DK1332_half 8/13/04 12:55 PM Page 1

Female Urology,
Urogynecology,
and Voiding
Dysfunction
DK1332_title 8/16/04 3:31 PM Page 1

Female Urology,
Urogynecology,
and Voiding
Dysfunction

Edited By
Sandip P. Vasavada, M.D.
Cleveland Clinic Foundation,
Cleveland, Ohio, U.S.A

Rodney A. Appell, M.D.

Baylor College of Medicine,
Houston, Texas, U.S.A.

Peter K. Sand, M.D.

Northwestern University,
Evanston, Illinois, U.S.A.

Shlomo Raz, M.D.

David Geffen School of Medicine at UCLA,
Los Angeles, California, U.S.A.

Marcel dekker New York

v Contents

Although great care has been taken to provide accurate and current information, neither the author(s) nor
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iii
 Contents xi

Preface

There has been a convergence of the sub-specialties of female urology and urogynecology over
the last several years. This development has resulted in improved care for women, as we have
had to “escalate” our own knowledge and abilities. Recently, we have even seen fellowship
training transcend towards this multidisciplinary goal by the creation of joint accredited
fellowship programs in female urology and urogynecology. These programs have as their
primary aim to create the thought leaders of tomorrow in women’s health by creating a unique
group of physicians who see the “whole” patient and can treat them accordingly. It is evident that
there is a strong need for more subspecialization in the field with the aging population and
prevalence of incontinence and pelvic floor disorders that is present worldwide. This book
speaks to the combined nature of our practices that has emanated from this approach.
We have sought to have some of the top thought leaders and experts from around the world
to contribute to this publication. Furthermore, these authors embody some of the exact
principles, which establish our sub-specialties as being progressive and forward thinking in their
approaches to the various disease processes and disorder that we treat. One of the prevailing
undertones of our book speaks to the fact that there are many ways in which to treat any single
disorder. We have, therefore, had several chapters written by physicians or subspecialists who
may do things differently to present contradictory views. The purpose is more than to be
controversial, but rather to give an entrance point for those wishing to advance the field and aim
for the utopian dream of literal cures for incontinence and other women’s disorders.
We all have much to learn in this area of urinary incontinence and pelvic floor disorders. It
is our hope that this book will help to build on the currently existing framework and provide a
platform towards better understanding of the disease processes that affect so many of our
patients.

Sandip P. Vasavada, M.D.

Rodney A. Appell, M.D.
Peter K. Sand, M.D.
Shlomo Raz, M.D.

iii
Introduction

Times have changed and so should our intellectual basis for the management of diseases and
conditions. Once thought of as an anatomic structure containing disparate and unrelated viscera,
the human pelvis is now appreciated as a functional syncytium as complex as any within the
human body. The dysfunctions of urinary, genital, and gastrointestinal elements which
constitute this complex functional–anatomic arrangement require comprehensive and inclusive
management strategies.
None of us is capable of mastering the vagaries of function and structure of all the
elements of the human pelvis and therefore it is requisite that expertise be drawn from
collaborative fields of endeavor so that as complete a management schema as is possible be
developed. Additionally, the very real superimposition of behavioral, vascular and neurologic
dysfunctions further make the inclusive “team” approach concept a mandatory one. This
textbook represents a superb example of the inclusive approach for management. The interaction
between colorectal (and gastroenterologic), urogynecologic, and urologic specialists can and
does produce the best possible outcome for individual patients as well as for entire populations
of individuals.
The concept of pelvic medicine remains not only viable, but one that reflects the
aforementioned global interaction and collaboration of similarly motivated specialists whose
primary concern is the attainment of the best outcome possible for women severely afflicted by
conditions which are disruptive and destructive to quality of life and, in some cases, to well
being and life expectancy. This book should be viewed in the context of intellectual instruction
and exchange which will make the pelvic medicine endeavor that much more successful from
both the patient and medical standpoint. The editors of the authors of the text represent the best
and their achievement should serve as a model for subsequent efforts in cross specialty
collaboration and, possibly more importantly, harmony.

Roger Dmochowski, M.D., F.A.C.S.

Department of Urology
Vanderbilt University Medical Center
Nashville, Tennessee, U.S.A.

v
Introduction

Over the last 10 years, all of you who care for women in your practice have been impressed with
the increasing call to provide services for urinary incontinence and pelvic organ prolapse. These
pelvic floor disorders are becoming more prevalent within our practices as the number of women
in the age groups most affected by these disorders increases. Also, women now coming into
these age groups have a more proactive approach to their own health care than did their mothers
and their sophistication and expectations demand optimal care.
It is estimated that the demand for pelvic floor disorders care will double in the next 25
years. This increasing demand combined with the remarkable growth in high quality research is
both encouraging and intimidating. Intimidating in that as we learn more, we realize how much
more we have to learn and encouraging as we watch great strides in both basic science and
outcomes research take hold.
This text embraces one of the fundamental concepts that leaders within both female
urology and urogynecology have come to understand—that women with pelvic floor disorders
are best served by an approach that acknowledges the wisdom and experience of both of these
developing subspecialties. Thus, these varied accounts by divergent authors give the reader the
opportunity to consider these issues from many points of view. This will inevitably lead to a
richness of understanding that a single doctrine could not provide.
As we face the challenge of training our residents, fellows and colleagues, we will come to
appreciate this text as an excellent resource and frequent reference. These in depth discussions of
both basic and complex components of Female Urology, Urogynecology and Voiding
Dysfunction offer us an opportunity to both reflect and to look forward. As all involved in
research and providing care in this growing field combine forces, the wisdom and philosophy
embodied in this work will enable us to expand the foundation of physicians able to join in the
process toward the ultimate goal of improving the quality of the care that these women receive.

Karl M. Luber, M.D.

University of California, San Diego
Southern California Permanente Medical Group
San Diego, California, U.S.A.

vii
v Contents
Contents

Preface iii
Introduction Roger Dmochowski v
Introduction Karl M. Luber vii
Contributors xv
Basic Concepts
1. Anatomy of Pelvic Support 1
Nirit Rosenblum, Karyn S. Eilber, Larissa V. Rodrı́guez, and Shlomo Raz
2. Neurophysiology of Micturition 23
Gamal M. Ghoniem and John C. Hairston
3. Epidemiology of Female Urinary Incontinence 45
Christopher Saigal and Mark S. Litwin
4. Quality-of-Life Issues in Incontinence 53
David F. Penson and Mark S. Litwin
5. Female Sexual Dysfunction 65
Kathleen E. Walsh and Jennifer R. Berman
6. Hormonal Influence on the Lower Urinary Tract 79
Dudley Robinson and Linda Cardozo
7. Obstetric Issues and the Female Pelvis 95
Roger P. Goldberg and Peter K. Sand

SECTION I. INCONTINENCE
Evaluation of Incontinence
8. History and Physical Examination in Pelvic Floor Disorders 119
Sanjay Gandhi and Peter K. Sand
Urodynamic Assessment
9. Urodynamic Assessment: Urethral Pressure Profilometry and PTR 141
ix
x Contents

Stacey J. Wallach and Donald R. Ostergard

10. Leak Point Pressures 157
Shahar Madjar and Rodney A. Appell
11. Videourodynamics 167
Jennifer Gruenenfelder and Edward J. McGuire
12. Pharmacologic and Surgical Management of Detrusor Instability 191
H. Henry Lai, Michael Gross, Timothy B. Boone, and Rodney A. Appell

Management of Urinary Incontinence

13. Pharmacologic Management of Urinary Incontinence 215
Alan J. Wein and Eric S. Rovner
14. Behavioral Treatments 233
Diane K. Newman
15. Pessaries and Vaginal Devices for Stress Incontinence 267
G. Willy Davila and Minda Neimark
16. Current Role of Transvaginal Needle Suspensions 279
Firouz Daneshgari
17. Anterior Vaginal Wall Suspension 283
Tracey Small Wilson and Philippe E. Zimmern
18. Retropubic Urethropexy 291
Jeffrey L. Cornella
19. Laparoscopic Treatment of Urinary Stress Incontinence 309
Thomas L. Lyons
20. Insertion of Artificial Urinary Sphincter in Women 319
H. Roger Hadley
21. Urethral Injectables in the Management of SUI and Hypermobility 329
Sender Herschorn and Adonis Hijaz

Vaginal Sling Surgery: Overview and history

22. Vaginal Sling Surgery: Overview, History, and Sling Material 345
Keith J. O’Reilly and Kathleen C. Kobashi

Vaginal Sling Surgery: Techniques

23. Use of Cadaveric Fascia Lata Allograft for Pubovaginal Slings 357
Matthew B. Gretzer and E. James Wright
24. Autologous Fascia Lata Sling Cystourethropexy 367
Karl J. Kreder
25. The In Situ Anterior Vaginal Wall Sling 379
Howard B. Goldman
26. CATS: Cadaveric Transvaginal Sling 387
 Contents xi

Dawn M. Bodell and Gary E. Leach

27. Tension-Free Vaginal Tape: An Innovative, Minimally Invasive
Pubovaginal Sling for Female Stress Urinary Incontinence 399
Vincent R. Lucente and Marisa A. Mastropietro
28. Distal Urethral Polypropylene Sling 417
Larissa V. Rodrı́guez
29. Transvaginal Cooper’s Ligament Sling for the Treatment of Stress
Urinary Incontinence and Low-Pressure Urethra 429
Sanjay Gandhi and Peter K. Sand
30. Management of Postoperative Detrusor Instability and Voiding Dysfunction 437
Peter O. Kwong and O. Lenaine Westney
31. Postoperative Complications of Sling Surgery 447
Elizabeth A. Miller and George D. Webster

Management of Refractory Detrusor Instability

32. Detrusor Myomectomy 457
Patrick J. Shenot
33. Management of Refractory Detrusor Instability: Anterior Flap
Extraperitoneal Cystoplasty 465
Eric S. Rovner, David A. Ginsberg and Shlomo Raz
34. Laparoscopic Enterocystoplasty 473
Raymond R. Rackley and Joseph B. Abdelmalak
35. Management of Refractory Detrusor Instability: Sacral Nerve Root Stimulation 485
Patrick J. Shenot

SECTION II. PELVIC ORGAN PROLAPSE

36. Physical Exam and Assessment of Pelvic Support Defects 497
Steven Swift
37. Radiographic Evaluation of Pelvic Organ Prolapse 507
Craig V. Comiter
38. Surgical Therapy of Uterine Prolapse 525
Karyn Schlunt Eilber, Nirit Rosenblum, and Shlomo Raz
39. Vaginal Hysterectomy and Other Operations for Uterine Prolapse 545
Paul M. Fine and Dallas Johnson
40. Advanced Anterior Vaginal Wall Prolapse (Stage III and IV) 561
Christina H. Kwon and Peter K. Sand
41. Anterior Vaginal Wall Prolapse: Mild/Moderate Cystoceles 575
Harriette M. Scarpero and Victor W. Nitti
42. Diagnosis and Treatment of the Stage IV Cystocele 595
xii Contents

Nancy B. Itano, Fernando Almeida, Larissa V. Rodrı́guez, and Shlomo Raz

43. Surgical Correction of Paravaginal Defects 615
Matthew D. Barber
44. Paravaginal Repair: A Laparoscopic Approach 631
John R. Miklos, Robert Moore, and Neeraj Kohli
45. Transvaginal Levator Myorraphy for Vaginal Vault Prolapse 641
Gary E. Lemack and Philippe E. Zimmern
46. Sacrospinous Ligament Suspension for Vaginal Vault Prolapse 651
Roger P. Goldberg and Peter K. Sand
47. Surgical Treatment of Vaginal Apex Prolapse: Transvaginal Approaches 663
Mark D. Walters and Tristi W. Muir
48. Abdominal Sacrocolpopexy for the Correction of Vaginal Vault Prolapse 677
J. Christian Winters, Richard Vanlangendonck, and R. Duane Cespedes
49. Laparascopic Abdominal Sacral Colpopexy 691
Marie Fidela R. Paraiso
50. Colpocleisis for the Treatment of Severe Vaginal Vault Prolapse 701
R. Duane Cespedes and J. Christian Winters
51. Rectocele Repair/Posterior Colporrhaphy 717
Nirit Rosenblum, Karyn S. Eilber, and Larissa V. Rodriguez
52. Evaluation and Management of Rectoceles 735
Jeffrey L. Segal and Mickey M. Karram

SECTION III. RECONSTRUCTION

53. Vesicovaginal Fistula: Complex Fistulae 761
Karyn Schlunt Eilber, Nirit Rosenblum, and Larissa V. Rodrı́guez
54. Vesicovaginal Fistula: Abdominal Approach 783
Martin B. Richman and Howard B. Goldman
55. Urethrovaginal Fistula 797
John B. Gebhart and Raymond A. Lee
56. Female Urethral Diverticula 811
Sandip P. Vasavada and Raymond R. Rackley
57. Urethral Reconstruction in Women 841
Jerry G. Blaivas and Adam J. Flisser
58. Radical Cystectomy and Orthotopic Neobladder Substitution in the Female 859
David A. Ginsberg and John P. Stein

SECTION IV. OTHER

59. Interstitial Cystitis 889
Marie-Blanche Tchetgen, Raymond R. Rackley, and Joseph B. Abdelmalak
 Contents xiii

60. Chronic Pelvic Pain in Interstitial Cystitis 903

James Chivian Lukban and Kristene E. Whitmore
61. Fecal Incontinence 919
Tracy Hull

Index 931
Contributors

Joseph B. Abdelmalak Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

Fernando Almeida* University of California, Los Angeles, California, U.S.A.

Rodney A. Appell, M.D. Head, Section of Female Urology and Voiding Dysfunction, F.
Brantley Scott Chair. Professor of Urology and Gyneocology, Baylor College of Medicine,
Houston, Texas, U.S.A.

Matthew D. Barber, M.D., M.H.S. Section of Urogynecology, Pelvic Reconstruction

Surgery, Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

Jennifer R. Berman Female Sexual Medicine Center, David Geffen School of Medicine at
UCLA, Los Angeles, California, U.S.A.

Jerry G. Blaivas Joan and Sanford Weil College of Medicine, Cornell University, New York,
New York, U.S.A.

Dawn M. Bodell Fellow, Tower Urology Institute for Continence, Los Angeles, California,
U.S.A.

Timothy B. Boone, M.D., Ph.D. Professor and Chairman, Scott Department of Urology,
Baylor College of Medicine, Houston, Texas, U.S.A.

Linda Cardozo, M.D., F.R.C.O.G. Professor of Urogynaecology, Department of Obstetrics

and Gynaecology, King’s College Hospital, London, England

R. Duane Cespedes, M.D. Chairman, Department of Urology, Wilford Hall Medical Center,
Lackland AFB, Texas, U.S.A.

*Current affiliation: Senior Associate Consultant, Department of Urology, Mayo Clinic Scottsdale,
Scottsdale, Arizona, U.S.A.

xv
xvi Contributors

Craig V. Comiter University of Arizona Health Sciences Center, Tucson, Arizona, U.S.A.

Jeffrey L. Cornella Mayo Clinic Scottsdale, Scottsdale, Arizona, U.S.A.

Firouz Daneshgari Director, Center for Female Pelvic Medicine and Reconstructive Surgery,
The Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

G. Willy Davila Cleveland Clinic Florida, Weston, Florida, U.S.A.

Karyn Schlunt Eilber, M.D. † Department of Urology, University of California, Los Angeles,
California, U.S.A.

Paul M. Fine Baylor College of Medicine, Houston, Texas, U.S.A.

Adam J. Flisser Joan and Sanford Weil College of Medicine, Cornell University, New York,
New York, U.S.A.

Sanjay Gandhi, M.D. Research Fellow, Department of Obstetrics and Gynecology,

Northwestern University, Evanston, Illinois, U.S.A.

John B. Gebhart Mayo Clinic and Mayo Clinic College of Medicine, Rochester, Minnesota,
U.S.A.

Gamal M. Ghoniem, M.D., F.A.C.S. Head, Section of Voiding Dysfunction and Female
Urology, Cleveland Clinic Florida and the Cleveland Clinic Foundation Health Sciences Center
of OSU, Weston, Florida, U.S.A.

David A. Ginsberg Assistant Professor of Urology, Department of Urology, University of

Southern California School of Medicine, Los Angeles, California, U.S.A.

Roger P. Goldberg, M.D., M.P.H. Director of Urogynecology Research, Evanston

Continence Center, Northwestern University Medical School, Evanston, Illinois, U.S.A.

Howard B. Goldman, M.D. Assistant Professor of Urology, Department of Urology and

Reproductive Biology, University Hospitals of Cleveland, CASE School of Medicine,
Cleveland, Ohio, U.S.A.

Matthew B. Gretzer The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A.

Michael Gross Fellow in Neurourology, Scott Department of Urology, Baylor College of

Medicine, Houston, Texas, U.S.A.

Jennifer Gruenenfelder University of Michigan, Ann Arbor, Michigan, U.S.A.

H. Roger Hadley, M.D. Professor and Chief, Division of Urology, Loma Linda University,
Loma Linda, California, U.S.A.

†
Current affiliation: Assistant Attending, Department of Urology, Memorial Sloan-Kettering Cancer
Center, New York, New York, U.S.A.
 Contributors xvii

John C. Hairston, M.D. Assistant Professor of Urology, Division of Urology, University of

Texas Medical School at Houston, Houston, Texas, U.S.A.

Sender Herschorn University of Toronto and Sunnybrook and Women’s Health Sciences
Centre, Toronto, Ontario, Canada

Adonis Hijaz University of Toronto and Sunnybrook and Women’s Health Sciences Centre,
Toronto, Ontario, Canada

Tracy L. Hull, M.D. Staff Surgeon, Department of Colon and Rectal Surgery, Cleveland
Clinic Foundation, Cleveland, Ohio, U.S.A.

Nancy B. Itano § University of California, Los Angeles, California, U.S.A.

Dallas Johnson Baylor College of Medicine, Houston, Texas, U.S.A.

Mickey M. Karram, M.D. Director Urogynecology, Professor OBGYN, Department of

OBGYN, Good Samaritan Hospital, Cincinnati, Ohio, U.S.A.

Kathleen C. Kobashi, M.D. Co-Director, Urology and Renal Transplantation, Continence

Center, Virginia Mason Medical Center, Seattle, Washington, U.S.A.

Neeraj Kohli, M.D. Associate Professor; Director, Division of Urogynecology, Brigham and
Womens Hospital, Harvard University, Boston, Massachusetts, U.S.A.

Karl J. Kreder, M.D. Professor and Clinical Vice Chair, Department of Urology, University
of Iowa, Iowa City, Iowa, U.S.A.

Christina H. Kwon Evanston Continence Center, Northwestern University, Evanston,

Illinois, USA

Peter O. Kwong, M.D. Fellow in Female Urology and Urinary Tract Reconstruction,
Department of Surgery=Urology, University of Texas Health Science Center, Houston, Texas,
U.S.A.

H. Henry Lai, M.D. Resident, Scott Department of Urology, Baylor College of Medicine,
Houston, Texas, U.S.A.

Gary E. Leach Director, Tower Urology Institute for Continence, Los Angeles, Califonia,
U.S.A.

Raymond A. Lee Mayo Clinic and Mayo Clinic College of Medicine, Rochester, Minnesota,
U.S.A.

Gary E. Lemack, M.D. Associate Professor of Urology, Southwestern Medical Center,

University of Texas, Dallas, Texas, U.S.A.

§
Current affiliation: Senior Associate Consultant, Department of Urology, Mayo Clinic Scottsdale,
Scottsdale, Arizona, U.S.A.
xviii Contributors

Mark S. Litwin, M.D., M.P.H. Professor, Department of Urology, David Geffen School of
Medicine at UCLA and UCLA School of Public Health, Los Angeles, California, U.S.A.

Vincent R. Lucente, M.D., M.B.A. } Pennsylvania State University, College of Medicine,

Hershey, Pennsylvania, U.S.A.

James Chivian Lukban Urogynerology Associates of Colorado, Denver, Colorado, U.S.A.

Thomas L. Lyons, M.S., M.D. Director, Center for Women’s Care and Reproductive Surgery,
Atlanta, Georgia, U.S.A.

Shahar Madjar Northern Michigan Urology at Bell, Bell Memorial Hospital, Marquette
County, Michigan, U.S.A.

Marisa A. Mastropietro, M.D.** Lehigh Valley Hospital, Allentown, Pennsylvania, U.S.A.

Edward J. McGuire University of Michigan, Ann Arbor, Michigan, U.S.A.

John R. Miklos, M.D. Director Urogynecology, Atlanta Urogynecology Associates, Atlanta,

Georgia, U.S.A.

Elizabeth A. Miller Duke University Medical Center, Durham, North Carolina, U.S.A.

Robert D. Moore, D.O. Assistant Director Urogynecology, Atlanta Urogynecology

Associates, Atlanta, Georgia, U.S.A.

Tristi W. Muir, M.D. Assistant Chief, Female Pelvic Medicine and Reconstructive Surgery,
Department of Obstetrics and Gynecology, Brooke Army Medical Center, Fort Sam Houston,
Texas, U.S.A.

Minda Neimark Cleveland Clinic Florida, Weston, Florida, U.S.A.

Diane K. Newman University of Pennsylvania Medical Center, Philadelphia, U.S.A.

Victor W. Nitti New York University School of Medicine, New York, U.S.A.

Keith J. O’Reilly †† Tripler Army Medical Center, Honolulu, Hawaii, U.S.A.

Donald R. Ostergard, M.D. University of California, Irvine, and Long Beach Memorial
Medical Center, Long Beach, California, U.S.A.

Marie Fidela R. Paraiso Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

}
Current affiliation: Medical Director, Institute for Female Pelvic Medicine and Reconstructive Surgery,
Allentown, Pennsylvania, U.S.A.
**Current affiliation: Director of Gynecologic Services, Lincoln Hospital, Bronx, New York, U.S.A.
††
Current affiliation: Department of Urology, Madigan Army Hospital, Tacoma, Washington, U.S.A.
 Contributors xix

David F. Penson, M.D., M.P.H. §§ Section of Urology, 112-UR, University of Washington

School of Medicine, VA Puget Sound HCS, Seattle, Washington, U.S.A.

Shlomo Raz, M.D. Professor, Department of Urology, David Geffen School of Medicine at
UCLA, Los Angeles, California, U.S.A.

Raymond R. Rackley, M.D. Co-Head, Section of Female Urology, Urological Institute,

Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

Martin B. Richman, M.D. Department of Urology, Case Western Reserve University,

University Hospitals of Cleveland, Cleveland, Ohio, U.S.A.

Dudley Robinson, M.D., M.R.C.O.G. Sub-speciality Trainee—Urogynaecology, Depart-

ment of Obstetrics and Gynaecology, King’s College Hospital, London, England

Larissa V. Rodrı́guez, M.D. Assistant Professor, Co-director of Division of Female Urology,

Reconstructive Surgery and Urodynamics, Department of Urology, University of California, Los
Angeles, California, U.S.A.

Nirit Rosenblum, M.D. }} Department of Urology, University of California, Los Angeles,

California, U.S.A.

Eric S. Rovner Assistant Professor Urology, Department of Surgery, Division of Urology,

University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.

Christopher Saigal, M.D., M.P.H. Assistant Professor, Department of Urology, David

Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.

Peter K. Sand, M.D. Professor, Department of Obstetrics and Gynecology, Evanston

Continence Center, Northwestern University, Evanston, Illinois, U.S.A.

Harriette M. Scarpero New York University School of Medicine, New York, U.S.A.

Jeffrey L. Segal, M.D. Clinical Instructor OBGYN, Fellow Urogynecology, Department of

OBGYN, Good Samaritan Hospital, Cincinnati, Ohio, U.S.A.

Patrick J. Shenot Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A.

John P. Stein Department of Urology, University of Southern California, Los Angeles,

California, U.S.A.

Steven Swift, M.D. Associate Professor, Department of Obstetrics and Gynecology, Medical
University of South Carolina, Charleston, South Carolina, U.S.A.

§§
Current affiliation: Associate Professor Urology and Preventive Medicine, Keck School of Medicine,
University of Southern California, Los Angeles, Califonia, U.S.A.
}}
Current affiliation: Assistant Professor, Department of Urology, NYU School of Medicine, New York,
New York, U.S.A.
xx Contributors

Marie-Blanche Tchetgen Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

Richard Vanlangendonck, M.D. Director of Minimally Invasive Surgery, Department of

Urology, Ochsner Clinic Foundation, New Orleans, Louisiana, U.S.A.

Sandip P. Vasavada, M.D. Co-Head, Section of Female Urology, Urological Institute,

Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

Stacey J. Wallach, M.D.*** University of California, Irvine, and Long Beach Memorial
Medical Center, Long Beach, California, U.S.A.

Kathleen E. Walsh Female Sexual Medicine Center, David Geffen School of Medicine at
UCLA, Los Angeles, California, U.S.A.

Mark D. Walters, M.D. Head, Section of Urogynecology and Reconstructive Pelvic Surgery,
Department of Obstetrics and Gynecology, Cleveland Clinic Foundation, Cleveland, Ohio,
U.S.A.

George D. Webster Duke University Medical Center, Durham, North Carolina, U.S.A.

O. Lenaine Westney, M.D. Assistant Professor, Department of Surgery=Urology, University

of Texas Health Science Center, Houston, Texas, U.S.A.

Alan J. Wein Chair, Division of Urology, Department of Surgery, University of Pennsylvania

School of Medicine, Philadelphia, Pennsylvania, U.S.A.

Kristene E. Whitmore Graduate Hospital, Philadelphia, Pennsylvania, U.S.A.

Tracey Small Wilson University of Texas Southwestern Medical Center, Dallas, Texas,
U.S.A.

J. Christian Winters, M.D. Director of Female Urology, Department of Urology, Ochsner

Clinic Foundation, New Orleans, Louisiana, U.S.A.

E. James Wright The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A.

Philippe E. Zimmern, M.D. Professor of Urology, Southwestern Medical Center, University

of Texas, Dallas, Texas, U.S.A.

***Current affiliation: Assistant Professor, Department of Obstetrics and Gynecology, University of

California, Sacramento, California, U.S.A.
1
Anatomy of Pelvic Support

Nirit Rosenblum,* Karyn S. Eilber,† Larissa V. Rodrı́guez, and Shlomo Raz

University of California, Los Angeles, California, U.S.A.

I. INTRODUCTION

Female pelvic anatomy is a complex combination of muscles, ligaments, nerves, and blood
vessels that act dynamically to provide support for the urethra, bladder, uterus, and rectum. An
understanding of normal mechanisms of pelvic support are essential in the evaluation of women
with voiding complaints, urinary incontinence, and bowel dysfunction related to pelvic floor
relaxation. Thus, the treatment of female urinary incontinence often involves recognition and
treatment of concurrent pelvic pathophysiology such as cystocele, uterine prolapse, enterocele,
rectocele, and perineal laxity. Identification of the various components of pelvic floor
dysfunction is aided by diagnostic tools such as video urodynamics and magnetic resonance
imaging of the pelvis. This chapter will focus on normal female pelvic anatomy, including
the supporting structures relevant to voiding dysfunction and incontinence, as well as the
pathophysiology of pelvic floor relaxation, with a description of the various components of
pelvic organ prolapse.

II. PELVIC SUPPORTING STRUCTURES

A. Bone
Passive support of the pelvic floor is provided by the bony structures, which act as anchors for
the important muscular and fascial structures comprising the pelvic floor. The pubic rami, ischial
spines, and sacrum represent the anchoring points of the true bony pelvis, which is made up of
pubis, ilium, ischium, sacrum, and coccyx (1). The pelvic floor is diamond-shaped with the pubic
symphysis and sacrum at the anterior and posterior apices while the ischial spines serve as lateral
anchors. The pelvic floor can be further subdivided into anterior and posterior compartments by
drawing a line between the two ischial spines.

B. Ligaments
The sacrospinous ligaments span the posterior portion of the pelvic floor, from the ischial spines
to the anterolateral aspect of the sacrum and coccyx. The coccygeus muscle is found between the

*Current affiliation: NYU School of Medicine, New York, New York, U.S.A.
†
Current affiliation: Memorial Sloan-Kettering Cancer Center, New York, New York, U.S.A.

1
2 Rosenblum et al.

ischial spines and the lateral aspect of the sacrum and coccyx, overlying the sacrospinous
ligament and is an important landmark in vaginal surgery. Above the coccygeus muscle lies the
sciatic nerve and its plexus, while the pudendal nerve and vessels lie lateral (Alcock’s canal).
Medially, the sacrospinous ligament fuses with the sacrotuberous ligament (2). Anteriorly, the
tendinous arc, a curvilinear condensation of pelvic fascia arising from the obturator internus
muscle, runs between the ischial spines and the lower portion of the pubic symphysis. This
crucial structure provides a musculofascial origin for the majority of the anterior pelvic
diaphragm, allowing its attachment to the bony pelvis. The arcus tendinous flanks the urethra
and bladder neck anteriorly and rectum posteriorly, providing lateral attachment of the pelvic
diaphragm and its ligaments (1).
The perineal body is a tendinous structure located in the midline of the perineum between
the anus and the vaginal introitus, which provides a central point of fixation for the transverse
perineal musculature (3). This anchoring site provides a second level of pelvic support to the
posterior vaginal wall and rectum, incorporating the levator ani and transverse perineal
musculature as well as the external anal sphincter.

C. Musculature
The striated musculature comprising the pelvic floor acts as a supporting structure for the
visceral contents of the abdominopelvic cavity as well as a dynamic organ involved in
maintenance of urinary and fecal continence. The pelvic diaphragm is composed of the levator
ani and coccygeus muscles. The levator ani muscle group and its fascia provide the most critical
support for the pelvic viscera, acting as the true muscular pelvic floor. The levator ani group
is composed of the pubococcygeus, ischiococcygeus, and iliococcygeus, named according to
their origin from the pelvic sidewall (4). This broad sheet of muscular tissue extends from
the undersurface of the pubic symphysis to the pelvic surface of the ischial spines, taking
origin from the tendinous arc laterally. The anterior muscle group, primarily made up of
pubococcygeus (puborectalis) with its overlying endopelvic fascia, directly attaches to the
bladder, urethra, vagina, uterus, and rectum, actively contributing to visceral control (Fig. 1).
This important muscular support mechanism is crucial during times of suddenly increased intra-
abdominal pressure (1).
The posterior muscle group consists of the posterior portion of the levator ani and the
coccygeus muscle. Their points of origin include the more posterior portions of the tendinous
arc and the ischial spines. The two sides fuse in the midline posterior to the rectum and attach
to the coccyx. This plate of horizontal musculature spans from the rectal hiatus to the coccyx
and allows maintenance of the normal vaginal and uterine axis. The upper vagina and uterine
cervix lie on this horizontal plane created by the levator plate. This posterior muscle group is
active at rest and contracts further during rectus abdominis contraction, maintaining proper
vaginal axis (1).
Midline apertures in the levator ani group, collectively referred to as the levator hiatus,
allow passage of the urethra, vagina, and rectum. Adjacent fascial attachments provide support
to these pelvic viscera as they exit the pelvis, fashioning a “hammock” of horizontal support (5).
The bladder, proximal vagina, and rectum rest on the levator floor and become coapted against it
during periods of increased intra-abdominal pressure. Resting tone of the levator muscle, as well
as reflex and voluntary contraction, acts to pull the vagina and rectum forward, thereby
preventing incontinence of both urine and stool. These active mechanisms of pelvic floor support
maintain both urinary and fecal continence.
 Anatomy of Pelvic Support 3

Figure 1 Schematic diagram of the striated musculature of the pelvic floor. PR, puborectalis; PC,
pubococcygeus; IC, iliococcygeus; O, obturator muscle; TA, tendinous arc of the obturator muscle.

III. ANTERIOR VAGINAL SUPPORT

The fascia overlying the pelvic floor musculature plays a critical role in pelvic support. The
abdominal portion of the fascia is referred to as endopelvic fascia and represents a continuation
of the abdominal transversalis fascia (1). The levator ani muscle is covered superiorly and
inferiorly by a fascial layer (Fig. 2). The two fascial layers split at the levator hiatus to cover the
pelvic organs that traverse it. The superior or intra-abdominal segment (endopelvic fascia) and
the inferior or vaginal side of the levator fascia together constitute the pubocervical fascia in
the classical anatomic descriptions. This levator fascia is divided into discrete areas of
specialization, depending on the associated organ it supports. The specialization of levator fascia
around the urethra, the pubourethral ligament, represents a fusion of the periurethral fascia and
endopelvic fascia attaching to the tendinous arc. The levator fascia associated with the bladder,
the vesicopelvic ligament or fascia, represents the fusion of perivesical and endopelvic fascia
attached to the tendinous arc. Such condensations of the endopelvic fascia create “ligamentous”
structures that support the pelvic viscera, such as the pubourethral ligaments, urethropelvic
ligaments, pubocervical fascia, and cardinal and uterosacral ligaments (Fig. 3). These represent
discrete supportive structures that are part of a continuum of connective tissue surrounding the
pelvic organs and serve as important surgical and physiologic landmarks. An understanding of
their individual contribution to pelvic visceral support is essential in reconstructive surgery.
Therefore, these four fascial structures will be discussed in detail as a basis for understanding the
pathophysiology of pelvic organ prolapse.
4 Rosenblum et al.

Figure 2 Schematic diagram of the pelvic floor, specifically the levator ani musculature and its fascial
condensations. The endopelvic fascia represents the abdominal side of the levator fascia. The arcus
tendineus represents the insertion of the levator muscle into the obturator muscle of the lateral pelvic
side wall.

A. Pubourethral Ligaments
The pubourethral ligaments are a condensation of levator fascia connecting the inner surface of
the inferior pubis to the midportion of the urethra. They provide support and stability to the
urethra and its associated anterior vaginal wall. These ligaments divide the urethra into proximal
and distal halves; the proximal or intra-abdominal portion is responsible for passive or
involuntary continence. The striated external urethral sphincter is located just distal to the
pubourethral ligaments so that the midurethra becomes primarily responsible for active or

Figure 3 Schematic diagram of the levator muscle fascia viewed from the vaginal side, with specifically
named condensations which form supportive ligamentous structures for the urethra, bladder, and uterus.
 Anatomy of Pelvic Support 5

voluntary continence. The distal one-third of urethra is simply a conduit and does not
significantly change continence when damaged or resected. Weakening or detachment of the
pubourethral ligament causes separation of the urethra from the inferior ramus of the pubic
symphysis. This pathologic process has an unclear role in continence.

B. Urethropelvic Ligaments
The urethropelvic ligaments are composed of a two-layer condensation of levator fascia, which
provides the most important anatomic support of the bladder neck and proximal urethra to the
lateral pelvic wall (Fig. 4). The first layer is known as the periurethral fascia (vaginal side) and is
located immediately beneath the vaginal epithelium, apparent as a glistening white layer
surrounding the urethra. The second layer of the urethropelvic ligament consists of the levator
fascia covering the abdominal side of the urethra (endopelvic fascia), which fuses with the
periurethral fascia. The two layers attach as a unit to the tendinous arc of the obturator fascia
along the pelvic sidewall (Fig. 5). These lateral fusions of the levator and periurethral fascia
provide important, elastic musculofascial support to the bladder outlet, thereby maintaining
passive continence in women. Voluntary or reflex contractions of the levator or obturator
musculature increase the tensile forces across these ligaments, increasing outlet resistance and
continence. Thus, these ligamentous structures are critically important in the surgical correction
of stress incontinence.

C. Pubocervical Fascia (Vesicopelvic Ligament)

The pubocervical fascia is a continuous sheet of connective tissue support from pubic symphysis
to cervix, including the periurethral, perivesical, and endopelvic fascia, which fuse to support the
bladder to the lateral pelvic wall (Fig. 6). It is formed by the fusion of fascia from the bladder
wall and anterior vaginal wall in the region of the bladder base. It is continuous distally with the
periurethral fascia and proximally with the uterine cervix and cardinal ligament complex. This
fascial condensation, sometimes referred to as the vesicopelvic ligament, fuses laterally with the

Figure 4 Schematic diagram demonstrating the urethropelvic ligaments, a two-layer condensation of

levator fascia which envelops the urethra and surrounding neurovascular structures and attaches to the
lateral side wall.
6 Rosenblum et al.

Figure 5 Intraoperative photograph of the urethropelvic ligament, as it attaches laterally to the tendinous
arc.

endopelvic fascia, attaching to the pelvic sidewall at the tendinous arc and supporting the
bladder base and anterior vaginal wall (Fig. 7). Attenuation of this lateral bladder support results
in a lateral cystocele defect (paravaginal).

IV. UTERINE AND VAGINAL VAULT SUPPORT

The cardinal ligaments are thick, triangular condensations of pelvic fascia that originate from
the region of the greater sciatic foramen. They insert into the lateral aspects of a fascial ring
encircling the uterine cervix and isthmus as well as the adjacent vaginal wall, providing
important uterine and apical vaginal support. In addition, the cardinal ligaments are an
important mechanism of support for the bladder base and can be seen extending to the
perivesical fascia. It is often difficult to differentiate the two structures surgically, and sharp
dissection is required. These ligaments contain numerous blood vessels branching from the
hypogastrics that supply the uterus and upper vagina (1). The cardinal ligaments fuse
posteriorly with the uterosacral ligaments (sacrouterine), which stabilize the uterus, cervix,
and upper vagina posteriorly toward the sacrum. They originate from the second, third, and
fourth sacral vertebrae and insert into the posterolateral aspect of the pericervical fascia and
lateral vaginal fornices (6). The fascial unit comprising cardinal ligaments, uterosacral
ligaments, and pubocervical fascia spreads out posterolaterally on each side of the vaginal
apex, uterus, and cervix to the pelvis (7).
The broad ligaments provide additional uterine support and are located more superiorly,
covered by anterior and posterior sheets of peritoneum. They attach the lateral walls of the
uterine body to the pelvic sidewall and contain the Fallopian tubes, round and ovarian ligaments,
and uterine and ovarian vessels.
 Anatomy of Pelvic Support 7

Figure 6 Schematic diagram of the vaginal fascial condensations from the pubic symphysis to the
cervix, including the periurethral fascia, perivesical fascia, and cardinal ligaments. This continuous sheet of
fascial support is also known as the pubocervical fascia.

Figure 7 Schematic diagram of the vesicopelvic ligament, the fascial condensation providing lateral
support to the bladder base and anterior vaginal wall.
8 Rosenblum et al.

V. POSTERIOR VAGINAL AND PERINEAL SUPPORT

A. Rectovaginal Septum
The rectovaginal septum represents a fascial extension of the peritoneal cul-de-sac between the
vaginal apex and the anterior rectal wall. This septum comprises two distinct layers, the posterior
vaginal fascia and the prerectal fascia, which fuse distally at their insertion into the perineal
body. More proximally, these fascial layers fuse with the cardinal-uterosacral complex to
provide support for the posterior vaginal apex. The proximal posterior vagina and intrapelvic
rectum are supported by the pubococcygeus portion of the levator ani group, which inserts into
the midline raphe between the vagina and rectum.

B. Perineum
The perineal body, a tendinous structure located between the anus and vagina in the midline,
provides a central point of musculofascial insertion. This acts as an additional level of pelvic
support, which is elastic in nature, thereby allowing significant distortion and recoil during
childbirth and intercourse (1). Two paired superficial transverse perineal muscles run on each
side of the perineal body to the ischial tuberosities laterally, with a similar deeper pair of
transverse perineal muscles found more superiorly. Voluntary contraction of these transverse
perineal muscles causes lateral vaginal compression as well as stability of the perineum during
acute increases in intra-abdominal pressure.
The perineum can be conceptually divided into anterior and posterior triangular
compartments by drawing a line between the two ischial tuberosities. The anterior urogenital
triangle in the female contains the clitoris, urethra, and vaginal vestibule in the midline. The
ischiocavernosus muscles cover the clitoral crura at their attachments to the pubis. The bulbo-
cavernosus muscles run on each side of the vaginal vestibule beneath the labia between the
clitoris and the perineal body. The anal canal is found in the center of the posterior anal triangle.
The external anal sphincter is composed of two layers of fibers, the deeper layer completely
encircling the anal canal and fusing with the pubococcygeus-puborectal muscles superiorly.

VI. PATHOPHYSIOLOGY OF PELVIC FLOOR DYSFUNCTION

Disruption of the normal supporting structures of the pelvis can occur secondary to numerous
processes. Congenital defects are rare and will usually present in early childhood. Iatrogenic or
traumatic injury as well as heavy physical labor may cause various degrees of pelvic floor
relaxation. Furthermore, nulliparous women may experience pelvic floor dysfunction related to
postmenopausal tissue atrophy (8). Neuromuscular damage of the pelvic floor can be caused by
chronic constipation with straining, childbirth, and pelvic organ prolapse. Such denervation
injury leads to levator ani and coccygeal muscular atrophy and dysfunction, contributing to
pelvic floor relaxation and urinary and fecal incontinence (9).
Deficiency of pelvic support is most commonly related to childbirth or hysterectomy.
Aging is associated with both loss of tissue elasticity and neuronal mass, additional factors
contributing to loss of pelvic support. Genitourinary and bowel manifestations of pelvic floor
relaxation do not routinely occur immediately following childbirth, but often present soon after
menopause, when the hormonal milieu changes. This adds further evidence to the importance of
dynamic changes in pelvic musculature and connective tissue following hormonal alterations,
which contribute to loss of pelvic support. The initial symptom associated with pelvic floor
dysfunction in women is usually stress urinary incontinence. However, bowel, urinary, and
 Anatomy of Pelvic Support 9

sexual functions are all significantly affected by loss of pelvic support. Bladder outlet resistance
is compromised, allowing intravesical pressures to exceed those of the urethra and bladder neck
and leading to urinary incontinence. Thus, the mechanisms of maintaining bladder outlet
resistance in women are an important and integral component of pelvic floor dysfunction.

A. Mechanisms of Urethral Continence in Women

Bladder outlet resistance in women is attained by several factors working together to provide
continence at rest and during stress maneuvers. Urethral anatomy, including functional length and
elastic closure, is an important determinant of continence. In addition, activity of the muscular
pelvic floor with its associated connective-tissue elements helps to maintain outlet resistance
during times of increased intra-abdominal pressure. The anatomic position of the urethra is
another factor contributing to continence. Each of these entities will be discussed separately in
order to provide a basis for understanding the pathophysiology of pelvic floor relaxation.

B. Urethral Length
The distance between internal meatus and external urethral meatus in a female determines
anatomic length. Congenital anomalies and traumatic injuries may result in significant urethral
loss with subsequent incontinence. Functional urethral length is determined by urethral pressure
profilometry where the total urethral length is assessed by urethral pressure exceeding bladder
pressures (10). The clinical utility of urethral length has not been consistently proven. Funneling
of the bladder neck and proximal urethra during straining cystography is seen in up to 50% of
continent women (11). Furthermore, surgical incision of the bladder neck and Y-V plasty do not
cause incontinence in women with otherwise normal outlets. In addition, resection of the distal
one-third of the urethra does not produce incontinence. However, despite these observations, a
critical length of healthy urethra is necessary to provide the coaptation for passive continence
and continence during increases in abdominal pressure. Bladder neck suspensions may restore
functional urethral length, thereby improving continence.

