anatomy and advances in surgical techniques, success is variable, and recurrence rates vary from 20% to 40%.1 Recent literature has suggested that the interposition of graft material over the fascial defect to repair both central and lateral defects of the anterior vaginal wall may increase the success rate of surgery. The purpose of the graft is to allow for replacement or regeneration of fascia by providing a matrix into which in-growth of support tissue will occur.2 A variety of graft materials are available for such pelvic floor reconstruction. The properties of an ideal implant (graft material) were described by Cumberland3 and Scales4 more than 50 years ago, and the principles remain true today. These characteristics include the proposal that the implant should be elastic or supple, should be easily tailored, and it should have good tensile strength. Additionally, the implant should cause minimal foreign body reaction and allow for good tissue incorporation and collagen in-growth while promoting permanent tissue repair. Finally, the graft must be tolerated in an infected environment and cause minimal wound complications. To date, the graft that meets all of the above criteria remains elusive. Currently available grafts are most easily classified as biologic or synthetic. Biologic grafts can be further described as autologous, allograft (cadaveric fascia and dermis), or xenograft (e.g., porcine dermis, porcine small intestine submucosa). Synthetic grafts and some biologic biomaterials are discussed elsewhere in the text; this chapter discusses the use of dermal allografts and xenografts for the treatment of anterior vaginal wall prolapse.

Biomaterials Access Assurance Act was passed by the U.S. Congress in July 1998 to provide some protection to manufacturers as well as encourage development of new materials.6 In the United States, the Food and Drug Administration (FDA) regulates medical devices, but not biomaterials, unless they are a component of a medical device. In Europe, any device or apparatus intended for human use is required to have a CE mark, indicating that safety and performance criteria have been met for a particular indication.7 Although most would agree that the ideal biomaterial should be reproducible, biocompatible, biodegradeable, and nontoxic, less is understood about the properties required to facilitate the colonization and integration of cells into a functional tissue.8 A principal factor in the success of a new material is its ability to perform with an appropriate host response in a specific application (i.e., its tissue biocompatibility). Tissue reactions to implanted materials vary widely, and the response determines to a great extent whether the material will be biocompatible.9 In the urologic and urogynecologic community, there are a broad range of uses for biomaterials. Biomaterials are used in artificial urinary sphincters, in testicular and penile prostheses, and as injectables for stress incontinence. Additionally, they can be used for the restoration of function or structure (i.e., grafts for Peyronie’s disease, bladder augmentation) and for reinforcement of the vaginal wall in prolapse/reconstructive procedures.7 The most commonly used natural materials available for prolapse repair include autograft (rectus fascia), allograft (cadaveric fascia,) and xenografts. Xenografts may be either nonabsorbable (i.e., Pelvicol) or absorbable collagen (small intestine submucosa [SIS]). NONABSORBABLE PORCINE COLLAGEN

BIOMATERIALS The United States National Institutes of Health (NIH) defines a biomaterial as “any substance (other than a drug) or a combination of substances, synthetic or natural in origin, which can be used for any period of time, as a whole or a part of a system which treats, augments, or replaces any tissue, organ, or function of the body.”5 Currently, there are five types of biomaterials being used in the medical environment: polymers (i.e., in catheters), composites, metals and alloys, ceramics, and biologic materials.6 Each material offers unique capabilities and advantages based on its composition, its architecture, and whether it is biodegradable. The concern over possible costly litigation resulted in a worldwide shortage of biomaterials in the mid-1990s. In response, the

Pelvicol (C.R. Bard, Covington, GA) is the most frequently researched and implanted xenograft collagen. It was developed at the University of Dundee in the United Kingdom and was designed for permanent implantation in humans for use in pubovaginal slings, vaginal wall repair, cystoplasty, and phalloplasty.7 Pelvicol was licensed for use in Europe in 1998 and received approval from the U.S. FDA in 2000. When the tissue is used for applications outside urology and urogynecology, it is distributed under the name Permacol. Porcine collagen is 95% homologous to human collagen, and it appears to provide a strong, nonallergenic scaffold for human tissue growth.10 Pelvicol is derived from porcine dermis. A patented process removes all fats and cellular materials, including cells, cell components, and nucleic acids, through a series of organic and enzy655

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Section 7 FEMALE ORGAN PROLAPSE

matic extractions that leave the material without any DNA.11,12 The final stage of the processing involves stabilizing the matrix with an approved cross-linking agent to maintain strength and provide permanence. Gamma sterilization of the tissue ensures sterility. Originally, the grafts were cross-linked with glutaraldehyde. However, this agent was associated with significant calcifications,13 so now diisocyanate, which has less graft mineralization, is used as the cross-linking agent.10,14 Ultimately, this final product is a piece of fibrous, acellular, cross-linked porcine dermal collagen that is nonallergenic, is nontoxic, and does not elicit a foreign body response.15 Also, the resulting material conserves the original three-dimensional architecture of the collagen matrix with a small amount of elastin.12 The treated tissue is free of DNA remnants as well as foot and mouth disease,16 and the manufacturing process has been demonstrated to remove the viral and bacteriologic load from Pelvicol implants. Reoviruses are reduced by more than 12 logs and porcine parvoviruses by 6.7 logs, levels that are acceptable to both the FDA and the European United (EU) regulatory authorities.17 Once implanted in to human tissue, the implant has been shown to be a biocompatible, sterile, and strong biologic matrix that is permanently incorporated into the host tissue.15 The graft is available in several sizes depending on its clinical use. There are other nonabsorbable xenograft collagens produced by other companies, but, as of this publication, human use of these grafts has not been reported. One such graft, Cytrix Soft Tissue Repair Matrix (TEI Biosciences, Boston, MA) is a bovine dermis that does not undergo cross-linking.18 Whether this difference in processing alters graft strength remains to be seen. In a rat model, Rosenblatt showed that this graft was populated by host fibroblasts and a supporting vasculature. Over 15 months, the implant collagen was remodeled and replaced by the host into collagen that repaired the iatrogenic muscle defect.18 Fate of the Graft: Porcine Collagen Although rejection of porcine dermis has not been reported, case studies suggest an unpredictable tissue response once the graft is implanted. Cole identified a completely encapsulated porcine dermis sling during urethrolysis at 6 months after surgery. Grossly, the sling was intact, and histologically, it was acellular and did not show evidence of human tissue proliferation.19 Salomon and assocuates reported on 1 patient who underwent exploratory surgery 1 year after implantation of a transobturator Pelvicol graft for cystocele repair. At the time of surgery, there was no inflammation around the graft which was easily freed from surrounding tissues. Histologic evaluation showed colonization by fibroblasts and blood vessels with minimal inflammatory response.17 Gandhi and colleagues reviewed the tissue specimens of seven patients with a prior porcine dermal sling and found limited collagen remodeling and evidence of a foreign body–type reaction in patients with postoperative retention. In cases of recurrent stress incontinence, implants appeared to be completely replaced by dense fibroconnective tissue and moderate neovascularization without evidence of inflammation or graft remnants. The authors concluded that this variable tissue reaction raises questions of tolerability and efficacy and may contribute to unpredicitable clinical outcomes.20 After implantation, there is a migration of cells, in-growth of tissue, neovascularization, and collagen formation in and around

the graft. Although it is unclear what the ultimate biomechanical properties will be like once the graft is implanted, some researchers believe that this connective tissue surrounding the implant adds to its strength.21 On the other hand, Dora and coworkers demonstrated in a rat model that porcine dermis and porcine SIS show a marked decreased in tensile strength and stiffness after being implanted for 12 weeks on the abdominal rectus fascia.22 Whether this mechanical change is of clinical significance remains unknown. In still another animal study, Macleod and colleagues evaluated Permacol 20 weeks after implantation in the SpragueDawley rat. Although the graft maintained its thickness over the 20 weeks, there was a decrease in mean collagen density. These findings suggest an overall loss of collagen over the 20 weeks.9 Although it appears that there is not one specific factor that is paramount for porcine dermis graft success, attempts have been made to evaluate the integral pieces necessary for success. One belief is that the graft relies, to some degree, on its capacity to be colonized by host cells, and when recurrence occurs, it may be because of compromised native tissue and vascularity contributing to poor graft behavior.23 In another evaluation of the tissue, Boon and coworkers implanted the graft subcutaneously in a rat model and found minimal fibroblast in-growth into cross-linked collagen. They suggested that cross-linked collagen may be considered for use in situations where neither incorporation nor dissolution of the biomaterial is desired.24 Others have also seen a low inflammatory response to the Pelvicol.21 This “tolerance” may contribute to a more ordered deposition of collagen,21 perhaps allowing the graft to behave similar to autologous tissue. With respect to vaginal examination after porcine dermis implantation, we are in agreement with the assessment by others that the Pelvicol implant is difficult to palpate postoperatively, whereas that is not always true with some mesh materials.2 Additionally, there is minimal to no shrinkage of the material, a key factor in sexually active women and in those with preoperative vaginal stenosis. Some authors have shown that perforating the porcine dermis improves the graft take and decreases wound infections by allowing for increased tissue in-growth and revascularization of the vaginal epithelilum overlying the graft. Tensile strength and suture pull-out strength were maintained in the perforated graft.25

RESULTS: PORCINE COLLAGEN Long-term data for porcine dermis in cystocele repair are generally lacking, but early results are promising (Table 65-1). De Ridder compared the Raz classic cystocele repair using polyglactin mesh with a modified Raz technique using a Pelvicol implant as an overlay graft material. Follow-up was only 9.3 months, but there were no recurrences or erosions in the Pelvicol group.2 Fischer used Pelvicol implant for cystocele repair in 14 patients, for rectocele repair in 80 patients, and for combined repair in 10 patients.26 With follow-up of at least 6 months, there were no cases of extrusion, recurrence, shrinkage, induration, dyspareunia, or urgency-frequency syndrome. Gomelsky used porcine dermis for cystocele repairs with and without anti-incontinence surgery or vault suspension in 70 patients. With follow-up of at

Chapter 65 CYSTOCELE REPAIR USING BIOLOGIC MATERIAL

Table 65-1

Results of Porcine Dermis Implants for the Correction of Anterior Vaginal Wall Prolapse

Study (Ref. No.) De Ridder (2) Fischer (26) Gomelsky et al (10)

N

Follow-up (Mo)

28 104 70

9.3 >6 24

Leboeuf et al (23)

15

Adverse Events

None Not provided 8.6% grade 2, 4.3% grade 3

No erosions No extrusion Superficial wound separation treated conservatively (1 case) 4.7% postoperative retention; 11.7% de novo urge incontinence Each preoperative stage of prolapse showed significant improvement postoperatively Placed via transobturator approach, combined with bilateral sacrospinous fixation; 1 graft removed because of pain at transfixing vaginal stitch 2 wound breakdowns

Pelvicol

2 poor wound healing managed as outpatient; no graft infection/rejection No infection, erosion, or rejection 1 expulsion; 1 small graft erosion 24% anaerobic infection No infection, erosion, or rejection 1 erosion

Pelvicol

93%

6.9% (2 pts grade 2, 1 pt grade 3)

69%

26% first degree (BadenWalker); 4.9% second degree

81

Salomon et al (17)

27

14

81%

1 pt stage 1, 4 pts stage 2; all pts had stage 3 or 4 preoperatively

Ruparelia et al (29)

48

20

2% reoperation rate

Kocjancic et al (30)

79

85% pt satisfaction rate, 78% symptomatic improvement 73% optimal anatomic outcomes

6.5

8

1 pt stage 1

Graul et al (32)

37

Flam (33)

59

None

Paparella et al (34)

45

1 pt stage 2

Cervigni et al (35)

6

8.8

68% anatomic cure

Implant Trade Name

Recurrence

Steinberg et al (27)

Verleyen et al (31)

8.5

Objective Cure

Intexen

Pelvicol

Porcine dermis (company not stated)

Pelvicol

Pelvicol

Pelvicol Pelvicol Pelvicol Pelvicol

pt, patient; pts, patients.

least 12 months, 9 patients (12.9%) had asymptomatic recurrent cystoceles that were managed conservatively.10 Steinberg used a 6 × 12 cm trapezoid piece of porcine dermis to perform vaginal paravaginal repair. When patients were analyzed stage for stage, there was a statistically significant improvement from preoperative to postoperative stage of prolapse.27 Besides anatomic improvement with the use of a graft, Sundar showed that the use of porcine collagen provides a significant overall improvement in quality of life.28

SMALL INTESTINE SUBMUCOSA SIS is harvested from porcine jejunum and is composed of the stratum compactum of the tunica mucosa, the tunica muscularis mucosa, and the tunica submucosa.9 Processing leaves the extracellular collagen matrix intact, thus allowing the presence of collagen, growth factors, glycosaminoglycans, proteoglycans, and glycoproteins to promote host cell proliferation through SIS layers.36 Theoretically, the SIS scaffold should be entirely remod-

657

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Section 7 FEMALE ORGAN PROLAPSE

eled and replaced by the host’s connective tissue in 90 days.37 SIS for pelvic reconstruction is currently available in 1-ply and 4-ply sheets for prolapse repairs (SurgiSIS and SurgiSIS ES, Cook Inc., Bloomington, IN). To date, there are few published data available on the use of porcine SIS for the treatment of pelvic organ prolapse. In one small human study, eight patients underwent SurgiSISaugmented vaginal prolapse surgery. At follow-up, there was adequate support of the vaginal wall, and symptom scores showed improvement.38 Although the database for pelvic reconstruction is small, SIS has been used as a pubovaginal sling39,40 and for the treatment of abdominal wall hernias, where it was effective in both clean and clean-contaminated repairs.41 As with other biologic materials, in vivo human studies for prolapse repair are lacking. Therefore, response of the implant in this application must be extrapolated from its use in pubovaginal sling surgery. In three humans requiring exploration after SIS pubovaginal sling placement, Weidemann and Otto found minimal SIS implant and no inflammatory or foreign body reaction.42 These results were in stark contrast to the significant inflammatory reaction found after an 8-ply SIS graft was placed as a sling.43,44 In an attempt to limit the inflammatory response, modifications to the graft and instructions for its use have been made. A number of animal studies evaluating SIS have been performed. Other authors have used a rat model to show that SIS initially shows a moderate degree of chronic inflammation that falls to minimal levels in a 20-week period of implantation.9 In a rabbit model, porcine SIS was shown to decrease in surface area by 41%.22 The clinical implications for this finding with respect to anterior vaginal wall repair were not expanded on and in reality are unknown. In a canine model, a piece of SIS was used to replace a portion of bladder wall. Immunohistochemical examination of the regenerated bladder at 15 months showed normal histology (epithelium, muscle, and serosa) and presence of nerves and other constituents (calcitonin gene-related peptide and substance P immunoreactive nerve fibers). Of note, in vitro testing of the new bladder wall for compliance and contractility showed it to be similar in function to the original bladder wall. To date, there have been no clinical trials.45 It remains to be seen how this knowledge can be incorporated into the use of SIS for the generation of a graft for prolapse repair. Using a rabbit model, Claerhout and colleagues evaluated various materials including SIS and Pelvicol in abdominal wall defects. By 3 months, the SIS appeared as a thin, almost transparent membrane. For SIS, the point of weakness was determined

to be the material itself, whereas for Pelvicol the maximum point of weakness was the interface between graft and native tissue.46 HUMAN DERMIS The most common cadaveric dermis used in pelvic reconstructive surgery is AlloDerm (LifeCell Corp, Branchburg, NJ); Duraderm (C.R. Bard Inc, Murray Hill, NJ) has less information for prolapse repair available.47 Cadaveric dermis is an acellular and immunologically inert biologic biomaterial that works by acting as a biologic scaffold for tissue remodeling.48 Graft preparation involves decellularization to remove the epidermis and dermis while preserving the basement membrane complex.49 The graft then undergoes freeze-drying such that the collagen, elastin, and proteoglycans are maintained.48 The biomechanical properties of dermal grafts have been shown to be similar to those of autologous rectus fascia and solvent-dehydrated cadaveric fascia.50 Although intact DNA has been found in acellular cadaveric dermis,51 it has not been associated with disease transmission in recipients. The American Association of Tissue Banks is the organization responsible for maintaining screening and procurement standards. Dermal allograft has been used for many different surgical procedures,52,53 including pelvic floor reconstruction.54-57 One potential benefit of the tissue is its ability to maintain elasticity. However, it remains unclear whether this characteristic prevents recurrence by allowing the vaginal wall to stretch with Valsalva maneuvers and then return to its original position, or whether the elasticity contributes to failure because it may be stretched too far.57 Histologically, it appears that dermal allograft completely incorporates into the host fibromuscular layer, with no significant inflammation and no identifiable graft 2 years after implantation.58 Variations in processing may affect success rates with cadaveric fascia, but studies with cadaveric dermis are lacking.59 If complications such as graft extrusion occur, they can be managed conservatively with topical estrogen cream.60 Human studies for anterior wall reconstruction are limited; results are shown in Table 65-2. BOVINE PERICARDIUM Experience with bovine pericardium for cystocele repair is extremely limited, and indeed, in our opinion, very suspect. McLennan used this graft in 61 patients undergoing vaginal paravaginal repair. With a mean follow-up of 7.25 months, 6.5% of

Table 65-2 Results of Cadaveric Dermal Graft for the Treatment of Anterior Vaginal Wall Prolapse Study (Ref. No.)

N

Follow-up (Mo)

Outcome

Complications

18.4

44% stage 0-1

20% site granulation tissue (includes posterior repairs)

16% objective failure 41% objective failures (stage >2); 3% subjective failures 2 failures defined as stage 2 or greater

Jelovsek et al (54)

9

Chung et al (55) Clemonset al (57)

19 33

28 18

Graul & Hurst (61)

67

10.2

No erosion/rejection 1 erosion treated conservatively; 1 graft expulsion

Chapter 65 CYSTOCELE REPAIR USING BIOLOGIC MATERIAL

patients had a stage 2 or greater anterior wall prolapse. There were no cases of graft erosion, and the authors noted that by 6 weeks vaginal tissue was supple and normal.62 However, when bovine pericardium was used for pubovaginal sling procedures, the rate of erosion was much more significant.63,64 SURGICAL TECHINIQUE Surgery is performed with the patient under either general or spinal anesthesia. Sequential compression devices are placed preoperatively, and prophylactic antibiotic coverage is given on call to the operating room. The patient is placed in dorsal lithotomy position with Allen stirrups. Concominant procedures such as a hysterectomy or pubovaginal sling can be performed at the same sitting. Usually, prolapse repair is completed before anti-incontinence surgery or rectocele repair and after hysterectomy. If the patient has had a prior hysterectomy, the uterosacral ligaments are sutured and tagged for easier identification. The vaginal epithelium is injected with 0.25% Marcaine. Incision of the vaginal epithelium is usually in the midline. Lateral vaginal flaps are elevated superficial to the pubocervical fascia, all the way to the obturator fascia laterally and the uterosacral/cardinal ligaments proximally. The endopelvic fascia is perforated, and dissection is carried into the space of Retzius bilaterally. The arcus tendineus fascia pelvis is identified laterally where it attaches to the obturator internus fascia. The native fascia may be brought together in the midline with absorbable or nonabsorbable suture depending on surgeon preference. The graft is prepared on the back table according to the manufacturer’s recommendations and then brought into the vagina and trimmed to an appropriate size. Initial tapering should err on the large side so as not to foreshorten the graft. The graft is secured to the vaginal cuff and uterosacral ligaments proxi-

mally at the vaginal apex and then laterally to the obturator fascia, using interrupted 2-0 polyglycolic acid suture. Distally, the graft should be affixed to the arcus or the fascia overlying the inferior ramus of the pubis at the level of the bladder neck. Tailoring of the graft shape is accomplished as the graft fixation progresses distally. Copious antibiotic irrigation may be used throughout the procedure. Cystoscopy is performed to confirm integrity of the bladder and ureters. After the graft has been secured in place, redundant vaginal epithelium is trimmed, and the vaginal wall is closed with interrupted absorbable suture. If an anti-incontinence procedure is necessary, it may be performed at this time via a separate incision. CONCLUSION Biologic biomaterials may have a valuable role in reconstructive procedures for anterior vaginal wall prolapse. When graft material is required, the surgeon must identify the positive properties of each option and determine the most appropriate material for the individual patient. Future technologic advancements may one day provide the ideal graft material that meets all the necessary criteria for long-term durability and success. Disclaimer The authors have been asked to review the use of particular biologic materials in the repair of anterior vaginal wall defects and to provide comment. This does not represent endorsement of use of such materials, and it should be stated that “the jury is still out” regarding the optimal approach and materials one should use to enhance the success of repairs of the anterior vaginal compartment.

References 1. Macer GA:Transabdominal repair of cystocele, a 20 year experience, compared with the traditional vaginal approach. Am J Obstet Gynecol 131:203-207, 1978. 2. De Ridder D:The use of biomaterials in reconstructive urology. Eur Urol 1(Suppl):7-11, 2002. 3. Cumberland VH: A preliminary report on the use of prefabricated nylon weave in the repair of ventral hernia. Med J Aust 1:143-144, 1952. 4. Scales JT: Materials for hernia repair. Proc R Soc Med 46:647-652, 1953. 5. National Institutes of Health: Clinical applications of biomaterials. NIH Consensus Statement 4(5):1-19, 1982. 6. Science and Technology Policy Institute: Biomaterials availability: Potential effects on medical innovation and health care. [Issue paper.] Rand IP-194:1-60, 2000. 7. Lloyd SN, Cross W: The current use of biomaterials in urology. Eur Urol 1(Suppl):2-6, 2002. 8. Kimuli M, Eardley I, Southgate J: In vitro assessment of decellularized porcine dermis as a matrix for urinary tract reconstruction. BJU Int 94:859-866, 2004. 9. Macleod TM, Williams G, Sanders R, Green CJ: Histological evaluation of Permacol™ as a subcutaneous implant over a 20week period in the rat model. Br J Plast Surg 58:518-532, 2005. 10. Gomelsky A, Rudy DC, Dmochowski RR: Porcine dermis interposition graft for repair of high grade anterior compartment defects with or without concomitant pelvic organ prolapse procedures. J Urol 171:1581-1584, 2004.

11. Oliver RF, Barker H, Cooke A, et al: Dermal collagen implants. Biomaterials 3:38-40, 1982. 12. Grosh SK, Hanke CW, DeVore DP, Gibbons DG: Variables affecting the results of xenogenic collagen implantation in an animal model. J Am Acad Dermatol 13:792-798, 1985. 13. McPherson JM, Sawamura S, Armstrong R: An examination of the biologic response to injectable glutaraldehyde cross-linked collagen implants. J Biomed Res 20:93, 1986. 14. Oliver RF: Scar and collagen implantation. Burns 13:S49-S55, 1987. 15. Harper C: PermacolTM: clinical experience with a new biomaterial. Hosp Med 62:90-95, 2001. 16. Data on File: PelvicolTM acellular collagen matrix foot and mouth disease. Tissue Science Laboratories, PLC, Manufacturers Statement, March 2001. 17. Salomon LJ, Detchev R, Barranger E, et al: Treatment of anterior vaginal wall prolapse with porcine skin collagen implant by the transobturator route: Preliminary results. Eur Urol 45:219-225, 2004. 18. Rosenblatt P: Repair of abdominal muscle defects with implants composed of xenogenic fetal collagen: Long term (15 month) in vivo evaluation of implant reconstitution and remodeling. Presented at the International Continence Society Annual Meeting, Paris, France, August, 2004. 19. Cole E, Gomelsky A, Dmochowski RR: Encapuslation of a porcine demris pubovaginal sling. J Urol 170:1950, 2003. 20. Gandhi S, Kubba LM, Abramov Y, et al: Histopathologic changes of porcine dermis xenografts for transvaginal suburethral slings. Am J Obstet Gynecol 192:1643-1648, 2005.

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21. Zheng F, Lin Y, Verbeken E, et al: Host respons after reconstruction of abdominal wall defects with porcine dermal collagen in a rat model. Am J Obstet Gynecol 191:1961-1970, 2004. 22. Dora CD, Dimarco DS, Zobitz ME, Elliott DS: Time dependent variations in biomechanical properties of cadaveric fascia, porcine dermis, porcine small intestine submucosa, polypropylene mesh and utologous fascia in the rabbit model: implications for sling surgery. J Urol 171:1970-1973, 2004. 23. Leboeuf L, Miles RA, Kim SS, Gousse AE: Grade 4 cystocele repair using four-defect repair and porcine xenograft acellular matrix (Pelvicol): Outcome measures using SEAPI. Urology 64:282-286, 2004. 24. Boon ME, Ruijgrok JM, Vardaxis MJ: Collagen implants remain supple not allowing fibroblast ingrowth. Biomaterials 16:1089-1093, 1995. 25. Taylor G, Moore R, Miklos J, Mattox T: Posterior repair with perforated porcine dermal graft. Presented at International Continence Society Annual Meeting, Paris, France, 2004. 26. Fischer A: Prolapse surgery using biomaterials. Eur Urol Suppl 1:2932, 2002. 27. Steinberg AC, Oyama IA, Feloney M, et al: Vaginal paravaginal repair with the use of porcine dermis. J Pelvic Med Surg 11:88, 2005. 28. Sundar K, Pain S, Ruparelia B: Quality of life (QOL) after pelvic floor repair with porcine collagen. Int Urogynecol J Pelvic Floor Dysfunct 12(Suppl 1):10-11, 2002. 29. Ruparelia BA, Gunasheela S, Sundar K: Anterior and posterior vaginal prolapse repairs with porcine skin collagen (Pelvicol™) implant. Int Urogynaecol J 11(Suppl 1):FDP33 S45, 2000. 30. Kocjancic E, Meshia M, Pifarotti P, et al: Multicentre randomized trial of Pelvicol™ implant in the treatment of cystocele. J Urol 173:233, 2005. 31. Verleyen P, Filip C, Bart K, et al: A prospective randomized trial comparing Pelvicol™ and Vicryl™ cystocele repair in the Razcolposuspension. Presented at Annual International Continence Society Meeting, Paris, France, August 2004. 32. Graul EA, Hurst B, Abbott T: Porcine allograft in the repair of anterior and posterior vaginal wall defects. Int Urogynecol J Pelvic Floor Dysfunct 13(Suppl 1):7, 2002. 33. Flam F: Pelvicol™ implant for the operative treatment of prolapse. Int Urogynecol J Pelvic Floor Dysfunct 13(Suppl 1):5, 2002. 34. Paparella P, Ercoli A, Marturano M, et al: The use of porcine dermal implant in the vaginal surgical repair of stage II-IV anterior vaginal wall prolapse: Feasibility, short term complications and results. Presented at the International Continence Society 33rd Annual Congress, October 2003, Florence, Italy. 35. Cervigni M, Natale F, Weir J, et al: Prospective randomized trial of two new materials for the correction of anterior compartment prolapse: Pelvicol and Prolene Soft. Presented at the 35th Annual Meeting of the International Continence Society Meeting, Montreal, Canada, September 2005. 36. Voytik-Harbin SL, Brightman AO, Kraine MR, et al: Identification of extractable growth factors from small intestinal submucosa. J Cell Biol 67:478-491, 1997. 37. Sandusky GE, Lantz GC, Badylak SF: Healing comparison of small intestine mucosa and ePTFE grafts in the canine carotid artery. J Surg Res 58:415-420, 1995. 38. Ellerkmann RM, Dunn JS, Blomquist JL, et al: Evaluation of graft biomaterial in reconstructive pelvic surgery: A pilot study. Proceedings of the 23rd annual meeting of the American Urogynecologic Society, San Francisco, CA, Oct 17-19, 2002. 39. Rutner AB, Levine SR, Schmaelzle JF: Processed porcine small intestine submucosa as a graft material for pubovaginal slings: Durability and results. Urology 62:805-809, 2003. 40. Jones JS, Cherullo EE, Abdelmalak JB, et al: Small intestine submucosa (SIS): Minimally invasive non-synthetic sling. Presented at the American Urological Association Annual Meeting, Orlando, FL, May 25-30, 2002.

41. Helton WS, Fisichella PM, Berger R, et al: Short-term outcomes with small intestinal submucosa for ventral abdominal hernia. Arch Surg 140:549-560, 2005. 42. Wiedemann A, Otto M: Small intestinal submucosa for pubourethral sling suspension for the treatment of stress incontinence: First histopathological resuls in humans. J Urol 172:215-218, 2004. 43. Ho KLV, Witte MN, Bird ET: Eight-ply small intestinal submucosa tenstion-free sling: Spectrum of postoperative inflammation. J Urol 171:268-271, 2004. 44. Kalota S: Small intestinal submucosa tenstion-free sling: Postoperative inflammatory reactions and additional data. J Urol 172:13491350, 2004. 45. Kropp BP, Sawyer BD, Shannon HE, et al: Characterization of small intestinal submucosa regenerated canine detrusor: assessment of reinnervation, in vitro compliance and contractility. J Urol 156(2S):599-607, 1996. 46. Claerhout F, Deprest J, Zheng F, et al: Long term evaluation of the tissue response and mechanical properties of two collagen based and polypropylene implants and a rabbit model for abdominal wall repair. Presented at the 33rd Annual Congress of the International Incontinence Society, Florence, Italy, October 2003. 47. Owens DC, Winters JC: Pubovaginal sling using Duraderm graft: Intermediate follow-up and patient satisfaction. Neurourol Urodyn 23:115-118, 2004. 48. AlloDerm regenerative tissue matrix. LifeCell Corporation. Available at: http://www.lifecell.com (accessed August 15, 2007). 49. Livesey S, Atkinson Y, Call T, et al: An acellular dermal transplant processed from human cadaver skin retains normal extracellular matrix components and ultrastructural characteristics. The American Association of Tissue Banks (AATB) Conference, Boston, Massachusetts, August 1994. 50. Lemer ML, Chaiken DC, Blaivas JG: Tissue strength analysis of autologous and cadaveric allografts for the pubovaginal sling. Neurourol Urodyn 18:497-503, 1999. 51. Choe JM, Bell T: Genetic material is present in cadaveric dermis and cadaveric fascia lata. J Urol 166:122-124, 2001. 52. Wainwright DJ: Use of an acullular allograft dermal matrix (Alloderm) in the management of full-thickness burns. Burns 21:243248, 1995. 53. Chaplin JM, Costantino PD, Wolpoe ME, et al: Use of an acellular dermal allograft for dural replacement: An experimental study. Neurosurgery 45:320-327, 1999. 54. Jelovsek JE, Amundsen C, Addison WA, Weidner AC: Outcomes of pelvic organ prolapse surgery with Alloderm™ graft. Proceedings of the 23rd annual meeting of the American Urogynecologic Society, San Francisco, California, October 17-19, 2002. 55. Chung SY, Franks M, Smith CP, et al: Technique of combined pubovaginal sling and cystocele repair urisn a single piece of cadaveric dermal graft. Urology 59:538-541, 2002. 56. Miklos JR, Kohli N: Rectovaginal fistula repair utilizing a cadaveric dermal allograft. Int Urogynecol J Pelvic Floor Dysfunct 10:405-406, 1999. 57. Clemons JL, Myers DL, Aguilar VC, Arya LA: Vaginal paravaginal repair with an AlloDerm graft. Am J Obstet Gynecol 189:1612-1619, 2003. 58. Graul EA, Hurst B, Abbott T: Disposition of dermal allograft tissue two years after implantation. Proceedings of the 23rd annual meeting of the American Urogynecologic Society, San Francisco, California, October 17-19, 2002. 59. Crivellaro S, Smith JJ, Kocjancic E, Bresette JF: Transvaginal sling using acellular human dermal allograft: Safety and efficacy in 253 patients. J Urol 172:1374-1378, 2004. 60. Drake NL, Weidner AC, Webster GD, Amundsen CL: Patient characteristics and management of dermal allograft extrusions. Int Urogynecol J Pelvic Floor Dysfunct 16:375-377, 2005.

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61. Graul EA, Hurst B: An alternative technique for the repair of pelvic prolapse. Int Urogynecol J Pelvic Floor Dysfunct 12(Suppl 1):3, 2002. 62. McLennan M, Leong FC, Melick C: Bovine pericardium augmentation graft for vaginal paravaginal defect repair of the anterior segment. Presented at the Annual Meeting of the International Continence Society, Paris, France, August 2004.

63. Martucci RC, Ambrogini A, Calado AA, et al: Pubovaginal sling with bovine pericardium for treatment of stress urinary incontinence. Braz J Urol 26:208-214, 2000. 64. Candido EB, Triginelli SA, Silva Filho AL, et al: The use of bovine pericardium in the pubovaginal sling for the treatment of stress urinary incontinence. Rev Bras Ginecol Ostet 25:525-528, 2003.

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TENSION-FREE CYSTOCELE REPAIR USING PROLENE MESH Mauro Cervigni and Franca Natale Pelvic organ prolapse (POP) is one of the emerging problems in women, considering the aging population in Western countries together with already known risk factors such as race, genetic predisposition, pregnancy, parity, obstetric trauma, menopause, and previous gynecologic surgery. Among these factors, certainly white Caucasian women have a higher odds ratio (1.0) with respect to African American and Hispanic women (0.6 and 1.2, respectively).1 Considering the different segments involved in the development of POP, the anterior vaginal wall, and in particular the bladder, represented the site most frequently affected in a study of 27,000 American women; the posterior segment (rectocele) was present in 19%, and uterine prolapse in 14%.1 Mant and colleagues, in 1997, studied a group of 17,000 women and observed that the incidence of anterior colporrhaphy was 37%, compared with a 24% rate of vaginal hysterectomy.2 Numerous surgical procedures have been proposed in the last century to correct all types of anterior vaginal wall defects (central, paravaginal, combined), using either an abdominal or vaginal approach. Despite improved understanding of pelvic anatomy and organ function and the advancement of surgical techniques, the long-term success rate is still variable. Recurrence rates for the various surgical procedures used to treat anterior vaginal prolapse range from 3%3 to 20%4 after single anterior colporrhaphy, from 22%5 to 92%6 if the anterior colporrhaphy is combined with other procedures (sacrospinous ligament suspension), from 2%7 to 59%8 after four-corner suspension, and from 5%9 to 50%10 after vaginal paravaginal repair. The reasons for such discrepancies are several and include poor patient selection, suboptimal surgical technique, inappropriate choice of suture material, and persistence of predisposing risk factors for prolapse (constipation, chronic respiratory disease).11 Moreover, Farrell and colleagues emphasized that the very existence of the pubocervical fascia used during anterior colporrhaphy is doubtful. They observed in samples obtained during surgical procedures for the correction of anterior defect that the so-called fascia is adequately identified only 58% of the time and concluded that this finding calls into question techniques that rely on isolated fascia for the repair of anterior and posterior defects.12 In addition, recent information on the biochemical and ultrastructural composition of the connective tissue of the pelvic floor has provided new insight into its role in stabilization of the pelvic organs and in the healing processes after surgery.

EVOLUTION OF SURGICAL PROCEDURES In the last 20 years, the repair of anterior vaginal wall prolapse has shifted from a classic anterior repair to a more detailed surgi662

cal procedure (site-specific repair) with an attempt to identify the precise localization of the tissue defect. For example, Richardson and associates proposed the vaginal paravaginal repair using native tissues to restore the anatomy.13 These concepts were further explored in surgery of the posterior compartment. However, despite encouraging results, the anterior segment (i.e., the connective tissue supporting the bladder) remained the site of least durability.14,15 Moreover, the rate of complications was not insignificant (11% ureteral occlusion), and the conclusions of Barber and Bump were that a correct vaginal reconstruction is best accomplished in women with severe stress conditions (severe constipation, chronic pulmonary disease, occupation and recreational straining, severe compromise of pelvic floor neuromuscular function) with techniques that do not rely solely on the patient’s native tissue for support and that this is often achieved with the use of synthetic mesh or tissue graft substitution.

CONNECTIVE TISSUE AND ITS ROLE IN THE PELVIC FLOOR Connective tissue is analogous to a fiber-reinforced composite, containing fibrous elements (collagen and elastin) and a viscoelastic matrix including proteoglycans (large polysaccharides attached to proteins). The cells in the connective tissues, which form about 20% of the tissue volume, are embedded in the extracellular matrix. The biomechanical properties of a soft tissue are determined by the various extracellular matrix components. Collagen, which accounts for a large proportion of tissue strength, is a protein produced by fibroblasts with a specific pattern that is remarkable for its consistency. The amino acid glycine allows collagen to form a tight helix, one of its important attributes. Two other amino acids are present in its structure, namely proline and hydroxyproline. These amino acids form cross-links that stabilize the collagen chains. The collagen fibers responsible for the tensile strength of the tissue are a family of 16 different types distributed in different parts of the body. Of these, type I (the most common and strongest) and type III (smaller and randomly organized with type I), are found in tissue that requires strength and flexibility. Elastin and laminin are two other glycoproteins that may play a role in elasticity of the ground substance. Elastin provides the ability of a tissue to be stretched and is found not only in the bladder as a component of compliance but also in the urethra. Elastin is degraded by elastase, which is part of a proteaseantiprotease control mechanism found in the plasma. It has recently been demonstrated that there is an increase in the percentage activity of elastase in women with stress urinary inconti-

Chapter 66 TENSION-FREE CYSTOCELE REPAIR USING PROLENE MESH

nence (SUI) compared with aged-matched controls.16 Several factors, such as age, stress, hormones, and growth factors, are involved in the regulation of connective tissue metabolism.17 Collagen turnover slows down with increasing age, and the concentration increases after menopause.18-21 The changes during menopause seem to generate a connective tissue with a higher collagen concentration but with alterations in cross-linking,22 and there is also an increase in fibril diameter in the cardinal and uterosacral ligament in patients with POP and SUI. This produces a tissue with an increased load-bearing ability but decreased elasticity.23 Based on biochemical assays, Sayer and colleagues24 reported modification of cross-linking in women with bladder neck prolapse and SUI. A reduction of collagen in the pubocervical fascia25 and in nonsupportive pelvic tissue has also been observed.26 Recent studies indicate that women of fertile age with SUI demonstrate changes in the extracellular matrix of the paraurethral connective tissue resulting in a stiffer and less supportive connective tissue and a defect in the connective tissue glue.27-30 In women with genital prolapse after menopause, there seems to be a difference in collagen metabolism suggesting a change in the degradation of collagen related to matrix metalloproteinases and with a significant reduction in the ratio of type I to type III collagen.31 Therefore, it is not the amount of collagen but the amount of fresh elastic collagen that is important for the mechanical strength of supporting fascia layers. HEALING PROCESS AFTER SURGICAL REPAIR When a wound is created, such as an anterior vaginal wall and pubocervical fascia incision, fibrous protein synthesis and remodeling reestablish tissue strength. Collagen is a central factor in wound healing. The first day after injury, immature fibroblasts synthesize and secrete collagen and proteoglycans. A weaker and more elastic flexible type III collagen is the principal type found in early wounds. After 2 weeks, the majority of regenerated tissue is composed of type III collagen, which accounts for only 7% of its final tensile strength. With maturation of the scar, a stronger type I gradually replaces the type III collagen. In this way, an organized cross-linked pattern regains some tensile strength, but the new tissue is never as strong as the original tissue.32 The factors that influence healing and scar maturation are still incompletely understood, even though we know that the gene for type III collagen seems to be activated more than the gene for type I collagen.33 Elastin is a protein that the body does not seem to be able to synthesize and remodel, as it does collagen. Lack of elastin and high amounts of the less strong type III collagen may explain why new scars lack strength and elasticity.

Mesh: in-growth tissue

PMN Fibroblasts Macrophage Fibrin Capillars

1

2

5

10 Day

Figure 66-1 In-growth of tissue in mesh implants. PMN, polymorphonuclear cells.

(angiogenesis) with in-growth of capillaries. These modifications lead to synthesis of collagen and then to maturation of these new fibers (cross-linking). These events happen as a result of the interaction between the graft materials (biologic or synthetic) and the tissue interface, which is of prime importance; for this reason, we need to reduce the intensity and time of the inflammatory period, in particular with regard to reducing potential complications (erosion and extrusion) (Fig. 66-1). Once the prosthetic material has been implanted, there are four types of tissue reactions: minimal response with a thin layer of fibrosis around the implant; chemical response with a severe and chronic inflammatory reaction around the implant; physical response with an inflammatory reaction to certain materials and the presence of giant cells; and necrotic tissue, a layer of necrotic debris produced as a result of in situ exothermic polymerization.34 WHAT MATERIALS ARE CURRENTLY AVAILABLE FOR THE SURGICAL REINFORCEMENT OF PELVIC TISSUE? The following materials are currently available for the surgical reinforcement of pelvic tissue: synthetic material, which acts as a substitute for natural tissue; autograft, which is tissue obtained from another area of the patient’s body; allograft, which is tissue obtained from a human donor; and acellular collagen matrix, such as dermal (skin) tissue from pigs. PROPERTIES OF SYNTHETIC BIOMATERIALS

WHAT HAPPENS WHEN A MESH IS IMPLANTED IN THE BODY When a graft is introduced into a biologic tissue, there is a strong immediate (antibody-mediated) foreign body reaction, followed by blood flow increase, temperature rise, macrophage migration, and attempted phagocytosis of the foreign body. The graft incorporation process includes a cascade of events: first, there is a rapid activation of polymorphonuclear cells and macrophages; 60 hours later, there is fibroblast proliferation with a subsequent slow phenomenon of fibroplasia and blood vessel proliferation

Biocompatibility is the capability of a material to provoke a favorable reaction when introduced into a living system. Consequently, a biomaterial is any material, natural or man-made, or any biomedical device that performs, augments, or replaces a natural function. One definition of biocompatibility is “the utopian state where a biomaterial presents an interface with a physiologic environment without the material adversely affecting that environment or the environment adversely affecting the material.” The biomaterials employed can come close to this utopian state, but we must accept compromises between the

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Section 7 FEMALE ORGAN PROLAPSE

Figure 66-2 Type I synthetic mesh: monofilament polypropylene.

Figure 66-3 Type I synthetic mesh: Marlex.

benefits and the undesired reactions caused to the living system by the material. Cumberland35 and Scales36 delineated a series of properties of an “ideal” synthetic biocompatible materials: ■ ■ ■ ■ ■ ■ ■

Chemically and physically inert Noncarcinogenic Mechanically strong Does not cause allergic or inflammatory reactions Can be sterilized No physical modification by body tissue Convenient and affordable format for clinical use

At the present time none of the synthetic meshes meet all of these criteria. Although from the chemical point of view all of the synthetic meshes are completely biocompatible, some physical and structural properties of the prosthesis are associated with certain complications. Prevention of biomaterial-related complications requires a profound knowledge of the physical properties of prostheses, of which the porosity (pore size) of the materials are of paramount importance. Based on their pore size, the most common synthetic meshes can be classified into four types: Type I: totally macroporous materials such as Atrium, Marlex, Prolene, and Trelex. These meshes contain pores larger than 75 μm (microns), which is the required size for admission of macrophages, fibroblasts (fibroplasia), blood vessels (angiogenesis), and collagen fibers into the pores (Figs. 66-2 and 66-3).37,38 Type II: totally microporous materials such as expanded polytetrafluoroethylene (PTFE; Gore-Tex), Surgical Membrane, and Dual-mesh. These meshes contain pores smaller than 10 μm in at least one of their three dimensions (Fig. 66-4). Type III: macroporous materials with multifilamentous or microporous components, such as PTFE mesh (Teflon), braided Dacron mesh (Mersilene), braided polypropylene mesh (Surgipro), and perforated PTFE patch (MycroMesh) (Figs. 66-5 and 66-6).

Figure 66-4 Type II synthetic mesh: Gore-Tex (expanded PTFE).

Figure 66-5 Type III synthetic mesh: polytetrafluroethylene (PTFE).

Chapter 66 TENSION-FREE CYSTOCELE REPAIR USING PROLENE MESH

Type IV: biomaterials with submicronic pore size, such as Silastic, Cellgard (polypropylene sheeting), Preclude Pericardial membrane, and Preclude Dura-substitute. Another important property is the composition of fibers (Table 66-1). Polypropylene meshes are monofilaments, whereas the other commonly used meshes are multifilaments. One theoretical disadvantage of multifilament meshes is that the interstices are smaller than 10 μm; this allows small bacteria to infiltrate and proliferate, but macrophages and neutrophilic granulocytes that could eliminate the bacteria are too large to enter a 10-μm tridimensional pore.39-41 In addition, because of their wide pores, type I materials (but not types II and III) allow rapid in-growth of vascularized fibrous tissue, as was demonstrated by Chvapil and colleagues42; this leads to fibroplasia and angiogenesis, which not only prevent infection but also form fibrous connections to the surrounding tissue. Therefore, pore size is a key factor in determining inflammatory response and the growth of fibrocollagenous tissue. Flexibility or stiffness is another important property that appears to be related to pore size. Marlex has higher flexural rigidity (stiffness) than Mersilene or Teflon. Marlex is also shown to wrinkle more than Mersilene. Prolene is composed of knitted filaments of polypropylene, as is Marlex; however, it has a pore size twice as large as that of Marlex (1500 versus 600 μm) and therefore is more flexible.43 Because of this property, Prolene seems to have a lower erosion rate through the vagina and adja-

Surgipro side–B

Figure 66-6 Type III synthetic mesh: multifilament mesh.

cent viscera, but up to now there are insufficient data to prove it. Atrium mesh, because of its intermediate pore size (800 μm), is more pliable and thinner than Marlex or Prolene. Table 66-2 reports data about mean stiffness and mean peak load of the main synthetic materials. COMPLICATIONS OF SYNTHETIC MATERIALS Biomaterial-related complications frequently encountered are infection and sinus tract formation, seroma, intestinal adhesion, erosion and fistula formation, and shrinkage. Infection and sinus tract formation is caused by infiltration and proliferation of bacteria; it is frequently due to the use of multifilamentous suture materials for fixation of the mesh, although it may be mistaken as being caused by the mesh itself.44-46 The reported infection rate ranges from 9.6% to 50% in type II/III prostheses,47,48 whereas in type I it has never been reported. More important, with type I mesh, infection may be managed simply by drainage of the infected area, followed by local wound care.49-51 On the contrary, total removal of type II and at least partial removal of type III is required to manage infection. Prosthetic-related seroma formation is caused by the host inflammatory reaction to the prosthesis and by the dead space created between the artificial mesh and host tissue. Types I and III allow a rapid penetration of host proteinaceous materials into their pores,52 with rapid fibrinous fixation. Therefore, the chance of seroma formation is minimized.53 Type II, because of its inadequate pore size, has a higher rate of seroma formation ranging, from 9.6% to 14.6%. At the present time, all available artificial meshes, absorbable or nonabsorbable, adhere to the intestine.54-56 Covering the mesh on its intestinal side with a layer of absorbable material such as Vycril or expanded-PTFE patch partially solves this problem. Composites that combine type I and type IV mesh can prevent these complications. A dangerous side-effect is erosion or migration of the artificial mesh when it is in direct contact with organs that do not have a serosal covering, such as rectum, bladder, and the intestinal tract. Contraction of the mesh fibers during the scarring process leads to shrinkage of the mesh by approximately 20% compared to the original shape. Table 66-3 shows the main complications related to each type of mesh.

Table 66-1 Composition and Types of Fibers Chemical Component

Trade Name (Manufacturer)

Type

Polypropylene

Marlex (CR Bard, Branston, RI) Prolene (Ethicon, Sommerville, NJ) Atrium (Atrium Medical, Hudson, NH) Teflon (CR Bard, Haverhill, MA) Gore-Tex (WL Gore, Flagstaff, AZ) Mersilene (Ethicon, Somerville, NJ) Dexon (absorbable) (Davis and Geck, American Cyanamid, Danbury, CT) Vicryl (absorbable) (Ethicon, Somerville, NJ)

Monofilament Monofilament Monofilament Multifilament Multifilament Multifilament Multifilament Multifilament

Polytetrafluoroethylene (PTFE) Expanded PTFE Polyethylene tetraphthalate Polyglycolic acid Polyglactin 910

Adapted in part from Chu and Welch, John Wiley & Sons, p 907. Reprinted by permission of John Wiley & Sons, Inc.

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Table 66-2 Peak Load and Stiffness of Common Synthetic Materials Material TVT SPARC Prolene Mersilene IVS tape Gore-Tex MycroMesh Nylon

Mean Stiffness (N/mm)

Mean Peak Load (N)

0.23 0.53 0.53 1.17 1.58 2.61 6.83

68.1 52.1 56.4 50.3 46.2 71.3 422.0

Adapted from Dietz HP, Vancaillie P, Svehla M, et al: Mechanical properties of urogynecologic implant materials. Int Urogynecol J 14:241, 2003.

Table 66-3 Main Complications by Type of Mesh Complication Infection Seroma Adhesion Erosion

Type I

Type II

Type III

+ + +++ +++

+++ ++ + +

++ + ++ ++

Adapted from Debodinance P, Delporte P, Engrand JB, Boulogne M: [Development of better tolerated prosthetic materials: Applications in gynecological surgery.] [In French.] J Gynecol Obstet Biol Reprod 31:527540, 2002.

TECHNIQUES The Pioneers A recent metanalysis of the European Union Hernia Trialists Collaboration compared mesh versus nonmesh methods of open groin hernia repair in 4005 patients. They concluded that mesh repair was associated with fewer recurrences (1.4% versus 4.4%; P < .001). This concept, using synthetic mesh applied “tensionfree,” and the long-term successful outcome incited researchers to transfer an analogous rationale to pelvic surgery. Therefore, surgeons, in the early fifties, introduced synthetic materials to correct the anatomic position of the visceral organs in the pelvic cavity. In 1955, tantalum mesh was used to reinforce tissues in patients with POP.57 In 1970, collagen mesh was proposed for the treatment of pelvic descensus.58 The “fashion” for using polypropylene to repair prolapse started in 1992, with the first published data on Marlex appearing in 1996.59 Evolving Concepts The goal of prosthetic surgery, compared with site-specific autologous tissue repair, is to replace the damaged visceral fascia, restoring cohesion between visceral and parietal fascia and rebuilding the hammock connected to the arcus tendineous fascia pelvis (ATFP), thus respecting the bladder neck and stabilizing the bladder hammock. Initial experience used an overlaid synthetic mesh reinforcing a traditional anterior colporraphy.60 Meanwhile, the new concept of transvaginal suspension of pelvic floor repair was introduced by the four-corner suspension.7 The

Figure 66-7 Tension-free cystocele repair.

evolution of this technique included a prosthetic reinforcement of the central segment, using a mesh applied with a doubleneedle suspension.61 The new “tension-free” concept acquired by general surgeons in treating abdominal hernia and the revolution in the treatment of female SUI brought about by the tension-free vaginal tape (TVT) were translated into POP repair. A new proposal was developed that used a Prolene mesh applied below the bladder inserted “tension-free” without any fixation.62 Since then, other authors have proposed various transvaginal “tension-free” mesh repairs.63-65 In 2001, a new approach, using the transobturator route, was proposed to treat SUI patients in the same tension-free manner as TVT.66 The excellent preliminary results incited the development of a wider concept of transperineal pelvic floor repair.67-69 Therefore, studies employing larger meshes covering all the pelvic defects, using Prolene material (soft or traditional) applied “tension-free,” extended to stronger pelvic structures: transobturator foramina and sacrospinous ligaments. The Italian Experience In 1998, Cervigni and coworkers developed a tension-free cystocele repair (TCR) technique applying a traditional Prolene mesh below the bladder with two wings inserted paraurethrally without any fixation.62 The rationale of this technique was to use a wider mesh to cover all the bladder, avoiding any specific site defect evaluation, to reinforce pubocervical and endopelvic fascia. Because the mesh is applied tension-free, there is a reduction of anatomic distortion, which reduces future sequelae in the other vaginal segments (Fig. 66-7). Nicita published a Prolene technique mesh repair that was anchored with stitches to the arcus tendineous levator ani and sacrospinous ligaments with a central hole to allow a pelvic reconstruction with the uterus in situ.70 Migliari and Usai, using the Raz concepts, developed a four-corner suspension using a Prolene mesh to reinforce a central defect.61

Chapter 66 TENSION-FREE CYSTOCELE REPAIR USING PROLENE MESH

The Australian Experience In 1990, Petros and Ulmsten published the Integral Theory to explain the mechanism of incontinence and other pelvic dysfunction.71 They postulated that all pelvic floor defects start from fascial, ligamentous, and muscular deficiency. There are forward forces (pubococcygeus and puborectalis muscles) and backward/ downward forces (levator plate and ileococcygeus muscles) that could be impaired. A new surgical proposal based on this concept, developed by Farnsworth, uses a Prolene mesh with the aim to restore the normal anatomy by a complete prosthetic fascial substitution.72 The mesh is sutured tension-free in the normal anatomic insertion of the native fasciae, restoring the three levels of vaginal support described by DeLancey.73 The French Experience In 2000, a group of nine surgeons developed a transvaginal POP repair using Prolene soft, a wide mesh with four arms introduced into the transobturator canal for the anterior compartment and two arms transfixing the sacrospinous ligaments for the posterior compartment, which they inserted tension-free with the straps transferred using a long curved needle without any fixation. To reduce the risk of shrinkage, they put the four arms at the more distal part of the ATFP, and to avoid the risk of erosion, they used midline colpectomy instead of a “T” incision and the vaginal wall is not trimmed.74 A different approach, called the “triple perineal operation,” used posterior IVS for the suspension of the vaginal vault; an interposition of mesh in the vesicovaginal space for the correction of cystocele, fixed posteriorly to the cervix; and a third mesh in the rectovaginal space to treat rectocele, fixed to the posterior IVS and distally to the fibrous central nucleus of the perineum.75

THE NEW TRANSOBTURATOR CYSTOCELE REPAIR Transobturator cystocele repair can be accomplished in several ways. With the transvaginal mesh repair (TVM), Prolene soft (Gynemesh) is delivered with the use of a single, reusable, long curved needle and anchored with low tension (friction) in a Velcro effect. The mesh is placed tension-free in the vesicovaginal space, the space of Retzius, and the paravesical space. The two superficial and two deeper arms are positioned apically and distally at the ATFP (Fig. 66-8). With the Perigee transobturator repair system, polypropylene is delivered with the use of four Deschamps nonreusable needles connected with a special connector. A low-tension (friction) anchoring system is used (Velcro effect). The mesh is applied tension-free in the vesicovaginal space, the space of Retzius, and the paravesical space. The two superficial and two deeper arms are positioned apically and distally at the ATFP (Fig. 66-9). The Avaulta system uses polypropylene covered by collagen in the central part. This is positioned like the Perigee and TVM systems, with he use of a single, reusable curved needle (Fig. 66-10).

TRANSVAGINAL MESH CYSTOCELE REPAIR In 1996, Julian first published a study assessing the efficacy and complications of Marlex mesh in repairing severe recurrent ante-

rior vaginal wall prolapse.59 Twenty-four patients entered the study and were divided into control and treatment groups. Transvaginal repair was similar between groups except for reinforcement of the anterior vaginal wall with synthetic mesh. After 2 years, four patients in the control group and none in the treatment group had recurrent anterior vaginal wall prolapse (P < .05). A similar technique was carried out by Flood and colleague in a more consistent group of patients.60 They obtained the same cure rate of prolapse with a longer follow-up; there was also a concomitant treatment of SUI in 74% of their patients. Mage76 had the same results using a polyester mesh sutured to the vaginal angles. Migliari and Usai applied the same principle, using mixed fiber mesh to correct grade 4 cystocele; the mesh was positioned during a modified four-corner procedure.61 With this technique, there was no recurrence of cystocele except in 1 patient, and 13 of 15 patients were continent. Nicita proposed a new method to support female prolapsed pelvic organs, using a hammock-shaped Prolene mesh anchored transversally between the two arcus tendineous portions of the endopelvic fascia and between the bladder and uterine neck.70 He treated 44 patients presenting with various degrees of incontinence and combinations of cystocele and pelvic prolapse. All patients affected by incontinence or vaginal prolapse were satisfied; uterine prolapse partially recurred in three patients. Another original technique, the TCR, was proposed by Cervigni and associates in 1998. This approach uses a Prolene mesh in a double wing shape applied without sutures between the pubocervical fascia and vagina. The procedure was carried out in 138 women; after a mean follow-up of 18 months, there was a complete anatomic recovery in 135 patients (97.8%).77 In a further experience with a longer follow-up, the success rate (cystocele grade 10/day) n = 27 (63%)* P < .005

Nocturia (>2/night)

Urge Incontinence (>2/day)

Abnormal Emptying

Pelvic Pain

n = 47 (83%)* P < .005

n = 36 (78%)* P < .005

n = 53 (73%)* P < .005

n = 46 (86%)* P < .005

*Symptom change with surgery (percent cure in parentheses).

Chapter 69 USE OF A POSTERIOR SLING FOR VAGINAL VAULT PROLAPSE

Figure 69-13 The vaginal trampoline. The vagina is suspended by the pubourethral ligaments (PUL), arcus tendineus fasciae pelvis (ATFP), and uterosacral ligaments (USL). Red arrows represent pelvic muscle forces. White arrows indicate the central inhibitory mechanism. (From Petros P: The Female Pelvic Floor. New York, Springer-Verlag, 2004.)

Figure 69-12 The pictorial diagnostic algorithm summarizes the relationships between structural damage in the three zones of vaginal support and symptoms. The size of the bar gives an approximate indication of the prevalence (probability) of the symptom. The same connective tissue structures in each zone may cause prolapse and abnormal symptoms. B, bladder; EAS, external anal sphincter; PB perineal body; PCM, m. pubococcygeus; PRM, m. puborectalis; PS, pubic symphysis; PUL, pubourethral ligament; R, rectum; RVF, rectovaginal fascia S, spine; USL, uterosacral ligament; UT, uterus. (From Petros P: The Female Pelvic Floor. New York, Springer-Verlag, 2004.)

Twenty-eight of these patients had only minor posterior zone prolapse, Table 69-2. Lax ligaments may cause urge, frequency, and nocturia. In the normal patient, the cortex coordinates urinary retention and micturition (Fig. 69-13).3 As the bladder fills, the stretch receptors send afferent impulses to the cortex.12 If it is inconvenient to micturate, the impulses are blocked by the inhibitory centers and by contraction of the three pelvic muscle forces. These stretch the vaginal membrane like a trampoline to support the hydrostatic pressure of the urine, relieving the pressure on the receptors, thereby diminishing the afferent impulses to the cortex. Like a trampoline with loose springs, lax ligaments may not allow the muscles to tension the vaginal membrane, and the

receptors (see Fig. 69-13) fire, activating the micturition reflex prematurely. The sequence of events in patients with urodynamically demonstrated detrusor instability (Fig. 69-14) was similar13 to that in normal patients about to micturate: sensory urgency, urethral relaxation, detrusor contraction (Fig. 69-15), and urine loss.14 This “premature micturition” may be symptomatically expressed as frequency, urgency, and nocturia. The rationale for surgical cure of these symptoms is that firm ligaments and fascia permit the vagina (see Fig. 69-13) to be stretched sufficiently to offer support. This concept can be confirmed as an office procedure using the technique of simulated operations.15 The patient’s bladder needs to be sufficiently full for her to have urge symptoms in the supine position. In its simplest form, the vagina is supported below bladder base digitally, by a ring forceps, or by gentle compression of the vaginal tissue just behind bladder neck with a Littlewood forceps. Unmyelinated nerves run along the USLs. A lax ligament may not be able to support these nerves, and they become subjected to the force of gravity. This explains the dragging nature of the pain experienced and symptom relief on lying down. Compared with a normal patient at rest (Fig. 69-16), it has been demonstrated radiologically and electromyographically4 that after relaxation of the forward force, the bladder base and urethra are pulled open (i.e., funneling), apparently by pelvic contraction, during micturition (Fig. 69-17). The downward force acts against the USLs, and lax USLs diminish the opening forces. As the intraurethral resistance varies inversely with the fourth power of the radius, failure of the pelvic muscles (see Fig. 69-17) to open the urethra increases the resistance geometrically, which is perceived as obstructed micturition. For example, if the radius of the urethra in a normal patient (see Fig. 69-17) is

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Figure 69-15 Control of detrusor instability by stretching the vagina. Some seconds after the release of vaginal tension, the detrusor begins to contract. (From Petros P: The Female Pelvic Floor. New York, Springer-Verlag, 2004.) Figure 69-14 Detrusor instability: premature activation of the micturition reflex, The arrows indicate synchronous pressure variations in the urethra and bladder. B, bladder pressure; c to c1, rise in detrusor pressure; CP, closure pressure; r to r1, fall in urethral pressure; U, urethral pressure. (From Petros P: The Female Pelvic Floor. New York, Springer-Verlag, 2004.)

R, expelling urine through a urethra which can open only to a radius of R/2, will require an expulsion pressure 16 times greater than that required for R. CONCLUSIONS AND FUTURE DIRECTIONS The use of posterior slings for vault and uterine prolapse repair is becoming well accepted. The future challenge is to explore their use in patients with major symptoms and minimal prolapse to more accurately assess which other connective tissue structures may contributing to dysfunction and how best to repair these structures.

Figure 69-16 Lateral radiograph of a normal patient at rest. Bv, attachment of the bladder base to the vagina; CX, cervix; LP, levator plate; PUL, pubourethral ligament; R, rectum; U, urethra; USL, uterosacral ligament; V, vagina.

Chapter 69 USE OF A POSTERIOR SLING FOR VAGINAL VAULT PROLAPSE

Figure 69-17 Lateral x-ray view of micturition in a normal patient. Backward and downward muscle forces (arrows) act against the pubourethral and uterosacral ligaments to stretch the vagina and bladder base to actively open the outflow tract. CX, cervix; LP, levator plate; PUL, pubourethral ligament; R, rectum; U, urethra; USL, uterosacral ligament; V, vagina.

References 1. Petros PE, Ulmsten U: The posterior fornix syndrome: A multiple symptom complex of pelvic pain and abnormal urinary symptoms deriving from laxity in the posterior fornix. Scand J Urol Nephrol 27(Suppl 153):89-93, 1993. 2. Petros PE: Vault prolapse. II. Restoration of dynamic vaginal supports by the infracoccygeal sacropexy, an axial day-care vaginal procedure. Int Urogynecol J Pelvic Floor Dysfunct 12:296-303, 2001. 3. Petros PEP: The Female Pelvic Floor: Function, Dysfunction and Management, According to the Integral Theory. Heidelberg, Springer, 2004, pp 14-47. 4. Petros PE, Ulmsten U: Role of the pelvic floor in bladder neck opening and closure. I. Muscle forces. II. Vagina. Int Urogynecol J Pelvic Floor Dysfunct 8:69-80, 1997. 5. Brown JS, Sawaya G, Thorn DH, Grady D: Hysterectomy and urinary incontinence: A systematic review. Lancet 356:535-539, 2000. 6. Sturmdorf A: The levator ani muscle. In Gynoplastic Technology. Philadelphia, FA Davis, 1919, pp 109-114. 7. Petros PE: Vault prolapse. I. Dynamic supports of the vagina. Int Urogynecol J Pelvic Floor Dysfunct 12:292-295, 2001. 8. Nichols DH, Randall CL: Massive eversion of the vagina. In Nichols DH & Randall CL (eds): Vaginal Surgery, 3rd ed. Baltimore, Williams & Wilkins, 1989, pp 328-357.

9. Sze EH, Karram MM: Transvaginal repair of vault prolapse: A review. Obstet Gynecol 89:466-475, 1997. 10 Petios PEP, Richardson PA: The TFS posterior sling for repair of uterine/vault prolapse—a preliminary report. ANZJOG 45:372-375, 2005. 11. Farnsworth BN: Posterior intravaginal slingplasty (infracoccygeal sacropexy) for severe posthysterectomy vaginal vault prolapse—A preliminary report. Int J Urogynecol 13:4-8, 2002. 12. Petros PE: Detrusor instability and low compliance may represent different levels of disturbance in peripheral feedback control of the micturition reflex. Neurourol Urodyn 18:81-91, 1999. 13. Petros PE, Ulmsten U: Bladder instability in women: A premature activation of the micturition reflex. Neurourol Urodyn 12:235-239, 1993. 14. Tanagho EA: The anatomy and physiology of micturition. Clin Obstet Gynaecol 5:1, 3-25, 1978. 15. Petros PEP: The Female Pelvic Floor: Function, Dysfunction and Management, According to the Integral Theory. Heidelberg, Springer, 2004, pp 48-76.

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TRANSVAGINAL REPAIR OF APICAL PROLAPSE: THE UTEROSACRAL VAULT SUSPENSION Raymond T. Foster, Sr., and George D. Webster For decades, the reconstructive treatment of uterine prolapse or post-hysterectomy vaginal cuff descent has included suspension of the vaginal apex. Reconstructive urologists and gynecologists have developed many techniques, including abdominal, laparoscopic, and vaginal routes of surgery, for the correction of apical descent.1 Our understanding about which technique or approach is superior with regard to efficacy, safety, and durability is limited by a relative lack of level I evidence. Although many well-designed, retrospective reports (each with a large study population and long-term follow-up) exist to give us useful information about particular procedures for the correction of vault descent,2-17 we are still unsure which procedure is best for any particular patient. The techniques used to treat pelvic organ prolapse are largely shaped by each surgeon’s experience and

training and not necessarily influenced by prospective, outcomesbased research. To compound the problem of sparse well-designed and executed, randomized surgical trials, we are also handicapped by confounding, coexisting pelvic support problems. It is difficult to study apical prolapse in isolation, because most patients present for treatment with many support defects (Fig. 70-1) and associated pelvic floor dysfunction (e.g., urinary incontinence, defecatory dysfunction, pelvic pain, difficulty with sexual intercourse). We are, for example, unsure of how our choice of treatment for cystocele or urethral hypermobility may affect the outcome of our vault suspension. Operative technique in other fields is often driven by an understanding of the cause and natural history of the surgical

A. PS

B

Apical Enterocele

PCF

Pt

PS

SB B

Pt

RVF

PCF R

RVF

B. PS

R

B

PCF RVF

Pt

SB

R

Figure 70-1 Prolapse of the vaginal vault with associated apical enterocele. A, Vaginal vault prolapse with cystocele. B, Vaginal vault prolapse with a proximal rectocele.

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Chapter 70 TRANSVAGINAL REPAIR OF APICAL PROLAPSE

Promoting factors • Constipation • Recreation • Surgery • Menstrual cycle • Occupation • Smoking

Inciting factors • Childbirth • Nerve damage • Muscle damage • Radiation • Tissue disruption • Radical surgery

Decompensating factors

Normal support or function Predisposing factors • Gender • Anatomic • Collagen • Cultural

• Ageing • Debility • Medications

Abnormal support or function

• Racial • Neurologic • Muscular • Environmental

• Menopause • Infection • Chronic cough • Obesity • Lung disease • Medications

• Dementia • Disease • Environment

Intervene • Surgical • Pharmacologic

• Behavioral • Devices

Figure 70-2 Model developed by Bump and Norton18 to propose a mechanism for the development and progression of pelvic floor dysfunction, including pelvic organ prolapse.

problem, and this often helps guide surgical therapy. Unfortunately, we are still uncertain about these variables in pelvic organ prolapse. Bump and Norton18 have provided a useful model with which we can consider how prolapse develops and progresses (Fig. 70-2), but in their own words, the model is “based mainly on expert opinion and supported by limited epidemiologic and clinical evidence. None of the factors has been studied in a longitudinal fashion in a representative study.” The surgical goal in treating pelvic organ prolapse is to select a technique that can maximize the chance of anatomic and functional cure and minimize the occurrence of intraoperative injury or complication, but we must recognize that surgeons have preferred techniques based on training and experience. We favor a transvaginal surgical correction of apical prolapse, and our goal is to review the history of the uterosacral ligament vault suspension, a procedure that is often considered to be the gold standard in transvaginal surgery for apical prolapse. HISTORY Written history of gynecologic surgery documents that uterosacral ligaments have been used in vaginal reconstructive surgery for at least the past century, but it is difficult to say who was the first person to conceive of the importance of these structures in supporting the uterus and vaginal apex. John Burns, a renowned Scottish anatomist and surgeon, was the first person to write about the importance of the uterosacral ligaments. In his 1839 book, The Principles of Midwifery including the Diseases of Women and Children, Burns19 wrote: By experiments made on the dead subject, we find that prolapsus is chiefly prevented by the fascia passing off from the cavity of the pelvis to the upper part of the vagina, and thence reflected to the face of the rectum. It is also prevented by the fascia of the outlet of the pelvis, and levator ani, which contribute to support the vagina. . . . The greatest aid,

however, is afforded by the levator ani and the pelvic fascia, particularly that part of it which is deep in the cavity of the pelvis. Burns published earlier editions to this enormously popular text in 1810, 1813, 1814, 1817, 1824, 1831, 1832, and 1837. In some earlier editions (1810 and 1813), he was discouraged that apical prolapse could not be created in cadavers by disrupting the round ligaments and applying traction to the cervix through the vagina, but he and his students continued their cadaver work, and their writings became exponentially more informed. The first mention of the use of uterosacral ligaments to suspend the vaginal apex as treatment for prolapse was by the American gynecologist Norman F. Miller, who in 1927 described the placement of a “no. 2 chromic catgut suture on a small full curved needle passed through the peritoneum and underlying fascial and muscular structures at the base of the sacro-uterine ligament, approximately 11/2 inches below the promontory of the sacrum.” Since this report, the use of the uterosacral ligament for apical prolapse has been described by other surgeons. McCall first described his transvaginal culdoplasty technique for treating enterocele with associated vault prolapse in 1957.20 Lee and Symmonds21 published what became known as the Mayo modification in 1972. As vaginal surgeons made developments in the treatment of apical prolapse with the uterosacral ligament (among other attachment sites, including the iliococcygeus fascia22 and the sacrospinous ligament23) throughout the 20th century, parallel progress was being made in the abdominal24, 25 and laparoscopic26 approaches to vault prolapse. In the later half of the 20th century, less attention was attributed to a vaginal uterosacral vault suspension as other techniques and approaches became widely used with acceptable results. Four prominent gynecologic surgeons—Cullen Richardson (1923-2001), William Saye, Tom Elkins (1950-1998), and Bob Shull—met in Atlanta in the fall of 1992 to review videos of laparoscopic support procedures and discuss surgical strategies for the treatment of pelvic organ prolapse (interview with B. Shull,

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2005). Richardson had previously stressed the importance of finding specific fascial defects and repairing them to achieve optimal restoration of pelvic anatomy.27 After working together, Richardson and Saye developed what is now known as the Richardson-Saye laparoscopic technique of enterocele repair and vault suspension, which applies the principles of site-specific repair26 to the laparoscopic approach. During their meeting in 1992, it occurred to the assembled group that they could find specific fascial defects, repair them, and resuspend the newly reconstructed vault to the uterosacral ligaments from a vaginal approach. In 2000, Shull and colleagues6 published their technique and experience with this approach in 302 consecutive women. With only minor modifications, this is the surgical technique that we now use for the transvaginal correction of apical prolapse, and it is this procedure that we describe in this chapter. TECHNICAL ASPECTS OF THE UTEROSACRAL LIGAMENT VAULT SUSPENSION We are inclined to offer transvaginal repair to most of our patients. In our hands, this route of surgery has been safe, efficacious, and durable.3 We have developed a bias, however, in that we prefer the abdominal sacral colpopexy to treat apical prolapse in our younger and more physically active patients. We are also likely to consider abdominal sacral colpopexy in patients with complete vaginal vault inversion. Preoperatively, we discuss with the patient the reported incidence of complications associated with such major surgery in general and with this technique in particular. The ureteral obstruction rate is between 0% and 11%.2,4-6 Intraoperative or postoperative blood transfusion may be required in up to 1% of patients.2,4-6 It is important that the patient have realistic expectations of what can be achieved and that recurrent prolapse of the vault or the development of other vaginal defects is not uncommon. Interference with sexual function, in particular loss of vaginal depth and caliber, is not uncommon. Patients are placed in the dorsal lithotomy position using padded, adjustable (Allen) stirrups and wearing sequential compression hose. The rectum is packed with an open, wet Kerlix sponge to the level of the ischial spines to aid the identification of the rectum and decrease the incidence of intraoperative injury during placement of the uterosacral suspensory sutures. A selfretaining vaginal retractor (Lone Star Medical Products, Houston, TX) and a weighted speculum are used to obtain good visualization. If the patient is being treated for uterine prolapse, a vaginal hysterectomy is performed as previously described by Lee28 with minor modifications. In patients being treated for vault descent alone, a silk marking suture is placed in the vaginal epithelium at 3-o’clock and 9-o’clock positions at the vaginal apex for later reference. At these positions, the surgeon usually can see an epithelial dimple indicating the prior attachment point of the uterosacral ligaments to the vaginal cuff. The vaginal epithelium is incised in the midline along the extent of the prolapsed vaginal segments. The dissecting scissors are used to separate the vaginal epithelium from the underlying pubocervical and rectovaginal connective tissues as needed to expose the entire fascial defect, including the enterocele sac. With the patient in Trendelenburg position, the enterocele sac is identified and opened sharply. A wet Kerlix sponge is used to pack the bowel out of the operative field into the upper peritoneal

cavity. We have learned by experience to protect the posterior peritoneum (with an instrument such as a Breisky-Navratil retractor) to avoid tearing the peritoneum during the packing process, which invariably leads to bleeding and poor visualization of anatomic structures along the pelvic side wall. For correct and safe placement of the uterosacral suspensory sutures, good exposure is critical. To provide adequate illumination in this deep cavity, we are accustomed to using a surgical headlight or a cool lighting system adherent to our retractor that is designed to be placed within the pelvis (LightMat surgical illuminator, Lumitex, Inc., Strongsville, OH). Various techniques have been used to expose the pelvic side wall, but we have been most satisfied using Breisky-Navratil retractors. Three BreiskyNavratil retractors are placed anteriorly, laterally, and posteriorly so that the bladder, ureter, and rectum, respectively, are protected while the uterosacral ligament is easily visualized. The posterior retractor, placed in the angle between the packed and easily identifiable rectum and the pelvic side wall, can be used to sweep the rectum to the contralateral side during placement of the uterosacral suspensory suture. By placing light tension on the uterosacral ligament, by traction on the earlier placed silk suture at the dimples at the vaginal cuff, identification of this ligament becomes much easier. A no. 1 polyglactin suture is passed through the uterosacral ligament medial and cephalad to the ischial spine. We have had excellent anatomic outcomes using a single absorbable suture through each uterosacral ligament, but this procedure has been described by others with as many as three suspensory sutures through each uterosacral ligament (Fig. 70-3). Tension placed on each uterosacral suspensory suture is used to confirm placement at a sturdy location and to visualize an attachment point in the proximal uterosacral ligament. After a suture has been placed through each uterosacral ligament, the sutures are held with a tag for later use in suspending the vaginal apex. At this point, the patient is given 5 mL of intravenous indigo carmine dye and 5 mg of intravenous furosemide. The Foley catheter is removed, and a 70-degree cystoscope is used to inspect for spill of blue urine from each ureteral orifice while the uterosacral suspensory sutures are held on tension. If ureteral obstruction is suspected, the ipsilateral suspensory suture is released to confirm ureteral efflux. If necessary, the suspensory suture is removed and replaced in a more medial position. The anterior arm of each suspensory suture is passed through the apical portion of the pubocervical connective tissue, and the posterior arm of each suture is passed through the apical portion of the rectovaginal connective tissue. A Mayo needle is used where necessary (see Fig. 70-3). Both ends of each suspensory suture are passed through the vaginal epithelium near the silk marking sutures that were placed at the outset of the procedure. Once satisfied with placement of the uterosacral suspensory sutures, attention is directed toward site-specific repair of any remaining prolapse defects. Typically, we use an anterior colporrhaphy to correct cystocele and a posterior colporrhaphy with or without allograft material (i.e., cadaveric dermis) to correct rectocele. Anterior and posterior colporrhaphy work well to reestablish a clearly defined transverse (apical) portion of the pubocervical and rectovaginal connective tissue. Colporrhaphy also aids in the preservation of acceptable vaginal length. Besides repair of the anterior and posterior defects, we commonly perform high ligation and excision of the enterocele sac using a 2-0 polyglactin suture. If stress urinary incontinence was a preoperative complaint or if a positive stress test result or urodynamic evidence of stress urinary incontinence existed with the

Chapter 70 TRANSVAGINAL REPAIR OF APICAL PROLAPSE

B

PS

PCF USL

AD

RVF R

A

Double–Armed Suture Through Pubocervical Fascia Retrovaginal Fascia, and Left Uterosacral Ligament

Figure 70-3 A and B, By passing one end of the each uterosacral suspensory suture through the apical (transverse) portion of the pubocervical connective tissue and the opposite end through the apical (transverse) portion of the rectovaginal connective tissue, the surgeon can elevate the vaginal cuff and reapproximate the endopelvic fascia simultaneously with two or more such sutures. AD, Apical Defect; B, Bladder; PCF, Pubocervical Fascia; USL, Uterosacral Ligament.

prolapse replaced, a pubovaginal sling also is performed. Sling tension is adjusted after the uterosacral sutures have been tied and after completion of the anterior repair. The uterosacral suspensory sutures are then tied to close and suspend the vaginal cuff to the point of retroperitoneal uterosacral ligament fixation. The surgeon is reassured of excellent placement of these sutures if the knots seat in a posterior direction toward the sacral hollow. Redundant vaginal epithelium (after associated anterior and posterior repair by fascial plication or allograft placement) is excised and the epithelium closed. A digital vaginal examination is next performed to assess the axis and depth of the vaginal canal (Fig. 70-4). A vaginal pack is placed if deemed necessary, and a digital rectal examination is performed at completion to confirm the absence of suture material in the rectal lumen. POSTOPERATIVE CARE AND PATIENT INSTRUCTIONS Although patients are able to ambulate and tolerate a diet on the evening of the day of surgery, we usually leave in the Foley cath-

eter in place until the morning of postoperative day 1. With few exceptions, we consistently use scheduled dosing of oral narcotic analgesics in lieu of intravenous narcotics (i.e., patient-controlled analgesia by intravenous morphine pump). Our typical postoperative pain control regimen includes a 12-hour dosing schedule of controlled-release oxycodone combined with a 6-hour dosing schedule of intravenous ketorolac or oral ibuprofen. Anecdotally, we observe less postoperative nausea, pruritus, and respiratory depression when we avoid using narcotics through an intravenous pump. On the morning of postoperative day 1, the nursing staff is instructed to fill the patient’s bladder with 300 mL of fluid (i.e., normal saline or sterile water) through the Foley catheter. The Foley catheter is removed, and the patient is instructed to void. The amount of urine voided is measured. If the postvoid residual urine volume exceeds the amount voided, the patient is sent home with instructions to do self-catheterization as necessary; patients are taught how to perform selfcatheterization preoperatively. If the patient can spontaneously empty more than 50% of the total bladder contents, she is dismissed without an indwelling catheter or self-catheterization program.

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Figure 70-3 cont’d

B

We use printed discharge instructions that outline answers to common questions patients have in the postoperative period. The instruction sheet covers postoperative activity level (we discourage heavy lifting and straining for 90 days), constipation management, bathing, driving, vaginal bleeding, catheter program parameters, and other areas of interest and frequent concern to our patients. Patients usually are followed in the clinic after vaginal reconstructive surgery at 6 weeks, 6 months, and 1 year postoperatively. We typically allow patients to resume intravaginal intercourse and employment activities after the first postoperative visit. At the 6-month and 1-year postoperative visit, we reassess the patient’s pelvic support using the Pelvic Organ Prolapse Quantification (POP-Q) scoring system.29 The POP-Q

score is compared with our preoperative evaluation so that we can assess the efficacy and durability of surgery.

CONCLUSIONS AND FUTURE DIRECTIONS Transvaginal suspension of the vaginal vault to the uterosacral ligament for the treatment of apical prolapse is a safe, efficacious, and durable procedure.2-6 Although reports have been published comparing the treatment of apical prolapse using the vaginal and abdominal approaches with mixed outcomes,30,31 we believe that in our hands, transvaginal surgery affords most patients

Chapter 70 TRANSVAGINAL REPAIR OF APICAL PROLAPSE

PS B

PCF USL

R

RVF

Suspension of Pubocervical and Rectovaginal Fascia to Uterosacral Lgaments

Figure 70-4 At the conclusion of the procedure, a digital vaginal examination is performed to assess the vaginal axis and depth. B, Bladder; PCF, Pubocervical Fascia; R, Rectum; RVF, Rectovaginal Fascia; USL, Uterosacral Ligament.

the best chance of cure with the least morbidity and shortest convalescence. The care of patients with prolapse will continue to evolve as our understanding of the natural history of this disease becomes more informed. Pelvic organ prolapse, including apical prolapse, is a widespread problem among women in the United States and abroad. The lifetime risk for pelvic organ prolapse surgery in women is reported to be more than 11%.32 Pelvic organ prolapse often coexists with urinary and fecal incontinence, sexual dysfunction, and defecatory dysfunction. Despite myriad procedures to correct the anatomic circumstances arising with pelvic organ prolapse, there is often poor correlation between the anatomic and functional outcomes of surgery. The best operation designed to restore normal pelvic anatomic relationships can leave women with suboptimal functional outcomes. The best therapies therefore are measures taken to prevent prolapse in asymptomatic women. The most efficient way to employ preventive measures is to identify women at risk and intervene in that group of patients. Little has been written about the epidemiology of pelvic floor dysfunction, including pelvic organ prolapse.29 Our current understanding of the development of prolapse correlates this problem with risk factors that include vaginal parity, age, race, obesity, and chronic constipation. Pelvic organ prolapse, urinary incontinence, and fecal incontinence have been associated with denervation injury of the pelvic

floor muscles during vaginal childbirth.33 Vaginal childbirth may be a time in the early stages of the natural history of pelvic organ prolapse when intervention could significantly prevent prolapse later in life. Some have advocated elective cesarean section as an intervention. It may be possible, however, to treat nerves damaged during vaginal childbirth so that denervation of the pelvic floor may be minimized or eliminated. We are involved in ongoing research with the squirrel monkey model of pelvic organ prolapse to define the role of parturition-induced nerve injury and to eventually propose pharmacologic intervention that would decrease the risk of permanent nerve injury after pelvic floor trauma, such as that incurred during vaginal childbirth. Until the results of research in humans and animal models are available to help us understand the cause of prolapse, we will continue to treat prolapse with conservative, nonsurgical techniques and with invasive procedures designed to provide anatomic and functional cure. The procedure described in this chapter has a reported efficacy between 87%6 and 100%,5 with patients followed for up to 4 years. The morbidity and postoperative recovery associated with the transvaginal uterosacral vault suspension is acceptable and satisfying to surgeons and patients. We believe that this particular procedure will continue to be the gold standard for the treatment of apical prolapse in the hands of experienced vaginal surgeons for many years to come.

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References 1. Flynn BJ, Webster GD: Surgical management of the apical vaginal defect. Curr Opin Urol 12:353-358, 2002. 2. Karram M, Goldwasser S, Kleeman S, et al: High uterosacral vaginal vault suspension with fascial reconstruction for vaginal repair of enterocele and vaginal vault prolapse. Am J Obstet Gynecol 185:13391342; discussion 1342-1343, 2001. 3. Amundsen CL, Flynn BJ, Webster GD: Anatomical correction of vaginal vault prolapse by uterosacral ligament fixation in women who also require a pubovaginal sling. J Urol 169:1770-1774, 2003. 4. Barber MD, Visco AG, Weidner AC, et al: Bilateral uterosacral ligament vaginal vault suspension with site-specific endopelvic fascia defect repair for treatment of pelvic organ prolapse. Am J Obstet Gynecol 183:1402-1410; discussion 1410-1411, 2000. 5. Jenkins VR 2nd: Uterosacral ligament fixation for vaginal vault suspension in uterine and vaginal vault prolapse. Am J Obstet Gynecol 177:1337-1343; discussion 1343-1344, 1997. 6. Shull BL, Bachofen C, Coates KW, Kuehl TJ: A transvaginal approach to repair of apical and other associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 183:1365-1373; discussion 1373-1374, 2000. 7. Cruikshank SH, Muniz M: Outcomes study: A comparison of cure rates in 695 patients undergoing sacrospinous ligament fixation alone and with other site-specific procedures—A 16-year study. Am J Obstet Gynecol 188:1509-1512; discussion 1512-1515, 2003. 8. Addison WA, Livengood CH 3rd, Sutton GP, Parker RT: Abdominal sacral colpopexy with Mersilene mesh in the retroperitoneal position in the management of posthysterectomy vaginal vault prolapse and enterocele. Am J Obstet Gynecol 153:140-146, 1985. 9. Cook JR, Seman EI, O’Shea RT: Laparoscopic treatment of enterocele: A 3-year evaluation. Aust N Z J Obstet Gynaecol 44:107-110, 2004. 10. Culligan PJ, Murphy M, Blackwell L, et al: Long-term success of abdominal sacral colpopexy using synthetic mesh. Am J Obstet Gynecol 187:1473-1480; discussion 1481-1482, 2002. 11. Guner H, Noyan V, Tiras MB, et al: Transvaginal sacrospinous colpopexy for marked uterovaginal and vault prolapse. Int J Gynaecol Obstet 74:165-170, 2001. 12. Lantzsch T, Goepel C, Wolters M, et al: Sacrospinous ligament fixation for vaginal vault prolapse. Arch Gynecol Obstet 265:21-25, 2001. 13. Limb J, Wood K, Weinberger M, et al: Sacral colpopexy using Mersilene mesh in the treatment of vaginal vault prolapse. World J Urol 23:55-60, 2005. 14. Nieminen K, Heinonen PK: Sacrospinous ligament fixation for massive genital prolapse in women aged over 80 years. BJOG 108:817-821, 2001. 15. Ross JW: Laparoscopic approach for severe pelvic vault prolapse. J Am Assoc Gynecol Laparosc 3:S43, 1996. 16. Timmons MC, Addison WA, Addison SB, Cavenar MG: Abdominal sacral colpopexy in 163 women with posthysterectomy vaginal vault

17. 18. 19. 20. 21. 22.

23. 24. 25. 26. 27. 28.

29. 30.

31.

32. 33.

prolapse and enterocele. Evolution of operative techniques. J Reprod Med 37:323-327, 1992. Comiter CV, Vasavada SP, Raz S: Transvaginal culdosuspension: Technique and results. Urology 54:819-822, 1999. Bump RC, Norton PA: Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 25:723-746, 1998. Burns J: The Principles of Midwifery, including the Diseases of Women and Children. New York, CS Francis, 1839. McCall M: Posterior culdeplasty; surgical correction of enterocele during vaginal hysterectomy: A preliminary report. Obstet Gynecol 10:595-602, 1957. Lee RA, Symmonds RE: Surgical repair of posthysterectomy vault prolapse. Am J Obstet Gynecol 112:953-956, 1972. Shull BL, Capen CV, Riggs MW, Kuehl TJ: Bilateral attachment of the vaginal cuff to iliococcygeus fascia: An effective method of cuff suspension. Am J Obstet Gynecol 168:1669-1674; discussion 16741677, 1993. Zweifel P: Vorlesungen uber klinische Gynakologie. Berlin, Hirschwald, 1892, p 407. Arthure HG, Savage D: Uterine prolapse and prolapse of the vaginal vault treated by sacral hysteropexy. J Obstet Gynaecol Br Emp 64:355-360, 1957. Falk HC: Uterine prolapse and prolapse of the vaginal vault treated by sacropexy. Obstet Gynecol 18:113-115, 1961. Carter JE, Winter M, Mendehlsohn S, et al: Vaginal vault suspension and enterocele repair by Richardson-Saye laparoscopic technique: Description of training technique and results. JSLS 5:29-36, 2001. Richardson AC, Lyon JB, Williams NL: A new look at pelvic relaxation. Am J Obstet Gynecol 126:568-573, 1976. Lee RA: Combined compartment defects: Vaginal hysterectomy with repair of enterocele, cystocele, and rectocele. In Rock JA, Thompson JD (eds): Te Linde’s Operative Gynecology. Philadelphia, Lippincott-Raven, 1997. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. Benson JT, Lucente V, McClellan E: Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: A prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 175:1418-1421; discussion 1421-1422, 1996. Maher CF, Qatawneh AM, Dwyer PL, et al: Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: A prospective randomized study. Am J Obstet Gynecol 190:20-26, 2004. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-506, 1997. Swash M, Snooks SJ, Henry MM: Unifying concept of pelvic floor disorders and incontinence. J R Soc Med 78:906-911, 1985.

Chapter 71

VAGINAL HYSTERECTOMY IN THE TREATMENT OF VAGINAL PROLAPSE Christopher M. Rooney and Mickey M. Karram Hysterectomy continues to be one of the most commonly performed surgical procedures in the United States, second only to cesarean section. Approximately 800,000 hysterectomies are performed annually in the United States.1 According to the National Center for Health Statistics, 3,525,237 hysterectomies were performed in the United States between 1994 and 1999, at a rate of 5.5 per 1000 women. The most common indication for hysterectomy continues to be uterine leiomyoma, accounting for approximately 38% of all hysterectomies. Endometriosis accounts for 18% of all hysterectomies, followed by uterine prolapse (16%) and endometrial hyperplasia (4%).1 As the population of women older than 65 years continues to rise, the practitioner can anticipate an increase in the number of women presenting with these indications.2 Most hysterectomies are performed by the abdominal route, with the rate of vaginal hysterectomy remaining stable over the past several decades.1 Vaginal hysterectomy in the appropriately selected patient has been reported to result in a shorter hospital stay, less operative blood loss, and less postoperative pain compared with the abdominal route of hysterectomy. Patients presenting for evaluation and surgical correction of pelvic organ prolapse are particularly appropriate candidates for vaginal hysterectomy.

ANATOMY OF PELVIC SUPPORT Normal pelvic support is a complex interaction between the muscular and fascial structures that line the pelvic cavity, collectively known as the pelvic floor. The levator ani complex (i.e., coccygeus, iliococcygeus, and pubococcygeus) stretches from the coccyx to the symphysis pubis anteriorly in the erect woman. Laterally, the levator complex attaches to the arcus tendineus fasciae pelvis (“white line”). The arcus tendineus fasciae pelvis extends from the symphysis pubis to the ischial spines bilaterally. The levator ani complex is typically described in two parts: the diaphragmatic portion (i.e., coccygeus and iliococcygeus) and the pubovisceral portion (i.e., pubococcygeus). The coccygeus muscles run bilaterally from the sacrum and coccyx to the ischial spines and are associated with the sacrospinous ligaments. The iliococcygeus muscles pass laterally from the symphysis pubis to the arcus tendineus fasciae pelvis, where they attach and turn medially to join the coccygeus at the coccyx, forming the levator plate. The pubovisceral portion, or pubococcygeus, is associated with the puborectalis, arising from the posterior surface of the symphysis pubis and extending back to the ventral surface of the coccyx.3 Normal pelvic support is provided by the pelvic floor and by the connective tissue attachments. The pelvic organs rest on the pelvic floor and are stabilized by the connective tissues. In 1992,

DeLancey described the stabilization of the vagina in levels. Level 1 support is derived from the cardinal-uterosacral complex and is responsible for holding the upper vagina and cervix in a superior position in relation to the genital hiatus. Level II support is responsible for lateral support of the midvagina to the arcus tendineus fasciae pelvis. Level III support is responsible for distal support of the lower vagina by means of connections to the perineal body and perineal membrane4 (Fig. 71-1). PELVIC ORGAN PROLAPSE The cause of pelvic organ prolapse is multifactorial. Uterovaginal prolapse results from damage to the cardinal-uterosacral complex, or level I support.5 The uterus and upper vagina normally lie over the pelvic floor and are directed to the hollow of the sacrum. Increased intra-abdominal pressure is directed toward the levator ani complex. Attenuation of the levator ani complex may result in inadequate support to the overlying pelvic organs. Such attenuation may be the result of childbirth and some connective tissue disorders. Conditions or maneuvers that result in repeated increases in intra-abdominal pressure may lead to attenuation of the pelvic floor and aggravate pelvic organ prolapse. These conditions may include occupations that require heavy lifting or medical conditions such as chronic constipation resulting in excessive straining or chronic obstructive pulmonary disease with chronic coughing. Age also has been implicated as an etiologic factor in pelvic organ prolapse. Age is widely accepted to be associated with decreased muscle tone and decreased quality of underlying fibroblasts and collagen fibers, both of which can aggravate the underlying prolapse. Postmenopausal women who are not receiving hormone replacement therapy may also present with signs and symptoms of pelvic organ prolapse. PELVIC ORGAN PROLAPSE Diagnosis Patients with uterovaginal prolapse may present with a multitude of symptoms. A carefully tailored history and physical examination are important in gaining insight into the complaint and any affect on the patient’s quality of life. Patients may present with a vaginal mass, sometimes described by them as a bulge. They may complain of pelvic pain, pressure, or dyspareunia. Patients may describe urinary urgency or frequency or incontinence. In cases of severe prolapse, patients may complain of urinary retention, because of the effect of the prolapse on the anatomy of the lower urinary tract. The typical patient describes symptoms that are 705

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Section 7 FEMALE ORGAN PROLAPSE

I II III

Ischial spine and sacrospinous ligament

Level I

Level II Levator ani Pubocervical fascia

III

Rectovaginal fascia

Figure 71-1 Levels of support of the upper and middle vagina. Level I support represents the apical support of the vagina by means of the uterosacral-cardinal complex. Level II support represents the lateral support of the vagina by means of attachments to the arcus tendineus fasciae pelvis. (From DeLancey JOL: Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 166:1717, 1992.)

worse with standing or activity and that improve on assuming a supine position. If the diagnosis of pelvic organ prolapse is obscure, it is important to consider performing the examination of the patient at the end of the day, when the prolapse is likely to be at its worst. Physical Examination The result of physical examination remains one of the most important pieces of information in the evaluation of pelvic organ prolapse. The diagnosis of uterovaginal prolapse is confirmed by significant descensus of the uterus on pelvic examination. A bimanual examination is important to ascertain the size and mobility of the uterus and any underlying pathology such as uterine leiomyoma or adnexal masses. The caliber of the genital hiatus is measured to predict the success of a vaginal hysterectomy. The coexistence of anterior or posterior vaginal wall prolapse should be determined. In our experience, it is advisable to evaluate the patient with uterovaginal prolapse in the supine and standing positions. The patient should be examined with an empty bladder because the prolapse may not be fully appreciated in the presence of a subjectively full bladder.6 It is important to evaluate for the sign of stress incontinence with the bladder full and the prolapse reduced to its normal anatomic location to exclude potential or occult stress incontinence.

Classification The severity of pelvic organ prolapse is described to standardize findings among examiners. For decades, the Baden-Walker system was used to describe the presence of pelvic organ prolapse.7 The Baden-Walker system, still in use today, is also known as the halfway system. It involves description of the most dependent position of the pelvic organs during a maximum Valsalva maneuver or during standing in relation to the hymenal ring (Table 71-1). In 1996, Bump and colleagues8 standardized the terminology of female pelvic organ prolapse for the International Continence Society (ICS). The Pelvic Organ Prolapse Quantification (POPQ) system involves measurement of six anatomic points (in centimeters) in relation to the hymenal ring, as well as the genital hiatus, perineal body, and total vaginal length. The hymenal ring, defined as zero, is chosen as the reference point because it is a fixed anatomic point from which interobserver variability can be standardized. Prolapse distal to the hymenal ring is described in positive centimeters from the hymenal ring. Prolapse proximal to the hymenal ring is defined in negative centimeters from the hymenal ring. The six anatomic points can be divided into two points on the anterior vaginal wall (Aa and Ba), two points on the posterior vaginal wall (Ap and Bp), and two points in the superior vagina (C and D) (Fig. 71-2). The genital hiatus (gh) is measured from the posterior fourchette to the middle of the urethral meatus. The perineal body

Chapter 71 VAGINAL HYSTERECTOMY FOR VAGINAL PROLAPSE

(pb) is measured from the posterior fourchette to the middle of the anus. Total vaginal length (tvl) is measured with point C and point D reduced to their normal anatomic positions. Table 71-2 represents the stages of pelvic organ prolapse as defined by the POP-Q system. Because of the use of measure-

Table 71-1 Baden-Walker Classification of Pelvic Organ Prolapse Cystocele

Uterine or vaginal vault prolapse

Rectocele

Enterocele

First degree: Anterior vaginal wall and bladder descend halfway to the hymen. Second degree: Anterior vaginal wall and bladder descend to the hymenal ring. Third degree: Anterior vaginal wall and bladder are outside the hymen. First degree: Cervix or vaginal apex descends halfway to the hymen. Second degree: Cervix or vaginal apex extends to the hymen or over the perineal body. Third degree: Cervix and uterine corpus extend beyond the hymen, or the vaginal vault is everted and protrudes beyond the hymen. First degree: Posterior vaginal wall descends halfway to the hymen. Second degree: Posterior vaginal wall descends to the hymen. Third degree: Posterior vaginal wall extends beyond the hymen. Presence of the enterocele sac, relative to the hymen, should be described anatomically, with the patient in the supine and standing positions during a Valsalva maneuver.

Figure 71-2 Six anatomic sites (points Aa, Ba, C, D, Bp, and Ap), the genital hiatus (gh), perineal body (bp), and total vaginal length (tvl) are used to describe the degree of pelvic organ prolapse. (From Bump RC, Mathiason A, Bo K, et al: The Standardization of Terminology of Female Pelvic Organ Prolapse and Pelvic Floor Dysfunction. Am J Obstet Gynecol 175:10, 1996.)

ments revolving around fixed anatomic landmarks, the POP-Q system is a much more precise method of defining pelvic organ prolapse compared with previous systems. Interexaminer variability is markedly reduced, which is important for clinical standardization and for the purposes of research. VAGINAL HYSTERECTOMY AND RELATED PROCEDURES Indications The most frequent indication for hysterectomy is the leiomyomatous uterus. Patients with uterine fibroids may complain of pelvic pain or pressure. Other patients may complain of low back pain or urinary symptoms. Dysfunctional uterine bleeding is a common complaint of the woman with uterine fibroids. The

Table 71-2 Stages of Pelvic Organ Prolapse Stage 0

Stage 1 Stage 2

Stage 3

Stage 4

No evidence of pelvic organ prolapse. Points Aa, Ba, Ap, and Bp are all defined at −3 cm. Points C and D are located within 2 cm of the tvl (i.e., ≤ tvl − 2 cm). Most distal portion of the prolapse is > 1 cm above the level of the hymen (i.e., ≤ 1 cm). Most distal portion of the prolapse within 1 cm of the hymenal ring, proximal or distal (i.e., ≥ −1cm but ≤ +1 cm) Most distal portion of the prolapse is more than 1 cm distal to the hymenal ring but not more than 2 cm less than the tvl (i.e., > +1 cm but not more than tvl − 2 cm). Complete eversion of the tvl

tvl, total vaginal length.

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patient with symptomatic uterine fibroids is a safe candidate for vaginal hysterectomy assuming the uterus is mobile and the total uterine size is less than 12 weeks’ gestational size.9 Vaginal hysterectomy is particularly appropriate for the patient with symptomatic uterine prolapse when additional pelvic reconstruction may be indicated. These patients rarely present with isolated uterine prolapse, often having coexistent prolapse of the anterior or posterior vaginal walls, requiring a tailored and thoughtful pelvic reconstruction. Other indications for vaginal hysterectomy include adenomyosis, pelvic pain, and endometrial hyperplasia. Contraindications With an appropriate understanding of pelvic anatomy, the experienced surgeon encounters few contraindications to the vaginal route of hysterectomy. Even the large fibroid uterus can be removed vaginally in the hands of a skilled surgeon. Uterine immobility can make a vaginal hysterectomy difficult if abdominopelvic adhesions or scarring are present. A narrow, or stenotic, vaginal introitus can complicate removal of the uterus vaginally, and consideration should be given to an abdominal approach in this case. Selected cases of endometriosis are a contraindication to the vaginal route of hysterectomy. In 1995, Kovac10 assigned 617 women to abdominal, vaginal, or laparoscopically assisted vaginal hysterectomy based on uterine size and risk factors suggesting pelvic disease. In his series, 548 women were able to undergo successful vaginal hysterectomy. In the case of laparoscopically assisted vaginal hysterectomy, all but 2 of the 63 cases could have undergone successful vaginal hysterectomy based on laparoscopic findings. In his series, Kovac reported a 99.5% success rate for the vaginal route of hysterectomy using the techniques of morcellation, bivalving, and uterine coring (discussed later).10 The suspicious adnexal mass and high-grade endometrial carcinoma present absolute contraindications to the urogynecologic surgeon. In some cases, low-grade endometrial carcinoma may be managed with a vaginal hysterectomy. Technique For a simple vaginal hysterectomy, after the patient is in the operating suite, anesthesia is administered. The patient is then appropriately placed in the dorsal lithotomy position. We prefer the use of candy cane stirrups. A careful examination of the anesthetized patient is performed to confirm the findings of the previous examination. The patient is then prepared using a povidone-iodine solution or chlorhexidine gluconate and is draped in the usual fashion. The bladder is allowed to drain after placement of a 16-Fr, 5-mL Foley catheter. After complete drainage, the catheter is clamped using a Kelly clamp. Simms retractors are used to retract the anterior and posterior vaginal walls to fully visualize the cervix. The cervix is then grasped at the 3-o’clock and 9-o’clock positions with single-tooth tenaculums. The uterus is mobilized downward toward the introitus by traction on the tenaculums. Careful attention is paid to the location of the bladder. A solution of 1% lidocaine with epinephrine is then injected into the cervicovaginal junction in a circumferential fashion. The injection solution serves two purposes. First, it aids in hydrodissection, allowing the appropriate plane to be entered more efficiently. Second, the injection solution results in vasoconstriction, which facilitates visualization because of decreased operative blood loss.

Figure 71-3 Using a scalpel, the initial incision begins circumferentially at the reflection of the vaginal mucosa and the cervix.

An incision is made from the 9-o’clock position anteriorly to the 3-o’clock position. A similar incision is made posteriorly around the cervix (Fig. 71-3). Appropriate traction is applied to the cervix in the direction opposite the incision to facilitate separation of the underlying cervical stroma from the overlying vaginal wall. Side wall retractors are used by the assistants to aid in visualization. The full-thickness vaginal mucosa is dissected off of the underlying connective tissues using curved Mayo scissors. A right angle Heaney retractor or Deaver retractor can be used to retract the anterior vagina away from the underlying cervix to correctly identify the plane of cleavage. Posteriorly, a similar dissection is undertaken, completely separating the full thickness posterior vaginal mucosa from the overlying cervix (Fig. 71-4). After the peritoneum of the posterior cul-de-sac can be palpated, a posterior colpotomy is performed, and entrance into the peritoneal cavity is confirmed using a finger (Fig. 71-5). A right-angle Heaney retractor is used to deflect the rectosigmoid colon away from the operative field. Assuming the bladder has been sufficiently mobilized cephalad, the uterosacral ligaments can be secured to release the natural pelvic support of the cervix. We prefer the latter method because release of the uterosacral attachments facilitates anterior dissection (Fig. 71-6). Care must be taken to adequately retract the bladder away from the clamps. Heaney clamps are used to secure the uterosacral ligaments, incorporating the posterior peritoneum. The Heaney clamps are rotated laterally so that the tips of

Chapter 71 VAGINAL HYSTERECTOMY FOR VAGINAL PROLAPSE

Figure 71-4 Posteriorly, the full-thickness vaginal mucosa is sharply or bluntly dissected from the cervix. Figure 71-6 The uterosacral ligaments are clamped to gain access to the vesicouterine space.

Figure 71-5 The posterior cul-de-sac is sharply entered using Mayo or Metzenbaum scissors.

the clamp are almost perpendicular with the plane of the cervix. The results in shortening of the uterosacral ligaments and helps avoid injury to the bladder and ureters laterally. The uterosacral ligaments are then released from the uterus using Mayo scissors. The pedicles are then secured using a suture ligature of a 1-0 absorbable suture. At this point, attention is turned anteriorly. The full-thickness vagina is separated from the underlying cervix with the Mayo scissors. The dissection ultimately leads to the vesicouterine space (Fig. 71-7). A history of cesarean section may lead to scarification. Elevating the cesarean scar with forceps allows the surgeon to separate the scar from the underlying lower uterine segment. In this fashion, the vesicouterine space is entered. A right-angle Heaney retractor or Deaver retractor is then used to deflect the bladder anteriorly to identify the vesicouterine fold. The vesicouterine fold can be visualized as a semilunar, white line. The vesicouterine fold is then elevated, and the peritoneum is incised below the level of the forceps with Mayo scissors (Fig. 71-8). Entrance into the anterior cul-de-sac is confirmed by palpation. A retractor is used to deflect the bladder away from the surgical field. Lateral dissection using Mayo scissors aids in separation of the vaginal wall from the cervix. Heaney clamps are then used to secure the uterine vessels bilaterally as they run in the cardinal ligament. The pedicles are released from the uterus and secured using a 1-0 absorbable suture. We prefer to use a suture ligature, incorporating the previous uterosacral ligament pedicle. With this technique, the dead space between pedicles is obliterated, preventing tearing of tissue and bleeding from the small cervical

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Figure 71-7 The anterior vaginal wall is dissected from the cervix using Mayo or Metzenbaum scissors. This plane will ultimately lead to the vesicouterine space.

branches (Fig. 71-9). The cardinal ligament is secured in successive bites as previously described, ensuring that the anterior peritoneum and posterior peritoneum are incorporated. This technique fuses the anterior and posterior leaves of the broad ligament, preventing extensions of the peritoneal incisions into the vasculature of the broad ligament. Care must be taken to clamp medial to the previous pedicle to avoid ureteral injury. With adequate descensus, the fundus of the uterus is reached. An adequate examination should be performed to exclude pelvic adhesions or abnormal pathology. The utero-ovarian ligaments are then clamped with Heaney clamps (Fig. 71-10). The surgeon must proceed with caution to avoid bowel injury. The pedicles are released from the uterus using Mayo scissors. The uterine specimen is then submitted for pathologic analysis. The uteroovarian pedicles are secured first using a free tie of a 1-0 absorbable suture, followed by a distal suture ligature of a 1-0 absorbable suture. At this time, all of the pedicles are inspected for hemostasis. Packing the bowel with moist tail sponges or the use of a sponge stick can aid in visualization. The ovaries should be palpated to look for abnormal pathology.

Figure 71-8 The vesicouterine fold is elevated and entered sharply using Metzenbaum scissors.

tions for oophorectomy at the time of abdominal hysterectomy. After vaginal hysterectomy, the ovaries are not as accessible, leading to a more technically difficult procedure than oophorectomy at the time of abdominal hysterectomy.11 However, adhering to the surgical principles of mobilization and adequate visualization can lead to successful adnexectomy in more than 90% of cases, without increased morbidity.12 At the start of the procedure, the adnexa are identified. Using gentle traction on the round ligaments often affords the surgeon adequate visualization. Alternatively, a Babcock clamp can be used to grasp the adnexa, which are then brought into the surgical field. A finger can be used to palpate the ipsilateral ureter through the broad ligament. A curved clamp, such as a Heaney or Satinsky vascular clamp, can be used to clamp across the infundibulopelvic ligament (Fig. 71-11). Care should be taken to clamp as close to the ovary as possible to avoid ureteral injury. After adnexectomy, we prefer to secure the infundibulopelvic ligament with a free tie of 1-0 Vicryl, followed by a transfixion suture of 1-0 Vicryl placed distal to the free tie. The pedicle should be held until adequate hemostasis has been ensured to avoid retraction of an inadequately secured infundibulopelvic ligament high into the pelvis.

Managing the Adnexa The decision to proceed with vaginal oophorectomy at the time of hysterectomy is a controversial topic and should involve a thoughtful preoperative discussion with the patient. The indications for vaginal oophorectomy should be similar to the indica-

Vaginal Vault Suspension After vaginal hysterectomy, the cul-de-sac should be routinely evaluated to determine if an enterocele coexists. Based on the size of the enterocele and the degree of vault prolapse, the appropriate

Chapter 71 VAGINAL HYSTERECTOMY FOR VAGINAL PROLAPSE

Figure 71-9 Proper technique for clamping the uterine vessels. The vascular pedicle is suture ligated to the previously ligated pedicle. This technique ensures that the dead space between pedicles is obliterated and guards against bleeding from small cervical branches.

Figure 71-10 A finger is placed behind the utero-ovarian pedicle to prevent injury to the hollow viscus or other structures while the pedicle is cut with scissors.

procedure to obliterate the cul-de-sac and support or suspend the vaginal apex can be determined. With the bowel packed away using moist tail sponges and the patient in a slight Trendelenburg position, an assessment can be made about the presence or absence of an enterocele by simple digital palpation of the posterior cul-de-sac. An identifiable pocket confirms the presence of an enterocele and determines the need for excision of redundant peritoneum and posterior vaginal wall. Subsequently, the excess vaginal mucosa and peritoneum may be removed in a wedgelike fashion using Mayo scissors or Bovie cautery (Fig. 71-12). Allis clamps are then used to grasp the peritoneum and corresponding vaginal mucosa at the 5o’clock and 7-o’clock positions. Outward traction and elevation of the Allis clamps at a 45-degree angle in relation to the patient allow the surgeon to palpate the uterosacral ligaments coursing back toward the sacrum. With the same finger, the surgeon can palpate the position of the ipsilateral ureter in relation to the uterosacral ligament. The ureter can be found ventral and lateral to the ischial spine. The McCall culdoplasty was first described in 1957 by Milton McCall. In the initial description, McCall used several nonabsorbable sutures to plicate the uterosacral ligaments in the midline, incorporating the intervening, redundant peritoneum. This resulted in effective obliteration of the posterior cul-de-sac. External absorbable, McCall sutures were placed through the full-thickness vagina, incorporating the ipsilateral uterosacral ligament and intervening peritoneum before crossing the midline and incorporating the contralateral uterosacral ligament and passing back through the full-thickness vagina (Figs. 71-13 and

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Figure 71-11 The infundibulopelvic ligament is secured using a curved Haney or Satinsky vascular clamp. The pedicle is secured first using a free tie of a =0 absorbable suture followed by a suture ligament.

Figure 71-12 A finger in the posterior cul-de-sac can be used to confirm the presence of an enterocele. The redundant wedge of posterior vaginal wall and peritoneum can then be excised.

Figure 71-13 The technique of McCall culdoplasty. Two internal sutures (permanent) and two external sutures (absorbable) have been placed.

71-14). After tying the external McCall sutures, cystoscopy is performed to confirm ureteral patency. Some patients have more advanced vaginal vault prolapse. In these cases, it may be appropriate to perform a more formal vaginal vault suspension, such as a sacrospinous fixation, high uterosacral ligament suspension, or iliococcygeus suspension. To more adequately reestablish level I support, a high uterosacral ligament suspension can be performed. The bowel is packed away as previously described, and a Heaney retractor is used to lift the bowel out of the posterior cul-de-sac. Traction on the previously placed Allis clamps enables palpation of the remnants of the uterosacral ligaments. For the right-handed surgeon, the left index finger is used to deflect the sigmoid colon medially. As the assistant places traction on the patient’s left uterosacral ligament, the surgeon places a figure-of-eight 1-0 absorbable suture through the left uterosacral ligament (lateral to medial) at the level of the ischial spine. With traction on the first suture, the surgeon then places a second figure-of-eight 1-0 absorbable suture through the left uterosacral ligament approximately 1 cm proximal to the first suture. This throw is higher and slightly more medial than the first suture because of the natural course of the uterosacral ligament. A similar procedure is performed on the opposite site, with careful attention to the location of the ureter. These four sutures are tagged and held. We prefer to use

Chapter 71 VAGINAL HYSTERECTOMY FOR VAGINAL PROLAPSE

Complete Uterine Procidentia The technical aspects of vaginal hysterectomy in the patient with complete procidentia are the same as those for the simple vaginal hysterectomy. However, a careful preoperative evaluation must be performed to determine whether the prolapse represents a true procidentia or an elongated cervix. Severe descensus of the uterus in the case of procidentia results in anatomic distortion of the entire pelvis. The surgeon must remember that the course of the ureters is likely distorted in the wake of chronic traction associated with a large cystocele. If it is determined preoperatively that the prolapse represents a severely elongated cervix with the uterus in a normal anatomic location, the surgeon must be careful not to amputate the cervix prematurely, because this will complicate the remainder of the procedure. Alternatively, the surgeon should take successive extraperitoneal bites until the anterior and posterior peritoneal reflections are reached (Fig. 71-15). After the anterior and posterior cul-de-sacs have been entered, the vaginal hysterectomy proceeds in a normal fashion. Narrow Vaginal Introitus

Figure 71-14 Cross section of the upper vagina before and after the McCall sutures have been tied down toward the hollow of the sacrum.

1-0 nonabsorbable sutures to obliterate the posterior cul-de-sac by plicating the distal portions of the uterosacral ligaments across the midline. The nonabsorbable sutures are then tied down, obliterating the posterior cul-de-sac. At this point, it is essential to confirm ureteral patency by cystoscopy after administration of intravenous indigo carmine. In the absence of anterior or posterior vaginal wall prolapse, the high uterosacral ligament suspension sutures are passed out through the full-thickness vagina. The bowel packing is removed, and the vaginal cuff is closed using interrupted figure-of-eight 1-0 absorbable sutures in a transverse or longitudinal fashion. If an anterior repair is needed, the cuff is usually closed after the colporrhaphy. After hemostasis is confirmed, the vaginal mucosa is pushed toward the hollow of the sacrum, around the vault suspension sutures. The suspension sutures are then tied down. Examination should allow 2 fingerbreadths to be comfortably passed through the vaginal introitus toward the vaginal apex. The ultimate vaginal length should be a minimum of 8 cm. THE DIFFICULT VAGINAL HYSTERECTOMY Vaginal hysterectomy can be complicated in the face of pelvic floor relaxation or coexistent pelvic pathology.

A lack of uterine descensus or a narrow vaginal introitus, particularly in a nulliparous patient, are not contraindications to the vaginal route of hysterectomy. A thorough examination under anesthesia should be performed to determine the size and mobility of the uterus to assess the feasibility of a successful vaginal hysterectomy. A relaxing episiotomy may be necessary to afford the surgeon more room in the pelvis. If necessary, the surgeon may use a Schuchardt incision, which is made into the lateral vaginal wall and carried down to the perineal body. The Schuchardt incision resembles a sulcal tear after an operative vaginal delivery. These techniques alter the integrity of the perineal muscles and the levator muscles. The surgeon must ensure that normal anatomy has been restored after vaginal hysterectomy. Obliterated Vesicouterine Fold A history of multiple cesarean sections or endometriosis may complicate vaginal hysterectomy by obliterating the vesicouterine fold. As long as the bladder has been sufficiently dissected off of the cervix, anterior colpotomy is not mandatory. Alternatively, the surgeon may proceed with successive bites posteriorly until the fundus is palpated with a finger. Passing a finger around the fundus anteriorly may expose the anterior peritoneum, allowing the surgeon to safely enter the anterior cul-de-sac and effectively avoiding inadvertent cystotomy (Fig. 71-16). If the surgeon suspects an obliterated cul-de-sac based on patient history or exam under anesthesia, the dissection should proceed sharply, rather than bluntly. Blunt dissection follows the path of least resistance, tearing into the bladder. Obliterated Cul-de-Sac of Douglas A history of pelvic surgery, endometriosis, or pelvic inflammatory disease may result in an obliterated cul-de-sac of Douglas. This scenario predisposes to rectal injury or injury to the small bowel during attempted posterior colpotomy. If necessary, the anterior cul-de-sac should be entered first, and a finger wrapped should be around the fundus to palpate for adhesions or scarifi-

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Figure 71-15 Technique of removal of an elongated cervix. Successive extraperitoneal bites are taken until the anterior and posterior peritoneal reflections are reached.

cation. In their absence, the posterior-cul-de-sac can then be entered safely without fear of rectal injury.

Massive Leiomyomatous Uterus The uterus measuring less than 12 weeks’ gestational size poses few problems for the vaginal route of hysterectomy, provided the surgical principles outlined earlier are followed. The uterus measuring more than 12 weeks’ gestational size is not an absolute contraindication to the vaginal route of hysterectomy in the hands of a skilled surgeon. The large leiomyomatous uterus poses several difficulties to the surgeon. The leiomyomatous uterus may be enlarged to the point that en bloc removal of the uterus by the vaginal route is impossible. In this situation, several techniques may be used to facilitate vaginal hysterectomy, including morcellation, bivalving of the

uterus, or intramyometrial coring. Ligation of the major blood supply to the uterus, the uterine arteries, is a prerequisite for the use of these techniques. It is prudent to enter the anterior and posterior cul-de-sac to prevent injury to the bladder and rectum. After the uterine vessels have been secured, morcellation may begin. The cervix is amputated with a scalpel. Tenacula are used to grasp the posterior aspect of the uterus, which is brought down into the surgical field. A scalpel or Mayo scissors is then used to remove the tissue within the tenacula en bloc (Fig. 71-17). The entire body of the uterus is then morcellated. After the fundus has been identified, the remainder of the uterus can be bivalved, securing the lateral pedicles as outlined earlier (Fig. 71-18). In patients with a massive uterus because of leiomyomas or adenomyosis, the fundus may not be deliverable posteriorly. In this case, intramyometrial coring is particularly appropriate (Fig. 71-19).

Chapter 71 VAGINAL HYSTERECTOMY FOR VAGINAL PROLAPSE

A

B

C Figure 71-16 An obliterated vesicouterine fold. A, Adhesions are seen between the bladder and anterior cervix. B, Blunt dissection in this setting may lead to inadvertent cystotomy, because a finger will follow the path of the least resistance. C, Passing a finger around the fundus of the uterus often leads to identification of the appropriate plane of the dissection.

COMPLICATIONS OF VAGINAL HYSTERECTOMY Complications of vaginal hysterectomy are uncommon but can include bleeding, infection, or inadvertent injury to the bladder, ureters, or bowel. Postoperative complications can include hematoma or abscess formation. Risk factors include previous abdominal surgery, a history of endometriosis or pelvic malignancy, cervical or broad ligament myomas, congenital anomalies, the presence of inflammation or pelvic adhesions, or a history of pelvic irradiation. Patient factors such as large uterine size or morbid obesity can reduce visualization. An inexperienced surgeon or inadequate retraction or lighting can add to the risks posed during the vaginal hysterectomy. Inadvertent cystotomy remains one of the most common complications of vaginal hysterectomy. The incidence of inadvertent cystotomy during vaginal hysterectomy is reported to be between 1% and 1.8%. In 2002, Carley and colleagues13 performed a retrospective review of 590 vaginal hysterectomies. The rate of inadvertent cystotomy was 1.9%. Cases were matched with five controls with similar procedures performed. Patients who suffered inadvertent cystotomy had a longer operative time and greater intraoperative blood loss than similarly matched controls.13 As the rate of cesarean section continues to rise, concerns have surfaced regarding the risk of inadvertent cystotomy because of scarification in the lower uterine segment. Rooney and associates14 performed a retrospective analysis of more than 5000

hysterectomies in 2004. They found an odds ratio of incidental cystotomy of 3.00, which approached statistical significance for women undergoing a total vaginal hysterectomy who had a history of prior cesarean section. The odds ratio for incidental cystotomy at the time of laparoscopically assisted vaginal hysterectomy in women with a history of prior cesarean section was found to be significant at a value of 7.50.14 One of the most serious complications of gynecologic surgery is iatrogenic injury to the ureters. The literature reports an incidence of iatrogenic ureteral injury of 0.02% to 0.8% during vaginal hysterectomy.15 The ureters can be burned, clipped, ligated, kinked, or partially or completely transected. Intraoperative recognition is essential because of the subsequent risk of fistula formation or hydronephrosis resulting in loss of renal function. Most iatrogenic ureteral injuries occur when securing the uterine vessels. Particular care should be taken to keep the surgical clamps medial to the uterosacral ligament pedicles when performing the vaginal hysterectomy. Iatrogenic injury to the ureter is the most common complication of the vaginal vault suspension, whether the surgeon has performed a traditional McCall culdoplasty or a high uterosacral ligament suspension. Karram and colleagues16 reported a 2.4% risk of iatrogenic ureteral injury during 168 high uterosacral ligament suspensions. Barber and coworkers reported an 11% risk of ureteral injury during the same procedures.16 Intraoperative cystoscopy with intravenous indigo carmine must be used to verify ureteral patency after the procedure. Webb and colleagues

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B

A Figure 71-17 Technique of morcellation in the massively leiomyomatous uterus. A, An elliptical wedge of tissue is excised from the posterior uterus. B, The edges of the incision are brought together with the tenacula. A second wedge of tissue is removed in a similar fashion. The procedure is repeated until the fundus is reached and the uterus is delivered.

described 660 women who underwent a modified Mayo McCall culdoplasty in 1998.16 In addition to ureteral injury, lacerations to the bowel and rectum were reported in 2.3% of cases. Other complications of the McCall culdoplasty include vault hematoma in 1.3% and cuff abscess or infection in 0.6% of patients. Webb reported a blood transfusion rate of 2.2%.16 Injuries to the rectum during vaginal hysterectomy are rare, with most occurring during attempted entry into the pouch of Douglas. Mathevat and colleagues17 performed a retrospective review of more than 3000 vaginal hysterectomies with or without additional procedures. They reported five rectal injuries, all of

which occurred during attempted entry to the posterior cul-desac.17 Posterior colporrhaphy also poses a risk of rectal injury. In the same series, Mathevat and colleagues17 reported 11 rectal injuries associated with posterior colporrhaphy. The overall incidence of rectal injury in their series was 0.45%.17 Hematoma formation is a rare complication of vaginal hysterectomy and is usually the result of inadequate hemostasis at the end of the procedure. Particular attention must be given to the pedicles in the post-hysterectomy patient to confirm hemostasis is adequate. After the vaginal hysterectomy with or without concomitant reconstructive procedures, we prefer to pack the

Chapter 71 VAGINAL HYSTERECTOMY FOR VAGINAL PROLAPSE

B

A Figure 71-18 Technique of hemisection of the uterus. A, The midportion of the uterus. B, Lateral view demonstrates many uterine myomas.

A

B

Figure 71-19 Technique of intramyometrial coring. A, A scalpel is used to create a cylinder of tissue. B, Lateral view of the technique of intramyometrial coring. Downward traction on the cervix will deliver the specimen, everting the uterine fundus.

vagina with 2-inch iodoform gauze to apply pressure to small amounts of venous oozing. The packing is removed the next morning, and hemostasis is confirmed. CONCLUSIONS As the population continues to increase, the gynecologist can expect a concurrent rise in the number of women presenting for

hysterectomy. Currently, the rate of abdominal hysterectomy exceeds the rate of vaginal hysterectomy. Reducing the rate of abdominal hysterectomy could result in a reduction in hospital stay and postoperative recovery. With appropriate patient selection and in the hands of an experienced surgeon, vaginal hysterectomy represents a useful adjunct in the treatment of pelvic organ prolapse.

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References 1. Keshavarz H, Hillis SD, Kieke BA, et al: Hysterectomy surveillance— United States 1994-1999. MMWR CDC Surveill Summ 51:1-8, 2002. 2. U.S. Census Bureau: U.S. Interim Projections by Age, Sex, Race, and Hispanic Origin. Available at http://www.census.gov/ipc/www/ usinterimproj/ Accessed March 18, 2004. 3. Walters MD, Weber AM: Anatomy of the lower urinary tract, rectum and pelvic floor. In Walters MD, Karram MM (eds): Urogynecology and Reconstructive Pelvic Surgery, 2nd ed. St. Louis, Mosby, 1999, pp 3-13. 4. DeLancey JOL: Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 166:1717, 1992. 5. Shull BL, Bachofen CG: Enterocele and rectocele. In Walters MD, Karram MM (eds): Urogynecology and Reconstructive Pelvic Surgery, 2nd ed. St. Louis, Mosby, 1999, pp 221-234. 6. Silva WA, Kleeman SD, Segal J, et al: Effects of a full bladder and patient positioning on pelvic organ prolapse assessment. Obstet Gynecol 104:37-41, 2004. 7. Baden WF, Walker T, Lindsey JH: The vaginal profile. Tex Med 64:56, 1968. 8. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. 9. Friedman AJ, Haas ST: Reply to letter of Fruchter. Am J Obstet Gynecol 170:259, 1994.

10. Kovac SR: Guidelines to determine the route of hysterectomy. Obstet Gynecol 85:18-23, 1995. 11. Nichols DH, Randall CL: Vaginal hysterectomy. In Vaginal Surgery, 4th ed. Baltimore, Williams & Wilkins, 1996, pp 151-212. 12. Sheth SS: The place of oophorectomy at vaginal hysterectomy. Br J Obstet Gynecol 98:662-666, 1991. 13. Carley ME, McIntire D, Carley JM, et al: Incidence, risk factors and morbidity of unintended bladder or ureter injury during hysterectomy. Int Urogynecol J 13:18-21, 2002. 14. Rooney CM, Crawford AT, Kleeman SD, Karram MM: Is prior cesarean section a risk factor for incidental cystotomy at the time of hysterectomy? A case-controlled study. Am J Obstet Gynecol 193:2041-2044, 2005. 15. Visco AG, Taber KH, Weidner AC, et al: Cost-effectiveness of universal cystoscopy to identify ureteral injury at hysterectomy. Obstet Gynecol 97:685-692, 2001. 16. Karram MM, Kleeman SK: Vaginal vault prolapse. In Rock JA, Jones HW (eds): Te Linde’s Operative Gynecology, 9th ed. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 999-1025. 17. Mathevet P, Valencia P, Cousin C, et al: Operative injuries during vaginal hysterectomy. Eur J Obstet Gynecol Reprod Biol 97:71-75, 2001.

Chapter 72

LAPAROSCOPIC SACRAL COLPOPEXY Marie Fidela R. Paraiso Laparoscopic sacral colpopexy was first reported by Nezhat and colleagues in 1994.1 Adoption of this procedure has increased in the past decade and has evolved to include robotic assistance. The possible advantages of laparoscopic surgery are improved visualization of anatomy of the peritoneal cavity because of laparoscopic magnification, insufflation effects, and improved hemostasis; shortened hospitalization resulting in potential cost reduction; decreased postoperative pain and more rapid recovery and return to work; and better cosmetic appearance of smaller incisions. Disadvantages of laparoscopic surgery include a steep learning curve in acquiring suturing skills, technical difficulty of presacral dissection, increased operating time early in the surgeon’s experience, and possibly greater hospital cost because of increased operating room time and the use of disposable surgical instruments. These disadvantages, inadequate experience in advanced laparoscopy in residency and fellowship programs, surgeon preference for vaginal route surgery, and recently introduced minimally invasive apical suspension procedures have thwarted widespread adoption of laparoscopic surgery for pelvic organ prolapse. The indications for laparoscopic vaginal apex prolapse and enterocele repair are identical to those for vaginal and abdominal routes. The choice of laparoscopic route is determined by the preferences of the surgeon and patient and by the laparoscopic skill of the surgeon. Additional factors that should be considered include history of pelvic or anti-incontinence surgery, previous failed transvaginal colpopexy, short vagina, severe abdominopelvic adhesions, the patient’s age and weight, the need for concomitant pelvic surgery, and the patient’s ability to undergo general anesthesia. The technique of laparoscopic sacral colpopexy described in this chapter follows standard procedures for operative laparoscopy for access and is identical to the more proven open abdominal sacral colpopexy (see Chapter 73). Clinical outcome and complications are summarized.

ANATOMY Thorough knowledge of the anatomy of the anterior abdominal wall is mandatory for safe and effective trocar insertion. The umbilicus is approximately at the L3-to-L4 level, and the aortic bifurcation is at the L4-to-L5 level. In obese women, the umbilicus is caudal to the bifurcation. The intraumbilical trocar should be introduced at a more acute angle toward the pelvis in thin women and closer to 90 degrees in obese women. The left common iliac vein courses over the lower lumbar vertebrae from the right side and may be inferior to the umbilicus. Common iliac arteries course 5 cm before bifurcating into the internal and external iliac arteries. The ureter crosses the common iliac artery at or above its bifurcation.

The superficial epigastric artery, a branch of the femoral artery, courses cephalad and can be transilluminated. The inferior epigastric artery branches from the external iliac artery at the medial border of the inguinal ligament and runs lateral to and below the rectus sheath at the level of the arcuate line. It is accompanied by two inferior epigastric veins. When considering the anatomy of the repair of pelvic organ support, a surgeon must keep in mind the three levels of support of the vagina described by DeLancey in 1992.2 The upper fourth of the vagina (level I) is suspended by the cardinal-uterosacral complex, the middle half (level II) is attached laterally to the arcus tendineus fasciae pelvis and the medial aspect of the levator ani muscles, and the lower fourth (level III) is fused to the perineal body. The endopelvic fascia laterally blends with the muscularis of the vagina. All pelvic support defects, whether anterior, apical, or posterior, represent a break in the continuity of the endopelvic fascia or vaginal muscularis and a loss of its suspension, attachment, or fusion to adjacent structures. The goals of pelvic reconstructive surgery are to correct all symptomatic defects, thereby reestablishing vaginal support at all three levels, and to maintain or restore normal visceral and sexual function. The key anatomic landmarks of sacral colpopexy are the middle sacral artery and vein; the sacral promontory with anterior longitudinal ligament; the aortic bifurcation and the vena cava, which are at the level of L4 to L5; the right common iliac vessels and right ureter, which are at the right margin of the presacral space; and sigmoid colon, which is at the left margin. The left common iliac vein is medial to the left common iliac artery and can be damaged during dissection or retraction. The sacral foramina are only 1 to 1.5 cm from the midline, and the sympathetic chain is lateral. The ureter, which crosses over the common iliac artery bifurcation and courses along the pelvic sidewall, is approximately 1 to 1.5 cm lateral to the uterosacral ligament as it passes underneath the uterine artery. The anatomic landmarks during laparoscopic sacral colpopexy graft attachment are the pubocervical fascia (i.e., anterior vaginal muscularis with overlying endopelvic fascia) and the rectovaginal muscularis (i.e., fibromuscular layer of the posterior vaginal wall above the rectovaginal septum). The rectovaginal septum is ideally the posterior point of attachment of the sacral colpopexy mesh, allowing continuity with the perineal body.

