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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
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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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Chapter 1
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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Section 1 BASIC CONCEPTS
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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Section 1 BASIC CONCEPTS
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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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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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
183
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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.
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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.
Chapter 16 IDIOPATHIC URINARY RETENTION IN THE FEMALE
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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Chapter 17
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.
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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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Section 5 STRESS INCONTINENCE
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
353
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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
370
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
450
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
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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
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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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Chapter 57
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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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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Section 7 FEMALE ORGAN PROLAPSE
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 p