C. Urethral Closure
The urethra is made up of three functional anatomic components that result in an elastic, dynamic
conduit with mucosal coaptation. The urethral mucosa is a transitional epithelium with numerous
infoldings that allow distensibility and closure with excellent coaptation. Beneath the mucosa is
a spongy tissue made up of vascular networks analogous to the corpus spongiosum in the male.
Surrounding the spongy tissue is a thin musculofascial envelope, the periurethral fascia, which
appears as a glistening white membrane. These three components create a coaptive seal.
Urethral closure is also affected by surrounding connective tissue structures. The
pubourethral ligaments provide stability to the midurethra, especially during increases in intra-
abdominal pressure. In addition, the tensile forces of the urethropelvic ligaments along with the
adjacent levator musculature facilitate compression of the proximal and midurethra. Finally, the
striated musculature of the midurethral complex adds resting tone to the urethra, further
effecting closure. Surrounding the sphincteric unit is skeletal musculature that provides an
important additional mechanism for urethral closure. The striated musculature provides resting
urethral tone as well as an involuntary reflex contraction in response to stress that increases
coaptation. Furthermore, voluntary contraction also helps to prevent loss of urine by improving
urethral closure. These mechanisms increase urethral resistance, as measured by leak point
pressures, but may not directly affect urethral pressures.
10 Rosenblum et al.

D. Pelvic Floor Activity During Increased Intra-Abdominal Pressure

Female continence is maintained during increases in intra-abdominal pressure by several distinct
mechanisms. Abdominal pressure is passively transmitted to the proximal urethra followed by an
active contraction of the striated external sphincter musculature (12). Furthermore, the suburethral
supportive layer, made up of periurethral fascia, anterior vaginal wall, and levator ani muscles,
provides a firm backboard against which the urethra is compressed rapidly during increases in
intra-abdominal pressure (13). Both the levator musculature and the urogenital diaphragm undergo
reflex contraction, resulting in increased midurethral pressure. Furthermore, voluntary contraction
of the levator and obturator muscles increases tension on the urethropelvic ligaments. These factors
act in concert to promote urethral continence during changes in position and abdominal pressure.

E. Anatomic Position
Both the bladder neck and the urethra are normally maintained in a high retropubic position
relative to the more dependent bladder base, creating a valvular effect. The bladder neck and
urethra are supported by a musculofascial layer that suspends these structures from the pubic
bone and pelvic sidewalls, thereby preventing their descent during increases in intra-abdominal
pressures (14). A limited degree of bladder base rotation against a well-supported urethra occurs
with increased abdominal pressures, further creating a valvular effect between these two
structures (5). Furthermore, direct transmission of intra-abdominal forces to a well-supported
proximal urethra increases its resistance and promotes coaptation (15).
This complex set of compensatory mechanisms in a normal healthy woman allows
maintenance of sufficient outlet resistance to promote continence, especially during episodes of
abdominal stress such as coughing, sneezing, walking, and straining. Any process that results in
deterioration of these mechanisms can result in incontinence. Urethral function can be
compromised by atrophy of its spongy tissue secondary to menopausal hormonal deficiency,
altered neuromuscular function, or intrinsic damage from surgery, radiation, or trauma. In
addition, a weakening of the levator musculature impairs the compensatory increases in
midurethral pressures during stress. Although these physiologic changes can adversely impact
on continence, the most common etiology of impaired outlet resistance in women is the loss of
anatomic support of the bladder neck and urethra. Relaxation of the pelvic floor as well as
weakening of the urethropelvic ligaments and midurethral complex produces significant
posterior and downward rotation of the urethra and bladder neck (Fig. 8).
This anatomic repositioning of the urethra and bladder neck to a more dependent pelvic
position eliminates the valvular effect. Sudden increases in intra-abdominal forces facilitate
funneling and opening of a poorly supported bladder outlet. The extra-abdominal location of the
poorly supported proximal urethra and the loss of the backboard of strong normal support of
the urethropelvic ligaments do not allow effective transmission of abdominal forces. Although
such anatomic changes can lead to incontinence, urethral hypermobility does not always
correlate with incontinence. Many asymptomatic women with urethral hypermobility on
physical examination do not report urinary incontinence. Thus, the anatomic position of the
urethra alone does not correlate with the degree of incontinence. A component of intrinsic
sphincter deficiency must be present along with these anatomic changes to create incontinence.
The factors responsible for pelvic floor relaxation rarely affect isolated anatomic areas.
Thus, stress urinary incontinence resulting from urethral and bladder neck hypermobility is
often accompanied by associated defects of pelvic support. The identification of these
concomitant defects is crucial to planning effective therapy, with restoration of pelvic support,
anatomic vaginal axis, and outlet resistance. Defects in pelvic support can be organized
 Anatomy of Pelvic Support 11

Figure 8 Schematic diagram demonstrating weakness of the urethropelvic ligament, allowing posterior
and downward rotation of the urethra.

according to their effects on various pelvic organs and structures, in order to allow a more
systematic approach to treatment planning (5). The vaginal compartment contains a confluence
of urinary, genital, and bowel organs. The goal of pelvic reconstructive surgery is to restore both
anatomy and function. However, the restoration of anatomy does not always correlate with
restoration of function.

VII. ANTERIOR VAGINAL WALL PROLAPSE

A. Bladder Neck and Urethra
Bladder neck hypermobility associated with stress incontinence most commonly results from
attenuation of the urethropelvic ligaments or their attachment to the pelvic sidewall at the level of
the tendinous arch of the obturator fascia. Furthermore, intrinsic sphincter deficiency (ISD) in
addition to hypermobility gives way to incontinence. Normally, loss of anatomic position can be
compensated for by the balance of forces that maintain continence: urethral length, urethral
closure, and changes in urethral function that take place during episodes of stress (the valvular
effect, increased urethral resistance secondary to levator contraction, and the transmission of intra-
abdominal forces). Failure of these compensatory mechanisms will lead to stress incontinence.
Recently, more attention has been given to midurethral function as an etiologic factor in
the development of stress incontinence. Normally, the bladder neck acts as the primary
mechanism of continence. However, with intrinsic sphincter deficiency, the midurethral
complex becomes the main compensatory mechanism maintaining continence. Much of our
current armamentarium for curing stress incontinence is aimed at improving mid to distal
urethral function and competence (i.e., transvaginal tape or sling). Although it is unclear how
such methods correct incontinence in this segment of the urethra, we do know that anatomy and
hypermobility have not necessarily been corrected.
In patients with stress incontinence and urethral hypermobility, there is rotational descent
of the bladder neck and urethra under the pubic symphysis. The bladder neck funnels with
Valsalva maneuvers, facilitating the loss of urine. However, the degree of rotational descent
12 Rosenblum et al.

does not correlate with the degree of incontinence. The urethra rotates beyond the pubourethral
ligament, often with separation of the midurethral complex from the inferior pubic ramus. The
significance of this anatomic finding is unclear, but it is thought to play a role in midurethral
function. Videourodynamic evaluation confirms separation of the midportion of the urethra from
its normal attachment to the underside of the symphysis pubis as well as bladder neck and
urethral hypermobility in women with stress incontinence and loss of pelvic support. Based on
these findings we have altered our surgical approach in treating stress incontinence, by focusing
on the midurethral complex during attempts at restoring support.
Although restoration of both anatomic position and underlying support are critical in the
treatment of stress incontinence, it is important to recognize that the majority of women with
bladder neck hypermobility do not experience significant incontinence. Intrinsic urethral
function contributes significantly to continence and may be the determining factor in
compensating for loss of bladder neck and urethral support. Therefore, women with stress
incontinence and bladder outlet hypermobility must have some component of intrinsic urethral
dysfunction. Anatomic support alone is not sufficient to achieve continence if urethral resistance
remains inadequate.

B. Intrinsic Urethral Dysfunction

The plasticity of the highly efficient mucosal seal mechanism found in the urethra allows perfect
continence. Infolding and deformity of the inner mucosal layer create a seal mechanism and
provide a leak-proof mechanism. Minimal extraurethral forces are necessary for continence if
this inner layer is intact. The intrinsic urethral tissues are affected by trophic hormonal
influences. Thus, the lack of estrogen following menopause may lead to thinning and flattening
of the urethral epithelium as well as atrophy of the spongy vascular tissue, which is replaced by
fibrous tissue. Additional factors, which may impair the ability of the urethra to achieve or
maintain a perfect seal, include numerous surgical procedures, pelvic trauma, radiation therapy,
and neurogenic disease.
Incontinence related to the bladder outlet was previously categorized into anatomic
incontinence, due to inadequate support of the bladder neck and urethra, and intrinsic sphincter
dysfunction, due to inadequacy of urethral resistance. However, this differentiation is no longer
important because we now recognize that every woman with stress incontinence has a
component of ISD. Thus, surgical therapy is aimed not only at correcting the anatomical defect
but also at restoring coaptation and urethral closure (16). With compromise of intrinsic urethral
function, stress incontinence may result despite adequate pelvic support. Thus, simple
suspension of the bladder neck or urethra will be insufficient in restoring continence, and
treatment must be aimed at restoring urethral coaptation and compression as well as anatomic
support. Such treatments include sling procedures, injection of urethral bulking agents, or
implantation of artificial sphincter devices.

C. Cystocele
Loss of bladder neck and urethral support represents only one component of anterior vaginal wall
prolapse. A significant number of women with stress incontinence will also have a cystocele,
which may require surgical correction as well. A cystocele is defined as descent of the bladder
base below the inferior ramus of the symphysis pubis, either at rest or with straining (17). Several
systems of classification are in use that grade cystoceles based on degree of descent. We utilize a
system of cystocele grading that includes four degrees of anterior vaginal wall prolapse. Grades I
and II cystourethroceles are described as a mild to moderate degree of anterior vaginal wall
 Anatomy of Pelvic Support 13

hypermobility during straining, usually ,2 cm. As a solitary entity, these are usually
asymptomatic unless associated with significant bladder neck and urethral hypermobility,
leading to stress incontinence. A grade III cystourethrocele is described as descent of the bladder
base and anterior vaginal wall to the introitus during straining, while a grade IV cystourethrocele
is descent of the bladder base and anterior vaginal wall beyond the introitus at rest. These higher
degrees of cystocele are more frequently symptomatic, with complaints of dyspareunia,
a sensation of a painful or painless vaginal bulge, recurrent urinary tract infections, nonspecific
back pain, renal failure, and difficulty walking. Importantly, retention of urine may occur
secondary to kinking at the level of the bladder neck, especially if the urethra has been fixed by
previous surgery (17). Many patients will describe the need to manually reduce the cystocele in
order to facilitate voiding. Silent hydroureteronephrosis can develop as a result of ureteral
obstruction, often confounded by a patient’s delay in seeking treatment.
Anterior vaginal wall support defects are further categorized by location of the primary
anatomic defect. Weakness or disruption of the lateral attachments of the vesicopelvic or
cardinal ligaments to the pelvic sidewall, at the level of the tendinous arch of the obturator,
causes lateral cystocele defects. These lateral defects account for 70 –80% of all anterior vaginal
wall prolapse (17). Central cystocele defects result from attenuation of the vesicopelvic fascia in
the midline, allowing herniation of the bladder base into the vagina (5) (Fig. 9). Isolated central
cystoceles account for 5– 15% of all cystocele defects (17). Commonly, the two support defects
occur in conjunction and are often found in women with high-grade prolapse, such as grade IV
cystoceles (Fig. 10). Both the lateral and the central defects must be corrected at the time of
surgical repair in order to restore anatomic position and prevent progression or recurrence of the
cystocele defect.
The anterior vaginal wall is supported in a rectangular configuration by the cardinal-
sacrouterine ligament complex combined with the periurethral fascia and vesicopelvic
ligaments. The superior aspect of the rectangle is the periurethral fascia, the lateral walls are the
vesicopelvic ligaments, and the inferior aspect (base) is made up of the cardinal ligaments. The
fibers of the pubocervical fascia fuse bilaterally with the anterior aspect of the cardinal

Figure 9 Schematic diagram of a central defect cystocele, resulting from attenuation of the vesicopelvic
fascia in the midline.
14 Rosenblum et al.

Figure 10 Intraoperative photograph of high-grade cystocele following dissection of the perivesical

fascia from the overlying vaginal wall.

ligaments. Thus, in women with good uterine support as a result of strong cardinal ligaments, the
base of this rectangle will be short and centrally located. On the other hand, in cases of uterine
prolapse or significant laxity of the cardinal-sacrouterine ligament complex following
hysterectomy, there will be elongation and separation of the rectangular base and widening of
the levator hiatus. These defects in support allow formation of a central cystocele defect (5).
Thus, the first maneuver during surgical correction of a cystocele involves reapproximation of
the cardinal and uterosacral ligaments to the midline, essentially narrowing the base of the
rectangle to prevent further cystocele progression.

VIII. VAGINAL VAULT PROLAPSE

A. Uterus and Vaginal Vault
The most critical supporting structures of the uterus and vaginal vault are the sacrouterine and
cardinal ligament complex. Relaxation of these structures results not only in anterior vaginal
wall prolapse, but also in vault and uterine prolapse as well as enterocele formation. Uterine
prolapse is described as uterine descent at rest or with straining and is further classified in a
manner similar to cystocele grading, as previously described. Grade I uterine prolapse is
described as minimal mobility, grade II as uterine descent to the level of the midvagina with
straining, grade III as descent to the vaginal introitus with straining, and grade IV, or procidentia,
as prolapse through the introitus. Grades I and II uterine prolapse are often asymptomatic, but
when symptomatic present with back pain aggravated by standing. More severe grades of uterine
 Anatomy of Pelvic Support 15

prolapse are associated with a vaginal mass, pelvic pain, dyspareunia, urinary retention, and
incontinence (17).
Initially, weakness of the sacrouterine ligaments allows anterior movement of the cervix,
compromising the position of the uterus over the horizontal levator plate. The uterine axis
gradually changes, leading to retroversion with the corpus falling backward. Abdominal
pressures are transmitted to the anterior surface of the uterus, causing progression of uterine
prolapse (17). Following hysterectomy, deficient sacrouterine and cardinal ligamentous support
may result in prolapse of the vaginal dome and cuff. Uterine prolapse rarely occurs as an isolated
defect of pelvic support and is treated either by uterine suspension procedures or by
hysterectomy, with treatment of the accompanying defects in pelvic support. Vault prolapse or
eversion requires fixation of the apex to the sacrum, sacrospinous ligament or ileococcygeus
muscle, often in conjunction with repair of anterior and posterior vaginal wall defects (18).

B. Enterocele
An enterocele is defined as a herniation of peritoneum and its contents at the level of the vaginal
apex. Enteroceles occur in the upper, posterior portion of the vagina in association with the cul-
de-sac of Douglas. Most enteroceles are acquired following hysterectomy, caused by separation
of the cardinal-sacrouterine complex and described as a “pulsion” defect at the vaginal dome
(19). Enteroceles are classically divided into four types: Congenital enteroceles result from
failure of fusion of the layers of peritoneum at the level of the rectovaginal septum and are not
associated with cystocele or rectocele. Traction enteroceles occur when prolapse of the vaginal
vault or uterus pulls the peritoneum in a caudal direction. Pulsion enteroceles form as a result of
chronic pressure exerted on the vaginal vault. This force creates a hernia sac and pushes the
vaginal vault caudally, causing a sliding herniation of the vault and anterior vaginal wall along
the surface of the rectum. Pulsion enteroceles are very rarely associated with uterine prolapse.
Iatrogenic enteroceles form following a surgically induced change in the vaginal axis, where the
cul-de-sac of Douglas is left unprotected. Classically, this type of enterocele is seen after
colposuspension, with an incidence of 26.7% following Burch colposuspension (17).
Furthermore, enteroceles can be classified based on associated anatomic findings at the
time of examination, in order to guide the course of treatment. Simple enteroceles exist without
concomitant vault prolapse, and the vaginal cuff is well supported. In addition, no cystocele or
rectocele is present. Complex enteroceles are associated with vault or uterine prolapse, with poor
support of the vaginal cuff. Prolapse may include the anterior vaginal wall (cystocele) or the
posterior vaginal wall (rectocele) (17). In patients with complex enteroceles there are two
discrete defects: separation of the prerectal from the perivesical fascia, and descent of the vault
due to weakness of the sacrouterine and cardinal ligaments. Both of these defects must be
addressed during vault prolapse repair.
In general, enteroceles are minimally symptomatic until descent reaches the level of the
hymen. The patient may complain of a sensation of fullness in the perineal area or sensation of a
vaginal bulge. Dyspareunia, vaginal discomfort, and low back pain accentuated in the upright
position are also common. In rare instances, complications of bowel obstruction may be seen.
Concomitant cystocele and/or rectocele may produce bowel and bladder symptoms (17).
Diagnosis of an enterocele is made by physical examination, often with observation of a vaginal
mass bulging through the introitus. Bimanual rectovaginal examination during straining may
reveal an impulse of the peritoneal sac against the examining fingertip. Furthermore, thickness of
the proximal rectovaginal septum may be appreciated. Radiographic imaging can be utilized to
confirm the suspected diagnosis of an enterocele. Plain film radiography may reveal bowel gas
within a prolapsing mass below the pubic symphysis. A voiding cystourethrogram during
16 Rosenblum et al.

straining will exclude the bladder as the source of a mass (17). Magnetic resonance imaging of
the pelvis during both a relaxed and straining state can elucidate the presence of an enterocele.
Fat, small intestine, fluid, and bowel gas can be identified within a protruding vaginal mass well
below the pubococcygeal line (20). Enterocele repair commonly involves repair of concomitant
pelvic prolapse defects as well as resuspension of the vaginal vault.

IX. POSTERIOR VAGINAL WALL PROLAPSE AND PERINEUM

Two distinct levels of musculofascial support, the pelvic floor (the pubococcygeal portion of the
levator ani musculature) and the perineum, make up the posterior vaginal wall in addition to
the prerectal and pararectal fasciae. The perineum is made up of the bulbocavernosus muscle, the
superficial and deep transverse perineal muscles, the external anal sphincter, and the central
tendon of the perineum (21,22) (Fig. 11). In the normal upright female, the proximal two-thirds
of the vagina is 1108 from the horizontal plane compared with the distal one-third.
The transition from proximal to distal vagina occurs at the point where the vagina crosses the
pelvic floor, influenced by the degree of support of the levator musculature and urogenital
diaphragm. Thus, the proximal half of the vagina is oriented horizontally, lying over the levator
plate (Fig. 12). Levator contraction pulls the vagina forward and increases the angulation
between proximal and distal posterior vagina. Changes in intra-abdominal pressure tend to
further close and support the posterior vaginal wall, thereby preventing prolapse. When the
posterior vaginal wall axis is altered, i.e., following bladder neck suspension, intra-abdominal

Figure 11 Schematic diagram of perineal musculature, providing support to posterior vaginal wall
and rectum.
 Anatomy of Pelvic Support 17

Figure 12 Schematic diagram representing a sagittal view of the pelvis with a normal vaginal axis. The
proximal portion of the vagina lies horizontally, resting on the levator plate, providing support for the
uterus, rectum, and bladder base.

forces tend to push the posterior vaginal wall forward, increasing the tendency for rectocele
formation. The levator musculature and the perineal body support the distal aspect of the
vagina (17).
Damage to or relaxation of the levator musculature results in widening and elongation
of the levator hiatus and disappearance of the normal proximal vaginal axis. The posterior
vaginal wall becomes flattened, and intra-abdominal forces will tend to make the posterior
vaginal wall prolapse forward (17). There are several components of posterior vaginal wall
support to take into consideration: the presence of a rectocele; separation of the levator hiatus;
relaxation and widening of the introitus; and relaxation and herniation of the perineum. In
addition, damage to the perineal support mechanisms results in further widening of the
vaginal introitus, with an increase in the distance between the urethra and the posterior
fourchette. Perineal tears may also be present in varying degrees, the most severe form being
direct continuity between the posterior vaginal wall and underlying rectum. The result of
these anatomic changes is the development of a rectocele, possibly a posterior and high
enterocele and perineal laxity.
The importance of the rectovaginal septum as a supporting structure for the rectum has
been emphasized by Richardson (23). Milley and Nichols described this layer of fascia after
performing both surgical and cadaveric dissections. This fascial layer envelops the posterior
vaginal wall, merging into the uterosacral ligaments and adhering to the cul-de-sac peritoneum.
Distally, it merges into the perineal body fusing with the fibers of the deep transverse perineal
muscle. Laterally, this fascial layer fuses with the iliococcygeus and pubococcygeus muscles
just below the arcus tendineus (23). The rectovaginal septum acts to separate the rectal
compartment from the urogenital compartment.
18 Rosenblum et al.

A. Rectocele
A rectocele is described as intravaginal herniation of the rectum through an attenuated
rectovaginal septum. In addition, defects in the prerectal and pararectal fasciae are also
associated with rectocele formation. Isolated breaks in the rectovaginal septum facilitate
rectocele formation. Generally, there are several areas along the rectovaginal septum where
breaks are commonly found. The most common site is a transverse separation immediately above
the attachment of this septum to the perineal body, resulting in a low rectocele (seen just inside
the introitus). A midline vertical defect is equally common and most likely represents a
poorly repaired or poorly healed episiotomy. Rarely, one can see lateral separation on one side
(23).
Symptoms of rectocele are often related to bowel function and sexual intercourse; they
include a sensation of fullness in the vagina, a mass bulging through the introitus, difficulty with
rectal evacuation, constipation, the need for manual reduction to improve bowel emptying, and
interference with intercourse (17).
The diagnosis of a posterior vaginal wall support defect is made by physical examination.
A rectocele manifests as a bulge extending from the posterior vaginal wall, which can be better
identified by placing a half-speculum anteriorly to support the anterior vaginal wall and bladder
during straining maneuvers. Bimanual rectovaginal examination reveals significant attenuation
of the rectovaginal septum. In addition, loss of the normal right-angle configuration between the
proximal and distal vaginal segments is exhibited. Similar to enteroceles, rectoceles can be
diagnosed radiographically by the presence of bowel gas below the inferior pubic ramus on plain
radiography or by magnetic resonance imaging of the pelvis during relaxed and straining
conditions (Fig. 13).
It is rare to find an isolated posterior wall defect, or rectocele. One must identify associated
defects in pelvic floor support prior to planning surgical correction. Perineal tears are commonly
seen in conjunction with severe rectoceles in multiparous women. Type I defects have an intact,
but thin, perineum with a defect in the anterior muscle fibers of the external anal sphincter, the
puborectalis muscle and perirectal fascia, and the transverse perineal muscles. Type II defects
result in total loss of the perineal body secondary to obstetric trauma. Type III defects present
with a rectovaginal fistula in the lower rectovaginal wall following a history of obstetric trauma.
In type IV defects, a fistula is present in the bottom third of the vaginal wall with an intact
perineum. This usually results from a partially healed fourth-degree laceration during delivery.
These defects in the perineum, with resultant widening of the levator hiatus, may lead to
progressive loss of control of both gas and feces (24). Further discussion of external anal
sphincter defects as well as perineal herniation is found in subsequent sections.

B. Perineal Laxity
Perineal herniation or laxity results most commonly from obstetric trauma, with attenuation of
the central tendon of the perineum. The discrete anatomic defect results in an increase in
the distance from the posterior fourchette to the anus as well as an outward convexity of the
perineum during straining. In addition, perineal laxity contributes further to widening of the
vaginal introitus. This defect in perineal support can be seen either with or without a concomitant
rectocele. Symptoms or signs specifically associated with perineal body defects can include
incontinence of stool, incontinence of flatus, or severe constipation requiring perineal pressure to
facilitate defecation. In general, this is a relatively rare condition and is often associated with a
severe degree of posterior vaginal wall prolapse.
 Anatomy of Pelvic Support 19

Figure 13 Magnetic resonance imaging of the pelvis in a sagittal plane during straining. A large, dark
structure is seen below the both the pubococcygeal line and puborectalis muscular sling, representing a
high-grade rectocele.

C. Anal Sphincter
Damage to the external anal sphincter can also result from obstetric trauma, such as grade IV
perineal tear involving the rectum and/or anus or injury to the central tendon of the perineum as
previously mentioned. Furthermore, anal sphincter laxity or defects can be a result of neurologic
injury. This defect will lead to fecal incontinence, incontinence of flatus, poor sphincter tone on
physical examination, and a palpable anatomic defect in the external anal sphincter. This defect
is often present when signs of perineal laxity are found in addition to high-grade pelvic prolapse.
Reconstruction of the anal sphincter involves transperineal plication of the levator ani
musculature and the external anal sphincter as well as reapproximation of the transverse perineal
musculature to the external anal sphincter.

X. CONCLUSIONS

A complete and thorough understanding of pelvic floor anatomy provides a basis for the goals of
vaginal and pelvic reconstructive surgery. First, identification of all pelvic floor pathology and
organ prolapse is necessary to plan a definitive therapeutic approach to reconstruction.
Diagnostic imaging of pelvic prolapse is a useful adjunct to physical examination, specifically
haste sequence magnetic resonance imaging during relaxed and strained states. Concurrent
20 Rosenblum et al.

pelvic organ pathology, including ovarian and uterine abnormalities as well as hydronephrosis,
can be identified and subsequently addressed at the time of surgical intervention. Repair of all
elements of pelvic floor prolapse must be achieved with special emphasis given to restoration of
vaginal axis. The normal posterior curvature of the proximal vagina must be restored to allow
intra-abdominal forces to cause vaginal coaptation and prevent subsequent or recurrent organ
prolapse. This goal of reconstructive surgery cannot be overemphasized.

REFERENCES

1. Klutke CG, Siegel CL. Functional female pelvic anatomy. Urol Clin North Am 1995;
22:487– 498.
2. De Lancey JO. Surgical anatomy of the female pelvis. In: Rock JA, Thompson JD, eds. Te Linde’s
Operative Gynecology. Philadelphia: Lippincott-Raven, 1997:63 – 93.
3. Tanagho EA. Anatomy of the lower urinary tract. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED,
eds. Campbell’s Urology. Philadelphia: W.B. Saunders, 1992:40 –69.
4. Redman JF. Surgical anatomy of the female genitourinary system. In: Buchsbaum HJ, Schmidt JD,
eds. Gynecologic and Obstetric Urology. Philadelphia: W.B. Saunders, 1993:25 – 60.
5. Raz S, Little NA, Juma S. Female urology. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED, eds.
Campbell’s Urology. Philadelphia: W.B. Saunders, 1992:2782 – 2829.
6. De Lancey JOL, Richardson AC. Anatomy of genital support. In: Hurt WG, ed. Urogynecologic
Surgery. Gaithersburg, IL; Rockville, MD: Aspen Publishers, 1992:19 – 33.
7. Baden WF, Walker T. The anatomy of uterovaginal support. In: Baden WF, Walker T, eds. Vaginal
Defects. Philadelphia: Lippincott, 1992:25 – 50.
8. Stanton SL. Vaginal prolapse. In: Raz S, ed. Female Urology. Philadelphia: W.B. Saunders,
1983:229– 240.
9. Strohbehn K. Normal pelvic floor anatomy. Obstet Gyn Clin North Am 1998; 25:683 –705.
10. Bruskewitz R. Urethral pressure profile in female lower urinary tract dysfunction. In: Raz S, ed.
Female Urology. Philadelphia: W.B. Saunders, 1983:112 – 122.
11. Versi E, Cardozo LD, Studd JWW, Brincat M, O’Dowd TM, Cooper DJ. Internal urinary sphincter in
maintenance of female continence. B M J 1986; 292:166 – 167.
12. Steers WD. Physiology and pharmacology of the bladder and urethra. In: Walsh PC, Retik AB,
Vaughan ED, Wein AJ, eds. Campbell’s Urology. Philadelphia: W.B. Saunders, 1998:870 – 915.
13. Wein AJ. Pathophysiology and categorization of voiding dysfunction. In: Walsh PC, Retik AB,
Vaughan ED, Wein AJ, eds. Campbell’s Urology. Philadelphia: W.B. Saunders, 1998:917 – 926.
14. Blaivas JG, Romanzi LJ, Heritz DM. Urinary incontinence: pathophysiology, evaluation, treatment
overview, and nonsurgical management. In: Walsh PC, Retik AB, Vaughan ED, Wein AJ, eds.
Campbell’s Urology. Philadelphia: W.B. Saunders, 1998:1007 – 1043.
15. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand
1961; 276:3.
16. Raz S, Siegel AL, Short JL, Snyder JA. Vaginal wall sling. J Urol 1989; 141:43– 46.
17. Raz S, Stothers L, Chopra A. Vaginal reconstructive surgery for incontinence and prolapse. In:
Walsh PC, Retik AB, Vaughan ED, Wein AJ, eds. Campbell’s Urology. Philadelphia: W.B. Saunders,
1998:1059 –1094.
18. Raz S. The anatomy of pelvic support and stress incontinence. In: Raz S, ed. Atlas of Transvaginal
Surgery. Philadelphia: W.B. Saunders, 1992:1 –22.
19. Zacharin RF. Pulsion enterocele: review of the functional anatomy of the pelvic floor. Obstet Gynecol
1980; 55:135 –140.
20. Rodriguez LV, Raz S. Diagnostic imaging of pelvic floor dysfunction. Curr Opin Urol 2001;
11:423– 428.
 Anatomy of Pelvic Support 21

21. Huisman AB. Aspects of the anatomy of the female urethra with special relation to urinary
continence. Contrib Gynecol Obstet 1983; 10:1 – 31.
22. Joseph J. Female genital structure and function. The bones, joints, and ligaments of the female pelvis.
In: Phillip E, Barnes J, Newton M, eds. Scientific Foundations of Obstetrics and Gynecology.
Chicago: Year Book, 1986:86 – 94.
23. Richardson AC. The rectovaginal septum revisited: its relationship to rectocele and its importance in
rectocele repair. Clin Obstet Gynecol 1993; 36:976 –983.
24. Wiskind AK, Thompson JD. Fecal incontinence and rectovaginal fistulas. In: Rock JA, Thompson JD,
eds. Te Linde’s Operative Gynecology. Philadelphia: Lippincott-Raven, 1997:1207 – 1236.
2
Neurophysiology of Micturition

Gamal M. Ghoniem
Cleveland Clinic Florida and the Cleveland
Clinic Foundation Health Sciences Center of OSU, Weston, Florida, U.S.A.
John C. Hairston
University of Texas Medical School at Houston, Houston, Texas, U.S.A.

I. INTRODUCTION

The lower urinary tract has two essential functions: the low-pressure storage of urine in a
continent reservoir, and the timely expulsion of stored urine in a coordinated, efficient, and
complete fashion. These two mutually exclusive functions are ultimately determined by the
activity of the smooth and striated musculature of the bladder, urethra, and external urethral
sphincter under the control of various neural circuits in the brain and spinal cord. Although a
result of complex interplay between both the central and peripheral nervous systems, these
functions are also influenced by several anatomic factors such as integrity of the pelvic floor
support and dynamic relationship of the bladder and its outlet to various points in the bony
pelvis and adjacent organs during voiding. In addition, as our understanding of lower urinary
tract neurophysiology grows, so grows the list of neurotransmitters and receptors identified as
having a role in voiding function and dysfunction. Voiding dysfunction can occur as a result
of neurologic disease or injury, disturbance of anatomical relationships within the pelvis and
urinary organs, or as an unwanted, often unrecognized pharmacologic effect of medical
therapy for other diseases. Voiding dysfunction also occurs as a result of normal aging and
is affected by changes in the viscoelastic properties of the bladder wall. As with other
neurologic systems, innervation of the lower urinary tract is not static; it changes in
response to disease and aging. This phenomenon is known as neural plasticity. More often
than not, the etiology of voiding dysfunction is multifactorial, so a fundamental under-
standing of the neuroanatomy and neurophysiologic mechanisms of the lower urinary tract is
essential.

II. PROPERTIES OF DETRUSOR MUSCLE AND BLADDER WALL

A. Excitation-Contraction Coupling
The process of force generation of muscle in response to ligand binding has been termed
excitation-contraction coupling. It is a very complex process that results from molecular changes
23
24 Ghoniem and Hairston

induced by a neurotransmitter crossing the postsynaptic cleft. The details of these intricate
events are beyond the scope of this chapter and best left to a major physiology text, but the
central concepts can be summarized as follows.
Smooth muscle cell morphology differs from that of striated muscle in that the major
contractile protein in smooth muscle is actin, whereas myosin predominates in striated muscle.
Nevertheless, force is ultimately generated by interaction of these two myofilaments. Cardiac
muscle and striated muscle have been studied to a much larger extent than smooth muscle,
but much of what we know about smooth-muscle physiology comes from the fields of
gastroenterology and obstetrics. The molecular events leading to smooth-muscle contraction are
shown in Figure 1. The first step in this process is smooth-muscle cell excitation by either ligand
binding (neurotransmitter with its associated receptor) or membrane depolarization. This leads
to an increase in free cytosolic calcium. Free cytosolic calcium ion levels are usually ,0.1 mM.
Total intracellular calcium concentrations are much higher, indicating a considerable pool of
stored calcium. The increase in cytosolic calcium may come from influx across the cell
membrane of extracellular calcium through specific voltage-sensitive channels or via release of
intracellular stores. The release of intracellular stores can be triggered by second messengers
such as inositol trisphosphate (IP3), cyclic AMP, or guanosine triphosphate (GTP). The excess
of free cytosolic calcium binds with calmodulin, altering this molecule and allowing it to bind to
the enzyme myosin light-chain kinase. Myosin light-chain kinase causes phosphorylation of
the myosin light chain, which then interacts with actin, causing a conformational change of these
proteins and allowing them to slide over each other, thus shortening the muscle. Adenosine
triphosphate (ATP) is a necessary cofactor for this step. This process can be repeated over and
over as long as there is a stimulus for contraction.
The process of muscle relaxation also depends highly on ATP. A significant amount of
energy is expended by certain ATP-dependent pumps (ATPases) as they act to pump calcium
(often against tremendous gradients) out of the cell or into storage sites thus allowing calcium
homeostasis and cell repolarization.

Figure 1
 Neurophysiology of Micturition 25

B. Compliance
The ability of the bladder to accommodate increasing volumes of urine at low pressures is
termed bladder compliance. In mathematical terms, it is measured as a change in unit volume
per change in pressure (C ¼ DV/DP). A bladder that can hold large volumes of urine at low
pressures is “highly” compliant. At physiologic rates of filling (,10 mL/min), bladder pressure
rarely rises above 10 cm H2O up to a capacity of 400 –500 cc. This phenomenon is unique to the
bladder as an organ if one considers that bladder smooth muscle must undergo a 100 –200%
displacement in slack length to create this kind of compliance. The vena cava, in contrast, need
only undergo 25 – 50% displacement to produce significant changes in vessel diameter (1).
Compliance is a product of both the neuromechanical and viscoelastic properties of the bladder
wall. The fact that even acutely denervated bladders maintain adequate compliance underscores
the importance of the passive viscoelastic properties in maintaining adequate bladder com-
pliance. The human bladder wall is composed of detrusor smooth muscle interspersed with
islands of connective tissue or extracellular matrix (ECM). The ECM is composed of proteins
such as collagen, proteoglycans, elastin, and many other molecules that are now being identified.
Because bladder muscle does not have a “skeleton” on which to exert force, these ECM proteins
are extremely important with regard to energy transmission. They are also crucial to compliance,
and any alteration in the composition of the ECM can result in decreased compliance. Such
alterations can occur with chronic inflammation, injury, obstruction, or chronic denervation and
typically result in increased collagen content and fibrosis. There is no agreement yet on the
definition of abnormal compliance values. Ghoniem suggested that a value of ,10 mL/cm H2O
is severely impaired compliance and dangerous to the upper urinary tracts, 10– 20 mL/cm H2O
is moderately impaired and .20 mL/cm H2O is normal.

III. LOWER URINARY TRACT INNERVATION

The pelvic and hypogastric nerves supply the bladder and urethra with efferent parasympathetic
and sympathetic neurons, and both convey afferent (sensory) neurons from these organs to the
spinal cord. The storage phase of micturition is controlled primarily by sympathetic, and void-
ing phase by parasympathetic, vesicourethral innervation. The somatic innervation is important
mainly in regard to the musculature of the pelvic floor and the external or striated urethral
sphincter (EUS), and is supplied via efferents in the pudendal nerve (2 – 4).

A. Parasympathetic Supply
The parasympathetic efferent supply is classically described as originating in the
intermediolateral region of the gray matter of the spinal cord segments S 2 – 4 and emerges as
preganglionic fibers in the ventral roots and exits as the pelvic nerve. This nerve courses deep in
the pelvis on each side of the rectum as three or four trunks in human. Bilaterally, at a variable
distance from the bladder and urethra, the pelvic and hypogastric nerves meet and branch to
form the pelvic plexus, sometimes known as the inferior hypogastric plexus, or plexus of
Frankenhauser. This is a plexus of freely interconnected nerves in the pelvic fascia that is lateral
to the rectum, internal genitalia, and lower urinary organs. Divergent branches of this plexus
innervate these pelvic organs. The hypogastric and pelvic nerves also carry afferent autonomic
nerve impulses to synapses in the dorsal column of the lumbosacral spinal cord (2,3).
26 Ghoniem and Hairston

B. Sympathetic Supply
The sympathetic innervation to the lower urinary tract originates in the intermediolateral nuclei
of the thoracolumbar spinal cord in segments from T11 through L2 or L3. They traverse the
lumbar sympathetic ganglion and join the presacral nerve (superior hypogastric plexus). The
hypogastric plexus lies anterolateral to the great vessels at the level of third lumbar to first sacral
vertebrae and gives rise to the left and right hypogastric nerves which are really elongated nerve
plexuses. These nerve plexuses join the pelvic nerves to form the plexuses of Frankenhauser,
from which they spread out to innervate the pelvic organs (5).
As demonstrated by Gilepsie, two nerve bundles extended from the inferior hypogastric
plexus (plexus of Frankenhauser), each accompanied by artery derived from the vaginal artery
(6). The first bundle (vesicoureteric plexus) parallels the inferior border of the ureter until it
reaches the cardinal ligament, from where, some fibers supply the dorsum of the bladder, while
the remaining nerve fibers continue to parallel the ureter to pierce the bladder at the level of the
interureteric ridge of the trigone. The destruction of this plexus (vesicoureteric plexus) was
found effective in the treatment of women with hypersensitive bladder disorders. The second
nerve bundle passes downward to the junction of the urethra with the anterior wall of the vagina.
However, more anatomical dissections are needed for this area.
Classically, the autonomic nervous system has been regarded as a two-neuron system
composed of two neuron models; preganglionic and postganglionic neurons. Elbadawi has
nicely reviewed the anatomic aspects of the contemporary modifications of classical autonomic
nervous system (7 –11). He stated that the muscular innervation of the lower urinary tract is
derived exclusively from postganglionic neurons of what is called the urogenital short neuron
system. Although paraganglia and preganglia exist, actual innervation predominantly emanates
from peripheral ganglia that are at a short distance from, adjacent to, or within the organs they
innervate, thus the name short. The ganglia are composed of three cell types: cholinergic
principal neurons, adrenergic principal neurons, and small intensely fluorescent (SIF) cells. The
SIF cells are thought to play an important role in modulation of interganglionic vasomotor
function and ganglionic transmission. In addition, there are complex intraganglionic networks of
cholinergic and adrenergic fibers. Thus, there is a wide variety of modulating synaptic relays. In
addition, postganglionic neurons do not necessarily terminate in the peripheral end organ, but
many actually terminate within the ganglia of some systems. Increasing scientific work is
revealing that the neural control of the lower urinary tract is more complex than had previously
been thought.

C. Somatic Supply
The somatic supply arises from motorneurons in the anterior horn of S2, S3, and S4, clustered in
an area known as Onuf’s nucleus. There are contradictory views of the neural supply of the
striated sphincter. The EUS is composed of an extramural and intramural component that differ
physiologically and will be discussed later. However, most authors agree that the striated
sphincter, including both components, is innervated only through motor end plates, implying
purely somatic innervation, through there may be differences in opinions regarding the actual
nerve trunks carrying these fibers (4,12). In a recent neuroanatomical study, Hollabaugh et al.
described an intrapelvic branch of the pudendal nerve that joins the pelvic nerve branch at the
level of the proximal urethral sphincter (13). The morphologic evidence of autonomic
innervation of the striated sphincter has not been definitively demonstrated in other species or in
human. However, Elbadawi and Atta (11) reported that there is evidence for triple innervation
(somatic plus cholinergic and adrenergic autonomic) of the intramural striated sphincter of the
 Neurophysiology of Micturition 27

male cat. This finding is supported by electrophysiologic studies (14). These conclusions are
applicable only to the intramural portion of the striated sphincter, and other authors’ conclusions
regarding the intramural component may have been erroneously drawn from specimens from the
adjacent extramural component.

IV. NEUROTRANSMISSION AND RECEPTORS

A. General
In both the parasympathetic and sympathetic systems, the preganglionic neurotransmitter is
acetylcholine, which affects nicotinic cholinergic receptors. The primary postganglionic
parasympathetic neurotransmitter is also acetylcholine, which affects muscarinic cholinergic
receptors, while the postganglionic sympathetic neurotransmitter is a catecholamine,
norepinephrine, which affects the adrenergic receptors. Newer scientific data are supporting
the existence of many other neurotransmitters and receptors responsible for lower urinary tract
function. These include ATP, nitric oxide (NO), dopamine, serotonin, glutamine, gamma amino
butyric acid (GABA), various neuropeptides, and prostanoids. Representative parasympathetic
and sympathetic nerve terminals are depicted in Figures 2 and 3.