SURGICAL TECHNIQUE Operative Laparoscopy for Pelvic Organ Prolapse: Setup, Instrumentation, and Trocar Placement Ideal stirrups for combined laparovaginal cases are the Allen stirrups and Yellofins (Allen Medical Systems, Acton, MA), which have levers that can quickly convert the patient from low to high 719

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lithotomy position while preserving sterility of the field. A sterile pouch attached to each thigh is equipped with commonly used instruments such as unipolar scissors, bipolar cautery, blunttipped graspers, bowel graspers, and suction irrigation. The monitor screens should be placed lateral to the legs in direct view of the surgeon standing on the opposite side of the table. The scrub nurse should be centered between the two monitor screens that are used; otherwise, the scrub nurse is located behind one surgeon and the electrosurgical unit or harmonic scalpel on the opposite side. After the three-way Foley catheter and uterine manipulator (if needed) have been placed, the vaginal tray with cystoscope can be set aside for later use. For standard suturing technique, needle holder preference is determined by comfort of the surgeon. Conventional and 90degree, self-righting German needle holders (Ethicon EndoSurgery, Cincinnati, OH) have ratchet spring handles, and the Talon curved needle drivers with spring handles (Cook OB/GYN, Spencer, IN) self-right the needle at an angle of 45 or 90 degrees to the needle driver shaft, depending on the style chosen. The Storz Scarfi needle holder and notched assistant needle holder (Karl Storz Endoscopy, Culver City, CA) are most like conventional needle holders used during laparotomy. However, the handles are difficult to maintain and may pop open after extended use. The needle holder tips may become magnetized, which hampers needle grasping. Disposable suturing devices that have been introduced include the Endo-stitch (U.S. Surgical Corp., Norwalk, CT) and the Capio CL (Microvasive Boston Scientific, Natick, MA; CL refers to Cooper’s ligament). Suturing devices are not recommended when performing laparoscopic sacral colpopexy because the depth of stitch placement in the vaginal muscularis is difficult to gauge tactically with these devices. Extracorporeal knot tying is preferred because of technical facility and the ability to hold more tension on the suture, although some surgeons prefer intracorporeal suturing. When robotically assisted laparoscopic sacral colpopexy is performed, all suturing is done in an intracorporeal fashion. The choice of an open-ended or close-ended knot pusher for extracorporeal knot tying depends on surgeon preference. Our suture of choice is the single- or double-armed 1-0 Ethibond 36-inch suture on a CT-1 needle (Ethicon, Somerville, NJ). Our alternative choice for suture is 1-0 Gore-Tex (W.L. Gore and Associates, Phoenix, AZ). A 48-inch suture is preferred when suturing from ports at the level of the umbilicus. Sterile steel thimbles may be used by the surgeon or assistant when elevating the vagina while the surgeon is placing the stitches in the vaginal wall. However, vaginal manipulation when placing sutures is best achieved with endoanal anastomosis (EAA) sizers or fiberglass stents. Intraumbilical or infraumbilical incisions depend on the anatomy of the umbilicus. Many variations of the accessory trocar sites have been described. For laparoscopic sacral colpopexy, we use three to four additional trocars: a 5- to 12-mm disposable trocar with reducer in the right and left lower quadrants lateral to the inferior epigastric vessels and a reusable 5-mm port or an additional 5- to 12-mm disposable trocar with reducer in the left upper quadrant at least 8 cm lateral to the umbilicus. Trocars are placed lateral to the rectus muscle, approximately 3 cm medial to and above the anterior superior iliac spine. Based on an anatomic study by Whiteside and coworkers3 in 2003, we know that ilioinguinal and iliohypogastric nerve entrapment during fascial closure may be reduced if the ports are placed at least 2 cm cephalad to the anterior superior iliac spines. For more

extensive reconstructive surgery, an additional 5-mm port may be placed on the principal surgeon’s side so that he or she can operate with two hands. Reusable and disposable ports may be secured with circumferential screws to prevent port slippage. Versa Step Plus trocars (U.S. Surgical Corp.) allow easy introduction of needles, maintain pneumoperitoneum during extracorporeal knot tying, and prevent port slippage because of the expandable sleeve. General Intraoperative and Postoperative Procedures The patient is instructed to take one bottle of magnesium citrate or equivalent bowel preparation and limit her diet to clear liquids on the day before surgery. Placing an orogastric or nasogastric tube to decompress the stomach at the time of surgery is also helpful. Patients receive prophylactic intravenous antibiotic therapy 30 minutes before surgery. Pneumatic compression stockings are routinely used. The operations are performed under general anesthesia in the low lithotomy position. A 16-Fr, threeway Foley catheter with a 20- to 30-mL balloon is attached to continuous drainage, and the irrigation port is connected to sterile water or saline. After all sutures are placed and tied, transurethral cystoscopy or suprapubic teloscopy is done to document ureteral patency and absence of sutures in the bladder. A suprapubic catheter is placed, if desired. The surgeon must again inspect the pelvis for bleeding while reducing the carbon dioxide insufflation. Routine closure of the peritoneum is performed based on the surgeon’s preference. All ports are removed under direct visualization, and the peritoneum and fascia of all 5- to 12-mm incisions are reapproximated with the fascial closure instrument (Karl Storz, Tuttingen, Germany) or the Grice needle (New Ideas in Medicine, Clearwater, FL). The skin is closed in a subcuticular fashion. The fascia and subcutaneous fat can be infiltrated with a long-acting local anesthetic, such as 0.5% bupivacaine hydrochloride. Postoperative care consists of oral pain medication (intravenous, if needed), rapid diet advancement, and ambulation. If an anti-incontinence procedure is concomitantly performed, voiding trials begin as soon as the patient is ambulatory. Intermittent self-catheterization protocols can begin immediately, especially if the patient was taught the technique preoperatively. Some patients are able to go home on the same day if adequately counseled preoperatively. Preoperative teaching includes discussion of postoperative analgesics, the need for a caretaker at home during the immediate recovery period, instruction in catheter care or intermittent self-catheterization, and explanation of goals to be reached before outpatient discharge. Patients are instructed to refrain from sexual intercourse and lifting objects heavier than 10 pounds for at least 8 weeks. They are cautioned to heed to these instructions despite rapid recovery. Technique of Laparoscopic Sacral Colpopexy Vaginal obturators, spongesticks, or equivalent vaginal manipulators (EEA Sizer, U.S. Surgical Corp.; CDH, Ethicon EndoSurgery) are used for delineation of the vaginal apex and rectum. After all ancillary ports are placed, the presacral space is dissected (Fig. 72-1). If exposure of the sacral promontory and presacral space is not adequate, the patient should be tilted to her left and a reusable snake retractor (Snowden Pencer, Tucker, GA) or fan retractor (Origin Medsystems, Menlo Park, CA) placed through

Chapter 72 LAPAROSCOPIC SACRAL COLPOPEXY

Figure 72-1 Dissection of the presacral space.

Figure 72-3 Anterior attachment of polypropylene mesh to the muscularis of the vaginal apex.

Figure 72-2 Dissection of the rectovaginal space.

Figure 72-4 Fixation of two separate polypropylene meshes during sacral colpopexy.

an ancillary port. A suture may be placed through the sigmoid epiploicae and placed on traction outside of the abdomen lateral to the left lower quadrant port to keep the sigmoid colon retracted throughout the surgery, thereby freeing an operative port. The peritoneum overlying the sacral promontory is incised longitudinally with laparoscopic scissors or harmonic scalpel (Gynecare, Somerville, NJ) and extended to the cul-de-sac. A laparoscopic dissector or hydrodissection is used to expose the periosteum of the sacral promontory. If blood vessels are encountered during the dissection, coagulation or clip placement is used to achieve hemostasis. Some surgeons prefer to dissect the presacral space first, eliminating the most technically difficult portion of the procedure. A Halban procedure or Moschcowitz culdoplasty may be performed based on the surgeon’s preference or when a deep cul-de-sac is encountered. When a concomitant culdoplasty is performed, it is completed after posterior mesh placement. To dissect the rectovaginal septum, the peritoneum between the vaginal apex and rectum is placed on countertraction by manipulating the EAA sizers, pointing the vagina toward the pubic bone and the rectum toward the sacrum (Fig. 72-2). Anterior dissection is performed after the bladder is filled with 300 ml

of sterile water. Dissection is extended to the bladder base. This dissection can be very difficult if a patient has undergone a previous anterior colporrhaphy or vaginal suspension procedure. Our technique incorporates two pieces of 15 × 4 cm polypropylene mesh or biologic tissue. We sew the posterior mesh on first. The most caudal stitch is placed on the posterior vaginal wall and rectovaginal fascia. After placement of the first stitch, the mesh is threaded through the stitch before introducing the mesh into the peritoneal cavity. The corresponding contralateral stitch is taken and threaded through the mesh to anchor the inferior border of the mesh to the rectovaginal septum or perineum (a 15- to 18-cm mesh length may be required for laparoscopic sacral colpoperineopexy). The sutures are tied extracorporeally as they are placed. Care is taken to place the stitches through the entire thickness of the vaginal wall, excluding the epithelium. The mesh is sutured to the posterior vaginal apex and rectovaginal septum with three to four similar rows of suture and to the vaginal apex anteriorly with two to three pairs of No. 0 nonabsorbable sutures (Figs. 72-3 and 72-4). The surgeon sutures the mesh to the longitudinal ligament of the sacrum with two

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Figure 72-5 Attachment of the mesh to the anterior longitudinal ligament of the sacrum without tension.

Figure 72-6 Biologic mesh implantation in sacral colpopexy.

No. 0 nonabsorbable sutures (Fig. 72-5). No undue tension is placed on the mesh. Titanium tacks or hernia staples may also be used to attach the mesh to the anterior longitudinal ligament of the sacrum. The redundant portion of the mesh is excised. Biologic tissue may also be used, especially when concomitant bowel resection is performed (Fig. 72-6). The peritoneum is reapproximated over the mesh with 2-0 polyglactin suture. If the mesh remains exposed, sigmoid epiploic fat may be sutured over it. CLINICAL RESULTS AND COMPLICATIONS The current gynecologic literature for laparoscopic sacral colpopexy is sparse and consists of case series from surgeons subspecializing in advanced laparoscopy and urogynecologic surgery. Comparative, adequately powered studies of laparoscopic surgery for vaginal apex prolapse do not exist. In 1994, Nezhat and colleagues1 reported a series of 15 patients who underwent laparoscopic sacral colpopexy for whom the

mean operative time was 170 minutes (range, 105 to 320 minutes) and the mean blood loss was 226 mL (range, 50 to 800 mL). The mean hospital stay was 2.3 days, excluding a case converted to laparotomy because of presacral hemorrhage. The cure rate for apical prolapse was 100% at 3 to 40 months. In 1995, Lyons and Winer 4 reported 4 laparoscopic sacrospinous fixations and 10 laparoscopic sacral colpopexies with operative times comparable to those for vaginal and abdominal approaches. He reported less intraoperative and postoperative morbidity with the laparoscopic route; this was attributed to a superior anatomic approach and visualization of anatomic structures. Nezhat and associates1 and Lyons and Winer4 used mesh and suture, and they sometimes stapled the mesh into the longitudinal ligament of the anterior sacrum. In 1997, Ross5 evaluated 19 patients with post-hysterectomy vaginal apex prolapse prospectively with extensive preoperative and postoperative testing, including multichannel urodynamics and transperineal ultrasound. All patients underwent sacral colpopexy, Burch colposuspension, and modified culdoplasty. Paravaginal defect repair and posterior colporrhaphy were added as indicated. Ross reported seven complications: three cystotomies, two urinary tract infections, one seroma, and one inferior epigastric vessel laceration. Five patients had recurrent defects that were all less than grade 2 (two paravaginal defects and three rectoceles). Vaginal length ranged from 10.8 to 12.1 cm, and all sexually active patients reported no sexual dysfunction. All but four patients voided spontaneously, and none required more than 4 days of catheterization. All were discharged within 24 hours. The cure rate at 1 year was 100% for vaginal apex prolapse and 93% for stress incontinence, although two patients were lost to follow-up. In another study reported in 2004, Ross6 prospectively analyzed 51 cases of laparoscopic sacral colpopexy for grade III or IV apical vaginal vault prolapse. Forty-three patients demonstrated an objective cure rate of 93% at the vaginal apex during their 5-year follow-up visit. Complications included one partial small-bowel obstruction resulting from bowel adherence to the mesh and two locally treated mesh erosions. Ross concluded that patient recovery was greatly enhanced, with most patients requiring only overnight hospitalization. The largest series of laparoscopic sacral colpopexies is a retrospective cohort of 83 patients published by Cosson and associates7 in the French literature. The investigators performed concomitant laparoscopic supracervical hysterectomy in 60 patients and converted six cases to laparotomy. Operative time decreased from 292 to 180 minutes with increased experience. One patient required reoperation for prolapse, and two patients underwent procedures for stress incontinence. The median length of follow-up was 343 days. In 2004, Gadonneix and coworkers7 reported the use of two separate meshes for laparoscopic sacral colpopexy with or without Burch colposuspension in 46 consecutive patients with primary vaginal apex prolapse with or without primary stress incontinence. Mean operating time was 171 minutes, and mean hospital stay was 4 days. Median follow-up was 24 months (range, 12 to 60 months). Eleven percent of patients required conversion to laparotomy. Complications included de novo urge incontinence in 5% of patients, laparoscopically treated bladder injury in 7%, and recurrent rectoceles in 12% (occurring only in women who had undergone laparoscopic Burch colposuspension compared with no colposuspension, P = .036). One patient developed obstructed defecation, which the study authors attributed to excessive mesh tension.

Chapter 72 LAPAROSCOPIC SACRAL COLPOPEXY

At the Cleveland Clinic Foundation, we compared our first 56 consecutive laparoscopic sacral colpopexies with 61 consecutive open sacral colpopexies performed during the same period.9 Mean follow-up was 14 and 16 months for the laparoscopic and open groups, respectively. Laparoscopic sacral colpopexy and concomitant procedures required a significantly longer operating room time compared with open sacral colpopexy, with mean operating room times of 269 and 218 minutes, respectively. However, mean hospital stay was significantly longer for the open group than the laparoscopic group (4 versus 1.8 days). We found similar clinical outcomes and reoperation rate. Our sample size was too small to determine differences in complications. CONCLUSIONS Laparoscopy is a means of achieving less invasive surgical access, and its use is expanding rapidly in all surgical specialties. The technique for laparoscopic sacral colpopexies should be as close as possible to the operative technique for open sacral colpopexy. Bladder injury is probably more common with laparoscopy, but the risk of cystotomy decreases with surgical experience. Complications associated with laparotomies, such as wound infection and hernias, are rare with the laparoscopic route.

The benefits of improved visualization of anatomic structures and the small incisions associated with the laparoscopic approach are desirable, particularly in obese patients. The advantages of less postoperative pain, shorter hospitalization, a shortened recovery period, and earlier return to work are very popular with patients, but these advantages are partially offset by increased operating time and possibly by increased cost. The operating time and cost will likely decrease as surgeons gain experience with the advanced laparoscopic techniques of suturing and knot tying. Laparoscopic approaches for pelvic organ prolapse may be somewhat underused because of the greater technical difficulty associated with surgical dissection and laparoscopic suturing. The emergence of vaginal mesh kit procedures and tunneling techniques may thwart widespread adoption of laparoscopic sacral colpopexy. However, the greatest potential for laparoscopic advances and innovations may be in operations for prolapse. We believe that laparoscopic sacral colpopexy will gain popularity because abdominal sacral colpopexy remains the most proven and effective surgery for cure of severe apical prolapse. Pelvic floor surgeons in specialized centers strive to offer their patients pelvic reconstruction by laparoscopic route, many employing robotic assistance. More comparative studies and prospective clinical trials with long-term follow-up are warranted.

References 1. Nezhat CH, Nezhat F, Nezhat C: Laparoscopic sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 84:885, 1994. 2. DeLancey JO: Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 166:1717, 1992. 3. Whiteside JL, Barber MD, Walters MD, et al: Anatomy of ilioinguinal and iliohypogastric nerves in relation to trocar placement and low transverse incisions. Am J Obstet Gynecol 189:1574, 2003. 4. Lyons TL, Winer WK: Vaginal vault suspension. Endosc Surg 3:88, 1995. 5. Ross JW: Techniques of laparoscopic repair of total vault eversion after hysterectomy. J Am Assoc Gynecol Laparosc 4:173, 1997.

6. Ross JW: The role of laparoscopy in the treatment of severe vaginal vault prolapse: 6 to 10 year outcome [abstract]. J Am Assoc Gynecol Laparosc 11:S4, 2004. 7. Cosson M, Bogaert E, Narducci F, et al: Laparoscopic sacral colpopexy: Short-term results and complications in 83 patients. J Gynecol Obstet Biol Reprod (Paris) 29:746-750, 2000. 8. Gadonneix P, Ercoli A, Salet-Lizee D, et al: Laparoscopic sacrocolpopexy with two separate meshes along the anterior and posterior vaginal walls for multicompartment pelvic organ prolapse. J Am Assoc Gynecol Laparosc 11:29, 2004. 9. Paraiso MF, Walters MD, Rackley RR, et al: Laparoscopic and abdominal sacral colpopexies: A cohort study. Am J Obstet Gynecol 192:1752, 2005.

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OPEN ABDOMINAL SACRAL COLPOPEXY Chi Chiung Grace Chen and Marie Fidela R. Paraiso Pelvic organ prolapse is a condition that physicians are likely to encounter as women are living longer and more emphasis is placed on maintaining their physique and capacity for sexual activity. It has been estimated that more than 300,000 surgeries are being performed annually to correct pelvic organ prolapse at a cost of greater than $1 billion dollars.1 The number of women seeking attention for these disorders is projected to increase by 45% in the future.2 Management of pelvic organ prolapse depends on the goals and expectations of the patient and on the patient’s comorbidities. For example, women who have minimal symptoms or those with prolapse that does not extend beyond the hymen may benefit from pelvic floor exercises and behavioral modifications. Patients who have many comorbidities and are poor surgical candidates may benefit from vaginal pessaries. Women who do not desire preservation of sexual capacity may benefit from a less morbid obliterative procedure, such as colpocleisis. When contemplating the surgical correction of pelvic organ prolapse, the surgeon must also consider the existence of other support defects and any dysfunction of bladder or bowel. The surgeon must decide whether to approach these repairs abdominally, vaginally, or laparoscopically. In this chapter, we will focus on abdominal sacral colpopexy or suspension of the vagina to the sacral promontory, which is considered the gold standard procedure for correcting pelvic organ prolapse. Abdominal sacral colpopexy should be considered if the patient has severe vaginal apical prolapse and requires concomitant pelvic or anti-incontinence surgery by the abdominal route. Other indications include previous failed transvaginal colpopexy, foreshortened vagina, weakened pelvic floor, and chronic increases in abdominal pressure as a result of medical comorbidities (e.g., chronic obstructive pulmonary disease, chronic constipation) or occupation (e.g., heavy manual labor). Some pelvic surgeons also prefer abdominal sacral colpopexy for young patients with severe apical prolapse.

“GENERAL INTRAOPERATIVE PRODURES” TO “ANATOMY AND GENERAL INTRAOPERATIVE PRODURES” As the relevant abdominal and pelvic anatomic landmarks for open sacral colpopexy are the same as for laparoscopic sacral colpopexy, please refer to Chapter 72. Furthermore, some general intraoperative considerations are also the same and include placement of the patients in low lithotomy position under general anesthesia, prophylactic intravenous antibiotics before initiation of surgery, pneumatic compression stockings on the patients’ lower extremities, and placement of a 16-Fr three-way Foley catheter to continuous drainage with the irrigation port attached to sterile water or saline to facilitate retrograde filling of the 724

bladder to assist in dissection of the bladder off the vaginal apex during surgery.

SURGICAL TECHNIQUE General Intraoperative Procedures Specifically, the ideal stirrups for combined abdominovaginal cases are the Allen stirrups and Yellofins (Allen Medical Systems, Acton, MA), which have levers that can quickly convert the patient from low to high lithotomy position while preserving sterility of the field. A transverse or vertical laparotomy incision is made based on surgeon preference or concomitant procedures. For obese patients, a Maylard incision may be useful for improved exposure compared with a Pfannenstiel incision. The patient is placed in a Trendelenburg position. The small bowel is packed upward, and the sigmoid colon is packed to the left paracolic gutter. The Bookwalter retractor or Balfour retractor is placed to hold the sides of the incision open, giving exposure to the operative field. The Bookwalter retractor is ideal for obese patients. Sterile towels are placed below the lateral points of the Balfour retractor to decrease compression of the psoas muscle, safeguarding against femoral neuropathy. The sacral promontory is palpated, and the respective landmarks of the presacral space are delineated. The presacral peritoneum is tented and incised down to the level of the posterior cul-de-sac. The peritoneum may be retracted laterally by placing tagged 2-0 absorbable sutures, which can be tied together after the procedure is complete for closure of the peritoneum. Alternatively, a tunnel can be made in the right pararectal peritoneum from sacral promontory to the posterior cul-de-sac rather than completely incising the peritoneum. Kittners (i.e., endoscopic, blunt dissectors with radiopaque tips) are used to clear away the areolar tissue of the sacral promontory, delineating the anterior longitudinal ligament of the sacrum and the middle sacral vessels. Care must be taken to avoid trauma to the presacral vessels because these vessels retract easily, and life-threatening hemorrhage may ensue. If bleeding does occur, pressure, hemostatic clips, cautery, fibrin glue, and Gelfoam may be applied. If these measures are not successful, bone wax and sterile thumbtacks should be used. The presacral nerve should be preserved to decrease the risk of temporary postoperative urinary retention and constipation. Manipulators are placed in the vagina and rectum for delineation. For example, fiberglass obturators or endoanal anastomosis (EAA) sizers may be placed in the vagina and rectum for traction in opposite directions to delineate the rectovaginal space. The peritoneum is incised, rectovaginal space entered, and blunt dissection performed along the length of the posterior vaginal wall. In cases of abdominal sacral colpoperineopexy, this dissection is extended to the perineum. The bladder is filled with 300 mL in

Chapter 73 OPEN ABDOMINAL SACRAL COLPOPEXY

a retrograde fashion with a three-way Foley catheter hooked to irrigation to delineate the superior border of the bladder. The bladder peritoneum is incised, and the bladder is sharply dissected downward to the bladder base off the vagina. Palpation of the Foley catheter bulb aids in this dissection. Care should be taken not to cauterize the bladder and vagina to a great extent. Peritoneum should be preserved at the vaginal apex if possible to decrease risk of mesh erosion. After dissection of the bladder and preparation of the rectovaginal space, several rows of 1-0 nonabsorbable suture are stitched into the posterior vaginal muscularis. The most distally placed sutures are at the perineum during colpoperineopexy. The stitches should be placed at least halfway down the length of the posterior vagina for a sacral colpopexy. It is preferable to avoid through-and-through stitches into the vaginal epithelium. Each row of sutures should be placed 2 cm apart. The sutures are tagged, and after all sutures are placed, the ends of the suture are brought through the pores of a 4 × 15 cm polypropylene mesh. Polypropylene suture is easy to work with in this setting; when cut, it is easily passed through the pores. A longer piece of polypropylene mesh is required for the sacral colpoperineopexy. The sutures are then tied without strangulating the tissue to decrease erosion. If a Halban or Moschcowitz procedure is performed to obliterate the pouch of Douglas, these sutures can be placed before or after posterior mesh placement, but they should not be tied until the posterior mesh is placed. A 2-0 nonabsorbable suture is adequate for the culdoplasty procedures. Approximately two or three rows of 1-0 nonabsorbable suture are placed on the anterior vaginal wall. The ends of the sutures are then brought through the pores of a second 4 × 15 cm piece of polypropylene mesh and tied. The vaginal manipulator is used to place the vagina under no tension in the right pararectal space. The securing point of the mesh to the anterior longitudinal ligament at the S1 or S2 level is then marked. Two or three polypropylene sutures are placed transversely into the anterior longitudinal ligament. The suture ends are then brought through the pores of both leafs of mesh so that each leaf can be secured without tension. After the mesh is tied down and hemostasis ensured, the peritoneum is reapproximated over the mesh with a 3-0 absorbable suture. This is an important step to decrease risk of smallbowel obstruction below the mesh and mesh adhesion to viscera. Care must be taken not to kink the right ureter or the rectosigmoid. Sigmoid epiploica and bladder peritoneum may be used to cover the mesh. After all sutures are placed and tied, transurethral cystoscopy or suprapubic teloscopy is done to document ureteral patency and absence of sutures in the bladder. The incision is closed in the customary fashion after concomitant abdominal procedures are performed. Vaginal route procedures, if necessary, are completed after the abdominal procedures are performed (see Chapter 72 for photographs of the procedure). Postoperative care consists of intravenous analgesia for the first 12 to 24 hours after surgery. Oral pain medication, diet advancement, and ambulation are the rule on the first postoperative day. If an anti-incontinence procedure is concomitantly performed, voiding trials begin as soon as the patient is ambulatory. Preoperative teaching includes a discussion about postoperative analgesics, the need for a caretaker at home during the immediate recovery period, instruction in catheter care or intermittent selfcatheterization, and the goals to be reached before discharge. Patients are able to go home on postoperative day 2 or 3. Patients

are instructed to refrain from sexual intercourse and lifting objects heavier than 10 pounds for at least 8 weeks. Clinical Results The effectiveness of abdominal sacral colpopexy to correct pelvic organ prolapse can be examined from two perspectives: patient satisfaction or resolution of symptoms and restoration of normal anatomy (Table 73-1). The rate of patient satisfaction or resolution of symptoms in different studies range from 85% to 100%. Unfortunately, many of these studies do not include a description of the outcome tools used to assess satisfaction. In one study, a visual analogue score using a 10-point scale was used to determine that the overall patient satisfaction rate was 85% with a follow-up interval of 3 years.3 In another study with patient follow-up assessments ranging from 1 to 13 years (median, 4 years), 29% of patients experienced “no improvement,” 39% experienced “considerable improvement,” and 32% felt that they were “fully cured.”4 To examine anatomic success, common measures of vaginal support include the Baden-Walker grading scale and the Pelvic Organ Prolapse Quantification (POP-Q) system (see Chapter 54).5,6 In a review article by the Pelvic Floor Disorders Network, abdominal sacral colpopexy resulted in the cure of vaginal apex prolapse in 78% to 100% and the cure of prolapse in all vaginal segments in 58% to 100%, with follow-up ranging from 6 months to 3 years.7 The success rate of sacral colpopexy drops when it is defined as the absence of all vaginal prolapse regardless of apical, anterior, or posterior location. It is therefore important when looking at outcomes to consider recurrent or de novo anterior and posterior vaginal wall prolapse. For example, one study found that only 7% of patients after surgery experienced recurrent apical prolapse, whereas 30% developed new enterorectoceles.8 The investigators thought that this discrepancy reflected the inconsistent use of culdoplasty and consequently recommended that this procedure be routinely performed with all sacral colpopexies. Brubaker9 reported that 29% (19 of 65) of patients with a follow-up of 3 months had new or persistent anterior prolapse despite having undergone sacral colpopexy with a posterior graft attachment and a separate anterior compartment repair. However, only two patients were symptomatic. Sacral colpopexy is an effective method to correct apical prolapse, but its effects on other compartment defects and the optimal management of those defects remain unclear. The need for reoperation to correct persistent, recurrent, or de novo pelvic organ prolapse may depend on factors other than surgical techniques. These factors include vaginal tissue quality, coexisting defects, and medical conditions such as chronic obstructive pulmonary disease. In one large data series, it was found that one of three patients who underwent a procedure for urinary incontinence or prolapse had to undergo reoperation within 4 years.10 The Pelvic Floor Disorders Network reported the median reoperation rate to be 4.4%, with follow-up intervals between 6 months and 3 years.7 The reoperations predominately were for anterior or posterior prolapse and not for apical defects. Patients after abdominal sacral colpopexy for pelvic organ prolapse are also at risk for persistent or de novo stress urinary incontinence. The Pelvic Floor Disorders Network reported the rate of operations for stress incontinence to be 4.9% after sacral colpopexy.7

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Table 73-1 Clinical Outcomes of Abdominal Sacral Colpopexy Study

No. of Patients

Follow-up (mo)

Success Rate (%)

Snyder and Krantz, 1991

147

43

93

Sullivan et al, 2001 Culligan et al, 2002 Brizzolara and Pillai-Allen, 2003 Timmons et al, 1992 Lecuru et al, 1994 De Vries et al, 1995

236 245 124

64 61 36

100 85 98

163 203 101

33 33 48

99 87-100 32

Ocelli et al, 1999 Patsner, 1999 Lindeque and Nel, 2002

271 175 262

66 ≥12 ≥16

98 97 99

Criteria for Success No recurrence of symptoms for at least 6 months No recurrence of vaginal or rectal prolapse Any POPQ point < stage II No recurrent vault prolapse Good vaginal vault support Anatomically good results Fully cured (patient satisfaction based on questionnaire) Cured for prolapse No mesh failures No vaginal vault prolapse

POPQ, Pelvic Organ Prolapse Quantification system.

It is also pertinent to compare the effectiveness of open abdominal sacral colpopexy with vaginal procedures to correct pelvic organ prolapse. In a retrospective case series of 80 abdominal sacral colpopexies compared with 130 attempted vaginal sacrospinous vault suspensions (five were abandoned because of technical difficulties), the incidence of recurrent prolapse was not statistically different (1.3% and 2.4%, respectively) (Table 73-2).11 The complication rates were similar in both groups, except that the mean estimated blood loss was higher in the abdominal sacral colpopexy group compared with the vaginal sacrospinous vault suspension group (745 versus 567 mL, P = .04). Moreover, in the sacral colpopexy group, one patient developed stress incontinence; this complication was not seen after sacrospinous suspension. Concomitant incontinence and other gynecologic procedures were performed with various frequencies in the different groups. The results must be interpreted in light of these inconsistencies. Three randomized trials compared open abdominal sacral colpopexy and vaginal procedures for pelvic organ prolapse and had different results (Table 73-3). Benson and colleagues12 and Lo and Wang found that sacral colpopexy was more effective at correcting pelvic organ prolapse than sacrospinous suspension. However, Maher and coworkers13 found that the abdominal and vaginal approaches were equally efficacious at correcting pelvic organ prolapse. It is difficult to compare efficacy in the different studies because most of these operations were performed simultaneously with various combinations of different incontinence and gynecologic procedures. There are also no consistencies between the different studies with regard to a propensity for complications with the abdominal or vaginal approach. COMPLICATIONS Intraoperative complications of abdominal sacral colpopexies include those associated with any gynecologic laparotomies, such as enterotomy, proctotomy, cystotomy, and ureteral injury. The Pelvic Floor Disorders Network found that enterotomy or proctotomy occurred in 1.6%, cystotomy in 3.1%, and ureteral injury in 1.0% of operations. Although uncommon, one of the most morbid complications associated with this procedure is hemorrhage from the presacral

vessels. Hemostasis is especially difficult to achieve in this area because the vessels form a complex interlacing network above and underneath the sacral periosteum. Once lacerated, these vessels retract, making it even more impossible to isolate single vessels. The presacral vessels often form communications with adjoining pelvic vessels, especially the left common iliac vein, resulting in even more extensive hemorrhage if they are damaged. Although the incidence of presacral vascular injury in the literature has not been specifically addressed, the requirement overall rate of hemorrhage with or without transfusion is 4.4%. Management of this complication include packing the presacral space, which is often only a temporizing measure and has the added possibility of lacerating more of these delicate vessels as the pack is removed. Other measures include using electrocautery, sutures, and metallic vascular clips. These procedures are especially successful if the lacerations are small or individual vessels that can be visualized. If these strategies are not successful, other interventions include using bone wax and orthopedic bone thumbtacks.14 To avoid this complication, some surgeons recommend minimal dissection of the presacral space by attaching the graft to the ligament,15 and others advocate careful, extensive dissection of this space to prevent inadvertent injury to unseen vessels. Postoperative complications include urinary tract infection, ileus and small bowel obstruction, deep venous thrombus or pulmonary embolus, extrafascial wound problems, and granulation tissue in the vagina. Urinary tract infection was the most commonly reported complication in the literature, occurring in 2.5% to 25.9% of patients. Postoperative ileus occurred in 3.6% of cases, and reoperation for small bowel obstruction occurred in 1.1% of operations. Deep venous thrombus or pulmonary embolus was reported in 3.3% of cases. Extrafascial wound complications such as hematoma, infection, or superficial separation occurred in 4.6% of operations, and 5.0% of procedures resulted in incisional hernias requiring subsequent repairs. Other uncommon complications reported in the literature include femoral, obturator and sciatic neuropathies, fascial dehiscence, vertebral osteomyelitis, and gluteal necrotizing myofascitis. One of the most discussed but uncommon postoperative complication is mesh erosion. In one retrospective series of 155 abdominal sacral colpopexies using Mersilene mesh (Johnson & Johnson) with a median follow-up of 6.5 months (range, 1 to 87

Chapter 73 OPEN ABDOMINAL SACRAL COLPOPEXY

Table 73-2 Trials of Abdominal Sacral Colpopexy and Vaginal Procedures for Pelvic Organ Prolapse No. Patients

Follow-up (months)

Success Rate (%)

Criteria for Success

125

47

99

No recurrence vault prolapse

Sacrospinous vault suspension Sacral colpopexy and paravaginal repair

80

26

98

38

30

58

Sacrospinous vault suspension and paravaginal repair Sacral colpopexy

42

30

29

47

24

76% objective 94% subjective

48

24

69% objective 91% subjective

Study

Procedure

Hardiman and Drutz, 1996

Sacral colpopexy

Benson et al, 1996

Maher et al, 2004

Sacrospinous vault suspension

Asymptomatic and vaginal apex support above levator plate

Objective: no prolapse beyond the halfway point Subjective: no symptoms

Data from Nygaard IE, McCreery R, Brubaker L, et al: Abdominal sacrocolpopexy: A comprehensive review. Am J Obstet Gynecol 104:805-823, 2004.

Table 73-3 Erosion Rates with Different Mesh Materials Mesh Material

Manufacture

Polypropylene

Prolene Ethicon Endo-Surgery, Inc. Mersilene Johnson & Johnson W.L. Gore & Associates, Inc. E.I. DuPont de Nemours & Co. Marlex Phillips Sumika Polypropylene Co.

Polyethylene terephthalate Gore-Tex Teflon Polyethylene

Reported Rates of Erosion 0.5% 3.1% 3.4% 5.5% 5.0%

Data from Nygaard IE, McCreery R, Brubaker L, et al: Abdominal sacrocolpopexy: A comprehensive review. Am J Obstet Gynecol 104:805-823, 2004.

months), the erosion rate was 3.2%, with a median time to the appearance of erosion of 15.6 months (range, 2 to 33 months).16 Although the true incidence of this complication is unknown because most reported studies have short follow-up intervals, the Pelvic Floor Disorders Network found that the reported rate to be 3.4% at 6 months to 3 years.7 Moreover, the reported rate of reoperations for mesh-related complications, including

erosion and infection, is 3.0%. Although mesh erosion has been reported with all available synthetic graft materials (see Table 73-3), there are no published randomized trials comparing the erosion rates of these different graft materials. Not surprisingly, case series involving nonsynthetic grafts such as autologous, cadaveric fascia or dura mater reported no cases of erosion.

References 1. Subak LL, Waetjen LE, van den Eeden S, et al: Cost of pelvic organ prolapse surgery in the United States. Obstet Gynecol 98:646-651, 2001. 2. Luber KM, Boero S, Choe JY: The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 184:1496-1501, 2001. 3. Virtanen H, Hirvonen T, Makinen J, Kiilholma P: Outcome of thirty patients who underwent repair of posthysterectomy prolapse of the vaginal vault with abdominal sacral colpopexy. J Am Coll Surg 178:283-287, 1994.

4. de Vries MJ, van Dessel TH, Drogendijk AC, et al: Short-term results and long-term patients’ appraisal of abdominal colposacropexy for treatment of genital and vaginal vault prolapse. Eur J Obstet Gynecol Reprod Biol 59:35-38, 1995. 5. Baden WF, Walker TA: Genesis of the vaginal profile: a correlated classification of vaginal relaxation. Clin Obstet Gynecol 15:10481054, 1972. 6. Bump RC, Mattiasson A, Bø K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996.

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7. Nygaard IE, McCreery R, Brubaker L, et al: Abdominal sacrocolpopexy: A comprehensive review. Am J Obstet Gynecol 104:805-823, 2004. 8. Geomini PM, Brolmann HA, van Binsbergen NJ, Mol BW: Vaginal vault suspension by abdominal sacral colpopexy for prolapse: A follow-up study of 40 patients. Eur J Obstet Gynecol Reprod Biol 94:234-238, 2001. 9. Brubaker L: Sacrocolpopexy and the anterior compartment: support and function. Am J Obstet Gynecol 173:1690-1696, 1995. 10. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-506, 1997. 11. Hardiman PJ, Drutz HP: Gynecology: sacrospinous vault suspension and abdominal colposacropexy: success rates and complications. Am J Obstet Gynecol 175:612-616, 1996.

12. Benson JT, Lucente V, McClellan E: Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: A prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 175:1418-1422, 1996. 13. Maher CF, Qatawneh AM, Dwyer PL, et al: Abdominal sacrocolpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 190:20-26, 2004. 14. Lane FE: Modified technique of sacral colpopexy. Am J Obstet Gynecol 142:933, 1982. 15. Sanz LE, Verosko J: Modification of the abdominal sacrocolpopexy using a suture anchor system. J Reprod Med 48:496-500, 2003. 16. Visco AG, Weidner AC, Barber MD, et al: Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 184:297-302,

Part C POSTERIOR VAGINAL WALL Chapter 74

POSTERIOR WALL PROLAPSE: SEGMENTAL DEFECT REPAIR Tristi W. Muir Pelvic organ prolapse is common in women. The lifetime risk for undergoing an operation for prolapse or urinary incontinence is estimated to be 11.1%.1 The posterior wall of the vagina primarily provides support over the anterior rectum and posterior cul-desac. Prolapse of the posterior vaginal wall may result from the presence of an enterocele, sigmoidocele, rectocele, or a combination of these entities. This chapter focuses on the herniation of the anterior rectum into the posterior vaginal wall as the cause of the prolapse. A variety of surgical procedures are available for the management of posterior vaginal wall prolapse, including posterior colporrhaphy, site-specific defect repair, posterior fascial replacement, transanal or transperineal repair, and a sacral colpoperineopexy Posterior colporrhaphy and site-specific defect repair for surgical repair of posterior wall prolapse are discussed. ANATOMY AND PATHOPHYSIOLOGY The support of the vagina is provided by an interaction of the bony pelvis, pelvic floor musculature (i.e., levator ani and coccygeus muscles), and the connective tissue supports. The vagina is a fibromuscular tube, which must maintain its position but have enough mobility to accommodate urinary, sexual, and defecatory functions. This vaginal tube also must distend to allow for childbirth. The pelvic floor muscles are composed of two functional components, one horizontal and the other vertical. The coccygeus muscle and horizontal portion of the levator ani muscles provide a backstop of support of the abdominal contents. The urethra vagina and rectum exit the abdominal cavity through the levator hiatus. A muscular sling that is chronically contracted to close this hiatus but capable of relaxing open to allow for urinary, defecatory, and sexual function is provided by the puborectalis portion of the levator ani. A continually contracted levator ani muscle closes the levator hiatus and angulates the rectal and vaginal tubes toward the pubic symphysis. Anatomically, there are no native fibers of the levator ani muscles traversing the rectovaginal space. The connective tissue supports of the posterior vaginal wall are in continuity from the apical support of the vaginal vault (originating at the sacrum) to the perineal body. The apical portion of the anterior and posterior vaginal wall is provided by the suspensory support of the cardinal-uterosacral ligaments. The cardinal-uterosacral ligaments provide a mesentery of

support directed toward the sacrum (S2 to S4) and pelvic side wall. The broad posterior fan of support directs the proximal (apical) portion of the vaginal axis posteriorly, and the contracted levator ani muscles direct the midportion of the vagina and rectum anteriorly toward the pubic symphysis. This orients the proximal vagina and rectum in a horizontal plane, supported over the pelvic floor muscles rather than a vertical orientation through the levator hiatus.2 The connective tissue attachments of the midsection of the posterior vaginal wall are directed laterally and cranially to the levator ani muscular side wall.3 The proximal halves of the posterior and anterior vaginal wall are attached to the same condensation of endopelvic fascia on the levator ani muscles, the arcus tendineus fasciae pelvis. The distal half of the posterior vaginal wall has a separate, caudal attachment to the pelvic side wall, the arcus tendineus fasciae rectovaginalis.4 These separate lines of attachment of the anterior and posterior vaginal wall give the distal portion of the vagina an H shape (Fig. 74-1). The perineal body is the central connection between the two sides of the perineal membrane, which originates bilaterally on the medial portion of the ischiopubic rami. Within the perineal body lie the bulbocavernosus muscle, superficial transverse perinei muscle, and the external anal sphincter and the rectovaginal septum, or Denonvilliers’ fascia. Extending from the posterior cul-de-sac to the perineal body, the rectovaginal septum is the fused, endopelvic fascial remnant of the embryonic posterior cul-de-sac.5,6 The role of the perineal body is to resist caudally directed force provided by the rectum and provide a physical barrier between the vagina and rectum. The perineal body’s mobility is limited by an intact connective tissue support within the vagina from the sacrum to the perineal body and an intact perineal membrane from ischiopubic ramus to ischiopubic ramus.3 An increase in intra-abdominal pressure, such as a Valsalva maneuver, flattens the horizontally oriented upper vagina against the rectum and pelvic floor musculature. In the distal vagina, a Valsalva maneuver causes an equal increase in pressure against the anterior and posterior vaginal walls. No net strain is placed on the connective tissue support of the vaginal wall (Fig. 74-2). However, if the levator hiatus is widened or not closed, two things may happen. First, the vagina may lose the horizontal orientation of its axis. As the vagina becomes more vertically oriented, intra-abdominal pressure pushes the pelvic organs through the levator hiatus and toward the genital hiatus. The 729

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Figure 74-1 Lateral attachment of the anterior and posterior vaginal walls. The lateral support of the anterior wall fuses at the arcus tendineus fasciae pelvis (ATFP), which extends from the back of the pubic bone to the ischial spine (IS). The distal lateral connection of the posterior vaginal wall is more posterior, the arcus tendineus fasciae rectovaginalis (ATFR). The proximal connection of the posterior vaginal wall is the ATFP. (Courtesy of the Cleveland Clinic Foundation.)

Figure 74-3 Rectocele. In a woman with an open vagina, the pressure within the rectum is met by atmospheric pressure. The anterior vaginal wall does not provide equilibrating force, and there is stress (arrow) placed on the posterior vaginal wall’s connective tissue. This may lead to rectocele formation. (Courtesy of the Cleveland Clinic Foundation.)

the posterior vaginal wall, or it may uncover damage done by a prior event, such as childbirth. Anything that damages the pelvic floor musculature, its innervation, or the connective tissue of the posterior vaginal wall may result in prolapse. Damage to the levator ani muscles or innervation may be traumatic (usually related to childbirth) or be a result of neuromuscular diseases or aging. Connective tissue may be damaged through trauma (i.e., childbirth or constant straining with defecatory dysfunction), congenital disease, or aging. A combination of these factors is the likely recipe for the manifestation of prolapse. SIGNS AND SYMPTOMS

Figure 74-2 Equalization of pressure in the anterior and posterior vaginal walls (arrows). The pressure on the anterior vaginal wall and the posterior vaginal wall (PVW) is equal, and no strain is placed on the connective tissue supports of the vaginal walls. The perineal body (PB) is intact and resists the downward intrarectal force. ARW, anterior rectal wall. (Courtesy of the Cleveland Clinic Foundation.)

anterior and posterior vaginal walls then do not lie in apposition. An increase in intra-abdominal or intrarectal pressure, such as that obtained with straining for a bowel movement, is not met with an equal measure of pressure of the anterior vaginal wall. Instead, the posterior vaginal wall pressure meets the atmospheric pressure present in the open vagina (Fig. 74-3). In both situations, an increase in abdominal pressure places a net force on the connective tissue supports of the posterior vaginal wall. This force on the connective tissue supports may attenuate or break

Many women with posterior wall prolapse are asymptomatic. Women who have prolapse that protrudes beyond the hymenal ring are more likely to be symptomatic.7 This bulge may be associated with vaginal pressure or pain, which worsens as the day progresses or with abdominal straining. This bulge may affect urinary, sexual, and defecatory functions. As the posterior vaginal wall balloons upward toward the anterior vaginal wall and outward toward the genital hiatus or beyond, urinary function may be altered. Inside the vagina, the distended posterior vaginal wall may provide additional support of the urethra and mask or decrease the severity of urinary incontinence. Urodynamic investigations, with and without reduction of the posterior wall prolapse, have demonstrated that when the posterior wall prolapse is retracted, there are significant decreases in the maximum urethral closure pressure and functional urethral length and an increase in leak volumes.8 Beyond the genital hiatus, posterior wall prolapse may partially obstruct the external urethral meatus, altering the stream of urine. Sexual function is a complicated issue involving both partners’ psychological and physical well-being. Prolapse protruding beyond the genital hiatus may lead to an altered body image and self-esteem. This may be worsened by fear of urinary or anal incontinence. Prolapse may be significant enough to require

Chapter 74 POSTERIOR WALL PROLAPSE

reduction before even attempting to have vaginal intercourse. A widened genital hiatus may decrease sensation for both partners during intercourse. The woman’s partner may also be concerned about causing pain or discomfort or about contributing to worsening of the prolapse. Defecatory dysfunction and pelvic organ prolapse often coexist in women. A ballooning of the anterior rectum into the posterior vaginal wall or perineal body may alter the process of defecation. Stool may be trapped in the distended rectal pouch, leading to incomplete rectal emptying. Women may employ digitally placed pressure in the vagina, on the perineal body, or within the rectum to evacuate the stool. Some woman may perceive this as constipation (i.e., straining to have a bowel movement or an unproductive urge to defecate). However, constipation is often unrelated to a rectocele, such as that related to irritable bowel syndrome, slow-transit colon, or secondary constipation related to medications or neurologic disorders. Determining if the woman’s defecatory dysfunction is related to her posterior prolapse may be difficult to discern. Weber and colleagues9 examined bowel function and severity of posterior wall prolapse and found no correlation. If a woman’s sole defecatory complaint is incomplete rectal emptying that resolves with vaginal splinting, she is likely to have functional improvement after surgical correction. A thorough history, including direct questions about fecal incontinence, should be obtained. Fecal incontinence may also coexist with posterior vaginal wall prolapse. There is an association with a rectocele, which protrudes beyond the hymen and anal incontinence.10 A descending perineum may provide stretch on the pudendal nerve, which innervates the external anal sphincter. This stretch injury may lead to denervation of the external anal sphincter and fecal incontinence. Prior obstetric trauma that injures the external anal sphincter may also result in fecal incontinence. The goal of the physical examination is to recreate the woman’s symptoms. A validated measure of pelvic organ prolapse is the Pelvic Organ Prolapse Quantification (POPQ) system.11 The POPQ examination includes measures of the uterus or vaginal cuff, posterior cul-de-sac, anterior and posterior vaginal walls, perineal body, and genital hiatus at maximal strain. Total vaginal length is assessed at rest. The posterior vaginal wall may be visualized with the posterior blade of a bivalve speculum or with a Sims speculum with the woman in the dorsal lithotomy or semirecumbent position. In most women, there is excellent correlation between the dorsal lithotomy and standing positions.12 Confirmation of the recreation of the woman’s maximal protrusion can be facilitated with a hand-held mirror. If a woman describes prolapse that is more significant than that observed in the supine or sitting positions, a standing examination may be employed. A rectovaginal examination should accompany the physical examination. The tone of the external anal sphincter at rest and with squeeze may be assessed. With digital pressure directed toward the anterior rectal wall, areas of weak support and perineal body mobility can be evaluated. The clinical examination for identifying site-specific defects through a rectovaginal examination was found to be inaccurate when compared with site-specific defects found intraoperatively.13 However, the rectovaginal examination may help to differentiate an enterocele from a rectocele. Palpation of loops of bowel between the rectum and vagina is consistent with an enterocele. This may be more evident in the standing position or with a Valsalva maneuver. Digital pressure placed on the posterior wall of the vagina directed toward the rectum may uncover rectal prolapse.

A focused neurologic examination to evaluate S2 to S4 should accompany the physical examination. Sensation may be determined by asking the patient to discriminate between sharp and dull sensations. Pelvic floor strength may be determined with the examiner’s two fingers in the vagina and asking the patient to contract the pelvic floor (i.e., perform a Kegel exercise). Strength and duration of this contraction can be determined. Tenderness or spasm of the levator ani muscles may be uncovered on clinical examination. If a woman is unable to relax the levator ani muscles, anismus may be the cause of her obstructed defecation. Anismus, or paradoxical puborectalis contraction, often responds to biofeedback or botulinum toxin.14,15 Reflex testing of the bulbocavernosus reflex and anal wink may be performed. Ancillary tests may be considered in the evaluation. Urodynamics with prolapse reduction may be indicated in a woman with complaints of urinary incontinence or for evaluation of potential urinary incontinence. Anorectal or colonic transit studies may help differentiate the potential causes of defecatory dysfunction. If the woman’s primary complaint is related to her defecatory dysfunction rather than the bulge of the posterior vaginal wall, further defecatory testing should be performed before surgery. Incomplete emptying of the rectum may be caused by a paradoxical puborectalis contraction or slow-transit colon. Endoanal ultrasonography is useful in a woman with fecal incontinence to determine whether there is an anatomic defect in the external and internal anal sphincters. Imaging studies such as defecography and magnetic resonance imaging are used uncommonly for further elucidation of the anatomy of the prolapse. TECHNIQUE The vaginal epithelium is opened with a transverse incision at the posterior fourchette. The posterior vaginal epithelium is then opened in the midline to a level proximal to the bulge and dissected away from the underlying fibromuscularis. The dissection is extended laterally to the endopelvic fascial attachment of the posterior vaginal wall to the arcus tendineus fasciae pelvis and arcus tendineus fasciae rectovaginalis (Fig. 74-4). Posterior Colporrhaphy The underlying fibromuscularis of the posterior vaginal wall is exposed. A posterior colporrhaphy uses interrupted sutures to reduce the redundancy of the posterior fibromuscularis (Fig. 74-5). A delayed-absorbable 2-0 suture is used. A vertically oriented suture may reduce the length and width of the posterior vaginal wall. Care should be taken to maintain adequate vaginal caliber (i.e., approximately 3 fingerbreadths) and to avoid ridging of the posterior vaginal wall. If a suture constricts the vagina or creates a ridge, the suture should be removed and replaced. The vaginal epithelium is trimmed and closed with a 2-0 absorbable suture. It is important to avoid over-trimming the vaginal epithelium, particularly in a postmenopausal woman with vaginal atrophy or a woman with prior vaginal surgery and a constricted vagina. A perineorrhaphy may be performed to correct perineal body defects. A plication of the levator muscles in the midline has been performed in conjunction with a posterior colporrhaphy in some patients. This may be indicated in a woman with a significantly widened levator hiatus. This is not the anatomic position of the

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Figure 74-4 Dissection of the posterior vaginal wall epithelium. The underlying fibromuscularis of the posterior vaginal wall is exposed, and the perineal body is opened in the midline. (Courtesy of the Cleveland Clinic Foundation.)

Figure 74-5 Posterior colporrhaphy. A midline plication of the fibromuscularis of the posterior vaginal wall is performed with interrupted sutures. (Courtesy of the Cleveland Clinic Foundation.)

levator ani muscles, but it may further narrow the vaginal caliber. A levator plication has been suggested to be a contributor to postoperative dyspareunia in women undergoing this procedure.16 A vaginal pack and Foley catheter are placed for 2 to 24 hours postoperatively. Voiding trials should be performed postoperatively to ensure that the patient is able to void adequately. Site-Specific Defect Repair After dissection of the posterior vaginal epithelium off the underlying fibromuscularis, the fibromuscularis (i.e., rectovaginal fascia) is carefully inspected to identify breaks. Irrigation and a digital rectal examination, placing upward pressure in the anterior rectal wall, may facilitate identification of the defects in the fibromuscularis (Fig. 74-6). Defects of the posterior vaginal wall may occur as isolated defects in the lateral, distal, midline, and superior portions of the wall or as a combination of defects (Fig. 74-7). The identified breaks are individually isolated and repaired (Fig. 74-8). Delayed-absorbable or nonabsorbable 1-0 or 2-0 suture may be used. If the fibromuscularis of the posterior wall has lost apical attachment, the fibromuscularis should be reattached to the apical support (through reattachment to a wellsupported vaginal apex or attachment to the concurrent apical support procedure, such as a sacrospinous or uterosacral vaginal vault suspension). Apical lateral support may be obtained with a unilateral or bilateral iliococcygeal suspension of the fibromuscularis. The suture is placed through the iliococcygeus fascia on

Figure 74-6 Identification of site-specific defects. After dissection of the posterior vaginal wall epithelium, a rectovaginal examination is helpful in the identification of defects in the fibromuscularis of the posterior vaginal wall. (Courtesy of the Cleveland Clinic Foundation.)

Chapter 74 POSTERIOR WALL PROLAPSE

Figure 74-7 Location of site-specific defects in the fibromuscularis of the posterior vaginal wall. Transverse defects (T) may be apical or distal. Lateral defects (L) may occur as the fibromuscularis separates from its lateral attachment. Midline defects (M) may also occur. Often, a combination of these defects is found. (Courtesy of the Cleveland Clinic Foundation.)

Figure 74-9 Perineorrhaphy. After the completion of the posterior repair, the perineal body is reconstructed by plicating the bulbocavernosus muscles and the transverse perinei muscles. (Courtesy of the Cleveland Clinic Foundation.)

Perineorrhaphy

Figure 74-8 Repair of a left lateral defect with interrupted sutures. (Courtesy of the Cleveland Clinic Foundation.)

the lateral side wall (distal to the ischial spine) and then through the ipsilateral apical portion of fibromuscularis. If a distal defect is present, such as a separation of the fibromuscularis from the perineal body, the defect is repaired with absorbable suture in an attempt to reduce the incidence of postoperative dyspareunia. The vaginal epithelium is closed without significant trimming. Perineal body defects are also repaired with interrupted sutures. A levator plication is not performed. A vaginal pack and Foley catheter are placed for 2 to 24 hours postoperatively. Voiding trials should be performed postoperatively to ensure that the patient is able to void adequately.

The perineal body should be in continuity with the posterior vaginal wall repair. The perineal body may be opened with a midline, vertical incision. In a woman with a very short perineal body, a transverse or curvilinear incision may be made to expose the perineal body. The bulbocavernosus muscles are identified bilaterally and plicated. Similarly, the superficial transverse perinei muscles are plicated (Fig. 74-9). The plicated bulbocavernosus muscles may be reattached to the repaired rectovaginal fibromuscularis with an interrupted suture. With these sutures, the perineal membrane is reestablished, and the perineal body is in continuity with the support of the vagina. SURGICAL OUTCOMES The goals of pelvic reconstructive surgery are to correct the anatomic defect, improve function, and avoid complications. The difficulty in achieving these goals lies in function. The woman’s defecatory dysfunction may coexist with her prolapse rather than

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Table 74-1 Surgical Outcomes for Posterior Colporrhaphy

Study

No. of Patients at Follow-up

Mean Follow-up (mo)

Anatomic Cure Rate (%)

Preop (%)

177 22 25 171 24 14 38 183

≥24 ≥24 12 42.5 9 8 12.5 12

94 77 80 76 100 71 87 96

20 48 27 68 100 100 30¶

Francis and Jeffcoate, 1961 Arnold et al, (1990)* Mellgren et al, 1995 Kahn and Stanton, 1997 Lopez et al, 2002† Sloots et al, 2003 Maher et al, 2004 Abramov et al, 2005‡

Incomplete Evacuation Postop (%)

0 38 36 29 16 34¶

Sexual Dysfunction Preop (%)

Postop (%)

7

50 23 19 27 23 29§ 5 17

6 18 18 21 37 8

*Cure defined as % satisfied. † Anatomic cure rate of 100% on clinical examination; 84% cure rate by defecography. ‡ Cure defined as no prolapse beyond the hymenal ring. § Includes one sexually inactive woman with postoperative de novo pelvic pain. ¶ Defined as constipation.

Table 74-2 Surgical Outcomes for Site-Specific Defect Repair

Study Cundiff et al, 1998 Glavind et al, 2000 Kenton et al, 1999 Porter et al, 1999 Singh et al, 2003* Abramov et al, 2005†

Incomplete Evacuation or Splinting

No. of Patients at Follow-up

Mean Follow-up (mo)

Anatomic Cure Rate (%)

Preop (%)

Postop (%)

Preop (%)

Postop (%)

43 65 46 89 33 124

12 3 12 18 18 12

82 100 77 82 92 89

39 40 30 24 57 33‡

25 5 15 14 27 37‡

29 12 28 67 31 8

19 6 2 46 24 16

Sexual Dysfunction

*Cure defined as resolution of symptom of “feeling of vaginal protrusion.” † Cure defined as no prolapse beyond the hymenal ring. ‡ Defined as constipation.

be a symptom of her prolapse. In this case, anatomic correction will be unlikely to improve her function. Surgical correction may interfere with defecatory and sexual functions. Historically, efficacy has been related to anatomic cure, but evaluating functional outcomes is equally important. The posterior colporrhaphy was introduced in the 19th century. The goals of this procedure were to narrow the vaginal tube and genital hiatus and to create a shelf of support. It has remained a commonly performed surgical procedure for posterior wall prolapse. The traditional posterior colporrhaphy has an anatomic cure rate of 71% to 100% (Table 74-1).16-23 The site-specific defect repair approach to rectocele repair relies on theory advocated by A. Cullen Richardson, that the herniation of the rectum into the vagina is the result of identifiable defects in the fibromuscularis (rectovaginal fascia) or its attachment to the pelvic side wall.24 The anatomic cure rate of the site-specific posterior repair is 77% to 100% (Table 74-2).23,25-29 The primary reason that this method of repair of posterior wall prolapse has been embraced is that it more often avoids the risk of postoperative dyspareunia. With the exception of the retrospective review by Abramov and colleagues23 of women undergoing a site-specific posterior repair, there was no change or a

decrease in dyspareunia in the series involving site-specific posterior repairs (see Table 74-2).25-29 Abramov and colleagues23 were the first to compare anatomic and functional outcomes in women who underwent a site-specific posterior repair (undertaken in women with specific defects identified in the fibromuscularis intraoperatively) with those who had undergone a posterior colporrhaphy without a levator plication (undertaken in women without identifiable breaks in the fibromuscularis) during the same time period.23 Objective and subjective anatomic outcomes were better for the women undergoing a posterior colporrhaphy compared with those undergoing a site-specific repair. Functional outcomes were similar for the two groups. Improvement in defecation has also been described with this method of repair (see Table 74-2).23,25-29 Cundiff and coworkers25 did not perform a perineorrhaphy in women who underwent a site-specific posterior repair. However, the perineal body was stabilized through reestablishment of the continuity of connective tissue support within the posterior vaginal wall from the sacrum to the perineal body. The stabilization of the perineal body was reflected in a significant reduction in the size of the genital hiatus despite not having performed a perineorrhaphy (4.8 cm preoperatively versus 2.5 cm postoperatively, P < .0001).25

Chapter 74 POSTERIOR WALL PROLAPSE

COMPLICATIONS Short-term complications associated with a posterior colporrhaphy or site-specific posterior repair include pain, constipation, and temporary urinary retention. Hematoma, infection, and inclusion cyst formation occasionally occur with all vaginal operations. Injury to the rectum with subsequent development of a rectovaginal or rectoperitoneal fistula is uncommon. Recurrent prolapse and de novo defecatory complaints may occur. Postoperative development of dyspareunia is widely reported after a posterior colporrhaphy (see Table 74-1).16-23 This complication paved the road of acceptance of the site-specific posterior repair. Postoperative sexual dysfunction related to prolapse repair, primarily dyspareunia, has been reported for decades. Francis and Jeffcoate17 reported that 70 (50%) of 140 women who had undergone an anterior and posterior colporrhaphy with perineorrhaphy said they had apareunia or dyspareunia. Most (43 of 70)of the women with postoperative apareunia or dyspareunia were found to have a significantly narrowed postoperative vagina that would admit only one finger. Kahn and Stanton16 found an increase in the number of women with dyspareunia from 18% (preoperative evaluation) to 27% (postoperative evaluation) after an anterior and posterior colpoperineorrhaphy. The investigators routinely plicated the levator ani muscles and proposed that pressure atrophy of the levator ani and resultant scar formation contributed to the development of postoperative dyspareunia. Haase and Skibsted30 reported that 5 (21%) of 24 women who underwent a prolapse operation that included a posterior colpoperineorrhaphy experienced worsening or de novo dyspareunia. The appeal of the site-specific posterior repair is that ridging or excessive narrowing of the posterior vaginal wall can be avoided, which decreases the likelihood of the postoperative development of dyspareunia. Although most studies of women undergoing a posterior colporrhaphy or site-specific defect repair have found an improvement in rectal emptying (see Tables 74-1 and 74-2), rectocele repair has been associated with postoperative fecal incontinence. Kahn and Stanton16 reported that de novo fecal

incontinence occurred in 14 (8%) of 171 women after a posterior colporrhaphy. A strong association was found between fecal incontinence and a history of more than one posterior colporrhaphy.16 CONCLUSIONS The posterior vaginal wall is composed of interactions among the bony pelvis, pelvic floor muscles, and connective tissue supports. Alterations or injuries to these support units may lead to prolapse. Posterior vaginal wall prolapse may be asymptomatic and require no treatment. Women with symptoms of vaginal protrusion, pressure or pain, defecatory dysfunction (specifically outlet obstruction leading to incomplete evacuation or need to splint to have a bowel movement), or sexual dysfunction may desire surgical management. Surgical options commonly employed include posterior colporrhaphy (with and without a levator plication) and site-specific defect repair. Both of these posterior vaginal wall repairs may be performed with or without the addition of a perineal body repair (i.e., perineorrhaphy). Posterior colporrhaphy is effective at reducing the vaginal mass of the rectocele, but some studies have associated this anatomic improvement with an increased incidence of de novo dyspareunia and fecal incontinence. Levator plication may increase the risk of dyspareunia. It is essential to maintain adequate vaginal caliber and to avoid ridging of the vaginal tube when performing a posterior colporrhaphy. Sitespecific defect repair is also effective at correcting prolapse, although Abramov and colleagues23 suggest that it is not as anatomically successful as the posterior colporrhaphy. The vaginal caliber usually is maintained with a site-specific defect approach, and the risk of postoperative de novo dyspareunia is lower than with a posterior colporrhaphy. Augmentation of prolapse repair surgery has been performed using biologic and synthetic grafts. Prospective, randomized trials are needed to compare techniques and their outcomes, including anatomic and functional efficacy and complication rates.

References 1. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-506, 1997. 2. Nichols DH: Posterior colporrhaphy and perineorrhaphy: Separate and distinct operations. Am J Obstet Gynecol 164:714-721, 1991. 3. DeLancey JOL: Structural anatomy of the posterior pelvic compartment as it relates to rectocele. Am J Obstet Gynecol 180:815-823, 1999. 4. Leffler KS, Thompson JR, Cundiff GW, et al: Attachment of the rectovaginal septum to the pelvic sidewall. Am J Obstet Gynecol 185:41-43, 2001. 5. Milley PS, Nichols DH: A correlative investigation of the human rectovaginal septum. Anat Rec 163:443-452, 1969. 6. Van Ophoven A, Roth S: The anatomy and embryological origins of the fascia of Denonvilliers: A medico-historical debate. J Urol 157:39, 1997. 7. Swift SE, Tate SB, Nicholas J: Correlation of symptoms with degree of pelvic organ support in a general population of women: what is pelvic organ prolapse? Am J Obstet Gynecol 189:372-379, 2003. 8. Myers DL, LaSala CA, Hogan JW, Rosenblatt PL: The effect of posterior wall support defects on urodynamic indices in stress urinary incontinence. Obstet Gynecol 91:710-714,1998.

9. Weber AM, Walters MD, Ballard LA, et al: Posterior vaginal prolapse and bowel function. Am J Obstet Gyencol 179:1446-1450, 1998. 10. Meschia M, Buonaguidi A, Pifarotti P, et al: Prevalence of anal incontinence in women with symptoms of urinary incontinence and genital prolapse. Obstet Gynecol 100:719-723, 2002. 11. Bump RC, Mattiasson A, Bo K, et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 175:10-17, 1996. 12. Swift SE, Herring M: Comparison of pelvic organ prolapse in the dorsal lithotomy compared with the standing position. Obstet Gynecol 91:961-964, 1998. 13. Burrows LJ, Sewell C, Leffler KS, Cundiff GW: The accuracy of clinical evaluation of posterior vaginal wall defects. Int Urogynecol J 14:160-163, 2003. 14. Lau CW, Heymen S, Alabaz O, et al: Prognostic Significance of rectocele, intussusception, and abnormal perineal descent in biofeedback treatment for constipated patients with paradoxical puborectalis contraction. Dis Colon Rectum 43:478-482, 2000. 15. Ron Y, Avni Y, Lukovetski A, et al: Botulinum toxin type-A in therapy of patients with anismus. Dis Colon Rectum 44:1821-1826, 2001.

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16. Kahn MA, Stanton SL: Posterior colporrhaphy: Its effects on bowel and sexual function. Br J Obstet Gynaecol 104:82-86, 1997. 17. Francis WJA, Jeffcoate TNA: Dyspareunia following vaginal operations. J Obstet Gynaecol Br Commonw 68:1-10, 1961. 18. Arnold MW, Stewart WR, Aguilar PS: Rectocele repair: Four years’ experience. Dis Colon Rectum 33:684-687, 1990. 19. Mellgren A, Anzén B, Nilsson BY, et al: Results of rectocele repair. Dis Colon Rectum 38:7-13, 1995. 20. López A, Anzén B, Bremmer S, et al: Cystodefecoperitoneography in patients with genital prolapse. Int Urogynecol J 13:22-29, 2002. 21. Sloots CEJ, Meulen AJ, Felt-Bersma RJF: Rectocele repair improves evacuation and prolapse complaints independent of anorectal function and colonic transit time. Int J Colorectal Dis 18:342-328, 2003. 22. Maher CF, Qatawneh AM, Baessler K, Schluter PJ: Midline rectovaginal fascial plication for repair of rectocele and obstructed defecation. Obstet Gynecol 104:685-689, 2004. 23. Abramov Y, Gandhi S, Goldberg RP, et al: Site-specific rectocele repair compared with standard posterior colporrhaphy. Obstet Gynecol 105:314-318, 2005.

24. Richardson AC, Lyon JB, Williams NL: A new look at pelvic relaxation. Am J Obstet Gynecol 126:568-573, 1976. 25. Cundiff GW, Weidner AC, Visco AG, et al: An anatomic and functional assessment of the discrete defect rectocele repair. Am J Obstet Gynecol 179:1451-1457, 1998. 26. Kenton K, Shott S, Brubaker L: Outcome after rectovaginal fascia reattachment for rectocele repair. Am J Obstet Gynecol 181:13601363, 1999. 27. Porter WE, Steele A, Walsh P, et al: The anatomic and functional outcomes of defect-specific rectocele repairs. Am J Obstet Gynecol 181:1353-1358, 1999. 28. Glavind K, Madsen H: A prospective study of the discrete fascial defect rectocele repair. Acta Obstet Gynecol Scand 79:145-147, 2000. 29. Singh K, Cortes E, Reid WMN: Evaluation of the fascial technique for surgical repair of isolated posterior vaginal wall prolapse. Obstet Gynecol 101:320-324, 2003. 30. Haase P, Skibsted L: Influence of operations for stress incontinence and/or genital descensus on sexual life. Acta Obstet Gynecol Scand 67:659-661, 1988.

Chapter 75

POSTERIOR REPAIR USING CADAVERIC FASCIA Sarah A. Rueff and Gary E. Leach Traditional posterior colporrhaphy for symptomatic rectoceles has been associated with failure rates as high as 35% and de novo dyspareunia rates ranging from 6% to 41%.1 The technique involves midline plication of the levator muscles and rectovaginal fascia to obliterate the fascial defect and perineorrhaphy to reapproximate the central tendon and perineal body.2 Inherent problems exist with traditional posterior repair. First, the success of the repair relies on the patient’s own tissue, which has already shown a propensity for weakness. Second, by attempting to obliterate the fascial defects, the patient’s anatomy is inevitably distorted, and the procedure can result in vaginal narrowing and dyspareunia. The patient may complain of constriction of the vaginal tube or may feel a ridge in the midline of the posterior wall due to suture placement. The use of defect-specific rectocele repair is an attempt to alleviate the vaginal narrowing and dyspareunia associated with traditional repair. The technique involves identification of fascial tears and plicating nearby durable fascia over the defect. Recurrence rates of 18% to 23% with mean follow-up periods of 12 to18 months have been reported along with variable improvements in bowel habits.3-5 As with traditional colporrhaphy, the repair relies on the patient’s inherently weak tissues to repair fascial defects. By failing to address the entire posterior vaginal wall, all areas of fascial weakness may not be identified, increasing the likelihood of failure. Rectocele repair with cadaveric fascia attempts to address the inherent problems of traditional and defect-specific rectocele repair. First, by graft interposition, all areas of weakness within the posterior compartment are addressed simultaneously. Second, the use of solvent-dehydrated, nonfrozen cadaveric fascia lata avoids the use of the patient’s own weak tissues. Third, the fascia is secured to the levator complex without tension, as is often necessary with traditional repair, preventing vaginal narrowing. Fourth, avoidance of tissue plication prevents the patient from feeling a ridge in the midline and preserves the width of the introitus. For these reasons, we think rectocele repair with cadaveric fascia offers several advantages over traditional posterior vaginal reconstruction techniques.

gens and viruses, solvent dehydration, and gamma irradiation. The tensile strength and tissue stiffness of nonfrozen cadaveric fascia lata has been investigated, and it is comparable to that of autologous fascia lata.7 Studies have compared solventdehydrated and freeze-dried cadaveric fascia lata, another commercially available preparation. Solvent-dehydrated fascia lata has significantly greater stiffness, maximum load to failure, and maximum load per unit of graft compared with freeze-dried fascia lata.8 All commercially available cadaveric fascia lata is not the same. The method used to prepare the tissue ultimately affects its tensile strength and subsequent surgical outcomes. We prefer the use nonfrozen cadaveric fascia to commercially available synthetic mesh material, which carries inherent risks of erosion and infection. Milani and colleagues9 described 31 women who underwent posterior repair with Prolene mesh who had an erosion rate of 6.5%. Other studies have reported similar findings, with erosion rates as high as 48%.10 PREOPERATIVE EVALUATION Before undergoing rectocele repair, a thorough history is obtained focusing on the symptoms associated with posterior prolapse. Based on the results of a series of questions in the Rectocele Symptom Inventory (Table 75-1), patients are assigned a preoperative score that correlates with the degree of symptoms. Questions focus on three areas of symptoms bowel function with symptoms that include straining, stool trapping, the need to manually reduce the rectocele to facilitate defecation, or a feeling of incomplete emptying after defecation; prolapse symptoms, which include vaginal pressure or the feeling of sitting on a ball; and sexual function, which includes dyspareunia and overall sexual satisfaction. We do not routinely repair rectoceles that are asymptomatic or low grade because the theoretical risks of surgery or its side effects outweigh the benefit gained. For patients who present with constipation or bowel dysfunction that does not correlate with the severity of posterior prolapse, referral to a gastroenterologist or colorectal surgeon may be beneficial before considering surgical repair.

CADAVERIC FASCIA The choice of fascia for rectocele repair with cadaveric fascia is of utmost importance in determining surgical outcome. Fascia lata is strong, regardless of a patient’s age or medical condition, and it has three to four times more tensile strength than rectus fascia.6 Our choice of fascia is Tutoplast (Mentor Corp., Santa Barbara, CA). Tutoplast is prepared by a five-step process that involves screening of donors, cleansing, denaturization of anti-

Physical Examination A systematic examination of the anterior, apical, and posterior compartments is performed with the patient in the dorsal lithotomy position. The posterior blade of a Graves speculum is used to displace the anterior vaginal wall and examine the posterior wall at rest and with straining. A simultaneous rectal examination using the index finger is performed to push the posterior vaginal 737

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Table 75-1 Rectocele Symptom Inventory In the past month, how often have you experienced the stated symptoms? I have to push or strain to have a bowel movement I feel the stool “gets stuck” when having a bowel movement I assist my rectum by placing my finger in the vagina or pressing on the skin outside of the vagina to have a bowel movement I feel that I have not completely emptied my bowels after having a bowel movement I feel the sensation of pressure in my rectum or vagina or have the sensation of “sitting on a ball” I have pain with sexual relations My ability to have sexual relations is satisfactory to me

Scoring* All of the time (4)

Most of the time (3)

Some of the time (2)

Rarely (1)

Never (0)

Not sexually active (0)

Most of the time (0)

Some of the time (2)

Not satisfactory (4)

*On the Rectocele Symptoms Inventory (RSI), the total score may range between 0 and 28.

Table 75-2 Baden-Walker Rectocele Classification Anatomic Grade

Description

Grade 1

Posterior wall protrusion with strain Posterior wall protrusion with strain Posterior wall protrusion introitus with strain Posterior wall protrusion introitus at rest

Grade 2 Grade 3 Grade 4

Figure 75-1 Examination of the posterior compartment with the index finger inserted into the rectum. Using the finger to push the posterior vaginal wall forward may reveal posterior wall weakness consistent with rectocele.

toward introitus to the introitus outside of the outside of the

(e.g., rectal prolapse or intussusception, large hemorrhoids, skin tags). The perineal body should be evaluated for associated defects. Patients who present with a widened vaginal introitus or a shortened perineum, signified by a decreased distance between the posterior margin of the vagina and the anterior margin of the anus, may benefit from a simultaneous perineal repair. We use the Baden-Walker system to classify rectoceles preoperatively (Table 75-2). In most cases, grade 1 rectoceles are incidental findings and asymptomatic. Only patients with grade 2 to grade 4 rectoceles and associated symptoms of stool trapping or the need to splint the vagina or perineum to facilitate defecation are considered candidates for surgical repair. Ancillary Testing

wall forward (Fig. 75-1). Finger examination allows simultaneous assessment of the integrity of the rectovaginal fascia and the integrity of the external anal sphincter. Sphincter evaluation is especially important in patients who complain of fecal incontinence, and it can rule out other causes of defecatory dysfunction

No further evaluation is necessary in patients who present with symptomatic posterior prolapse without complicating factors. Patients with associated voiding complaints or anterior wall prolapse should undergo urodynamic evaluation before surgical intervention.

Chapter 75 POSTERIOR REPAIR USING CADAVERIC FASCIA

When patients have anatomic abnormalities (e.g., sigmoidocele, rectal prolapse, internal hemorrhoids) that can cause overlapping symptoms, defecating proctography may provide additional anatomic information. The study can also provide functional information regarding the efficiency of rectal emptying.10 In other situations, given the patient’s body habitus or limitations in lower extremity mobility, it may be difficult to delineate the exact compartment of prolapse. Dynamic magnetic resonance imaging (MRI)provides additional information that enables the appropriate treatment recommendation to be made. The study is performed with the patient in the standing position and consists of rapid-sequence MRI of the pelvis at rest and during Valsalva maneuvers. By simultaneous examination of all intrapelvic compartments, for example, an enterocele can be distinguished from a high rectocele and the appropriate operative procedure recommended.

Figure 75-2 The rectum is dissected off of the posterior vaginal wall until the levator complex is exposed bilaterally.

PREOPERATIVE PREPARATION Before performing prolapse repair, the urine is confirmed to be sterile. Patients are not routinely instructed on self-catheterization unless simultaneous transvaginal sling or cystocele repair is planned or the patient has incomplete emptying preoperatively. Preferably, patients should be started on stool softeners preoperatively in an attempt to regulate bowel function. Patients with vaginal wall atrophy should use estrogen vaginal cream for 4 to 6 weeks before surgery. Patients are instructed to use one third of an applicator of estrogen cream three times each week to improve the quality of tissue and postoperative healing properties. A povidone-iodine vaginal douche and a Fleet enema are performed the night before and the morning of surgery. Perioperative antibiotics are administered, preferably using a firstgeneration cephalosporin, ampicillin, or vancomycin (if allergic to penicillin) combined with an aminoglycoside. When indicated, simultaneous transvaginal repair of associated anterior or apical prolapse is performed with the rectocele repair with cadaveric fascia. When multiple repairs are to be done, the rectocele repair with cadaveric fascia is performed last. A thorough discussion of the risks and complications of the procedure is undertaken with the patient before repair. Patients are counseled regarding the goals of surgery, which include restoration of anatomy, improvement of or relief from associated symptoms, and maintenance or restoration of visceral and sexual function.11 Paraiso and coworkers12 evaluated preoperative and postoperative symptoms that may predict outcome after a traditional posterior colporrhaphy. They found that preoperative constipation or straining to defecate predicted poor outcome after rectocele repair.12 OPERATIVE PROCEDURE The procedure is performed with the patient in the dorsal lithotomy position. A Foley catheter is placed, and a Scott retractor (Lonestar, Houston, TX) is secured to the medial buttocks with towel clamps. When other procedures will be performed (e.g., transvaginal sling, cystocele repair, vaginal hysterectomy, enterocele repair, vaginal vault suspension), the procedures are completed, and the vaginal epithelium is closed before rectocele repair. To begin, a 1-0 silk suture is used to mark the apex of the rectocele, and the posterior vaginal wall is infiltrated with saline.

Figure 75-3 Two 1-0 polydioxanone sutures are placed within the levator complex on each side for attachment to the nonfrozen cadaveric fascia.

A midline incision is made in the posterior vaginal wall from the marking suture to the vaginal introitus. Using Metzenbaum scissors, the posterior vaginal wall is dissected off of the rectum on the white, shiny layer of the inner aspect of the vaginal wall. Dissection is continued until the levator complex, consisting of the levator ani musculature and the remaining rectovaginal fascia, is exposed bilaterally (Fig. 75-2). Four 1-0 polydioxanone attachment sutures (two per side) are placed laterally into the levator complex (Fig. 75-3), a fifth suture is placed at the apex of the rectocele near the previously placed marking suture, and a sixth suture is placed distally within the perineal body (Fig. 75-4). A 4 × 7 cm piece of nonfrozen cadaveric fascia lata (Tutoplast), presoaked in antibiotic solution, is used to close the

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Figure 75-4 Sutures are in place within the levator complex bilaterally. Sites for apical suture and distal perineal suture are exposed. Figure 75-6 The remaining sutures are passed through the fascia and tied with the proper amount of tension.

Figure 75-5 Sutures on one side are passed through the folded fascial edge and tied.

rectovaginal fascial defect. The edges of the fascia are folded over to minimize chances of suture pull-through.13 The previously placed sutures are passed through the fascia on one side and tied (Fig. 75-5). The contralateral fascia edge is folded over, and the site for suture placement is measured to allow for proper tension. The contralateral sutures, apical suture, and distal suture are then passed through the fascia and tied (Fig. 75-6). Irrigation with antibiotic solution is performed throughout the procedure. After hemostasis is obtained, redundant vaginal epithelium is trimmed, and the incision is closed with running 2-0 absorbable suture. Care should be taken to avoid excess trimming of the vaginal epithelium and resultant tension on the vaginal closure, which can result in wound separation or vaginal narrowing postoperatively.

Figure 75-7 Vaginal width and depth are maintained after the rectocele repair with cadaveric fascia.

In patients with whom perineal reconstruction is indicated, Allis clamps are placed on the posterior fourchette at the 5o’clock and 7-o’clock positions. The mucocutaneous junction and the underlying tissue are excised to expose the underlying perineal body. Vertical mattress sutures using 1-0 absorbable sutures are placed to reapproximate the central tendon, which is formed by the bulbocavernosus, superficial, and deep transverse perinei muscles (i.e., the urogenital diaphragm) and the external anal sphincter musculature at their junction with the levator ani musculature.14 A subcuticular stitch is used to reapproximate the perineal skin. At the conclusion of the repair, the vagina should comfortably admit two or three fingers (Fig. 75-7). A Foley catheter and a Betadine-soaked vaginal pack are left in place.

Chapter 75 POSTERIOR REPAIR USING CADAVERIC FASCIA

35 30 25 No. of pts (n=39)

20 15 10 5 0

Preop Post op

Strain with BM

Stool trapping

Splinting

Incomplete emptying

Vaginal pressure

Dyspareunia

Figure 75-8 Rectocele Symptom Inventory: preoperative to postoperative changes. BM, bowel movement.

POSTOPERATIVE CARE The vaginal packing and Foley catheter are removed on the morning of the first postoperative day. Fluid intake is restricted to 1500 mL per day. A voiding trial is administered, and residual urine measurement is obtained by means of intermittent catheterization. If residual urine measurements are more than 100 mL, patients are again instructed on self-catheterization. Urinary retention is a temporary complication reported for up to 12.5% of patients after posterior repair.15 Patients are continued on intravenous antibiotics for 24 hours postoperatively and then begun on an oral antibiotic (cephalexin or fluoroquinolone) for 1 week to minimize the risk of wound infection. Patients are routinely discharged on postoperative day one with oral analgesics. Stool softeners are continued for 1 month, and patients are counseled to avoid straining with defecation. Patients with elevated postvoid residual volumes are instructed to continue to monitor at home by self-catheterization until residual urine volumes are consistently less than 100 mL. If a patient is unable to learn or is uncomfortable performing selfcatheterization, she can be discharged home with a Foley catheter and return for a trial of void in the office. At time of discharge, patients are instructed to avoid heavy lifting or straining and to observe pelvic rest (i.e., no intercourse, no tampons) for 6 weeks postoperatively. Patients are seen for follow-up at 1 week, 6 weeks, 6 months, 12 months, and yearly thereafter. Evaluation consists of urinalysis, postvoid residual urine measurement, and physical examination. Patients are administered the confidential Rectocele Symptom Inventory preoperatively and at 6-month intervals postoperatively, the results of which are entered into a prospective database (see Table 75-1).

have had symptomatic rectocele recurrences (one grade 2 rectocele and one grade 3 rectocele). Symptom Outcomes Thirty-nine patients (74%) have at least 6 months of questionnaire follow-up (range, 6 to 50 months; mean, 25.1 months). A comparison of preoperative to postoperative symptoms based on questionnaire responses is provided in Figure 75-8. Specifically, 33 (85%) of 39 patients complained of significant symptoms of stool trapping preoperatively, and 13 (33%) of 39 complained of the need to perform vaginal or perineal splinting or postural changes to facilitate defecation preoperatively. Postoperatively, only 11 (28%) of 39 and 6 (15.4%) of 39 described stool trapping or need to splint, respectively. In regard to overall bowel function, 15 (38%) of 39 patients described their bowel function as “significantly improved,” and 10 (25.6%) of 39 stated that they continued to have trouble with their bowel function. Twenty-six patients were sexually active before the procedure. In regard to overall sexual function, 106 (38%) of 26 stated their sexual function was “significantly improved,” and 12 (46%) of 26 stated their sexual function was “unchanged, not a problem,” resulting in 22 (85%) of 26 of patients having stable or improved sexual function. Nine patients complained of significant dyspareunia preoperatively, which improved in 5 (55.6%) of the 9 patients. Only 2 (7.7%) of 26 developed de novo dyspareunia. Overall, patient satisfaction with the procedure has been excellent, with 32 (82%) of 39 patients giving a satisfaction rating of 50% or more and 33 (85%) of 39 stating they would undergo the procedure again.

COMPLICATIONS RESULTS Prolapse Outcomes Rectocele repair with cadaveric fascia has been performed on a total of 53 patients between the ages of 31 and 86 years (mean, 59.7 years). Forty patients (75%) had at least 6 months’ follow-up (range, 6 to 54 months; mean, 19.6 months). All patients had symptomatic grade 2 to 4 rectoceles preoperatively. For 29 (72.5%) of 40 patients, rectoceles were grade 3; for 7 (17.5%) of 40 patients, rectoceles were grade 4; and for 4 (10%) of 40 patients, rectoceles were grade 2. Only 2 (50%) of 40 patients

Most complications have been minor. Seven patients developed wound separation or granulation tissue, which healed with observation. Fecal urgency developed in one patient and was successfully treated with biofeedback. One patient suffered a mild cerebrovascular accident postoperatively and subsequently required transfer to a rehabilitation center. One patient had a rectotomy recognized intraoperatively that was repaired primarily. Despite intraoperative repair, the patient developed a postoperative rectovaginal fistula, which healed spontaneously with close observation and did not require operative intervention.

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CONCLUSIONS Rectocele repair with cadaveric fascia, using nonfrozen cadaveric fascia lata for posterior vaginal wall reconstruction, offers several advantages over traditional posterior colporrhaphy. Incorporation of durable graft tissue prevents a reliance on the patient’s own tissue, which has an established propensity for weakness. By

avoiding tissue plication and obliteration of the tissue in the midline, the degree of vaginal narrowing is minimal after rectocele repair with cadaveric fascia. In this way, complaints of postoperative dyspareunia are minimized, and patient satisfaction has been excellent. The avoidance of synthetic materials prevents subsequent graft erosion and wound infection associated with their use.

References 1. Kobashi KC, Leach GE, Frederick R, et al: Initial experience with rectocele repair using nonfrozen cadaveric fascia lata interposition. Urology 66:1203-1207; discussion 1207-1208, 2005. 2. Rosenblum N, Eilber KS, Rodriguez LV: Rectocele repair/posterior colporrhaphy. In Vasavada SP, Appell RA, Sand PK, Raz S (eds): Female Urology, Urogynecology, and Voiding Dysfunction. New York, Marcel Dekker, 2005. 3. Cundiff GW, Weidner AC, Visco AG, et al: An anatomic and functional assessment of the discrete defect rectocele repair. Am J Obstet Gyncol 179:1451-1457, 1998. 4. Porter WE, Steele A, Walsh P, et al: The anatomic and functional outcomes of the defect-specific rectocele repairs. Am J Obstet Gynecol 181:1353-1358, 1999. 5. Kenton K, Shott S, Brubaker L: Outcome after rectovaginal fascia reattachment for rectocele repair. Am J Obstet Gynecol 181:13601364, 1999. 6. Lemer ML, Chaikin DC, Blaivas JG: Tissue strength analysis of autologous and cadaveric allografts for the pubovaginal sling. Neurourol Urodyn 18:497-503, 1999. 7. Crawford JS: Nature of fascia lata and its fate after transplantation. Am J Opthamol 67:900, 1969. 8. Jinnah RH, Johnson C, Warden K, Clarke HJ: A biochemical analysis of solvent-dehydrated and freeze dried human fascia lata allografts. A preliminary report. Am J Sports Med 20:607-612, 1992.

9. Milani R, Salvatore S, Soligo M, et al: Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with Prolene mesh. BJOG 112:107-111, 2005. 10. Birch C, Fynes M: Mesh erosion complicating vaginal surgery for the correction of posterior compartment prolapse. Poster presentation at the 34th annual meeting of the International Continence Society and the International Urogynecological Association Colloquium (ICS/IUGA), August 23-27, 2004, Paris, France. 11. Segal JL, Karram MM: Evaluation and management of rectoceles. In Vasavada SP, Appell RA, Sand PK, Raz S (eds): Female Urology, Urogynecology, and Voiding Dysfunction. New York, Marcel Dekker, 2005. 12. Paraiso MF, Weber AM, Walters MD: Anatomic and functional outcome after posterior colporrhaphy. J Pelvic Surg 129:524-529, 2001. 13. Sutaria PM, Staskin DR: A comparison of fascial “pull-through” strength using four different suture fixation techniques [abstract]. J Urol 161:79, 1999. 14. Babiarz JW, Raz S: Pelvic floor relaxation. In Raz S (ed): Female Urology. Philadelphia, WB Saunders, 1996. 15. Rovner ES, Gindsberg DA: Posterior vaginal wall prolapse: Transvaginal repair of pelvic floor relaxation, rectocele, and perineal laxity. Tech Urol 7:161-168, 2001.

Chapter 76

PERINEAL HERNIA AND PERINEOCELE Christian Twiss and Nirit Rosenblum Perineal hernia is an uncommon condition that was once thought to be incurable because of the difficulty in closing the hernia defect and the high recurrence rate.1 The past century witnessed the development of a plethora of techniques to repair perineal hernias and an improved understanding of the anatomic defects, leading to their classification. Despite the knowledge gained, much remains to be discovered about perineal hernias. There are no controlled studies to guide the clinician in the choice of optimal therapy. Perineocele is an even less studied and less welldefined clinical problem. Both conditions are discussed in this chapter. PERINEAL HERNIA Definition and Classification Perineal hernias occur through focal defects within the pelvic floor, and they are classified by primary cause and by anatomic region. Primary perineal hernias are focal, acquired defects within the pelvic floor that typically occur in women as a result of pelvic relaxation associated with vaginal parity or chronic conditions involving increased abdominal pressure (e.g., chronic cough, constipation, ascites). Secondary perineal hernias are true incisional hernias within the pelvic floor that result from prior pelvic (typically exenterative) surgery. Herniation can occur through the anterior or posterior compartments of the pelvic floor. Anterior perineal hernias (i.e., pudendal hernias, pudendal enteroceles, or levator hernias) occur within the urogenital triangle anterior to the superficial transverse perineal muscles, and they occur exclusively in women; no confirmed cases in men have been reported. Anterior perineal hernias occur through the urogenital diaphragm within the triangular regions lateral to each side of the vaginal vestibule defined by the medial border of the ischiocavernosus muscle, the lateral border of the bulbocavernosus muscle, and the anterior border of the superficial transverse perineal muscle (Fig. 76-1). Posterior perineal hernias occur in within the anal triangle posterior to the superficial transverse perineal muscles and anterior to the ventral borders of the gluteus maximus muscles. They typically occur midway between the anus and the ischial tuberosity within a levator ani defect, in the space between the pubococcygeus and iliococcygeus portions of the levator ani muscle, or in the space between the levator ani and coccygeus muscles (see Fig. 76-1). Translevator and supralevator hernias are anatomically distinct.2 A translevator perineal hernia sac passes through the focal defect within the levator ani musculature, whereas a supralevator hernia sac remains superior to the levator ani but exists as a focal outpouching of the weakened levator ani muscle that extends beyond the plane of the levator plate. Despite the anatomic difference, the principles of hernia repair remain the same.

The hernia sac of a perineal hernia may be empty (i.e., peritoneum) or may contain one or more of the abdominopelvic viscera, including small or large bowel, bladder, omentum, ovary, and fallopian tube. Because intraperitoneal and extraperitoneal structures may herniate, a true hernia sac may not always be present.1 Etiology and Epidemiology Anterior perineal hernias can be primary or secondary (i.e., after surgery or obstetric procedures). Anterior perineal hernias are rare, with fewer than 17 well-described cases in the English literature.1,3-6 Most reported perineal hernias are posterior perineal hernias. The largest reported series of anterior perineal hernias is that of Chase in 1922, reporting 13 cases.1 However, only 10 of these 13 cases were described in enough detail to be confirmed cases of anterior perineal hernia. All of the well-described cases of anterior perineal hernia appear to have occurred in the setting of multiple prior pelvic operations for pelvic prolapse or urinary incontinence or of difficult and prolonged labor, often requiring forceps delivery. Both causes involve direct trauma to the pelvic floor musculature, which is thought to be the primary cause of anterior perineal hernias. Most anterior perineal hernias are secondary. Posterior perineal hernias may be primary or secondary. Primary perineal hernias are rare, and their true incidence is unknown. They typically occur between the ages of 40 and 60 years, and they occur more commonly in women, with a female preponderance of threefold to fivefold higher than for men.7,8 This female preponderance is attributed to female pelvic floor trauma encountered during childbirth9 and the phenomenon

Bulbospongiosus m. Ischiocavernosus m. Deep transverse perineal m. (urogenital diaphragm)

1

Superficial transverse perineal m. 2 External anal sphincter m. 3

Levator ani m. Gluteus maximus m.

Coccygeus m.

Figure 76-1 Anatomy of perineum and typical locations of perineal hernias. (Modified from Cali RL, Pitsch RM, Blatchford GJ, et al: Rare pelvic floor hernias. Dis Colon Rectum 35:604, 1992.).

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Table 76-1 Risk Factors for Perineal Hernias

Table 76-2 Differential Diagnosis of Perineal Hernia

Primary perineal hernia Female gender Vaginal childbirth Prolonged or difficult labor Pelvic organ prolapse or pelvic floor descent Recurrent infections of pelvic floor Chronic cough Chronic constipation Obesity Abdominal ascites

Diagnosis

Secondary perineal hernia Female gender Abdominoperineal resection Open postoperative perineal wound Pelvic exenteration Radical cystourethrectomy Coccygectomy Anti-incontinence surgery Hysterectomy Pelvic organ prolapse surgery Perineal prostatectomy Pelvic irradiation Excessive length of small bowel mesentery

of pelvic relaxation.10 A study by Gearhart and colleauges10 demonstrated a 15% incidence of levator ani hernia in a group of 80 patients who underwent dynamic pelvic magnetic resonance imaging (MRI) for the evaluation of symptomatic pelvic organ prolapse. Forty-two percent of these patients had undergone prior pelvic surgery, and approximately 60% (or 9% of the entire group) are presumed to be primary levator ani hernias associated with symptomatic pelvic organ prolapse. Other conditions are also thought to contribute to the formation of primary perineal hernia, including recurrent pelvic floor infections and conditions involving increased abdominal pressure such as chronic cough, chronic constipation, obesity, and ascites (Table 76-1).8,11,12 Secondary posterior perineal hernias occur through defects in the pelvic floor resulting from surgery, and they usually manifest within 1 year after the initial surgery.9 Most secondary perineal hernias occur after pelvic exenterative surgery, requiring corrective surgery after approximately 0.7% of abdominoperineal resections13 and 3% of pelvic exenterations.14 The true incidence of perineal hernia after these procedures is likely higher, and most are asymptomatic. Hullsiek15 found a 7% incidence of perineal hernia after abdominoperineal resection by means of barium x-ray films, and most were asymptomatic. Secondary posterior16 and anterior3,5,6 perineal hernias have been reported after surgery for pelvic prolapse and urinary incontinence. However, their overall incidence after prolapse and incontinence surgery is unknown. It is difficult to determine whether these hernias result from the prolapse surgery or the pathophysiologic process of pelvic prolapse itself. Presumably, it is a combination of both because a significant proportion (42%) of perineal hernias associated with symptomatic pelvic prolapse occur in the absence of a history of pelvic surgery.10 Table 76-1 summarizes the types of operations associated with secondary perineal hernias. Poor perineal tissue quality and

Anterior perineal masses Anterior perineal hernia Inguinal hernia Bartholin gland abscess

Lipoma or sarcoma Hematoma Cystocele, rectocele, enterocele Posterior perineal masses Posterior perineal hernia Sciatic hernia Rectal prolapse

Perineocele

Clinical Features Labial mass reduces into pelvic floor medial to pubic ramus Labial mass reduces into inguinal canal across pubic ramus Labial mass irreducible, fluctuant, signs of inflammation Labial mass, irreducible Labial mass, irreducible, history or signs of perineal trauma Introital mass, associated urinary or fecal symptoms Soft, reducible, posterior to perineum Emerges on inferior border of gluteus maximus Emerges from anus, associated constipation or fecal incontinence Pelvic descent, increased anovaginal distance

factors that hinder wound healing such as diabetes and pelvic irradiation also predispose to perineal hernia. One of the most significant predisposing factors for perineal hernia after abdominoperineal resection was found to be a partial or complete open perineal wound in the postoperative period.17 Symptoms and Clinical Findings Anterior perineal hernia typically manifests as a reducible labial mass, usually in the posterior aspect of the labia majora. This may be accompanied by a heavy sensation within the perineum.4 The mass is characteristically covered with vaginal mucosa on its medial border and the labial integument on its lateral border. An anterior perineal hernia is also characteristically reducible into the pelvic floor medial and inferior to the pubic ramus, whereas an inguinal hernia within the labia reduces into the inguinal canal by crossing over the pubic ramus. The reducibility of the hernia also distinguishes it from irreducible labial masses such as Bartholin’s gland abscesses or cysts, benign labial cysts, labial lipomas and sarcomas, and labial hematomas (Table 76-2). Careful vaginal and perineal examination is needed to avoid inadvertent incision into a perineal hernia that many contain bladder or bowel. It is not uncommon for anterior perineal hernias to contain bladder because defects within the anterior pelvic floor more often contain bladder.3 This can result in urinary sequelae, including urinary incontinence, weak urinary stream, and incomplete bladder emptying with high postvoid residual volumes.4,6 Patients with concurrent urinary symptoms should undergo diagnostic cystoscopy and imaging of the lower urinary tract. Posterior perineal hernias typically manifest as soft, reducible masses within the posterior perineum (posterior to the perineal

Chapter 76 PERINEAL HERNIA AND PERINEOCELE

body), usually occurring in the region between the anus and ischial tuberosity, but they may also emerge just ventral to the gluteus maximus, in which case they must be distinguished from a sciatic hernia, which is rare.12 They are often asymptomatic,10 but they may be accompanied by a heavy or dragging feeling within the perineal region and pain with sitting. Perineal hernias usually do not incarcerate or strangulate because the pelvic floor defect is often large and the hernia remains easily reducible. However, there are reports of postoperative perineal hernia that have been accompanied by bowel obstruction and perineal skin breakdown.18,19 Often, the bowel obstruction is intermittent and occurs because of bowel compression when the patient is sitting. Evaluation There is no consensus on the workup of perineal hernias beyond a careful history and vaginal, perineal, and rectal examinations. The examination should focus on diagnosing the hernia and evaluate the possibility of cystocele, rectocele, or rectal prolapse, because some perineal hernias occur in the setting of pelvic organ prolapse. In suspected cases of anterior perineal hernia with accompanying urinary symptoms, cystourethrography and cystoscopy are recommended to confirm the presence of bladder within the hernia and to determine whether the trigone is involved in the hernia. This seems reasonable because the bladder is more commonly involved in anterior perineal hernias. If cystourethrography is performed solely to confirm presence of bladder within the perineal hernia, other modalities such as computed tomography (CT) or pelvic MRI could derive the same information. Further imaging of the suspected hernia is warranted to confirm the diagnosis and to provide additional information for surgical planning, such as which pelvic contents are present within the hernia, where the hernia emerges from the pelvic floor, and an estimation of the size of the defect. It is arguable whether a careful physical examination can derive all this information except for the exact contents of the hernia sac. However, the most conservative approach is to obtain the most information about the hernia through careful examination and pelvic imaging before its repair. Plain radiographs of the pelvis and barium enema are able to demonstrate bowel within the hernia sac.20 Dynamic proctography, typically used to evaluate defecatory dysfunction, is able to demonstrate the extent and involved segment of perineal rectal herniation.7 The presumed advantage over barium enema is applicable for cases in which the perineal herniation occurs only during straining and defecation. CT evaluation of the pelvic floor is more definitively able to identify the contents of the hernia sac and the location and extent of the associated pelvic floor defect.11 MRI is gaining acceptance as a preferred method of evaluation of the pelvic floor because of its excellent resolution of pelvic floor21,22 and perianal23 structures and the ability to visualize the prolapsing pelvic organs in real time by dynamic pelvic MRI. In addition to its utility in visualizing pelvic organ prolapse with an anatomic staging system,24 dynamic pelvic MRI was able to detect unsuspected levator ani hernias in 15% of patients undergoing evaluation for symptomatic pelvic organ prolapse.10 Pelvic MRI was also able to preoperatively detect a large unsuspected posterior perineal hernia associated with recurrent vaginal vault

prolapse, thereby changing operative management.2 These two studies highlight some important considerations. They confirm that perineal hernias occur in conjunction with pelvic organ prolapse and that clinicians treating these patients should maintain a degree of clinical suspicion about the diagnosis. As MRI evaluation of pelvic organ prolapse increases, the number of unsuspected perineal hernias can also be expected to increase. This ultimately presents a need and an opportunity to create patient cohorts to study and further define a protocol for the management of perineal hernia that occurs in the setting of pelvic organ prolapse. Treatment The treatment for perineal hernias is surgical, but there is no clearly defined protocol for their management. Because they rarely incarcerate and strangulate, the primary indication for the repair of perineal hernias is patient discomfort. The general principles remain the same as for any hernia: exposure of the sac and the musculofascial defect, opening of the sac with reduction of its contents, and high ligation of the sac followed by closure of the musculofascial defect. There remain two important caveats. First, there is not always a clearly defined sac, because not all pelvic contents (especially bladder) are completely covered by peritoneum. Second, the fascial defect encountered can be quite extensive, especially in post-exenterative perineal hernias requiring advanced reconstructive maneuvers. There are three basic approaches to repair: perineal, abdominal, and a combined perineal and abdominal approach. Two reports described a laparoscopic mesh repair technique.25,26 There are no controlled studies demonstrating the superiority of any one approach. However, the combined experience of several surgeons demonstrates the applicability of each approach to management. A key concept that determines the goals and techniques of repair is whether the hernia has occurred after pelvic exenterative surgery (i.e., pelvic exenteration or abdominoperineal resection). The repair of perineal hernias in this setting typically involves the repair of a large pelvic floor defect requiring an extensive reconstruction of the pelvic floor (Table 76-3). Cancer recurrence and bowel adhesions are additional considerations that affect the operative goals at the time of repair. Perineal hernias after nonexenterative surgery are typically more localized defects in the pelvic floor that do not require advanced reconstructive techniques. Because the pelvic organs are still in place, most pelvic reconstructive techniques described for the repair of postexenterative perineal hernias are not feasible in the absence of prior pelvic exenterative surgery. However, because pelvic relaxation and pelvic organ prolapse are predisposing factors of perineal hernias, their surgical correction needs to be considered at the time of repair. The perineal approach (or translabial approach in the case of anterior perineal hernias) remains the least invasive one with the advantages of less morbidity and success in most cases.17 The perineal approach also allows resection of residual perineal skin that may accompany sizable perineal hernias.27 However, the exposure is limited, allowing less access to sac contents, adhesions, recurrent cancer, or injured viscera or vasculature.28 Recurrences have also been reported with the perineal approach.6,17,28 In the small series of postoperative perineal hernias reported by So and coworkers,17 the perineal approach carried a 23% recurrence rate, compared with no recurrences after repairs using the

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Table 76-3 Techniques of Perineal Hernia Repair Year 1944 1951 1960 1963 1967 1973 1975 1980 1981 1981 1982 1984 1985 1987 1987 1989 1995 1997 2002 2002

Study

Method 31

Cattel and Cunnigham Koontz8 Kelly19 Cawkwell54 Bach-Nielsen55 Buchsbaum and White56 Alexander et al57 Bell et al58 Hurwitz and Walton35 Leuchter et al59 Sarr et al37 Giampapa et al60 Brotschi et al33 Beck et al28 Delmore et al32 Frydman and Polglase29 Erdmann and Waterhouse38 So et al17 Franklin et al25 Ghellai et al26

Uterus to uterosacral ligaments Local muscle and fascia Fascia lata Nylon mesh Uterus to sacrum and pelvic wall Omental sling Mesenteric leaf Gracilis myocutaneous flap Gluteal thigh flap Bulbocavernosus myocutaneous flap Marlex mesh Rectus abdominis muscle flap Gracilis muscle sling Marlex mesh Human dura Polypropylene mesh Rectus abdominis flap Gore-Tex patch Laparoscopic Vicryl mesh Laparoscopic polypropylene mesh

Modified from Abdul Jabbar AS: Postoperative perineal hernia. Hernia 6:188, 2002.

abdominal or combined approach. Perineal repairs have been performed with4,27,29,30 and without5,6,17 mesh repair of the hernia defect. Because of its simplicity, the perineal approach has been recommended as the best initial approach for straightforward cases,4,17,27 reserving the abdominal and abdominoperineal approach for recurrent cases, cases of strangulation of the hernia contents, or situations in which primary closure of the defect is complex. The perineal technique involves a skin incision over the site of the hernia defect after sterile preparation of the perineum. In the case of anterior perineal hernias, this is directly over or alongside the involved major labium. If bladder (especially trigonal) involvement is suspected, prophylactic ureteral stents also may be placed. This is followed by careful dissection of the sac from the skin and then the margins of the hernia defect itself. In the case of post-exenterative hernias, the dissection during this step must be meticulous because it is a frequent source of bowel injuries.18 In cases of small hernia defects in which there is a clearly defined sac, the hernia sac is opened, the contents are reduced, and the sac is ligated and excised. Any additional nonperitonealized hernia contents, such as bladder, are also reduced. This is followed by repair of the hernia defect using a simple layered closure with or without mesh reinforcement on the pelvic side of the hernia defect. When the pelvic viscera are in place, larger defects that cannot be closed primarily require mesh repair. Interposition of uterus has been reported.31 In cases of large post-exenterative hernias, simple closure of the levator ani defect is usually not possible, and pelvic floor reconstruction is required using synthetic mesh, free fascial grafts, or pedicled flaps (see Table 76-3).27-29,32-35 The abdominal approach has been recommended as the best first approach by some surgeons, 3,8,9,12,28 primarily because of better exposure of the anatomic defect and hernia sac. This is especially true in the cases of large pelvic floor defects requiring

mesh reconstruction of the pelvic floor.9,27,28 The abdominal approach facilitates proper fixation of the mesh to the pelvic and sacral support structures, and it assists simultaneous treatment of bowel adhesions and cancer recurrence after exenterative surgery.28 The abdominal approach also facilitates sacral resuspension of pelvic contents such as herniated rectum36 or prolapsed vaginal vault,2 and it permits closure of the cul-de-sac to prevent abdominal contents from accessing the area of the repaired hernia defect.6 In cases of strangulation of the hernia contents, the abdominal approach is required to address the need for possible resection or repair of the hernia contents. For the abdominal approach, the patient should be placed in the modified lithotomy position to allow simultaneous access to the perineum. This enables perineal traction to be applied to assist in the dissection and allows vaginal access to assist in identification of the vaginal cuff. It also permits conversion to a combined approach and possible placement of ureteral stents.28 Access is obtained through a lower midline incision, followed by possible exploration for recurrent cancer in post-exenterative cases. The hernia sac is identified, and the sac is dissected free from the margins of the defect. A small defect can be repaired with layered closure or mesh, whereas larger post-exenterative defects typically require more complex reconstruction of the pelvic floor as previously discussed. The abdominoperineal or combined approach provides maximal exposure of the hernia sac and hernia defect. It is especially useful in cases in which the pelvic floor defect is difficult to access by the abdominal route3 and in cases of large perineal hernias in which the redundant skin if the perineum must be resected.36,37 A laparoscopic combined approach has also been described25 in which the hernia contents are mobilized by a laparoscopic intraperitoneal approach, followed by open perineal repair of the levator defect and subsequent laparoscopic reinforcement of the repair with polypropylene mesh on the pelvic side of the repair.

Chapter 76 PERINEAL HERNIA AND PERINEOCELE

The list of methods that have been used to address the hernia defect is extensive (see Table 76-3), but there are no controlled trials demonstrating the superiority of any approach. In general, small defects with healthy tissue can be addressed by closing the levator defect primarily with nonabsorbable sutures. This can also be reinforced with mesh. When this is not possible or simple closure has failed, the use of synthetic mesh has produced durable repairs regardless of the surgical approach.6,25,28,36,37 However, when the tissue is infected, the tissue quality is poor, or the mesh has failed, the transposition of healthy, well-vascularized tissue by flap reconstruction is often required.17 Flap repairs using gracilis,33,34 fascia lata,18 rectus abdominis,38 and gluteus maximus35 have been described. There is no single correct approach to the repair of a perineal hernia. The choice ultimately depends on the size of the defect, the patient’s surgical history, the condition of the tissues, the condition and extent of the hernia sac contents, and the comfort level of the surgeon. PERINEOCELE Definition Perineocele is typically synonymous with perineal hernia.39 However, perineal hernia is a misnomer because many perineal hernias occur as labial swellings or swellings close to the buttocks and not on the perineum. Although perineal hernias remain focal defects within the pelvic floor, there is a related but separate clinical entity involving a diffuse weakening and bulging of the entire perineum itself due to an acquired attenuation of the perineal central tendon (Figs. 76-2 and 76-3).40,41 This has a symptom complex and treatment strategy that differs from the perineal hernias previously described. We think that perineocele is the term most appropriate for this condition because it is a pelvic floor herniation of the perineum itself and a clinical entity that differs from a classic perineal hernia. The two anatomic defects associated with perineoceles are convex deformity plus descent of the perineum with abdominal straining and widening of the distance between the posterior

Pubic bone Vagina

Rectum

Figure 76-3 Physical examination for perineocele. (From Raz S: Repair of perineal hernia. In Atlas of Transvaginal Surgery, 2nd ed. Philadelphia, WB Saunders, 2002.).

vaginal fourchette and the anus.40,41 Whereas the typical distance between the posterior fourchette and anus is 3 cm,42 this distance can increase to as much as 8 to 14 cm in large perineoceles.40,41 These defects are caused by a musculofascial disruption of the perineal body itself. Etiology and Epidemiology The true incidence of perineocele has not been reported. Perineocele is thought to result from the process of pelvic floor relaxation, which is associated with the pelvic floor damage that occurs during childbirth. Lacerations to the perineum occur when the pelvic floor and perineum are stretched excessively during the second stage of labor.43,44 Childbirth also lowers the position of the perineum,45 which can take up to 5 years to return to its normal position.46 It is unclear whether perineocele results from direct pelvic floor damage from childbirth or from the condition of abnormal perineal descent, or both. Symptoms and Clinical Features

Perineum

Figure 76-2 Schematic diagram of the anatomic defect of a perineocele. (Modified from Raz S: Repair of perineal hernia. In Atlas of Transvaginal Surgery, 2nd ed. Philadelphia, WB Saunders, 2002.).

In addition to having a perineal bulge between the anus and vagina, patients with perineoceles present with additional symptoms distinct from perineal hernias. They have a feeling of perineal pressure, and they typically present with chronic constipation and a possible need to apply perineal pressure to defecate.40,41 The descending perineum syndrome, first described by Parks and associates,47 is characterized by downward descent of the perineum during straining efforts and is associated with chronic constipation hallmarked by excessive straining with bowel movements and perineal pain. Fecal or urinary incontinence and vaginal prolapse may also be associated. The continued downward displacement of the perineum in descending perineum syndrome causes chronic stretching of the pudendal

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A

B

Figure 76-4 The goal of standard perineorrhaphy is to lengthen the perineum and shorten a widened genital hiatus. (Modified from Nichols DH: Posterior colporrhaphy and perineorrhaphy: Separate and distinct operations. Am J Obstet Gynecol 164:714, 1991.).

nerve, leading to worsening of the pelvic floor tone and anal tone.48-50 Perineocele and the descending perineum syndrome share some of the same clinical features, and it is interesting to postulate that they are in the same clinical spectrum. However, further investigation is required to determine whether perineoceles are perineal hernias with a distinct location and distinct clinical features or are dynamic defects in the pelvic floor that lead to progressive pelvic floor neuropathy and the descending perineal syndrome. Treatment The treatment of perineocele is surgical. Because there is no focal defect within the pelvic floor through which to reduce the sac and repair, the surgical technique differs from that of a typical perineal hernia. The goal of repair is to reconstruct the perineal body such that distance between the posterior vaginal fourchette and the anus, the perineal body length, is returned to its normal length of approximately 3 cm. This differs from the goal of standard perineorrhaphy, which is to repair the perineum in such a manner as to lengthen the attenuated perineal body while simultaneously reducing the anteroposterior length of the widened genital hiatus (Fig. 76-4).51 There is scant literature on the repair of perineoceles because it remains a relatively understudied clinical entity. Raz41 has described a perineal site-specific technique for the repair of perineocele in which the levator musculature anterior to the anal sphincter is reapproximated to the transverse perineal muscles using a series of interrupted horizontal mattress sutures (Fig. 76-5). This technique is used to repair the anatomic defect and its associated symptoms, including constipation. There are no long-term data on the durability of this repair. Other investiga-

tors have made efforts to specifically address the perineum and perineal descent in the repair of pelvic floor prolapse by affixing the perineum to the sacrum with synthetic mesh while repairing vaginal vault prolapse.52,53 However, it is not clear whether these techniques are applicable to the repair of perineocele because they correct perineal descent and its symptoms but do not address the condition of the widened perineum itself. Perineocele, although a poorly studied condition, is a clearly defined anatomic defect of the pelvic floor that is distinct from classically described anterior and posterior perineal hernias. It is typically associated with chronic constipation, and it remains unclear whether it also carries the pelvic neuropathic sequelae of abnormal perineal descent. The study of a large group of these patients with respect to risk factors, possible associated pelvic floor defects and neuropathy, and durability of repair is needed. CONCLUSIONS The anatomic defects of perineal hernia and perineocele are well defined, and a careful history, clinical suspicion, and physical examination remain tantamount to their diagnosis. Modern imaging techniques such as CT and MRI provide excellent and precise visualization of perineal hernias to assist in preoperative planning. Although there are few surgical repairs described for perineocele, there are several surgical approaches and repair techniques described for perineal hernia repair. However, there are no controlled trials directing clinicians to the optimal surgical approach or repair technique. Surgical treatment remains individualized, depending on the size and nature of the hernia defect, the condition of the tissues, and the comfort level and judgment of the surgeon.

Chapter 76 PERINEAL HERNIA AND PERINEOCELE

A

C

B

D

Figure 76-5 The goal of a perineocele repair is to shorten and strengthen the widened perineum by reapproximating the anal sphincter toward the superficial transverse perineal muscles. A, A 5-cm perineocele. B, Inverted Y incision to expose the defect. C, Suturing of the levator ani just anterior to the anus to the transverse perineal muscles. D, Repaired perineocele.

References 1. Chase HC: Levator hernia (pudendal hernia). Surg Gynecol Obstet 35:717, 1922. 2. Singh K, Reid WMN, Berger LA: Translevator gluteal hernia. Int Urogynecol J 12:407, 2001. 3. Hermann G: Pudendal (labial) hernia: Report of a case. N Engl J Med 265:435, 1961. 4. Anderson WR: Pudendal hernia. Unusual cause of labial mass. Obstet Gynecol 32:802, 1968. 5. Brodak PP, Juma S, Raz S: Levator hernia. J Urol 148:872, 1992. 6. Zimmern PE, Miyazaki F: Pudendal enterocele with bladder involvement. Urology 44:918, 1994.

7. Poon FW, Lauder JC, Finlay IG: Perineal herniation. Clin Radiol 47:49, 1993. 8. Koontz AR: Perineal hernia: Report of a case with many associated muscular and fascial defects. Ann Surg 133:255, 1951. 9. Pearl RK: Perineal hernia. In Nyhus LM, Condon RE (eds): Hernia, 4th ed. Philadelphia, JB Lippincott, 1995, pp 451-454. 10. Gearhart S, Pannu HK, Cundiff GW, et al: Perineal descent and levator ani hernia: A dynamic magnetic resonance imaging study. Dis Colon Rectum 47:1298, 2004. 11. Lubat E, Gordon RB, Birnbaum BA, et al: CT diagnosis of posterior perineal hernia. Am J Radiol 154:761, 1990.

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12. Cali RL, Pitsch RM, Blatchford GJ, et al: Rare pelvic floor hernias. Dis Colon Rectum 35:604, 1992. 13. McMullin ND, Johnson WR, Polglase AL, et al: Post-proctectomy perineal hernia: Case report and discussion. Aust N Z J Surg 55:69, 1985. 14. Rutledge FN, Smith JP, Wharton JT, et al: Pelvic exenteration: Analysis of 296 patients. Am J Obstet Gynecol 129:881, 1973. 15. Hullsiek HE: Perineal hernia following abdominoperineal resection. Am J Surg 92:735, 1956. 16. Silva-Filho AL, Santos-Filho AS, Figueiredo-Netto O, et al: Uncommon complications of sacrospinous fixation for treatment of vaginal vault prolapse. Arch Gynecol Obstet 271:358, 2005. 17. So JB, Palmer MT, Shellito PC: Postoperative perineal hernia. Dis Colon Rectum 40:954, 1997. 18. Ego-Aguirre, E, Spratt JS, Butcher HR. et al: Repair of perineal hernias developing subsequent to pelvic exenteration. Ann Surg 159:66, 1964. 19. Kelly AR: Surgical repair of post-operative perineal hernia. Aust N Z J Surg 29:243, 1960. 20. Trackler RT, Koehler PR: The radiographic findings in posterior perineal hernia. Radiology 91:950, 1968. 21. Kelvin FM, Maglinte DDT, Hale DS, et al: Female pelvic organ prolapse: A comparison of triphasic dynamic mr imaging and triphasic fluoroscopic cystocolpoproctography. Am J Radiol 174:81, 2000. 22. Barbaric ZL, Marumoto AK, Raz S: Magnetic resonance imaging of the perineum and pelvic floor. Top Magn Reson Imaging 12:83, 2001. 23. Morren GL, Beets-Tan RG, van Engelshoven JM: Anatomy of the anal canal and perianal structures as defined by phased-array magnetic resonance imaging. Br J Surg 88:1506, 2001. 24. Comiter CV, Vasavada SP, Barbaric ZL, et al: Grading pelvic prolapse and pelvic floor relaxation using dynamic magnetic resonance imaging. Urology 54:454-457, 1999. 25. Franklin ME, Abrego D, Parra E: Laparoscopic repair of postoperative perineal hernia. Hernia 6:42, 2002. 26. Ghellai AM, Islam S, Stoker ME: Laparoscopic repair of postoperative perineal hernia. Surg Laparosc Endosc Percutan Tech 12:119, 2002. 27. Abdul Jabbar AS: Postoperative perineal hernia. Hernia 6:188, 2002. 28. Beck DE, Fazio VW, Jagelman DG, et al: Postoperative perineal hernia. Dis Colon Rectum 30:21, 1987. 29. Frydman GM, Polglase AL: Perineal approach for polypropylene mesh repair of perineal hernia. Aust N Z J Surg 59:895, 1989. 30. Venzo A, Elberg JJ, Hjortrup A: Recurrent perineal hernia repair with transperineal approach: A case report. J Pelvic Med Surg 10:205, 2005. 31. Cattell RB, Cunningham RM: Postoperative perineal hernia following resection of the rectum. Surg Clin North Am 24:679, 1944. 32. Delmore JE, Turner DA, Gershenson DM, et al: Perineal hernia repair using human dura. Obstet Gynecol 70:507, 1987. 33. Brotschi E, Noe JM, Silen W: Perineal hernias after proctectomy. Am J Surg 149:301, 1985. 34. Hansen MT, Bell JL, Chun JT: Perineal hernia repair using gracilis myocutaneous flap. South Med J 90:75, 1997. 35. Hurwitz DJ, Walton RL: Closure of chronic wounds of the perineal and sacral regions using the gluteal thigh flap. Ann Plast Surg 8:375, 1981. 36. Salum MR, Prado-Kobata MH, Saad SS, Matos D: Primary perineal posterior hernia: An abdominoperineal approach for mesh repair of the pelvic floor. Clinics 60:71, 2005. 37. Sarr MG, Stewart R, Cameron JC: Combined abdominoperineal approach to repair of postoperative perineal hernia. Dis Colon Rectum 25:597, 1982.

38. Erdmann MWH, Waterhouse N: The transpelvic rectus abdominis flap: Its use the reconstruction of extensive perineal defects. Ann R Coll Surg Engl 77:229, 1995. 39. Spraycar M (ed): Stedman’s Medical Dictionary, 26th ed. Baltimore, Williams & Wilkins, 1995. 40. Rosenblum N, Rodriguez LV, Eilber KS, et al: Central tendon defects causing abnormal perineal support: Physical exam, perineal length, and magnetic resonance image (MRI) evaluation. Paper presented at the American Urological Association meeting, Orlando, FL, 2002. 41. Raz S: Repair of perineal hernia. In Atlas of Transvaginal Surgery, 2nd ed. Philadelphia, WB Saunders, 2002. 42. Bourcier AP, Juras JC, Villet RM: Office evaluation and physical examination. In Bourcier AP, McGuire EJ, Abrams P (eds): Pelvic Floor Disorders. Philadelphia, Elsevier Saunders, 2004, pp 133-148. 43. Walfisch A, Hallak M, Harlev S, et al: Association of spontaneous perineal stretching during delivery with perineal lacerations. J Reprod Med 50:23, 2005. 44. Baessler K, Schuessler B: Pregnancy, childbirth, and pelvic floor damage. In Bourcier AP, McGuire EJ, Abrams P (eds): Pelvic Floor Disorders. Philadelphia, Elsevier Saunders, 2004 pp 33-42. 45. Small KA, Wynne JM: Evaluating the pelvic floor in obstetric patients. Aust N Z J Obstet Gynecol 30:41, 1990. 46. Snooks SJ, Swash, M, Mathers SE, et al: Effect of vaginal delivery on the pelvic floor: A 5-year follow-up. Br J Surg 77:1358, 1990. 47. Parks AG, Porter NH, Hardcastle J: The syndrome of the descending perineum. Proc R Soc Med 59:477, 1966. 48. Benson JT: Physiology of anal continence and defecation. In Benson JT (ed): Female Pelvic Floor Disorders. New York, Norton Medical Books, 1992, pp 380-389. 49. Harewood GC, Coulie, B, Camilleri M, et al: Descending perineum syndrome: Audit of clinical and laboratory features and outcome of pelvic floor retraining. Am J Gastroenterol 94:126, 1999. 50. Dominguez JM, Saclarides TJ: Preprolapse syndromes. In Brubaker LT, Saclarides TJ (eds): The Female Pelvic Floor: Disorders of Function and Support. Philadelphia, FA Davis, 1996, pp 283-288. 51. Nichols DH: Posterior colporrhaphy and perineorrhaphy: Separate and distinct operations. Am J Obstet Gynecol 164:714, 1991. 52. Link RE, Su LM, Bhayani SB, et al: Laparoscopic sacral colpoperineopexy for treatment of perineal body descent and vaginal vault prolapse. Urology 64:145, 2004. 53. Cundiff GW, Harris RL, Coates K, et al: Abdominal sacral colpoperineopexy: A new approach for correction of posterior compartment defects and perineal descent associated with vaginal vault prolapse. Am J Obstet Gynecol 177:1345, 1997. 54. Cawkwell I: Perineal hernia complicating abdominoperineal resection of the rectum. Br J Surg 50:431, 1963. 55. Bach-Nielsen P: New surgical method of repairing sacral hernia following abdominoperineal resection of the rectum. Acta Chir Scand 133:67, 1967. 56. Buchsbaum HJ, White AJ: Omental sling for management of the pelvic floor following exenteration. Am J Obstet Gynecol 117:407, 1973. 57. Alexander JC, Beazley RM, Chretien PB: Mesenteric leaf repair of pelvic defects following exenterative operations. Ann Surg 182:767, 1975. 58. Bell JG, Weiser EB, Metz P, et al: Gracilis muscle repair of perineal hernia following pelvic exenteration. Obstet Gynecol 56:377, 1980. 59. Leuchter RS, Lagasse LD, Hacker NF, et al: Management of postexenteration perineal hernias by myocutaneous axial flaps. Gynecol Oncol 14:15, 1981. 60. Giampapa V, Keller A, Shaw WW, et al: Pelvic floor reconstruction using the rectus abdominis muscle flap. Ann Plast Surg 13:56, 1984.

Chapter 77

COMPLICATIONS OF VAGINAL SURGERY Raymond T. Foster, Sr., Cindy L. Amundsen, and George D. Webster Urologists and gynecologists use the vaginal approach to surgically correct many of the pelvic organ problems of women, including urinary incontinence, uterine and vaginal prolapse, vesicovaginal fistula, and urethral diverticulum. As surgeons continue to seek new ways to surgically treat women without laparotomy, it is important that vaginal surgeons remain informed about potential surgical complications, some of which are unique to this route of surgery. In this chapter, we review the potential complications of vaginal surgery, highlight patient characteristics and specific techniques that may be associated with a higher frequency of surgical complications, and outline strategies that may reduce the likelihood of a serious intraoperative or postoperative complication. Because this textbook is dedicated to a readership interested in female urology, we focus our discussion on complications related to urologic and pelvic reconstructive procedures. BLEEDING Problematic bleeding is undoubtedly the most feared problem that a surgeon encounters during or immediately after a surgical procedure. During the procedure, intraoperative bleeding compromises the surgeon’s ability to adequately complete the task at hand. The reported incidence of bleeding during vaginal surgery varies by specific procedure, and to some degree, reported rates of hemorrhage depend on the investigator’s definition of excessive blood loss. Most surgeons consider the need for blood transfusion a reliable definition of excessive surgical bleeding, but less blood loss can still interfere with surgical outcome and prolong hospitalization. Reported rates of such intraoperative hemorrhage are between 0% and 2% for most vaginal procedures, but these rates likely underestimate the incidence of problematic bleeding. Several investigators have reported low transfusion rates even when multiple vaginal reconstructive repairs, including hysterectomy and pubovaginal slings, are performed during the same operation. One of the largest series of patients undergoing multiple vaginal prolapse and incontinence procedures was reported by Shull and colleagues.1 Three hundred and two patients underwent a uterosacral vault suspension in combination with other support defects involving the urethra, bladder, posterior cul-desac, or rectum. The mean intraoperative blood loss for all patients in this study was 243 mL, and the blood transfusion rate was 1%. Other studies have reported similarly low rates of blood transfusion and blood loss between 200 and 350 mL when performing multiple vaginal prolapse repairs with a uterosacral vault suspension.2-5 In one report looking at a series of patients undergoing vaginal reconstructive procedures, each of which included uterosacral vault suspension, the investigator found that when he com-

pared blood loss between those having a hysterectomy at the time of repair with patients having only reconstructive procedures, hysterectomy did not significantly increase operative blood loss or the risk of significant bleeding.3 One of the attractive features of the uterosacral vault suspension for apical prolapse is its low incidence of troublesome bleeding. However, most published data are reported by experts in the field and may not accurately reflect the experience of the generalist surgeon. Although the reports cited found major intraoperative blood loss to be uncommon even when an apical prolapse procedure was performed, correction of the vaginal apex with a sacrospinous ligament fixation has been often associated with the potential for increased bleeding. This procedure, originally described by Richter,6 has been studied repeatedly in the past decade with regard to surgical complications in general and bleeding in particular. The incidence of excessive bleeding reported in most series has been between 0.5% and 3.5%.7-9 An important aspect of these statistics, however, is that maneuvers to control bleeding in this area have been reported to promote injury to adjacent structures, including the rectum and nerves. Nieminen and Heinonen9 reported a higher transfusion rate (28% of 25 women) when performing a sacrospinous ligament fixation in a population of patients older than 80 years. In an attempt to define the optimal surgical strategy for controlling intraoperative hemorrhage associated with sacrospinous ligament fixation, Barksdale and coworkers.10 conducted an anatomic study with 10 female cadavers to map the vascularity in the region of the sacrospinous ligament and propose surgical strategies for controlling hemorrhage. Their report detailed various combinations and permutations of vascular anastomoses in the area of the sacrospinous ligament (i.e., superior gluteal, inferior gluteal, internal pudendal, vertebral, middle sacral, lateral sacral, and external iliac by way of the circumflex femoral artery system). They concluded that because of the vascular anastomoses, the heroic approach of laparotomy with surgical ligation of the internal iliac artery was unlikely to be of significant benefit. They also determined the inferior gluteal artery to be the most likely artery responsible for hemorrhage related to the sacrospinous ligament fixation. Based on anatomic considerations, bleeding from the inferior gluteal artery is optimally controlled by any combination of packing and vascular clips by means of the vaginal approach or arterial embolization by invasive radiology techniques. We have become less hesitant to employ surface hemostatic factors, such as FloSeal (Baxter International, Deerfield, IL). Very few studies have evaluated factors associated with increased blood loss during vaginal surgery, such as surgeon skill level, surgical techniques, obesity, and the impact of prior pelvic surgery. Coates and associates11 reported surgical outcomes in 289 women undergoing a vaginal prolapse repair. In 154 of these operations, the senior staff member was the primary surgeon 751

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(mean blood loss, 248 mL), and in the remaining 135 procedures, a senior gynecology resident was the primary surgeon (mean blood loss, 234 mL). The difference in operative bleeding between the senior staff surgeon and the surgical trainee was not clinically or statistically significant. One retrospective review of surgical outcomes in obese women (i.e., body mass index [BMI] > 30 kg/ m2) compared surgical complications in 189 subjects undergoing abdominal hysterectomy and in 180 women having a vaginal hysterectomy.12 Both groups of obese women had a mean change in hemoglobin of 1.7 g and a 13% transfusion rate, which established obesity as risk factor for hemorrhage in female pelvic surgery, regardless of the chosen surgical approach. Besides patient characteristics and surgical experience, surgical equipment may also impact the occurrence of unacceptable bleeding. Good surgical exposure and lighting is paramount to achieving surgical goals and avoiding and controlling bleeding. The Lonestar retractor (Lone Star Medical Products, Stafford, TX) is invaluable in this regard because it retains an open introitus and allows the surgeon to maintain visualization of the vaginal apex. The use of a surgical headlight or a cool lighting system that is adherent to the retractor and placed within the pelvis (LightMat, Lumitex, Strongsville, OH) provides sufficient light for operating in a deep body cavity. In addition to the traditional ways of controlling bleeding, such as suture ligation and electrocautery, other user-friendly techniques have been introduced. In the United Kingdom, Hefni and colleagues13 randomized 116 patients to vaginal hysterectomy with traditional suture ligation (n = 59) or to vaginal hysterectomy with the LigaSure (Valleylab, Boulder, CO) vessel sealing system (n = 57).13 Mean intraoperative blood loss was 100 mL in both groups, but perioperative bleeding complications in the suture ligation group neared statistical significance (P = .0571). More than other approaches to surgery, the transvaginal approach may be technically challenging in the setting of previous surgery. Boukerrou and coworkers14 reported surgical outcomes of 741 women undergoing vaginal hysterectomy. Seventy-one (9.58%) of their subjects had undergone previous cesarean section, and the remaining 670 (90.41%) had not. Mean blood loss was 181.69 mL in the group of patients with previous cesarean section and 145.96 mL in the control group (P = .05). Among women with a history of cesarean section, 11.3% had intraoperative hemorrhage (i.e., blood loss in excess of 500 mL), compared with only 2.5% of women without a history of previous cesarean section. It is intuitive to surgeons that prior procedures in the same area render subsequent operations more difficult and prone to complications such as bleeding, but few articles report this conclusion. In addition to vaginal prolapse procedures, transvaginal incontinence procedures, such as pubovaginal slings, may also cause intraoperative bleeding. Even though the traditional bladder neck pubovaginal slings required more extensive transvaginal surgical dissection, including digital and usually blind dissection of the retropubic space, several large pubovaginal sling series have demonstrated rare intraoperative bleeding complications.15-18 The increasingly popular minimally invasive or midurethral sling is placed by passing a trocar blindly through the retropubic or obturator space. Although there are rare reports of iliac artery injuries published on the MAUDE database, most case series report a 1% to 3% increased bleeding rate resulting in pelvic or perineal hematomas. Abouassaly and associates19 reviewed 241 patients who had undergone placement of a tension-

free vaginal tape. These patients, recruited from six medical centers, had an intraoperative hemorrhage rate of 2.5% (16 patients). Four patients (1.9%) developed a pelvic hematoma within the first 24 hours after surgery. In another series, Krauth and colleagues20 described 604 patients undergoing placement of a minimally invasive suburethral sling by the transobturator approach. They reported a 0.8% incidence of intraoperative hemorrhage and postoperative development of two (0.33%) perineal hematomas, one of which resolved without intervention, and the other, believed to be associated with a concomitant prolapse repair (not the transobturator sling), required revision surgery. In summary, surgeons are wise to consider each patient’s individual risk factors for operative bleeding before surgery. Intuitively, obese women and women with a history of prior pelvic surgery may have an elevated risk for excessive surgical bleeding, and extra precautions should be taken in the operating room (e.g., good surgical assistants and exposure, blood products available on short notice). We evaluate bleeding time and platelet function for patients who provide us a history of prior intraoperative or postoperative hemorrhage. Any medication that can affect bleeding should be stopped 7 to 10 days before surgery when this can be safely accomplished. Surgeons who are managing patients who require some level of anticoagulation, such as a patient with a history of heart valve replacement or atrial fibrillation, are wise to obtain hematologic advice for the perioperative management of anticoagulation agents. INJURY TO THE URINARY TRACT Operating in the vagina places the surgeon close to the urinary tract, and great care must be taken to avoid its injury. As with any effort to avoid surgical complication, a sound surgical plan and good exposure are important, as is a thorough understanding of the anatomy within the surgical field. It is encouraging to consider that most injuries to the urinary tract during vaginal surgery are problematic only if unrecognized. Injuries to the urethra, bladder, or ureters that are identified at the time of surgery and primarily repaired most often heal without incident or further significant consequence to the patient.21 For this reason, we rarely perform vaginal surgery without a cystoscopic evaluation of the lower urinary tract and confirmation of bilateral ureteral spill after the administration of intravenous indigo carmine. In addition to absent ureteral spill, other abnormalities sought are suture transfixation or sling penetration of the bladder and surgical entry to the bladder, each of which would necessitate re-exploration for removal or repair. We also look for bladder wall ecchymosis, which may suggest the need for a longer period of postoperative catheterization. Several published studies have confirmed the importance of intraoperative cystoscopy when pelvic reconstructive procedures, including incontinence procedures, are performed. Harris and associates22 reviewed the records of 224 consecutive patients undergoing urogynecologic and reconstructive pelvic surgery. Based on a 4% rate of injury to the urinary tract, which would have been unrecognized without intraoperative cystoscopy, they concluded that cystoscopy should be included in all incontinence and pelvic reconstructive procedures. Another large, prospective study, in which intraoperative cystourethroscopy was performed universally on 471 women undergoing hysterectomy, documented a 7.6% rate of injury to the urinary tract.23 Of the patients in this

Chapter 77 COMPLICATIONS OF VAGINAL SURGERY

report, 144 (31%) had a vaginal hysterectomy. Among those patients having vaginal hysterectomy, 11 (7.6%) experienced an injury to their urinary collecting system; 6 of the 11 had concurrent prolapse surgery. Of the 11 injuries, 2 were ligated ureters, 7 were cystotomies, 1 was a suture in the bladder, and 1 was bladder abrasion. Concurrent prolapse surgery was therefore found to be an independent risk factor for injury to the urinary system. When controlling for prolapse and incontinence surgery, there was not a significant increase in the risk of urinary tract injury based on route of hysterectomy, age, BMI, race, blood loss, uterine size, and history of previous cesarean section. However, the standard of care in community practice is to not routinely perform cystoscopy at the end of hysterectomy or pelvic organ prolapse surgery. Transvaginal vault suspensions, specifically uterosacral vault suspensions, have been associated with urinary tract injuries, especially injuries involving one or both ureters. Because this vault suspension involves placement of sutures intraperitoneally above the level of the ischial spines, the ureter is near the suture placement. A cadaveric study by Buller and colleagues24 demonstrated the strength of the uterosacral ligament at various locations in the pelvis and its proximity to the ureter at the site of customary suture placement. Based on their findings after necropsy of 11 female cadavers, the ureter is, on average, 2.3 ± 0.9 cm from the uterosacral ligament at the level of the ischial spine. This finding led Buller and his colleagues to claim, “The proximity of the ureter to the distal uterosacral ligament warrants concern during vaginal vault repairs that use the ligament.”24 Several surgical series of uterosacral vault suspension have reported a 0% to 11% incidence of injury to the ureter.1-5 In each of these series, the injuries were identified at the time of surgery after confirming an absence of ureteral spill on cystoscopic evaluation. Management usually involved removal of the uterosacral suspensory sutures with or without ureteral stent placement; however, some injuries, presumably transections, required ureteroneocystotomy. In these reports, all injuries were detected by intraoperative cystoscopy at the time of surgery, and as a result, none of the patients had permanent or long-term urinary tract sequelae. In addition to ureteral injury, cystotomy may occur during transvaginal surgical entry into the peritoneal cavity and may be repaired and the operation continued in most circumstances.4 Aronson and colleagues25 reported the ureteral injury rate using a modified “deep” Mayo-McCall uterosacral ligament plication for vaginal vault suspension. The technique for placement of suture through the uterosacral ligament described by the investigators resulted in a uterosacral anchoring point much more dorsal and posterior than previously described. In this retrospective report of 411 consecutive patients, they observed three ureteral injuries, only one of which was attributable to the vault suspension procedure (0.24% [range, 0.01% to 1.35%]). Injury to the lower urinary tract is not uncommon in vaginal procedures designed to treat stress urinary incontinence, and the data depend on the procedure used. Factors such as anesthetic technique (i.e., regional or local versus general anesthesia) and the use of hydrodissection in the retropubic space were previously thought to affect bladder injury rate, but a report from Ghezzi and coworkers26 disputes these assumptions. The minimally invasive techniques for placement of midurethral slings are associated with the highest rate of bladder injury,

with some articles describing cystotomy rates greater than 10%.27-29 However, in one study that surveyed members of the American Urogynecologic Society and members of the Society for Urodynamics and Female Urology, only 10% to 15% of those surveyed from both groups admitted to cystotomy rates higher than 5%. More than 90% of the members in both societies would replace the trocar at the time of surgery, and more than 80% of the members in both societies would drain the bladder transurethrally for at least 24 hours if a cystotomy was made with the trocar.30 Some investigators have described risk factors associated with inadvertent cystotomy. Bodelsson and associates27, in their series of 177 patients undergoing a tension-free vaginal tape procedure, were able to show a statistically and clinically significant difference in the occurrence of cystotomy and urethrotomy among surgeons with different levels of experience. Another potential contributing factor to operative morbidity, including urinary tract injury, is obesity. However, Rafii and colleagues29 performed a midurethral sling in 38 consecutive patients with a BMI greater than 30 and compared outcomes with 149 age- and paritymatched controls with a BMI of 30 or less.29 They found no difference in estimated blood loss, operative times, bladder injuries, postoperative urgency, and voiding disorders. This study also found no difference between the two groups in objective and subjective cure rates. Lovatsis and coworkers28 studied 35 patient pairs (BMI = 35 kg/m2 versus BMI = 30 kg/m2) undergoing placement of tension-free vaginal tape. The patients were matched according to age and history of previous incontinence surgery. In this series, obesity was protective against injury to the lower urinary tract (0% versus 14%, P = .03). It may be that although obesity complicates vaginal access, it protects the bladder by virtue of the fat separation of the bladder from the symphysis pubis. Rardin and associates31 looked at surgical complications related to placement of tension-free vaginal tape as a primary procedure (n = 157) or as a secondary procedure for recurrent stress urinary incontinence (n = 88). The cystotomy rates were similar (3.2% versus 3.4%). In summary, surgical experience appears to be related to the occurrence of injury to the urinary tract during placement of retropubic midurethral slings. However, obesity and prior incontinence surgery do not appear to increase the risk of cystotomy or urethrotomy. We prefer to use a 70-degree cystoscope to evaluate the bladder and a 30-degree cystoscope to visualize the urethra after passing the trocars through the retropubic space but before the sling is placed. During cystoscopy, we are careful to fully expand the bladder with 400 to 500 mL of clear fluid, and we pay particular attention to the 11- and 8-o’clock and the 1- and 4-o’clock positions, which are the most likely areas to be penetrated during trocar passage. We are encouraged by failure to visualize a perforation with a fully expanded bladder and by the absence of hematuria. If a bladder perforation is identified, we remove the offending trocar and replace it, with an exaggerated emphasis on “hugging” the pubic bone during passage of the trocar. Cystoscopy is repeated to ensure adequate trocar placement is obtained on the second passage. After cystotomy, we leave a catheter for 24 to 72 hours postoperatively. Recognizing the need for a safer suburethral sling system that may not obligate the surgeon to cystoscopy, Delorme32 introduced a transobturator midurethral sling in 2001. Although there are few safety and efficacy data on this relatively new approach for sling placement, Cindolo and colleagues33 experienced a single

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bladder neck laceration, which was repaired intraoperatively, and no occurrence of bladder perforation after placing a midurethral sling in 80 women. However, cystoscopy was not used to definitively document the absence of bladder injury. In a similar series of 71 patients, Dargent and coworkers34 reported no instance of bladder perforation with the transobturator technique, despite cystoscopic examination at the time of surgery. Conversely, Minaglia and associates35 reported three bladder perforations in 61 patients and concluded that “routine intraoperative cystoscopy is therefore recommended for the identification of bladder injuries during the transobturator sling procedure.” Anecdotally, we have also seen a patient with an intraurethral sling after this approach. Vesicovaginal fistula (VVF) may occur after vaginal surgery, most commonly after hysterectomy (0.5% to 2% of cases).36,37 Examination of this occurrence shows that it more commonly follows the abdominal rather than the vaginal approach. The symptoms of continuous urinary leakage, usually developing between 1 and 6 weeks after surgery, are ominous and should lead to evaluation for fistula by vaginal examination, tampon test, and cystoscopy. Less commonly, the ureter is the source of a postoperative vaginal fistula. When suspecting a ureterovaginal fistula, usually heralded by urinary leakage emanating from the vaginal cuff, the physician should pursue further investigation with an excretory urogram. The intraoperative events that lead to VVF remain unknown, and the fact that the cervix must be dissected from the bladder adds to the inherent risk because the bladder wall may be thinned. Inadvertent entry into the bladder during this maneuver must be carefully repaired in layers, and a Foley catheter is left for sufficient time to allow healing. This area is close to the vaginal cuff closure, and any breakdown will promote fistula formation. Suture transfixation of the bladder by the cuff closure sutures has been suggested as a factor in the genesis of fistula, although animal experiments cast doubt on this theory. The proximity of the cuff and bladder at this location make this event almost unavoidable on some occasions, particularly when the patient is obese, hemostasis is poor, or exposure, lighting, and assistance are suboptimal. Cystoscopy may help identify the bladder injury that may lead to fistula formation, but it is not performed in most cases of hysterectomy. The timing of VVF repair has been reported to be successful at all intervals after discovery, and some advocate immediate surgical repair. However, a more judicious approach includes a period of catheterization, hoping for spontaneous healing. The size of the fistula affects the likelihood of success with this approach and how long it should be pursued. We time our intervention based on the status of the vaginal cuff tissue, and our preference is to monitor inflamed and edematous tissue at weekly intervals until the cuff reveals a healthy, mature fistulous tract. Vaginal repair usually can be performed by 6 weeks after hysterectomy. In summary, transvaginal surgical treatment of prolapse and incontinence is a significant risk factor for injuring the urinary tract in women. We believe that careful surgical planning and intraoperative cystoscopy is an advisable element for most vaginal surgeries that seek to correct these problems. We recognize that patients experience poor long-term outcomes after urinary tract injury when the problem is undetected at the time of occurrence. However, patients are likely to recover from surgery without incident when the urinary system is repaired at the time of the primary surgery.