Figure 2
28 Ghoniem and Hairston

Figure 3

B. Cholinergic Mechanisms
The voiding phase of the micturition cycle is primarily controlled by the parasympathetic
nervous system. Stimulation of the pelvic nerves produces a strong, sustained bladder
contraction that leads to bladder emptying. Cholinergic receptors are ubiquitous throughout
the bladder body but scarce at the region of the bladder neck and the ventral part of the urethra.
They are absent in an area called the superficial trigonal muscle. The human bladder has two
muscarinic cholinergic receptor subtypes, M2 and M3. M2 receptors predominate immuno-
histochemically (80% overall), but functional studies show that bladder contractions are
mediated primarily by M3 receptors through hydrolysis of phosphoinositol and the resultant
release of intracellular calcium (15,16). M1, M2, and M4 receptors are also present
prejunctionally on nerve terminals in the bladder and are thought to play a modulating role
through amplification (M1) and inhibition (M2 and M4) of acetylcholine release (17,18). Drugs
with anticholinergic properties such as propantheline, dicyclomine, imipramine, and oxybutynin
have been used for many years to suppress overactive detrusor contractions. The usefulness of
these medicines, however, has been somewhat limited owing to their lack of specificity with
regard to mucscarinic receptors. Muscarinic receptors are also present extensively in salivary
glands, bowel, and the accommodation apparatus of the eye, with M3 receptors predominating
in the salivary glands. As a result, the use of standard antimuscarinic drugs often leads to
intolerable side effects such as dry mouth, constipation and visual disturbances.
Newer, more selective muscarinic antagonists are being developed. Tolterodine, a
competitive antagonist that binds all receptor subtypes, was shown in clinical studies to be equal
in efficacy to oxybutynin in reducing micturition frequency and urge incontinence episodes
while having a lower incidence of dry mouth (19). The apparent bladder selectivity of these
newer agents may be due to several factors. The action of these drugs on prejunctional
muscarinic receptors may play a larger role than initially thought. In addition, heterogeneity of
the M3 receptor population has been postulated. In fact, radioligand-binding studies showed
tolterodine and oxybutynin to have similar affinities for M3 receptors in the bladder, but
oxybutynin had an eightfold higher affinity for parotid gland M3 receptors. These types of
 Neurophysiology of Micturition 29

sensitivity differences have also been detected with other M3-selective antagonists, darifenacin
and zamifenacin (15,20).
Botulinum toxin, now commonly used for treatment of skeletal muscle spasticity, inhibits
acetylcholine release from cholinergic nerve terminals. It has been used successfully in the
treatment of detrusor-sphincter dyssynergia in spinal cord-injured men by injecting it into the
external sphincter to lower outlet resistance (21). It is also showing promise as a treatment for
bladder hyperreflexia and possibly overactive bladder. Injection of the toxin into detrusor muscle
has been effective in suppressing contractions in these patient populations, and further studies
are eagerly awaited (22).
Bethanechol chloride, a cholinergic agonist, has been used rather commonly to enhance
voiding, and this seems theoretically sound. Although cholinergic agonists may raise baseline
bladder pressure, the use of such agents does not appear to be clinically useful in promoting
bladder emptying (23 –25). There are several reasons for this. Cholinergic agonists appear to
cause a reflex sympathetic urethral constriction, prohibiting coordinated voiding (26). Further-
more, cholinergic activation leads to a feedback mechanism via the aforementioned pre-
junctional M2 and M4 receptors, inhibiting further acetylcholine release. Finally, bethanechol
is poorly absorbed from the gastrointestinal tract, necessitating subcutaneous administration or
prohibitively high oral doses to achieve pharmacologic effect.

C. Adrenergic Mechanisms
The adrenergic receptors (a and b) have different distributions in the lower urinary tract. The a
receptors are distributed mainly in the urethra and bladder neck. They are further subclassified
into a1 (postsynaptic) and a2 (presynaptic) receptors. Stimulation of a1 receptors regulates
vasoconstriction and smooth muscle contraction, whereas stimulation of a2 receptors inhibits
the release of norepinephrine from nerve terminals through a negative feedback mechanism.
Several subtypes of the a1 receptor have been identified. Studies have shown that a1 receptors
in the urethras of humans are of the a1a subtype (27,28). In addition, radioligand binding has
suggested the majority of a receptors in female animals are a2, whereas a1 receptors pre-
dominate in the male (29).
Phentolamine and phenoxybenzamine are both nonspecific a-adrenergic antagonists and
are not routinely used in the treatment of voiding disorders. Prazosin, doxazosin, and terazosin
are relatively selective antagonists of a1 receptor sites and are commonly used in the treatment
of outlet obstruction in males secondary to benign prostatic hyperplasia because of their relax-
ing effect on prostatic smooth muscle. The use of these agents is somewhat limited by
cardiovascular side effects owing to the presence of a1 receptors throughout the vascular tree.
Tamsulosin, an a1a-selective antagonist, targets urethral smooth muscle with a decreased
incidence of cardiovascular side effects such as postural hypotension. Although sometimes used
to treat female bladder outlet obstruction, the efficacy of these drugs in this capacity has not been
definitively established, chiefly owing to a lack of standardized criteria to define this entity in
women. Any lack of efficacy may also be explained by the deficiency of a1 receptors in the
female urethra. a-Stimulating drugs such as phenylpropranolamine and ephedrine will increase
the tone of urethra and bladder neck by stimulating smooth muscle contraction at these sites.
In fact, over-the-counter cold medications and decongestants are a common cause of urinary
retention in elderly males. It is also for this reason that these drugs have been used in the
pharmacologic treatment of stress incontinence in women (30).
There have been conflicting animal studies regarding the role of a receptors in the spinal
cord, with data to support both inhibitory and facilitative influences. Some studies have indicated
an excitatory role for a1 receptors at both the end-organ level and in the spinal cord. These
30 Ghoniem and Hairston

effects include the release of NO, the enhancement of acetylcholine release (a1a), and direct
excitatory effects on bladder smooth muscle (a1b/a1d) (31,32). This last postjunctional
excitatory effect is hardly present in younger animals but becomes prominent in older animals,
supporting the concept of neural plasticity and change of adrenergic receptor expression over
time. In addition, the intrathecal administration of doxazosin (a1 antagonist) has been shown to
suppress bladder hyperactivity and decrease the amplitude of bladder contractions in rats (33).
This effect was more pronounced in the setting of chronic bladder outlet obstruction, again
suggesting the plastic nature of neural control of the diseased bladder. There is other evidence to
support age-related changes in lower urinary tract adrenergic receptor expression, an intriguing
concept that may hold promise for future research.
b-Adrenergic receptors in the urinary tract (b2) tend to cluster in the bladder body, as
opposed to the bladder base and neck. They appear to modulate smooth-muscle relaxation;
b stimulants, e.g., terbutaline, cause bladder relaxation and may contribute to urinary retention
when given in high doses for premature labor. Unfortunately, b agonists do not appear to be
clinically useful in treating detrusor instability (DI) (34).
The role of the sympathetic nervous system in the lower urinary tract is a matter of dispute.
However, many authors advocate its major role in the lower urinary tract. The sympathetic
nervous system acts primarily to facilitate the filling and/or storage phase of micturition and
does so by three mechanisms: (a) increasing accommodation by stimulation of b-adrenergic
receptors in the bladder body; (b) increasing outlet resistance by stimulation of the
predominantly a-adrenergic receptors in the bladder base and proximal urethra and by causing
an increase in activity of striated muscle of the pelvic floor (“guarding reflex”); and (c) inhibiting
bladder contractility by means of a blocking effect on parasympathetic ganglionic transmission
(35,36). Edvardsen postulated a spinal reflex in the cat—with afferents in the pelvic nerves and
efferents in the hypogastric nerves—causing bladder relaxation during filling and therefore an
increased volume threshold for micturition (37,38). Consistent with this hypothesis is the fact
that in the cat b-adrenergic blockade or surgical sympathectomy has been reported to increase
bladder activity, decrease bladder capacity, and produce a shift to the left of the accommodation
limb of the cystometric curve (39,40).

D. Nonadrenergic, Noncholinergic Mechanisms

The fact that not all bladder contractile activity can be blocked by atropine even with massive
doses (the phenomenon of atropine resistance) has led to the postulation of nonadrenergic,
noncholinergic (NANC) neurotransmitter system, which is responsible for part of the
neurotransmission in the bladder. Experimental studies on bladder muscles have shown that the
bladder contraction is biphasic. Only the contraction of the second phase can be blocked by
atropine; not the first phase. ATP and other substances are responsible for the contraction of
the first phase (41,42). More recently, numerous substances have been shown to play a role in
regulation of the lower urinary tract. These substances acting as neurotransmitters or
neuromodulators, include an extensive list, e.g., opioids, vasoactive intestinal polypeptide (VIP),
serotonin, dopamine, glutamic acid, GABA, ATP, and prostaglandins (F2, E, E2). Many of these
substances exhibit both inhibitory and facilitative influence on the micturition cycle at the spinal
cord level and higher. These developments have significant potential implications for the future
development of drugs affecting nervous control mechanisms in the urinary tract and elsewhere
(43,44). However, the role of NANC mechanisms in the contractile activation of the human
bladder is still disputed. In normal human detrusor, atropine was found to cause .95%
inhibition of electrically evoked contraction (45). In detrusor strips from patients with a
diagnosis of unstable bladder or from patients with benign prostatic hyperplasia, atropine
 Neurophysiology of Micturition 31

resistance was found in up to 65% (46). These apparently conflicting data may be explained by
differences in the tissues investigated. Ghoniem found a significant atropine-resistant component
to the electrically induced detrusor contraction of meningomyelocele patients undergoing
augmentation cystoplasty, which was absent in normal bladders of patients undergoing ureteral
reimplantation (47). Most probably, normal human detrusor muscle exhibits little atropine
resistance while abnormal detrusor exhibits high atropine resistance, making study of NANC
mechanisms more attractive in disease states. There is much research being done in this regard,
and these studies are eagerly awaited.

E. Purinergic Mechanisms
Purinergic receptors are classified as P1 and P2 based on their affinity for either adenosine or
ATP respectively. ATP-sensitive P2 receptors can be subclassified into P2X and P2Y receptor
families based on whether the mechanism is ion channel gated (P2X) or G-protein coupled
(P2Y). The P2X family can be further subclassified into seven subtypes (P2X1, P2X2, etc.).
Levin suggested that purinergic stimulation initiates a bladder contraction (first phase) whereas
cholinergic stimulation leads to sustained bladder emptying (48). Chancellor showed that ATP
generated a more forceful smooth muscle contraction than a cholinergic agonist, a finding that
was corroborated by Sneddon, who showed that purinergic mediated contraction is more
forceful in neonates (49,50). Theobald demonstrated a greater rise in bladder pressure in cats
treated with purinergic agonists versus cholinergic agonists (51). These findings have not been
consistent, however, as others have shown decreased bladder emptying with purinergic agonists
(52). Animal studies have implied the presence of multiple types of purinergic (P2X and P2Y)
receptors in the bladder and that the response of detrusor muscle to purinergic stimulation is
itself biphasic depending on the receptor stimulated (P2X, fast response; P2Y, slow, sustained
response) (53). P2X1 receptors have been shown to be dominant in rat detrusor and vascular
smooth muscle (54). O’Reilly and coworkers studied P2X receptors and their role in idiopathic
DI in human females. They found that P2X2 receptors were increased and other P2X subtypes
were decreased in women with idiopathic DI, again demonstrating the trend toward atropine
resistance in abnormal bladders (55). These data hold promise as the search for novel approaches
to the treatment of overactive bladder and other bladder disorders continues.
It is likely that purinergic mechanisms also play an excitatory role at higher sites,
including parasympathetic ganglia and afferent nerve terminals in dorsal root ganglia. P2X3
receptors have been identified in neurons in dorsal root ganglia in addition to subepithelial
afferent nerves plexuses in the bladder and ureteral wall (54,56). Intravesical administration of
ATP activates bladder afferent fibers and desensitization of these afferents with suramin, a
purinergic antagonist, decreased reflex bladder activity (57,58). Afferent activity induced by
bladder distention was reduced in P2X3 knockout mice (53). These data argue that purinergic
mechanisms play a sensory role in the lower urinary tract as well and could provide potential
targets for therapy of disorders such as sensory urgency and interstitial cystitis.

F. Dopaminergic Mechanisms
Central dopaminergic pathways appear to exhibit both inhibitory and excitatory influences on
micturition, based on the site and receptor type stimulated. D1 or D1-like receptors mediate
inhibition whereas D2 or D2-like receptors mediate excitatory reflexes. Activation of D1
receptors in the substantia nigra causes suppression of reflex bladder activity in cats (59).
Bladder hyperreflexia produced in monkeys through destruction of these pathways (inducing
Parkinson-like motor symptoms) was also suppressed using a D1-like agonist in one study (60).
32 Ghoniem and Hairston

From a clinical standpoint, however, treatment in humans with standard anti-Parkinsonian

medications does not appear to correlate well with improvement in bladder symptoms or
urodynamic findings (61). These patients often require treatment with anticholinergics to control
bladder hyperreflexia, underscoring the complex nature of voiding dysfunction.
The diversity of dopaminergic influence on micturition is demonstrated by the fact that
stimulation of D2-like receptors in animals in both the pontine micturition center (PMC) and in
the spinal cord can induce bladder hyperactivity (62,63). It is likely that central dopaminergic
pathways play a significant role in micturition, but the translational value of current basic
science knowledge to the clinical arena has yet to be realized.

G. Serotonergic Mechanisms
It is possible that serotonin (5HT) has an impact on neural control of the lower urinary tract at
both the central and peripheral levels, although the degree of this impact is still largely unknown.
This uncertainty is a product of the multiple receptors that have been identified coupled with the
lack of specific drugs with which to target them. There have been at least seven different 5HT
receptors identified (5HT1, 5HT2, etc.). Nonetheless, immunohistochemical studies have
identified 5HT-containing neurons in the pelvic ganglia. Similarly, 5HT-containing neurons in
the raphe nucleus of the caudal brainstem project to the dorsal horn in addition to the autonomic
and sphincter motor nuclei in the lumbosacral cord. In cats, activation of these 5HT neurons in
the cord inhibits reflex bladder activity and decreases firing of sacral efferents to the bladder
(62,64). Administration of 5HT antagonists in animals blocks these effects and causes a
decreased functional bladder capacity indicating that descending serotonergic pathways cause
tonic inhibition of the afferent limb of the micturition reflex (65). Of interest is the possible role
of serotonergic pathways in enuresis or overactive bladder. Tricyclic antidepressants are often
used in the treatment of nocturnal enuresis. The efficacy of these agents may be explained by
decreased 5HT reuptake, increasing levels available for suppression of reflex detrusor activity. Is
has also been shown that the incidence of overactive bladder and urge incontinence is greater in
individuals with depression, a condition associated with low levels of 5HT.
Peripherally, 5HT has been shown to induce bladder contractions as well as facilitate
acetylcholine release from nerve terminals in the bladder via activation of prejunctional
receptors (66,67). Anatomically, the sympathetic autonomic nuclei and sphincter motor nuclei
receive serotonergic input, and there is evidence to show that sphincter reflexes are facilitated by
activation of 5HT receptors as in the case of duloxetine, a combined 5HT and norepinephrine
reuptake inhibitor (68,69).

H. Glutaminergic Mechanisms
Glutamic acid or glutamate plays an important role as a facilatory transmitter in the central
pathways controlling micturition. It is present in visceral afferents in the dorsal horn of the
lumbosacral cord, spinal interneurons, and the descending pathway from the PMC to the sacral
parasympathetic plexus (70,71). Glutamate appears to facilitate bladder function at all of these
levels via either NMDA (N-methyl-D-aspartate) or AMPA (a-amino-3-hydroxy-5-methyl-4-
isoxazoleproprionic acid) receptors. NDMA antagonists depress reflex bladder activity and
sphincter electromyographic activity in anesthetized animals as well as animals with cord
transection at the midthoracic level (72). This indicates that the spinal reflex pathways
controlling micturition rely on glutaminergic transmitter mechanisms. Studies also indicate that
differences in bladder and external sphincter sensitivity to glutaminergic suppression may be
 Neurophysiology of Micturition 33

explained by differing receptor expression at each site. In situ hybridization studies have
revealed high messenger RNA for AMPA receptor subunits GluR-A and GluR-B in sacral
parasympathetic preganglionic neurons, but not NR2 NMDA receptor subunits. Conversely,
high levels of messenger RNA for all four AMPA receptor subunits (GluR-A thru D) as well as
the NR1 NMDA subunit are expressed in the motorneurons of the EUS (53).

I. GABA Inhibitory Mechanisms

GABA is a well-known inhibitory transmitter in the central nervous system. It appears to
influence micturition at both spinal and supraspinal sites via both GABA-A and GABA-B
receptors. In animal studies, injection of a GABA-A agonist into the PMC suppressed reflex
bladder activity and intrathecal administration of either GABA-A or GABA-B antagonists
increased bladder capacity and decreased voiding pressure (73).

V. SENSORY INNERVATION

Afferent nerve fibers have been demonstrated in the pelvic, pudendal, and hypogastric nerves
(74). In the cat, the afferents subserving the sensation of distension (and active therefore in
evoking micturition) are more prominent in muscularis propria layer and are distributed
evenly to all regions of the bladder, but the afferents subserving the sensations of pain and
conscious touch are more prominent in the submucosa in the regions of trigone and anterior
bladder neck. Both pelvic and hypogastric afferent pathways carry nociceptive afferents,
whereas afferent pathways from the striated sphincter and from the urethra transmit sensations
of temperature, pain, wall distension (urethra), urine passage, and travel in the pudendal
nerve (74).
Anatomical and electrophysiological studies have shown that sacral afferent fibers
projecting from the bladder to the spinal cord are either myelinated (A-delta with fast conduction
up to 30 m/sec) or unmyelinated (C-fibers with slow conduction 0.3 m/sec) (75,76). Figure 4
represents a schematic of sensory pathways. A large body of evidence suggests that substance P
(SP) and other tachykinins are likely to be involved in afferent neurotransmission in the lower
urinary tract via vanilloid receptor (VR1). Exposure of bladder mucosa to the neurotoxin
capsaicin, the pungent ingredient in hot pepper, causes the release of SP and produces smooth
muscle contraction that can be blocked by SP antagonists and the neurotoxin tetrodoxin.
Systemic use of capsaicin produces either partial or complete denervation of capsaicin-sensitive
afferents, depending on the dose, species, and the age of experimental animal (77). In rats,
intravesical administration of capsaicin causes neuroanatomic or functional changes that prevent
bladder afferents from transmitting nociceptive input (78). In humans, capsaicin-sensitive
nerves have been postulated. A concentration-dependent reduction in first sensation and
bladder capacity occurs following acute administration of intravesical capsaicin. It causes
desensitization of C-fiber sensory afferents inducing reversible suppression of sensory neuron
activity. These pharmacological data support the use of capsaicin or other neurotoxins to treat
painful bladder disorders (79).
Resiniferatoxin (RTX), a substance isolated from the cactus plant Euphorbia resinifera, is
1000 times more potent than capsaicin. In contrast, however, RTX has weaker initial excitatory
effects than capsaicin on bladder afferents thus eliciting less discomfort. This agent holds
significant promise as an alternative to capsaicin in the treatment of both painful bladder
disorders as well as detrusor hyperreflexia (80,81).
34 Ghoniem and Hairston

Figure 4

VI. PHYSIOLOGY OF THE EXTERNAL URETHRAL SPHINCTER (EUS)

There are two types of muscle fibers in the striated sphincter or EUS. The first one is the strongly
reactive fast-twitch muscle fibers, and the second is the weekly reactive slow-twitch muscle
fibers. Speed of contraction seems to correlate with histochemical reaction for ATP. Resistance
to fatigue is directly related to the intensity of oxidative enzyme staining in the same fibers.
Slow-twitch fibers are high in oxidative enzyme activity and relatively fatigue resistant. Fast-
twitch fibers may be fatigable or relatively fatigue resistant (82).
The entire intramural (intrinsic) striated sphincter is composed of slow-twitch fibers,
whereas the extramural (extrinsic) component consists of both slow-twitch and fast-twitch
fibers. Telealogically, this would be convenient because the intramural striated component
would then consist of specialized fibers functionally capable of maintaining tension over
prolonged time periods without fatigue. The structure of the extramural component might be
related to a role played by this muscle in activity supporting the pelvic viscera and that the slow-
twitch fibers are responsible for (background activity) during electromyographic recording. The
fast-twitch population of the extramural component is functionally associated with rapid,
forceful muscle contraction. It is these fibers then that are recruited to increase the force and
speed of contraction of the levator ani during those events that might otherwise cause stress
 Neurophysiology of Micturition 35

incontinence by raising intra-abdominal pressure (83). However, Bazeed and colleagues,

studying the dog, reported a different fiber distribution in the intramural component of the
striated sphincter (84). They found that the slow-twitch fatigue resistant fibers are only 35%,
fast-twitch fatigue-resistant 20%, and fast-twitch fatigable fibers 45% of the intramural striated
sphincter. The fast-twitch fibers (fatigable) can convert to slow-twitch fibers by physiotherapy
(e.g., electrical stimulation). This is also a theoretical advantage of pelvic floor exercises and
behavioral modifications. Some authors explain the success of these therapies for the treatment
of urinary incontinence on the basis of changes in the oxidative characteristics of striated
muscle. However, other authors have shown that these types of therapies more successfully treat
urge incontinence rather than stress incontinence, raising doubt as to the validity of alterations in
muscle morphology (85).

VII. CENTRAL NERVOUS CONNECTIONS OF THE

LOWER URINARY TRACT

It has yet to be resolved whether voiding is the result of a segmental reflex arc that is facilitated and
inhibited by supraspinal neurologic pathways, or a long routed reflex that is integrated at higher
nervous system levels (86,87). However, in the cat, it appears that the most fundamental
micturition reflex is a spinal reflex occurring largely in the sacral micturition center (SMC) at S 2–
4 (88). The spinal cord itself has complex patterns of facilitation and inhibition that take place
among the ascending and descending pathways at the spinal cord level. Above the level of the
cord, the PMC is located. It is the most important facilitative motor center for micturition, and it is
believed that this center serves as the final common pathway for all bladder motor neurons. The
region is known as Barrigton’s center and is present in the anterior pons. The cerebellum serves as
a major center for coordinating pelvic floor relaxation and force of detrusor contraction. There are
extensive cerebellar interconnections with the brainstem reflex centers (87,89).
Above this level, the basal ganglia exert inhibitory function on detrusor contractility.
Consequently, detrusor hyperactivity is frequently seen in Parkinson’s disease. The cerebral
cortex, particularly the frontal lobes and genu of the corpus callosum, exerts primarily inhibitory
influences on the micturition reflex. Thus, facilitative influences that release inhibition occur in
the upper cortex and permit the anterior PMC to send efferent impulses through the spinal cord
allowing a sacral micturition reflex to occur with resultant bladder emptying. Any lesion in these
centers can produce a disturbance in bladder function characterized by a reflex coordinated
contraction with complete emptying (87,89). A simplified overview of micturition reflexes is
shown in Figures 5 and 6.

A. Bradley’s Loop Concept

Bradley et al. described a concept of neurological control of the lower urinary tract in the cat
(90). This concept described four loops and circuits that are interconnected by axons, and their
integrated output contributes to the determination of the threshold of the detrusor reflex and
coordinated synchronized opening of the urethra and relaxation of the urinary bladder. Most of
the micturition reflex requires a balanced contribution by all four loops.

Loop I: Cerebral-Brainstem Circuit

This loop consists of pathways to and from the frontal lobes to the pontine mesencephalic
reticular formation, with contribution from the thalamic nuclei in the basal ganglia and
36 Ghoniem and Hairston

cerebellum. This loop coordinates volitional control of micturition. It matures during infancy,
and may account for voluntary control over the micturition reflex in the childhood. This loop
integrity can be demonstrated during cystometry by asking the patient to voluntarily suppress
detrusor contraction. Interruption of this circuit severs the micturition reflex from volitional
control, e.g., in brain tumor, trauma, cerebrovascular disease (91).

Loop II: The Brainstem Sacral Loop

This loop consists of pathways from the brainstem (pontine-mesencephalic reticular formation)
to the sacral micturition area. Additionally, sensory afferents from the bladder musculature
travel directly in the spinothalamic tract to the brainstem without synapsing in the sacral
micturition area. These sensory afferent fibers are responsible for the normal sensation of desire
to micturate. Loop II is responsible for the occurrence of a coordinated detrusor reflex of
adequate duration to produce total evacuation of the intravesical content. Partial interruption
of loop II, as in spinal cord injury, results in detrusor reflex of low threshold and the presence of
postvoiding residual urine. While abrupt and complete interruption (in spinal shock) produce
areflexia and urinary retention. With recovery, uninhibited detrusor reflex contractions appear in
the cystogram (92,93).

Figure 5
 Neurophysiology of Micturition 37

Figure 6

Loop III: Vesical-Sacral Sphincter Loop

This loop consists of the detrusor nuclei and pudendal nuclei in the gray matter of the sacral
spinal cord with their neurons. Sensory afferents in the detrusor muscle travel the detrusor
nucleus and influence the closely located pudendal motor nucleus. Pudendal motor neurons
terminate in the striated muscular component of the urethral sphincter. Loop III provides the
circuit for coordination of detrusor and urethral muscular activity during voiding. Dysfunction
of this loop will be manifested in electromyographic recording as either detrusor sphincter
dyssynergia or uninhibited sphincter relaxation (94).

Loop IV: Cerebral-Sacral Loop

This loop consists of two components: (a) supraspinal and (b) segmental innervation of the
peripheral striated muscle. The supraspinal component consists of sensory pathways originating
from muscle spindles and tendon organs in the pelvic floor musculature. These axons course
through the posterior column and synapse in the thalamus, to reach the pudendal area of the
sensorimotor cortex. From there, the motor fibers originate and travel to terminate by synapsing
on motor neurons on the pudendal nucleus in the spinal cord. The segmental portion of the loop
consists of sensory axons arising from the muscle spindles and tendon organs, which end by
38 Ghoniem and Hairston

synapsing on pudendal motor neurons. The pudendal neurons give origin to efferent axons to
innervate the pelvic floor musculature and to regulate the sensitivity of spindle stretch receptors.
Electromyographic evidence of voluntary contraction of the external sphincter demonstrate an
intact loop IV (90,95).

B. Integral Theory of Voiding Reflexes

Mahoney et al. described another concept of micturition as a reflex event that occurs largely in
the peripheral autonomic nervous system, permitted to do so by the central nervous system (96).
They proposed 12 reflexes operating among bladder, urethra, brainstem micturition center, and
spinal cord micturition center. These reflexes could be grouped into four groups according to
their function.

1. Storage-Favoring Reflexes (Four Reflexes)

a. Sympathetic-Detrusor Inhibition Reflex (SDIR). The afferent is the pelvic nerve; the
efferent is the hypogastric nerve. This reflex is activated by bladder wall stretch during filling
and its function is to inhibit detrusor contraction.
b. Sympathetic Sphincter Constrictor Reflex (SSCR). This reflex consists of the same
stimulus and pathway as SDIR, but the target organ is the smooth muscle component of the
urethral sphincter. It produces an increase in the tone of the sphincter during bladder filling.
Together, these two reflexes comprise the “sympathetic stabilizing reflexes” favoring continence
of urine (97).
c. Perineodetrusor Inhibitory Reflex (PDIR). Stimulation of the stretch receptors of the
perineum and pelvic floor muscles produces impulses that travel through pudendal nerve
afferents to the SMC. Efferent impulses travel via the pelvic nerve, and the function is inhibition
of the detrusor contraction.
d. Urethrosphincteric Guarding Reflex (USGR). The stimulus is an increase in mural
tension in the trigone and bladder neck during filling or escape of urine into proximal urethra.
The afferent limb is via the pelvic nerve to the SMC, and the efferent is via the pudendal nerve to
the striated component of the external urethral sphincter producing contraction.

2. Initiation of Micturition Reflexes (Two Reflexes)

a. Perineobulbar Detrusor Facilitative Reflex (PBDFR). The stimulus is the voluntary
contraction of the diaphragm and abdominal wall muscles with simultaneous relaxation of the
pelvic floor muscles. The impulse travels through the pudendal nerve and other somatic nerves
cranially to the brainstem and brain cortex, which in turn produce stimulation of the SMC.
b. Detrusodetrusor Facilitative Reflex (DDFR). An increase in detrusor mural tension
produces an impulse that travels via the pelvic nerve to the PMC. The PMC sends facilitative
impulses via the lateral reticulospinal tract to the SMC. From here, stimulatory impulses are sent
to the detrusor muscle via pelvic nerve efferents producing a detrusor contraction.

3. Intramicturition Reflexes (Five Reflexes)

These reflexes are concerned with maintaining a strong detrusor contraction with synchronous
relaxation of the sphincter during the voiding phase to provide complete and efficient emptying
of the bladder.
a. Detrusourethal Inhibitory Reflex (DUIR). The impulse from the detrusor stretch
receptors travels via the pelvic nerve to the SMRC producing stimulation, then via the pelvic
 Neurophysiology of Micturition 39

nerve again to the bladder neck and smooth muscle component of the external urethral sphincter
producing relaxation.
b. Detrusosphincteric Inhibitory Reflex (DSIR). An inhibitory impulse via the pelvic
nerves to the “pudendal nucleus” producing relaxation of the striated component of the external
urethral sphincter is generated in response to a stimulus from the stretch receptors in the detrusor
muscle.
c. Urethrodetrusor Facilitative Reflexes (UDFR). Both of these reflexes originate in
the proximal urethra and produce detrusor contractions via efferents from the SMC. There are
two reflex pathways proposed, one with a brainstem component and one without. Both may act
to cause a detrusor contraction in response to the presence of urine in the proximal urethra.
d. Urethrosphincteric Inhibitory Reflex (USIR). This reflex has both its afferent and
efferent limbs in the pudendal nerves. It is responsible for the prompt synchronous relaxation of
the external sphincter at the onset of micturition and is additive to the effect of the DSIR in
this regard.

4. Micturition Cessation Reflex (One Reflex)

a. Perineobulbar Detrusor Inhibitory Reflex (PBDIR). At the end of micturition,
inhibitory impulses from the stretch receptors in the perineum and pelvic muscles travel to the
brainstem. Efferent inhibitory impulses are then sent to the SMC, thus reestablishing the storage
reflexes (Group I).

VIII. SUMMARY

Much controversy still abounds regarding the exact processes of the micturition cycle, but most
experts would agree that it involves two relatively discrete phases: (a) bladder filling and
storage, and (b) bladder emptying. From a clinical standpoint, most disorders of voiding can be
categorized into a failure of either one of these discrete processes, although quite often there is a
combination of the two. While some of the basic concepts of pathways and neural circuits have
been around for decades, our understanding of the details of these pathways and circuits has
grown tremendously in the past several years. With the advent of functional MRI and PET
scanning, as well as the continued discovery of new neurotransmitters and receptors, this
knowledge base will continue to develop allowing more effective diagnosis and treatment of
voiding dysfunction well into the future.

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3
Epidemiology of Female Urinary Incontinence

Christopher Saigal
David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
Mark S. Litwin
David Geffen School of Medicine at UCLA and UCLA School of Public Health, Los Angeles,
California, U.S.A.

I. INTRODUCTION

Urinary incontinence, defined as the involuntary passage of urine per urethra, can be divided into
four clinical entities, as defined by the Agency for Healthcare Research and Quality’s clinical
practice guidelines (1). These are stress incontinence, in which a rapid increase in intra-
abdominal pressure causes urine leakage; urge incontinence, in which precipitous, uninhibited
detrussor contractions result an urgent need to void and leakage of urine; mixed stress and urge
incontinence; and overflow incontinence, in which chronic retention of urine results in passive
loss of small amounts of urine as the bladder is filled beyond capacity.
Recent estimates of the societal costs attributable to urinary incontinence are as high as
$26.3 billion (1995 dollars), in the over-65-year-old population alone (2). Others have estimated
the current costs of urinary incontinence to be $16.3 billion (1995 dollars), with 76% of those
costs attributable to female incontinence (3). In the latter study, for women, routine care
comprised the majority of the cost (70%), although nursing-home admissions (14%) and
treatment (9%) were also major contributors. Others have confirmed that urinary incontinence is
a significant reason for nursing-home admissions, with incontinent women having twice the risk
of admission as continent women (4). Given the burden of this condition on the health and
economy of the nation, much work has been done to create a descriptive epidemiology of urinary
incontinence.

II. RISK FACTORS

A. Age
Increasing age was accepted as one of the risk factors for urinary incontinence at the 1988
National Institutes of Health consensus panel on urinary incontinence (5). Several studies have
since documented an increasing prevalence and severity of urinary incontinence with advanced
age (6 – 9). This increased prevalence in elderly women may be due to age-related laxity of
pelvic musculature and connective tissue supporting the urethra. Additionally, factors in the
45
46 Saigal and Litwin

elderly such as impaired mobility and/or declining mental status can increase the risk of
incontinent episodes. The elderly suffer from significant rates of fecal impaction and
constipation, both clinically associated with urinary incontinence (10).

B. Heredity
Some researchers have questioned whether there is a genetic basis for the connective tissue
atrophy and weakness that contribute to stress urinary incontinence. Mushkat and colleagues
examined the prevalence of stress urinary incontinence in first-degree relatives of 259 female
probands (11). As a control, they collected data on the first-degree relatives of 165 women
(matched for age, parity, and weight) without stress urinary incontinence being seen in a
gynecology clinic. Prevalence of stress urinary incontinence was almost three times higher
(20.3% vs. 7.8%) in first-degree female relatives of women with stress urinary incontinence
themselves. These data suggest that there may be familial transmission of traits that can lead to
an increased incidence of stress urinary incontinence.

C. Obesity
Several studies have documented an increased risk for urinary incontinence in women with high
body mass indices (BMIs). Estimates of odds ratios for urinary incontinence range from 1.5
(95% confidence interval, 1.15 –1.95) in a study of women using a criteria for high BMI of
.26 kg/m2 (12), to 3.0 (95% CI 1.8, 5.0) in a study examining those in the heaviest quartile of
BMI (13). Several other studies have suggested a relationship between weight and incontinence
(9,14,15). One prospective study of women undergoing a surgical procedure for obesity found a
reduction in incontinence after weight loss (16).

D. Hysterectomy
Data on the risk hysterectomy confers on the development of subsequent urinary incontinence
are conflicting. In one large, systematic review of the literature published from 1966 to 1997,
Brown and colleagues constructed a summary estimate of the increased odds for development of
urinary incontinence in women who undergo hysterectomy (17). They found that among women
.60 years of age, those who had a history of hysterectomy had an odds ratio of 1.6 (95% CI
1.4 –1.8) compared to those without such a history. There was not a similar increase in odds for
women younger than 60. They concluded that urinary incontinence following hysterectomy
might not be seen until many years after the procedure.

E. Pregnancy and Parity

Several studies suggest that parity is a risk factor for urinary incontinence (18 – 20). Investigators
have documented incidence rates for urinary incontinence occurring after pregnancy as high as
26% at 6 months, although most women recover continence with time (21). Possible
explanations for this relationship lie in pelvic floor denervation due to compression during
pregnancy and delivery and stretching or tearing of pelvic floor connective tissue and
musculature during pregnancy and delivery.
A Danish study which followed a cohort of 278 women for 5 years after delivering their
first child found a 5-year prevalence of International Continence Society –defined stress urinary
incontinence of 30%, and 5-year incidence of 19%. Use of vacuum extraction or episiotomy
during delivery was found to increase the risk of stress urinary incontinence (22). Although in
 Epidemiology of Female Urinary Incontinence 47

another analysis of this group of women, a second delivery did not increase the risk for stress
urinary incontinence (23), others have found a linear relationship between number of deliveries
and risk of stress urinary incontinence (13).
The relative effect of pregnancy itself versus the process of vaginal delivery on the
development of urinary incontinence has been debated. One study addressed this issue with a
comprehensive physical exam and medical history on 189 women being seen for menopausal
symptoms in a gynecology clinic (24). Ninety-eight of the patients were found to have urinary
incontinence, and multivariate analysis revealed that the risk of urinary incontinence was almost
five times higher among women with at least one pregnancy than in women who had never been
pregnant. The risk was 3.5 times higher among women who had had only cesarean sections than
in women who had never been pregnant. These data suggest that pregnancy itself confers risk for
urinary incontinence, and calls into question the use of cesarean section to mitigate this risk.
However, in a prospective study of 595 nulliparous women undergoing first pregnancy, in whom
continence status had been ascertained prior to pregnancy, the relative risk of urinary
incontinence when a woman delivered vaginally versus via cesarean section was 2.8 (21).

F. Tobacco Use
Some evidence links stress urinary incontinence and urge incontinence with cigarette smoking in
women. In a case control study, Bump and McClish examined 606 women with known smoking
history (current, former, or never) and recorded the results of urodynamic tests for the 322
women who were incontinent. Urinary incontinence was significantly more prevalent in current
and former smokers than in nonsmokers. The odds ratio for urodynamically proven stress
urinary incontinence in current female smokers was 2.48 (95% CI 1.60 – 3.84), while the odds
ratio for current female smokers with urodynamically proven urge incontinence was 1.89 (95%
CI 1.19– 3.02) (25). In further study of the urodynamic characteristics of stress urinary
incontinence in smoking and nonsmoking women, Bump and McClish found that smokers were
at increased risk despite having stronger urethral sphincters (26). They speculated that increased
and more forceful coughing associated with smoking “likely promotes the earlier development
of the anatomic and pressure transmission defects that allow genuine stress incontinence and
overcomes any protective advantage of a stronger urethral sphincter.” However, other work has
not supported a link between smoking and urinary incontinence (15).

G. Race
Some evidence suggests that African-American women have a lower prevalence of urinary
incontinence than Caucasian women. In a population-based study of elderly (.70 years old)
noninstitutionalized Americans, 16% of African-American women reported an episode of
urinary incontinence in the past year, versus 23% of Caucasian women, a statistically significant
difference (27). In a population-based survey of 1922 health maintenance organization
members, Thom found a significant association between Caucasian race and the reporting of an
incontinent episode in the last year (odds ratio 1.8, 95% CI 1.2– 2.8) (13).
In addition to racial variation in the prevalence of urinary incontinence in women, race
appears to play a role in the distribution of types of incontinence in incontinent women. In a
study of 200 consecutive patients with urinary incontinence who were subject to a comprehensive
physical exam and urodynamic testing, significant differences were found in the distributions of
stress urinary incontinence, urge incontinence, and mixed incontinence between African-
American and Caucasian patients (28). Stress urinary incontinence was found in 27% of
incontinent African-American women, versus 61% of incontinent Caucasian women. Urge
48 Saigal and Litwin

incontinence was found in 56% of African-American women, versus 28% of Caucasian women.
Similar results were obtained in a study by Graham and Mallet, who examined urodynamic
findings in 183 African-American and 132 Caucasian women with urinary incontinence (29).
African-American women had a significantly lower prevalence of stress urinary incontinence
and higher prevalence of urge incontinence than Caucasian women. In stepwise logistic
regression, race emerged as a stronger predictor of stress urinary incontinence than age, obesity,
tobacco use, parity, and other risk factors.
These studies were not population based, as the women studied sought care for their
condition. However, if these differences in the distribution of incontinence type reflect the
population at large, the higher prevalence of urge incontinence in African-American women
may make them a group well served by more intensive urodynamic evaluation of their
incontinence. Research examining differences in distribution of the type of incontinence in
Hispanic and Caucasian women has not uncovered significant differences with urodynamic
evaluation (30).

III. PREVALENCE

Estimates of the prevalence of urinary incontinence in non-institutionalized adults vary

considerably, from 2% to 55% (31). Variation in published prevalence and incidence rates for
this condition may be related to the variety of definitions of incontinence employed in the
population-based studies examining the issue. For some studies, urinary incontinence is defined
as any involuntary loss of urine per urethra, regardless of frequency, while other studies use
definitions with minimum frequency or volume criteria. Another source of variation in the
estimates can be attributed to the different populations included in these studies. Urinary
incontinence rates are higher in older women and in those confined to nursing homes; studies
with a preponderance of either group of women may arrive at higher estimates for prevalence
and incidence of the disease. Additionally, variation in response rates to surveys regarding
urinary incontinence may produce different estimates of prevalence owing to response bias.

A. Urinary Incontinence in Younger Women

Although urinary incontinence is often perceived as a problem primarily of elderly women,
evidence suggests that it has a significant impact on women as young as 18. In a study of 1250
women between the ages of 18 and 44, Turan found the prevalence of urinary incontinence to
be 24% (32). In a population-based study of 436 Swedish women between the ages of 20
and 59, investigators followed subjects for 5 years, and administered a gynecologic exam
and incontinence questionnaire at the beginning and end of the study. The prevalence of urinary
incontinence in the population was 23.6% at baseline and 27.5% at follow-up (33). Similarly, in
two large studies of active-duty female Army soldiers, the reported prevalence of urinary
incontinence during exercise or work activity was 33% (34,35). Fitzgerald and colleagues sent
a urinary incontinence questionnaire to 2000 women who were randomly selected from a
population of 4000 employed women (36). The response rate in this study was 57%. Defining
urinary incontinence as “the accidental loss of urine at least monthly,” including incontinence
both with and without associated increased intra-abdominal pressure or urgency, they found a
urinary incontinence prevalence rate of 17.6% in women ,50 years old. In this study, fewer than
half of affected women reported urinary incontinence as a problem to their health care provider,
underscoring the consistent finding that urinary incontinence is an underreported and
undertreated condition.
 Epidemiology of Female Urinary Incontinence 49

B. Urinary Incontinence in Older Women

In an effort to address the variation in reported estimates of the prevalence of urinary
incontinence in older women, Thom et al. performed an extensive literature search and reviewed
90 articles relating to the issue (31). Of these, 21 met inclusion criteria (e.g., they were
population based, not limited to institutionalized women, and reported in English). Study sizes
ranged from 388 to 18,084 subjects. The median study response rate was 76%. Prevalence data
were abstracted and combined, and calculations were made for the prevalence rates in several
populations. The mean prevalence of urinary incontinence that occurred “ever” or “ever in the
last year” in “older women” (50 years and older) was 34%. The mean prevalence of urinary
incontinence occurring on a daily basis in older women was 14%. Thom found that in studies in
which it was possible to distinguish between these types of incontinence the proportion of all
urinary incontinence attributable to stress incontinence ranged from 30% to 80%.

C. Incidence
Fewer studies have addressed the issue of incidence of urinary incontinence. The overall
incidence rate in the population-based study of 436 Swedish women described above (33) was
2.9% in these younger women, while the incidence of urinary incontinence occurring weekly or
more was 0.5%. One study of continent middle-aged women found the incidence of urinary
incontinence (occurring monthly) to be 8% at 3 years (37). Nygaard found a 3-year incidence
rate of urinary incontinence of 28.6% in a community-based sample of rural elderly women. In
his study, a significant number of women had remission of disease, although data were not
adjusted for incontinence treatment (8). Another community-based investigation, “The Medical,
Epidemiologic, and Social Aspects of Aging” study, found a 1-year incidence rate of 20% in
women .60 years of age (38).
Urinary incontinence is a common and costly national health problem. Epidemiological
data have identified risk factors for urinary incontinence, such as obesity and smoking, which
might serve as targets for preventive health interventions. Other data from studies on race and its
relationship to specific types of urinary incontinence may help physicians tailor diagnosis and
treatment efforts. Data regarding the prevalence of the condition in both younger and older
women serve to remind health care providers to be diligent in querying these patients regarding
symptoms. Given the many successful therapeutic options open to women with urinary
incontinence, an overlooked diagnosis represents a missed opportunity to improve health.

REFERENCES

1. Agency for Healthcare Research and Quality. Overview: Urinary Incontinence in Adults, Clinical
Practice Guideline Update. 1996. http://www.ahrq.gov/clinic/uiovervw.htm
2. Wagner TH, Hu TW. Economic costs of urinary incontinence in 1995. Urology 1998; 51(3):355– 361.
3. Wilson L, Brown JS, Shin GP, Luc KO, Subak LL. Annual direct cost of urinary incontinence. Obstet
Gynecol 2001; 98(3):398– 406.
4. Thom DH, Haan MN, Van den Eeden SK. Medically recognized urinary incontinence and risks of
hospitalization, nursing home admission and mortality. Age Ageing 1997; 26(5):367– 374.
5. National Institutes of Health. NIH Consensus Statement Online: Urinary Incontinence in Adults; 1988
Oct 3 – 5. http://odp.od.nih.gov/consensus/cons/071/071_statement.htm (date accessed September
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6. Milsom IEP, Molander U. The influence of age, parity, oral contraception, hysterectomy and the
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50 Saigal and Litwin

7. JC B. Urinary incontinence in the community-analysis of a MORI poll. BMJ 1993; 306:832 –834.
8. Nygaard IE, Lemke JH. Urinary incontinence in rural older women: prevalence, incidence and
remission. J Am Geriatr Soc 1996; 44(9):1049– 1054.
9. Schmidbauer J, Temml C, Schatzl G, Haidinger G, Madersbacher S. Risk factors for urinary
incontinence in both sexes. Analysis of a health screening project. Eur Urol 2001; 39(5):565– 570.
10. Cheater FM, Castleden CM. Epidemiology and classification of urinary incontinence. Baillieres Best
Pract Res Clin Obstet Gynaecol 2000; 14(2):183– 205.
11. Mushkat Y, Bukovsky I, Langer R. Female urinary stress incontinence—does it have familial
prevalence? Am J Obstet Gynecol 1996; 174(2):617– 619.
12. Sherburn M, Guthrie JR, Dudley EC, O’Connell HE, Dennerstein L. Is incontinence associated with
menopause? Obstet Gynecol 2001; 98(4):628– 633.
13. 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 1997; 90(6):983– 989.
14. Resnick NM. Geriatric incontinence. Urol Clin North Am 1996; 23(1):55 – 74.
15. Brown JS, Seeley DG, Fong J, Black DM, Ensrud KE, Grady D. Urinary incontinence in older
women: who is at risk? Study of Osteoporotic Fractures Research Group. Obstet Gynecol 1996;
87(5 Pt 1):715 –721.
16. Bump RSH, Fantl A, McClish D. Obestiy and lower urinary tract function in women: effect of
surgically induced weight loss. Am J Obstet Gynecol 1992; 167:392 –399.
17. Brown JS, Sawaya G, Thom DH, Grady D. Hysterectomy and urinary incontinence: a systematic
review. Lancet 2000; 356(9229):535– 539 (Comment In: Lancet. 2000 Dec 9;356(9246):2012-3 UI:
21013012 Comment In: Lancet. 2000 Oct 7;356(9237):1275 UI: 20523126.)
18. Foldspang AMS, Lam GW, Elving L. Parity as a correlated of adult female urinary incontinence
prevalence. J Epidemiol Community Health 1992; 46:595.
19. Milson IEP, Molander U, Arvidsson L, Areksoug B. The influence of age, parity, oral contraception,
hysterectomy and menopause on the prevalence of urinary incontinence in women. J Urol 1993;
149:1459.
20. Foldspang A, Mommsen S, Djurhuus JC. Prevalent urinary incontinence as a correlate of pregnancy,
vaginal childbirth, and obstetric techniques. Amer J Public Health 1999; 89(2):209– 212.
21. Farrell SA, Allen VM, Baskett TF. Parturition and urinary incontinence in primiparas. Obstet Gynecol
2001; 97(3):350– 356.
22. Viktrup L, Lose G. The risk of stress incontinence 5 years after first delivery. Am J Obstet Gynecol
2001; 185(1):82– 87.
23. Viktrup L, Lose G. Lower urinary tract symptoms 5 years after the first delivery. Int Urogynecol J
Pelvic Floor Dysfunct 2000; 11(6):336– 340.
24. Faúndes A, Guarisi T, Pinto-Neto AM. The risk of urinary incontinence of parous women who
delivered only by cesarean section. Int J Gynaecol Obstet 2001; 72(1):41 –46.
25. Bump RMD. Cigarette smoking and urinary incontinence in women. Am J Obstet Gynecol 1992;
167(5):1213– 1218.
26. Bump R. Cigarette smoking and pure genuine stress incontinence of urine: a comparison of risk
factors and determinants between smokers and nonsmokers. Am J Obstet Gynecol 1994; 170(2):
579– 582.
27. Fultz NH, Herzog AR, Raghunathan TE, Wallace RB, Diokno AC. Prevalence and severity of urinary
incontinence in older African American and Caucasian women. J Gerontol Ser A Biol Sci Med Sci
1999; 54(6):M299– M303.
28. Bump R. Racial comparisons and contrasts in urinary incontinence and pelvic organ prolapse. Obstet
Gynecol 1993; 81(3):421– 425.
29. Graham CA, Mallett VT. Race as a predictor of urinary incontinence and pelvic organ prolapse. Am J
Obstet Gynecol 2001; 185(1):116– 120.
30. Mattox TF, Bhatia NN. The prevalence of urinary incontinence or prolapse among white and Hispanic
women. Am J Obstet Gynecol 1996; 174(2):646 –648.
31. Thom D. Variation in estimates of urinary incontinence prevalence in the community: effects of
differences in definition, population characteristics, and study type. J Am Geriatr Soc 1998;
46(4):473– 480.
 Epidemiology of Female Urinary Incontinence 51

32. Turan C, Zorlu CG, Ekin M, Hancerlio N, Saraço F. Urinary incontinence in women of reproductive
age. Gynecol Obstet Invest 1996; 41(2):132 –134.
33. Samuelsson EC, Victor FT, Svärdsudd KF. Five-year incidence and remission rates of female urinary
incontinence in a Swedish population less than 65 years old. Am J Obstet Gynecol 2000; 183(3):568–
574.
34. Sherman RA, Davis GD, Wong MF. Behavioral treatment of exercise-induced urinary incontinence
among female soldiers. Mil Med 1997; 162(10):690– 694.
35. Davis G, Sherman R, Wong MF, McClure G, Perez R, Hibbert M. Urinary incontinence among
female soldiers. Mil Med 1999; 164(3):182– 187.
36. Fitzgerald ST, Palmer MH, Berry SJ, Hart K. Urinary incontinence. Impact on working women.
Aaohn J 2000; 48(3):112 –118.
37. Burgio K, Matthews K, Engel B. Prevalence, incidence and correlates of UI in healthy, middle-aged
women. J Urol 1991; 146:1255 –1259.
38. Herzog AR, Fultz NH. Prevalence and incidence of urinary incontinence in community-dwelling
populations. J Am Geriatr Soc 1990; 38(3):273– 281.
4
Quality-of-Life Issues in Incontinence

David F. Penson*
University of Washington, Seattle, Washington, U.S.A.
Mark S. Litwin
David Geffen School of Medicine at UCLA and UCLA School of Public Health, Los Angeles,
California, U.S.A.

I. INTRODUCTION

Urinary incontinence is a common condition in older women (1). However, unlike other
common medical conditions, such as coronary artery disease or cancer, one cannot measure the
public health impact of urinary incontinence in terms of years of life lost or overall mortality.
Nonetheless, there is little doubt that urinary incontinence has a considerable impact on patients’
health, well-being, and overall quality of life. The problem facing clinicians and researchers
alike is finding ways to measure outcomes objectively in women with this common condition.
Objective measures, such as urodynamic assessments and urinary pad tests, often used
when studying urinary incontinence, may provide important clinical information during the
diagnostic evaluation of urinary incontinence. However, they are not always meaningful to
patients. For example, some women who report urinary leakage at home cannot reproduce their
symptoms during urodynamic evaluation (2). Others may experience minimal leakage during
pad testing but find even the smallest leak to be a problem (3). Finally, some patients may
present with symptoms such as urgency or dysuria, which cannot be easily quantified with
objective tests (4). These observations underscore the need to find ways to measure patient
experience in urinary incontinence accurately, as the ultimate goal of treatment for this condition
is to improve quality of life.
Advances in research methodology now allow reliable collection of meaningful data on
patients’ health-related quality of life (HRQOL). HRQOL includes both objective evaluation of
functional status and patients’ perceptions of their own health and its impact on their existence.
In the past decade, several valid and reliable questionnaires have been developed that are
specifically designed to measure HRQOL in urinary incontinence. These instruments can be used
to quantify the qualitative, subjective outcomes, allowing us to capture the public health impact
of urinary incontinence on women and better assess the effectiveness of existing therapies for
this common condition.

*Current affiliation: Keck School of Medicine, University of Southern California, Los Angeles, California,
U.S.A.

53
54 Penson and Litwin

The goal of this chapter is to provide background on HRQOL research as it applies to

urinary incontinence and to present an overview of the existing instruments available for patients
with urinary incontinence. In addition, we will summarize the literature on the impact of urinary
incontinence on quality of life.

II. HEALTH-RELATED QUALITY-OF-LIFE RESEARCH

HRQOL encompasses a wide range of human experience, including the daily necessities of life,
such as food and shelter, intrapersonal and interpersonal responses to illness, and activities
associated with professional fulfillment and personal happiness (5). Most importantly, HRQOL
involves patients’ perceptions of their own health and ability to function in life. HRQOL is
often confused with functional status (6). While functional status is an important dimension
of HRQOL, other aspects of HRQOL, such as role function, vitality, mental health, and
psychosocial interactions, are equally important.
Health-related quality of life is a patient-centered variable, measured using questionnaires
or surveys (also known as instruments), which are administered directly to patients in an
objective, nonjudgmental manner. The principles of psychometric test theory are used to design
instruments that measure HRQOL in a reproducible, quantifiable manner (7). HRQOL
instruments typically contain questions, or items, that are organized into scales. Each scale
measures a different aspect, or domain, of HRQOL. Responses to the items in a given scale are
tabulated to produce a numerical score within that domain, which can then be used for statistical
testing. Numerical values typically range from 0 to 100, the higher numbers representing better
outcomes.
Many health care providers mistakenly believe that they can accurately estimate a
patient’s quality of life during the clinical interaction, obviating the need for patient-centered
data collection. In one study of 2252 men with localized prostate cancer, patients’ self-
assessment of urinary HRQOL was compared with physicians’ assessment. While 97% of
patients reported some impairment due to urinary incontinence, only 21% of physicians reported
that their patients were impaired by this problem (P , .0001). Similar findings were noted when
assessing impairment due to urinary frequency (97% of patients as opposed to 19% of
physicians, P , .0001) or due to decreased stream (97% vs. 14%, P , .0001) (8). This study
demonstrates the difficulty providers have when trying to assess their patients’ quality of life and
underscores the need to use patient-centered instruments when assessing this outcome.
HRQOL instruments may be general or disease specific. General HRQOL domains
address the components of overall well-being, while disease-specific domains focus on the
impact of particular organ dysfunctions that affect HRQOL (9). General HRQOL instruments
typically address general health perceptions, sense of overall well-being, and function in the
physical, emotional, and social domains. Disease-specific HRQOL instruments for patients with
urinary incontinence focus on more directly relevant domains, such as urinary leakage, urgency,
and lifestyle changes due to urinary problems or distress/anxiety caused by urinary dysfunction.
When studying quality of life in urinary incontinence, it is important to measure both general and
disease-specific domains to obtain a complete portrait of the patient’s experience.

III. DEVELOPMENT AND EVALUATION OF NEW INSTRUMENTS

The development and validation of a new HRQOL instruments is a long and arduous process that
should not be undertaken lightly. Therefore, it is always preferable to use established
instruments when available. An added advantage of using existing HRQOL instruments is that it
 Quality-of-Life Issues in Incontinence 55

allows clinicians to compare their results to other, previously studied populations and assess
their own outcomes.
When instruments are developed, they are first pilot tested to ensure that the target
population can understand and complete them with ease. Pilot testing may reveal problems that
might otherwise go unrecognized by researchers. For example, many commonly used medical
terms are poorly understood by patients. This may result in missing data if patients leave
questions blank. Furthermore, because many patients with urinary incontinence are older and
may have poor eyesight, pilot testing often identifies easily corrected visual barriers such as type
size and page layout. Pilot testing is a necessary and valuable phase of instrument development.
Instruments are also evaluated for the two fundamental psychometric statistical properties of
reliability and validity.
Reliability refers to how reproducible the scale is—in other words, what proportion of a
patient’s test score is true and what proportion is due to individual variation. Test-retest
reliability is a measure of response stability over time. It is assessed by administering scales to
patients at two separate time points, usually a short period apart. If too long an interval
transpires, real change in the variable may artificially deflate test-retest reliability coefficients.
The correlation coefficients between the two scores reflect the stability of responses. Internal
consistency reliability is a measure of the similarity of an individual’s responses across
several items, indicating the homogeneity of a scale (7). The statistic used to quantify the
internal consistency, or unidimensionality, of a scale is called Cronbach’s coefficient alpha (10).
Generally accepted standards dictate that reliability statistics measured by these two methods
should exceed 0.70 (11).
Validity refers to how well the scale or instrument measures the attribute it is intended to
measure. Validity provides evidence to support drawing inferences about HRQOL from the scale
scores. Three types of validity are usually evaluated in scales and instruments. Content validity
involves a nonquantitative assessment of the scope and completeness of a proposed scale (12).
Although more superficial, it is always included in the early stages of instrument development.
Criterion validity is a more quantitative approach to assessing the performance of scales and
instruments. It requires the correlation of scales scores with other measurable health outcomes
(predictive validity) and with results from other established tests (concurrent validity). For
example, the predictive validity of a new HRQOL scale for physical function might be correlated
with the number of subsequent physician visits or hospitalizations. Likewise, the concurrent
validity of a new urinary function scale might be correlated with daily pad use in a urinary pad
test. A new emotional HRQOL scale might be correlated with an established mental health
index. Generally accepted standards dictate that validity statistics should exceed 0.70 (11).
Construct validity is the most valuable yet most difficult way of assessing a survey
instrument. It is often determined only after years of experience with a survey instrument. It is a
measure of how meaningful the scale or survey instrument is when in practical use. Often, it is
not calculated as a quantifiable statistic. Rather, it is frequently seen as a Gestalt of how well a
survey instrument performs in a multitude of settings and populations over a number of years.
Construct validity requires much effort over many years of evaluation.

IV. HEALTH-RELATED QUALITY-OF-LIFE INSTRUMENTS AVAILABLE

FOR USE IN URINARY INCONTINENCE
A. General HRQOL Instruments
Although there are over 50 established and published instruments designed to measure general
HRQOL, few have been used in the specific setting of primary urinary incontinence. These
56 Penson and Litwin

include only the RAND 36-item Health Survey (SF-36), the Sickness Impact Profile (SIP), and
the Nottingham Health Profile.
Many researchers feel that the SF-36 is the “gold standard” for measuring general HRQOL
in medical research (6). Developed during the Medical Outcomes Study, a large study that
examined health-related aspects of daily life in many different types of patients (13), it is a
36-item, self-administered instrument that takes ,10 min to complete and quantifies HRQOL in
eight multi-item scales that address different health concepts: physical function, social function,
bodily pain, emotional well-being, energy/fatigue, general health perceptions, and role
limitation due to physical or emotional problems. Two summary scales, a physical health
composite and a mental health composite, may also be calculated (14). Each of the eight
individual scales is scored from 0 to 100, with higher scores corresponding to better outcomes.
The composite scales are standardized to a population mean of 50 with a population standard
deviation of 10. Importantly, the SF-36 has been used in prior studies of patients with urinary
incontinence and has been shown to perform well in this patient group (15). There is also a
shortened version of the SF-36, known as the SF-12, which can be used in place of the SF-36 if
the researcher wishes to reduce the respondent burden. Although the results are not reported in
eight distinct domains, as with the SF-36, the two summary domains generated in the SF-12 are
still acceptable in many research settings.
The SIP is considerably longer (136 items) than the SF-36. However, the greater number
of questions results in more domains—12—which may allow for a more comprehensive view of
general HRQOL. Individual summary scores can be generated for each of these domains (16,17).
The Nottingham Health Profile contains six domains comprising a total 38 items that the subject
responds to with binary (yes/no) answers (18). It has been used primarily in the United Kingdom
to measure general HRQOL in a number of disease processes (19 – 21). While not as widely used
in the general population as the SF-36, both of the Nottingham Health Profile and the SIP have
been successfully utilized to measure general HRQOL in women with incontinence (22,23). In a
recent review of HRQOL instruments for use in incontinence, Corcos and colleagues (24)
concluded that these three generic HRQOL instruments were not responsive to change in
incontinent patients. This observation underscores the need for valid, reliable, and responsive
disease-specific HRQOL instruments in incontinence.

B. Disease-Specific HRQOL Instruments

There are now numerous HRQOL instruments designed specifically to look at the impact of both
stress and urge incontinence on HRQOL. No one instrument has been demonstrated to be
superior to another, and the choice of outcome measure should be based upon one’s particular
clinical or research goals. Most of these questionnaires are available in the public domain.
Interested clinicians and researchers can therefore review the items in an instrument and select
the established questionnaire that best suits their purposes.
The Incontinence Impact Questionnaire (IIQ) and the Urogenital Distress Inventory (UDI)
are two of the most common questionnaires used to measure disease-specific HRQOL in urinary
incontinence. Developed in the mid 1990s, the original versions of these questionnaires were
relatively long (roughly 53 items combined) (25). The two questionnaires had the advantage of
adequately capturing both dysfunction and bother due to urgency, frequency and incontinence,
etc. The IIQ generates four domain subscores: physical activity, travel, social, and emotional.
The IIQ and UDI were specifically designed for females with urinary incontinence and have
been extensively tested in this population and shown to be valid and reliable. The IIQ has been
shown to perform well in both English- and French-speaking women (26). In clinical practice,
however, the questionnaires were cumbersome to complete, which limited their utility. This was
 Quality-of-Life Issues in Incontinence 57

remedied with the development of short-form versions of these questionnaires—the IIQ-7 and
the UDI-6. Although the information obtained is not as detailed, it is adequate and still provides
a relatively comprehensive measure of disease-specific HRQOL in women with urinary
incontinence. In addition, the IIQ-7 and UDI-6 have been shown to be responsive to change. In a
group of 55 women with pelvic organ prolapse, FitzGerald et al. (27) found that women who
reported subjective continence following surgery for this condition also reported lower IIQ-7
and UDI-6 scores (better HRQOL) when compared to baseline. Finally, although not originally
developed for men, the IIQ-7 and UDI-6 have since been used in a population of older men and
have performed well (28,29).
The IIQ and UDI instruments have also been modified for use in various subsets of patients
with specific forms of urinary dysfunction. Lubeck et al. (30) developed and validated modified
versions of the IIQ and UDI specifically for use in patients with urge incontinence and overactive
bladder, known as the Urge-Incontinence Impact Questionnaire (U-IIQ) and the Urge-Urinary
Distress Inventory (U-UDI). The U-IIQ and the U-UDI are longer (42 items) than the IIQ-7 and
UDI-6, but have the advantage of measuring the impact of urgency, frequency, and urge
incontinence on HRQOL in much greater detail. HRQOL is measured in seven domains: severity
of urge symptoms, and impact on travel, activities, feelings, physical activities, relationships,
and sexual function. The instrument has good psychometric properties and appears to capture
most of the psychosocial concerns of patients with overactive bladder. Similarly, Barber and
colleagues (31) modified the IIQ and UDI instruments for use in women with pelvic floor
disorders. The new instruments, known as the Pelvic Floor Distress Inventory (PFDI) and the
Pelvic Floor Impact Questionnaire (PFIQ), contain six scales. The PFDI consists of 61 items and
generates scores in three domains: distress due to urinary incontinence, distress due to
colorectal-anal dysfunction; and distress due to pelvic organ prolapse. The PFIQ includes 93
items and measures life impact in the same three domains. While the new scales have been
shown to have acceptable criterion validity, further use in the clinical and research setting is
needed to determine if the total number of items on the PFIQ and PFDI will affect subject’s
willingness to complete the questionnaire.
The Bristol Female Lower Urinary Tract Symptoms (BFLUTS) instrument is a modified
version of the ICSmale survey questionnaire that was developed to measure lower urinary tract
symptoms (LUTS) in males (32). To develop the BFLUTS, the majority of the items on voiding
symptoms in the ICSmale questionnaire were replaced with items quantifying the frequency and
extent of urinary incontinence. The new questionnaire contains 20 items that address urinary
incontinence, voiding symptoms in the voiding and storage phase, sexual function, and other
aspects of quality of life. The BFLUTS was shown to be valid and reliable in a population of 85
incontinent women from the United Kingdom. It has the advantage of capturing both function
and bother in the urinary domains, which are both important components of HRQOL. Although
the BFLUTS has not been formally validated in men, a modified version of the questionnaire has
been administered to males and was shown to perform well (33).
Kelleher et al. developed a 21-item survey, known as the King’s Health Questionnaire, to
assess HRQOL in incontinent women (34). This questionnaire measures the domains of general
health perception, incontinence impact, urinary symptoms, severity of disease, role limitations,
physical limitations, social limitations, personal limitations, emotional problems, and sleep
disturbances. It has been shown to be valid and reliable and correlates well with outcomes from
the SF-36.
Black and colleagues (35) developed two instruments, a Symptom Severity Index (SSI)
and a Symptom Impact Index (SII), to assess the impact of incontinence on women’s HRQOL.
They developed their instruments in a population of 442 women undergoing surgery for stress
urinary incontinence. The new questionnaires have the advantage of being brief (eight items
58 Penson and Litwin

total), yet able to generate to distinct summary scores that show acceptable validity and
reliability. Research is ongoing to assess the responsiveness of these instruments to change.
Patrick et al. (36) have developed the I-QOL, a 22-item questionnaire, that specifically
examines HRQOL in three domains, avoidance and limiting behavior due to incontinence, social
embarrassment, and psychosocial impact of incontinence. This instrument has the advantage of
being developed and test in both sexes and has been cross-culturally adapted for use in numerous
countries in various languages (37). As it does not capture urinary function well, it should be
used with a functional scale, such as a voiding diary or the SSI.
The York Incontinence Perceptions Scale (YIPS) is a simple eight-item questionnaire that
is specifically designed to capture a subject’s psychosocial adjustments to urinary incontinence
(38). This instrument, like most of the others described so far, tends to focus on stress
incontinence, and is therefore of less utility when studying urge incontinence or overactive
bladder. If the YIPS were to be used in this setting, it would need to be accompanied by other
instruments that capture the impact of urgency and frequency on HRQOL. The 24-item Urge
Impact Scale (URIS) (39) has the added advantage of examining urge incontinence in particular,
although it doesn’t specifically capture the impact of urgency or overactive bladder on HRQOL.

V. IMPACT OF URINARY INCONTINENCE ON GENERAL

HEALTH-RELATED QUALITY OF LIFE

Although urinary incontinence is traditionally thought of as a condition that affects quality of

life, there are few studies that quantify the impact of this health problem on general health-
related quality of life. However, the studies that have been performed clearly demonstrate that
this condition has a broad effect on quality of life. Using the Nottingham Health Profile, Grimby,
et al. (40) measured general HRQOL in 120 elderly women (mean age 75.4 years) with urinary
incontinence. As a comparison group, 313 age-matched women without urinary incontinence
also completed the questionnaire. They found that incontinent women experienced greater
emotional disturbance and social isolation than the age-matched controls. When they compared
women with either stress or urge incontinence to the control group, they found that the women
with urge incontinence had significantly greater emotional disturbance than the controls, while
no differences were noted between women with stress incontinence and controls in this domain.
Both groups (stress and urge incontinence) reported more social isolation than the controls.
Direct comparisons between women with stress and urge incontinence were hindered by sample
size issues. Although these data demonstrate that all types of urinary incontinence have a broad
impact on women’s daily lives and cause significant social isolation, they also underscore the
fact that the quality-of-life impact of urge incontinence is uniquely different from that of stress
incontinence.
In another study, Haggland et al. (41) used a population-based approach to assess the
impact of stress and urge incontinence on HRQOL (as measured by the SF-36) in Surahammar,
Sweden. HRQOL data were available in 596 women without incontinence, 440 women with
stress incontinence, and 71 women with urge incontinence. Incontinent women, regardless of
type, reported significantly lower general HRQOL scores in all eight domains of the SF-36.
However, when stratified by type of incontinence, women with urge incontinence reported
significantly worse general HRQOL in all domains even when compared to women with stress
incontinence. The magnitude of difference in general HRQOL scores between women with
stress, as opposed to urge, incontinence was particularly striking, 10– 20 points lower in all
domains, and underscores the clinical importance of these findings. Similarly, Hunskaar and
Visnes used the Sickness Impact Profile to specifically compare women with urge incontinence
 Quality-of-Life Issues in Incontinence 59

to those with stress incontinence and found that the group with urge incontinence had
significantly worse HRQOL in the sleep and social interaction domains of the SIP. In addition,
they divided their cohort by age, comparing HRQOL in 36 incontinent women aged 40– 60 years
and 40 women age 70 years, while controlling for type of incontinence. Younger women had
worse HRQOL than older women, particularly in the domains of emotional behavior and effect
on recreation and pastimes. This study demonstrates that the effect of incontinence on general
HRQOL is affected not only by the type of incontinence but also by the age of the patient.
Interestingly, it is not simply incontinent episodes that affect quality of life in urge
incontinence. In a telephone study of overactive bladder (OAB), Liberman and colleagues
administered the SF-36 to 483 subjects with OAB symptoms and 191 controls. After adjusting
for age, sex, and use of medical care, subjects with incontinent OAB (n ¼ 185) had worse
HRQOL in the physical function, role-functional, bodily pain, health perceptions, social
functioning, and mental health domains of the SF-36 when compared to controls. However, in
the subgroup of patients with overactive bladder symptoms and no incontinence (n ¼ 298),
significantly lower HRQOL scores were still noted in the role-functioning, mental health, health
perception, and bodily pain domains. The investigators further divided this population into
continent OAB patients with frequency only (n ¼ 175), urgency only (n ¼ 80), and both
frequency and urgency symptoms (n ¼ 43). Of these three subgroups, only patients with
continent OAB who experience both frequency and urgency have significant lower HRQOL
scores than controls. This association was noted in all domains except for social function. This
study, and others (42) indicate that, while much of the quality of life impact of urge incontinence
is due to the actual leakage episodes, the combination of frequency and urgency symptoms, in
and of itself, also affects quality of life.
It is also notable that urinary incontinence can have a significant impact on psychological
health, which may in turn impact general HRQOL. In a study of 668 adults seen in 41
community primary care practices in North Carolina, 43% of patients who reported urinary
incontinence also noted depressive symptoms, as opposed to 30% in patients without urinary
incontinence. Furthermore, in the 230 subjects who reported urinary incontinence, lower domain
scores in physical and mental health, life satisfaction, and the perception that incontinence
interfered with daily life were significant predictors of depression (43). Other studies have found
a similar relationship between urinary incontinence and depression and social isolation (44,45).
In conclusion, urinary incontinence and lower urinary-tract symptoms appear to impact health-
related quality of life extensively, affecting physical, psychological, and emotional domains to a
greater degree than clinicians might expect.

VI. THE IMPACT OF INCONTINENCE TREATMENT ON HRQOL

Given the broad impact of urinary incontinence on health-related quality of life as described
above, it is important that we document that treatment for urinary incontinence result in improved
quality of life for our patients. Although the field of health-related quality-of-life research in
urinary incontinence is still young, several authors have used validated HRQOL instruments to
document that successful incontinence treatment results in improved quality of life.

A. Behaviorally Based and Other Noninvasive Interventions

A number of investigators have explored the impact of noninvasive approaches for urinary
incontinence on health-related quality of life. These studies have all used validated instruments
to demonstrate that quality of life in incontinent women can be improved with the use of
60 Penson and Litwin

behaviorally based or other non invasive interventions. For example, Bo and colleagues (46)
randomized 59 women with stress incontinence to either pelvic floor muscle exercises or no
intervention for a period of 6 months. General HRQOL was assessed using a modified version of
an existing Norwegian quality-of-life instrument, while disease-specific HRQOL was assessed
using the BFLUTS instrument. Although there were no differences in general HRQOL at the end
of the trial, women in the behavioral intervention arm experienced a significant improvement
in disease-specific HRQOL. In particular, patients in the pelvic floor exercise group had
significantly fewer problems with interference with social life (4% vs. 41% in controls), fewer
problems with interference with physical activity (44% vs. 79% in controls), less overall
influence of incontinence with life (58% vs. 82% in controls), and less dissatisfaction if the
subject had to spend the rest of her life with her current urinary symptoms (4% vs. 38% in
controls). While the study could be criticized as having a placebo effect, as there is no way to
blind patients to a behavioral intervention, it still demonstrates that women who use pelvic floor
muscle exercises for urinary incontinence can expect to have improved disease-specific quality
of life.
A number of studies have examined the impact of urinary control inserts on quality of life.
Sand et al. (47) used the SF-36 to assess HRQOL in 63 women who used the Reliance urinary
control insert. Fully 79% of patients reported that they were completed dry with this device.
Importantly, patients reported significant improvement in the physical function domain of the
SF-36. The SF-36 and the IIQ were used in another study that assessed the impact of a vaginal
device (continence guard) on urinary incontinence and HRQOL. In this study of 55 women
with stress incontinence, no differences were noted in the general domains of the SF-36,
but significant improvements were seen in disease-specific HRQOL as measured by the IIQ.
Other studies have noted similar findings (48). Taken as a whole, it appears that the behaviorally
based or noninvasive therapies for urinary incontinence appear to have little impact on general
HRQOL, but result in dramatic improvements in disease-specific HRQOL. Further research is
needed to confirm or refute these preliminary observations.

B. Medical Management of Urinary Incontinence

Medical therapy has an important role in the treatment of urge incontinence and overactive
bladder. Prior to the introduction of disease-specific HRQOL questionnaires in the past 5 years,
little information was available regarding the impact of these medications on the quality of life
of patients with these conditions. However, the majority of recent randomized clinical trials of
new agents for this condition include HRQOL, measured with validated instruments, as an
important outcome measure.
For example, Dmochowski et al. (49) recently completed a double-blind randomized
clinical trial (RCT) of the safety and efficacy of a transdermal oxybutynin patch in subjects with
urge and mixed incontinence. There were three groups of patients receiving active agent of
varying doses (n ¼ 125 – 133), and one placebo group (n ¼ 132). Outcomes included number of
weekly incontinence episodes, adverse events, and changes in HRQOL, as measured by the IIQ.
Patients in the highest dosing group (3.9 mg daily) reported improvement in all functional
measures, such as number of weekly incontinence episodes and average daily urinary frequency,
when compared to placebo but, importantly, also reported a significant improvement in disease-
specific HRQOL, with a reduction in mean IIQ score from 144 at baseline to 89 at the end of the
3-month trial.
Similarly, Naglie et al. (50) performed an RCT to assess the efficacy of a calcium channel
blocker, nimodipine, in detrusor instability and overactive bladder. Like the prior study, they
assessed functional outcomes and HRQOL using the IIQ. Again, significant improvements in
 Quality-of-Life Issues in Incontinence 61

disease-specific HRQOL were noted in the active treatment arm of the study. Other authors have
used the IIQ-7 (51) and the I-QOL instruments (52) to demonstrate the beneficial impact of
effective medical therapies for urinary incontinence on quality of life. Given these prior studies,
and the wide availability of disease-specific HRQOL instruments for urinary incontinence, it is
safe to say that any future randomized clinical trial of new agents for this condition would be
considered incomplete without the inclusion of HRQOL as an important endpoint.

C. Surgical Treatment of Urinary Incontinence

Health-related quality of life can and should be assessed following surgical therapy for urinary
incontinence. Like other treatment modalities for this condition, there are few published studies
to date that have used validated instruments to assess this outcome, but this number should
increase in the coming years. To date, there have been studies assessing HRQOL following
Burch colposuspension (53), pubovaginal sling procedures (54), and tension-free vaginal tape
placement (55).
Bidmead et al. (53) assessed videourodynamic and HRQOL outcomes in 83 consecutive
women who underwent the Burch procedure at a single institution. HRQOL was measured using
the King’s Health Questionnaire. Ninety-two percent of women were “objectively cured”
according to videourodynamic testing. Accordingly, 95% of women reported improved
HRQOL, although only 28% of women reported 50% improvement in HRQOL. This study
demonstrates the importance of measuring both “objective” and “subjective” outcomes
following surgical treatment for urinary incontinence, as patients who may be “objectively
cured” may still experience minor decrements in quality of life that may be amendable to
additional, nonsurgical therapy.
Morgan et al. (54) used a cross-sectional design to study the long-term efficacy of
pubovaginal sling in 247 women who underwent this procedure in the mid-1990s. In addition to
assessing efficacy, the investigators also measured HRQOL outcomes using the UDI-6
instrument. With a mean follow-up of 51 months, the overall objective continence rate was 88%,
with 26% of patients who experienced urge incontinence preoperatively having persistent
symptoms, and 7% of patients reporting de novo urge incontinence. Summary scores from the
UDI-6, usually reported on a scale from 0 to 18 with lower scores being better quality of life,
were transformed into a 0 – 100 scale. Ninety-two percent of patients reported transformed scores
of ,20 (implying good quality of life), closely mirroring the overall objective continence rate.
Surprisingly, patients with de novo urge incontinence also reported reasonable HRQOL (mean
score 24) while those with persistent urge incontinence reported significantly worse HRQOL
(mean score 44). These results demonstrate that patients’ expectations can play an important
role in HRQOL outcomes, as patients with similar objective urge incontinence symptoms
had differing HRQOL experiences, depending upon whether these symptoms were present
preoperatively.

VII. CONCLUSIONS

As urinary incontinence is a highly prevalent condition that has a significant impact on quality of
life, it is important that we measure this outcome when studying this incontinence. In the past
decade, numerous valid and reliable HRQOL instruments have been developed for use in urinary
incontinence. These instruments have been used in various patient populations and are readily
available for use in both clinical and research settings. While the exact role of these
questionnaires at the bedside is still evolving, it is clear that there is a pressing need for further
62 Penson and Litwin

research on the impact of various treatments for urinary incontinence on HRQOL. With
information on how these treatments affect quality of life, we can better counsel our patients on
which therapy is best for them and what to expect after treatment. This, in turn, will result in
better outcomes and better care for incontinent patients.

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5
Female Sexual Dysfunction

Kathleen E. Walsh and Jennifer R. Berman

Female Sexual Medicine Center, David Geffen School of Medicine at UCLA,
Los Angeles, California, U.S.A.

I. INTRODUCTION

Sexuality is one of the most important quality-of-life issues in both men and women. Societal,
religious, family, and individual belief systems can significantly influence an individual’s
sexuality. Female sexual dysfunction has been recognized as a common medical problem in all
age groups. Basic science research in the anatomy and physiology of normal female sexual
response and the pathophysiology of female sexual dysfunction has been limited. However,
recent advances in understanding male sexual dysfunction and treatment options have facilitated
interest in women’s health issues and the study of female sexual dysfunction.
Sexual dysfunction is highly prevalent in both sexes, ranging from 25% to 63% of women
and from 10% to 52% of men. Data from the National Health and Social Life Survey (NHSLS), a
study of adult sexual behavior in the United States, found that sexual dysfunction (SD) is more
prevalent in women (43%) than in men (31%). They also found an association between SD and
various demographic characteristics, including age, education and race (1). In a study of 329
women, aged 18– 73, a standardized sexual function questionnaire identified 38.1% with anxiety
or inhibition during sexual activity, 16.3% lacked sexual pleasure, and 15.4% had difficulty
achieving orgasm (2). A survey of 448 women over the age of 60 found that 12% of married
women had difficulty with intercourse and 14% experienced pain with intercourse. Two-thirds of
the women surveyed were sexually inactive. Sexual activity was strongly correlated with marital
status (3).
In 1998, the American Foundation of Urologic Disease (AFUD) Consensus Panel
classified female sexual dysfunction into 4 categories: desire, arousal, orgasmic, and sexual pain
disorders (4).

1. Hypoactive sexual desire disorder: the persistent or recurring lack of sexual fantasies/
thoughts and/or receptivity to sexual activity
2. Sexual arousal disorder: the persistent or recurring inability to attain or maintain
sufficient sexual excitement
3. Orgasmic disorder: the persistent or recurring difficulty, delay in, or absence or
attaining orgasm following sufficient sexual stimulation and arousal
4. Sexual pain disorders: includes dyspareunia (genital pain with intercourse),
vaginismus (involuntary muscle spasms of the outermost third of the vagina), and
other (genital pain caused by noncoital sexual stimulation)
65
66 Walsh and Berman

Pelvic floor disorders can also contribute to female sexual dysfunction. Disorders of
the pelvic floor include incontinence, cystocele, rectocele, enterocele, and vaginal and uterine
prolapse. It is estimated that 10– 58% of adult women have symptoms of urinary incontinence
(5). Studies have shown that urinary incontinence can be a significant contributing factor to
female sexual dysfunction (6,7). Recent data have identified high rates of sexual dysfunction in
patients with pelvic prolapse (8).

II. FEMALE SEXUAL RESPONSE CYCLE

The definition of sexual dysfunction has included both psychological and physiological
components. Masters and Johnson first characterized the female sexual response cycle in 1966
(9). The cycle consisted of four consecutive phases: excitement, plateau, orgasmic, and
resolution. Kaplan proposed a three-phase model in 1974, which included desire, arousal, and
orgasm (10). Both of these cycles depict excitement or sexual desire as a spontaneous force that
by itself stimulates sexual arousal. In contrast to these cycles, a five-phase model focusing on
intimacy has been proposed by Basson (11) (Fig. 1). Basson suggests that for a large majority of
women, the wish to enhance intimacy is the driving force of the female sexual response cycle.
The cycle begins with basic intimacy needs, which may include mutuality, respect, and
communication. When these needs are met, a woman will seek out and will be more receptive to
sexual stimuli. The model hypothesizes a receptive type of desire, which stems from arousal and
a woman’s conscious choice of sexual stimuli. If there is an overall positive emotional and
physical interaction, the woman’s intimacy is enhanced and the cycle strengthened.

III. NEUROGENIC MEDIATORS OF THE FEMALE SEXUAL RESPONSE

The medial preoptic, anterior hypothalamic, and related limbic-hippocampal regions are areas
within the central nervous system that are responsible for sexual arousal. Once stimulated, these
regions will emit signals to both the sympathetic and parasympathetic nervous systems.

Figure 1 Alternative model of the female sexual response cycle.

 Female Sexual Dysfunction 67

A. Nonadrenergic/Noncholinergic Mediated Responses

Neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), nitric oxide synthetase (NOS),
cyclic gyanylate monophosphate (cGMP), and substance P have all been identified in human
vaginal tissue nerve fibers (12,13). Recent studies suggest that nitric oxide (NO) and VIP are
involved in altering vaginal relaxation and secretory processes (14,15). In organ bath analysis of
rabbit clitoral cavernosal smooth muscle strips, enhanced relaxation was demonstrated in
response to sodium nitroprusside and L-arginine (both NO donors). Using the same model, VIP
was found to cause dose-dependent relaxation of clitoral and vaginal muscle (16). Phospho-
diesterase type 5 (PDE5) has also been isolated in human clitoral, vestibular, and vaginal smooth
muscle cultures (17,18). PDE5 is the enzyme responsible for degradation of cGMP and
NO production. Sildenafil (Viagra), a PDE5 inhibitor, promotes intracellular cGMP
synthesis and accumulation, thus allowing for enhanced relaxation of clitoral and vaginal
smooth muscle (19).

B. Alpha-1-and Alpha-2-Adrenergic Responses

Alpha-adrenergic agents have been shown to be effective treatment for male erectile
dysfunction. The adrenergic receptors associated with penile erection, libido, and erection are
located in the male brain. Alpha-adrenergic mediators may also play a role in female sexual
arousal (20). In preliminary organ chamber experiments using rabbit vaginal tissue, exogenous
norepinephrine (alpha-1 and alpha-2 agonist) was found to cause dose-dependent contraction of
vaginal smooth muscle. In addition, both alpha-1- (prazosin and tamsulosin) and alpha-2-
(delequamine) selective antagonists inhibit smooth muscle contraction (21). These findings
suggest that adrenergic nerves mediate contractile response. There also appears to be a
difference in the quality of contractile responses in upper and lower vaginal segments, reflective
of their different innervation and embryologic origin.

IV. HORMONAL INFLUENCE ON FEMALE SEXUAL FUNCTION

AND RESPONSE
A. Testosterone
Only 1– 2% of total testosterone circulates unbound. The remainder is bound by sex hormone –
binding globulin (SHBG) or albumin. The nonbound (free) testosterone is biologically active.
Within the central nervous system, testosterone has been shown to affect female sexual behavior
(22,23). Low levels of testosterone are associated with decreased sexual arousal, libido, sexual
responsiveness, genital sensation, and orgasm (24,25). Recent evidence suggests that
testosterone may help promote the expression of endothelial NOS, the enzyme responsible for
production of NO (26).
There is no direct regulator, stimulator, or feedback mechanism of androgen production in
women. An increase in ovarian activity or adrenal activity has been shown to cause a rise in
androgen production (27). Androgen deficiency in women can be caused by a number of factors
including adrenal, pituitary, or ovarian surgery. Conditions such as hypopituitarism, adrenal
insufficiency, anorexia nervosa, exercise-induced amenorrhea, and premature ovarian failure
can also cause androgen deficiency. Lower androgen levels can occur in women taking
exogenous corticosteroids and in women with chronic illness. Oral administration of hormones
that elevate SHBG levels and reduce bioavailable androgens must also be considered to place
women at risk of androgen deficiency. Increased levels of estradiol such as in the oral
68 Walsh and Berman

contraceptive pill or hormone replacement therapy (HRT) can increase SHBG, thus decreasing
biologically available testosterone (28,29). Current commercial assays measuring total and free
testosterone levels were developed to measure the much higher circulating concentrations in
males.

B. Estrogen
Female sexual function is strongly influenced by estrogen. Both the neurological and vascular
systems are affected by circulating levels of estrogen. In postmenopausal women, estrogen
replacement was found to restore clitoral and vaginal vibration and pressure thresholds to levels
to premenopausal levels (30). The vasoprotective and vasodilatory effects of estrogen have also
been demonstrated. ERT has been shown to increase in vaginal, clitoral, and urethral arterial
flow (31). Low estradiol levels are associated with thinning of mucosal epithelium, atrophy of
vaginal wall smooth muscle, and an increase in vaginal pH. The less acidic environment within
the vaginal canal can lead to vaginal infections, incontinence, urinary tract infections, and sexual
dysfunction (32). Levels of estradiol ,50 pg/mL have been directly correlated with increased
sexual complaints (33).
Estrogen has also been shown to play a role in regulating vaginal and clitoral NOS (34). In
animal models, aging and surgical castration are associated with decreased vaginal and clitoral
NOS expression and apoptosis vaginal smooth muscle and mucosal epithelium. Estrogen
replacement restored vaginal mucosal health, NO expression, and decreased vaginal cell death
(35). These findings suggest that medications such as sildenafil (Viagra), which increases levels
of NO, may have a role in the treatment of female sexual dysfunction, in particular sexual
arousal disorder.

V. MEDICAL RISK FACTORS ASSOCIATED WITH SEXUAL DYSFUNCTION

Current evidence suggests that up to 80% of cases of sexual dysfunction have some organic
component. Conditions associated with sexual dysfunction are listed in Table 1.