BOWEL INJURY Complications involving the bowels most commonly occur during rectocele repair, although the high rectum is vulnerable during all varieties of vaginal vault suspension. For this reason, we prefer a low bowel preparation preoperatively and the placement of a rectal pack at the commencement of some procedures to aid in the identification of surgical landmarks. Injury to the bowel is a relatively uncommon occurrence during vaginal surgery. Hoffman and coworkers,38 at the University of South Florida, reported nine rectal injuries (0.7%) from their database of 1346 patients who underwent vaginal surgery between 1987 and 1998.38 Of the nine, six were being treated for prolapse, one for cervical dysplasia, one for fibroid uterus, and one for gender dysphoria. In another large study from a vaginal surgery database, Mathevet and colleagues39 reported 14 (0.45%) rectal injuries in 3076 patients undergoing vaginal surgery. Most (62.5%) of the 14 patients were undergoing surgery for the primary indication of genital prolapse. In the study of Isik-Akbay and associates12 comparing abdominal and vaginal routes of surgery in obese women undergoing hysterectomy, the investigators found five bowel injuries in the abdominal group (2.7%) and none among women having vaginal surgery. Although the difference was not statistically significant, this report suggests fewer rectal injuries in obese patients when surgery was performed vaginally.12 During rectocele repair, injury is most likely to occur in women undergoing repeat surgery. When the rectum is prepared before surgery and injury occurs, it is generally appropriate to repair the defect primarily. Even though the published rate of rectal injuries is low, we routinely perform a digital rectal examination at the conclusion of vaginal prolapse procedures that involve some risk of rectal injury to ensure that there is no blood on the examining finger and that there has been no suture transfixation. As with urinary tract injury, the best time to identify injury is at the time of the primary surgery. If a rectovaginal fistula does occur postoperatively, as with vesicovaginal fistula, the timing of repair is individualized and is dictated primarily by the status of the tissues. If the fistula is large, a temporary diverting colostomy is required to afford the patient the highest probability of a successful repair. Such decisions are individualized based on severity. INFECTION The hallmark clinical sign of postoperative infection is fever, and in surgical training, we are taught to investigate the cause of fever with physical examination, radiographic images, and laboratory studies. Historically, surgeons have treated postoperative fever with antibiotics even in the absence of an obvious cause after a comprehensive evaluation. More contemporary evidence, however, calls into question the medical necessity of treating an unidentified postoperative infection in most patients. In 1983, Freischlag and Busuttil40 reported their experience following 464 patients after abdominal surgery. They defined postoperative fever as a rectal temperature of 38.5°C or higher in the first 6 postoperative days. Seventy-one patients (15%) had postoperative fever. Only 19 (27%) of these 71 patients had an identifiable source of infection after a radiographic and laboratory evaluation. They concluded that routine evaluations of fever do not alter the outcome most patients and are not cost-effective.

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Shackleford and associates41 examined the predictive value of postoperative fever for infection in patients recovering from vaginal surgery. Febrile morbidity was defined in their series as an oral temperature greater than 38.0°C on two separate occasions, excluding the first 24 hours after surgery. They retrospectively examined outcomes of 431 vaginal surgery patients. Forty-three percent of these patients had vaginal hysterectomy alone, and the remaining 57% had a procedure for prolapse with (27%) or without (30%) vaginal hysterectomy. Fifty-four women (12.5%) had postoperative febrile morbidity. Thirty-five infections were definitively identified (8.1%), but only 13 of these infections occurred in the 54 patients with postoperative fever. Among the identified infections were 20 urinary tract infections (4.6%), five infections at the suprapubic catheter site (1.2%), three cases of vaginal cuff cellulites (0.7%), three “pelvic infections” (0.7%), and two cases of Clostridium difficile colitis. Two women had infection unrelated to their vaginal surgery; one was diagnosed with sinusitis and the other with bronchitis. Based on their findings, the investigators calculated the sensitivity of febrile morbidity for postoperative infection to be 40%, with a specificity of 98%, a positive predictive value of 26%, and a negative predictive value of 94%. Univariate analysis was performed, and they found that women with febrile morbidity were older, had longer procedures, lost more blood, were higher parity, and had lower uterine weights and longer hospital stays than women without febrile morbidity. Their data also demonstrated that women with proven infection had prolonged surgery, weighed less, had lower uterine weights, and stayed in the hospital longer than women without infections. Women who had hysterectomy done at the time of prolapse surgery were the most likely to have postoperative infection compared with women who had vaginal hysterectomy alone or prolapse surgery without hysterectomy. Vaginal surgery is a clean-contaminated procedure. Some investigators have become interested in the vaginal flora at the time of surgery. The assumption of these clinical scientists is that an understanding of how to manipulate the vaginal flora at the time of surgery (e.g., decrease the bacterial colony count) would aid in the prevention of postoperative infection for patients undergoing vaginal procedures. Culligan and colleagues42 published an observational study in 2003 that reported the rate of vaginal contamination (defined as an aerobic or anaerobic culture result of 5000 colony-forming units/mL) at given time intervals during vaginal reconstructive surgery. All patients in their study had preoperative antibiotic prophylaxis and a standard 5-minute surgical scrub with povidone iodine. The first set of cultures, obtained 30 minutes after the surgical scrub, revealed a 52% contamination rate in the surgical field, whereas the cultures collected at 90 minutes only had a 41% contamination rate. After this initial study that defined vaginal contamination as a surrogate end point for postoperative infection, Culligan and his group43 published their results of a randomized trial that evaluated povidone iodine and chlorhexidine gluconate as surgical scrub solutions for vaginal surgery. Fifty patients were enrolled in the study that demonstrated a clinically and statistically significant difference between the contamination rates of surgical fields prepared with povidone iodine (63% contaminated) and chlorhexidine gluconate (22% contaminated) at 30 minutes (P = .003; relative risk = 6.12; 95% CI: 1.7 to 21.6). Surgical infection is a problem that is often easier to prevent than to treat. In an era of prophylactic, broad-spectrum antibiot-

ics, we are rarely confronted with wound infections at the surgical site after vaginal procedures. Postoperative febrile morbidity and postoperative infections at sites remote from the vagina remain areas of some concern, especially in elderly patients, those with above-average blood loss, and patients who undergo prolonged surgical procedures.

COMPLICATIONS RELATED TO GRAFT MATERIALS USED IN THE VAGINA Reported rates of recurrent or de novo vaginal wall prolapse range from 15% to 30%44 and for this reason, many clinicians implant synthetic or organic (allograft or xenograft) material to address this problem. This position is supported by the fact that surgeons have known for a long time that the efficacy and durability of hernia repair is improved by the use of a graft material. However, long-term data associated with the use of the various graft materials, including complications and success rates for prolapse repair, are limited. Vaginal surgery is performed in a clean-contaminated field, and this adds the potential risk of infection and erosion when synthetic material is used. There are also concerns about whether the inclusion of grafts or synthetics in vaginal repairs may compromise vaginal caliber or elasticity and thereby compromise sexual function. There have been few well-designed studies to provide evidence that the risks of placing the mesh are balanced by a longer durability of the vaginal repair, but this continues to be the trend. Synthetic material may be absorbable or permanent. Two randomized studies evaluated the use of an absorbable synthetic graft to reinforce the vaginal prolapse repair, and they had opposing views on the success of the material. Neither, however, reported significant complications associated with the material. Sand and collegues45 randomized women to polyglactin 910 mesh (with anterior colporrhaphy) or to anterior colporrhaphy alone. Thirty women (43%) without mesh and 18 women (25%) with mesh had recurrent cystocele beyond the mid-vaginal plane (P = .02). The study authors concluded that polyglactin mesh was useful in the prevention of recurrent cystoceles. In 2001, Weber and coworkers46 compared standard colporrhaphy, standard colporrhaphy with polyglactin 910 mesh, and ultralateral anterior colporrhaphy. They analyzed 109 patients randomized to one of the three treatment arms, with a mean follow-up of 23.3 months (range, 4.5 to 44.4 months) and found no difference in the three groups with respect to the anterior vaginal wall. A single vaginal mesh erosion was the only mesh-related complication in this study. There seems not to be widespread interest in absorbable mesh to enhance prolapse repair. The most commonly reported permanent synthetic mesh used for vaginal prolapse has been polypropylene. Randomized, controlled studies are lacking, but several published case series using polypropylene mesh report a rate of recurrent prolapse not exceeding 6%.47-49 The same reports document mesh erosion rates between 7% and 13%, and postoperative, new-onset dyspareunia in 14% to 63% of patients. Management of vaginal exposure of the mesh should begin with conservative therapy such as intravaginal conjugated equine estrogen cream, but surgical resection of the exposed portion of mesh is commonly required. Organic materials such as cadaveric dermal or fascia lata grafts have also been used for vaginal prolapse reinforcement. In a

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randomized study evaluating the success of solvent-dehydrated fascia lata versus a standard anterior colporrhaphy, 21% of the allograft-reinforced group had recurrent prolapse, compared with 29% in the control group. This finding did not reach statistical significance. No vaginal erosions were reported among the 76 patients in the allograft group.50 We notice a surprising lack of literature to document the erosion rate of allograft material when used in transvaginal prolapse surgery, and there seems to be little evidence to guide management strategies when erosion does occur. In our own experience (69 women), we have found a 10.9% vaginal exposure rate of dermal allograft material when used in anterior or posterior repairs.51 We also documented a 100% rate of resolution of this problem with vaginal conjugated equine estrogen cream. The median time to complete healing in our series was 13 weeks. Xenograft material has been marketed for use in prolapse repair. Available materials include porcine dermis and porcine small intestinal submucosa. As with the materials discussed previously, there have been variable results, with recurrent prolapse reported in 8% to 39% of patients.52,53 Vaginal exposure of the graft appears to be relatively common, similar to that seen with cadaveric dermis, with a reported incidence of 15% and a healing time of up to 3 months with conservative therapy. Porcine dermis has several suggested beneficial characteristics, including the fact that it is 95% homologous to human collagen, possibly providing a nonallergenic scaffold for human tissue ingrowth. When considering complications such as vaginal graft erosion, infection, and postoperative dyspareunia, the physician may be wise to consider that the graft itself is not always the determining cause for these suboptimal outcomes. Surgical techniques of graft placement must always be considered, and it is inappropriate to always blame the product for a bad outcome; however, we have no way to control for the surgeon’s performance. Minimally invasive techniques used to place the material may produce complications related to blind passage of a trocar. Although the techniques are new with infrequent reports of complications, placement of augmented synthetic mesh using a trocar approach could cause rectal and bladder injury with the potential for rectovaginal fistula and vesicovaginal fistula.54 We await development of this field, which promises to simplify the repair of vaginal organ prolapse if the techniques can achieve good functional results and prove to be safe.55 INJURY TO THE PERIPHERAL NERVOUS SYSTEM Peripheral nerve injury resulting from vaginal surgery is an unexpected but reported complication after pelvic surgery. It is a potentially debilitating problem for the patient and a great concern for the surgeon. Most neuropathies that occur in reconstructive pelvic surgery are neurapraxic, and they heal with time. Physical therapy and neuroleptic medications plays a role in managing these patients, and rarely is surgery required for relief of symptoms. The nerve injuries most commonly reported have been sciatic nerve injuries and are largely thought to be caused by positioning in free-hanging stirrups.56-58 Injury to the sciatic nerve has been reported after sacrospinous ligament fixation in which the nerve was thought to be entrapped by the suture.8 Symptoms are usually buttock pain radiating down the posterior thigh, and if the cause is related to sacrospinous ligament fixation, removal of the suture often resolves the pain.

We have managed patients with temporary postoperative sciatic pain after undergoing transvaginal uterosacral cuff suspension by removal of the suture or expectant management with analgesics, anti-inflammatory agents, and neuroleptic medication. Recovery time for expectant management may be several months. Use of padded Allen stirrups with an extended padded lower leg support provides a secure and stable positioning for the patient’s legs, and we believe this added precaution reduces the risk of lower extremity neural injuries. Symptoms of femoral nerve injury include weakness with hip flexion, leg extension, and sensory loss over the anteromedial thigh and leg. These are uncommon but may follow prolonged lithotomy with the legs markedly abducted or a retractor blade compression injury after retropubic surgery.59 Injury to the common peroneal nerve may occur if pressure is placed on the lateral part of the lower part of leg where the nerve wraps around the fibular head or if there is hyperflexion of the thigh. The almost routine use of sequential compression hose, which raise the lower leg from the stirrup periodically, probably reduces this complication. Common symptoms of peroneal nerve injury are footdrop and sensory loss to the anterior leg and dorsal foot. In pelvic surgery, injury may occur to branches of the ilioinguinal and iliohypogastric nerves in the suprapubic location. These branches are susceptible to injury where the nerve runs on the undersurface of the external and internal abdominal oblique fascia above the symphysis, where they may become entrapped or involved by the fixation of pubovaginal slings. Patients present with sharp or burning pain and paresthesia in the suprapubic region that may radiate to the groin, and it can be quite problematic. Treatment may be by local injection of the trigger point, and occasionally, the site must be explored surgically to release the suture, lyse the fibrosis, or excise a neuroma. Obturator nerve injury may occur during vaginal, paravaginal, or transobturator prolapse surgery. The patient has difficulty adducting the leg (and therefore complains about problems walking) and may have sensory loss to the medial thigh. Injury to branches of the pudendal nerve, including the dorsal genital nerve to the clitoris and the perineal branch to the urethral sphincter, perineal skin, and anal sphincter, may occur during any anterior vaginal dissection. These unfortunate injuries therefore may occur during incontinence or prolapse surgery. Common symptoms of these uncommon injuries include sharp, burning pain to the perineal area or worsening of urinary and fecal incontinence. Important measures to reduce the incidence of neural injury include proper patient positioning, surgical technique to avoid known nerve locations, careful use of retractors and, avoidance of prolonged surgery. Even when all these preventative strategies are followed, neuropathies will occur. Postoperatively, clinical symptoms and physical examination allows the physician to make the diagnosis. If motor deficits are identified, a neurology consultation may be obtained for baseline testing and management options. CONCLUSIONS The possible complications associated with vaginal surgery are numerous and tend to be underestimated. Reducing complications is probably largely a product of the technical skills of the surgeon and the application of good surgical principles, but some events remain unavoidable. Variables contributing to the occur-

Chapter 77 COMPLICATIONS OF VAGINAL SURGERY

rence of adverse events in vaginal surgery that are beyond the immediate control of the surgeon include obesity, medical comorbidities, and undiagnosed bleeding dyscrasias. However, by good surgical planning and execution, the surgeon may reduce

the occurrence of complications. Vaginal surgery, when performed correctly and safely, remains one of the most rewarding aspects of surgical practice for female urologists and gynecologists.

References 1. Shull BL, Bachofen C, Coates KW, Kuehl TJ: A transvaginal approach to repair of apical and other associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 183:1365-1373; discussion 1373-1374, 2000. 2. Karram M, Goldwasser S, Kleeman S, et al: High uterosacral vaginal vault suspension with fascial reconstruction for vaginal repair of enterocele and vaginal vault prolapse. Am J Obstet Gynecol 185:133942; discussion 1342-1343, 2001. 3. Jenkins VR 2nd: Uterosacral ligament fixation for vaginal vault suspension in uterine and vaginal vault prolapse. Am J Obstet Gynecol 177:1337-1343; discussion 1343-1344, 1997. 4. Barber MD, Visco AG, Weidner AC, et al: Bilateral uterosacral ligament vaginal vault suspension with site-specific endopelvic fascia defect repair for treatment of pelvic organ prolapse. Am J Obstet Gynecol 183:1402-1410; discussion 1410-1411, 2000. 5. Amundsen CL, Flynn BJ, Webster GD: Anatomical correction of vaginal vault prolapse by uterosacral ligament fixation in women who also require a pubovaginal sling. J Urol 169:1770-1774, 2003. 6. Richter K: The surgical anatomy of the vaginae fixatio sacrospinalis vaginalis. A contribution to the surgical treatment of vaginal blind pouch prolapse [in German]. Geburtshilfe Frauenheilkd 28:321327, 1968. 7. David-Montefiore E, Garbin O, Hummel M, Nisand I: Sacro-spinous ligament fixation peri-operative complications in 195 cases: Visual approach versus digital approach of the sacro-spinous ligament. Eur J Obstet Gynecol Reprod Biol 116:71-78, 2004. 8. Lantzsch T, Goepel C, Wolters M, et al: Sacrospinous ligament fixation for vaginal vault prolapse. Arch Gynecol Obstet 265:21-25, 2001. 9. Nieminen K, Heinonen PK: Sacrospinous ligament fixation for massive genital prolapse in women aged over 80 years. BJOG 108:817-821, 2001. 10. Barksdale PA, Elkins TE, Sanders CK, et al: An anatomic approach to pelvic hemorrhage during sacrospinous ligament fixation of the vaginal vault. Obstet Gynecol 91:715-718, 1998. 11. Coates KW, Kuehl TJ, Bachofen CG, Shull BL: Analysis of surgical complications and patient outcomes in a residency training program. Am J Obstet Gynecol 184:1380-1383; discussion 1383-1385, 2001. 12. Isik-Akbay EF, Harmanli OH, Panganamamula UR, et al: Hysterectomy in obese women: A comparison of abdominal and vaginal routes. Obstet Gynecol 104:710-714, 2004. 13. Hefni MA, Bhaumik J, El-Toukhy T, et al: Safety and efficacy of using the LigaSure vessel sealing system for securing the pedicles in vaginal hysterectomy: Randomised controlled trial. BJOG 112:329333, 2005. 14. Boukerrou M, Lambaudie E, Collinet P, et al: A history of cesareans is a risk factor in vaginal hysterectomies. Acta Obstet Gynecol Scand 82:1135-1139, 2003. 15. Amundsen CL, Visco AG, Ruiz H, Webster GD: Outcome in 104 pubovaginal slings using freeze-dried allograft fascia lata from a single tissue bank. Urology 56:2-8, 2000. 16. Groutz A, Blaivas JG, Hyman MJ, Chaikin DC: Pubovaginal sling surgery for simple stress urinary incontinence: Analysis by an outcome score. J Urol 165:1597-600, 2001. 17. Morgan TO Jr, Westney OL, McGuire EJ: Pubovaginal sling: 4-year outcome analysis and quality of life assessment. J Urol 163:18451848, 2000. 18. Carbone JM, Kavaler E, Hu JC, Raz S: Pubovaginal sling using cadaveric fascia and bone anchors: Disappointing early results. J Urol 165:1605-1611, 2001.

19. Abouassaly R, Steinberg JR, Lemieux M, et al: Complications of tension-free vaginal tape surgery: A multi-institutional review. BJU Int 94:110-113, 2004. 20. Krauth JS, Rasoamiaramanana H, Barletta H, et al: Sub-urethral tape treatment of female urinary incontinence—morbidity assessment of the trans-obturator route and a new tape (I-STOP): A multi-centre experiment involving 604 cases. Eur Urol 47:102-106; discussion 106-107, 2005. 21. Mattingly RF, Borkowf HI: Acute operative injury to the lower urinary tract. Clin Obstet Gynaecol 5:123-149, 1978. 22. Harris RL, Cundiff GW, Theofrastous JP, et al: The value of intraoperative cystoscopy in urogynecologic and reconstructive pelvic surgery. Am J Obstet Gynecol 177:1367-1369; discussion 1369-1371, 1997. 23. Vakili B, Chesson RR, Kyle BL, et al: The incidence of urinary tract injury during hysterectomy: A prospective analysis based on universal cystoscopy. Am J Obstet Gynecol 192:1599-604, 2005. 24. Buller JL, Thompson JR, Cundiff GW, et al: Uterosacral ligament: Description of anatomic relationships to optimize surgical safety. Obstet Gynecol 97:873-879, 2001. 25. Aronson MP, Aronson PK, Howard AE, et al: Low risk of ureteral obstruction with “deep” (dorsal/posterior) uterosacral ligament suture placement for transvaginal apical suspension. Am J Obstet Gynecol 192:1530-1536, 2005. 26. Ghezzi F, Cromi A, Raio L, et al: Influence of the type of anesthesia and hydrodissection on the complication rate after tension-free vaginal tape procedure. Eur J Obstet Gynecol Reprod Biol 118:96100, 2005. 27. Bodelsson G, Henriksson L, Osser S, Stjernquist M: Short term complications of the tension free vaginal tape operation for stress urinary incontinence in women. BJOG 109:566-569, 2002. 28. Lovatsis D, Gupta C, Dean E, Lee F: Tension-free vaginal tape procedure is an ideal treatment for obese patients. Am J Obstet Gynecol 189:1601-1604; discussion 1604-1605, 2003. 29. Rafii A, Darai E, Haab F, et al: Body mass index and outcome of tension-free vaginal tape. Eur Urol 43:288-292, 2003. 30. Romero AA, Webster GD, Amundsen CL: Comparison of practice patterns when using the minimally invasive sling. J Pelvic Med Surg 11:76, 2005. 31. Rardin CR, Kohli N, Rosenblatt PL, et al: Tension-free vaginal tape: Outcomes among women with primary versus recurrent stress urinary incontinence. Obstet Gynecol 100:893-897, 2002. 32. Delorme E: Transobturator urethral suspension: Mini-invasive procedure in the treatment of stress urinary incontinence in women [in French]. Prog Urol 11:1306-1313, 2001. 33. Cindolo L, Salzano L, Rota G, et al: Tension-free transobturator approach for female stress urinary incontinence. Minerva Urol Nefrol 56:89-98, 2004. 34. Dargent D, Bretones S, George P, Mellier G: Insertion of a suburethral sling through the obturating membrane for treatment of female urinary incontinence [in French]. Gynecol Obstet Fertil 30:576-582, 2002. 35. Minaglia S, Ozel B, Klutke C, et al: Bladder injury during transobturator sling. Urology 64:376-377, 2004. 36. Hadley HR: Vesicovaginal fistula. Curr Urol Rep 3:401-407, 2002. 37. Harkki-Siren P, Sjoberg J, Tiitinen A: Urinary tract injuries after hysterectomy. Obstet Gynecol 92:113-118, 1998. 38. Hoffman MS, Lynch C, Lockhart J, Knapp R: Injury of the rectum during vaginal surgery. Am J Obstet Gynecol 181:274-277, 1999.

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39. Mathevet P, Valencia P, Cousin C, et al: Operative injuries during vaginal hysterectomy. Eur J Obstet Gynecol Reprod Biol 97:71-75, 2001. 40. Freischlag J, Busuttil RW: The value of postoperative fever evaluation. Surgery 94:358-363, 1983. 41. Shackelford DP, Hoffman MK, Davies MF, Kaminski PF: Predictive value for infection of febrile morbidity after vaginal surgery. Obstet Gynecol 93:928-931, 1999. 42. Culligan P, Heit M, Blackwell L, et al: Bacterial colony counts during vaginal surgery. Infect Dis Obstet Gynecol 11:161-165, 2003. 43. Culligan PJ, Kubik K, Murphy M, et al: A randomized trial that compared povidone iodine and chlorhexidine as antiseptics for vaginal hysterectomy. Am J Obstet Gynecol 192:422-425, 2005. 44. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501-506, 1997. 45. Sand PK, Koduri S, Lobel RW, et al: Prospective randomized trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Am J Obstet Gynecol 184:1357-1362; discussion 13621364, 2001. 46. Weber AM, Walters MD, Piedmonte MR, Ballard LA: Anterior colporrhaphy: A randomized trial of three surgical techniques. Am J Obstet Gynecol 185:1299-1304; discussion 1304-1306, 2001. 47. Dwyer PL, O’Reilly BA: Transvaginal repair of anterior and posterior compartment prolapse with Atrium polypropylene mesh. BJOG 111:831-836, 2004. 48. Milani R, Salvatore S, Soligo M, et al: Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with Prolene mesh. BJOG 112:107-111, 2005. 49. Yan A, Anne M, Karine A, et al: Cystocele repair by a synthetic vaginal mesh secured anteriorly through the obturator foramen. Eur J Obstet Gynecol Reprod Biol 115:90-94, 2004.

50. Gandhi S, Goldberg RP, Kwon C, et al: A prospective randomized trial using solvent dehydrated fascia lata for the prevention of recurrent anterior vaginal wall prolapse. Am J Obstet Gynecol 192:16491654, 2005. 51. Drake NL, Weidner AC, Webster GD, Amundsen CL: Patient characteristics and management of dermal allograft extrusions. Int Urogynecol J Pelvic Floor Dysfunct 16:365-377, 2005. 52. Altman D, Lopez A, Gustafsson C, et al: Anatomical outcome and quality of life following posterior vaginal wall prolapse repair using collagen xenograft. Int Urogynecol J Pelvic Floor Dysfunct 16:298303, 2005. 53. Gomelsky A, Rudy DC, Dmochowski RR: Porcine dermis interposition graft for repair of high grade anterior compartment defects with or without concomitant pelvic organ prolapse procedures. J Urol 171:1581-1584, 2004. 54. Jelovsek JE, Sokol AI, Walters MD, Barber MD: Anatomic relationships of infracoccygeal sacropexy (posterior intravaginal slingplasty) trocar insertion. J Pelvic Med Surg 11:60, 2005. 55. Biertho I, Dallemagne B, Dewandre JM, et al: Intravaginal slingplasty: Short term results. Acta Chir Belg 104:700-704, 2004. 56. Batres F, Barclay DL: Sciatic nerve injury during gynecologic procedures using the lithotomy position. Obstet Gynecol 62:92s-94s, 1983. 57. Burkhart FL, Daly JW: Sciatic and peroneal nerve injury: A complication of vaginal operations. Obstet Gynecol 28:99-102, 1966. 58. McQuarrie HG, Harris JW, Ellsworth HS, et al: Sciatic neuropathy complicating vaginal hysterectomy. Am J Obstet Gynecol 113:223232, 1972. 59. Flanagan WF, Webster GD, Brown MW, Massey EW: Lumbosacral plexus stretch injury following the use of the modified lithotomy position. J Urol 134:567-568, 1985.

Chapter 78

PATHOPHYSIOLOGY, DIAGNOSIS, AND TREATMENT OF DEFECATORY DYSFUNCTION Tracy Hull and Massarat Zutshi The domain of defecatory disorders is vast, and their treatment can be frustrating for the surgeon and the patient. Except for straightforward surgically correctible disorders, most diseases in this category have many causes and need treatment that encompass medical, behavioral, and surgical modalities. These patients often go from physician to physician seeking a cure for these complex disorders. ANATOMY Pathogenesis of the defecatory disorders can be a function of abnormal anatomy at the outlet. The anal sphincter complex is composed of the puborectalis, the internal anal sphincter, and the external anal sphincter. The puborectalis and the external anal sphincter are striated muscles that are primarily responsible for the process of defecation by voluntary relaxation. They are innervated by the S3 and S4 nerves. The internal anal sphincter accounts for about two thirds of the resting tone and is composed of smooth muscle. It is innervated by the autonomous nervous system. The external anal sphincter accounts for one third of the resting tone. Any process that causes a change in this normal physiology can lead to defecatory disorders. MECHANISM OF DEFECATION Storage is a function of the transverse colon. When the sigmoid colon is filled, the process of defecation commences with the propagation of stool into the rectum. Defecation occurs in response to the sensory stimulus generated by rectal distention that is received by receptors in the pelvic floor and anal transition zone; the rectum itself is not richly innervated by sensory nerves. The sensation of filling is normally perceived at a volume of 50 mL, and the maximum tolerated volume normally is about 200 mL. Rectal pressures should be more than the anal pressures for evacuation to take place, which is usually achieved by increasing the intra-abdominal pressure. The external anal sphincter and puborectalis relax, allowing fecal contents to be evacuated. If it is socially unacceptable at that time, the external anal sphincter contracts, and the sensation of the need to evacuate disappears.

lored to the patient’s presenting symptoms. All patients should be asked about their current medications, and a history should be sought for all medical problems, especially diabetes, thyroid disorders, scleroderma, multiple sclerosis, stroke, dementia, food intolerance, and inflammatory bowel disease. The evaluation of a female patient with fecal incontinence should include a detailed obstetric history, including the number of vaginal deliveries, tears and episiotomies, unusual presentations, and prolonged labor. Other pertinent points are pad usage and number of accidents, symptoms of urinary incontinence, previous perineal surgery, back injuries, irradiation, and effect of symptoms on sexual behavior. Patients undergoing evaluation for constipation should be specifically asked about the duration of symptoms, the use of digitation to relieve symptoms, and factors that relieve or alleviate symptoms. Physical examination of a patient with fecal incontinence should focus on the sphincters and pelvic floor. Scars are looked for, and the anal opening is assessed for any gaping. The anocutaneous reflex can be evaluated, providing a crude assessment of the nerves. The patient may then be asked to strain. Perineal descent and prolapsed hemorrhoids or prolapsed rectum should be looked for. A digital rectal examination with the patient squeezing assesses the tone, obvious defects, and muscle fatigue. For a patient with constipation, the digital rectal examination evaluates increased tone with paradoxical contractions when straining and the presence of an internal intussusception and rectocele. In cases of rectal prolapse, inspection is important to differentiate a true rectal prolapse from prolapsing hemorrhoids, mucosal prolapse, or an anal or rectal polyp. Enema A tap-water enema in the office is a good and simple test to evaluate the sphincter tone in an incontinent patient. After administering the enema, the nurse documents the time the patient can hold the 100 mL of water. A patient with a suspected rectal prolapse is examined on the commode after the enema is given. The rectal prolapse may be seen while the patient strains on the commode. In a patient with irritable bowel syndrome, it may demonstrate urgency in the presence of normal tone. Anal Physiology Testing

DIAGNOSIS History and Physical Examination A detailed history and physical examination is the first step in diagnosing any defecatory disorder. The history should be tai-

Anal physiology testing has two parts. The first is manometry, which records resting and squeeze pressures and evaluates rectal sensation by documenting the time of first sensation of rectal filling and maximum tolerated volume. Rectal compliance also can be calculated. Paradoxical pressures in the rectum can be 761

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Figure 78-1 Normal anal ultrasound. EAS, external anal sphincter; IAS, internal anal sphincter.

Figure 78-3 Defect in the internal and external anal sphincters.

demonstrable. After sphincteroplasty, the repaired sphincter can be evaluated with this test. Colon Transit Study Transit studies specifically demonstrate slow-transit constipation. This assessment reflects motility of the colon but not the rectum. The patient swallows capsules with radiopaque markers. The markers are followed on day 1, 2, 4, and 7. Demonstration of markers in the right and left colon on day 7 indicates slow transit of the fecal matter on the right side, supporting a diagnosis of colonic inertia. If markers are aggregated on the left side, the problem may be redundancy of the left colon or outlet obstruction. Defecating Proctogram Figure 78-2 Defect in the external anal sphincter.

recorded during squeeze and strain, and they also can be demonstrated on electromyography by identifying the external anal sphincter contraction. Balloon expulsion tests can demonstrate rectal inertia or loss of coordination among the rectum, pelvic floor, and anal sphincters. The second part of the test evaluates pudendal nerve terminal motor latency. The test uses the St. Marks electrode and records electrical impulses when the pudendal nerve is stimulated. The amplitude of the wave reflects the voltage, which is low or absent in neurologic disorders. Anorectal Ultrasound Endoluminal ultrasound is the single most important test to demonstrate sphincter defects. The normal sphincter is shown in Figure 78-1. Sphincter defects may be those of the internal anal sphincter or external anal sphincter (Fig. 78-2), or both (Fig. 78-3). Thinning of the internal anal sphincter is easily

Patients with constipation and symptoms suggesting obstructive defecation syndrome are subjected to a test in which contrast is instilled in the rectum, small bowel, vagina, and bladder. Patients defecate in a radiolucent commode, and serial radiographs are taken to demonstrate perineal descent, cystocele, enterocele, internal intussusception, and rectal prolapse. Dynamic Magnetic Resonance Imaging Dynamic magnetic resonance imaging (MRI) is a test that replaces the defecating proctogram. Contrast is instilled in the vagina and rectum, and serial MR images are taken with the patient straining. Newer imaging techniques use upright MRI scans with the patient seated and evacuating in the sitting position. This test can evaluate pelvic descent, rectal diameter before and during straining, the width of the pelvic hiatus, presence of enteroceles and sigmoidoceles, and prolapse of the uterus and bladder.1 It may become the confirmatory test for obstructive defecation. Cine radiography can give a dynamic picture of the process of evacuation, and it can demonstrate prolapse of the anterior wall of the rectum.

Chapter 78 DEFECATORY DYSFUNCTION

Colonoscopy Fecal incontinence after failed medical treatment and biofeedback and no IBD

All colonic pathology must be excluded before undertaking formal treatment of any defecatory disorder. Colonoscopy should be part of the workup of all patients older than 50 years and patients with any suspicion of mucosal pathology.

Anal ultrasound Anal physiology testing

Barium Enema A barium enema is warranted when the anatomy of the colon needs to be defined. It may be of use in cases of rectal prolapse to demonstrate a redundant sigmoid colon, necessitating a sigmoid colectomy. FECAL INCONTINENCE Pathophysiology Injury to the muscle complex or the nerves that supply them can result in a loss of continence. The most common etiologic factor is childbirth injury. Other causative factors are listed in Table 78-1. Treatment of Fecal Incontinence The treatment of fecal incontinence is based on the severity of symptoms, the anatomy of the sphincter mechanism, and the presence of nerve damage. An algorithm for management is provided in Figure 78-4, but treatment options depend on

Sphincter defect

Sphincteroplasty Unsuccessful Re-repair

Unsuccessful

No sphincter defect

Consider • Secca procedure • Post anal Repair • Graciloplasty • Sacral stimulation • Artificial anal sphincter • Colostomy Consider • Sacral stimulation • Artificial anal sphincter • Colostomy

Figure 78-4 Algorithm for the management of fecal incontinence. Sacral stimulation has been used successfully in some centers. Although listed, graciloplasty no longer available in the United States. IBD, irritable bowel disease. *Sacral stimulation has been used successfully in some centers. **Not available in the US.

the availability of certain procedures and on the patient’s comorbidities. Table 78-1 Causes of Fecal Incontinence Sphincter injury Childbirth trauma Surgical trauma Rectal injury, traumatic Irradiation Congenital causes Imperforate anus Colonic causes Fecal impaction Colitis, proctitis Rectal prolapse Tumors Decreased rectal compliance Neurogenic causes Peripheral disorders (e.g., diabetes) Central disorders Trauma Stroke Tumors Dementia Multiple sclerosis Functional causes Other causes Diarrhea Myopathy

Treatment of Minor Incontinence A thorough history and physical examination are the first step in treatment to rule out inflammatory bowel disease, irritable bowel disease, and neurologic disorders. Minor incontinence can be treated with medical management2 using bulking agents, which can change the consistency of stool and lead to evacuation as a mass movement. They are started in small doses to prevent abdominal distention and bloating, and they are gradually increased to achieve the desired effect. Other agents that are used slow the gastrointestinal motility. They tend to constipate the patients because they decrease the bulk of the stool during the increased transit time. Loperamide hydrochloride (Imodium) is the commonly used medication, and it may be started in doses of 2 mg before breakfast and advanced to a maximum of 16 mg daily as warranted. Diphenoxylate hydrochloride (Lomotil) is another drug that may be used, especially if diarrhea is the main symptom. It is started in doses of 1 tablet once or twice daily and may be advanced to 1 or 2 tablets three or four times daily. Amitriptyline3 has been used for idiopathic fecal incontinence. It acts through an anticholinergic mechanism, increasing intrarectal pressures. Phenylephrine cream is an α1-adrenergic blocker that has not been approved by the U.S. Food and Drug Administration (FDA). Used in some studies in strengths of 10% to 40%, it has been shown to increase resting pressures for 1 to 2 hours.4 Other treatment modalities include the use of regular (even daily) enemas, which evacuate the rectum until it fills again. Bulking agents may be used in conjunction to prevent seepage between enemas.

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Biofeedback and Kegel Exercises Kegel exercises are an integral part of the treatment of fecal incontinence, but they are ineffective as the sole treatment. They may benefit to patients with very mild incontinence and those with easy fatigability of the sphincter and no sphincter defect. Biofeedback training consists of retraining the patient’s response using visual, auditory, and sensory stimuli. It consists of strength training of the external sphincter, retraining the sphincter to coordinate rectal distention with external anal sphincter contraction, and sensory training of the rectal mucosa to be able to sense earlier when the rectum receives contents. It is done in the office by a trained therapist using the electromyographic apparatus to retrain and strengthen the sphincter, and a rectal balloon is used for sensory stimulation training. Some studies have shown improvement after biofeedback therapy.5 Biofeedback has been shown to benefit patients after sphincter repair.6 Treatment of Moderate Fecal Incontinence with an Intact Sphincter Secca Procedure The Secca procedure involves radiofrequency stimulation of the muscular layer of the anal canal and lower rectum. It has been hypothesized that the procedure causes stimulation of collagen deposition and remodeling over time, which can improve symptoms of fecal incontinence. The procedure is done under conscious sedation. After local anesthesia is injected, radiofrequency is delivered by means of a specialized probe that contains needles that pierce the mucosa and submucosa. In about 64 separate punctures, the radiofrequency is applied beneath the mucosal surface. Contraindications to this procedure include inflammatory bowel disease, a history of depression, collagen vascular disease, acute infections, pudendal neuropathy, and a history of pelvic irradiation.7 Sacral Stimulation Sacral nerve stimulation is FDA approved in the United States for stress urinary incontinence, and it is being evaluated under a research protocol for fecal incontinence. It produces constant stimulation of the sacral nerves, resulting in an increase in resting tone and squeeze pressures. In this procedure, a temporary stimulator is implanted as a first step, and if the patient improves, a permanent device is implanted. It has gained popularity in Europe, where it has been available for many years.8 Perianal Bulking Agents Bulking agents instilled in the perianal area are being studied.9 They work by increasing the internal bulk of the sphincter, preventing seepage of stool. An optimal bulking agent should be nonbiodegradable, should not migrate, and should be removable if the need arises. Treatment of Moderate to Severe Fecal Incontinence due to a Defect in the Sphincter Mechanism Overlapping Sphincter Repair: Sphincteroplasty Any fixable defect of the sphincter complex should be considered for repair. Because it is difficult to determine which patient will benefit, consideration should be given to all those with a defect. The technique involves a semicircular incision about 1 to 1.5 cm beyond the anal verge. For obstetric injuries, this arc spans about 200 degrees in a semicircular fashion, mirroring the anus. The branches of the pudendal nerves that innervate the external

sphincter approach the muscle from the posterolateral position. To avoid nerve injury, the arc of the incision should not extend to the extreme posterolateral position. The rectovaginal septum is dissected, and care is taken to avoid making buttonhole defects in the anal canal or rectum. Occasionally, the only part of the perineal body that remains is the vaginal and anal mucosa, and dissection in this situation can be difficult. The dissection is carried laterally to the ischiorectal fat. A finger placed in the vagina or rectum and dissecting from lateral to medial may facilitate the dissection. Any tears in the anal mucosa are repaired with 4-0 chromic suture. The ends of the sphincter are usually dissected with scar in the midline (or midportion of the injury). This scar is divided in the middle, leaving two ends of sphincter with scar attached. It is important to divide the scar but to not trim it from the ends of the sphincter, because this will provide tensile strength when the repair is done. If the internal and external muscles are injured, it is preferable to repair them as one unit. If the internal sphincter is intact, divide and repair only the external sphincter. The levator ani muscles may be plicated at this point using 1-0 or 2-0 delayed absorbable sutures. This may lengthen the anal canal. The vagina should be checked after the levator plication to ensure that a ridge or narrowing did not occur with levator plication, because this may contribute to dyspareunia. If the internal anal sphincter was intact, plication can be done before the sphincteroplasty if there is redundant internal sphincter. The sphincter ends that have been sufficiently mobilized to allow overlapping of the muscle are grasped. Some authorities10,11 advocate merely approximating the muscles, but if possible, overlapping the muscle ends is preferred using 2-0 polyglactin sutures, placing mattress sutures for the sphincteroplasty. Approximately six sutures (three on each side) are used. The repair tightens the anal canal such that only an index finger may be admitted. During the procedure, the wound may be irrigated with antibiotic solution. The skin edges are closed in a V-Y fashion, starting laterally and leaving the center open for drainage. If there is a significant amount of dead space, a 0.5-inch Penrose drain can be inserted and then removed postoperatively. Postoperatively, we keep patients on intravenous antibiotics for 2 to 3 days and withhold oral intake. Because sitz baths macerate the skin edges, they are avoided, but showers are permitted. We do not use constipating drugs. The Foley catheter is removed on postoperative day 2, and the patient is allowed a high-fiber diet just before discharge. At discharge, patients are placed on Metamucil, Citrucel, or Konsyl daily. Additionally, they take 1 ounce of mineral oil each morning. If they do not move their bowels by postoperative day 7, they take 1 ounce of milk of magnesia twice daily until their bowels begin to function. Because they undergo a complete bowel cleansing before surgery, patients may not move their bowels for several days after surgery. A diverting stoma is used at the discretion of the surgeon. Preoperatively, this should be discussed with patients who have had previous failed repairs, have concomitant inflammatory bowel disease, have severe diarrhea, or need an extremely complicated repair. A stoma does not ensure success but may aid a successful outcome in such patients.12 Initial functional improvement can be anticipated in 80% to 90%13-15 of patients. Pudendal nerve damage is associated with suboptimal results.13 Age does not seem to significantly affect results,12 although erratic bowel problems such as urgency and diarrhea may lead to continued incontinence. Wound infection occurs in up to a fourth of patients15 but does not usually adversely

Chapter 78 DEFECATORY DYSFUNCTION

affect the outcome unless the sphincter repair sutures become disrupted. Complete disruption of the skin sutures usually heals by secondary intention with adequate wound care. Long-term follow-up suggests that about 40% of patients undergoing a repair are expected to be continent without further surgery.16 In patients needing a repeat overlapping sphincter repair due to disruption of the initial repair, evidence suggests that satisfactory outcome can be achieved.17

Colostomy or Ileostomy When the symptoms are severe, the quality of life is greatly affected, and all other avenues have been unsuccessfully explored, a colostomy or ileostomy is a viable option. Although this procedure may sound drastic, it improves the quality of life for these patients, who otherwise become prisoners in their homes. CONSTIPATION

Dynamic Graciloplasty Graciloplasty is no longer available in the United States, because the stimulator is no longer supplied by the manufacturer. Indications for this procedure include sphincter defects from obstetric or traumatic injury, congenital defects, and idiopathic incontinence. Contraindications are diseases with a neurologic basis, such as multiple sclerosis. Dynamic graciloplasty has been an excellent choice for patients who have no alternative but to have a stoma. Success has been reported in about 40% to 65% patients undergoing this procedure.18,19 Treatment of Moderate to Severe Incontinence with an Intact Sphincter and No Neurologic Deficit Postanal Repair Postanal surgical repair is indicated in patients with an intact sphincter but no neurologic incontinence.20 The aim of this procedure is to increase the length of the anal canal, reestablish the anorectal angle, and tighten the anal canal. The operation is done through an inverted-V-shaped incision made 5 to 6 cm from the anal verge posteriorly. Flaps are raised, and the intersphincteric plane is identified. Dissection is carried in this plane cephalad to Waldeyer’s fascia, which is divided to expose the mesorectal fat. Figure-of-eight, 2-0 polypropylene sutures are placed to draw the two sides of the iliococcygeus muscle together. The sides do not approximate because of the distance, and the sutures are tied with minimal tension to form a lattice. The pubococcygeus muscle is the next muscle encountered. Sutures are placed and tied to again to form a lattice, especially posteriorly, although anteriorly, the ends may be approximated. The last layer plicated is the puborectalis and external sphincter. The skin is closed with absorbable suture in a V-Y fashion. Postoperative care is similar to that for sphincteroplasty. Postanal repair has lost popularity because of poor overall improvement results. Treatment of Severe Fecal Incontinence due to Failed Repairs or Neurologic Causes Artificial Anal Sphincter The artificial anal sphincter evolved from the artificial urinary sphincter. The device has three parts. The first is an inflatable cuff that encircles the anal orifice. The second is a pump with a valve that controls the fluid entering and exiting the cuff. It is placed in the labia or the scrotum. The third part a balloon that is placed in the space of Retzius. When the valve is activated, fluid flows from the cuff to the balloon, allowing defecation. Over the next 7 minutes, reverse flow from the storage balloon to the anal cuff produces occlusion of the anus. If evacuation is incomplete, the valve can be activated again. Continence is restored completely in the immediate postoperative period. The main problems associated with this procedure are the rate of infections and device malfunction. These problems can affect as many as 33% of patients, even after a period of learning how to operate the device.21,22

Pathophysiology It is difficult to define constipation. It often is defined by reference to bowel frequency, because this is the most convenient way to assess and document the condition. Bowel frequency of less than three movements per week is considered to be constipation, but this is not the only criterion. Excessive straining at stools and hard stools are other symptoms that should be considered. The pathophysiology of constipation is disordered motility of the colon and rectum rather than delayed motility. The transit time may not be vastly delayed, but the patient may be still be constipated. The many causes of constipation are listed in Table 78-2. It is important to differentiate constipation from obstructive defecaTable 78-2 Causes of Constipation Idiopathic causes Drugs Antidepressants Anticholinergics Antispasmodics Antipsychotics Iron supplements Calcium Antacids Opiates Antihypertensives Anticonvulsants Metabolic causes Diabetes mellitus Hypothyroid Hypercalcemia Pregnancy Neurogenic causes Hirschsprung’s disease Neurofibromatosis Hypoganglionosis Intestinal pseudo-obstruction Ganglioneuromatosis Neurologic causes Spinal cord lesions Parkinson’s disease Trauma to nervi erigentes Multiple sclerosis Collagen and vascular disorders Dermatomyositis Systemic sclerosis Amyloidosis

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tion syndrome because this changes the workup and treatment of these patients. A thorough history should include associated symptoms such as cramping, bloating, straining, use of digitation and pressure around the anus or in the vagina during evacuation, medications, presence of metabolic disorders, and cerebral and neurologic causes. The physical examination should include a digital rectal examination, which assesses prolapse of the anterior rectal wall, paradoxical contractions of the anal muscles, and rectal lesions. Most patients are referred to a surgeon after exhausting all medical treatments. A full workup includes excluding all metabolic causes listed in Table 78-2. Colon transit studies using radiopaque markers (i.e., sitz markers) are ordered for all patients with long-standing constipation not responding to medical treatment. Anal manometry is ordered for patients in whom an outlet obstruction is suspected. Manometry can demonstrate paradoxical contractions of the anal muscles, which may respond to biofeedback training. For patients suspected of having rectal prolapse or obstructive defecation syndrome, a defecating proctogram or dynamic MRI may be helpful. These studies provide valuable information regarding rectal dilatation during straining, pelvic descent, and the presence of obstructing sigmoidoceles or enteroceles. In patients with suspected adult Hirschsprung’s disease, a full-thickness biopsy is indicated for diagnosis if a rectal anal inhibitory reflex is not helpful (done as a part of anal manometry). Medical Management Recent-onset constipation may be treated with diet modification; increasing fiber with bulk laxatives (containing psyllium); saline laxatives such as magnesium citrate, magnesium sulfate, and hyperosmolar laxatives such as lactulose, sorbitol, and polyethylene glycol. Emollient laxatives such as mineral oil, docusate salts, stimulant laxatives such as castor oil, anthraquinones (e.g., senna, cascara sagrada, phenolphthalein, and bisacodyl are avoided for long-term use. Patients who have paradoxical contractions can be treated with biofeedback sessions23 and can be taught to use the right muscles to be able to initiate the process of defecation. Surgical Management For patients who have exhausted medical treatment, surgical treatment requires defining the problem as colonic inertia or obstructive defecation. The algorithm for treatment is provided in Table 78-2. Long-standing constipation due to colonic inertia is treated with a total colectomy with an ileorectal anastomosis or occasionally with a cecorectal anastomosis. Because preservation of the sigmoid colon is associated with postoperative constipation,24,25 an ileosigmoid anastomosis is not considered a good option. Laparoscopic colectomy is gaining popularity because of the decreased morbidity, shorter hospital stay, and better cosmetic result.26,27 Patients who undergo colectomy with ileorectal anastomosis have increased number of bowel movements, although many patients complain of incontinence and persistent symptoms of abdominal pain and bloating.28 Quality-of-life scores are usually not elevated although the symptoms of constipation are successfully treated.29,30 A less popular procedure is the antegrade continent enema (ACE) described by Malone in 1990. This procedure was described for children and later used in adults.31 Through a surgically con-

structed retrograde appendicostomy, washout of the colon is accomplished, although it can also induce high-amplitude waves and mass movement. Although this procedure has good results, it is marred by complications such as intestinal obstruction and perforation, and it may require many surgical revisions. A newer technique that is showing potential in treating constipation is neuromodulation. Sacral nerve stimulation, which is unavailable in the United States, has produced some promising results in studies conducted in Europe.32 Further research and newer techniques in neuromodulation may be the future treatment of choice for colonic inertia. Patients with obstructive defecation may respond to biofeedback,33 relaxation therapy, and retraining. This requires a dedicated therapist and a motivated patient. Results of biofeedback therapy are encouraging in carefully selected patients.23 Those with symptoms that do not respond to biofeedback have been improved with the stapled transanal rectal resection (STARR) procedure.34 This is widely used in Europe and uses a circular stapler to excise a full thickness of the rectal wall at a distance of about 6 to 9 cm from the anal verge. Surgery for constipation is appropriate for only selective patients and in patients with severe symptoms. Patients usually dictate the timing of the surgery, but they should be warned that not all preoperative symptoms are relieved. Usually, bowel frequency is a symptom that does improve.30 Figure 78-5 is an algorithm for management of patients with chronic constipation.

IRRITABLE BOWEL SYNDROME Pathophysiology Irritable bowel syndrome (IBS) is a disease of symptoms with no single pathologic entity. The prevalence has been estimated at 10% to 15% in the Western population,35,36 with only 3.3% being medically diagnosed.37 The Rome II criteria are commonly used (Table 78-3).38 The common symptoms are abdominal pain and altered bowel habits. Patients can develop symptoms with diarrhea (IBS-D) or constipation (IBS-C) as a predominant symptom or have a combination of diarrhea and constipation. There have been no studies that demonstrate a change in myoelectric activity in the colon and small intestine. Current studies are focusing on the role of visceral sensory abnormalities in IBS.39 This disease has been associated with various emotional disorders, and this has led to the speculation of being associated with a disorder of the central nervous system. However, it is uncertain whether this is a primary central nervous system disorder that affects gut motility or a primary gut disorder with inappropriate input from the central nervous system.40 Associations between sexual and physical abuse,41 abnormal psychiatric features,42 and IBS have been reported. Other factors are a history of prior gastrointestinal infection, malabsorption, and food intolerance. Treatment of Irritable Bowel Syndrome The diagnosis of IBS is essentially one of exclusion of organic causes. A workup should include a thorough history and physical examination, a complete blood cell count, sedimentation rate, thyroid profile, and stool analysis for parasites. For patients with diarrhea-predominant symptoms, a hydrogen breath test to rule out lactose intolerance is considered. IBS has been known to remit spontaneously.

Chapter 78 DEFECATORY DYSFUNCTION

Constipation Check medications and metabolic profile Rule out structural lesions via barium enema /Colonoscopy

Long-standing

Figure 78-5 Algorithm for the management of chronic constipation. IRA, ileorectal anastomosis; MRI, magnetic resonance imaging; ODS, obstructive defecation syndrome; STARR, stapled transanal rectal resection.

Recent Diet modification, fiber supplement, exercise

Medical treatment

No improvement

Colon transit study/anal manometry/dynamic MRI

Improvement

Medical treatment

Paradox

Slow transit

No improvement

Improvement

ODS Biofeedback

Colectomy + IRA

Diet The treatment of IBS is frustrating for the physician and the patient because it consists of a trial-and-error approach. The initial management is dietary guidance and counseling. It is important to have an in-depth dietary history that rules out food allergies, lactose intolerance, foods that cause increased gas production, and foods that induce an immune response, which contribute to mucosal inflammation. Diet is modified in accordance with symptoms. Fiber may help constipation-prone patients, and limiting fiber, salads, fresh fruit, and some vegetables may help those that are diarrhea prone. However, most patients with IBS rarely adhere to a strict dietary or supplementary regimen.43 Foods commonly found to help patients when excluded from the diet are milk, eggs, and wheat and, less commonly, coffee, nuts, and peas. Exclusion of wheat, potatoes, onions, and dairy products has been shown to decrease the amount of gas production. Lactose-free diets have not had any benefit in adult patients, except in selected groups of patients or cultures44 (e.g., Norwegian) in which the lactose intake is high. Drugs Causing Decreased Bowel Motility Antidiarrheal agents have been widely used in IBS-D patients. They delay transit time, increase anal pressures, and decrease rectal sensation, causing the stool to be dehydrated. Loperamide

STARR

is the most commonly used antidiarrheal and has been shown to decrease fecal urgency, borborygmi, and diarrhea.45 Other agents commonly used are cholestyramine, which is a resin that binds bile acids, and ondansetron,46 which is a serotonin receptor antagonist. Antispasmodic agents have a wide application in IBS. They range from anticholinergics such as dicyclomine to calcium channel blockers and peppermint oil, which is a naturally occurring carminative. Drugs for Irritable Bowel Syndrome with Constipation The 5-hydroxytryptamine type 4 (5-HT4) receptor agonist tegaserod stimulates peristaltic activity and increases small and large intestinal transit time. The dosage used has been (6 mg twice daily) has provided significant improvement of bloating, abdominal discomfort, and constipation (during first and repeated symptoms).47,48 The common side effects are diarrhea and headaches. Antidepressants Amitriptyline has been used in the IBS-D patients. In addition to its mood-lifting activity, it has a physiologic effect by inhibiting the motor activity of the gut. These effects are particularly helpful in patents with pain-predominant symptoms.

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Table 78-3 ROME II Criteria for the Diagnosis of Irritable Bowel Syndrome For at least 12 weeks (which need not be consecutive) of the preceding 12 months, abdominal discomfort or pain that has two of three of the folowing features* † 1. Pain relieved with defecation 2. Onset of pain associated with a change in frequency of stool 3. Onset of pain associated with a change in form (appearance) of stool Symptoms that cumulatively support the diagnosis of IBS 1. Abnormal stool frequency (more than three bowel movements per day; less than three bowel movements per week) 2. Abnormal stool form (lumpy or hard; loose or watery) 3. Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation) 4. Bloating or feeling of abdominal distention Symptoms are not typical of IBS 1. Pain that awakens or interferes with sleep 2. Diarrhea that awakens or interferes with sleep 3. Blood in the stool (visible or occult) 4. Weight loss 5. Fever Symptoms that further aid the diagnosis of IBS A. Fewer than three bowel movements a week B. More than three bowel movements a day C. Hard or lumpy stools D. Loose or watery stools E. Straining during a bowel movement F. Urgency G. Feeling of incomplete bowel movement H. Passing mucus during a bowel movement I. Abdominal fullness, bloating, or swelling Categoration of of IBS based on symptoms‡ Diarrhea-predominant IBS: At least one of B, D, and F but none of A, C, and E, or at least two of B, D, and F plus one of A or E Constipation-predominant IBS: At least one of A, C, and E but none of B, D, and F, or at least two of A, C, and E plus one of B, D, and F *Rome I criteria not included in this algorithm. The diagnosis of IBS relies on meeting Rome II inclusion criteria (updated by Rome III criteria) and excluding other illnesses based on the history, physical examination, and laboratory testing. † In addition to meeting these positive criteria, patients have initial laboratory testing with a complete blood cell count, basic chemistry panel, and an erythrocyte sedimentation rate. The diagnostic accuracy for IBS is more than 95% when the Rome II criteria are met, the history and physical examination results do not suggest any other cause, and initial laboratory test results are negative. ‡ An update to these criteria was issued at the Rome III conference and published in May 2006. The preferred terms were changed to IBS with diarrhea (from diarrhea-predominant IBS) and to IBS with constipation (from constipation-predominant IBS). In this categorical system, many people whose features place them close to a subtype boundary (e.g., IBS with alternating stool pattern) can change pattern without a major change in pathophysiology.

Other Drugs Prokinetic drugs such as cisapride (which has been taken off the market) have been used in IBS-C patients.49 Other drugs that have been used are anxiolytics, antigas preparations, and mast cell degranulation inhibitors such as disodium chromoglycolate. Probiotics have been studied, and the results are conflicting.50 The probiotic commonly used is Lactobacillus plantarum. Alosetron (Lotronex), a 5-HT3 receptor antagonist, decreases small and large intestine motility and transit time. It has been used to treat severe IBS-D patients for control of diarrhea and abdominal discomfort.51,52 The use of alosetron has been limited because of its association with ischemic colitis53 and serious complication of constipation.54 Other Therapies Other treatment modalities that have been helpful are relaxation therapy,55 psychotherapy,56 and hypnotherapy.57 Patients with IBS frequently present with symptoms of constipation or fecal incontinence. These patients most often fail surgical corrections unless the symptoms of IBS are brought under control first. RECTAL PROLAPSE Overt rectal prolapse is the prolapse of the entire thickness of the rectal wall through the anal orifice. This is usually a problem seen in older women. A multitude of treatment modalities have been described, highlighting the fact that treatment is controversial and that no one treatment or surgery is entirely successful. Etiopathology The cause of rectal prolapse is unknown, but several theories have been postulated. The first of these, described by Moschowitz,58 attributes rectal prolapse to a sliding hernia through a defect in the pelvic fascia. The second theory by Brodin and Snellman59 postulates that rectal prolapse is an intussusception of the rectum starting about 3 inches above the anal verge. Radiologic findings that the prolapse starts well above the pelvic floor rules out the possibility of this being a sphincter disorder. Predisposing factors are intractable constipation, chronic diarrhea, neurologic diseases, anatomic defect due to pregnancies, previous surgeries, and psychiatric illness. Rectal prolapse has been categorized as complete or full-thickness (Fig. 78-6) wall prolapse through the sphincters or intussusception that has not protruded beyond the sphincter complex. It should be differentiated from mucosal prolapse (Fig. 78-7). Workup The confirmatory test is a clinical demonstration of a rectal prolapse and the exclusion of prolapsing hemorrhoids. Other tests are done for associated symptoms and to rule out colonic pathology. These tests may include a barium enema to look for a redundant colon, anorectal manometry and dynamic MRI (when obstructive defecation is suspected), transit studies in patients with constipation, and a colonoscopy. Treatment of Rectal Prolapse The earliest operation for rectal prolapse was described by Thiersch in 1891. It involved encircling the anus with a silver

Chapter 78 DEFECATORY DYSFUNCTION

Figure 78-6 Complete rectal prolapse.

Figure 78-7 Mucosal prolapse of rectum.

wire, thereby decreasing the anal opening. This procedure has largely been abandoned. The current operative procedures are divided into abdominal and perineal procedures. The abdominal procedures are based on fixing the rectum to the sacrum; the perineal procedures aim at excision of the prolapsed rectum. Abdominal Procedures The principles of abdominal procedures are based on rectal mobilization and fixation, with or without resection of the sigmoid colon based on the patient’s symptoms. Rectal mobilization is described subsequently, and the various methods of rectal fixation are discussed. Abdominal Mobilization of the Rectum Rectal mobilization is carried out through a Pfannenstiel or midline incision. The extent varies among surgeons but usually involves posterior mobilization to the coccyx and incision anteriorly to the upper third of the vagina. Lateral mobilization is controversial, and at least one lateral stalk may be preserved to avoid new evacuation problems.

Rectal Fixation Rectal fixation can be achieved by using mesh (i.e., Ripstein’s procedure) or a foreign material (i.e., Ivalon sponge repair) or suture rectopexy. Ripstein’s procedure is more frequently done outside the United States. Ripstein and Lante60 thought that the rectal prolapse was caused by loss of attachment of the rectum, which makes it lose its posterior curvature and become a straight tube. Massive straining causes the rectal walls to intussuscept, which begins at the rectosigmoid junction and finally protrudes through the anus. They did not believe that the pelvic defects were the primary cause and did not see the need to repair them. Rectal fixation was achieved initially by fascia lata and later changed to Marlex mesh61 and Gore-Tex mesh.62 In this procedure, the rectum is mobilized to the tip of the coccyx posteriorly. The lateral stalks may be divided. The free end of a 5-cm Marlex or Gore-Tex mesh is fixed to the sacrum with nonabsorbable sutures, which are placed 1 cm from the midline, taking care to avoid any presacral bleeding. The mesh is wrapped around the rectum anteriorly, and the free end is sutured to the other side in a similar fashion. The sling should be loose enough to admit two fingers. The peritoneum is then closed over the sling. Intraoperative complications of this procedure include presacral bleeding. Postoperative complications include hemorrhage and pelvic abscesses.63 Late complications include persistent constipation, new onset of constipation, recurrence, erosion of the mesh, and strictures. The recurrence rate has been cited as 2% to 10%.64,65 Some investigators66 have recommended this procedure be performed with a sigmoid resection in patients with a longstanding history of constipation. However, others are hesitant to resect large intestine in the face of introducing mesh at the same procedure.63 Ivalon sponge repair was described by Wells67 in 1959 and was popular in Europe. After rectal mobilization, a rectangular piece of Ivalon sponge is moistened and fixed to the sacrum in the midline using nonabsorbable sutures. The mobilized rectum is then pulled upward in front of the sponge, and the sponge is wrapped around the rectum and sutured to the anterior wall, leaving one third of the circumference free anteriorly. The sponge is then buried under the peritoneum. The predominant complication is pelvic abscess, which occurs in about 16% of the patients.68 Even though an abscess usually necessitated removal of the sponge, inflammatory scarring of the rectum on many occasions fixes the rectum to the sacrum, thereby curing the prolapse. This procedure is not performed in the United States. Suture rectopexy was first described by Pemberton and Stalker.69 It fixes the rectum to the sacrum posteriorly. After mobilization of the rectum posteriorly, proctopexy is achieved using two or three nonabsorbable sutures on either side to fix the rectum to the presacral fascia, taking care to avoid the presacral vessels, which can result in bleeding. Suture rectopexy has been associated with a mortality rate of 0% to 6.7% and a recurrence rate of 0% to 20%.70 In many, the incontinence decreases in time after rectopexy.71 Abdominal Rectopexy with or without Resection of the Sigmoid Colon Sigmoid resection alone has not been popular for rectal prolapse. However, resection of the sigmoid colon has been advocated when constipation is a predominant symptom preoperatively

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and a redundant sigmoid colon has been demonstrated by imaging studies. In some cases, this improves after sigmoid resection.72 Resection and the subsequent fibrosis that occurs in the area of the anastomosis may add to the fibrosis that occurs with a rectopexy. Laparoscopic Rectopexy The laparoscopic approach is theoretically similar to the open procedure, and results should be comparable, but the technique is still evolving. The advantage of the laparoscopic technique is a reduction in pain at the incision site and hospital stay.73 Laparoscopically assisted rectopexy has acceptable results, with a morbidity rate of 9%, leak rate of less than 1%, and a recurrence rate of 2.5% for a full-thickness and 18% for a mucosal prolapse.74 Studies have demonstrated that laparoscopic resection has a short-term benefit in the length of stay and is comparable to open prolapse surgery in the long term for continence and constipation and recurrence rates.14 Perineal Procedures Perineal Rectosigmoidectomy Perineal rectosigmoidectomy was initially described in 1889 and popularized by Miles75 in 1933. Subsequently, Altemeier76 championed its use in the United States. The indication for surgery is the high-risk individual who may not tolerate the anesthesia needed for an abdominal approach. Some institutions have advocated this approach for young men in whom the abdominal procedures may carry a higher risk of sexual dysfunction.77 It can be done under local, regional, or general anesthesia in the lithotomy position. The anastomosis can be hand-sewn or stapled. A circumferential incision is carried out 1 to 2 cm above the dentate line, and of the rectum is mobilized. The mesentery of the rectum is clamped and divided until the bowel cannot be pulled down anymore. The bowel is then transected and anastomosed to the distal cut end. Before the anastomosis, the levator muscles may be plicated in an effort to lengthen the anal canal to improve continence. Complications include bleeding from the suture line, dehiscence of the suture line, anastomotic stricture, injury to the small bowel, and an increase in morbidity due to pulmonary and cardiac complications in fragile patients.78 Delorme Procedure The Delorme79 procedure is another perineal procedure. It has become more popular in recent years. A circular incision is made in the mucosa about 1 cm above the dentate line, and the mucosa is carefully lifted away, taking care to cauterize any bleeding vessels on the way. This continues until there exists no further redundancy. The redundant mucosa is amputated, and the

mucosal ends are then brought together and sutured. Recurrence rates vary from 5% to 20%.80 Abdominal versus Perineal Procedures The abdominal procedure is the procedure of choice for the medically fit patient in most institutions because of the lower recurrence rates. Perineal procedures are usually offered to frail patients with comorbidities. The choice of perineal procedure usually rests with the surgeon and depends on his or her level of experience. The perineal rectosigmoidectomy has a lower recurrence rate than the Delorme procedure.81 The Delorme procedure may be a choice when there is insufficient length to do a perineal rectosigmoidectomy. Concomitant levatoroplasty after a perineal rectosigmoidectomy has been shown to improve continence.81 The most common abdominal procedure is rectopexy with or without resection. The abdominal procedures are associated with better continence than the perineal procedures.82 Suture rectopexy has acceptable results, and the addition of mesh posteriorly does not seem to offer any distinct advantage. The addition of a sigmoid resection is of value in patients with a redundant colon and symptoms of constipation. The Ivalon sponge has been associated with an increase in infection and has been abandoned. The Ripstein’s procedure has been associated with new-onset constipation due to the mesh configuration. Laparoscopic rectopexy is gaining popularity, and with time and development of new instruments, it will be performed more.73 Emphasizing the mental algorithm in approaching patients with rectal prolapse Kim and colleagues83 reviewed 188 perineal rectosigmoidectomy and 160 abdominal rectopexy patients. They found no significant differences in morbidity but found a higher recurrence rate with perineal procedures. Recurrent rectal prolapse is treated by a repeat repair, and both abdominal and perineal repairs have been advocated. However, care should be taken to delineate the previous anastomosis. It is important to consider all previous operations in an attempt to avoid rendering a section of bowel ischemic due to division of blood vessels at the previous repair. CONCLUSIONS Evaluation of the individual patient is the key to treating defecatory disorders and fecal incontinence. There is no perfect cure for these ailments, and much patience and time goes into making a diagnosis and reaching an individual treatment plan that can help these patients. Newer treatment options are emerging, and the modalities of treatment may change in the future.

References 1. Pannu HK: Magnetic resonance imaging of pelvic organ prolapse. Abdom Imaging 27:660-673, 2002. 2. Scarlett Y: Medical management of fecal incontinence. Gastroenterology 126:S55-S63, 2004. 3. 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 43:1676-1681, 2000. 4. Cheetham MJ, Kamm MA, Phillips RKS: Topical phenylephrine increases anal canal resting pressure in patients with fecal incontinence. Gut 48:356-359, 2001.

5. Ozturk R, Niazi S, Stessman M, Rao SS: Long-term outcome and objective changes in anorectal function after biofeedback therapy for fecal incontinence. Aliment Pharmacol Ther 20:667-674, 2004. 6. Jensen LL, Lowry AC: Biofeedback improves functional outcome after sphincteroplasty. Dis Colon Rectum 40:197-200, 1997. 7. Efron JE, Corman Ml, Fleshman J, et al: Safety and effectiveness of temperature controlled radiofrequency energy delivery to the anal canal. Dis Colon Rectum 46:1606-1616, 2003. 8. Conaghan P, Farouk R: Sacral nerve stimulation can be successful in patients with ultrasound evidence of external anal sphincter disruption. Dis Colon Rectum 48:1610-1614, 2005.

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9. Vaizey CJ, Kamm MA: Injectable bulking agents for treating faecal incontinence. Br J Surg 92:521-527, 2005. 10. Arnaud A, Sarles JC, Sielezneff I, et al: Sphincter repair without overlapping for fecal incontinence. Dis Colon Rectum 9:744-747, 1991. 11. Tjandra JJ, Han WR, Goh J, et al: Direct repair vs overlapping sphincter repair: A randomized controlled trial. Dis Colon Rectum 46:937-942, 2003. 12. Young C. J, Mathur MN, Eyers AA, Solomon MJ: Successful overlapping anal sphincter repair relationship to patient age, neuropathy and colostomy function. Dis Colon Rectum 41:344-349, 1998. 13. Fang DT, Nivatongs S, Vernuelen FD, et al: Overlapping sphincteroplasty for acquired anal incontinence. Dis Colon Rectum 27:720722, 1984. 14. Solomon MJ, Young CJ, Eyers AA, Roberts RA: Randomized clinical trial of laparoscopic versus open abdominal rectopexy for rectal prolapse. Br J Surg 89:35-39, 2002. 15. Young CJ, Mathur MN, Eyers AA, Solomon MJ: Successful overlapping sphincter repair: Relationship to age, neuropathy and colostomy formation. Dis Colon Rectum 41:344-349, 1998. 16. Gutirrez AB, Madoff RD, Lowery AC, et al: Long-term results of anterior sphincteroplasty. Dis Colon Rectum 47:727-731, 2003. 17. Vaizey CJ, Norton C, Thornton MJ, et al: Long-term results of repeat anal sphincter repair. Dis Colon Rectum 47:858-863, 2004. 18. Baeten CG, Geerdes BP, Adang EMM, et al: Anal dynamic graciloplasty in the treatment of intractable fecal incontinence. N Engl J Med 332:1600-1605, 1995. 19. Wexner SD, Gonzalea-Padron A, Rius J, et al: Stimulated gracilis neosphincter operation: Initial experience pitfalls, and complications. Dis Colon Rectum 39:957-964, 1996. 20. Rainey JB, Donaldson DR, Thompson JP: Post-anal repair: Which patients derive most benefit? J R Coll Surg Edinb 35:101-105, 1990. 21. Casal E, San Ildefonso A, Carracedo R, et al: Artificial bowel sphincter in severe anal disease. Colorectal Dis 6:180-185, 2004. 22. Wong D, Jensen LL, Bartolo DC, et al: Artificial anal sphincter. Dis Colon Rectum 39:1345-1351, 1996. 23. Chiaroni G, Salandini L, Whitehead WE: Biofeedback benefits patients only patients with outlet dysfunction not patients with isolated slow transit constipation. Gastroenterology 129:86-97, 2005. 24. Pemberton JH, Rath DM, Ilstrup DM: Evaluation and surgical treatment of severe chronic constipation. Ann. Surg 214:403-411, 1991. 25. Beck DE, Fazio VW, Jagleman DG, Lavery IC: Surgical management of colonic inertia. South Med J 82:305-309, 1989. 26. Sample C, Gupta R, Bambriz F, Anvari M: Laparoscopic subtotal colectomy for colonic inertia. J Gastrointest Surg 9:803-808, 2004. 27. Wexner SD, Daniel N, Jagleman DG: Colectomy for constipation: physiological investigation is the key. Dis Colon Rectum 34:851-856, 1991. 28. Webster CMD: Results of colectomy for colonic inertia: A sixteen year experience. Am J Surg 182:639-644, 2001. 29. 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 46:1720-1721, 2003. 30. Thaler K, Dinnewitzer A, Oberwalder M, et al: Quality of life after colectomy for colonic inertia. Tech Coloproctol 9:133-137, 2005. 31. Hill J, Scott S, MacLennan I, et al: Antegrade enemas for the treatment of severe idiopathic constipation. Br J Surg 81:1490-1491, 1994. 32. Malouf AJ, Wiesel PH, Nicholls T, et al: Short term effects of sacral nerve stimulation for idiopathic slow transit constipation. World J Surg 26:166-170, 2001. 33. Bassotti G, Chistolini F, Sietchiping-Nzepa F, et al: Biofeedback for pelvic floor dysfunction in constipation. Br J Surg 328:393-396, 2004. 34. Bosscanta P, Venturi M, Salamina G, et al: New trends in the surgical treatment of outlet obstruction: Clinical and functional results of

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two novel transanal stapled techniques from a randomised controlled trial. Int J Colorectal Dis 19:539-369, 2004. Drossman DA, Cammilleri M, Mayer EA, et al: AGA technical review of irritable bowel syndrome. Gastroenterology 123:21082131, 2002. Talley NJ: Irritable bowel syndrome: Definition, diagnosis and epidemiology. Baillieres Best Pract Res Clin Gastroenterol 13:371-384, 1999. Hungin APS, Chang L, Locke GR, et al: Irritable bowel syndrome in the United States prevalence, symptoms patterns and impact. Aliment Pharmacol Ther 21:1365-1375, 2005. Boyce PM, Koloski NA, Talley NJ: Irritable bowel syndrome according to varying diagnostic criteria: Are the Rome II criteria unnecessarily restrictive for research and practice? Am J Gastroenterol 95:3176-3183, 2000. Poitras P, Riberdy PM, Boivin M, Verrier P: Evolution of visceral sensitivity in patients with irritable bowel syndrome. Dig Dis Sci 47:914-920, 2002. Wingate DL: The irritable bowel syndrome. Gastroenterol Clin North Am 20:351-365, 1991. Drossman DA, Leserman J, Nachman G, et al: Sexual and physical abuse in women with functional or organic gastrointestinal disorders. Ann Intern Med 113:828-833, 1990. Walker EA, Katon WJ, Jemelka RP, et al: Comorbidity of gastrointestinal complaints, depression, and anxiety in the Epidemiologic Catchment Area (ECA) study. Am J Med 92:26S-30S, 1999. Rees GA, Davies GJ, Parker M, Trevan M: Gastrointestinal symptoms and diet of members of an irritable bowel self-help group. J R Soc Health 14:222-227, 1994. Bohmer CM, Tuynman HE: The clinical relevance of lactose malabsorption in irritable bowel syndrome. Eur J Gastroenterol Hepatol 8:1013-1016, 1996. Cann PA, Read NW, Holdsworth CD, Barends D: Role of loperamide in the management of irritable bowel syndrome. Dig Dis Sci 1984; 29:239. Steadman CJ, Talley NJ, Phillips SF, Zinsmeister AR: Selective 5hydroxytryptamine type 3 receptor antagonism with ondansetron as treatment for diarrhea predominant irritable bowel syndrome—A pilot study. Mayo Clin Proc 67:732-738, 1992. Schonfield P: Efficacy of current drug therapies in Irritable bowel Syndrome: What works and does not work. Gastroenterol Clin North Am 34:319-335, 2005. Tack J, Müller-Lissner, Bytzer P, et al: A randomised controlled trial assessing the efficacy and safety of repeated tegaserod therapy in women with irritable bowel syndrome and constipation (IBS-C). Gut 54:1701-1713, 2005. Van Outryve M, Milo R, Toussaint J, Van Eeghem P: Prokinetic treatment of constipation-predominant irritable bowel syndrome a placebo controlled study of cisapride. J Clin Gastroenteral 13(1): 49-57, 1991. Madden JA, Hunter JO: A review of the role of gut microflora in irritable bowel syndrome and the effects of probiotics. Br J Nutr 88: S67-S72, 2002. Lembo T, Wright RA, Bagby B, et al: Alosetron controls bowel urgency and provides global symptom improvement in women with diarrhea prone IBS. Am J Gastroenterol 96:2662-2670, 2001. Cammilleri M, Northcutt AR, Kong S, et al: The efficacy and safety of alosetron in female patients with IBS. Am J Gastroenterol 355:1035-1040, 2000. Freidel D, Thomas R, Fisher RS: Ischemic colitis during treatment with alosetron. Gastroenterology 121:231-232, 2001. Cammilleri M, Chey WY, Mayer EA, et al: A randomized controlled clinical trial of the serotonin type 3 receptor antagonist alosetron in women with diarrhea-predominant irritable bowel syndrome. Arch Intern Med 61:1733-1740, 2001. Heymen-Monnikes I, Arnold R, et al: The combination of medical treatment plus multicomponent behavioural therapy is superior to

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56. 57. 58. 59. 60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70.

medical treatment alone in the treatment of irritable bowel syndrome. Am J Gastroenterol 95:981-994, 2000. Svedlund J: Psychotherapy in irritable bowel syndrome: A controlled outcome study. Acta Psychiatr Scand Suppl 306:67-86, 1983. Whorwell PI, Prior A, Faragher EB: Controlled trial of hypnotherapy in the treatment of severe refractory irritable bowel syndrome. Lancet 2:1232-1234, 1984. Moschowitz AV: The pathogenesis and cure of the prolapse of the rectum. Surg Gynecol Obstet 15:7-21, 1912. Broden B, Snellen B: Procedentia of the rectum studied with cine radiography: A contribution to the discussion of causative mechanism. Dis Colon Rectum 11:330-347, 1968. Ripstein CB, Lanter B: Etiology and surgical therapy of massive prolapse of the rectum. Ann Surg 157:259-264, 1963. Keighley MR, Fielding JW, Alexander-Williams J: Results of Marlex mesh abdominal rectopexy for rectal prolapse in 100 consecutive patients. Br J Surg 70:229-232. 1983. Cicconi M, Romanelli P, Cardelli M, et al: Abdominal Wells rectopexy with patch micromesh PTFE (Goretex) [in Italian]. G Chir 24:46-52, 2003. Athanasidis S, Weynad G, Heilgers J, et al: The risk of infection of three synthetic materials used in rectopexy with or without colonic resection for rectal prolapse. Int J Colorectal Dis 11:42-44, 1996. Gordon PH, Hoexter B: Complication of Ripstein’s procedure. Dis Colon Rectum 21:277-280, 1978. Biehl AJ, Pay JE, Gathright JB: Repair of rectal prolapse: Experience with the Ripstein sling. South Med J 71:923-925, 1978. Tjandra JJ, Fazio VW, Church JM, et al: Ripstein’s procedure is an effective procedure for treatment of rectal prolapse without constipation. Dis Colon Rectum 36:501-507, 1993. Wells C: New operation for rectal prolapse. Proc R Soc Med 32:602603, 1959. Kupfer CA, Goligher JC: One hundred consecutive cases of complete rectal prolapse of the rectum treated by operation. Br J Surg 57:481487, 1970. Backer OG, Baden H: The Pemberton-Stalker rectopexy. Dis Colon Rectum 86:421-422, 1964. Loygue J, Nordinger B, Cunci O, et al: Rectopexy to the promontory for the treatment of rectal prolapse. Dis Colon Rectum 27:356-359, 1984.

71. Blachford GJ, Perry RE, Thorson AG, et al: Rectopexy without resection for rectal prolapse. Am J Surg 158:574-576, 1989. 72. Mckee RF, Lauder JC, Poon FW, et al: A prospective randomized study of abdominal rectopexy with and without sigmoidectomy in rectal prolapse. Surg Gynecol Obstet 174:145-148, 1992. 73. Boccasanta P, Rosati R, Venturi M, et al: Comparison of laparoscopic rectopexy with open technique in the treatment of complete rectal prolapse: Clinical and functional results. Surg Laparosc Endosc 8:460-465, 1998. 74. Ashari LHS, Lumley JW, Stevenson ARL, Sitz RW: Laparoscopicallyassisted resection rectopexy for rectal prolapse: ten year experience. Dis Colon Rectum 48:982-987, 2004. 75. Miles WE: Rectosigmoidectomy as a method of treatment for procidentia recti. Proc R Soc Med 26:1445-1452, 1933. 76. Altemeier WA, Culbertson WR, Schowengerdt C, Hunt J: Nineteen years experience with the one stage perineal repair for rectal prolapse. Ann Surg 173:993-1006, 1971. 77. Yakut M, Kayamakcioglu N, Simsek A, et al: Surgical treatment of rectal prolapse. A retrospective analysis of 94 cases. Int Surg 83:5355, 1998. 78. Williams JG, Rothenberger DA, Madoff RD, Goldberg SM: Treatment of rectal prolapse in the elderly by perineal proctosigmoidectomy. Dis Colon Rectum 35:830-834, 1992. 79. Delorme E: On the treatment of total prolapse of the rectum by excision of the rectal mucous membranes or retrocolic. Dis Colon Rectum 28:544-553, 1985. 80. Lechaux JP, Atienza P, Goasguen N, et al: Prosthetic rectopexy to the pelvic floor and sigmoidectomy for rectal prolapse. Am J Gastroenterol 182:465-469, 2001. 81. Agachan F, Reissmann P, Pfeifer J, et al: Comparison of three perineal procedures for the treatment of rectal prolapse. South Med J 90:925-992, 1997. 82. Watts JD, Rothenberger DA, Buls JG, et al: The management of rectal procidentia: 30 years experience. Dis Colon Rectum 28:96102, 1985. 83. Kim DS, Tsang CB, Wong WD, et al: Complete rectal prolapse: Evolution management and results. Dis Colon Rectum 42:460-466, 1999.

Chapter 79

URETHROVAGINAL FISTULA Jason P. Gilleran and Philippe E. Zimmern Urethrovaginal fistula (UVF) presents a challenging diagnostic and therapeutic dilemma for the reconstructive surgeon. Because of its uncommon occurrence, much of what is known about this entity is derived from small series and case reports. Consequently, most UVFs are seen and treated in specialized centers, whether they manifest alone or in combination with a vesicovaginal fistula. The underlying cause, number of prior repairs, and damage to the continence mechanism are key factors in approaching the patient with a UVF. This chapter reviews the common causes, diagnostic modalities, and therapeutic options for UVFs. ETIOLOGY Postoperative Iatrogenic Factors Traumatic fistulas resulting from obstetric deliveries account for most UVFs in underdeveloped nations, whereas in industrialized nations,1 UVFs occur as a complication of urethral diverticulectomy, anterior colporrhaphy, or other periurethral procedures. Some direct injuries are recognized at the time of the original surgery. In this instance, closure of the urethral lumen without verifying water-tightness, overlapping suture lines, lack of consideration for tissue interposition, insufficient bladder drainage, or a combination of these factors can contribute to the secondary formation of a UVF. Indirect mechanisms are less common but have been reported after periurethral collagen injection2 and an anterior colporrhaphy during which tight suburethral plication resulted in tissue necrosis and secondary fistula formation.3 An unrecognized urethral injury, which can occur during urethrolysis and particularly in the setting of dense periurethral scar tissue after a sling procedure, is another indirect mechanism. Most contemporary series on synthetic slings using tension-free vaginal tape or transobturator tape report a low incidence of urethral injuries and secondary urethral erosions, which can result in UVFs.4-6 Radiation Therapy Although the incidence of vaginal fistulas occurring after irradiation for pelvic malignancies is significantly lower than in the past because of technical advances in radiation delivery, the profound long-term effects of radiation on surrounding tissues can promote fistula formation. Repair with flap interposition should be considered, but a supravesical diversion may be the only remaining option for heavily radiated tissues. Other Causes Vaginal lacerations after pelvic trauma, if ignored or inadequately repaired, can lead to UVF formation. Primary closure of vaginal

lacerations is advocated to prevent fistula formation; regardless of the approach, these lacerations are susceptible to wound dehiscence if not properly débrided before repair.1 Although rare, a neoplasm arising from a urethral diverticulum7 can extend locally and manifest as a UVF. Likewise, radiation therapy for urethral cancer can lead to tumor necrosis and a secondary UVF. DIAGNOSIS History and Physical Examination Presenting symptoms may provide some insight as to the location and size of a UVF. Fistulas distal to the urethral continence mechanism may be entirely asymptomatic, or they may manifest as a split urinary stream or vaginal voiding. Occasionally, recurrent urinary tract infections are the main presenting symptoms. Women with larger fistulas or with fistulas involving the proximal urethra and bladder neck region present with continuous incontinence. It is important to review the prior operative notes, evaluate tissue quality (i.e., multi-operated, densely scarred, or atrophic tissues), and look for risk factors for deficient healing (e.g., immunosuppression, malnutrition, irradiation). Physical examination should identify the size and location of the fistula and any other associated fistulas or tissue changes. However, smaller tracts may be challenging to recognize, requiring endoscopy and imaging for exact determination. In some cases, a high index of suspicion despite thorough negative investigations may lead to urethrocystoscopy under anesthesia to establish the diagnosis. Imaging Visualization of the fistula tract may be accomplished by voiding cystourethrography8,9 or by double-balloon urethrography, but these techniques require high resolution to see the tract and true lateral views (Fig. 79-1). Upper tract imaging may be necessary for large or multiple fistulas to exclude ureteral obstruction or an associated ureterovaginal fistula. Urethral magnetic resonance imaging is of limited benefit to identify a fistula tract and is occasionally helpful in case of suspected residual diverticulum pocket associated with a UVF after urethral diverticulectomy. Endoscopy Direct visualization of the fistula opening on the floor of the urethral lumen with a short-beaked female urethroscope or a flexible scope can confirm the diagnosis.10 It is important to document the size of the opening and its location in the urethra in relation to the continence mechanism. The status of the bladder neck, trigone, and ureteric orifices should be observed, as well as the condition of the surrounding tissues for changes 775

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Table 79-1 Perioperative Checklist High lithotomy (or prone) position Short-beaked female cystourethroscope (consider guidewire and open-ended ureteral catheter) Suprapubic tube placement (Lowsley retractor or percutaneous kit) Headlight Vaginal retractor (Scott Lone Star, Turner-Warwick) Injectable saline and marking pen

Fine urethral instruments and sutures Access to autologous sling harvest (rectus fascia, fascia lata) Interposing graft (Martius labial fat pad, gracilis muscle) Soft urethral catheter Magnifying loupes (optional) Vaginal pack, antibiotics and anticholinergic medications (belladonna and opium suppository)

Surgical Repair

Figure 79-1 Lateral view from voiding cystourethrography (VCUG) of a woman with a urethrovaginal fistula at the mid-urethra demonstrates a fistula tract, with contrast seen in the vagina. Good resolution and true lateral voiding films are important in visualizing the tract on VCUG.

suggesting inflammation or neoplasm. A biopsy may be indicated for friable and irregular fistula edges or in case of a palpable induration around the fistula site. After vaginal laceration or urethral tear, the urethra may be completely strictured and the UVF located proximal to the site of urethral injury. Transvaginal endoscopy can help accessing the fistula tract and possibly the bladder by advancing a small flexible scope through the tract. MANAGEMENT The decision on how and when to best manage a UVF largely depends on the cause of the fistula, the quality of the surrounding tissues, the correction of risk factors for poor tissue healing whenever possible, and the number of prior repairs. Experience with urethral reconstruction procedures is paramount to achieving a good technical outcome. A large armamentarium of additional procedures to secure continence and prevent fistula recurrence should be available to the repairing surgeon. Observation Small fistulas in the distal urethra may be discovered incidentally and observed if minimally or asymptomatic. Spontaneous resolution of UVF with short-term catheter drainage has been reported.11 Most patients, however, choose surgical repair.

The goals of UVF repair are to close the tract, prevent recurrence of the fistula, and restore continence as indicated. In the case of a small distal fistula tract producing a split urinary stream with minimal or no incontinence, a simple marsupialization procedure to create a hypospadiac opening (i.e., Spence procedure) may correct the problem.12 We review two scenarios for transvaginal repair of a UVF, one involving a simple primary closure for a small nonirradiated UVF and the other a larger UVF necessitating more advanced techniques of urethral reconstruction and flap interposition for continence and closure. Primary Closure with a Vaginal Flap A primary repair using layered closure was first described by Collis,13 and it is ideal in the setting of a small to medium-sized UVF in nonirradiated tissues. Sterile urine must be obtained preoperatively, and antibiotic administration must be continued perioperatively. Several elements are necessary to facilitate a successful repair, as listed in Table 79-1. Patient positioning varies between advocates of the prone position14 and those preferring a high lithotomy position. Maximum perioperative urinary drainage is best achieved with a urethral and a suprapubic catheter. Exposure is facilitated by a Lonestar retractor (Lone Star Medical Products, Stafford, TX) or other self-retaining retractor, a weighted vaginal speculum, a headlight, and even magnifying glasses if available. Passage of a Teflon guidewire over a 5-Fr open-ended ureteral catheter through the tract can facilitate the dissection of the tract (Fig. 79-2). Hydrodissection with normal saline can aid in separating the vagina from the urethral wall. A broad-base, inverted-U-shaped incision is made in the anterior vaginal wall. This broad-base flap permits secondary tissue interposition (e.g., autologous sling, Martius labial fat pad graft15) (Fig. 79-3). After raising the anterior vaginal flap, the fistula opening on the vaginal wall is closed with fine absorbable sutures. In our experience, which follows the principles recommended by Raz for a vaginal repair of a vesicovaginal fistula, the wellcircumscribed UVF tract is not excised. This decision prevents enlarging the fistula site and creating further bleeding and urethral compromise. Closure of the tract is performed with two running absorbable sutures started at each corner of the fistula

Chapter 79 URETHROVAGINAL FISTULA

tract and run toward the midpoint. After water-tightness of the repair is verified,16 it is frequently necessary to interpose a layer over the urethral repair to minimize the risk of recurrence. We routinely use an autologous sling (i.e., rectus or fascia lata) interposition, which serves the dual purpose of restoring continence and minimizing recurrence. After the sling is secured in place at the undersurface of the urethra and over the UVF closed site, the initially raised anterior vaginal wall flap is advanced to complete the vaginal closure. Use of a fibrin adhesive as a protective layer between suture lines has been reported.17 A vaginal pack with antibiotic ointment is placed for 24 hours, and anticholinergic medications are administered to avoid secondary bladder spasms.

Figure 79-2 Passage of a 5-Fr ureteral catheter over a Teflon guidewire facilitates identification of the fistula tract during dissection. Additional hooks as part of the self-retaining retractor (lateral) are important to adequately visualize the surgical field.

A

Urethral Reconstruction In advanced cases involving a severely damaged urethra from many previous urethral procedures, a more complex surgical repair may be necessary. At the time of consent, it is essential to explain to the patient and her family the challenges posed by repairing a large urethral defect with often scarred, thin, and poorly vascularized tissues or making a neo-urethra. A large defect always compromises the continence mechanism; closing

B

Figure 79-3 A, An inverted-U-shaped anterior vaginal wall flap incision is made, with the fistula outlined. Creating a broad vaginal flap is essential to avoid flap necrosis and allow for adequate mobilization. B, The flap is advanced and the fistula tract closed, with tissue interposition between the two (transparent) to prevent recurrence.

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A

C

B

the defect alone will lead to an incontinent pipe-stem urethra, and urethral support with a nonsynthetic sling can aid in restoring continence. Despite these precautions, a secondary UVF fistula can occur, and even after a technically successful repair, various degrees of stress or urge incontinence, secondary urethral narrowing, or even voiding dysfunction can remain challenging issues to manage. Before deciding which technique to employ, a careful examination under anesthesia is needed to determine the precise location and extent of the urethral loss, the quality and length of the anterior vaginal wall, and the condition of the labia minora and the labia majora. Traditionally, the options for repair are limited to the creation of an anterior vaginal wall flap or a tube graft from the labia minora. When the defect extends into the bladder neck and trigone, placement of ureteral stents is recommended. After the tissues are adequately mobilized, our preference to create a neo-urethra or a segmental inferior urethral plate is to roll labia

Figure 79-4 Construction of a neo-urethra in a large urethrovaginal fistula involving extensive tissue loss (A). Vaginal flaps are mobilized and tubularized over a soft urethral catheter (B), with labial tissue used for flap coverage of the neo-urethra (C).

minora flaps medially and suture them with invagination of the mucosal layer18 around a 14- or 16-Fr, soft, Silastic urethral catheter (Fig. 79-4). Then a second layer of tissue (i.e., Martius or sling, or both) is interposed before vaginal closure. Using the vagina to create a urethra usually is our second choice, and it can be considered when the anterior vaginal wall is long enough or the risk of foreshortening is not a concern in a patient who is not sexually active. Beyond these two scenarios are a multitude of complex reconstructions involving poor-quality tissues, occasionally damage from radiation exposure, total or near-total urethral loss, or refractory UVFs, for which other techniques may need to be considered, including an anterior bladder wall flap, other interposition tissues (e.g., gracilis, rectus muscle,19 omental flap), or vaginal wall closure with an island of bulbocavernous musculocutaneous flap20 with attached skin. However, in such advanced cases, consideration should be given to transvaginal or abdomi-

Chapter 79 URETHROVAGINAL FISTULA

nal21 bladder neck closure or a continent or noncontinent urinary diversion.22 Postoperative Care Broad-spectrum antibiotic coverage is continued, and the vaginal pack is removed after 24 to 48 hours. Uninterrupted postoperative bladder drainage with urethral and suprapubic catheters is imperative. Anticholinergic medications are administered during this period to limit bladder spasms and to prevent catheter expulsion. After approximately 3 to 4 weeks, voiding cystourethrography should be used to document urethral integrity and exclude a fistula recurrence. Return to sexual activity is delayed until complete healing of the vagina has occurred. RESULTS Because of the rarity of UVF, no large case-control series or randomized trials are available. Most case series consist of heterogenous UVFs managed with different techniques. One series divided 34 women into three groups based on the degree of urethral damage and type of surgical repair. In women with intact urethras who underwent a primary, transvaginal, layered closure, 23 (88%) of 26 experienced a successful anatomic and functional outcome.12 Five women with destruction of the posterior urethra underwent extensive reconstruction, with all having successful anatomic outcomes, but only two of five were continent postoperatively. In another series of nine women with UVF, there was a 100% anatomic success rate after primary repair with a Martius labial graft interposition, with no cases of recurrent fistula or stricture.18 However, two patients required additional surgery for stress incontinence. Similar success rates were reported in a series of 24 patients who underwent UVF repair using a Martius fat pad for reinforcement.11 The systematic use of a Martius labial fat pad interposition for all UVF repairs is arguable. In a report of 11 women with UVF, 7 who had undergone primary or vaginal flap closure without a Martius procedure had recurrences and subsequently underwent secondary repair with a labial fat pad.1 The four remaining patients who underwent a Martius procedure had excellent anatomic results. In another retrospective study of 12 women with UVF, 3 of 4 patients who were repaired primarily alone had recurrences, compared with only 1 of 8 whose closures were reinforced with a Martius labial fat pad.23 Women in this series who had multiple or recurrent UVFs and underwent Martius along with UVF repair fared better than those women repaired without a Martius flap. Repair with a rectus abdominis muscle flap was reported for six women with refractory and complex UVFs. In this series, no patient had fistula recurrence at a mean follow-up of 23 months, and five of six women were continent and voiding to completion.19 Similarly, a series of four “giant” vesicourethrovaginal fistulas were repaired by a suprapubic approach with fistula excision and omental interposition or a modified Tanagho bladder wall flap urethral reconstruction.24 Two of these patients remained totally incontinent due to deficient sphincteric mechanism. PREVENTION “An ounce of prevention is worth a pound of cure” is applicable to urethral surgery and UVF formation. Technical considerations

to help avoid this complication altogether are addressed in the following sections. Urethral Diverticulectomy Beyond patient positioning, adequate visualization of the tissues during urethral diverticulectomy can be facilitated by the use of a headlight and magnifying glasses. Careful dissection to limit the size of the urethral defect after complete excision of the diverticulum pocket, particularly along the inside wall of the diverticulum adjacent to the urethral lumen, can decrease the risk of fistula formation.25 After the urethral defect is closed with fine absorbable sutures, the integrity of the closure is tested with a 5-Fr feeding tube or ureteral catheter in the lumen, occluding the distal outlet and bladder neck. Any visual leak should be further controlled with absorbable sutures. For a large defect, strong consideration should be given to tissue interposition (i.e., Martius or sling). Pubovaginal Sling and Urethrolysis Procedures The risk of urethral injury is of particular concern in the midurethra because the plane between urethra and vagina (Fig. 79-5A) is thinner compared with that in the proximal urethra (see Fig. 79-5B). Hydrodissection can aid in discerning this fairly avascular plane; venous bleeding from the urethral side may suggest an otherwise subtle urethral injury. Urethroscopy at the end of the vaginal dissection may be useful to identify such an injury, which should be repaired before sling placement. With a midline longitudinal incision common to many of the synthetic sling procedures, there is a risk of lateral urethral injury early in the dissection. The tips of the scissors should be pointed laterally and away from the undersurface of the urethra. In case of obstruction from a synthetic sling, it is preferable to stay lateral rather than just underneath the urethra to incise the sling.26 Sling excision exposes the patients to urethral injury, especially when the sling is under tension and encroaches on the suburethral tissues. Anterior Colporrhaphy Early reports described UVF formation caused by overplication of tissues around a urethral catheter using silk sutures.11 Although the use of permanent suture material or distal urethral plication has been abandoned for the most part, plication at the bladder neck or proximal urethra can still result in fistula formation. Palpation through the vaginal wall to identify the location of the Foley catheter balloon at the bladder neck is an important step to avoid extending the dissection underneath the urethra. CONCLUSIONS UVFs have different causes, locations, sizes, and associated factors. These aspects and the patient’s symptoms dictate the selection of a surgical technique. Each repair is unique and challenging, and it is best performed by an experienced reconstructive surgeon. Adherence to time-honored principles of fistula repair can help ensure satisfactory anatomic results in most instances. Patients should be counseled that functional results are not always perfect in regard to continence and voiding function postoperatively.

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A

B

Figure 79-5 A, Transverse view on T2-weighted magnetic resonance imaging(MRI) at the mid-urethra demonstrates the proximity of the urethral and vaginal tissue (outlined), with no discernible gap between the two. Dissection here is more likely to result in urethral injury and contribute to urethrovaginal fistula formation. B, Similar transverse MRI at the proximal urethra (one cut distal to the bladder neck) shows an identifiable gap between the urethra and vaginal tissue (outlined).

References 1. Webster GD, Sihelnik SA, Stone AR: Urethrovaginal fistula: A review of the surgical management. J Urol 132:460-462, 1984. 2. Carlin BI, Klutke CG: Development of urethrovaginal fistula following periurethral collagen injection. J Urol 164:124, 2000. 3. Blaivas JG: Reconstruction of the severely damaged female urethra. In Glenn’s Urologic Surgery, 5th ed. Philadelphia, Lippincott-Raven; 1998, pp 415-424. 4. Clemens JQ, DeLancey JO, Faerber GJ, et al: Urinary tract erosions after synthetic pubovaginal slings: Diagnosis and management strategy. Urology 56:589-594, 2000. 5. Madjar S, Tchetgen MB, Van Antwerp A, et al: Urethral erosion of tension-free vaginal tape. Urology 59:601, 2002. 6. Flisser AJ, Blaivas J: Outcome of urethral reconstructive surgery in a series of 74 women. J Urol 169:2246-2269, 2003. 7. Ghoniem G, Khater U, Hairston J, et al: Urinary retention caused by adenocarcinoma arising in recurrent urethral diverticulum. Int Urogynecol J Pelvic Floor Dysfunct 15:363-365, 2004. 8. Zimmern PE: The role of voiding cystourethrography in the evaluation of the female lower urinary tract. Probl Urol 5:23-41, 1991. 9. Lemack G, Zimmern PE: Voiding cystourethrography and magnetic resonance imaging of the lower urinary tract. In Corcos J, Schick E (eds): The Urinary Sphincter. New York, Marcel Dekker, 2001, pp 407-421. 10. Blander DS, Zimmern PE: Diagnosis and management of female urethral diverticula and urethrovaginal fistula. In Stanton SL, Zimmern PE (eds): Female Pelvic Reconstructive Surgery. London, Springer, 2003, pp 299-311. 11. Keettel WC, Sehring FG, DeProsse CA, et al: Surgical management of urethrovaginal and vesicovaginal fistulas. Am J Obstet Gynecol 131:425-431, 1978.

12. Tancer ML: A report of thirty-four instances of urethrovaginal and bladder neck fistulas. Surg Gynecol Obstet 177:77-80, 1993. 13. Collis MH: Further remarks upon a new successful mode of treatment for vesicovaginal fistula. Dublin Q J 31:302-316, 1861. 14. Turner-Warwick R, Chapple C: The surgical access option for urethral reconstruction. In Functional Reconstruction of the Urinary Tract and Gynaeco-Urology. Oxford, Blackwell, 2002, pp 491-498. 15. Leach GE: Urethrovaginal fistula repair with Martius labial fat pad graft. Urol Clin North Am 18:409-413, 1991. 16. Dmochowski R: Surgery for vesicovaginal fistula, urethrovaginal fistula, and urethral diverticulum. In Walsh P, Retik A (eds): Campbell’s Urology. Philadelphia, Elsevier, 2002, pp 1195-1217. 17. Krogh J, Kay L, Hjortrup A: Treatment of urethrovaginal fistula. Br J Urol 63:555, 1989. 18. Patil U, Waterhouse K, Laungani G: Management of 18 difficult vesicovaginal and urethrovaginal fistulas with modified IngelmanSundberg and Martius operations. J Urol 123:653-656, 1980. 19. Bruce RG, El-Galley RE, Galloway NT: Use of rectus abdominis muscle flap for the treatment of complex and refractory urethrovaginal fistulas. J Urol 163:1212-1215, 2000. 20. Candiani P, Austoni E, Campiglio GL, et al: Repair of a recurrent urethrovaginal fistula with an island bulbocavernous musculocutaneous flap. Plast Reconstr Surg 92:1393-1396, 1993. 21. Litwiller SE, Zimmern PE: Closure of bladder neck in the male and female. In Graham SD, Glenn JF (eds): Glenn’s Urologic Surgery, 5th ed. Philadelphia, Lippincott-Raven, 1999, pp 407-414. 22. Venn SN, Mundy TR: Diversion and bladder neck closure. In Stanton SL, Zimmern PE (eds): Female Pelvic Reconstructive Surgery. London, Springer, 2003, pp 261-273.

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23. Rangnekar NP, Imdad Ali N, Kaul SA, et al: Role of the Martius procedure in the management of urinary-vaginal fistulas. J Am Coll Surg 191:259-263, 2000. 24. Bissada NK, McDonald D: Management of giant vesicovaginal and vesicourethrovaginal fistulas. J Urol 130:1073-1075, 1983. 25. Blander DS, Zimmern PE: Diagnosis and management of female urethral diverticula and urethrovaginal fistula. In Stanton SL,

Zimmern PE (eds): Female Pelvic Reconstructive Surgery. London, Springer, 2003, pp 306-307. 26. Sweat SD, Itano NB, Clemens JQ, et al: Polypropylene mesh tape for stress urinary incontinence: Complications of urethral erosion and outlet obstruction. J Urol 168:144-146, 2002.

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RECONSTRUCTION OF THE ABSENT OR DAMAGED URETHRA Jerry G. Blaivas and Jaspreet S. Sandhu Damage to the female urethra requiring surgical intervention is rare. It is most commonly seen in underdeveloped countries where obstetric injuries predominate because of prolonged labor, particularly when there is maternal-fetal disproportion. It is postulated that the fetal head compresses the bladder neck and urethra against the undersurface of the pubis, causing pressure necrosis.1 With the advent of modern obstetric techniques, the most common causes of urethral injury are shearing injuries from scarring that occurs between the urethra and cervix in response to cerclage sutures, prior cesarean section, or other sources. In industrialized countries, surgical trauma from antiincontinence surgery is the most common cause. Less common causes include damage from urethral diverticula, pressure necrosis from long-term indwelling catheters, pelvic fracture injury, and invasion from adjacent malignancies. Iatrogenic injuries may occur during urethral diverticulectomy, anti-incontinence surgery, anterior colporrhaphy, and vaginal hysterectomy. Erosions of synthetic slings and sutures from anti-incontinence surgery are seen with increasing frequency and may manifest years after the original surgery. This is fast becoming the most common reason for damage to the urethra, requiring various degrees of urethral reconstruction.2-6 The most likely cause is the increased use of synthetic materials and technical issues, such as dissecting too close to the urethra or tying the sling too tightly. In our experience, urethral diverticulectomy continues to be the most common cause of extensive urethral damage.7,8 This most likely results from failure to obtain a tension-free closure of the urethral defect that results from excision of the diverticulum. During bladder neck suspension, an inadvertent (and unrecognized) injury to the bladder or urethra may occur, or an errant suture may result in fistula formation or tissue necrosis. We have also seen several patients who sustained extensive tissue loss after a seemingly simple Kelly plication. It is postulated that the plication sutures were tied too tightly around a urethral catheter, resulting in pressure necrosis. Long-term indwelling urethral catheters may cause pressure necrosis of the urethra, and less commonly, trauma to the pelvis may result in fracture or separation of the symphysis pubis, which lacerates the urethra or vesical neck, or both. There may be local invasion of the urethra or bladder neck from carcinoma of vagina or cervix. There can be extensive fibrosis or fistula of the urethra as a consequence of radiation treatment of adjacent cancers. Regardless of the cause of urethral damage, the diagnostic and therapeutic challenges are considerable. The goals of surgical correction are to create a continent urethra that permits the volitional, painless, and unobstructed passage of urine. It should be of appropriate length to ensure that the patient does not void into 782

the vagina or over the toilet bowl, which can occur if the urethra is too long. We think these goals can almost always be accomplished with a single transvaginal procedure.

DIAGNOSIS Although urethral damage is rare, it should be suspected in certain clinical scenarios: 1) urinary incontinence after pelvic surgery, particularly urethral diverticular surgery, incontinence surgery, anterior colporrhaphy, and Kelly plication; 2) large urethral diverticula; 3) urinary incontinence or other lower urinary tract symptoms after pelvic fracture; 4) urinary incontinence that occurs around an indwelling urethral catheter; and 5) urinary incontinence or lower urinary tract symptoms in patients who have undergone pelvic irradiation. Most patients with significant damage to the urethra have urinary incontinence, but they occasionally present with overactive bladder or voiding symptoms. In patients who have undergone recent synthetic sling placement, urethral erosion should be suspected when the patient has intractable vaginal or urethral pain, recurrent urinary tract infections, vaginal discharge, or hematuria. For patients with incontinence, the first step in diagnosis is physical examination with a comfortably full bladder; the physician should witness urethral leakage of urine with his or her own eyes before a definitive diagnosis of sphincteric incontinence is made. On more than one occasion, we have diagnosed a urethra-vagina fistula in a woman already scheduled for antiincontinence surgery because the fistula was misdiagnosed as sphincteric incontinence. When incontinence is observed from the urethral meatus and there is reason to suspect a fistula, the examination should be repeated with a finger obstructing the meatus to observe for leakage more proximally from the fistula itself. Conversely, some women with urethrovaginal fistula have no symptoms, particularly when the fistula is in the distal half of the urethra and the vesical neck remains intact. These fistulas usually are discovered incidentally on physical examination and need no treatment. For examination, we find it best to use the posterior blade of a vaginal retractor to depress the posterior vaginal wall downward. In many instances, the anatomic deformity is obvious, or urinary leakage may be seen proximal to the urethral meatus. The next step in diagnosis is cystourethroscopy to evaluate the extent of the fistula and to assess the remainder of the urethra, particularly the length, viability, and sphincteric function of the proximal urethra. Visualization of the urethra is best accomplished with a 0- or 30-degree lens and a cystoscope with a 90degree beak or flexible cystoscope. Cystourethroscopy is the

Chapter 80 RECONSTRUCTION OF THE URETHRA

modality of choice for diagnosing urethral erosions after sling placement. When a urethral injury is diagnosed, an equally high index of suspicion should be maintained for concomitant abnormalities such as vesicovaginal or ureterovaginal fistula, ureteral obstruction, vesicoureteral reflux, and sphincteric deficiency. A careful evaluation to exclude each of these conditions should be undertaken before surgery. Detrusor function may be compromised in the form of low bladder compliance, impaired detrusor contractility, or detrusor overactivity. However, it is difficult to diagnose these conditions preoperatively, and even when present, they should not be surgically treated when the damaged urethra is repaired because most subside spontaneously after successful repair of the urethra. Urethral stricture is a rare complication of pelvic fracture or other trauma, multiple urethral dilations, prior surgery, and pelvic irradiation. This condition is usually diagnosed by cystoscopy, but it is occasionally found by urodynamic study.

MANAGEMENT Indications for Surgery The mere presence of extensive urethral damage is not an indication for surgery. The two main indications for reconstruction are sphincteric incontinence and urethral obstruction, but neither is an absolute indication. Urethral erosions after urethral synthetic sling surgery are a definite indication for surgery because of the presence of foreign material in contact with the urinary tract. If there is an associated condition such as a vesicovaginal fistula, it should be repaired at the same time. Urethral reconstruction is technically demanding and requires a considerable degree of experience and skill. In inexperienced hands, the risks may be prohibitive, and when there is insufficient local tissue for reconstruction, it may be more prudent to consider urinary diversion than urethral reconstruction, particularly when complications of radiation therapy are suspected. When sphincteric incontinence is present preoperatively, we believe that it should be surgically corrected at the time of urethral reconstruction. We prefer to construct an autologous fascial pubovaginal sling9,10 with an interposed labial fat pad flap7,9,11,12 between the sling and the reconstructed vesical neck. Others have recommended transvaginal bladder neck suspension,13 but in our experience, this has a failure rate of about 50%.9 Although it is tempting to use a synthetic sling, we do not recommend it because of the possibility of infection or erosion. It may be prudent to use allograft or xenograft tissue for the sling, but because of lack of long-term follow-up and some early failures, we have chosen these kinds of tissue grafts very selectively.4,8 There are three general approaches to urethral reconstruction: anterior bladder flaps,13,14 posterior bladder flaps,15 and vaginal wall flaps.1,7,12,16-18 These techniques appear to be comparable with respect to creation of a neo-urethra. However, when the vesical neck and proximal urethra are involved, which is usually the case, postoperative incontinence rates of about 50% are to be expected unless a concomitant anti-incontinence procedure is performed.13-15 We believe that vaginal reconstruction is considerably easier and faster, is much more amenable to concomitant anti-incontinence surgery, and is associated with much less morbidity than the bladder flap operations.

Timing of Surgery and Preoperative Management In the past, much controversy surrounded the timing of surgical repair. For decades, it had been taught that surgery should be delayed for 3 to 6 months or even longer to allow adequate time for tissue inflammation and edema to subside. In our experience, surgery can be safely performed as soon as the vaginal wound is free of infection and inflammation and the tissues are reasonably pliable. Principles of Surgical Technique In women with damaged urethras, the vaginal tissue is often scarred, fibrotic, and ischemic. Before surgery, careful examination of the vagina is necessary to determine the actual extent of urethral tissue loss and to assess the availability of local tissue for use in the reconstruction. In most instances, there is sufficient tissue in the anterior or lateral vaginal wall that can be mobilized and used for the reconstruction.1,7,9,12,13,16-18 Occasionally, it may be necessary to use an adjacent labial16,19 or thigh flap.20,21 Alternatively, an anterior bladder flap can be used.13 In patients undergoing urethral reconstruction for urethral erosion after synthetic sling placement, attempts should be made to remove all synthetic material, including nonabsorbable mesh and sutures.2 When infection is absent, bone anchors can be left in place because of the difficulty in retrieving them. However, if infection exists, it is advisable and usually straightforward to identify and remove bone anchors. The urethra usually can then be reconstructed primarily. After reconstruction of the urethra, it is often advisable to interpose a well-vascularized pedicle flap over the site of the repair. Sources include labial,9,13,22 rectus abdominal,17,23 gracilis,7 and thigh tissue.20,21 In most patients, nothing more than a labial fat pad graft is necessary (Fig. 80-1). The most important principles of surgical repair include clear visualization and exposure of the operative site; creation of a tension-free, multilayered closure; an adequate blood supply; and adequate bladder drainage. Bladder drainage is best accomplished with a suprapubic catheter, which should be placed at the beginning of the procedure to avoid damaging the reconstructed urethra. We use a urethral catheter as a stent postoperatively. The catheter must be sewn to the anterior abdominal wall in a gentle curve to avoid putting tension of the suture line. Surgical Technique There are four basic techniques for urethral reconstruction: primary closure, laterally based (tube) flaps, advancement flaps, and labia minora pedicle grafts. The choice of incision depends on the local anatomy of the tissue loss and whether a pubovaginal sling or other anti-incontinence procedure is planned. If a pubovaginal sling is planned, it is best to complete the urethral reconstruction first; the sling then is completed. In our prior publications on urethral reconstruction, we made the opposite recommendation, but in subsequent operations, we encountered some instances in which the vaginal dissection for the sling interfered with subsequent incisions for the reconstruction.7,9 Before incising the vaginal wall for passage of the sling, it is important to select the site and shape of the initial incisions for vaginal reconstruction to be sure that no options are sacrificed. On several occasions, we inadvertently burned some bridges and hope others can learn from our mistakes. If an inverted-U-shaped

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A

C

B

Figure 80-1 Labial fat pad graft—a Martius flap. A, A vertical incision is made over the labia majora, and the fat pad is mobilized. The initial dissection should begin beneath Scarpa’s fascia. If the plane is more superficial than that, troublesome bleeding may be encountered from thin, wide, flat veins that are difficult to visualize. The fat pad is mobilized anteriorly, suture ligated and divided, and the end of the suture is left long. B, A tunnel is made underneath the vaginal epithelium, and the fat pad is pulled into place with the long suture (arrow). C, It is sewn in place over the suture lines of the neo-urethra. (Modified from Mattingly RF, Thompson JD: Ch. 27. In Mattingly RF, Thompson JD [eds]: TeLinde’s Operative Gynecology, 6th ed. Philadelphia, JB Lippincott, 1985, p 665.)

Chapter 80 RECONSTRUCTION OF THE URETHRA

incision is made in the anterior vaginal wall in anticipation of advancing it to cover the reconstruction, that tissue can no longer be used as an advancement flap for urethral reconstruction if needed. Accordingly, an inverted-U-shaped incision should be made only after it is clear that an advancement flap will not be necessary. If two parallel incisions are made alongside the intended site of the urethra to roll the flaps into a tube graft, it is important to be sure that the distance between the two incisions is sufficient to allow the flaps to cover the entire circumference of the catheter and that they can be sutured together over the catheter without any tension. The tissue lateral to the incisions should not be undermined until it is clear that a laterally based flap will not be needed to cover the wound. Primary Closure If the defect is small and the tissue pliable enough to achieve a loose, tension-free closure over a 16-Fr catheter, primary closure should be considered (Fig. 80-2). We prefer chromic catgut to longer-acting synthetic absorbable sutures for urethral closure because the latter often make subsequent voiding or urethral instrumentation painful. Only after the repair has been completed is the decision made about how to cover the wound. In some instances, it is possible to elevate laterally based flaps and suture them in the midline over the wound, but when this is not possible, a U-shaped or inverted-U-shaped flap usually suffices. If a Martius labial fat pad graft is needed, it is prepared before

closure of the wound (see Fig. 80-1); if a pubovaginal sling is also necessary, the fat pad graft is placed between the sling and urethra. The vaginal incision is closed with 2-0 or 3-0 chromic catgut (Fig. 80-3). Advancement Flap If there is insufficient tissue on the anterior vaginal wall at the site of the urethra to mobilize lateral flaps, it may be possible to repair the urethra and cover the repair with an advancement flap from the anterior vaginal wall cranial to the damaged urethra (see Fig. 80-3). Tube Graft If there is circumferential loss of the urethra and sufficient vaginal wall tissue on the anterior vaginal wall, a tube graft should be considered (Fig. 80-4). Parallel incisions are made over the site of the neo-urethra, and tissue is loosely rolled into a tube over a 16-Fr urethral catheter and closed with interrupted sutures of 3-4 chromic catgut. If there is a urethral fistula, we prefer to retain the remaining bridge of urethral tissue and close the fistula primarily to preserve local blood supply. Labia Minora Pedicle Graft When there is insufficient local vaginal wall tissue, a labia minora pedicle graft may be possible (Fig. 80-5). An oval incision is made in an adjacent hair-free portion of the labia minora as close to

Vaginal mucosa

Margin or urethral roof

Line of incision

Urethral orifice

A

B

Figure 80-2 Primary closure of the urethra. A, The fistula is circumscribed. B, Lateral and cranial vaginal wall flaps are elevated, but the edges of the fistula are not excised because that would likely comprise the size of the reconstructed urethral lumen.

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D

C

E Figure 80-2, cont’d C, The urethra is closed primarily with interrupted sutures of 3-0 or 4-0 chromic catgut, and the vaginal wall is closed with lateral flaps. D and E, If there is insufficient mobility of the lateral tissue, an inverted-U-shaped graft of anterior vaginal wall (arrow) may be used. (Modified from Blaivas JG: Vaginal flap urethral reconstruction: An alternative to the bladder flap neo-urethra. J Urol 141:542-545, 1996.)

Chapter 80 RECONSTRUCTION OF THE URETHRA

A

B

C

D

Figure 80-3 Advancement flap. A, The vertical distance from the planned meatus to the base of the defect should be measured, and a U-shaped incision is made so that the apex of the U reaches the site of the new meatus without any tension. B, The U-shaped flap is mobilized and rotated 180 degrees. Its lateral edges are sutured to the vaginal wall over the catheter for form the neo-urethral tube using interrupted sutures of 3-0 or 4-0 chromic catgut. C, An inverted-U-shaped graft of anterior vaginal wall is made so that its tip reaches the new meatus without tension. D, The flap is undermined, advanced, and sutured in place with 3-0 chromic catgut. If there is insufficient tissue for this, a full labial graft may be used (see Fig. 80-6). (Modified from O’Conor VJ, Kropp KA: Ch. 13. In Glenn JF, Boyce WH [eds]: Urologic Surgery. New York, Hoeber Medical Division, Harper & Row, 1969, p 568.)

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A

B

C

D

Figure 80-4 Tube graft. A, A bridge of tissue separates the fistula into two openings. The proximal opening is circumcised, and an invertedU-shaped incision is made in the anterior vaginal wall with the apex of the U at the vesical neck, just proximal to first fistula. B, Fullthickness vaginal wall flaps are developed around the fistula. C, The proximal fistula is closed with interrupted sutures of 4-0 chromic catgut. D, A rectangular incision is made. The horizontal distance should be measured to be sure that it is wide enough to cover a 16-Fr Foley catheter. The vertical distance is defined by the site of the new urethral meatus.

Chapter 80 RECONSTRUCTION OF THE URETHRA

E

F

Figure 80-4 E, The lateral edges of the incision are undermined medially and laterally and then rolled over and approximated in the midline over the Foley catheter, creating the neo-urethra. If necessary, A vertical incision is made over the labia majora for access to the labial fat pad graft. F, The vaginal wall is closed by advancing a U-shaped flap, but if this is not possible, any of the other techniques previously discussed may be used. (Modified from Blaivas JG: Vaginal flap neo-urethra: An alternative to bladder flap urethral reconstruction. J Urol 141:542 -545, 1989.)

the site of the urethra as possible (Fig. 80-6). The size of the incision should be large enough to roll into a tube around a 16-Fr catheter or to be used as a patch graft over the catheter and allow loose approximation over the catheter. The incision is deepened around labial incision, and a pedicle graft is raised on an anteriorly or posteriorly based blood supply. The graft is passed beneath the vaginal wall and rotated so that the mucosal surface forms the inner wall of the reconstructed urethra. In some patients, it is not possible to create a tunnel for passage of the graft because of extensive scarring. In this instance, an incision is made in the vaginal wall between the site of the new urethra and the graft. It is usually possible to elevate flaps to cover the graft. Alternative Closures If it is not possible to close the vaginal incision primarily, there are several alternatives. The most straightforward is to create an inverted-U-shaped or lateral broad-based flap (Fig. 80-2(d&e). If that is not feasible, a labia minora pedicle graft may be taken and rotated so that the skin is on the outside (Figure 80-5). Alternatively, a modification of the Martius flap using full-thickness vaginal wall can be used (see Fig. 80-6). Other techniques include gracilis myocutaneous, rectus pedicle, and Singapore flaps (19-

21), but in approximately 100 cases, we have found an alternative approach to be necessary only two times. At the conclusion of the procedure using any technique, the Foley catheter is sutured to the anterior abdominal wall with a gentle loop to ensure that undue tension is not placed on the urethra. Failure to maintain a correct position of the catheter may result in necrosis of the urethra.

Postoperative Care If a Martius flap is used, the Penrose drain is removed as soon as there is minimal drainage, which usually is on the first or second postoperative day. The urethral wound and catheter are checked frequently to be sure that there is no tension or pressure on the suture line. The urethral catheter is removed as soon as feasible, usually within the first 2 to 5 days, but always before discharge from the hospital. Voiding cystourethrography is performed though the suprapubic catheter at about day 14. If the patient voids satisfactorily and there is no extravasation, the suprapubic tube is removed. If not, the tube is left in place, and another voiding trial is undertaken in about 2 weeks.

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A

B

Figure 80-5 Labia minora pedicle graft for creation of a neo-urethra. A, An oval incision is made in the hair-free labia minora, and the incision is deepened to include a vascularized pedicle, similar to that obtained for a Marius flap, except that the labial skin is left intact. A U-shaped incision is made at the site selected for the neo-urethra. B, The pedicle graft is tunneled beneath the vaginal wall, and the skin surface of the pedicle flap is wrapped around the catheter and sutured to the incisions that were made in the vaginal wall to form the neo-urethra. The vaginal and labial wounds are closed primarily.

Table 80-1 Reconstruction of Damaged Urethras: Study Results Study Rovner and Wein,24 2003 Tanello et al,16 2002 Bruce et al,23 2000 Leng et al,27 1998 Elkins et al,28 1969 Elkins et al,11 1990 Flisser and Blaivas,8 2003 Gray,1 1968 Hamlin and Nicholson,12 1969 Morgan et al,29 1978 Patel et al,30 1980 Symmonds and Hill,22 1978

No. of Patients

Continence (%)

Cure or Improved (%)

Successful Repair (%)

Obstruction (%)

9 2 6 4 6 20 74 10 50 9 9 20

75 100 83 75 10 50 87 50 80 56 — 65

88 100 100 75 83 55 93 50 84 89 78 90

75 100 100 100 67 90 93 — 98 100 100 85

13 — 0 — 17 10 1 — 12 11 0 —

RESULTS Because of the rarity of the condition, there have been few studies concerning reconstruction of the severely damaged urethra. Combining all the series we could find in the English language literature, there were fewer than 500 patients. Overall, successful anatomic reconstructions were reported in 67% to 100% of women (Table 80-1). Most study authors emphasized the need

for well-vascularized pedicle flaps to ensure a successful outcome. Continence, however, was achieved in only 55% to 92% after a single operation, and postoperative urethral obstruction was reported in 2% to 17% of patients. In most studies, the criteria for incontinence and urethral obstruction were not specified, and in view of lack of follow-up, the results cited should be considered overly optimistic. It does seem evident that an antiincontinence procedure should be performed at the same time

Chapter 80 RECONSTRUCTION OF THE URETHRA

A

B

Figure 80-6 Technique of obtaining a full-thickness labial fibrofatty pedicle graft to cover the reconstructed urethra when there is insufficient local vaginal wall tissue. A, A U-shaped incision is made in the labia minora large enough to cover the defect. The incision is carried down through the labial fat pad (see Fig. 80-1), and the posterior end of the flap is suture ligated. B, The vaginal wall is closed primarily with running sutures of 3-0 or 400 chromic catgut. (Modified from Mattingly RF, Thompson JD: Ch. 27. In Mattingly RF, Thompson JD [eds]:TeLinde’s Operative Gynecology, 6th ed. Philadelphia, JB Lippincott, 1985, p 665.)

as the urethral reconstruction. Failure to do so resulted in incontinence rates ranging from 50% to 84%. The results of many series indicated that secondary procedures to correct incontinence were successful in most patients. The first report of a large series was published in 1969 by Hamlin,12 a dedicated pioneer of fistula repair who worked in West Africa. Excellent anatomic repair was achieved in 49 of the 50 childbirth injuries, but 8 (16%) had severe incontinence, and many more had lesser degrees of incontinence. The incontinence was usually cured after a second procedure. Symmonds22 described 50 women undergoing neo-urethra procedures using tubularized vaginal wall. Follow-up ranged from 1 to 15 years, and using an independent examiner, he reported that 37 of 50 patients were dry (i.e., no pads and said they were cured) and that 7 of 50 patients considered the operation successful, even though they had “some” stress incontinence. We have operated on more than 100 women with extensive anatomic vesical neck and urethral defects; results for 74 have been reported.8 The causes of the injury are given in Table 80-2. All but one patient underwent a vaginal reconstruction (one patient had a Tanagho anterior bladder flap that failed). One patient with squamous cell carcinoma of the distal third of the urethra underwent wide excision and urethral reconstruction with adjacent local flaps. In the remainder, we used a Martius flap in all except three—one had a successful repair with a gracilis flap, and two women with childbirth injuries underwent cutaneous labial pedicle grafts. One of the latter patients was successful; the other failed because of wound necrosis and underwent con-

Table 80-2 Causes of Urethral Pathology Pathology Diverticula or injury from diverticulectomy Urethral injury from prior incontinence surgery Anterior colporrhaphy Fistula or erosion associated with synthetic material Fistula from other gynecologic surgery Urethral obstruction from prior surgery Trauma Obstetric injury Ectopic ureter Primary urethral stricture Total

No. of Patients* 28 18 10 5 3 3 3 2 1 1 74

*Women who underwent operations because of extensive anatomic vesical neck and urethral defects.

tinent urinary diversion. A successful anatomic outcome was achieved in 93%, and continence was achieved in 87% of patients who had preoperative incontinence; no patient developed de novo incontinence. Early in our series,7 we did not routinely perform concomitant pubovaginal slings, and 50% of the women who underwent a modified Pereyra procedure had persistent sphincteric incontinence; all were subsequently cured or improved by an autologous fascial pubovaginal sling. No patient required

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intermittent catheterization except for the patients with anatomic failures, who underwent continent urinary diversion. One had a previously unrecognized vesicovaginal fistula. Rovner and Wein24 recommended that women with large, circumferential urethral diverticula undergo complete excision of the diverticulum and partial urethrectomy by transecting the urethra to gain access to its dorsal wall. Urethral continuity was restored by end-to-end urethroplasty or by tubularizing the anterior wall of the diverticulum to construct a neo-urethral segment. Autologous fascial slings were used selectively. With only shortterm follow-up, they reported that six of the eight patients were dry (i.e., no pads), one was using two or three pads per day, and the remaining one reported urgency and the use of one pad each day. Complications included one distal fistula and one stricture. Tanello and colleagues16 described two women undergoing urethral reconstruction using a pedicle skin flap from the labia minora. They cited a 2-year follow-up and reported that both patients were dry. Bruce and coworkers23 described six women with multiple previous urethral operations who underwent reconstruction. The surgical technique used a pedicled rectus abdominis flap interposed between the fistula closure and the vaginal suture line. The follow-up period was 23 months. Five of six patients were dry and able to void; one had urge incontinence. Many investigators have reported the results of urethral reconstruction after urethral erosion resulting from mid-urethral sling placement. Amundesen and colleagues2 described nine patients who presented with urethral erosion. All were repaired primarily with a multilayered closure, followed by a Martius flap in two patients. All were repaired adequately, but 66% of patients with preoperative urge urinary incontinence or stress urinary incontinence had continued incontinence. Others have reported results with similar rates of incontinence, prompting some surgeons to perform concomitant anti-incontinence procedures with interposed vascularized tissue, such as a Martius flap.3,4

A

B

C

D

BLADDER FLAP TECHNIQUES We believe that bladder flap reconstructions are almost never necessary in these patients. The single patient in whom we performed this procedure failed because of refractory detrusor instability. There are two basic techniques: anterior and posterior bladder flaps. The anterior technique is depicted in Figure 80-7. More information is available in the original descriptions and the excellent work of the late Vincent O’Conor.25 In the latest and most extensive series, Elkins13 and associates reported their experience with a Tanagho-like procedure in 20 West African women with extensive urethral damage after obstructed labor. These patients had large vesicovaginal fistulas, and because of extensive scarring, they were not suitable for vaginal flap techniques. The procedure was performed entirely through the vaginal approach. The anterior and lateral fistula edges are dissected sharply away from the pubic bone beneath the arch of the pubic ramus, and the retropubic space is entered from the vagina. The anterior bladder wall is then dissected free of surrounding tissues to the level of the peritoneal reflection. After the anterior bladder is mobilized, a 3 × 3 cm flap is raised and rolled into a tube over a 16-Fr catheter. The new urethra is sutured to the remaining distal urethra or at the site of the new meatus. The posterior edges of the vesicovaginal fistula are approximated and "fixation sutures are placed through the top portion of the neo-urethra to reattach the urethra to the base of

E Figure 80-7 Technique of performing anterior bladder flap urethroplasty (i.e., Tanagho procedure). A, An anterior bladder wall flap is selected, mobilized, and held with suspension sutures. B, The urethra is transected at site of fistula. C, The bladder flap is tubularized. D, The posterior bladder is closed. E, The neo-urethra is sutured to the distal urethra. (Modified from Tanagho EA: Bladder neck reconstruction for total urinary incontinence: 10 years of experience. J Urol 125:321, 1981.)