A. Vascular
Males and females can experience sexual dysfunction secondary to diabetes, cardiovascular
disease, hypertension, peripheral vascular disease, and tobacco use (36,37). Diminished blood
flow of the iliohypogastric/pudendal arterial bed leads to significant compromise of the vascular
bed in both male and female genitalia (38,39). In females this is termed clitoral and vaginal
vascular insufficiency syndromes (40). Sufficient blood flow is crucial for maintaining vascular
and muscular integrity, both components integral in sexual arousal. Diminished blood flow can
lead to vaginal wall and clitoral smooth muscle fibrosis that can result in symptoms of vaginal
dryness and dyspareunia. Pelvic fractures, blunt trauma, surgical disruption, radiation, or chronic
perineal pressure from bicycle riding can all lead to diminished vaginal and clitoral blood flow
and sexual dysfunction.

B. Hormonal
In females, the most common causes of primary endocrine abnormalities are menopause,
surgical or medical castration, premature ovarian failure, dysfunction of the hypothalamic/
pituitary axis, and chronic birth control use. The percentage of women with a primary endocrine
 Female Sexual Dysfunction 69

Table 1 Medical Risk Factors Associated With Sexual Dysfunction

Vascular
Diabetes mellitus
Atherosclerosis
Hypertension
Lipid disorders
Peripheral vascular disease
Hormonal
Hypogonadism
Hyperprolactinemia
Hypo/hyperthyroidism
Neurogenic
Spinal cord injury
Multiple sclerosis
Musculogenic
Pelvic floor muscle hyper/hypotonicity
Medications (see Table 2)
Psychogenic
Depression
Anxiety/obsession-compulsive disorder
Social stressors
Religious inhibitions
Posttraumatic sexual experiences
Dysfunctional attitudes about sex
Other
Autoimmune disorders
Renal disease (dialysis)
Bowel disease (colostomy)
Bladder disease (incontinence, cystitis)
Skin disorders (contact dermatitis, eczema)

dysfunction responsible for their sexual dysfunction is unknown. Estrogen and testosterone play
a significant role in regulating female sexual function.
There is a decline in both estrogen and testosterone levels with age, although the decline in
testosterone is much less pronounced (28). A decrease in estrogen levels is associated with
adverse neurovascular events affecting vaginal, clitoral, and urethral tissues. Low testosterone
levels in females have been associated with a decline in sexual arousal, genital stimulation,
libido, and orgasm. Therapy with combination estrogen-androgen compared with estrogen alone
has shown to enhance libido, sexual desire and motivation, and overall sense of well-being (41).

C. Neurogenic
Neurogenic sexual dysfunction can occur in both men and women with spinal cord injury (SCI)
or disease of the central or peripheral nervous system. In a study comparing premenopausal
women with SCI, ,50% of women with SCIs were able to achieve orgasm, compared with
100% of able-bodied women. They also reported that only 17% of women with complete lower
70 Walsh and Berman

motor neuron dysfunction affecting the S2 –S5 spinal segments were able to achieve orgasm,
compared with 59% of women with other levels of SCI. Time to orgasm was also significantly
increased in women with SCIs (42). Women with complete upper motor neuron injuries
affecting sacral spinal segments had difficulty achieving psychogenic lubrication (43). Focus
group studies examining diabetes and female sexuality identified complaints of increased
fatigue, vaginitis, decreased sexual desire, decreased vaginal lubrication, and an increased time
to reach orgasm (44,45).

D. Musculogenic
The levator ani and perineal membrane make up the pelvic floor musculature that influences
female responsiveness during sexual activity. The perineal membrane consists of the
bulbocavernous and ischiocavernosus muscles. These muscles contract both voluntarily and
involuntarily, intensifying sexual arousal and orgasm. The levator ani muscles are involved in
modulating motor responses during vaginal receptivity and orgasm. Hypertonicity in the
muscles can occur secondary to trauma (surgery, radiation, childbirth) and aging. This can cause
vaginal hypoanesthsia, coital anorgasmia, or urinary incontinence during sexual intercourse or
orgasm. Hypertonicity of the levator ani muscles can cause sexual pain disorders such as
vaginismus that leads to dyspareunia.

E. Psychogenic
For many women who experience symptoms of sexual dysfunction, a combination of
psychogenic and organic causes can be established. Psychogenic issues may include poor
partner communication, performance anxiety, low self-esteem, social stressors, and religious
inhibitions (46). Psychological disorders such as depression, posttraumatic sexual experiences,
obsessive-compulsive disorder, or anxiety disorder can also have a significant impact on sexual
function (47,48).

F. Medications
There are 1.5 billion prescriptions written every year in the United States. One or more new
prescriptions are written in over two-thirds of physician office visits (49). While many
prescription medications have been implicated in causing sexual dysfunction, antihyperten-
sive, antidepressant, and antipsychotic medications are the most frequently cited (50).
Controlled research is limited for the majority of medications and substances believed to
cause female SD. Many articles present only subjective evidence or case reports. The classes
of medications most commonly associated with causing sexual dysfunction are listed in
Table 2.

VI. EVALUATION OF THE FEMALE SEXUAL RESPONSE

A. Psychosocial/Psychosexual
Diagnosis of sexual dysfunction begins with sensitive and comprehensive questioning regarding
sexual history. The Brief Index of Sexual Function in Women (BISF-W) is a validated 21-item,
self-reported inventory of sexual interest, activity, satisfaction, and preference. This instrument
can be used to differentiate among depressed, sexually dysfunctional, and healthy patients. This
 Female Sexual Dysfunction 71

Table 2 Common Classes of Medications With Sexual Side Effects

Class Examples

Antihypertensive agents a1 and 2 blockers (clonidine, reserpine, prasozin)

b-blockers (metoprolol, propranolol)
Calcium channel blockers (diltiazem, nifedipine)
Diuretics (hydrochorothiazide)
Chemotherapeutic Alkylating agents (busulfan, chlorambucil, cyclophosphamide)
Central nervous Anticholinergics (diphenhyramine)
system agents Anticonvulsants (carbamazepine, phenobarbital, phenytoin)
Antidepressants (MOAIs, TCAs, SSRIs)a
Antipsychotics (phenothiazines, butyrophenones)
Narcotics (oxycodone)
Sedatives/anxiolytics (benzodiazepines)
Agents that affect Antiandrogens (cimetidine, spironolactone)
hormones Antiestrogens (tamoxifen, raloxifene)
Oral contraceptives
a
MAOIs, monoamine oxidase inhibitors; TCAs, tricylcic antidepressants; SSRIs, selective serotonin reuptake inhibitors.

subjective report from the patient is crucial to understanding whether or not psychotherapy and/
or medical therapy is useful. Studies have shown that physicians are reluctant to address sexual
topics. The physicians cited several reasons including awkwardness with sex language, fear of
insulting the patient, feeling uncomfortable with the topic, and not knowing what questions to
ask or how to ask them (51,52). Evidence suggests, however, that patients believe sexual
function is an appropriate topic and are relieved when it is discussed with their physician (53).
Patients may feel pressure to live up to an idealized standard of performance and have unrealistic
expectations for themselves or their partner. Many men and women question where they fit on
the continuum from normality to dysfunction. Open-ended and/or direct questioning can help
guide the physician and patient to understanding the patient’s sexual dysfunction.

B. Physical Exam
Every patient complaining of sexual dysfunction should undergo a thorough physical exam,
including an external and internal gynecological exam. During the external gynecological exam,
assessment of muscle tone, skin color, turgor and texture, and pubic hair distribution can identify
conditions such as vaginismus, vulvar dystrophy, dermatitis, and atrophy. Examination of the
posterior forchette and hymenal ring can help recognize episiotomy scars and possible strictures.
The monomanual exam should include palpation of the rectovaginal surface, levator ani, and
bladder/urethra in order to identify any rectal disease, levator ani myalgia, vaginismus,
urethritis, cystitis, or urinary tract infections. Cervical motion tenderness may indicate infection
or peritonitis. Palpation of the uterus and adnexa are included in the bimanual exam and assist
in the identification of uterine retrogression, fibroids, adnexal masses/cysts, and possible
endometriosis.
Finally, the speculum exam is utilized to evaluate for discharge, pH, vaginal mucosa,
Papanicolaou smear, and prolapse. In females, vaginal pH, an indirect measurement of
lubrication, can be measured using a digital pH probe. Decreased pulses, bruits, elevated blood
72 Walsh and Berman

pressure, and cool extremities are suggestive of vascular disease. Assessment should include a
lipid profile and Doppler exams.
The suggested baseline hormonal profile includes follicle-stimulating hormone (FSH),
luteinizing hormone (LH), total and free testosterone levels, SHBG, and estradiol and prolactin
levels. Measurements of FSH and LH can assist in evaluating for primary versus secondary
hypogonadism. High levels of FSH and LH are indicative of primary gonadal failure, and low or
normal levels suggest hypothalamic or pituitary disease. Decreased levels of estrogen and
testosterone have been associated with decreased libido, decreased sensation, vaginal dryness,
dyspareunia, and decreased arousal. Hyperprolactemia can be seen in patients with decreased
libido, galactorrhea, visual complaints, and headaches. Physical examination is positive for
bitemporal hemianopsia. A CT or MRI may be needed to assess the pituitary gland.
Fatigue and cold intolerance are seen in patients with hypothyroidism. Examination for
a possible goiter, myxedema, dry skin, and coarse hair is warranted. An increased TSH
and decreased free T4 are seen on laboratory tests. Hyperthyroidism can present with heat
intolerance, weight loss, diaphoresis, and palpitations. Lid lag, exophthalamos, hyperreflexia,
tremor, and tachycardia may be present on clinical exam. Laboratory values include a decreased
TSH and an increased free T4.
Cushing’s syndrome is diagnosed on clinical exam by easy bruising, weight gain, truncal
obesity, “moon face,” “buffalo hump,” and striae. An elevated overnight dexamethasone
suppression test is needed for confirmation of clinical exam. Diabetic patients should be
evaluated for peripheral neuropathy, retinopathy, and abnormal body mass index.
A thorough neurological exam is necessary in patients who have known or suspected SCI,
nerve injury (prostate surgery, hysterectomy, childbirth), peripheral neuropathy, multiple
sclerosis, or Parkinson’s disease. The neurologic exam may uncover sensory or motor
impairment that will account for residual urine (neuropathic bladder) or incontinence. Since the
bladder and its sphincter are innervated by the second to fourth sacral segments. Somatic
function of the sacral cord levels S2 – 4 is assessed by touching the perianal skin or placing a
finger in the patient’s rectum and noting contraction of the external anal sphincter muscles. This
is termed the bulbocavernosus reflex.

VII. TREATMENT

In patients in whom an underlying medical condition has been diagnosed, treatment for
correction or to control progression is appropriate. However, patients should be made aware that
treatment of their condition does not guarantee the elimination of their sexual dysfunction.
Consideration should be given to discontinuation of any medication suspected of contributing to
sexual dysfunction or, if possible, switching to an alternative medication. For patients with a
component of psychogenic dysfunction, referral to a psychologist or psychiatrist with expertise
in sexual dysfunction may be beneficial.

A. Estrogen
Medical management of sexual dysfunction in women has focused on hormonal treatment. Both
estrogen and testosterone are being used alone and in combination. In postmenopausal women,
estrogen replacement has been found to improve clitoral and vaginal sensitivity, increase libido,
restore vibratory and pressure thresholds, and decrease symptoms of vaginal dryness and pain
during intercourse (33,54). Estrogen is available in several forms including oral pill, dermal
 Female Sexual Dysfunction 73

patch, vaginal ring, and cream. The vaginal ring is a therapeutic option for women with breast
cancer who are unable to take oral or transdermal estrogen.
Estrogen, especially when begun early in menopause, has been shown to be beneficial in
the prevention and treatment of osteoporosis. ERT has also been shown to significantly reduce
the risk for colon cancer, but not rectal cancers (55). Postmenopausal estrogen replacement,
with or without progestin therapy, has a generally favorable impact on lipids, improves
endothelial function, and has anti-inflammatory and antioxidant effects. However, the results
of the Heart and Estrogen/Progestin Replacement Study (HERS) trial found no overall
reduction in coronary events among women assigned to active hormone treatment. It is also
suggested that there may be a transitory increase in coronary risk after starting hormone
therapy in women with established coronary heart disease and a decreased risk thereafter (56).
Prospective studies are under way to try to delineate how estrogen impacts Alzheimer’s
disease. Potential risks of HRT include gallbladder disease, thromboembolism, and breast
cancer.

B. Testosterone
Testosterone supplementation has been shown to improve mood and well-being in naturally
menopausal and surgical postmenopausal women (41,57,58). Women treated with testosterone
and intramuscular E2 were found to have improvements in sexual desire, fantasy, arousal, and
orgasm (25,30,59). Decreased testosterone levels can be seen in women with premature ovarian
failure and following natural, surgical or post-chemotherapy-induced menopause.
For replacement purposes, testosterone is available in lozenger pill form, sublingual,
dermal patch, and cream. Oral methyltestosterone is available in the United States either alone or
in combination with estrogen (Estratest). In postmenopausal women who experience inhibited
desire, dyspareunia, or lack of vaginal lubrication, testosterone can be prescribed in combination
with estrogen. The transdermal testosterone patch is under clinical investigation. The patches
contain 150 mg testosterone. Two patches are applied simultaneously twice a week. Preliminary
results have been promising (60,61).
Testosterone topical cream has been approved for treatment of vaginal lichen planus.
Topical preparations can be make in 1%, 2%, and 3% formulations and can be applied up to
three times per week. Benefits from testosterone therapy include improved libido, increased
vaginal and clitoral sensitivity, increased vaginal lubrication, and heightened arousal. Side
effects of testosterone use that need to be monitored for in women include weight gain, clitoral
enlargement, increased facial hair, and hypercholesterolemia. Measurement of testosterone
levels before and after therapy, lipid panels (cholesterol, triglyceride, HDL, LDL), and liver
function tests are recommended (62,63). Whether or not testosterone therapy in premenopausal
women is beneficial is under investigation.

C. Investigational Medications/Devices
Secondary to the increase in both clinical and biological research in female sexual dysfunction,
several new investigational medications and devices are now available. See Table 3.

VIII. SUMMARY

Female sexual dysfunction is a multicausal medical problem. Evaluation of the patient should
include a comprehensive and collaborative effort between a physician and a psychologist.
74 Walsh and Berman

Table 3 Investigational Medications

Treatment Company Ingredient Already used for Side effects

Alista (cream) Vivus Inc. Topical Sexual arousal Transient burning in

Alprostadil/ disorder men; in trials in
PGE 1 women now
Androsorb Novavax Testosterone Hormone booster for Early stages of clinical
(cream) hypogonadal men trial; may heighten
libido in
postmenopausal
women
EROS-CTD Urometrics Clitoral therapy Arousal disorder Increased sensation
device and blood flow to
clitoris via gentle
suction
Estratest (pill) Solvay Pharm. Estrogen- HRT Heightens libido in
testosterone some women; side
combination effects include acne
and hair growth
Femprox (cream) NexMed, Inc. Blood vessel Sexual arousal Improves blood flow to
dilator disorder genitals; enhances
arousal
Intrinsa (patch) Proctor & Testosterone Hypoactive sexual Increases sexual
Gamble desire disorder activity and pleasure
Watson Labs
Livial (pill) Organon Synthetic Osteoporosis, HRT Approved in Europe
steroid for menopause
symptoms;
improved mood and
libido
Argimax NitroMed Yohimbine Arousal disorder Increases vaginal blood
African tree flow in
bark fortified postmenopausal
with L-Argine women; may
enhance arousal
Premarin or Wyeth-Ayerst Estrogen Osteoporosis, vaginal Vaginal dryness and
Estrace Warner 17-b estradiol atrophy, HRT discomfort; not for
(cream) Chilcott use in women with
history of blood clots
or breast or
endometrial cancer
Steryl- Senetek PLC Synthetic Arousal disorder Enhances vaginal
Norleucine version of lubrication,
VIP (cream) VIP sensation, and
genital engorgement
Testosterone Off-label Testosterone New product Not FDA approved;
(cream) prescriptions side effects include
from weight gain, hair
compounding growth, oily skin,
pharmacies enlarged clitoris

(continued )
 Female Sexual Dysfunction 75

Table 3. Continued

Treatment Company Ingredient Already used for Side effects

Tostrelle (gel) Cellegy Testosterone Hormone booster for Early study:

hypogonadal men testosterone levels in
women on HRT
jumped to levels of
teenage girls
Uprima (pill) Tap Pharm. Apomorphine Sexual arousal Targets the brain and
disorder and stimulates the
low desire release of dopamine;
side effects: nausea,
vomiting, not yet
FDA approved
Vagifem Pharmacia Estrogen Vaginal atrophy Improves dryness and
Upjohn irritation; not
absorbed
systemically
Vasofem (pill) Zonagen Blood vessel Sexual arousal Increases blood flow to
dilator disorder genitals
Viagra (pill) Pfizer Blood vessel Male erectile Increases blood flow to
dilator dysfunction and genitals; enhances
female sexual arousal
arousal disorder
Levitra Bayer Blood vessel Male erectile Increases blood flow to
dilator, smooth dysfunction and genitals; enhances
muscle relaxer female sexual arousal
arousal disorder

Although there are anatomic similarities between male and females, the complexity of female
sexual dysfunction remains distinct from that of a man. The context in which a woman
experiences her sexuality is equally as if not more important than the physiologic outcome she
experiences. It is imperative that issues regarding how a woman views her sexuality be
addressed before beginning medical therapy or determining treatment efficacies.

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6
Hormonal Influence on the Lower
Urinary Tract
Dudley Robinson and Linda Cardozo
King’s College Hospital, London, England

I. INTRODUCTION

The female genital and lower urinary tract share a common embryological origin, arising from
the urogenital sinus. Both are sensitive to the effects of female sex steroid hormones. Estrogen is
known to have an important role in the function of the lower urinary tract throughout adult life,
with estrogen and progesterone receptors demonstrated in the vagina, urethra, bladder, and
pelvic floor musculature (1 –4). This is supported by the fact that estrogen defiency occurring
following the menopause is known to cause atrophic changes within the urogenital tract (5) and
is associated with urinary symptoms such as frequency, urgency, nocturia, incontinence, and
recurrent infection. These may also coexist with symptoms of vaginal atrophy such as
dyspareunia, itching, burning, and dryness. This chapter will review the role of estrogen and
progesterone on lower urinary tract function in addition to assessing the role of estrogens in the
management of lower urinary tract dysfunction.

II. ESTROGEN RECEPTORS AND HORMONAL FACTORS

The effects of the steroid hormone 17b-estradiol are mediated by ligand-activated transcription
factors known as estrogen receptors. These are glycoproteins and share common features with
both androgen and progesterone receptors and can be divided into several functional domains
(6). The classic estrogen receptor (ERa) was first discovered by Jensen in 1958 and cloned from
uterine tissue in 1986 (7), although it was not until 1996 that the second estrogen receptor (ERb)
was identified (8). The precise role of the two different receptors remains to be elucidated
although ERa appears to play a major role in the regulation of reproduction whilst ERb has a
more minor role (9).
Estrogen receptors have been demonstrated throughout the lower urinary tract and are
expressed in the squamous epithelium of the proximal and distal urethra, vagina, and trigone of
the bladder (3,10), although not in the dome of the bladder, reflecting its different embryological
origin. Pubococcygeus and the musculature of the pelvic floor have also been shown to be
estrogen sensitive (11), although estrogen receptors have not yet been identified in the levator
ani muscles (12).
79
80 Robinson and Cardozo

The distribution of estrogen receptors throughout the urogenital tract has also been
studied, with both a and b receptors being found in the vaginal walls and uterosacral ligaments
of premenopausal women, although the latter were absent in the vaginal walls of
postmenopausal women (13). In addition, a receptors are localized in the urethral sphincter
and when sensitised by estrogens are thought to help maintain muscular tone (14).
In addition to estrogen receptors, both androgen and progesterone receptors are expressed
in the lower urinary tract although their role is less clear. Progesterone receptors are expressed
inconsistently, having been reported in the bladder, trigone, and vagina. Their presence may be
dependent on estrogen status (5). While androgen receptors are present in both the bladder and
urethra, their role has not yet been defined (15). Interestingly, estrogen receptors have also been
identified in mast cells in women with interstitial cystitis (16,17) and in the male lower urinary
tract (18).
More recently, the incidence of both estrogen and progesterone expression has been
examined throughout the lower urinary tract in 90 women undergoing gynecological surgery; 33
were premenopausal, 26 postmenopausal without hormone replacement therapy (HRT), and 31
postmenopausal and taking HRT (19). Biopsies were taken from the bladder dome, trigone,
proximal urethra, distal urethra, vagina, and vesicovaginal fascia adjacent to the bladder neck.
Estrogen receptors were found to be consistently expressed in the squamous epithelia, although
were absent in the urothelial tissues of the lower urinary tract of all women, irrespective of
estrogen status. Progesterone receptor expression, however, showed more variability, being
mostly subepithelial, and was significantly lower in postmenopausal women not taking
oestrogen replacement therapy.

III. HORMONAL INFLUENCES ON LOWER URINARY TRACT SYMPTOMS

To maintain continence, the urethral pressure must remain higher than the intravesical pressure
at all times except during micturition (20). Estrogens play an important role in the continence
mechanism, with bladder and urethral function becoming less efficient with age (21). Elderly
women have been found to have a reduced flow rate, increased urinary residuals, higher filling
pressures, reduced bladder capacity, and lower maximum voiding pressures (22). Estrogens may
affect continence by increasing urethral resistance, raising the sensory threshold of the bladder,
or increasing a adrenoreceptor sensitivity in the urethral smooth muscle (23,24). In addition,
exogenous estrogens have been shown to increase the number of intermediate and superficial
cells in the vagina of postmenopausal women (25). These changes have also been demonstrated
in the bladder and urethra (26).
More recently, a prospective observational study has been performed to assess cell
proliferation rates throughout the tissues of the lower urinary tract (27). Fifty-nine women were
studied of whom 23 were premenopausal, 20 were postmenopausal and not taking HRT, and 20
were postmenopausal and taking HRT. Biopsies were taken from the bladder dome, trigone,
proximal urethra, distal urethra, vagina, and vesicovaginal fascia adjacent to the bladder neck.
The squamous epithelium of oestrogen replete women was shown to exhibit greater levels of
cellular proliferation than in those women who were estrogen deficient.
Cyclical variations in the levels of both estrogen and progesterone during the menstrual
cycle have been shown to lead to changes in urodynamic variables and lower urinary tract
symptoms, with 37% of women noticing a deterioration in symptoms prior to menstruation (28).
Measurement of the urethral pressure profile in nulliparous premenopausal women shows there
is an increase in functional urethral length midcycle’ and early in the luteal phase corresponding
to an increase in plasma estradiol (29). Furthermore, progestogens have been associated with an
 Hormonal Influence on the Lower Urinary Tract 81

increase in irritative bladder symptoms (30,31) and urinary incontinence in those women taking
combined hormone replacement therapy (32). The incidence of detrusor overactivity in the
luteal phase of the menstrual cycle may be associated with raised plasma progesterone following
ovulation, and progesterone has been shown to antagonize the inhibitory effect of estradiol on rat
detrusor contractions (33). This may help to explain the increased prevalence of detrusor
overactivity found in pregnancy (34).
The role of estrogen replacement therapy in the prevention of ischemic heart disease has
recently been assessed in a 4-year randomized trial, the Heart and Estrogen/Progestin
Replacement Study (35). In the study 55% of women reported at least one episode of urinary
incontinence each week, and were randomly assigned to oral conjugated estrogen plus
medroxyprogesterone acetate or placebo daily. Combined HRT was associated with worsening
stress and urge urinary incontinence, although there was no significant difference in daytime
frequency, nocturia, or number of urinary tract infections.
Finally, the role of estrogen therapy in the management of women with fecal incontinence
has also been investigated in a prospective observational study using symptom questionnaires
and anorectal physiological testing before and after 6 months of ERT. At follow-up, 25% of
women were asymptomatic and a further 65% were improved in terms of flatus control, urgency,
and fecal staining. In addition, anal resting pressures and voluntary squeeze increments were
significantly increased following estrogen therapy, although there were no changes in pudendal
nerve terminal latency. The authors conclude that estrogen replacement therapy may have a
beneficial effect, although larger studies are needed to confirm these findings (36).

IV. HORMONAL INFLUENCES ON URINARY TRACT INFECTION

Urinary tract infection is also a common cause of urinary symptoms in women of all ages. This is
a particular problem in the elderly, with a reported incidence of 20% in the community and
.50% in institutionalized patients (37,38). Pathophysiological changes such as impairment of
bladder emptying, poor perineal hygiene, and both fecal and urinary incontinence may partly
account for the high prevalence observed. In addition, changes in the vaginal flora due to
estrogen depletion lead to colonization with gram-negative bacilli which in addition to causing
local irritive symptoms also act as uropathogens. These microbiological changes may be
reversed with estrogen replacement following the menopause, offering a rationale for treatment
and prophylaxis.

V. HORMONAL INFLUENCES ON LOWER URINARY TRACT FUNCTION

A. Neurological Control
Sex hormones are known to influence the central neurological control of micturition, although
their exact role in the micturition pathway has yet to be elucidated. Estrogen receptors have been
demonstrated in the cerebral cortex, limbic system, hippocampus, and cerebellum (39,40), while
androgen receptors have been demonstrated in the pontine micturition centre and the preoptic
area of the hypothalamus (41).

B. Bladder Function
Estrogen receptors, although absent in the transitional epithelium at the dome of the bladder, are
present in the areas of the trigone that have undergone squamous metaplasia (10). Estrogen is
82 Robinson and Cardozo

known to have a direct effect on detrusor function through modifications in muscarinic receptors
(42,43) and by inhibition of movement of extracellular calcium ions into muscle cells (44).
Consequently, estradiol has been shown to reduce the amplitude and frequency of spontaneous
rhythmic detrusor contractions (45), and there is also evidence that it may increase the sensory
threshold of the bladder in some women (46).

C. Urethra
Estrogen receptors have been demonstrated in the squamous epithelium of both the proximal and
distal urethra (10), and estrogen has been shown to improve the maturation index of urethral
squamous epithelium (47). It has been suggested that estrogen increases urethral closure
pressure and improves pressure transmission to the proximal urethra, both promoting continence
(48 – 51). Additionally, estrogens have been shown to cause vasodilatation in the systemic and
cerebral circulation, and these changes are also seen in the urethra (52 –54).
The vascular pulsations seen on urethral pressure profilometry secondary to blood flow in
the urethral submucosa and urethral sphincter have been shown to increase in size following
estrogen administration (55), while the effect is lost following estrogen withdrawal at the
menopause. The urethral vascular bed is thought to account for around a third of the urethral
closure pressure, and estrogen replacement therapy in postmenopausal women with stress
incontinence has been shown to increase the number of periurethral vessels (56).

D. Collagen
Estrogen are known to have an effect on collagen synthesis, and they have been shown to have a
direct effect on collagen metabolism in the lower genital tract (57). Changes found in women
with urogenital atrophy may represent an alteration in systemic collagenase activity (58), and
genuine stress incontinence and urogenital prolapse have been associated with a reduction in
both vaginal and periurethral collagen (59 –61). Furthermore, there is a reduction in skin
collagen content following the menopause (62), with rectus muscle fascia being shown to
become less elastic with increasing age, resulting in a lower energy requirement to cause
irreversible damage (63). Changes in collagen content have also been identified, the
hydroxyproline content in connective tissue from women with stress incontinence being 40%
lower than in continent controls (64).

VI. LOWER URINARY TRACT SYMPTOMS

A. Urinary Incontinence
The prevalence of urinary incontinence is known to increase with age, affecting 15 –35% of
community dwelling women over the age of 60 years (65) and other studies reporting a
prevalence of 49% in women over 65 years (66). In addition, rates of 50% have been reported in
elderly nursing-home residents (67). A recent cross-sectional population prevalence survey of
146 women aged 15– 97 years found that 46% experienced symptoms of pelvic-floor dysfunc-
tion defined as stress or urge incontinence, flatus or fecal incontinence, symptomatic prolapse,
or previous pelvic-floor surgery (68).
Little work has been done to examine the incidence of urinary incontinence, although a
study in New Zealand of women over the age of 65 years found 10% of the originally continent
developed urinary incontinence in the 3-year study period (69).
 Hormonal Influence on the Lower Urinary Tract 83

Epidemiological studies have implicated estrogen deficiency in the etiology of lower

urinary tract symptoms, with 70% of women relating the onset of urinary incontinence to their
final menstrual period (5). Lower urinary tract symptoms have been shown to be common in
postmenopausal women attending a menopause clinic, with 20% complaining of severe urgency
and almost 50% complaining of stress incontinence (70). Urge incontinence in particular is more
prevalent following the menopause, and the prevalence would appear to rise with increasing
years of estrogen deficiency (71). There is, however, conflicting evidence regarding the role of
estrogen withdrawal at the time of the menopause. Some studies have shown a peak incidence in
perimenopausal women (72,73), while other evidence suggests that many women develop
incontinence at least 10 years prior to the cessation of menstruation, with significantly more
premenopausal women than postmenopausal women being affected (74).

B. Urogenital Atrophy
Urogenital atrophy is a manifestation of estrogen withdrawal following the menopause, and
symptoms may appear for the first time more than 10 years after the last menstrual period (75). In
addition, increasing life expectancy has led to an increasingly elderly population, and it is now
common for women to spend a third of their lives in the estrogen-deficient postmenopausal state
(76), with the average age of the menopause being 50 years (77).
Postmenopausal women comprise 15% of the population in industrialised countries, with a
predicted growth rate of 1.5% over the next 20 years. Overall, in the developed world 8% of the
total population have been estimated to have urogenital symptoms (78), this representing 200
million women in the United States alone.
It has been estimated that 10– 40% of all postmenopausal women are symptomatic (79),
although only 25% are thought to seek medical help. In addition, two out of three women report
vaginal symptoms associated with urogenital atrophy by the age of 75 years (80). However, the
prevalence of symptomatic urogenital atrophy is difficult to estimate since many women accept
the changes as being an inevitable consequence of the aging process and thus do not seek help
leading to considerable under reporting.
A study assessing the prevalence of urogenital symptoms in 2157 Dutch women has been
recently reported (81). Overall, 27% of women complained of vaginal dryness, soreness, and
dyspareunia, while the prevalence of urinary symptoms such as leakage and recurrent infections
was 36%. When considering severity, almost 50% reported moderate to severe discomfort,
although only a third had received medical intervention. Interestingly, women who had
previously had a hysterectomy reported moderate to severe discomfort more often than those
who had not.
The prevalence of urogenital atrophy and urogenital prolapse has also been examined in a
population of 285 women attending a menopause clinic (82). Overall, 51% of women were
found to have anterior vaginal wall prolapse, 27% posterior vaginal prolapse, and 20% apical
prolapse. In addition, 34% of women were noted to have urogenital atrophy, 40% complaining
of dyspareunia. While urogenital atrophy and symptoms of dyspareunia were related to
menopausal age, the prevalence of prolapse showed no association.
However, while urogenital atrophy is an inevitable consequence of the menopause,
women may not always be symptomatic. A recent study of 69 women attending a gynecology
clinic were asked to fill out a symptom questionnaire prior to examination and undergoing
vaginal cytology (83). Urogenital symptoms were found to be relatively low and were poorly
correlated with age and physical examination findings although not with vaginal cytological
maturation index. Women who were taking estrogen replacement therapy had higher symptom
scores and physical examination scores.
84 Robinson and Cardozo

From this evidence it would appear that urogenital atrophy is a universal consequence of
the menopause, although elderly women may be minimally symptomatic. Hence, treatment
should not be the only indication for replacement therapy.

VII. MANAGEMENT OF LOWER URINARY DYSFUNCTION

A. Estrogens in the Management of Incontinence
Estrogen preparations have been used for many years in the treatment of urinary incontinence
(84,85), although their precise role remains controversial. Many of the studies performed have
been uncontrolled observational series examining the use of a wide range of different prepara-
tions, doses, and routes of administration. The inconsistent use of progestogens to provide
endometrial protection is a further confounding factor, making interpretation of the results
difficult. To clarify the situation a meta-analysis from the Hormones and Urogenital Therapy
(HUT) committee has been reported (86). Of 166 articles identified that were published in
English between 1969 and 1992, only six were controlled trials and 17 were uncontrolled series.
Meta-analysis found an overall significant effect of estrogen therapy on subjective improvement
in all subjects and for subjects with urodynamic stress incontinence alone. Subjective
improvement rates with estrogen therapy in randomized controlled trials ranged from 64% to
75%, although placebo groups also reported an improvement of 10 –56%. In uncontrolled series
subjective improvement rates were 8 –89%, with subjects with urodynamic stress incontinence
showing improvement of 34 –73%. However, when assessing objective fluid loss, there was no
significant effect. Maximum urethral closure pressure was found to increase significantly with
estrogen therapy, although this outcome was influenced by a single study showing a large effect
(87).

B. Estrogens in the Management of Stress Incontinence

In addition to the studies included in the HUT meta-analysis, several authors have also
investigated the role of estrogen therapy in the management of urodynamic stress incontinence
only (Table 1). Oral estrogens have been reported to increase the maximum urethral pressures
and lead to symptomatic improvement in 65– 70% of women (88,89), although other work has
not confirmed this (90,91). More recently, two placebo-controlled studies have been performed
examining the use of oral estrogens in the treatment of urodynamic stress incontinence in
postmenopausal women. Neither conjugated equine estrogens and medroxyprogesterone (92)

Table 1 Summary of Randomized Controlled Trials Assessing the Use of Estrogens in

the Management of Urinary Incontinence

Study Year Type of incontinence Estrogen Route

Henalla et al. (87) 1989 Stress incontinence Conjugated estrogen Vaginal

Hilton et al. (96) 1990 Stress incontinence Conjugated estrogen Vaginal
Beisland et al. (95) 1984 Stress incontinence Estriol Vaginal
Judge (120) 1969 Mixed incontinence Quinestradol Oral
Kinn and Lindskog (121) 1988 Stress incontinence Estriol Oral
Samsioe et al. (97) 1985 Mixed incontinence Estriol Oral
Walter et al. (91) 1978 Urge incontinence Estradiol and estriol Oral
Walter et al. (122) 1990 Stress incontinence Estriol Oral
Wilson et al. (90) 1987 Stress incontinence Piperazine estrone sulfate Oral
 Hormonal Influence on the Lower Urinary Tract 85

nor unopposed estradiol valerate (93) showed a significant difference in either subjective or
objective outcomes. Furthermore, a review of eight controlled and 14 uncontrolled prospective
trials concluded that estrogen therapy was not an efficacious treatment for stress incontinence
but may be useful for symptoms of urgency and frequency (94).
From the available evidence estrogen does not appear to be an effective treatment for
stress incontinence, although it may have a synergistic role in combination therapy. Two
placebo-controlled studies have examined the use of oral and vaginal estrogens with the
a-adrenergic agonist phenylpropanolamine used separately and in combination. Both studies
found that combination therapy was superior to either drug given alone, although while there
was subjective improvement in all groups (95), there was only objective improvement in the
combination therapy group (96). This may offer an alternative conservative treatment for women
who have mild urodynamic stress incontinence.
Estrogens have been used in the treatment of urinary urgency and urge incontinence for
many years, although there have been few controlled trials to confirm their efficacy (Table 1). A
double-blind placebo controlled crossover study using oral estriol in 34 postmenopausal women
produced subjective improvement in eight women with mixed incontinence and 12 with urge
incontinence (97). However, a double-blind multicenter study of the use of estriol (3 mg/d) in
postmenopausal women complaining of urgency has failed to confirm these findings (98),
showing both subjective and objective improvement but not significantly better than placebo.
Estriol is a naturally occurring weak estrogen that has little effect on the endometrium and does
not prevent osteoporosis although it has been used in the treatment of urogenital atrophy.
Consequently, it is possible that either the dosage or route of administration in this study was not
appropriate in the treatment of urinary symptoms, and higher systemic levels may be required.
The use of sustained release 17b-estradiol vaginal tablets (Vagifem, Novo Nordisk) has
also been examined in postmenopausal women with urgency and urge incontinence or a
urodynamic diagnosis of sensory urgency or detrusor overactivity. These vaginal tablets have
been shown to be well absorbed from the vagina and to induce maturation of the vaginal
epithelium within 14 days (99). However, following a 6-month course of treatment, the only
significant difference between active and placebo groups was an improvement in the symptom of
urgency in those women with a urodynamic diagnosis of sensory urgency (100). A further
double-blind, randomized, placebo-controlled trial of vaginal 17b-estradiol vaginal tablets has
shown lower urinary tract symptoms of frequency, urgency, urge, and stress incontinence to be
significantly improved, although no objective urodynamic assessment was performed (101). In
both of these studies the subjective improvement in symptoms may simply represent local
estrogenic effects reversing urogenital atrophy rather than a direct effect on bladder function.
More recently a randomized, parallel-group, controlled trial has been reported comparing
the estradiol-releasing vaginal ring (Estring, Pharmacia, Uppsala, Sweden) with estriol vaginal
pessaries in the treatment of postmenopausal women with bothersome lower urinary tract
symptoms (102). Low-dose vaginally administered estradiol and estriol were found to be equally
efficacious in alleviating lower urinary tract symptoms of urge incontinence (58% vs. 58%),
stress incontinence (53% vs. 59%), and nocturia (51% vs. 54%), although the vaginal ring was
found to have greater patient acceptability.
To try to clarify the role of estrogen therapy in the management of women with urge
incontinence, a meta-analysis of the use of estrogen in women with symptoms of “overactive
bladder” has been reported by the HUT committee (103). In a review of 10 randomized placebo-
controlled trials, estrogen was found to be superior to placebo when considering symptoms of
urge incontinence, frequency, and nocturia, although vaginal estrogen administration was found
to be superior for symptoms of urgency. In those taking estrogens there was also a significant
increase in first sensation and bladder capacity as compared to placebo.
86 Robinson and Cardozo

C. Estrogens in the Management of Recurrent Urinary Tract Infection

Estrogen therapy has been shown to increase vaginal pH and reverse the microbiological
changes that occur in the vagina following the menopause (104). Initial small uncontrolled
studies using oral or vaginal estrogens in the treatment of recurrent urinary tract infection
appeared to give promising results (105,106), although unfortunately this has not been supported
by larger randomized trials. Several studies have been performed examining the use of oral and
vaginal estrogens although these have had mixed results (Table 2).
Kjaergaard and colleagues (107) compared vaginal estriol tablets with placebo in 21
postmenopausal women over a 5-month period and found no significant difference between the
two groups. However, a subsequent randomized, double-blind, placebo-controlled study
assessing the use of estriol vaginal cream in 93 postmenopausal women during an 8-month
period did reveal a significant effect (108).
Kirkengen randomized 40 postmenopausal women to receive either placebo or oral estriol
and found that although initially both groups had a significantly decreased incidence of recurrent
infections, after 12 weeks estriol was shown to be significantly more effective (109). However,
these findings were not confirmed subsequently in a trial of 72 postmenopausal women with
recurrent urinary tract infections randomized to oral estriol or placebo. Following a 6-month
treatment period and a further 6-month follow-up estriol was found to be no more effective than
placebo (110).
More recently a randomized, open, parallel-group study assessing the use of an estradiol-
releasing silicone vaginal ring (Estring; Pharmacia, Uppsala, Sweden) in postmenopausal
women with recurrent infections has been performed which showed the cumulative likelihood of
remaining infection free was 45% in the active group and 20% in the placebo group (111).
Estring was also shown to decrease the number of recurrences per year and to prolong the
interval between infection episodes.