Chapter 80 RECONSTRUCTION OF THE URETHRA

the pubic periosteum." In the last three patients in the series, a modified Pereyra procedure was performed instead. A Martius fat pad graft was then placed beneath the suture lines. Eighteen of the 20 women so treated had a satisfactory anatomic repair of the fistula, but 4 of the 18 had persistent stress incontinence that required further surgery. Two others had refractory detrusor instability or low bladder compliance. OTHER TECHNIQUES Park and Hendren26 reported a series of seven girls with severely fibrotic urethras. Urethral reconstruction was accomplished with a 2 × 4 cm full-thickness buccal mucosa graft after splitting the pubis and excising the fibrotic urethra. Causes of the urethral pathology included complications from operations for cloacal extrophy and other cloacal malformations. The investigators reported that five of seven patients were continent and that two were being treated with periurethral bulking agents. After the follow-up period of 12 to 58 months (mean, 34.7 months), all seven patients were continent, but two required bulbing agents for continence.

CONCLUSIONS Reconstruction of the severely damaged urethra is a technically challenging undertaking that requires considerable surgical expertise and decision-making. Most women with traumatic injuries have sufficient vaginal tissue for a vaginal flap reconstruction, and we believe that the vaginal approach offers the best chance for a successful outcome. However, for those with extensive vaginal scarring that precludes a local tissue repair, bladder flap techniques or free grafts with or without gaining access by splitting the pubis may prove useful. The most important principles to keep in mind are clear visualization and exposure of the operative site; careful selection of the initial vaginal incision to ensure that there is adequate blood supply if pedicle flaps become necessary; removal of all foreign material; creation of a tension-free, supple, multilayered closure; an adequate blood supply and soft tissue base with a Martius flap; a concomitant pubovaginal sling when antiincontinence surgery is indicated; adequate bladder drainage; and suturing of the urethral catheter to the anterior abdominal wall and meticulous attention to catheter care to prevent pressure necrosis.

References 1. Gray LA: Urethrovaginal fistulas. Am J Obstet Gynecol 101:28, 1968. 2. Amundsen CL, Flynn BJ, Webster GD: Urethral erosion after synthetic and nonsynthetic pubovaginal slings: Differences in management and continence outcome. J Urol 170:134, 2003. 3. Clemens JQ, DeLancey JO, Farber GJ, et al: Urinary tract erosions after synthetic pubovaginal slings: Diagnosis and management strategy. Urology 56:589, 2000. 4. Kobashi KC, Dmochowski R, Mee SL, et al: Erosion of woven polyester pubovaginal sling. J Urol 162:2070, 1999. 5. Sweat SD, Itano NB, Clemens JQ, et al: Polypropylene mesh tape for stress urinary incontinence: Complications of urethral erosion and outlet obstruction. J Urol 168:144, 2002. 6. Tsivian, A, Kessler O, Mogutin B, et al: Tape related complications of the tension-free vaginal tape procedure. J Urol 171:762, 2004. 7. Blaivas JG: Vaginal flap urethral reconstruction: An alternative to the bladder flap neo-urethra. J Urol 141:542, 1996. 8. Flisser AJ, Blaivas JG: Outcome of urethral reconstruction cases in a series of 74 women. J Urol 169:2246, 2003. 9. Blaivas JG: Female urethral reconstruction. In Webster G (ed): Reconstructive Urology. Boston, Blackwell Scientific, 1993, pp 873-886. 10. Chaikin DC, Rosenthal J, Blaivas JG: Pubovaginal fascial sling for all types of stress urinary incontinence: long-term analysis. J Urol 160:1312, 1998. 11. Elkins TE, DeLancey JO, McGuire EJ: The use of modified Martius graft as an adjunctive technique in vesicovaginal and rectovaginal fistula repair. Obstet Gynecol 75:727, 1990. 12. Hamlin RHJ, Nicholson EC: Reconstruction of urethra totally destroyed in labor. Br Med J 1:147, 1969. 13. Elkins TE, Ghosh TS, Tagoe GA, et al: Transvaginal mobilization and utilization of the anterior bladder wall to repair vesicovaginal fistulas involving the urethra. Obstet Gynecol 79:455, 1992. 14. Tanagho EA: Bladder neck reconstruction for total urinary incontinence: 10 years of experience. J Urol 125:321, 1981. 15. Leadbetter GW Jr: Surgical correction of total urinary incontinence. J Urol 91:261, 1964.

16. Tanello M, Frego E, Simeone C, et al: Use of pedicle flap from the labia minora for the repair of female urethral strictures. Urol Int 69:95, 2002. 17. Ellis LR, Hodges CV: Experience with female urethral reconstruction. J Urol 102:214, 1969. 18. Symmonds RE: Loss of the urethral floor with total urinary incontinence: A technique for urethral reconstruction. Am J Obstet Gynecol 103:665, 1968. 19. Hoskins WJ, Park RC, Long R, et al: Repair of urinary tract fistulas with bulbocavernosus myocutaneous flaps. Obstet Gynecol 63:588, 1984. 20. Wee JT, Joseph VT: A new technique of vaginal reconstruction using neurovascular pudendal-thigh flaps: A preliminary report. Plast Reconstr Surg 83:701, 1989. 21. Zinman, L: Use of myocutaneous and muscle interposition flaps in management of radiation-induced vesicovaginal fistula. In MCdougal WS (ed): Difficult Problems in Urologic Surgery. Chicago, Yearbook Medical Publishers, 1989, pp 143-163. 22. Symmonds RE, Hill LM: Loss of the urethra: A report on 50 patients. Am J Obstet Gynecol 130:130, 1978. 23. Bruce RG, El-Galley RES, Galloway NTM: Use of rectus abdominis muscle flap for the treatment of complex and refractory urethrovaginal fistulas. J Urol 163:1212, 2000. 24. Rovner E, Wein AJ: Diagnosis and reconstruction of the dorsal or circumferential urethral diverticulum. J Urol 170:82, 2003. 25. O’Conor VJ Jr: Repair of vesicovaginal fistula with associated urethral loss. Surg Gynecol Obstet 146:251, 1978. 26. Park J, Hendren HJ: Construction of female urethra using buccal mucosa graft. J Urol 166:640, 2001. 27. Leng WW, Amundsen CL, Mcguire EJ, Management of Female Genitourinary Fistulas: Transvesical or Transvaginal Approach, Jurol, 160:1995, 1998. 28 Morgan JE, Farrow GA, Sims RH: The Sioughed Urethra syndrome, Am J Obstet Gynecol, 130:521, 1978. 29. Patel U, Waterhouse K, Laungani G: Management of 18 Difficult Urethrovaginal Fistula with Modified Ingelman-Sundberg and Martius Operations. J Urol, 123:653, 1980.

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VESICOVAGINAL FISTULA: VAGINAL APPROACH Matthew P. Rutman, Larissa V. Rodríguez, and Shlomo Raz Vesicovaginal fistula (VVF) is one of the most significant and distressing complications in female urology and urogynecology. A VVF is an abnormal communication between the bladder and vagina that results in continuous urine leakage from the vagina. VVFs have been recognized and described since ancient times, but successful repair was not documented until James Marion Sims’ first paper in 1852.1 He used a transvaginal technique to perform the repair, including the use of silver wire suture. Many principles he described are still applicable. Subsequent modifications and advances included the first layered repair by Mackenrodt2 and the interposed labial fat graft of Martius3 in the late 1920s. In developing countries, birth trauma remains the most common cause of VVF. Prolonged and obstructed labor leads to pressure necrosis of the anterior vaginal wall and the underlying bladder neck and urethra. In industrialized nations, most fistulas result from complications of gynecologic and other pelvic surgery. Regardless of the cause, surgical repair remains the gold standard and primary treatment of VVF.

include prior cesarean section, endometriosis, previous cervical conization, and radiation treatment.6 The bladder is most often injured during the dissection of the posterior bladder wall from the anterior surface of the uterus at the level of the vaginal cuff during abdominal hysterectomy. Placement of an indwelling Foley catheter and meticulous sharp dissection can minimize inadvertent injury. Iatrogenic injuries can be unavoidable in difficult reoperations and in patients with dense adhesions that obliterate normal surgical planes. Careful attention should be paid to diagnose and repair the injury intraoperatively. Filling the Foley catheter with methylene blue dye to check for leakage is a simple and effective method of checking bladder integrity. If a bladder injury is recognized, two-layer repair is required after adequate exposure is provided. A drain should be placed. The catheter should be left in longer than the usual 1 or 2 days after hysterectomy. An interposition flap can provide an additional layer of coverage.

DIAGNOSIS ETIOLOGY In the United States and other developed nations, VVFs occur as a result of surgical trauma, most commonly at the time of abdominal or vaginal hysterectomy. Unrecognized suture placement into the bladder during closure of the vaginal cuff results in tissue necrosis and subsequent fistula formation. Excessive blunt dissection of the bladder can result in ischemia or an unrecognized tear in the posterior bladder wall. Approximately 75% of VVFs are reported to occur after hysterectomy for benign disease.4 The incidence of VVF after hysterectomy is between 0.5% and 1%.5 VVFs also occur after anterior colporrhaphy, sling procedures for stress incontinence, cystocele repair, colposuspension procedures, and urethral or bladder diverticulectomy. Approximately 90% of VVFs in North America result from gynecologic procedures. The other 10% are caused by advanced local malignancy (i.e., cervical, vaginal, and endometrial), radiation therapy, inflammatory bowel disease, foreign bodies, and infectious processes of the urinary tract.

History Patients typically present with continuous urinary drainage (day and night) from the vagina after gynecologic or pelvic surgery. Any patient with urinary incontinence immediately after pelvic surgery should be evaluated to rule out a VVF. The fistula may manifest immediately postoperatively, but it often becomes clinically apparent days to weeks later. Ureterovaginal fistulas tend to manifest later than VVFs. Ten percent of patients with a VVF have an associated ureterovaginal fistula.7 Early in the postoperative course, patients may present with fevers, abdominal pain, hematuria, ileus, and lower urinary tract symptoms. Patients with VVF related to prior radiation therapy may present 6 months to 20 years later.8 Fluid draining from the vagina may be urine, lymph, peritoneal fluid, fallopian tube fluid, or vaginal secretions. Important considerations in the differential diagnosis of VVF include urethrovaginal fistula, ureterovaginal fistula, ectopic ureter, peritoneal fluid drainage, and vaginal cuff infection. Diagnostic Tests

PREVENTION Recognizing that most VVFs are iatrogenic, it is paramount that the treating surgeon takes the necessary precautions to prevent their occurrence. Risk factors reported for fistula development 794

To confirm that the leaking fluid from the vagina is urine, the fluid can be sent for creatinine analysis. Elevated levels (relative to serum) establish the diagnosis of a communication between the vagina and urinary tract. Physical examination is paramount in the evaluation of a woman with a suspected fistula. The

Chapter 81 VESICOVAGINAL FISTULA: VAGINAL APPROACH

diameter, depth, mobility, and mucosa of the vagina must all be assessed. Concomitant prolapse, urethral hypermobility, and stress incontinence should also be evaluated. Vaginal examination with a speculum can isolate the point of leakage. The most common location for VVF (after a hysterectomy) is at the level of the vaginal cuff. Pooling of urine at the apex and the fornices is commonly seen. Surrounding vaginal mucosa may appear edematous and erythematous, making it difficult to identify the opening. Placing a Foley catheter into the bladder can assist by visualizing the balloon. If all of these measures fail to identify a fistula, dye tests can be used for confirmation. Instilling methylene blue dye through the Foley catheter, with concomitant inspection of the vagina for leakage of blue fluid, can help identify a VVF. Requesting the patient to ambulate with a vaginal pack in place may stain the packing blue. If a VVF is still not identified, the patient should be given oral phenazopyridine, which stains the urine orange. The vagina is then packed, and orange staining confirms a fistula. A positive phenazopyridine test result with a negative methylene blue test result strongly suggests a ureterovaginal fistula. All patients with a diagnosis of a urinary fistula should undergo upper tract evaluation and cystoscopy. Upper tract evaluation can be done with intravenous pyelography (IVU) or retrograde pyelography. Ureteral involvement can be demonstrated by hydronephrosis or extravasation on IVU, although the ipsilateral kidney can appear normal with prompt drainage. Retrograde pyelography remains the most sensitive test to evaluate ureteral involvement in the presence or absence of a VVF. Cystoscopy should identify the location and size of the fistula and determine its relation to the ureteral orifices. It is important to ascertain that there is adequate bladder capacity and to rule out foreign body as the source of the fistula. Surveillance for multiple fistulas is imperative, because this finding would alter operative repair. Patients with a radiation- or malignancy-associated fistula must undergo biopsy of the site before repair. A voiding cystourethrogram (VCUG) can help identify the presence and location of a fistula. Coexisting vesicoureteral reflux, urethral diverticulum, stress incontinence, and cystocele can also be identified, which may alter the surgical plan. VCUG can help elucidate fistulas involving the rectum or uterus, and vaginoscopy can assist in identifying the vaginal communication.

TREATMENT Conservative Management Small VVFs may close spontaneously with continuous Foley catheter drainage (up to 10% of cases). This has usually been attempted by the time patients have sought consultation with a specialist. Three weeks of drainage is a reasonable option if the fistula is discovered early in the postoperative period. Mature fistula tracts are unlikely to resolve with this technique. Prolonged catheter drainage requires coverage with antibiotics. Another conservative treatment option includes fulgurating the lining of the fistula tract. This should not be attempted with large fistulous tracts. Stovsky and colleagues9 reported closure in 11 of 17 patients with fulguration of fistulas less than 3 mm long and with 2 weeks of catheter drainage. Reports have shown success with fibrin therapy in treating small VVFs.10 Most conservative measures ultimately fail in the attempt to cure VVFs. For larger, complex, and radiation-induced fistulas, there is no

role for conservative treatment, and formal repair remains the gold standard. Operative Management Preoperative Considerations Before formal repair of a VVF, many factors must be considered to optimize the chances of a successful repair. Historically, most surgeons advocated waiting 3 to 6 months before surgical repair to allow the fistula to completely mature.11,12 They theorized that this allowed maximal healing during the post-hysterectomy inflammatory stage. However, patients with VVFs experience enormous social, physical, and psychological stress during this period that greatly hinders their quality of life. Contemporary surgeons have reported excellent results with early repair, and the strategy avoided patients’ distress throughout a waiting period.13,14 Typically, early transvaginal repair is performed 2 to 3 weeks after the time of injury. This is most commonly done in women with fistulas that form after hysterectomy using an abdominal approach. Patients with vaginal cuff infections or pelvic abscesses must be treated long-term with antibiotics before any repair attempt. Patients with previously failed repairs or radiationrelated fistulas are not candidates for early intervention. They should wait a minimum of several months before repair. VVFs after traumatic delivery are ischemic in origin and require a longer period of conservative management. The most appropriate approach to formal surgical repair of a VVF is the one most familiar to the surgeon. The choice between an abdominal or vaginal approach depends on the surgeon’s experience, training, and comfort level with the procedure. The highest success rates are associated with the first operation, regardless of the approach. Traditionally, the fistula’s location dictated the surgical approach. Infratrigonal and bladder neck fistulas were repaired vaginally, whereas supratrigonal fistulas were repaired transabdominally. Even complex high VVFs can be repaired using a transvaginal approach with adherence to good surgical technique and tissue interposition. The advantage of an abdominal approach is the ability to perform simultaneous procedures for coexisting intra-abdominal pathology, including augmentation cystoplasty, ureteral reimplantation, and repair of bowel fistulas. The vaginal approach avoids an abdominal incision and possible bladder bivalving. It is associated with decreased morbidity, shorter hospital stay, and quicker patient convalescence. We use the transvaginal approach for most VVFs. Many principles are integral to fistula repair, regardless of the approach chosen. Excellent exposure with watertight, tensionfree closure using multiple, nonoverlapping sutures lines provide an approximately 90% chance of cure on the first attempt. Continuous catheter drainage postoperatively is mandatory. Interpositional grafts optimize the chance for cure if the integrity of the repair is in question. Preoperative preparation includes prescribing antibiotics to clear any infection and provide a sterile environment for repair. Urine culture should document absence of infection before surgery. Broad-spectrum, intravenous antibiotics are provided preoperatively. Preoperative estrogen-containing vaginal cream is used in the postmenopausal or post-hysterectomy patient to improve the quality of the vaginal tissues. Traditional repair of VVF included excision of the tract to provide clean and vascular edges. This was thought to increase chances for cure. Raz and associates15,16 demonstrated excellent results without excising the fistulous tract with no adverse effects.

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Excising the fistula enlarges the tract, and it may cause iatrogenic bleeding, requiring hemostatic measures that may inhibit healing. Excising fistulous tracts located near the ureteral orifices may require ureteral reimplantation. Before surgical repair, the surgeon should be familiar with several techniques for interposition of tissue. Although these grafts are often necessary in large, complex, post-radiation, and failed primary repairs, it is difficult to accurately predict which fistulas will require the additional layer of coverage to avoid a tenuous repair. Preoperative evaluation should attempt to identify patients who have coexisting stress urinary incontinence. Simultaneous sling procedure or bladder neck suspension can be performed, avoiding the need for a second procedure. Concomitant repair for stress incontinence does not increase the fistula recurrence rate.17 It is also important to consider the sexual function of the patient and ensure preservation of vaginal depth in the sexually active patient. This can require rotational flaps in patients with large fistulas and vaginal stenosis. Local estrogen replacement should be used in patients with vaginal atrophy. Vaginal Technique We routinely repair VVFs by means of a vaginal approach and describe the technique for transvaginal repair of VVFs. The surgery is performed on an outpatient basis and avoids the morbidity of a laparotomy. Step 1 is patient preparation. The patient is placed in the low lithotomy position and prepped in standard fashion. A headlight provides excellent visualization for the surgeon. Cystoscopy with ureteral catheterization is done when the fistula is located near the trigone and the ureteral orifices. A curved Lowsley retractor aids in placement of a 16-Fr suprapubic catheter through a small suprapubic incision. A posterolateral episiotomy (i.e., relaxing incision) may be necessary in a patient with a narrow vagina. The labia minora are sutured apart, and a ring retractor is positioned for optimal exposure. A urethral catheter is placed to ensure maximal urinary drainage. An Allis clamp is used to elevate the anterior vaginal wall, and a weighted speculum is placed posteriorly. Step 2 is isolation of fistula. The fistulous tract is identified and catheterized with an 8- or 10-Fr Foley catheter. This aids retraction throughout the dissection. Metal sounds may be necessary to dilate the tract before catheter placement. An inverted-J incision is made with care taken to circumscribe the fistulous tract (Fig. 81-1). The long end of the J should extend to the apex of the vagina, which facilitates rotation and advancement of a posterior flap at the later stages of the procedure. Fistulas located high in the vaginal cuff may require an inverted incision, with the base of the flap facing the urethral meatus. Step 3 is the creation of flaps. Anteriorly and posteriorly based vaginal flaps are dissected on each side of the fistulous tract, starting with healthy tissue located away from the fistula itself (Fig. 81-2). This usually provides a healthy plane of dissection and helps prevent enlargement of the fistulous tract or inadvertent bladder perforation. The ring of vaginal tissue at the opening of the fistula is left intact. The flaps should be developed at least 2 to 4 cm away from the fistulous tract, exposing the underlying perivesical fascia. The flaps are then retracted with the hooks of the ring retractor. Lateral dissection of the vaginal wall 2 to 4 cm from the fistulous tract allows complete exposure of the perivesical fascia.

Figure 81-1 Inverted-J-shaped incision around the fistulous tract. (From Raz S, Little NA, Juma S: Female urology. In Walsh PC, Retik AB, Stamey TA, Vaughan ED Jr [eds]: Campbell’s Urology, 6th ed. Philadelphia, WB Saunders, 1992, pp 2782-2828.)

Figure 81-2 Development of vaginal flaps.

Step 4 is closure of the fistula. The standard VVF repair is done in three layers. The first layer closes the epithelialized edges of the fistula tract and a few millimeters of the surrounding tissue (including bladder wall) with interrupted, absorbable, 2-0 sutures (Vicryl or Dexon) in a transverse fashion (Fig. 81-3). The fistula catheter is removed, and the sutures are secured, closing the fistulous tract. The second layer of the repair incorporates the perivesical fascia and deep muscular bladder wall using the same suture material (Fig. 81-4). The sutures are placed at least 1 cm from the prior suture line and secured in a tension-free fashion. The sutures are placed in a line 90 degrees from the first suture

Chapter 81 VESICOVAGINAL FISTULA: VAGINAL APPROACH

Figure 81-5 Third layer of repair: vaginal flap advancement.

Figure 81-3 First layer of repair: transverse closure of a fistulous tract without excision.

Figure 81-4 Second layer of repair: imbricated first layer with perivesical fascia.

layer to minimize overlapping suture lines. The second layer of sutures completely covers the first layer of closure. The bladder is filled with indigo carmine diluted in saline to ensure repair integrity. Step 5 is completion of the operation. In a standard VVF repair (without interposition), the procedure is completed. The previously raised posterior flap is rotated beyond the fistula closure site by at least 3 cm. The excess vaginal flap tissue is

excised. The vaginal wall is closed using a running, locking, absorbable, 3-0 suture (Vicryl or Dexon). This covers the tract with healthy vaginal tissue and provides a third layer of closure with no overlapping suture lines. (Fig. 81-5) An antibioticimpregnated vaginal pack is placed, and the urethral and suprapubic catheters are left to dependent drainage. Most cases of uncomplicated VVF require only a three-layer, tension-free repair. Complicating factors that mandate additional protection include prior irradiation, failed prior surgery, and poor tissue quality. These conditions require tissue interposition. In most cases of high VVF after hysterectomy, we perform the interposition of a peritoneal flap between the first two layers of fistula closure and the advancement of the vaginal wall flap. The tissue is readily available, requires minimal additional dissection, and creates a more secure closure of the fistulous tract. Other Techniques The abdominal approach is beyond the objectives of this chapter. We use the abdominal approach only in selected patients requiring concomitant abdominal procedures such as augmentation cystoplasty or ureteral reimplantation. The Latzko operation, originally described in 1942, uses partial colpocleisis to treat the VVF.18 The operation consists of denudement of the vaginal wall around the fistula without excising the fistulous tract. A separate layered closure is performed that includes the bladder, fistula, and vagina. A major concern with this procedure is vaginal shortening. However, success rates of 93% and 95% have been reported in two series of 43 and 20 patients, respectively, with no significant patient-reported vaginal shortening or sexual dysfunction.19,20 Many gynecologists still use this technique because of its technical ease and minimal morbidity. Transurethral suture cystorrhaphy without fistula tract excision has been described as a minimally invasive alternative for smaller fistulas (5 to 8 mm) located away from the ureteral orifices. The technique requires fulguration of the tract and surrounding bladder mucosa before combined transurethral and abdominal endoscopic suture placement. A minimum 2- to 3-

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week period of bladder drainage is required. Eight (73%) of 11 patients treated with this technique were cured.21 With the recent upsurge in minimally invasive surgery, VVF repair also has been done laparoscopically.22 The approach was first described in 1994 and has since undergone various modifications, including use of endostaplers, omental interposition, and layered closure.23 Management of Complex Fistulas Complex VVFs include those associated with prior irradiation or malignancy, recurrent fistulas, fistulas of large size (>3 cm), fistulas involving the bladder neck and trigone, and those associated with poor tissue quality or difficult closure. In these cases, the standard transvaginal repair must be modified. Many techniques of tissue interposition have been described. These provide an additional layer of closure and enhance the quality of the reconstructive repair. Radiation-Induced Fistulas Radiation-induced VVFs require special consideration. The site of fistula formation is typically in the trigone region; it is in a relatively fixed position and radiation effects are more likely. Between 1% and 5% of patients treated for cervical or uterine carcinoma develop radiation-induced fistulas. The fistulas most commonly manifest in a delayed fashion, sometimes 15 to 20 years later.15 Fistulas associated with prior irradiation should always be biopsied to rule out recurrence of the primary malignancy. Radiation-induced fistulas result from obliterative endarteritis in the irradiated field.24 The injury compromises healing. The surrounding tissues are also affected by the endarteritis, complicating an already difficult repair. Video urodynamics and cystoscopy are mandatory before surgery. They allow assessment of bladder capacity and compliance. With adequate capacity and compliance, transvaginal repair is performed with modifications, including tissue interposition and prolonged postoperative catheter drainage. If the bladder has poor compliance and small capacity, augmentation cystoplasty is required, and an abdominal approach is taken. Careful inspection of the bowel is necessary to ensure use of a nonirradiated segment for the augmentation. Martius Graft The Martius graft (i.e., fibrofatty labial flap) was first described in 1928.3 This technique is commonly used in pelvic and perineal reconstructive surgery, and it has great utility in treating VVF, rectovaginal fistula, and urethrovaginal fistula and in urethral reconstruction. It has high reported success rates in complex fistula repair25 and is a convenient source of interposition in transvaginal repair. We use a Martius flap in cases of trigonal or urethral fistula. For fistula located high in the vaginal vault (after hysterectomy), the peritoneum is our preferred source of tissue interposition in these cases. The Martius graft is a long band of adipose tissue from the labia majora. It has excellent strength and vascularity. The blood supply is threefold. Branches of the external pudendal artery supply the graft superiorly and anteriorly. Obturator branches enter the graft at its lateral border. The inferior labial artery and vein supply the graft inferiorly. The graft may be mobilized superiorly or inferiorly, depending on the desired location of transfer.

The first two layers of the fistula are closed as described earlier. The vaginal flaps are left intact, and the labial retraction suture is removed. A vertical incision is then made over the labia majora, and the subcutaneous tissues are dissected laterally to the lateral border of the dissection, the labiocrural fold. The flap is then dissected posteriorly to the Colles fascia and medially to the labia minora and bulbocavernosus muscle. The main vascular supply is at the base, and the entire thickness of the fat pad is carefully encircled by a Penrose drain. The superior and anterior segment of the graft is clamped, transected, and suture ligated. The remaining dissection is completed, freeing the flap, except at its base (Fig. 81-6A). A tunnel is then made between the perivaginal tissues and vaginal wall. The graft is then passed from the labial area to the vaginal area (through the tunnel) with the aid of a hemostat (see Fig. 81-6B). The Martius graft is placed over the fistula site and secured with interrupted, absorbable suture in a tension-free fashion. The vaginal flap is advanced and closed as previously described, providing a fourth layer of closure. A light pressure dressing may be applied, and ice packs are routinely applied. Eilber and colleagues26 reported a 97% cure rate with transvaginal repair using Martius graft interposition in 34 patients with complex fistulas. We have performed an in situ technique for the creation of a Martius flap, avoiding a labial incision. After the creation of the vaginal flaps in the distal vagina, we dissect a tunnel under the vaginal wall in the direction of the fibrofatty tissue in the labia. The medial and lateral segments of the Martius flaps are isolated using a Penrose drain, the upper segment of the Martius flap is dissected free, and the flap is mobilized and transferred to cover the fistula closure. Peritoneal Flap We use a peritoneal flap in the repair of high fistulas located at the vaginal vault, which are seen most commonly after hysterectomy. Extending a Martius graft to this location may be difficult and inadvertently result in vaginal shortening. A peritoneal flap is an easily available, well-vascularized tissue that can be harvested without the morbidity of a second incision. The fistula repair begins as described in the first three steps of the transvaginal technique. The fistula is circumscribed, and vaginal flaps are prepared. A catheter in the fistula can help in dissection of the flap. Sharp dissection is used to expose the peritoneum and preperitoneal fat. The fistulous tract is then closed in two layers, as previously described. The preperitoneal fat and peritoneum are advanced to cover the fistula repair and secured to the perivesical fascia with tension-free, interrupted sutures. The vaginal flap is then advanced and closed. Raz and coworkers27 reported a 91% success rate in their initial experience using a peritoneal flap in 11 patients with VVFs. Eilber and associates26 reported a 96% cure rate using a peritoneal flap in 83 patients who underwent complex fistula repair. This approach has high success rates, minimal morbidity, and outcomes similar to those of a Martius graft but without a second incision. Omental Interposition Omental interposition is primarily used in the abdominal approach for fistula repair, although it can be accessed transvaginally in women who have had previous procedures. This technique results in an omental graft that can be placed between the bladder and vagina for an additional layer of protection.

Chapter 81 VESICOVAGINAL FISTULA: VAGINAL APPROACH

A

B

Figure 81-6 A, Mobilization of a Martius flap based on an inferior pedicle. B, Transfer of a Martius flap to cover a fistula repair (B, from Raz S: Atlas of Transvaginal Surgery. Philadelphia, WB Saunders, 1992.)

Rotational Full-Thickness Labial Flap In selected complex cases with loss of the vaginal wall, insufficient vaginal epithelium may preclude primary vaginal closure. A fullthickness labial flap can be rotated to substitute for the missing vaginal wall. The advantage of this flap is that combines the use of the fibrofatty tissue of the Martius with a well-vascularized skin flap to cover the deficient or absent vaginal wall. The fistula is closed as previously described, and the vascularized flap is rotated to provide full-thickness skin coverage. After closure of the fistula, a U-shaped incision is made over the labia, including the lateral labial skin and underlying tissue. The apex of the flap is created at the level of the posterior fourchette and the base at the upper segment of the labia majora. The flap is dissected from the fascia overlying the pubic bone and then rotated to cover the repair. After closure of the fistula, the fatty tissue covers the fistula closure, and the skin of the labia is sutured to the edge of the vaginal flaps. Interrupted, absorbable sutures are used to secure the edges in place.28 Small series have reported excellent results. Carr and Webster29 reported excellent outcomes for four patients. Postoperative complications include sensory deficit at the harvest site, poor cosmetic result, wound infection, and flap sloughing.

Gluteal Skin Flap Gluteal skin flaps are used predominantly in patients with radiation-induced fistulas or severe vaginal wall atrophy with no other viable skin source. In cases of severe radiationinduced fistula, the vaginal canal is very narrow, and access to the fistulous tract can be extremely difficult. Before the repair, a lateral episiotomy, starting at the posterior fourchette (5- or 7-o’clock) is performed and extended toward the vaginal cuff. The first two layers of the fistula are closed, and the vaginal flaps are raised as previously described. The edges of the vaginal wall incision are dissected laterally to widen the vaginal canal and make room for the flap interposition. From the end of the episiotomy incision, the incision is continued in an invertedU-shaped fashion toward the gluteal area. The skin is then undermined, and the flap is rotated and advanced into the vaginal canal to cover the fistula. The flap contains skin and fatty tissue and is broad based. The flap is secured with interrupted, absorbable sutures, and the vaginal flaps are secured to the skin flap edges.30 Complications include wound infection, sloughing of the flap, and injury to the anal sphincter.31 Meticulous surgical technique is mandatory to avoid the sphincter injury.

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Myocutaneous Gracilis Flap The gracilis muscle–based myocutaneous flap is frequently described in association with repair of radiation-induced VVFs in patients with vaginal atrophy or absence. The gracilis muscle is a long, slender muscle hat extends from the inferior pubic symphysis to the medial condyle of the femur. It is an accessory muscle (used for thigh adduction and knee flexion), and it can be sacrificed with no loss in function. It sits between the adductor magnus medially and the adductor longus laterally. The blood supply is derived from the medial femoral circumflex artery, a branch of the deep femoral artery. The flap is harvested with a tennis racquet incision on the medial aspect of the thigh over the gracilis muscle. It begins around 10 cm below the pubic tubercle and extends 20 cm toward the knee. The skin and underlying muscle are mobilized, and care is taken to preserve the vascular supply. The gracilis is transected at its distal insertion. A tunnel is then created underneath the medial aspect of the thigh and labia, and the flap is transferred to the vaginal area, providing additional coverage of the fistula tract and reconstruction of the vaginal canal. This can result in considerable cosmetic scarring, but there is no functional defect.

INTRAOPERATIVE COMPLICATIONS Bleeding and ureteral injury represent the two major intraoperative complications. Hemostasis is critical throughout the dissection and can be controlled with fine, absorbable sutures. Electrocautery should be avoided to preserve the vascularity of the tissues and promote healing. Lack of excellent hemostasis can lead to hematoma formation and possible disruption of the fistula repair. Ureteral catheterization is recommended for fistulas close to the trigone because of the higher risk of iatrogenic ureteral injury. Fistulas located elsewhere do not usually require this maneuver. If there is any concern about ureteral violation, cystoscopy is performed after intravenous indigo carmine is administered. Ureteral catheterization can be done if any question remains about ureteral patency.

POSTOPERATIVE MANAGEMENT The vagina is packed with an antibiotic-impregnated gauze, which is left in place for several hours. Surgery is mostly performed on an outpatient basis. The suprapubic and Foley catheters (joined to a Y connector) are left to dependent drainage, typically for 3 weeks. Anticholinergics are given to minimize bladder spasm and increase the patient’s comfort. An oral cephalosporin or quinolone is continued until the catheters are removed. Patients are instructed to resume normal activity except for strenuous exercise. Sexual intercourse is prohibited for 12 weeks. The urethral catheter is removed 3 weeks after surgery, and a suprapubic cystogram is performed. If the cystogram

demonstrates no extravasation, the suprapubic catheter is removed. OUTCOMES Many factors must be considered when assessing patient outcomes. Morbidity, patient satisfaction, and cure rate are critical factors in determining the best approach and the likelihood of success. There have been no prospective, randomized studies comparing vaginal and abdominal approaches in VVF repair. Many series have shown success rates of 90% to 100% with both approaches.15,32-34 The best approach remains the one with which the surgeon has the most expertise and comfort, giving the patient the best chance at cure with the first repair. POSTOPERATIVE COMPLICATIONS Early Complications Vaginal bleeding, bladder spasms, and vaginal infection must be treated aggressively and immediately to prevent fistula recurrence. Secondary vaginal bleeding is treated with repacking and bed rest. Prophylactic anticholinergics should minimize bladder spasms. Belladonna and opium suppositories (e.g., B & O Supprettes) can be used if required. Perioperative antibiotics are continued in the postoperative period to prevent vaginal infections. Delayed Complications The most important delayed complication is fistula recurrence. Others include vaginal shortening, vaginal stenosis, and unrecognized ureteral injury. Tension-free, multilayered closure with tissue interposition (as needed) results in a greater than 95% success rate. If the fistula recurs, a second vaginal repair may be performed with a Martius graft or peritoneal flap. A minimum waiting period of 3 months after the previous repair allows for resolution of postoperative inflammation. Avoiding excessive resection of the vaginal wall minimizes the odds of significant shortening and stenosis. Secondary vaginoplasty is required in selected cases. Unrecognized ureteral injury manifests more commonly as an obstruction process than a leak. An antegrade approach with percutaneous nephrostomy is preferred to a retrograde procedure because of the possible disruption of the repair by a transurethral approach. CONCLUSIONS VVF remains a significant source of morbidity after gynecologic and pelvic surgery. Transvaginal VVF repair is an outpatient procedure associated with minimal morbidity, short convalescence times, and high cure rates. It is our preferred method of repair unless concomitant abdominal surgery is required.

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References 1. Sims JM: On the treatment of vesico-vaginal fistula [originally published in Am J Med Sci 23:59-82, 1852]. Int Urogynecol J Pelvic Floor Dysfunct 9:236-248, 1998. 2. Mackenrodt A: Die operative Heiling grosser Blasencheindenfisteln. Zentralbl Gynakol 8:180-184, 1894. 3. Martius H: Uber die Behandlung von Blasenscheidenfisteln, insbesondere met Hilfe einer Lappenplastik. Geburtshilfe Gynakol 103:2234, 1932. 4. Lee RA, Symmonds RE, Williams TH: Current status of genitourinary fistula. Obstet Gynecol 72:313-319, 1998. 5. Drutz HP, Mainprize TC: Unrecognized small vesicovaginal fistula as a cause of persistent urinary incontinence. Am J Obstet Gynecol 158:237-240, 1988. 6. Kursh ED, Morse RM, Resnick MI, et al: Prevention of the development of a vesicovaginal fistula. Surg Gynecol Obstet 166:409-412, 1988. 7. Symmonds RE: Incontinence: Vesical and urethral fistulas. Obstet Gynecol 27:499-514, 1984. 8. Graham JB: Vaginal fistulas following radiotherapy. Surg Gynecol Obstet 120:1019-1030, 1965. 9. Stovsky MD, Ignaroff JM, Blum MD, et al: Use of electrocoagulation in the treatment of vesicovaginal fistulas. J Urol 152:1443-1444, 1994. 10. Morita T, Tokue A: Successful endoscopic closure of radiation induced vesico-vaginal fistula with fibrin glue and bovine collagen. J Urol 162:1689, 1999. 11. O’Conor VJ: Review of experience with vesico-vaginal fistula repair. J Urol 123:367-369, 1980. 12. Wein AJ, Malloy TR, Carpiniello VL, et al: Repair of vesico-vaginal fistula by a suprapubic transvesical approach. Surg Gynecol Obstet 150:57-60, 1980. 13. Blaivis JG, Heritz DM, Romanzi LJ: Early versus late repair of vesicovaginal fistulas: Vaginal and abdominal approaches. J Urol 153:1110-1112, 1995. 14. Raz S, Little NA, Juma S: Female urology. In Walsh PC, Retik AB, Stamey TA (eds): Campbell’s Urology, 6th ed. Philadelphia, WB Saunders, 1992, pp 2782-2828. 15. Zimmern PE, Hadley HR, Staskin DR, Raz S: Genitourinary fistulae: Vaginal approach for repair of vesicovaginal fistulae. Urol Clin North Am 12:361-367, 1985. 16. Leach GE, Raz S: Vaginal flap technique: A method of transvaginal vesicovaginal fistula repair. In Raz S (ed): Female Urology. Philadelphia, WB Saunders, 1992, pp 372-377. 17. Arrowsmith SD: Genitourinary reconstruction in obstetric fistulas. J Urol 152:403-406, 1994.

18. Latzko W: Postoperative vesicovaginal fistulas; genesis and therapy. Am J Surg 58:211-228, 1942. 19. Tancer ML: The post-total hysterectomy (vault) vesicovaginal fistula. J Urol 123:839-840, 1980. 20. D’Amico AM, Lloyd KL: Latzko repair of vesicovaginal fistula. J Urol 161(Suppl):202, 1999. 21. Mckay HA: Vesicovaginal fistula repair: Transurethral suture cystorrhaphy as a minimally invasive alternative. J Endourol 18:487-490, 2004. 22. Ou C, Huang U, Tsuang M, Rowbotham R: Laparoscopic repair of vesicovaginal fistula. J Laparoendosc Adv Surg Tech 14:17-20, 2004. 23. Nezhat CH, Nezhat F, Nezhat C, et al: Laparoscopic repair of vesicovaginal fistula: A case report. Obstet Gynecol 83:899-901, 1994. 24. Perez Ca, Grigsby PW, Lockett MA, et al: Radiation therapy morbidity in carcinoma of the uterine cervix: Dosimetric and clinical correlation. Int J Radiat Oncol Biol Phys 44:855-866, 1999. 25. Margolis T, Elkins TE, Seffah J, et al: Full-thickness Martius grafts to preserve vaginal depth as an adjunct in the repair of large obstetric fistulas. Obstet Gynecol 84:148-152, 1994. 26. Eilber KS, Kavaler E, Rodriguez LV, et al: Ten-Year experience with transvaginal vesicovaginal fistula repair using tissue interposition. J Urol 169:1033-1036, 2003. 27. Raz S, Bregg KJ, Nitti VW, et al: Transvaginal repair of vesicovaginal fistula using a peritoneal flap. J Urol 150:56-59, 1993. 28. Raz S: Atlas of Transvaginal Surgery. Philadelphia, WB Saunders, 2002. 29. Carr LK, Webster GD: Full-thickness cutaneous Martius flaps: A useful technique in female reconstructive urology. Urology 48:461463, 1996. 30. Stothers L, Chopra A, Raz S: Vesicovaginal fistula. In Raz S (ed): Female Urology, 2nd ed. Philadelphia, WB Saunders, 1996, pp 490-506. 31. Wang Y, Hadley HR: The use of rotated vascularized pedicle flaps for complex transvaginal procedures. J Urol 149:590-592, 1993. 32. Langkilde NC, Pless TK, Lundbeck F, et al: Surgical repair of vesicovaginal fistulae—A ten-year retrospective study. Scand J Urol Nephrol 33:100-103, 1999. 33. Diaz CE, Calatrava GS, Caldentey GM, et al: Surgical repair of vesico-vaginal fistulae with abdominal-transvesical approach. Comments on this technique with long-term results. Arch Esp Urol 50:55-60, 1997. 34. Frohmuller H, Hofmockel G: Transvaginal closure of vesicovaginal fistulas. Urologe A 37:102, 1998.

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ABDOMINAL APPROACH FOR THE TREATMENT OF VESICOVAGINAL FISTULA Mariangela Mancini and Walter Artibani An abdominal approach can be used to repair a vesicovaginal fistula (VVF). A VVF, an abnormal communication between the bladder and the vagina, is located outside the abdomen. The peritoneum reflects over the bladder dome anteriorly and the lower third of the uterus posteriorly (Fig. 82-1). The lamina of connective tissue interposed between the bladder and the vagina, whose destruction is associated with the formation of the VVF (Fig. 82-2), is found well outside the abdominal cavity. From an anatomic perspective, it appears to be more intuitive and, indeed, to reach a VVF through the vaginal route instead of through the abdomen, specific technique for VVF repair originally was mastered by the vaginal approach. Nevertheless, the abdominal approach for treatment of the VVF has its own indications and can offer specific advantages over the vaginal route. The history of the development of this surgical technique can help us understand the part that the abdominal approach plays in VVF surgery.

The first surgeons who tried to correct a VVF did so through the vaginal approach. In 1663, Hendrik van Roonhuyse recommended transvaginal repair with the patient in the lithotomy position. Stiff swan quills were passed to the edges of the wound, and the bladder and surrounding tissues were widely mobilized. Van Roonhuyse’s book was published in 1676.1

The first two successful cases treated with this technique were reported by Johann Fatio in 1675.2 Despite these preliminary and isolated successful experiences, the presence of a VVF was commonly considered an incurable situation in the years that followed. An important innovation was introduced by Antoine Jobert the Lamballe in 1834, when he performed his first operation of transvaginal closure of a VVF by resection of the margins and coverage of the loss of substance with a cutaneous autograft obtained from the labia or the internal face of the thigh.3 The first operation was unsuccessful because of necrosis of the graft, but the patient was successfully cured on the second attempt with the same technique. Further developing the technique, Jobert pioneered later a method of tissue mobilization that widely detached the bladder from the vagina, which he called vesicovaginal autoplasty (autoplastie vesico-vaginale par glissement). He used this approach to avoid traction on the margins before suturing the edges of the fistula, and thereby obtained several successes in difficult VVF cases.4 In 1839, George Hayward5 reported the first cure of a VVF in the United States. He underscored the importance of accurate dissection of the vagina from the bladder before closing the fistula with stitches and pioneered the flap-splitting technique.5 In 1852, James Marion Sims6 published his first report of successful primary repair of a VVF, which was again performed transvaginally. This interesting paper has been recently republished in the medical literature.6 The correct surgical technique, the use of a

Figure 82-1 Sagittal section of the female lower abdomen and pelvis. The peritoneum (bold line) lines the floor of the abdominal cavity, leaving the vagina and posterior face of the bladder below it.

Figure 82-2 Female pelvic organs with their subperitoneal sheaths. The connective pillow layer interposed between the vagina and the bladder and urethra is indicated by cross-hatching. Damage to this tissue is associated with the formation of a vesicovaginal fistula.

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new speculum designed by him, the search for the optimal patient position for exploration of the vagina, and an understanding of the importance of postoperative bladder drainage led to a high success rate for VVF treatment through the vaginal route and to international popularity for Sims. This brief historical review shows that the basic principles stated by Sims and his predecessors for correct fistula treatment are still valid and that few modifications have been made by the surgeons who followed.7 However, in 1868, Thomas Addis Emmet, who succeeded Sims as chief surgeon of the Woman’s Hospital in New York, described some cases in which extensive scarring of the vagina and proximal location of the fistula compromised optimal access during transvaginal repair, indicating the need for higher access in these situations.8,9 Some years later, the abdominal approach for the treatment of VVF was introduced. The suprapubic transperitoneal-transvesical route was first described by Friedrich Trendelenburg in 1881,10 and in 1893, Von Dittel introduced the approach extraperitoned suprabubic for access to the VVF route.11 In 1902, Howard Kelly recommended a transperitoneal approach in the treatment of VVFs formed after hysterectomy that were too high in the bladder to be safely reached transvaginally.12 In 1914, Legueu13 described in more detail the transperitoneal-transvesical approach.13 To improve the chance of success in the most difficult cases, the omental graft technique was introduced by Hiltebrant in 1929 and further developed by Bastiaanse in the attempt to cure the challenging cases of postirradiation fistulas.14 In 1951, O’Conor and Sokol15 described the complete range of possible procedures for successful treatment of VVFs, from conservative measures to vaginal or suprapubic closure to urinary diversion.15 They emphasized the importance of careful selection of patients for each procedure. In some patients who had endured repeated previous failures, the fistulous opening was too high and too far from the bladder floor and the vagina too scarred to allow a vaginal approach. In these cases, a suprapubic procedure, preferably extraperitoneal, was described with bisection of the bladder down to the fistula opening and wide mobilization of the bladder from the vagina. A transperitoneal approach was selected when exposure was difficult because of previous operations, a history of cancer, or when the omentum needed to be used. With proper application of this technique, many successes were reported by O’Conor16,17 in the following years. However, the suprapubic approach was not used by O’Conor17 in 35% of his cases, for which a less invasive procedure was chosen. This information underscores the importance of case selection. With the many possibilities available, VVF often can be treated successfully by tailing the approach to the patient’s condition. It took almost 300 years of surgical research and extended practice with VVF patients, including enormous suffering and great rewards, to achieve this important goal. The history of the approaches to treatment demonstrates that flexibility is the key to successful management of this challenging pathologic condition. ABDOMINAL APPROACH Indications An abdominal approach for the treatment of a VVF can be chosen for several reasons. Theoretically, the abdominal approach should be used when a less invasive approach is not feasible, but practically, this can have different meanings in different settings. At

least four factors enter into the decision: the kind of fistula, the patient, the situation in which treatment takes place, and the surgeon. Fistulas are not all the same, and treatment must be individualized. Case selection is important.18,19 The abdominal approach was developed to treat fistulas that were too high or too far from the bladder floor to be reached transvaginally. Moreover, in some cases, especially after several previous attempts, the vagina can be severely scarred and cannot be used for access to the fistula. Application of this concept depends on the surgeon’s experience. Surgeons who have extensive experience with transvaginal surgery perform most repairs in this way, finding treatment of most fistulas amenable to the transvaginal approach.20,21 Even the most complex fistulas can be repaired with the use of a peritoneal flap.22 There have been no abdominal repairs in the Addis Ababa Fistula Hospital in the past 4 years, during which about 4500 patients have been repaired transvaginally. However, one case of a high cervicovaginal fistula was operated on in another hospital. The patient had previously undergone a cesarean section, and in this particular case it was necessary to switch from the vaginal to the abdominal route because the fistula could not be reached safely from the vagina (A Browing, personal communication, 2005). Similarly, in patients who have been treated more than once with less invasive procedures without success, an attempt through a different route may be a reasonable choice. Some patients may express a preference for the abdominal route to increase the likelihood of cure. Some patients may need adjunctive procedures, such as ureteral reimplantation, bladder augmentation, or omental grafting, which need to be performed through the abdominal route. The treatment setting also can influence operative decisions. In some tropical countries, for example, general anesthesia is not commonly available, which makes widespread use of the abdominal approach almost impossible.23,24 In this situation, the technical level of hospitals encourages the use of less invasive procedures that can be performed safely under spinal anesthesia.25,26 The surgeons’ preferences are based on general surgical experience, familiarity with the procedure, and personal opinions about the case. Box 82-1 summarizes the indications for the abdominal approach that are consistently reported. Timing The best time to intervene and repair a fistula is unknown. Initially, treatment delay was advocated by some surgeons,16,27,28 but later data indicate that immediate treatment is beneficial.26 Treatment decisions are complicated by the fact that fistulas can be completely different pathologic entities, from the small, clear-cut opening produced during pelvic surgery, which is suitable for Box 82-1 Indications for the Abdominal Approach too high in the bladder to be reached • Fistula vagina • Inaccessible preference • Patient’s Previously failed multiple attempts or failed less invasive • attempt of other concurrent transabdominal procedures • Necessity setting • Hospital • Surgeon’s preference

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immediate repair,29 to the large, necrotic loss of substance, which results from hours of ischemic injury to the bladder during obstructed labor.30 Timing should be tailored to the specific situation.31,32 It seems reasonable that a fistula should be treated as soon after diagnosis as possible, with timing modified according to the individual case. In the developed world, there often is no reason to postpone treatment.29,31,33-35 Exceptions include the presence of infection or significant edema or a massive hematoma at the site of the fistula, which should be resolved before surgery. Taking care of coexistent problems usually requires not more than a few weeks, during which regular cystoscopic evaluation may be advisable.36 The possibility of spontaneous closure should be considered, especially for small, clean, postoperative fistulas, because spontaneous closure has been described in several cases after a trial of observation for 3 to 4 weeks.26,37-39 After a conservative trial is started, we avoid using an indwelling catheter during the period, to minimize local infection and edema. Large fistulas, fistulas recurring after previous attempts at repair, multiple fistulas, or those associated with other conditions that require surgical treatment are not prone to spontaneous closure, and there is no reason to consider a conservative approach. These cases are more often treated with the abdominal approach. Box 82-2 addresses the suggested timing of VVF management. Preoperative Preparation The following guidelines for the preoperative preparation of the patient are based on published data and our personal opinions and experience. Preoperative preparation should not delay surgery, unless there is infection, massive hematoma, or significant edema at the site of the fistula (see Box 82-2). The performance status and nutritional status of some patients may require time for improvement. This situation may be more common in countries with a high incidence of VVF among poor patients. In these cases, preoperative preparation to improve the general condition of the patient is indicated, as emphasized in several reports.14,23,30,40 Box 82-3 summarizes the issues concerning preoperative preparation of VVF patients.

Box 82-2 Timing Sequence

• Diagnosis evaluation • Cystoscopic conservative trial (when appropriate) • Quick • Surgery Postpone surgery for infection, hematoma, or significant • edema

As soon as the patient is ready for surgery the issue of antibiotic prophylaxis must be considered. A randomized control trial, which reported the results for 79 VVF in 1998, showed that antibiotic prophylaxis (500 mg of ampicillin IV) at the start of the operation did not produce benefit in terms of success rates, but it seemed to reduce postoperative urinary infections and the need for long-term antibiotic therapy.41 Consistent with this first experience, in a large series from Nigeria Waaldjik, reported a success rate of 98% for 1716 cases of VVF without the use of antibiotic prophylaxis.26 Postoperative wound infection was not never seen, and antibiotic use does not seem to be mandatory according to these data. However, when economic restrains are not severe, antibiotic prophylaxis may be considered and continued postoperatively when necessary or in cases involving surgical manipulation of the intestines. Another consideration is the use of cortisone. Collins and associates42 reported the use of oral corticosteroids (100 mg, three times daily for 10 to 12 days preoperatively) in the treatment of fistulas to reduce edema and fibrosis. Cortisone use is not widely accepted before surgery for VVF because it may compromise healing. It is difficult on the basis of the available data to justify the use of steroids before fistula repair. Local application of estrogen creams has been advocated as a preoperative measure.17,43,44 Estrogens can improve the cellular proliferation rate and blood supply of the vaginal wall, which contains estrogen receptors in the epithelial layer. Estrogen receptors are also found in the connective tissue of the female pelvis between the bladder and the vagina. This tissue undergoes atrophy with hypoestrogenism. It therefore seems wise to recommend the local use of preoperative estrogen creams, particularly in postmenopausal or post-hysterectomy patients. Even in premenopausal women, the use of estrogen creams has helped in healing postcesarian VVFs soon after delivery.45 Consistently, the use of tamoxifen, an anti-estrogen drug, has been associated with poor local healing after gynecologic surgery.46 However, the epithelium that lines the fistulous tract itself contains estrogen and progesterone receptors in vesicouterine fistulas.47 Estrogen stimulation in this case could antagonize spontaneous closure of the fistula by maintaining the lining epithelium. Jozwik and Jozwik48 reported spontaneous closure of vesicouterine fistulas with hormonal suppression by induction of amenorrhea, supporting the role of estrogens in the maintenance of this kind of fistula. There are few data on the histology of VVFs. It is not known whether estrogen receptors are present in the epithelium lining VVFs. A case of persistent VVF associated with endometriosis has been reported,49 but endometriotic tissue was not found on histologic analysis of the fistula’s epithelium. In a few cases, estrogens may maintain the fistula’s epithelium, but this seems more common in vesicouterine fistulas and has never been demonstrated in VVFs. Surgical Technique

Box 82-3 Preoperative Preparation of patient's performance status (when • Improvement necessary) prophylaxis • Antibiotic treatment (when indicated) • Antibiotic treatment (not supported by evidence) • Cortisone • Local estrogens (useful)

The patient is positioned supine on the operating table with the hips abducted and mildly flexed. An appropriate degree of headdown tilt is advisable. The abdomen and perineum are prepared for the operation. Even when the operative approach is through the abdomen, sterile access to the perineum should be provided for catheterization, preoperative cystoscopy (if required), access to the vagina for finger or tampon aid during separation of the vagina from the bladder, or in case a combined perinealabdominal approach becomes necessary.

Chapter 82 ABDOMINAL APPROACH FOR VESICOVAGINAL FISTULA

Figure 82-4 View of the internal surface of the bladder after an anterior cystotomy during the anterior transvesical approach. Suspension sutures retract the bladder walls for exposure. The ureters have been catheterized. The fistula opening is shown just behind them. The bladder wall is excised around the fistula in a racquet fashion (dashed line).

Figure 82-3 Patient position and incision lines for the abdominal approach to treating vesicovaginal fistula. Cutaneous incisions can be on the midline or horizontal (i.e., Pfannenstiel incision). The rectal fascia incision should be performed vertically on the midline in both cases. A Pfannenstiel incision can be combined with a short epigastric incision in case omental mobilization is required. The infra-umbilical median incision can be extended upward.

sion is truncated with a 4-cm horizontal tract at the level of the pubic symphysis. After the incision is completed, the procedure can take place through the anterior transvesical approach or the classic O’Conor technique by means of the extraperitoneal or intraperitoneal route. The former is described first.

A catheter is placed in the bladder. The surgical instruments are those used during classic pelvic surgery. Autostatic retractors are useful. Laparotomy can be performed by a lower midline incision or by a Pfannenstiel incision, especially when a previous operation used this route (Fig. 82-3). When needed, both incisions can be extended to the upper abdomen to obtain access for omental preparation. The median incision is extended upward, and the Pfannenstiel incision can be integrated with an extrashort epigastric median incision. Sometimes, reaccessing a previous Pfannenstiel incision may not guarantee proper exposure of the pelvis. In this case, the suprapubic cross incision or a suprapubic V-shaped incision, as described by Turner-Warvick and Chapple50,51 and Turner-Warvick and coworkers52 can be a suitable choice. This is particularly valid when the patient previously had surgery by the Pfannenstiel route. An additional midline incision would leave this patient with a double-cross–like scar and a long-lasting memory of the VVF. The suprapubic cross incision allows reopening of the skin though the previous incision, but after dissecting the subcutaneous tissue away from the rectal fascia, it must be transected vertically on the midline up to the umbilicus, not along the previous horizontal fascial incision. The V-shaped incision is a variant, in which after a Pfannenstiel skin incision, the rectus sheath is opened upward and laterally toward the anterior superior iliac spine; distally, the fascial inci-

Anterior Transvesical Approach After the fascia is open, the Retzius space is entered. Dissection of the Retzius space allows preparation of the preperitoneal surface of the bladder, separating it from the surrounding structures. A self-retaining retractor can be placed at this point to keep the abdominal wall stabilized laterally. A vertical anterior cystotomy is performed, which allows visualization of the internal surface of the bladder with the fistula and the ureteral openings. If fistula and ureteral openings are close, ureteral catheters can be passed in the ureters at this point. A delicate retractor or suspension sutures can be used to separate the bladder walls (Fig. 82-4). The operation proceeds with a racquet-shaped excision of the bladder wall around the fistula opening in the bladder and of the fistulous tract until clean, well-vascularized margins are obtained (Fig. 82-5). Some methods can help to gain traction on the fistula and facilitate its dissection, including use of a Foley catheter with an inflated balloon44 and specially designed devices passed through the fistula53,54 from the bladder opening to the vaginal opening. Dissection of the bladder from the vagina around the fistula is carried out to obtain free lateral margins, which can be then sutured without traction. Meticulous hemostasis is recommended during these maneuvers, with care taken to avoid ischemic damage to the tissue, which may compromise the repair. At this stage, sutures are placed, starting deeply from the vaginal site. Interrupted, absorbable, 2-0 or 3-0 sutures are

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Figure 82-5 The vagina is sutured, and then the bladder is sutured. The sutures can be placed in directions perpendicular to each other, but the best strategy is to suture the vagina and the bladder according to the lines that allow the least tension on the margins.

recommended. One layer is enough at the vaginal site. For fistulas located at the bladder neck, it may be feasible to close the vaginal end of the fistula from the vagina, using a combined abdominoperineal approach.55 The bladder end of the fistula is then closed with a double layer (muscular layer and mucosal layer) of interrupted or continuous sutures (see Fig. 82-5). Absorbable sutures should be used. The ureteral catheters are removed, and the anterior cystotomy can be closed in a similar double-layered fashion. A drain is left in the Retzius space, along with a suprapubic cystostomy or a transurethral catheter, or both. The catheter’s balloon is not inflated or inflated with only 4 to 5 mL to avoid balloon compression on the suture lines. The key points of the technique are wide excision of the fistulous tract until well-vascularized margins are achieved; generous dissection to ensure no tension on sutures; perfect hemostasis; a three-layered suture that includes the vagina, detrusor, and bladder mucosa; and a watertight suture of the bladder. O’Conor Technique The O’Conor technique is based on complete bisection of the bladder and wide separation of it from the vagina. In its original description, it was performed extraperitoneally, but intraperitoneal access sometimes is required.15,16 The bladder is exposed extraperitoneally with as much dissection as necessary to free its posterior wall. The peritoneum can be opened when the extraperitoneal posterior exposure of the bladder is insufficient, when additional procedures or omental interposition is required, or when the patient has undergone previous operations for carcinoma.17 After the peritoneum has been opened at the midline, the abdominal cavity can be explored. The bowel is evaluated in case an augmentation cystoplasty has been planned, and the omentum is inspected and measured to verify its ability to reach the pelvis. Adhesions can be separated, and the bladder dome and the Douglas space are reached and prepared. In the extraperitoneal

Figure 82-6 The posterior cystotomy is extended downward to include the fistula opening during the O’Conor procedure. Excision of the bladder wall is continued posteriorly widely around the fistula, which is totally excised on the vaginal side to obtain healthy free edges (dashed line).

and intraperitoneal approaches, the bladder is fully mobilized before incising it. A generous vertical cystotomy is performed on the posterior surface of the bladder, from the dome down to the site of the fistula, which is included in the distal part of the incision. To facilitate later closure of the cystotomy, the posterior incision of the bladder can be curved laterally so that the two edges will approximate more comfortably at the end of the operation. The bladder is practically bisected on the posterior wall with this long incision, which reaches the fistula opening. Suspension sutures can be placed along the separated bladder halves to keep them separate and guide the surgeon later during closure. The interior surface of the bladder is inspected, and the ureters can be catheterized. The bladder wall around the fistula is sectioned circularly, and the fistula is excised to obtain free, healthy margins (Fig. 82-6). All necrotic and nonviable tissue is excised; a wide, lateral dissection of the bladder from the vagina is obtained; and the bladder is moved upward and anteriorly, with careful hemostasis to prevent postoperative ischemia (Fig. 82-7). The suturing begins at this point. Transverse vaginal closure is achieved with a single or double layer (double layer in the O’Conor’s description of the procedure15) of absorbable continuous or interrupted sutures (Fig. 82-8). Longitudinal bladder closure is then achieved with a double layer of absorbable interrupted or continuous sutures. The bladder closure starts from the distal apex of the cystotomy and walks upward (Fig. 82-9). Interposition tissue such as peritoneum or fat can be placed over the top of the vaginal suture to reinforce it. Unlike the original description, the vaginal site of the fistula is not always closed, because some surgeons think that closure can prevent drainage of hematomas from the widely dissected intervesicovaginal space.56 A drain is left in the retropubic space before closing the abdomen, along with a cystostomy or a transurethral catheter, or both.

Chapter 82 ABDOMINAL APPROACH FOR VESICOVAGINAL FISTULA

Figure 82-7 The dissection plane lies between the bladder anteriorly and the vagina posteriorly during the O’Conor procedure (dashed line). This plane is carefully developed after the fistulectomy has been performed to obtain full separation of the bladder from the vagina.

Figure 82-9 The last step of the procedure is closure of the bladder wall. This can be performed in one or two layers, starting from the distal end of the posterior cystotomy. The initial curved line of the bladder incision facilitates closure of the bladder wall without tension.

line or when proximity between the fistula and the ureteral meatus does allow primary closure of the bladder without ureteral reimplantation. Interposition grafts can be used during any abdominal surgical procedure, and they vary in terms of location, vascularization, and type of tissue used. Free Bladder Mucosa A simple procedure using free bladder mucosa can be applied easily during a limited anterior transvesical approach. A patch of bladder mucosa is harvested from the bladder dome in a size proportional to the size of the fistula, and it is then placed between the bladder and vagina, with the mucosal surface directed toward the vagina or the bladder, and it is fixed in place with a few stitches. The bladder wall is then sutured over the graft. The patch is harvested, leaving the underlying detrusor muscle intact. The donor bed fully re-epithelizes after a few weeks.59 This method has shown good results in avoiding reimplantation of the ureters when they were close to the fistula opening in the vagina, because no attempt is made to separate the vaginal and vesicle layers of the fistula60 or close the vaginal or bladder site of the tract.61,62 Figure 82-8 Closure of the vagina with interrupted sutures. The wide mobilization performed earlier allows closure without tension on the margins.

Interposition Grafts Interposition grafts are used in VVF surgery because experience indicates that this tissue promotes the success of the procedure, especially in cases of multiple failures and necrotic and poorly vascularized tissues, as in postirradiation fistulas.57,58 Another indication for interposition grafts is when the loss of substance after fistulectomy is too wide to guarantee a tension-free suture

Sliding Bladder Wall Gil-Vernet63 described a technique to advance downward a portion of full-thickness bladder wall to close a large loss of substance after fistulectomy. It is a type of vesical autoplasty that has been successful in resolving complex VVFs, especially when the fistula is close to the ureteral meatus. In this procedure, a flap obtained from the posterior bladder wall is moved down to replace the mucosa excised during the fistulectomy. After closing the vaginal site, the bladder wall is bilaterally incised from the fistula opening upward, allowing a flap to be brought down to the bladder neck and sutured to the distal bladder wall in a single layer. In this way, the vaginal suture line can be completely

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covered. This technique is easy to perform, and it limits the need to use omentum in cases of large, complex fistulas when the bladder cannot be closed primarily. It has the advantage of replacing bladder with bladder.64 Dura Mater A graft of solvent-dehydrated human dura mater can be used for interposition during the extraperitoneal approach, even in cases of limited exposure and when the fistula has not been excised. After closure of the vaginal site, the dura mater graft is placed over the suture and fixed with interrupted, absorbable suture. Subsequently, the bladder is closed in two layers.65 The use of dura mater as a bladder or ureteral wall substitute has been successfully demonstrated.66 Abdominal Wall Fat When abdominal wall fat is used for interposition, an extraperitoneal approach is undertaken in the usual fashion. The fistula is excised, and the free graft of abdominal wall fat is placed over the vaginal suture line before closing the bladder site. This simple technique can be performed easily in cases of limited exposure.67 Rectus Abdominis Muscle Flap A rectus abdominis muscle flap can be raised during an extraperitoneal approach; blood for the flap is supplied by the inferior epigastric artery. This muscle has excellent vascularization, and it can be rotated easily and brought down into the pelvis in cases of complex fistulas, especially when the omentum is not available for interposition. A rectus abdominis myofascial flap has been used successfully in one patient with a large postirradiation VVF.68 In another case of postirradiation VVF, a rectus abdominis myocutaneous flap covered a large loss of substance in the bladder after fistulectomy adjacent to the ureteral meatus, with the skin side of the graft covering the bladder inner wall.69 Rectus abdominis myocutaneous flaps have been used successfully in a complex cases of irradiated pelvic wounds and pouch-vaginal fistulas, for which several previous transvaginal and transabdominal approaches had failed.70 Successful use of rectus abdominis muscle flaps has been reported for four other cases of difficult, recurrent VVFs.71,72 Gracilis Muscle Flap In complex cases when the omentum is not available, the gracilis muscle can be considered for tissue interposition during an abdominal repair. The access is extraperitoneal. The muscle is harvested from the thigh based on the profunda femoris artery, and the flap is transposed between the bladder and the vagina. Two cases of recurrent VVFs were successfully treated with this technique.73 Peritoneal Flap When using a flap of peritoneum for interposition, access is gained through the transperitoneal route. After incision of the bladder and excision of the fistula, a flap of peritoneum with an appropriate pedicle is raised from the lateral pelvic wall. The vaginal site is closed, and the flap is placed between the bladder and the vagina and fixed with interrupted absorbable sutures. The bladder wall is closed over the flap. Care is taken at the end of the procedure to suture the peritoneal lateral edges from which the flap has been harvested, but this is not always necessary. This simple technique can be used successfully to repair recurrent or postirradiation fistulas.74 One possibility when using the

peritoneum is to harvest a flap of the peritoneum that lines the broad ligament. A portion of the anterior surface of the broad ligament can be raised and moved medially to cover the vaginal site of a VVF in case of a large fistula.75 An epiploic appendix can be used as interposition tissue and be brought behind the bladder when using an intraperitoneal or an extraperitoneal approach; in the latter case, access is gained by cutting a small opening in the peritoneum.76 Seromuscular Intestinal Graft A patch of seromuscular intestinal graft obtained from a segment of small bowel can be used to repair VVFs. This technique requires intraperitoneal access and interruption of the bowel for harvesting the intestinal segment. The loop obtained is opened along the antimesenteric border, and the mucosal lining is mechanically removed, obtaining a seromuscular graft of small intestine. This patch is then used as interposition tissue between the bladder and the vagina, with the seromuscular face positioned toward the bladder. Complete re-epithelization of the seromuscular face of the graft with transitional epithelium occurs after a few weeks, and a 100% cure rate has been reported for treating complex postirradiation fistulas in four patients.77 Omentum The omentum has excellent capacity for tissue healing, revascularization, lymphatic drainage, and anti-inflammatory activity. Unlike other tissues such as muscle, the omentum does not undergo atrophy or fibrosis after transposition. A transperitoneal approach always allows access to the omentum. However, this does not necessarily mean that the omentum can be used, because in some cases, it may be retracted or not available for interposition because of previous surgical procedures. Availability of the omentum can be established only after opening of the peritoneum. The omentum reaches directly into the pelvis in only 30% of patients.78 In 70%, omental mobilization is required. A complete description of the surgical technique for omental interposition was published by Turner Warwick.50 The key point is maintenance of the vascularization of the omentum by careful preparation of its vascular pedicle. Vascularization of the omentum is based on the gastroepiploic arteries. The right artery usually is larger. The two arteries form an arch along the greater curvature of the stomach, which needs to be mobilized for elongation of the omentum when this is needed. Because mobilization should be based on the right gastroepiploic artery, the omentum should be released from the greater curvature, starting high on the left and moving down to the right. Variations of this procedure may vary from a limited tract to the entire length of the greater curvature. The prepared omental apron is displaced in the pelvis and interposed between the bladder and the vagina, where it is secured in place with a few stitches. It is important to protect the passage of the omentum by mobilizing the ascending colon and placing the omentum behind it.51 Suction drainage of the stomach can protect it from postoperative overdistention that could put the sutures on the small vessels along the greater curvature under tension. Complex Repairs Combined grafting with omentum and a gastric segment has been described in a case of postirradiation VVF with large sub-

Chapter 82 ABDOMINAL APPROACH FOR VESICOVAGINAL FISTULA

stance loss. The gastro-omental graft was based on the right gastroepiploic pedicle. The gastric wall was used successfully to replace the posterior bladder wall, and the omentum closed the vaginal defect, which was not sutured.79 Large postirradiation fistulas may require bladder augmentation during repair. An ileocystoplasty can be successfully performed in these cases; it can be combined with omental interposition, without closure of the vaginal site when this is not possible.80,81 Augmentation cystoplasty should be performed when the bladder capacity is small as a consequence of previous failed repairs, because it may prevent the necessity of urinary diversion.82 However, urinary diversion as a final option in the treatment of VVF can be employed with good functional results. Continent diversions are more acceptable to patients, especially in countries when the local culture does not accept external diversions or the economic and clinical support for the external incontinent stoma is not available.83 Continent urinary diversions performed with the Mitrofanoff procedure can be a valuable technique to restore continence in the most difficult patients.84,85 When good anal continence is preserved, an ureterosigmoidostomy, such as a Mainz II pouch, can be considered.86,87 A colon pouch can be similarly used for a continent external diversion.88 Laparoscopic Repair Laparoscopic repair of a VVF fistula is a less invasive strategy than the open abdominal approach. This is especially true when the VVF resulted from a previous laparoscopic procedure. Successful laparoscopic repair of a VVF was first described by Nezhat and colleagues89 in 1994 in a patient who had been previously treated laparoscopically for an ovarian remnant syndrome. Subsequently, more experience with this technique were published.90-96 Preoperative cystoscopy and ureteral catheterization are advisable before laparoscopy. During cystoscopy, a ureteral catheter or a Foley catheter can be passed through the fistula into the vagina and retrieved outside through the introitus. This helps with identification of the fistula during dissection. Leaving the cystoscope in the bladder with the light on can facilitate identification of the fistula during the operation.96 The patient is placed in the low lithotomy position. For access, one 10-mm infraumbilical incision is made to insert the video laparoscope and the CO2 laser, and three additional 5- to 10-mm incisions are made in the lower abdomen for the suction-irrigation probe, the grasping forceps, and the bipolar forceps. The principles of laparoscopic surgery do not differ from those of open surgery. A classic O’Conor technique is reproducible laparoscopically.95,96 Cystotomy on the posterior bladder wall and careful dissection of the bladder from the vagina are performed under direct vision, with the advantage of magnification provided by the laparoscopic approach. An inflated glove or a wet sponge in the vagina can help to maintain the pneumoperitoneum after the vagina has been opened. The pneumoperitoneum can also help to distend the bladder after the cystotomy has been performed After excision of the fistula and mobilization of the bladder from the vagina, the vagina and then the bladder are each sutured with one layer of interrupted or continuous absorbable sutures using extracorporeal knotting. Intracorporeal knotting has also been performed,93 as has double-layered closure of the bladder.94,96 A flap of parietal peritoneum can be used for interposition.89 The omentum can be mobilized with staplers and interposed without closure of the vaginal site91 or after the vagina

has been sutured.92-96 Patients can be discharged on the first or second postoperative day. Additional intra-abdominal procedures, such as ureteral reimplantation or nephrectomy, can be performed during the laparoscopic approach.93,96 Two large series of patients treated laparoscopically have been reported,95,96 consisting of 6 (plus 2 cases of vesicouterine fistulas) and 15 cases of VVFs. Success rates of 100% and 93% were reported for these series. Robotic Repair A robotic system can be used as an alternative to laparoscopy in VVF repair, especially during the reconstructive period. Robotic surgical systems offer several technical advantages: high magnification, three-dimensional imaging, and a degree of freedom in movement that surpasses the possibilities of the human hand and laparoscopic instruments. Successful repair of VVFs using the Da Vinci robotic system is possible. The first case managed with this technique was reported in 2005.97 The patient is placed in the low lithotomy position. Preoperative cystoscopy with ureteral catheterization is performed. The patient is then moved into an extreme Trendelenburg position, and the ports are placed. Port placement does not differ from the technique used in robotic-assisted radical prostatectomy.98 In the first part of the operation, exposure of the bladder and cystotomy on the posterior bladder wall are performed, with identification of the fistula and excision of the fistulous tract, using a standard laparoscopic technique. The Da Vinci system is docked for the reconstructive part of the operation. The vaginal layer is closed with a single layer of sutures, and the bladder is then closed in two layers. The patient is discharged on the second postoperative day. It is probable that robotic repair of VVFs will become more common in the future. The hope is that technologic improvements, such as the Da Vinci robot, can help surgeons successfully manage the more difficult cases with less invasive procedures and faster postoperative recovery while maintaining or improving the standards for proper surgical repair. POSTOPERATIVE CARE The key aspect of postoperative care in VVF surgery is continuous bladder drainage.6 This can be accomplished by a transurethral or a suprapubic catheter, or both, placed at the end of the operation. Prevention of kinking and obstruction by blood or mucus of the catheter is crucial. The transurethral catheter balloon should not be inflated or inflated with no more than 5 mL to prevent compression on the suture lines, especially if the fistula was at the level of the bladder neck. Suprapubic and transurethral urine drainage can be beneficial in case one catheter stops functioning. Maintenance of a high urine output with adequate fluid intake is a good postoperative measure to keep the patient hydrated and prevent blockage of the catheter.26,99 Bladder drainage should be maintained for a minimum of 10 days100 and, more often, for 2 weeks. The timing of catheter removal varies and must consider the patient’s circumstances. More prolonged catheterization is required for extension of the bladder sutures and for poor tissue quality.101 The transurethral catheter can be removed before or after the suprapubic catheter. The suprapubic catheter should be

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Box 82-4 Postoperative Care

Box 82-5 Differences in Fistula Cases

bladder drainage • Adequate High fl uid intake • Intra-abdominal drainage • Temporary gastricfluid drainage after omentum mobilization • Avoidance of traction on the sutures: no tampons, no sex • for 2 months therapy: antibiotics, anticholinergic agents, • Adjuvant estrogens

• Cause of fistula • Location Hospital setting • First versus subsequent treatments • Quality of surrounding tissue • Associated lesions • published experiences and our own experience with the abdominal approach to VVF repairs.

clamped before removal is attempted to check for effective voiding. A voiding cystogram is obtained before removing the last catheter to make sure that there is no leak from the bladder. If incomplete closure is suspected, the catheter can be left in place for 1 or 2 weeks longer. A drain in the paravesical space can be left at the end of the operation to ensure drainage of blood or fluids from the pelvis. An intraperitoneal drain can be placed during transperitoneal procedures or when the omentum has been mobilized. Drains can be removed starting 5 or 6 days after the operation. It may be advisable to leave the paravesical drains longer. Ureteral catheters can usually be removed at the end of the operation, unless the ureters have been reimplanted. After a transperitoneal procedure, especially when the omentum was mobilized, temporary gastric drainage may be advisable, to prevent gastric overdistention. Alternatively, a gastrostomy performed at the time of surgery may be a more comfortable option for the patient.50,102 A vaginal pack is removed on the first postoperative day. Bed rest may be advised in cases of large, necrotic fistulas and poor vascularization of surrounding tissues.24 In other cases, ambulation on the first or second postoperative day is encouraged. Postoperative antibiotic prophylaxis is administered for 10 days or until the drains are removed, but antibiotics are not always mandatory. Oral or local estrogen treatment may be useful in postmenopausal women. Mechanical stress or tension on the suture line should be avoided. The use of vaginal tampons is discouraged for a few weeks, and sexual intercourse is not allowed for 2 months after surgery. Anticholinergic drugs may help to reduce bladder spasms that can put tension on the sutures.99,103 These drugs should be stopped 24 hours before obtaining the voiding cystogram. Postoperative care issues are summarized in Box 82-4. RESULTS It is difficult and sometimes impossible to compare published series of VVF repair. In all cases, patient selection is critical, and different series may be not comparable in terms of patients, hospital setting, strategy used, and the type of fistulas involved. Cure rates are not always intended as closure at the first operation. The relevant clinical characteristics of VVF cases are provided in Box 82-5. They should be taken into account when comparing cases and series. Tables can be found in the medical literature that compare reported series.104,105 This approach to comparing series is common, but it sometimes is impossible to summarize in a table all the information for a reported experience. For this reason, in the next sections, we provide brief descriptions of some

Review of Reported Series El-Imam and colleagues,106 2005: Thirty of 50 cases of VVF were selected for the abdominal approach (20 operated vaginally). The fistulas are described as large, recurrent, high fistulas occurring in older women. Causes included obstructed labor and hysterectomy. The success rate for repairs using the abdominal approach was 99%. Vyas and coworkers,60 2005: Twenty-two VVFs were treated. Causes included : obstetric issues in 15 and post-hysterectomy fistula formation in 7. All were operated using the transabdominal extraperitoneal approach (some through a combined abdominoperineal approach) and free bladder mucosa autograft. Five patients had undergone previous repairs; of these, two had recurrences. The success rate was 91%. Naru and associates,107 2004: Fifty-six VVFs were treated. In these cases, 72.4% had obstetric causes, and 26.4% occurred after gynecologic surgery. A transabdominal approach was chosen in 69% of the cases. In one case, a ureterosigmoid diversion was performed. The overall success rate was 83.8% (79.4% at first attempt). In this report, one ureterosigmoid diversion was done, and the patients lost at follow-up were considered as failures. Alagol and colleagues,65 2004: Eleven VVFs were treated. All cases were caused by hysterectomy for benign disease. Two patients had undergone previous repair attempts. The approach was transabdominal extraperitoneal with interposition of a dura mater free graft. The success rate was 100%. Navarro Sebastian and coworkers, 108 2003: Eighteen VVFs and two vesicouterine fistulas were treated. Causes included postoperative formation in 83% (13 hysterectomies, 1 cesarean section) and cancer in 17% of patients. Twelve patients were operated transabdominally, nine using an intraperitoneal approach and peritoneal graft (six cases) or omental interposition (three cases), and three operations used an extraperitoneal transvesical approach. The success rate was 88.5%. Rafique,109 2002: Thirty-six VVFs and two 2 vesicouterine fistulas were treated. The cause in all cases was obstetric. Twentynine patients were operated using a transabdominal, transvesical approach with bladder bisection. Omentum interposition was used in all cases. Two ureteral reimplantations and two hysterectomies were performed. The success rate was 89.6%. Kam and associates,110 2003: Twenty VVFs were treated. Fourteen VVFs occurred after gynecologic surgery. Four patients were operated using the transvaginal approach, seven using the extraperitoneal transabdominal approach, and eight using an intraperitoneal approach with bladder bisection. In one case, a urinary diversion (i.e., ileal conduit) was performed. Interposition flaps

Chapter 82 ABDOMINAL APPROACH FOR VESICOVAGINAL FISTULA

were used in six cases. The success rate was 85%. Three failures were reoperated using the extraperitoneal approach with complete success. Wook Bai and colleagues,111 2003: Twenty-six VVFs were treated. The fistulas were caused by hysterectomy or delivery. A transabdominal extraperitoneal approach was selected in 11 cases, and a combined abdominoperineal approach was used 7. The success rate for the first attempt was 90%, and for the second attempt, 80%. Benchekroun and coworkers,112 2003: In this large report of 1050 cases of urogenital fistulas, 48% were VVFs. Obstetric causes accounted for 93% of the VVFs. The patients were operated preferentially transvaginally, but the abdominal route was preferred when the fistulas were high or posterior, if other procedures or omental interposition were planned, or in case of severe vaginal sclerosis. The success rate was 95%. Sharifi and associates,62 2002: Fourteen VVFs were treated. Thirteen occurred after hysterectomy, and one was caused by obstructed labor. The access was transvesical extraperitoneal, and free bladder mucosa autograft was used. In 12 of 14, there was immediate success, but 2 required prolonged catheterization. Kochakarn and colleagues,113 2000: The surgeons treated 230 VVFs. Known causes included hysterectomy in 195, obstructed labor in 10, and irradiation in 9. Thirty-five patients had undergone previous attempts at repair. The transvesical extraperitoneal approach was performed in 168 cases (73%), including 29 reoperations and 139 first operations. The success rates were 78% (109 of 139) for the first-operation group and 62% (18 of 29) for the reoperation group. Of the 30 failures in the first-operation group, 15 were postirradiation fistulas. The O’Conor technique with bladder bisection was performed in 30 patients (success rate of 93.3%). Twenty patients were operated transvaginally (success rate of 100%). Urinary diversion (i.e., ileal conduit, colon conduit, or bilateral ureterostomies) was performed in 10 patients. Evans and associates,58 2001: Thirty-seven VVFs were treated. Twenty-five resulted from gynecologic surgery. A transperitoneal O’Connor procedure was used. In some cases, interposition flaps were used (with 100% success), and the others were operated without flaps (63% success rate). Mondet and colleagues,56 2001: Thirty VVFs in 28 patients were treated. Causes included gynecologic surgery in 78%, of which 86% occurred after hysterectomy, and cesarean section in 14%. In 30% of the patients, previous procedures had been performed. A transperitoneal-transvesical approach was used. The vaginal site was not closed in 66% of the cases. In 10 cases (83% of the trigonal fistulas), ureteral reimplantation was necessary. The overall success rate was 85%; success rates were 93% for supratrigonal and 75% for trigonal fistulas. Postoperative voiding disorders were documented in 38% of the patients. The failures were treated with urinary diversion in three cases (one transileal noncontinent cutaneous ureterostomy and two ureterosigmoidostomies). In one case, a second transperitoneal operation was undertaken with ureteral reimplantation (not performed in the first procedure), and it was successful. Flores-Carreras and coworkers,114 2001: The surgeons treated 153 VVFs. Fistulas resulted from hysterectomy in 90%, cesarean section in 3.9%, and Burch procedures in 1.9%. Thirty-two (20.9%) patients had been previously operated. In 113 patients (68%), a vaginal approach was chosen, with a success rate of 90% at the first attempt and 100% at the second or third attempt. Thirty-three percent pf the patients underwent a transvesical

suprapubic procedure (success rate of 91% at the first attempt). Of three failures, two were reoperated, and the third patient refused reoperation (final success rate of 97%). The transperitoneal approach was used in eight patients, with two failures (75% success rate); one had a successful second operation using the transvesical approach. Langkilde and associates,115 1999: Fifty-five patients VVFs were treated, 49 of whom had operations. Fistulas resulted from pelvic surgery (23 after hysterectomy) in 30 patients, cesarean section in 4, Burch procedures in 2, and radiation treatment in 19. Eight patients had undergone previous attempts. Among the 30 postoperative cases, 23 patients underwent an abdominal procedure (with transperitoneal-transvesical access), and 7 had a vaginal procedure. In four patients, reimplantation of the ureter was necessary. The success rate was 90% at the first attempt and 100% at the second (treatment of failures included two abdominal and one vaginal approach). Among those with postirradiation fistulas, 12 patients underwent urinary diversions (five ureterocutaneostomies and seven ileal conduits), 2 had an abdominal procedure, and 5 had a vaginal procedure (with a high failure rate in the postirradiation group: 6 of 7 cases). Nesrallah and colleagues,104 1999: Twenty-nine VVFs were treated. All fistulas were supratrigonal in this group. Fistulas resulted from hysterectomy in 28 patients (25 operations for benign disease, 2 after irradiation plus hysterectomy, and one cesarean section). Nine (34%) of 29 had undergone previous operations. In all cases, the transperitoneal approach was used, and an O’Conor procedure was performed, often with omental interposition. Four ureteral reimplantations were added. The success rate was 100%. Ostad and coworkers,61 1997: Six VVFs were treated. All fistulas resulted from hysterectomies. A transabdominal approach with free bladder mucosa graft was chosen. The success rate was 100%. Brandt and associates,591997: Eighty VVFs were treated. Fistulas resulted from gynecologic surgery for benign disease. Three patients had undergone previous attempts at repair. The approach was extraperitoneal with free bladder mucosa autograft. The success rate was 96%, and there were no late failures. Blaivas and colleagues,31 1995: Twenty-four VVFs were treated. Most fistulas resulted from previous surgery (15 from hysterectomy, 2 from anterior colporrhaphy, 2 from urethral diverticulectomy, and 1 from an anti-incontinence procedure). Procedures included 16 vaginal repairs with a Martius flap, 1 with a gracilis flap, and 7 suprapubic transvesical repairs with omentum. In two patients, the procedure was started vaginally and then switched to the abdominal route because of poor exposure. The overall success rate was 96%. Kristensen and Lose,116 1994: Eighteen VVFs were treated. All fistulas were caused by hysterectomies. A total of 27 previous attempts had been performed. An O’Conor procedure with a transperitoneal approach was performed in all cases. In four, ureteral reimplantation was necessary, of which one was bilateral. Only 1 of 18 had a recurrence, with successful repair on the second attempt with interposition of omentum. Arrowsmith,24 1994: Ninety-eight VVFs were treated. Fistulas resulted from obstetric causes in 93 patients, surgery in 4, and trauma in 1. Twenty-five cases were treated abdominally with the O’Conor procedure (omentum was used in nine cases), three used a combined abdominoperitoneal approach, and the rest used a vaginal approach. Nineteen percent underwent multiple procedures. The success rate was 96%. Larger fistulas did not fare

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worse than smaller fistulas (P = .87). However, treatment failure was significantly associated with bladder neck damage (P < .015) or severe vaginal scarring (P < .005). Blandy and coworkers,29 1991: Twenty-five VVFs were treated. Fistulas resulted from hysterectomy in 24 patients and transvaginal uterine prolapse surgery in 1 patient. A transperitoneal transvesical approach was chosen, with interposition of omentum. The success rate was 100%. Motiwala and associates,117 1991: Sixty-eight VVFs were treated. Fistulas resulted from hysterectomy in 48 patients, cesarean section in 15, and labor in 5. Fifty-one were supratrigonal fistulas. Four patients had undergone previous repairs. A transperitoneal-transvesical approach was chosen, with omentum grafts in 10 cases, and 58 used an extraperitoneal approach. Two ureteral reimplantations were necessary. The success rate was 95% for the extraperitoneal procedures and 90% for the transperitoneal cases. Gil-Vernet and colleagues,63 1989: Forty-two VVFs were treated. Fistulas resulted from gynecologic operations in 28 patients, obstetric causes in 11, and irradiation in 3. All the patients had undergone previous surgical attempts at repair. An extraperitoneal approach was performed, with the sliding bladder wall technique described previously. The success rate was 100%. Lee and coworkers,19 1988: The surgeons treated 182 VVFs. Fistulas resulted from hysterectomy in 156 patients, obstetric operations in 19, malignancy in 10, and trauma in 6. Ninety-one patients had undergone previous attempts at repair. The approach chosen was abdominal in 37 cases (20%) and transvaginal in 145. The success rate was 98%. Udeh and associates, 55 1985: Thirty-one VVFs were treated. All fistulas resulted from obstructed labor. Twenty-one patients had undergone previous attempts at repair. Two underwent elective diversion, and 29 were operated abdominally with an anterior transvesical approach. The success rate was 86%.

Personal Experience Patients Eighty-four patients with urinary fistulas have been operated using the abdominal approach at the Department of Urology of the University of Padova, Italy, between May 1979 and March 2003, under the chairmanship of Professor Francesco Pagano. Patients’ data have been collected and analyzed retrospectively. Sixty-five of 84 patients developed a VVF after hysterectomy for benign or malignant disease; 7 of them had received adjuvant radiation treatment for cancer. Two patients had undergone radiotherapy alone. Four patients developed a VVF after vaginal delivery, one after cesarean section, one after a bladder biopsy, one after bladder diverticulectomy, one after resection of a urethral lesion, one after a vaginoplasty procedure, one after sacral colpopexy, and one after radical cystectomy and orthotopic ileal neobladder. In five cases, the patients’ records were incomplete for cause. In one case, a clear reason for the fistula could not be identified. The most common onset symptoms were recorded for 82 of 84 patients: vaginal leakage with a preserved micturition pattern was present in 58 patients and complete urinary incontinence through the vagina in 24. The patients received a preoperative evaluation, including cystoscopy, endovenous pyelography, retrograde ureterography, voiding cystography, vaginoscopy, and pressure-flow studies (for

seven). Seventy-six (90%) of 84 patients presented with a VVF, 5 with a VVF and associated rectovaginal fistula, 2 with a ureteroVVF, and 1 with an orthotopic neobladder-vaginal fistula. In 56 patients, the fistula was supratrigonal; in 15, it was at the trigonal level; in 5, it was at the bladder neck; and in 3, it was on the lateral bladder wall. In five cases, fistula localization was not described. Before coming to our attention, 21 (25%) patients had received previous unsuccessful treatments in other institutions (with a median delay in this group of 25 weeks from onset of symptoms): 14 had undergone one previous attempt (2 patients had been treated endoscopically with collagen injection or diathermocoagulation of the fistulous tract), 11 had been operated using the vaginal approach, and 7 had been treated using the abdominal approach. One patient had been treated for cervical malignancy and had received an “external diversion” that was not better described. The other seven patients had undergone two previous attempts in another institution, two endoscopically with collagen or Teflon infiltration, two treated transvaginally, and three treated transabdominally. Surgical Technique In 64 of 84 patients, the fistula was corrected using an extraperitoneal transvesical approach, and in 14 of 84, a transperitoneal approach was used; omental interposition was performed in three of these cases. Additional intraperitoneal procedures were performed in 12 cases: augmentation ileocystoplasty in 6 cases and ureteral reimplantation in 6 cases (four bilateral and two monolateral procedures). Urinary diversion was performed as the first procedure in six patients (i.e., one continent ileal reservoir with a Mitrofanoff procedure and five external noncontinent diversions, three with colon, one with ileum, and one ureterocutaneostomy). The bladder catheter was maintained for an average period of 10 days after surgery. Outcomes Excluding the patients treated with urinary diversion (6 of 84), successful closure was obtained in 94% (73) of the 78 other patients in whom abdominal repair was performed. Five patients had fistula recurrences between 0 and 95 weeks; two were successfully reoperated transvaginally, with one using a Martius flap interposition. Two were treated endoscopically with collagen or silicone injection (one failed, requiring after 12 weeks a second successful abdominal repair with ureteral reimplantation and omentum interposition). One had a ureteral-sigmoid-cutaneous diversion. Long-Term Follow-Up Long-term follow-up was possible for 62 of 84 patients. The minimum follow-up in this group was 2 years (average, 12.5 ± 8.4 years). All patients were satisfied with their situation; 61 of 62 patients were dry, and 1 complained about mild urinary incontinence but declined further treatment. CONCLUSIONS The ideal treatment for a VVF is the one that provides rapidly the best result with the least invasive approach. The abdominal approach for treatment of VVF, which is an invasive approach, has several indications, and when properly selected, it can provide the definitive solution to VVFs not treatable with less invasive procedures. New techniques, such as laparoscopy or robotic

Chapter 82 ABDOMINAL APPROACH FOR VESICOVAGINAL FISTULA

surgery, can reduce the invasiveness of the open abdominal approach and make the procedure more acceptable to the patient. Some of the strategies for repair highlighted in this chapter can increase the chances of success. These strategies, which are independent of the approach used, are summarized in Box 82-6. Using these strategies, we think that major improvements can be made in the treatment of this undesirable clinical condition can be made in the near future.

Box 82-6 Strategies for Success selection • Case Surgical training opportunities • Choice ofexperience, less invasive • Steps taken to minimizeprocedures of failure • Use of interposition flapschances when possible • Prioritization of postoperative uninterrupted bladder • drainage • Correct analysis of comparable series

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41. Tomlinson AJ, Thornton JG: A randomized controlled trial of antibiotic prophylaxis for vesicovaginal fistula repair. Br J Obstet Gynecol 105:397-399, 1998. 42. Collins CG, Pent D, Jones FB: Results of early repair of vesicovaginal fistula with preliminary cortisone treatment. Am J Obstet Gynecol 80:1005-1012, 1960. 43. Little NA, Juma S, Raz S: Vesicovaginal fistulae. Semin Urol 7:7885, 1989. 44. Cortesse A, Colau A: Vesicovaginal fistula. Ann Urol (Paris) 38:5266, 2004. 45. Goh JT, Howat P, De Costa C: Oestrogen therapy in the management of vesicovaginal fistula. Aust N Z J Obstet Gynaecol 41:333334, 2001. 46. Caputo RM, Copeland LJ: Gynecologic effects of tamoxifen: Case reports and review of the literature. Int Urogynecol J Pelvic Floor Dysfunct 7:179-184, 1996. 47. Jozwik M, Jozwik M, Sulkowska M, et al: The presence of sex hormone receptors in the vesicouterine fistula. Gynecol Endocrinol 18:37-40, 2004. 48. Jozwik M, Jozwik M: Spontaneous closure of vesicouterine fistula. Account for effective hormonal treatment. Urol Int 62:183-187, 1999. 49. Lovatsis D, Drutz HP: Persistent vesicovaginal fistula associated with endometriosis. Int Urogynecol J Pelvic Floor Dysfunct 14:358359, 2003. 50. Turner-Warvick R, Chapple C (eds): Functional reconstruction of the urinary tract and Gyneco-Urology. Oxford, Blackwell Science, 2002. 51. Chapple C, Turner-Warwick R: Vesico-vaginal fistula. BJU Int 95:193-214, 2005. 52. Turner Warwick R, Worth P, Milroy E, Duckett J: The suprapubic V-incision. Br J Urol 46:39-45, 1974. 53. Mobilio G, Cosciani Cunico S: An instrument for the surgical repair of a vesicovaginal fistula. J Urol 117:231, 1977. 54. Landes RR: Simple transvesical repair of vesicovaginal fistula. J Urol 122:604-606, 1979. 55. Udeh F: Simple management of difficult vesicovaginal fistulas by anterior transvesical approach. J Urol 133:591-593, 1985. 56. Mondet F, Chartier-Kastler EJ, Conort P, et al: Anatomic and functional results of transperitoneal—Transvesical vesicovaginal fistula repair. Urology 58:882-886, 2001. 57. Fitzpatrick C, Elkins TE: Plastic surgical techniques in the repair of vesicovaginal fistulas: A review. Int Urogynecol J Pelvic Floor Dysfunct 4:287-295, 1993. 58. Evans DH, Madjar S, Politano VA, et al: Interposition flaps in transabdominal vesicovaginal fistula repairs: Are they really necessary? Urology 57:670-674, 2001. 59. Brandt FT, Lorenzato FR, Albuquerque CD: Treatment of vesicovaginal fistula by bladder mucosa autograft technique. J Am Coll Surg 186:645-648, 1998. 60. Vyas N, Nandi PR, Mahmood M, et al: Bladder mucosal autografts for repair of vesicovaginal fistula. BJOG 112:112-114, 2005. 61. Ostad M, Uzzo RG, Coleman J, Young GP: Use of a free bladder mucosal graft for simple repair of vesicovaginal fistulae. Urology 52:123-126, 1998. 62. Sharifi-Aghdas F, Ghaderian N, Payvand A: Free bladder mucosal autograft in the treatment of complicated vesicovaginal fistula. BJU Int 89:54-56, 2002. 63. Gil-Vernet JM, Gil-Vernet A, Campos JA: New surgical approach for treatment of complex vesicovaginal fistula. J Urol 141:513-516, 1989. 64. Couvelaire R: Les fistules vesico-vaginales complexes. J Urol 88:353, 1982. 65. Alagol B, Gozen AS, Kaya E, Inci O: The use of human dura mater as an interposition graft in the treatment of vesicovaginal fistula. Int Urol Nephrol 36:35-40, 2004. 66. Kelami A: Lyophilised human dura as a bladder wall substitute: Experimental and clinical results. J Urol 105:518-521, 1971.

67. El-Lateef Moharram AA, El-Raouf MA: Retropubic repair of genitourinary fistula using a free suporting graft. BJU Int 93:581-583, 2004. 68. Salup RR, Julian TB, Liang MD, et al: Closure of large postirradiation vesicovaginal fistula with rectum abdominis myofascial flap. Urology 44:130-131, 1994. 69. Viennas LK, Alonso AM, Salama V: Repair of radiation-induced vesicovaginal fistula with a rectus abdominis myocutaneous flap. Plast Reconstr Surg 96:1435-1437, 1995. 70. Horch RE, Gitsch G, Schultze-Seemann W: Bilateral pedicled myocutaneous vertical rectus abdominus muscle flaps to close vesicovaginal and pouch-vaginal fistulas with simultaneous vaginal and perineal reconstruction in irradiated pelvic wounds. Urology 60:502-507, 2002. 71. Perata E, Severoni S, Schietroma M, et al: Post partum vesicovaginal fistula: Abdominal muscle strip treatment. Minerva Ginecol 53:165-170, 2001. 72. Menchaca A, Akhyat M, Gleicher N, et al: The rectus abdominis muscle flap in a combined abdominovaginal repair of difficult vesicovaginal fistuale. J Reprod Med 35:565-568, 1990. 73. Fleischmann J, Picha G: Abdominal approach for gracilis muscle interposition and repair of recurrent vesicovaginal fistulas. J Urol 140:552-554, 1988. 74. Eisen M, Jurkovic K, Altwein JE, et al: Management of vesicovaginal fistulas with peritoneal flap interposition. J Urol 112:195-198, 1974. 75. Singh RB, Pavitran NM, Nanda S: Plastic reconstruction of a mega vesicovaginal fistula using broad ligament flaps—A new technique. Int Urogynecol J Pelvic Floor Dysfunct 14:62-63, 2003. 76. Lytton B: Vesicovaginal fistula: Postsurgical. In Resnick MI, Kursh E(eds): Current Therapy in Genitourinary Surgery. Philadelphia, BC Decker, 1992, pp 261-265. 77. Mraz J, Sutory M: An alternative in surgical treatment of postirradiation vesicovaginal and rectovaginal fistulas: The seromuscular intestinal graft (patch). J Urol 151:357-359, 1994. 78. Turner-Warwick R: The use of the omental pedicle graft in urinary tract reconstruction. J Urol 116:341-347, 1976. 79. Bissada SA, Bissada NK: Repair of active radiation-induced vesicovaginal fistula using combined gastric and omental segments based on the gastroepiploic vessels. J Urol 147:1368- 1370, 1992. 80. Tabakov ID, Slavchev BN: Large post-hysterectomy and postirradiation vesicovaginal fistulas: Repair by ileocystoplasty. J Urol 171:272-274, 2004. 81. Hsu TH, Rackley RR, Abdelmalak JB, et al: Novel technique for combined repair of postirradiation vesicovaginal fistula and augmentation ileocystoplasty. Urology 59:597-599, 2002. 82. Gan E, Li MK: Repair of complex uretrovaginal and vesicovaginal fistulas with ileal cystoplasty and ureteric reimplantation into an antireflux ileal nipple valve—A case report. Ann Acad Med Singapore 27:707-709, 1998. 83. Naude JH: Reconstructive urology in the tropical and developing world: A personal prespective. BJU Int 89:31-36, 2002. 84. Mitrofanoff P: Trans-appendicular continent cystostomy in the management of the neurogenic bladder. Chir Pediatr 21:297-305, 1980. 85. Hodges AM: Vesico-vaginal fistula associated with uterine prolapse. Br J Obstet Gynaecol 106:1127-1128, 1999. 86. Zincke H, Segura JW: Ureterosigmoidostomy: Critical review of 173 cases. J Urol 113:324-7, 1975. 87. Fisch M, Klinkowski U, Wammack R, Hohenfellner R: The sigmarectum pouch (Mainz II). Critical analysis after 3 years of clinical experience [abstract]. J Urol 153:61A, 1995. 88. Leissner J, Black P, Fisch M, et al: Colon pouch (Meinz pouch III) for continent urinary diversion after pelvic irradiation. Urology 56:798-802, 2000. 89. Nezhat CH, Nezhat F, Nezhat C, Rottenberg H: Laparoscopic repair of a vesicovaginal fistula: A case report. Obstet Gynecol 83:899-901, 1994.

Chapter 82 ABDOMINAL APPROACH FOR VESICOVAGINAL FISTULA

90. Phipps J: Laparoscopic repair of posthysterectomy vesico-vaginal fistula: Two case reports. Gynecol Endosc 5:123-124, 1996. 91. Von Theobald P, Hamel P, Febbraro W: Laparoscopic repair of a vesicovaginal fistula using an omental J flap. BJOG 105:1216-1218, 1998. 92. Miklos JR, Sobolewski C, Lucente V: Laparoscopic management or recurrent vesicovaginal fistula. Int Urogynecol J Pelvic Floor Dysfunct 10:116-117, 1999. 93. Nabi G, Hemal AK: Laparoscopic repair of vesicovaginal fistula and right nephrectomy for nonfunctioning kidney in a single session. J Endourol 15:801-803, 2001. 94. Ou CS, Huang UC, Tsuang M, Rowbotham R: Laparoscopic repair of vesicovaginal fistula. J Laparoendosc Adv Surg Tech 14:17-21, 2004. 95. Chibber PJ, Shah NH, Jain P: Laparoscopic O’Conor’s repair for vesico-vaginal and vesico-uterine fistulae. BJU Int 96:183-186, 2005. 96. Sotelo R, Mariano MB, Garcia-Segui A, et al: Laparoscopic repair of a vesicovaginal fistula. J Urol 173:1615-1618, 2005. 97. Melamud O, Eichel L, Turbow B, Shanberg A: Laparoscopic vesicovaginal fistula repair with robotic reconstruction. Urology 65:163-166, 2005. 98. Pick DL, Lee DI, Skarecky DW: Anatomic guide for port placement of the Da Vinci robotic system radical prostatectomy. J Endourol 18:572-575, 2004. 99. Smith GL, Williams G: Vesicovaginal fistula. BJU Int 83:564-569, 1999. 100. Miller EA, Webster GD: Current management of vesicovaginal fistulae. Curr Opin Urol 11:417-421, 2001. 101. Margolis T, Mercer LJ: Vesicovaginal fistula. Obstet Gynecol Surv 49:840-847, 1994. 102. Woo HH, Rosario DJ, Chapple CR: The treatment of vesicovaginal fistulae. Eur Urol 29:1-9, 1996. 103. Carr LK, Webster GD: Abdominal repair of vesicovaginal fistulas. Urology 48:10-11, 1996.

104. Nesrallah LJ, Srougi M, Gittes RF: The O’Connor technique: The gold standard for supratrigonal vesicovaginal fistula repair. J Urol 161:566-568, 1999. 105. Angioli R, Penalver M, Muzii L, et al: Guidelines of how to manage vesicovaginal fistula. Crit Rev Oncol Hematol 48:295-304, 2003. 106. El-Imam M, El-Hassan el-HM, Adam I: Vesicovaginal fistula in Sudanese women. Saudi Med J 26:341-342, 2005. 107. Naru T, Rizvi JH, Talati J: Surgical repair of genital fistulae. J Obstet Gynaecol Res 30:293-296, 2004. 108. Navarro Sebastián FJ, García González JI, Castro Pita M, et al: Treatment approach for vesicovaginal fistula. Retrospective analysis of our data. Actas Urol Esp 27:530-537, 2003. 109. Rafique M: Genitourinary fistulas of obstetric origin. Int Urol Nephrol 34:489-493, 2002-2003. 110. Kam MH, Tan YH, Wong MY: A 12-year experience in the surgical management of vesicovaginal fistulae. Singapore Med J 44:181-184, 2003. 111. Wook Bai SW, Kim SH, Kwon HS, et al: Surgical outcome of female genital fistula in Korea. Yonsei Med J 43:315-319, 2002. 112. Benchekroun A, al Alj HA, el Sayegh H, et al: Vesico vaginal fistula: Report of 1050 cases. Ann Urol 37:194-198, 2003. 113. Kochakarn W, Ratana-Olarn K, Viseshsindh V, et al: Vesico vaginal fistula: Experience of 230 cases. J Med Assoc Thai 83:1129-1132, 2000. 114. Flores-Carreras O, Cabrera JR, Galeano PA, Torres FE: Fistulas of the urinary tract in gynecologic and obstetric surgery. Int Urogynecol J 12:203-214, 2001. 115. Langkilde NC, Pless TK, Lundbeck F, Nerstrom B: Surgical repair of vesicovaginal fistulae—A ten-year retrospective study. Scand J Urol Nephrol 33:100-103, 1999. 116. Kristensen JK, Lose G: Vesicovaginal fistulas: The transperitoneal repair revisited. Scand J Urol Nephrol Suppl 157:101-105, 1994. 117. Motiwala HG, Amlani JC, Desai KD, et al: Transvesical vesicovaginal fistula repair: A revival. Eur Urol 19:24-28, 1991.

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RECTOVAGINAL FISTULA Matthew P. Rutman, Larissa V. Rodríguez, Donna Y. Deng, and Shlomo Raz A rectovaginal fistula consists of an abnormal, epithelium-lined communication between the rectum and the vagina. It represents an extremely distressing problem for the patient and a surgical challenge for the physician. The reconstructive pelvic surgeon must have a full understanding of rectovaginal fistula to provide the patient with the most appropriate treatment option. PATHOPHYSIOLOGY It is important to consider the underlying cause of the rectovaginal fistula in preparing for a successful repair. The most common cause of rectovaginal fistula remains obstetric trauma,1,2 usually caused by an unrecognized injury with traumatic vaginal delivery, wound infection, or an inadequate repair of a third- or fourth-degree perineal laceration. Up to 5% of vaginal deliveries result in these lacerations. Most heal when repaired at the time of labor. Prolonged labor and compression can result in ischemic necrosis of the vaginal septum, predisposing the delivering woman to development of a rectovaginal fistula. This is a greater concern in developing nations and likely not a large factor in industrialized countries such as the United States and Canada. Vaginal, rectal, and pelvic operations, such as rectocele repair, low anterior resection, and hemorrhoidectomy, may lead to rectovaginal fistula as a result of intraoperative injury or postoperative infection. Rectovaginal fistula can result from nonobstetric blunt and penetrating trauma. Inflammatory processes of the bowel, such as diverticulitis, Crohn’s disease, and ulcerative colitis, can produce a rectovaginal fistula. Rectal, cervical, uterine, and vaginal malignancy and radiation therapy are known causes of rectovaginal fistulas. The incidence of rectovaginal fistula after irradiation is 0.3% to 6%.3,4 The fistula may occur up to 2 years after irradiation because of progressive radiation damage. Any fistula associated with radiation therapy and malignancy must be biopsied to rule out recurrent malignancy before formal repair. Inflammatory or infectious processes near the rectovaginal septum or cul-de-sac may result in formation of a rectovaginal fistula. Prolonged use of a vaginal pessary can result in a rectovaginal fistula. The location of rectovaginal fistulas may mandate a particular surgical approach. The fistula may be in the high, middle, or low rectal region. Most fistulas associated with obstetric trauma are classified as low types. Diverticular disease and other intraabdominal pathologic conditions are associated with higher rectovaginal fistula. The high fistula usually is associated with intra-abdominal conditions such as diverticulitis or abscess formation, and it may require a laparotomy. The low fistula of rectal origin can be repaired transvaginally, avoiding the morbidity of an abdominal approach. 816

EVALUATION The diagnosis is obvious in patients with a large rectovaginal fistula because bowel content is evacuated through the vagina. Patients with a smaller fistula may be completely asymptomatic. A thorough history and physical examination are mandatory for every patient suspected of having a fistula. The interview should include questions about prior malignancy, radiation therapy, complicated obstetric history, inflammatory bowel disease, and prior anorectal surgery. Physical examination should reveal the size, location, and number of fistulous tracts. The perineal body must be examined to determine the function and tone of the anal sphincter. Bimanual examination allows the physician to palpate the thickness of the perineal body and identify the fistula. Multiple fistulas and perianal fissures may suggest Crohn’s disease. If the fistula is not easily identified, vaginal speculum examination should be performed. If the diagnosis is still in doubt, a dye test can be performed. Methylene blue dye is instilled into the rectum, and a tampon or sponge inserted into the vagina. Staining of the pad confirms the diagnosis and can be helpful in identifying a small fistula. Proctoscopy, colonoscopy, barium examination, and computed tomography should be performed if indicated. Any area of suspicious inflammation, ulceration, or mass should be biopsied to rule out a malignant process or recurrence. Examination under anesthesia can be performed to make the diagnosis if all of the previous measures fail and the physician still suspects a fistula. Before formal repair, it is necessary to evaluate the patient for fecal incontinence. A review of 52 patients at the University of Minnesota revealed a 48% incidence of coexistent fecal incontinence.5 Among women who develop rectovaginal fistula after obstetric trauma, the incidence is probably much higher. It is essential to assess the function of the anal sphincter before surgical repair. Endoanal ultrasonography, anal manometry, and pudendal nerve terminal motor latency testing remain valuable tools to aid with the clinical evaluation. Ultrasound can easily identify defects in the internal anal sphincter. Defects in the external anal sphincter are more difficult to identify because of the hyperechoic pattern. Manometry can help quantify the resting and squeezing pressures of the sphincter muscle. Pudendal nerve testing helps identify underlying neuropathy. PREOPERATIVE CONSIDERATIONS Management of rectovaginal fistulas depends on several factors: cause, size, number, and location of the fistulas and the surgeon’s preference. Anal sphincter integrity and prior operations

Chapter 83 RECTOVAGINAL FISTULA

influence the choice of treatment. Regardless of the approach chosen, several principles require consideration before repair. Antibiotic coverage and topical hormonal replacement help optimize the health of local tissues and decrease any associated infection and inflammation. The health of the surrounding tissues influences the waiting period before surgical repair. Any inflammation or infection should be resolved. Waiting 3 to 6 months in these cases allows resolution and increases the chance of successful repair. In patients with prior failed repair, a longer waiting period may be necessary. In patients with postirradiation rectovaginal fistulas, a much longer waiting period may be required. Patients with complex fistulas (e.g., large size, radiation induced, neoplasm induced, multiple failed repairs) may require a diverting colostomy before formal repair. After diversion, a waiting period of 2 to 3 months before vaginal repair allows local tissue healing. Complete bowel preparation is given before surgery. Excellent exposure allows good mobilization of tissue flaps. The fistulous tract should be exposed in its entirety and left intact. We tend to not excise the tract. This prevents iatrogenic enlargement of the fistula and allows us to use it in our repair. The rectal opening is closed in multiple, tension-free layers. Interposition of healthy tissue between the rectum and vagina should be used routinely. Common sources include labia fatty tissue (i.e., Martius flap), labial skin and underlying fatty tissue, gluteal skin, gracilis muscular flaps, and omentum. Case reports have described pudendal thigh fasciocutaneous island flaps and gluteal-fold flap repairs to aid in rectovaginal fistula repair.6,7 Several common techniques of tissue interposition can be found in Chapters 81 and 82. After closure of the fistula, anal sphincter defects should be addressed to restore normal sphincter function.

Figure 83-1 The fistulous tract is catheterized.

SURGICAL REPAIRS Surgical options can be divided into transvaginal repair, transanal repair, transperineal repair, and abdominal repair. Reconstructive urologists and gynecologists typically use a transvaginal approach, whereas colorectal surgeons prefer a transanal approach. An abdominal approach is often used in treating radiation-induced rectovaginal fistulas. We use a multilayered transvaginal approach, avoiding the morbidity of a laparotomy, in most rectovaginal fistula repairs. Complete bowel preparation is done, and antibiotics are given preoperatively. The patient is given general or spinal anesthesia and placed in the high lithotomy position. A Foley catheter is placed in the bladder. Use of a surgeon’s headlight and a ring retractor help to optimize exposure. A Foley catheter is inserted into the fistulous tract (Fig. 83-1). A circumferential incision is made around the Foley catheter, and the tract is dissected to the rectal wall (Fig. 83-2). A flap of distal vaginal is also prepared. The fistulous tract is then excised, leaving the rectal wall with an indwelling catheter (Fig. 83-3). The rectal wall is closed in two layers using 2-0 absorbable sutures (Fig. 83-4). The levator musculature is included in the closure. A Martius flap is prepared. A vertical incision is made lateral to the labia, and a fibrofatty flap is developed and isolated, preserving the inferior vascular pedicle (Fig. 83-5). The flap is then tunneled through the vagina and rotated to cover the fistula. Interrupted sutures are used to fix the flap to the rectal wall. The wound is then closed in layers, advancing the vaginal wall distally

Figure 83-2 The circumferential incision is dissected to the rectal wall.

and ensuring new tissue covers the area of the fistula (Fig. 83-6). Vaginal packing is left for a few hours, and the patient resumes a regular diet. Oral antibiotics are continued for 1 week. For patients who had a prior diverting colostomy, we routinely wait 3 to 6 months before takedown. Physical examination and a radiographic contrast study confirm complete healing of the fistula. Intraoperative complications are rare. If tissue quality is poor intraoperatively (because of infection or irradiation), the surgery should be aborted and a diverting colostomy performed to allow tissue healing. Postoperative complications include recurrent

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Figure 83-5 The Martius flap is based on an inferior vascular pedicle. Figure 83-3 Excision of a fistulous tract.

Figure 83-6 The vaginal wall flap is advanced to cover the fistula. Figure 83-4 Closure of the rectal wall.

fistula. Recurrent fistula requires a diverting colostomy, if not previously performed, before re-exploration. A second transvaginal approach includes inversion of the fistula. The patient is placed in the lithotomy position as described earlier. The vaginal mucosa is incised in a circumferential fashion around the fistula and mobilized in all directions. After excising the fistulous tract, a purse-string suture is placed around the opening of the rectovaginal septum, and the suture is secured, inverting the fistula into the rectum. The muscle and vaginal mucosa are then closed, resulting in three layers of repair.8 Case reports have reported successful use of cadaveric dermal allograft9 interposition and porcine dermal graft interposition10 Dexon mesh has been used to separate the suture lines between

the vaginal and rectal walls.11 These may be viable alternatives to traditional autologous flaps. Although not commonly used by urologists and gynecologists, colorectal surgeons often advocate a transanal approach. The most common of the approaches uses an advancement flap.12 The patient is given standard antibiotics and mechanical bowel preparation preoperatively. After general anesthesia is provided, the patient is placed in the prone jackknife position. The vagina and perineum are cleansed in standard sterile fashion. Proctoscopy identifies the fistula and allows irrigation of the lower rectum to clear any residual fecal contents. Rectal retractors help optimize exposure. Injectable Xylocaine with epinephrine is infiltrated into the dissection planes. A trapezoidal flap consisting of mucosa, submucosa, and internal sphincter (i.e., circular muscle) is raised

Chapter 83 RECTOVAGINAL FISTULA

around the fistula and mobilized 4 to 5 cm cephalad. The flap should easily advance to cover the fistula tract, and any tension should be avoided. Excess flap, including the fistula itself, is excised, and the remaining flap is advanced and sutured with 3-0 absorbable sutures. The vaginal aspect of the fistula is left open for drainage. Layered closure can be performed transanally.13 A transverse elliptical incision is made around the fistula through the rectovaginal septum. It is dissected circumferentially for about 3 cm. The fistula tract is excised, and a two-layer closure is performed. The rectal mucosa is then advanced distal to the deeper portion of the repair and reapproximated. Transperineal approaches can be organized into three categories: fistulotomy, perineoproctotomy, and sphincteroplasty. Fistulotomy converts a fistula into a fourth-degree perineal laceration, resulting in fecal incontinence due to sphincter damage. This procedure is not recommended as a solo primary approach. Perineoproctotomy with layered closure is a commonly used transperineal technique.1 It is often used by obstetricians for repair of lower vaginal rectovaginal fistulas. The patient is prepared with standard antibiotics and bowel preparation and placed in the lithotomy position. The fistula is identified, and the bridge of skin, sphincter, and perineal body between the posterior fourchette and fistula are divided. The fistula becomes a fourth-degree perineal laceration. The fistulous tract is excised, and the defect is then closed in standard layered fashion (i.e., vaginal wall, sphincter muscle, and rectal mucosa). The perineal body is reconstructed. Postoperative complications include vaginal stenosis and dyspareunia. Fecal incontinence may result with scarring of the transected anal sphincter. Sphincteroplasty performed through a transperineal approach allows correction of any underlying sphincter defect.14 The patient is prepared as previously described and placed under general anesthesia. A Foley catheter is placed, and the patient is placed prone in the jackknife position. A curvilinear incision is made through the perineum. A flap of anoderm distally and mucosa and submucosa proximally is raised. The ends of the sphincter (external and internal) muscles are identified laterally and left intact. Levatoroplasty is often needed at this stage of the surgery if the injury involves the deep external sphincter muscle. The ends of the mobilized sphincter muscles are sutured in an overlapping manner using horizontal mattress sutures. This reconstructs the sphincter mechanism. Tissue is then interposed between the rectum and vagina. The endorectal flap is sutured to the reconstructed sphincter muscle, and the perineal incision is closed. The vaginal mucosa is left open to drain. Transabdominal procedures to repair rectovaginal fistula are necessary for complex fistulas resulting from irradiation, inflammatory bowel disease, and failed previous repairs. Surrounding tissues are often poorly vascularized, and local repair is a poor option. Abdominal approaches leave the anal sphincter intact and allow easy interposition of well-vascularized tissues. In patients with a high fistula location and normal surrounding tissues (i.e., no irradiation or inflammatory bowel disease), simple abdominal repair can be performed. A laparotomy is performed, and the rectovaginal septum is mobilized. The diseased segment is divided, and layered closure of the rectal and vaginal defects is performed. Omentum is interposed between the rectum and the vagina. Most commonly, an abdominal approach is chosen because of poor local tissue quality. These approaches are typically per-

formed after a primary diverting colostomy has been done or concomitantly with fecal diversion. The abdominal approach allows repair of the fistula with concomitant bowel resection. The patient undergoes complete bowel preparation, is given antibiotics, and is placed under general anesthesia. A laparotomy is performed. The splenic flexure, left colon, and sigmoid colon are fully mobilized down to the levator hiatus. The diseased bowel segment is resected. At this point, a coloanal anastomosis is performed by a pull-through15,16 or sleeve anastamosis.17 A non-resectional onlay patch technique was introduced by Bricker and Johnson in 1979 for radiation-induced rectovaginal fistula.18 The rectosigmoid colon is divided and an endsigmoid colostomy performed. The distal end is then folded and sutured to the exposed and débrided edges of the fistulous opening in the rectum. At a later stage, after healing is confirmed, the colostomy is taken down and anastomosed to the side of the folded loop of the rectosigmoid. The major downfall of this procedure is that it leaves behind irradiated tissue, and it is rarely used today. For patients with a fistula resulting from a neoplasm, abdominoperineal resection and vaginectomy are typically required. Patients with severe inflammatory bowel disease may ultimately require proctocolectomy. Patients with terminal malignancies or major medical comorbidities (i.e., unfit for major surgery) and symptomatic rectovaginal fistulas may be best served by a diverting colostomy. ALTERNATIVE TREATMENTS Alternative procedures for rectovaginal fistula have been described in the literature. Fibrin glue has been injected into the fistulous tract, with reported success rates of 74% and 80%.19,20 In patients with Crohn’s disease, several medical regimens have been studied. Sands and colleagues21,22 reported fistula closure with infliximab infusion in 13 of 29 patients after 14 weeks of follow-up. Similar improvements have been reported with intravenous and oral cyclosporine.23,24 Metronidazole and 6-mercaptopurine have been used to effectively treat rectovaginal fistula resulting from Crohn’s disease.25 The Latzko technique used in vesicovaginal fistula repair can also be used to repair a high rectovaginal fistula located at the apex of the vagina. The anterior and posterior vaginal walls are denuded, and an incision is made around the fistula margins. Three layers of closure invert the fistula, close the rectal muscle and fascia, and close the vaginal mucosa. RESULTS The many different approaches to repair of rectovaginal fistula have various success rates and outcome measures. Success should be evaluated according to objective measures and the results of self-reported questionnaires about patient satisfaction. Successful repair of the fistula sounds great, but secondary fecal incontinence or dyspareunia may alter the outcome. The existing literature primarily reports success or failure based on healing of the rectovaginal fistula. Future reports should report on fistula healing, fecal continence, sexual function, and quality of life. Transvaginal repairs using a layered closure have success rates of 84% to 100%.2,26-28 Advancement flaps placed by means of a

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transanal approach have success rates in the range of 78% to 100%.29-31 The rates were higher for patients undergoing initial repair.32 Success rates of 88% to 100% have been reported for perineoproctotomy and layered closure.1,2,8,33-35 The combination of sphincteroplasty and levatoroplasty has a success rate of 93%.32 Transabdominal repairs also have high cure rates, in the range of 80% to 100%.4,17,36

CONCLUSIONS The management of rectovaginal fistulas remains a challenge for the reconstructive pelvic surgeon. The decision-making algorithm must include the size, location, and cause of the fistula. The health of the patient and judgment of the treating physician greatly influence successful repair and a good outcome.

References 1. Mazier WP, Senagore AJ, Schiesel EC: Operative repair of anovaginal and rectovaginal fistulas. Dis Colon Rectum 38:4, 1995. 2. Hibbard LT: Surgical management of rectovaginal fistulas and complete perineal tears. Am J Obstet Gynecol 130:139, 1978. 3. Allen-Mersh, TG, Wilson, EJ, Hope-Stone, HF, et al: The management of late radiation-induced rectal injury after treatment of carcinoma of the uterus. Surg Gynecol Obstet 164:521, 1987. 4. Cooke SA, de Moor NG: The surgical treatment of the radiationdamaged rectum. Br J Surg 68:488, 1981. 5. Tsang CB, Madoff RD, Wong WD, et al: Anal sphincter integrity and function influences outcome in rectovaginal fistula repair. Dis Colon Rectum 41:1141, 1998. 6. Monstrey S, Blondeel P, Van Landuyt K, et al: The versatility of the pudendal thigh fasciocutaneous flap used as an island flap. Plast Reconstr Surg 107:719, 2001. 7. Kosugi C, Saito N, Kimata Y, et al: Rectovaginal fistulas after rectal cancer surgery: Incidence and operative repair by gluteal-fold flap repair. Surgery 137:329, 2005. 8. Given FT Jr: Rectovaginal fistula: A review of 20 years’ experience in a community hospital. Am J Obstet Gynecol 108:41, 1970. 9. Miklos JR, Kohli N: Rectovaginal fistula repair utilizing a cadaveric dermal allograft. Int Urogynecol J Pelvic Floor Dysfunct 10:405, 1999. 10. Moore RD, Miklos JR, Kohli N: Rectovaginal fistula repair using a porcine dermal graft. Obstet Gynecol 104:1165, 2004. 11. Walfisch A, Zilberstein T, Walfisch S: Rectovaginal septal repair: Case presentations and introduction of a modified reconstruction technique. Tech Coloproctol 8:192, 2004. 12. Rothenberger DA, Christenson CE, Balcos EG, et al: Endorectal advancement flap for treatment of simple rectovaginal fistula. Dis Colon Rectum 25:297, 1982. 13. Greenwald JC, Hoexter B: Repair of rectovaginal fistulas. Surg Gynecol Obstet 146:443, 1978. 14. Russell TR, Gallagher DM: Low rectovaginal fistulas. Approach and treatment. Am J Surg 134:13, 1977. 15. Cutait DE, Figliolini FJ: A new method of colorectal anastomosis in abdominoperineal resection. Dis Colon Rectum 4:335, 1961. 16. Turnbull RB Jr, Cuthbertson A: Abdominorectal pull-through resection for cancer and for Hirschsprung’s disease: Delayed posterior colorectal anastomosis. Cleve Clin Q 28:109, 1961. 17. Parks AG, Allen CL, Frank JD, et al: A method of treating postirradiation rectovaginal fistulas. Br J Surg 65:417, 1978. 18. Bricker EM, Johnston WD: Repair of postirradiation rectovaginal fistula and stricture. Surg Gynecol Obstet 148:499, 1979. 19. Hjortrup A, Moesgaard F, Kjaergard J: Fibrin adhesive in the treatment of perineal fistulas. Dis Colon Rectum 34:752, 1991.

20. Abel ME, Chiu YS, Russell TR, et al: Autologous fibrin glue in the treatment of rectovaginal and complex fistulas. Dis Colon Rectum 36:447, 1993. 21. Sands BE, Blank MA, Patel K, et al: Long-term treatment of rectovaginal fistulas in Crohn’s disease: Response to infliximab in the ACCENT II Study. Clin Gastroenterol Hepatol 2:912, 2004. 22. Sands BE, Anderson FH, Bernstein CN, et al: Infliximab maintenance therapy for fistulizing Crohn’s disease. N Engl J Med 350:876, 2004. 23. Lichtiger S, Present DH, Kornbluth A, et al: Cyclosporine in severe ulcerative colitis refractory to steroid therapy. N Engl J Med 330:1841, 1994. 24. Present DH, Lichtiger S: Efficacy of cyclosporine in treatment of fistula of Crohn’s disease. Dig Dis Sci 39:374, 1994. 25. Stein BL, Gordon PH: Perianal inflammatory conditions in inflammatory bowel disease. Curr Opin Gen Surg nv:141, 1993. 26. Lawson J: Rectovaginal fistulae following difficult labour. Proc R Soc Med 65:283, 1972. 27. Lescher TC, Pratt JH: Vaginal repair of the simple rectovaginal fistula. Surg Gynecol Obstet 124:1317, 1967. 28. Tancer ML, Lasser D, Rosenblum N: Rectovaginal fistula or perineal and anal sphincter disruption, or both, after vaginal delivery. Surg Gynecol Obstet 171:43, 1990. 29. Belt RL Jr: Repair of anorectal vaginal fistula utilizing segmental advancement of the internal sphincter muscle. Dis Colon Rectum 12:99, 1969. 30. Hoexter B, Labow SB, Moseson MD: Transanal rectovaginal fistula repair. Dis Colon Rectum 28:572, 1985. 31. Hilsabeck JR: Transanal advancement of the anterior rectal wall for vaginal fistulas involving the lower rectum. Dis Colon Rectum 23:236, 1980. 32. Lowry AC, Thorson AG, Rothenberger DA, et al: Repair of simple rectovaginal fistulas. Influence of previous repairs. Dis Colon Rectum 31:676, 1988. 33. Pepe F, Panella M, Arikian S, et al: Low rectovaginal fistulas. Aust N Z J Obstet Gynaecol 27:61, 1987. 34. Watson SJ, Phillips RK: Non-inflammatory rectovaginal fistula. Br J Surg 82:1641, 1995. 35. Thiele H, Wesch G, Nusser CJ: Surgical therapy of enterovaginal fistulae following gynecologic primary procedures [in German, author’s translation]. Langenbecks Arch Chir 357:35, 1982. 36. Nowacki MP, Szawlowski AW, Borkowski A: Parks’ coloanal sleeve anastomosis for treatment of postirradiation rectovaginal fistula. Dis Colon Rectum 29:817, 1986.

Chapter 84

URETEROVAGINAL FISTULA David Ginsberg

DEFINITION AND INCIDENCE A ureterovaginal fistula is an abnormal communication between the distal ureter and the vagina that results in urinary incontinence. Formation is often preceded by pelvic surgery, with an unrecognized ureteral injury occurring at the time of surgery. Damage to the ureter can lead to ureteral obstruction or leakage of urine at the site of injury. The urine often makes its way out through the vaginal cuff, which ultimately results in the formation of the ureterovaginal fistula. Ureteral injury has occurred in about 0.5% to 1% of all pelvic surgeries.1 Total abdominal hysterectomy is the most common procedure leading to injury to the ureter and subsequent ureterovaginal fistula, accounting for 75% of all cases in one study.2 Enlarged uteri, pelvic adhesions, and significant intraoperative bleeding also appear to increase the risk of ureteral injury at the time of gynecologic surgery.3 Other operations that may lead to ureterovaginal fistula include anterior colporrhaphy, colorectal surgery, and oophorectomy. Obstetric causes rarely lead to ureterovaginal fistula formation and are primarily attributed to cesarean section (especially after prior cesarean section),3 although traumatic vaginal delivery has been reported as a cause of ureterovaginal fistula.4 Other unusual causes of ureterovaginal fistula include vaginal foreign body5 and residual stone fragments after shockwave lithotripsy.6 Radiation therapy by itself or in conjunction with surgery can place a patient at risk for ureteral injury and subsequent formation of ureterovaginal fistula.7 Persistent urinary leakage resulting from an injury to the ureter during any of these procedures places the patient at risk for developing an ureterovaginal fistula. Later series looking at laparoscopic pelvic surgery found a rate of ureteral injury of less than 1% to 2%, with a much lower incidence of injury associated with diagnostic laparoscopy compared with laparoscopic intervention.8,9 The injury to the ureter usually occurs in the distal third. Types of injury include ischemia, transaction, excision, and ligation. Ischemia is most commonly associated with radical (Wertheim’s) hysterectomy, which requires the ureter to be stripped from its fascial encasement in the broad ligament. More commonly, the ureter is injured by a suture, with resultant extravasation leading to fistula formation. The left ureter is much more at risk, and most prior series reveal ureterovaginal fistula formation on the left three to five times more often than on the right side. This increased risk to the left ureter is related to its course, which places it much closer to the cervix than the right ureter. Another common site of injury is at the level of the pelvic brim, where the ureter crosses the iliac vessels. Injury at this site is thought to occur during the manipulation and division of the infundibulopelvic ligament.3 Patients with pelvic inflammatory disease, prior pelvic surgery, and other conditions that can distort

the normal pelvic anatomy may be at greater risk for ureteral injury and subsequent fistula formation.

PRESENTATION In most series, patients with ureterovaginal fistula present 1 to 4 weeks after pelvic surgery with an acute onset of continuous incontinence. Many also void normally despite the continuous leak, because the bladder continues to fill normally through the contralateral ureter, which is usually uninvolved (bilateral ureterovaginal fistulas are rare). The presentation of ureteral injury alone in the absence of fistula formation is often missed because the symptoms are nonspecific. The most common symptoms of ureteral injury include abdominal pain, flank pain, and nausea, all of which can be easily overlooked and confused with postoperative complaints after the initial surgery or masked by postoperative narcotic use. Because symptoms of ureteral injury are nonspecific, a high degree of suspicion should be maintained for any patient with these complaints and prior pelvic surgery. Complains about urinary incontinence should result in an evaluation to look for problems such as a vesicovaginal or ureterovaginal fistula.

EVALUATION Renal ultrasound may be helpful as a screening tool, but the result may be normal if distal obstruction is absent. The most commonly used modality to evaluate for ureteral injury is intravenous urography (IVU). It can identify n ureteral injury in most cases, and it enables evaluation of renal function and potential obstruction on the affected side (Fig. 84-1). IVU may not identify a ureterovaginal fistula in every patient. Lask and colleagues10 evaluated iatrogenic ureteral injuries in 44 patients, 10 of whom had a ureterovaginal fistula. The fistula was identified in only 3 of 10 patients undergoing IVU.10 These findings highlight the importance of retrograde pyelography, which may be required to identify the fistula in some patients.11 This is especially true if the IVU result is abnormal but does not reveal ureterovaginal fistula and the patient complains of urinary incontinence after recent pelvic surgery. Any obstruction at the level of the injury should be identified because an untreated distal blockage makes spontaneous healing of the fistula extremely unlikely. If conservative attempts at therapy are to be attempted, such as placement of a ureteral stent as discussed in the next section, the retrograde pyelogram can be done simultaneously. Computed tomography should be considered for patients who are systemically ill to evaluate for possible 821

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ENDOSCOPIC THERAPY

Figure 84-1 Intravenous urography (IVU), with coned down view of the pelvis. The patient underwent total abdominal hysterectomy 2 weeks earlier and now complains of flank pain and urinary incontinence. IVU demonstrates fullness of the distal ureter and an injury that has resulted in a ureteral leak and subsequent ureterovaginal fistula.

urinoma or abscess formation, which should be percutaneously drained. In addition to radiographic evaluation, the double-dye test can be used. This was initially described using intravenous indigo carmine,12 but it has been modified to eliminate the need for intravenous access to perform the test. With the modified test, a patient is given Pyridium orally until the urine turns orange. A tampon is placed vaginally, and the bladder is emptied with a catheter. Through that catheter, the bladder is filled with a mixture of 300 mL of normal saline and 5 mL of methylene blue dye. After 5 minutes, the bladder is emptied, and the tampon is removed and inspected. An orange stain at the top of the tampon indicates a ureterovaginal fistula, a blue stain in the middle of the tampon indicates a vesicovaginal fistula, and a blue stain at the distal tip of the vagina indicates leakage of urine through the urethra.13

A variety of minimally invasive therapies have been described for the management of ureterovaginal, and they have a wide range of results. The least invasive option is observation. This has been reported with periodic success in the past and was primarily used before the use of fluoroscopy and modern endoscopic equipment made ureteral stent placement commonplace.11,14,15 Clinical and radiographic features that are likely to predict a successful outcome with nonsurgical management of a ureterovaginal fistula include minimal to moderate obstruction on the affected side, a mild degree of periureteral extravasation, upper tract improvement on subsequent follow-up studies, adequate control of urinary tract infection, and the use of absorbable suture material at the time of the initial procedure that caused the injury to the ureter.14 The risk of expectant management is stricture formation, which may require regular dilations or, if not followed carefully, can lead to chronic obstruction, loss of kidney function, and the need for subsequent nephrectomy.16 Physicians had some success with a nephrostomy tube alone when a stent could not be passed by the area of ureteral occlusion. Nephrostomy tube placement protects the upper tracts if the patient is obstructed and has successfully led to ureterovaginal fistula resolution in a small number of patients.10,11 This should be the first option if the patient is too ill to undergo anesthesia and an attempt at retrograde stent placement. This technique protects the renal unit while the patients improves and can therefore allow stent placement at a later date through an antegrade approach.10 The increased likelihood of fistula resolution with stent placement (and not nephrostomy drainage alone) was elucidated by Dowling and coworkers.17 In this series, all six of the ureterovaginal fistulas that had a stent placed successfully (antegrade or retrograde) required no further therapy; all three patients managed with nephrostomy alone failed the primary mode of therapy and subsequently required surgical intervention.17 Further evidence that nephrostomy drainage alone is insufficient was reported by Schmeller and associates18 in a review of 11 patients with ureterovaginal fistula. With this mode of management, six patients had a persistent fistula, and two had issues of ureteral stricture.18 It is unlikely that nephrostomy tube drainage alone will lead to spontaneous resolution of a ureterovaginal fistula if the ureter is obstructed distally. The goal of all minimally invasive therapy should be placement of a stent across the fistula and site of injury. This protects the kidney from potential damage from distal obstruction and can lead to spontaneous healing of the fistula. Some studies have reported resolution of up to 100% of ureterovaginal fistulas if the stent was left in place for an appropriate length of time.19,20 If the stent is successful, it is important to remember that these patients are at risk for ureteral stricture in the future, and they should be followed in the early period after stent removal with regular renal ultrasound examinations. This approach allows appropriate evaluation for the presence of de novo hydronephrosis, which can indicate stricture formation. With current endourologic techniques, it is likely that a stricture could be managed with endoscopic techniques alone, avoiding the need for open intervention.19 The primary difficulty with most of these patients is stent placement. The injury that led to ureterovaginal fistula formation is often obstructing and does not allow easy, retrograde passage of a ureteral stent. An antegrade approach can allow for stent

Chapter 84 URETEROVAGINAL FISTULA

passage when this cannot be done in a retrograde fashion.21 Chang and colleagues20 report successful resolution of ureteral fistula with an antegrade stent approach in 10 of 12 patients and recommend a stent diameter of 8 to 12 Fr to minimize the risk of subsequent ureteral stricture formation. If the stent cannot be passed by a retrograde or antegrade approach, a combined approach can be performed. Ureteroscopic assistance may be invaluable22 and can be used in a “cut to the light” approach if the ureteral lumen is completely occluded.23 This can be done with ureteroscopes proximal and distal to the level of the occlusion. If access to the kidney has yet to be obtained, this can be done with the patient in the prone split-leg position.23 However, if access to the kidney has already been obtained and a percutaneous nephrostomy tube is in place, this can be done with the patient in a modified flank position to allow for simultaneous retrograde and antegrade approaches. Stents have been placed with passage of a wire from above through the strictured proximal segment and then retrieval from below with a ureteroscope; this technique requires only one ureteroscope and one surgeon, compared with cutting to the light, which is a two-surgeon procedure.24 Fluoroscopy should be used, and after continuity is reestablished, the strictured segment should be incised proximal and distal to the lesion. All of these techniques were successful with strictures less than 2 cm long, and they should be performed by surgeons comfortable with the various endoscopic techniques that may be required.

ureterovaginal fistula spontaneously healing if leakage continues after a stent is in good position, and most fistulas that heal with drainage alone do so within 4 to 8 weeks after stent placement.19 After it is clear that open surgery will be required, there is no reason to wait. Patients are bothered by the constant urinary leakage that occurs with this fistula, and evidence supports the success of early surgical intervention.7,25,26 Surgical options include ureteroureterostomy, ureteroneocystostomy (often with a psoas hitch ureteral reimplant or Boari flap), ileal ureter, transureteroureterostomy, and nephrectomy. Surgical tenets that have been recommended in the past when repairing a ureterovaginal fistula include the sacrifice of all abnormal ureter, no attempt to stay extraperitoneal, reestablishment of continuity between the ureter and bladder, and adequate postoperative drainage.25 Excision of the affected segment of ureter and ureteroureterostomy is rarely indicated. The injury tends to be in the distal portion of the ureter, which does not lend itself to primary reanastomosis, and if done, it often results in postoperative ureteral stricture. The most commonly performed intervention for the treatment of the ureterovaginal fistula is a ureteroneocystostomy. This allows for the injured distal area to be bypassed, obviating the need for to localize and dissect the injured portion of the ureter. The method of ureteroneocystostomy depends on the level of ureteral injury or fistula, the level at which healthy ureter is found distally, and the degree of bladder mobility. Most patients can be managed with a psoas hitch ureteral reimplant (Fig. 84-2). This allows a tension-free anastomosis in most patients, with the psoas hitch also decreasing any risk of ureteral kinking caused by excessive bladder mobility. Goodwin and Scardino7 had a success rate of 100% for the 16 patients in their series treated with ureteroneocystostomy. Bleland25 found that reimplantation of the ureter with an anti-refluxing technique is preferable; however, a

SURGICAL THERAPY Open surgical intervention is indicated for patients who cannot be stented or in those who have failed attempts at minimally invasive therapy. How to define a failure of conservative therapy has not been addressed in the literature. It is hard to imagine a

IVC

Ao

Psoas major m. R. ureter Psoas minor tendon Genitofemoral n.

A

B

C

Figure 84-2 Diagram of psoas hitch ureteral reimplantation. A, The lateral attachments to the bladder on the side contralateral to the reimplantation side are taken down to allow for sufficient bladder mobility. A wide-based anterior bladder wall flap is made with a curvilinear incision. B, The bladder wall is mobilized superiorly. The posterosuperior bladder wall is secured to the psoas tendon with interrupted sutures. C, The ureter is reimplanted, and the bladder incision is closed. (Modified from Payne CK, Raz S: Ureterovaginal and related fistulae. In McAninch JW [ed]: Traumatic and Reconstructive Urology. Philadelphia, WB Saunders, 1996.)

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ureteroneocystostomy without tunneling is unnecessary and is equally successful in regard to fistula resolution.27,28 More important than an anti-refluxing anastomosis is a tension-free connection between the bladder and the ureter. Extra bladder mobility can be achieved with a psoas hitch by taking down the lateral attachments to the bladder on the side contralateral to the hitch. If a psoas hitch is unable to reach the ureter without tension, another option is a Boari flap. One indication for using this primarily is the finding of a pelvic abscess at the time of reconstruction. The Boari flap allows the surgeon to perform the ureteroneocystostomy away from the infected field of the abcess.11 More complex procedures such as transureteroureterostomy, renal autotransplantation and ileal ureter interposition are available, but they are rarely needed for this patient population. Nephrectomy is a last resort and is rarely needed for these patients, as shown in the evolution of literature. Lee and Symonds29 reported a nephrectomy rate of 48% in their review, with most nephrectomies performed before 1958. This rate

decreased to 5% as reported by Goodwin and Scardino in 1980,7 and in current series, the rate is essentially zero among patients able to maintain appropriate follow-up.10,19 CONCLUSIONS Ureterovaginal fistula is a rare complication of pelvic surgery. It is most commonly seen after total abdominal and radical hysterectomy. Because symptoms of ureteral injury can be vague in the initial postoperative period, the physician should remain alert to the possibility, especially in patients with new-onset incontinence 1 to 2 weeks after pelvic surgery. The diagnosis can be made radiographically with IVU or retrograde pyelography or though the use of the double-dye test. Initial therapy with stent placement allows healing of the fistula in a high percentage of patients. If this is not possible, definitive therapy can be achieved with ureteroneocystostomy, usually in conjunction with a psoas hitch, with a high rate of success.

References 1. Mattingly RF, Borkowf HI: Acute operative injury to the lower urinary tract. Clin Obstet Gynaecol 5:123, 1978. 2. Symmonds RE: Ureteral injuries associated with gynecologic surgery: Prevention and management. Clin Obstet Gynecol 19:623, 1976. 3. Meirow D, Moriel EZ, Zilberman M, Farkas A: Evaluation and treatment of iatrogenic ureteral injuries during obstetric and gynecologic operations for nonmalignant conditions. J Am Coll Surg 178:144, 1994. 4. Hosseini SY, Roshan YM, Safarinejad MR: Ureterovaginal fistula after vaginal delivery. J Urol 160:829, 1998. 5. Binstock MA, Semrad N, Dubow L, Watring W: Combined vesicovaginal-ureterovaginal fistulas associated with a vaginal foreign body. Obstet Gynecol 76:918, 1990. 6. Kumar RV, Kumar A, Banerjee GK: Ureterovaginal fistula: An unusual complication of stone fragments after extracorporeal shock wave lithotripsy in situ. J Urol 152:2096, 1994. 7. Goodwin WE, Scardino PT: Vesicovaginal and ureterovaginal fistulas: A summary of 25 years of experience. J Urol 123:370, 1980. 8. Wang PH, Lee WL, Yuan CC, et al: Major complications of operative and diagnostic laparoscopy for gynecologic disease. J Am Assoc Gynecol Laparosc 8:68, 2001. 9. Harkki-Siren P, Sjoberg J, Kurki T: Major complications of laparoscopy: A follow-up Finnish study. Obstet Gynecol 94:94, 1999. 10. Lask D, Abarbanel J, Luttwak Z, et al: Changing trends in the management of iatrogenic ureteral injuries. J Urol 154:1693, 1995. 11. Mandal AK, Sharma SK, Vaidyanathan S, Goswami AK: Ureterovaginal fistula: Summary of 18 years’ experience. Br J Urol 65:453, 1990. 12. Raghavaiah NV: Double-dye test to diagnose various types of vaginal fistulas. J Urol 112:811, 1974. 13. O’Brien WM, Lynch JH: Simplification of double-dye test to diagnose various types of vaginal fistulas. Urology 36:456, 1990. 14. Peterson DD, Lucey DT, Fried FA: Nonsurgical management of ureterovaginal fistula. Urology 4:677, 1974. 15. Hulse CA, Sawtelle WW, Nadig PW, Wolff HL: Conservative management of ureterovaginal fistula. J Urol 99:42, 1968.

16. Millin T: The ureter, the gynaecologist and the urologist. Proc R Soc Med 42:37, 1949. 17. Dowling RA, Corriere JN Jr, Sandler CM: Iatrogenic ureteral injury. J Urol 135:912, 1986. 18. Schmeller NT, Gottinger H, Schuller J, Marx FJ: Percutaneous nephrostomy as primary therapy of ureterovaginal fistula. Urologe A. 22:108, 1983. 19. Selzman AA, Spirnak JP, Kursh ED: The changing management of ureterovaginal fistula. J Urol 153:626, 1995. 20. Chang R, Marshall FF, Mitchell S: Percutaneous management of benign ureteral strictures and fistulas. J Urol 137:1126, 1987. 21. Lang EK: Diagnosis and management of ureteral fistulas by percutaneous nephrostomy and antegrade stent catheter. Radiology 138:311, 1981. 22. Koonings PP, Huffman JL, Schlaerth JB: Ureteroscopy: A new asset in the management of postoperative ureterovaginal fistulas. Obstet Gynecol 80:548, 1992. 23. Lingeman JE, Wong MYC, Newmark JR: Endoscopic management of total ureteral occlusion and ureterovaginal fistula. J Endourol 9:391, 1995. 24. Tsai CK, Taylor FC, Beaghler MA: Endoscopic ureteroureterostomy: long-term follow-up using a new technique. J Urol 164:332, 2000. 25. Beland G: Early treatment of ureteral injuries found after gynecological injury. J Urol 118:25, 1977. 26. Blandy JP, Badenoch DF, Fowler CG, et al: Early repair of iatrogenic injury to the ureter or bladder after gynecological surgery. J Urol 146:761, 1991. 27. Kihl B, Nilson AE, Pettersson S: Uretero-neocystostomy in the treatment of postoperative uretero-vaginal fistula. Acta Obstet Gynecol 61:341, 1982. 28. Murphy DM, Grace PA, O’Flynn JD: Ureterovaginal fistula: A report of 12 cases and review of the literature. J Urol 128:924, 1982. 29. Lee RA, Symmonds RE: Ureterovaginal fistula. Am J Obstet Gynecol 109:1032, 1971.

Chapter 85

URETHRAL DIVERTICULA Eric S. Rovner Diverticula of the female urethra present some of the most challenging diagnostic and reconstructive problems in female urology. These cases can be simultaneously fascinating and frustrating. Urethral diverticula have a bewildering variety of clinical manifestations, ranging from completely asymptomatic, incidentally noticed lesions identified on physical examination or radiographs to very debilitating, painful vaginal masses associated with incontinence, stones, or tumors. Anatomic variations between patients and in the location, size and complexity of these lesions ensure that each case is unique (Fig. 85-1). Although described as early as the 19th century,1 the modern era of diagnosing and treating female urethral diverticula began in 1956 with the advent of positive-pressure urethrography introduced by Davis and Cian.2 Over the next several years, there was a dramatic increase in number of cases of urethral diverticula reported in the literature. Davis and Telinde’s3 series of 121 cases published in 1958 approximately doubled the number of cases reported during the previous 60 years. Development of adjuvant imaging techniques such as ultrasound and magnetic resonance imaging (MRI) during the past 3 decades has contributed greatly to understanding of urethral diverticula. With the expanding use of these imaging modalities, the diagnosis and evaluation of this condition continues to evolve. After the diagnosis is confirmed, definitive therapy often consists of operative excision and reconstruction. Successful surgical excision and reconstruction requires a detailed knowledge of the relevant operative anatomy, adherence to basic surgical tenets, and an ability to be creative and sometimes even improvisational in the operating room.

they are most prominent over the distal two thirds, with most glands draining into the distal one third of the urethra. Skene’s glands are the largest and most distal of these glands. These glands drain outside the urethral lumen, lateral to the urethral meatus. Most acquired female urethral diverticula originate from pathologic processes involving the periurethral glands. The urethra has several muscular layers: an internal longitudinal smooth muscle layer, an outer circular smooth muscle layer, and a skeletal muscle layer. The skeletal muscle component spans much of the length of the urethra but is more prominent in the middle third. It has a U-shaped configuration and is deficient dorsally. Ventral to the urethra but separated from it by the periurethral fascia lies the anterior vaginal wall. Arterial inflow to the urethra derives from two sources. The proximal urethra has a similar blood supply as the adjacent bladder, whereas the distal urethra derives its blood supply from

ANATOMY OF THE FEMALE URETHRA The normal female urethra is a musculofascial tube approximately 3 to 4 cm long. It extending from the bladder neck to the external urethral meatus, and it is suspended from the pelvic side wall and pelvic fascia (i.e., tendinous arc of the obturator muscle) by a sheet of connective tissue called the urethropelvic ligament. The urethropelvic ligament is composed of two layers of fused pelvic fascia that extend toward the pelvic side wall bilaterally (Fig. 85-2). This structure can be considered to have an abdominal side (i.e., endopelvic fascia) and a vaginal side (i.e., periurethral fascia). Within and between these two leaves of fascia lies the urethra. The urethral lumen is lined by an epithelial layer that is a transitional cell type proximally and a nonkeratinized stratified squamous cell type distally. The urethra can be considered to be a rich, vascular, spongy cylinder surrounded by an envelope of consisting of smooth and skeletal muscle and fibroelastic tissue.4 Within the thick, vascular lamina propria-submucosal layer are the periurethral glands (Fig. 85-3). These tubuloaveolar glands exist over the entire length of the urethra posterolaterally, but

Figure 85-1 The postvoid film after voiding cystourethrography demonstrates a collection of contrast below the bladder that suggests a urethral diverticulum.

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Urethropelvic ligament (endopelvic and periurethral fascia) Tendinous arc of obturator

Urethropelvic ligament (endopelvic and periurethral fascia) Tendinous arc of the obturator

Urethra (with Foley) Levator

Urethral diverticulum

Levator

Ostia or neck of the UD

Vaginal wall

Vaginal wall

Figure 85-2 Representative anatomy of the mid-urethra in a coronal plane.

Figure 85-4 Diagram of a urethral diverticulum. The urethral diverticulum forms within and between the layers of the urethropelvic ligament.

Urethral “envelope” Urethral diverticulum Periurethral glands

Bladder lumen

Saddlebag urethral diverticulum m ral lu Ureth

en

Circumferential urethral diverticulum

Figure 85-3 Periurethral glands are located within the submucosa of the urethra deep to the muscular envelope. They drain distally but arborize proximally.

the terminal branches of the inferior vesical artery through the vaginal artery, which runs along the superior lateral aspect of the vagina. Lymphatic drainage of the female urethra is to the sacral lymph nodes, internal iliac nodes, and inguinal lymph nodes. Innervation to the female urethra is from the pudendal nerve (S2 to S4), and afferents from the urethra travel by means of the pelvic splanchnic nerves. URETHRAL DIVERTICULA Pathophysiology and Etiology As conceptualized by Raz and colleagues,4 a urethral diverticulum represents an epithelialized cavity dissecting within the confines of the fascia of the urethropelvic ligament. This defect is often an isolated cystlike appendage with a single, discreet connection to the urethral lumen, called the neck or ostia (Fig. 85-4). However, complicated anatomic patterns may exist, and in certain cases, the urethral diverticula may extend partially (i.e., saddlebag urethral diverticula) around the urethra, anterior to the urethra,5 or circumferentially about the urethra (Fig. 85-5).6

Figure 85-5 Different morphologies of urethral diverticula may exist.

The exact origin of urethral diverticula is unknown. A major debate in the earlier part of the 20th century focused on whether urethral diverticula were congenital or acquired lesions.7-9 Although this condition exists in children, it may represent a different clinical entity from adult female urethral diverticula. Scattered reports of congenital urethral diverticula in female infants have been described.10 Marshall11 reported five cases of urethral diverticula in young females, and three diverticula underwent spontaneous regression. Congenital anterior urethral diverticulum is a well-described entity in boys,12-14 but this is considered to be a different clinical entity from urethral diverticula in the female. Congenital Skene’s glands cysts have been reported15,16 but are considered to be rare. Diverticula in the pediatric population have been attributed to a number of congenital anomalies, including an ectopic ureter draining into a Gartner’s duct cyst and a form fruste of urethral duplication.17-19 Most urethral diverticula are likely to be acquired and are diagnosed in female adults. In two large series of urethral diverticula, there were no patients reported who were younger than 10 years old,20,21 arguing against a congenital origin for these lesions. Although it is possible that there exists a congenital defect in patients that results in or represents a precursor to urethral diver-

Chapter 85 URETHRAL DIVERTICULA

ticula that becomes symptomatic only later in life, it remains unproven. There are many theories regarding the formation of acquired urethral diverticula. For many years, acquired urethral diverticula were thought to be most likely caused by trauma from vaginal childbirth.22 It was postulated that mechanical trauma during vaginal delivery resulted in herniation of the urethral mucosa through the muscular layers of the urethra, with the subsequent development of a urethral diverticula. However, 20% to 30% of patients in some urethral diverticula series are nulliparous,23,24 which may significantly discount parity as a risk factor. Trauma with forceps delivery, however, has been reported to cause urethral diverticula,25 as has the endoscopic injection of collagen.26 The periurethral glands are the probable site of origin of acquired urethral diverticula.4 Huffman’s27 anatomic work with wax models of the female urethra were critical to the early theories regarding the pathophysiology of urethral diverticula and the involvement of the periurethral glands. By reviewing 10-μm transverse sections, he refuted earlier anatomic descriptions of the glandular anatomy of the female. He characterized the periurethral glands as located primarily dorsolateral to the urethra, arborizing proximally along the urethra and draining into ducts located in the distal one third of the urethra (see Fig. 85-3). He found that periductal and interductal inflammation was common. In support of these observations and an infectious (acquired) cause of urethral diverticula, in more than 90% of urethral diverticula cases, the ostium is located posterolaterally in the middle or distal urethra, which corresponds to the location of the periurethral glands.28,29 Although there are probably other factors that facilitate the initiation, formation, or propagation of urethral diverticula, infection of the periurethral glands seems to be the etiologic factor in most cases. Peters and Vaughn30 found a strong association between concurrent or previous infection with Neisseria gonorrhea and urethral diverticula. However, the initial infection and especially subsequent reinfections may be caused by a variety of organisms, including E. coli, other coliform bacteria, and vaginal flora. Urethral diverticula have been historically attributed to recurrent infection of the periurethral glands with obstruction, suburethral abscess formation, and subsequent rupture of these infected glands into the urethral lumen. Continual filling and pooling of urine in the resultant cavity may result in stasis, recurrent infection, and eventual epithelialization of the cavity, forming a permanent urethral diverticulum. This concept was first popularized by Routh31 more than a century ago, and it has become the most widely accepted theory regarding the formation of female urethral diverticula. Reinfection, inflammation, and recurrent obstruction of the neck of the cavity are theorized to result in patients’ symptoms and in enlargement of the diverticulum. This proposed pathophysiology appears to adequately explain the anatomic location and configuration of most urethral diverticula and is supported by the work of Huffman.27 However, Daneshgari and colleagues32 have reported noncommunicating urethral diverticula diagnosed by MRI. Whether this lesion represents a forme fruste of urethral diverticula or simply an obstructed urethral diverticula ostium is unclear. Raz and colleagues4 formulated a modern hypothesis regarding the pathogenesis of urethral diverticula through extensive clinical experience with this entity, including the diagnosis, imaging, and surgical repair of urethral diverticula. These inves-

tigators propose that acquired urethral diverticula result from infection and obstruction of the periurethral glands. These glands are normally found in the submucosal layer of the spongy tissue of the distal two thirds of the urethra. Repeated infection and abscess formation in these obstructed glands eventually result in enlargement and expansion. Initially, the expanding mass displaces the spongy tissue of the urethral wall and then enlarges to disrupt the muscular envelope of the urethra. This results in herniation into the periurethral fascia. The enlarging cavity can then expand and dissect within the leaves of the periurethral fascia and urethropelvic ligament. This expansion occurs most commonly ventrally, resulting in the classic anterior vaginal wall mass palpated on physical examination in some patients with urethral diverticula. However, the lesions may also expand laterally or even dorsally about the urethra. Eventually, the abscess cavity ruptures into the urethral lumen, resulting in the communication between the urethral diverticula and the urethral lumen. An appreciation of the anatomy and pathophysiology of urethral diverticula is important in understanding the surgical approach to the excision and reconstruction of these lesions. Prevalence Moore33 stated that urethral diverticula as an entity is “found in direct proportion to the avidity with which it is sought.” Although no longer considered a rare lesion, fewer than 100 cases of urethral diverticula were reported in the literature before 1950. With the development of sophisticated imaging techniques, including positive-pressure urethrography in the 1950s, the diagnosis of urethral diverticula became increasingly common. The true prevalence of female urethral diverticula is unknown, but it is reported to occur in up to 1% to 6% of adult females in some series. Determining the true prevalence of urethral diverticula would require appropriate screening and imaging of a large number of symptomatic and asymptomatic adult female subjects in a primary care setting, which has not been done. Bruning34 found urethral diverticula in 3 of 500 female autopsy specimens. In 1967, Andersen reported the results of positive-pressure urethrography on 300 women with cervical cancer but without lower urinary tract symptoms and found urethral diverticula in 3%.35 Aldridge36 reported a prevalence of urethral diverticula in 1.4% of women presenting with incontinence and related symptoms. Stewart37 found urethral diverticula in 16 of 40 highly symptomatic females investigated with positive-pressure urethrography. Endorectal coil MRI was performed on 140 consecutive female patients with lower urinary tract symptoms, and the incidence of urethral diverticula was approximately 10%.38 However, this represented a series of symptomatic females at a tertiary referral center, which probably did not reflect the general population. Some series have suggested a definite racial predilection, with blacks being as much as six times as likely to develop urethral diverticula as their white counterparts.20 The reasons for this racial distribution is not well understood. It has not been confirmed in some modern case series, and it may reflect referral bias at the urban academic centers in the original reported series.39 Diverticular Anatomy Most commonly, urethral diverticula represent an epithelialized cavity with a single connection to the urethral lumen. The size of

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A

B

C

the lesion may vary from only a few millimeters to several centimeters. The size may vary over time because of inflammation and intermittent obstruction of the ostia with subsequent drainage into the urethral lumen. The epithelium of urethral diverticula may be columnar, cuboidal, stratified squamous, or transitional. In some cases, the epithelium is absent, and the wall of the urethral diverticula consists of only fibrous tissue. These lesions are found within the periurethral fascia bordered by the anterior vaginal wall ventrally. Urethral diverticula are most often located in the sagittal plane, and they are centered at the level of the middle third of the urethra, with the luminal connection or ostia located posterolaterally. They may extend distally along the vaginal wall almost to

Figure 85-6 T2-weighted magnetic resonance images demonstrate a large urethral diverticulum extending to the trigone of the bladder in the sagittal (A), axial (B), and coronal planes (C).

the urethral meatus or proximally up to and beyond the bladder neck, underneath the trigone of the bladder (Fig. 85-6). A bewildering array of configurations can be identified on imaging and at surgical exploration (Table 85-1). In the axial plane, the urethral diverticula cavity may extend laterally along the urethral wall, and in some cases, they may extend around to the dorsal side of the urethra or wrap circumferentially around the entire urethra. Urethral diverticula may be bilobed (i.e., dumbbell shaped), extending across the midline in a so-called saddlebag configuration (see Fig. 85-5). Multiple loculations are not uncommon, and at least 10% of patients have multiple urethral diverticula at presentation. Various degrees of sphincteric compromise may exist because of the location of diverticulum relative to the

Chapter 85 URETHRAL DIVERTICULA

Table 85-1 Diverticular Morphology and Characteristics Series 28

Lang and Davis Hoffman and Adams45 Pavlica et al146 Kim et al147 Leach et al99

Axial Location (%)

Number (%)

No. of Patients

Size Range (cm)

Anterior

Lateral

Posterior

Single

Multiple

108 60 47 16 61

N/A 0.5-5.0 0.5-6.0 0.9-4.5 0.2-5.0

N/A N/A 3 (6) 5 (31)* N/A

N/A N/A 6 (13) N/A N/A

N/A N/A 38 (81) 11 (69) N/A

N/A N/A 41 (87) N/A 55 (90)

N/A N/A 6 (13) N/A 6 (10)

Coronal Location Proximal 11 (10) 4 (7) 3 (6) 4 (25) 15 (25)

Mid 50 29 39 10 37

(46) (48) (83) (63) (60)

*Anterior and lateral. N/A, not available. Adapted from Westney OL, Leng WW, McGuire EJ: The Diagnosis and Treatment of Female Urethral Diverticulum, vol 20, lesson 37. Houston, TX, AUA Update Series, 2001, p 291.

Box 85-1 Signs and Symptoms of Urethral Diverticula Symptoms Vaginal or pelvic mass Pelvic pain Urethral pain Dysuria Urinary frequency Postvoid dribbling Dyspareunia Urinary urgency Incontinence Urinary hesitancy Vaginal or urethral discharge Double voiding Sense of incomplete emptying Signs Recurrent urinary tract infections Hematuria Vaginal or perineal tenderness Urinary retention Vaginal mass Urethral discharge with stripping of anterior vaginal wall

proximal and distal urinary sphincter mechanisms. This is a consideration for surgical repair. Presentation Most patients with urethral diverticula present between the third and seventh decade of life.7,23,33,40,41 The presenting symptoms and signs of patients with urethral diverticula are protean (Box 85-1). The classic presentation of urethral diverticula has been described historically as the three Ds: dysuria, dyspareunia, and dribbling (postvoid). However, individually or collectively, these symptoms are neither sensitive nor specific for urethral diverticula. Although presentation is highly variable, the most common symptoms are irritative (e.g., frequency, urgency) lower urinary tract symptoms, pain, and infection.20,21,30,42 Dyspareunia is reported by 12% to 24% of patients.20,21 Approximately 5% to 32% of patients complain about postvoid dribbling.20,23 Recur-

rent cystitis or urinary tract infection is a frequent presentation in one third of patients,20,23 likely due to urinary stasis in the urethral diverticula. Multiple bouts of recurrent cystitis should alert the clinician to the possibility of a urethral diverticulum. Other complaints include pain, a vaginal mass, hematuria, vaginal discharge, obstructive symptoms or urinary retention, and stress or urge incontinence. Up to 20% of patients diagnosed with urethral diverticula may be completely asymptomatic. Patients may present with complaints of a tender or nontender anterior vaginal wall mass, which on gentle compression may reveal retained urine or purulent discharge through the urethral meatus. Although spontaneous rupture of these lesions is rare, urethrovaginal fistula may result under these circumstances.43 The size of the urethral diverticula does not correlate with symptoms. In some cases, very large urethral diverticula may result in minimal symptoms, and some urethral diverticula that are not palpable may result in considerable patient discomfort and distress. Symptoms may wax and wane and even resolve for long periods. The reasons for these exacerbations and remissions are poorly defined but may be related to periodic and repeated episodes of infection and inflammation. Because many of the symptoms associated with urethral diverticula are nonspecific, patients may be misdiagnosed and treated for years for a number of unrelated conditions before the diagnosis of urethral diverticula is made. This may include therapies for interstitial cystitis, recurrent cystitis, vulvodynia, endometriosis, vulvovestibulitis, and other conditions. In one series of 46 consecutive women eventually diagnosed with urethral diverticula, the mean interval from onset of symptoms to diagnosis was 5.2 years.44 In this series, women consulted with an average of nine physicians before the definitive diagnosis was made, despite the fact that 52% of women had a palpable mass on examination. This underscores the importance of a baseline level of suspicion and a thorough pelvic examination in female patients complaining of lower urinary tract symptoms or other symptoms that may be associated with urethral diverticula. Evaluation and Diagnosis The diagnosis and complete evaluation of urethral diverticula can be made with a combination of a thorough history; physical examination; appropriate urine studies, including urine culture and analysis; endoscopic examination of the bladder and urethra; and selected radiologic imaging. A urodynamic study may also be used in selected cases.

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incontinence should be performed, and the presence or absence of vaginal prolapse should be assessed. Urine Studies Urinalysis and urine culture should be performed. The most common organism isolated in patients with urethral diverticula is Escherichia coli. However, other gram-negative enteric flora and Neisseria gonorrhea, Streptococcus, and Staphylococcus are often present.3,45 A sterile urine culture does not exclude infection because these patients are often on antibiotic therapy at presentation. For patients with irritative symptoms or when a malignancy is suspected, urine cytology can be performed.

Figure 85-7 Large anterior vaginal wall mass. The urethral catheter is seen superiorly and a weighted vaginal speculum is seen inferiorly. Scott retractor hooks are seen exposing the anterior vaginal wall in this operating room photo.

Physical Examination During physical examination the anterior vaginal wall should be carefully palpated for masses and tenderness. The location, size, and consistency of suspected urethral diverticula should be recorded. Most urethral diverticula are located ventrally over the middle and proximal portions of the urethra, corresponding to the area of the anterior vaginal wall 1 to 3 cm inside the introitus (Fig. 85-7). However, urethral diverticula also may be located anterior to the urethra or extend partially or completely around the urethral lumen. These particular configurations may have significant implications when undertaking surgical excision and reconstruction. Urethral diverticula may extend proximally toward the bladder neck. The urethral diverticula may produce distortion of the bladder outlet and trigone of the bladder on cystoscopy or on radiographic imaging, and special care should be taken during surgical excision and reconstruction because of concerns about intraoperative bladder and ureteral injury and the potential for development of postoperative voiding dysfunction and urinary incontinence. More distal vaginal masses or perimeatal masses may represent other lesions, including abnormalities of Skene’s glands. The differentiation between these lesions sometimes cannot be made on the basis of a physical examination alone and may require additional radiologic imaging. A particularly hard anterior vaginal wall mass may indicate a calculus or cancer within the urethral diverticula, and it mandates further investigation. During physical examination, the urethra may be gently stripped or milked distally in an attempt to express purulent material or urine from within the urethral diverticula cavity. Although often described for the evaluation of urethral diverticula, this maneuver is not successful in producing the diagnostic discharge through the urethral meatus in most patients.39 The vaginal walls are assessed for atrophy, rugation, and elasticity. Poorly estrogenized, atrophic tissues are important to identify if surgical treatment is being considered. These tissues are often surgically mobilized and may be used for flaps during excision and reconstruction. The distal vagina and vaginal introitus are also assessed for capacity. These factors may influence surgical planning because a narrow introitus can make surgical exposure difficult and may mandate an episiotomy. During the physical examination, a provocative maneuver to elicit stress

Cystourethroscopy Cystourethroscopy is performed in an attempt to visualize the urethral diverticular ostia and to rule out other causes of the patient’s lower urinary tract symptoms. A specially designed female cystoscope can be helpful in evaluating the female urethra. The short beak maintains the discharge of the irrigation solution immediately adjacent to the lens, which aids in distention of the relatively short (compared with the male) urethra, permitting improved visualization. It may also be advantageous to compress the bladder neck while simultaneously applying pressure to the diverticular sac with an assistant’s finger. Luminal discharge of purulent material can often be seen with this maneuver or with simple digital compression of the urethral diverticula during urethroscopy. The urethral diverticular ostium is most often located posterolaterally at the level of the mid-urethra, but it can be very difficult to identify in some patients. The success rate in identifying a diverticular ostium on cystourethroscopy is highly variable and is reported to be between 15% and 89%.20,23,39 Patients with urethral diverticula are often highly symptomatic, and endoscopic examination can be difficult to initiate or complete. A positive examination result may help in surgical planning, but the failure to locate an ostium on cystourethroscopy should not influence the decision to proceed with further investigations or surgical repair. Urodynamics For patients with urethral diverticula and urinary incontinence or significant voiding dysfunction, a urodynamic study can be helpful.46-48 Urodynamics may document the presence or absence of stress urinary incontinence before repair. Approximately 50% of women with urethral diverticula are found to have stress urinary incontinence on urodynamic evaluation.23,49 A video urodynamic study combines a voiding cystourethrogram and a urodynamic study, consolidating the diagnostic evaluation and decreasing the number of required urethral catheterizations during the patient’s clinical workup. For patients undergoing surgery for urethral diverticula with coexistent, symptomatic stress urinary incontinence demonstrated on physical examination or by urodynamic study or for those found to have an open bladder neck on preoperative evaluation, concomitant antiincontinence surgery can be offered. Many investigators have described successful concomitant repair of urethral diverticula and stress incontinence in the same operative setting.23,49-51 Alternatively, on urodynamic evaluation, a small number of patients may have evidence of bladder outlet obstruction due to the obstructive or mass effects of the urethral diverticula on the urethra. Stress urinary incontinence may coexist with obstruction,52 but both conditions can be treated successfully with a carefully planned and executed operation. Urethral pressure pro-

Chapter 85 URETHRAL DIVERTICULA

filometry has also been used by some physicians to assess or diagnose patients with urethral diverticula by noticing a biphasic pattern at the level of the lesion during the study.47,48,53 Imaging Critically important to the success of surgical treatment of female urethral diverticula is high-quality preoperative imaging. Along with its utility as a diagnostic entity, radiologic imaging should provide an accurate reflection of the anatomy of the urethral diverticulum, including its relationship to the proximal urethra and bladder neck. Several imaging techniques have been applied to the study of female urethral diverticula, and no single study can be considered the gold standard for this purpose. Each technique has relative advantages and disadvantages, and the ultimate choice of diagnostic study in many centers depends on several factors, including local availability, cost, and the experience and expertise of the radiologist. Available techniques for the evaluation of urethral diverticula include double-balloon positive-pressure urethrography (PPU), voiding cystourethrography (VCUG), intravenous urography (IVU), ultrasonography, and magnetic resonance imaging (MRI) with or without an endoluminal coil (eMRI). Positive-Pressure Urethrography, Voiding Cystourethrography, and Intravenous Urography Classically, double-balloon PPU had been considered to be the best study for the diagnosis and assessment of female urethral diverticula.2,21,23,54 With this technique, a highly specialized catheter with two balloons separated by several centimeters is inserted into the female urethra (Fig. 85-8). This catheter contains a channel within the catheter that exits through a side hole between the two balloons. One balloon is positioned adjacent to the external urethral meatus, and the other balloon is situated at the bladder neck. Both balloons are inflated, sealing the urethral lumen. Contrast is then infused through the channel under slight pressure, distending the urethral lumen between the two balloons and forcing contrast into the urethral diverticula, thereby opacifying the cavity. This highly specialized study provides outstanding images of the urethra and urethral diverticula, and unlike

VCUG, it does not depend on the patient successfully voiding during the study. However, PPU is not widely performed clinically. It is a complicated study requiring a very specific type of modified urethral catheter and expertise in the performance and interpretation of the study by the radiologist. It is invasive, requiring catheterization of the urethra, and in the setting of acute inflammation commonly seen with female urethral diverticula, it can cause considerable patient discomfort and distress. Noncommunicating urethral diverticula32 and loculations within existing urethral diverticula cannot be visualized with PPU because the contrast does not enter and fill these areas in the absence of a connection to the urethral lumen. As an alternative to PPU, VCUG may provide excellent imaging of urethral diverticula (Fig. 85-9). It is widely available and is a familiar diagnostic technique to most radiologists. Sensitivity for urethral diverticula with this technique varies from 44% to 95%.23,55 After a scout film, the bladder is filled through a urethral catheter. The catheter is removed at bladder capacity, and images of the bladder and bladder neck are obtained. Ideally, voiding images are obtained in the anteroposterior, lateral, and oblique projections. A postvoid film is obtained. Although VCUG is probably the most widely used study for the diagnosis and evaluation of patients with known or suspected urethral diverticula, it has several limitations. VCUG is invasive, requiring catheterization of the urethra for bladder filling. This can result in considerable patient discomfort and may risk translocating bacteria from an infected urethral diverticulum into the bladder during catheterization, resulting in bacterial cystitis. This is also a risk of PPU. Successful imaging of the urethral diverticulum occurs only during the voiding phase of the VCUG with subsequent filling of the urethra. Occasionally, only the postvoid film demonstrates the urethral diverticulum.56-58 Not uncommonly, patients are somewhat inhibited or otherwise unable to void during VCUG for a variety of reasons, including pain from the initial urethral catheterization. Unfortunately, in the absence of contrast entering the urethra, opacification of the diverticulum does not occur. An inability to generate an adequate flow rate

Contrast

UD

Figure 85-8 Diagram of a double-balloon catheter. Balloons are inflated at the bladder neck and external urethral meatus. Contrast is then infused through an additional port, and it exits through a side hole between the balloons, distending the urethral lumen under pressure and filling the urethral lumen and diverticulum (UD).

Figure 85-9 A voiding cystourethrogram demonstrates a urethral diverticulum (UD).

831

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A

B

C

D

Figure 85-10 Voiding cystourethrography (VCUG) and magnetic resonance imaging (MRI) demonstrated a large, circumferential urethral diverticulum (UD). VCUG (A) shows poor opacification of the proximal urethra with suboptimal distention of the urethral diverticulum due to a poor voiding effort. Endoluminal MRI demonstrates the full extent and complexity of the lesion on the T2-weighted axial (B), midline sagittal (C), and parasagittal (D) images.

during the VCUG results in suboptimal filling of the urethral diverticulum and an underestimation of its size and complexity (Fig. 85-10). Some urethral diverticula may not opacify after a technically successful VCUG because of acute inflammation of the ostium or neck of the diverticulum or because the diverticulum does not otherwise communicate with the urethral lumen. These noncommunicating urethral diverticula exist within the

urethropelvic ligament and can be successfully imaged with cross-sectioning techniques such as MRI.32 Three studies have compared VCUG with PPU and concluded that PPU is a more sensitive test for urethral diverticula than VCUG.55,59,60 In one study of 32 patients, VCUG failed to demonstrate the urethral diverticula in 69% of patients, whereas PPU failed to demonstrate the lesion in only 6%.55

Chapter 85 URETHRAL DIVERTICULA

A

B

Figure 85-11 Surface coil, T2-weighted magnetic resonance imaging demonstrates a urethral diverticulum in the sagittal (A) and axial (B) planes.

IVU may be considered in patients in whom it is necessary to delineate the upper urinary tract or to rule out an ectopic ureterocele.61 The postvoid film of the urogram can be helpful for the diagnosis of urethral diverticula in some patients.56,57 Ultrasound Ultrasound has been advocated for the preoperative assessment of urethral diverticula.62-71 Abdominal, transvaginal, translabial, and transurethral techniques have been described. Transvaginal imaging often provides information regarding the size and location of urethral diverticula. On ultrasonographic imaging, the urethral diverticulum appears as an anechoic or hypoechoic area with enhanced through transmission. Ultrasound is relatively noninvasive and does not expose the patient to radiation. Another significant advantage of ultrasound is that successful imaging of urethral diverticula does not require voiding. However, ultrasound may not produce detailed, high-resolution images that demonstrate precise surgical anatomy. This study can be somewhat operator dependent. Transurethral ultrasound techniques are evolving and may provide an incremental improvement in resolution. Similar to PPU and VCUG, the transurethral techniques are invasive because the ultrasound probe is placed per urethra and can cause patient discomfort and bacterial seeding of the lower urinary tract.

Magnetic Resonance Imaging As an alternative to the radiologic investigations described previously, MRI permits relatively noninvasive, high-resolution, multiplanar imaging of urethral diverticula. Urethral diverticula appear as areas of decreased signal intensity on T1-weighted images compared with the surrounding soft tissues, and they have high signal intensity on T2-weighted images (see Fig. 85-10). Additional advantages of MRI compared with PPU and VCUG are that successful imaging of urethral diverticula is wholly independent of voiding and free from ionizing radiation. Surface-coil (Fig. 85-11)72,73 and endoluminal techniques38,60,74,75 have been described. Endoluminal imaging (eMRI) places the magnetic coil into a body cavity adjacent to the area of interest. This location produces an improved signal-to-noise ratio and high-resolution imaging of these areas.74,75 For the evaluation of urethral diverticula, the coil is placed intravaginally or intrarectally (Fig. 85-12). Surface-coil MRI and eMRI appear to be superior to VCUG and PPU in the evaluation of urethral diverticula,74,76,77 but the technology is expensive and not widely available. The few contraindications to MRI for urethral diverticula include metallic foreign body fragments, claustrophobia, and an inability to tolerate the endoluminal probe.

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Axial

Sagittal Pubis

Urethra

UD

Vaginal coil

Figure 85-12 Sagittal and axial, T2-weighted endoluminal magnetic resonance images show the relevant anatomy of a patient with a urethral diverticulum (UD).

Figure 85-13 Large anterior vaginal wall leiomyoma.

Differential Diagnosis of Urethral Diverticula: Periurethral Masses Other Than Urethral Diverticula Periurethral masses other than urethral diverticula comprise a wide spectrum of conditions that must be differentiated from each other and urethral diverticula. It may be possible to make a definitive diagnosis based on the history and physical examination alone; in other cases, judicious use of radiographic and cystoscopic studies is necessary to exclude urethral diverticula. Vaginal Leiomyoma Vaginal leiomyoma is a benign, mesenchymal tumor of the vaginal wall that arises from smooth muscle elements. It commonly manifests as a smooth, round mass on the anterior vaginal wall (Fig. 85-13). It is an uncommon lesion; approximately 300 cases have been reported in the literature.78 In a series of 79 patients with periurethral masses, 4 (5%) were found to have leiomyoma.79 These benign tumors were apparent on physical examination as freely mobile, nontender masses on the anterior vaginal wall. They may be misdiagnosed as urethral diverticula.80 Symptoms, if they exist, are usually related to the size of the lesion

Figure 85-14 Skene’s gland cyst in a 19-year-old woman. Notice the large periurethal mass with displacement of the urethral meatus.

and include a mass effect, obstruction, pain, and dyspareunia. They commonly present in the fourth to fifth decade. Like uterine leiomyomas, these lesions are usually estrogen dependent and have been demonstrated to regress during menopause.81 Excision or enucleation78 using a vaginal approach is often curative and is recommended to confirm the diagnosis, exclude malignant histology, and alleviate symptoms. Skene’s Gland Abnormalities Skene’s gland cysts and abscesses are similar lesions that are differentiated based on clinical findings (Fig. 85-14). Both lesions manifest as small, cystic masses just lateral or inferolateral to the urethral meatus. They may be lined with transitional or stratified

Chapter 85 URETHRAL DIVERTICULA

squamous epithelium. Abscesses may be extremely tender and inflamed, and in some cases, purulent fluid can be expressed from the ductular orifice. Unlike urethral diverticula, these lesions do not communicate with the urethral lumen. Skene’s gland cysts may be seen in neonatal girls and young to middleaged female patients.16 Symptoms may include dysuria, dyspareunia, obstruction, and pain. Differentiation from urethral diverticula can often be made on the basis of the physical examination, because these lesions are located relatively distally on the urethra, often distorting the urethral meatus, compared with urethral diverticula, which most commonly occur over the middle and proximal urethra. Various treatments for Skene’s glands abnormalities have been described, including aspiration, marsupialization, incision and drainage and simple excision. Adenocarcinoma arising in Skene’s glands has been reported. Because of homology of these glands with the prostate, these patients may demonstrate elevated prostate-specific antigen (PSA) levels, which normalize with treatment.82 Gartner’s Duct Cysts Gartner’s duct cysts represent mesonephric remnants and are found on the anterolateral vaginal wall from the cervix to the introitus. Because they are mesonephric remnants, they may drain ectopic ureters from poorly functioning or nonfunctioning upper-pole moieties in duplicated systems. They have been reported with single-system ectopia, although this is much less common in female patinets.83,84 It is not clear what proportion of patients with Gartner’s duct cysts have ipsilateral renal abnormalities, but upper tract evaluation is recommended. In contrast, approximately 6% of subjects with unilateral renal agenesis have a Gartner’s duct cyst.85 Up to 50% of patients with Gartner’s duct cysts and renal dysplasia may also have ipsilateral müllerian duct obstruction.86 Treatment depends on symptoms and association with ectopic ureters. If the lesions are asymptomatic and are associated with a nonfunctioning renal moiety, they can be observed. Aspiration and sclerotherapy have been successful.87 Simple excision or marsupialization has been recommended for symptomatic lesions. If the cyst is associated with a functioning renal moiety, treatment must be individualized. Vaginal Wall Cysts Vaginal wall cysts usually manifest as small, asymptomatic masses on the anterior vaginal wall.88 They may arise from multiple cell types: mesonephric (Gartner’s duct cysts), paramesonephric (müllerian), endometriotic, urothelial, or epidermoid (inclusion cyst) tissues. A specific diagnosis cannot be reliably made until the specimen is removed and examined by a pathologist. The histologic subtype is usually of little consequence, although epidermoid cysts are usually associated with previous trauma or vaginal surgery. Pradhan and Tobon89 described the pathologic characteristics of 43 vaginal cysts removed from 41 women over a 10-year period. The derivation of the cyst was müllerian in 44%, epidermoid in 23%, and mesonephric in 11%. The others were Bartholin gland, endometriotic, and indeterminate types. As with other periurethral masses, they must be differentiated from urethral diverticula. Treatment is usually by simple excision in symptomatic patients. Urethral Mucosal Prolapse Urethral prolapse manifests as a circumferential herniation or eversion of the urethral mucosa at the urethral meatus. The pro-

lapsed mucosa commonly appears as a beefy red, doughnutshaped lesion that completely surrounds the urethral meatus. It may be asymptomatic or manifest with bleeding, spotting, pain, or urinary symptoms. It is commonly seen in two populations: postmenopausal women and prepubertal girls. Although thought to be more common in young African American girls, later series do not confirm this predilection.90,91 In children, it is often causally related to a Valsalva maneuver or constipation. Eversion of the mucosa may occur because of a pathologically loose attachment between smooth muscle layers of the urethra.92 The cause is much less clear for postmenopausal women, although it has been epidemiologically linked to estrogen deficiency. Treatment may be medical or surgical. Medical treatment involves topical creams (e.g., estrogen, anti-inflammatory ointment) and sitz baths. Various surgical techniques have been described, including cauterization, ligation around a Foley catheter, and complete circumferential excision. Circumferential excision with suture reapproximation of the remaining urethral mucosa to the vaginal wall can be performed with few complications. Rudin and colleagues91 reported outcomes for 58 girls with urethral prolapse. Medical treatment was initially successful in 20 patients, among whom there were five recurrences. The remaining 38 patients failed initial conservative management and underwent surgical excision, with four complications, including urethral stenosis in two. Jerkins and coworkers93 found superior results in surgically treated patients compared with medical management or catheter ligation. Urethral Caruncle Urethral caruncle is an inflammatory lesion of the distal urethra that is most commonly diagnosed in postmenopausal women. It usually appears as a reddish, exophytic mass at the urethral meatus that is covered with mucosa. These lesions are often asymptomatic and identified incidentally on gynecological examination. When irritated, they may cause underwear spotting or become painful. Less commonly, they may cause voiding symptoms. They are etiologically related to mucosal prolapse. Chronic irritation contributes to hemorrhage, necrosis, and inflammatory growth of the tissue, which corresponds to the histology of excised lesions. If the lesion is atypical in appearance or behavior, excision may be warranted to exclude other entities. Intestinal metaplasia, tuberculosis, melanoma, and lymphoma have been reported to coexist with or mimic urethral caruncles.94-98 There is a paucity of literature regarding optimal treatment of urethral caruncle. Most urologists recommend initial conservative management with topical estrogen or anti-inflammatory creams and sitz baths. Large or refractory lesions may be managed with simple excision. The tip of the lesions should be grasped and traction employed to fully expose the base of the caruncle. The lesion can then easily be excised. If a large defect remains, the mucosa may be reapproximated with absorbable suture. In most instances, the urethral mucosa heals around a Foley catheter, which may be left in place for several days. Classification of Urethral Diverticula Although not widely adopted, a classification system for urethral diverticula has been proposed by Leach and associaties.99 This staging system for urethral diverticula, called the L/N/S/C3 classification system, is similar to that used for cancer staging and is based on several characteristics of urethral diverticula, including location, number, size, anatomic configuration, site of commu-

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nication to the urethral lumen, and continence status of the patient. This system attempts to standardize description of urethral diverticula, but it has not been prospectively applied or validated by other investigators. Another proposed classification scheme uses the location of the urethral diverticula as the primary determinant of surgical approach, with distal lesions undergoing marsupialization and more proximal lesions undergoing excision and reconstruction.40 A classification system proposed by Leng and McGuire100 divides urethral diverticula into two categories based on the presence or absence of a preserved periurethral fascial layer. In some patients with urethral diverticula who have undergone prior vaginal or urethral surgery, the periurethral fascial layer may be deficient, resulting in a pseudodiverticulum. These investigators suggest that the recognition of this anatomic configuration has important implications for surgical reconstruction. Patients may require additional reconstruction or interposition of a tissue flap or graft to buttress the repair and prevent recurrence or postoperative urethrovaginal fistula formation.

SURGICAL REPAIR OF FEMALE URETHRAL DIVERTICULA Indications for Repair Although often highly symptomatic, not all urethral diverticula mandate surgical excision. Some patients may be asymptomatic at presentation, and the lesion is incidentally diagnosed on imaging for another condition or incidentally identified on routine physical examination. Other patients may be unwilling or medically unable to undergo surgical removal. Very little is known regarding the natural history of untreated urethral diverticula. Whether these lesions will progress in size, symptoms, or complexity with time is unknown. For these reasons and because of the lack of symptoms in selected cases, some patients may not desire surgical therapy. However, there are many reports in the literature of carcinomas arising in urethral diverticula,101-110 and it is possible that certain carcinomas arising in urethral diverticula are asymptomatic and may not be prospectively identified on radiologic imaging. Counseling and ongoing monitoring is necessary for patients who elect primary nonoperative management. Symptomatic patients, including those with dysuria, refractory and bothersome postvoid dribbling, recurrent urinary tract infections, dyspareunia, and pelvic pain in whom the symptoms can be attributed to the urethral diverticula, may be offered surgical excision. Those with urethral diverticula and symptomatic stress urinary incontinence can be considered for a concomitant anti-incontinence procedure at the time of urethral diverticular excision (discussed later). Techniques for Repair Alternative Techniques A variety of surgical interventions for urethral diverticula have been reported since 1805, when Hey1 described transvaginal incision of the urethral diverticula and packing of the resulting cavity with lint. Approaches have included transurethral20 and open111,112 marsupialization, endoscopic unroofing,113,114 fulguration,115 incision and obliteration with oxidized cellulose116 or polytetrafluoroethylene,117 coagulation,117 and excision with

Box 85-2 Principles of Transvaginal Urethral Diverticulectomy of a well-vascularized anterior vaginal wall • Mobilization flap (or flaps) of the periurethral fascia • Preservation cation and excision of the neck of the urethral • Identifi diverticulum or ostia entire urethral diverticulum wall or sac • Removal (mucosa) urethral closure • Watertight Multilayered, non-overlapping closure with absorbable • suture of dead space • Closure • Preservation or creation of continence

reconstruction. Most commonly, complete excision and reconstruction are performed as described subsequently. However, for distal lesions, a transvaginal marsupialization as described by Spence and Duckett111,118 and Roehrborn112 may reduce operative time, blood loss, and recurrence rate. During this procedure, care must be taken to avoid aggressively extending the incision proximally, which could result in vaginal voiding or potentially damage the proximal and distal sphincteric mechanism, resulting in stress urinary incontinence. This approach is probably applicable only to urethral diverticula in selected cases involving the distal one third of the urethra. It is not commonly performed. Excision and Reconstruction Excision and reconstruction is probably the most common surgical approach to urethral diverticula in the modern era. The principles of the urethral diverticulectomy operation have been well described (Box 85-2). There are a few issues about which some surgeons may disagree, including the type of vaginal incision (inverted U versus inverted T), whether it is necessary to remove the entire mucosalized portion of the lesion, and the optimal type of postoperative catheter drainage (urethra only versus urethra and suprapubic). These are, however, minor points, and they are addressed subsequently. Complex urethral reconstructive techniques for the repair urethral diverticula have been described. Fall119 described the use of a bipedicled vaginal wall flap for urethral reconstruction in patients with urethral diverticula and urethrovaginal fistula. Laterally based vaginal flaps have also been used as an initial approach to urethral diverticula.120,121 Complex anatomic configurations may exist, and many novel approaches have been described for complicated, anteriorly located or circumferential lesions.5,6,122 The technique described here is similar to that described by Leach and Raz42 and based on earlier work by Benjamin and colleagues123 and Busch and Carter.124 Preoperative Preparation Prophylactic antibiotics can be used for a period preoperatively to ensure sterile urine at the time of surgery. Patients can also be encouraged to strip the anterior vaginal wall after voiding, thereby consistently emptying the urethral diverticulum and preventing urinary stasis and recurrent urinary tract infections. This may not be possible in those with noncommunicating urethral diverticula or in those who have significant pain related to the urethral

Chapter 85 URETHRAL DIVERTICULA

diverticula. Application of topical estrogen creams for several weeks before surgery may be beneficial in some patients with postmenopausal atrophic vaginitis in improving the overall quality of the tissues with respect to dissection and mobilization. Preoperative parenteral antibiotics are often administered, especially for those with recurrent or persistent urinary tract infections. Patients with symptomatic stress urinary incontinence can be offered simultaneous anti-incontinence surgery. Preoperative video urodynamics may be helpful in evaluating the anatomy of the urethral diverticula, assessing the competence of the bladder neck, and confirming the diagnosis of stress urinary incontinence. In patients with stress urinary incontinence and urethral diverticula, Ganabathi and coworkers23 and Lockhart and associates125 have described excellent results with concomitant needle bladder neck suspension in these complex cases. Pubovaginal fascial slings have been used in patients with urethral diverticula and stress urinary incontinence with satisfactory outcomes.44,50,51 Further complicating these cases may be associated symptoms such as pain, dyspareunia, voiding dysfunction, urinary tract infections, and urinary incontinence. These associated symptoms often are improved or eliminated with surgical repair. The importance of appropriate preoperative patient counseling regarding surgery and postoperative expectations of cure cannot be overemphasized. Procedure The patient is placed in the lithotomy position with all pressure points well padded. The use of padded adjustable stirrups for the lower extremities greatly enhances operative access to the female perineum. A standard vaginal antiseptic preparation is applied. A weighted vaginal speculum and Scott retractor with hooks aid in exposure. A posterolateral episiotomy may be beneficial in some patients for additional exposure, although the mid-urethral (and therefore somewhat distal in the vaginal canal) location of most urethral diverticula usually precludes the need for this type of adjunctive procedure. A Foley catheter is placed through the urethra, and a suprapubic tube may be used for additional unobstructed postoperative urinary drainage. Often, a small-caliber urethral catheter is used during the case, and the placement of a suprapubic tube during the procedure ensures adequate postoperative urinary drainage. If desired, a suprapubic tube is placed at the start of the procedure using the Lowsley retractor or percutaneously under direct transurethral cystoscopic visual guidance. Placement of the suprapubic tube at the end of the case is not advisable because it requires traversing the fresh urethral suture line, which risks disruption of the repair. An inverted U is marked out along the anterior vaginal wall, with the base of the U at the level of the distal urethra and the limbs extending to the bladder neck or beyond (Fig. 85-15). Care is taken to ensure that the limbs of the U are progressively wider proximally (toward the bladder neck) to ensure adequate vascularity at the distal lateral margins of the anterior vaginal wall flap. Unlike the inverted-T-shaped incision, the inverted-U-shaped incision provides excellent exposure laterally at the level of the midvagina, and it can be extended proximally as needed for lesions that extend beyond the bladder neck. Injectable saline can be infused along the lines of the incision to facilitate dissection. An anterior vaginal wall flap is created by careful dissection in the potential space between the vaginal wall and the periurethral fascia. The use of sufficient countertraction during this portion

Figure 85-15 An inverted-U-shaped incision (dashed line) on the anterior vaginal wall. Retraction is aided by the use of Allis clamps and a ring retractor with hooks.

of the procedure is important in maintaining the proper plane of dissection. Care is taken to preserve the periurethral fascia and to avoid inadvertent entry into the urethral diverticula. A distinct layer of periurethral fascia is usually interposed between the vaginal wall and the urethral diverticula. Preservation and later reconstruction of this layer is important to prevent recurrence, close dead space, and avoid urethrovaginal fistula formation postoperatively. Pseudo-diverticula have been described where this layer of tissue is considerably attenuated or even absent.100 In these patients, an interpositional flap or graft such as a pubovaginal sling may be used for reconstruction. The periurethral fascia is incised transversely (Fig. 85-16). Proximal and distal layers of periurethral fascia are carefully developed avoiding entrance into the urethral diverticula. The urethral diverticula is then grasped and dissected back to its origin on the urethra within the leaves of the periurethral fascia (Fig. 85-17). In many cases, it is necessary to open the urethral diverticulum to facilitate dissection from the surrounding tissues. The ostium or connection to the urethra is identified, and the walls of the urethral diverticulum are completely removed. Every effort should be made to remove the entire mucosalized surface of the urethral diverticulum to prevent recurrence.23,65 This may involve removing small, adherent or inflamed portions of the urethral wall, especially in the ostial area (Fig. 85-18). All abnormal tissue in the area of the ostium should be removed if possible to ensure that no mucosal elements of the urethral diverticular wall remain, which can result in postoperative urine leakage and

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Figure 85-16 After reflection of the anterior vaginal wall, a transverse incision (dashed line) is made in the periurethral fascia.

Figure 85-17 The periurethral fascia is incised and dissected from the underlying urethral diverticulum.

recurrence. Elaborate methods of identifying the full extent of the urethral diverticular cavity have been described, including catheterization of the urethral diverticulum with urinary33,126 and Fogarty127 catheters, packing the urethral diverticulum with gauze,128 infusing and staining the urethral diverticulum with methylene blue,8 and the use of silicone129 or cryoprecipitate130 to create a solid mass and ease dissection. However, these measures are mostly of historical interest and are usually unnecessary in modern urethral diverticular surgery.23,39 The Foley catheter is usually seen after complete excision of a urethral diverticulum (Fig. 85-19). The urethra can be reconstructed over as small as a 12-Fr Foley catheter without long-term risk of urethral stricture,4 and it should be closed in a watertight fashion with absorbable suture (Fig. 85-20). The closure should be tension free. Uncommonly, a urethral diverticulum may extend circumferentially around the urethra and require segmental resection of the involved portion of the urethra and complex reconstruction.6,131 The periurethral fascial flaps are reapproximated with absorbable suture in a perpendicular orientation to the urethral closure line to minimize overlap and the risk of postoperative urethrovaginal fistula formation (Fig. 85-21). Care is taken to secure the periurethral fascial flaps to close all dead space. If desired, a fibrofatty labial (Martius) flap can be harvested at this point and placed over the periurethral fascia as an additional layer of closure.64 Indications for such a flap are not universally agreed on. However, in patients with poor-quality tissues

or attenuated periurethral fascia or in whom significant inflammation is encountered intraoperatively, a well-vascularized adjuvant flap (e.g., Martius flap) may reduce the risk of wound breakdown and subsequent complications such as urethrovaginal fistula. The anterior vaginal wall flap is then repositioned and reapproximated with absorbable suture (Fig. 85-22). This completes a three-layer closure (four layers if a Martius flap is used). An antibiotic-impregnated vaginal pack is placed. Postoperative Care Antibiotics are continued for 24 hours postoperatively. The vaginal packing is removed and the patient discharged home with closed urinary drainage. Antispasmodics are used liberally to reduce bladder spasms. Pericatheter VCUG is obtained at 14 to 21 days postoperatively. If there is no extravasation, the catheters are removed. If extravasation is seen, repeat pericatheter VCUG is performed weekly until resolution is documented. In most cases, extravasation resolves in several weeks with this type of conservative management.132 Complications Careful adherence to the principles of transvaginal urethral diverticulectomy should minimize postoperative complications. Nevertheless, complications may arise (Box 85-3). One small series suggested that large diverticula (>4 cm) or those associated with a lateral or horseshoe configuration may be associated with

Chapter 85 URETHRAL DIVERTICULA

Figure 85-18 The urethral diverticulum sac is freed from the periurethral fascia.

Figure 85-20 The urethra is closed with absorbable suture.

Box 85-3 Complications of Transvaginal Urethral Diverticulectomy Urinary incontinence (1.7-16.1)* Urethrovaginal fistula (0.9-8.3) Urethral stricture (0-5.2) Recurrent urethral diverticulum (1-25) Recurrent urinary tract infection (0-31.3) Other Hypospadias or distal urethral necrosis Bladder or ureteral injury Vaginal scarring or narrowing (e.g., dyspareunia) *The range of reported incidence (%) is given within parentheses. Adapted from Dmochowski R: Surgery for vesicovaginal fistula, urethrovaginal fistula, and urethral diverticulum. In Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds): Campbell’s Urology, 8th ed. Philadelphia, WB Saunders, 2002, p 1214.

Figure 85-19 The urethral catheter is seen after complete excision of the urethral diverticulum sac.

a greater likelihood of postoperative complications.133 Common complications include recurrent urinary tract infections, urinary incontinence, and recurrent urethral diverticula. Urethrovaginal fistula is a devastating complication of urethral diverticulectomy and deserves special mention. A fistula located beyond the sphincteric mechanism should not be associated with symptoms other than perhaps a split urinary stream and or vaginal voiding. As such, an asymptomatic distal urethrovaginal fistula may not require repair, although some patients may request repair. Conversely, a proximal fistula located at the

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Figure 85-21 The periurethral fascia is closed with care to obliterate any dead space.

bladder neck or at the mid-urethra in patients with an incompetent bladder neck will likely result in considerable symptomatic urinary leakage. These patients should undergo repair with the use of an adjuvant tissue flap such as a Martius flap to provide a well-vascularized additional tissue layer. The timing of the repair relative to the initial procedure is controversial. Meticulous attention to surgical technique, good hemostasis, avoidance of infection, preservation of the periurethral fascia (Fig. 85-23), a well-vascularized anterior vaginal wall flap, and multilayered closure with nonoverlapping suture lines should minimize the potential for postoperative urethrovaginal fistula formation. Persistence of Symptoms after Urethral Diverticulectomy Some patients have persistence or recurrence of their preoperative symptoms postoperatively. The finding of a urethral diverticulum after a presumably successful urethral diverticulectomy may occur as a result of a new medical problem (e.g., urinary tract infection), a new urethral diverticulum, or recurrence of the original lesion. A urethral diverticulum may recur because of incomplete removal of the urethral diverticulum, inadequate closure of the urethra or residual dead space, or other technical factors. Lee134 identified a recurrent urethral diverticulum in 8 of 85 patients at follow-up of between 2 and 15 years from resection of the initial urethral diverticulum.134 Repeat urethral diverticulectomy can be challenging due to altered anatomy, scarring, and the difficulty in identifying the proper anatomic planes.

Figure 85-22 The anterior vaginal wall flap is advanced over the periurethral suture line and secured with running, interlocking absorbable suture.

Urethral diverticulum (periurethral fascia opened and preserved, with excision of the epithelial lining of the diverticulum)

A

Urethral diverticulum excised (defect closed in periurethral fascia)

B Figure 85-23 Diagrams demonstrate the importance of preserving and reconstructing the periurethral fascia. A, Defect in the periurethral fascia after removal of the epithelial lining of the urethral diverticulum. B, Closure of the urethra and periurethral fascia.

Chapter 85 URETHRAL DIVERTICULA

Urethral Diverticula and Associated Conditions Malignant and benign tumors may be found in urethral diverticula. Both are rare, and fewer than 100 cases of carcinoma within urethral diverticula have been reported in the English language literature.106 The most common malignant pathology in urethral diverticula is adenocarcinoma, followed by transitional cell and squamous cell carcinomas.106 This contrasts with primary urethral carcinoma, in which the primary histologic type is squamous cell carcinoma. Some investigators have suggested that urethral diverticulum is associated with the development of urethral adenocarcinoma in women.135 If this is true, nonexcisional therapy of urethral diverticula, such as marsupialization or endoscopic incision, should always be combined with a biopsy to rule out malignancy.136 There is no consensus on proper treatment in these cases, and recurrence rates are high with local treatment alone.106 The incidental finding of malignancy can be particularly troubling when found intraoperatively or on the postoperative pathology report. It has not been conclusively demonstrated that any particular preoperative imaging modality such as ultrasound or MRI can reliably and prospectively diagnose a small malignancy arising in a urethral diverticula. When considering curative therapy, it is unclear whether extensive surgery, including cystourethrectomy with or without adjuvant external beam radiotherapy, is superior to local excision followed by radiotherapy.104 Many benign lesions, including nephrogenic adenoma and endometriosis, have been described within urethral diverticula.137-140 Pathologically, nephrogenic adenoma can be difficult to differentiate from adenocarcinoma. Calculi within urethral diverticula may be diagnosed in 4% to 10% of cases,44,141,142 and they are most likely caused by urinary stasis or infection. This may be suspected by physical examination findings or found incidentally on imaging evaluation. The presence of a stone does not significantly alter the evaluation or surgical approach, and it can be considered an incidental finding (Fig. 85-24). Urethral diverticula have manifested during pregnancy. Moran143 reported four cases of urethral diverticula diagnosed during pregnancy. Conservative treatment included antibiotics and aspiration or incision and drainage. Two women delivered vaginally, and the other two delivered by cesarean section for unrelated reasons. In one patient, drainage was performed during labor to facilitate delivery. Three of the four women had definitive repair performed after delivery. It is not known whether pregnancy is associated with formation of urethral diverticula, although patients may be more likely to become symptomatic during this period. Usually, conservative management with antibiotics may be desirable until after delivery to avoid precipitating premature labor, although successful surgical treatment during pregnancy has been reported.144

A

B Figure 85-24 Large calculus within a urethral diverticulum. A, Voiding cystourethrographic scout film demonstrates a midline, calcified density overlying the symphysis pubis. B, Voiding image shows filling of the urethra and a cavity adjacent to the urethra surrounding the calcification, confirming that this represents a stone in a urethral diverticulum.

References 1. Hey W: Practical Observations in Surgery. Philadelphia, James Humphries, 1805, pp 304-305. 2. Davis HJ, Cian LG: Positive pressure urethrography: A new diagnostic method. J Urol 68:611-616, 1952. 3. Davis HJ, TeLinde RW: Urethral Diverticula: An assay of 121 cases. J Urol 80:34-39, 1958.

4. Young GPH, Wahle GR, Raz S: Female urethral diverticulum. In Raz S (ed): Female Urology. Philadelphia, WB Saunders, 1996, pp 477-489. 5. Vakili B, Wai C, Nihira M: Anterior urethral diverticulum in the female: Diagnosis and surgical approach. Obstet Gynecol 102:11791183, 2003.

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6. Rovner ES, Wein AJ: Diagnosis and reconstruction of the dorsal or circumferential urethral diverticulum. J Urol 170:82-86, 2003. 7. Johnson CM: Diverticula and cyst of the female urethra. J Urol 39:506-516, 1938. 8. Gilbert CR, Rivera Cintron FJ: Urethral diverticula in the female: Review of the subject and introduction of a different surgical approach. Am J Obstet Gynecol 67:616-627, 1954. 9. Pinkerton JH: Urethral diverticula in women. Br Med J 5366:12041205, 1963. 10. Glassman TA, Weinerth JL, Glenn JF: Neonatal female urethral diverticulum. Urology 5:249-251, 1975. 11. Marshall S: Urethral diverticula in young girls. Urology 17:243-245, 1981. 12. Kaneti J, Sober I, Bar-Ziv J, et al: Congenital anterior urethral diverticulum. Eur Urol 10:48-52, 1984. 13. Kirks DR, Grossman H: Congenital saccular anterior urethral diverticulum. Radiology 140:367-372, 1981. 14. Lau JT, Ong GB: Congenital diverticulum of the anterior urethra. Aust N Z J Surg 51:305-306, 1981. 15. Kimbrough HM Jr, Vaughan ED Jr: Skene’s duct cyst in a newborn: Case report and review of the literature. J Urol 117:387-388, 1977. 16. Lee NH, Kim SY: Skene’s duct cysts in female newborns. J Pediatr Surg 27:15-17, 1992. 17. Boyd S, Raz S: Ectopic ureter presenting in midline urethral diverticulum. Urology 41:571-574, 1993. 18. Silk MR, Lebowitz JM: Anterior urethral diverticulum. J Urol 101:66-67, 1969. 19. Vanhoutte JJ: Ureteral ectopia into a Wolffian duct remnant presenting as a urethral diverticulum in two girls. Am J Roentgenol Radium Ther Nucl Med 110:540-545, 1970. 20. Davis BL, Robinson DG: Diverticula of the female urethra: Assay of 120 cases. J Urol 104:850-853, 1970. 21. Davis HJ, TeLinde RW: Urethral Diverticula: An assay of 121 cases. J Urol 80:34-39, 1958. 22. McNally A: Diverticula of the female urethra. Am J Surg 28:177, 1935. 23. Ganabathi K, Leach GE, Zimmern PE, et al: Experience with the management of urethral diverticulum in 63 women. J Urol 152:1445-1452, 1994. 24. Lee RA: Diverticulum of the urethra: Clinical presentation, diagnosis, and management. Clin Obstet Gynecol 27:490-498, 1984. 25. Klyszejko C, Ilnicki W, Klyszejko D, et al: Development of a urethral diverticulum after forceps delivery. Ginekol Pol 56:766-769, 1985. 26. Clemens JQ, Bushman W: Urethral diverticulum following transurethral collagen injection. J Urol 166:626, 2001. 27. Huffman JW: The detailed anatomy of the paraurethral ducts in the adult human female. Am J Obstet Gynecol 55:86, 1948. 28. Lang ED, Davis HJ: Positive pressure urethrography: A roentgenographic diagnostic method for urethral diverticula in the female. Radiology 72:410, 1959. 29. MacKinnon M, Pratt JH, Pool T: Diverticulum of the female urethra. Surg Clin North Am 39:953-962, 1959. 30. Peters W III, Vaughan ED Jr: Urethral diverticulum in the female. Etiologic factors and postoperative results. Obstet Gynecol 47:549552, 1976. 31. Routh A: Urethral diverticula. BMJ 1:361-362, 1890. 32. Daneshgari F, Zimmern PE, Jacomides L: Magnetic resonance imaging detection of symptomatic noncommunicating intraurethral wall diverticula in women. J Urol 161:1259-1261, 1999. 33. Moore TD: Diverticulum of the female urethra. An improved technique of surgical excision. J Urol 68:611-616, 1952. 34. Bruning EJ: Die Pathologie der weiblichen Urethra und des Parurethrium. Stuttgart, Enke, 1959. 35. Andersen MJ: The incidence of diverticula in the female urethra. J Urol 98:96-98, 1967.

36. Aldridge CW Jr, Beaton JH, Nanzig RP: A review of office urethroscopy and cystometry. Am J Obstet Gynecol 131:432-437, 1978. 37. Stewart M, Bretland PM, Stidolph NE: Urethral diverticula in the adult female. Br J Urol 53:353-359, 1981. 38. Lorenzo AJ, Zimmern P, Lemack GE, et al: Endorectal coil magnetic resonance imaging for diagnosis of urethral and periurethral pathologic findings in women. Urology 61:1129-1133, 2003. 39. Leach GE, Bavendam TG: Female urethral diverticula. Urology 30:407-415, 1987. 40. Ginsburg D, Genadry R: Suburethral diverticulum: Classification and therapeutic considerations. Obstet Gynecol 61:685-688, 1983. 41. Pathak UN, House MJ: Diverticulum of the female urethra. Obstet Gynecol 36:789-794, 1970. 42. Leach GE, Schmidbauer CP, Hadley HR, et al: Surgical treatment of female urethral diverticulum. Semin Urol 4:33-42, 1986. 43. Nielsen VM, Nielsen KK, Vedel P: Spontaneous rupture of a diverticulum of the female urethra presenting with a fistula to the vagina. Acta Obstet Gynecol Scand 66:87-88, 1987. 44. Romanzi LJ, Groutz A, Blaivas JG: Urethral diverticulum in women: Diverse presentations resulting in diagnostic delay and mismanagement. J Urol 164:428-433, 2000. 45. Hoffman MJ, Adams WE: Recognition and repair of urethral diverticula: A report of 60 cases. Am J Obstet Gynecol 92:106-111, 1965. 46. Reid RE, Gill B, Laor E, et al: Role of urodynamics in management of urethral diverticulum in females. Urology 28:342-346, 1986. 47. Summitt RL Jr, Stovall TG: Urethral diverticula: Evaluation by urethral pressure profilometry, cystourethroscopy, and the voiding cystourethrogram. Obstet Gynecol 80:695-699, 1992. 48. Bhatia NN, McCarthy TA, Ostergard DR: Urethral pressure profiles of women with urethral diverticula. Obstet Gynecol 58:375378, 1981. 49. Bass JS, Leach GE: Surgical treatment of concomitant urethral diverticulum and stress urinary incontinence. Urol Clin North Am 18:365-373, 1991. 50. Faerber GJ: Urethral diverticulectomy and pubovaginal sling for simultaneous treatment of urethral diverticulum and intrinsic sphincter deficiency. Tech Urol 4:192-197, 1998. 51. Swierzewski SJ III, McGuire EJ: Pubovaginal sling for treatment of female stress urinary incontinence complicated by urethral diverticulum. J Urol 149:1012-1014, 1993. 52. Bradley CS, Rovner ES: Urodynamically defined stress urinary incontinence and bladder outlet obstruction can coexist in women. J Urol 171:757-761, 2004. 53. Wagner U, Debus-Thiede G, Christ F: Significance of the urethral pressure profile in the diagnosis of urethral diverticulum [in German]. Geburtshilfe Frauenheilkd 46:456-458, 1986. 54. Greenberg M, Stone D, Cochran ST, et al: Female urethral diverticula: Double-balloon catheter study. AJR Am J Roentgenol 136:259-264, 1981. 55. Jacoby K, Rowbotham RK: Double balloon positive pressure urethrography is a more sensitive test than voiding cystourethrography for diagnosing urethral diverticulum in women. J Urol 162:2066-2069, 1999. 56. Stern AJ, Patel SK: Diverticulum of the female urethra. The value of the post-void bladder film during excretory urography. Radiology 121:222, 1976. 57. Goldfarb S, Mieza M, Leiter E: Postvoid film of intravenous pyelogram in diagnosis of urethral diverticulum. Urology 17:390-392, 1981. 58. Houser LM, Von Eschenbach AC: Diverticula of female urethra. Diagnostic importance of postvoiding film. Urology 3:453-455, 1974. 59. Golomb J, Leibovitch I, Mor Y, et al: Comparison of voiding cystourethrography and double-balloon urethrography in the diagnosis of complex female urethral diverticula. Eur Radiol 13:536-542, 2003.

Chapter 85 URETHRAL DIVERTICULA

60. Wang AC, Wang CR: Radiologic diagnosis and surgical treatment of urethral diverticulum in women. A reappraisal of voiding cystourethrography and positive pressure urethrography. J Reprod Med 45:377-382, 2000. 61. Blacklock ARE, Shaw RE, Geddes JR: Late presentation of ectopic ureter. Br J Urol 54:106-110, 1982. 62. Baert L, Willemen P, Oyen R: Endovaginal sonography: New diagnostic approach for urethral diverticula. J Urol 147:464-466, 1992. 63. Chancellor MB, Liu JB, Rivas DA, et al: Intraoperative endoluminal ultrasound evaluation of urethral diverticula. J Urol 153:72-75, 1995. 64. Dmochowski R: Urethral diverticula: Evolving diagnostics and improved surgical management. Curr Urol Rep 2:373-378, 2001. 65. Fortunato P, Schettini M, Gallucci M: Diagnosis and therapy of the female urethral diverticula. Int Urogynecol J 12:51-57, 2001. 66. Gerrard ER Jr, Lloyd LK, Kubricht WS, et al: Transvaginal ultrasound for the diagnosis of urethral diverticulum. J Urol 169:13951397, 2003. 67. Lee DI, Bagley DH, Liu JB: Experience with endoluminal ultrasonography in the urinary tract. J Endourol 15:67-74, 2001. 68. Martensson O, Duchek M: Translabial ultrasonography with pulsed colour-Doppler in the diagnosis of female urethral diverticula. Scand J Urol Nephrol 28:101-104, 1994. 69. Vargas-Serrano B, Cortina-Moreno B, Rodriguez-Romero R, et al: Transrectal ultrasonography in the diagnosis of urethral diverticula in women. J Clin Ultrasound 25:21-28, 1997. 70. Wexler JS, McGovern TP: Ultrasonography of female urethral diverticula. AJR Am J Roentgenol 134:737-740, 1980. 71. Lee TG, Keller FS: Urethral diverticulum: Diagnosis by ultrasound. AJR Am.J.Roentgenol 128:690-691, 1977. 72. Hricak H, Secaf E, Buckley DW, et al: Female urethra: MR imaging. Radiology 178:527-535, 1991. 73. Kim B, Hricak H, Tanagho EA: Diagnosis of urethral diverticula in women: Value of MR imaging. AJR Am J Roentgenol 161:809-815, 1993. 74. Blander DS, Rovner ES, Schnall MD, et al: Endoluminal magnetic resonance imaging in the evaluation of urethral diverticula in women. Urology 57:660-665, 2001. 75. Siegelman ES, Banner MP, Ramchandani P, et al: Multicoil MR imaging of symptomatic female urethral and periurethral disease. Radiographics 17:349-365, 1997. 76. Kim B, Hricak H, Tanagho EA: Diagnosis of urethral diverticula in women: Value of MR imaging. AJR Am J Roentgenol 161:809-815, 1993. 77. Neitlich JD, Foster HE Jr, Glickman MG, et al: Detection of urethral diverticula in women: Comparison of a high resolution fast spin echo technique with double balloon urethrography. J Urol 159:408-410, 1998. 78. Young SB, Rose PG, Reuter KL: Vaginal fibromyomata: two cases with preoperative assessment, resection, and reconstruction. Obstet Gynecol 78:972-974, 1991. 79. Blaivas JG, Flisser AJ, Bleustein CB, et al: Periurethral masses: Etiology and diagnosis in a large series of women. Obstet Gynecol 103:842-847, 2004. 80. Shirvani AR, Winters JC: Vaginal leiomyoma presenting as a urethral diverticulum. J Urol 163:1869, 2000. 81. Liu MM: Fibromyoma of the vagina. Eur J Obstet Gynecol Reprod Biol 29:321-328, 1988. 82. Dodson MK, Cliby WA, Keeney GL, et al: Skene’s gland adenocarcinoma with increased serum level of prostate-specific antigen. Gynecol Oncol 55:304-307, 1994. 83. Currarino G: Single vaginal ectopic ureter and Gartner’s duct cyst with ipsilateral renal hypoplasia and dysplasia (or agenesis). J Urol 128:988-993, 1982. 84. Gadbois WF, Duckett JW Jr: Gartner’s duct cyst and ipsilateral renal agenesis. Urology 4:720-721, 1974.

85. Eilber KS, Raz S: Benign cystic lesions of the vagina: A literature review. J Urol 170:717-722, 2003. 86. Sheih CP, Li YW, Liao YJ, et al: Diagnosing the combination of renal dysgenesis, Gartner’s duct cyst and ipsilateral mullerian duct obstruction. J Urol 159:217-221, 1998. 87. Abd-Rabbo MS, Atta MA: Aspiration and tetracycline sclerotherapy: A novel method for management of vaginal and vulval Gartner cysts. Int J Gynaecol Obst 35:235-237, 1991. 88. Deppisch LM: Cysts of the vagina: Classification and clinical correlations. Obstet Gynecol 45:632-637, 1975. 89. Pradhan S, Tobon H: Vaginal cysts: A clinicopathological study of 41 cases. Int J Gynecol Pathol 5:35-46, 1986. 90. Fernandes ET, Dekermacher S, Sabadin MA, et al: Urethral prolapse in children. Urology 41:240-242, 1993. 91. Rudin JE, Geldt VG, Alecseev EB: Prolapse of urethral mucosa in white female children: Experience with 58 cases. J Pediatr Surg 32:423-425, 1997. 92. Lowe FC, Hill GS, Jeffs RD, et al: Urethral prolapse in children: insights into etiology and management. J Urol 135:100-103, 1986. 93. Jerkins GR, Verheeck K, Noe HN: Treatment of girls with urethral prolapse. J Urol 132:732-733, 1984. 94. Atalay AC, Karaman MI, Basak T, et al: Non-Hodgkin’s lymphoma of the female urethra presenting as a caruncle. Int Urol Nephrol 30:609-610, 1998. 95. Indudhara R, Vaidyanathan S, Radotra BD: Urethral tuberculosis. Urol Int 48:436-438, 1992. 96. Khatib RA, Khalil AM, Tawil AN, et al: Non-Hodgkin’s lymphoma presenting as a urethral caruncle. Gynecol Oncol 50:389-393, 1993. 97. Lopez JI, Angulo JC, Ibanez T: Primary malignant melanoma mimicking urethral caruncle: Case report. Scand J Urol Nephrol 27:125126, 1993. 98. Willett GD, Lack EE: Periurethral colonic-type polyp simulating urethral caruncle: A case report. J Reprod Med 35:1017-1018, 1990. 99. Leach GE, Sirls LT, Ganabathi K, et al: L N S C3: A proposed classification system for female urethral diverticula. Neurourol Urodyn 12:523-531, 1993. 100. Leng WW, McGuire EJ: Management of female urethral diverticula: A new classification. J Urol 160:1297-1300, 1998. 101. Gonzalez MO, Harrison ML, Boileau MA: Carcinoma in diverticulum of female urethra. Urology 26:328-332, 1985. 102. Hickey N, Murphy J, Herschorn S: Carcinoma in a urethral diverticulum: Magnetic resonance imaging and sonographic appearance. Urology 55:588-589, 2000. 103. Marshall S, Hirsch K: Carcinoma within urethral diverticula. Urology 10:161-163, 1977. 104. Patanaphan V, Prempree T, Sewchand W, et al: Adenocarcinoma arising in female urethral diverticulum. Urology 22:259-264, 1983. 105. Prudente DT, Dias Montellato NI, Arap S, et al: Carcinoma in diverticulum of female urethra. Urol Int 33:393-398, 1978. 106. Rajan N, Tucci P, Mallouh C, et al: Carcinoma in female urethral diverticulum: Case reports and review of management. J Urol 150:1911-1914, 1993. 107. Seballos RM, Rich RR: Clear cell adenocarcinoma arising from a urethral diverticulum. J Urol 153:1914-1915, 1995. 108. Tesluk H: Primary adenocarcinoma of female urethra associated with diverticula. Urology 17:197-199, 1981. 109. Thomas RB, Maguire B: Adenocarcinoma in a female urethral diverticulum. Aust N Z J Surg 61:869-871, 1991. 110. Tines SC, Bigongiari LR, Weigel JW: Carcinoma in diverticulum of the female urethra. AJR Am J Roentgenol 138:582-585, 1982. 111. Spence HM, Duckett JW Jr: Diverticulum of the female urethra: Clinical aspects and presentation of a simple operative technique for cure. J Urol 104:432-437, 1970.

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112. Roehrborn CG: Long term follow-up study of the marsupialization technique for urethral diverticula in women. Surg Gynecol Obstet 167:191-196, 1988. 113. Lapides J: Transurethral treatment of urethral diverticula in women. Trans Am Assoc Genitourin Surg 70:135-137, 1978. 114. Spencer WF, Streem SB: Diverticulum of the female urethral roof managed endoscopically. J Urol 138:147-148, 1987. 115. Saito S: Usefulness of diagnosis by the urethroscopy under anesthesia and effect of transurethral electrocoagulation in symptomatic female urethral diverticula. J Endourol 14:455-457, 2000. 116. Ellick M: Diverticulum of the female urethra: A new method of ablation. J Urol 77:243-246, 1957. 117. Mizrahi S, Bitterman W: Transvaginal, periurethral injection of polytetrafluoroethylene (polytef) in the treatment of urethral diverticula. Br J Urol 62:280, 1988. 118. Spence HM, Duckett JW Jr: Motion picture: simple operation for cure of diverticula of female urethra. Trans Am Assoc Genitourin Surg 61:78-79, 1969. 119. Fall M: Vaginal wall bipedicled flap and other techniques in complicated urethral diverticlum and urethrovaginal fistula. J Am Coll Surg 180:150-156, 1995. 120. Appell RA, Suarez BC: Experience with a laterally based vaginal flap approach for urethral diverticulum. J Urol 127:677-678, 1982. 121. Woodhouse CR, Flynn JT, Molland EA, Blandy JP: Urethral diverticulum in females. Br J Urol 52:305-310, 1980. 122. Clyne OJ, Flood HD: Giant urethral diverticulum: A novel approach to repair. J Urol 167:1796, 2002. 123. Benjamin J, Elliott L, Cooper JF, et al: Urethral diverticulum in adult female. Clinical aspects, operative procedure, and pathology. Urology 3:1-7, 1974. 124. Busch FM, Carter FH: Vaginal flap incision for urethral diverticula. Paper presented at the Western Section Meeting, American Urological Association, Honolulu, June 29, 1973. 125. Lockhart JL, Ellis GF, Helal M, et al: Combined cystourethropexy for the treatment of type 3 and complicated female urinary incontinence. J Urol 143:722-725, 1990. 126. Kohorn EI, Glickman MG: Technical aids in investigation and management of urethral diverticula in the female. Urology 40:322325, 1992. 127. Wear JB: Urethral diverticulectomy in females. Urol Times 4:2-3, 1976. 128. Hyams JA, Hyams MN: A new operative procedure for the treatment of diverticulum of the female urethra. J Urol 43:573-577, 1939. 129. Hirschhorn RC: A new surgical technique for removal of urethral diverticula in the female patient. J Urol 92:206-209, 1964. 130. Feldstein MS: Cryoprecipitate coagulum as an adjunct to surgery for diverticula of the female urethra. J Urol 126:698-699, 1981.

131. Tamada S, Iwai Y, Tanimoto Y, et al: Urethral diverticula surrounding the urethra in women: report of 2 cases [in Japanese]. Hinyokika Kiyo 46:639-642, 2000. 132. Schwab CW, Rovner ES: Utility of radiologic imaging and prolonged catheterization following complex lower urinary tract reconstruction. Paper presented at the Mid-Atlantic AUA sectional meeting, Boca Raton, FL, October 26, 2003. 133. Porpiglia F, Destefanis P, Fiori C, et al: Preoperative risk factors for surgery female urethral diverticula: Our experience. Urol Int 69:711, 2002. 134. Lee RA: Diverticulum of the female urethra: Postoperative complications and results. Obstet Gynecol 61:52-58, 1983. 135. Oliva E, Young RH: Clear cell adenocarcinoma of the urethra: A clinicopathologic analysis of 19 cases. Mod Pathol 9:513-520, 1996. 136. McLoughlin MG: Carcinoma in situ in urethral diverticulum: Pitfalls of marsupialization alone. Urology 6:343, 1975. 137. Paik SS, Lee JD: Nephrogenic adenoma arising in an urethral diverticulum. Br J Urol 80:150, 1997. 138. Palagiri A: Urethral Diverticulum with endometriosis. Urology 11:271-272, 1978. 139. Peterson LJ, Matsumoto LM: Nephrogenic adenoma in urethral diverticulum. Urology 11:193-195, 1978. 140. Piazza R, Aragona F, Pizzarella M, et al: Nephrogenic adenoma in urethral diverticulum: An unusual finding. Urol Int 42:69-70, 1987. 141. Ward JN, Draper JW, Tovell HM: Diagnosis and treatment of urethral diverticula in the female. Surg Gynecol Obstet 125:12931300, 1967. 142. Ginesin Y, Bolkier M, Nachmias J, et al: Primary giant calculus in urethral diverticulum. Urol Int 43:47-48, 1988. 143. Moran PA, Carey MP, Dwyer PL: Urethral diverticula in pregnancy. Aust N Z J Obstet Gynaecol 38:102-106, 1998. 144. Wittich AC: Excision of urethral diverticulum calculi in a pregnant patient on an outpatient basis. J Am Osteopath Assoc 97:461-462, 1997. 145. Westney OL, Leng WW, McGuire EJ: The diagnosis and treatment of female urethral diverticulum. In Ball TP Jr (ed): AUA Update Series, vol 20. Houston, TX, AUA Office of Education, 2001, pp 290-295. 146. Pavlica P, Viglietta G, Losinno F, et al: I diverticoli dell’uretra femminile: Studio radiologico ed ecografico. Radiol Med 75:521527, 1988. 147. Kim B, Hricak H, Tanagho EA: Diagnosis of urethral diverticula in women: Value of MR imaging. AJR Am J Roentgenol 161:809-815, 1993. 148. Dmochowski R: Surgery for vesicovaginal fistula, urethrovaginal fistula, and urethral diverticulum. In Walsh PC, Retik AB, Vaughan ED Jr, et al (eds): Campbell’s Urology, vol 8. Philadelphia, WB Saunders, 2002.

Chapter 86

URINARY TRACT INFECTIONS IN WOMEN Amanda M. Macejko and Anthony J. Schaeffer EPIDEMIOLOGY Urinary tract infections (UTIs) are the most common bacterial infections and account for a substantial number of office and emergency room visits as well as hospital admissions each year. Additionally, UTI is the most common cause of nosocomial infection.1 The morbidity of UTIs varies widely, from self-limited to life-threatening conditions. The focus of this chapter is on UTI in women, who make up a significant proportion of UTI sufferers. The annual incidence among women is 12.1%. Peak incidence in women occurs between the ages of 20 to 24 years.2 Health care costs attributed to UTIs are substantial. The estimated overall costs of UTI among ambulatory women in the United States exceeds $1 billion annually.3 Pathogenesis The interaction between bacterial virulence and host defense factors can ultimately result in UTI. More virulent bacteria are necessary to infect healthy hosts with a normal urinary tract, whereas less virulent bacteria may easily infect compromised hosts. Laboratory studies of uropathogenic strains of Escherichia coli (UPEC) have helped to obtain a better understanding of the pathogenesis of UTIs. The initial step is bacterial adherence to the urothelium. Type 1 pili are filamentous adhesive organelles encoded by almost all UPEC, and they are significant virulence factors associated with UTIs. FimH is an adhesin molecule at the tip of type 1 pili that specifically binds to the luminal surface of the bladder.4 Bacterial colonization then precipitates a host inflammatory response, which includes neutrophil influx followed by apoptosis and exfoliation of the bladder’s epithelial cells in an effort to rid the bladder of bacteria. Despite the host’s response, however, high titers of UPEC persist in the bladder for several days.5

How are the bacteria able to elude the host defenses? Recent research has shown that UPEC avoids clearance by invading and replicating within the epithelial cells. They form “bacterial factories” that are refuges in which bacteria may persist and form biofilms. Bacteria within a biofilm are resistant not only to host defenses but also to typical courses of antimicrobials.5 These bacteria may subsequently reemerge and cause recurrent acute infections.6 Historically, the vagina and intestine have been accepted as UPEC reservoirs; however, this new paradigm demonstrates that the bladder itself may be a reservoir for UPEC. Host Factors Host factors include genetic, anatomic, functional, and behavioral factors that affect the host’s susceptibility to uropathogens and its ability to overcome them (Table 86-1). Vaginal Colonization In order for a UTI to occur, the infecting organism must first obtain access to the urinary tract. In the 1960s, Stamey hypothesized that bacteria that cause UTIs originate in the rectal flora and colonize the vaginal and urethral mucosa before ascending to the bladder.7 Vaginal colonization has proved to be a crucial step in the pathogenesis of UTI. Many factors that increase the risk of UTI do so by facilitating vaginal colonization with uropathogens.8 Women (in comparison to men) are particularly at risk based simply on differences in anatomy. Women have a moist periurethral space, a shorter distance between the anus and urethral opening, and a shorter urethra. These factors increase exposure to uropathogens and enhance the ability of these pathogens to colonize the urinary tract.2 Why are some women more susceptible to vaginal colonization, and therefore recurrent UTI, than others? There is substantial evidence that vaginal colonization is determined by genetic factors. In 1977, Fowler and Stamey discovered that E. coli

Table 86-1 Host Factors Genetic

Anatomic/Functional

Behavioral

Blood group antigen Nonsecretor status Density of adhesin receptors Maternal history of UTI

Congenital abnormalities Urinary obstruction Urinary incontinence Calculi Residual urine Catheters or foreign bodies Atrophic vaginitis

Sexual activity Diaphragm use Spermicide use Antimicrobial use

UTI, urinary tract infection. Modified from Ronald A: The etiology of urinary tract infection: Traditional and emerging pathogens. Am J Med 113(Suppl 1A):14S-9S, 2002.

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adhered more avidly to vaginal epithelial cells of women with recurrent UTI.9 Follow-up studies by Schaeffer showed that high vaginal cell receptivity was correlated with high buccal cell receptivity, suggesting that epithelial cell receptivity is actually a genotypic trait.10 The concept of hereditary susceptibility was further investigated by Schaeffer and associates, who demonstrated that the prevalence of the human leukocyte antigen (HLA) A3 subtype was greater in women with recurrent UTIs.11 In addition, carbohydrate structures bound to cell membranes known as blood group antigens make up a significant component of the uroepithelial cell membrane. Certain blood group antigens have been associated with susceptibility to UTI. Sheinfeld and colleagues determined that women with Lewis blood group Le(a−b−) or Le(a+b−) (nonsecretor) had a significantly higher incidence of recurrent UTIs than women with the Le(a−b+) (secretor) phenotype.12 E. coli bind to mannose residues, which are more available in nonsecretor mucosa.13 Sexual Activity Vaginal and oral intercourse help to propagate potential pathogens into the vagina and urinary tract. Additionally, vaginal intercourse may cause trauma of the vaginal epithelium, rendering it more susceptible to bacterial adherence and vaginal colonization.14 Several studies have linked sexual activity with vaginal colonization and UTI. Foxman and colleagues found that vaginal colonization with E. coli was inversely associated with the number of days since sexual activity.15 Hooton and coworkers reported that urine cultures in the immediate postcoital period show a transient bacteriuria.16 It has been proposed that voiding immediately after intercourse is protective, although there are no current data that support this conjecture.1 Spermicide and Diaphragm Use Spermicide and diaphragm use has been found to greatly increase the risk of vaginal colonization with uropathogens and UTI, independent of sexual activity. Nonoxynol-9, the active ingredient in most spermicides, has a bactericidal effect on the normal vaginal flora and therefore enhances the growth of E. coli.2,8 Estrogen Estrogen withdrawal in postmenopausal women alters the normal vaginal flora. In a randomized, double-blind, placebo-controlled trial of postmenopausal women with recurrent UTI, Raz and Stamm found that topically applied intravaginal estriol cream lowered the vaginal pH, restored lactobacilli in 61% of vaginal cultures, and reduced the incidence of UTI 10-fold. He concluded that intravaginal estrogen replacement restores an acidic environment that is more hospitable to premenopausal flora.17 However, these results have not been replicated in studies evaluating oral estrogens. Cardozo and associates evaluated the effects of low-dose, oral estrogen replacement but were unable to establish a significant protective effect.18 Recent Antimicrobial Use Another factor that contributes to UTI susceptibility is recent antimicrobial use. Smith and coworkers, in a prospective study, found that antimicrobial use up to 4 weeks before the onset of a UTI increased the relative risk for that UTI by 2.57 to 5.83 times. It has been proposed that recent antimicrobial use increases a woman’s risk of UTI by altering the normal urogenital flora.19 The most offending antimicrobials are β-lactams, whereas tri-

methoprim and nitrofurantoin seem to have much less of an effect on the normal vaginal flora.8

DIAGNOSTIC TOOLS History A thorough history is an essential component of obtaining the proper diagnosis. It is important to clarify the onset and the presence or absence of symptoms including dysuria, urinary frequency, hematuria, suprapubic tenderness, flank pain, fever, and nausea/vomiting. Has the patient had previous UTIs as a child or as an adult? If so, were her previous UTIs associated with fever? A complete medical and surgical history is also important. Does the patient have a history of nephrolithiasis or previous urinary tract surgery? Is the patient pregnant? Does the patient diabetic? The answers to these questions will direct further workup and management. Physical Examination The physical examination is not considered diagnostic of UTI but can be helpful in certain cases. The findings may assist in differentiating between lower urinary tract (cystitis) and upper urinary tract (pyelonephritis) infection. Is the patient febrile? Is there costovertebral tenderness? Findings such as a urethral diverticulum may occasionally reveal a potential source of recurrent UTI. The physical examination may also help to rule out other causes of patient symptomatology. For example, the presence of vaginal discharge has a strong association with vaginal infection rather than a UTI.20 Urinalysis Women should provide a midstream voided urine for analysis after spreading the labia and wiping from front to back with a clean sponge.7 The urinalysis provides information about pyuria, bacteriuria, and hematuria. Urine dipstick analysis is a quick and inexpensive test that is often used in the clinical setting. Testing for leukocyte esterase, an enzyme produced by polymorphonuclear cells, and nitrite, a byproduct of bacterial growth, it provides an indirect measurement of both pyuria and bacteriuria.21 If either the nitrite assay or the leukocyte esterase test is positive, the dipstick test has a sensitivity of 75% and a specificity of 82%.22 False-negative results can occur when the infecting organism does not produce nitrites.23 It is important to note that, although the dipstick test can be useful for screening, it is not as sensitive as microscopic examination.7 Pyuria on microscopic examination has a high sensitivity (95%) and a relatively low specificity (71%).24 The presence of bacteria on microscopic examination has a lower sensitivity (40% to 50%) yet a higher specificity (85% to 95%).24 Urine Culture The Infectious Diseases Society of America (ISDA) defines cystitis as greater than or equal to 105 cfu/mL of midstream urine. However, studies by Stamm and Hooton demonstrated that greater than or equal to 102 cfu/mL for a catheterized urine specimen in a symptomatic patient is significant.25 It is not necessary

Chapter 86 URINARY TRACT INFECTIONS IN WOMEN

to obtain a urine culture in all patients. Appropriate patient selection for urine culture is addressed in a later section. Imaging Techniques Multiple radiographic techniques are available for imaging the urinary tract. Plain abdominal films may demonstrate radiopaque calculi. Intravenous pyelography, although not typically used in the setting of UTI, can be useful to determine the site of an obstruction.7 Renal ultrasonography may demonstrate stone, hydronephrosis, or perirenal abscess. Advantages of ultrasound are that it does not expose the patient to radiation or contrast material; however, ultrasound results are dependent on operator experience.7 Computed tomography (CT) and magnetic resonance imaging (MRI) demonstrate excellent anatomic detail and are more sensitive than intravenous pyelography and ultrasonography.7 Although numerous imaging techniques are available, most UTIs do not warrant radiologic evaluation. The appropriateness of imaging in the setting of a UTI is discussed later.

TREATMENT Antimicrobial Principles The successful treatment of a UTI depends on two important principles. First, the treatment should result in elimination of bacteriuria. This typically occurs hours after initiation of treatment.7 Second, the urine concentration of the antimicrobials must exceed the minimal inhibitory concentration (MIC) of the bacteria.26 It is important to keep in mind that hospital microbiology laboratories typically report bacterial sensitivities based on serum levels that may be several-fold lower than the urine levels of a particular agent. Antimicrobial Resistance The most common reason for unresolved bacteriuria is bacterial resistance to the chosen antimicrobial agent. There are several

ways in which bacteria may be resistant. In natural resistance, certain bacteria simply lack a drug-susceptible substrate, rendering an entire species of bacteria resistant to a particular antimicrobial. Examples include Proteus resistance to nitrofurantoin and Enterococcus faecalis resistance to cephalexin.7 Resistance can also occur when the antimicrobial therapy actually selects for resistant mutants. This mode of resistance occurs within the urinary tract and can typically be avoided by choosing an agent with a urine concentration that exceeds the MIC by the greatest margin, adequate dosing, and stressing the importance of compliance with therapy.7 The third mechanism of resistance is extrachromosomal plasmid-mediated resistance, also known as transferable resistance. This mode of resistance takes place within the bowel and produces multiple resistant strains. To date, transferable resistance has not been demonstrated with nitrofurantoin or fluoroquinolones, and therefore these two drugs are good options for patients exposed to other antimicrobials.27 Antimicrobial Selection In selecting an antimicrobial agent, it is necessary to understand the efficacy, spectrum of activity, resistance patterns, side effects, dosing, and cost.28 Individual antimicrobials are discussed later. Costs for a complete course of therapy of the antimicrobials based on 2001 wholesale prices are listed in Table 86-2. Trimethoprim-sulfamethoxazole Trimethoprim-sulfamethoxazole (TMP-SMX) blocks folic acid metabolism of bacteria, thereby preventing bacterial growth. TMP is effective as a single agent in uncomplicated UTI, has fewer side effects, and is safe for patients with sulfa allergies.29 SMX has a synergistic bactericidal effect that improves the efficacy of the treatment of upper tract infections.30 The combination of TMP-SMX is active against most aerobic gram-positive and gram-negative organisms. It is not active against enterococci or Pseudomonas aeruginosa.23 Dosage is one double-strength tablet twice daily for 3 days for uncomplicated cystitis. Side effects may include rash, gastrointestinal upset, and photosensitivity.31 Serious adverse events may include Stevens-Johnson syndrome.23

Table 86-2 Antimicrobial Cost Antimicrobial Sulfonamides TMP-SMX TMP

Dose (mg)

Cost ($)

160/800 two times daily × 3 days 100 two times daily × 3 days

6.30-8.80 0.90-1.40

100-250 two times daily × 3 days 250-500 daily × 3 days

17.20-25.00 21.90-25.60

Fluoroquinolones Ciprofloxacin Levofloxacin Nitrofurantoin macrocrystals Macrodantin Macrobid

100 four times daily × 7 days 100 two times daily × 7 days

b-lactams Amoxicillin Cefixime Cefpodoxime

250-500 three times daily × 3 days 400 daily × 3 days 100 two times daily × 3 days

SMX, sulfamethoxazole; TMP, trimethoprim. Modified from Jancel T, Dudas V: Management of uncomplicated urinary tract infections. West J Med 176:51-55, 2002.

47.00 23.00 6.40-11.50 23.20 18.30

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TMP-SMX should be avoided in pregnant patients as well as those taking warfarin.7 TMP-SMX has historically been the most widely used antimicrobial in the treatment of uncomplicated UTI, which may account for its high resistance rates. A recent study by Gupta and colleagues highlighted the fact that antimicrobial susceptibility patterns are dependent on geographic distribution. E. coli resistance to TMP-SMX ranged from 10% in the northeastern United States to 22% in the western United States.32 Risk factors for resistance to TMP-SMX include previous use of TMP-SMX and current use of other antimicrobials, as well as diabetes and recent hospitalization.23 Nitrofurantoin Nitrofurantoin inhibits several bacterial enzyme systems and is bactericidal. It is active against E. coli and most species of Klebsiella, Enterobacter, Staphylococcus, and Enterococcus. It is not effective against Pseudomonas or Proteus species.33 A 7-day course of therapy is recommended for uncomplicated UTI, and it is also frequently used for UTI prophylaxis.23 The agent does not penetrate urinary tract tissue or achieve bactericidal levels in blood and therefore is not recommended for complicated UTIs or pyelonephritis.34 It also should not be used in patients with poor renal function, because adequate urine concentration levels will not be achieved.7 Side effects may include gastrointestinal upset, peripheral polyneuropathy, hemolysis in patients with glucose6-phosphate dehydrogenase deficiency, and pulmonary reactions ranging from cough to fibrosis.7 Nitrofurantoin exhibits very low levels of resistance.23 b-Lactams The β-lactam family includes penicillins, aminopenicillins, cephalosporins, and aztreonam. These antimicrobials inhibit bacterial cell wall synthesis.23 The aminopenicillins (ampicillin, amoxicillin ± clavulanate) are useful against Streptococcus, Enterococcus, E. coli, and Proteus mirabilis. Recommended treatment length is 7 days. The most common adverse reactions are hypersensitivity and diarrhea. Extended-spectrum penicillin derivatives including piperacillin are often active against typically ampicillin-resistant gramnegative bacilli.7 There are three generations of cephalosporins. Typically, the first-generation agents are active against Streptococcus, Staphylococcus, E. coli, Proteus, and Klebsiella species. Second-generation cephalosporins have similar activity to first-generation agents with additional activity against anaerobes. Third-generation cephalosporins have decreased activity against gram-positive cocci and increased activity against gram-negative bacilli. Some third-generation cephalosporins are active against P. aeruginosa and are often used for nosocomial infections caused by gramnegative organisms. It is important to note that none of the cephalosporins is active against enterococci. Similar to the aminopenicillins, adverse reactions include hypersensitivity and gastrointestinal upset. These agents should not be used in patients with immediate hypersensitivity to penicillins.7 Aztreonam is active only against gram-negative aerobes. This drug has a less than 1% incidence of cross-reactivity in penicillin-allergic patients, and its use is mainly limited to those patients with allergies to penicillin.7 Fluoroquinolones Ciprofloxacin and levofloxacin are the fluoroquinolones most commonly used against UTI in the United States. They are avail-

able in both oral and intravenous forms. The mechanism of action of these drugs is to inhibit DNA gyrase. They are active against enterobacteria and P. aeruginosa.7 These agents are often used as first-line therapy for UTIs in regions with high levels of bacterial resistance to ampicillin and TMP-SMX.23 Side effects are uncommon but include gastrointestinal upset, dizziness, lightheadedness, photosensitivity, and tendon rupture. Fluoroquinolones should be avoided in pregnant women. Sucralfate should not be used concomitantly, because it decreases oral absorption.7 Resistance to fluoroquinolones is low in the United States,32 but this is not the case worldwide. Spain and Portugal have high rates of resistance to ciprofloxacin, 14.7% and 5.8% respectively.23 This is perhaps due to the wider use of fluoroquinolones in Europe. In a recent paper, Hooton and colleagues expressed concern regarding increasing fluoroquinolone resistance and recommended discouraging the routine use of fluoroquinolones for treatment of mild-to-moderate acute uncomplicated cystitis.35 Aminoglycosides Aminoglycosides inhibit ribosomal protein synthesis and are active against Staphylococcus and most gram-negative pathogens. They are the drugs of choice in patients with urosepsis when used in combination with ampicillin.7 Once-daily dosing at 7 mg/kg has been shown to maximize bacterial killing and to reduce nephrotoxicity, a common adverse effect.36 These agents should be avoided in pregnant patients and in those with impaired renal function or diabetes.7

PRACTICAL APPROACHES TO PATIENT ASSESSMENT Classification of Urinary Tract Infections UTIs can be classified in several different ways. The location of the infection is one method of classification. For example, UTIs may involve the lower tract (cystitis) or the upper tract (pyelonephritis). Texts also describe UTIs as uncomplicated or complicated. Uncomplicated infections occur in healthy women who are without physiologic or anatomic urinary tract abnormalities or recent urologic surgery or instrumentation. Women with uncomplicated infections are not pregnant or immunocompromised and have not recently taken antimicrobials.7 Complicated infections occur when there is poor response to therapy, the patient is not healthy or is otherwise compromised (e.g., pregnant), or there is a structural or functional abnormality of the urinary tract that increases the risk of therapy failure.8 Unfortunately, the category into which a patient fits is not always readily apparent. This section attempts to help the clinician recognize patient characteristics that should guide patient categorization. Uncomplicated Acute Cystitis A typical patient with uncomplicated acute cystitis is a premenopausal, sexually active, nonpregnant woman. She reports recent onset of symptoms including dysuria, frequency, urgency, and possibly suprapubic discomfort and hematuria.37 The differential diagnosis for acute cystitis includes vaginitis and sexually transmitted diseases. Some authors report that a history, physical examination, and urinalysis should be all that is needed to ascertain the appropriate diagnosis.38 Others report that treating acute, uncomplicated cystitis in low risk women by telephone consultation to be safe and effective.39

Chapter 86 URINARY TRACT INFECTIONS IN WOMEN

Table 86-3 Pathogens Cultured in Uncomplicated Urinary Tract Infections Escherichia coli Staphylococcus saprophyticus (premenopausal women) Klebsiella species Enterococcus faecalis Proteus mirabilis

70-95% 5-20%

Modified from Hooton TM, Stamm WE: Diagnosis and treatment of uncomplicated urinary tract infection. Infect Dis Clin North Am 11:551581, 1997.

Box 86-1 Situations in which it is Appropriate to Obtain a Urine Culture in Acute Uncomplicated Cystitis Symptoms and/or urinalysis not consistent with cystitis Recent antimicrobial therapy UTI symptoms >7 days Age >65 yr Diabetes Pregnancy Recurrent UTI UTI, urinary tract infection. Modified from Schaeffer AJ: Infections of the urinary tract. Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds). Campbell’s Urology. Philadelphia, WB Saunders, 2002, pp 516-602.

Box 86-2 When to use Fluoroquinolones as First-Line Therapy for Uncomplicated Acute Cystitis Allergic to TMP-SMX Recent antimicrobial exposure High rate of TMP-SMX resistance in the community (>20%) Unresolved UTI without prior fluoroquinolone therapy Recurrent UTI TMP-SMX, trimethoprim-sulfamethoxazole; UTI, urinary tract infection.

For the patient with uncomplicated UTI, urine cultures are usually not necessary, because most acute, community-acquired, uncomplicated infections in the United States and abroad are caused by predictable organisms (Table 86-3) and respond to empiric therapy. The routine use of urine cultures in uncomplicated cases has been shown to increase the cost of care by 39% without significant benefit to patient outcomes.28 However, it is important to recognize situations in which it is appropriate to perform urine cultures in uncomplicated acute cystitis. These are included in Box 86-1. Evidence-based guidelines for the treatment of acute uncomplicated cystitis were published by the Infectious Diseases Society America (IDSA) in 1999. According to these guidelines, TMP alone or TMP-SMX for 3 days is considered the current standard therapy. However, fluoroquinolones should be used as initial empiric therapy in specific situations, as outlined in Box 86-2.7,40

There has been renewed interest in nitrofurantoin in the treatment of uncomplicated cystitis because of its low resistance rates. However, it is not as effective as TMP-SMX or the fluoroquinolones.41 The IDSA found that nitrofurantoin had lower cure rates (approximately 85%) than other first-line agents (90% to 95%).40 Most women experience marked improvement in symptoms within 24 hours.28 Response to therapy is primarily measured by clinical resolution of symptoms, and further follow-up is usually unnecessary.7 Unresolved Urinary Tract Infection If the patient’s symptoms do not resolve with empiric therapy, the clinician should consider these questions: Has the patient been compliant with treatment? Is the UTI caused by a resistant organism? Are symptoms due to a UTI or another diagnosis altogether? A urine culture should be obtained, and the patient should be switched to a fluoroquinolone if she is not taking one already. The patient should be monitored to ensure that her symptoms resolve and that her urine culture is negative at the end of treatment. Recurrent Urinary Tract Infections Recurrent UTI is noted when a premenopausal, sexually active, nonpregnant woman presents with her third episode of urgency, frequency, and dysuria in the same year. Reports show that 25% to 50% of women experience recurrent UTI, defined as three or more symptomatic UTIs in 1 year or two UTIs within 6 months.42 Recurrent UTIs usually occur in the absence of anatomic urinary tract abnormalities and represent a new infection from bacteria outside of the urinary tract.7 Reinfections typically occur at long intervals and usually are caused by different uropathogens, whereas relapses secondary to bacterial persistence are commonly caused by the same organism and typically occur at close intervals.7 A study by Scholes and colleagues aimed at determining the risk factors for recurrent UTI determined that lifetime sexual activity and sexual activity within the last year were the most important risk factors for recurrence.42 Other risk factors included spermicide use, a new sexual partner within the past year, first UTI at 15 years of age or younger, and having a mother with a history of UTIs.8 As indicated in Box 86-1, when a patient has recurrent UTIs, is appropriate to obtain a urine culture, because it is vital to document that these recurrent episodes are in fact infectious. If the patient’s symptoms are not caused by infection, the clinician needs to consider alternative diagnoses, including urethritis, vaginitis, interstitial cystitis, and carcinoma in situ. Further urologic workup is usually not necessary in patients with recurrent UTIs. There are three different strategies for antimicrobial prophylaxis for patients with recurrent UTIs. Low-Dose Prophylaxis Continuous antimicrobial prophylaxis involves daily administration of a low-dose antimicrobial such as TMP, TMP-SMX, or nitrofurantoin.1 These agents are ideal because they have minimal adverse effects on the fecal and vaginal flora and have been shown to decrease recurrence rates by 95%.43 Low-dose prophylaxis is well suited for patients with three or more UTIs annually and is well tolerated.1 Postcoital Prophylaxis As mentioned previously, sexual intercourse is a significant risk factor for acute cystitis. Postcoital antimicrobial administration is appropriate for patients with UTI recurrence associated with

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intercourse. Single doses of nitrofurantoin, cephalexin, or TMPSMX have been shown to be effective.44 Self-Start Therapy A patient on self-start therapy is provided a culture kit as well an antimicrobial preparation so that she may culture her urine and begin therapy promptly after the onset of symptoms. Fluoroquinolones are typically used in self-start therapy. The patient sees her physician after therapy to assess the response. This method has been found to be safe, effective, and economical.45 Uncomplicated Acute Pyelonephritis A young, sexually active woman without recent antimicrobial use or urologic instrumentation presents with symptoms of flank pain, nausea, vomiting and fever and has costovertebral angle tenderness on examination; this patient most likely has acute pyelonephritis. Treatment for acute pyelonephritis may occur in an outpatient or inpatient setting, depending on patient presentation (Table 86-4). Table 86-4 Patient Classification in Acute Pyelonephritis Outpatient Therapy

Inpatient Therapy

Not pregnant Compliant Non–toxic-appearing No nausea or vomiting

Pregnant Noncompliant Septic Unable to tolerate oral therapy

From Hooton TM, Stamm WE: Diagnosis and treatment of uncomplicated urinary tract infection. Infect Dis Clin North Am 11:551-581, 1997.

Figure 86-1 depicts the appropriate algorithm for the management of acute uncomplicated pyelonephritis, which has a similar etiologic profile to uncomplicated acute cystitis (see Table 86-3). For outpatient therapy, the ISDA recommends a 7-day course of an oral fluoroquinolone.40 ISDA guidelines for inpatient therapy include a parenteral fluoroquinolone, an aminoglycoside with or without ampicillin, or an extended-spectrum cephalosporin with or without ampicillin. Ampicillin/sulbactam with or without an aminoglycoside is recommended if the offending species is a gram-positive organism.40 Antimicrobials should be given for a total of 10 to 14 days. The patient may be switched to oral antimicrobials once there has been documented improvement within 72 hours.7 When is it Appropriate to Obtain Imaging? If the patient does not improve clinically within 72 hours, the clinician should give serious consideration to obtaining a CT scan or ultrasound study.46 Some patients may require intervention in addition to antimicrobials. This may include ureteral stenting or placement of a percutaneous nephrostomy to bypass an obstruction, or perhaps drainage of a perinephric abscess. Imaging may also be helpful in determining whether there is a urologic abnormality, such as struvite stones, foreign bodies, urethral diverticula, or perivesical fistula, that is causing bacterial persistence.7 A complete list of patient characteristics that should direct the clinician to obtain imaging is included in Box 86-3. Complicated Urinary Tract Infection As mentioned previously, a complicated infection is classified as either an infection that has responded poorly to therapy or one that is associated with host factors that increase the risk of therapy

Symptoms of pyelonephritis

Meets outpatient criteria

Labs Urine gram stain and culture

Treatment PO Fluoroquinolone x 7 days

Meets inpatient criteria

Labs Blood and urine cultures

Treatment Start parenteral therapy with: Ampcillin + gentamicin Fluoroquinolone 3rd generation cephalosporin

Improvement within 72 hours

Switch to PO therapy Complete 10-14 days of therapy

Figure 86-1 Algorithm for uncomplicated pyelonephritis. (Adapted from Schaeffer AJ: Infections of the urinary tract. In Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ [eds]: Campbell’s Urology. Philadelphia, WB Saunders, 2002, pp 516-602.)

Chapter 86 URINARY TRACT INFECTIONS IN WOMEN

Table 86-5 Host Risk Factors for Complicated Urinary Tract Infection Structural/Functional Abnormality

Compromised Host by History

Virulent Bacteria

Obstruction Congenital urinary tract abnormality

Pregnancy Diabetes Spinal cord injury

Recent antimicrobial use Hospitalized or nursing home patient Recent urinary tract instrumentation

Data from Hooton TM: Pathogenesis of urinary tract infections: An update. J Antimicrob Chemother 46(Suppl 1):1-7; discussion 63-65, 2000; Bent S, Nallamothu BK, Simel DL, et al: Does this woman have an acute uncomplicated urinary tract infection? JAMA 287:2701-2710, 2002; Ronald A: The etiology of urinary tract infection: Traditional and emerging pathogens. Am J Med 113(Suppl 1A):14S-19S, 2002.

Box 86-3 When Is It Appropriate to Obtain Imaging?

Table 86-6 Pathogens Cultured in Complicated Urinary Tract Infections

On initial assessment, history or findings suggestive of: Ureteral obstruction (may include stone, stricture, tumor, history of genitourinary surgery, or congenital obstruction) Sepsis/fever Severe diabetes mellitus Neurogenic bladder Papillary necrosis (sickle cell, diabetes, analgesic abuse) Polycystic kidney disease on dialysis

Gram-negative organisms Escherichia coli Proteus mirabilis Klebsiella species Citrobacter species Enterobacter species Pseudomonas aeruginosa Other

• • • • • •

After initial treatment: Pyelonephritis with poor response to therapy after 72 hr Unusual infecting organism (urea-splitting organism, tuberculosis, fungus)

• •

Modified from Schaeffer AJ: Infections of the urinary tract. Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds): Campbell’s Urology. Philadelphia, WB Saunders, 2002, 516-602.

failure.8 It is important to recognize patients with complicated UTIs, because there are implications for the workup and treatment. What are the factors that lead to the classification of a complicated UTI? These factors may be classified as structural or functional abnormalities, conditions that compromise host response, and conditions that promote infection with virulent bacteria (Table 86-5). The pathogenic organisms cultured in complicated UTIs vary from those seen in uncomplicated UTIs (Table 86-6). If the patient is well enough to be treated as an outpatient, then a fluoroquinolone should be chosen as first-line therapy. However, if the patient has a severe infection requiring admission, then broad-spectrum antimicrobials should be initiated.7 In general, treatment requires at least 14 to 21 days of antimicrobial therapy.40 Individual scenarios of complicated infections are discussed in the following paragraphs. Obstruction Case: A 32-year-old woman with a history of nephrolithiasis presents with right-sided flank pain and fever. Calcium oxalate stones can cause ureteral obstruction and may become secondarily colonized. Other than stones, urinary tract obstruction may also be caused by tumor, clot, or papillary necrosis. Urea-Splitting Bacteria that Cause Struvite Stones Case: A 25-year-old woman with recurrent UTI has recently completed a course of antimicrobials after suffering from a UTI

Gram-positive organisms Coagulase-negative staphylococci Enterococci Group B streptococci Staphylococcus aureus Other

21-54% 1-10% 2-17% 5% 2-10% 2-19% 6-20% 1-4% 1-23% 1-4% 1-2% 2%

From Nicolle LE: Recurrent urinary tract infection in adult women: Diagnosis and treatment. Infect Dis Clin North Am 1:791-806, 1987.

caused by P. mirabilis. A post-therapy urine culture is obtained and grows the same organism. She is currently asymptomatic. P. mirabilis causes alkalinization of the urine, leading to precipitation of calcium, magnesium, ammonium, and phosphate salts and subsequent struvite stone formation. These stones have become known as staghorn calculi because they tend to be large stones that take on the shape of the renal collecting system. Bacteria persist within these struvite stones, and bacteriuria tends to recur almost immediately on discontinuation of antimicrobial therapy. Struvite stones often contain minimal calcium and may not be evident on plain film radiographs.7 Congenital Urinary Tract Anomalies Case: An 18-year-old woman with a known history of ureteropelvic junction obstruction presents with a history of recurrent UTIs. In patients with anomalies of the urinary tract and UTI, recurrent bacteriuria with the same organism typically occurs until the anomalous structure is surgically corrected. Such anomalies include ureteral duplication with ectopic ureter, pericalyceal diverticula, urachal cysts, unilateral medullary sponge kidneys, and congenital obstructions with nonfunctioning kidneys.7 Pregnancy Case: A 29-year-old pregnant woman in her third trimester presents with fever, left-sided flank pain, nausea, and vomiting.

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Box 86-4 Urinary Tract Changes in Pregnancy Collecting system Decreased peristalsis of the collecting system and ureters Mechanical obstruction of the ureters secondary to enlarging uterus

• •

Bladder Displaced superiorly and anteriorly

•

Kidneys Increased glomerular filtration rate (GFR) by 30-50%

•

From Waltzer WC: The urinary tract in pregnancy. J Urol 125:271-276, 1981.

Although it has been shown that the incidence of bacteriuria in pregnant women is similar to that in their nonpregnant counterparts, the incidence of acute pyelonephritis is significantly increased in pregnant women compared with nonpregnant women.47 This is perhaps due to the numerous anatomic and physiologic changes that occur in the urinary tract during pregnancy (Box 86-4). Not surprisingly, pyelonephritis is most commonly seen in the third trimester, when stasis and hydronephrosis are most evident.7 Before the advent of antimicrobial therapy, pregnant women with pyelonephritis had an increased rate of infant prematurity and perinatal mortality. Today, there is continued debate in the literature as to whether gestational pyelonephritis leads to prematurity and subsequent perinatal mortality. In any case, patients with pyelonephritis during pregnancy should be admitted and treated with parenteral agents.7Antimicrobials that are safe to use during pregnancy include penicillins, cephalosporins, and nitrofurantoin. The latter, however, should not be used in pyelonephritis, because it does not achieve adequate tissue penetration. Agents that may be harmful to the developing fetus should be avoided. Fluoroquinolones may impair cartilage development, and TMP-SMX is associated with antifolate teratogenicity in the first trimester and with neonatal hyperbilirubinemia in the third trimester.48 After treatment, women should either be given prophylaxis or monitored closely throughout the remainder of the pregnancy, because there is an increased risk of repeated episodes of pyelonephritis.49 Diabetes Mellitus Case: A 45-year-old woman with poorly controlled diabetes is admitted to the hospital with acute pyelonephritis. Despite parenteral antimicrobial therapy for 3 days, she continues to have high, spiking temperatures. The incidence of UTI in diabetic women has been shown to be substantially higher than in nondiabetic women.50 Treatment may be more difficult if glomerulopathy is present, because urine concentration of antimicrobials may be less than optimal.7 Diabetes is also associated with specific entities such as intrarenal and perirenal abscess, emphysematous pyelonephritis and cystitis, xanthogranulomatous pyelonephritis, and papillary necrosis.8 Further discussion of these entities is beyond the scope of this chapter. Spinal Cord Injuries Case: A 27-year-old woman with a history of a thoracic spinal cord injury presents with fevers and foul-smelling urine. She manages her bladder with clean intermittent catheterization.

The method of bladder management plays a large role in UTI in these patients. Patients with indwelling urethral or suprapubic catheters have high rates of infection.51 Clean intermittent catheterization was introduced in 1972 and revolutionized bladder management of patients with spinal cord injury. It has been shown to reduce the risk factors for UTI by decreasing intravesical pressure and the incidence of stones.52 Nevertheless, UTI is a common problem in spinal cord–injured patients and is often difficult to diagnose. Because of loss of sensation, patients do not present with the typical symptoms of frequency, urgency, or dysuria. Additionally, urinalysis in these patients often demonstrates bacteriuria and pyuria regardless of the presence of infection. Therefore, the diagnosis is often clinical, based on symptoms of flank, back, or abdominal discomfort; leakage between catheterizations; fever; increased spasticity; and/or cloudy, malodorous urine.7 A urine culture must be obtained before therapy is initiated, because there is a high probability of bacterial resistance.7 Spinal cord–injured patients with recurrent UTI should undergo urinary tract imaging, urodynamic testing, and a review of their bladder management program.53

SPECIAL CONSIDERATIONS Urinary Tract Infection Prophylaxis A nonantimicrobial treatment that prevents UTIs would be extremely useful for women who suffer from recurrent UTIs. Cranberry Two compounds in cranberries, fructose and proanthocyanidin, have been found to inhibit E. coli adhesins in vitro.54 This finding is likely the basis for the widespread belief among laypersons that cranberries prevent UTIs. Despite a number of clinical trials, at this time there is no compelling evidence that cranberries or cranberry products prevent UTIs.55 Lactobacilli Lactobacillus probiotics have been proposed as means of enhancing the natural host defenses by restoring the presence of a normal vaginal microflora.56,57 Various properties of lactobacillus are believed to be protective against uropathogenic organisms. These include maintenance of an acidic pH, direct killing of pathogens through the production of H2O2, and competitive inhibition of bacterial adherence.58 Multiple small trials have been conducted using Lactobacillus species to recolonize the vaginas of women with recurrent UTI. These studies have produced mixed results, and further research in this area is needed.57 Vaccine Several vaccines to provide protection against UTI caused by E. coli or other uropathogens are currently under development. Preliminary studies are promising for short-term protection from recurrences, but it remains to be seen whether long-term efficacy can be demonstrated.57 Asymptomatic Bacteriuria of Pregnancy Asymptomatic bacteriuria occurs in 4% to 6% of both pregnant and nonpregnant women.59Despite these similar rates, the number of pregnant women who develop pyelonephritis is sig-

Chapter 86 URINARY TRACT INFECTIONS IN WOMEN

nificantly higher than in nonpregnant women. It has been reported that as many as 20% to 40% of pregnant women with asymptomatic bacteriuria subsequently develop acute pyelonephritis.60,61 Treatment of bacteriuria early in pregnancy has been shown to decrease the incidence of pyelonephritis by 90%.62 The American College of Obstetricians and Gynecologists currently recommends screening for asymptomatic bacteriuria in

pregnancy.60,63 Obtaining a urine culture once at the end of the first trimester is sufficient. Repeated screening of women with initial negative urine cultures is not recommended, because the risk of pyelonephritis is low.63 If the urine culture is positive, a repeat specimen for culture should be obtained and treatment initiated. After treatment, women should have periodic urine cultures to identify recurrent bacteriuria throughout the remainder of the pregnancy.64

References 1. McLaughlin SP, Carson CC: Urinary tract infections in women. Med Clin North Am 88:417-429, 2004. 2. Foxman B, Brown P: Epidemiology of urinary tract infections: transmission and risk factors, incidence, and costs. Infect Dis Clin North Am 17:227-241, 2003. 3. Foxman B, Barlow R, D’Arcy H, et al: Urinary tract infection: selfreported incidence and associated costs. Ann Epidemiol 10:509-515, 2000. 4. Mulvey MA, Lopez-Boado YS, Wilson CL, et al: Induction and evasion of host defenses by type 1-piliated uropathogenic Escherichia coli. Science 282:1494-1497, 1998. 5. Anderson GG, Palermo JJ, Schilling JD, et al: Intracellular bacterial biofilm-like pods in urinary tract infections. Science 301:105-107, 2003. 6. Mulvey MA, Schilling JD, Hultgren SJ: Establishment of a persistent Escherichia coli reservoir during the acute phase of a bladder infection. Infect Immun 69:4572-4579, 2001. 7. Schaeffer AJ: Infections of the urinary tract. In Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds): Campbell’s Urology. Philadelphia, WB Saunders, 2002, pp 516-602. 8. Hooton TM: Pathogenesis of urinary tract infections: an update. J Antimicrob Chemother 46(Suppl 1):1-7; discussion 63-65, 2000. 9. Fowler JE Jr, Stamey TA: Studies of introital colonization in women with recurrent urinary infections. VII. The role of bacterial adherence. J Urol 117:472-476, 1977. 10. Schaeffer AJ, Jones JM, Duncan JL, et al: Adhesion of uropathogenic Escherichia coli to epithelial cells from women with recurrent urinary tract infection. Infection 10:186-191, 1982. 11. Schaeffer AJ, Radvany RM, Chmiel JS: Human leukocyte antigens in women with recurrent urinary tract infections. J Infect Dis 148:604, 1983. 12. Sheinfeld J, Schaeffer AJ, Cordon-Cardo C, et al: Association of the Lewis blood-group phenotype with recurrent urinary tract infections in women. N Engl J Med 320:773-777, 1989. 13. Schaeffer AJ: New concepts in the pathogenesis of urinary tract infections. Urol Clin North Am 29:241-250, xii, 2002. 14. Eschenbach DA, Patton DL, Hooton TM, et al: Effects of vaginal intercourse with and without a condom on vaginal flora and vaginal epithelium. J Infect Dis 183:913-918, 2001. 15. Foxman B, Manning SD, Tallman P, et al: Uropathogenic Escherichia coli are more likely than commensal E. coli to be shared between heterosexual sex partners. Am J Epidemiol 156:1133-1140, 2002. 16. Hooton TM, Roberts PL, Stamm WE: Effects of recent sexual activity and use of a diaphragm on the vaginal microflora. Clin Infect Dis 19:274-278, 1994. 17. Raz R, Stamm WE: A controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections. N Engl J Med 329:753-756, 1993. 18. Cardozo L, Benness C, Abbott D: Low dose oestrogen prophylaxis for recurrent urinary tract infections in elderly women. Br J Obstet Gynaecol 105:403-407, 1998. 19. Smith HS, Hughes JP, Hooton TM, et al: Antecedent antimicrobial use increases the risk of uncomplicated cystitis in young women. Clin Infect Dis 25:63-68, 1997.