D. Estrogens in the Management of Urogenital Atrophy

Symptoms of urogenital atrophy do not occur until the levels of endogenous estrogen are lower
than that required to promote endometrial proliferation (112). Consequently, it is possible to use
a low dose of estrogen replacement therapy in order to alleviate urogenital symptoms while
avoiding the risk of endometrial proliferation and removing the necessity of providing
endometrial protection with progestogens (113). The dose of estradiol commonly used in
systemic estrogen replacement is usually 25 –100 mg, although studies investigating the use of
estrogens in the management of urogenital symptoms have shown that 8 –10 mg of vaginal
estradiol is effective (114). Thus, only 10 – 30% of the dose used to treat vasomotor symptoms
may be effective in the management of urogenital symptoms. Since 10 – 25% of women
receiving systemic HRT still experience the symptoms of urogenital atrophy (115), low-dose
local preparations may have an additional beneficial effect.
A recent review of estrogen therapy in the management of urogenital atrophy has been
performed by the HUT committee (116). Ten randomized trials and 54 uncontrolled series were
examined from 1969 to 1995 assessing 24 different treatment regimens. Meta-analysis of 10
placebo-controlled trials confirmed the significant effect of estrogens in the management of
urogenital atrophy (Table 3).
The route of administration was assessed, and oral, vaginal, and parenteral (transcutaneous
patches and subcutaneous implants) were compared. Overall, the vaginal route of administration
was found to correlate with better symptom relief, greater improvement in cytological findings,
and higher serum estradiol levels.
Table 2 Summary of Randomized Controlled Trials Assessing the Use of Estrogens in the Management of Recurrent Lower Urinary Tract

Study Type of Route of Duration of

Study group estrogen delivery therapy Results

Kjaergaard et al. 1990 (107) 21 postmenopausal Estradiol Vaginal tablets 5 months Number of positive cultures not
women with statistically different between the
recurrent cystitis two groups.
10 active group
11 placebo
Kirkengen et al. 1992 (109) 40 postmenopausal Estriol Oral 12 weeks Both estriol and placebo significantly
women with reduced the incidence of UTIs
recurrent UTIs (P , .05).
20 active group After 12 weeks estriol was
20 placebo significantly more effective than
placebo (P , .05).
Raz and Stamm 1993 (108) 93 postmenopausal Estriol Vaginal cream 8 months Significant reduction in the incidence
women with of UTIs in the group given estriol
recurrent UTIs compared to placebo (P , .001).
50 active group
43 placebo
Cardozo et al. 1998 (110) 72 postmenopausal Estriol Oral 6-month treatment period Reduction in urinary symptoms and
women with with a further 6 months incidence of UTIs in both groups.
recurrent UTIs follow-up Estriol no better than placebo.
36 active group
36 placebo
Eriksen 1999 (111) 108 women with Estradiol Estring 36 weeks for the active Cumulative likelihood of remaining
recurrent UTIs group 36 weeks or until free of infection was 45% in active
Hormonal Influence on the Lower Urinary Tract

53 active group first recurrence for the group and 20% in control group
55 no treatment controls (P ¼ .008).
87
88 Robinson and Cardozo

Table 3 Summary of Randomized Controlled Trials Assessing the Use of Estrogens

in Urogenital Atrophy

Study Year Estrogen Route

Bellatoni et al. (123) 1991 Estradiol Transdermal

Campbell et al. (124) 1977 Conjugated estrogen Oral
Campbell et al. (124) 1977 Conjugated estrogen Oral
Erikson and Ramussen (101) 1992 Estradiol Pessary
Felding et al. (125) 1992 Estradiol Pessary
Foidart et al. (126) 1991 Estriol Vaginal cream
Laufer et al. (127) 1983 Estradiol Transdermal
Mettler and Olsen (113) 1991 Estradiol Pessary
Molander et al. (128) 1990 Estriol Oral
Raz and Stamm (108) 1993 Estriol Vaginal cream
Van der Linden et al. (129) 1993 Estriol Oral

With regard to the type of estrogen preparation estradiol was found to be most effective in
reducing patient symptoms, although conjugated estrogens produced the most cytological
change and the greatest increase in serum levels of estradiol and estrone.
Finally, the effect of different dosages was examined. Low-dose vaginal estradiol was
found to be the most efficacious according to symptom relief, although oral estriol was also
effective. Estriol had no effect on the serum levels of estradiol or estrone, while vaginal estriol
had minimal effect. Vaginal estradiol was found to have a small effect on serum estrogen,
although not as great as systemic preparations. In conclusion, it would appear that estrogen is
efficacious in the treatment of urogenital atrophy, and low-dose vaginal preparations are as
effective as systemic therapy.
More recently, the use of a continuous low dose estradiol-releasing silicone vaginal ring
(Estring; Pharmacia, Uppsala, Sweden) releasing estradiol 5 –10 mg/24 h has been investigated
in postmenopausal women with symptomatic urogenital atrophy (111). There was a significant
effect on symptoms of vaginal dryness, pruritis vulvae, dyspareunia, and urinary urgency with
improvement being reported in .90% of women in an uncontrolled study; the maturation of
vaginal epithelium was also significantly improved. The patient acceptability was high, and
while the maturation of vaginal epithelium was significantly improved, there was no effect on
endometrial proliferation.
These findings were supported by a 1-year multicenter study of Estring in postmenopausal
women with urogenital atrophy that found subjective and objective improvement in 90% of
patients up to 1 year. However, there was a 20% withdrawal rate with 7% of women reporting
vaginal irritation, two having vaginal ulceration, and three complaining of vaginal bleeding
although there were no cases of endometrial proliferation (117). Long-term safety has been
confirmed by a 10-year review of the use of the estradiol ring delivery system that has found its
safety, efficacy, and acceptability to be comparable to other forms of vaginal administration
(118). A comparative study of safety and efficacy of Estring with conjugated equine estrogen
vaginal cream in 194 postmenopausal women complaining of urogenital atrophy found no
significant difference in vaginal dryness, dyspareunia, or resolution of atrophic signs between
the two treatment groups. Furthermore, there were similar improvement in the vaginal mucosal
maturation index and a reduction in pH in both groups, with the vaginal ring being found to be
preferable to the cream (119).
 Hormonal Influence on the Lower Urinary Tract 89

VIII. CONCLUSIONS

Estrogens are known to have an important physiological effect on the female lower genital tract
throughout adult life, leading to symptomatic, histological, and functional changes. Urogenital
atrophy is the manifestation of estrogen withdrawal following the menopause, presenting with
vaginal and/or urinary symptoms. The use of estrogen replacement therapy has been examined
in the management of lower urinary tract symptoms as well as in the treatment of urogenital
atrophy, although only recently has it been subjected to randomized placebo-controlled trials
and meta-analysis.
Estrogen therapy alone has been shown to have little effect in the management of
urodynamic stress incontinence, although when used in combination with an a-adrenergic
agonists it may lead to an improvement in urinary leakage. When considering the irritive
symptoms of urinary urgency, frequency, and urge incontinence, estrogen therapy may be of
benefit, although this may simply represent reversal of urogenital atrophy rather than a direct
effect on the lower urinary tract. The role of estrogen replacement therapy in the management of
women with recurrent lower urinary tract infection remains to be determined although there is
now some evidence that vaginal administration may be efficacious. Finally, low-dose vaginal
estrogens have been shown to be have a role in the treatment of urogenital atrophy in
postmenopausal women and would appear to be as effective as systemic preparations.

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7
Obstetric Issues and the Female Pelvis

Roger P. Goldberg and Peter K. Sand

Northwestern University, Evanston, U.S.A.

I. BACKGROUND

Urinary incontinence, anal incontinence, pelvic organ prolapse, and sexual dysfunction—the
major disorders of the female pelvic floor—are associated with a substantial public health
burden. And for many women, pregnancy, labor, and delivery represent the most important
physiological events predisposing to these conditions. Although many aspects of obstetrical
pelvic floor injury have yet to be fully understood, our knowledge of etiological mechanisms and
epidemiological risk factors has markedly expanded over the past several years. This chapter
will explore the effects of pregnancy and childbirth on the pelvic floor, and the impact of
obstetrical events on these prevalent postreproductive disorders.

II. PELVIC FLOOR DURING PREGNANCY, LABOR, AND DELIVERY

A. Evolutionary Strains and Anatomic Adaptations
From an evolutionary standpoint, certain anatomic trends have produced a maternal pelvic floor
that is highly vulnerable to injury during pregnancy and childbirth. One factor was the increasing
size of the newborn cranium to accommodate an enlarging brain, resulting in disproportion with
the maternal pelvic outlet. With enhanced nutrition resulting in larger offspring, the maternal-fetal
disproportion further increased. This trend was magnified by changes in locomotion and posture,
as the upright bipedal stance (first adopted by the Australopithecines) shifted the pelvic outlet
directly beneath the abdominopelvic contents. The female pelvis became increasingly
foreshortened in the anterior-posterior plane, and laterally, more anterior and prominent ischial
spines presented a further obstacle to delivery (1). The maternal pelvic floor can be viewed as an
evolutionary response to these anatomical selection pressures—a transformation of vertically
oriented “tail-wagging” muscles into a horizontal platform supporting the abdominopelvic
organs. In the normal female pelvis, the major foundation consists of the paired levator ani
muscles (2,3), whose position is maintained by endopelvic connective tissue and tone is preserved
by nerves arising from the lumbosacral roots. All of these components—muscular anatomy,
connective tissue supports, and nerve supply—are exposed to acute physical strains during
childbirth, and also chronic wear and tear resulting from intraperitoneal forces. Pelvic floor
dysfunction, in its various forms, can be viewed as a consequence of these conflicting demands.
95
96 Goldberg and Sand

During pregnancy and delivery, both maternal and fetal adaptations serve to mitigate the
full impact of anatomical strains on the maternal pelvis. On the fetal side, “molding” results in
reduction of the fetal head circumference. On the maternal side, estrogen-mediated smooth
muscle hypertrophy, connective tissue relaxation, and increased lubrication result in an
accentuation of vaginal length, skin thickness, and soft tissue compliance. Relaxin may be
responsible for a variety of connective tissue changes within the bony pelvis, including increased
mobility of the sacroiliac joint and pubic symphysis (4 – 6). Animal models have demonstrated
relaxin-mediated collagen reorganization in the pubic symphysis (7). After the return of the
nongravid hormonal milieu during the postpartum period, normal rigidity of the bony pelvis is
resumed.
Despite these and other compensatory adaptations, the potential for injury to the pelvic
floor cannot be avoided even for “normal” childbirth. For nulliparas the first stage of labor may
involve tissue compression for 20 or more. The second stage of labor, though substantially
shorter, involves pressures between the fetal head and vaginal wall averaging 100 mm Hg and
reaching as high as 230 mm Hg. As a benchmark for comparison, consider that compressive
forces of only 20 –80 mm Hg will cause blood perfusion to cease in the setting of orthopedic
compartment syndrome, leading to permanent tissue damage if sustained. Unsurprisingly,
obstetrical forces up to three times that intensity within the maternal pelvis, applied over many
hours, may often result in physical sequelae.

B. Perineum and Anal Sphincter

In the nulliparous female the bulbocavernosis muscles, transverse perineal muscles, and anterior
portion of the external anal musculature contribute to normal introital tone and anal sphincter
pressure. Attenuation, widening or descent of the perineum after childbirth—whether resulting
from episiotomy or a spontaneous injury—may result in bulging or laxity near the vagina and
rectum, loss of vaginal sensation during intercourse, and/or anal incontinence. Perineal
lacerations involving the anal sphincter have been reported in 10% of first vaginal deliveries,
and 0.3% of subsequent births (8). Apart from the presence or absence of perineal laceration,
descent of the perineal plane relative the ischial tuberosities is common following vaginal
delivery and appears to correlate with anal sphincter dysfunction (9), but has the potential for
resolving to the normal antenatal position in some women. Excessive descent of the perineal
body during voluntary straining may represent a marker for persistent neuromuscular
dysfunction after childbirth (10). However, the degree of perineal trauma evident after delivery
has not been shown to accurately predict subsequent pelvic floor symptoms (11). One
prospective study (12), using anal manometry in primiparous women prenatally and at 4– 6
weeks postnatally, found vaginal delivery to be associated with significantly reduced squeeze
pressure (SP: prenatal 269 cmH2O vs. postnatal 204 cmH2O; P ¼ .004). Cesarean section was
not associated with any significant change in anal pressures. Thus, normal vaginal deliveries
with no evidence of sphincter injury are associated with a significant effect on postpartum anal
function.
External anal sphincter lacerations complicate up to 20% of vaginal deliveries (13) and
represent a major risk factor for reduced squeeze pressure (14) and anal incontinence, which will
be subsequently reported in 4 – 50% of cases (8,15 – 20). Incontinence of flatus is reported six
times more often by women who experienced anal sphincter injury during delivery (15). Vaginal
delivery is independently associated with anal incontinence (21), and the risk is increased with
prolonged labor, operative vaginal delivery, and episiotomy (22). Although in the absence of a
visible anal sphincter injury the incidence of subsequent anal incontinence is ,3%, a normal
perineum on clinical examination does not exclude underlying anal sphincter damage (23).
 Obstetric Issues and the Female Pelvis 97

Postpartum endoanal ultrasound has demonstrated external anal sphincter defects in 20– 53% of
women after normal vaginal delivery (24 –28).
Unfortunately, even a complete repair of visible anal sphincter lacerations, at the time of
delivery, may be associated with suboptimal long-term results. According to postpartum ultra-
sonography, external anal sphincter separations can be detected in 11 –85% of cases after
primary obstetrical repair of a sphincter injury (14,29). Among women with anal incontinence
and a past history of repaired episiotomy or perineal laceration, up to 95% may have persistent
external or internal anal sphincter defects visible by transanal ultrasound (30). Sixty-five percent
of residual defects in this study were found in the mid or upper anal canal, suggesting an
important role for internal anal sphincter injuries. The internal anal sphincter extends an
additional 12 mm cranial to the external sphincter margin, is prone to disruption with severe
perineal lacerations, and may be commonly overlooked during primary obstetrical repair (31).
Using transanal ultrasonography, Sultan et al. (32) demonstrated internal anal sphincter lace-
rations in 17% of primiparas experiencing no visible perineal injury at the time of delivery.
Posterior anal sphincter injuries, though far less common than anterior injuries, may also escape
notice during perineal repair.
Finally, neurological injury to the anal sphincter may play a role. Prolonged motor
latencies may persist in the internal (upper) anal sphincter, for up to 5 months after vaginal
delivery (33). Denervation of the internal anal sphincter system after vaginal delivery may
persist even after the restoration of anal squeeze pressures, and may be associated with later
development of fecal incontinence. Some surgeons advocate overlapping sphincteroplasty rather
than end-to-end sphincter repair for the primary management of third- to fourth-degree perineal
lacerations (34). Long-term outcomes following overlapping external anal sphincter repair are
still being evaluated; however, recent case series have reported failure rates exceeding 50%, and
the potential for decreased efficacy over time (35,36). Success rates appear to be lower among
individuals with demonstrably abnormal pudendal nerve function preoperatively (16% vs. 62%)
(37). Because of the limitations associated with the surgical repair of severe perineal injuries,
primary prevention of obstetrical trauma should be regarded as the most effective approach for
reducing the incidence of postreproductive perineal and anal sphincter dysfunction.

C. Effects of Episiotomy
Episiotomies were introduced from Europe during the early 1900s and have subsequently
become the most common obstetrical operation. In the United States, 1.2 million are performed
each year, with midline episiotomy performed in up to 60% of vaginal deliveries (13). In
decades past, the routine use of episiotomy was thought to provide an array of maternal benefits
including preservation of pelvic muscle tone and sexual function, improved perineal healing,
and a reduced risk of anal sphincter injury. Since then, however, a steadily growing number of
observational studies support the conclusion that episiotomies increase rather than decrease the
risk of pelvic floor dysfunction.
Rectal injuries appear to be more often associated with than prevented by episiotomies,
with the risk of anal sphincter laceration increasing by 1 –11%. Midline episiotomy in particular
has been associated with a sharply elevated risk of severe lacerations into the vagina, perineum,
and rectum, in primiparous women (38 – 40). Mediolateral episiotomies confer only a 1 –2%
likelihood of anal or rectal injury, but may be associated with a greater risk of postpartum and
sexual pain. During second, third, or later deliveries, an even higher proportion of severe
perineal injuries are preceded by episiotomy, though the absolute incidence is decreased in
comparison to a first delivery.
98 Goldberg and Sand

Episiotomies appear to be associated with slower recovery of pelvic floor muscle strength
compared with an intact perineum after delivery and also spontaneous perineal lacerations
(41,39). One Argentine study randomized .2000 women to undergo episiotomy either
“routinely” or “selectively” if a significant perineal injury appeared to be imminent, and found
pain and healing complications to be more common within the routine episiotomy group (42).
Another randomized trial of selective episiotomy found that multiparous women in the selective
group more often gave birth with an intact perineum (31% vs. 19%) (43). Nearly all perineal
lacerations involving the anal sphincter were associated with midline episiotomy (46/47 in
primiparous women and 6/6 among multiparous women). No differences were found between
groups with respect to postpartum perineal pain, antepartum, and 3-month postpartum EMG
perineometry, and urinary and pelvic floor symptoms. The authors concluded that restriction of
episiotomy use among multiparous women results in significantly less perineal injury. With
respect to anal incontinence, one retrospective cohort study (44) found midline episiotomy to be
associated with an elevated risk of fecal incontinence at 3 (odds ratio 5.5) and 6 (3.7) months
postpartum compared with women with an intact perineum. Compared with women with a
spontaneous laceration in this cohort, episiotomy tripled the risk of fecal incontinence at 3
months (95% confidence interval 1.3 – 7.9) and 6 months (0.7 –11.2) postpartum, and doubled
the risk of flatal incontinence at 3 months (1.3 – 3.4) and 6 months (1.2 –3.7) postpartum.
The effects of episiotomy on sexual function have not been definitively established. One
study demonstrated that at 3 months postpartum, sexual satisfaction appears to be highest among
women without perineal injury, and lowest among women with an episiotomy that had extended
during birth (39). A more recent study also found highest satisfaction among women with an
intact perineum during delivery, but no difference between those who had undergone episiotomy
or spontaneous perineal laceration (45).
In summary, although selective episiotomies maintain a valid role in obstetrical
management room, the scientific evidence does not support their routine use. A Cochrane report
(46) concluded that the practice of routine episiotomy increases the overall risk of maternal
trauma and complications during vaginal delivery. Even during forceps or vacuum-assisted
delivery, previously regarded as an absolute indication for episiotomy, the selective use of
episiotomy has become increasingly common (47,48). The American College of Obstetricians
and Gynecologists (ACOG) formally stated in March 2000 that routine episiotomy should not be
considered a part of current obstetrical practice.

D. Levator Ani Muscles and Childbirth

The levator muscles represent the most important foundation of pelvic floor support, a broad
muscular complex counteracting the constant downward force of the pelvic and abdominal
organs. The iliococcygeous components form a shelflike barrier across the urogenital hiatus—
supporting the uterus, vagina, bladder, and other pelvic organs, and allowing the pelvic viscera
to compress against a muscular floor rather than prolapsing through the urogenital hiatus with
increased intra-abdominal pressure. The pubococcygeous and puborectalis muscles encircle the
anal and urethral sphincters in the manner of a sling, augmenting intrinsic smooth muscle tone
and maintaining tonic and phasic pressures. When intra-abdominal pressure is increased, reflex
contraction of these muscular components contributes to urethral and anal sphincter tone,
promoting continence.
Injuries to the levator ani muscles and their nerve supply may, in many instances, represent
the seminal obstetrical events ultimately leading to pelvic prolapse or urinary incontinence.
Several forms of trauma to the levator ani may occur. Direct injury may include attenuation of
the musculature, detachment of individual muscle components from their insertion points along
 Obstetric Issues and the Female Pelvis 99

the pelvic sidewalls, or both. Indirect changes may involve generalized atrophy of the levator
muscles resulting from pudendal neuropathy. Finally, diminished basal tone of the levator
muscles may result in widening of the urogenital hiatus and descent of the levator plate from its
horizontal position, thus orienting the pelvic viscera more directly over the widened urogenital
hiatus (49) and shifting the burden of their support to connective tissues and ligaments. With
cumulative intra-abdominal stress over time, weakening of these “secondary” endopelvic
connective tissue supports may lead to pelvic organ prolapse (50) years after the initial
neuromuscular insult.
Diminished levator ani function after childbirth is common, but the severity of change
varies according to the timing of postpartum assessment. Sampselle et al. (51) evaluated pelvic
floor muscle strength using digital palpation before deliver and again at 3 months postpartum in
a small cohort of primiparous women. Diminished levator strength was found to be associated
with the onset of urinary stress incontinence. Peschers et al. (52) evaluated levator ani function
before and after childbirth using intravaginal perineometry, and found that pelvic muscle
strength was significantly reduced 3– 8 days postpartum following vaginal birth, but not after
cesarean delivery, and returned to normal values within 2 months for most women. Allen and
Hosker (53), using perineometry, also demonstrated a significant and persistent reduction in
pelvic floor contraction strength. Prolonged EMG motor duration was associated with urinary
incontinence postpartum, and appeared to be more likely after a long second stage of labor or
vaginal delivery of a macrosomic baby.

E. Pudendal Nerve and Neuropathic Changes

The majority of the important pelvic floor support structures, including the levator ani and
sphincter muscles, receive their innervation from S2 –S4 anterior sacral nerve roots with motor
branches coursing along the cranial surface of the pelvic floor. The pudendal nerve, arising from
these same nerve roots, supplies the external anal and urethral sphincter, and perineum.
Compression and stretching of the pudendal during childbirth appears to be a major risk factor
associated with diminished levator muscle function afterwards. With delayed conduction, the
slinglike components of the levator complex, such as the pubococcygeous muscle, may fail to
reflexively contract and elevate sphincter pressure during a cough or sneeze. Basal tone of the
shelflike levator plate and perineal body, as previously mentioned, may also diminish as a result
of neuropathic changes.
The pudendal nerve and its three branches supply most of the anatomic structures helping
to maintain pelvic support and continence—including the perineum and vagina, levator muscle
complex, and anus. Stretching and compression of the pudendal nerve appears to be particularly
vulnerable as the fetus descends past the ischial spine in the midpelvis. Apart from the pudendal
nerve, a recent cadaveric study by Barber et al. (54) suggested that the levator ani musculature
may receive substantial innervation from independent “levator nerve” components arising from
the lumbosacral nerve roots. In 1986, Snooks and Swash (55) reported that partially reversible
pudendal nerve injury occurs commonly with vaginal birth. Pudendal nerve terminal motor
latency measurements indicate decreased conduction in women with vaginal birth compared
with nulliparous controls, an effect that appears to be prevented by cesarean delivery (114). The
likelihood of nerve injury is increased by forceps delivery, multiparity, increased duration of the
second stage of labor, third-degree perineal tear, and macrosomia (53,56). Pelvic floor
neuromuscular function can also be measured by concentric needle electromyography or single-
fiber electromyography, providing a quantitative measure of pelvic floor denervation.
Denervation changes within the pubococcygeous and striated anal sphincter muscles have
been observed following 42 –80% of vaginal deliveries (55). While some degree of
100 Goldberg and Sand

reinnervation by surrounding nerves will frequently occur, loss of muscle function is common.
Evidence of denervation injury appears to increase with parity, and can be demonstrated 5– 6
years after delivery (57,58). Cesarean delivery appears to effectively prevent denervation
injuries when performed electively, but does not confer full protection if performed after the
onset of labor.
For many women, pelvic neuropathy will have no clinical consequences; for others, these
nerve injuries initiate a pathophysiologic cascade eventually leading to incontinence, prolapse,
and pelvic floor dysfunction. Women with stress incontinence have delayed pudendal
conduction relative to controls on motor latency testing. Increased pudendal nerve terminal
motor latency has been associated with genuine urinary stress incontinence. (59,60) and lower
maximal urethral closure pressure (60) compared to asymptomatic controls. However,
electromyography of the urethral sphincter has not demonstrated increased denervation among
stress-incontinent subjects (61) and has also failed to correlate sphincter denervation with a
reduction in urethral closure pressures (62). Smith et al. (63) showed that partial denervation of
the pelvic floor after childbirth is associated with both genital prolapse and urinary incontinence.
A 5-year follow-up by Snooks et al. (58) demonstrated that denervation-reinnervation patterns
on electromyography may become more pronounced over time, and indicate higher risks of
urinary and fecal incontinence. Others have found anal incontinence to be associated with pelvic
floor neuropathy in 75– 80% of cases (64,65). Among multiparas, levator denervation appears to
be more common among those with prolapse, according to histological and electromyelographic
study, occurring in up 50% of women with symptomatic pelvic organ prolapse (66,67). To what
extent these changes to the levator ani musculature represent a direct cause of pelvic organ
prolapse, or its consequence, is not fully certain. In summary, pelvic floor neuropathy is a
common repercussion of childbirth—less often recognized than vaginal and perineal injury, but
arguably more significant with respect to the etiology of subsequent pelvic floor dysfunction.
Our understanding of the mechanisms of neuromuscular injury, and its repercussions, continues
to evolve.

F. Connective Tissues, Ligaments, and Bony Pelvis

Some element of injury to the connective tissues of the pelvic floor is inevitable during
childbirth. And in the etiology of pelvic floor disorders after childbirth, endopelvic connective
tissue injuries have an established role (68). Investigations into the etiology and treatment of
pelvic organ prolapse have sought to identify “site-specific” breaks and detachments of the
endopelvic connective tissue from their anatomical insertion sites, as the origins for pelvic organ
prolapse (69). These include paravaginal defects in the anterior vaginal compartment, site-
specific defects in the rectovaginal (Denonvillier’s) fascia, and ligamentous/fascial detachments
of the vaginal apex. Attenuation injuries to the endopelvic connective tissue during childbirth
may account for a variety of other forms of prolapse, including central cystoceles, rectoceles,
and uterine prolapse resulting from laxity of the uterosacral ligaments.
Bony pelvic anatomy may have an important relationship to the progress of childbirth, the
physical ease or difficulty encountered during childbirth, and the amount of pressure, stretch, and
potential injury to the soft-tissue structures of the pelvic floor. Among the pelvic shapes
described in the 1930s, the “gynecoid” pelvis is most common among women, and also best
suited for childbirth owing to its generous anterior-posterior and lateral dimensions with a wide
pubic arch. “Android” features present a greater challenge for vaginal delivery and may exist to
some degree in up to 24% of women undergoing x-ray pelvimetry before labor (70). The
relatively narrow pubic arch, prominent ischial spines, and anterior-posterior foreshortening
resulting from the protuberant sacrum create a heart-shaped passageway. The “anthropoid”
 Obstetric Issues and the Female Pelvis 101

pelvis resembles a narrow oval, restricted laterally by convergent sidewalls and prominent
spines. “Platypoid” pelvises resemble a horizontal oval, and are the least commmon shape in the
female population.
Although it remains unclear which specific bony pelvic features signal a higher risk of
pelvic floor injury, certain shapes would seem, at least in theory, to be of potential significance.
For instance, a narrow pubic arch (android, anthropoid) may indicate less anterior space for the
fetal vertex, and thus a greater likelihood of posterior injury to the perineum and anal sphincter.
A wide pubic arch (gynecoid, platypoid) or prominent coccyx may force the fetal head from
posterior to anterior, increasing the risk of compression injury to the bladder and urethra. Finally,
in the case of a narrow midpelvic region due to prominent ischial spines or convergent pelvic
sidewalls (anthropoid), the pudendal nerves may be exposed to an increased risk of compression
near Alcock’s canal. However, these potential “pelvic factors” in maternal injury have not been
scientifically evaluated. Spinal anatomy may also influence the risk of pelvic prolapse according
to one case control study of 92 women. When compared with patients with a normal curvature,
patients with an abnormal spinal curvature were 3.2 times more likely to have development of
pelvic organ prolapse (71). A loss of lumbar lordosis appeared to be the most significant risk
factor in the development of pelvic organ prolapse. Another matched observational study of bony
pelvic anatomy concurred that women with advanced uterovaginal prolapse have less lumbar
lordosis and a pelvic inlet that is oriented less vertically than women without prolapse (72). The
impact of specific pelvic shapes on postreproductive pelvic floor dysfunction, and the proper role
of pelvic anatomy assessment in obstetrical decision making, warrants future investigation.

III. OBSTETRICAL CORRELATES OF URINARY INCONTINENCE

The symptom of stress urinary incontinence occurs in 32– 85% of pregnant women, peaking in
the third trimester (73 –75). Francis showed an intrapartum prevalence of 85% in multiparas and
53% in nulliparas, with nearly half of these patients noting some degree of incontinence before
the observed pregnancy. Several other investigators have observed that stress incontinence,
arising with pregnancy and childbirth, may often fail to resolve. Stanton et al. (76) prospectively
studies 181 women in the third trimester and through the puerperium. Of the 83 nulliparas, 38%
had stress incontinence during the third trimester and 6% had persistent postpartum
incontinence. Among 98 multiparas, 10% had stress incontinence symptoms prior to pregnancy,
42% had stress incontinence in the third trimester, and 11% had persistent postpartum
incontinence. Meyer et al. (77) examined 149 women during pregnancy, and again at 9 weeks
postpartum. The rates of stress urinary incontinence were 31% and 7%, respectively, meaning
that 22% of patients with stress incontinence during pregnancy had persistence after delivery.
Several investigators have observed that mode delivery may have a profound impact on
the persistence of incontinence for the long term. Viktrup et al. (73) prospectively studied
urinary incontinence symptoms before, during, and after pregnancy in 305 primiparous women.
The multivariate analysis identified the length of second stage, fetal head circumference,
episiotomy, and birth weight as risk factors for postpartum stress incontinence, whereas cesarean
section was protective against incontinence. Among women with stress incontinence during
pregnancy, 21 of 167 women (13%) had persistent incontinence postpartum compared to none of
the 35 delivered by cesarean (P , .05). At 3 months postpartum, only 4% of these women had
persistent stress incontinence complaints; after 1 year, only 3% still had stress incontinence. In
subsequent pregnancies, however, it appears that these patients are at greater risk for more
severe incontinence with earlier onset and persistence beyond the puerperium. And in a 5-year
follow-up study, Viktrup and Lose (78) questioned 278 of the 305 women (91%) comprising
102 Goldberg and Sand

their original cohort, and found a 30% prevalence of stress incontinence. Nineteen percent of
women who were not incontinent in the original trial developed stress incontinence in the
ensuing 5 years. Again, cesarean section was found to significantly decrease the risk of stress
incontinence. The proper role of elective cesarean delivery, for preventing urinary incontinence,
remains uncertain. Iosif and Ingemarsson (1) showed that stress urinary incontinence does occur
following elective cesarean delivery, but to a much lesser degree than after vaginal birth. Among
204 of 264 women who had undergone an elective cesarean section 1– 6 years earlier, 4.7% had
persistent stress urinary incontinence after primary cesarean section, and 4.1% after a second
cesarean section.
Several mechanisms may contribute to the relationship among pregnancy, childbirth, and
urinary incontinence. An increased prevalence of urethral hypermobility is one important
change (79,80) known to be associated with genuine stress urinary incontinence. Peschers and
colleagues (81) studied the anatomic effects of vaginal delivery and found that bladder neck
support was significantly weaker after vaginal delivery than following cesarean section
(P , .001) or compared to a group of 25 nulliparous controls (P , .001). They also found that
bladder neck descent during Valsalva was significantly increased after vaginal delivery
compared to cesarean section in both primiparous and multiparous women (P , .001).
Diminished intrinsic urethral function, immediately after childbirth or later on also plays an
important role in the development of genuine stress incontinence (82). Van Geelen et al. (83)
demonstrated an association between vaginal delivery and decreased urethral closure pressure
and functional length; the absence of these changes after cesarean delivery highlights the
importance of birth mode rather than only pregnancy. Meyer et al. (77), in a prospective study of
149 women, found similar changes in functional urethral length, and intravaginal and intra-anal
pressure, 9 weeks after vaginal delivery compared to antepartum values. None of these changes
were found in the 33 women who had delivered by cesarean. As previously mentioned, vaginal
delivery can produce neurological changes in the pelvic floor, adversely affecting pudendal
nerve conduction velocity, vaginal contraction strength, and urethral closure pressure.
Presumably, these alterations may account for persistent or new-onset genuine stress
incontinence in women after vaginal delivery. After cesarean section, these pathophysiological
changes are far less pronounced.
Whether or not pelvic floor damage leading to persistent stress urinary incontinence is
cumulative for multiparous women—“from delivery to delivery”—has been controversial.
Mallett et al. (84) demonstrated that absolute parity and further childbearing did not further
influence pelvic floor neurophysiology, and concluded that most pudendal nerve damage occurs
during the first vaginal delivery. Hojberg et al. (85) studied 1781 primiparas at 16 weeks’
gestation and showed an odds ratio of 5.7 for stress incontinence after vaginal delivery compared
to 1.3 with cesarean delivery. Within their cohort, the first vaginal delivery was a major risk
factor for developing urinary incontinence; subsequent deliveries did not increase the risk
significantly. However, other population-based observational studies and prospective trial have
shown strong associations between vaginal delivery and increasing parity with stress
incontinence. Persson et al. (86) studies 10,074 women in Sweden having surgery for stress
incontinence and found a strong association with stress incontinence and parity, and also that the
odds ratio of prior cesarean section versus vaginal delivery was 0.21. Moller et al. (87) studie
502 women with lower urinary tract symptoms and 742 controls. They found an association of
parity and stress incontinence with an odds ratio of 2.2 after one vaginal delivery, 3.9 after a
second vaginal delivery, and 4.5 after a third delivery. Marshall et al. (88) studied 7771 women
early in the pueperium and found a strong association between parity and stress incontinence. A
1989 consensus conference of the National Institutes of Health identified parity as an established
risk factor for urinary incontinence (89).
 Obstetric Issues and the Female Pelvis 103

IV. PREVENTION OF OBSTETRICAL PELVIC FLOOR INJURY

From the standpoint of pelvic injury a great number of obstetrical complications of previous
generations are now fully preventable. Obstetrical fistulae, for instance, are today exceedingly
rare due to the recognition and prevention of obstructed labor. Unfortunately, the more
commonplace pelvic floor disorders—urinary incontinence, anal incontinence, and pelvic
prolapse—remain largely overlooked.
It could be argued that pelvic floor disorders are natural consequences of childbirth just as
skin cancer is a natural consequence of sun exposure. Both are associated with identifiable risk
factors, both can affect quality of life greatly, and both, in many cases, are preventable. During
and after pregnancy, strategies for reducing the risk of subsequent pelvic floor dysfunction
should be considered.

A. During Pregnancy
1. Pelvic Floor Exercises, Perineal Massage, and General Health
Daily pelvic floor exercises may consist of 20 –30 daily repetitions throughout pregnancy.
Increased muscle “reserve” before delivery may help to decrease the risk of injury during
childbirth and accelerate healing afterward. Improved muscular tone, and awareness of muscular
location, may enhance the patient’s ability to voluntarily relax the pelvic floor musculature
during labor and delivery. Two controlled trials of antenatal pelvic floor exercises have
demonstrated reduced urinary stress incontinence postpartum, but no discernible differences in
pelvic muscle strength according to perineometry (90,91). Prenatal pelvic floor exercises may
reduce the likelihood of incontinence symptoms after delivery (90).
Perineal massage represents another strategy for the prevention of obstetrical injury,
which involves gentle stretching of the lubricated perineum in preparation for delivery. The
protective effects of perineal massage remain a subject of debate, with some investigators
concluding no benefit when performed only during labor (92). However, two studies of perineal
massage begun during the third trimester have reported a decreased risk of perineal laceration.
One found that among women aged 30 or older, massage increased the chances of an intact
perineum by 12%. Another study, involving over 1500 women, found that for those without a
previous vaginal birth, 3 weeks of perineal massage routine increased the likelihood of an intact
perineum by 9% (93). A follow-up analysis (94) 1 year later reported on subsequent symptoms
within the same cohort; among women with a previous vaginal birth, perineal massage reduced
the odds of perineal pain at 3 months postpartum from 94% to 86%. For women without a
previous vaginal birth, no differences were found between the two groups.
Maintaining a moderate exercise routine during pregnancy, and optimal body weight, may
reduce the strain of pregnancy and childbirth on the pelvic floor. One study demonstrated that
although transient urinary incontinence during pregnancy improving postpartum is common,
persistent leakage is more likely among women gaining more weight before delivery. Excess
body weight has been identified as a risk factor for postpartum stress urinary incontinence and
urgency (95), with a body mass index .30 conferring an elevated risk (96). A reasonable target
for weight gain is 2 – 4 pounds during the first trimester and 1 pound per week thereafter,
translating into 25 –35 pounds for a full-term pregnancy. For women who are overweight before
pregnancy, significantly less weight gain is acceptable. Exercise during pregnancy should be
tailored to specific consideration, including changes in posture, balance, and coordination;
altered respiratory patterns; increased joint and ligament mobility due to relaxin; and increased
vulnerability of the pelvic floor beneath the gravid uterus.
104 Goldberg and Sand

Finally, preventing constipation is an important cornerstone for minimizing pelvic floor

strain during pregnancy, as gastrointestinal motility decreases owing to the effects of
progesterone and iron supplementation. Maintaining regular bowel movements, with proper
consistency, helps to reduce straining with defecation and thus reduces stress on the pelvic floor
supports. Dietary fiber should be accompanied by adequate hydration, regular exercise, and stool
softeners.

2. Predicting Pelvic Floor Injury: Maternal and Fetal Factors

Predicting the ease or difficulty of childbirth, and forecasting which women are at highest risk
for pelvic floor dysfunction, has challenged physicians and midwives for centuries. In the 1940s,
for instance, some obstetricians maintained that a large number of abdominal striae indicated an
increased risk of pelvic injury. More recently, double-jointed fingers and distensible skin have
been implicated as markers for generalized connective tissue disorders predisposing to pelvic
floor dysfunction. Specific demographic factors may have an impact on the risk of pelvic floor
injury. One report of .50,000 women, from the University of Miami, found maternal age might
relate to be predictive of severe lacerations involving the anal sphincter or rectum; older women
during their first delivery were found to be most at risk, especially with delivery of a large baby
(97). Within a cohort to African mothers, women ,150 cm tall were more likely to experience
cephalopelvic disproportion leading to a failed labor. Short stature (,10th centile) within this
group was associated with a twofold risk of cesarean delivery, and 15 times the usual risk of
requiring forceps or vacuum assistance. Urethral and bladder neck hypermobility, defined by
transvaginal ultrasound before delivery, has also been associated with an elevated risk of
postpartum incontinence (98).
Fetal head engagement may influence the relationship between childbirth and the pelvic
floor. For nulliparous women, engagement before the onset of labor is regarded as an indicator of
good maternal-fetal “fit.” Conversely, a lack of fetal head engagement at term may reflect
cephalopelvic disproportion and higher risk for arrest of labor. One study assessed .1200
women carrying their first pregnancy, demonstrating that the risk of cesarean section nearly
tripled if fetal head engagement had not yet occurred at the start of active labor (99). Another
study found that lack of fetal head engagement was associated with both a longer second stage of
labor and an elevated risk of cesarean, from 6.9% to 27%. Other studies have reported equal
success at achieving vaginal delivery even if the fetal head is floating above the pelvic inlet. The
relationship of fetal engagement to the maternal pelvic floor, and postreproductive body,
remains uncertain. If an unengaged fetus portends a longer labor, more physical effort, or greater
odds of an operative delivery, it could represent a risk factor for subsequent pelvic floor
dysfunction.
Pelvimetry during pregnancy or labor has been used to help determine the most important
features of the bony pelvis. Unfortunately, pelvimetry—whether performed clinically or with
radiological imaging—has not been found to reliably predict the course of labor and delivery, or
obstetrical pelvic injury. Forecasting pelvic floor injuries and postreproductive problems based
on pelvic shape remains a medical area posing more questions than answers.

B. During Labor and Delivery

During the second stage of labor, many elements of childbirth are viewed as inevitable. But in
fact, a number of important decisions may have implications for subsequent pelvic floor
function. Recognizing modifiable risk factors for pelvic floor injury is an important aspect of
routine obstetrical care.
 Obstetric Issues and the Female Pelvis 105

1. Pushing Positions and Techniques

Whereas some women will be instructed to push immediately after reaching “full” cervical
dilatation, others will be advised to wait until feeling the strong urge created by fetal descent,
and still others are encouraged to wait until the urge is unbearable. Determining the most
appropriate technique and time parameters for second stage from the standpoint of the maternal
pelvic floor—and the relative impact of “active” versus “passive” laboring—remains an area of
women’s health warranting attention. “Full dilatation,” after all, refers exclusively to the cervix;
from the standpoint of the major pelvic floor supports, an enormous degree of tissue dilatation
has yet to occur for most women. It has been suggested that premature active pushing before full
cervical dilatation may create sever stress against the pelvic floor, by advancing the cervix and
its surrounding attachments ahead of the fetal vertex (100).
Lithotomy is the most common position used by women choosing regional analgesia,
with the lower extremities held fully flexed and abducted during each contraction. Although
some practitioners suspect that the “uphill” orientation of this pushing style may increase the
difficulty of delivery, specific disadvantages for pelvic floor function have not been proven.
Squatting is purported to increase the diameter of the pelvic outlet compared with the lying-
down position, and help to shift the tail bone posteriorly. Studies have shown reduced rates of
forceps delivery and perineal lacerations compared with semirecumbent position (101). One
study of 300 women (102) showed squatting to be associated with a decreased risk of perineal
laceration and episiotomy. The effects of squatting on the deeper pelvic floor supports are
unknown.
Other, less common delivery positions may have a positive or negative impact on the
pelvic floor. Sitting has been associated with more rapid delivery; however, studies evaluating
birthing chairs have shown perineal swelling and labial lacerations to be more likely, and blood
loss increased. Lateral positioning (“side lying”) may be useful for multiparous women with an
already relaxed introitus, by improving control over the speed of fetal expulsion at the end of
second stage, and thereby helping to avoid perineal injury caused by a precipitous delivery.
Upright positioning has been advocated as a means to shorten the duration of labor and reduce
the need for forceps or vacuum assistance. Randomized trials have found the upright position to
be associated with lower rates of perineal injury, postpartum pain, and risk of undergoing
episiotomy compared with lithotomy (103). A Cochrane analysis concluded similar benefits of
upright or lateral, compared with supine, positioning (104). The upright, sitting, and squatting
positions should be avoided if significant perineal swelling develops. Finally, the “hands and
knees” position may help to correct fetal malposition—for instance, rotation from occiput
posterior, which has been associated with higher rates of anal sphincter injury (105). This
position may also help to shift the pressure of the fetal vertex from posterior to anterior, if an
imminent perineal injury appears likely. Management of the “final push,” at the time of fetal
crowning, may occasionally take on significance to pelvic floor injury, with shallow breathing
and pelvic relaxation, rather than straining, allowing the fetal head to ease gradually past the
introitus. There is evidence that the common hands-on approach, including counterpressure
against the fetal head and “guarding” of the perineum with the practitioner’s second hand, may
be of little benefit to preventing perineal injury (106). Hyperflexion of the lower extremities may
increase the risk of a sudden laceration as the fetal head rapidly distends the perineum, and
should therefore be avoided in most cases.

2. Second-Stage Labor Strategies

Directed Valsalva pushing starting at full cervical dilatation is the most common second-stage
labor strategy, its advocates arguing that the duration of labor grows too long in the absence of a
106 Goldberg and Sand

constant maternal expulsive effort, introducing more stress for the baby and a greater likelihood
of maternal neuromuscular injury. Critics of active pushing, on the other hand, maintain that it
shortens labor and delivery less than is often assumed while increasing maternal exhaustion,
stressing the pelvic floor supports, and possibly increasing the risk for pelvic injury. Among
primigravid women, active pushing for .1 h has been shown to confer an increased risk of
pudendal neuropathy and denervation injury; however, prolonging the passive (nonpushing)
second stage may not increase the risk of injury.
“Delayed” pushing involves resisting the urge to push, while allowing the fetus to
passively descend past the pelvic supports. One 1998 randomized controlled trial of delayed
pushing demonstrated a nonsignificant trend with fewer instrumental vaginal deliveries. More
recently, a multicenter study (107) conducted at 12 different sites throughout Canada,
Switzerland, and the United States evaluated a delayed pushing strategy among 1862 nulliparous
women, all with epidural analgesia, randomized to either immediate pushing at full dilatation or
delayed pushing for up to 2 h before pushing. “Difficult deliveries” were less likely in the
delayed pushing group, and forceps assistance was less often necessary. The benefits of delayed
pushing were greatest for women whose fetus was at a high station, or in the occiput posterior
position, when full cervical dilatation was determined. Notably, the 41% episiotomy rate in this
study may limit the external validity of its conclusions. A more recent randomized controlled
trial of delayed pushing found no increase in adverse events, despite prolongation of second
stage of up to 4.9 h (108). “Physiologic” (or “spontaneous”) pushing is similar to the delayed
pushing approach, entailing the delay of expulsive efforts until the onset of an overwhelming
physical urge. A 1999 survey compared spontaneous to directed pushing and found that
advanced perineal lacerations were less likely, and an intact perineum more likely, in the
“spontaneous pushing” group (109). A randomized trial of 350 women in Denmark found no
differences between women “actively” or “spontaneously” pushing, with respect to perineal
injury or duration of labor (110). A shorter active (pushing) phase and less maternal fatigue have
also been cited as potential benefits (111).
The effects of pushing styles on pelvic floor function are largely unknown. Increased
terminal nerve motor latency may be associated with a longer pushing stage. One study (112)
evaluated the effect of pushing time on anal function, comparing primiparous women with a
second stage shorter than 2 h to those with a second stage exceeding 3 12 h. The “long labor”
group had a significantly higher rate of new-onset flatal incontinence (73% vs. 44%). Finally, in
some cases a prolonged active second stage may predispose to maternal exhaustion. If this
results in a greater likelihood of operative delivery by forceps or vacuum, the increased risk for
pelvic floor injury resulting from these interventions should be recognized.