20. Bent S, Saint S: The optimal use of diagnostic testing in women with acute uncomplicated cystitis. Dis Mon 49:83-98, 2003. 21. Semeniuk H, Church D: Evaluation of the leukocyte esterase and nitrite urine dipstick screening tests for detection of bacteriuria in women with suspected uncomplicated urinary tract infections. J Clin Microbiol 37:3051-3052, 1999. 22. Hurlbut TA 3rd, Littenberg B: The diagnostic accuracy of rapid dipstick tests to predict urinary tract infection. Am J Clin Pathol 96:582-528, 1991. 23. Nickel JC: Management of urinary tract infections: Historical perspective and current strategies. Part 2: Modern management. J Urol 173:27-32, 2005. 24. Fihn SD: Clinical practice: Acute uncomplicated urinary tract infection in women. N Engl J Med 349: 259-266, 2003. 25. Stamm WE, Hooton TM: Management of urinary tract infections in adults. N Engl J Med 329:1328-1334, 1993. 26. Klastersky J, Daneau D, Swings G, Weerts D: Antibacterial activity in serum and urine as a therapeutic guide in bacterial infections. J Infect Dis 129:187-193, 1974. 27. Schaeffer AJ: The expanding role of fluoroquinolones. Am J Med 113(Suppl 1A):45S-54S, 2002. 28. Hooton TM, Stamm WE: Diagnosis and treatment of uncomplicated urinary tract infection. Infect Dis Clin North Am 11:551-581, 1997. 29. Johnson JR, Stamm WE: Urinary tract infections in women: Diagnosis and treatment. Ann Intern Med 111:906-917, 1989. 30. Burman LG: Significance of the sulfonamide component for the clinical efficacy of trimethoprim-sulfonamide combinations. Scand J Infect Dis 18:89-99, 1986. 31. Cockerill FR, Edson RS: Trimethoprim-sulfamethoxazole. Mayo Clin Proc 66:1260-1269, 1991. 32. Gupta K, Sahm DF, Mayfield D, Stamm WE: Antimicrobial resistance among uropathogens that cause community-acquired urinary tract infections in women: A nationwide analysis. Clin Infect Dis 33:89-94, 2001. 33. Iravani A: Advances in the understanding and treatment of urinary tract infections in young women. Urology 37:503-511, 1991. 34. Wilhelm MP, Edson RS: Antimicrobial agents in urinary tract infections. Mayo Clin Proc 62:1025-1031, 1987. 35. Hooton TM, Besser R, Foxman B, et al: Acute uncomplicated cystitis in an era of increasing antibiotic resistance: A proposed approach to empirical therapy. Clin Infect Dis 39:75-80, 2004. 36. Nicolau DP, Freeman CD, Belliveau PP, et al. Experience with a once-daily aminoglycoside program administered to 2,184 adult patients. Antimicrob Agents Chemother 39:650-655, 1995. 37. Bent S, Nallamothu BK, Simel DL, et al: Does this woman have an acute uncomplicated urinary tract infection? JAMA 287:2701-2710, 2002. 38. Komaroff AL: Acute dysuria in women. N Engl J Med 310:368-375, 1984. 39. Barry HC, Hickner J, Ebell MH, Ettenhofer T: A randomized controlled trial of telephone management of suspected urinary tract infections in women. J Fam Pract 50:589-594, 2001. 40. Warren JW, Abrutyn E, Hebel JR, et al: Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelo-

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41. 42. 43. 44.

45. 46. 47. 48. 49. 50. 51.

nephritis in women. Infectious Diseases Society of America (IDSA). Clin Infect Dis 29:745-758, 1999. Hooton TM, Winter C, Tiu F, Stamm WE: Randomized comparative trial and cost analysis of 3-day antimicrobial regimens for treatment of acute cystitis in women. JAMA 273:41-45, 1995. Scholes D, Hooton TM, Roberts PL, et al: Risk factors for recurrent urinary tract infection in young women. J Infect Dis 182:1177-1182, 2000. Nicolle LE, Ronald AR: Recurrent urinary tract infection in adult women: Diagnosis and treatment. Infect Dis Clin North Am 1:793806, 1987. Stapleton A, Latham RH, Johnson C, Stamm WE: Postcoital antimicrobial prophylaxis for recurrent urinary tract infection: A randomized, double-blind, placebo-controlled trial. JAMA 264:703-706, 1990. Schaeffer AJ, Stuppy BA: Efficacy and safety of self-start therapy in women with recurrent urinary tract infections. J Urol 161:207-111, 1999. Soulen MC, Fishman EK, Goldman SM, Gatewood OM: Bacterial renal infection: Role of CT. Radiology 171:703-707, 1989. Sweet RL: Bacteriuria and pyelonephritis during pregnancy. Semin Perinatol 1:25-40, 1977. Weiser AC, Schaeffer AJ: The use and misuse of antimicrobial agents in urology. AUA Update Series 31:137, 2002. Gilstrap LC, Leveno KJ, Cunningham FG, et al: Renal infection and pregnancy outcome. Am J Obstet Gynecol 141:709-716, 1981. Ooi BS, Chen BT, Yu M: Prevalence and site of bacteriuria in diabetes mellitus. Postgrad Med J 50:497-499, 1974. Tambyah PA, Maki DG: Catheter-associated urinary tract infection is rarely symptomatic: A prospective study of 1,497 catheterized patients. Arch Intern Med 160:678-682, 2000.

52. Stover SL, Lloyd LK, Waites KB, Jackson AB: Urinary tract infection in spinal cord injury. Arch Phys Med Rehabil 70:47-54, 1989. 53. Cardenas DD, Hooton TM: Urinary tract infection in persons with spinal cord injury. Arch Phys Med Rehabil 76:272-280, 1995. 54. Zafriri D, Ofek I, Adar R, et al: Inhibitory activity of cranberry juice on adherence of type 1 and type P fimbriated Escherichia coli to eucaryotic cells. Antimicrob Agents Chemother 33:92-98, 1989. 55. Raz R, Chazan B, Dan M: Cranberry juice and urinary tract infection. Clin Infect Dis 38:1413-1419, 2004. 56. Reid G: The scientific basis for probiotic strains of Lactobacillus. Appl Environ Microbiol 65:3763-3766, 1999. 57. Stapleton A: Novel approaches to prevention of urinary tract infections. Infect Dis Clin North Am 17:457-471, 2003. 58. Reid G, Bruce AW: Selection of lactobacillus strains for urogenital probiotic applications. J Infect Dis 183(Suppl 1):S77-S80, 2001. 59. Stamey TA: Pathogenesis and Treatment of Urinary Tract Infections. Baltimore, Williams & Wilkins, 1980. 60. Millar LK, Cox SM: Urinary tract infections complicating pregnancy. Infect Dis Clin North Am 11:13-26, 1997. 61. Patterson TF, Andriole VT: Detection, significance, and therapy of bacteriuria in pregnancy: Update in the managed health care era. Infect Dis Clin North Am 11:593-608, 1997. 62. Gratacos E, Torres PJ, Vila J, et al: Screening and treatment of asymptomatic bacteriuria in pregnancy prevent pyelonephritis. J Infect Dis 169:1390-1392, 1994. 63. Stenqvist K, Dahlen-Nilsson I, Lidin-Janson G, et al: Bacteriuria in pregnancy: Frequency and risk of acquisition. Am J Epidemiol 129:372-379, 1989. 64. Nicolle LE: Asymptomatic bacteriuria: When to screen and when to treat. Infect Dis Clin North Am 17:367-394, 2003.

Chapter 87

VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE Andrea J. Rapkin and Monica Lee DEFINITION OF VULVODYNIA AND CURRENT NOMENCLATURE The purpose of this chapter is to outline the anatomy and physiology of vulvar and vaginal pain syndromes and to explore the differential diagnosis and management of vulvar and vaginal pain and dyspareunia (Tables 87-1 and 87-2), including the roles of medication, surgery, psychotherapy, and multidisciplinary pain management. The differential diagnosis and management of abnormal vaginal discharge is also discussed. Vulvar pain syndromes are characterized by unexplained burning or any combination of stinging, irritation, itching, pain or rawness anywhere from the mons pubis to the anus that causes physical, sexual, and psychological distress. A multitude of terms have been used in the literature to describe vulvar pain syndromes. Vulvodynia was first described in 1889 by A. J. C. Skene1 but received little attention until the 1970s. The International Society for the Study of Vulvovaginal Diseases (ISSVD) abandoned the term “burning vulva syndrome,” first described in 1984,2 and introduced a classification wherein the two principal divisions were vulvar vestibulitis syndrome (VVS) and dysesthetic or essential vulvodynia.3 The most recent classification of vulvar pain, which was agreed on at the October 2003 Congress of the ISSVD, consists of two major categories4: 1. Vulvar pain related to a specific disorder a. Infection b. Inflammation c. Neoplasm d. Neurologic disease 2. Vulvodynia: vulvar discomfort, usually described as burning pain, occurring in the absence of a specific disorder a. Generalized (involving the entire vulva) or localized (involving a portion or component of the vulva, such as the vestibule, clitoris, or hemivulva) b. Provoked (i.e., by sexual and/or nonsexual contact), unprovoked (i.e., spontaneous), or mixed (provoked and unprovoked). The term vestibulitis signifies the presence of inflammation, which was thought to be misleading because much evidence suggests no such presence. Therefore, the ISSVD voted to discontinue use of this term.

INCIDENCE AND EPIDEMIOLOGY OF VULVODYNIA The typical patient with vulvodynia used to be described as a nulliparous woman in her 20s or early 30s who often may have developed symptoms suddenly.5 The true prevalence of vulvo-

dynia is uncertain due to its recent recognition; however, a 1991 study of 210 consecutive patients seen at a private practice for general gynecology found that 37% had some degree of positive testing for vulvar discomfort, and 15% met full criteria.6 A survey of more than 4900 women aged 18 to 64 years reported that 16% of the 3000 respondents had experienced vulvar pain lasting at least 3 months; 7% had vulvar pain at the time of the survey, and many had seen up to five different doctors for this problem.7 Unexplained vulvar pain was found to be of similar incidence among white and African American women. Hispanic women were 80% more likely than white women to have experienced chronic vulvar pain.

ANATOMY OF THE VULVA AND VAGINA The vulva is the part of female anatomy located between the genitocrural folds laterally and between the mons pubis anteriorly and the anus posteriorly (Fig. 87-1).8 It is composed of the labia majora, labia minora, mons pubis, clitoris, vestibule, urinary meatus, vaginal orifice, hymen, Bartholin’s glands, Skene’s ducts, and vestibulovaginal bulbs. The labia majora form the lateral boundaries of the vulva and consist of two large folds of adipose and fibrous tissue. Anteriorly, the labia majora fuse into the mons pubis; posteriorly, they become narrower and flatter and terminate 3 to 4 cm anterior to the anus, where they are united by the posterior commissure or fourchette. The skin of the labia majora is usually darker than the adjacent skin. The skin has an outer lining of stratified squamous epithelium. Within the dermis are numerous hair follicles and sebaceous, sweat (eccrine), and apocrine glands. The labia minora lie between the labia majora and consist of two flat folds of connective tissue containing little or no adipose tissue. They are covered by skin on their lateral aspects and partially so on their medial aspects. Hart’s line separates the medial boundary of the minora from the vestibule and is the line of demarcation between the skin and mucous membrane; it runs along the base of the inner aspect of each labia minora, passes into the fossa navicularis, and separates the skin boundary of the fourchette from the mucous membrane of the hymen. The labia minora are 4 to 5 cm in length and 0.5 cm in thickness. Anteriorly, each divides into two parts, one passing over the clitoris to form the prepuce and the other joining the clitoris to form the frenulum. Posteriorly, they tend to become smaller and blend with the medial surfaces of the labia majora or unite anterior to the posterior commissure to form the fourchette. The skin and mucosa of the labia minora are extremely rich in sebaceous glands. During sexual excitement, the labia minora frequently 857

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Table 87-1 Differential Diagnosis of Dyspareunia Fissure

Pruritus

Ulcer

Erythema

Mass/tumor/swelling

Urinary tract lesions

Dryness

No vulvar lesions

Anal fissure Posterior fourchette fissure Enteroperineal fissure (Crohn’s disease) Lichen sclerosus Vaginal atrophy Vulvovaginitis Dermatitis Human papillomavirus infection Lichen planus Lichen sclerosus Lichen simplex chronicus Seminal plasma allergy Vaginal atrophy Vulvovaginitis Behçet’s syndrome Chancroid Herpes simplex virus infection Lichen planus Bartholin’s abscess Dermatitis Desquamative inflammatory vaginitis Hemorrhoids Seminal plasma allergy Vulvar vestibulitis Vulvovaginitis Bartholin’s abscess Bartholin’s cyst Hemorrhoids Labial hypertrophy Radiation Urethral caruncle Urethral diverticulum Urethral caruncle Urethral diverticulum Urethritis Inadequate sexual arousal/lubrication Radiation Vaginal atrophy Episiotomy scar Female circumcision Inadequate sexual arousal/lubrication Rigid hymeneal ring Vaginismus Vulvar neuroma Vulvar vestibulitis Vulvodynia Vulvovaginitis

become swollen and congested and take on the appearance of erectile tissue. The clitoris is the female homologue of the penis. It consists of two cylindrical erectile bodies, called the corpora cavernosa, that terminate in the vestibule as the glans. The body of the clitoris is approximately 2 cm long, is formed by the fusion of the two corpora cavernosa, and extends posteriorly from the pubic arch to the glans. The glans of the clitoris is covered by a mucous membrane containing many special nerve end organs.

Entry dyspareunia

Deep dyspareunia

Bartholin’s gland cyst or abscess Behçet’s syndrome Chancroid Dermatitis: allergy, vulvovaginitis, atopic vulvitis Desquamative inflammatory vaginitis Episiotomy scar Female circumcision Fissure: anal, posterior fourchette, enteroperineal (Crohn’s) Hemorrhoids Herpes simplex or zoster Inadequate sexual arousal and lubrication Labial hypertrophy Lichen planus Lichen sclerosus Lichen simplex chronicus Mullerian abnormality Post-traumatic pubic symphysis pain Radiation damage Rigid hymenal ring Seminal plasma allergy Urethral caruncle Urethral diverticulum Urethritis Vaginal atrophy Vaginismus Vulvar vestibulitis Vulvodynia Vulvovaginitis Adenomyosis Endometriosis Fixed uterine retroversion Inflammatory bowel disease Interstitial cystitis Irritable bowel syndrome Leiomyomas Ovarian pathology Pelvic adhesions Pelvic floor relaxation Pelvic inflammatory disease Radiation-induced vaginal scarring Rectocele Shortened vagina Urethral syndrome

The vestibule is the portion of the vulva that extends from the clitoris to the fourchette and is visible on separation of the labia majora. Hart’s line represents the outer perimeter of the vulvar vestibule, and the inner margin of the vestibule is the hymen. The vestibule is covered by nonpigmented, nonkeratinized squamous epithelium and is devoid of skin adnexa. It contains mucussecreting minor vestibular glands. The ductal orifices of Bartholin’s glands, the periurethral gland complexes of Skene, and the urethral meatus all empty onto the vestibular surface. The vagina opens into the vestibule. The hymen is the thin membrane of

Chapter 87 VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE

Table 87-2 Evaluation of Patients with Vulvar or Vaginal Pain History Vulvar examination

Vaginal examination

Bimanual examination

Rectovaginal examination Additional diagnotic tests as needed

Create differential or specific diagnoses

Detailed pain history, obstetric/gynecologic, sexual, medical, surgical, psychosocial, medications, allergies, habits, trauma Inspection: lesions (macules, papules, ulcers, nodules), fissures, fistulas, inflammation (edema, erythema), discharge, tumors, anatomic abnormalities (surgical, congenital, traumatic). Palpation: localize pain with cotton swab, identify specific neural distribution, vestibule, Bartholin’s, Skene’s, hymenal caliber, urethra Biopsy and/or culture suspicious lesions (e.g., VIN, ulcers, verrucae, white or red plaques); colposcopic magnification of lesions if indicated Speculum examination: inspect mucosa (color, rugations, lesions) pH of discharge Wet mount saline and KOH: infection, atrophy Culture (fungal, bacterial): vagina, cervix Cystocele, rectocele, enterocele, uterine prolapse, cervical discharge, lesions Palpate, attempt to reproduce pain: hymen, bladder, individual pelvic floor muscles, ischial spine area for pudendal nerves, inferior hypogastric plexus (paracervical), cervical motion tenderness Assess ability to contract and relax muscles Uterus: size, shape, position, mobility, tenderness, uterosacral ligament thickening/ nodularity, tenderness, adnexal masses, tenderness, mobility Cervical motion tenderness Rectal masses, stool guaiac, nodules/fibrosis in cul-de-sac Pelvic floor MRI, pelvic ultrasound, pudendal nerve conduction velocity, diagnostic nerve blocks (local, pudendal, inferior hypogastric), cystourethroscopy, sigmoidoscopy, physical therapist evaluation of pelvic floor, psychological/stress/couples evaluation, HSV serology, urine analysis and culture Specific infectious, inflammatory, or anatomic pathology. Treat per diagnosis (e.g., pharmacologic, surgical) Neuroplastic or neuropathic/neuromuscular pain requires a multidisciplinary approach: physical therapy, psychology (cognitive/behavioral/biofeedback/sexual), series of specific nerve blocks, pharmacologic (medications to alter nerve conduction or for depression/ anxiety, such as antidepressants, anticonvulsants, local anesthetics, or muscle relaxants [Botox])

HSV, herpes simplex virus; KOH, potassium hydroxide; MRI, magnetic resonance imaging; VIN, vulvar intraepithelial neoplasm.

connective tissue over the entrance of the vagina into the vestibule. Bartholin’s glands lie deep beneath the fascia, one on each side of the vestibule, posterolaterally to the vaginal orifice. The cells lining the acini contain mucin, which is secreted during sexual excitement and contributes to lubrication of the vaginal orifice. The main ducts of Bartholin’s glands open into the vestibule at approximately the 5 and 7 o’clock positions, outside the hymenal ring. The urethra opens into the vestibule just anterior to the vaginal introitus. Arterial blood supply to the vulva comes from the internal pudendal artery, which derives from the internal iliac artery (hypogastric artery), and from branches of the external pudendal artery, which derives from the femoral artery. The veins of the vulva form a large plexus, which empties into the internal and external pudendal veins. Innervation of the vulva is supplied by the cutaneous branches of the ilioinguinal nerve anterosuperiorly and by the pudendal branches of the femoral cutaneous nerve posteroinferiorly (Fig. 87-2). The three roots of the pudendal nerve derive from the second, third, and fourth sacral nerves; they unite approximately 1 cm proximal to the ischial spine, then leave the pelvic cavity by passing though the greater sciatic foramen.9 The pudendal nerve subsequently passes posterior to the junction between the ischial

spine and the sacrospinous ligament, then reenters the pelvic cavity through the lesser sciatic foramen and proceeds anteriorly through Alcock’s canal. The major cutaneous nerve supply of the perineum is provided by the branches of the pudendal nerve.9 The inferior hemorrhoidal nerve supplies the posterior portion; the superficial branch of the perineal nerve divides into medial and lateral parts known as the posterior labial nerves, and the dorsal nerve of the clitoris innervates the clitoral area. The vagina extends from the vestibule to the uterus and is directed obliquely upward and backward at an angle approximately 45 degrees to the horizontal axis. Its long axis is parallel to the plane of the pelvic brim and at a right angle to the uterus. The upper one third of the vagina is in contact with the base of the bladder, and the entire lower two thirds is in contact with the urethra. The vagina consists of three principal layers: an outer fibrous layer that derives from pelvic fascia, a middle muscular layer, and an inner mucosal layer. The pelvic floor muscles include the levator ani, pubococcygeus, and coccygeus muscles. All of the fasciae investing the muscles form a continuum of connective tissue that joins the fascial covering of the pelvic viscera above with the fascia of the perineum below.9 The levator ani muscle is a broad, thin structure that is attached to the inner surface of the side of the

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Mons pubis

Prepuce of clitoris Labium majus Glans of clitoris Frenulum of clitoris

Urethral orifice Labium minus Vaginal orifice

Vestibule Orifice of Bartholin's Gland Genitocrural fold

Hymen Posterior fourchette

Anus

Perineum

rectal nerve or from the perineal branch of the pudendal nerve. The function of the levator ani muscle is constriction of the lower end of the rectum and vagina, and probably fixation of the perineal body as well. The levator ani, together with the coccygei, form a muscular diaphragm that supports the pelvic viscera and opposes itself to the downward thrust produced by any increase in intra-abdominal pressure. The coccygeus muscle is posterosuperior in the same tissue plane as the levator ani muscle. It consists of a triangular sheath of muscular and tendinous fibers, arising by its apex from the pelvic surface of the spine of the ischium and sacrospinous ligament. It is attached at its base to the margin of the coccyx and the side of the S5 segment. The muscle receives its nerve supply through branches of the S4 and S5 spinal nerves. The coccygeus functions in pulling forward and supporting the coccyx after it has been pressed backward during defecation or parturition. The coccygeus, together with the levator ani and piriformis muscles, closes the posterior part of the pelvic outlet. The chief sources of blood supply to the vagina are the uterine, pudendal, and middle hemorrhoidal arteries, which arise from the internal iliac arteries. They form a plexus around the vagina. The upper portion is supplied by a descending branch of the uterine artery, the cervical-vaginal artery. The lower half of the vagina is supplied by ascending branches of the middle hemorrhoidal arteries; the dorsal artery, which originates from the internal pudendal, supplies the clitoris.

EVALUATION Figure 87-1 Vulvar anatomy. (Redrawn from Kaufman RH: Benign Diseases of the Vulva and Vagina, 5th ed. St. Louis, Elsevier Mosby, 2005.)

true pelvis.9 It is attached anteriorly to the pelvic surface of the body of the pubis, lateral to the symphysis; behind, to the medial surface of the spine of the ischium; and between these two points, to the obturator fascia. Morphologically, the levator ani can be divided into the pubococcygeus and the iliococcygeus muscles. The pubococcygeus muscle arises from the posterior surface of the pubis and from the anterior part of the obturator fascia. Its fibers are directed backward, almost horizontally, along the line of the anal canal and become attached to the front of the coccyx by a tendinous plate that is continuous with the anterior sacrococcygeal ligament. The medial coccygeal muscle arises from the ischial spine and from the posterior part of the tendinous arch of the levator ani muscle. Its fibers attach to the sides of the coccyx and to the opposite muscle in the median raphe on the undersurface of the tendinous plates of the pubococcygeus that contribute to the anococcygeal ligament. The superior or pelvic surface of the levator ani is separated by its covering fascia from the bladder, rectum, and perineum, whereas its inferior and or perineal surface forms the medial boundary of the ischiorectal fossa and is covered by the inferior fascia of the pelvic diaphragm. Its posterior border is free and is separated from the coccygeus muscle by areolar tissue, whereas the medial borders of the two muscles are separated by the visceral outlet, an interval through which the urethra, vagina, and anorectum pass from the pelvis. The nerve supply of the levator ani muscle includes a branch from the S4 nerve, a branch that arises either from the inferior

History Obtaining a thorough history is critical in the evaluation and management of vulvar or vaginal pain and dyspareunia (see Table 87-2). Pain symptoms must be well characterized to assess the onset, type of pain (burning, itching, stinging, irritating), timing (constant or cyclic), associated activities (e.g., intercourse, exercise, stress), inciting agents (perfume, lotions, detergents, clothing), and relieving factors (e.g., antifungal medications). A daily pain diary may better define these characteristics. Pain should be quantified on each visit on a scale of 1 (no pain) to 10 (maximal pain imaginable). Concurrent gynecologic, genitourinary, and gastrointestinal symptoms should be identified. In addition, past or current infections (human papillomavirus [HPV], herpes, Candida), medications, local and systemic dermatologic disorders, neurologic disorders (e.g., herniated disk, herpes zoster, pudendal or genitofemoral neuralgia), urologic disorders (interstitial cystitis, urethral syndrome), physical trauma (vaginal deliveries, episiotomy, vaginal surgery), and fibromyalgia should be ascertained. Sexual history evaluating arousal, lubrication, ability to achieve orgasm, whether pain is primary or secondary, and a history of sexual, physical, or emotional abuse should be addressed.10 Physical Examination In many cases, the vulva appears normal. However, careful inspection should be performed to evaluate for discoloration (erythema, hypopigmentation, or hyperpigmentation), lesions (ulcers and fissures) and atrophy (white epithelium consistent with lichen sclerosis or absence of well-estrogenized tissue). On examination, tenderness (hyperesthesia) at the periurethral or

Chapter 87 VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE

Anterior labial nerve (from ilioinguinal nerve) Dorsal nerve of clitoris Posterior labial nerves Superficial Deep

Branches of perineal nerve

Perineal branch of posterior femoral cutaneous nerve

Dorsal nerve of clitoris passing superior to perineal membrane Perineal nerve Pudendal nerve in pudendal canal (Alcock’s) (dissected) Inferior clunial nerves Gluteus maximus muscle (cut away) Sacrotuberous ligament Perforating cutaneous nerve Inferior anal (rectal) nerves Anococcygeal nerves

Figure 87-2 Nerves of perineum and external female genitalia. (Redrawn from © Netter images “Nerves of Perineum and External Genitalia Female.” www.netter images.com).

Bartholin’s glands and the vulvar vestibule should be outlined using a cotton-tipped swab, scored (on a scale from 0, no pain, to 10, severe pain), and recorded. The hymeneal ring should be assessed for remnants or tight annular hymen which could tear with intercourse and cause dyspareunia. Tone and tenderness and trigger points of the pelvic floor muscles should be assessed. Pudendal nerves proximal to the ischial spines should be palpated for tenderness. It should be determined whether the pain is within the distribution of a particular branch of the pudendal, genitofemoral, ilioinguinal, or inferior hypogastric nerve. Vaginal pH, whiff test, and microscopic examination of the vaginal secretions with saline and potassium hydroxide (KOH) should be performed to rule out vaginitis, vaginosis, and vaginal atrophy. Vaginal fluid may be cultured for Candida (because microscopic evaluation reveals candidiasis in only 50% of cases), bacterial culture and immunoglobulin E (to evaluate for local allergy). All lesions or discolorations should be further evaluated

by colposcopy or biopsy to evaluate for an underlying dermatosis or an infectious or neoplastic process.10

DIFFERENTIAL DIAGNOSIS OF VULVAR OR VAGINAL PAIN Vaginitis The vaginal mucosa has only a few nerve endings needed for the sensations of pain and light touch.11 For this reason, many vaginal infections are asymptomatic until the discharge reaches the vulva, where there is abundant somatic innervation. The problem is then perceived as vulvar itching, burning, or pain. Vaginal Ecology In childhood and menopause, in the absence of estrogen, the vaginal epithelium is thin and undifferentiated.11 Estrogen causes

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thickening of the epithelium and a differentiation into wellrecognized layers (basal, intermediate, and superficial). The percentage of superficial cells on a vaginal smear is indicative of the amount of estrogen activity. The vagina has a large amount of glycogen, second only to the liver, and it is most available in the superficial layers. Estrogen effects the formation and deposition of glycogen in the vagina. Glycogen is important as a substrate for a series of enzymatic and fermentative processes that result in the production of lactic and acetic acid. Normal vaginal flora, consisting largely of lactobacilli and acidogenic corynebacteria, produce lactic and acetic acid from glycogen and its breakdown products. These organisms exist in a delicate balance with a small amount of Candida. The result of this symbiosis is a low vaginal pH, a milieu that is highly selective for bacterial growth and favors only the lactobacilli, corynebacteria, and Candida organisms. Changes in the vaginal flora pH or inoculum of a large amount of foreign bacteria can change this delicate equilibrium and lead to overgrowth of foreign invaders. At a low pH (3.5 to 4.1), normal vaginal flora predominate, but as the pH rises, various pathogens replace them. Interruption of the delicate balance of the vaginal flora can result from antibiotic treatments, pregnancy, oral contraceptives, intercourse, and menses. The vaginal pH is increased with vaginitis, bacterial vaginosis, and atrophy.

Vaginitis: Description, Diagnosis, Treatment Bacterial Vaginosis Bacterial vaginosis, the leading cause of abnormal vaginal discharge (according to the American College of Obstetricians and Gynecologists [ACOG], 1996) is a polymicrobial syndrome in which synergistic activity occurs among a characteristic set of bacterial species (Gardnerella vaginalis and anaerobic bacteria).12 Risk factors for bacterial vaginosis infection include multiple or new sexual partners (male or female), early age at first coitus, douching, cigarette smoking, and use of an intrauterine contraceptive device. Approximately 50% to 75% of women who have bacterial vaginosis are asymptomatic. Symptomatic bacterial vaginosis is associated with a “fishy” odor, thin white or gray discharge, absence of pruritus, and inflammation with rare dysuria and dyspareunia. Diagnosis of bacterial vaginosis is by clinical criteria. Three of the four Amstel criteria have been traditionally needed for diagnosis of bacterial vaginosis. However, a recent study showed that use of only two of the four criteria does not change the specificity or sensitivity of diagnosis.13 The Amstel criteria include the following: 1. Homogeneous, grayish-white discharge 2. Vaginal pH greater than 4.5 3. Positive whiff-amine test, defined as the presence of a fishy odor when 10% KOH is added to vaginal discharge samples 4. Clue cells on saline wet mount. (Vaginal culture plays no role in diagnosis, because the organisms are detected in 50% to 60% of healthy asymptomatic women.) Treatment of bacterial vaginosis is indicated for patients with symptomatic infection, those with asymptomatic infection before abortion or hysterectomy, and asymptomatic women with previous preterm births. It is not necessary to treat sexual partners. The condition spontaneously resolves in up to one third of

women. Treatment regimens include metronidazole or clindamycin, orally or intravaginally. Metronidazole is the most successful therapy, with cure rates of greater than 90% in 1 week and 80% at 4 weeks.14,15 The recommended dose is 500 mg twice a day for 7 days.16 Topical vaginal therapy with 0.75% metronidazole gel, 5 g once daily for 5 days, is just as effective as the oral regimen.16,17 A single oral dose of 2 g of metronidazole is an alternative regimen with higher relapse rate but a similar immediate rate of response.16 Clindamycin appears to be less effective but is a reasonable alternative to metronidazole. It is available as topical vaginal therapy 2% cream, 5 g once daily for 7 days, or oral therapy at 300 mg twice daily for 7 days, or ovules 100 mg once daily for 3 days. Other, less effective therapies include triplesulfa creams, erythromycin, tetracycline, acetic gel, povidoneiodine pouches, ampicillin, and amoxicillin. Candida Candida vulvovaginitis accounts for approximately one third of vaginitis cases. Studies suggest that 75% of women will suffer an attack at least once in their life.8 The infection is less common in postmenopausal women unless they take estrogen therapy. About half of those infected experience more than one episode. Candida albicans infection accounts for 80% to 90% of candidiasis cases; the remainder are evenly split between Candida glabrata and Candida tropicalis. The presence of estrogen, directly or indirectly, enhances candidal growth.18 The organism thrives in many body locations, such as vaginal fluid,19 as well as unsterile saliva.20 In one study, one half of infected patients were found to harbor Candida in the mouth, and about one third had Candida in the anorectal tract; one fourth were found to be colonized in the vagina.21 Besides the gut and vagina, intertriginous skin areas are especially susceptible including the vulva, groin, axillae, coronal sulcus, and the skin folds of the breast and panniculus. The organism needs warmth and moisture and does not survive long on dry skin. Tight-fitting clothing, especially if made of synthetic fabric, is more conducive to Candida than loose clothing is. The mechanism by which Candida species cause symptomatic disease is complex, and includes the host inflammatory response to invasion and yeast virulence factors (e.g., elaboration of proteases). Factors predisposing to symptomatic infection include diabetes, immune suppression, pregnancy, oral contraceptives, antibiotics, metabolic factors (hypothyroidism, anemia, zinc deficiency), and diet. Pregnancy is the most common predisposing factor, with the incidence and severity of infection increasing with the duration of gestation. The increased glycogen content and high hormone levels constitute a favorable environment for the growth of candidal organisms. The newer oral contraceptives have lower estrogen levels and do not seem to predispose patients to Candida infection. Furthermore, one study found that only pill-using women with active herpetic, condylomatous, or anaerobic vaginal infections had increased prevalence of candidiasis.22 Antimicrobials are thought to act as predisposing factors by reducing the number of protective resident bacteria. Some studies have shown that those patients who go on binges of dietary sweets suffer from recurrence of candidiasis and have high levels of urinary sugars derived from lactose and sucrose. By restricting lactose intake, 90% of these patients were able to maintain disease free intervals for longer than 1 year. If a patient has chronic refractory candidiasis, one may consider the possibility of acquired immunodeficiency syndrome (AIDS). Candidiasis has not been traditionally considered a sexually transmitted disease

Chapter 87 VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE

(STD), especially because it does occur in celibate women. However, it may be linked to orogenital sex.23 Vulvar pruritus is the main symptom of candidiasis. Some women notice itching only before menses, and others complain of symptoms only after intercourse. Burning is also a common complaint, particularly on urination, and it is often experienced in those who scratch. Some patients develop reflexive urinary urgency and frequency. The combination of these symptoms can often be mistakenly diagnosed as cystitis. Dyspareunia can be present. Physical examination reveals erythema of the vulva (sometimes with erythematous papules or satellite lesions) and vaginal mucosa. The discharge is classically described as thick, adherent, and “cottage-cheese like,” but it can also be thin and loose. Diagnosis is by vaginal pH, wet-mount, KOH, and culture. Candidal vaginal pH is 4 to 4.5. A pH value of 4.7 or higher essentially limits the diagnosis to candidiasis or physiologic discharge. The diagnosis is confirmed by KOH wet mount and microscopic examination of vaginal material. The addition of 10% KOH destroys cellular elements and facilitates recognition of budding yeast and pseudohyphae. Because microscopy is negative in up to 50% of patients with confirmed vulvovaginal candidiasis, culture should be performed for patients with persistent or recurrent symptoms. Treatment of candidiasis is indicated for relief of symptoms. Those who harbor Candida but are asymptomatic do not require therapy. Most patients (90%) have uncomplicated infections. The most commonly used antifungal agents are the azoles. There are both oral and vaginal preparations. The only oral preparation recommended is fluconazole: a 150-mg dose of fluconazole is as effective as multiple doses of intravaginal clotrimazole and oral butoconazole. Complicated infections occur in women with uncontrolled diabetes, immunosuppression, or a history of recurrent vulvovaginal candidiasis, and in those who are infected with Torulopsis (Candida) glabrata, or C. tropicalis. These women are less likely to respond to short courses of antimycotic drugs and may require 7 to 14 days of topical therapy or two doses of oral therapy 72 hours apart. Between 65% and 70% of those infected with C. glabrata respond to intravaginal boric acid (600 mg daily for 2 weeks), or a cure rate of more than 90% may be achieved with flucytosine cream (5 g nightly for 2 weeks).24 Documented recurrent infections warrant testing for human immunodeficiency virus (HIV) infection and glucose tolerance testing and may require weekly and then monthly therapy for 4 to 6 months.

women. The infection is associated with a high prevalence of coinfection with other STDs. There is a positive association between trichomonas infection and HIV infection.29 Trichomonads can survive in an aqueous environment between 20 and 30 degrees and can remain infectious for up to 24 hours.30 Women can deposit the trichomonads on toilet seats, on which the organism can survive up to 45 minutes.31 There are several signs and symptoms of trichomoniasis. One pathognomonic sign is abundant green, frothy, foul-smelling discharge with an alkaline pH (>6). Sometimes, generalized erythema is the only gross change in the vaginal tissue. “Strawberry vagina” is also associated with trichomoniasis, when the presence of swollen papillae project through a layer of discharge. Pruritus, or itching, is the second most common manifestation of trichomoniasis. Other symptoms include dyspareunia, urinary symptoms from urethrocystitis, discharge from the urethra and Skene’s ducts, and erythema of the vulva. The most practical and cost-effective diagnostic test available is still the saline wet mount done in a clinic setting.8 However, motile trichomonads are found only in 50% to 70% of cultureconfirmed cases. Culture on Diamond’s medium is 95% sensitive and more than 95% specific but should only be used if there is a high clinical suspicion despite a negative wet mount result, or wet mount is unavailable. Diagnosis with classic Pap smears is not recommended, but diagnosis with liquid-based pap smears has been shown to be highly specific (99%) and sensitive (61%).32 Treatment is indicated in all nonpregnant women diagnosed with Trichomonas vaginitis and their sexual partners. Trichomonas is associated with preterm rupture of membranes and prematurity in pregnant women, but treatment has not been shown to decrease these complications.33 Oral metronidazole is the treatment of choice; it is preferred over the vaginal route, because systemic administration achieves therapeutic drug levels in the urethra and periurethral glands, which serve as sources for endogenous recurrence. There is no need to identify the source in the male partner before treating him. It has been shown that a single 2-g dose to both sexual partners is as effective as the classic regimen, 500 mg twice a day for 7 days.34 The advantages of the single-dose regimen include better compliance, a lower total dose, shorter period of alcohol avoidance (due to the disulfiram-like effect of metronidazole), and possibly decreased Candida superinfection. In the event of treatment failure, the 7-day regimen should be prescribed before resistance is suspected; many cases of “failure” result from reinfection, possibly from a different or untreated partner.8

Trichomonas The prevalence of Trichomonas infection depends greatly on the population studied. Trichomonas was found in 3% of unselected, asymptomatic college women,25 15% of private patients with leukhorrea,26 6% to 8.9% of pregnant women,27 and 34% of pregnant inner-city adolescents.28 Nevertheless, there seems little justification for screening low-risk, nonpregnant, asymptomatic individuals. Trichomonas vaginalis is a unicellular protozoan flagellate, round or almond-shaped, slightly larger than a polymorphonuclear leukocyte.8 Under high-power microscopy, four flagella can be seen to protrude from the forward end of the trichomonad. They are found in the vagina, urethra, and paraurethral glands. This disorder is almost always sexually transmitted and can be identified in 30% to 40% of male sexual partners of infected

Desquamative Vaginitis Desquamative inflammatory vaginitis (DIV) is not a diagnosis in itself and may be the presentation of a range of blistering disorders, including pemphigus vulgaris, lichen planus, and mucous membrane pemphigoid.35 The existence of an idiopathic subset of DIV remains controversial. It is a rare but disabling condition and manifests in women of any age with a history of discomfort, irritation, and dyspareunia. Women who develop DIV are different from those who typically develop STDs, being older, married, and with higher levels of education. Patients may complain of increased yellow vaginal discharge. Examination of the vulva is normal, but erythematous regions on the vaginal walls are evident, with increased vaginal secretion. Repeated cultures are negative for pathogenic bacteria, viruses, and yeast. Microscopic examination of the vaginal discharge shows an increased number of immature epithelial cells, typical

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rounded parabasal cells, and an increase in polymorphonuclear leukocytes. Gram staining shows an absence of lactobacilli and occasionally increased levels of gram-positive cocci. The vaginal pH is increased from normal to 7.4. A biopsy of the erythematous portion of the vaginal wall for histology and immunofluorescence is necessary to exclude any underlying cause of DIV. This sterile inflammatory vaginitis is difficult to treat, but successful therapy has been reported with steroids and clindamycin. Studies have found that 2% clindamycin suppositories or high-potency intravaginal steroids alone or in combination with oral clindamycin for 4-6 weeks have been effective.36,37 Estrogen deficient women need supplementary vaginal estrogen therapy to maintain remission. Herpes Simplex Virus In the United States, the frequency of genital herpes simplex virus (HSV) is increasing. There are two types of HSV infection; it is reported that HSV-2 causes the most genital infections, and HSV-1 causes the most labial infections. However, HSV-1 genital infections are very common. Prevalence of HSV is high: 21.9% were positive among 13,094 individuals surveyed by the Third National Health and Nutrition Examination.8 HSV is more commonly associated with women, African Americans, single marital status, higher number of sex partners, prior history of an STD, and urban residence.8 Infection is transmitted by direct sexual contact, most commonly when an active virus-secreting lesion is present. HSV has been recovered from asymptomatic male carriers and from the cervix of asymptomatic women. Subclinical shedding is common, occurring in 55% of women with HSV-2 and 29% of women with HSV-1.38 In 70% of patients, transmission was linked to sexual contact during periods of asymptomatic viral shedding. Transmission of genital HSV was documented in 14 couples, and the risk was greater with male than female source partners (17% versus 4%).12 The types of genital HSV infection are primary, nonprimary first episode, and recurrent. The clinical manifestations of genital HSV are variable, depending on the type of infection.39,40 In acute primary and recurrent infections, the initial presentation can be severe, with painful ulcers, dysuria, fever, tender inguinal lymphadenopathy, and headache. Other patients have a mild presentation or are entirely asymptomatic.39,41 Recurrent infections are typically less severe than primary or nonprimary first-episode infections because of preexisting immunity. In turn, a nonprimary first episode is typically less severe than the primary infection, because the antibodies to one HSV type offer some protection against the other. Recurrent infections are more common with HSV-2 than HSV-1: 60% versus 14% in patients with a first symptomatic episode of genital herpes.42 Recurrent lesions are fewer in number and are more often unilateral than bilateral.39 In a primary infection, the average incubation period is 4 days.40 Patients usually have multiple, bilateral, ulcerating, pustular lesions that resolve after a mean of 9 days. Other symptoms include systemic headache, malaise, fever, and myalgia (67%); local pain and itching (98%); dysuria (63%); and tender lymphadenopathy (80%). Virus is very often isolated in the urethra and cervix of women with first-episode infection.39 Extragenital manifestations of HSV include orolabial symptoms, aseptic meningitis, urinary bladder retention, distant skin lesions, herpetic whitlow, and proctitis. The clinical manifestations of HSV in immunocompromised patients are more extensive and include

mucocutaneous involvement, variable appearance of genital lesions, and the development of chronic and recurrent ulcers. Patients may have prolonged viral shedding. In addition to genital symptoms, patients may also have more neurologic complications, such as aseptic meningitis, sacral radiculopathy, and transverse myelitis.43 The differential diagnoses of HSV include syphilis, chancroid, Behçet’s disease, and drug eruptions. Diagnosis based on history and physical examination is often inaccurate, and laboratory testing is required. Diagnostic tests include viral culture, polymerase chain reaction (PCR), and direct fluorescence antibody (DFA). Viral cultures can be obtained with active lesions; the vesicle should be unroofed for sampling of the vesicular fluid. The overall sensitivity of viral culture is 50%,44,45 and the highest yield is in the early vesicular stages rather than the later, crusted stages.46 HSV PCR is a more sensitive method for samples taken from genital ulcers, mucocutaneous sites, and cerebrospinal fluid, and it is particularly useful in detecting asymptomatic viral shedding.47-49 DFA is specific, reproducible, and less expensive than PCR. Serology is important because it is type-specific and antibodies persist indefinitely in the serum. Because HSV is a viral disease, there is no cure; however, drug treatment can shorten the duration of symptoms, and, in patients with frequent recurrences, medicine can be used as prophylactic therapy. There are three main drugs used in the treatment of HSV: acyclovir, famciclovir, and valacyclovir. In 2002, the Centers for Disease Control published treatment guidelines for the various types of HSV infection.16 Recommended regimens for individuals with first episode are acyclovir (400 mg PO three times daily or 200 mg PO five times a day), famciclovir (250 mg PO three times daily), or valacyclovir (1 g PO twice daily) for 7 to 10 days. Recommended regimens for individuals for suppressive therapy are acyclovir (400 mg PO twice daily), famciclovir (250 mg PO twice daily), or valacyclovir (1 g PO daily or 500 mg PO daily). Recommended regimens for individuals with recurrent episodes are acyclovir (400 mg PO three times daily or 200 mg PO five times a day or 800 mg PO twice daily), famciclovir (125 mg PO twice daily), or valacyclovir (1 g PO daily) for 5 days or valacyclovir (500 mg PO twice daily) for 3 to 5 days. Postherpetic neuralgia due to HSV has not been well documented, although the herpes virus can increase the risk of vulvodynia due to recurrent herpes prodromal symptoms or pudendal neuropathy. Prodromal symptoms may be accompanied by positive HSV immunoglobulin M antibody serology; they respond to antiviral agents, whereas the pudendal neuropathy does not. Human Papillomavirus HPV infection can lead to vulvar itching and pain through its anogenital manifestations. Condylomata acuminata usually manifest as single or multiple papules on the vulva, cervix, vagina, perineum, or anal region. The most common sites in women are the posterior introitus, followed by the labia majora and labia minora. External HPV lesions are frequently associated with cervical lesions. The lesions are flesh-colored, hyperkeratotic, exophytic, and either sessile or pedunculated.50 HPV subtypes, other than the low-risk types 6 and 11, are also closely associated with squamous intraepithelial lesions of the cervix. Diagnosis begins with a clinical examination supplemented with histologic examination of suspicious lesions. Biopsy is recommended in atypical cases or if the benign nature of the lesion is unclear.

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There are several treatments for anogenital warts. For home therapy, podophyllotoxin or imiquimod may be used. For office therapy, podophyllin or 40% trichloroacetic acid may be used. Surgical options include cryotherapy, laser therapy, electrosurgery, and surgical excision. Atrophic Vaginitis Estrogen-deficient vaginal and vestibular epithelium can be associated with itching, burning, and dyspareunia, due not just to decreased lubrication but also to fissuring from thin epithelium and poor compliance. Perimenopause or postmenopause status, use of hormonal contraceptives, and breastfeeding are the most common circumstances leading to atrophy. The vaginal epithelium loses its glycogen-rich superficial epithelial cells; the vaginal walls loose rugation and become pale or subject to petechial hemorrhage on contact; and the vaginal pH is elevated to 5.5. A yellow discharge reveals increased intermediate and parabasal cells under saline wet mount microscopy. Treatment is with 14 days of vaginal estrogen cream or suppository, followed by therapy twice weekly or use of an estrogen-secreting vaginal ring. Improvement can be expected in 2 months, but full estrogenization may take up to 18 months. Systemic absorption is present but is minimal. Dermatoses Lichen Sclerosus Lichen sclerosus is a benign, chronic, progressive dermatologic condition characterized by marked inflammation, epithelial thinning, and distinctive dermal changes.51 This disorder usually occurs in the anogenital area (85% to 98% of cases), where it causes itching and burning.52,53 In 20% of patients, identical lesions appear elsewhere on the body.8 Extragenital lichen sclerosus is most commonly found on the neck and shoulders and is usually asymptomatic. Pertaining to the vulva, the disorder can involve any or all areas, including the perianal skin, the skin folds adjacent to the thighs, and the inner aspects of the buttocks approximating the anus. The disorder usually occurs in postmenopausal women. However, 10% to 15% of cases occur in children, most of which involve female genitalia.54 Even though the disease is reported to occur mostly in white females, lichen sclerosus has also been reported in Native Africans, Asians, and dark-skinned patients. Multiple signs and symptoms are associated with lichen sclerosus. A prodrome to the gross lesions includes nonspecific, dull, painful vulvar discomfort in some women. Other women are asymptomatic. The major symptoms of the disorder include vulvar pruritus (which can be so intense as to disrupt sleep), pruritus ani, painful defecation, anal fissures, rectal bleeding, dysuria, and difficulty voiding. Dyspareunia is associated with introital stenosis, fissures, or posterior deflection of fused labia. On physical examination, the lesions typically begin as white papules that are irregularly outlined and may coalesce into welldefined plaques.8 Classic lesions consist of thin, white, “cigarette paper,” wrinkled skin localized to the labia minora and/or labia majora, although the whitening may extend over the perineum and around the anus in a keyhole fashion. Fissures may be found perianally, in the intralabial folds, or around the clitoris. Excoriations and lichenification may be observed, often associated with edema of the labia minora and the prepuce. Relatively minor

rubbing or intercourse may lead to hemorrhage and/or petechiae with purpura and ecchymoses due to the fragility of the involved skin. Early in the course of the disease, vulvar architecture remains intact; however, phimosis of the clitoris and obliteration of the labia minora and periclitoral structures may be seen later in the course of the disease. There is an increased risk of malignancy in patients with lichen sclerosus, of 4% to 6%. However, proof that lichen sclerosus causes cancer as a precursor lesion is lacking. The skin of patients with vulvar lichen sclerosus should be examined at least yearly. Biopsy should be performed of any thickened plaque that fails to thin with corticosteroid treatment or any persistently open or nonresolving lesion. Diagnosis is by clinical characteristics and histologic confirmation. Before treatment is initiated, if is important that confirmation be made by histologic diagnosis. Multiple punch biopsies should be taken from the vulva, especially from sites of fissuring, ulceration, induration, and thick plaques.8 Treatment is for relief of symptoms and discomfort, to prevent further anatomic changes, and to possibly prevent malignant transformation. Therapy comprises education, behavioral modification, support, and medication. Surgery is reserved for small subset of cases. Patients should first be educated about the chronicity of the disease and reassured that the condition is manageable. A discussion about the possibility of malignancy and the need for yearly monitoring should take place. Patients should be told about good vulvar hygiene and to stop scratching the lesion. The treatment with the best evidence of efficacy is superpotent corticosteroid ointment, clobetasol propionate 0.05% daily for 6 to 12 weeks and then one to three times a week for maintenance.55 Longstanding treatment with clobetasol does not appear to cause untoward skin effects. With the eradication of pruritus, hyperplastic lesions may improve or disappear entirely. There is no role for estrogen, progesterone, or testosterone cream in the treatment of lichen sclerosus. Surgical intervention is indicated only for postinflammatory sequelae of the disease and when malignancy is present. Introital stenosis, posterior fissuring, and scarring of the fourchette are treated with perineoplasty. Surgical treatment for lichen sclerosus results in a recurrence rate that is extremely high, making the operation contraindicated in the absence of significant atypia.8 Lichen Planus Lichen planus is a relatively common papulosquamous disorder of unknown etiology. It has its highest incidence in patients 30 to 60 years of age. It occurs most often on flexor surfaces of the extremities and the trunk. It can also affect nails, mucous membranes including the mouth, esophagus, conjunctivae, bladder, nose, larynx, stomach, and anus. It can be isolated to the vulva or be a part of a more generalized skin eruption. The prevalence of vulvar lichen planus is considered uncommon; it occurs in fewer than 10% of women who have lichen planus over a 3-year period.56 Patient complaints usually include irritating vaginal discharge, vulvar pruritus, burning, and dyspareunia with postcoital bleeding. Physical examination findings differ depending on the type of lesion. Papulosquamous lichen planus consists of small, intensely pruritic papules with a violaceous hue that arise on keratinized and perianal skin. Hypertrophic lichen planus is characterized by hyperkeratotic, rough lesions on the perineum and perianal region.57 The appearance is similar to squamous cell carcinoma. Erosive lichen planus refers to glassy, brightly

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erythematous erosions with white striae or a white border (Wickham’s striae) often visible along the margins. It can occur on the labia minora and vestibule as isolated lesions on an otherwise normal vulva or in association with marked architectural destruction, including loss of the labia minora and narrowing of the introitus. Vaginal involvement is reported in up to 70% of patients with erosive lichen planus, whereas vaginal involvement is not seen in lichen sclerosus.57 The vaginal lining may be friable, easily bleeding. The vagina may be massively inflamed and denuded with seropurulent exudates, pseudomembrane, or serosanguineous discharge. In severe cases, adhesions and synechiae develop that can lead to narrowing or obliteration of the vagina. The vulvo-vaginal-gingival syndrome is a variant of erosive lichen planus. It involves the epithelium of the vulva, vestibule, vagina, and mouth. The lesions may not be concurrent; for example, lesions in the mouth can proceed or follow lesions in the genital area for months or years.8 The diagnosis of lichen planus is based on characteristic clinical manifestations. Classic histopathologic features include irregular acanthosis of the epidermis, liquefactive degeneration of the basal cell layer, and band-like dermal infiltrate of lymphocytes in the upper dermis. Hyperkeratosis is present in areas of keratinized skin. Typical histopathologic features are not found in mucosal lesions. Also, tissue biopsies are not specific except in the erosive type. The oral and genital lesions of lichen planus, especially lichen planus, are persistent and resistant to therapy. There is no single effective therapy for erosive vulvar lichen planus, which is extremely difficult to treat. On the other hand, hypertrophic and papulosquamous lichen planus respond well to therapy. Patients should be told to maintain good vulvar hygiene and to stop scratching. The first line and mainstay of therapy is corticosteroids: topical, interlesional, and oral corticosteroids are all used. For erosive lichen planus, ultrapotent topical steroids (clobetasol or halobetasol propionate 0.05% ointment) can be applied nightly for 3 to 6 weeks, depending on the severity of disease. The ultrapotent steroid can then be reduced to twice per week, with a midpotency ointment of low potency ointment added, one to three times per week, for maintenance. It may be necessary to experiment to find the best course. Vaginal corticosteroids in the form of suppositories can be used for vaginal lesions. In one study, 16 of 17 patients improved with 25 mg hydrocortisone suppositories inserted in the vagina twice daily for 2 months.58 In another study of 60 patients, 80% improved by taking 12.5 to 25 mg of hydrocortisone suppositories twice a day for several months, tapering to a symptom-free maintenance dose once or twice weekly.59 Lichen Simplex Chronicus Lichen simplex chronicus is also called leukoplakia and hyperplastic dystrophy.8 The condition is caused by histologic changes in the vulvar dermis after persistent rubbing or scratching, usually in women who experience chronic irritation and/or pruritus. The condition is characterized by epithelial thickening and hyperkeratosis. There is an enhancement of the normal crosshatch markings of the skin, called lichenification.60,61 Labial skin folds appear greatly exaggerated, often edematous, and pubic hair can be broken or sparse. The lesions tend to occur on the mons pubis and labia majora. The most important element about diagnosing lichen simplex chronicus is to perform a biopsy to distinguish it from lichen

sclerosus, lichen planus, and carcinoma. Treatment is discussed in the section on allergic dermatitis. Neoplasm Vulvar cancer is the fourth most common gynecologic cancer (after uterine, ovarian, and cervical cancer) and comprises 5% of malignancies of the female genital tract.62 Vulvar carcinoma is most frequently found in postmenopausal women, with the mean age at diagnosis being 55 to 65 years. The signs and symptoms of all histologic types of vulvar malignancy are similar. Presentation usually includes a unifocal vulvar nodule, plaque, ulcer, or mass on the labia majora (40%), labia minora (20%), clitoris (10%), mons (10%), or perineum (15%). Lesions are multifocal in 5% of cases. The most common presenting symptom is pruritus. Other symptoms include vulvar bleeding or discharge, dysuria, or enlarged groin lymph node, but many patients are asymptomatic at time of diagnosis. There are two main categories of vulvar neoplasms, that of the squamous cell type and Paget’s disease.8 In 1984 and 1987, the ISSVD further subdivided these two classifications. Squamous cell type was divided into vulvar intraepithelial neoplasm (VIN) I (mild dysplasia), VIN II (moderate dysplasia), and VIN III (severe dysplasia to carcinoma in situ). The other category included Paget’s disease and melanoma in situ. More than 90% of vulvar malignancies are squamous cell. Two subtypes exist. The first (classic or Bowenoid type, VIN) is predominantly associated with HPV-16 and -18 and is found in younger women.63,64 Risk factors for this subtype include early coitarche, multiple sexual partners, HIV infection, and cigarette smoking. The second, more common subtype (keratinized, differentiated, or simplex type) occurs in older women and is not related to HPV infection. The gross appearance of VIN lesions is usually quite distinct: they are well localized, delineated, slightly elevated, white, and rough. The tissues may have a red or brown hue, and both red and white patches may be noted. These changes can be seen anywhere on the vulva but are most commonly found in the region of the fourchette and perineum. Squamous cell carcinoma in situ is a superficial, noninvasive, intraepithelial carcinoma characterized by chronicity, pruritus, burning, and a variable gross appearance. The diagnosis can be established only by histopathologic study, and biopsies should be taken from more than one site. Some sources say that the biopsy should be taken from the center of the lesion, because those taken from the leading edge do not reflect the most severe histology of the lesion. The best means of detecting an intraepithelial lesion is by careful inspection of the vulva. Surgical extirpation is the primary treatment for earlystage vulvar carcinoma. Paget’s Disease Pruritus is the most common symptom of Paget’s disease, occurring in 70% of patients. The appearance of the Paget’s lesion is variable. Typically, it manifests as an erythematous, eczematoid lesion with scales and a crust scattered over the surface. It may also appear as a grayish-white lesion and frequently with moist and oozing ulcerations that bleed readily on contact. The disease is usually multifocal and occurs anywhere on the vulva, mons, perineum/perianal area, or inner thigh. Diagnosis is by biopsy of the lesion, looking for characteristic histopathology. Vulvar biopsies should be performed for patients with suspicious lesions, including those with persistent

Chapter 87 VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE

pruritic eczematous lesions that fail to resolve with 6 weeks of therapy. Patients should also be evaluated for invasive carcinoma: two series found a 4% to 17% rate of invasive carcinoma within or beneath the surface of the Paget’s lesion.65,66 Women with this disease should also be evaluated for synchronous neoplasms, because approximately 20% to 30% of these patients have a noncontiguous carcinoma (breast, rectum, bladder, urethra, cervix, or ovary).67 Treatment includes wide local excision of the disease. The local recurrence rate is high, 12% to 58%. Recurrence may occur despite negative margins, probably because of the multicentricity of the disease and microscopic extension of disease beyond clinically visible margins.66 Recurrence after initial therapy and noncontiguous carcinoma are common. Vulvar Infection Folliculitis Folliculitis is a pyoderma of the hair follicles. Pyoderma is defined as a localized, purulent streptococcal infection of the skin. Predisposing factors to the development of folliculitis include nasal carriage of Staphylococcus aureus, use of swimming pools and hot tubs, and antibiotic administration and corticosteroid therapy predisposing to Candida. The most common pathogens are S. aureus, Pseudomonas aeruginosa, and Candida species. Other predisposing conditions include obesity, sweating, maceration, malnutrition, diabetes, seborrhea, poor hygiene, scabies, and pediculosis.8 Patients usually present with pain and tenderness, depending on the depth and extent of the lesions. Folliculitis lesions are typically small, less than or equal to 5 mm. They initially appear as papules that develop into vesicles, surrounded by a ring of erythema. Folliculitis does not cause systemic toxicity, and the lesions may spontaneously drain and resolve without scarring. Treatment includes the use of topical therapies. Warm saline compresses can accelerate pointing, at which time the lesion can be incised. Superficial folliculitis usually responds well to erythromycin-containing antibiotic lotion or cream and use of germicidal soaps. Antifungal agents are useful in the case of Candida infections. Mupirocin ointment should be considered for patients with frequent recurrences of folliculitis who are suspected of having nasal colonization with S. aureus. The ointment is applied to the anterior nares bilaterally twice a day for 5 days each month.68 Complications of folliculitis include recurrence and progression to furunculosis. Bartholin’s Gland Cyst or Abscess Bartholin’s duct cysts are seen in approximately 2% of new gynecologic patients.8 They arise in the duct system, and the occlusion is usually near the opening of the main duct into the vestibule. Chronic inflammation can obstruct the orifice and lead to cystic dilation of the duct, but not the gland, proximal to the obstruction. Bartholin’s cysts average 1 to 3 cm in size and are usually asymptomatic. Larger cysts are associated with vulvar pain, dyspareunia, or difficulty sitting or ambulating. Discomfort may be associated with rapid enlargement, as might be induced by repeated or prolonged sexual stimulation. The diagnosis is clinical and is based on the findings of a soft, painless mass in the medial labia majora or lower vestibular area.

Most cysts are unilateral and are detected during a routine pelvic examination of by the woman herself. No treatment is necessary for asymptomatic Bartholin’s cysts, except in postmenopausal women, in whom a biopsy or excision should be considered to rule out carcinoma. These cysts are usually sterile and therefore do not require antibiotic therapy.69 A cyst that is symptomatic or disfiguring requires treatment, of which there are several modes. The simplest procedure is an incision and drainage, with or without packing. However, if this procedure is done alone, there is a high likelihood of recurrence when the incised tissue edges reapproximate. Supplementation of the incision and drainage can be performed with a Word catheter. It is a balloon-tipped device that can be placed in the cavity after drainage. The bulb is inflated to keep the catheter in place for 2 to 4 weeks while the duct tract epithelializes. The end of the catheter is tucked in the vagina to minimize discomfort. An alternative procedure after failure of the Word catheter is marsupialization of the gland, whereby a new orifice is created. A fourth method involves sclerotherapy, in which silver nitrate sticks are inserted into the cyst cavity to necrotize the cyst wall after incision and drainage. Mild burning may occur. The patient returns after 48 hours for cleaning of the vulva. A randomized controlled trial found that silver nitrate insertion was as effective as excision of Bartholin’s cysts or abscesses.70 Excision of the entire Bartholin’s gland is the definitive procedure for both cysts and abscesses. It is usually considered after other methods have repetitively failed, because it is not an office procedure and has higher morbidity, including excessive bleeding, hematoma formation, cellulitis, and dyspareunia. Bartholin’s gland ducts and cysts can become infected and form abscesses. They are usually the result of polymicrobial infections, with the most common organisms being Escherichia coli, Neisseria gonorrhoeae, and Bacteroides species.71 Therefore, patients should have both routine cultures and those for gonorrhea and chlamydia. Symptoms for Bartholin’s abscess include pain and tenderness over the affected gland. Usually, these abscesses develop rapidly, within 2 to 3 days, and are associated with acute pain and tenderness. They tend to rupture spontaneously within 72 hours. Patients usually present with pain on intercourse or pain on walking and sitting. Examination reveals a lesion that appears as a large, tender, soft or fluctuant mass in the medial labia majora or lower vestibular area, occasionally with erythema, edema, and pointing of the abscess. Treatment entails drainage of the abscess, which provides immediate pain relief. Incision and drainage can be performed, followed by Word catheter placement, marsupialization, or silver nitrate insertion. Antibiotic regimens include one dose of ceftriaxone (125 mg IM) or cefixime (400 mg PO) to cover E. coli and N. gonorrhoeae plus clindamycin (300 mg PO four times a day for 7 days) to cover anaerobes. If Chlamydia trachomatis is present, azithromycin (1 g PO in a single dose) should be administered. Treatment with broad-spectrum antibiotics may easily delay ripening of the abscess. For women older than 40 years of age, some recommend complete excision of the gland to exclude underlying carcinoma.72 Allergic Dermatitis Contact dermatitis is an inflammatory reaction of the skin to a primary irritant or to an allergenic substance. Vulvar dermatitis (vulvar eczema) is the most common vulvar inflammatory skin

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disease in women. One third to one half of women’s vulvar complaints stem from this problem.73-75 Patients with this disorder have chronic irritation and pruritus, which leads to persistent rubbing and scratching. There are two types of vulvar dermatitis, endogenous and exogenous. Endogenous dermatitis is also called atopic dermatitis and has a familial disposition. It begins in childhood and may affect other parts of the body. Erythema found in labial folds, perianally, and in the skin between the buttocks suggests endogenous vulvar dermatitis. Exogenous dermatitis is also called contact dermatitis and results from external factors. Allergic dermatitis accounts for 20% of cases and results when an allergen induces an immune response. In irritant contact dermatitis (80% of cases), the trigger directly damages the skin. The history is important for differentiating among atopic, allergic, and contact dermatitis. What is the intensity of the pruritus, and when is it the worst? What kind of feminine products are used? Does the patient wear occlusive clothing that predisposes to Candida? Does she use any type of medication or scented soaps or deodorants? A patch test may be required to distinguish between atopic and contact dermatitis; biopsy is not helpful. Positive patch tests for relevant substances occur in 25% to 60% of women with vulvar pruritus. Biopsy, however, should be obtained to rule out other possible causes. Coexistent infections should also be diagnosed so they can be treated. Treatment involves behavioral modification and medications. First, the patient must modify any hygiene or clothing habits that facilitate dermatitis. Then, she must eliminate known or suspected allergens and irritants. She should be warned to refrain from scratching. Wet compresses or soaking in warm water must be undertaken for a day or two in order to restore the natural physiologic environment of the vulva. After this, the patient is ready for topical application of corticosteroid cream or lotion. For mild cases, use of a low- or medium-potency steroid is usually effective (hydrocortisone or triamcinolone), twice a day for 2 to 4 weeks, then twice a week and taper to pruritic symptoms. For severe cases, high-potency steroids may be necessary (clobetasol propionate or betamethasone dipropionate) every night for 30 days and then re-evaulate. Potent steroids can be used for up to 12 weeks on the vulva without adverse effects.76,77 Trauma Trauma to the vulva and vagina may lead to vulvar pain, dyspareunia, vulvar and vaginal lesions, and discharge. Accidental injuries are seldom seen in the vulva and vagina because of their anatomic location.8 The injuries seen in prepubertal girls result most commonly from straddling objects such as bench rails, gymnasium equipment, bicycle frames, baths, and toilet seats. In adults, these injuries can be secondary to automobile and motorcycle accidents, bicycle accidents, sexual trauma, snowboarding, or physical assault. Some injuries may result from placing inanimate objects into the vagina. Most of these lesions manifest as hematomas and lacerations. Lacerations of the vulva or vagina commonly occur from a violent fall on a slender object. Examples include falling on a stake, picket fence, handlebars of a bicycle, or the binding of a snowboard.78 Lacerations may extend into the rectum, bladder, urethra, or the peritoneal cavity through the cul-de-sac. The area must be inspected carefully for remnants of glass, metal, or plastic. Anterior, posterior, and lateral radiographs including the

vaginal area should be taken to locate metallic or other radiopaque objects. Lacerations can cause profuse hemorrhage, pain, and shock. Treatment includes restoration of normal anatomic relationships. Bleeding vessels should be ligated and tissue edges carefully reapproximated with absorbable suture. Large traumatized areas require copious irrigation and débridement. Other concomitant injuries should be ruled out. Sexual injuries are a major source of damage to the vulva and vagina. The right and posterior fornices of the vaginal vault are frequent sites of injury for parous women, whereas lower vaginal and introital injuries are often caused by defloration.79 Rape and insertion of foreign bodies are additional sources of vulvar and vaginal injury. Genital injuries as a result of consensual intercourse are rare. Most introital injuries associated with consensual first coitus are minor and lead to minimal bleeding.8 These injuries can be managed conservatively with compression. If the injury involves an extensive laceration of the hymenal ring that extends into the vagina with profuse bleeding, suturing of the laceration is indicated. It has been postulated that vigorous intercourse increases abdominal pressure, causing tensing of the cul-de-sac and decreasing the elasticity of the posterior fornix, which results in a higher likelihood of laceration. Fissuring of the posterior fourchette (vulvar granuloma fissuratum) repeatedly with intercourse may cause a nonhealing granuloma that requires primary excision and closure.80 Foreign objects can cause trauma of the vulva or vagina. With certain sexual techniques, patients have been known to insert molded phalluses, glass objects, tops of aerosol cans, and occasionally metal objects into the vagina, which can cause laceration. If glass objects are the cause, it is important to inspect the tissue for the presence of residual foreign bodies, with subsequent irrigation and removal. Patients also occasionally forget to remove tampons. If the tampon remains in the vagina for a long period, there is often a foul, copious, brownish discharge. A simple examination usually demonstrates the presence of the tampon. Removal of the tampon is usually sufficient unless it has been retained for more than 10 days, at which point it is appropriate to give antibiotic therapy. Vaginal pessaries are also a main culprit of vaginal trauma. They are usually used by elderly women with extensive vaginal vault prolapse and may cause erosive conditions in these patients. The patient usually complains of malodor and bloody discharge, which is indicative of abrasion and erosion of the vaginal mucosa. The use of intravaginal estrogen to prevent vaginal tissue thinning helps prevent erosion. Prolapse Pelvic organ prolapse refers to a hernia of one of the pelvic organs (uterus, vaginal apex, bladder, rectum) and its associated vaginal segment from its normal location. Pelvic prolapse occurs, in part, because of site-specific fascial defects that result in anterior, apical, or posterior segment weakness. Risk factors include multiparity, operative vaginal delivery, obesity, advanced age, estrogen deficiency, neurogenic dysfunction of the pelvic floor, connective tissue disorders, prior pelvic surgery, and chronically increased intra-abdominal pressure. The displacement of the pelvic organs is graded on a scale of 0 to 4, with 0 referring to no prolapse; 1, halfway to the hymen; 2, at the hymen; 3, halfway out of the hymen; and 4, total prolapse (procidentia). There are also different prolapsed organs. Cystocele is herniation of the bladder with associated descent of the

Chapter 87 VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE

anterior vaginal segment. Cystourethrocele is cystocele combined with distal prolapse of the urethra with or without associated urethral hypermobility. Uterine prolapse is descent of the uterus and cervix into the lower vagina, to the hymenal ring, or through the vaginal introitus. Vaginal vault prolapse is descent of the vaginal apex (after hysterectomy) into the lower vagina, to the hymenal ring, or through the vaginal introitus. Rectocele is hernia of the rectum with associated descent of the posterior vaginal segment. Enterocele is herniation of the small bowel/peritoneum into the vaginal lumen, most commonly after hysterectomy in conjunction with vaginal vault prolapse. The most common symptoms are a sensation of pressure and heaviness or protrusion of tissue from the vagina. Patients may also complain of low back pain and a feeling of heaviness that is relieved with lying down and worsens as the day progresses. Loss of anterior support can lead to urinary stress incontinence. A large anterior vaginal prolapse with vaginal vault eversion can lead to urinary retention. A rectocele can cause defecatory dysfunction. Sexual dysfunction may accompany prolapse of any of the compartments. Because there may be protrusion of the vaginal mucosa, irritation can occur and bleeding may be reported. Diagnostic evaluation includes examination of the vaginal support from both upright and recumbent positions. The traditional speculum examination should be supplemented with a site-specific examination with a single-bladed speculum or one half of a Graves speculum. This allows for a better view of the vaginal walls when looking for specific defects of vaginal support. A rectovaginal examination should be performed with the patient in standing position for detecting an enterocele, because the small bowel, if present, can be palpated easily in the cul-de-sac between thumb and forefinger. Magnetic resonance imaging is a useful diagnostic tool. Treatment of mild prolapse is with pelvic floor exercises, physical therapy, or behavioral modification. Women with moderate prolapse or who are not surgical candidates may benefit from a pessary. Surgical treatment is usually necessary for severe prolapse. Surgery can be associated with an up to 30% rate of recurrence/reoperation.81 Rigid Hymenal Ring The hymen varies in thickness and elasticity. It may be quite elastic and easily stretched without laceration at initial sexual intercourse, or it may be tough and rigid so as to cause dyspareunia or even prevent intercourse. Attention may be drawn to this problem when the patient is unable to insert a tampon. Treatment with appropriate estrogen cream, small dilators, or hymenoplasty can correct the problem and prevent unnecessary laceration of the hymen and introitus due to trauma from intercourse.8 Vulvar Neuroma Vulvar neuroma, which is usually caused by traumatic or iatrogenic transaction of peripheral nerve fibers, can cause dyspareunia and vulvar pain. It is postulated that dyspareunia related to episiotomy may be associated with disorganized proliferation of proximal nerve stumps. Patients can be in all age groups. There have been scarce case reports in the literature, but vulvar neuromas are often associated with episiotomy repairs and, in one case report, with female genital cutting.82 The patient usually describes

a deep pain of gradual onset that becomes more intense with time. The pain is usually unilateral without dyspareunia. Diagnosis is point tenderness that duplicates the pain. Frequently, a tiny nodule is palpable in the soft tissue, and most often patients can put their finger right on this area. There is no reliable efficacious treatment that ensures no recurrence. Treatment modalities include cryotherapy, chemical ablation, radiofrequency ablation, and surgical excision of the neuroma.83 Localized Vulvar Pain of Vestibule (Vestibulodynia or Vulvar Vestibulitis) Vulvar vestibulitis syndrome (VVS) orvestibulodynia is characterized by discomfort and hypersensitivity in the vulvar vestibule in the absence of physical findings except for varying degrees of erythema.84 Some investigators have proposed that there are two forms, primary and secondary. Primary VVS refers to introital dyspareunia dating from initiation of sexual activity or intolerable pain consistently present on insertion of a tampon or vaginal speculum.6,85 It accounts for 20% of cases.86 Secondary VVS describes introital dyspareunia that develops after a period of comfortable sexual relations, tampon use, or speculum examinations. The standard diagnostic criteria for VVS in the medical literature are as follows: severe pain on vestibular touch or attempted vaginal entry; tenderness to pressure localized within the vulvar vestibule; and no evidence of physical findings except for varying degrees of erythema.87 Spontaneous pain is minimal or absent. The pain is associated with intercourse, tampon use, binding clothes, and bicycle riding. In one study, one third of women had constant burning in the vestibule, three quarters had excessive vaginal discharge, and 10% had chronic urinary tract symptoms.88 This phenomenon is more prominent in premenopausal women.89 Risk factors related to some aspects of sexual reproductive history have been identified in women with VVS; they include early contraceptive use (before 17 years of age),90 early intercourse (before 16 years), and early menarche (before 12 years). Candida infection and STDs, on the other hand, have not been associated with increased risk of VVS.84 Other studies have proposed an autoimmune association between Candida and VVS.91 Excessive urinary oxalate excretion has been proposed as an etiology of vulvar pain, based upon a case report of one patient in whom complete remission of symptoms occurred with low oxalate diet.92 A controlled study of urinary oxalate excretion, however, did not show differences in women with and without pain.88 Another theory is that allergy causes VVS, because levels of immunoglobulin E consistent with vaginal allergy have been detected in vaginal fluid; however, treatment with antihistamines has not been effective.88 It has been suggested that some women have a genetic deficiency that impairs their immune system’s ability to stop the inflammatory response triggered by exposure to agents such as infection or chemicals.94 VVS is also associated with interstitial cystitis, which makes sense when one considers that the vestibule, bladder mucosa, and urethra share a common embryologic derivation from the urogenital sinus.95,96 On examination, there is tenderness to gentle cotton swab pressure in the vestibule (allodynia). The diagnosis is made when touching the vulva with a cotton-tipped applicator produces pain only in the vestibule.85 Some say that the Q-tip test is the sine qua non of diagnosing vestibulitis.83 While gentle tactile stimulation is applied to specific areas of the vestibule, the patient can rate

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her discomfort. Starting at 12 o’clock (just below the clitoris and above the urethra) and proceeding clockwise, the most tender areas may be at 4 and 8 o’clock. Other diagnoses must be ruled out, and estrogenization should be assessed with vaginal wet mount, looking for predominance of intermediate or parabasal cells instead of the normal, well estrogenized superficial cells. The most common conditions mimicking VVS are Candida infection, poor estrogenization, pudendal neuropathy, dermatitis, rigid hymen, and vaginismus/ pelvic floor muscle tension myalgia. The first step in treatment of VVS, once a diagnosis is made, is to validate the patient’s pain and reassure her that it is not psychological in nature and is not caused by cancer. The next step is to ensure adequate vulvar care. Patients should avoid scents, dyes, and chemicals, including fabric softener, bubble bath, body wash, and so on. Clothing should be cotton, comfortable and loose. Activities that may be abrasive to the vulvar area, such as biking, should be eliminated. Hydration by sitz baths may help. Use of natural lubricants, such as olive oil and Astroglide, may help. For burning, ice packs may provide relief. Because anecdotal evidence has supported eliminating foods high in oxalate, the patient may want to try this avenue. Topical anesthetics such as Xylocaine 2% jelly or 5% ointment89 or the compounded triple therapy (prilocaine, lidocaine, tetracaine: 3.5%/2.5%/1%) in a lipoderm base can provide relief if applied three times per day and liberally 20 minutes before sexual activity. This treatment useful because it “numbs the vulva,” but it probably works via its pharmacologic effect of blocking sodium channels and altering neural plasticity. Capsaicin has also been tried in a number of studies, but it has not been widely successful and is painful when first applied.97 Another study showed great improvement with injections of methyl prednisolone acetate and lidocaine cloridrate, with complete remission in 7 of 22 women and marked improvement in 3.98 Triple nerve block therapy using caudal, pudendal, and local anesthetic blocks over 8 weeks has also demonstrated success.98a One of the first-line therapies for VVS, because it appears to be a “neuroplastic pain syndrome,” are the tricyclic antidepressants, which are standard therapy for neuroplastic/neuropathic pain.89 Amitriptyline and desipramine improve pain substantially in patients who can tolerate doses of 50-75 mg.99 Patients should be counseled that the drug is known primarily for its antidepressant effect but is also widely used for pain, so that patients do not feel deceived. Dosing should start at 10 mg and gradually be increased to minimize side effects, until the total dose is 150 mg or the symptoms are controlled. If patients continue to experience drowsiness with amitriptyline despite decreasing doses for a week, then nortriptyline or desipramine should be substituted, using a similar dosing schedule (less sedation and fewer anticholinergic side effects). Tricyclics take at least 4 weeks to have an effect and should be tried for 3 months at 100 to 150 mg before moving on to another agent. Gabapentin or other anticonvulsants should be considered in those who cannot tolerate tricyclics or if those medications fail.89 Patients should be started slowly at 100 mg at bedtime of gabapentin and then increased by 100 mg every 2 days until at least 1800 mg and up to 3600 mg/day is being taken in three divided doses or nightly. Side effects include drowsiness, fatigue, dizziness, and ataxia. Up to 1200 mg can be given at night to decrease drowsiness. Interferonα has been reported to be beneficial, primarily when injected locally.100,101 The most common regimen is 1

million units injected three times per week for 4 weeks circumferentially at the periphery of the vestibule. Side effects include flu-like symptoms, fever, malaise, myalgias; pretreatment with acetaminophen or ibuprofen may help. These patients may also experience significant injection-site pain and may benefit from pretreatment for 20 to 30 minutes with a topical anesthetic. Surgical excision of the vestibule (Woodruff procedure) is another treatment option for patients with VVS. The affected area is mapped and excised, then covered with undermined vaginal epithelium. Many surgeons remove all areas of the vestibule, including those areas that are not painful, because failure can recur in areas of remaining vulvar tissue. One study showed an 85% cure rate.102 Complications include dehiscence, recurrence of symptoms, and occasionally worsening of pain. So, although vestibulectomy was once the treatment of choice for VVS, the discomfort of the procedure, the possibility of incomplete success or worsening of pain, and the success of less aggressive therapies have relegated this procedure to second- or third-line therapy.89 One study compared group cognitivebehavioral therapy (12-week trial), surface electromyographic biofeedback (12-week trial), and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis.103 This study found that, although vestibulectomy was superior to the other treatment modalities, all three groups significantly improved on measures of psychological adjustment and sexual function. Another study by the same group demonstrated that physical therapy is a promising treatment modality for dyspareunia associated with vulvar vestibulitis.104 Dysesthetic Vulvodynia or Generalized Vulvodynia It is likely that this syndrome is a variant of pudendal neuropathy or, at the least, neuropathic pain, and it is best diagnosed and treated as such. Pudendal Neuropathy Pudendal neuropathy, or “essential vulvodynia,” was a label given to patients who complained of constant or almost constant vulvar burning and had a paucity of physical findings.105 Pudendal canal syndrome (PCS) is induced by the compression or stretching of the pudendal nerve in Alcock’s canal.106 Causes of PCS are by sources of compression (biking, long-time sitting, horseback riding, hematoma) or stretching (descending perineum, surgery, delivery) of the pudendal nerve in the patient’s history. A change in the shape or orientation of the ischial spine induced by some athletic activities may also explain some cases.107 Pudendal neuralgia can also be found in patients with multiple sclerosis and postherpetic neuralgia. The complete syndrome manifests with pain, hypoesthesia or hyperesthesia, and sometimes anal or urinary incontinence. However, motor symptoms are actually rare. Patients can present with an unprovoked, persistent, superficial, burning sensation that is frequently accompanied by a deep, aching component or a rare, paroxysmal lancinating pain over a large area.105 Patients with less severe involvement may complain of an itch-burn sensation or a feeling of rawness. Some patients have burning pain with light touch and complain of dyspareunia not only on penile penetration but also during and after intercourse. Patients may also have rare, symptom-free periods that last for days or weeks. Because of the various areas supplied by the pudendal nerve, the following structures can be involved: cutaneous surfaces of the

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labia minora and majora, clitoris, urethral meatus, vulvar vestibule, perineum, and perianal skin. Physical findings are sparse. There is normally no evidence of infection. Focal vestibular erythema with or without tenderness is sometimes seen. Positive findings include thickened surgical scars, presence of palpable tumor, or evidence of genital herpes. Some patients have a weak anal reflex.108 Pudendal neuropathy is usually a diagnosis of exclusion. However, a pudendal nerve block can be used as both a diagnostic and a therapeutic measure. The pain usually disappears for only 1 to 2 days after injection. The block is repeated every third day for a total of four blocks. Computed tomography–guided blockade may be more accurate.109 Other tests sometimes found to be abnormal in PCS include electromyography (EMG) and pudendal nerve terminal motor latency (PNTML). There is diminished EMG activity of the external anal sphincter, external urethral sphincter, and levator ani. There is a significant increase in PNTML in women with severe PCS. Depending on the severity of the problem, there are several modalities of treatment. Nonsteroidal anti-inflammatory agents are frequently used but are not helpful in most cases. In mild cases, tricyclic antidepressants may be helpful.105 Anticonvulsants such as carbamazepine, phenytoin, and gabapentin have also been found to be helpful.110 As described earlier, serial pudendal blocks with a local anesthetic can be used. However, if none of these measures are helpful, another PNMLT is abnormal, there is evidence that surgical decompression of the pudendal canal may lead to improvement.108,111 Pelvic Floor Muscle Disorders: Myalgia and Trigger Points Trigger points are discrete, focal, hyperirritable spots located in a taut band of skeletal muscle.112 The spots are painful on compression and can produce referred pain, referred tenderness, motor dysfunction, and autonomic phenomena. Acute trauma or repetitive microtrauma may lead to the development of stress on muscle fibers and the formation of trigger points. Patients may have regional, persistent pain resulting in a decreased range of motion in the affected muscles. These include muscles used to maintain body posture, such as those in the neck, shoulders, and pelvic girdle. Trigger points may also manifest as tension headache, tinnitus, temporomandibular joint pain, decreased range of motion in the legs, and low back pain. Trigger points can also be found in the pelvis, causing pelvic pain. Palpation of a hypersensitive bundle or nodule of muscle fiber of harder than normal consistency is the physical finding typically associated with a trigger point. Palpation of the trigger point elicits pain directly over the affected area and/or causes radiation of pain toward a zone of reference and a local twitch response. Various treatment modalities, such as the spray and stretch technique, ultrasonography, manipulative therapy, and local anesthetic injection, are used to inactivate trigger points. Techniques for rehabilitation include the avoidance of perpetuating factors, rehabilitation of extrapelvic abnormalities, use of manual techniques and needling to promote resolution of connective tissue problems, closure of diastasis recti, and transvaginal/transrectal manual release of muscular trigger points and contractures.113 Trigger-point injection has been shown to be one of the most effective treatment modalities to inactivate trigger points and provide prompt relief of symptoms.

Vaginismus Vaginismus is an involuntary spasm of pelvic muscles that partially closes the vagina. The Diagnostic and Statistical Manual of Mental Disorders, 4th Revision (DSM-IV), defines vaginismus as repeated and persistent involuntary spasm of the vaginal muscles that interferes with intercourse. This condition causes penetration to be difficult and painful, or even impossible. Vaginismus is considered a sexual dysfunction although the patient may often have pain with tampon insertion and gynecologic examinations as well. It is a complex condition with several possible causes that may result from past sexual trauma or abuse, other psychological factors, or a history of discomfort with sexual intercourse. Causes can also be congenital or infectious.114 Sometimes no cause can be determined. Women with varying degrees of vaginismus often develop anxiety regarding coitus and penetration, and intercourse is usually painful. However, this does not mean that they cannot achieve or sustain sexual arousal. Many are very sexually responsive and can have orgasms through clitoral stimulation. Difficulty or inability to allow vaginal penetration for intercourse is the primary symptom. Vaginal pain with attempts at intercourse or during attempted pelvic examination is common. A gynecologic examination can confirm the diagnosis of vaginismus. The health care provider will note whether there is an involuntary muscle contraction when fingers are inserted into the vagina, and this usually reproduces the pain the woman feels with intercourse. Other causes of dyspareunia should also be ruled out. The treatment of choice with vaginismus is an extensive therapy program that combines education and counseling with behavioral exercises. Exercises include pelvic floor muscle contraction and relaxation (Kegel exercises) to improve voluntary control. Vaginal dilation exercises are recommended using plastic dilators. This should be done under the direction of a sex therapist or other health care provider, and treatment should involve the partner. This treatment should gradually include more intimate contact, ultimately resulting in intercourse. Psychosocial Factors Psychosocial factors are important in the management of vulvar and vaginal pain, both as a cause and as an effect of the pain. Patients with chronic vaginal or vulvar pain often experience progressively limited professional and social lives. Patients often become frustrated with the multiple physician visits, diagnostic tests, and treatment regimens including surgeries. If the medical treatment is not conclusive or successful, patients may be told it is “all in their head.” This may lead to further stress, depression, and sexual dysfunction. Most studies indicate that an average of 20% to 30% of women with pelvic pain have experienced childhood trauma or sexual abuse. If the pain is “nonsomatic” or of “unknown etiology,” the frequency of abuse is found to be much higher. The impact of historical factors in causing pain is controversial but may exacerbate a patient’s experience of pain. Chronic Pelvic Pain with Resultant Dyspareunia Chronic pelvic pain (CPP) is frequently associated with dyspareunia. CPP is a common problem, and it presents a major challenge to health care providers because of its unclear etiology,

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complex natural history, and poor response to therapy. A significant number of these patients have various associated problems, including bladder or bowel dysfunction, sexual dysfunction, and other systemic or constitutional symptoms. Other associated conditions, such as depression, anxiety, and drug addiction, also may coexist. Studies have shown that women with CPP are more likely to have a history of sexual and physical abuse than are other groups of women.115 The most common causes of CPP are endometriosis, irritable bowel syndrome, interstitial cystitis, abdominal wall and pudendal neuropathy, pelvic floor muscle tension myalgia, and fibromyalgia. Residual symptomatology after accurate diagnosis and focused treatment is best managed with a multidisciplinary approach.116 The diagnosis and management of CPP is beyond the scope of this chapter. Abnormal Vaginal Discharge Normal vaginal discharge is 1 to 4 mL over 24 hours, white or transparent, thick and odorless. Physiologic discharge is formed by mucoid endocervical secretions in combination with sloughing epithelial cells, normal bacteria, and vaginal transudate. Discharge may be more noticeable during pregnancy, oral contraceptive use, or at midmenstrual cycle, close to the time of ovulation. Physiologic leukorrhea has a pH of 4.0 to 4.5, has a ratio of polymorphonuclear leukocytes to vaginal epithelial cells that is less than 1, and contains many squamous cells.117 Vaginitis and vaginosis were discussed in earlier sections of this chapter. Cervicitis can lead to abnormal vaginal discharge. Gonorrhea Cervicitis Gonorrhea is one of the most frequently diagnosed STDs and remains a significant cause of preventable and treatable morbidity. The peak incidence occurs in 15- to 19-year-old women.118 N. gonorrhoeae is a gram-negative diplococcus, first described by Neisser in 1879.119 The most concerning complications of gonorrhea infection relate to female reproduction. Scarring from pelvic inflammatory disease can interfere with fertilization in 20% of cases. There is also a 9% risk of ectopic pregnancy and an 18% risk of chronic abdominal pain.120 Women can also infect newborn infants during birth, causing neonatal ophthalmia. The incubation period for urogenital gonococcal infection is approximately 10 days in the female patient.8 The typical symptoms are increased vaginal discharge, dysuria, intermenstrual uterine bleeding, postcoital bleeding, and menorrhagia.50,121 Infection in women is often asymptomatic, whereas men are asymptomatic only 10% of the time.122 Gonorrhea in women can infect the cervix, urethra, anus, rectum, or oropharynx or can be disseminated. The most common site of infection is the cervix; approximately 50% of affected women are asymptomatic. Symptoms include vaginal pruritus and mucopurulent discharge from runny or scant to copious. Patients may also complain of new postcoital spotting or dyspareunia. On examination, the cervix may appear normal or show signs of frank discharge. The cervix may be friable, and there may be abdominal pain with upper genital tract disease. Gonococcal vulvitis and vaginitis are infrequent, because the stratified squamous epithelium of the vagina is resistant to invasion by the gonococcus.8 The symptoms for urethritis are initially urinary frequency and burning.8 Infection of the trigone is accompanied by increased dysuria, and the patient often has tenesmus. The urethral meatus is often edematous and erythematous with purulent discharge with the urethral epithelium everted.

Patients may have severe pain from Skene’s duct abscess and be unable to void. There can also be infection of Bartholin’s gland, and pus may drain from that site, but if the duct is occluded, then an abscess will form. Anorectal infection can be asymptomatic or associated with clinical proctitis. In about 4% of patients with anorectal involvement, it is the sole site of infection.123 Symptoms include anal itching, rectal discharge, rectal fullness, tenesmus, and painful defecation. Pharyngitis results from fellatio with a male partner who has gonococcal urethritis or from cunnilingus.124 The pharynx is infected in 10% to 20% of individuals. Symptoms include fever and cervical lymphadenopathy. There are several methods of diagnosing gonorrhea infection. The “gold standard” is culture on modified Thayer-Martin medium. This is very sensitive in symptomatic women but only 65% to 85% sensitive in asymptomatic women.125 Cultures are 100% specific and allow testing for antibiotic resistance. Gram stains are less sensitive but allow for an earlier diagnosis and treatment. DNA probes have accuracy similar to that of culture, with high sensitivity, specificity, and positive and negative predictive values.126 Enzyme immunoassay is not widely used, because its positive predictive value is acceptable only in populations with a high prevalence of infection. There are also commercially available nucleic acid amplification tests (NAATs). They are more rapid to perform than culture, returning results within hours, but are much more expensive. NAATs have also been shown to be more sensitive than culture, being able to detect as little as one organism per sample, whereas the threshold for conventional methods is approximately 1000 organisms.127 There are many accepted regimens for gonorrhea. The use of one-time, observed therapy is recommended, because compliance with multiple doses is lower. Also, because 42% of patients with gonorrhea are found to have dual infection with chlamydia,128 concurrent treatment for both organisms is recommended. The recommended treatments of uncomplicated cervical, urethral, or anorectal infection are ceftriaxone 125 mg IM once, ciprofloxacin 500 mg PO once, ofloxacin 400 mg PO once, levofloxacin 250 mg PO once, and spectinomycin 2g IM once.16 Pregnant women should not be treated with quinolones or tetracyclines. The partner should also be treated. Chlamydia Cervicitis Chlamydia is the most common agent of sexually transmitted genital infections leading to cervicitis and often abnormal vaginal discharge. Chlamydia is a true bacterium, an obligate intracellular parasite. The organism is transmitted primarily by sexual contact. The organism cannot be transmitted across intact skin or mucous membranes. Risk factors for infection are young age, black race, multiple sex partner, recent new sex partner, low rates of barrier contraception, and history of STD.129,130 Chlamydia has been implicated in urethritis, Bartholin’s abscess, cervicitis, endometritis, salpingitis, conjunctivitis, and pneumonitis of the newborn. The ultimate sequelae in the female that may involve chlamydial infection are ectopic pregnancy, infertility, and complex salpingitis that may lead to formation of a tubo-ovarian abscess and eventually hysterectomy.8 Most patients with cervicitis are asymptomatic. If symptoms are present, they may include vaginal spotting with intercourse, vaginal discharge, poorly differentiated abdominal pain, or lower abdominal pain. Examination may reveal the presence of mucopus or hypertrophy of the endocervical epithelium with a copious clear discharge, or the cervix may bleed briskly when

Chapter 87 VULVAR AND VAGINAL PAIN, DYSPAREUNIA, AND ABNORMAL VAGINAL DISCHARGE

touched with cotton-tipped applicator. Approximately 30% of women with Chlamydia infection develop pelvic inflammatory disease if left untreated.131 Traditional methods of diagnosis include cervical swabs requiring a full pelvic examination, but new diagnostic techniques include cervical swabs, urine, or self-administered vaginal swabs. Antigen detection by DFA and enzyme-linked immunosorbent assay (ELISA) still requires a swab from the cervix or urethra and is 80% to 95% sensitive compared to culture. Genetic probe methods based on direct specimen swab from the cervix or urethra are also 80% to 95% sensitive compared with culture. Nucleic acid amplification, PCR, and ligase chain reaction (LCR) are being studied and have high sensitivity and specificity.132 Clinical practice guidelines strongly recommend routine Chlamydia screening for sexually active women younger than 25 years of age.16,133 Azithromycin (1 g PO as a single dose) and doxycycline (100 mg PO twice daily for 7 days) are the two recommended regimens. Alternative regimens include 7 days of erythromycin base (500 mg PO four times daily), erythromycin ethylsuccinate (800 mg PO), ofloxacin (300 mg PO twice daily), or levofloxacin (500 mg PO once daily).16,134 Test of cure is not recommended, except for patients with persisting symptoms and those with suspect compliance. Test of cure should be done 3 weeks after the completion of therapy.16 Cervical and Vaginal Lesions Vesicovaginal Fistula Vesicovaginal fistula is a communication between the vagina and a part of the urinary tract (ureter, bladder, or proximal urethra). Continual wetness, odor, and discomfort cause serious social problems. The main causes include obstructed labor and surgical trauma, and 10% of the cases are caused by irradiation, locally advanced pelvic tumors, and pelvic pathologies (e.g., inflammation, foreign bodies).

Classically, vesicovaginal fistulas manifest with continuous incontinence after a recent pelvic operation.135 If the fistula is small, then watery discharge from the vagina accompanied by normal voiding may be the only symptom. Diagnostic tests can be done by passing a small ureteric catheter through the fistular tract to see if it enters the vagina. Other means of diagnosis are by retrograde and voiding cystourethrography. A high creatinine level of the discharge can confirm urinary leakage. Colovaginal, Rectovaginal, and Coloperineal Fistulas Colovaginal and rectovaginal fistulas are thought to be a relatively uncommon occurrence, but they can cause distressing symptoms depending on the severity, site, location, and etiology.136 The most common cause of colovaginal fistulas is diverticular disease. They also occur as a result of irradiation, pelvic surgery, malignancy, abdominal hysterectomy, abscess formation, perforation by a foreign body, inflammatory bowel disease, and trauma. Fistulas develop in 2% of patients with diverticulitis. Most patients have colovaginal fistulas secondary to diverticular disease, Crohn’s disease, or pelvic surgery, particularly hysterectomy. The passage of feces per vagina is diagnostic of a fistula between the bowel and internal genitalia. Putting a tampon in the vagina may assist in the diagnosis. Most patients present with abnormal discharge, which may not be recognized as frank feces. Colovaginal fistula may also manifest as vaginal flatus. With small bowel–vaginal fistulas, severe excoriation may be seen secondary to the presence of digestive enzymes. Physical examination with a speculum usually reveals an opening or granular area at the apex of the vagina that appears red and is usually on the left. The next examination usually requested is a barium enema, but this is ineffective. Vaginography may be useful, however. Other diagnostic tools include colposcopy, colonovaginoscopy, and computed tomography.

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42. Reeves WC, Corey L, Adamd HG, et al: Risk of recurrence after first episodes of genital herpes: Relation to HSV type and antibody response. N Engl J Med 305:315, 1981. 43. Mommeja-Marin H, Lafaurie M, Scieux C, et al: Herpes simplex virus type 2 as a cause of severe meningitis in immunocompromised adults. Clin Infect Dis 37:1527, 2003. 44. Schomogyi M, Wald A, Corey L: Herpes simplex virus-2 infection: An emerging disease? Infect Dis Clin North Am 12:47, 1998. 45. Lafferty WE, Coombs RW, Benedetti J, et al: Recurrences after oral and genital herpes simplex virus infection: Influence of site of infection and viral type. N Engl J Med 316:1444, 1987. 46. Moseley RC, Corey L, Benjamin D, et al: Comparison of viral isolation, direct immunofluorescence, and indirect immunoperoxidase techniques for detection of genital herpes simplex virus infection. J Clin Microbiol 13:913, 1981. 47. Ramaswamy M, McDonald C, Smith M, et al: Diagnosis of genital herpes by real time PCR in routine clinical practice. Sex Transm Infect 80:406, 2004. 48. Filen F, Strand A, Allard A, et al: Duplex real-time polymerase chain reaction assay for detection and quantification of herpes simplex virus type 1 and herpes simplex virus type 2 in genital and cutaneous lesions. Sex Transm Dis 31:331, 2004. 49. Kimberlin DW, Lakeman FD, Arvin AM, et al: Application of the polymerase chain reaction to the diagnosis and management of neonatal herpes simplex virus disease: National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. J Infect Dis 174:1162, 1996. 50. Bonnez W, Reichman R: Papillomaviruses. In Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of infectious Diseases, 5th ed. Philadelphia, Churchill Livingstone, 2000, p 1630. 51. Black MM, McKay M, Braude PR: Color Atlas and Text of Obstetric and Gynecologic Dermatology. London, Mosby Wolfe, 1995, p 119. 52. Ridley CM, Neill SM: Non-infective cutaneous conditions of the vulva. In Ridley CM, Neill SM (eds): The Vulva. Oxford, Blackwell Science, 1999, p 121. 53. Thomas RH, Ridley CM, McGibbon DH, Black MM: Anogenital lichen sclerosus in women. J R Soc Med 89:694, 1996. 54. Loening-Bucke V: Lichen sclerosus et atrophicus in children. Am J Dis Child 145:1058-1061, 1991. 55. Zellis S, Pincus SH: Treatment of vulvar dermatoses. Semin Dermatol 15:71, 1996. 56. Fischer GO: The commonest causes of symptomatic vulvar disease: A dermatologist’s perspective. Australas J Dermatol 37:12, 1996. 57. Lewis FM: Vulval lichen planus. Br J Dermatol 138:569, 1998. 58. Mann MS, Kaufmann RH: Erosive lichen planus of the vulva. Clin Obstet Gynecol 34:605, 1991. 59. Anderson M, Kutzner S, Kaufmann RH: Treatment of vulvovaginal lichen planus with vaginal hydrocortisone suppositories. Obstet Gynecol 100:359, 2002. 60. Marren P, Wojnarowska F: Dermatitis of the vulva. Semin Dermatol 15:36, 1996. 61. Lynch PJ: Dermatology. Baltimore, Williams & Wilkins, 1994, p 4. 62. Jemal A, Murray T, Ward W, et al: Cancer statistics 2005. CA Cancer J Clin 55:10, 2005. 63. Hildesheim A, Han CL, Brinton LA, et al: Human papillomavirus type 16 and risk of preinvasive and invasive vulvar cancer: Results from a seroepidemiological case-study. Obstet Gynecol 90:748, 1997. 64. Iwasawa A, Nieminen P, Lehtinen M, Paavonen J: Human papillomavirus in squamous cell carcinoma of the vulva by polymerase chain reasction. Obstet Gynecol 89:81, 1997. 65. Parker LP, Parker JR, Bodurka-Bevers D, et al: Paget’s disease of the vulva: Pathology, pattern of involvement, and prognosis. Gynecol Oncol 77:183, 2000. 66. Fanning J, Lambert HC, Hale TM, et al: Paget’s disease of the vulva: Prevalence of associated vulvar adenocarcinoma, invasive Paget’s

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67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91.

disease, and recurrence after surgical excision. Am J Obstet Gynecol 180:24, 1999. Feuer GA, Shevchuk M, Calanog A: Vulvar Paget’s disease: The need to exclude an invasive lesion. Gynecol Oncol 38:81, 1990. Raz R, Miron D, Colodner R, et al: A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection. Arch Intern Med 156:1109, 1996. Lee YH, Rankin JS, Alpert S, et al: Microbiological investigation of Bartholin’s abscesses and cysts. Am J Obstet Gynecol 129:150-153, 1977. Mungan T, Ugur M, Yalcin H, et al: Treatment of Bartholin’s cyst and abscess: Excision versus silver nitrate insertion. Eur J Obstet Gynecol Reprod Biol 63:61, 1995. Brook I: Aerobic and anaerobic microbiology of Bartholin’s abscess. Surg Gynecol Obstet 169:32, 1989. Droegemueller W: Comprehensive gynecology. Mosby, St. Louis, 1992, p 637. Ball SB, Wojnarowska F: Vulvar dermatoses: Lichen sclerosus, lichen planus, and vulvar dermatitis/lichen simplex chronicus. Semin Cutan Med Surg 17:182, 1998. Fischer G, Spurrett B, Fischer A: The chronically symptomatic vulva: Aetiology and management. Br J Obstet Gynaecol 102:773, 1995. Fischer GO: The commonest causes of symptomatic vulvar disease: A dermatologist’s perspective. Australas J Dermatol 37:12, 1996. Dalziel KL, Wojnarowska F: Long-term control of vulvar lichen sclerosus after treatment with a potent topical steroid cream. J Reprod Med 38:25, 1993. Dalziel KL, Millard PR, Wojnarowska F: The treatment of vulval lichen sclerosus with a very potent topical steroid (clobetasol propionate 0.05%) cream. Br J Dermatol 124:461, 1991. Kanai M, Osada R, Maruyama K, et al: Warning from Nagano: Increase of vulvar hematoma and/or lacerated injury caused by snowboarding. J Trauma 50:328-331, 2001. Sau AK, Dhar KK, Dhall GI: Nonobstetric lower genital tract trauma. Obstet Gynaecol 33:433-435, 1993. Kennedy CM, Dewdney S, Galask RP: Vulvar granuloma fissuratum: A description of fissuring of the posterior fourchette and the repair. Obstet Gynecol 105(5 Pt 1):1018-1023, 2005. Olsen AL, Smith VJ, Bergstrom JO, et al: Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 89:501, 1997. Fernandez-Aguilar S, Noel JC: Neuroma of the clitoris after female genital cutting. Obstet Gynecol 101(5 Pt 2):1053-1054, 2003. Perry PC: Vulvodynia. In Howard FM, Perry PC, Carter JE, et al (eds): Textbook of pelvic pain: Diagnosis & Management. Philadelphia, Lippincott Williams & Wilkins, 2000, pp 204-210. Masheb RM, Nash JM, Brondolo E, Kerns RD: Vulvodynia: An introduction and critical review of a chronic pain condition. Pain 86:3-10, 2000. Bazin S, Bouchard C, Brisson J, et al: Vulvar vestibulitis syndrome: An exploratory case-control study. Obstet Gynecol 83:47-50, 1994. Witkin SS, Gerber S, Ledger WJ: Differential characterization of women with vulvar vestibulitis syndrome. Am J Obstet Gynecol 187:589, 2002. Friedrich EG: Vulvar vestibulitis syndrome. J Reprod Med 32:110114, 1987. Ledger WJ, Kessler A, Leonard GH, Witkin SS: Vulvar vestibulitis: A complex clinical entity. Infect Dis Obstet Gynecol 4:269, 1996. Edwards L: New concepts in vulvodynia. Am J Obstet Gynecol 189(3 Suppl):S24-S30, 2003. Bouchard C, Brisson J, Fortier M, et al: Use of oral contraceptive pills and vulvar vestibulitis: A case control study. Am J Epidemiol 156:254, 2002. Ashman RB, Ott AK: Autoimunity as a factor in recurrent vulvovaginal candidosis and the minor vestibular gland syndrome. J Reprod Med 34:264, 1989.

92. Solomons CC, Melmed MH, Heitler SM: Calcium citrate for vulvar vestibulitis: a case report. J Reprod Med 36:879, 1991. 93. Baggish MS, Sze EH, Johnson R: Urinary oxalate secretion and its role in vulvar pain syndrome. Am J Obstet Gynecol 177:507, 1997. 94. Jeremias MS, Ledger WJ, Witkin SS: Interleukin 1 receptor antagonist gene polymorphism is women with vulvar vestibulitis. Am J Obstet Gynecol 182:283, 2000. 95. McCormack WM: Two urogenital sinus syndromes: Interstitial cystitis and focal vulvitis. J Reprod Med 35:873, 1990. 96. Fitzpatrick CC, DeLancey JO, Elkins TE, McGuire EJ: Vulvar vestibulitis and interstitial cystitis: A disorder of urogenital sinusderived epithelium? Obstet Gynecol 81:860, 1993. 97. Bergeron S, Binik YM, Khalife S, et al: Vulvar vestibulitis syndrome: A critical review. Clin J Pain 13:27, 1997. 98. Murina F, Tassan P, Roberti P, Bianco V: Treatment of vulvar vestibulitis with submucous infiltrations of methylprednisolone and lidocaine: An alternative approach. J Reprod Med 46:713, 2001. 98a. Rapkin AJ, McDonald JS, Morgan M: Multilevel local anesthetic nerve blockade for the treatment of vulvar vestibulitis syndrome. Am J Obstet Gynecol, 2007. In press. 99. McKay M: Dyesthetic (“essential”) vulvodynia: Treatment with amitryptiline. J Reprod Med 38:9-13, 1993. 100. Horowitz BJ: Interferon therapy for condylomatous vulvitis. Obstet Gynecol 73:446-448, 1989. 101. Marinoff SC, Turner ML, Hirsch RP, Richard G: Intralesional alpha interferon: Cost-effective therapy for vulvar vestibulitis syndrome. J Reprod Med 38:19-24, 1993. 102. McCormack WM, Spence MR: Evaluation of the surgical treatment of vulvar vestibulitis. Eur J Obstet Gynecol Reprod Biol 86:135-138, 1999. 103. Bergeron S, Binik YM, Khalife S, et al: A randomized comparison of group cognitive–behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Pain 91:297-306, 2001. 104. Bergeron S, Brown C, Lord MJ, et al: Physical therapy for vulvar vestibulitis syndrome: A retrospective study. J Sex Marital Ther 28:183-192, 2002. 105. Turner ML, Marinoff SC: Pudendal neuralgia. Am J Obstet Gynecol 165(4 Pt 2):1233-1236, 1991. 106. Shafik A: Pudendal canal syndrome: Description of a new syndrome and its treatment—Report of 7 cases. Coloproctology 13:102-110, 1991. 107. Antolak SJJ, Hough DM, Pawlina W, Spinner RJ: Anatomical basis of chronic pelvic pain syndrome: The ischial spine and pudendal nerve entrapment. Med Hypotheses 59:349-353, 2002. 108. Shafik A: Pudendal canal syndrome as a cause of vulvodynia and its treatment by pudendal nerve decompression. Eur J Obstet Gynecol Reprod Biol 80:215-220, 1998. 109. McDonald JS, Spigos DG: Computed tomography–guided pudendal block for treatment of pelvic pain due to pudendal neuropathy. Obstet Gynecol 95:306-309, 2000. 110. Swerdlow M: Anticonvulsant drugs and chronic pain. Clin Neuropharmacol 7:51, 1984. 111. Becos J, Climov D, Bex M: Pudendal nerve decompression in perineology: A case series. BMC Surgery 4:15, 2004. 112. Alvarez DJ, Rockwell PG: Trigger points: Diagnosis and management. Am Fam Physician 65:653-660, 2002. 113. FitzGerald MP, Kotarinos R: Rehabilitation of the short pelvic floor. II: Treatment of the patient with the short pelvic floor. Int Urogynecol J Pelvic Floor Dysfunct 14:269-275; discussion 275, 2003. Epub 2003 Aug 7. 114. McDonald JS, Rapkin AJ: Pelvis, perineum and genitalia: General considerations. In Loeser JD (ed): Bonica’s Management of Pain, 3rd ed. Philadelphia, Williams & Wilkins, 2000, p 1369. 115. Rapkin AJ, Kames LD, Darke LL, et al: History of physical and sexual abuse in women with chronic pelvic pain. Obstet Gynecol 76:92-96, 1990.

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116. Rapkin AJ, Jolin J: Chronic pelvic pain. In Weiner RS (ed): Pain Management, 6th ed. Washington, DC: CRC Press, 2002, p 251. 117. Sobel JD. Vaginitis. N Engl J Med 337:1896-1903, 1997. 118. Gonorrhea—United States, 1998. MMWR Morb Mortal Wkly Rep 49:538, 2000. 119. Neisser ALS: Uber eine der Gonorrhea eigentumliche Micrococcusform. Abl Med Wiss 17:497, 1879. 120. Platt R, Rice P, McCormack W: Risk of acquiring gonorrhea and prevalence of abnormal adnexal findings among women recently exposed to gonorrhea. JAMA 250:3205, 1983. 121. Noble RC: Characterization of Neisseria gonorrhoeae from women with simultaneous infections at two sites. Br J Vener Dis 56:3, 1980. 122. Sherrard J, Barlow D: Gonorrhoea in men: Clinical and diagnostic aspects. Genitourin Med 72:422, 1996. 123. Klein EJ, Fisher LS, Chow AW, Guze LB: Anorectal gonococcal infection. Ann Intern Med 86:340, 1977. 124. Sackel SG, Alpert S, Fiumura NJ, et al: Orogenital contact and the isolation of Neisseria gonorrhea, Mycoplasma hominis, and Ureaplasma urealyticum from the pharynx. Sex Transm Dis 6:64, 1979. 125. Schink JC, Keith LG: Problems in the culture diagnosis of gonorrhea. J Reprod Med 30:244, 1985. 126. Kouman EH, Johnson RE, Knapp JS, St Louis ME: Laboratory testing for Neisseria gonorrheae by recently introduced nonculture tests: A performance review with clinical and public health considerations. Clin Infect Dis 27:1171, 1998. 127. Van Dyck E, Ieven M, Pattyn S, et al: Detection of Chlamydia trachomatis and Neisseria gonorrheae by enzyme immunoassay,

culture, and three nucleic acid amplification tests. J Clin Microbiol 39:1751, 2001. 128. Lyss SB, Kamb ML, Peterman TA, et al: Chlamydia trachomatis among patients infected with and treated for Neisseria gonorrheae in sexually transmitted disease clinics in the United States. Ann Intern Med 139:178, 2003. 129. Gaydos CA, Howell MR, Pare B, et al: Chlamydia trachomatis infections in female military recruits. N Engl J Med 339:739, 1998. 130. Cook RL, St George K, Lassak M, et al: Screening for Chlamydia trachomatis infection in college women with polymerase chain reaction assay. Clin Infect Dis 28:1002, 1999. 131. Cates W Jr, Wasserheit JN: Genital chlamydial infections: Epidemiology and reproductive sequelae. Am J Obstet Gynecol 164:1771, 1991. 132. Marrazzo JM, Johnson RE, Green TA, et al: Impact of patient characteristics on performance of nucleic acid amplification tests and DNA probe for detection of Chlamydia trachomatis in women with genital infections. J Clin Microbiol 43:577-584, 2005. 133. Howell MR, Quinn TC, Gaydos CA: Screening for Chlamydia trachomatis in asymptomatic women attending family planning clinics. Ann Intern Med 128:277, 1998. 134. Drugs for sexually transmitted infections. Treat Guidel Med Lett 2:67, 2004. 135. Romcs I, Kelemen ZS, Fazakas ZS: The diagnosis and management of vesicovaginal fistula. BJU Int 89:764-766, 2002. 136. Bahadursingh A, Longo W: Colovaginal fistulas: Etiology and management. J Reprod Med 48:489-495, 2003.

Chapter 88

BENIGN CYSTIC LESIONS OF THE VAGINA AND VULVA Karyn Schlunt Eilber Benign cystic lesions of the female external genitalia are frequently encountered in gynecologic and female urologic practices. True cystic lesions of the vagina and vulva originate from vaginal and vulvar tissues, respectively, but lesions arising from the urethra and surrounding tissues can appear as cystic lesions of the vagina and vulva as well. Most cysts of the female genitalia are located within the vagina, and their prevalence has been estimated to be 1 in 200 women; however, this figure is probably an underestimation, because most cysts are asymptomatic and therefore not reported.1 Cysts arising within the vulvar vestibulum are much less common. Vaginal cysts typically occur in the third and fourth decades and are rarely found in prepubertal females except in countries where female circumcision in performed.2 Pradhan and Tobon reviewed the histology of 43 vaginal cysts over a 10-year period. In their study, the incidence of cyst types in decreasing order was müllerian cysts (44%), epidermal inclusion cysts (23%), Gartner’s duct cysts (11%), Bartholin’s gland cysts (7%), and endometriotic type (7%).3 The remaining types of cystic lesions include those of urethral or paraurethral origin and other rare lesions (Table 88-1).

PATIENT EVALUATION Cysts of the vagina and vulva are usually asymptomatic, and their presence is usually noted as an incidental finding on physical examination. In patients whose cysts are discovered because of symptomatology, mild discomfort, patient detection of a mass, or urinary symptoms such as incontinence or obstructive voiding symptoms are common presenting symptoms. In most cases, the appropriate diagnosis is made by history and physical examination alone; other cases are diagnosed only after excision and histologic examination of the tissue. Patient history should include the onset and duration of symptoms and the presence of pain, dyspareunia, voiding complaints, and prior urologic or gynecologic procedures. A history of recurrent urinary tract infections and/or intermittent incontinence may indicate the presence of a urethral diverticulum, whereas continuous incontinence may represent an ectopic ureterocele. During physical examination, the lesion should be assessed for location, mobility, tenderness, definition (smooth versus irregular), and consistency (cystic versus solid). The presence of

Table 88-1 Vaginal Wall Cyst Location and Histology Diagnosis

Location

Histology

Müllerian (paramesonephric) cyst

Pseudostratified columnar, mucinous

Gartner’s (mesonephric) cyst Skene’s (paraurethral) duct cyst Bartholin’s gland cyst Adenosis Cyst of canal of Nuck (hydrocele) Urethral caruncle Urethral diverticulum Inclusion cyst

Anywhere, usually anterolateral vaginal wall Same as müllerian cyst Floor of distal urethra Lateral introitus, medial to labia minora Vaginal fornices and upper walls Superior to labia majora or inguinal canal Urethral meatus Periurethral, anterior vaginal wall Area of previous surgery

Endometriosis

Anywhere, usually posterior fornix

Ectopic ureterocele Vaginitis emphysematosa Hidradenoma Dermoid cyst

Periurethral Upper two thirds of vagina Interlabial sulcus Paravaginal

Aggressive angiomyxoma

Vagina and vulva

Ciliated cyst Pigmented follicular cyst

Anywhere in vagina, vulvar vestibulum Vulva

Low columnar, nonciliated, nonmucinous Stratified squamous Transitional or columnar, mucinous Columnar, ciliated, mucinous Flat cuboidal Loose connective tissue and vessels Transitional or squamous epithelium Stratified squamous epithelium around keratinous debris Two of three: endometrial glands, stroma, hemosiderin-laden macrophages Transitional or squamous epithelium Inflammatory and giant cells Papillomatous Keratinized squamous epithelium and dermal appendages Hypocellular, myxoid matrix of collagen and capillary-like vessels Müllerian-like columnar ciliated epithelium Stratified squamous epithelium with keratinization and pore

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the urogenital sinus begins to grow upward and replace the original pseudostratified columnar epithelium with squamous mucosa. In addition to the lower two thirds of the vagina, the urogenital sinus derivatives in the female are Skene’s glands and Bartholin’s glands.4 Müllerian Cysts

A

During the process of replacement of the müllerian (pseudostratified columnar) epithelium with squamous epithelium of the urogenital sinus, müllerian epithelial tissue can persist anywhere in the vaginal wall, although it typically rests within the anterolateral wall. Consequently, müllerian cysts tend to be located along the anterolateral aspect of the vagina.5 Müllerian derivatives are the most common type of vaginal cyst; they are lined predominantly by mucinous epithelium but may be lined by any epithelium of müllerian origin: endocervical, endometrial, or fallopian.4,6 Clinically, the distinction between müllerian and mesonephric (Gartner’s duct) cysts is of little importance. Müllerian cysts range in size from 1 to 7 cm.4 The great majority are asymptomatic and require no treatment. Occasionally, a müllerian cyst may become large enough that symptoms warrant excision. Gartner’s Duct Cysts

B Figure 88-1 A, Voiding cystourethrogram (VCUG) demonstrates obstruction of distal urethra. B, Magnetic resonance imaging (MRI) confirms that the obstructing lesion is a cyst.

malignancy must always be considered. Pelvic organ prolapse, such as cystocele or enterocele, can mimic a vaginal cyst and should be ruled out. Pelvic imaging by means of ultrasound, voiding cystourethrogram (VCUG), computed tomography (CT), or magnetic resonance imaging (MRI) may be required to characterize the lesion further (Fig. 88-1). Although each of these modalities has been useful in the diagnosis of vaginal cysts, pelvic MRI is the preferred modality for diagnosing both cystic lesions and a variety of other genitourinary abnormalities, including pelvic organ prolapse, urethral diverticula, ovarian abnormalities, and uterine pathology. CYSTS OF EMBRYONIC ORIGIN During the eighth week of embryologic development, the paired müllerian (paramesonephric) ducts fuse distally and develop into the uterus, cervix, and upper third of the vagina, which are lined by a pseudostratified columnar (glandular) epithelium. Wolffian (mesonephric) ducts normally regress in the female, and their remnants include Gartner’s duct, epoöphoron and paroöphoron. Beginning at week 12, a squamous epithelial plate derived from

Although it is clinically irrelevant to distinguish Gartner’s duct cysts from müllerian cysts, true Gartner’s duct cysts arise from vestigial remnants of the mesonephric (wolffian) ducts. Gartner’s duct extends from the mesosalpinx via the broad ligament to the cervix, so these cysts are usually located along the anterolateral vaginal wall.4,6 Typically, they are small, with an average diameter of 2 cm, but the cysts may enlarge to the point where they are mistaken for other structures, such as a cystocele or urethral diverticulum (Fig. 88-2A).4 The largest Gartner’s duct cyst reported was 16 × 15 × 8 cm.7 An association between Gartner’s duct cysts and abnormalities of the metanephric urinary system exists, and cases of ectopic ureter, unilateral renal agenesis, and renal hypoplasia have all been reported in association with Gartner’s duct cysts.8-10 Currarino reported on five children with a Gartner’s duct cyst and either ipsilateral renal hypoplasia or dysplasia,9 and Sheih and colleagues found that 6% of female children with unilateral renal agenesis had a Gartner’s duct cyst.10 Although such abnormalities usually present in childhood, awareness of this association should prompt the clinician to image the urinary tract when evaluating adults who present with Gartner’s duct cysts. MRI is especially useful, both for evaluation of the characteristics of the cyst and to rule out communication with the urinary tract (see Fig. 88-2B). Gartner’s duct cysts are synonymous with simple cysts and are lined by cuboidal or low columnar, nonciliated, nonmucinous cells. They can be distinguished from müllerian cysts by the presence of a basement membrane and smooth muscle layer; however, clear distinction between the two can be made only on the basis of histochemical staining: müllerian cysts are periodic acid–Schiff (PAS) and mucin positive, whereas mesonephric cysts are devoid of cytoplasmic mucicarmine or PAS-positive material.5,6 If a Gartner’s duct cyst is large and symptomatic, excision is indicated (see Fig. 88-2C). Successful treatment with cyst aspiration and 5% tetracycline injection has been reported but without long-term follow-up.11

Chapter 88 BENIGN CYSTIC LESIONS OF THE VAGINA AND VULVA

A

B

C

Skene’s Duct Cysts Skene’s (paraurethral) glands are bilateral prostatic homologues located in the floor of the distal urethra. Obstruction of the ducts is presumed to occur in response to skenitis, of which gonorrhea is the most common cause.5,12 Because Skene’s ducts are embryologically derived from the urogenital sinus, these cysts are lined by stratified squamous epithelium.12 Clinically significant cysts of Skene’s ducts are rare, but cysts larger than 2 cm often cause patients to seek treatment for urinary symptoms such as dysuria or obstructive voiding symptoms (Fig. 88-3A).13 In this situation, a Skene’s duct cyst must be distinguished from a urethral diverticulum. Dysuria, history of urinary tract infections, and postvoid dribbling are common in the presence of a urethral diverticulum. Furthermore, on physical examination, compression of a Skene’s duct cyst should not result in fluid extravasation. Both MRI and cystourethroscopy are useful to determine whether there is a communication between the lesion and the urethra (see Fig. 88-3B). It is of paramount importance to determine whether a vaginal cyst is of urethral origin. Unless a urethral diverticulum is suspected, urethral injury during cyst excision may occur, and a urethrovaginal fistula can result if the urethra is not adequately repaired and postoperative catheter drainage instituted.

Figure 88-2 A, Large Gartner’s duct cyst mimics a urethral diverticulum. B, Magnetic resonance imaging confirms cystic nature and absence of communication with the urinary tract. C, Excision.

Small Skene’s duct cysts can be observed. Excision is recommended for larger, symptomatic cysts. Marsupialization is not necessary, and the duct itself need not be preserved.5 Acute infection is a contraindication for excision; incision and drainage are advocated in this setting. Bartholin’s Duct Cysts Bartholin’s glands are also of urogenital sinus origin and are homologous to bulbourethral glands in males. Ductal obstruction, due to previous infection or inspissated mucus, is a prerequisite to cyst formation. Size and rapidity of growth depend on the accumulation of secretions from Bartholin’s gland, which is influenced by sexual stimulation.4 Although most patients have no symptoms or only mild dyspareunia, repeated sexual stimulation may be associated with rapidly enlarging, painful lesions. Pain may also indicate infection of the cyst. Bartholin’s gland is composed of acini lined by columnar, mucus-secreting epithelium and ducts lined by transitional epithelium. Larger ducts may contain areas of stratified squamous epithelium.4 The origin of a Bartholin’s duct cyst is indicated by its histology: cysts arising from the main duct are lined by transitional or squamous epithelium, whereas cysts originating in an acinus are lined by mucinous columnar epithelium.5,14

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Cysts associated with pain, recurrent abscess formation, or introital obstruction require surgical intervention. Excision of Bartholin’s duct cysts has been described, but the preferred treatment is marsupialization to preserve function and prevent cyst or abscess reformation (see Fig. 88-4C). Incision and drainage is indicated for Bartholin’s abscesses, with definitive treatment deferred until a period of quiescence. Vaginal Adenosis

A

Vaginal adenosis is the presence of glandular epithelium within the vagina. It is attributed to failure of the squamous epithelium to replace the columnar epithelium in the vagina and ectocervix during embryogenesis.15 It can be found in infants, children, and adults, and it is the most common lesion in women exposed to diethylstilbestrol (DES).16 As with müllerian cysts, the lesions may represent any müllerian derivation and may include endocervical, endometrial, or tubal-type mucous cells (Fig. 88-5).6,17 Vaginal adenosis is commonly an incidental finding on examination of a DES-exposed woman and may resemble cervical ectropion. The classic appearance of adenosis is red, grape-like mucosa in the vaginal fornices and upper walls.5 Identification of adenosis may be facilitated by its lack of staining with iodine solution.4,5 Symptoms may include excessive mucoid vaginal discharge or mild postcoital bleeding. No specific therapy is recommended for the treatment of adenosis, because the lesion may spontaneously regress. Routine examination of these lesions is recommended, because metaplastic conversion is well documented. Cysts of the Canal of Nuck (Hydrocele) The processus vaginalis, also referred to as the canal of Nuck, is a rudimentary peritoneal sac that accompanies the round ligament through the inguinal canal into the labia majora. During the first trimester, the canal of Nuck normally becomes obliterated. Persistence of the canal is associated with inguinal hernias, and occlusion at any point can lead to the formation of a cyst that is analogous to a hydrocele of the spermatic cord. Cysts of the canal of Nuck are found in the superior aspect of the labia majora or inguinal canal. Their size may be several centimeters, and they are associated with an inguinal hernia in one third of cases.18 Most of these cysts are diagnosed intraoperatively, but if a cyst of the canal of Nuck is suspected preoperatively, the surgical approach should be that for an inguinal herniorrhaphy.

B Figure 88-3 A, Vaginal mass causing distal urethral obstruction which proved to be a Skene’s duct cyst. B, Preoperative magnetic resonance image demonstrates a cystic lesion arising in the urethra, consistent with a Skene’s duct cyst.

Bartholin’s duct cysts typically range from 1 to 4 cm in diameter. Most are unilateral, nontender, cystic masses located in the lateral introitus, medial to the labia minora (Fig. 88-4A). These lesions are detectable by ultrasound, CT, and MRI (see Fig. 88-4B). If small and asymptomatic, they require no treatment.

CYSTS OF URETHRAL ORIGIN It is important to determine whether a cystic lesion in the vagina is of urethral origin, because excision of urethral lesions requires postoperative catheter drainage to prevent fistula formation. Urethral Caruncle The term caruncle refers to a wide variety of lesions protruding from the urethral meatus. Urethral caruncles typically occur in postmenopausal women and most likely represent ectropion of the urethral wall due to postmenopausal regression of the vaginal

Chapter 88 BENIGN CYSTIC LESIONS OF THE VAGINA AND VULVA

A

B

C

mucosa. Urethral prolapse is often mistakenly diagnosed as a caruncle in a child. On physical examination, a urethral caruncle is seen as a solitary, red, polypoid lesion protruding from one segment of the urethral meatus (Fig. 88-6). Most caruncles measure only a few millimeters in diameter. Symptoms range from mild bleeding to extreme discomfort. Based on histology, caruncles are classified as either papillomatous, angiomatous, or granulomatous.4 All types consist of a core of loose connective tissue and blood vessels covered by a transitional or squamous epithelium. Classification depends on the degree of associated inflammatory reaction. Treatment is expectant for small, asymptomatic lesions. Excision is performed for lesions with significant symptoms or in cases in which carcinoma must be ruled out.

Figure 88-4 A, Bartholin’s duct cyst on physical examination. B, Magnetic resonance image. C, Marsupialization.

Urethral Diverticulum A urethral diverticulum typically manifests as a cystic lesion in the anterior vaginal wall along the distal urethra (Fig. 88-7A). It most likely forms as a consequence of the rupture of infected periurethral glands into the lumen. Common symptoms include postvoid dribbling, dyspareunia, and recurrent urethritis or cystitis. Compression of the cyst may cause expulsion of urine or purulent material. Cystourethroscopy is often the initial test when evaluating a patient with a suspected urethral diverticulum, but it may not be diagnostic if the neck of the diverticulum is small. In this case, imaging is invaluable. Neitlich and colleagues demonstrated that high-resolution, fast-spin echo technique MRI has a high sensitivity for detecting diverticula and a higher negative

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EPIDERMAL CYSTS Epidermal inclusion cysts secondary to buried epithelial fragments after episiotomy or other surgical procedures are the most common nonembryologic type of vaginal cysts.4 In Nigeria, epidermal inclusion cysts are common in the first decade of life, and this has been attributed to the practice of prepubertal female circumcision.2 Inclusion cysts vary in size from a few millimeters to several centimeters in diameter. Their location correlates with an area of previous surgery, and their contents appear cheese-like and may even resemble a thick, purulent exudate. Imaging of these lesions by MRI reveals a cystic structure containing heterogeneous fluid. On histologic examination, inclusion cysts are lined with stratified squamous epithelium and contain sebaceous-appearing material that represents desquamated epithelial cells. Cysts lined by squamous epithelium but not associated with buried skin fragments are simply termed epidermal cysts. Because these cysts are usually asymptomatic, they may be observed. ENDOMETRIOSIS Figure 88-5 Microscopic appearance of vaginal adenosis.

Endometriosis is the ectopic implantation of endometrial glands and stroma. Primary occurrence in the vulva and vagina is rare and usually represents a secondary manifestation of pelvic disease. On gross examination, these cysts are mucoid and may appear brown or black. Nodules of endometriosis are located in the posterior fornix and appear red-blue to yellow-brown (“chocolate cyst”). The patient may complain of cyclic enlargement, dysmenorrhea, dyspareunia, pelvic pain, or dysuria. Two of the following three characteristics must be present to make the diagnosis: endometrial glands, stroma, and hemosiderin-laden macrophages. Foreign body giant cells may be found.4 Treatment is destruction or excision of the lesions. ECTOPIC URETEROCELE

Figure 88-6 Urethral caruncle.

predictive rate than double-balloon urethrography.19 A combination of both VCUG and MRI can be used to accurately diagnosis the condition and localize the lesion or lesions (see Fig. 88-7B,C). Transvaginal excision with postoperative urethral catheter drainage is the preferred treatment, although endoscopic incision has been described.

A ureterocele is a cystic dilatation of the distal ureter. Ureteroceles are commonly associated with the upper pole of a duplicated collecting system; if present with an ectopic ureter, they may manifest as a cystic vaginal mass. Although diagnosis is usually made at an early age, an ectopic ureterocele may manifest as incontinence in an older female child or young woman. Clinically, most ureteroceles are diagnosed by prenatal ultrasound examination, but they may also be found as a cystic vaginal mass on physical examination. An endoscopic or open surgical approach is dictated by factors such as the presence of duplication, reflux, and parenchymal function of the upper pole associated with the ectopic ureterocele. PELVIC ORGAN PROLAPSE Prolapse of pelvic organs (e.g., cystocele, rectocele) can manifest as a vaginal cystic lesion. Symptoms can range from mild vaginal pressure to urinary incontinence or retention. Diagnosis is by history and physical examination. MRI is often helpful. All of the options for treatment are beyond the scope of this chapter and

Chapter 88 BENIGN CYSTIC LESIONS OF THE VAGINA AND VULVA

C A

B

will not be discussed, but in general treatment depends on the patient’s symptoms, health status, and degree of prolapse. RARE CYSTIC LESIONS Vaginitis Emphysematosa Vaginitis emphysematosa is a rare, benign process characterized by gas-filled cysts in the vaginal wall, first described by Zweifel in 1877.20 Fewer than 200 cases have been reported in the literature. Most patients present with symptoms of vaginitis, but an audible popping sound during intercourse has been reported by some.21

Figure 88-7 A, Large urethral diverticulum. B, Imaging of urethral diverticulum by voiding cystourethrogram (VCUG). C, Magnetic resonance image.

No definitive infectious etiology has been found, but most cases are associated with Trichomonas vaginalis.22 Diagnosis can be made by physical examination. The cysts are usually found in the upper two thirds of the vagina but may extend to the lower vagina, and rarely to the vulva. On physical examination, the cysts are seen to be discrete, tense, and smooth, and they may create a popping sound when ruptured during a vaginal examination. On histologic examination, the cysts are found to contain pink hyaline-like material, and they are lined by foreign body giant cells and other inflammatory cells.23 The condition is self-limited and does not require specific treatment.

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Hidradenoma Hidradenomas of the vagina are well-circumscribed, freely mobile nodules found mainly on the medial aspect of the labia majora in the interlabial sulcus. The majority are smaller than 1 cm. The presence of granular, papillomatous tissue is suggestive of the diagnosis. Microscopic examination is remarkable for a cystic lesion filled with papillomatous growths.4 Treatment is by local excision.

Ciliated Cyst A ciliated cyst is a cyst lined with columnar ciliated epithelium. Ciliated cysts are rare and are probably of müllerian origin. They occur in women 25 to 35 years of age and have been associated with pregnancy, exogenous progesterone, and chronic inflammation.27 Resection is indicated for symptomatic lesions. Pigmented Follicular Cyst

Dermoid Cyst Only two cases of dermoid cysts involving the vagina have been reported.24,25 In both cases, the cyst originated in the paravaginal space and diagnosis was delayed. Histology is remarkable for a cyst lined by keratinized squamous epithelium and containing dermal appendages. Aggressive Angiomyxoma Aggressive angiomyxoma is a rare myofibroblastic tumor of the pelvic and genital soft tissues with just over 110 cases reported in the literature. It is typically found in women 35 to 40 years of age, although it can develop in men and children as well.26 The term “aggressive” refers to its pattern of local infiltration and recurrent growth. Most are large (>10 cm), and surgical resection after imaging to determine the extent of disease is recommended.

Pigmented follicular cysts are rare, occur predominantly in adult men, are composed of stratified squamous epithelium with epidermoid keratinization, and have a pore-like opening to the skin surface. Only one case of pigmented follicular cyst of the vulva has been reported, and treatment of this lesion was with CO2 laser.28 CONCLUSIONS Cystic lesions of the vagina and vulva are a relatively common occurrence and represent a spectrum of disease from embryologic derivatives to preneoplastic lesions. Familiarity with the different diagnoses is essential for any clinician involved in gynecologic or female urologic practice in order to arrive at the correct diagnosis and treatment plan.

References 1. Smith RP (ed): Netter’s Obstetrics, Gynecology and Women’s Health. Toronto, Canada, MediMedia, Inc., 2002. 2. Junaid TA, Thomas SM: Cysts of the vulva and vagina: A comparative study. Int J Gynaecol Obstet 19:239-223, 1981. 3. Pradhan S, Tobon H: Vaginal cysts: A clinicopathological study of 41 cases. Int J Gynecol Pathol 5:35, 1986. 4. Kaufman RH, Faro S (eds): Benign Diseases of the Vulva and Vagina. Stouis: Mosby, 1994. 5. Zaino RJ: Cysts. In Kurman RJ (ed): Blaustein’s Pathology of the Female Genital Tract, 4th ed. New York, Springer-Verlag, 2001. 6. Wilkinson EJ (ed): Pathology of the Vulva and Vagina. New York, Churchill Livingstone, 1987. 7. Hagspiel KD: Giant Gartner duct cyst: Magnetic resonance imaging findings. Abdom Imaging 20:566, 1995. 8. Youssef AF (ed): Atlas of Gynecology Diagnosis. New York, Churchill Livingstone, 1984. 9. Currarino G: Single vaginal ectopic ureter and Gartner’s duct cyst with ipsilateral renal hypoplasia and dysplasia (or agenesis). J Urol 128:988, 1982. 10. Sheih CP, Lu WT, Liao YJ, et al: Renal hypoplasia, Gartner’s duct cyst and imperforated hemivagina: Report of a case. J Formos Med Assoc 93:531, 1994. 11. Abd-Rabbo MS, Atta MA: Aspiration and tetracycline sclerotherapy: A novel method for management of vaginal and vulvar Gartner’s cysts. Int J Gynaecol Obstet 35:235, 1991. 12. Satani H, Yoshimura N, Hayashi N, et al: A case of female paraurethral cyst diagnosed as epithelial inclusion cyst. Hinyokika Kiyo 46:205, 2000. 13. Miller EV: Skene’s duct cyst. J Urol 131:966, 1984. 14. Evans DM, Paine CG: Tumors of the vulva and vagina: Bartholin’s cysts and paraurethral lesions. Clin Obstet Gynecol 8:997, 1965. 15. Fenoglio CM, Ferenczy A, Richart RM, Townsend D: Scanning and transmission electron microscopic studies of vaginal adenosis and

16. 17. 18. 19.

20. 21. 22. 23. 24. 25. 26. 27. 28.

the cervical transformation zone in progeny exposed in utero to diethylstilbestrol. Am J Obstet Gynecol 126:170, 1976. Robboy SJ, Kaufman RH, Prat J, et al: Pathologic findings in young women enrolled in the National Cooperative Diethylstilbestrol Adenosis (DESAD) Project. Obstet Gynecol 53:309, 1974. Antonioli DA, Burke L: Vaginal adenosis: Analysis of 325 biopsy specimens from 100 patients. Am J Clin Pathol 64:625, 1974. Anderson CC, Broadie TA, Mackey JE, Kopecky KK: Hydrocele of the canal of Nuck: Ultrasound appearance. Am Surg 61:959, 1995. Neitlich JD, Foster HE Jr, Glickman MG, Smith RC: Detection of urethral diverticula in women: Comparison of a high resolution fast spin echo technique with double balloon urethrography. J Urol 159:408, 1998. Zweifel P: Die vaginitis emphysematosa ode colpo hysterplasia cystica nach winckel. Arch Gynäkol 12:39, 1877. Close JM, Jesurun HM: Emphysematous vaginitis: Report of a case. Obstet Gynecol 19:513, 1962. Gardner HL, Fernet P: Etiology of vaginitis emphysematosa. Am J Obstet Gynecol 88:680, 1964. Kramer K, Tobon H: Vaginitis emphysematosa. Arch Pathol Lab Med 111:746, 1987. Livengood CH, Addison WA, Hammond CB: Epidermoid cyst of the paravaginal space located only by computerized axial tomography: A case report. J Reprod Med 3:176, 1982. Hirose R, Imai A, Kondo H, et al: A dermoid cyst of the paravaginal space. Arch Gynecol Obstet 249:39, 1991. Gungor T, Zengeroglu S, Kaleli A, Kuzey GM: Aggressive angiomyxoma of the vulva and vagina. A common problem: Misdiagnosis. Eur J Obstet Gynecol Reprod Biol 112:114, 2004. Hamada M, Kiryu H, Ohta T, Furue M: Ciliated cyst of the vulva. Eur J Dermatol 14:347, 2004. Chuang Y, Hong H, Kuo T: Multiple pigmented follicular cysts of the vulva successfully treated with CO2 laser: Case report and literature review. Dermatol Surg 30:1261, 2004.

Chapter 89

PATHOPHYSIOLOGY OF PELVIC PAIN Ursula Wesselmann

Chronic pelvic pain syndromes belong to the category of visceral pain. Chronic pelvic pain is a common and debilitating problem that can significantly impair a woman’s quality of life. Patients with chronic pelvic pain are usually evaluated and treated by urologists, gynecologists, gastroenterologists, and internists. The clinical presentation is often considered to be a diagnostic dilemma, because many urologic, gastrointestinal, and gynecologic disorders appear to cause or are associated with chronic pelvic pain.1 Although these patients seek medical care because they are looking for help to alleviate their pelvic discomfort and pain, in clinical practice much emphasis has been placed on finding a specific cause and specific pathologic markers for pelvic disease. These patients typically undergo many diagnostic tests and procedures. Often, however, the examination and workup remain unrevealing and no specific cause of the pain can be identified. In these cases, it is important to recognize that pain is not only a symptom of pelvic disease, but that the patient is suffering from a chronic pelvic pain syndrome, in which “pain” is the prominent symptom of the chronic visceral pain syndrome.2,3 The purpose of this chapter is to review the pathophysiology of chronic nonmalignant pelvic pain, a chronic visceral pain syndrome. Because of the anatomic location of the viscera, they do not lend themselves easily to experimental manipulation, but recognition of the existence of the chronic pelvic pain syndromes has resulted in the development of novel animal models to study the pathophysiologic mechanisms of chronic pelvic pain4 and of clinical studies to assess pain treatment options. Knowledge of the neurophysiologic characteristics of visceral pain will guide the physician in making a diagnosis of chronic pelvic pain and in sorting it out from the lump diagnosis of idiopathic pain.3 A basic understanding of the neurobiology is paramount to gain further insights into the mechanisms of the pelvic pain disorders and contributes greatly to the development of effective clinical management strategies for patients presenting with these syndromes.

DEFINITIONS: WHAT IS CHRONIC PELVIC PAIN? Definitions are important if a body of reliable information is to be built up in the scientific literature that will eventually lead to a better understanding of the pathophysiology of chronic pelvic pain. At present, one of the major problems of research into chronic pelvic pain is the lack of agreed definitions, which would allow comparisons among studies. On the other hand, lack of understanding of the pathophysiologic mechanisms of the pelvic pain syndromes makes it difficult to decide on criteria to define chronic pelvic pain conditions.5

Pain is defined by the International Association for the Study of Pain (IASP) as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or is described in terms of such damage.6 There is no generally accepted definition of chronic pelvic pain. The IASP defines chronic pelvic pain without obvious pathology as chronic or recurrent pelvic pain that apparently has a gynecologic origin but for which no definitive lesion or cause is found.6 This definition is problematic from a clinical perspective, because it implies absence of pathology, which might not necessarily be the case (for example, many patients with endometriosis suffer from pelvic pain). It also excludes cases in which pathology is present but not necessarily the cause of pain (for example, some patients with endometriosis do not have pelvic pain). As in many other pain conditions, the relationship of the pain complaint to the presence of pathology is often unclear in patients with chronic pelvic pain. The proportion of women with chronic pelvic pain and a specific diagnosis (or diagnoses) varies greatly in the literature. A large primary care study from Great Britain found that diagnoses related to urinary and gastrointestinal tracts are more common than gynecologic causes (30.8% urinary, 37.7% gastrointestinal, 20.2% gynecologic). Further, 25% to 50% of women with chronic pelvic pain who received medical care in primary care practices had more than one diagnosis.7,8 Several medical societies have recently published consensus statements revising definitions of chronic pelvic pain. The International Continence Society has defined “pelvic pain syndrome” as the occurrence of persistent or recurrent episodic pelvic pain associated with symptoms suggestive of lower urinary tract, sexual, bowel, or gynecologic dysfunction in the absence of proven infection or other obvious pathology.9 The European Association of Urology suggested extending this definition by considering two subgroups based on the presence or absence of well-defined conditions that produce pain.10 In the gynecologic literature, chronic pelvic pain is often referred to as pelvic pain in the same location for at least 6 months. The American College of Obstetricians and Gynecologists has proposed the following definition: chronic pelvic pain is noncyclic pelvic pain of 6 or more months’ duration that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocks and is of sufficient severity to cause functional disability or lead to medical care. A lack of physical findings does not negate the significance of a patient’s pain, and normal examination results do no preclude the possibility of finding pelvic pathology.1 Definitions of chronic pelvic pain will probably continue to be revised, as knowledge about the pathophysiology of pelvic pain is increasing based on basic science and clinical research. When reviewing literature on chronic pelvic pain, it is crucial for the reader to realize which definition of chronic pelvic was actually used for the study. 885

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HOW COMMON IS CHRONIC PELVIC PAIN? EPIDEMIOLOGIC DATA Chronic pelvic pain is more common than previously thought. Epidemiologic data from the United States showed that 14.7% of women in their reproductive years reported chronic pelvic pain, and the estimated number of female pelvic pain sufferers was 9.2 million in the United States alone.11 Analysis of a large primary care database from the United Kingdom demonstrated that the annual prevalence rate of chronic pelvic pain in women was 38/1000, which is comparable to the prevalence rates of asthma and low back pain.7 Although this study found a high prevalence of pain, many women had never had the condition diagnosed.12 NEUROANATOMY OF THE PELVIS The purpose of this section is to provide an overview of the innervation of the pelvis and urogenital floor.13,14 Although this summary attempts to derive as much information as possible from investigations involving humans, it is important to note that some generalizations are necessarily taken from animal studies, recognizing that much research in this field is still in its infancy. All viscera, including the pelvic visceral organs, are dually innervated by both divisions of the autonomic nervous system, the sympathetic and parasympathetic divisions, as well as by the somatic and sensory nervous systems. In a broad anatomic view, dual projections from the thoracolumbar and sacral segments of the spinal cord carry out this innervation, converging primarily into discrete peripheral neuronal plexuses before distributing nerve fibers throughout the pelvis (Fig. 89-1). Interactive neuronal pathways routing from higher origins in the brain through the spinal cord add to the complexity of neuronal regulation in the pelvis. Although it is important to appreciate the influence of supraspinal centers in the coordination of pelvic organ activities, it is beyond the scope of this section to discuss these interactions in further detail; for review, see Bors and Comarr,15 Morrison,16 de Groat et al,17 de Groat,18 and Berkley and Hubscher.19 The nomenclature of the various plexuses, ganglia, and nerves in the pelvic cavity (see Dail20) is varied, and sometimes there are confusing presenting designations from both Nomina Anatomica21 and clinical usage (see Baljet and Drukker22). In this review and in Figure 89-1, the anatomic nomenclature is used, with the clinical usage given in parentheses: superior hypogastric plexus (presacral nerve), hypogastric plexus (hypogastric nerve), inferior hypogastric plexus (pelvic plexus), and pelvic splanchnic nerve (pelvic nerve). Within the pelvis, the inferior hypogastric plexus is regarded as the major neuronal integrative center. Neuroanatomic studies have confirmed its retroperitoneal location adjacent to each lateral aspect of the rectum, with interconnections between the left and right inferior hypogastric plexuses at the posterior aspect of the rectum.23-26 It innervates multiple pelvic organs, including the urinary bladder, proximal urethra, distal ureter, rectum, and internal anal sphincter, as well as genital and reproductive tract structures.27 The anterior part of the inferior hypogastric plexus, which is associated with the distal extent of the hypogastric plexus (hypogastric nerve), is referred to as the paracervical ganglia in females.28 The paracervical ganglia part of the inferior hypogas-

tric plexus in the female, situated in the parametrium lateral to the cervix and the upper part of the vagina, distributes nerve fibers to the corpora cavernosa of the clitoris, vagina, and periurethral tissues.28 Neuronal input to the inferior hypogastric plexuses involves dual input through the sympathetic and parasympathetic divisions of the autonomic nervous system. Sympathetic nerves originate in the thoracolumbar segments of the spinal cord (T10L2) and condense into the superior hypogastric plexus located just inferior to the aortic bifurcation. Preganglionic efferents originate largely in the intermediolateral cell column, whereas afferents have their cell bodies located in dorsal root ganglia of these segments. Nerve fibers project from the superior hypogastric plexus as paired hypogastric plexuses (hypogastric nerves) and fuse distally before diverging bilaterally into branches destined for the inferior hypogastric plexuses. Additional sympathetic innervation to genitourinary organs may involve preganglionic nerves that synapse on postganglionic nerves originating in sympathetic chain ganglia; these postganglionic nerves join sacral nerves and course to their destinations via pelvic somatic neuronal pathways.29 Parasympathetic preganglionic nerve efferents are thought to arise from cell bodies of the sacral parasympathetic nucleus located in the intermediolateral gray matter of the sacral spinal cord (S2-S4) and to fuse as the pelvic splanchnic nerve before entering the inferior hypogastric plexus.30,31 Parasympathetic afferents have cell bodies located in the S2-S4 dorsal root ganglia and course also within the pelvic splanchnic nerve. In addition to its parasympathetic efferent and afferent component, the pelvic splanchnic nerve also receives postganglionic axons from the caudal sympathetic chain ganglia.18 A distinctive distribution of pelvic autonomic innervation is recognized at the urogenital organ level. Lower urinary tract smooth muscle, including that of the proximal urethra, urinary bladder, and lower ureter, receives direct postganglionic efferent projections from the inferior hypogastric plexus, although vesical or intramural ganglia also serve as origins for postganglionic axons.32 The inferior hypogastric plexus additionally provides afferent input to the lower urinary tract and internal reproductive organs, with proximal afferent fibers predominantly projecting through the hypogastric plexuses (hypogastric nerves) (see Jänig and Koltzenburg33). The autonomic innervation of the female genitalia has been less well studied than the male counterpart. It involves inferior hypogastric plexus projections deriving primarily from the paracervical ganglia part of the plexus. Conspicuous nerve trunks run in the adventitia of the vagina parallel to its long axis, sending off anterior branches that course to the clitoris and periurethral tissues and local branches that enter the vaginal smooth muscle walls.22,34 A network of nerve fibers tends to follow vascular distributions and conspicuously terminates at the junction between the subepithelial connective tissue and the vaginal epithelium as well as within the epithelium.34 Nerve density is observed to be greater in the distal vagina than in the proximal regions.34 Although the rectum and the anal sphincters are closely situated anatomically, their exact sources of innervation differ. Not surprisingly, a division of neural control is characterized on the basis of morphologic and functional differences. The smooth muscle of the rectum and internal anal sphincter (a thickened continuation of the circular smooth muscle fibers of the rectal wall) is influenced by the autonomic nervous system and receives innervation directly from sympathetic and parasympathetic

Chapter 89 PATHOPHYSIOLOGY OF PELVIC PAIN

T10 - L2 CEL

SCG

G

DR

Aorta

SHP

S2 - S4

HG P

Uterus

G

DR

SA

C

N

PS

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IHP SA

Rectum PU D Vag.

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Figure 89-1 Schematic drawing showing the innervation of the pelvic area in the human female. CEL, celiac plexus; DRG, dorsal root ganglion; HGP, hypogastric plexus (hypogastric nerve); IHP, inferior hypogastric plexus (pelvic plexus); PSN, pelvic splanchnic nerve (pelvic nerve); PUD, pudendal nerve; SA, short adrenergic projections; SAC, sacral plexus; SCG, sympathetic chain ganglion; SHP, superior hypogastric plexus (presacral nerve); Vag = vagina. (From Wesselmann U, Burnett AL, Heinberg LJ: The urogenital and rectal pain syndromes. Pain 73:269-294, 1997. With permission of the International Association for the Study of Pain.)

origins coursing through or synapsing within the inferior hypogastric plexus.35 Rectal branches from this plexus accompany the middle rectal vessels to the lateral sides of the rectum, within condensations of connective tissue referred to as the lateral ligaments of the rectum.35 At the level of the intestinal wall, innervation continues according to the pattern observed throughout the gastrointestinal tract, which involves two ganglionic plexuses, the myenteric plexus lying between the longitudinal and circular muscle layers and the submucosal plexus.27 In contrast, the striated muscle of both the external anal sphincter and the levator ani (including the puborectalis muscle) is generally under the control of the somatic nervous system. Somatic efferent and afferent innervation to the pelvis is generally understood to involve the sacral nerve roots (S2-S4) and their ramifications. Somatic efferents arise within Onuf’s nucleus situated in the ventral horn of the S2-S4 spinal cord, and afferents reach the dorsal horn with their cell bodies in dorsal root ganglia

of these segments.32 Central projections of somatic afferents overlap with pelvic nerve afferents within the spinal cord, which theoretically allows coordination of somatic and visceral motor activity.29 The sacral nerve roots emerge from the spinal cord, forming the sacral plexus,36 from which the pudendal nerve diverges (S2-S3) along with the sciatic nerve, between an initial division of sacral nerves that branch to the levator muscle and a subsequent division of fibers that intermingle with autonomic pelvic nerves coursing to the inferior hypogastric plexus.37-39 The pudendal nerve also receives postganglionic axons from the caudal sympathetic chain ganglia.18 In general, the pudendal nerve runs medial to the internal pudendal vessels along the lateral wall of the ischiorectal fossa, dorsal to the sacrospinous ligament. An initial branch then splits off destined to innervate the clitoris, and the remaining pudendal nerve fibers distribute branches in various directions, which include medial branches to

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the anal canal (external anal sphincter and puborectalis muscle), dorsal branches to the urethral sphincter, and dorsolateral branches primarily to anterior perineal musculature (including bulbospongiosus and ischiocavernosus muscles). Nerves originating predominantly from sacral level S4 supply the posterior perineal musculature, and branches of S4-S5 nerve roots forming the coccygeal plexus distribute to perineal, perianal, and labial skin.39 Nociception and pain arising from within the pelvis and pelvic floor involve diverse neuronal mechanisms. In general, sensations from the pelvic viscera are conveyed within the sacral afferent parasympathetic system, with a far lesser afferent supply from thoracolumbar sympathetic origins.33 Functionally, this dual innervation contributes to differential processing of visceral stimuli by different regions of the neuraxis. For example, in a model of colonic pain it was demonstrated that the pelvic nerve and lumbosacral spinal cord process acute or transient colorectal pain with recruitment of the splanchnic innervation during inflammation of the colon.40,41 Pelvic nerve afferents innervate the deeper layers of hollow organs, including mucosa and submucosa as well as the muscle and serosa.42 Receptive fields in the perineum are understood to be carried out primarily by sensorymotor discharges associated with pudendal nerve afferents.17,33 While the interactions of sensory afferents are quite complex, likely possibilities by which these pathways exert effects on autonomic efferent function include mediatory effects on spinal cord reflexes and modulatory effects on efferent release in peripheral autonomic ganglia and in peripheral organs. These neural structures in the periphery comprise the first of numerous relays of sensory neurons that transmit painful sensations from the abdominal/pelvic cavity to the brain. Traditionally, it was thought that ascending pathways for visceral and other types of pain were mainly the spinothalamic and spinoreticular tracts. Recently, three previously undescribed pathways that carry visceral nociceptive information have been discovered: the dorsal column pathway, the spino(trigemino)parabrachio-amygdaloid pathway, and the spinohypothalamic pathway (see review in Cervero and Laird43). The dorsal column pathway plays a key role in the processing of pelvic pain, and neurosurgeons have successfully used punctate midline myelotomy to relieve pelvic pain due to cancer (see review in Willis and Westlund44). In addition, descending facilitatory influences may contribute to the development of maintenance of hyperalgesia, thus contributing to the development of chronic pelvic pain.45 VISCERAL NOCICEPTION: VISCERAL NOCICEPTORS, VISCERAL SENSITIZATION, AND REFERRED PAIN MECHANISMS Chronic visceral pain is a much greater clinical problem than that from skin, however, until relatively recently, the focus of experimental work on pain mechanisms mainly related to cutaneous sensation. Although it was often assumed that concepts derived from cutaneous studies could be transferred to the visceral domain, there are emerging experimental data indicating that the neural mechanisms involved in pain and hyperalgesia of the skin are different from the mechanisms involved in painful sensations from the viscera.46,47 This is supported by differences between somatic and visceral pain based on clinical observation. In contrast to somatic pain, visceral pain cannot be evoked from all

viscera and is not necessarily linked to visceral tissue injury. Further, visceral pain tends to be a diffuse and poorly localized sensation, whereas somatic pain can be localized exactly. Different from somatic pain, visceral pain can be referred to other visceral structures and somatic structures of the same segmental level. For example, patients with chronic pelvic pain typically report multiple pelvic pain problems, and they present with pain radiating to the lower back and legs.7,8 The visceral innervation is not as dense as the somatic innervation. It is assumed that at most 5% to 8% of the total afferent input to the spinal cord is contributed by spinal visceral nerves.48 This rather sparse afferent input to the spinal cord from the viscera is compensated for by an extensive divergence in the central nervous system. In addition, recent studies have suggested that some visceral afferents innervate more than one organ. About 20% of dorsal root ganglion cells retrogradely labeled from the colon were double-labeled from the bladder.49 The physiologic role of the bifurcating afferents is not clear, because recordings from colon or bladder afferents failed to provide evidence of excitation of the other organ.50,51 It is possible that these bifurcating afferents become active after inflammation. This hypothesis is supported by the observation that colonic inflammation in a rat model results in plasma extravasation in an otherwise normal bladder.52 These neuroanatomic and neurophysiologic observations might explain why visceral pain tends to be diffuse and poorly localized, providing a diagnostic challenge to the health care provider who is trying to ascertain the origin of the pain. There are two components of visceral pain, which were already described more than 100 years ago53: “true visceral pain,” which is deep visceral pain arising from inside the body, and “referred visceral pain,” which is pain that is referred to segmentally related somatic and also other visceral structures. Secondary hyperalgesia usually develops at the referred site.4 Although several mechanisms have been entertained to explain the referred pain phenomenon over the last 70 years, the most convincing experimental evidence is provided by the observation of convergence. Convergence of afferent input is a typical characteristic of secondorder neurons in the spinal cord that receive visceral input. These visceroceptive spinal neurons receive convergent somatic input from skin and musculature.54 In addition, viscerovisceral convergence of input onto second-order spinal neurons is common (e.g., colon and bladder). This mechanism offers a ready explanation for the segmental nature of referred pain, but it does not address explicitly the issue of hyperalgesia in the referred zone. To interpret “referred pain with hyperalgesia,” two main theories have been proposed, which are not mutually exclusive. The first is known as convergence-facilitation theory. It proposes that the abnormal visceral input produces an irritable focus in the relative spinal cord segment, thus facilitating messages from somatic structure. The second theory postulates that the visceral afferent barrage induces the activation of a reflex arc whose afferent branch is presented by visceral afferent fibers and efferent branch by somatic efferents and sympathetic efferents toward the somatic structures (muscle, subcutis, and skin). The efferent impulses toward the periphery sensitize nociceptors in the parietal tissues of the referred area, thus resulting in the phenomenon of hyperalgesia. When examining and treating a woman with chronic pelvic pain, it is important to consider the true and referred aspects of the visceral pain syndrome, including the pain deep in the pelvic cavity and pain referred to somatic structures (lower back and

Chapter 89 PATHOPHYSIOLOGY OF PELVIC PAIN

legs) and other visceral organs. The mechanisms of referred viscerovisceral pain might explain the substantial overlap observed in epidemiologic studies between chronic pelvic pain and other abdominal symptoms.12,55 Considering the concept of referred visceral pain and realizing that the visceral innervation is sparse, but compensated for by extensive divergence in the central nervous system, will allow the health care provider to look at the global picture of visceral dysfunction, rather than “chasing” one aspect of the visceral pain syndrome out of context. The existence of visceral nociceptors has been debated for a long time, in part because of the difficulty of defining and applying physiologically relevant noxious stimuli to the viscera (for review, see Bielefeldt and Gebhart54). The functional properties of visceral afferent neurons have been studied by recording afferent fiber activity and responses to controlled visceral stimuli in teased fiber preparations in which one or a few axons are recorded. These experiments have shown that several kinds of sensory receptors exist in most internal organs and that different pain states are mediated by different neurophysiologic mechanisms.56 Acute, brief visceral pain seems to be triggered initially by the activation of high-threshold visceral afferents and by the high-frequency bursts that these stimuli evoke in intensity-coding afferent fibers, which are afferents with a range of responsiveness in the innocuous and noxious ranges. However, more prolonged forms of visceral stimulation, including those leading to hypoxia and inflammation of the tissue, result in sensitization of high-threshold receptors and the bringing into play of previously unresponsive afferent fibers, termed “silent nociceptors.” This is a special class of mechano-insensitive C-fiber nociceptors that has been found in almost all tissues, including in animal models of visceral pain.57 Silent afferents are activated only in the presence of tissue damage or inflammation, which might explain why visceral pain cannot be evoked from all viscera and is not necessarily linked to every type of visceral tissue injury. There are several potential molecular substrates that may play key roles in the peripheral sensitization of nociceptor terminals in viscera. Messengers for tetrodotoxin (TTX)-resistant sodium channels, specifically Na 1.8, are primarily found in smalldiameter neurons with unmyelinated axons, which typically play an important role in nociception. Essentially all visceral sensory neurons have unmyelinated or thinly myelinated axons. Capsaicin and protons bind the vanilloid TRPV1 receptor. TRPV1 is coexpressed with calcitonin gene-related peptide (CGRP) and substance P in 60% to 80% of visceral afferents.58 TRPV1 expression in sensory fibers was correlated positively with the degree of hypersensitivity in patients with rectal hypersensitivity.59 In addition, urothelial cells (non-neuronal tissue) have been shown to express TRPV1 receptors as well, and these can be activated by vanilloids to produce the release of adenosine triphosphate (ATP), which then can activate P2X3 receptors in sensory afferent fibers.60 (Birder et al. 2001). This mechanism might account for the enhanced bladder sensitivity observed in patients with interstitial cystitis. Prostaglandins are synthesized in response to tissue injury by cyclooxygenase. They sensitize sensory fibers to mechanical and thermal stimuli and contribute to spinal processing of visceral pain.61 In studies of central contributions to visceral sensitization, the main focus has been the spinal cord. Intrathecal application of N-methyl-d-aspartate (NMDA) and non-NMDA receptor antagonists significantly attenuates visceral hypersensitivity in behavioral models, and spinal application of NMDA agonists increases the magnitude and duration of visceral

pain responses.62,63 NMDA receptors are expressed in primary afferents and in dorsal horn neurons. SEX, GENDER, AND GONADAL HORMONAL STATUS A distinguishing feature of many of the pelvic pain syndromes is the overwhelming burden reported by women in their reproductive years. For example, population prevalence estimates in patients with interstitial cystitis indicate a female-to-male ratio of 9:1.64 Interestingly, and in support of the hypothesis that the gonadal hormonal milieu influences pain perception, several pain syndromes are more common in women than in men.65,66 There is growing evidence from studies in animals and humans that the response to noxious stimuli may be influenced by the gonadal hormonal milieu and varies across different phases of the estrous (rodents) or menstrual (humans) cycle.65,67-69 However, the variations observed in different studies are inconsistent70 and cannot be linked to only one phase of the cycle. CLINICAL IMPLICATIONS Because epidemiologic data have confirmed the widespread existence of chronic pelvic pain in the female population in last 10 years, there is growing interest in the pharmaceutical industry to expand basic science and clinical research efforts for this underserved patient population. Controlled clinical trials are desperately needed to design improved pharmacologic treatment strategies. To date, most reports on the pharmacologic treatment of chronic pelvic pain are anecdotal. Currently used pharmacologic treatment approaches have mainly been evaluated for other chronic pain syndromes, and not specifically for chronic pelvic pain. Several different pharmacologic classes of medications have been demonstrated to be effective in alleviating pain in patients with chronic pain syndromes: nonsteroidal anti-inflammatory drugs (NSAIDs), antidepressants, anticonvulsants, local anesthetic antiarrhythmics, and opioids (for review, see Wesselmann71). Although clinical trials and case reports on the pharmacologic management of chronic pain syndromes provide general guidelines as to which drug to choose, currently we have no method to predict which drug is most likely to alleviate pain in a given patient. Therefore, it is a “trial and error” method of prescribing drugs. As the pathophysiologic mechanisms of visceral pain explored in basic science research have provided explanations for some of the clinical phenomena observed in patients, additional, revived and new concepts of chronic pelvic pain have emerged. First, a spectrum of different insults might lead to chronic pelvic pain. Second, different underlying pathogenic pain mechanisms may require different pain treatment strategies for patients presenting with pelvic pain. And third, multiple different pathogenic pain mechanisms may coexist in the same patient presenting with chronic pelvic pain, requiring several different pain treatment strategies (perhaps concomitantly) to successfully treat visceral pain.3

Acknowledgment Ursula Wesselmann is supported by NIH grants DK066641 (NIDDK), HD39699 (NICHD, Office of Research for Women’s Health) and the National Vulvodynia Association.

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References 1. American College of Obstetricians and Gynecologists: ACOG Practice Bulletin No. 51: Chronic pelvic pain. Obstet Gynecol 103:589605, 2004. 2. Wesselmann U: A call for recognizing, legitimizing and treating chronic visceral pain syndromes. Pain Forum 8:146-150, 1999. 3. Wesselmann U: Guest Editorial: Pain—The neglected aspect of visceral pain. Eur J Pain 3:189-191, 1999. 4. Giamberardino MA, Vecchiet L: Experimental studies on pelvic pain. Pain Rev 1:102-115, 1994. 5. Wesselmann U: Obstetric and gynaecological pain. In Schmidt RF, Willis WD: Encyclopedic Reference of Pain, 1st ed. Heidelberg, Springer-Verlag, 2006. 6. Merskey H, Bogduk N: Classification of Chronic Pain. Seattle, IASP Press, 1994. 7. Zondervan KT, Yudkin PL, Vessey MP, et al: Prevalence and incidence of chronic pelvic pain in primary care: Evidence from a national general practice database. Br J Obstet Gynaecol 106:11491155, 1999. 8. Zondervan KT, Yudkin PL, Vessey MP, et al: Patterns of diagnosis and referral in women consulting for chronic pelvic pain in UK primary care. Br J Obstet Gynaecol 106:1156-1161, 1999. 9. Abrams P, Cardozo L, Fall M, et al: The standardization of terminology of lower urinary tract function: Report from the Standardization Sub-committee of the International Continence Society. Neurourol Urodyn 21:167-178, 2002. 10. Fall M, Baranowski AP, Fowler CJ, et al: EAU guidelines on chronic pelvic pain. Eur Urol 46:681-689, 2004. 11. Mathias SD, Kuppermann M, Liberman RF, et al: Chronic pelvic pain: Prevalence, health-related quality of life, and economic correlates. Obstet Gynecol 87:321-327, 1996. 12. Zondervan KT, Yudkin PL, Vessey MP, et al: Chronic pelvic pain in the community: Symptoms, investigations, and diagnoses. Am J Obstet Gynecol 184:1149-1155, 2001. 13. Burnett AL, Wesselmann U: History of the neurobiology of the pelvis. Urology 53:1082-1089, 1999. 14. Burnett AL, Wesselmann U: Neurobiology of the pelvis and perineum: Principles for a practical approach. J Pelvic Surg 5:224232, 1999. 15. Bors E, Comarr AE: Neuro-anatomy and neuro-physiology. In Bors E, Comarr AE (eds): Neurological Urology. New York, Karger, 1971, pp 61-128. 16. Morrison JFB: Role of higher levels of the central nervous system. In Torrens M, Morrison JFB (ed): The Physiology of the Lower Urinary Tract. London, Springer-Verlag, 1987, pp 237-274. 17. de Groat WC, Booth AM, Yoshimura N: Neurophysiology of micturition and its modification in animal models of human disease. In Maggi CA (ed): Nervous Control of the Urogenital System. Chur, Switzerland, Harwood Academic Publishers, 1993, pp 227-290. 18. de Groat WC: Neurophysiology of the pelvic organs. In Rushton DN (ed): Handbook of Neuro-Urology. New York, Marcel Dekker, 1994, pp 55-93. 19. Berkley KJ, Hubscher CH: Visceral and somatic sensory tracks through the neuraxis and their relation to pain: Lessons from the rat female reproductive system. In Gebhart GF (ed): Visceral Pain. Vol. 5: Progress in Pain Research and Management. Seattle, WA, IASP Press, 1994, pp 195-216. 20. Dail WG: Autonomic innervation of male reproductive genitalia. In Maggi CA (ed): Nervous Control of the Urogenital System. Chur, Switzerland, Harwood Academic Publishers, 1993, pp 69-101. 21. Nomina Anatomica, 4th ed. Amsterdam, Excerpra Medica, 1977. 22. Baljet B, Drukker J: The extrinsic innervation of the pelvic organs in the female rat. Acta Anat (Basel) 107:241-267, 1980. 23. Walsh PC, Donker PJ: Impotence following radical prostatectomy: Insight into etiology and prevention. J Urol 167:1005-1010, 2002.

24. Lue TF, Zeineh SJ, Schmidt RA, et al: Neuroanatomy of penile erection: Its relevance to iatrogenic impotence. J Urol 131:273-280, 1984. 25. Lepor H, Gregerman M, Crosby R, et al: Precise localization of the autonomic nerves from the pelvic plexus to the corpora cavernosa: A detailed anatomical study of the adult male pelvis. J Urol 133:207212, 1985. 26. Zorn BH, Watson LR, Steers WD: Nerves from pelvic plexus contribute to chronic orchidalgia. Lancet 343:1161, 1994. 27. Burnstock G: Innervation of bladder and bowel. In Bock G, Whelan J (eds): Neurobiology of Incontinence, Ciba Foundation Symposium. Chichester, UK, Wiley, 1990, pp 2-26. 28. Jänig W, McLachlan EM: Organization of lumbar spinal outflow to distal colon and pelvic organs. Physiol Rev 67:1332-1404, 1987. 29. McKenna KE, Nadelhaft I: The organization of the pudendal nerve in the male and female rat. J Comp Neurol 248:532-549, 1986. 30. Hancock MB, Peveto CA: Preganglionic neurons in the sacral spinal cord of the rat: An HRP study. Neurosci Lett 11:1-5, 1979. 31. Nadelhaft I, Booth AM: The location and morphology of preganglionic neurons and the distribution of visceral afferents from the rat pelvic nerve: A horseradish peroxidase study. J Comp Neurol 226:238-245, 1984. 32. Lincoln J, Burnstock G: Autonomic innervation of the urinary bladder and urethra. In Maggi CA (ed): Nervous Control of the Urogenital System. Chur, Switzerland, Harwood Academic Publishers, 1993, pp 33-68. 33. Jänig W, Koltzenburg M: Pain arising from the urogenital tract. In Maggi CA (ed): Nervous Control of the Urogenital System. Chur, Switzerland, Harwood Academic Publishers, 1993, pp 525-578. 34. Hilliges M, Falconer C, Ekman-Ordeberg G, et al: Innervation of the human vaginal mucosa as revealed by PGP 9.5 immunohistochemistry. Acta Anat (Basel) 153:119-126, 1995. 35. Ger R: Surgical anatomy of the pelvis. Surg Clin North Am 68:12011216, 1988. 36. Elbadawi A: Neuromorphologic basis of vesicourethral function: I. Histochemistry, ultrastructure and function of intrinsic nerves of the bladder and urethra. Neurourol Urodyn 1:3-50, 1982. 37. Dietemann JL, Sick H, Wolfram-Gabel R, et al: Anatomy and computed tomography of the normal lumbosacral plexus. Neuroradiology 29:58-68, 1987. 38. Juenemann KP, Lue TF, Schmidt RA, et al: Clinical significance of sacral and pudendal nerve anatomy. J Urol 139:74-80, 1988. 39. Matzel KE, Schmidt RA, Tanagho EA: Neuroanatomy of the striated muscular anal continence mechanism: Implications for the use of neurostimulation. Dis Colon Rectum 33:666-673, 1990. 40. Traub RJ: Evidence for thoracolumbar spinal cord processing of inflammatory, but not acute colonic pain. Neuroreport 11:21132116, 2000. 41. Traub RJ, Murphy A: Colonic inflammation induces fos expression in the thoracolumbar spinal cord increasing activity in the spinoparabrachial pathway. Pain 95:93-102, 2002. 42. Brierley SM, Jones RC 3rd, Gebhart GF, et al: Splanchnic and pelvic mechanosensory afferents signal different qualities of colonic stimuli in mice. Gastroenterology 127:166-178, 2004. 43. Cervero F, Laird JM: Visceral pain. Lancet 353:2145-2148, 1999. 44. Willis WD Jr, Westlund KN: The role of the dorsal column pathway in visceral nociception. Curr Pain Headache Rep 5:20-26, 2001. 45. Gebhart GF: Descending modulation of pain. Neurosci Biobehav Rev 27:729-737, 2004. 46. Gebhart GF: Visceral nociception: Consequences, modulation and the future. Eur J Anaesthesiol Suppl 10:24-27, 1995. 47. McMahon SB, Dmitrieva N, Koltzenburg M: Visceral pain. Br J Anaesth 75:132-144, 1995. 48. Cervero F: Sensory innervation of the viscera: Peripheral basis of visceral pain. Physiol Rev 74:95-138, 1994.

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49. Bielefeldt K, Christianson JA, Davis BM: Basic and clinical aspects of visceral sensation: Transmission in the CNS. Neurogastroenterol Motil 17:488-499, 2005. 50. Sengupta JN, Gebhart GF: Characterization of mechanosensitive pelvic nerve afferent fibers innervating the colon of the rat. J Neurophysiol 71:2046-2060, 1994. 51. Sengupta JN, Gebhart GF: Mechanosensitive properties of pelvic nerve afferent fibers innervating the urinary bladder of the rat. J Neurophysiol 72:2420-2430, 1994. 52. Winnard KP, Dmitrieva N, Berkley KJ: Estrous influences about how acute inflammation of the uterus and colon affects vascular permeability of the bladder via the hypogastric nerve. Society for Neuroscience Abstract Viewer, 52.5, 2005. 53. Head H: On the disturbances of sensation with especial reference to the pain of visceral disease. Brain 16:1-133, 1893. 54. Bielefeldt K, Gebhart GF: Visceral pain: Basic mechanisms. In McMahon SB, Koltzenburg M (eds): Textbook of Pain, 5th ed. New York, Churchill Livingstone, 2006, pp 721-736. 55. Alagiri M, Chottiner S, Ratner V, et al: Interstitial cystitis: Unexplained associations with other chronic disease and pain syndromes. Urology 49:52-57, 1997. 56. Cervero F, Janig W: Visceral nociceptors: A new world order? Trends Neurosci 15:374-378, 1992. 57. Habler HJ, Janig W, Koltzenburg M: A novel type of unmyelinated chemosensitive nociceptor in the acutely inflamed urinary bladder. Agents Actions 25:219-221, 1988. 58. Hwang SJ, Oh JM, Valtschanoff JG: Expression of the vanilloid receptor TRPV1 in rat dorsal root ganglion neurons supports different roles of the receptor in visceral and cutaneous afferents. Brain Res 1047:261-266, 2005. 59. Chan CL, Facer P, Davis JB, et al: Sensory fibres expressing capsaicin receptor TRPV1 in patients with rectal hypersensitivity and faecal urgency. Lancet 361:385-391, 2003.

60. Birder LA, Kanai AJ, de Groat WC, et al: Vanilloid receptor expression suggests a sensory role for urinary bladder epithelial cells. Proc Natl Acad Sci U S A 98:13396-13401, 2001. 61. Svensson CI, Yaksh TL: The spinal phospholipase-cyclooxygenaseprostanoid cascade in nociceptive processing. Annu Rev Pharmacol Toxicol 42:553-583, 2002. 62. Rice AS, McMahon SB: Pre-emptive intrathecal administration of an NMDA receptor antagonist (AP-5) prevents hyper-reflexia in a model of persistent visceral pain. Pain 57:335-340, 1994. 63. McRoberts JA, Coutinho SV, Marvizon JC, et al: Role of peripheral N-methyl-D-aspartate (NMDA) receptors in visceral nociception in rats. Gastroenterology 120:1737-1748, 2001. 64. Jones CA, Nyberg LM: Epidemiology of interstitial cystitis. Urology 49 (Suppl 5A):2-9, 1997. 65. Berkley KJ: Sex differences in pain. Behav Brain Sci 20:371-380; discussion 435-513, 1997. 66. Unruh AM: Gender variations in clinical pain experience. Pain 65:123-167, 1996. 67. Fillingim RB, Ness TJ: Sex-related hormonal influences on pain and analgesic responses. Neurosci Biobehav Rev 24:485-501, 2000. 68. Riley JL 3rd, Robinson ME, Wise EA, et al: A meta-analytic review of pain perception across the menstrual cycle. Pain 81:225-235, 1999. 69. Wesselmann U, Garrett-Mayer E, Kaplan Gilpin AM, et al: Vulvodynia: Changes in vaginal pain perception across the menstrual cycle. Society for Neuroscience Abstract Viewer, 52.1, 2005. 70. Bradshaw HB, Temple JL, Wood E, et al: Estrous variations in behavioral responses to vaginal and uterine distention in the rat. Pain 82:187-197, 1999. 71. Wesselmann U: Chronic pelvic pain. In Turk DC, Melzack R (ed): Handbook of Pain Assessment, 2nd ed. New York, Guilford Press, 2001, pp 567-578.

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NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN C. A. Tony Buffington The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” The awareness of acute pain motivates those experiencing it toward withdrawal and guarding to permit avoidance of further injury and activation of repair processes. In some cases of chronic pain, however, the situation may be somewhat different, in that the severity of signs loses its usual tight correlation with symptoms. In chronic visceral pain states such as interstitial cystitis (IC) and chronic pelvic pain (CPP), the endocrine system also may be involved in maintaining the sensation of pain (Fig. 90-1),1,2 although the extent to which (or in which patients) this results from an underlying genetic or developmental predisposition and to what extent it results from the etiology of the disease process cannot yet be determined. The aims of this chapter are to describe some of the neuroendocrine abnormalities that occur in women with IC and CPP and to suggest the possibility of underlying neuroendocrine abnormalities in some of these patients. IC is a lower urinary tract syndrome of unknown cause and no generally accepted treatment.3 The symptoms of IC include variable combinations of pain referable to the urinary bladder, as well as increased frequency and urgency of urination. IC may affect more than 700,000 American women,4 and a significant (potentially comparable) number of men diagnosed with sterile prostatitis or prostatodynia.5 The quality of life of IC patients is significantly degraded; in one study, these patients scored much lower (P < .001) than healthy control subjects did in all eight domains of health assessed by the Medical Outcomes Study Short Form-36 Health Survey.3 Since 1993, my laboratory has investigated a common lower urinary tract disorder of domestic cats, feline interstitial cystitis (FIC), that represents a naturally occurring model of IC. We have found that cats with FIC meet all the criteria promulgated by the National Institutes of Health for diagnosis of IC that can be applied to animals, and we have shown that cats with FIC and humans with IC have comparable bladder, sensory afferent, central, sympathetic, and endocrine abnormalities, to the extent they have been investigated. Recent findings in these cats3,6 are consistent with and extend the neuroendocrine abnormalities identified in humans with IC. The National Institutes of Health classifies IC as a CPP syndrome, which has been defined as nonmenstrual pain of at least 6 months’ duration that is severe enough to cause functional disability or necessitate medical or surgical treatment.7 As many as 39% of women of reproductive age seen by primary care physicians report the presence of CPP “always,” “often,” or “some892

times.”8 Women with CPP use more medications, have more nongynecologic operations, and are five times more likely to have a hysterectomy than are women without CPP. These patients also are more likely to have a history of abuse and to suffer from depression, impaired sexual functioning, and reduced overall quality of life.9 A recent comprehensive review7 listed some 70 disorders (15 extrauterine and 8 uterine, 11 urologic, 8 gastrointestinal, 17 musculoskeletal, and 11 “other”) that may be associated with CPP in women, including IC, irritable bowel syndrome, and fibromyalgia. The comorbidity of some of these diseases was suggested by the results of a recent mail questionnaire survey in England, which found that 24% of women aged 18 to 49 years reported CPP during the previous 3 months. Of these women, 52% had CPP only, 24% had CPP and irritable bowel syndrome, 9% had CPP and urinary frequency and urgency, and 15% had all three.10 These results suggest that patients with CPP have variable combinations of organ involvement, raising the question of the extent to which a different etiology affects each organ individually, or whether some common underlying etiology affects a variety of organs, which then respond in their own characteristic ways. Two subtypes of IC currently are recognized based on cystoscopic evaluation of the bladder. In most patients (90%), only submucosal petechial hemorrhages (glomerulations) are observed (type I), whereas mucosal (“Hunner’s”) ulcers, with or without glomerulations, are identified in a minority (type II). The two types also appear to differ in patient epidemiology, histologic findings, and response to treatment, further suggesting that they

Input

Integration

Output

CNS Sensory afferents

External events

Sensing cells

Endocrine organs

SNS

Peripheral tissue

Figure 90-1 General plan of communication between the central nervous system and peripheral structures. CNS, central nervous system; SNS, sympathetic nervous system.

Chapter 90 NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN

may be distinct entities.11 One important difference between the two types is that many patients with type II IC report significant symptomatic relief after supratrigonal cystectomy and cystoplasty, whereas the pain in patients with type I IC is not usually diminished by this procedure.12 This difference in patient response to removal of the bladder may provide an important clue to the underlying causes of pain associated with IC: the cause of the pain in patients with type II disease may be nociceptive, whereas the pain of patients with type I IC may be neuropathic. Nociceptive pain results from persistent activity of sensory afferent fibers innervating the affected area and is relieved by removal of the stimulus. Examples of nociceptive pain include toothache, which is relieved by extraction, and osteoarthritis of the hip joint, which is relieved by hip replacement.13 In contrast, neuropathic pain arises from some abnormality related to the nervous system; although generally attributed to a body structure, it can remain after desensitization of nociceptive afferents14,15 or even removal of the structure.16,17 Such results have been reported for endometriosis, where removal of identified abnormalities does not always lead to resolution of the CPP.18

Cortex

Thalamus

Amygdala

BNST Sensory Input Hypothalamus CRF Anterior Pituitary

ACTH

THE STRESS RESPONSE SYSTEM The presence of neuropathic pain may be related to abnormalities and imbalances of the neuroendocrine system, which is activated in response to threats to homeostasis. One commonality among some IC and CPP patients appears to be a relative predominance of activation of the sympathetic nervous system (SNS) limb of the stress response system (SRS), compared to the responses of the hypothalamic-pituitary-adrenal (HPA) and -gonadal (HPG) axes.19 A schematic diagram of some of the features this complex system20 is presented in Figure 90-2. Once the system is stimulated by central nervous system structures responding to sensory inputs (conscious or unconscious21) that are perceived as a threat to homeostasis, corticotropin-releasing factor (CRF) is released from the paraventricular nucleus of the hypothalamus. CRF acts as a neurotransmitter, to activate sympathetic premotor neurons in the pontine locus coeruleus and brainstem nuclei, and as a hormone, to stimulate the anterior pituitary. In some patients, the SNS arm of the response appears to be uncoupled from the HPA and HPG axes in that SNS outflow increases in the absence of activation of the HPA axis and in the presence of reduced HPG function. Sympathoneural Output Even though the neuroendocrine features of the stress response have not been thoroughly studied in humans with IC and CPP, the available data support the presence of a comparable abnormality in at least a subset of these patients. Although plasma catecholamine concentrations have yet to be reported patients with IC, the findings of abnormal vasomotor tone,22 increased density of bladder neurons staining for tyrosine hydroxylase (the rate-limiting enzyme for catecholamine synthesis),23,24 and increased urine norepinephrine excretion25 that have been reported suggest increased SNS activity. Recent studies have begun to map the pathways that transduce activation of the SRS into cellular dysfunction via the SNS. Events external to the central nervous system, from both within and without the body, are transmitted to the brain by the sensory

LC & Brainstem nuclei

Cortisol SNS

Cortisol Adrenal Cortex

CNS Inhibition Excitation

Neurrosteroids Sex steroids

Bladder, other organs

Figure 90-2 Afferent (sensory input), integrative (thalamus, cortex, amygdala, BNST, and motor (hypothalamus and beyond) components of the stress response system. ACTH, adrenocorticotropic hormone; BNST, bed nucleus of the stria terminalis; CRF, corticotropin-releasing factor; LC, locus coeruleus; SNS, sympathetic nervous system.

neurons. These signals are conveyed to the thalamus, where they are evaluated and usually forwarded to the cerebral cortex for further processing before activation of the appropriate motor program (see Fig. 90-2).26 Potentially threatening events, however, can activate the SRS directly via the thalamic activation of the amygdala, bypassing cortical inhibitory control.27 Activation of the SNS results in sympathoneural release of norepinephrine. A 2003 study28 traced this pathway from the external environment through to norepinephrine-mediated induction of the transcription factor nuclear factor kappa B (NFκB), which is thought to play a role in mediating the urothelial inflammatory response of IC.29 In vitro stimulation of human promonocytic (THP-1) cells with physiologic amounts of norepinephrine for 10 minutes resulted in a dose- and timedependent induction of NF-κB and NF-κB-dependent gene expression; only norepinephrine induced this response, which was reduced by both α1- and β-adrenergic receptor antagonists. The authors concluded that norepinephrine-mediated activation of NF-κB represented a downstream effector of the neuroendocrine response to stressful psychosocial events, linking changes in

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the environment to a bewildering array of cellular responses through activation of the SRS.30 Activation of the SRS also can increase epithelial permeability, permitting environmental agents greater access to sensory afferent neurons,31 which could result in both increased sensory afferent firing and local inflammation. Sympathetic neural-epithelial interactions appear to play an important role in urothelial permeability. For example, Birder and colleagues showed that application of β-adrenergic receptor agonists to urinary bladder strips induced release of nitric oxide (NO) from urinary bladder epithelium, raising the possibility that norepinephrine from adrenergic nerves in the bladder (which may not be present in normal individuals)23,24 or circulating catecholamines could influence bladder function by acting on β-adrenergic receptors in the urothelium to release NO and possibly other neurotransmitters, such as adenosine triphosphate (ATP).32 Application of capsaicin, the pungent principle in hot peppers, also resulted in release of NO from epithelium as well as nervous tissue in the urinary bladder.33 In light of reports that NO may increase urothelial permeability,34,35 these results suggest that some of the sympathetically mediated alterations in permeability may be mediated by norepinephrine via this mechanism. The increased permeability related to increased SNS activation does not require direct interaction with epithelial cells, nor is it restricted to the urinary bladder.36 Moreover, neural release of norepinephrine37 is but one of a variety of mechanisms whereby SRS-induced increases in efferent SNS output can activate local inflammatory cells such as mast cells, which can in turn also increase epithelial permeability.36 Afferent sensory neurons, too, may increase epithelial permeability by releasing neurotransmitters at the peripheral process of the nerve via sympathetic-sensory coupling, dorsal root reflexes, and axon reflexes.38 Recently, increased sensitivity to potassium chloride instillation, a test thought by some to indicate increased urothelial permeability, was reported in 244 female patients with CPP. Eighty-one percent of patients, with clinical diagnoses that included endometriosis, vulvodynia, and pelvic pain, showed a positive (painful) response to potassium instillation into the bladder.39 However, patient’s sensitivity to potassium instilled into other organs (vagina, uterus, colon, or peritoneum) was not assessed, so the specificity of the response cannot be evaluated. This may be an important control procedure, because a number of studies have reported that abnormalities in one visceral organ may affect responses in another, a process called viscerovisceral convergence.40-42 In cats with FIC, we recently reported43,44 sensitization and abnormal properties of dorsal root ganglion cells of axons that provide innervation not only to the bladder but throughout the lumbosacral (L4-S3) region, suggesting that generalized hypersensitivity may a mediating mechanism for viscerovisceral convergence in animals with naturally occurring as well as induced disease. Moreover, one must recall that the presence of inflammation, or altered permeability, is not well correlated with pain, as anyone who has had a superficial bruise knows from personal experience. In the bladder, we have reported the presence of submucosal petechial hemorrhages in cats with no signs referable to the lower urinary tract,45 and others have identified petechial hemorrhages in healthy women,46 as well as urothelial disruption and increased presence of inducible nitric oxide synthase (iNOS), and presumably increased permeability, in elderly men with bladder outlet obstruction.47 Moreover, emotional and environmental factors such as stress or depression can modulate the experience of pain through

descending pathways from the midbrain.48 Therefore, even the recently reported increased firing rate of afferent nerves noted in cats with FIC49 could result in differences in perceived sensations arising from the bladder, depending on the effects of the emotional state of the animal on descending inhibitory and facilitory balance. Hypothalamic-Pituitary-Adrenal Axis The HPA axis of the SRS acts at multiple levels to coordinate and modulate the body’s response to perceived threats. Glucocorticoids tend to antagonize the effects of the SNS, both centrally and peripherally,20 and they appear to play a complex role in epithelial permeability. Corticosterone has long been known to decrease capillary permeability to proteins in the brain,50 skin,51 and lung,52 and cortisol has been shown to reduce in vitro permeability by enhancing tight junction integrity.53 The effects of stress on glucocorticoid-mediated alterations in permeability are more complex and may be dose dependent. For example, stress created by a brief forced swim increased the permeability of the bloodbrain barrier in adult FVB/N mice, whereas no evidence of a stress-potentiated effect was found when restraint, forced swim, or a combination of restraint and forced swim stressors were applied to Long-Evans or Wistar rats.54 Moreover, stress-induced increases in intestinal epithelial permeability disappeared after adrenalectomy or pharmacologic blockade of glucocorticoid receptors, and dexamethasone treatment of control animals increased gastrointestinal permeability and mimicked the effects of stress.55 Differences in tissues studied, rodent strain, type of stress, glucocorticoid studied, and the specifics of the experimental protocol all could influence interpretation of these discordant results. The response to glucocorticoids also is likely to be hormetic (Fig. 90-3); that is, there is an inverse-U–shaped function wherein both deficiencies and excesses may produce abnormalities, which sometimes are relatively similar, further complicating interpretation of the results.56 Glucocorticoids also tend to inhibit activation of NF-κB.57,58 This and other adrenocortical steroidrelated protective mechanisms, such as inhibition of the SRS and modulation of neuronal excitability,59-61 may be less efficient in states of reduced function of cortisol and other steroids (see later discussion) such as IC and other stress-related bodily disorders.62

+ Response

894

Dose

–

Figure 90-3 Hormetic responses are those that move from inadequate function with deficient doses of a substance, to satisfactory function at intermediate doses, to inadequate function again with excessive doses. This pattern is common to many nutrients and hormones.

Chapter 90 NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN

In a 2002 study of IC patients and healthy controls, Lutgendorf and colleagues63 reported that, although mean urinary or salivary cortisol did not differ between the groups, IC patients who had higher morning salivary cortisol concentrations had significantly reduced pain and urgency, and those with higher urinary free cortisol concentrations reported less overall symptomatology (P < .05). This relationship also was observed when comorbid conditions such as fibromyalgia, chronic fatigue syndrome (CFS), and rheumatoid arthritis were controlled for. Patients with morning salivary cortisol concentrations less than 12.5 nmol/L (0.45 μg/dL) were 12.8 times more likely to report high urinary urgency than those with values above this cutoff point. An increased ratio of adrenocorticotropic hormone (ACTH) to cortisol also was reported in women with IC by Lutgendorf and associates.64 Hypocortisolism has been reported in women with CPP, CFS and a variety of other disorders, often related to increased activity of the SRS.62 The causes of the decrease in cortisol have yet to be identified in patients with IC but have been investigated in patients with CPP62,65 and CFS.66 Although diagnostic laparoscopy may be normal in some patients with CPP, psychological studies have identified a high frequency of psychopathology and increased prevalence of chronic stress and traumatic life events, such as sexual and physical abuse, in women with CPP, suggesting a relationship between post-traumatic stress disorder (PTSD) and CPP. Heim and colleagues65 explored stress history, psychopathology, and HPA axis alterations in 16 female patients with CPP and 14 pain-free, infertile controls. An increased prevalence of abuse experiences and PTSD was identified in women with CPP, as well as a higher total number of major life events, although symptoms of depression were within the normal range. Women with CPP also had normal to low diurnal salivary cortisol concentrations and normal plasma ACTH but reduced salivary cortisol response to a CRF stimulation test and enhanced suppression of salivary cortisol by dexamethasone. The authors concluded that a lack of protective properties of cortisol may be of relevance for the development of bodily disorders in chronically stressed or traumatized individuals, although other hormones were not measured. It is not necessary to show such extreme examples of abuse to find correlations between early adverse experience and disease, which also may result from environmental instability and parenting variables.67,68 In patients with CFS, Demitrack and associates66 concluded, after comprehensive study of the HPA axis, that the data were most compatible with a mild central adrenal insufficiency secondary to either a deficiency of CRF (although this was not identified) or some other central stimulus to the pituitary-adrenal axis. Scott and coauthors later reported that the adrenal glands of patients with CFS were some 50% smaller than those of control subjects based on computed tomography.69 Although they studied patients who had low cortisol responses to ACTH, these authors subsequently found comparable results in CFS patients with normal cortisol responses to ACTH.70 A more recent study did not find any difference from normal in adrenal gland volume in another group of CFS patients,71 leaving the question of the role of adrenal volume in the observed abnormalities still open. Additionally, Kizildere and associates72 recently identified a β-adrenergic receptor–mediated inhibition of CRF-stimulated adrenal steroid secretion in healthy humans. They found that administration of 10 mg propranolol (a nonspecific β-adrenergic receptor antagonist) 2 hours before administration of 100 μg human CRF

decreased heart rate and diastolic blood pressure by 20%. Propranolol treatment also reduced plasma ACTH concentrations by about 40% and increased serum cortisol by approximately 70%, which decreased the ACTH-to-cortisol ratio by twofold. These results suggest that increased sympathetic tone also may reduce adrenocortical responsiveness to ACTH. Moreover, ACTH release can be enhanced by α-adrenergic receptor activation, as well as by vasopressin, which also can modulate SRS activity.73 There is convincing evidence that the adrenal cortex is hypoactive in some circumstances in a variety of chronic disorders other than IC and CPP, including asthma, chronic fatigue syndrome, fibromyalgia, panic disorder, PTSD, and rheumatoid arthritis. Moreover, flares in disease activity in these disorders have been related to stress. Although hypocortisolism appears to be a frequent and widespread phenomenon, the nature of the underlying mechanisms and the homology of these mechanisms within and across clinical groups remain speculative. Potential mechanisms underlying the observed hypocortisolism include dysregulation of function at any level of the HPA axis, genetic vulnerability, previous stressful experiences, and individual coping and personality styles.62 In neuroendocrine investigations comparing healthy cats to cats with FIC in a basal state, we found higher plasma catecholamine concentrations in cats with FIC but could not identify a difference in response of ACTH and cortisol to CRF between affected and healthy cats.74 Based on some anomalous responses to a naturalistic stressor obtained during experiments with a CRF receptor antagonist in cats with FIC,75 we began to look more closely at adrenal function during activation of the SRS and found increased concentrations of CRF76,77 and ACTH75 in the absence of a comparable increase in plasma cortisol concentrations, suggesting the presence of mild primary adrenal insufficiency or decreased adrenocortical reserve. We also found that adrenal gland size was significantly smaller in cats with FIC than in healthy cats.78 Microscopic examination of the glands did not reveal any obvious hemorrhage, inflammation, infection, fibrosis, or necrosis as causes of the reduced size. The primary abnormality identified was a reduced size of the fasciculata and reticularis zones of the adrenal cortex. These results suggest that any adrenocortical abnormality might be unmasked more readily in response to a moderate, salient stressor and may not be identifiable in patients studied under basal circumstances, a conclusion about these systems that has also been drawn by others studying human patients.79,80 The simplest explanation for the combination of increased CRF, ACTH, and SNS activity in the presence of reduced adrenocortical response and small adrenal fasciculata and reticularis zones without other apparent abnormalities seems to be the presence of an underlying genetic disorder or developmental anomaly (or some combination of the two). These relationships are depicted in Figure 90-4. When a woman is exposed to a sufficiently harsh stressor during pregnancy, the hormonal products of the ensuing stress response may cross the placenta and affect the course of fetal development. Prenatal and postnatal stressors can result in persistently increased central CRF activity in animals.81 For example, in both continuous and last-trimester paradigms, prenatal dexamethasone (0.1 mg/kg) treatment increased CRF messenger RNA levels specifically in both the hypothalamus and central nucleus of the amygdala, key loci for the effects of the neuropeptide on the expression of fear and anxiety.82

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Birth Interstitial cystitis, CPP?, other disorders?

Sensitive period

Genetic predisposition

Prenatal maternal stress → ↑ CRF, SNS, and ↓adrenal cortex size in fetus

Provocative environment disease, trauma, etc.

Figure 90-4 Potential trajectories to some cases of interstitial cystitis and chronic pelvic pain (CPP). Variable combinations of these factors could result in differences in disease severity among patients. CRF, corticotropin-releasing factor; SNS, sympathetic nervous system. (Adapted from Compagnone NA, Mellon SH: Neurosteroids: Biosynthesis and function of these novel neuromodulators. Front Neuroendocrinol 21:1, 2000.)

Matthews recently suggested that the biological “purpose” of transmitting this response to the fetus is to program the development of the fetal SRS and associated behaviors toward enhanced vigilance to increase the probability of survival.83 The effects of stressors on the fetal HPA axis seem to depend on the timing and magnitude of exposure to products of the maternal stress response in relation to the developmental “programs” that determine the maturation of the various body systems during gestation and early postnatal development. If the fetus is exposed before initiation of a developmental program, there may be no effect. With exposure during the critical period while the adrenocortical maturation program is running, however, adrenal size in the developing fetus may be reduced, as shown by studies in Long-Evans rats,84 guinea pigs,85 blue fox,86 rhesus monkeys,87 and baboons.88 If a sufficiently severe stress response occurs after the critical period of adrenocortical development, including during postnatal development, subsequent adrenocortical responses to stress and adrenal size may be increased.83 In either case, however, the biologic outcome might be similar. Raison and Miller56 recently concluded from a review of the pertinent literature that inadequate biologic activity of glucocorticoids can occur either as a result of decreased hormone bioavailability or from reduced hormone sensitivity due to agonist-mediated receptor desensitization. Regardless of the cause, decreased biologic activity of adrenocortical steroids may have a variety of adverse effects on bodily function, possibly related to their role in restraining activation of the immune system and other components of the stress response, including the SNS and CRF. The lack of long-term benefit of glucocorticoid therapy in most patients with IC89 (but see Hosseini and colleagues90 for results of a small, uncontrolled study of patients with type II IC given 5 mg/day oral prednisolone) suggests that the most appropriate dose has not yet been identified, that inadequate production of other steroids also might play a role in the pathophysiology of IC, and/or that SNS output needs to be attenuated. Most doses of glucocorticoid, although possibly appropriate for acute phases

of the disease,91 may be excessive for chronic therapy. As shown in Table 90-1, the daily production of cortisol in humans is in the range of 8 to 25 mg, much lower than doses of glucocorticoid sometimes suggested. In a recent open trial, 10 mg/day hydrocortisone was administered orally for 1 month to three patients with PTSD in a double-blind, placebo-controlled, crossover design. A significant treatment effect was observed in all patients, with cortisol-related reductions of at least 38% in one of the daily rated symptoms of traumatic memories, as assessed by selfadministered rating scales. Although very preliminary, these results suggest that physiologic glucocorticoid replacement may have a role in some patients with CPP, if only in those with concurrent PTSD.92 Available evidence also suggests that part of the stress response may include maintaining production of cortisol (Δ4 pathway) at the expense of the 17,20-lyase (Δ5 pathway) products of the 17-α hydroxylase enzyme (Fig. 90-5) such as dehydroepiandrosterone sulfate (DHEAS, the longer-lived metabolite of DHEA)72 if the stressor is severe or adrenocortical reserve is inadequate.93,94 DHEAS also is a neurosteroid, a term used to describe steroids that are synthesized in the central and peripheral neurons and in glial cells. The concept of neurosteroids was introduced by Baulieu in 198195 to describe a steroid hormone (DHEAS) he found at high levels in the brain long after gonadectomy and adrenalectomy. Androstenedione, pregnenolone, and a variety of other steroids were later also identified as neurosteroids.96 These compounds can act as allosteric modulators of ion-gated neurotransmitter receptors, such as γ-aminobutyric acid (GABA)-A and N-methyl-d-aspartate (NMDA) receptors, which are the primary inhibitory and excitatory receptors, respectively, in the nervous system. Neurosteroid concentrations vary according to environmental and behavioral circumstances, such as stress, sex recognition, and aggressiveness. In the peripheral nervous system, neurosteroids also may play a role in neuronal repair after injury. Abnormal neurosteroid function may underlie some functional disturbances of the nervous system.96-98

Chapter 90 NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN

PREGS

↔

Cholesterol ↓ PREG

ALLO

α5 ←

↓ PROG

THDOC

←

↓ DOC

→ a →

17-OHPREG ↓ 17-OHPROG Δ4 ↓ Cortisol

Δ5 →

DHEA

↔

DHEAS

b →

↓ ASD

↔

Testosterone

→

DHT

↔

↓ Estradiol

3α, 5α-diol ↓ Androsterone

Figure 90-5 The output of the adrenal cortex includes variable combinations of glucocorticoids, sex steroids, and neurosteroids. Other sources of sex steroids and neurosteroids include the gonads and neural tissue. Some examples in women are presented in Table 90-1. The cytochrome P450 c17 enzyme (a) performs the 17α-hydroxylase reaction equally well using PREG or PROG as substrate, but the 17,20-lyase reaction (b) occurs 50 to 100 times more efficiently using 17-OH-PREG as substrate, rather than 17-OH-PROG. Therefore, conversion of 17-OH-PROG to ASD is minimal, and DHEA is the principal precursor of sex steroid synthesis. 3α,5α-diol, 3α-androstanediol; ALLO, 3α,5α-tetrahydroprogesterone; ASD, androstenedione; DOC, 11-deoxycorticosterone; DHT, dihydrotestosterone; DHEA, dehydroepiandrosterone; DHEAS, dehydroepiandrosterone sulfate; 17-OH-PREG, 17-hydroxy-pregnenolone; 17-OH-PROG, 17-hydroxyprogesterone; PREG, pregnenolone; PREGS, pregnenolone sulfate; PROG, progesterone; THDOC, 3α,5α-tetrahydrodeoxycorticosterone. (Adapted from Compagnone NA, Mellon SH: Neurosteroids: Biosynthesis and function of these novel neuromodulators. Front Neuroendocrinol 21:1, 2000.)

Table 90-1 Sources, Production Rates, and Plasma Concentrations of Selected Steroids in Women Steroid 142

Cortisol

Source

Production (mg/day)

Plasma Concentration Range (nmol/L)

AC zona fasciculata

8-25*

AM:

3.5-20* (declines with age) 6-8* (declines with age)

1350-5518 690-2758 3,000-12,000 5.6-27.8

1.4-6.2

2-8

0.1-0.4 (declines with age)

0.5-2.4

—

Follicular phase: 0.8 ± 0.30 (mean ± SEM, n = 81)145 Luteal phase: 3.7 ± 1.0 (mean ± SEM, n = 108)145

PM:

DHEAS143 DHEA143

ASD143 Testosterone143

Allopregnanolone

AC ZR AC ZR 50% Ovarian theca 20% Circulating DHEAS 30% AC ZR 50% Ovarian stroma 50% AC ZR 25% Ovarian stroma 25% Circulating ASD 50% AC144 Ovary Neural tissue

*No change during menses. AC, adrenal cortex; ASD, androstenedione; DHEA, dehydroepiandrosterone; DHEAS; dehydroepiandrosterone sulfate; SEM, standard error of the mean; ZR, zona reticularis.

We recently measured serum free cortisol and DHEAS concentrations in patients with moderate to severe IC during flare and remission. During flare, the concentration of serum free cortisol was half, and that of DHEAS was 20%, of the concentration found in patients not in a flare (Fig. 90-6). During their flare, two patients were deficient in serum free cortisol, and four patients were deficient in DHEAS (adjusted for age).99 In addition to suggesting that neuroendocrine function may be altered in IC during flare, the results of studies of cats with FIC, and of human patients with IC and other unexplained clinical conditions,100 document that neuroendocrine abnormalities may not be identifiable by evaluation of basal neuroendocrine function and may be unmasked only by appropriate provocative testing paradigms. Adrenocortical function also has been evaluated in patients with CFS by measuring the cortisol-to-DHEAS ratio,101 which

was twofold to threefold higher in CFS patients than in controls. Kizildere and colleagues72 suggested that serum levels of DHEAS may be low in patients with inflammatory and noninflammatory diseases due to an activated SNS. They concluded that sympathetic hyperactivity may be a common denominator for low levels of DHEAS in both inflammatory and noninflammatory diseases. These abnormalities also suggest that some patients may have decreased availability of adrenocortical sex steroids and neurosteroids (see Fig. 90-5),98 which could adversely affect normal neural function.102,103 Hypothalamic-Pituitary-Gonadal Axis Patients with IC and CPP also may be at increased risk for inadequate biologic activity of the sex hormones, for a variety of reasons. Some patients in both groups have decreased circulating

897

Section 10 PELVIC PAIN AND INFLAMMATORY CONDITIONS

100th

(10)

(4)

(10)

100

(3)

75th Quartile

75th

50th

50th

25th

25th

Group

Figure 90-6 Effects of flare (F) and remission (R) of interstitial cystitis symptoms on serum free cortisol (SFC) and dehydroepiandrosterone sulfate (DHEAS). Parentheses (= no. of patients = no of dots in graph). (Adapted from Compagnone NA, Mellon SH: Neurosteroids: Biosynthesis and function of these novel neuromodulators. Front Neuroendocrinol 21:1, 2000.)

glucocorticoid concentrations, suggesting decreased adrenocortical availability of sex steroid precursors99,104; some have undergone oophorectomy and/or hysterectomy; and some may have inadequate pituitary function. Kalantaridou and associates105 recently reviewed the complex effects of activation of the SRS system on the female reproductive system. Increased CRF and β-endorphin release as a consequence of chronic activation of the SRS can inhibit release of gonadotropin-releasing hormone (GnRH), thus decreasing sex hormone availability. Increased glucocorticoid activity also can suppress function at all levels of the gonadal axis.105 Decreased estrogen activity has been recognized in some patients with CPP, as well as in patients with irritable bladder symptoms,106 and replacement therapy may be beneficial. Androgen activity also may be inadequate in some patients.107,108 Reported causes of androgen deficiency in women are presented in Table 90-2. Any of these causes may lead to variable combinations of the deficiency symptoms listed in Table 90-3. Dessein and colleagues109 investigated the concentrations of adrenal androgen metabolites and their relationship with health status in women with fibromyalgia, a syndrome that commonly occurs comorbidly with CPP and IC. Responses to the Fibromyalgia Impact Questionnaire and fasting blood samples were obtained from 57 women with fibromyalgia for measurement of DHEAS, free testosterone (T), cortisol, serotonin, and insulinlike growth factor-1. Normal values for DHEAS and T were obtained from 114 controls. Individual results for all patients were reported and are plotted in Figure 90-7. The individual values were divided by the uppermost value from the reference range to allow the results to be plotted as quartiles of the reference range. DHEAS concentrations were decreased significantly in both premenopausal and postmenopausal patients (P < .0001 and P < .0005, respectively). T concentrations were decreased significantly in premenopausal patients (P < .0001), and a trend could be identified in postmenopausal patients (P = .06). After

in ro to n Se

or tis ol C

IG

F1

e Te

st os te ro n

EA H

EA SR H D

D H EA SF

-R SF C

-F SF C

-S

0

0

D

Quartile

898

Hormone (n=57)

Figure 90-7 Fasting blood concentrations of selected hormones in women with fibromyalgia syndrome. DHEA-S, dehydroepiandrosterone sulfate; IGF-1, insulin-like growth factor 1. (Adapted from Dessein PH, Shipton EA, Joffe BI, et al: Hyposecretion of adrenal androgens and the relation of serum adrenal steroids, serotonin and insulin-like growth factor-1 to clinical features in women with fibromyalgia. Pain 83:313, 1999.)

Table 90-2 Causes of Androgen Insufficiency in Women Presentation

Causes

Inadequate adrenal function Inadequate ovarian function

Decreased adrenal reserve, adrenal failure, surgery Oophorectomy, hysterectomy, premature menopause after radiation therapy or chemotherapy Chronic stress response, hypercortisolism Exogenous oral estrogen, antiandrogen therapy, chronic glucocorticoid treatment Low bioavailable free testosterone

Inadequate pituitary function Iatrogenic

Normal aging

Data from Cameron DR, Braunstein GD: Androgen replacement therapy in women. Fertil Steri 82: 273, 2004; and Rivera-Woll LM, Papalia M, Davis SR, et al: Androgen insufficiency in women: Diagnostic and therapeutic implications. Hum Reprod Update 10: 421, 2004.

adjustment for age, the only significant correlations between hormone concentrations and Fibromyalgia Impact Questionnaire scores were between DHEAS and pain (r = −0.29, P < .001), and between T and physical functioning (r = .34, P = .002). Body mass index correlated positively with pain (r = .38, P < .001) and inversely with DHEAS level (r = −0.33, P = .006). Androgen insufficiency can occur even in regularly menstruating women. Guay recently reported measurement of total and free serum testosterone levels in 12 premenopausal women with complaints of decreased libido.110 Eight of the women had low or immeasurable levels of both testosterones despite having regular menstrual periods. Concentrations of DHEAS and androstenedione were in the low-normal to high-normal range. Treatment

Chapter 90 NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN

Table 90-3 Symptoms of Androgen Deficiency and Excess in Women Deficiency

Excess

Hormone

Signs

Symptoms

Signs

Symptoms

Estrogen

Hot flashes Dry vagina Lowered libido Painful intercourse Irritable bladder symptoms Fatigue Headache/migraine Night sweats Vaginal infections Urinary tract infections Incontinence Difficulty falling asleep Decreased concentration Episodes of rapid heart rate Decreased verbal skills Irregular vaginal bleeding

Depression Minor anxiety Emotional instability Feelings of despair Crying easily

Breast pain PMS Irregular bleeding Fluid retention Headache Breast adenoma Gall bladder problems Blood sugar problems Sugar cravings Fibroids Hormonal cancers Heavy menstruation Bloating Weight gain Nausea Endometriosis Thyroid problems Sleep disturbances

Nervousness Irritability Low libido Mood swings

Progesterone

Breast cysts/pain Fluid retention Reduced body temperature Hair loss Heavy periods Menstrual cramps Fibroids Hypothyroidism Bone loss Irregular cycle/Infertility

Testosterone

Decreased pubic hair Reduced lean body mass Osteopenia or osteoporosis Incontinence Thinning skin Genital thinning Reduced muscle tone

Anxiety Over-reacting Easily alarmed Easily stressed Feelings of confusion Mood swings Irritability Nervousness Depression PMS Headaches/migraine Endometriosis Sleep disturbances Blunted motivation Diminished well-being Flat mood Reduced libido

Acne/oily skin Facial hair Deepened voice Ovarian cysts Low blood sugar Midcycle pain Low HDL cholesterol Thinning scalp hair Increased breast cancer risk Painful nipples

Agitation Anger Irritability

HDL, high-density lipoprotein; PMS, premenstrual syndrome.

with oral DHEA, 50 to 100 mg per day, restored sexual desire in six of the eight women, gave partial improvement in one, and failed in one. It is important to note that DHEA currently is marketed as a “dietary supplement,” which means that the U.S. Food and Drug Administration does not certify the amount or quality of DHEA in the many commercially available preparations. Thompson and Carlson recently reported that determination of the DHEA content of 54 such supplements using a liquid chromatographic method revealed variation from 0% to 109.5% of the declared amount, with an overall mean value of 91%.111 This variability suggests that circulating DHEA concentrations should be moni-

tored in patients taking these products to ensure that intake is not inadequate or excessive. The most frequently reported side effects of excessive DHEA intake are increased facial hair and acne.107 Additionally, conversion of DHEA or DHEAS to androgens and estrogens may not occur normally in some patients.112 Most of the androgens in women, especially after menopause, are synthesized in peripheral tissues from adrenal DHEA and DHEAS by 17β-hydroxysteroid dehydrogenase enzymes in a process called intracrinology.113 Once synthesized, the sex steroids exert their action in the cells where they are synthesized without significant diffusion into the circulation, thus seriously limiting

899

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Section 10 PELVIC PAIN AND INFLAMMATORY CONDITIONS

the ability to interpret serum sex steroid concentrations. They also are inactivated locally into more water-soluble compounds that diffuse into the general circulation, where they can be measured.113,114 Dysfunctions in human 17β-hydroxysteroid dehydrogenases result in disorders of biology of reproduction and neuronal diseases, and these enzymes also are involved in the pathogenesis of various cancers. Abnormalities of this complex peripheral system may underlie some of the discordant results found in studies of DHEA and DHEAS replacement therapy. Recently, concern has been expressed that excessive biologic activity of estrogen and testosterone, both essential hormones, can increase the risk for breast cancer in women.115,116 On the other hand, patients with documented symptoms and laboratory evidence of hormone insufficiency have been shown to benefit from appropriate physiologic replacement therapy.107,117 The occurrence of abnormalities with both inadequate and excessive biologic activity of hormones demonstrates the hormetic nature of the biologic response to steroid hormones (see Fig. 90-3).118 The “dose-response” for hormones is similar to that for many essential nutrients, with deficiency signs occurring with inadequate intake, a variable plateau of satisfactory intake, and symptoms of toxicity with excessive intake.119 The diagnosis of androgen insufficiency should be made only in adequately and satisfactorily estrogenized women, because estrogen therapy alone may be sufficient to alleviate the symptoms in some patients.120 Adequately means replacement with physiologic doses that avoid potentially detrimental excesses. Satisfactorily means avoidance of oral preparations in this patient population, due to the effects on the liver of oral conjugated equine estrogens (or oral contraceptives). Oral forms of estrogens appear to stimulate hepatic production of both cortisol and sex hormone–binding globulin, reducing the availability of the free, biologically active forms of cortisol and testosterone. Oral conjugated equine estrogens also have been reported to increase high-density lipoproteins, triglycerides, and C-reactive protein, which may adversely affect cardiovascular health. Transdermal delivery of estradiol has not been associated with these potentially adverse changes.121 The Princeton consensus statement122 proposed the algorithm presented in Figure 90-8 for initiating androgen therapy in women. The age at onset of symptoms also supports the hypothesis that hormone deficiency may play a role in IC. Prevalence was greatest in age categories 41 to 45 years and 71 to 75 years, with the highest prevalence (266 per 100,000) observed in those age 41 to 45 years.123 Koziol also reported an average age at the time of onset of symptoms of IC of approximately 41 years, although almost 30% of patients were younger than 30 years of age at the time of onset.124 Further support comes from the observation that some patients with IC and CPP have significant symptom improvements during pregnancy, a time when concentrations of many of the steroid hormones increase.125 Inadequate sex hormone biologic activity in women also may increase SNS activity. Stoney and coworkers126 tested the effects of elective hysterectomy and/or bilateral salpingo-oophorectomy on cardiovascular risk factors, blood pressure, lipids, weight, and physiologic responses to stress in 29 middle-aged premenopausal women. After surgery, the 10 women who had undergone oophorectomy only had higher concentrations of stress-induced lipids and tended to have higher circulating concentrations of epinephrine and higher stress-induced systolic and diastolic blood pressure than did the 19 women who had undergone hysterectomy including removal of their ovaries. In rats, Ting and colleagues127

Signs and symptoms consistent with FAI?

NO – end evaluation

YES

Is there an alternative explanation for the symptoms (e.g., major depression, chronic fatigue syndrome in the pressence of normal androgen status)?

NO

Is the patient in an optimal estrogen state?

YES – manage as appropriate

NO – initiate estrogen replacement

YES

Is laboratory assessment consistent with FAI? Measure 2 of 3: total T, free T, SHBG. Values should be in the lowest quartile of reference range.

YES

Is a specific treatable cause for FAI present (e.g., oral estrogen, oral contraceptive use)?

NO – consider alternative treatment or referral

YES – treat specific cause

NO

Consider a trial of androgen replacement therapy.

Figure 90-8 Algorithm proposed by the Princeton consensus statement for initiating androgen therapy in women. FAI, female androgen insufficiency; SHBG, sex hormone–binding globulin; T, testosterone. (Adapted from Bachmann G, Bancroft J, Braunstein G, et al: Female androgen insufficiency: The Princeton consensus statement on definition, classification, and assessment. Fertil Steril 77:660, 2002.)

recently reported that ovariectomy resulted in a 59% elevation in vaginal nerve density. This change was attributable to increased densities of sympathetic (70%), cholinergic parasympathetic (93%), and nociceptive sensory nerves (84%); myelinated sensory innervation did not appear to be affected. Sustained administration of 17β-estradiol reduced innervation density to an extent comparable to that of estrus, suggesting that estrogen deficiency had mediated the increments in innervation. These findings indicate that some aspects of vaginal dysfunction during menopause may be attributable to changes in innervation. Increased sympathetic innervation may augment vasoconstriction and promote vaginal dryness, and nociceptive sensory afferent proliferation may contribute to symptoms of pain, burning, and itching associated with menopause and some forms of CPP. Documentation of widespread involvement of other organ systems124,128-132 also suggests a role for neuroendocrine involvement in at least some patients with IC and CPP. In particular, the prominence of autonomic symptoms in some patients with type I IC provides further evidence for the presence of persistently increased SNS activity in these patients. Even the somewhat unusual bladder histopathology found in patients with IC, vasodilatation, and vascular leakage in the absence of any significant mononuclear infiltrate could be the result of high local concentrations of norepinephrine.133,134

Chapter 90 NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN

IC and CPP are so complex that is seems unlikely that all, or even most, cases will be explained by a single underlying etiology. Separation of type I from type II patients in data analyses appears to be an important distinction and may suggest different underlying neuroendocrine abnormalities. Even if neuroendocrine imbalance explains only a subset of cases of IC, however, it could result in improved care for those patients. In the case of CPP, patients who have had their reproductive organs removed to treat the pain, without success, may be most likely to be affected.104 In susceptible individuals with IC or CPP, it may be prudent to assess adrenocortical function before elective surgical procedures or after significantly stressful experiences and to consider providing replacement therapy as indicated.135 Although adverse addisonian-like events have not been reported in these patients to the my knowledge, studies in other patient populations have suggested that inadequate adrenocortical function in stressed patients may predispose some individuals to development of PTSD.56,136 The direct and circumstantial evidence that neuroendocrine abnormalities may play an important role in the etiology, pathophysiology, and therapy of IC and CPP in some patients is tantalizing and incomplete. There are so many genetic, environmental,

and individual variables that finding a single “smoking gun” does not seem likely. To begin to tease apart the relative contributions of the SNS, HPA, HPG, and other systems may require measurement of a “panel” of markers of neuroendocrine function in patients, much like a serum biochemical profile. The most appropriate sample source (e.g., saliva,137 serum138), timing of collection (during flare or remission periods), and assay methodology139 for diagnosis and follow-up of neuroendocrine abnormalities remain unresolved questions, as do the amount, balance, and route of replacement therapy, when indicated. The sex and adrenal steroids arose hundreds of millions of years ago,140 and we are left to sort out the ensuing complexity. It may be that, by broadening our perspective, at least initially, to include additional systems, we may be better able to understand syndromes that at first appear to be restricted to isolated organs but in some patients are revealed on closer inspection to be system wide.141 Acknowledgment Dr. Buffingtion is supported by the National Institutes of Health P50 DK64539 Women’s Health and Functional Visceral Disorders Center, and DK47538.

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30. Kumar A, Takada Y, Boriek AM, et al: Nuclear factor-kappa B: Its role in health and disease. J Mol Med 82:434, 2004. 31. Veranic P, Jezernik K: The response of junctional complexes to induced desquamation in mouse bladder urothelium. Biol Cell 92:105, 2000. 32. Birder LA, Nealen ML, Kiss S, et al: Beta-adrenoceptor agonists stimulate endothelial nitric oxide synthase in rat urinary bladder urothelial cells. J Neurosci 22:8063, 2002. 33. Birder LA, Apodaca G, De Groat WC, et al: Adrenergic- and capsaicin-evoked nitric oxide release from urothelium and afferent nerves in urinary bladder. Am J Physiol Renal Physiol 44:F226, 1998. 34. Jezernik K, Romih R, Mannherz HG, et al: Immunohistochemical detection of apoptosis, proliferation and inducible nitric oxide synthase in rat urothelium damaged by cyclophosphamide treatment. Cell Biol Int 27:863, 2003. 35. Oter S, Korkmaz A, Oztas E, et al: Inducible nitric oxide synthase inhibition in cyclophosphamide induced hemorrhagic cystitis in rats. Urol Res 32:185, 2004. 36. Theoharides TC, Cochrane DE: Critical role of mast cells in inflammatory diseases and the effect of acute stress. J Neuroimmunol 146:1, 2004. 37. Elenkov IJ, Wilder RL, Chrousos GP, et al: The sympathetic nerve—An integrative interface between two supersystems: The brain and the immune system. Pharmacol Rev 52:595, 2000. 38. Wang J, Ren Y, Zou XJ, et al: Sympathetic influence on capsaicinevoked enhancement of dorsal root reflexes in rats. J Neurophysiol 92:2017, 2004. 39. Parsons CL, Dell J, Stanford EJ, et al: The prevalence of interstitial cystitis in gynecologic patients with pelvic pain, as detected by intravesical potassium sensitivity. Am J Obstet Gynecol 187:1395, 2002. 40. Houdeau E, Larauche M, Monnerie R, et al: Uterine motor alterations and estrous cycle disturbances associated with colonic inflammation in the rat. Am J Physiol Regul Integr Comp Physiol 288: R630, 2005. 41. Giamberardino MA, Berkley KJ, Affaitati G, et al: Influence of endometriosis on pain behaviors and muscle hyperalgesia induced by a ureteral calculosis in female rats. Pain 95:247, 2002. 42. Giamberardino MA: Recent and forgotten aspects of visceral pain. Eur J Pain (London) 3:77, 1999. 43. Sculptoreanu A, deGroat WC, Buffington CAT, et al: Abnormal excitability in capsaicin-responsive DRG neurons from cats with feline interstitial cystitis. Exp Neurol 193:437, 2005. 44. Sculptoreanu A, deGroat WC, Buffington CAT, et al: Protein kinase C contributes to abnormal capsaicin responses in DRG neurons from cats with feline interstitial cystitis. Neurosci Lett 381:42, 2005. 45. Chew DJ, Buffington CA, Kendell MS, et al: Amitriptyline treatment for severe recurrent idiopathic cystitis in cats. J Am Vet Med Assoc 213:1282, 1998. 46. Waxman JA, Sulak PJ, Kuehl TJ: Cystoscopic findings consistent with interstitial cystitis in normal women undergoing tubal ligation. J Urol 160:1663, 1998. 47. Romih R, Korosec P, Jezernik K, et al: Inverse expression of uroplakins and inducible nitric oxide synthase in the urothelium of patients with bladder outlet obstruction. BJU Int 91:507, 2003. 48. Fields H: State-dependent opioid control of pain. Nat Rev Neurosci 5:565, 2004. 49. Roppolo JR, Tai C, Booth AM, et al: Bladder A-delta afferent nerve activity in normal cats and cats with feline interstitial cystitis. J Urol 173:1011, 2005. 50. Long JB, Holaday JW: Blood-brain barrier: Endogenous modulation by adrenal-cortical function. Science 227:1580, 1985. 51. Leme JG, Wilhelm DL: The effects of adrenalectomy and corticosterone on vascular permeability responses in the skin of the rat. Br J Exp Pathol 56:402, 1975.

52. Boschetto P, Musajo FG, Tognetto L, et al: Increase in vascular permeability produced in rat airways by Paf: Potentiation by adrenalectomy. Br J Pharmacol 105:388, 1992. 53. Harhaj NS, Antonetti DA: Regulation of tight junctions and loss of barrier function in pathophysiology. Int J Biochem Cell Biol 36:1206, 2004. 54. Sinton CM, Fitch TE, Petty F, et al: Stressful manipulations that elevate corticosterone reduce blood-brain barrier permeability to pyridostigmine in the rat. Toxicol Appl Pharmacol 165:99, 2000. 55. Meddings JB, Swain MG: Environmental stress-induced gastrointestinal permeability is mediated by endogenous glucocorticoids in the rat. Gastroenterology 119:1019, 2000. 56. Raison CL, Miller AH: When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. Am J Psychiatry 160:1554, 2003. 57. Wen Y, Yang SH, Liu R, et al: Estrogen attenuates nuclear factorkappa B activation induced by transient cerebral ischemia. Brain Res 1008:147, 2004. 58. Hayashi R, Wada H, Ito K, et al: Effects of glucocorticoids on gene transcription. Eur J Pharmacol 500:51, 2004. 59. Turrin NP, Rivest S: Unraveling the molecular details involved in the intimate link between the immune and neuroendocrine systems. Exp Biol Med 229:996, 2004. 60. Nadeau S, Rivest S: Glucocorticoids play a fundamental role in protecting the brain during innate immune response. J Neurosci 23:5536, 2003. 61. Koulich E, Nguyen T, Johnson K, et al: NF-kappa B is involved in the survival of cerebellar granule neurons: Association of I kappa beta phosphorylation with cell survival. J Neurochem 76:1188, 2001. 62. Heim C, Ehlert U, Hellhammer DH: The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology 25:1, 2000. 63. Lutgendorf SK, Kreder KJ, Rothrock NE, et al: Diurnal cortisol variations and symptoms in patients with interstitial cystitis. J Urol 167:1338, 2002. 64. Lutgendorf S, Kreder K, Ratliff T, et al: Effects of stress reactivity on HPA function and symptoms in interstitial cystitis. Psychosom Med 62:1332, 2000. 65. Heim C, Ehlert U, Hanker JP, et al: Abuse-related posttraumatic stress disorder and alterations of the hypothalamic-pituitaryadrenal axis in women with chronic pelvic pain. Psychosom Med 60:309, 1998. 66. Demitrack MA, Dale JK, Straus SE, et al: Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metab 73:1224, 1991. 67. Lackner JM, Gudleski GD, Blanchard EB: Beyond abuse: the association among parenting style, abdominal pain, and somatization in IBS patients. Behav Res Ther 42:41, 2004. 68. Yehuda R, Halligan SL, Bierer LM: Cortisol levels in adult offspring of Holocaust survivors: Relation to PTSD symptom severity in the parent and child. Psychoneuroendocrinology 27:171, 2002. 69. Scott LV, Teh J, Reznek R, et al: Small adrenal glands in chronic fatigue syndrome: A preliminary computer tomography study. Psychoneuroendocrinology 24:759, 1999. 70. Dinan TG: Personal communication, 2003. 71. Calis M, Gokce C, Ates F, et al: Investigation of the hypothalamopituitary-adrenal axis (HPA) by 1 microg ACTH test and metyrapone test in patients with primary fibromyalgia syndrome. J Endocrinol Invest 27:42, 2004. 72. Kizildere S, Gluck T, Zietz B, et al: During a corticotropin-releasing hormone test in healthy subjects, administration of a betaadrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH. Eur J Endocrinol 148:45, 2003. 73. Aguilera G: Corticotropin releasing hormone, receptor regulation and the stress response. Trends Endocrinol Metab 9:329, 1998.

Chapter 90 NEUROENDOCRINE ROLE IN INTERSTITIAL CYSTITIS AND CHRONIC PELVIC PAIN IN WOMEN

74. Buffington CA, Pacak K: Increased plasma norepinephrine concentration in cats with interstitial cystitis. J Urol 165:2051, 2001. 75. Westropp JL, Buffington CAT: Effect of a corticotropin releasing factor (crf) antagonist on hypothalamic-pituitary-adrenal activation in response to crf in cats with interstitial cystitis. Presented at the Research Insights into Interstitial Cystitis, Alexandria, VA, 2003. 76. Westropp JL, Buffington CAT: Cerebrospinal fluid corticotrophin releasing factor and catecholamine concentrations in healthy cats and cats with interstitial cystitis. Presented at the Research Insights into Interstitial Cystitis, Alexandria, VA, 2003. 77. Welk KA, Buffington CAT: Effect of interstitial cystitis on central neuropeptide and receptor immunoreactivity in cats. Presented at the Research Insights into Interstitial Cystitis, Alexandria, VA, 2003. 78. Westropp JL, Welk KA, Buffington CAT: Small adrenal glands in cats with feline interstitial cystitis. J Urol 170:2494, 2003. 79. Liberzon I, Abelson J, Flagel S, et al: Neuroendocrine and psychophysiologic responses in PTSD: A symptom provocation study. Neuropsychopharmacology 21:40, 1999. 80. Wilkinson DJC, Thompson JM, Lambert GW, et al: Sympathetic activity in patients with panic disorder at rest, under laboratory mental stress, and during panic attacks. Arch Gen Psychiatry 55:511, 1998. 81. Coplan JD, Smith EL, Altemus M, et al: Variable foraging demand rearing: sustained elevations in cisternal cerebrospinal fluid corticotropin-releasing factor concentrations in adult primates. Biol Psychiatry 50:200, 2001. 82. Welberg LAM, Seckl JR: Prenatal stress, glucocorticoids and the programming of the brain. J Neuroendocrinol 13:113, 2001. 83. Matthews SG: Early programming of the hypothalamo-pituitaryadrenal axis. Trends Endocrinol Metab 13:373, 2002. 84. Fameli M, Kitraki E, Stylianopoulou F: Effects of hyperactivity of the maternal hypothalamic-pituitary-adrenal (HPA) axis during pregnancy on the development of the HPA axis and brain monoamines of the offspring. Int J Devel Neurosci 12:651, 1994. 85. Cadet R, Pradier P, Dalle M, et al: Effects of prenatal maternal stress on the pituitary adrenocortical reactivity in guinea-pig pups. J Dev Physiol 8:467, 1986. 86. Braastad BO, Osadchuk LV, Lund G, et al: Effects of prenatal handling stress on adrenal weight and function and behaviour in novel situations in blue fox cubs (Alopex lagopus). Appl Ani Behav Sci 57:157, 1998. 87. Challis JRG, Davies IA, Benirschke K, et al: The effects of dexamethasone on plasma steroid levels and fetal adrenal histology in the pregnant rhesus monkey. Endocrinology 95:1300, 1974. 88. Leavitt MG, Aberdeen GW, Burch MG, et al: Inhibition of fetal adrenal adrenocorticotropin receptor messenger ribonucleic acid expression by betamethasone administration to the baboon fetus in late gestation. Endocrinology 138:2705, 1997. 89. Pontari MA, Hanno PM: Oral therapies for interstitial cystitis. In Sant GR (ed): Interstitial Cystitis. Philadelphia, Lippincott-Raven, 1997, pp 173-176. 90. Hosseini A, Ehren I, Wiklund NP: Nitric oxide as an objective marker for evaluation of treatment response in patients with classic interstitial cystitis. J Urol 172:2261, 2004. 91. Schelling G: Effects of stress hormones on traumatic memory formation and the development of posttraumatic stress disorder in critically ill patients. Neurobiol Learn Mem 78:596, 2002. 92. Aerni A, Traber R, Hock C, et al: Low-dose cortisol for symptoms of posttraumatic stress disorder. Am J Psychiatry 161:1488, 2004. 93. Scott LV, Svec F, Dinan T: A preliminary study of dehydroepiandrosterone response to low- dose ACTH in chronic fatigue syndrome and in healthy subjects. Psychiatr Res 97:21, 2000. 94. Cardoso E, Persi G, Arregger AL, et al: Assessment of corticoadrenal reserve through salivary steroids. Endocrinologist 12:38, 2002. 95. Baulieu EE: Steroid hormones in the brain: Several mechanisms? In Fuxe K, Gustafson JA, Wetterberg L (eds): Steroid Hormone

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120. Davis SR: When to suspect androgen deficiency other than at menopause. Fertil Steril 77(Suppl 4):S68, 2002. 121. Minkin MJ: Considerations in the choice of oral vs. transdermal hormone therapy: A review. J Reprod Med 49:311, 2004. 122. Bachmann G, Bancroft J, Braunstein G, et al: Female androgen insufficiency: The Princeton consensus statement on definition, classification, and assessment. Fertil Steril 77:660, 2002. 123. Clemens JQ, Meenan RT, Rosetti MC, et al: Prevalence and incidence of interstitial cystitis in a managed care population. J Urol 173:98, 2005. 124. Koziol JA: Epidemiology of interstitial cystitis. Urol Clin North Am 21:7, 1994. 125. Masi AT, Feigenbaum SL, Chatterton RT: Hormonal and pregnancy relationships to rheumatoid arthritis: Convergent effects with immunological and microvascular systems. Semin Arthritis Rheum 25:1, 1995. 126. Stoney CM, Owens JF, Guzick DS, et al: A natural experiment on the effects of ovarian hormones on cardiovascular risk factors and stress reactivity: Bilateral salpingo oophorectomy versus hysterectomy only. Health Psychol 16:349, 1997. 127. Ting AY, Blacklock AD, Smith PG: Estrogen regulates vaginal sensory and autonomic nerve density in the rat. Biol Reprod 71:1397, 2004. 128. Zondervan KT, Yudkin PL, Vessey MP, et al: The community prevalence of chronic pelvic pain in women and associated illness behaviour. Br J Gen Pract 51:541, 2001. 129. Erickson DR, Morgan KC, Ordille S, et al: Nonbladder related symptoms in patients with interstitial cystitis. J Urol 166:557, 2001. 130. Alagiri M, Chottiner S, Ratner V, et al: Interstitial cystitis: Unexplained associations with other chronic disease and pain syndromes. Urology 49:52, 1997. 131. Clauw DJ, Schmidt M, Radulovic D, et al: The relationship between fibromyalgia and interstitial cystitis. J Psychiatr Res 31:125, 1997. 132. Aaron LA, Herrell R, Ashton S, et al: Comorbid clinical conditions in chronic fatigue: A co-twin control study. J Gen Intern Med 16:24, 2001.

133. Straub RH, Cutolo M: Involvement of the hypothalamic– pituitary–adrenal/gonadal axis and the peripheral nervous system in rheumatoid arthritis: Viewpoint based on a systemic pathogenetic role. Arthritis Rheum 44:493, 2001. 134. Buffington CAT, Teng BY, Somogyi GT: Norepinephrine content and adrenoceptor function in the bladder of cats with feline interstitial cystitis. J Urol 167:1876, 2002. 135. Cooper MS, Stewart PM: Corticosteroid insufficiency in acutely ill patients. N Engl J Med 348:727, 2003. 136. Schelling G, Kilger E, Roozendaal B, et al: Stress doses of hydrocortisone, traumatic memories, and symptoms of posttraumatic stress disorder in patients after cardiac surgery: A randomized study. Biol Psychiatry 55:627, 2004. 137. Granger DA, Shirtcliff EA, Booth A, et al: The ‘’trouble’’ with salivary testosterone. Psychoneuroendocrinology 29:1229, 2004. 138. Miller KK: Androgen deficiency in women. J Clin Endocrinol Metab 86:2395, 2001. 139. Holst JP, Soldin OP, Guo TD, et al: Steroid hormones: Relevance and measurement in the clinical laboratory. Clin Lab Med 24:105, 2004. 140. Baker ME: Co-evolution of steroidogenic and steroid-inactivating enzymes and adrenal and sex steroid receptors. Mol Cell Endocrinol 215:55, 2004. 141. Wessely S, White PD: There is only one functional somatic syndrome. Br J Psychiatry 185:95, 2004. 142. Greenspan FS, Gardner DG: Basic and Clinical Endocrinology, 6th ed. New York, McGraw-Hill, 2001, p 891. 143. Burger HG: Androgen production in women. Fertil Steril 77(Suppl 4):S3, 2002. 144. Corpechot C, Young J, Calvel M, et al: Neurosteroids: 3-Alphahydroxy-5-alpha-pregnan-20-one and its precursors in the brain, plasma, and steroidogenic glands of male and female rats. Endocrinology 133:1003, 1993. 145. Genazzani AR, Petraglia F, Bernardi F, et al: Circulating levels of allopregnanolone in humans: Gender, age, and endocrine influences. J Clin Endocrinol Metab 83:2099, 1998.

Chapter 91

FOCAL NEUROMUSCULAR THERAPIES FOR CHRONIC PELVIC PAIN SYNDROMES IN WOMEN Rodney U. Anderson Women have been suffering from chronic pelvic pain (CPP) syndromes presumably since the age of primate evolution. Except for endometriosis, there is little in the way of objective biologic findings to explain the pathophysiology of these complaints. In most instances, the diagnostic terms for disorders of pain in the pelvis relate to a specific organ with no identifiable mechanistic relationship. This chapter attempts to identify the common urologic/gynecologic disorders commonly considered CPP syndromes, explores the evidence for neuromuscular disorder, and reviews most of the local and focused therapeutic approaches that may be beneficial in the management of these conditions. I am specifically avoiding consideration of any pharmaceutical therapy. The objective is to suggest an integration of both physical and behavioral treatments to elicit relief from these life-altering conditions while we await more elucidation about the biologic mechanisms involved. BIOFEEDBACK THERAPY Biofeedback therapy for pelvic disorders has primarily been used to manage pelvic floor disorders and urinary incontinence, but

it has also become quite valuable for patients with pelvic pain disorders. Biofeedback and behavioral changes can play a role in effecting clinical improvement in urologic problems including pelvic pain (vulvar vestibulitis), irritative voiding symptoms, recurrent urinary tract infections, and urinary incontinence. Biofeedback for pelvic floor dysfunction involves the use of surface internal (vaginal and rectal) electrodes that transduce muscle potentials into visual and auditory signals; by this means, patients learn to be aware and control (increase or decrease) voluntary muscle activity. Physical exercises are then used to affect the pelvic floor muscles (Fig. 91-1). In the late 1940s, Dr. Arnold Kegel, an obstetrician/gynecologist, invented the first feedback device that was used for pelvic muscle rehabilitation to treat female urinary incontinence. The processes and procedures of biofeedback therapy have been described.1,2 A general overview for application to pain management was summarized by Tan and colleagues.3 Two major subtypes of biofeedback therapy are currently in practice. The traditional form is known as peripheral or somatic feedback, which assists in teaching patients to be more physiologically aware of abnormal muscle tension and adjust accordingly. Surface electromyography (EMG), heart rate and blood

Pubis Bulbiospongiosus m. Anterior iliac spine

Urethral orifice Vagina Ischiocavernous muscle

Ilium

Inferior layer of urogenital diaphragm (cut)

Acetabulum (hip socket) Transversus perinei superficialis

Transversus perinei profundus m.

Tuberosity of ischium

Perineal body Sphincter ani externus m.

Obturator fascia

Anus

Sacrotuberous ligament

Levator ani m., iliac part (iliococcygeus m.)

Levator ani m., pubic part (pubococcygeus m.)

Anococcygeal body (ligament) Coccygeus m. (ischiococcygeus m.

Coccygeal fascia

Figure 91-1 Pelvic floor muscles as seen from below in the supine female subject. (Redrawn from Travell JG, Simons DG: Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol 2, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 1998.)

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pressure, skin temperature, and galvanic skin responses are used. Applications of peripheral biofeedback include neuromuscular re-education (for patients after stroke), musculoskeletal therapy, urinary4 and fecal incontinence, and pelvic pain including CPP syndromes in men,5,6 vulvodynia,7 and dysmenorrhea.8,9 A second subtype of biofeedback therapy uses electroencephalography (EEG) and is classified as central biofeedback, neurofeedback, or neurotherapy. With the exception of migraine, most of the research with this therapy has been in areas other than pain, such as treatment of alcohol or additive disorders. Glazer and coworkers reported their experience in two separate open-ended, uncontrolled studies using EMG biofeedback of the pelvic floor musculature to treat patients with vulvar vestibulitis syndrome, a subset of vulvodynia.7,10 The rationale for study was based on the knowledge that patients with vulvar vestibulitis usually have hyperirritability of the pelvic floor muscles.7,11 The hypothesis has been put forward that destabilization of pelvic floor muscles is a factor in perpetuating the vulvar skin disturbances and accompanying pain. Travell and Simons reported that muscle disturbances are reflected in discord of EMG recordings.12 In the studies by Glazer and associates, patient diagnosis was confirmed by physical examination, and the initial pelvic floor EMG assessments were performed with a surface EMG single-user vaginal sensor; monthly evaluations followed during clinic visits.7,10 A portable EMG biofeedback device and instructions for pelvic floor rehabilitation exercises were provided to each patient for twice-daily in-home practice. Patient demographics were similar in both studies; average duration of symptoms was 3.5 years (range, 2 to 6 years), and most had abstained from sexual intercourse for an average of 1 year. In the first Glazer study of 33 women, symptoms ranged from only introital dyspareunia to chronic, intense pain provocation.7 After 16 weeks of practice, pelvic floor contraction increased by 95%, resting tension levels decreased by 68%, and muscle instability at rest decreased by 62%. Based on subjective reporting at each evaluation, maximum pain decreased from the previous evaluation to a average of 83%. Many patients (22 [79%] of 28) resumed intercourse. Half of the women remained pain free at follow-up 6 months later. In the second study, 29 women with level 2 and 3 vulvar vestibulitis were enrolled.10 Level 2 includes women who have pain with intercourse that requires interruption or discontinuance of coitus, and level 3 includes those who have pain with intercourse that prevents any attempt at insertion or coitus.13 With biofeedback therapy, increased muscle stabilization was associated with decreased pain; as pain decreased, patients were more likely to resume intercourse. After therapy, 85% (24 of 29) had negligible or mild pain, and 69% resumed sexual activity. Neuromuscular education of the pelvic floor muscles to ameliorate chronic pain has been supported by the studies in men with CPP syndromes. In a preliminary study of 19 patients using biweekly sessions of biofeedback and home exercises, significant decreases (approximately 50%) in pain and urgency scores were reported by Clemens and colleagues.5 However, only about half of the patients completed the full course of therapy. In the study by Cornel and colleagues, biofeedback rehabilitation of 25 men with type III CPP involved verbal guidance and feedback through palpation of pelvic floor muscles and EMG measurements to teach correct muscle contraction and relaxation.6 Significant improvements in the National Institutes of Health–Chronic Prostatitis Symptom Index (NIH-CPSI) total scores, with pain and micturition domains decreasing an average of 50%, were

associated with a significant 35% decrease in pelvic muscle tonus after treatment. MYOFASCIAL TRIGGER POINT RELEASE THERAPY Definition and Basic Science Investigation A long list of disorders in women has been shown to involve the musculoskeletal system; these include the levator ani syndrome, vulvodynia, vulvar vestibulitis syndrome, dyspareunia, vaginismus, coccygodynia, interstitial cystitis (IC) or painful bladder syndrome, pelvic floor tension myalgia, urge-frequency syndrome, urethral syndrome, inflammatory bowel disease, proctodynia, proctalgia fugax, and pudendal nerve entrapment,7,14-18 and, in men, nonbacterial prostatitis and CPP syndromes.19,20 Often overlooked and misunderstood as a musculoskeletal source of pelvic pain are myofascial trigger points (MTrPs). More than 50 years ago, Dr. Janet Travell introduced the phenomenon of referred pain and referred motor activity attributed to trigger points (TrPs) in skeletal muscles, which were later shown to be a causative factor in myofascial pain and dysfunction. Our understanding of MTrPs and their relation to myofascial pain syndromes continues to evolve, as shown in Table 91-1.

Table 91-1 Progress of Discovery and Understanding of Chronic Pain Syndromes and Myofascial Trigger Points ■

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1838 Recaimer—First describes syndrome of tension myalgia of pelvic floor in “Stretching massage and rhythmic percussion in the treatment of muscular contractions” 1937 Thiele—Describes tonic spasms of levator ani, coccygeus, and pyriformis muscles and their relationship to pain 1942 Travell et al—First describes myofascial trigger points as common cause of chronic muscle pain 1951 Dittrich—First recognizes pelvic pain occurring as a result of referral from trigger points in subfascial fat and perifascial tissue 1963 Thiele—Successful uses digital massage of spastic levator muscles subsequently described as “Thiele massage” 1977 Sinaki et al—Consolidates various syndromes of pelvic musculature under one terminology: tension myalgia of the pelvic floor; uses combined treatment with rectal diathermy, Thiele’s massage, and relaxation exercises 1983 Travell and Simons Publishes the first edition of Myofascial Pain and Dysfunction: The Trigger Point Manual; identifies external and internal muscles and areas of referred pain from myofascial trigger points 1984 Slocum—Treats trigger points related to the abdominal pelvic pain syndrome in women using locally injected anesthetic; indicates that emotional stress is frequently a potentiating factor, not a cause for chronic pelvic pain 1994 Hong—Develops rabbit animal model to identify myofascial trigger points; with colleagues, subsequently publishes 36 animal clinical and 12 basic science articles to advance understanding of myofascial trigger point 2004 Simons—Reviews the present understanding of myofascial trigger points as they relate to musculoskeletal dysfunction

Chapter 91 FOCAL NEUROMUSCULAR THERAPIES FOR CHRONIC PELVIC PAIN SYNDROMES IN WOMEN

An MTrP is defined as a highly localized and hyperirritable spot in a palpable taut band or tender nodule of skeletal muscle fibers.16,21 MTrPs can be located in one or more muscles, and common clinical characteristics exist.22-26 Muscles can become “knotted” and inelastic and unable to contract or relax. Stimulated by digital palpation or needling, active MTrPs characteristically elicit local pain or a referred pain similar to that of the patient’s complaint of pain or aggravation of existing pain. A local twitch response is also a confirmatory sign of an MTrP. Latent MTrPs are clinically asymptomatic and do not cause pain with compression. Both active and latent MTrPs are associated with muscle weakness on active contraction and reduced range of motion, and MTrPs can be perpetuated or aggravated by mechanical stress, metabolic, endocrine, and nutritional inadequacies, as well as psychological factors.21 Depression and chronic pain are often closely associated, and it should be appreciated that depression and anxiety are frequently consequent to unresolved symptoms. Recent reviews present the current understanding of MTrPs and an historical summary of the development of these concepts.27,28 An integrated hypothesis of the etiology of TrPs implicating local myofascial tissue, the central nervous system, and mechanical factors is proposed in the 1999 edition of Travell and Simons’ Myofascial Pain and Dysfunction: The Trigger Point Manual.29 The hypothesis postulates that a central MTrP has multiple fibers with end plates releasing excessive acetylcholine and shows histopathologic evidence of regional sarcomere shortening. The positive-feedback loop of events perpetuates these changes until the loop is interrupted. The putative steps were elegantly explained by Simons.28 Evidence contributing to the etiology of TrPs has evolved from two early studies. Mense and Simons reported that histologic examination of biopsied muscle tissue in the vicinity of TrPs reveals large, rounded, and darkly stained muscle fibers, as well as increased muscle fiber diameters.30 At physical examination for MTrPs, these changes are manifested as taut bands and palpable nodules. An EMG study by Hubbard and Berkoff showed greater activity in MTrPs than in adjacent nontender muscle.31 EMG activity was significantly higher in TrPs of patients with chronic tension headaches than in normal patients and could be reduced by injection of sympathetic blockers such as phenoxybenzamine. In another study, McNutley and colleagues reported that EMG activity within an MTrP was significantly increased in subjects involved in an experimental stress test, whereas contiguous nontender muscle showed no changes.32 This finding may have implications for the psychophysiology of stress contributing to pain and the association with MTrPs. Physical Examination and Mapping of Trigger Points A distinguishing feature of MTrPs is their location within a taut band of muscle or fascia as identified by palpation. They can be discovered with a careful external and internal pelvic examination. Compression of the MTrP results in a twitch response, a transient contraction from the band of fibers, and referred sensory and motor responses (e.g., tenderness, pain) occurring distant to the TrP. Two objective methods have been used to document MTrPs. Algometry provides a quantitative measurement of pressure thresholds to document the sensitivity of TrPs. Results from several studies have confirmed that MTrPs are more sensitive than contralateral muscle areas without TrPs or surrounding healthy tissue.33,34 A difference in pressure threshold

exceeding 20 newtons per square centimeter (2 kg/cm2) between a TrP and a contralateral point is considered abnormal.33 A second method, thermography, employs a noninvasive imaging technique to detect infrared radiation from body surfaces and heat distribution.35 Comparative imaging of subjects with clinical TrPs and asymptomatic controls revealed discrete thermal responses in muscles with suspected TrPs. Sensory referral areas for TrPs in symptomatic subjects showed significantly reduced temperatures from precompression levels during ischemic compression; no significant temperature changes were noted in asymptomatic areas after compression. It was assumed that the colder area was caused by a reduction in blood flow due to a sympathetic autonomic change associated with the myofascial pain syndrome. A review of the neuroanatomy of the pelvis, such as that as provided by Wesselmann and colleagues, assists in understanding the pathophysiology of urogenital and rectal pain syndromes and their management.36 The involvement of MTrPs in CPP can thereby be taken in perspective. Travell and Simons published the first manuals on TrPs and myofascial pain and dysfunction and provided specific details of the pelvic muscles to check internally.16,22 A subsequent edition of this manual was published in 1998.12 All of the muscles of the pelvis, both internal and external, must be thoroughly evaluated and subsequently treated. Muscles known to contain TrPs referring pain to an area that the patient is complaining about should be examined with extra care. Testing for MTrPs within the pelvis depends on the palpation skills of an experienced examiner, because no diagnostic standard has been established to identify intrapelvic MTrPs. The therapist must be trained in identifying TrPs and be able to feel for superficial and deep TrPs located in the belly and the attachments of the muscles. For the purpose of locating these MTrPs, the pelvic muscles can be grouped into three categories—perineal muscles, pelvic floor muscles, and pelvic wall muscles. Examination of intrapelvic muscles for MTrPs requires a vaginal or rectal approach, as appropriate for each muscle by establishing bony and ligamentous landmarks, and relating the direction of palpation to the direction of the muscle fibers. This was explained in detail by Travell and Simons, as was the relationship between symptoms and the location of associated MTrPs.12 Other MTrP associations have been gleaned from the experience of many physical therapists. Table 91-2 summarizes the internal pelvic muscles and external muscles referring pain to pelvis from MTrPs. Approaches for Inactivating Myofascial Trigger Points A variety of manual massage techniques have been reported to inactivate MTrPs.29 Manual therapy may involve active and passive rhythmic muscle releases based on the principle that tight or poorly relaxed muscles can exhibit released tension after moderate voluntary contraction. The active and passive release maneuvers take up the slack in the muscle by stretching it to the point of beginning resistance or discomfort. This is then followed by a patient-performed isometric contraction that is held in position by the patient or therapist. Direct transrectal massage was reported by Thiele for patients with coccygodynia with pain localized to the coccyx and the presence of spasms of the levator ani and coccygeus muscles.14 A modified Thiele massage was used by Oyama and colleagues in 21 women to treat IC and high-tone dysfunction of the pelvic

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Table 91-2 Internal and External Muscles and Referred Pain to Pelvis from Myofascial Trigger Points Muscle

Referred Pain Site

Symptom

Pelvic floor muscles Levator ani

Sacrococcygeal region, perineal region

Pain in perineum, vagina, anal sphincter; pain with sitting; aggravated by lying on back and by defecation Pain in vagina, dyspareunia, perineal ache

Bulbospongiosus Ischiocavernosus Transverse perinei Coccygeus

Perineal region and adjacent urogenital structures

Sphincter ani Obturator internus

Poorly localized aching in anal region Perineal region, outward toward hip, whole pelvic floor, posterior thigh, and hamstrings

Sacrococcygeal region

Muscles referring pain into pelvis Piriformis Sacroiliac joint, hip girdle, hamstrings, pelvic floor, buttock, low back Gluteus Iliopsoas Quadratus lumborum Abdominals Transverse Rectus Pectineus Pyramidalis Thoracolumbar Paraspinals

Hip girdle, buttock, sacrum, hamstrings Groin, anterior thigh, low back Sacroiliac joint and buttock, lower abdomen, groin Entire abdomen up into ribs Groin, inguinal ligament, detrusor, and urinary sphincter Across thoracolumbar back, xiphoid process, sacroiliac joints, and low back Groin area, bladder, and pubis Abdomen

Pain in coccyx, hip, or back; ischiococcygeus is likely cause of backache in late pregnancy and early labor Anal pain, painful bowel movement Pain in vagina, vulva, urethra, coccyx, posterior thigh; pain and feeling of fullness in rectum

Pain in rectum during defecation, dyspareunia; pain in referred areas worsens with palpation, standing, sitting, walking Pain in low back, hip, inguinal area Pain in groin, down anterior thigh, and in low back Pain in low back and with coughing, sneezing, and walking Groin pain, bladder pain, urinary frequency or retention Somatovisceral response, nausea, vomiting, diarrhea, intestinal colic, dysmenorrhea Pain in groin, bladder, urethra, and pubic area Visceral pain, sacral pain, pain in middle and lower back; pain can resemble renal colic

Data from references 12, 37, 38, and 39.

floor (e.g., dyspareunia, impaired bladder and bowl evacuation, pelvic pain exacerbated by physical activity or prolonged sitting).40 Subjects underwent 5 weeks of twice-weekly Thiele intravaginal massage, with massages of the affected hypertonic pelvic muscles, 10 to 15 times per session, from origin to insertion along the direction of muscle fibers. Additional short ischemic compression of tender points was applied as needed. IC symptom scores and pelvic floor muscle tone showed significant improvements, and pelvic tone remained improved at 4.5 months of followup in three of the four treated pelvic muscles, excepting the coccygeus. Weiss reported amelioration of symptoms in 42 patients with urgency-frequency syndrome with or without urethral pain (and in some patients with IC) using manual therapy of discrete MTrPs in the pelvic floor.18 Treatment continued one to two times weekly for 8 to 12 weeks until MTrPs and muscle tension decreased. A program of home therapy involving muscle stretches and strengthening, biofeedback, and Kegel exercises was also part of the treatment. In the 42 patients (39 women, 3 men) with urgency-frequency syndrome, 83% had moderate to marked improvements or complete resolution. Of the 10 patients with IC (6 women, 4 men), 70% had moderate to marked improvements. Injection with local anesthetics, saline, or water has been used for inactivation of MTrPs. An important sign of precise needle

placement in an MTrP is elicitation of a local twitch response. The resulting MTrP inactivation should result in immediate relief of pain and tightness.24 Specific targeted therapy with local anesthetic injections of TrPs in the abdominal wall has been used for treatment of CPP in women.41,42 Slocumb reported that approximately 50% of 122 women with pelvic pain had relief after treatment that consisted of TrP blocks in all patients; additional surgeries were performed in 13 women.41 Most patients (89%) had abdominal wall TrPs; pain was relieved in 89% after anesthetic injection. Patients with only vaginal TrPs had a response rate of 85% after injections. TrP identification with needling and therapy of active MTrPs with 0.5% procaine injections was reported to provide symptomatic relief in four female patients with pelvic pain, IC, and irritative voiding symptoms.37 Associated Stress and Psychological Factors CPP in women is a perplexing problem. Frequently, a physical cause of pain cannot be established, and, consequently, it is difficult to treat successfully. In the absence of a discrete physical cause, a psychopathologic causation has been considered. Many reports have associated CPP with personality and mood disturbances, childhood events including sexual abuse, and difficulties in sexual relationships; evidence, however, is inconclusive.43 Among the causes of CPP is tension myalgia of the pelvic

Chapter 91 FOCAL NEUROMUSCULAR THERAPIES FOR CHRONIC PELVIC PAIN SYNDROMES IN WOMEN

floor. Recent evidence indicates that TrPs associated with myofascial problems are not the cause of CPP but a sign of somatization of neurotic or psychosomatic problems in the pelvis.44-47 For example, Miller used stress management alone to effect symptom improvements in men with chronic prostatitis.48 Eighty-six percent (110 of 218) of the patients reported that they were better, much better, or cured. Miller focused on the person and not the prostate, reinforcing the relationship between managing stress in the patients’ lives and their symptoms. One hypothesis for CPP is that acute and chronic stress induces neuroendocrine disturbances and consequent neuroinflammatory stimulus-activating receptors and cytokines via neuropeptide release that give rise to CPP symptomatology. Stress triggers a cascade of pathophysiologic events that involve activation of two pathways: the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system. Chronic activation of the physiologic stress response induces putative glucocorticoid resistance and altered immunity, release of proinflammatory cytokines and prostaglandins that may contribute to pelvic tension myalgia, and, ultimately, cycling psychological distress. No systematic evaluation of the physiologic role of acute and chronic stress in pathogenesis of CPP in women has been undertaken. Over the years, clinicians have anecdotally observed that stress exacerbates symptoms, as has been shown for prostatitis,48 and chronic stress was shown to induce inflammatory histologic changes in the prostate of a rat model.49 Certain inherent personality traits (genetic and developmental factors) modulate reactivity to stress. Researchers at my institution have strong preliminary evidence from our male patients with CPP syndrome indicating that physiotherapeutic myofascial release and cognitive behavioral therapy, proven methods to relieve stress, can provide both curative and partial relief of pain in some patients with CPP syndrome.50,51 Physical and Mental Exercises Complementary to Management of Chronic Pelvic Pain Emerging evidence suggests the influence of psychosocial factors on physiologic function and health outcomes. Mind-body therapeutic interventions, including yoga (a body-based therapy), cognitive behavioral therapy, relaxation therapy, meditation, and imagery, have shown efficacy in several common conditions. A recent systematic analysis showed that mind-body therapy can serve as an effective adjunct to conventional medical therapies for chronic low back pain, headaches, incontinence, and cardiac rehabilitation.52 Hatha yoga has been proposed as a complimentary therapy for chronic urologic conditions involving pelvic floor dysfunction, to provide improved pain control and stress reduction. Specific yoga postures can contribute to the strengthening and relaxation of muscles that are associated with urologic symptoms resulting from hypotonicity (stress urinary incontinence) and hypertonicity (vulvodynia, IC) of pelvic floor muscles.53 In 1929, Edmund Jacobson published his method of “progressive relaxation,” which has been used in various forms in Western medicine ever since.54 He provided instructions to contract and relax muscles at the beginning of relaxation and, with Bell Telephone Laboratories, codeveloped the electromyograph to objectively verify the physiologic effects of tension and relaxation. He introduced the concept that relaxation of the gastrointestinal tract and arousal of the autonomic system, thought to be out of one’s control, could be voluntarily reduced. A modification of

progressive relaxation, the practice of “paradoxical relaxation” according to David Wise,39 has been used successfully in conjunction with MTrP release therapy to produce symptomatic relief in men with CPP syndrome.51 Operant behavioral and cognitive-behavioral approaches to chronic pain were introduced in the 1960s and 1980s, respectively, and often serve as a component of multidisciplinary treatment dealing with anatomic and physiologic factors.55 Aspects of these treatments include relaxation training, cognitive restructuring, interventions to change perception and emotional responses to pain, habit reversal, and maintenance and relapse prevention. These approaches are complementary for management of the psychosocial influences on a patient’s response to pain. Because pain is not entirely a response to nociception, therapies such as these attempt to influence the behavior of a patient in chronic pain. Clinical Experience with Combined Myofascial Trigger Point Release Therapy and Paradoxical Relaxation Therapy A recent study at Stanford University has integrated physiotherapy with myofascial trigger point release therapy (MFRT) to relieve pelvic floor myalgia and paradoxical relaxation therapy to achieve autonomic and pelvic floor self regulation.51 This study, although conducted in men with refractory CPP syndrome is nevertheless germane to both genders; it used multimodal therapy based on the potential etiology of pelvic pain as a manifestation of a neurobehavioral disorder.7,19,20,56 A team approach to therapy included a urologist, a physical therapist experienced in pelvic pain treatment, and a psychologist. The physiotherapist applied treatment to the patient in the lateral position. Individual muscle groups were palpated, and myofascial TrPs were identified. Positive myofascial TrPs induced pain on palpation that tends to reproduce symptoms at the site or referred to a nearby anatomic location. Pressure was held to each TrP for about 60 seconds to release.39 Additional physiotherapy techniques also used in conjunction with MFRT sessions included voluntary contraction and release, hold and relax, contract and relax, and reciprocal inhibition as well as deep tissue mobilization including stripping, strumming, skin rolling, and effleurage. MFRT physiotherapy was given weekly for 4 weeks, then biweekly for 8 weeks. Paradoxical relaxation therapy conducted by the psychologist coincided with physiotherapy. Patients received 1 hour of individual verbal instructions and a supervised practice session weekly for 8 weeks in progressive relaxation exercises. Training included the respiratory sinus arrhythmia breathing technique to quiet anxiety and relaxation training to have the patient focus attention on the effortless acceptance of tension in specific areas of the body. The therapy is called “paradoxical” because patients are directed to accepting their pelvic tension as a way of relaxing/releasing it.39 Daily home practice relaxation sessions of 1 hour were recommended for a minimum of 6 months using a series of audiotaped lessons. Symptoms were assessed with a Pelvic Pain Symptom Survey and the National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI). Patient-reported perceptions of overall effects of therapy were documented on a Global Response Assessment (GRA) questionnaire. A total of 138 men with refractory chronic pain or CPP syndrome (CP/CPPS) and median disease duration of 31 months

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were treated; their average age 40.5 years. Symptoms were rated as markedly improved or moderately improved by 72% of patients on the GRA questionnaire at the conclusion of therapy. This was associated with commensurate clinically significant decreases in NIH-CPSI total scores of 10.5 (46%) and 6.5 (24%), respectively. The number of treatments was variable; some patients had rapid responses occurring as early as after 1 week of treatment and either further improved or remained the same. After a median of five MFRT treatments, clinical improvements (≥25% decrease in symptom scores) were first observed. A few patients had intermittent therapy, based on need, throughout recurring episodes of pelvic pain. The combined MFRT and paradoxical relaxation therapy provided an effective approach for these chronic pain patients, resulting in pain and urinary symptom relief at least comparable to or better than that achieved with traditional pharmacologic therapy. The aspects of this treatment approach are amenable to the various expressions of pelvic pain in women. Each patient is unique in her objective and subjective clinical presentation. Thus, release of specific MTrPs that tend to recreate a patient’s symptoms and behavior modification to relax the pelvic muscles and modify the habit of focusing tension in the pelvis under stress could help to ameliorate pain. The patient can also become an active participant, partnering with her therapists in the healing process. ELECTRICAL STIMULATION FOR NEUROMODULATION Electrical stimulation has been entertained as a modality for treating pain since the distant past, when a man stepped on an eel at the beach and experienced an electrical shock that relieved his gout pain. Multiple attempts to introduce electrical energy have arisen, from Chinese acupuncture, through surface application using transcutaneous electrical nerve stimulation (TENS), to implantation of electrodes for continuous electrical stimulation of peripheral and spinal nerve roots and electrodes applied on the surface of the spinal cord itself. The gate control theory of controlling pain assumes that afferent nerve fibers may be influenced by continuous high-frequency electrical stimulation and thereby modulate the transmission of pain impulses. TENS has been used most successfully and was introduced for bladder urgency and urinary frequency as well as stress urinary incontinence. One disadvantage of this method may be the lack of specificity of the nerve branch or bundle of the afflicted nerve. Direct stimulation of the S3 nerve as it exits the sacrum has recently received approval from the U.S. Food and Drug Administration for management of frequency, urgency, and urge urinary incontinence refractory to medical therapy. Because pelvic pain, particularly that arising from IC, may represent a neuroinflammatory pathogenic condition, electrical modulation promises to exert favorable outcomes in pain management. The application of intravaginal electrical stimulation to treatment of CPP in women with levator ani syndrome was evaluated in a retrospective study of 66 patients.57 After digital vaginal palpation of the levator ani muscles for tenderness, a probe was placed in the patient’s vagina and pulsed electrical stimulation was given to muscles at variable settings (up to 50 mA for up to 20 minutes per session) for one to seven sessions. Pain symptoms were reported as improved in 34 (52%) of 66 patients; benefit

was sustained for more than 6 months after the last treatment. Electrical stimulation for management of vulvar vestibulitis including dyspareunia and vaginismus has been shown to be effective.58 A group of 29 women participated in a 10-week therapy program of stimulation (20 minutes once weekly) at the vestibular area and vagina introitus. Contractile ability and resting ability of the pelvic floor muscles significantly improved; pain was significantly reduced, and half of the women with vaginismus resumed coital activity. The therapeutic effects of high-frequency electrostimulation were also assessed in men with noninflammatory CPP syndromes using a urethroanal stimulation device.59 This approach was based on the supposition that chronic prostate pain may represent a chronic visceral pain,36 and the authors’ speculation that electrical stimulation might block afferent nerves supplying the pelvic floor and pelvic organs, thereby providing pain relief. This premise was supported by another study showing that sacral nerve stimulation can provide a dramatic and durable improvement in pain symptoms and urgency-frequency.60 The neuronal mechanisms associated with bladder inhibition during intravaginal electrical stimulation have been documented experimentally in the cat.61 Sacral neuromodulation is an approved treatment for management of refractory detrusor instability and nonobstructive voiding dysfunction; it has also been shown to be effective for amelioration of pelvic pain.62-64 An early study with TENS indicated the possibility for treatment of the chronic painful bladder syndrome, IC.65 Favorable responses to a percutaneous trial stimulation of the S3 sacral roots for as few as 5 days or up to 10 days have been shown for IC patients.66,67 Significant improvements occurred in urinary dysfunction, pelvic pain, and quality of life parameters. The test neuromodulation normalized urinary levels of heparin-binding epidermal growth factor and antiproliferative factor activity—factors known to be altered in patients with IC.66 The temporary nature of the percutaneous stimulation evaluation permits assessment of the potential efficacy and desirability of permanent sacral neurostimulation. Neuromodulation is the physiologic process by which the activity in a neural pathway alters preexisting activity in another pathway. It is theorized that sacral neurostimulation causes afferent inhibition of sensory processing in the spinal cord. The S2-S4 nerve roots provide the primary anatomic and somatic innervations to the pelvic floor, bladder, and urethra. Comiter indicated that the mechanism associated with the effectiveness of sacral nerve stimulation for IC involves both afferent (pelvic pain and sensory urgency) and efferent (motor frequency and urgency) modulation.68 Comiter evaluated the efficacy of sacral nerve stimulation for treatment of refractory IC in 25 patients.68 After a trial of nerve stimulation, 17 patients demonstrating at least 50% improvement in pain and urinary dysfunction qualified for permanent nerve stimulator implantation. Improvements were sustained in 16 of 17 patients for an average of 14 months’ follow-up after permanent implantation. In a retrospective study, the efficacy of long-term sacral neuromodulation was evaluated in 21 patients with refractory IC by Peters and Konstandt.69 Eighteen patients had used chronic narcotics for pain. After an average follow-up of 15 months after surgery for implantation of a permanent nerve stimulator, 20 patients reported marked improvements in pain, with a significant decrease (36%) in narcotic requirements; all narcotics were stopped in 4 of 18 patients.