3. Impact of Operative Vaginal Delivery: Forceps and Vacuum

Eighty years ago, episiotomies and forceps were routine elements of childbirth and were
advocated, until recently, as a means to avoid pelvic injury and provide a more “controlled”
delivery. However, the majority of existing research has debunked this viewpoint, and today it is
widely accepted that operative delivery tends to increase rather than decrease the risk of perineal
injury, and often has a negative impact on other pelvic floor structures (113). Although vacuum
and forceps procedures retain a valuable role in obstetrical care, they should not be routinely
performed.
Forceps delivery markedly increases the risk of third- and fourth-degree lacerations
(114) and also pelvic neuropathy—perhaps not surprising, since the average force of forceps
against the surrounding pelvic tissues has been estimated at 75 psi. Up to 80% of women who
undergo forceps delivery will have anal sphincter injuries detectable by transanal ultrasound
 Obstetric Issues and the Female Pelvis 107

(25). Forceps also confer an elevated risk of urinary incontinence. Within one cohort, the odds
of stress incontinence 7 years after childbirth were shown to be 10 times higher among
women with a previous forceps delivery (115). A prospective study evaluating the incidence
of new-onset urinary incontinence after forceps and vacuum delivery compared with
spontaneous vaginal delivery found that in primiparous women, urinary incontinence after
forceps delivery is more likely to persist compared with spontaneous vaginal or vacuum
delivery (116). At 6 months postpartum, the relative risk of urinary incontinence after forceps
has been estimated as 1.5 compared to spontaneous vaginal delivery (117). Women after
forceps delivery have significantly weaker levator and anal strength than those who had a
spontaneous vaginal birth (118).
Vacuum-assisted deliveries accounted for almost 6% of all deliveries in 1995. Although
vacuum application is not appropriate for all operative deliveries, there is evidence to suggest
that, compared with forceps, vacuum delivery is generally associated with lower rates of pelvic
trauma (119 – 121). Studies randomizing operative deliveries to either forceps or vacuum have
demonstrated lower rates of severe perineal lacerations, and anal injury, for the latter (122). One
1999 study randomized women undergoing operative delivery to one of these two instruments,
and found that anal sphincter injury was significantly more common after forceps (79% vs.
40%). Anal incontinence was also more common after forceps delivery (32% vs. 16%). The
incidence of occult anal sphincter injury is also increased after forceps, compared with vacuum
delivery (123). A Cochrane report concluded that vacuum delivery is associated with
significantly less risk of perineal injury compared with forceps (124).

4. Physical Effects of Macrosomia

Macrosomia is associated with a variety of potential fetal problems, including birth trauma,
shoulder dystocia, and lower Apgar scores. However, it is important not to overlook the potential
maternal complications including higher rates of spontaneous perineal injury and episiotomies,
increased nerve damage detected by EMG (53), an increased risk of perineal injuries involving
the anorectum (40,125 –127), pudendal nerve injury (128), and significantly weaker anal
squeeze pressures postpartum (129). Vaginal delivery of one or more babies weighing at least
4000 g raises the risk of long-term stress incontinence (130). Larger infants have been linked to a
60% increase in the risk of an episiotomy at delivery (131). Newborn head circumference has
been demonstrated as an independent risk factor for third-degree perineal injury during
childbirth (132).

5. Multiple Pregnancy and Childbirth: Effects on the Pelvic Floor

The effects of multiple gestation on pelvic floor injury, and postreproductive problems such as
incontinence, prolapse, and sexual dysfunction, were recently investigated (133). Among 733
mothers of multiples, with a mean age of 40 years, substantial rates of pelvic floor symptoms
were reported, including urinary stress incontinence by 45%, flatal incontinence by 28%, fecal
soiling among 12%, and fecal incontinence by 9.6%. A subanalysis of obstetrical risk factors
found that avoiding vaginal delivery resulted in a 50% reduction in the risk of urinary
incontinence, even after controlling for age, total parity, and body mass index. As the prevalence
of multiple gestation continues to increase in the modern obstetrical landscape, the risk factors
influencing the maternal pelvic floor, and the most rational strategies for the prevention of
significant injuries, need to be more precisely defined.
108 Goldberg and Sand

6. Other Factors: Fetal Position and Analgesia

Fetal position may also have prognostic significance for the effects of labor and delivery on the
pelvic floor. The occiput posterior fetal position, for instance, has been long associated with
childbirth that is more prolonged, and sometimes more painful, based on anecdotal experience.
One study from Ireland (134) validated these observations, analyzing a large number of
deliveries and comparing babies descending in the posterior and anterior positions. Occiput
posterior deliveries were associated with less favorable outcomes, including an increased
incidence of anal sphincter injuries, and higher rates of delivery by cesarean and forceps. Fewer
than half of occiput posterior deliveries ended in a spontaneous vaginal birth. Another study
found similar results, including higher rates of perineal injury and episiotomy (135).
The effects of epidural analgesia on the maternal pelvis have also been investigated. Some
investigators claim that epidurals may help to relax the pelvic floor musculature, facilitating a
smoother and less traumatic delivery. Others express concern that by producing a sensory
blockade, epidurals may increase the risk for stalled labor, leading to higher rates of forceps or
cesarean delivery and thus greater risks for pelvic floor injury. The potential effects of epidurals
on perineal injury were evaluated in a 1995 retrospective analysis (136). Within this sample of
nulliparous women, severe perineal lacerations occurred in 16% of women receiving epidurals
versus only 9.7% in women without one. Further analysis of this cohort, however, indicated that
this difference was the result of more frequent episiotomy and operative (forceps and vacuum)
assistance within the epidural group. Thus, avoiding these interventions whenever possible—
rather than avoiding the epidural per se—appeared to be the important principle for preventing
obstetrical pelvic floor injury. Other studies examining the effect of epidurals on pelvic floor
injury (137) have found no differences with respect to intrapartum trauma.

V. ELECTIVE CESAREAN DELIVERY FOR PROTECTING

THE PELVIC FLOOR

Opinions and attitudes regarding the appropriate use of cesarean section for the prevention of
pelvic injury vary widely. According to a 1996 survey of obstetricians published in the Lancet
(138), 31% of female obstetricians report that if faced with a normal full-term pregnancy, they
would personally select cesarean over vaginal delivery. Remarkably, 80% of these individuals
cited concern over perineal injury as the main rationale. Another survey of female gynecologists
reported, somewhat more modestly, that 16% would personally choose cesarean delivery for
delivery of their own full-term, nonmacrosomic infant; most respondents, again, cited a desire to
prevent incontinence and pelvic prolapse. A survey of 135 midwives, in contrast, found that only
6% would choose cesarean to protect their pelvic floor. Whether this reflects the fact that
midwives provide care only to women before and during childbirth—and not years later, when
the majority of pelvic floor symptoms arise—is an unexplored question.
Medically, it is important to emphasize that pregnancy itself may for some women be
enough to cause pelvic floor injury with the route of delivery playing only a minor role.
Nonetheless, cesarean birth clearly appears to reduce the likelihood of multiple pelvic floor
disorders. Pelvic nerve and muscle functions are generally protected by cesarean delivery (128),
the timing of intervention largely determining the degree of protection. When cesareans were
performed before the onset of their first labor, pudendal nerve injury is effectively prevented
(139). Yet the same study found that cesareans performed after the onset of labor resulted in rates
of nerve injury similar to vaginal birth. The most protective cesareans appear to be those
performed before the onset of a woman’s first labor.
 Obstetric Issues and the Female Pelvis 109

Stress urinary incontinence is less common after cesarean compared with vaginal birth,
though it is not fully eliminated (117,140,141). After a first vaginal delivery, the risk of
incontinence is increased up to 2.8 times compared with cesarean section (117). Among women
with a history of multiple gestation, delivery by cesarean-only confers a 50% reduction in the
risk of stress urinary incontinence after controlling for age, parity, and body mass index (133).
A randomized trial of vaginal versus cesarean delivery, for breech presentation, revealed
a significantly lower rate of urinary incontinence at 3 months postpartum in the cesarean
group (142).
Anal sphincter lacerations can follow cesarean deliveries performed late in labor (143) but
are nearly nonexistent after cesareans that are performed before the onset of labor. And yet since
anal incontinence is a relatively uncommon outcome, it remains uncertain under which
circumstances an elective cesarean delivery would be an appropriate consideration for
preventing anal injury. As mentioned, certain fetal position including “occiput posterior” may
represent another potential high-risk group, since the risk for anal and perineal trauma is
significantly increased (135).
The broader application of “elective cesarean at term,” in the absence of specific risk
factors, is a topic fraught with controversy. Even if the likelihood of postreproductive pelvic
floor dysfunction could be decreased for some women, it would be essential to factor the broad
medical impact and costs that would be required to achieve this narrow gain. Cesarean is by no
means always in the best interest of mother or baby. Therefore, despite the fact that up to 31% of
British female obstetricians would consider a cesarean delivery for themselves in order to
prevent pelvic floor injury, most societies remain appropriately ambivalent regarding each
woman’s “right to choose” cesarean birth. The full scope of issues regarding elective cesarean
delivery is well beyond the scope of this chapter, but will undoubtedly gain increasing attention.

VI. POSTPARTUM ISSUES

Despite the remarkable level of stress endured by the pelvic floor during labor and delivery, little
attention is devoted to its recuperation afterward. Immediately postpartum, strategies for pelvic
floor recuperation should be reviewed. Perineal care may include ice packs and lower-extremity
elevation to counteract swelling. Proper perineal hygiene is also important to avoid infection and
early suture breakdown. Lotions, ointments, and direct scrubbing of the perineal area should be
avoided. Breastfeeding may contribute to pelvic floor symptoms during the postpartum period,
as hypoestrogenic changes throughout the vagina and lower urinary tract result in diminished
urethral function, and occasionally increased severity of stress and urge incontinence. Estrogen-
dependent symptoms will improve after the cessation of breastfeeding, as normal ovarian
function resumes.
Rehabilitation for the deeper pelvic floor should include pelvic floor exercises, resumed
during the immediate postpartum period. An appropriate postpartum Kegel exercise routine may
consist of two to five daily sessions of 10– 20 slow levator contractions for up to 10 sec.
Exercising in the recumbent position may help to minimize caudal traction on the pelvic floor
supports before full involution of the uterine fundus. Strengthening the perineal and levator
musculature will help to improve vaginal tone and restore the ability to “brace” the pelvic
floor muscles during increased intra-abdominal pressure, a reflex that can be otherwise lost after
childbirth. Several studies have demonstrated the potential efficacy of postpartum pelvic
floor exercises in preventing incontinence and other pelvic floor symptoms (144). One study of
268 women, 3 months after their first delivery, demonstrated reduction in the rate of stress
incontinence from 33% to 19% (145). Morkved and Bo demonstrated that postpartum urinary
110 Goldberg and Sand

incontinence could be reduced by 8 weeks of structured group training combined with home
exercises three time weekly, and that benefits are still present at 1 year postpartum (146,147).
Supervised pelvic floor rehabilitation was also evaluated in a New Zealand study (148),
randomly assigning women with postpartum urinary incontinence to either “intensive” pelvic
exercises with personal instruction and multiple daily workouts, or “simple instruction.” At
1 year, the intensive group had less urinary incontinence, fecal incontinence, anxiety, and
depression. However, their improvement remained for only as long as the exercises were
continued. Trials randomizing women to either a structured pelvic floor exercise program or
routine postpartum care have demonstrated modest reductions in the rate of stress incontinence
with the structured treatment (149,150). When pelvic floor exercises are combined with with
biofeedback and electrostimulation, one study demonstrated a reduction in stress incontinence
for 19% of women, significantly .2% in the placebo group ( p ¼ .002) (151).
Proper bowel and bladder habits should be emphasized after childbirth. After episiotomy
or spontaneous perineal laceration, constipation and straining should be avoided to protect suture
integrity, and to minimize stress against the pelvic floor muscles. For multiparas with descent of
the perineal body, perineal branches of the pudendal nerve may be particularly prone to
cumulative stretch injury during straining efforts. Pudendal nerve terminal motor latencies
and descent of the perineum on straining are significantly associated in patients with fecal
incontinence (152); the cause-effect of this relationship is not fully understood. Dietary fiber and
stool softeners, along with occasional laxatives or suppositories, should be used as needed.
Finally, returning to exercise and physical activity after childbirth should take into consideration
the vulnerability of pelvic floor supports, with limited weight bearing to reduce abdominopelvic
straining. “Bracing” the pelvic floor during sudden physical stress may be useful for reducing
leakage episode and safeguarding the pelvic floor supports.

VII. AFTER PELVIC FLOOR INJURY: MANAGING THE NEXT PREGNANCY

After childbirth has resulted in pelvic floor dysfunction, appropriate guidelines for managing the
next pregnancy and delivery are often unclear. Perineal injuries represent one concern; although
they are most common during a woman’s first vaginal birth, “repeat” injuries can occur during
subsequent deliveries. Women with a history of severe perineal laceration during their first
delivery are up to 3.4 times likely to suffer a repeat injury in their next delivery (153). The same
study indicated the highest risk among women undergoing forceps, vacuum, or repeat
episiotomy in their second delivery—around one in five in this group—suffered a second severe
perineal injury. Perineal massage during pregnancy and labor, attention to fetal size and position,
and avoiding episiotomy and operative delivery whenever possible, appear to be the most
effective strategies whether it is a woman’s first childbirth or a subsequent one (154).
For pelvic prolapse following childbirth, there is no evidence suggesting that operative
intervention should be routinely considered. Pudendal nerve injury can accumulation with later
deliveries and presumably “set the stage” for the progression of prolapse, but it is unclear
whether specific obstetrical interventions can help to counteract the progression of these
changes. Patients should focus on symptom relief, consider the use of a pessary, and avoid
strenuous activity until later in pregnancy. By 18 – 20 weeks, as the gravid uterus rises above the
pelvic brim, prolapse symptoms will often improve for the remainder of pregnancy. Likewise,
there is no clear evidence to support the use of elective cesarean section for parous women
already affected by urinary incontinence. After previous stress incontinence surgery, elective
cesarean for subsequent deliveries has been suggested to reduce the risk of recurrence (155), but
 Obstetric Issues and the Female Pelvis 111

controlled trials are lacking. The risks and benefits need to be strongly considered for each
individual.
The management of childbirth after anal sphincter injuries represents another area of
debate. Ultrasonography demonstrates that occult anal sphincter injuries can occur during
second deliveries (156) and that the risk of anal incontinence increases, particularly among
women with a sphincter defect diagnosed after the first delivery (157). Thus, although the first
childbirth appears to be most important, postobstetrical pelvic floor injury can accumulate, with
subsequent deliveries potentially causing new symptoms to arise, old ones to recur, or existing
ones to worsen. A 1999 study (158) observed a cohort of Irish women experiencing some degree
of fecal incontinence after their first vaginal birth. Nearly all of those who remained
symptomatic at the time of their next pregnancy noticed that symptoms became more severe
following that next second pregnancy, the second birth still led to recurrence 40% of the time.
Pudendal nerve latency was significantly longer after second delivery in this cohort, a finding
corroborated by other studies (159).
Strategies for preventing repeat injury vary widely, with some experts suggesting that
event women with postpartum anal incontinence should be offered cesarean delivery since a loss
of bowel control is arguably one of childbirth’s most distressing repercussions. According to
survey data, up to 71% of colorectal surgeons would advise women with previous anal injuries
to deliver by cesarean, versus only 22% of obstetricians. Because a broad strategy of cesarean
delivery is not feasible, the identification of risk factors for injury is important. For instance, in
the setting of macrosomia diagnosed by prenatal ultrasound, elective cesarean delivery may
represent a sound strategy both medically and economically for the prevention of anal
incontinence. The use of episiotomy in the setting of a previously repaired anal sphincter is
another area of debate—recommended by only 1% of colorectal surgeons, compared with up to
30% of obstetricians. Future research will hopefully result in a broader consensus regarding the
best preventive obstetrical approach.

VIII. CONCLUSIONS

Pelvic floor dysfunction among postreproductive women has emerged as a major area of interest
in the realm of clinical practice and research. Our awareness of the numerous underlying
pathophysiologic mechanisms continues to increase, including neuropathic change and
anatomic alterations to muscular and connective tissue anatomy. A variety of procedures and
events during labor and delivery, including episiotomy and operative delivery, may have
implications for pelvic function afterward. These and other obstetrical practices should be
weighed against their potential long-term effects on the maternal pelvic floor. As future research
further clarifies the most significant determinants of obstetrical pelvic floor injury, efforts at
prevention will undoubtedly improve.

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8
History and Physical Examination in Pelvic
Floor Disorders
Sanjay Gandhi and Peter K. Sand
Northwestern University, Evanston, Illinois, U.S.A.

I. INTRODUCTION

Women with a pelvic floor disorder may present with a symptom, a previously identified
physical sign, or a previously identified diagnosis. A clinician must take each of these and start
a comprehensive inquiry into the patient’s medical history and constellation of symptoms.
Further evaluation includes a focused general examination and a comprehensive genitourinary
examination.
Most evaluations will focus on pelvic organ prolapse and on urinary and fecal
incontinence, but clinicians specializing in pelvic floor medicine will see a diverse range of
problems. Knowledge of urology, gynecology, gastroenterology, and neurology is crucial in
conducting an appropriate evaluation. A consistent methodology to evaluate patients with
urogenital tract symptoms is most important in establishing the underlying etiology of the
patient’s pelvic floor disorder. Effective treatment of pelvic floor disorders depends on an
accurate diagnosis and an understanding of the patient’s expectations of treatment.
The history, physical examination, and simple office testing may establish a preliminary
diagnosis on which a clinician may begin treatment or may serve as an excellent screening tool
to determine which individuals require further evaluation. If a complex or recurrent problem is
present, surgery is planned, or the patient’s symptoms do not improve with initial treatment,
specialized tests such as complex urodynamics should be employed to definitively establish
diagnoses. Urogenital, gastrointestinal, musculoskeletal, neurologic, and endocrinologic factors
may affect pelvic floor disorders, and a comprehensive history and physical examination begins
the process of evaluating these conditions. Other, more specific criteria to select patients for
further evaluation of urinary incontinence are listed in Table 1.

II. HISTORY

The history is an essential part of the evaluation of every female with a pelvic floor disorder. No
urogenital tract symptom is pathognomonic for an underlying condition. While the history is
limited in its specificity and is only the first step of the diagnostic inquiry into the patient’s
disorder, it defines the problem by identifying the symptoms that must be explained by the
119
120 Gandhi and Sand

Table 1 Criteria for Further Testing

1. Uncertain diagnosis and inability to develop a reasonable treatment plan based on the
basic evaluation. Uncertainty in diagnosis may occur when there is lack of correlation
between symptoms and clinical findings
2. Failure to respond to the patient’s satisfaction to an adequate therapeutic trial,
and the patient is interested in pursuing further therapy
3. Surgical intervention planned
4. Hematuria without infection
5. Presence of any of the following conditions:
Recurrent symptomatic UTI
Persistent symptoms of difficult bladder emptying
History of prior incontinence operation or radical pelvic surgery
Significant genital prolapse
Retention
Neurological condition (e.g., multiple sclerosis or spinal cord lesions/injury)

Source: Ref. 54.

evaluation. The clinician must evaluate information gathered from the patient history to
selectively choose which diagnostic tests will reveal a condition’s etiology.
A concise history may be obtained using premailed questionnaires providing the patient
time to consider her symptoms, past medical history, and family history and reconfirm them.
Bowel and bladder diaries or other chronological records of symptoms recorded at home may
provide further clarification of the patient’s symptoms. An office interview supplements this
initial history and should include an assessment of symptoms, risk factors for disease, and a
general medical and social history.
Most authors have found a medical history to be inadequate in establishing an accurate
etiology of incontinence (1 – 6), with only a few exceptions. Farrar et al. concluded that history
alone was accurate in establishing a diagnosis. Two of 56 women (3.6%) with stress
incontinence symptoms alone and 89% of the 110 women with symptoms of urge incontinence
were found to have detrusor overactivity on cystometry (7). Hastie and Moisey (8) also
concluded that a history of pure stress incontinence was 100% accurate in establishing the
diagnosis of genuine stress incontinence. In contrast, Jensen and colleagues (9) in a meta-
analysis of thousands of patients found that reliance on history alone to identify genuine stress
incontinence resulted in a misdiagnosis in 25% of patients. Patient history was an even less
accurate predictor of detrusor overactivity, with a misdiagnosis in 45% of patients with a history
of urge loss (9). In addition, advanced pelvic prolapse may mask underlying incontinence unless
the pelvic prolapse is reduced (10 – 12). Ghoneim and colleagues (12) found in a small cohort of
women that reducing the prolapse by a vaginal pack during urodynamic testing demonstrated
stress incontinence in 69% of women who were otherwise asymptomatic. Based on these
studies, a clinician cannot depend on a patient’s symptoms to accurately reflect the underlying
disorder. While the patient’s history will not be diagnostic, a complete assessment of symptoms
will serve as an outline to guide the clinician’s evaluation.

III. SYMPTOMS

Symptoms are the subjective indicator of disease or change in condition as perceived by the
patient, her caregiver, or partner and may lead her to seek help from health care professionals
(13). They are categorized separately from signs, conditions, and urodynamic observations (13).
 Pelvic Floor Disorders 121

Anatomic, physiologic, and pathologic factors within the lower urogenital tract as well as
nongenitourinary factors or conditions may result in pelvic floor disorders with a variety of acute
or chronic symptoms. Recurrent symptoms may represent acute exacerbations of chronic
disease. Women seeking care of a pelvic floor medicine specialist may present with symptoms of
disease in the lower or upper urinary tract, in the gynecologic or gastrointestinal organs, or in the
musculoskeletal or neurological system. Therefore, only a comprehensive review of systems
will assure the clinician that all aspects of the disease process are being assessed.

A. Systemic Manifestations
Systemic manifestations of urogenital tract disorders include fever and weight loss. While
simple acute cystitis typically does not cause a fever, acute pyelonephritis in adults typically
causes high fevers with rigors and costovertebral angle tenderness. In children, simply the
presence of fever should prompt the clinician to perform a bacteriologic evaluation of the urine,
as often no other localizing signs or symptoms of a renal infection may be present. Renal
infection may also present differently with recurrent fevers in the absence of other urinary tract
symptoms or with no fevers at all. Chronic pyelonephritis may only present with general
malaise. While infection is the typical cause of fevers, renal cell carcinoma may present with
fevers.
Weight loss and general malaise are nonspecific symptoms that may prompt one to
consider urogenital tract pathology such as advanced stages of cancer or renal insufficiency due
obstruction or infection.

B. Incontinence
The most common symptom of pelvic floor dysfunction is urinary incontinence—the
involuntary leakage of urine. Urinary incontinence should be described by type, frequency,
severity, precipitating factors, and impact on hygiene and on a patient’s social activities. The
clinician should understand the measures a patient uses to contain the leakage. Finally, it is
crucial for the clinician to assess the impact of the incontinence on a patient’s quality of life and
on her caregivers. Understanding a partner, caregiver, or patient’s expectations of treatment is
crucial to rendering effective care. The original ICS definition of incontinence—“Urinary
incontinence is the involuntary loss of urine that is a social or hygienic problem”—relates the
complaint of incontinence to quality of life issues. Whether or not the individual or their
caregiver seeks or desires help because of urinary incontinence should be known prior to
beginning an evaluation.

1. Stress Urinary Incontinence

The symptom of stress urinary incontinence is the involuntary loss of urine during coughing,
sneezing, laughing, or other physical activities that increase intra-abdominal pressure. Stress
incontinence, the sign, is the observation of involuntary leakage from the urethra with exertion,
coughing, or sneezing. Urodynamic stress incontinence, the condition, is defined as the
involuntary loss of urine during an increase in intra-abdominal pressure in the absence of a
detrusor contraction. This occurs when the bladder pressure exceeds the urethral pressure
because of decreased transmission of intra-abdominal pressure to the urethra. This is usually
secondary to urethral hypermobility. The decrease in transmission of intra-abdominal pressure
to the urethra relative to the bladder is referred to as a deficient extrinsic continence mechanism.
Incontinence can also occur secondary to deficient intrinsic urethral sphincteric function.
The smooth muscle, skeletal muscle, periurethral vasculature, and intrinsic urethral fibrous
122 Gandhi and Sand

tissue all contribute to the resting urethral resistance or tone. Intrinsic sphincteric deficiency is
the condition where the urethral sphincter is unable to generate enough resistance to retain urine
in the bladder. Intrinsic urethral function can be measured urodynamically by calculating the
resting urethral closure pressure. The leak point pressure is also used by some investigators to
measure both the extrinsic and intrinsic continence mechanisms. Although increased age and
multiparity are thought to increase the risk of stress incontinence, we know that even in
nulliparous women with a well-supported urethra and an intact sphincter (normal urethral
pressures), urinary incontinence may be present in as many as 50% of women (14,15). In elite
female athletes, urinary loss may be present in up to 52% during their sport (16,17).

2. Urge Urinary Incontinence

The symptom of urge urinary incontinence is the involuntary loss of urine accompanied by or
immediately preceded by a sudden compelling desire to pass urine, which is difficult to deter
(i.e., urgency). Women with urge incontinence often demonstrate, on urodynamics, involuntary
detrusor contractions, or detrusor overactivity. The prevalence of detrusor overactivity appears
to increase with age.

3. Mixed Urinary Incontinence

Women with symptoms of both urge and stress urinary incontinence are said to have mixed
urinary incontinence. Often one symptom is more bothersome than the other, and the clinician
should attempt to make this differentiation.

C. Pain
A patient may feel local pain near the involved organ. Acute pyelonephritis manifests with pain
in the costovertebral angle and the flank. In contrast, the spatial displacement of pain sensation
from the point of stimulation is known as referred pain. Convergence of many sensory inputs to a
single pain transmission neuron in the spinal cord underlies the phenomenon of referred pain.
The brain has no way of knowing the source of the pain and mistakenly projects the pain
sensation to a site distant from the original point of stimulation in the diseased organ (18).
Ureteral colic is a classic symptom with referred pain. In women, ureteral calculi may result in
pain felt in the vulva or inner thigh. Inflammation of the bladder trigone as seen in acute cystitis
often results in terminal dysuria felt at the urethral meatus.

1. Renal Pain
Renal pain or colic is typically felt in the area lateral to the sacrospinalis muscle and below the
12th rib. This pain may spread along the subcostal area around to the umbilicus or lower
abdomen (19). Such pain is typical in conditions that cause acute distension of the renal capsule
such as acute pyelonephritis or acute ureteral obstruction from urolithiasis. Many conditions,
however, are painless as they progress slowly without capsular distension including neoplasia,
chronic pyelonephritis, staghorn calculi, polycystic kidney disease, and hydronephrosis from
chronic ureteral obstruction (as seen in cervical cancer, massive fibroid tumors, or severe pelvic
organ prolapse).

2. Pseudorenal Pain (Radiculitis)

Musculoskeletal derangements of the thoracic spine may irritate costal nerves, causing pain that
mimics renal pain. Lifting of a heavy object, trauma to the flank, or a sudden fall may precipitate
 Pelvic Floor Disorders 123

such pain. Relief of this pain by changes in position and movement of the spine differentiates it
from true renal colic (19).

3. Ureteral Pain
Acute obstruction by calculi or blood clots typically results in ureteral pain. Renal capsular
distension causes back pain, and ureteral muscle spasm elicits severe colicky pain from the
costovertebral angle down toward the lower anterior abdominal quadrant along the course of the
ureter. Stones in the midportion of the ureter on the right side may simulate appendicitis with
referred pain to McBurney’s point, while on the left, ureteral pain may resemble diverticulitis. A
stone at the ureteral orifice may cause inflammation and edema in the bladder, producing lower
urinary symptoms such as urgency and frequency. Finally, if the calculus is small, it may not
even cause pain.

4. Vesical Pain
Overdistension of the bladder from acute retention causes severe suprapubic or retropubic pain.
Chronic retention from bladder outlet obstruction or an acontractile bladder typically does not
result in significant vesical pain even though the bladder may reach the level of the umbilicus.
Interstitial cystitis or bladder ulceration caused by tuberculosis or schistosomiasis infection may
cause suprapubic pain or discomfort when the bladder fills even to small volumes. Because these
conditions often result in diminished bladder capacities, voiding results in significant relief of
their suprapubic discomfort. Associated symptoms include urgency and frequency. Detrusor
overactivity, which also causes urgency and frequency, does not commonly cause bladder pain.
As stated earlier, bladder infection often results in referred pain to the distal urethra.

D. Abdominal and Gastrointestinal Symptoms of Urogynecolgic Disease

Gastrointestinal symptoms often accompany renal and ureteral disease. The gastrointestinal and
genitourinary systems share common autonomic and sensory innervations. Afferent stimuli from
the renal capsule may, by reflex, alter the tone of smooth muscle in the enteric tract leading to
gastrointestinal manifestations of renal disease. Enlargement of the kidneys may abut or displace
intraperitoneal organs (e.g., stomach, colon, liver, gallbladder), causing gastrointestinal
symptoms while inflammation may result in peritoneal irritation that results in muscle rigidity
and rebound tenderness on abdominal examination. Abdominal pain, distension, nausea, and
vomiting secondary to renointestinal reflexes are all common accompanying symptoms of acute
pyelonephritis and ureteral colic. The connection between severe pelvic organ prolapse and
abdominopelvic symptoms is less clear. Although anecdotally a large enterocele may lead to
peritoneal irritation that may produce abdominal pain and gastrointestinal distress, Heit and
Culligan (20) recently reported that pelvic organ prolapse was not associated with pelvic pain
when controlling for patient age and prior prolapse surgery.

E. Dyspareunia and Vulvodynia

Dyspareunia is pain in the pelvic area during or after intercourse. It occurs with vaginal
penetration—either at the introitus or deep in the vagina. Differentiation between locations of
pain with intercourse may point to distinct etiologies. Pain with deep penetration may suggest
endometriosis, vaginal infection, or interstitial cystitis, while pain with initial intromission is
more suggestive of vestibulitis, urethrotrigonitis, or vulvodynia.
124 Gandhi and Sand

Vulvodynia is chronic vulvar pain. It may be present constantly, intermittently, or only

with intromission during intercourse. Activities that cause friction or pressure on the vulva
aggravate the allodynic symptoms. Wearing tight pantyhose or jeans may elicit vulvar pain.
Urine-soaked pads, excessive perspiration, and allergens may cause inflammation of the small
vestibular glands and epithelium (i.e., vestibulitis) with secondary vulvodynia.

F. Medical and Social History

There are many medical conditions that may cause or aggravate urinary incontinence. The
clinician should exclude these when evaluating a woman with urinary incontinence. One should
take a medical, neurological, and genitourinary history including a detailed exploration of
symptoms. The medications and supplements used by the patient should be carefully reviewed.
The history should also include information on previous surgery, trauma, radiation therapy,
use of hormone replacement, past medical history, and current active medical conditions.
Information on previous urogynecologic treatments and assessment of their impact on current
symptoms may be helpful. Other associated pelvic floor dysfunction involving bowel or sexual
function is important to identify as these conditions may be interrelated with the patient’s lower
urinary tract symptomatology and may have been previously unrecognized. Correction of some
reversible causes of urinary incontinence may resolve or improve their incontinence (Table 2)
(21). Medications can often impact urinary symptoms such as incontinence or retention
(Table 3).
Assessment should include psychosocial and environmental questions. An understanding
of how a patient’s problem impacts her daily living is crucial to providing appropriate and timely
treatment. While pelvic prolapse may directly cause pain or discomfort and thus impact well-
being, incontinence has broad psychological effects that may prevent an otherwise functional or
healthy woman from leaving her home. An understanding of a patient’s environmental
conditions at home may help identify individuals with incontinence who are at risk for falls or
fractures (22). Urinary symptoms can often force the elderly to hastily move to the toilet in less
than ideal circumstances. A questionnaire can serve as a screening tool for psychosocial and
environmental conditions that impact the patient’s quality of life.
Knowledge of the amount and types of pads, briefs, and protective devices may provide
insight into the extent of debilitation caused by a patient’s incontinence. In elderly individuals, a
mental status evaluation and assessment of physical mobility is important. An understanding of a
patient’s access to toilets, especially at night, when the elderly may be at greater risk of falls and

Table 2 Reversible Causes of Incontinence

DIAPPERS
Delirium or confusion
Infection, urinary tract
Atrophic genital tract changes (vaginitis or urethritis)
Pharmaceutical agents (see Table 3).
Psychologic
Excess urine production (excess fluid intake, volume overload,
metabolic such as hyperglycemia or hypercalcemia)
Restricted mobility (chronic illness, injury, or restraint)
Stool impaction
 Pelvic Floor Disorders 125

Table 3 Drugs That May Affect Lower Urinary Tract

Impact on lower urinary tract

Class of drugs Side effect function
Psychotropic agents
Antidepressants Anticholinergic, sedation Urinary retention
Antipsychotics Anticholinergic, sedation Urinary retention
Sedatives/hypnotics Sedation, muscle relaxation, Urinary retention
confusion
Alcohol Sedation, impaired mobility Diuresis, frequency
Caffeine Urgency, frequency
Diuretics Polyuria, urgency, frequency
Narcotics Sedation, delirium Urinary retention, fecal impaction
ACE inhibitors Cough Aggravate preexisting stress
incontinence
Calcium-channel blockers Urinary retention, overflow
incontinence
Anticholinergic Urinary retention, overflow
incontinence
Alpha-adrenergic agonists Increased urethral tone Urinary retention
Alpha-adrenergic blockers Decreased urethral tone Stress incontinence
Beta-adrenergic agonists Inhibited detrusor function Urinary retention

injuries, of their living arrangements, and of the involvement of caregivers will help the clinician
plan an individualized treatment plan.
Signs of lower urinary tract dysfunction are observed by the physician to verify symptoms
and quantify them. Observations from bladder diaries, pad tests, and validated questionnaires are
examples of other instruments used to confirm and quantify symptoms.

IV. QUESTIONNAIRES

Filling out a standardized questionnaire at home before coming into the office may help patients
clarify and enhance their understanding of their symptoms. This gives patients time to delineate
their symptoms, increase the accuracy of their answers, and obtain information from other
family members if needed. It also speeds up their office evaluation.
Various validated questionnaires are useful not only to quantify the severity of symptoms
and their impact on quality of life, but to provide quantitative data for use in research studies and
outcomes analysis. Generalized health-related quality-of-life (HRQOL) instruments enable
researchers to compare groups with different diseases. However, condition-specific instruments
best allow the clinician to assess the impact of urogenital symptoms on a particular woman.
Table 4 presents a list of some of the numerous validated questionnaires that have been
developed for collecting and reporting subjective information about pelvic floor disorders in
women. Unfortunately, no single instrument has emerged as the preferred one since
questionnaires vary widely, depending on their intended purpose and target population (23).
Choosing the appropriate questionnaire—one that is comprehensive yet easy for patient to
complete—may be challenging. These questionnaires may be modified to meet the needs of a
specific clinician or practice and may be included in a general information packet.
126 Gandhi and Sand

Table 4 Validated Questionnaires

Generalized Medical Outcomes Survey Short Form-36 (SF-36) (55)

Condition-specific
Urinary incontinence Incontinence Impact Questionnaire (IIQ) (56)
Urinary Distress Inventor (UDI) (56)
IIQ-7 and UDI-6 (57)
Incontinence Quality of Life Measure (I-QOL) (58)
King’s Health Questionnaire (59)
Bristol Female Lower Urinary Tract Symptom Questionnaire (60)
York Incontinence Perception Scale (YIPS) (61)
Medical Epidemiologic and Social Aspects of Aging (MESA) Urinary
Incontinence Questionnaire (UIQ)
Sexual dysfunction Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire
(PISQ) (62), PISQ-12
Pelvic organ prolapse Pelvic Floor Dysfunction Inventory (PFDI) (63)
Defecatory dysfunction Fecal Incontinence Quality of Life Scale (64)
Pelvic Floor Dysfunction Inventory (PFDI) (63)
Interstitial cystitis Interstitial Cystitis Symptom Index (ICSI) and Interstitial Cystitis
Problem Index (ICPI) (65)

A. Bladder Diary
Bladder diaries assist in providing quantitative data on urinary frequency, voiding intervals, the
volume of continent voids, and the number of incontinent episodes. They also enable the
clinician to better understand triggers of incontinence such as coughing, exercises, Valsalva, or
strenuous activity. Bladder diaries (Fig. 1) help to accurately assess fluid intake patterns,
including the consumption of caffeine-containing fluids. The diary may help to establish voiding
patterns that can help clinicians select appropriate behavioral interventions, and may also serve
as a baseline of symptom severity for assessment of treatment efficacy. Seven-day bladder
diaries have been found to correlate well with actual symptoms and incontinence severity (24).
In addition, while filling out a diary may be tedious, the process of filling out a diary may in itself
be a form of bladder training, resulting in an improvement in incontinence symptoms.

B. Physical Examination
The physical examination attempts to identify neurological deficits, defects in pelvic support,
pelvic pathology, infection, estrogen deficiency, tenderness, and other urogenital problems. One
must employ a methodical approach to the evaluation of the urogenital tract for pathology. In
addition, a systematic general physical and neurological examination may also reveal other
causes (e.g., cardiac, endocrine) of urogynecologic symptoms.

1. Neurological Examination
The screening neurological examination should include an evaluation of mental status, gait, and
the lumbosacral nerves. A complete evaluation of the lumbosacral nerve roots includes testing of
deep tendon reflexes, sensation (Fig. 2), and strength in the lower extremities as well as the
bulbocavernosus and clitoral sacral reflexes (Fig. 3). Isolated deficits are often not a cause of
urogenital symptoms, and a comprehensive neurological examination may seem to be of low
Pelvic Floor Disorders 127

Figure 1 Bladder Diary.

128 Gandhi and Sand

Figure 2 Sensory dermatomes.

yield (Table 5). However, simple observations (e.g., deep tendon hyperreflexia, intention tremor,
or the presence of altered mental status) may identify women with predisposing functional
impairments (e.g., dementia, Parkinson’s disease, spinal cord disease, or previous strokes) that
explain their urinary symptoms. Urinary retention and/or incontinence may be the first sign of
multiple sclerosis in an otherwise healthy woman (25).

Figure 3 Examination of bulbocavernosus and clitoral reflexes.

 Pelvic Floor Disorders 129

Table 5 Significance of Abnormal Findings on Neurologic Testing

Examination Neurological level Significance of findings

Sensory testing around L2-S2 and peripheral Mapping altered sensations to follow either
knee (light touch, nerves dermatome or a peripheral nerve distribution
pin prick) determines level of injury
Deep tendon reflexes Upper and lower Hyperreflexia—UMN lesion
motor neurons Absent—LMN lesion
Babinski Corticospinal tracts Fanning and dorsiflexion; interruption of tracts
Muscle strength: Neuropathy or simply muscular weakness
Flexion extension (L3-L5)
knees
Flexion hips (L4-L5)
Extension hips (L2-L3)
Plantarflexion (S1-S2)
ankles
Dorsiflexion ankles (L4-L5)
Gait Cerebellum Cerebellar lesion: stroke or tumor
Bulbocavernosus/anal L5-S5 and pudendal Pudendal neuropathy or other sacral nerve injury (66)
wink nerve

Source: Ref. 34.

2. General Examination
All women presenting for evaluation of pelvic floor dysfunction should undergo age-appropriate
routine health checks and cancer screening according to the U.S. Preventive Services Task Force
(26 – 28). Pulmonary and cardiovascular examination may identify individuals with chronic
cough or those in need of diuretics for fluid overload. The back is examined for vertebral or flank
tenderness or paraspinal muscle spasm.
Masses, ascites, and organomegaly can influence intra-abdominal pressure and impact
urinary tract function. Visual inspection of the abdomen will reveal any scars from surgeries
unexplained by the patient’s history or unusual distention of the abdomen. In addition to
palpating the abdomen to assess for hepatosplenomegaly, masses, distention, and tenderness, a
Valsalva maneuver and cough will reveal any hernias. Palpation of the inguinal area may reveal
lymphadenopathy.

3. Gynecologic Examination
Inspection of the external genitalia will reveal any lesions or skin changes. “Rashes” may
indicate chronic irritation from urine or feces. Whitish skin changes, erythema, or loss of normal
architecture of the vulva may indicate hypoestrogenism or vulvar dystrophies. In women with
introital dyspareunia or vulvodynia, a careful examination of the vagina and vestibule to Hart’s
line is important. Hart’s line is the mucocutaneous junction where the outer vestibule meets the
squamous epithelium of the labia minora. A Q-tip and a pain scale may be used to elicit point
tenderness in this area. Asking the patient to rate the pain on a scale of 0 to 5 will enable the
clinician to identify the exact location of the pain and the point of maximal tenderness.
Speculum examination should include an inspection of the cervix or vaginal cuff and notations
of any lesions, discharge, inflammation, or atrophy.
Several gynecologic surgeons have attempted to develop classification systems to
categorize pelvic organ prolapse over the years. Figure 4 provides a comparison of major
 130
Gandhi and Sand

Figure 4 Comparison of pelvic organ classification systems.

 Pelvic Floor Disorders 131

prolapse classification systems. In 1996, the American Urogynecologic Society and the Society
of Gynecologic Surgeons adopted the International Continence Society’s Pelvic Organ Prolapse
Quantification (POP-Q) system (29). The system has been demonstrated to be learned easily and
performed quickly with highly reproducible findings between and within observers (30).
However, the classification lacks sensitivity to detect anterior and posterior wall prolapse in the
upper vaginal vault and may confuse redundant suburethral vaginal tissue or urethral
hypermobility with significant cystoceles. In addition, women with pelvic organ prolapse
experience symptoms that do not necessarily correlate with compartment-specific defects
identified by the POP-Q classification system (31). While many research centers have adopted
this system in favor of the Baden Half Way system, widespread use of the POP-Q system by all
practitioners that perform pelvic examinations is hampered by its relative complexity. Although
limitations of the POP-Q system exist, it is a sensitive measure of change in pelvic prolapse in an
individual patient. A uniform system of describing prolapse is necessary to facilitate
collaborative communications and research.