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Siegel and colleagues used sacral nerve stimulation to treat intractable pelvic pain in 10 patients (9 women, 1 man) without a primary complaint of voiding dysfunction.70 After successful percutaneous trial nerve stimulation, a neuroprosthetic sacral nerve stimulator device was surgically implanted, with leads placed in the S3 or S4 foramen. Follow-up was after a median of 19 months. Nine of 10 patients had decreased severity and frequency of pelvic pain; 6 had significant improvements in pain symptoms. No serious device complications were reported. Spinal cord stimulation (SCS) has been used since 1967 for the treatment of chronic lower back or lower extremity pain of diverse causes that is refractory to numerous conventional therapies. The work of Shealy and colleagues led to the development of this pain therapy, which was then used exclusively for failed back syndrome.71 As the clinical applications of SCS expanded in the following years, the outcomes were poor due to a lack of understanding of the appropriate clinical indications, SCS equipment technical failures, and the need for a trial stimulation period to identify patients who might achieve a long-term benefit. Based on increased knowledge, SCS outcomes throughout the last 2 decades were found to provide reasonable (>45% to 60%) longterm pain relief.72-75 There is a better understanding of the psychological factors that are predictive of SCS outcomes.74 Avoidance of implants in patients with severe untreated depression, untreated drug abuse, or borderline personality disorder has led to improved outcomes.76 A recent review presents the current and future trends of SCS.77 Technologic advances, which have widened the scope of applications for SCS, include multichannel leads, dual-lead configurations, multichannel devices, totally implantable generators, and new procedures for programming stimulators. The primary indication for treatment with SCS is neuropathic pain that has failed to be relieved by other conservative approaches. With the discovery of the dual-lead technology, the clinical applications have expanded. Acceptable relief was attained in 70% of patients with chronic axial low back and extremity pain.78 Several patients with intractable pain of the pelvis and rectum have been treated with the dual leads.79 SCS is a relatively simple and reversible treatment using greatly improved and clinically reliable equipment. It may serve as an option for patients with moderate to severe pain of the trunk or extremities when other pain relief methods have failed or are unacceptable. Studies of SCS for amelioration of CPP warrant further investigation. BOTULINUM A TOXIN Botulinum A toxin (BTX-A) is a neurotoxin derived from Clostridium botulinum that binds irreversibly to cholinergic, presynaptic membranes of the neuromuscular junction. When a minute amount is injected into a muscle, it prevents release of acetylcholine, thereby blocking neurotransmission and temporarily paralyzing affected muscles. It can provide symptomatic relief for up to 3 months. In the United States, BTX-A is approved for treatment of blepharospasm, strabismus, hemifascial spasm, and cervical dystonia in adults. In Europe, labeled indications are for cervical dysplasia and cerebral palsy. BTX-A has received much notoriety for its cosmetic use for facial wrinkles and in pain therapy to treat myofascial pain, low back pain, and headaches including migraine. BTX-A has been used clinically for more than 2 decades: there is continued accumulation of evidence for its application for a

variety of urologic conditions.80 Experience with BTX-A in neurourology began in the early 1990s with treatment of neurogenic-sphincter dyssynergia after spinal cord injury, neurogenic and non-neurogenic detrusor hyperactivity, and other dysfunctional voiding disorders.81 BTX-A injections have been used to treat voiding symptoms related to CPP syndromes in men.82 It has been hypothesized that interruption of the junction of somatic nerves with striated muscles may affect the central pain cycle. Zermann and coworkers used transurethral perisphinchteric injections of BTX-A in 11 patients with chronic prostatic pain.83 Injections resulted in pelvic floor muscle weakening and relief of pelvic pain and urethral hypersensitivity. A pilot study explored the use of BTX-A in the treatment of CPP associated with spasm of the levator ani muscles.84 The 12 women had a minimum 2-year history of pelvic pain and pelvic floor hypertonicity. BTX-A at one of three dilutions (10, 20, or 100 IU/mL) in groups of four patients was injected bilaterally into the puborectalis and pubococcygeus muscles under conscious sedation. Visual analogue pain scale scores were significantly improved for dyspareunia and dysmenorrhea at the 12-week follow-up. Pelvic floor muscle manometry had a 37% maximal reduction at week 4 and a statistically significant 25% reduction at week 12. Marked improvement in sexual activity was associated with significant reductions in discomfort and improved habit. No differences in response were noted with different dilutions of BTX-A; no medically adverse reactions occurred. A multicenter case series of 13 patients with recalcitrant IC was described using intravesical BTX-A.85 This study was based on evidence from a rat somatic pain model suggesting that BTXA may have an antinociceptive effect on both acute and chronic pain.86 Patients were injected submucosally with 10 RA to 20 RA IU/mL of BTX-A through a cystoscope into 20 to 30 sites to target dense sensory innervations in the trigone and bladder floor. Pain, daytime frequency, and nocturia measured by visual analogue scale scores decreased significantly (P < .01) by 79%, 44%, and 45%, respectively. First desire to void and maximal cystometric capacity also increased by more than 50% (P < .01). These observations, although preliminary, suggest the potential application of BTX-A for symptomatic and functional improvements in IC. BTX-A for treatment of urologic conditions has had a good safety profile with relatively few significant side effects. Leippold and colleagues have expressed their perspective on BTX-A as follows: “One cannot deny human ingenuity in transforming the lethal poison into a modern day therapeutic medicine.”87 Possible systemic side effects of BTX-A injection, although unusual, include nausea, vomiting, dysphagia, dry mouth, diplopia, and blurred vision, which may be due to unintentional distribution of the toxin. The incidence of systemic side effects treated in a variety of urologic conditions was reviewed by Maan and colleagues.80 A limited number of papers have reported on localized side effects associated with toxin diffusion and possible overdosing of the targeted tissue, including temporary stress incontinence in female patients treated for chronic retention, or urinary retention, or severe generalized muscle weakness (as reviewed by Leippold and colleagues87). Contraindications for BTX-A injections are pregnancy, breastfeeding, myasthenia gravis, muscular dystrophy, use of aminoglycosides or any drugs that interfere with neuromuscular transmission, and hemophilia or hereditary clotting factor deficiencies. Further research on BTX-A for treatment of CPP is warranted. Additional, larger studies are needed to explore the biologic and

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clinical effects of BTX-A including a placebo-control arm. Because the effects of the drug are temporary and most patients require repeat treatments, evaluation of the safety, benefits, and cost of repeated injections of the toxin are needed. In some cases, BTX-A given at high doses (>100 IU) for neurologic conditions has been shown to induce the development of antibodies (occurring in 250 mL). These patients seem to be more likely to have a large capacity under anesthesia and are therefore less likely to benefit from the procedure. In addition, it is probable that these patients might be adequately assessed by office cystoscopy when an evaluation is required for hematuria or some other reason. Patients with very small capacities on void diary (400 mL; 5/6 failures had cystectomy and diversion 14/17 (82%) success if 400 mL; recommend epidural to localize pain & psychological evaluation

Only patients without disease on trigone biopsy offered procedure

All had 3 mo Anesthetic capacity 150-550 mL, 16/19 right colon, some not detubularized, 4 with reflux 7/10 voided, 3 self-catheterized; all nonulcer patients successfully treated with Kock pouch and resection of trigone —

Comments

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continent form of diversion than with a conduit. As with supratrigonal cystectomy and augmentation, this form of reconstruction must be strictly limited to patients who are willing to perform self-intermittent catheterization. I have performed six neobladder operations in women with IC and contracted bladders. Five of the six are continent and pain free but have to self-catheterize three to six times per day due to incomplete voiding. The other patient developed persistent pain and stress incontinence very early in the postoperative period. 4. Continent diversion with or without cystectomy: Continent urinary diversion is the most complex reconstructive procedure and has the highest complication rate. The catheterizable stoma requires revision due to problems with catheterization or incontinence in approximately 20% to 30% of patients. The procedure is primarily indicated for the patient who seeks a more normal body image, without an external appliance, but is not able to perform selfcatheterization (due to urethral pain). The same issue as to whether a cystectomy should be performed applies as with a conduit diversion. In summary, radical surgical procedures offer tremendous relief to a small subset of IC patients with severe, refractory disease. These patients must be carefully screened in order to select those with the highest likelihood of benefit. There is no clear “best” reconstructive procedure, so the decision must be made based on individual patient preferences and the judgment of the surgeon. Pain Management Not all patients with IC complain of pain. Some describe an uncomfortable “pressure” in the bladder that generates urinary frequency while denying any “pain.” Nonetheless, most IC patients suffer from some degree of pain, and for many the pain is debilitating. Given that IC is not a curable disease at the current time, pain control becomes a legitimate and important goal in and of itself. Nevertheless, pain management tends to be poorly handled in IC (as in many chronic diseases) for a variety of reasons, some legitimate and some not. The impediments to proper pain control and strategies for improving pain management in IC/PBS are discussed in this section. Physicians are often reluctant to prescribe pain medication to IC patients. In contrast, most physicians feel comfortable prescribing pain medication to their postsurgical patients. This simple dichotomy highlights some of the important issues about pain in IC. Surgeons are trained in the management of acute pain. They understand the disease process, the expected course, and the range of responses that might be expected with various medications. Still, postoperative pain is often undertreated due to individual variation. Surgeons are much less comfortable treating chronic pain. Even when the disease process is understood, there is a reluctance to use adequate doses of chronic analgesics; this is in large part due to a lack of training and relatively limited exposure to this type of patient. The IC patient faces an even greater hurdle, the hurdle of “invisible disease.” In our current state of knowledge, IC is a diagnosis of exclusion, raising the specter of the patient as a malingerer and/or drug seeker. This is relevant because urologists have long been the target of such behavior, in the guise of the recurrent stone patient. Suspicion of motive, uncertainty of diagnosis, and a feeling of inadequacy can

interfere with the physician’s role. Finally, although lip service is paid to the importance of adequate pain control, physicians continue to see colleagues cited for improper prescription of controlled substances. Lawsuits have been filed for inadequate pain treatment but also for contributing to addiction. Many states place significant additional burdens on providers of common therapeutic narcotics. At the same time, we must acknowledge that treatment of acute pain in IC is quite difficult. Narcotics and nonsteroidal medications are often ineffective. It is therefore incumbent on the patient to try and address the issue of pain control proactively. In many instances, the “best” arrangement is for the patient to be referred to a pain specialist, typically an anesthesiologist or oncologist skilled in the evaluation and management of chronic pain. In this setting, the urologist continues to work with the patient with standard bladder treatments while the pain specialist uses alternative approaches. In the best of cases, this involves multimodality therapy, including narcotic and non-narcotic analgesics, physical therapy, and psychological counseling, nerve blocks, and so on. Some of the principles used in working with chronic pain are as follows. 1. Long-acting narcotics are preferable to short-acting narcotics. The dose of the long-acting drug is titrated up to a satisfactory level, and the patient is given a small amount of short-acting medication for breakthrough pain. 2. Combination medical therapy is usually superior to narcotics alone. Nonsteroidal anti-inflammatory medications, tricyclic antidepressants, and a wide variety of novel medications (often anticonvulsants) can be used to achieve a synergistic response. 3. Analgesic medications should be tied to concrete, functional outcomes. It is unlikely that a medication will provide complete resolution of the problem. Objective improvements can be assessed in any of a variety of role functions (e.g., work, home, sexual) as well as in urinary frequency and pain control. The most important principle is for the physician to care for the patient as a family member, using all diagnostic skill, all reasonable therapeutic modalities, and the utmost compassion. CONCLUSIONS IC presents a formidable challenge to the urologist. The disease continues to create diagnostic problems and to defy the development of universally effective therapy. Although it is easy for the clinician and patient to become frustrated, most patients can achieve substantial amelioration of their symptoms over time. Teamwork is required in the management of IC, more so than in almost any other disease faced by the urologist. The clinician must respect the integrity of the patient and the burden faced by those living with “invisible disease.” The patient must actively participate in seeking effective therapy. Although it is always reasonable to hope for a cure, realistic goals must be set with an aim to maximizing function. If behavioral techniques such as dietary modification, stress reduction, and bladder training fail to control the symptoms of IC, medical treatment is indicated. First-line therapies include bladder distention, DMSO bladder instillations, PPS, amitriptyline, and hydroxyzine. Most patients respond to one of these

Chapter 92 PAINFUL BLADDER SYNDROME AND INTERSTITIAL CYSTITIS

treatments. New treatments being investigated for refractory disease include instillations of BCG and hyaluronic acid and sacral nerve stimulation. The role of therapy directed at the pelvic floor muscles (myofascial release and biofeedback) is also being defined. Pain management is an underutilized tool for a disease in which daily pain is a common symptom. A multidisciplinary approach using the skills of a urologist, a physical therapist, and a pain specialist can produce excellent results. Ultimately, a small percentage of patients will go on to radical surgical treatment. Limited evidence suggests that those with a low bladder capacity

under anesthesia (80

30–39

40–49 50–59 60–69 Age decade, years

70–79

>80

60 50 40 30 20 10 0 19–29

(A) slow/poor stream; (B) straining (A) intermittency; (B) incomplete emptying (A) hesitancy; (B) dysuria

Figure 93-2 Relationships between age and type of stream (A) and bladder emptying symptoms (B) in women. (From Swithinbank LV, Abrams P: A detailed description, by age, of lower urinary tract symptoms in a group of community-dwelling women. BJU Int 85(Suppl2):19-24, 2000.)

suffer from overactive bladder with incontinence than men (2.6%). The prevalence and prevalence ratios were inversely related to increasing education, a pattern that was more apparent among women who had overactive bladder with urge incontinence. In women, but not in men, the prevalence of overactive bladder with urge incontinence increased in relation to increasing body mass index. The age-specific prevalence of overactive bladder was similar for men and women, but age patterns differed by sex and type of overactive bladder. The age-specific prevalence of overactive bladder without incontinence appears to plateau after age 44 years for women and after age 54 years for men. In contrast, agespecific prevalence of overactive bladder with urge incontinence continues to increase with increasing age, with women having a steeper age-related increase than men. These contrasting patterns suggest that overactive bladder without incontinence may precede the onset of overactive bladder with urge incontinence. Moreover, in the older ages, the transition rate from overactive bladder without to overactive bladder with urge incontinence may exceed the rate of occurrence of new cases of overactive bladder without incontinence. This may explain the plateau in prevalence of overactive bladder without incontinence. Longitudinal studies will be required to test this hypothesis. If confirmed, the incidence of overactive bladder with urge incontinence may be mitigated through secondary prevention efforts directed toward overactive bladder without urge incontinence. Women and men who have overactive bladder, with or without urge incontinence, have significantly poorer scores for health-related quality of life, mental health, and quality of sleep compared with sex- and age-matched controls. These differences were significant after adjusting for other covariates, including comorbid illnesses. CONCLUSIONS

Society (ICS) derived a consensus symptomatic definition of overactive bladder syndrome as urinary urgency, with or without urge incontinence, usually with urinary frequency and nocturia, in the absence of pathologic and metabolic factors that would explain the symptoms.1 Urodynamically, overactive bladder is characterized by the presence of involuntary bladder contractions that occur during bladder filling despite the patient’s attempt to suppress them. The National Overactive Bladder Evaluation (NOBLE) study was initiated to better understand the prevalence and impact of overactive bladder in a broad spectrum of the U.S. population.72 Using a clinically validated, computer-assisted telephone interview questionnaire, a sample population of adults, who were 18 years old or older and representative of the main population by sex, age, and geographic region, was surveyed. A surprising result from this study is the equal prevalence of urgency-related bladder control problems in men and women (16.0% and 16.9%, respectively), although more women (13.4%)

Urinary incontinence and voiding dysfunctions are prevalent conditions that can affect women of all ages. The incidence is especially high among the elderly, whether they are living in the community or in institutions. These conditions are associated with many medical correlates and have a tremendous effect on the psychological well-being of the afflicted. Urinary incontinence and voiding dysfunctions are very costly, with the expenditure similar to the more popularly recognized health concerns of the aging woman. The explosion of epidemiologic data has led to novel treatment and prevention strategies, although patient satisfaction about the outcome of surgery may not be as high as previously believed. Epidemiologic information about different racial and ethnic populations is now being reported. Our knowledge about the different issues of voiding dysfunctions is still inadequate, and our understanding of normal voiding parameters is still far from complete.

References 1. Abrams P, Cardozo L, Fall M, et al: The standardization of terminology in lower urinary tract function: Report from the Standardization Sub-committee of the International Continence Society. Neurol Urodyn 21:167. 2002. 2. Brocklehurst JC, Dillane JB, Griffiths, et al: The prevalence and symptomatology of urinary infection in an aged population. Gerontol Clin 10:242, 1968.

3. Thomas TM, Plymat KR, Blannin J, et al: Prevalence of urinary incontinence. BMJ 281:1243, 1980. 4. Hunskaar S, Gunnar L, Lars V, et al: Prevalence of stress incontinence in women in four European countries. Neurol Urodyn 21:275, 2002. 5. Hannestad YS, Rortveit G, Sandvik H, et al: A communitybased epidemiological survey of female urinary incontinence:

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The Norwegian EPINCONT study. J Clin Epidemiol 53:1150, 2000. 6. Diokno AC, Brock BM, Brown MB, et al: Prevalence of urinary incontinence and other urological symptoms in the noninstitutional elderly. J Urol 136:1022, 1986. 7. Kinchen K, Gohier J, Obenchain R, Bump R: Prevalence and frequency of stress incontinence among community-dwelling women. Eur Urol 85(Suppl 1):85, 2002. 8. Lapitan MC, Chye PL: Asia-Pacific Continence Advisory Board. The epidemiology of overactive bladder among females in Asia: A questionnaire survey. Int Urogynecol J 12:226, 2001. 9. U.S. Department of Health, Education and Welfare: Long-term Care Facility Improvement Study. Washington, DC, US Government Printing Office, 1975. 10. Van Nostrand JF, Zappolo A, Hing E, et al: The National Nursing Home Survey: Summary for the United States. DHEW publication no. 79-1794. Vital and Health Statistics, series 13, no. 43. Washington, DC, National Center for Health Statistics, Health Resources Administration, 1977. 11. Willington FL: Significance of incompetence of personal sanitary habits. Nurs Times 71:340, 1975. 12. Cheater FM, Castleden CM: Epidemiology and classification of Urinary incontinence. Clin Obstet Gynaecol 14:183, 2000. 13. Aggazzotti G, Pesce F, Grassi D, et al: Prevalence of urinary incontinence among institutionalized patients: A cross-sectional epidemiologic study in midsized city in northern Italy. Urology 56:245, 2000. 14. Brandeis GH, Baumann MM, Hossain M, et al: The prevalence of potentially remediable urinary incontinence in frail older people: A study using the minimum data set. J Am Geriatr Soc 45:179, 1997. 15. Sgadari A, Topinkova E, Bjornson J, et al: Urinary incontinence in nursing home residents: A cross-sectional comparison. Age Ageing 8:47, 1996. 16. Toba K, Ouchi H, Iimura O, et al: Urinary incontinence in elderly inpatients in Japan: A comparison between general and geriatric hospital. Aging 8:47, 1996. 17. Borie M, Davidson H: Incontinence in institutions: Costs and associated factors. Can Med Assoc J 147:322, 1992. 18. Ouslander JG, Palmer MH, Rovner BW, et al: Urinary incontinence in nursing homes: Incidence, remission and associated factors. J Am Geriatr Soc 41:1083, 1993. 19. Fonda D, for the Victorian Geriatricians Peer Review Group: Improving management of urinary incontinence in geriatric centres and nursing homes. Aust Clin Rev 10:1063, 1995. 20. Peet SC, Castleden CM: The prevalence of urinary and faecal incontinence in hospitals and residential and nursing homes for older people. BMJ 311:1063, 1995. 21. Hunskaar S, Arnold EP, Brugio K, et al: Epidemiology and natural history of urinary incontinent. In Abrams P, Khoury S, Wein A (eds): Incontinence. Plymouth, UK, Scientific International, 1999, p 197. 22. Thom DH, Haan MN, Van Den Eeden S: Medically recognized urinary incontinence and risks of hospitalization nursing home admission and mortality. Age Aging 26:237, 1997. 23. Fultz NH, Herzog AR, Raghunathan TE, et al: Prevalence and severity of urinary incontinence in older African American and Caucasian women. J Gerontol A Biol Sci Med Sci 54:M299-M303, 1999. 24.Dolan LM, Casson K, McDonald P, et al: Urinary incontinence in Northern Ireland: A prevalence study. BJU Int 83:760, 1999. 25. Bump RC, Norton PA: Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 25:723, 1998. 26. Howard D, Davies PS, Delancey JO, et al: Differences in perineal lacerations in black and white primiparas. Obstet Gynecol 96:622624, 2000. 27. Peacock LM, Wiskind AK, Wall LL: Clinical features of urinary incontinence and urogenital prolapse in a black inner city population. Am J Obstet Gynecol 171:1464, 1994.

28. Heyns OS: Bantu Gynaecology. Johhanesburg, Witwaterstrand University Press, 1956, p 98. 29. Skinner DP: Stress incontinence: A comparative racial study. Med Proc 9:189, 1963. 30. Knobel J: Stress incontinence in the black female. S Afr J Obstet Gynaecol 49:430, 1975. 31. Espino DV, Palmer RF, Miles TP, et al: Prevalence and severity of urinary incontinence in elderly Mexican-American women. J Am Geriatr Soc 51:1580, 2003. 32.Campbell AJ, Reinken J, McCosk L: Incontinence in the elderly: Prevalence and prognosis. Age Ageing 14:65, 1985. 33. Moller LA, Lose G, Jorgensen T: The prevalence and bothersomeness of lower urinary tract symptoms in women 40-60 years of age. Acta Obstet Gynecol Scand 79:298, 2000. 34. Samuelsson EC, Victor FT, Svardsudd KF: Five-year incidence and remission rates of female urinary incontinence in a Swedish population less than 65 years old. Am J Obstet Gynecol 183:568, 2000. 35. Hunskaar S, Burgio K, Diokno A, et al: Epidemiology and natural history of urinary incontinence in women. Urology 62(Suppl 4A):16, 2003. 36. Herzog AR, Fultz NH, Brock BM, et al: Urinary incontinence and psychological distress among older adults. Psychol Aging 3:115, 1988. 37. Herzog AR, Fultz NG Normolle DP, et al: Methods used in to manage urinary incontinence by older adults in the community. J Am Geriatr Soc 37:339, 1989. 38. Miller RL: Urinary incontinence in the community elderly: Functional status, cognitive function and depressive symptoms: Findings from the Yale Health and Aging study. Paper presented at the 113th annual meeting of the American Public Health Association, Washington, DC, 1985. 39. Diokno AC, Brock BM, Brown MB, et al: Medical correlates of urinary incontinence in the elderly. Urology 36:129, 1990. 40. Diokno AC, Brown MB, Herzog AR: Relationship between use of diuretics and continence status in the elderly. Urology 38:39, 1991. 41. Wells TJ, Brink CA, Diokno AC: Urinary incontinence in the elderly women: Clinical findings. J Am Geriatr Soc 35:933, 1987. 42. Ouslander JG: Diagnostic evaluation of geriatric urinary incontinence. Geriatr Med 2:715, 1986. 43. Shimp LA, Wells TJ, Brink CA, et al: Relationship between drug use and urinary incontinence in elderly women. Drug Intel Clin Pharmacol 22:786, 1988. 44. Jones KW, Schoenberg HW: Comparison of the incidence of bladder hyperreflexia in patients with benign prostatic hyperplasia and agematched female controls. J Urol 133:425, 1985. 45. Hilton P, Stanton SL: Algorithmic method for assessing urinary incontinence in elderly women. BMJ 282:940, 1981. 46. Brown JS, Waetjen LE, Subak LL, et al: Pelvic organ prolapse surgery in the United States. Am J Obstet Gynecol 186:712, 2002. 47. Leach GE, Dmowhowski RR, Appell RA, et al: Female stress urinary incontinence clinical guidelines panel summary report on surgical management of female stress urinary incontinence. J Urol158:875, 1997 48. Diokno AC, Burgio K, Fultz NH, et al: Prevalence and outcomes of continence surgery in community dwelling women. J Urol 170:507, 2003. 49. The Simon Foundation: Vital Issues. Consensus Statement of First International Conference for Prevention of Incontinence. Available at www.simonfoundation.org 50. Fantl JA, Wyman JF, McCish DK, et al: Efficacy of bladder training in older women with urinary incontinence. JAMA 265:609, 1991. 51. Fantl JA: Behavioral intervention for community dwelling individuals with urinary incontinence. Urology 51(Suppl):30, 1998. 52. Doherty MC, Dwyer JW, Pendergrast JF, et al: A randomized trial of behavioral management for continence with older rural women. Res Nurs Health 25:3, 2002.

Chapter 93 INCONTINENCE AND VOIDING DYSFUNCTION IN THE ELDERLY

53. Diokno AC, Yuhico M Jr: Preference, compliance and initial outcome of therapeutic options chosen by female patients with urinary incontinence. J Urol 154:1727, 1995. 54. Hay-Smith J, Herbison P, Morkved S: Physical therapies for prevention of urinary and faecal incontinence in adults. Cochrane Database Syst Rev (2):CD003191, 2002. 55. Morkved S, Bo K: Effect of postpartum pelvic floor muscle training in prevention of and treatment of urinary incontinence: A one-year follow-up. BJOG 107:1022, 2000. 56. Diokno AC, Sampselle CM, Herzog AR, et al: Prevention of urinary incontinence by behavioural modification program: A randomized, controlled trial among older women in the community. J Urol 171:1165, 2004. 57. Miller JM, Ashton-Miller JA, Delancey JO: A pelvic muscle precontraction can reduce cough-related urine loss in selected women with mild SUI. J Am Geriatr Soc 46:870, 1998. 58. Wagner TH, Hu TW: Economic costs of urinary incontinence in 1995. Urology 51:355, 1998. 59. US Dept of Health and Human Services. National Hospital Discharge Survey. Data from Vital and Health, series 13, no. 12. Hyattsville, MD, National Center for Health Statistics, 1994. 60. Liwin MS, Saigal CS (eds): Urologic Diseases in America. US Department of Health and Human Services, National Health Institute, National Institute of Diabetes and Digestive and Kidney Disease. Washington, DC, US Government Printing Office, pp 94-98, 2004. 61. Elbadawi A, Yalla SV, Resnick NM: Structural basis of geriatric voiding dysfunction. II. Aging detrusor: Normal versus impaired contractility. J Urol 150:1657, 1993. 62. Fitzgerald MP, Stablein U, Brubaker L: Urinary habits among asymptomatic women. Am J Obstet Gynecol 187:1384, 2002.

63. Jackson S, Donovan J, Brookes S, et al: Bristol Female Lower Urinary Tract Symptoms questionnaire: Development and psychometric testing. Br J Urol 77:805, 1996. 64. Swithinbank LV, Donovan JL, du Heaume JC, et al: Urinary symptoms and incontinence in women: relationships between occurrence, age and perceived impact. Br J Gen Pract 49:897, 1999. 65. Teasdale TA, Tuffet GE, Luchi RJ, Adam E: Urinary Incontinence in a community-residing population. J Am Geriatr Soc 36:600, 1988. 66. Brocklehurst JC, Fry J, Griffiths L, Kalton D: Dysuria on old age. J Am Geriatr Soc 19:582, 1971. 67. Somner P, Bauer T, Nielsen KK, et al: Voiding patterns and prevalence of incontinence in women. A questionnaire survey. Br J Urol 66:12, 1990. 68. Swithinbank LV, Abrams P: A detailed description, by age, of lower urinary tract symptoms in a group of community-dwelling women. BJU Int 85:19, 2000. 69. Lepor H, Machi G: Comparison of AUA symptom index in unselected males and females between fifty-five and seventy-nine years of age. Urology 42:36, 1993. 70. Chancellor MB, Rivas DA: American Urological Association symptom index specificity for benign prostatic hyperplasia. J Urol 150:1706, 1993. 71. Chai TC, Belville WD, McGuire EJ, Nyquist L: Specificity of American Urological Association voiding symptom index: Comparison of unselected and selected samples of both sexes. J Urol 150:1710, 1993. 72. Stewart WF, Van Rooyen JB, Cundiff GW, et al: Prevalence and burden of overactive bladder in the United States. World J Urol 20:327, 2003.

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Chapter 94

LOWER URINARY TRACT DISORDERS IN THE ELDERLY FEMALE Theodore M. Johnson, II, and Joseph G. Ouslander Aging is a continuous and inevitable process that affects everyone. It occurs at various rates in different individuals and in different organ systems within the same individual. The individual organism’s responses to the aging process are diverse and depend on many complex factors. The lower urinary tract, as much as any other organ system, is greatly influenced by the interactive and additive effects of age-related changes and the accumulation of many pathologic entities with increasing age. Symptoms of lower urinary tract dysfunction are common in elderly women. This chapter focuses on the age-related and age-associated changes that underlie lower urinary tract dysfunction in this population. We review in some detail the two most common

disorders of the lower urinary tract in elderly women—urinary incontinence and urinary tract infection (UTI). AGING AND THE FEMALE LOWER URINARY TRACT When considering the effects of increasing age on any organ system, a crucial distinction must be made between true agerelated changes that occur in everyone and age-associated changes resulting from the accumulation of pathologic conditions that do not occur in everyone. Table 94-1 lists age-related changes and age-associated factors that can influence lower urinary tract function and symptoms in elderly women. Because determining true

Table 94-1 Aging and the Female Lower Urinary Tract Change or Effect Age-related changes Altered cell function Decreased estrogen level Altered concentrations of central nervous system neurotransmitters; altered nerve conduction Altered immune function Altered bladder function Decreased capacity Increased uninhibited contractions Increased residual volume Lower urethral pressure Age-associated factors Cognitive and sensory impairment Locomotor disturbances and immobility Stroke Hip fracture Peripheral vascular disease Parkinson’s disease Poor fluid intake Central nervous system diseases affecting bladder function Stroke Dementia Parkinson’s disease Other diseases affecting bladder function Malignancy Atherosclerotic vascular disease Drug usage (see Table 94-2)

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Potential Effects Altered interstitial tissues and mucosal surfaces Increased likelihood of pelvic prolapse and urinary infection Thinner and more friable mucosa and interstitial tissues Increased likelihood of pelvic prolapse, urinary symptoms, and infection Increased likelihood of bladder and urethral dysfunction Increased susceptibility to infection Increased likelihood of urinary symptoms, incontinence, and infection

Increased likelihood of incontinence Decreased ability to relate symptoms More difficulty getting to a toilet; increased likelihood of fecal impaction and incontinence

Increased likelihood of fecal impaction and bacteriuria Increased likelihood of incontinence

Increased likelihood of bladder dysfunction

Increased likelihood of bladder or urethral dysfunction

Chapter 94 LOWER URINARY TRACT DISORDERS IN THE ELDERLY

age-related changes in the female lower urinary tract would involve invasive procedures (e.g., catheterization for urodynamic studies, cystoscopy) in continent elderly women without urinary symptoms, this type of information is rarely sought. Despite these difficulties in obtaining data, several types of age-related changes are known to have a prominent influence on lower urinary tract function. One of the most important age-related changes affecting the female lower urinary tract is the postmenopausal decline in estrogen. This remains true, even though evidence has suggested that oral estrogen supplementation is linked to worse continence outcomes.1 The bladder, urethra, and genital tract have a common embryologic origin, and the epithelium of all of these tissues responds to hormonal changes. When the influence of estrogen declines, the epithelium and supporting tissues of the pelvic area atrophy, resulting in a friable mucosa and a tendency toward prolapse. The lower glycogen content in the vaginal epithelium results in less lactic acid metabolism by Doderlein’s bacilli and an increase in the pH of vaginal secretions that may increase susceptibility to infection. Changes occur in the concentration of certain neurotransmitters in various locations in the central nervous system with increasing age. Given the important influence of the central nervous system on human bladder function, these age-related changes in central neurotransmitters may play a role in disorders of micturition in the elderly. Alterations in immune function also occur with increasing age. Although these changes have been seen mainly in cellular immunity, age-related changes in immune function, especially local immune activity in the lower urinary tract, may play an important role in susceptibility to bacteriuria and symptomatic UTI in older women. Certain functional changes appear to occur in the bladder and urethra with increasing age. In one study, abnormal cystometrographic results were found for 15 of 24 continent elderly women who were free of neurologic disease.2 Twelve of these 15 showed uninhibited contractions; 10 had a bladder capacity of less than 250 mL. Other studies have shown prevalence rates of 5% to 11% of abnormalities in continent older women.3,4 Some work has attempted to elucidate in the underlying anatomic basis of these changes. In a series of investigations in symptomatic and asymptomatic adults older than 65 years using urodynamics and electron microscopy of bladder biopsy specimens, investigators found that patients with detrusor activity had specific anatomic abnormalities, including a dysjunction pattern with protrusion junctions and ultraclose abutments. These changes are believed to be the anatomic explanation for the propagation of involuntary detrusor contractions in older patients.5-7 Maximal urethral pressure and functional urethral length are decreased in continent elderly women.8,9 In one study, the maximal urethral pressure in continent women fell from a mean of 87 cm H2O in the third decade to 42 cm H2O in the seventh decade, a value that overlapped that of younger women with stress incontinence.8 These age-related changes in lower urinary tract function should be considered when evaluating urodynamic findings in elderly women. One postmortem study of 25 bladders from women between the ages of 74 and 102 years revealed marked trabeculation, diverticula, and cellular formation.10 Another study demonstrated continuous loss of striated muscle cells of the rhabdosphincter due to apoptosis, which eventually may reach a critical mass, leading to reduced function of the muscle with resultant urinary incontinence.11 Histologic section of the bladder outlet showed a high incidence of chronic inflam-

mation, edema, and fibrosis, presumed to be related to chronically infected residual urine. The trabeculation in these bladders was thought to be the result of loss of elastic tissue and coalescence of muscle fiber and of muscle hypertrophy resulting from bladder outlet obstruction or frequent uninhibited bladder contractions against a closed sphincter, or both. Other investigators have reported that the bladder in elderly women is more often decompensated and thin walled and that hypertrophy does not occur with uninhibited contractions.12 Further research on the anatomic changes that occur in the aging lower urinary tract will help to clarify these issues. Several age-associated factors (Table 94-1) can have an important influence on lower urinary tract function and symptoms in elderly women. Although most elderly individuals are generally active and healthy, the incidence of several disorders does increase with age. Impairments of cognitive and sensory function are more common in the elderly than in younger populations. These impairments may make it difficult for the elderly to interpret and relate symptoms of lower urinary tract dysfunction accurately. Poor nutritional and fluid intake can predispose the elderly to fecal impaction and urinary infection. The prevalence of asymptomatic bacteriuria increases with age (discussed later), and this situation predisposes to symptomatic urinary infection. Locomotor disturbances are common in the elderly. The incidence of stroke, arthritis, osteoporosis with resultant hip fractures, peripheral vascular disease with claudication or resultant amputations, Parkinson’s disease, and other gait disorders increase with age. These disorders can make it difficult for the elderly to reach a toilet, especially in the setting of urinary frequency and urgency. Impaired mobility may play a prominent role in the development of incontinence in elderly women (discussed later). The incidence of diseases of the central nervous system, such as stroke, dementia, and Parkinson’s disease, increases with age. Given the important role of higher centers in the control of micturition, these diseases are frequently involved in urinary dysfunction in the elderly. An associated problem is that as a result of the high prevalence of so many diseases among the elderly, they are also likely to be taking a wide variety of drugs (often several different agents in complex dosage schedules), many of which can affect lower urinary tract function (Table 94-2). An important component of the assessment of older women with lower urinary tract symptoms is evaluation of the potential role of medications in causing or contributing to their symptoms. It is important to understand the potential effects of acetylcholinesterase inhibitors, given for dementia to stabilize cognitive decline, because these procholinergic agents can worsen or cause incontinence. Bladder relaxant agents may worsen cognition in some older adults.13 URINARY TRACT INFECTION IN ELDERLY WOMEN Asymptomatic and symptomatic UTIs are common in the elderly. The overall expenditures for the treatment of UTIs in women in the United States, excluding spending on outpatient prescriptions, were approximately $2.47 billion in 2000.14 The estimated lifetime risk for a woman to have a UTI is greater than 50%.14 The prevalence of bacteriuria increases with age; it is more common in elderly women than in men and in patients in nursing homes and hospitals than in elderly people residing at home. Compared with younger women, elderly women are at higher risk for hospitalization from a UTI14 and have twice the risk for

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Table 94-2 Medications That Can Negatively Affect Continence Type of Medication

Potential Effects on Continence

Diuretics Anticholinergics Acetylcholinesterase inhibitors (for dementia) Psychotropics Antidepressants Antipsychotics Sedatives and hypnotics Narcotic analgesics α-Adrenergic blockers α-Adrenergic agonists β-Adrenergic agonists Calcium channel blockers Alcohol

Polyuria, frequency, urgency Urinary retention, overflow incontinence, impaction Urgency, urge urinary incontinence Anticholinergic actions, sedation, rigidity, immobility Anticholinergic actions, sedation Sedation, delirium, immobility, muscle relaxation Urinary retention, fecal impaction, sedation, delirium Urethral relaxation Urinary retention Urinary retention Urinary retention Polyuria, frequency, urgency, sedation, delirium, immobility

Table 94-3 Prevalence of Bacteriuria in Elderly Women Setting of Population Community Nursing home Hospital

Women Affected (%) 11-17 23-27 32-50

developing bacteruria after urodynamic procedures,15 Table 94-3 summarizes several studies of the prevalence of bacteriuria in the elderly.16-26 Longitudinal studies of bacteriuria among older women have documented that the organisms change over time and that bacteriuria resolves and returns spontaneously in many women.20,24-26 Several factors have been implicated in the increased prevalence of bacteriuria in the elderly, including atrophic mucosal changes as a result of estrogen deficiency, increased residual urine volumes, immobility, the prevalence of fecal and urinary incontinence, and the relatively common use of indwelling catheters.27 Risk factors for bacteruria and UTIs in postmenopausal women include sexual activity, diabetes, urinary incontinence, and past UTIs.28 Symptoms common in elderly women that are usually associated with UTI, such as frequency, urgency, dysuria, and incontinence, do not reliably predict whether the urine is infected.17-19,21 Midstream urine specimens from elderly women are highly unreliable in predicting true bladder infection. The white blood cell count on urinalysis correlates poorly with bladder infection,10 and there is at least a 17% incidence of false-positive cultures when midstream urine specimens are repeated or compared with suprapubic aspirates.20,29 Growth of between 104 and 109 colonies/mL and contaminated specimens are also more common with midstream specimens. Taking two consecutive midstream specimens increases the reliability substantially. These factors can make the accurate diagnosis of true bladder infection difficult in elderly women. Asymptomatic bacteriuria is generally considered a benign condition in the elderly who are free of catheters. Studies have, however, shown a substantial incidence of potentially correctable lower urinary tract disease that can contribute to bacteriuria in asymptomatic elderly patients.22 One study found that bacteriuric elderly nursing home residents had a 30% to 50% lower sur-

vival rate (deaths from a variety of causes) when followed for 10 years compared with nonbacteriuric residents matched for age, blood pressure, smoking habits, hematocrit, and blood cholesterol levels.30 A second study of community-dwelling elderly also showed an association between bacteriuria and mortality,31 but a cause-and-effect relationship has not been documented. Two studies of treated asymptomatic bacteriuria in older institutionalized32 and ambulatory33 women have not documented substantial effects on mortality. In summary, therapy for asymptomatic bacteruria in older individuals has not produced improvements in survival or amelioration of genitourinary symptoms, but it has correlated with increased antimicrobial resistance and adverse drug effects. For these reasons, guideline consensus statements have recommended against the routine screening for and treatment of asymptomatic bacteriuria in older persons resident in the community elderly institutionalized residents of long-term care facilities.34 Symptomatic UTIs in elderly women should be treated with an antimicrobial that achieves a high concentration in the urine. Consensus guidelines recommend that trimethoprim/sulfamethoxazole (TMP/SMX) DS twice daily be first line therapy for UTIs, based on cost and efficacy considerations. Floxacins (i.e., ciprofloxacin and others) should be reserved for situations in which there are high rates of resistance (10% to 20%) to TMP/ SMX.34 In younger women, a 3-day regimen is associated with a 93% eradication rate. Longer courses are associated with higher eradication rates, which must be weighed against higher rates of adverse drug events.35 Because of the acknowledged higher rates of failure in 3-day treatment for older women, the consensus statement recommends a 7-day treatment course for uncomplicated symptomatic infections. Drug selection should be modified based on such factors as allergy, renal function, cost, and bacterial sensitivities (especially when infections are recurrent). Although age-related changes do occur in the kidney’s ability to eliminate these drugs, dosage adjustments usually are unnecessary unless the serum creatinine level is above 2.0 mg/dL. Compliance with drug regimens may be a problem for many elderly patients and should be kept in mind as a potential cause of treatment failure. Recurrent infections in elderly women usually are caused by reinfection with a different organism. Relapse with the same organism should prompt a search for a structural abnormality in the lower urinary tract. When relapse

Chapter 94 LOWER URINARY TRACT DISORDERS IN THE ELDERLY

Table 94-4 Prevalence of Urinary Incontinence Among Older Women Setting of Population

Women Affected (%)

Community

Approximately 33%: any incontinence* 4-6%: severe incontinence† Approximately 40% 50-70%

Acute care hospital Nursing home

*Positive response to questioning about any uncontrolled urine loss in the past year. † Incontinence that occurs more than once per week or requires the use of pads.

occurs in the absence of a structural abnormality, a 3- to 6-week course of drug therapy should be given. Infrequent symptomatic reinfections should be treated as separate episodes; frequent symptomatic infections can be managed by long-term prophylaxis. Nitrofurantoin (100 mg/day) and TMP/SMX (1/2 of a single strength (40 mg/200 mg) tablet/day) have been shown to prevent recurrent symptomatic infections36 and appear to be costeffective, especially in women who have three or more symptomatic infections per year.37 URINARY INCONTINENCE IN ELDERLY WOMEN Scope of the Problem Incontinence is a common, disruptive, and potentially disabling condition in the elderly. The prevalence of urinary incontinence is illustrated in Table 94-4. Incontinence is a heterogeneous condition among older women, ranging in severity from occasional episodes of dribbling small amounts of urine to continuous urinary incontinence with concomitant fecal incontinence. The prevalence of urinary incontinence among women increases with increasing age. The likelihood of having severe urinary incontinence also increases with increasing age; compared with 8% of women between 30 and 39 years old reporting severe urinary incontinence, 33% of women between 80 and 90 years old reported severe urinary incontinence.38 Although these general trends are clear, there are more subtle trends. The overall prevalence of urinary incontinence increases with rising age, but the prevalence of stress incontinence may peak at age 50 and then decrease slightly.39 Parity, which is a significant risk factor for stress incontinence in younger women, is a much less important risk factor for stress incontinence in older women.40,41 Not all incontinent elderly women are severely demented, bedridden, and in nursing homes. Many in institutions and in the community are ambulatory and have good mental function. Physical health, psychological well-being, social status, and the costs of health care can be adversely affected by incontinence. Physical consequences can include skin breakdown, UTIs, and fractures, which may result if patients fall when they are forced to get up in the middle of the night to urinate. The psychosocial effects can be even more devastating; many elderly patients may suffer intense embarrassment, loss of self-esteem, and feelings of helplessness, depression, and anxiety, resulting in a withdrawal from vital social contacts or at least a reluctance to go places or engage in activities that are not close to toilet facilities.42 The

financial impact of incontinence is also significant. It has been estimated that the cost of managing incontinence in elderly nursing home residents alone is close to $3 billion per year.43 Estimates put the U.S. Medicare cost of inpatient and outpatient treatment of urinary incontinence in women at $234.4 million (1998). Urinary incontinence as the main reason for physician care for a Medicare visit rose from 845 per 100,000 in 1992 to 1845 per 100,000 persons in 2000.39 Urinary incontinence is curable in many elderly patients, especially those who have adequate mobility and mental function. There is growing literature suggesting that for some individuals, urinary incontinence can be prevented or delayed by exercises and behavioral strategies.44 Even when urinary incontinence is not curable, incontinence can always be managed in a manner that keeps patients comfortable, makes life easier for caregivers, and minimizes the cost of caring for the condition and its complications. Acute, Reversible Incontinence versus Persistent Incontinence The distinction between acute, reversible forms of incontinence and persistent incontinence is clinically important in older women because incontinence is often contributed to or caused by factors outside the lower urinary tract in this population. Acute incontinence refers to situations in which the incontinence is of sudden onset, usually related to an acute illness or an iatrogenic problem, and subsides after the illness or medication problem has been resolved. Persistent incontinence refers to incontinence that is unrelated to an acute illness and persists over time. The causes of acute and reversible forms of urinary incontinence can be remembered by the acronym DRIP (Table 94-5). Many of the reversible factors listed in this table can also play a role in patients with persistent forms of incontinence. A search for these factors should be undertaken in all incontinent geriatric patients. Persistent forms of incontinence can be classified clinically into four basic types in the geriatric population: stress, urge, overflow, and functional. These types can overlap each other, and an individual patient may have more than one type simultaneously. Although this classification does not include all of the neurophysiologic abnormalities associated with incontinence (e.g., reflex or “unconscious” incontinence), it is helpful in approaching the clinical assessment and treatment of incontinence in the elderly.45 Stress incontinence is the most common type among women younger than 75 years, especially in ambulatory clinic settings.46-48 It may be infrequent and involve very small amounts of urine, and it may need no specific treatment in women who are not bothered by it. However, it may be so severe or bothersome that it requires surgical correction. It is most often associated with weakened supporting tissues and consequent hypermobility of the bladder outlet and urethra caused by lack of estrogen or by previous vaginal deliveries or surgery. Older adults with stress incontinence, compared with their continent older counterparts, are more likely to be white, have arthritis, be using oral estrogen therapy, have chronic obstructive pulmonary disease, and be obese.49 Parity appears to be a somewhat weaker risk factor among women 60 years old or older than among women younger than 60 years.30 Many older women also develop stress incontinence because of intrinsic urethral dysfunction after one or more lower urinary tract surgical procedures.

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Table 94-5 Reversible Factors That May Contribute to Urinary Incontinence DRIP Acronym

Definition

Description

D

Delirium

R

Restricted mobility Retention

I

Infection Inflammation Impaction

P

Polyuria Pharmaceuticals

New-onset urinary incontinence (UI) may be associated with delirium because of acute underlying conditions requiring diagnosis and treatment. Acute conditions causing immobility may precipitate UI; environmental manipulation and scheduled toileting are appropriate until the condition resolves. Urinary retention may be precipitated by many drugs (see Table 94-2) or may occur acutely because of anatomic obstruction; immobility and large fecal impactions may also contribute. Acute cystitis may precipitate urge UI. Otherwise asymptomatic bacteriuria may contribute to urinary frequency and should be eradicated before any urodynamic evaluations are carried out. Atrophic vaginitis and urethritis can cause irritative voiding symptoms, including UI. Fecal impaction and fecal incontinence may be associated with UI. Poorly controlled diabetes with glucosuria can contribute to urinary frequency and UI. Edema due to congestive heart failure or venous insufficiency can cause nocturia and exacerbate nocturnal UI (see Table 94-2)

Urge incontinence is the most common symptomatic and urodynamic type of incontinence in women older than 75 years, especially those in institutions, and it is commonly a component of the overactive bladder syndrome.50-52 Urge incontinence can be caused by a variety of lower genitourinary and neurologic disorders. Older incontinent individuals with urge incontinence are more likely than their older, continent counterparts to be white, have arthritis, be using oral estrogen therapy, have insulintreated diabetes, have depression, be older (within a 70- to 79year-old cohort), and have poor lower extremity physical performance.49 It is most often associated with detrusor motor instability or detrusor hyperreflexia. Some patients have a poorly compliant bladder without involuntary contractions (due to radiation or interstitial cystitis, both of which are unusual conditions in older women). Other patients have symptoms of urge incontinence but do not exhibit detrusor motor instability on urodynamic testing. This is usually called sensory instability or hypersensitive bladder; it is likely that some of these patients have detrusor motor instability in everyday life that is not documented at the time of the urodynamic study. However, some patients with neurologic disorders have detrusor hyperreflexia on urodynamic testing but may not have urgency and are incontinent without any warning symptoms (i.e., unconscious incontinence). These patients are generally treated as if they have urge incontinence if they can empty the bladder and do not have other correctable genitourinary pathology (discussed later). A subgroup of very elderly incontinent patients with detrusor hyperreflexia has been described who also have impaired bladder contractility; they empty less than a third of the bladder volume with involuntary contractions on urodynamic testing.51-53 The implications of this urodynamic finding for the pathophysiology and treatment of incontinence in the elderly are unclear and are being investigated. Urinary retention with overflow incontinence is relatively unusual among older women and can result from anatomic or neurogenic outflow obstruction, a hypotonic or acontractile bladder, or both (Box 94-1). Several types of drugs can also contribute to this type of incontinence (see Table 94-2). Stress, urge, and overflow incontinence can occur in combination. About one third of older women with stress incontinence

Box 94-1 Causes of Urinary Retention in Elderly Women Bladder outlet obstruction Mechanical compression Gynecologic malignancy Uterine fibroids Ovarian cyst Fecal impaction Fibrosis of bladder outlet (uncommon) secondary to chronic inflammation Urethral obstruction Stricture Prolapse and urethral distortion Hypotonic bladder Peripheral neuropathy Diabetes Alcoholism Mechanical interruption of motor innervation Tumor Herniated disk Trauma Overdistention injuries Detrusor-sphincter dyssynergy Drug-induced retention (see Table 94-2)

also have symptoms of urge incontinence and detrusor instability. Similarly, about one third of women with urge incontinence also have symptoms or signs of stress incontinence.46-48,54 These mixed types of incontinence can have important therapeutic implications, especially in decisions about surgery for stress incontinence. Functional incontinence results when an elderly person is unable or unwilling to reach a toilet on time. Distinguishing this type of incontinence from other types of persistent incontinence is critical to appropriate management. Factors that cause functional incontinence (e.g., inaccessible toilets, psychological disorders) can exacerbate other types of persistent incontinence.

Chapter 94 LOWER URINARY TRACT DISORDERS IN THE ELDERLY

Box 94-2 Diagnostic Evaluation of Urinary Incontinence in Older Women All Patients Focused history Targeted physical examination Urinalysis Postvoid residual determination Selected Patients Simple urodynamic test Complex urodynamic tests Dual-channel cystometrogram Pressure-flow study Urethral pressure profilometry Sphincter electromyography Video urodynamic evaluation Laboratory studies Urine culture Renal function tests Blood glucose Serum calcium Urine cytology Radiologic studies Renal ultrasound Voiding cystourethrography Urologic or gynecologic evaluation Cystourethroscopy

Patients with incontinence that appears to be predominantly related to functional factors may also have abnormalities of the lower genitourinary tract such as detrusor hyperreflexia. In some patients, it can be very difficult to determine whether the functional factors or the genitourinary factors predominate without a trial of specific types of treatment. It is therefore appropriate to consider functional incontinence as a diagnosis of exclusion among older patients. Cognitive impairment or impaired mobility should not preclude a trial of specific treatment for incontinence when indicated. Evaluation In patients with a sudden onset of incontinence (especially one associated with an acute medical condition and hospitalization), the possible causes (see Table 94-5) can be determined by a brief history, physical examination, and basic laboratory studies (e.g., urinalysis, culture, serum glucose or calcium level). Box 94-2 lists the basic components of the evaluation of persistent urinary incontinence. All patients should have a focused history, targeted physical examination, urinalysis, and a determination of postvoid residual urine volumes. The history should focus on the characteristics of the incontinence, current medical problems and medications, and the impact of incontinence on the patient and caregivers. Bladder records or voiding diaries are often helpful. Physical examination should focus on abdominal, rectal, and genital examinations and on evaluation of lumbosacral innervation. During the history and physical examination, special attention should be paid to factors such as mobility, mental status, medications, and accessibility of toilets that may be causing incontinence or interacting with urologic and neuro-

logic disorders to make the condition worse. A clean urine sample should be collected for urinalysis to exclude glucosuria, pyuria, bacteriuria, and hematuria. Persistent sterile microscopic hematuria (>5 red blood cells/high-power field) is an indication for further evaluation to exclude a tumor or other urinary tract abnormality. A series of simple tests of lower urinary tract function can be carried out in a clinic, hospital, nursing home, or even at home. They include observation of voiding, a pad test for stress incontinence, and simple cystometry.55 These tests are not necessary for all patients (discussed later). Like other diagnostic tests, they should be performed only if the results will change the patient’s management. When they are performed, they must be carried out and interpreted carefully in light of other information from the history and physical examination. Bladder capacity and stability as determined by simple cystometry are highly correlated with results of formal multichannel cystometrograms.56 Simple cystometry may be unnecessary to make a reasonable treatment plan in many elderly patients, such as those who have sterile urine and no atrophic vaginitis, meet none of the criteria given in Table 94-6, and who reliably give a history of stress incontinence without irritative or obstructive voiding symptoms, leak with stress maneuvers, and can empty the bladder completely (they can be treated for stress-type incontinence) or who reliably give a history of urge incontinence without symptoms of stress incontinence or voiding difficulty and can empty the bladder completely (they can be treated for urge-type incontinence). These tests are not essential for patients who are going to be treated initially with behavioral therapy alone, which can be used for stress, urge, mixed, and functional incontinence. The criteria for referral for further evaluation given in Table 94-6 have been shown to be reasonably sensitive but not very specific for identifying patients who require further evaluation for appropriate treatment.50 Management Several therapeutic modalities are used in managing incontinent older women. Special attention should be paid to the management of acute forms of incontinence, which are most common in elderly patients in acute care hospitals. These forms of incontinence are often transient if managed appropriately; however, inappropriate management may lead to a permanent problem. The most common treatment for incontinent elderly patients in acute care hospitals is indwelling catheterization. In some instances, this therapy is justified by the necessity for accurate measurement of urine output during the acute phase of an illness. In many instances, however, it is unnecessary and poses a substantial and unwarranted risk of catheter-induced infection. Although it may be more difficult and time consuming for caregivers, making toilets and toilet substitutes accessible combined with some form of scheduled toileting is probably a more appropriate approach to the treatment of patients who do not require indwelling catheters. Launderable or disposable and highly absorbent bed pads and undergarments may also be helpful in managing these patients. These products may be more costly than catheters but probably result in less morbidity and therefore lower overall cost in the long run. Specially designed incontinence undergarments and pads can be very helpful for many nonhospitalized patients but must be used appropriately. They are being marketed on television and are readily available in retail stores. Although they can be effective, several caveats should be

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Table 94-6 Criteria for Referral of Elderly Incontinent Women for Urologic, Gynecologic, or Urodynamic Evaluation Criteria History Recent history of lower urinary tract or pelvic surgery or irradiation Relapse or rapid recurrence of a symptomatic urinary tract infection

Physical examination Marked pelvic prolapse

Severe stress incontinence*

Severe hesitancy, straining, or interrupted urinary stream Postvoid residual Difficulty in passing a 14-Fr straight catheter Postvoid residual volume >200 mL†

Urinalysis Hematuria (sterile)

Failure to respond to nonsurgical management

Definition

Rationale

Surgery or irradiation involving the pelvic area or lower urinary tract within the past 6 months

A structural abnormality related to the recent procedure should be sought.

Onset of dysuria, new or worse irritative voiding symptoms, fever, suprapubic or flank pain associated with growth of more than 100,000 colony-forming units of a urinary pathogen; symptoms and bacteriuria that return within 4 weeks of treatment

A structural abnormality or pathologic condition in the urinary tract predisposing to infection should be excluded.

Pronounced uterine descent to or through the introitus; prominent cystocele that descends the entire height of the vaginal vault with coughing during speculum examination Prominent, bothersome stress incontinence that has failed to respond to adequate trials of nonsurgical therapy

Anatomic abnormality may underlie the pathophysiology of the incontinence and may require surgical repair.

Straining to begin voiding and a dribbling or intermittent stream when the patient’s bladder feels full Catheter passage impossible or requires considerable force or a larger or more rigid catheter Volume of urine remaining in the bladder within 5 to 10 minutes after the patient voids spontaneously in as normal a fashion as possible More than five red blood cells/high-power field on microscopic examination in the absence of infection After behavioral or drug therapy, or both, incontinence persists and the patient desires further evaluation and treatment.

Bladder neck suspension procedures are generally well tolerated and successful in properly selected elderly women who have stress incontinence that responds poorly to more conservative measures. Signs suggest obstruction or poor bladder contractility.

Anatomic blockage of the urethra or bladder neck may exist. Anatomic or neurogenic obstruction or poor bladder contractility may exist.

A pathologic condition in the urinary tract should be excluded. A formal urodynamic evaluation may help to better define and reproduce the symptoms associated with the patient’s incontinence and target treatment more effectively.

*If medical conditions preclude surgery or the patient is adamantly opposed to considering surgical intervention, the patient should not be referred. † Some patients with lesser degrees of urinary retention may require evaluation, depending on other findings.

mentioned. Garments and pads are a nonspecific treatment. They should not be used as a first response to incontinence or before some type of diagnostic evaluation is done. Many patients are curable if treated with specific therapies, and some have potentially serious factors underlying their incontinence that must be diagnosed and treated. Pants and pads can interfere with attempts at certain types of behaviorally oriented therapies (discussed later). Supportive measures are critical in managing all forms of incontinence and should be used in conjunction with other more specific treatment modalities. A positive attitude, education, environmental manipulations, appropriate use of toilet substitutes, avoidance of iatrogenic contributions to incontinence,

modifications of diuretic and fluid intake patterns, and good skin care are all important. To a large extent the optimal treatment of persistent incontinence depends on identifying the types of incontinence that exists. Table 94-7 outlines the primary treatments used for the basic types of persistent incontinence found among older incontinent women. Each treatment modality is briefly discussed in the following sections. Drug Treatment The efficacy of drug treatment has not been as well studied in the elderly as in younger populations,56,58 but for many patients, especially those with urge or stress incontinence, drug treatment

Chapter 94 LOWER URINARY TRACT DISORDERS IN THE ELDERLY

Table 94-7 Primary Treatments for Different Types of Urinary Incontinence in Elderly Women Type of Incontinence

Primary Treatment

Stress

Pelvic muscle (Kegel) exercises α-Adrenergic agonists Estrogen Biofeedback, bladder training Surgical intervention Bladder relaxants Estrogen topically (if vaginal atrophy is present) Behavioral intervention (e.g., bladder training, biofeedback) Surgical removal of pathologic lesions Surgical removal of obstruction Intermittent catheterization (if practical) Indwelling catheterization Behavioral therapies (e.g., prompted voiding, habit training) Environmental manipulations Incontinence undergarments and pads External collection devices Bladder relaxants (selected patients)† Indwelling catheters (selected patients)‡

Urge

Overflow*

Functional

*Overflow incontinence is no longer a recommended term (since 2002) by the International Continence Society, which favors the terminology of acute or chronic retention of urine.57 † Many patients with functional incontinence also have detrusor hyperreflexia, and some may benefit from bladder relaxant drug therapy. ‡ See Box 94-3.

may be very effective. Drug treatment can be prescribed in conjunction with one or more of the behavioral interventions discussed in the following section. Head-to-head comparisons of drug and behavioral therapy have shown that both are efficacious for treatment of urinary incontinence,59 and in practice. they often complement each other. Treatment decisions should be made on an individual basis and depend in a large part on the characteristics and preferences of the patient and the physician. For urge incontinence, drugs with anticholinergic and bladder smooth muscle–relaxing properties are used. All of them may cause bothersome systemic anticholinergic side effects, especially dry mouth, in the elderly, and they can precipitate urinary retention in some patients. The advantages of extended-release preparations (e.g., tolterodine LA, oxybutynin XL, oxybutynin transdermal) and newer drugs (e.g., trospium, darifenacin, solefenacin) for overactive bladder over older, cheaper, immediaterelease oxybutynin are more favorable side effect profiles (but no more efficacy). In animal models, these agents demonstrate more selectivity for the bladder than for the salivary glands, but some insist that the tolerability and effectiveness of agents are related to their antimuscarinic activity. Although use of immediaterelease oxybutynin in older patients who are tolerant of side effects is possible, consensus guidelines recommend against immediate-release oxybutynin.60 One newer agent, tolterodine, has been shown to have a slight decrease in efficacy and no decline in tolerability.61

The potential for severe anticholinergic side effects is much more likely in older adults than in younger adults. Patients with Alzheimer’s disease must be followed for the development of drug-induced delirium. Patients with cognitive impairment may be taking cholinesterase-inhibitor agents (i.e., medications for dementia that offer small gains in cognition and slower rates of cognitive decline). The potential interaction can be clinically evident at times; patients may have a worsening of their cognition with bladder relaxants (i.e., anticholinergic effect)13 or may have a worsening in their continence with acetylcholinesterase inhibitors (i.e., procholinergic effects). Research has shown that receptor targeting or properties that prevent a drug from crossing the blood-brain barrier may be important considerations in whether a medication will have effects on cognition. One study using darifenacin demonstrated in 129 nondemented patients that active drug did not have any significantly greater effect on cognition compared with placebo.62 Drugs specifically indicated for use in urinary incontinence or overactive bladder likely offer some advantage over other drugs with more pronounced systemic anticholinergic side effects.63 Several studies suggest that cognitive and physical functional impairments are associated with poor responses to bladder-relaxant drug therapy.64-66 The results of these studies should not preclude a treatment trial in this patient population. Some patients may respond, especially in conjunction with scheduled toileting or prompted voiding. The goal of treatment in these patients may not be to cure the incontinence but to reduce its severity and prevent discomfort and complications. For stress incontinence, drug treatment involves a combination of an α-adrenergic agonist, duloxetine67 (approved in Europe but not in the United States for treatment of stress incontinence), a selective serotonin reuptake inhibitor (SSRI) medication used in the treatment of depression, or topically applied estrogen, or both. Drug treatment is appropriate for motivated patients who have mild to moderate degrees of stress incontinence, do not have a major anatomic abnormality (e.g., large cystocele), and do not have any contraindications to these drugs. Although there are few published data on duloxetine in older patients, its inclusion here is merited because of the dearth of other medications for the treatment of stress urinary incontinence. Duloxetine generally enhances urine storage by facilitating the vesical sympathetic reflex pathway and inhibiting the parasympathetic voiding pathway. Duloxetine has been shown to increase significantly bladder capacity and sphincter tone without interfering with the normal voiding cycle. Duloxetine has also been evaluated for depression and lower urinary tract disease.67 α-Agonist medications that may be given for stress urinary incontinence have an effect on hypertension. The most commonly used over-the-counter medication previously used for stress urinary incontinence was phenylpropanolamine, which was removed from the market in 2000 because it was shown in women to be highly associated with intracranial hemorrhage when used as a dietary aid, which leaves pseudoephedrine as the over-the-counter agent. Pseudoephedrine may exacerbate hypertension and contribute to insomnia in some older patients. These patients may also respond to behavioral treatments (discussed later), and some data suggest that the two treatment modalities are roughly equivalent, with about three fourths of patients reporting improvement.68 A combination of these modalities can be a reasonable approach for some patients. Estrogen alone is not as effective as it is in combination with an α-agonist for stress incontinence. Estrogen is also used

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chronically or intermittently (i.e., 1- to 2-month courses) for the treatment of overactive bladder symptoms and urge incontinence in women with atrophic vaginitis and urethritis. Given that lack of estrogen results in conditions that make urinary incontinence more likely, several studies have examined estrogen as a preventive agent or therapy for urinary incontinence. In a large study of more than 20,000 women, oral estrogens (0.625 mg of conjugated equine estrogen, with and without progesterone) were shown to increase the risk of developing urinary incontinence at 1 year. Among women who were incontinent, estrogen treatment worsened the frequency of urinary incontinence.1 Despite the pessimism about using oral estrogens, there may still be a role for topical estrogen. Its administration has been shown to yield significant improvements in colposcopic findings, statistically significant increases in mean maximum urethral pressure and mean urethral closure pressure, and improvements in the abdominal pressure transmission ratio to the proximal urethra. The continence outcomes are less well understood.69 It is not possible to infer that because low estrogen levels are associated with physiologic changes, hormone replacement will reverse these changes, restore function, or reduce symptoms. Drug treatment for chronic overflow incontinence using a cholinergic agonist or an α-adrenergic antagonist is usually not effective, although anecdotal reports suggest α-blockers may be useful in some female patients. Bethanechol may be helpful when given for a brief period subcutaneously in patients with persistent

bladder contractility problems after an overdistention injury, but it is generally not effective when given orally over the long term.70 Symptomatically and urodynamically, many elderly women have a combination of urge and stress incontinence. In theory, a combination of estrogen and imipramine may be appropriate for these patients because imipramine has both anticholinergic and α-adrenergic effects. When urge incontinence is the predominant symptom, a combination of estrogen and oxybutynin would be appropriate. Behavioral interventions are also a reasonable approach to women with mixed incontinence. Behavioral Interventions Many types of behavioral procedures have been described for the management of urge and stress urinary incontinence.71,72 The nosology of these procedures has been somewhat confusing, and in much of the literature, the term bladder training is used to encompass a wide variety of techniques. It is important to distinguish between procedures that are patient dependent (i.e., require adequate function and motivation of the patient), in which the goal is to restore a normal pattern of voiding and continence, and procedures that are caregiver dependent and can be used for functionally disabled patients, in which the goal is to keep the patient and environment dry (Table 94-8). Pelvic muscle (Kegel) exercises consist of repetitive contractions of the pelvic floor muscles. This procedure is taught by having the patient interrupt voiding. This technique should be

Table 94-8 Behavioral Interventions for Urinary Incontinence in Elderly Women Procedure Patient dependent Pelvic muscle (Kegel) exercises Biofeedback

Bladder training

Bladder retraining

Caregiver dependent Scheduled toileting

Definition

Types of Incontinence

Comments

Repetitive contraction of pelvic floor muscles Use of bladder, rectal, or vaginal pressure recordings to train patients to contract pelvic floor muscles and relax bladder Use of educational components of biofeedback, bladder records, pelvic muscle, and other behavioral exercises Progressive lengthening or shortening of intervoiding interval, with adjunctive techniques* Intermittent catheterization used in patients recovering from overdistention injuries with persistent retention

Stress Stress and urge

Requires adequate function and motivation Requires equipment and trained personnel

Stress and urge

Requires trained therapist, adequate cognitive and physical function, and patient motivation Goal is to restore normal pattern of voiding and continence; requires adequate cognitive and physical function and patient motivation

Fixed toileting schedule

Prompted voiding

Regular opportunities to toilet with behavioral reinforcement

Habit training

Toileting based on established individual pattern with behavioral reinforcement

Acute (e.g., postcatheterization with urge or overflow, poststroke)

Urge and functional

Goal is to prevent wetting episodes Can be used in patients with impaired cognitive or physical functioning Requires staff or caregiver availability and patient motivation

*Techniques to trigger voiding (e.g., running water, stroking thigh, suprapubic tapping), completely emptying the bladder (e.g., bending forward, suprapubic pressure), and alterations of fluid or diuretic intake patterns may be helpful for some patients.

Chapter 94 LOWER URINARY TRACT DISORDERS IN THE ELDERLY

used only to identify the proper muscles, and patients should be discouraged from doing this repeatedly because of the potential risk of teaching patients dysfunctional voiding habits. To get a sense of the muscles used, the patient is asked to squeeze the examiner’s fingers during a vaginal examination (without doing a Valsalva maneuver, which is the opposite of the intended effect). One exercise consists of a several-second squeeze and a severalsecond relaxation. Once learned, the exercises should be practiced many times throughout the day (usually 75 exercises per day, broken down into three sessions of 25 exercises each), and they should be used in everyday life during situations (e.g., coughing, running water) in a variety of positions (e.g., sitting, standing, lying down) that can precipitate incontinence. Pelvic muscle exercises may be taught in conjunction with biofeedback procedures and can be especially helpful for women who bear down (i.e., increasing intra-abdominal pressure) when they attempt to contract the pelvic floor muscles. Vaginal cones (weights) may be useful adjuncts to pelvic muscle exercises in some patients. Biofeedback procedures involve the use of bladder, rectal, or vaginal pressure or electrical activity recordings to train patients to contract the pelvic floor muscles and relax the bladder. Studies have shown that these techniques can be very effective for managing stress and urge incontinence, even in the elderly.73 The use of biofeedback techniques may be limited by requirements for equipment and trained personnel; some of these techniques are relatively invasive and require the use of bladder or rectal catheters, or both. Some newer biofeedback techniques use surface electrodes and are less invasive. Electrical stimulation vaginally or rectally has also been used in the management of stress and urge incontinence. Research suggests that excellent results can be achieved in some older women in treating stress and urge incontinence without the use of electrical stimulation or computer-assisted biofeedback.74,75 In contrast to medication therapy, the degree of continence achieved with pelvic muscle exercises is not as highly correlated with an increase in bladder capacity.76 Other forms of patient-dependent training procedures include various forms of bladder training and bladder retraining. Bladder training procedures involve the educational components taught during biofeedback but not the use of biofeedback equipment. Patients are taught how to do pelvic muscle exercises, provided strategies for managing urgency, and instructed to regularly use bladder records. These techniques are highly effective in selected community-dwelling patients, especially women.77 Investigators have attempted to identify baseline characteristics that predict clinical success with behavioral techniques. It is probably more important to discuss factors that do not predict worse outcomes: greater age, greater parity, lower levels of education, and previous surgery (the latter two may actually predict greater success).78 The goal of caregiver-dependent behavioral interventions, such as prompted voiding and habit training, is to prevent incontinence episodes rather than restore the normal pattern of voiding and complete continence. These procedures have been shown to be effective in reducing incontinence in selected nursing home residents. In its simplest form, scheduled toileting involves toileting the patient at regular intervals, usually every 2 hours during the day and every 4 hours during the evening and night. Habit training involves a schedule of toiletings or prompted voidings that is modified according to the patient’s pattern of continent voids and incontinence episodes as demonstrated by a monitoring record. Positive reinforcement is offered for continent voids

and neutral reinforcement when incontinence occurs. Adjunctive techniques to prompt voiding (e.g., running tap water, stroking the inner thigh, suprapubic tapping) and to help empty the bladder completely (e.g., bending forward after completion of voiding) may be helpful for some patients. Prompted voiding has been the best studied of these procedures. It is a simple behavioral procedure that combines several of the elements mentioned earlier.79 The success of these procedures is largely dependent on the knowledge and motivation of the caregivers implementing them, rather than on the physical functional and mental status of the incontinent patient. These techniques are not feasible in home settings without available caregivers. For these types of procedures to be feasible and cost-effective in the nursing home setting, the amount of time generally spent by the nursing staff in changing patients after incontinence episodes should not be exceeded by the time and effort needed to implement such training procedures. Targeting these procedures to selected patients, such as those with less frequent voiding and larger bladder capacities or voided volumes, may enhance their cost-effectiveness.79 Quality assurance methods, based on principles of statistical quality control used in industry, have been shown to be helpful in maintaining the effectiveness of prompted voiding in nursing homes.80 Surgery Surgical interventions are described in detail in other chapters in this textbook. Surgery should be considered for elderly women with stress incontinence that continues to be bothersome after attempts at nonsurgical treatment have been made and in women with a significant degree of pelvic prolapse or intrinsic urethral dysfunction. As with many other surgical procedures, patient selection and the experience of the surgeon are critical to success. Several case series have demonstrated that with proper patient selection, even elderly adults can successfully undergo surgery, but the number of overall incontinence procedures in older women remains low. All women being considered for surgical therapy should have a thorough evaluation, including urodynamic tests, before undergoing the procedure. Women with mixed stress incontinence and detrusor motor instability may also benefit from surgery, especially if the clinical history and urodynamic findings suggest that stress incontinence is the predominant problem. Modified techniques of bladder neck suspension can be done with minimal risk and are highly successful in achieving continence, even in the elderly. Urinary retention can occur after surgery, but it is usually transient and can be managed by intermittent catheterization. Injection of bulking agents appears to be effective in older women, and age does not appear to correlate with outcomes.81 This procedure may be especially helpful for frail older women who have stress or mixed incontinence that has not responded to behavioral or drug therapy. Catheters and Catheter Care Three basic types of catheters and catheterization procedures are used for the management of urinary incontinence: external catheters, intermittent straight catheterization, and chronic indwelling catheterization. An external catheter for use in women is commercially available, but its safety and effectiveness have not been well documented in the elderly. Intermittent catheterization can help in the management of patients with urinary retention and overflow incontinence. The procedure can be carried out by the patient or a caregiver, and it involves straight catheterization two to four times daily, depending on residual urine volume. In

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Box 94-3 Indications for and Principles of Chronic Indwelling Catheter Use Indications 1. Urinary retention that Is causing persistent overflow incontinence, symptomatic infections, or renal dysfunction Cannot be corrected surgically or medically Cannot be managed practically with intermittent catheterization 2. Skin wounds, pressure sores, or irritations that are being contaminated by incontinent urine 3. Care of terminally ill or severely impaired patients for whom bed and clothing changes are uncomfortable or disruptive 4. Preference of patient or caregiver when patient has failed to respond to more specific treatments Catheter Care 1. Maintain sterile, closed, gravity drainage system; change the catheter every 4 to 8 weeks. 2. Avoid breaking the closed system. 3. Use clean techniques in emptying and changing the drainage system; wash hands between patients in institutionalized settings. 4. Secure the catheter to the upper thigh or lower abdomen to avoid perineal contamination and urethral irritation due to movement of the catheter.

the home, the catheter should be kept clean (but not necessarily sterile). Studies conducted largely among younger paraplegics have shown that this technique is practical and reduces the risk of symptomatic infection compared with chronic catheterization. Self-intermittent catheterization has been shown to be feasible for elderly women outpatients who are functional and are willing and able to catheterize themselves.82 However, studies carried out in young paraplegics and elderly female outpatients cannot automatically be extrapolated to frail elderly women or the institutionalized population. The technique may be useful in certain patients in acute care hospitals or nursing homes, such as those who have undergone bladder neck suspension, or in certain situations, such as after removal of an indwelling catheter in a bladder-retraining protocol. Nursing home residents, however, may be difficult to catheterize, and the anatomic abnormalities commonly found in elderly patients’ lower urinary tracts may increase the risk of infection because of repeated straight cathe-

5. Avoid frequent and vigorous cleaning of the catheter entry site; washing with soapy water once each day is sufficient. 6. Do not irrigate routinely. 7. If bypassing occurs in the absence of obstruction, consider the possibility of a bladder spasm, which can be treated with a bladder relaxant. 8. If catheter obstruction occurs frequently, increase the patient’s fluid intake and acidify the urine if possible. 9. Do not routinely use prophylactic or suppressive urinary antiseptics or antimicrobials. 10. Do not perform routine surveillance cultures to guide management of individual patients because all chronically catheterized patients have bacteriuria (which is often polymicrobial), and the organisms change frequently. 11. Do not treat infection unless the patient develops symptoms; symptoms may be nonspecific, and other possible sources of infection should be carefully excluded before attributing symptoms to the urinary tract. 12. If a patient develops frequent symptomatic urinary tract infections, a genitourinary evaluation should be considered to rule out pathology such as stones, periurethral or prostatic abscesses, or chronic pyelonephritis.

terizations. Use of this technique in an institutional setting (which may have an abundance of organisms that are relatively resistant to many commonly used antimicrobial agents) may yield an unacceptable risk of nosocomial infections, and the use of sterile catheter trays for these procedures would be very expensive. It therefore may be extremely difficult to implement such a program in a typical nursing home setting. Chronic indwelling catheterization is overused in some settings, and when used for periods of up to 10 years, it has been shown to increase the incidence of a number of other complications, including chronic bacteriuria, bladder stones, periurethral abscesses, and even bladder cancer. Elderly female nursing home residents managed by this technique are at relatively high risk for developing symptomatic infections.83 Given these risks, it seems appropriate to recommend limiting the use of chronic indwelling catheters to certain specific situations and to follow sound principles of catheter care when using indwelling catheterization to attempt to minimize complications (Box 94-3).

References 1. Hendrix SL, Cochrane BB, Nygaard IE, et al: Effects of estrogen with and without progestin on urinary incontinence [see comment]. JAMA 293:935-948, 2005. 2. Brocklehurst JC, Dillane JB: Studies of the female bladder in old age. I. Cystometrograms in non-incontinent women. Gerontol Clin 8:285-305, 1966. 3. Jones KW, Schoenberg HW: Comparison of the incidence of bladder hyperreflexia in patients with benign prostatic hypertrophy and agematched female controls. J Urol 133:425-426, 1985. 4. Diokno AC, Brown MB, Brock BM, et al: Clinical and cystometric characteristics of continent and incontinent noninstitutionalized elderly. J Urol 140:567-571, 1988.

5. Elbadawi A, Yalla SV, Resnick NM: Structural basis of geriatric voiding dysfunction. I. Methods of a prospective ultrastructural/ urodynamic study and an overview of the findings. J Urol 150(Pt 2): 1650-1656, 1993. 6. Elbadawi A, Yalla SV, Resnick NM: Structural basis of geriatric voiding dysfunction. III. Detrusor overactivity. J Urol 150(Pt 2): 1668-1680, 1993. 7. Elbadawi A, Hailemariam S, Yalla SV, Resnick NM: Structural basis of geriatric voiding dysfunction. VI. Validation and update of diagnostic criteria in 71 detrusor biopsies. J Urol 157:1802-1913, 1997. 8. Edwards L, Malvern J: The urethral pressure profile: Theoretical considerations and clinical application. British J Urol 46:325-335, 1974.

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9. Hendriksson L, Andersson KE, Ulmsten U: The urethral pressure profiles in continent and stress-incontinent women. Scand J Urol Nephrol 13:5-10, 1979. 10. Brocklehurst JC: The bladder. In Brocklehurst J (ed): Textbook of Geriatric Medicine and Gerontology. New York, Churchill Livingstone, 1992, pp 629-646. 11. Strasser H, Tiefenthaler M, Steinlechner M, et al: Urinary incontinence in the elderly and age-dependent apoptosis of rhabdosphincter cells [see comment]. Lancet 354:918-919, 1999. 12. McGuire EJ: Urinary dysfunction in the aged: Neurological considerations. Bull N Y Acad Med 56:275-284, 1980. 13. Tsao JW, Heilman KM: Transient memory impairment and hallucinations associated with tolterodine use. N Engl J Med 349:22742275, 2003. 14. Griebling TL: Urologic diseases in America project: Trends in resource use for urinary tract infections in women [see comment]. J Urol 173:1281-1287, 2005. 15. Yip SK, Fung K, Pang MW, et al: A study of female urinary tract infection caused by urodynamic investigation. Am J Obstet Gynecol 190:1234-1240, 2004. 16. Romano JM, Kaye D: UTI in the elderly: Common yet atypical. Geriatrics 36:113-115, 1981. 17. Akhtar AJ, Andrews G, Cairo F, et al: Urinary tract infection in the elderly: A population study. Age Ageing 1:48, 1972. 18. Brocklehurst JC, Dillane JB, Griffiths L, Fry J: The prevalence and symptomatology of urinary infection in an aged population. Gerontol Clin 10:242-253, 1968. 19. Brocklehurst JC, Fry J, Griffiths LL, Kalton G: Dysuria in old age. J Am Geriatr Soc 19:582-592, 1971. 20. Brocklehurst JC, Bee P, Jones D, Palmer MK: Bacteriuria in geriatric hospital patients its correlates and management. Age Ageing 6:240245, 1977. 21. Garibaldi RA, Brodine S, Matsumiya S: Infections among patients in nursing homes: Policies, prevalence, problems. N Engl J Med 305:731-735, 1981. 22. Gladstone JL, Friedman SA: Bacteriuria in the aged: A study of its prevalence and predisposing lesions in a chronically ill population. J Urol 106:745-749, 1971. 23. Jewett MA, Fernie GR, Holliday PJ, Pim ME: Urinary dysfunction in a geriatric long-term care population: Prevalence and patterns. J Am Geriatr Soc 29:211-214, 1981. 24. Sourander LB, Kasanen A: A 5-year follow-up of bacteriuria in the aged. Gerontol Clin 14:274-281, 1972. 25. Boscia JA, Kobasa WD, Knight RA, et al: Epidemiology of bacteriuria in an elderly ambulatory population. Am J Med 80:208-214, 1986. 26. Abrutyn E, Mossey J, Levison M, et al: Epidemiology of asymptomatic bacteriuria in elderly women. J Am Geriatr Soc 39:388-393, 1991. 27. Sobel JD, Kaye D: Host factors in the pathogenesis of urinary tract infections. Am J Med 76:122-130, 1984. 28. Hu KK, Boyko EJ, Scholes D, et al: Risk factors for urinary tract infections in postmenopausal women. Arch Intern Med 164:989993, 2004. 29. Moore-Smith B: Bacteriuria in elderly women. Lancet 2:827, 1972. 30. Dontas AS, Kasviki-Charvati P, Papanayiotou PC, Marketos SG: Bacteriuria and survival in old age. N Engl J Med 304:939-943, 1981. 31. Nordenstam GR, Brandberg CA, Oden AS, et al: Bacteriuria and mortality in an elderly population. N Engl J Med 314:1152-1156, 1986. 32. Nicolle LE, Mayhew WJ, Bryan L: Prospective randomized comparison of therapy and no therapy for asymptomatic bacteriuria in institutionalized elderly women. Am J Med 83:27-33, 1987. 33. Boscia JA, Kobasa WD, Knight RA, et al: Therapy vs no therapy for bacteriuria in elderly ambulatory nonhospitalized women. JAMA 257:1067-1071, 1987.

34. Nicolle LE, Bradley S, Colgan R, et al: Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin Infect Dis;40:643-654, 2005. 35. Warren JW, Abrutyn E, Hebel JR, et al: Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women. Infectious Diseases Society of America (IDSA). Clin Infect Dis 29:745-758, 1999. 36. Stamey TA, Condy M, Mihara G: Prophylactic efficacy of nitrofurantoin macrocrystals and trimethoprim-sulfamethoxazole in urinary infections. Biologic effects on the vaginal and rectal flora. N Engl J Med 296:780-783, 1977. 37. Stamm WE, McKevitt M, Counts GW, et al: Is antimicrobial prophylaxis of urinary tract infections cost effective? Ann Intern Med 94:251-255, 1981. 38. Melville JL, Katon W, Delaney K, Newton K: Urinary incontinence in US women: A population-based study. Arch Intern Med 165:537542, 2005. 39. Thom DH, Nygaard IE, Calhoun EA: Urologic diseases in America project: Urinary incontinence in women-national trends in hospitalizations, office visits, treatment and economic impact [see comment]. J Urol 173:1295-1301, 2005. 40. Grodstein F, Fretts R, Lifford K, et al: Association of age, race, and obstetric history with urinary symptoms among women in the Nurses’ Health Study. Am J Obstet Gynecol 189:428-434, 2003. 41. Rortveit G, Hannestad YS, Daltveit AK, Hunskaar S: Age- and typedependent effects of parity on urinary incontinence: The Norwegian EPINCONT study. Obstet Gynecol 98:1004-1010, 2001. 42. Ouslander JG, Abelson S: Perceptions of urinary incontinence among elderly outpatients. Gerontologist 30:369-372, 1990. 43. Hu TW: Impact of urinary incontinence on health-care costs. J Am Geriatr Soc 38:292-295, 1990. 44. Diokno AC, Sampselle CM, Herzog AR, et al: Prevention of urinary incontinence by behavioral modification program: A randomized, controlled trial among older women in the community. J Urol 171:1165-1171, 2004. 45. Ouslander JG: Geriatric urinary incontinence. Dis Mon 38:65-149, 1992. 46. Ouslander JG, Hepps K, Raz S, Su HL: Genitourinary dysfunction in a geriatric outpatient population. J Am Geriatr Soc 34:507-514, 1986. 47. Wells TJ, Brink CA, Diokno AC: Urinary incontinence in elderly women: Clinical findings. J Am Geriatr Soc 35:933-939, 1987. 48. Diokno AC, Wells TJ, Brink CA: Urinary incontinence in elderly women: Urodynamic evaluation. J Am Geriatr Soc 35:940-946, 1987. 49. Jackson RA, Vittinghoff E, Kanaya AM, et al: Urinary incontinence in elderly women: Findings from the Health, Aging, and Body Composition Study. Obstet Gynecol 104:301-307, 2004. 50. Ouslander J, Leach G, Staskin D, et al: Prospective evaluation of an assessment strategy for geriatric urinary incontinence. J Am Geriatr Soc 37:715-724, 1989. 51. Resnick NM, Yalla SV, Laurino E: The pathophysiology of urinary incontinence among institutionalized elderly persons [see comment]. N Engl J Med 320:1-7, 1989. 52. Pannill FC 3rd, Williams TF, Davis R: Evaluation and treatment of urinary incontinence in long term care. J Am Geriatr Soc 36:902910, 1988. 53. Resnick NM, Yalla SV: Detrusor hyperactivity with impaired contractile function. An unrecognized but common cause of incontinence in elderly patients. JAMA 257:3076-3081, 1987. 54. Fantl JA, Wyman JF, McClish DK, Bump RC: Urinary incontinence in community-dwelling women: Clinical, urodynamic, and severity characteristics. Am J Obstet Gynecol 162:946-951; discussion 951952, 1990. 55. Ouslander JG, Leach GE, Staskin DR: Simplified tests of lower urinary tract function in the evaluation of geriatric urinary incontinence. J Am Geriatr Soc 37:706-714, 1989.

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56. Ouslander JG, Sier HC: Drug therapy for geriatric urinary incontinence. Clin Geriatr Med 2:789-807, 1986. 57. Abrams P, Cardozo L, Fall M, et al: The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 21:167-178, 2002. 58. Agency for Health Care Policy and Research: Urinary incontinence in adults. Clin Pract Guidel Quick Ref Guide Clin (2)QR1-27, 1992. 59. Burgio KL, Locher JL, Goode PS, et al: Behavioral vs drug treatment for urge urinary incontinence in older women: A randomized controlled trial [see comment]. JAMA 280:1995-2000, 1998. 60. Fick DM, Cooper JW, Wade WE, et al: Updating the Beers criteria for potentially inappropriate medication use in older adults: results of a US consensus panel of experts [see comment] [erratum appears in Arch Intern Med 164:298, 2004]. Arch Intern Med 163:27162724, 2003. 61. Michel MC, Schneider T, Krege S, Goepel M: Does gender or age affect the efficacy and safety of tolterodine? J Urol 168:1027-1031, 2002. 62. Lipton RB, Kolodner K, Wesnes K: Assessment of cognitive function of the elderly population: Effects of darifenacin. J Urol 173:493-498, 2005. 63. Ouslander JG, Blaustein J, Connor A, et al: Pharmacokinetics and clinical effects of oxybutynin in geriatric patients. J Urol 140:47-50, 1988. 64. Castleden CM, Duffin HM, Asher MJ, Yeomanson CW: Factors influencing outcome in elderly patients with urinary incontinence and detrusor instability. Age Ageing 14:303-307, 1985. 65. Zorzitto ML, Jewett MAS, Fernie GR, et al: Effectiveness of propantheline bromide in the treatment of geriatric patients with detrusor instability. Neurourol Urodyn 5:133, 1986. 66. Tobin GW, Brocklehurst JC: The management of urinary incontinence in local authority residential homes for the elderly. Age Ageing 15:292-298, 1986. 67. Yoshimura N, Chancellor MB: Current and future pharmacological treatment for overactive bladder. J Urol 168:1897-1913, 2002. 68. Wells TJ, Brink CA, Diokno AC, et al: Pelvic muscle exercise for stress urinary incontinence in elderly women. J Am Geriatr Soc 39:785-791, 1991. 69. Dessole S, Rubattu G, Ambrosini G, et al: Efficacy of low-dose intravaginal estriol on urogenital aging in postmenopausal women [see comment]. Menopause 11:49-56, 2004.

70. Finkbeiner AE: Is bethanechol chloride clinically effective in promoting bladder emptying? A literature review. J Urol 134:443-449, 1985. 71. Burgio KL, Burgio LD: Behavior therapies for urinary incontinence in the elderly. Clin Geriatr Med 2:809-827, 1986. 72. Hadley EC: Bladder training and related therapies for urinary incontinence in older people. JAMA 256:372-379, 1986. 73. Burgio KL, Whitehead WE, Engel BT: Urinary incontinence in the elderly. Bladder-sphincter biofeedback and toileting skills training. Ann Intern Med 103:507-515, 1985. 74. Goode PS, Burgio KL, Locher JL, et al: Effect of behavioral training with or without pelvic floor electrical stimulation on stress incontinence in women: A randomized controlled trial [see comment]. JAMA 290:345-352, 2003. 75. Burgio KL, Goode PS, Locher JL, et al: Behavioral training with and without biofeedback in the treatment of urge incontinence in older women: A randomized controlled trial [see comment]. JAMA 288:2293-2299, 2002. 76. Goode PS, Burgio KL, Locher JL, et al: Urodynamic changes associated with behavioral and drug treatment of urge incontinence in older women. J Am Geriatr Soc 50:808-816, 2002. 77. Fantl JA, Wyman JF, McClish DK, et al: Efficacy of bladder training in older women with urinary incontinence. JAMA 265:609-613, 1991. 78. Burgio KL, Goode PS, Locher JL, et al: Predictors of outcome in the behavioral treatment of urinary incontinence in women. Obstet Gynecol 102(Pt 1):940-947, 2003. 79. Schnelle JF: Managing Urinary Incontinence in the Elderly. New York, Springer-Verlag, 1991. 80. Schnelle JF, Newman D, White M, et al: Maintaining continence in nursing home residents through the application of industrial quality control. Gerontologist 33:114-121, 1993. 81. Griebling T: Geriatric urology. In: Solomon DH, LoCicero J 3rd, Rosenthal RA, eds. New Frontiers in Geriatrics Research: An Agenda for Surgical and Related Medical Specialties. New York, American Geriatrics Society, 2004, pp 269-302. 82. Bennett CJ, Diokno AC: Clean intermittent self-catheterization in the elderly. Urology 24:43-45, 1984. 83. Warren JW, Damron D, Tenney JH, et al: Fever, bacteremia, and death as complications of bacteriuria in women with long-term urethral catheters. J Infect Dis 155:1151-1158, 1987.

Chapter 95

URODYNAMICS EVALUATION IN THE ELDERLY Pat O’Donnell Urodynamic studies are the most comprehensive objective clinical measures of bladder and urethra function available for the clinical evaluation of elderly women with urinary incontinence or any other voiding dysfunction. Although urodynamic studies have many limitations, the clinical information derived from these studies is invaluable for making reasonable long-term management decisions in the treatment of urinary incontinence in older women. Comprehensive urodynamic studies are accepted well by older women, and discomfort or complications related to the studies do not preclude performing studies, even in frail elderly women. Elderly incontinent women represent a group of patients who derive the most clinical benefit from urodynamic studies because of the complexity of voiding dysfunctions in this patient population and the impact that these voiding dysfunctions have on the quality of life in older women. Although the consequences of urinary incontinence in younger women are debilitating and life changing, it is primarily the elderly women who are placed in nursing homes because of it. Urodynamic studies represent a diagnostic evaluation available that has the potential to change the outcome of long-term incontinence therapy in older women. Successful treatment of voiding dysfunctions in older women has a profound impact on the quality of life of these patients, which emphasizes the importance of the diagnostic clinical information from urodynamic studies. Urodynamic studies provide the clinician with a basic understanding of the pathophysiology of the complex condition of incontinence in older women. The clinical value of urodynamic studies in elderly women reflects the magnitude of the problem of incontinence in this patient population. The incidence of incontinence is higher among older women than younger women. The personal impact of urinary incontinence on quality of life is so powerful that it can potentially take an older woman away from her home in a community-dwelling environment to the chronic-care environment of a nursing home. The life-changing consequences of incontinence are so great that aggressive evaluation should be considered as an initial part of management of these older patients. Changes in the bladder and urethral function, along with the changes in physical and mental function, that are associated with aging significantly complicate the diagnosis and management of incontinence in older women. Although voiding dysfunctions in this group represent a survival risk related to complications such as urinary tract infections or hip fractures associated with nocturia and urge urinary incontinence, the most common reasons to consider initial comprehensive urodynamic studies in elderly women are the quality-of-life concerns of the patient about activities that matter most in her daily life. These are the activities she needs to do each day to care for herself and the activities that she enjoys and that make life worthwhile. The long-term choices about evaluation and management are personal decisions by the individual patient that are based on the information provided to

her by the physician, the recommendations made to her by the physician, and how she chooses to use that information to live the rest of her life the best way possible. The diagnostic information provided by urodynamic studies is necessary for the physician to counsel the patient about the many decisions that she must make over time regarding the long-term management of her bladder symptoms. The mental functional status and physical functional status of an elderly individual determine to some extent to how she can participate in the choices about evaluation and therapy. The choices may be different if an elderly woman is in a communitydwelling, assisted-living, or chronic-care environment. The availability of family support is important in decisions about urodynamic studies and long-term management of urinary incontinence. If family members and the patient understand the value of urodynamic studies in clinical management decisions, the patient can commit to maximum personal participation in the procedure. The commitment by the patient and her family to the choice that she makes about comprehensive evaluation and long-term therapy is an essential component of the quality of the urodynamic studies and the clinical value of the information provided by the studies for the physician. Occasionally, family members of older women may have unrealistic expectations about treatment outcomes. The patient also may have treatment expectations that are not realistic. This situation is even more difficult for the physician when the family or the patient does not have a commitment to working through complications of therapy or treatment failure. In these circumstances, the urodynamic studies can be very helpful in providing objective information about the complexity of the clinical problem that can be communicated to the patient and her family. Urodynamic studies provide objective clinical information that allows realistic expectations about therapy and provide a basis for a personal commitment to therapy that needs to be made by the patient and her family. Urodynamic studies help the physician advise an older woman about her condition, explain the treatment choices that are reasonable, and help her to understand the possible treatment outcomes so that her expectations are realistic and she can become an active participant with the physician in the long-term management process. Because of the complexity of incontinence in older women, the partnership between the physician and the patient in the long-term management of urinary incontinence is an extremely important relationship. Complex urodynamic studies that are well performed have a positive impact on the relationship between the physician and the elderly patient. As a result, the physician is better able to recommend a practical approach to therapy, and the patient can become a confident partner in a process that is usually a long-term relationship. Urinary incontinence in older women rarely has a single therapeutic modality that results in complete resolution of bladder problems. Instead, voiding dysfunctions in older women usually require long-term 961

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treatment with a therapeutic goal of decreasing the severity of symptoms over time. Therapeutic choices and periodic changes in treatment need to be based on the best urodynamic studies available. Repeating the urodynamic studies during long-term management of older women can be valuable to the physician in altering the course of therapy. URODYNAMICS LABORATORY A laboratory for urodynamic evaluation of incontinence in elderly women needs to have the highest diagnostic capabilities possible and to be a very comfortable and congenial experience for the patient. The ambience of a urodynamics laboratory for older women is one of the most important aspects of the evaluation. Because the performance of the measurements alters the very functions that are being measured, the environment needs to feel as much like home to the patient as possible to minimize the measurement effect on the study results. A comfortable environment can make it possible for an older woman to be an active participant in the studies, and it enables the study results to provide the best possible information about her bladder and urethral function relative to symptoms experienced during her daily life. Another important aspect of the urodynamics laboratory is the relationship between the urodynamicist and the patient. Scheduling extra time in the laboratory before the studies is helpful in developing a personal relationship that is nurturing and congenial to minimize any feelings of fear and anxiety that the older patient may experience during the studies. Older women are often more difficult to engage in active participation in the studies than younger women. Because the complexity of bladder dysfunctions and functional impairment is greater in older women compared with younger women, the studies are considerably more difficult to perform and usually require more time to complete. When performing urodynamic studies in older women, the urodynamicist sometimes may feel like a flight attendant who says, “In the event of a sudden loss in cabin pressure, place the oxygen mask over your nose and mouth and breathe normally.” It is not likely that anyone would breathe normally under those conditions. Although it is necessary to recognize the artificial conditions of the urodynamics laboratory, the goal is to create an environment and testing experience that allows the measured behavior of the bladder in elderly women to be as normal as possible. It is one of the primary objectives during testing of older women to minimize the measurement effects of the urodynamic studies on normal bladder and urethral function. Comprehensive urodynamic studies in older women are not like an electrocardiogram of the bladder in the way the studies are performed and interpreted. Much of the information required for interpretation of urodynamic studies is recorded by the urodynamicist as the studies are being done by describing events and sensations experienced by the older patient. The training and experience of the urodynamicist is an integral part of the diagnostic capabilities of the urodynamics laboratory. The symptoms experienced by the older woman are less predictive of urodynamic findings than those in younger women.1 The voiding history and physical examination do not provide enough clinical information to make decisions about treatment in older women without the additional information provided by urodynamic studies. However, the urodynamicist needs to know

the clinical history and the observations made on physical examination to perform the best studies possible for the patient. Because urodynamic studies are more difficult to perform in older women and the results are so important in clinical management decisions for these patients, measurements often need to be repeated during the initial testing procedure to ensure that the clinical information provided is as complete and accurate as possible. It is a goal of the urodynamicist to duplicate the clinical symptoms described by the patient in the urodynamics laboratory. However, the symptoms experienced during the daily life of an older woman often do not occur during the urodynamic studies. In the elderly population, another approach to evaluation may be necessary. If the clinician can identify the symptoms experienced by the patient during her daily activities as completely and thoroughly as possible, the urodynamic studies can be used to better understand why she experiences those symptoms and what can be done to treat the symptoms based on the information provided by the studies. The diagnostic capabilities of the urodynamic testing equipment are frequently a concern of the physician. Physicians do not want to be limited in their diagnostic capabilities by the limitations of the equipment in the urodynamics laboratory. Although midlevel equipment from most manufacturers can provide the basic information needed for most patients, higher-level equipment is preferred for elderly women because of the complexity of the clinical problems. However, the most expensive equipment does not ensure high-quality studies. The ambience of the laboratory and the skill of the urodynamicist are as important as the capabilities of the equipment. Because elderly women usually have more complex voiding dysfunctions than younger women, the higher-level equipment is often required to meet the performance needs of the clinician in testing these patients. Urodynamic studies are objective measurements that require a significant knowledge of lower urinary tract function and clinical experience for interpretation. Similar knowledge and experience are required to clinically use the urodynamic studies to make reasonable recommendations for treatment in older women. Each study or test can provide only a fraction of the clinical data, and to see the complete clinical picture and make treatment decisions, especially for older patients, the physician needs comprehensive urodynamic studies. Urodynamic studies of older women are needed when considering pharmacologic, behavioral, or surgical therapy. It is much easier to change medications or combine pharmacologic therapy with behavioral therapy than it is to revise an operation. However, any long-term treatment needs to be based on the most complete clinical information available. Without urodynamic studies, the clinician is voluntarily relinquishing the most comprehensive objective measurements of bladder and urethral function that are available. Without urodynamic studies in this population, the opportunity of providing the most appropriate initial treatment is significantly decreased, even when nonsurgical therapy is recommended. An ineffective trial of pharmacologic therapy without urodynamic studies is rarely harmful in the long term, but the cost to the elderly woman is time and money at a moment in her life when she often feels she has little of either. NONINVASIVE URINARY FLOW STUDIES Noninvasive urinary flow studies are relatively easy to perform in younger women but can be difficult to perform in older women

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for many reasons. Older patients with urinary incontinence often have an impaired ability to inhibit involuntary detrusor contractions and an impaired ability to voluntarily initiate a bladder contraction.2 The older woman is usually instructed to arrive at the urodynamics laboratory with her bladder as full as possible so that the noninvasive urinary flow study can be done. She might have “had to go” just before coming to the urodynamics laboratory, or she might have had an “accident” just before arrival. She may be unable to voluntarily void even though she has not voided for hours. Catheterization of the bladder in an elderly woman who is unable to void often demonstrates a relatively large amount of urine in the bladder. The volume of urine obtained in this case is not a postvoid residual urine volume because the patient was unable to void. It is common for older women with urinary incontinence to be unable to prevent or initiate a bladder contraction. In contrast, young women can usually voluntarily void at almost any time. It is helpful to have a urinary flow unit in the office so that measurement of urinary flow rate can be done many times for older women to determine as closely as possible the urinary flow characteristics of the patient. An ultrasound postvoid residual volume measurement unit in the office allows the assessment to be done with each office visit to obtain multiple determinations. Ultrasound bladder volume measurements have been shown to have a high correlation with catheterized volume measurements in elderly patients.3 Although the measurement of the postvoid residual urine volume is a simple method to evaluate bladder emptying in elderly patients, it is not possible to predict the type of bladder dysfunction that the patient has without additional studies.4 Urethral Pressure Profile The maximum urethral pressure and urethral length decrease in continent women with increasing age.5 Clinical evaluation of urethral function in older women is one of the most important aspects of assessment of lower urinary tract function. However, urethral function remains one of the most elusive measurements of lower urinary tract function. Urethral dysfunction of some type is usually a component of urinary incontinence in older women. The urethral pressure profile (UPP) measurements in women significantly correlate with incontinence episodes and absorbent pad use.6 Although the UPP measurements have a significant correlation with incontinence severity, the UPP is a measurement of resting urethral pressure and not a direct measurement of continence. This distinction is important when using the UPP measurement in clinical decisions. Assessment of urethral sphincter dysfunction may require a composite of historic, urodynamic, anatomic, and clinical severity criteria.7 The composite of intrinsic sphincter deficiency has been suggested to include a maximum urethral closure pressure less than or equal to 20 cm/H2O, a Valsalva leak point pressure of less than or equal to 50 cm/H2O, and a stress urethral axis less than or equal to 20.7 The concept that intrinsic functional properties of the urethra exist that contribute to the integrity of the urethral continence mechanism resulted from many years of clinical work by McGuire and others.8,9 During the 1970s, McGuire and Lytton8 observed that women who had failed previous incontinence procedures had poor urethral function indicated by low urethral pressure. McGuire and colleagues9 subsequently categorized women who have poor urethral function as having type III incontinence. Type

III incontinence refers to a poorly closed proximal sphincter identified by video urodynamics and leak point pressure measurement. Intrinsic sphincter deficiency refers to a low-pressure urethra identified using UPP measurements recorded in the midurethral high-pressure zone. The UPP and abdominal leak point pressure (ALPP) assessments are performed differently and identify different characteristics of urethral function. Although the low-pressure urethra and the type III urethra identify different aspects of urethral function, the clinical objective of both studies is to recognize women who have severely compromised urethral function. Because clinical evaluation of urethral function in older women is important in the management of incontinence, the UPP and ALPP measurements can be used to better characterize urethral dysfunction. Although the UPP has many limitations, the measurements can contribute to the information obtained from ALPP assessment if the UPP is used appropriately. Elderly women who have intrinsic sphincter deficiency based on the UPP should be clinically identified and counseled about treatment because of the higher risk for failure of any therapeutic approach in this group.10,11 The maximum urethral closure pressure and the Valsalva leak point pressure are significantly decreased with increasing severity of the incontinence grade.13 Some studies have suggested a statistically significant relationship between the UPP and ALPP.12-15 From a clinical management perspective, the UPP and ALPP are different measurements of urethral function that can be useful in combination, but they are not comparable measurements. UPP measurements are usually performed using micro tip transducers. Although many techniques have been used, the microtip transducer remains the clinical standard for UPP measurements. A dual-channel microtip catheter is preferred. It has a microtip transducer located at the tip of the catheter for bladder pressure measurement and a microtip transducer located approximately 5 cm proximally for measurement of urethral pressure. The subtraction of intravesical pressure from urethral pressure produces the urethral closure pressure profile.16 The dual-channel microtip transducer allows the urodynamicist to perform stress UPP measurements. An electronic catheter puller is used to ensure a constant rate as the catheter passes through the urethra. Because of measurement variations in the UPP, many measurements are done to determine the maximum resting urethral pressure. The UPP measurement in older women is usually performed in the supine position because of measurement artifact that occurs in the standing position. A stress UPP is a measure of the difference between the intravesical pressure and intraurethral pressure during stress maneuvers such as coughing. A stress pressure profile is performed in the same way as a resting UPP with additional instructions for the patient to cough during the urethral pressure measurement. Usually, the patient is instructed to cough approximately six or more consecutive times as the UPP catheter is pulled through the functional urethra at a rate of approximately 1 mm per second. The pressure transmission ratios of a stress pressure profile measurement have been found to be sufficiently reproducible to be useful in characterizing stress sphincteric function.17 During coughing, an increase in urethral pressure occurs that is usually greater in magnitude than the increase in abdominal pressure, which indicates that active and passive compensatory pressure mechanisms are involved in continence. Denervation of the urethra, hypermobility of the urethra, and intrinsic dysfunction of the urethra are some of the reasons that the normal compensatory pressure mechanisms fail. A negative pressure

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gradient between the urethra and bladder during coughing indicates that the pressure compensatory mechanisms of the urethra are not functioning normally. Urethral function studies in healthy women compared with women having genuine stress incontinence show that the active closure mechanisms at the bladder neck and mid-urethra are significantly weakened in women with genuine stress incontinence, and the results do not support the concept that impaired passive pressure transmission to the urethra is an important pathophysiologic factor in genuine stress incontinence.18 A dynamic active closure mechanism has been demonstrated at the bladder neck in addition to the dynamic closure mechanism that is located in the middleurethra.18 Increases in urethral closure pressure during coughing probably occur because the urethra is compressed against a hammock supportive layer, rather than the urethra being truly intraabdominal.19 These observations do not support the concept of passive abdominal pressure transmission to an intra-abdominal urethra as the mechanism of urethral continence. Pelvic organ prolapse can produce obstructive symptoms and prevent or reduce urinary leakage.20 The resting urethral pressure is often higher than expected in women who have a cystocele. The resting UPP measurement is usually done initially without cystocele reduction. Repeat urethral pressure measurements are done after cystocele reduction. Results of the Scopettes (Birchwood Laboratories, Eden Prairie, MN) reduction technique to reduce prolapse revealed a 56% incidence of low-pressure urethra and stress urinary incontinence in 83% of patients with grade 4 vaginal prolapse.21 A statistically significant relationship exists between urethral incompetence and hypermobility of the urethra.22 If a significant decrease in resting urethral pressure occurs with reduction of the cystocele, surgical reduction of the cystocele can be expected to produce an even greater decrease in resting urethral pressure. The effect of a cystocele on the UPP can indicate relatively good urethral function even though the actual urethral function after surgical repair of the cystocele may be significantly compromised. The change in urethral pressure with cystocele reduction in the laboratory setting can be helpful for indicating changes in urethral function after surgical repair of the cystocele. However, in some older women, surgical reduction of a cystocele can result in a profound decrease in urethral function compared with preoperative manual reduction of the cystocele in the urodynamics laboratory. Abdominal Leak Point Pressures An ALPP is a measure of the lowest total bladder pressure at a known volume at which leakage occurs during prompted increases in abdominal pressure.23 The total bladder pressure is equal to the sum of the detrusor pressure and the abdominal pressure measured in the bladder. If the bladder compliance is normal, the abdominal pressure is usually approximately the same as the total bladder pressure at a low intravesical volume in the absence of a detrusor contraction. A simplified office technique for measuring ALPP in older women can be done during filling cystometry. The patient is placed in a semi-erect position, and bladder filling is stopped at 200 mL. The patient is instructed to strain progressively to the maximum abdominal pressure possible or until leaking occurs. The external urethral meatus is visually observed. When leaking is observed, the intravesical pressure is recorded. If leaking does not occur, the patient is instructed to cough progressively to a

maximum coughing pressure. The point at which leaking occurs with coughing is recorded. If leaking does not occur, the maximum abdominal pressure measured is recorded, and the absence of leaking is documented. At this point, filling cystometry is continued. This technique is particularly suited to officebased urodynamic studies in older women. The ALPP measured using this technique may have measurement error causing a higher ALPP value because the patient is not in a full standing position.12 It is more difficult to identify leaking using a visual technique compared with a fluoroscopic technique. If fluoroscopy is available, the measurement can be done in the semi-erect position or the standing position using the smallest catheter that is practical. A 5-Fr, double-lumen catheter can be used. One lumen is used to fill the bladder, and the other lumen is used to measure intravesical pressure. A 3-Fr microtip catheter can be used to measure ALPP fluoroscopically, but it is expensive and requires filling of the bladder with a separate catheter, which may not be practical for most urodynamics laboratories. A 20% iodinated contrast medium typically is used, although a 60% contrast medium can be used when better visualization of the urethra is required as in obese patients. An anteroposterior view of the urethra is often used, although a lateral view may provides better visualization of the bladder neck and midurethral continence mechanisms. When a lateral view is used, positioning the patient about 10 degrees off a line perpendicular to the x-ray table places the femoral heads out of alignment and allows a better radiographic view of the urethra. In this position, the urethra is usually centered between each femur, which makes leaking much easier to visualize. The measurement of ALPP in elderly women is an essential urethral function study. During the urodynamic studies, older women occasionally are unable physically to generate an abdominal pressure of 60 cm H2O, which is needed to identify type III incontinence if no leaking is seen. Some frail elderly women may have low abdominal pressures during most daily activities. Because women who have stress incontinence usually leak in the standing position, it is preferable to measure the ALPP in the standing position. Some older women may have difficulty standing and performing straining maneuvers at the same time. Although a semi-erect position is a compromise in the measurement technique, it is often a more feasible position to perform the ALPP measurement for older women. A cystocele can cause an error in the ALPP measurement, resulting in a higher abdominal pressure required for leaking. The ALPP can be measured with cystocele reduction using Scopettes, vaginal gauze packing, or a vaginal speculum.24 It is sometimes difficult to reduce the cystocele in older women enough in the urodynamics laboratory to be confident that the ALPP measurement accurately indicates urethral function. Women who demonstrate stress incontinence with the vaginal prolapse reduced and the urethra supported normally should be suspected of having type III incontinence.25 Placement of a pessary to reduce vaginal vault prolapse can obstruct the urethra and result in a measurement error. The clinical objective of ALPP measurement in older women is to determine the functional status of the urethra so that a reasonable clinical management recommendation can be made. Many older women have very complicated combinations of urethral dysfunction, bladder dysfunction, and vaginal prolapse. Vaginal vault prolapse can significantly complicate the measurement of urethral function. The ALPP is an essential piece of the clinical puzzle, and without the leak point pressure measure-

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ments, clinical evaluation of urethral function in older women is not complete. Cystometrogram The cystometrogram is a measure of the response of the bladder to being filled.26 Cystometry is the method by which the pressurevolume relationship of the bladder is measured.16 A medium filling rate typically is used when obtaining a cystometrogram in elderly women. A medium fill rate ranges from 10 to 100 mL per minute, which is a relatively wide range for older women. A lower filling rate in the medium filling range is preferred in older women to better evaluate the response of the bladder to filling. A filling rate of 30 mL per minute is usually satisfactory for older women. A slow filling rate of 10 mL per minute requires a long time to fill the bladder if the capacity is normal. Repeat filling of the bladder using a slow filling rate is a consideration for women who have severe detrusor instability or a very small bladder capacity. A common filling technique uses a small (5 to 7 Fr), doublelumen urethral catheter attached to a perfusion pump, and water or saline is the infusion medium. A 5-Fr urethral catheter is preferred because of the small size, although the small lumen may decrease the pump flow rate during filling. A larger urethral catheter (e.g., 6 Fr) has been shown to decrease the maximum urinary flow rate during pressure flow studies in women.27 The 5-Fr, double-lumen catheter allows filling cystometry and pressure flow studies to be done consecutively using the same catheter, which is an advantage for older women. A rectal catheter is a common method for measurement of abdominal pressure in older women. The intravesical catheter is a much more reliable initial measure of intra-abdominal pressure than the rectal catheter measurement. For this reason, the rectal catheter recording is adjusted to equal the bladder pressure recordings during resting and straining maneuvers at baseline before filling. Using a cough and strain maneuver, the rectal catheter recording usually can be adjusted to almost exactly match the bladder pressure recording at baseline. When the rectal pressure channel and the bladder pressure channel are reading as close to the same as possible during straining maneuvers, bladder filling is begun. During filling, small fluctuations in abdominal pressure can be seen that result from respiration, which assures the urodynamicist that both channels are working properly. Occasionally, a rectal contraction may cause the differential pressure measurement to have a negative value, which usually can be disregarded. Spontaneous rectal contractions usually disappear as the study progresses.28 Rectal contractions of some type occur in approximately 29% of patients having urodynamic studies, regardless of age.29 Persistent rectal contractions are a relatively uncommon event while obtaining the cystometrogram in older women. Bladder sensation during filling cystometry can be difficult to evaluate in older women because of the subjective nature of the measurement. The relationship of bladder sensation to bladder activity needs to be recorded, and identifying bladder sensation requires the patient to understand the importance of communicating awareness of bladder sensation to the urodynamicist. Unstable detrusor contractions may occur during the filling phase of cystometry in older women. The pressure resulting from involuntary detrusor contractions, the duration of the contractions, and the number of contractions during filling varies considerably among patients. When an involuntary detrusor

contraction occurs during filling, involuntary loss of urine usually occurs. A sensation of urinary urgency may precede an involuntary detrusor contraction, or the sensation of urgency may occur during the contraction. However, older women who have a history of urge urinary incontinence may not exhibit unstable detrusor contractions during filling. Elderly women who have had a previous stroke with residual neurologic deficits may exhibit detrusor hyperreflexia during filling cystometry. Suprapontine lesions in elderly patients can result in involuntary detrusor contractions during filling cystometry with associated electromyographic activity that has the appearance of detrusor sphincter dyssynergia. Involuntary loss of urine has occurred during phases of electromyographic relaxation in older patients who were studied using telemetry (Fig. 95-1).30 When continuous involuntary detrusor contractions occur during filling cystometry, the problem in some patients can be obtaining any further useful information from the studies. At that point, measurement of pressure flow studies during voluntary voiding would be useful, although measurements requiring voluntary voiding may not be possible. Further filling of the bladder should be discontinued during continuous involuntary contractions. After the bladder has stabilized, a slow filling rate of 10 mL per minute can sometimes allow filling to a volume adequate for voluntary voiding. Older women who cannot inhibit bladder contractions often have an inability to voluntarily initiate a bladder contraction. Sometimes, it is impossible to obtain a pressure flow study in older women who have continuous involuntary detrusor contractions, regardless of the techniques used for filling the bladder to a higher capacity. Same-session repeat cystometry and pressure flow studies have shown an increase in volume for the first desire to void and normal desire to void, whereas the maximum cystometric capacity remained unchanged in healthy women.31 However, for some older women who have a small capacity or detrusor instability, changing to a slow filling rate can increase the maximum cystometric capacity. If detrusor activity during filling cystometry remains stable, the first or normal desire to void is recorded, a strong desire to void is recorded, and the maximum cystometric capacity is recorded. At the maximum cystometric capacity, the passive bladder pressure is measured to determine compliance. Compliance is a measure of the change in volume per unit of change in pressure, and it is expressed in milliliters per centimeter of water.16 From a clinical management perspective, compliance is a measurement of the ability of the bladder to stretch without increasing pressure inside the bladder. A normal bladder can be filled to the maximum cystometric capacity with minimal change in the passive pressure within the bladder. In a study to determine the relationship of detrusor instability with changes in compliance in 270 women, 75% of the patients showed a compliance of greater than 130 mL/cm, 95% showed a compliance greater than 40 mL/cm, and women having compliance less than 40 mL/cm had a 16 times greater incidence of detrusor instability.32 Low bladder compliance can be a serious problem in older women who have had radiation therapy or previous pelvic surgery.33 Older women with abnormal bladder compliance often present with severe stress urinary incontinence. Although a significant abnormality in bladder compliance is relatively uncommon in older women, it is extremely important to recognize it. A sling procedure in an elderly woman with stress incontinence and low bladder compliance can result in increased bladder outlet resistance and passive bladder pressures of more than

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Figure 95-1 This 90-year-old woman has no known neurologic disease. She has detrusor instability with a high-pressure contraction and increased electromyographic activity. There is a delay in the onset of involuntary urine loss. The highest peak of electromyographic activity correlated with decreased the urinary flow, which was caused by outlet obstruction that resulted in an increase in detrusor pressure. The increased detrusor pressure appeared to overcome the opposing electromyographic activity, resulting in a sustained decline in electromyographic activity and an increase in urine flow that decreased bladder outlet resistance and decreased bladder pressure because of the outflow of urine. This pattern was previously observed during telemetric monitoring of incontinent elderly men.30

40 cm H2O, which can cause hydronephrosis and deterioration of renal function. Voiding Pressure Flow Studies Voiding pressure flow studies are useful for assessing older women. However, the clinical importance of pressure flow studies is not often emphasized in the management of older women. Voiding pressure flow studies identify three fundamental voiding states34: 1. Low detrusor pressure and high urinary flow rate (unobstructed) 2. High detrusor pressure and low urinary flow rate (obstructed) 3. Low detrusor pressure with low urinary low rate (poor detrusor contractility) Older women present with problems ranging from mixed incontinence with vault prolapse to recurrent urinary tract infections with incomplete bladder emptying. Although these are not precise categories, most older women with incontinence can be

classified by the results of pressure flow studies. These categories often are associated with similar symptoms but represent different clinical entities, and the approach to management usually is different for the three pressure flow categories. Older women who have had previous incontinence surgery usually present with complex combinations of lower urinary problems. For example, it is common for older women who have had a urethral suspension procedure to experience symptoms of mixed incontinence and symptoms of bladder outlet obstruction. Some degree of vaginal vault prolapse is a common physical finding in women with these symptoms. Only pressure flow studies can differentiate high detrusor pressure with a low urinary flow rate from low detrusor pressure with a low flow rate. Minimally invasive surgical procedures for the treatment of stress incontinence in women have reduced the morbidity of incontinence surgery enough that operative procedures often are offered to elderly women. Successful surgical treatment is available to many older women who would not have been advised to consider a surgical option in the past. However, older women with urinary incontinence are a complicated group of patients,

Chapter 95 URODYNAMICS EVALUATION IN THE ELDERLY

especially when surgical options are being considered, because the results of surgery in older women can be disappointing. Older women often have very poor urethral function (ALPP less than 60 cm H2O) with minimal urethral mobility. Although a pubovaginal sling placed without tension usually results in continence for women with good urethral function, a compressive sling is required to achieve continence in women with very poor urethral function. Pressure flow studies are important in the preoperative evaluation of bladder function in older women with urinary incontinence and poor urethral function because urinary retention can be a complication of a compressive sling procedure. The advent of minimally invasive surgery for urinary incontinence in older women has resulted in clinical diagnoses after surgical procedures in this population that were uncommon in the past. Pressure flow studies are invaluable in elucidating the pathophysiology of these unique clinical problems that occur after minimally invasive incontinence surgery in elderly women. When persistent voiding symptoms occur in these patients, comprehensive urodynamic studies performed preoperatively are invaluable for comparison with postoperative studies. The pressure flow studies are among the most valuable studies for clinical evaluation and formulating management strategies for these complicated clinical problems. Persistent voiding symptoms after minimally invasive surgical procedures in older women should be evaluated with comprehensive urodynamics studies. Bladder outlet obstruction in older women may occur after minimally invasive procedures for treatment of stress urinary incontinence, and pressure flow studies are the most important studies in the postoperative evaluation of these patients. The measurement parameters for bladder outlet obstruction in older

women after incontinence surgery have not been well defined. Voiding dysfunctions in elderly women after incontinence surgery need prompt urodynamic evaluation to plan long-term management. If bladder outlet obstruction is identified, a significant delay in urethrolysis after a sling procedure is associated with persistent bladder symptoms after urethrolysis,35 which suggests that changes in bladder activity after prolonged obstruction may not be reversible. De novo urge incontinence after minimally invasive sling procedures in older women needs to be evaluated with pressure flow studies to be sure that the overactive bladder symptoms are not caused by bladder outlet obstruction. The urethra has a different role in maintaining continence from that of the bladder. However, when considering the dynamics of voiding, the bladder and urethra appear to behave as a functional unit. Abnormalities of urethral function can affect bladder function, and abnormalities of bladder function can affect urethral function. Pressure flow studies are a measure of the dynamic functional unit of the bladder and urethra. Pressure flow studies are reproducible and provide consistent urodynamic measurements in women.36 Aging significantly alters the function of the urethra and the bladder. Elderly women who experience symptoms of stress urinary incontinence may have urinary flow rates that are considerably lower than would be expected based on the measured bladder pressure, even when the bladder pressure is low (Fig. 95-2). In these older women, it appears that the intrinsic urethral closing properties and the intrinsic urethral opening properties are deficient. The aging urethra seems to lose some of the dynamic properties that maintain continence and those required for normal voiding.

Figure 95-2 This elderly woman has severe symptoms of stress incontinence. The physical examination shows minimal hypermobility, no cystocele, and atrophic vaginitis. Her bladder is stable during filling. The urinary flow rate is low relative to the detrusor pressure. It appears as if the urethra has compromised dynamic properties related to voiding and continence.

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Figure 95-3 This older woman has symptoms of mixed urinary incontinence. Her bladder is stable during filling. She has bladder outlet obstruction that appears to be caused by a cystocele.

Voiding pressure flow studies allow the clinician to identify the dynamic relationships within the voiding functional unit of the bladder and urethra in elderly women. These studies are essential for any management decision, especially if a surgical procedure that could alter the functional dynamic relationship between the urethra and bladder is being considered. Bladder outlet obstruction is the association of a low urinary flow rate with a detrusor contraction of sufficient magnitude, duration, and speed to empty the bladder.34 This is an important definition because it requires the clinician to examine the pressure flow studies to assess the voiding dynamics of the patient. However, well-established parameters for voiding pressure flow studies in elderly women are not available. Bladder outlet obstruction can occur in women who have a cystocele (Fig. 95-3), and a low urinary flow rate may result from low detrusor pressure (Fig. 95-4). Voiding Pressure Flow Techniques A 5- to 7-Fr, double-lumen catheter is placed into the bladder for measurement of bladder pressure and infusion of fluid into the bladder. A balloon catheter is placed into the rectum for measurement of intra-abdominal pressure. Except in elderly women with severe physical or mental impairment, the pressure flow studies can be performed without significant discomfort or difficulty. Even though older women may have the neurologic capacity to voluntarily initiate voiding, that ability is often significantly impaired, and the patient may be unable to voluntarily initiate voiding in the urodynamics laboratory. Turning on a faucet in the room to allow the patient to hear the sound of running water can sometimes assist the patient to voluntarily initiate voiding. When an elderly woman is unable to voluntarily void for a study, it does not mean that she has an acontractile bladder.

The measurement of voiding pressure flow studies should be done during voluntary voiding. Elderly people who experience urge urinary incontinence usually void voluntarily most of the time.2,37 It may be possible to obtain a voluntary voiding pressure flow study by using a lower filling rate and allowing the patient a longer time to initiate voiding. Every effort should be made to obtain voluntary voiding pressure flow studies because the information has immense clinical value. The urodynamicist sometimes instructs the patient to voluntarily void as an involuntary detrusor contraction is in progress. This should not be considered a true voluntary voiding pressure flow study. Although it may be the best measurement that can be obtained under the circumstances, the information should be used carefully, and the limitations of the study should be recognized when making clinical decisions about management. Involuntary detrusor contractions in elderly patients do not appear to be normal bladder contractions that are uninhibited.2 Involuntary detrusor contractions in elderly people appear to be abnormal bladder contractions. In elderly patients with urinary incontinence due to detrusor hyperreflexia, cystometric measures of contractility vary considerably on repeating the study on the same occasion.38 Voiding pressure flow studies measured during an involuntary detrusor contraction therefore provide limited clinical information about the dynamics of normal voiding in that individual. Because the goal of treatment in elderly women is improvement of quality of life, the clinical objective is to incorporate the information obtained from urodynamic studies into reasonable, practical, and feasible clinical management decisions. Electromyography Measurement of the sphincteric electromyography in elderly women is important clinically, but the measurement can be

Chapter 95 URODYNAMICS EVALUATION IN THE ELDERLY

Figure 95-4 This elderly woman has symptoms of mixed incontinence. She has a low urinary flow rate because of poor bladder function.

technically difficult to perform. Although it is of immense clinical value to identify abnormal electromyographic activity, it is useful for the clinician to know that the sphincteric electromyographic activity during voiding is normal in elderly patients. For example, older patients may have central nervous diseases that result in an electromyographic appearance of detrusor sphincter dyssynergia.30 Older women who have had long-standing urge urinary incontinence caused by involuntary detrusor contractions may have a highly developed voluntary sphincteric contraction in response to the sensation of urinary urgency that has the appearance of detrusor sphincter dyssynergia. Although it may not be possible to differentiate these entities without neurourologic testing, both can be treated with biofeedback. Routine electromyographic measurement in elderly women is relatively uncomplicated after the technique has been developed and established for a particular urodynamics laboratory. The signal source is usually the external anal sphincter. Because the amplitude and frequency of electromyographic activity is usually lower in older women compared with younger women, the external anal sphincter is considered the best location for the signal source. Intravaginal surface electrodes and intraurethral surface electrodes are less reliable for electromyographic measurement39 and rarely provide an adequate signal for clinical evaluation in older women. Well-placed surface electrodes are preferred in elderly patients.40 Although needle electrodes are considered superior to surface electrodes in patients who may have neurologic disease, surface electrodes are more practical and desirable

for electromyographic studies in older women. Because needle electrodes easily become dislodged during the study, many attempts to replace a needle electrode are very uncomfortable for older women. Preparation of the skin and correct placement of surface electrodes are important to ensure an adequate signal is obtained.41 After the surface electrodes have been placed and the electromyographic activity is being monitored by the urodynamicist, the patient is instructed to perform a mild cough. If the electromyographic electrodes are properly placed, a mild cough will result in a sharp increase in electromyographic activity and an immediate return to baseline. With the bladder empty at rest, the gain on the electromyographic amplifier can be adjusted in response to a mild cough by the patient. Increasing the gain on the electromyographic amplifier is often required because of the low baseline electromyographic activity in this patient population. If the electronic gain on the amplifier becomes too high, a mild cough will produce a full-scale response on the electromyographic display. As the gain is increased, baseline electrical activity increases, which is usually caused by background electrical activity rather than the baseline sphincteric electromyographic activity. This baseline electromyographic artifact is usually caused by 60-cycle interference from the electrical power source. Interference from external electrical power sources is a much greater problem in these studies of older women because the electromyographic activity of the muscles measured is usually lower than in younger women, and it requires a higher electromyographic amplifier gain.

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Section 11 GERIATRIC UROLOGY

References 1. Ouslander J, Staskin D, Raz S, Su HL, Hepps K: Clinical versus urodynamic diagnosis in an incontinent geriatric female population. J Urol 137:68, 1987. 2. O’Donnell PD: Pathophysiology of urinary incontinence in elderly men. In Geriatric Urology. Boston, Little, Brown, 1994. 3. Chan H: Noninvasive bladder volume measurement. J Neurosci Nurs 25:309, 1993. 4. Starer P, Libow LS: The measurement of residual urine in the evaluation of incontinent nursing home residents. Arch Gerontol Geriatr 7:75, 1988. 5. Rud T: Urethral pressure profile in continent women from childhood to old age. Acta Obstet Gynecol Scand 59:331, 1980. 6. Theofrastous JP, Bump RC, Elser DM, et al: Correlation of urodynamic measures of urethral resistance with clinical measures of incontinence severity in women with pure genuine stress incontinence. The Continence Program for Women Research Group. Am J Obstet Gynecol 173:407; discussion 412, 1995. 7. Bump RC, Coates KW, Cundiff GW, et al: Diagnosing intrinsic sphincteric deficiency: Comparing urethral closure pressure, urethral axis, and Valsalva leak point pressures. Am J Gynecol 177:303, 1997. 8. McGuire EJ, Lytton B: Pubovaginal sling procedure for stress incontinence. J Urol 199:82, 1978. 9. McGuire EJ, Lytton B, Kohorn EI, Pepe V: The value of urodynamic testing in stress urinary incontinence. J Urol 124:256, 1980. 10. Kilicarslan H, Gokce G, Ayan S, et al: Predictors of outcome after in situ anterior vaginal wall sling surgery. Int Urogynecol J Pelvic Floor Dysfunct 14:339, 2003. 11. Rezapour M, Falconer C, Ulmsten U: Tension-Free vaginal tape (TVT) in stress incontinent women with intrinsic sphincter deficiency (ISD): A long-term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 12(Suppl 2):S12, 2001. 12. Nguyen JK, Gunn GC, Bhatia NN: The effect of patient position on leak point pressure measurements in women with genuine stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 13:9, 2002. 13. Nager CW, Schuz JA, Stanton SL, Monga A: Correlation of urethral closure pressure, leak-point pressure and incontinence severity measures. Int Urogynecol J Pelvic Floor Dysfunct 12:395, 2001. 14. McLennan MT, Melick CF, Bent AE: Leak-point pressure: Clinical application of values at two different volumes. Int Urogynecol J Pelvic Floor Dysfunct 11:136, 2000. 15. Almeida FG, Bruschini H, Srougi M: Correlation between urethral sphincter activity and Valsalva leak point pressure at different bladder distentions: Revisiting the urethral pressure profile. J Urol 174(Pt 1)1312, 2005. 16. Abrams P, Blaivas JG, Stanton SL, Andersen JT: The standardization of terminology of lower urinary tract function. Scand J Urol Nephrol 114(Suppl):5, 1988. 17. Cundiff GW, Harris RL, Theofrastous JP, Bump RC: Pressure transmission ratio reproducibility in stress continent and stress incontinent women. Neurourol Urodyn 16:161, 1997. 18. Lose G: Urethral pressure and power generation during coughing and voluntary contraction of the pelvic floor in females with genuine stress incontinence. B J Urol 67:580, 1991. 19. DeLancey JO: Structural support of the urethra as it relates to stress urinary incontinence: The hammock hypothesis. Am J Obstet Gynecol 173:346, 1995. 20. Long CY, Hsu SC, Wu TP, et al: Urodynamic comparison of continent and incontinent women with severe uterovaginal prolapse. J Reprod Med 49:33, 2004.

21. Veronikis DK, Nichols DH, Wakamatsu MM: The incidence of lowpressure urethra as a function of prolapse-reducing technique in patients with massive pelvic organ prolapse (maximum descent at all vaginal sites). Am J Obstet Gynecol 177:1305; discussion 1313, 1997. 22. Schick E, Jolivet-Tremblay M, Tessier J, et al: Observations on the function of the female urethra. III. An overview with special reference to the relation between urethral hypermobility and urethral incompetence. Neurourol Urodyn 23:22, 2004. 23. O’Connell HE, McGuire EJ: Leak point pressures. In O’Donnell PD (ed): Urinary Incontinence. St. Louis, Mosby, 1997. 24. Gallentine ML, Cespedes RD: Occult stress urinary incontinence and the effect of vaginal vault prolapse on abdominal leak point pressures. Urology 57:40, 2001. 25. Wall LL, Hewitt JK: Urodynamic characteristics of women with complete post hysterectomy vaginal vault prolapse. Urology 44:336; discussion 341, 1994. 26. Nitti VW: Cystometry and abdominal pressure monitoring. In Nitti VW (ed): Practical Urodynamics. Philadelphia, WB Saunders, 1998, pp 38-51. 27. Baseman AG, Baseman JG, Zimmern PE, Lemack GE: Effect of 6F urethral catheterization on urinary flow rates during repeated pressure-flow studies in healthy female volunteers. Urology 59:843, 2002. 28. Wall LL, Hewitt JK, Helms MJ: Are vaginal and rectal pressures equivalent approximation of one another for the purpose of performing subtracted cystometry? Obstet Gynecol 85:488, 1995. 29. Combs AJ, Nitti VW: Significance of rectal contractions noted on multichannel urodynamics. Neurourol Urodyn 14:73, 1995. 30. O’Donnell PD, Hannish H: Telemetric electromyographic monitoring in elderly inpatient men. J Neurourol Urodyn 11:115-121, 1992. 31. Brostrom S, Jennum P, Lose G: Short-term reproducibility of cystometry and pressure-flow micturition studies in healthy women. Neurourol Urodyn 21:457, 2002. 32. Harris RL, Cundiff GW, Theofrastous JP, Bump RC: Bladder compliance in neurologically intact women. Neurourol Urodyn 15:483, 1996. 33. Zoubek J, McGuire EJ, Noll F, DeLancey JO: The late occurrence of urinary tract damage in patients successfully treated by radiotherapy for cervical carcinoma. J Urol 141:1347, 1989. 34. Kim YH, Boone T: Voiding pressure flow studies In Nitti VW (ed): Practical Urodynamics. Philadelphia, WB Saunders, 1998, pp 52-64. 35. Leng WW, Davies BJ, Tarin T, et al: Delayed treatment of bladder outlet obstruction after sling surgery: Association irreversible bladder dysfunction. J Urol 172 (Pt 1):1379, 2004. 36. Digesu GA, Hutchings A, Salvatore S, et al: Reproducibility and reliability of pressure flow parameters in women. BJOG 110:774, 2003. 37. O’Donnell PD: The volume-interval relationship of incontinence episodes in elderly inpatient men. Urology 41:334-337, 1993. 38. Lord A, Eastwood H: Detrusor hyperreflexia? Are there two types? Age Ageing 23:32, 1994. 39. Brostrom S, Jennum P, Lose G: Motor evoked potentials from the striated urethral sphincter: A comparison of concentric needle an surface electrodes. Neurourol Urodyn 22:123, 2003. 40. O’Donnell PD, Beck C, Eubanks C: Surface electrodes in perineal electromyography. Urology 32:375, 1988. 41. O’Donnell PD: Pitfalls of urodynamic testing. Urol Clin North Am 18:257, 1991.

Chapter 96

USE OF BOWEL IN LOWER URINARY TRACT RECONSTRUCTION IN WOMEN Christoph Wiesner and Joachim W. Thüroff

The use of small and large bowel for bladder augmentation or substitution has been reported by surgeons since the first experimental report by Tizzoni and Foggi in 1888.1 Bladder enlargement by augmentation enterocystoplasty is predominantly offered to women with neuropathic and non-neuropathic bladder dysfunction who have not responded to pharmacologic regimens. Female patients in whom complete removal of bladder and urethra is mandatory because of urologic or gynecologic malignancies and those who have a bladder problem and irreparable loss of the functional urethra are candidates for urinary diversion. The underlying disease and the patient’s preference must be considered when deciding on the type of urinary reconstruction or diversion, such as bladder augmentation or orthotopic bladder substitution to the trigone or bladder neck, orthotopic bladder substitution to the urethra, continent cutaneous urinary diversion, or continent anal urinary diversion. Preoperative preparation in all female patients includes ultrasound of the upper urinary tract, evaluation of the renal function to judge the renal reserve to compensate for reabsorption of acids from an intestinal reservoir (i.e., renal isotope clearance >50% of the age-specific norm, serum creatinine level