C. POP-Q
The POP-Q system of assessing pelvic support unlike other prolapse grading systems quantifies
descent of the vaginal wall rather than speculating on what is on the other side of the vaginal
epithelium. It avoids specific labels such as cystocele, rectocele, or enterocele recognizing, for
example, that an anterior wall defect may not be the result of a cystocele. Table 6 and Figure 5
describe the different points used in the POP-Q system for describing prolapse, and Figure 6
shows the grid used to record the findings. Table 7 lists the stages of pelvic organ prolapse that

Table 6 POP-Q Points of Reference

Point Definition
Points A 3 cm proximal to or above the hymen in the midline, values from 23 cm
(no prolapse) to þ3 cm (maximal prolapse)
Aa Anterior, corresponds to location of the urethrovesical junction
Ba Posterior
Points B Lowest extent of the segment of the vagina between point A and the apex of
the vagina, values from 3 cm to TVL
location not fixed
If point A protrudes the most (situation in most women without severe
prolapse), then point B ¼ point A
Ba Anterior
Bp Posterior
C Most distal part of the cervix or in women after hysterectomy, the vaginal
cuff
D Posterior fornix
Omitted after hysterectomy
GH (genital hiatus) Distance (cm) from middle of the external urethral meatus to the posterior
midline hymen
PB (perineal body) Distance (cm) from the posterior midline hymen to the midanal opening
TVL (total vaginal length) Greatest depth of vagina (cm) when prolapse is fully reduced
Avoid excessive pressure or stretching
132 Gandhi and Sand

Figure 5 Reference points for POP-Q measurements.

are assigned based on the POP-Q examination when the full extent of the prolapse has been
demonstrated.
Performing a systematic pelvic examination enables the practitioner to consistently assess
patients and follow their progress longitudinally. We separate the speculum and place the lower
blade in posteriorly and hold a ruler or calibrated Q-tip 3 cm away from the urethral meatus.
While pulling the speculum blade posteriorly, we ask the patient to perform a Valsalva
maneuver and measure the descent of point Aa. At this time, the most dependent part of any
anterior wall prolapse is also measured (Ba). By inspecting the vaginal rugae of the anterior wall,
one may gain a hint of whether lateral and or central defects have caused anterior vaginal wall
prolapse. If the vaginal rugae appear to be prominent in the midline, it may be indicative of a
paravaginal defect. Direct assessment of the support of anterior lateral vaginal sulcus is used as a
more definitive marker of diagnosing a paravaginal defect unilaterally or bilaterally. This may be
 Pelvic Floor Disorders 133

Figure 6 Grid for recording prolapse measurements.

assessed during the speculum exam with the aid of ring forceps or a Baden defect analyzer
elevating the anteriorlateral vaginal sulcus to the level of the arcus tendineous and observing if
normal anterior vaginal wall support is restored. This may result in artifact and misdiagnosis if
the opened instrument is elevated above the level of the arcus tendineus.
In one study, while the sensitivity of the clinical assessment of paravaginal defects in
comparison with the operative confirmation of the defects was 92%, the specificity of 53% was
poor (32). We prefer a simpler, more consistent alternative to performing this assessment that
can avoid any potential over correction artifact. We take both halves of a Grave’s speculum and
insert them bilaterally along the lateral vaginal walls in the vertical axis. If the cystocele is
resolved completely, it is probably secondary to a unilateral or bilateral paravaginal defect.
Removing each blade with the other in place will elucidate whether it is a bilateral or unilateral
paravaginal defect. If the anterior vaginal wall descent is not completely corrected, it probably

Table 7 Staging of Pelvic Organ Prolapse Based on the POP-Q Examination

Stage Description
0 No descensus of pelvic structures during straining (Aa, Ap, Ba, Bp ¼ 23 and C or D
2([tvl 2 2])
I The leading surface of the prolapse does not descend below 1 cm above the hymenal ring (i.e.,
prolapse is not stage 0 and all points are ,21)
II The leading edge of the prolapse extends into the region from 1 cm proximal to the hymen to
1 cm distal to the hymen (i.e., most distal point is 21 but þ1)
III The leading edge of the prolapse extends 1 cm beyond the hymen, but there is not complete
vaginal eversion (i.e., most distal point is .þ1 but ,þ[tvl22])
IV Essentially complete eversion (i.e., most distal point is þ[tvl22])
134 Gandhi and Sand

represents a combination of central and paravaginal defects. This method is relatively quick and
may avoid the common overdiagnosis of paravaginal defects.
By rotating the speculum blade 1808 and reinserting it along the anterior vaginal wall, the
clinician can inspect the posterior wall and uterine or vaginal apex mobility. Digital examination
will help to measure vaginal length (TVL) as well as descent of the apex (C and/or D). Finally,
external examination will give measurements of the genital hiatus (GH) and perineal body (PB).
On bimanual examination, initial palpation of the posterior fourchette to assess for
tenderness at the introitus and palpation of the posterior vaginal wall and deeper pelvic
musculature to assess for tenderness or spasm of the levator ani muscle may help to identify
sources of dyspareunia. Palpation of the urethra and bladder neck may reveal tenderness or
masses that should be further evaluated with urethroscopy and cystoscopy. Routine assessment
of contour, size, and abnormalities of the pelvic organs is performed focusing on the presence of
pelvic tenderness or masses. Rectovaginal examination helps to assess the anal sphincter tone,
possible sphincter defects, fecal impaction, the presence of occult blood or rectal lesions, and
subtle distal rectoceles.
Asking the patient to contract her levator ani muscles during this examination will help the
clinician assess her ability to contract the muscles, the strength of the contraction, and the
duration of the contraction. The pelvic muscles have been considered integral to continence
since Kegel (33) observed that women with urinary incontinence experienced symptomatic
improvement by improving the strength of these muscles. The pubococcygeous and puborectalis
components of the levator ani form a hammock beneath the rectum and insert superiorly and
laterally upon the pubic rami. Contraction of these muscles, especially during strenuous physical
activity, compresses the rectum, vagina, and urethra, maintaining flatal, fecal, and urinary
continence (34). Although the utility of this assessment may be questioned, it is useful to grade
levator strength to better implement behavioral interventions such as pelvic floor muscle
exercises, biofeedback, or electrical stimulation. Many patients will have no ability to contract
their levator ani. Pelvic floor exercises without “biofeedback” in those women would be futile.
Various techniques to assess levator ani tone (35 – 42) have been studied, although no single
technique is widely accepted. The modified Oxford scale is presented in Table 8 (39). Given the
lack of a standardized scale, the clinician should adopt a single scale and consistently use it to
preserve internal consistency.

4. Measuring Urethral Hypermobility: Q-tip Test

If we believe that the underlying pathophysiology of most stress urinary incontinence
(previously identified as genuine stress incontinence) involves urethral hypermobility, then
some assessment of urethral mobility should be made. The Q-tip test is an excellent test to
document quantitatively the presence of urethral hypermobility (43,44). It was originally
designed to take the place of the bead chain cystourethrogram in the evaluation of the urethral

Table 8 Modified Oxford Scale for Measuring Pelvic Muscle Strength

Number Definition
0 No palpable muscle contraction
1 Flicker
2 Weak pelvic contraction
3 Moderate contraction with an element of lift
4 Good contraction with lift and holding power
5 Strong squeeze with good lift gripping examining hand
 Pelvic Floor Disorders 135

axis. Although the determination of urethral hypermobility is a poor predictor of the etiology of a
patient’s urinary incontinence (45 – 47), it has been included in the urogynecologic examination
to assess urethrovesical junction support. To perform the test, a sterile cotton applicator soaked
in 2% Xylocaine jelly is inserted into the urethra, and withdrawn slowly until slight resis-
tance indicates that the tip is at the bladder neck. A goniometer or compass (Fig. 7) provides a
measurement of the resting angle from the horizontal. The patient is then asked to repetitively
cough and perform Valsalva maneuvers while the maximum straining angle is measured (Fig. 8).
If the cotton tip is not in the bladder, the angle will be underestimated. A straining angle 308
has been arbitrarily suggested to indicate significant bladder neck mobility. Few normative
data are available regarding these measurements and factors during testing that may affect
measurements.
Walters and Diaz (48) reported that asymptomatic women with a mean parity of two and
mean age of 32 had an average maximum straining angle of 548. Although this was less than the
straining angle of 738 seen in a group of symptomatic women, there was considerable overlap
between groups (48). Fedorkow and colleagues (49) performed a receiver-operator characteristic
analysis and found the optimal diagnostic cutoff point for stress urinary incontinence to be 408
from the horizontal. At this cutoff, 84% of patients with genuine stress incontinence would have
a positive test. Thus, an arbitrary cutoff of 308 in parous women may be too low.
Handa and colleagues (50) noted that 71% of women diagnosed with urethral
hypermobility in the supine position did not have urethral hypermobility in the standing position.
This observation brings into question the reproducibility of the Q-tip test. Despite this
information, the test is still used by many in making decisions in selecting treatments for stress
incontinence primarily because the absence of a positive Q-tip test in someone diagnosed with

Figure 7 Goniometer used for measuring Q-tip angle.

136 Gandhi and Sand

Figure 8 Demonstration of resting and straining angles during the Q-tip test.

stress incontinence is important. Bergman and colleagues (51), using a Q-tip test cut-off point of
358, found a 50% failure rate in women with stress incontinence and negative Q-tip tests who
underwent Pereyra operations and a 55% failure rate for women who had Burch procedures.
By asking the patient to cough at this time, one can perform a supine empty stress test as a
screen for a low pressure urethra or a low leak point pressure (52,53). This simple test has been
identified as a very specific and reasonably sensitive test to assess for intrinsic sphincteric deficiency.
Finally, we repeat a vaginal examination while the patient bears down in the standing
position to reassess for the sign of stress incontinence and for increased genital prolapse with
gravity. Occasionally, pelvic organ descent may only be evident with the help of gravity.

V. CONCLUSIONS

A careful history and physical examination will guide the clinician in further evaluation of the
patient’s symptoms or allow them to begin empiric treatment in uncomplicated pelvic floor
disorders.

REFERENCES

1. Haylen BT, Sutherst JR, Frazer MI. Is the investigation of most stress incontinence really necessary?
Br J Urol 1989; 64:147 – 149.
2. Cundiff GW, Harris RL, Coates KW, Bump RC. Clinical predictors of urinary incontinence in
women. Am J Obstet Gynecol 1997; 177:262 – 266; discussion 266– 267.
3. Sand PK, Hill RC, Ostergard DR. Incontinence history as a predictor of detrusor stability. Obstet
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 Pelvic Floor Disorders 137

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9
Urodynamic Assessment: Urethral Pressure
Profilometry and PTR
Stacey J. Wallach* and Donald R. Ostergard
University of California, Irvine, and Long Beach Memorial Medical Center, Long Beach,
California, U.S.A.

I. INTRODUCTION

For a person to be continent, the pressure in the urethra must exceed the pressure in the detrusor
at all times. If bladder pressure should overcome urethral pressure, urine loss may result.
Researchers have devised different tests to assess the relationship between urethral and bladder
pressure. Their goal is to differentiate between patients with urinary incontinence based solely
on an anatomic loss of urethral support, from patients with a loss of ability to maintain urethral
pressure due to an incompetent urethral sphincter. Both urethral pressure profilometry and leak
point pressure look at urethral resistance to voiding. However, urethral pressure profiles are
static measurements along the length of the urethra thought to represent the intrinsic sphincter
mechanism, while leak point pressures are dynamic tests of the amount of pressure it takes to
overcome urethral resistance (1).
The female urethra is 3– 4 cm in length and is composed of a longitudinal layer of smooth
muscle surrounded by a circular layer of smooth muscle. These smooth muscle layers are, in
turn, encompassed by a circular sphincter of striated muscle. Lying beneath the urethral mucosa
is a vascular plexus that helps to produce a hermetic seal (2). The striated muscle, the vascular
bed, and the smooth muscle and connective tissue together generate the intrinsic urethral
pressure. Ulmsten et al. showed that each component is responsible for about a third of the
intraurethral pressure (3). Extrinsic factors can further augment urethral pressure. According to
DeLancey, the urethra itself lies on a hammock formed by the anterior vaginal wall (4). By
contracting the pelvic diaphragm, the urethra is compressed against the vagina further
augmenting urethral pressures.

II. HISTORY

In 1923, Victor Bonney (5) became the first person to measure urethral pressures. He used a
manometer to determine the pressure required to retrograde infuse fluid into the urethra. Since

*Current affiliation: University of California, Sacramento, California, U.S.A.

141
142 Wallach and Ostergard

that time, various methods to gauge urethral pressure have been devised. In 1940, Barnes (6)
used a fluid-filled balloon connected to a pressure transducer to evaluate the urethra’s resistance
to distension. In 1957, Lapides and colleagues (7) used a water manometer to quantify urethral
wall pressure at specific segments along the urethra.

A. Perfusion Catheters
Brown and Wickham (8) perfected the fluid perfusion technique developed by Toews (9) to
create an accurate and reproducible urethral pressure profile. A double- or triple-lumen catheter
allowed simultaneous recording of bladder and urethral pressure. Multiple circumferential side
holes minimized rotational error. A pump infused fluid at a constant rate of 2 mL/min while
a mechanical puller withdrew the catheter 1 –2 mm every second. The transducer measured
the pressure of the fluid required to lift the wall of the urethra off the side holes. Later on, other
researchers tried carbon dioxide gas as a perfusion medium but this was found to be less
accurate (10). (see Fig. 1).

B. Membrane Catheters
The accuracy of perfusion catheters depended on the ability of the urethra to create a seal around
the catheter. This shortcoming was remedied with the introduction of membrane catheters in the
1970s. These catheters had a cylindrical balloon or membrane over the infusion holes
thus preventing the loss of infusion media. They were more accurate but harder to use (11). All
air bubbles needed to be eliminated for accurate readings. The catheter was calibrated to

Figure 1 Perfusion catheter. (A) Before perfusion; (B) during infusion. The catheter measures resistance
to flow of the perfusion media. (From Ref. 66, p. 124.)
 Urodynamic Assessment 143

atmospheric pressure prior to insertion. The urethral pressure measured represented the average
pressure over the length of the membrane.

C. Microtransducer Catheters
All of the above methods were adequate for recording resting urethral pressure profiles but
lacked the ability to accurately measure rapid changes in pressure such as what happens during a
cough. In 1973, Millar and Baker (12) developed the microtip transducer. These catheters had a
pressure-sensitive piezoelectric unit mounted at the catheter tip and one mounted 6 cm proximal.
They were highly sensitive and very accurate and could record dynamic changes in intra-
vesicular pressure and urethral pressure simultaneously. On the downside, they were expensive,
extremely fragile, and prone to rotational error since the transducer was unidirectional. In reality,
the microtransducer measures a unidirectional force (not pressure) from contact of the
piezoelectric unit with the urethral wall (13).

D. Fiberoptic Catheters
Ten years after Millar and Baker (12) developed microtip transducers, Kyarstein and coworkers
adapted fiberoptic catheters for urodynamics (14). Fiberoptic catheters were more durable than
microtip catheters, did not require orientation, and, like microtip catheters, were able to record
dynamic changes in pressure. These catheters were marketed as a reliable and inexpensive way
for the average gynecologist/urologist to perform urodynamics. Fiberoptic catheters came in
both disposable and reusable forms. However, they tended to record lower than microtip
catheters, potentially leading to overdiagnosis of low-pressure urethras (15,16). Some fiberoptic
catheters also lacked the ability to record bladder pressure and urethral pressure simultaneously,
leaving them vulnerable to error should a bladder contraction occur during the urethral closure
pressure profile.

III. TECHNIQUE

The resting urethral pressure profile is performed with the patient in the sitting position with a
full bladder, often immediately after the cystometrogram. As with the cystometrogram, the
patient sits in a urodynamic chair. Surface electrodes are placed on either side of the anal
sphincter to measure pelvic floor muscle activity. The catheters are calibrated prior to insertion.
In the past, the transducers were zeroed at the level of the bladder, but this is no longer necessary
with some of the newer catheters. Any prolapse is reduced, with care taken not to apply pressure
on the urethra.
The intra-abdominal catheter is inserted into the vagina or rectum and secured. Then the
urethral meatus is cleaned and the dual-tipped microtransducer catheter is inserted into the
bladder. Before beginning the test, any residual urine is drained and the patient is filled with
warm saline to maximum bladder capacity. By convention, the dual-tipped catheter is oriented
with the transducer facing 9 o’clock and attached to the mechanical puller device. The
mechanical puller is set to withdraw the catheter at a rate between 1 and 2 mm/sec. Orienting the
catheter toward 12 o’clock will spuriously elevate urethral pressure, whereas orienting it toward
6 o’clock tends to record lower values (17,18). At the start of the procedure, both transducers on
the dual-tipped catheter begin inside the bladder. Therefore, the pressure recorded in the bladder
channel should equal the initial pressure recorded in the urethral channel.
144 Wallach and Ostergard

Once the patient is at maximum bladder capacity, the puller is turned on and the patient is
asked to cough to ensure the catheters are recording equally. The catheter is slowly drawn through the
urethra by the puller mechanism. The proximal transducer measuring intraurethral pressure will note
a progressive increase in pressure from the bladder neck to the midurethra followed by a progressive
decrease in pressure to zero as the transducer is pulled past the urethral meatus to outside atmospheric
pressure (Fig. 2) This test is repeated to ensure reproducibility, and the results are averaged.

Figure 2 Technique of static urethral pressure profilometry. The study begins with both microtip
transducers in the bladder (top), as the catheter is withdrawn through the urethra the proximal transducer
records urethral pressure. The urethral pressure increases to maximal urethral pressure near the midurethra
(middle), then decreases again (bottom) to zero as the proximal transducer is pulled out of the external
meatus to atmospheric pressure. (From Ref. 67, p. 83.)
 Urodynamic Assessment 145

IV. DEFINITIONS

Ideally, when performing a urethral closure pressure profile, six channels are recorded
simultaneously—EMG, intravesical pressure, intraabdominal pressure, intraurethral pressure, true
detrusor pressure, and urethral closure pressure (Fig. 3). Like true detrusor pressure, urethral closure
pressure is a subtracted channel created by deducting intravesical pressure from intraurethral
pressure. Thus, the urethral pressure profile differs from the urethral closure pressure profile in that
the latter has bladder pressure already subtracted. Rarely, the withdrawal of the catheter through the
urethra can cause a detrusor contraction. If bladder pressure is not measured simultaneously with
urethral pressure, one may erroneously label the urethral closure pressure as inadequate.
The urethral closure pressure profile (UCPP) graphically represents the pressure in
the urethra throughout its anatomic length. The maximal urethral closure pressure (MUCP) is the
highest amount of pressure attained in the urethra. Thus, the MUCP is the highest point on the
urethral closure pressure profile curve (Fig. 4). Anatomically, this point correlates to the area of

Figure 3 The static urethral closure pressure profile in the normal female. Intravesical pressure,
intraurethral pressure, and intrarectal pressure are measured simultaneously. The detrusor pressure channel
and urethral closure pressure channel are subtracted channels. (From Ref. 66, p. 127.)
146 Wallach and Ostergard

Figure 4 The static urethral pressure profile with ICS recommended nomenclature in the normal female.
(From Ref. 66, p. 646.)

the midurethra where the striated and smooth muscle sphincters overlap. Since the mechanical
puller device withdraws the transducer at a set rate, various distances can be calculated. The
length from the external urethral meatus to the point of maximum urethral pressure can be
determined based on the amount of time it takes the catheter to move from the point of MUCP to
the urethral meatus.
Functional urethral length and total urethral length can also be measured. Functional
urethral length is the length of the urethra along which urethral pressure exceeds bladder
pressure. Total urethral length includes the additional length needed to reach atmospheric
pressure, but this parameter has not been found to have clinical importance. Investigators have
also looked at the area under the urethral closure pressure curve termed the continence area
(Fig. 5). This area can be thought of as representing the intrinsic continence mechanism. The
space between the urethral closure pressure curve and the zero axis represents the patient’s
“margin to leakage,” or the pressure that must be overcome to cause equalization and urine loss.
Both the amount of fluid in the bladder and the patient’s position during the test can alter
the results of the urethral pressure profile (19 –21). The closure profile of a stress-incontinent
patient with a half-full bladder may still show positive pressure with a cough; thus, the patient
may not leak. This same person with stress at maximum bladder capacity may lose urine because
bladder pressure overcomes urethral pressure. A more upright position creates a larger
hydrostatic pressure, which leads to increased activation of urethral and pelvic floor skeletal
muscle. This results in higher urethral closure pressures and longer functional urethral lengths.
In the continent patient, there is a 25 –70% increase in the maximum urethral closure pressure
with standing. This increase is seen primarily in the mid to distal urethra corresponding to the
striated sphincter. The patient with genuine stress incontinence has a weakness in her
compensatory ability to augment urethral closure pressures by increasing activity of the striated
urethral sphincter. For this reason, urethral closure pressures decrease in the stress-incontinent
patient as the patient assumes a more upright position (22,23).
In addition, other factors may influence urethral closure pressures and functional urethral
length. Incontinent patients have lower maximum urethral closure pressures and shorter
 Urodynamic Assessment 147

Figure 5 The static urethral pressure profile in the normal female comparing urethral closure pressure to
total urethral pressure. (From Ref. 66, p. 128.)

functional urethral lengths than continent controls, although there is considerable overlap
(24,25). Maximum urethral closure pressure and functional urethral length decrease after
menopause (26 –28). Both of these parameters increase with the administration of estrogen to
postmenopausal women (29,30). Other medications, such as phenylpropanolamine and nore-
phedrine, also increase maximal urethral closure pressure (31,32). On the other hand, various
surgeries, e.g., radical hysterectomy, abdominalperineal resection, and internal urethrotomy,
have been shown to decrease urethral closure pressure and urethral length (33 –36).

A. Low Pressure Urethra

In fact, researchers noted that patients who failed previous incontinence procedures were at a
higher risk of a subsequent failure (37). McGuire was the first to document that these patients
had maximum urethral closure pressures ,20 cmH2O (38,39). Later on, Sand et al. showed
that patients with genuine stress incontinence (GSI) and low urethral closure pressures pre-
operatively were at a higher risk of failure (54% vs. 18% at 3-month follow-up) from a Burch
procedure (40). Other researchers concurred with their findings (41,42). Thus, the low-pressure
urethra is defined as one in which the maximal urethral closure pressure is 20 cmH2O. This
low-pressure urethra is considered to be associated with intrinsic sphincter deficiency.
Since patients with low-pressure urethras are at higher risk of surgical failure from
traditional retropubic suspension procedures, it is important to diagnose these patients
preoperatively. A suburethral sling is the current procedure of choice for these patients with low-
pressure urethras. Certain clues in the patient’s history may suggest that further evaluation
is necessary to rule out a low-pressure urethra. These include patients with previous failed
148 Wallach and Ostergard

Figure 6 The static urethral pressure profile superimposed onto a urethra with two diverticulum, one
proximal and one distal to the point of maximal urethral pressure. (From Ref. 66, p. 365.)

incontinence procedures, supine urine loss with an empty bladder, urine loss with a change
in position, presence of a meningomyelocele (43), previous pelvic radiation (44), history of
extensive pelvic surgery such as a radical hysterectomy (33), low anterior resection or
abdominalperineal resection (35), or age .50 (45).

B. Double-Peaked UCPPs
The urethral closure pressure profile may also help in detecting urethral kinking, a urethral
stricture, diverticulum, or fistula. If a sudden rapid elevation in urethral pressure is visualized
during the urethral closure pressure profile, the examiner should be on alert for urethral kinking
from a large prolapse or a urethral stricture (46,47). The opposite holds true for a urethral
diverticulum or fistula. As the catheter moves over the diverticular ostia or fistula opening, a
sudden drop in pressure will occur owing to the absence of the urethral wall. The urethral
pressure profile may have a double-peaked or biphasic appearance. Bhatia and coworkers used
the urethral closure pressure profile to determine the location of the urethral diverticulum in
relationship to the point of maximal urethral pressure (48) (Fig. 6). If the diverticular opening is
distal to the peak closure pressure, a Spence procedure can be performed. However, when the
diverticular ostia is proximal to the point of maximal closure pressure, a diverticulectomy should
be performed since a Spence procedure may result in genuine stress incontinence.

V. AUGMENTED UCPP

The augmented urethral closure profile reflects the patient’s ability to contract her periurethral
and levator ani muscles. This suggests an intact motor pathway from the brain down the spinal
cord and out the efferent motor neurons. Patients with motor lesions above the level of the sacral
 Urodynamic Assessment 149

spinal cord cannot control the striated sphincter. These patients lack the ability to relax their
external sphincter during voiding, called detrusor sphincter dyssynergia (49).
The study is performed in the same manner as the resting urethral closure pressure profile
except that the patient is asked to contract the muscles around her urethra as if she is holding her
urine while the catheter is withdrawn. Once this is accomplished, the same procedure is
performed again with the patient squeezing her rectum while the catheter is withdrawn. With
both of these procedures, the maximal urethral closure pressure and functional urethral length
should increase if the patient is able to contract her muscles. These tests are analogous to
performing a Kegel’s maneuver and are thus dependent on the patient’s understanding the
actions requested. Augmented urethral profiles have not been shown to have prognostic value for
women undergoing surgery (50).

VI. DYNAMIC UCPP

The dynamic or stress urethral closure pressure profiles reflect the patient’s ability to maintain
continence in the face of increases in intraabdominal pressure. In the continent patient, increases
in intra-abdominal pressure should be transmitted to both the bladder and proximal/midurethra.
(Pressure is not transmitted to the distal urethra because it is below the urogenital diaphragm.) In
patients with genuine stress incontinence, the dynamic urethral closure pressure profile equalizes
and urine loss occurs in the absence of a detrusor contraction.
There are two types of dynamic urethral closure pressure profiles, the Valsalva profile and
the cough profile. With the Valsalva profile, the patient is asked to give a maximal Valsalva
effort as the catheter is withdrawn through the urethra. The cough profile is performed in the
same manner except that the patient is asked to cough every 2 – 3 sec as the catheter is withdrawn
(Fig. 7). In both of these tests, the urethral meatus is observed for urine loss. As with static
urethral pressure profiles, dynamic urethral pressure profiles are performed at maximum bladder
capacity in the sitting position, as patients may be continent at lower bladder volumes.
In the continent patient, positive pressure is transmitted to the proximal urethra with each
cough. This can be seen as small spikes along the top of the urethral closure pressure profile and
represent a negative test. In patients with genuine stress incontinence, less pressure maybe
transmitted to the urethra with coughing than the bladder. This represents a failure in the
extrinsic continence mechanism, allowing bladder pressure to overcome urethral pressure and
urine loss to occur. For the cough urethral pressure profile to be considered positive, the cough
spikes must cross the zero axis. When this happens, the pressure in the urethra equalizes with
bladder pressure.
The functional urethral length is divided into four quarters. Investigators calculate
pressure transmission ratios in each quartile by comparing the amount of pressure transmitted to
the bladder to the amount of pressure transmitted to the urethra. The pressure transmission ratio
is defined as the change in urethral pressure divided by the change in intravesical pressure
multiplied by a hundred (Fig. 8). Thus, values .100% imply positive pressure transmission (the
urethral pressure spike exceeds the bladder pressure spike), whereas values ,100% suggest that
more pressure is transmitted to the bladder than the urethra.
As a group, patients with genuine stress incontinence have lower pressure transmission
ratios than continent controls (25,51). However, marked overlap exists between pressure trans-
mission ratios in continent and incontinent women, making it difficult to set cutoff values
(52,53). That said, most patients with genuine stress incontinence have pressure transmission
ratios ,90% (51). Pressure transmission ratios may be useful in excluding genuine stress
incontinence, but they lack the sensitivity to diagnose it (low sensitivity, high specificity) (54,55).
150 Wallach and Ostergard

Figure 7 The cough urethral pressure profile in the continent female (left) and incontinent female (right).
The curve on the left shows good pressure transmission with the space under the curve representing this
patient’s “margin to leakage.” The curve on the right equalizes with each cough and the patient leaks urine.
(From Ref. 67, p. 84.)
 Urodynamic Assessment 151

Figure 8 Calculation of pressure transmission ratios during a cough urethral pressure profile. (From Ref. 68.)
152 Wallach and Ostergard

No difference in pressure transmission ratios has been demonstrated between patients with
genuine stress incontinence and those with low urethral closure pressures (56).
Pressure transmission ratios increase after retropubic urethropexies and traditional slings
(57 – 61). The improved pressure transmission is theorized to be due to prevention of rotational
descent of the urethra (62,63). However, since pressure transmission ratios also increase after
the tension-free vaginal tape procedure, bladder neck support may not be the entire cause for
improved transmission ratios (64). Constantinou and colleagues showed that the urethral
pressure spike in continent patients precedes the intravesical pressure spike by several hundred
milliseconds (65). This relationship is lost in stress-incontinent women even after surgical
correction. Thus, there may be an active component to continence as well as the passive
transmission of pressure. The urethra may contract closing the bladder neck prior to the increase
in bladder pressure.

VII. MICTURITION UCPP

The micturition urethral closure pressure profile is used to detect outlet obstruction and its
location. The catheter is slowly withdrawn through the urethra as the patient voids. This study is
used primarily in men to look for obstruction at the bladder neck from a hypertrophied prostate.
In the case of obstruction in women, the distal urethra is a more common site. Causes for
obstruction in women vary from a urethral stricture, which can result from instrumentation, to
urethral kinking from a large prolapse.

VIII. ANCILLARY TESTS

A. Bulbocavernosus Reflex
The bulbocavernosus reflex is elicited by tapping the clitoris with a cotton swab. This results in
contraction of the bulbocavernosus and ischiocavernosus muscles. With a microtip transducer in
the urethra, the bulbocavernosus reflex is detected as a brisk increase in urethral pressure. This
reflex depends on the integrity of the pudendal nerve and the sacral spinal cord.

B. Anal Sphincter Reflex

The anal sphincter reflex can also be visualized with a pressure catheter in the urethra. The skin
next to the anus is stroked with a Q-tip, eliciting the reflex. An intact reflex indicates normal
function of L5 –S2.

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29. Rud T. The effects of estrogens and gestagens on the urethral pressure profile in urinary continent and
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31. Beisland HO, Fossberg E, Moer A, Sander S. Urethral sphincteric insufficiency in postmenopausal
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32. Ek A, Andersson KE, Ulmsten U. The effects of norephedrine and bethanechol on the human urethral
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33. Sasaki H, Yoshida T, Noda K, Yachiku S, Minami K, Kaneko S. Urethral pressure profiles following
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34. Farquharson DI, Shingleton HM, Orr JW, Hatch KD, Hester S, Soong SJ. The short-term effect of
radical hysterectomy on urethral and bladder function. Br J Obstet Gynaecol 1987; 94:351– 357.
35. Zanolla R, Campo B, Ordesi G, Martino G. Bladder urethral dysfunction after abdominoperineal
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37. Stanton SL, Cardozo L, Williams JE, Ritchie D, Allan V. Clinical and urodynamic features of failed
incontinence surgery in the female. Obstet Gynecol 1978; 51:515– 520.
38. McGuire EJ, Lytton B, Pepe V, Kohorn EI. Stress urinary incontinence. Obstet Gynecol 1976;
47:255– 264.
39. McGuire EJ. Urodynamic findings in patients after failure of stress incontinence operations. Prog Clin
Biol Res 1981; 78:351 – 356.
40. Sand PK, Bowen LW, Panganiban R, Ostergard DR. The low pressure urethra as a factor in failed
retropubic urethropexy. Obstet Gynecol 1987; 69:399– 402.
41. Bowen LW, Sand PK, Ostergard DR. Unsuccessful Burch retropubic urethropexy: a case controlled
urodynamic study. Am J Obstet Gynecol 1989; 160:451 – 458.
42. Koonings PP, Bergman A, Ballard CA. Low urethral pressure and stress urinary incontinence in
women: risk factor for failed retropubic surgical procedure. Urology 1990; 16:245– 248.
43. McGuire EJ, Woodside JR, Borden TA, Weiss RM. Prognostic value of urodynamic testing in
myelodysplastic patients. J Urol 1981; 126:205 – 209.
44. Parkin DE, Davis JA, Symonds RP. Urodynamic findings following radiotherapy for cervical
carcinoma. Br J Urol 1988; 61:213 – 217.
45. Horbach NS, Ostergard DR. Predicting intrinsic sphincter dysfunction in women with stress urinary
incontinence. Obstet Gynecol 1994; 84:188 – 192.
46. Richardson DA, Bent AE, Ostergard DR. The effect of uterovaginal prolapse on urethrovesical
pressure dynamics. Am J Obstet Gynecol 1982; 146:901– 905.
47. Højsgaard A. The urethral pressure profile in female patients with meatal stenosis. Scand J Urol
Nephrol 1976; 10:97 – 99.
48. Bhatia NN, McCarthy TA, Ostergard DR. Urethral pressure profiles of women with diverticula.
Obstet Gynecol 1981; 58:375 – 378.
49. Steele GS, Sullivan MP, Yalla SV. Urethral pressure profilometry: vesicourethral pressure
measurements under resting and voiding conditions. In: Nitti VW, ed. Practical Urodynamics.
Philadelphia: W.B. Saunders, 1998:113.
50. Sand PK, Bowen LW, Ostergard DR. The prognostic significance of augmentation of urethral closure
pressure and functional urethral length. Int J Gynaecol Obstet 1990; 33:135 – 139.
51. Bump RC, Copeland WE, Hurt WG, Fantl JA. Dynamic urethral pressure/profilometry pressure
transmission ratio determinations in stress-incontinent and stress-continent subjects. Am J Obstet
Gynecol 1988; 159:749 – 755.
52. Rosenzweig BA, Bhatia NN, Nelson AL. Dynamic urethral pressure profilometry pressure
transmission ratios: what do the numbers really mean? Obstet Gynecol 1991; 77:586 – 590.
53. Lose G, Thind P, Colstrup H. The value of pressure transmission ratio in the diagnosis of stress
incontinence. Neurourol Urodyn 1990; 9:323 – 324.
54. Richardson DA. Value of the cough pressure profile in the evaluation of patients with stress
incontinence. Am J Obstet Gynecol 1986; 155:808 – 811.
55. Hanzal E, Berger E, Koelbl H. Reliability of the urethral closure pressure profile during stress in the
diagnosis of genuine stress incontinence. Br J Urol 1991; 68:369 –371.
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56. Summitt RL, Sipes DR, Bent AE, Ostergard DR. Evaluation of pressure transmission ratios in women
with genuine stress incontinence and low urethral pressure: a comparative study. Obstet Gynecol
1994; 83:984 –988.
57. Faysal MH, Constantinou CE, Rother LF, Govan DE. The impact of bladder neck suspension on the
resting and stress urethral pressure profile: a prospective study comparing controls with incontinent
patients preoperatively and postoperatively. J Urol 1981; 125:55 –60.
58. Hilton P, Stanton SL. A clinical and urodynamic assessment of the Burch colposuspension for
genuine stress incontinence. Br J Obstet Gynaecol 1983; 90:934 – 939.
59. Weil A, Reyes H, Bischoff P, Rottenberg RD, Krauer F. Modifications of the urethral rest and stress
profiles after different types of surgery for urinary stress incontinence. Br J Obstet Gynaecol 1984;
91:46– 55.
60. Beck RP, McCormmick S, Nordstrom L. Intraurethral-intravesical cough-pressure spike differences
in 267 patients surgically cured of genuine stress incontinence of urine. Obstet Gynecol 1988;
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61. Baker KR, Drutz HP. Retropubic colpourethropexy: clinical and urodynamic evaluation in 289 cases.
Int Urogyncol J 1991; 2:196 – 200.
62. Bunne G, Obrink A. Influence of pubococcygeal repair on urethral closure pressure at stress. Acta
Obstet Gynaecol Scand 1978; 57:355– 359.
63. Barbic M, Kralj B. Effect of intra-abdominal position of the bladder neck and stability of its
supporting structures on pressure transmission ratio after colposuspension. Int Urogynecol J Pelvic
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64. Mutone N, Mastropietro M, Brizendine E, Hale D. Effect of tension-free vaginal tape procedure on
urodynamic continence indices. Obstet Gynecol 2001; 98:638 –645.
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urethral pressures in healthy women. J Urol 1982; 127:964 – 969.
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68. Karram MM. Urodynamics. In: Benson JT, ed. Female pelvic floor disorders: Investigation and
management. New York: Norton Medical Books, 1992.
10
Leak Point Pressures

Shahar Madjar
Northern Michigan Urology at Bell, Bell Memorial Hospital, Marquette County, Michigan,
U.S.A.
Rodney A. Appell
Baylor College of Medicine, Houston, Texas, U.S.A.

I. INTRODUCTION

The concept of leak point pressure (LPP) determination was introduced by McGuire et al. (1).
The first LPP to be defined was the detrusor or bladder leak point pressure (DLPP) and was
correlated with an increased risk of upper tract deterioration in children with meningomyelocele
(1). The definition of abdominal LPP (ALPP) was to follow (2), and it was used to categorize
patients into either anatomical or intrinsic sphincteric deficiency (ISD), the two types of stress
urinary incontinence. ALPPs can be further divided to ALPP measured during Valsalva
maneuver (VLPP) and ALPP measured during cough (CLPP). There is lack of standardization of
how LPPs are measured. Different entities of LPP and a great variation in the techniques used to
measure each of these entities have led to considerable confusion among professionals. The
clinical applicability of these tests is therefore still controversial, and interpretation of results is
difficult. The definitions of LPP, the techniques used for their measurement, and their clinical
applicability are described and discussed.

II. DEFINITIONS

The following definitions were made by the Standardization Committee of the Inter-
national Continence Society (ICS) and approved at the 28th annual meeting of the society in
Jerusalem (3).
Detrusor leak point pressure is the lowest value of detrusor pressure at which leakage is
observed in the absence of abdominal strain or a detrusor contraction. It is described as a static or
passive test to assess the storage function and detrusor compliance, particularly in patients with
neurogenic lower tract dysfunction.
Abdominal leak point pressure is the lowest of the intentional or actively increased
intravesical pressure that provokes urinary leakage in the absence of detrusor contraction.
Increased abdominal pressure can be induced by coughing (CLPP) or by a Valsalva maneuver

157
158 Madjar and Appell

(VLPP). ALPP is a dynamic test used to assess the severity and the type (anatomical vs. ISD) of
stress urinary incontinence.
The pressure measured in the bladder (Pves) is equal to the abdominal pressure plus the
pressure produced by the detrusor itself (Pves ¼ Pabd þ Pdet). ALPP is defined as an intravesical
pressure measurement at a time where no detrusor contraction appears (change in Pdet ¼ 0).
Therefore, the change in pressure measured at the bladder will be equal to that measured in the
abdomen (Pves ¼ Pabd). ALPP can thus be determined with no pressure measurement probe in
the bladder. This may allow for a true measurement of ALPP without interference of a urethral
catheter partially obstructing the bladder outlet.

III. ABDOMINAL LEAK POINT PRESSURE

A. Technique
Various techniques have been described to measure LPPs. These variations affect the actual
readings of LPP values. It is therefore recommended by the ICS that the location and access of
pressure sensors, position of the patient, the method by which the bladder is filled (diuresis or
catheter), and the volume at which the measurement is performed (both absolute and in relation
to maximum cystometric capacity) be specified. The mode of leak detection (e.g., direct or
fluoroscopic observation), the catheters used, and the measuring equipment for pressure
measurement should also be reported.
ALPP measurement is usually performed during urodynamic testing after cystometro-
graphy with an intraurethral catheter. Rectal or vaginal pressure sensors can be alternatively
used to prevent interference of the urethral catheter with urinary leakage. The bladder is filled to
200 mL, 250 mL, 50% of maximum cystometric capacity, or another predetermined fixed
volume. The patient is then asked to gradually increase his/her intra-abdominal pressure (in the
case of VLPP measurement) or to cough several times with increasing strength (CLPP). Some
laboratories use CLPP only when Valsalva maneuver has failed to produce leakage. The lowest
abdominal or vesical pressure at which leakage occurs is recorded and interpreted as ALPP.
Leakage can be detected using visual recording (4 – 6), video or fluoroscopy (1,7,8), or electric
conductance (9 – 11).

B. Study Conditions
Several factors have been described as influencing ALPP measurement and interpretation. The
following are variations and modifications in the technique used to measure ALPP and their
effect on ALPP values.

1. Catheter
VLPP measured by a urethral catheter was found to be higher than that measured with a rectal
catheter (12). This may result from the catheter’s partially occluding the bladder outlet. Catheter
size also affects LPP results, with larger-diameter catheters correlating with higher VLPP
measurement (4, 13). In a recent report by Bump et al., VLPP measurements were significantly
higher when an 8Fr catheter was used compared with a 3Fr catheter (4).

2. Bladder Volume
VLPP is correlated with bladder volume in the majority of clinical studies. Theofrastous (14)
reported on 120 women with genuine stress urinary incontinence who underwent serial VLPP
 Leak Point Pressures 159

determinations at bladder volumes of 100, 200, and 300 mL, and at maximum cystometric
capacity. Thirty-three women had leakage starting at a vesical volume of 100 mL, 18 at 200 mL,
19 at 300 mL, and 17 had leakage only at maximum cystometric capacity. The mean first
positive VLPPs were significantly higher than VLPPs at maximum capacity in all groups. It was
concluded that VLPP in women with stress urinary incontinence decreases significantly with
bladder filling. This was supported by the findings reported by Faerber and Vashi (15). Still
others found no correlation between bladder volumes (150, 300, maximal cystometric capacity)
and VLPP (16).

3. Cough Versus Valsalva Leak Point Pressures

Both Valsalva maneuver and cough have been used to provoke leakage in the determination of
ALPP. Peschers et al. (17) reported on their evaluation in 59 incontinent women: CLPP was
found to be significantly higher than VLPP (112.5 + 46.9 cm water vs. 58.9 + 27.6,
P , .0001). While CLPP was negative in two women only, VLPP was negative in 24 of 59
women evaluated (40.1%). If intrinsic sphincter deficiency (ISD) was defined as a leak point
pressure of 65 cm water, 16.9% of women fulfilled this criterion using the CLPP compared to
35.6% when VLPP is used. Therefore, coughing and Valsalva maneuver result in a different
classification of stress urinary incontinence into ISD and anatomical stress incontinence. A
similar correlation between CLPP and VLPP values was reported by Bump et al. (4).

4. Interpretation of Results
One of the debates concerning interpretation and the clinical applicability of VLPP
measurements is how they should be read. Should only the increase in intravesical pressure
(Pves) over baseline resting Pves (DVLPP) be accepted in the interpretation of the urodynamic
tracing or should the total increase in Pves (VLPPtot), meaning the resting baseline Pves þ the
increase in Pves during Valsalva, be accepted in the interpretation of urodynamic tracing?
Madjar et al. (18) studied 264 female patients who had undergone an anti-incontinence
procedure. Baseline Pabd varied between 10 and 55 cmH2O (mean ¼ 32.7 + 8.8) and was
significantly correlated with patient’s weight (P , .001) and patient’s body mass index
(P , .001). Higher VLPPtot significantly correlated with decreased age (P ¼ .004), less severe
incontinence (P ¼ .004), higher peak Valsalva pressure (P , .0001), and the ability to increase
abdominal pressure for a longer period of time (time to peak Pabd during Valsalva). VLPPtot and
DVLPP had similar statistical correlation with all the clinical variables examined, and neither
could predict the outcome of any anti-incontinence surgery. Using a VLPP of 60 cmH2O as a
cutoff to differentiate severe ISD from anatomical incontinence, 211 (67.4%) of the patients
would be categorized as having ISD according to their DVLPP, compared with only 106 (40.1%)
using the VLPPtot. Looking at VLPPtot and DVLPP will therefore result in a different
categorization of the type of incontinence in at least 25% of patients.

5. Alternatives to ALPP Measurement

Supine stress tests at empty bladder and at 200 mL were suggested as alternatives to the
VLPP measurement by McLennan (19) and Hsu et al. (20), respectively. McLennan reported
on 179 patients with a history of genuine stress incontinence confirmed with urodynamic
testing. All patients had a supine stress test performed after voiding. Residual urine
determinations were all ,100 cc. A vesical Valsalva leak point pressure determination (cough
and strain) was performed during multichannel urodynamics with 150 cc in the bladder. A
statistically significant relationship between a low leak point pressure and a positive supine
160 Madjar and Appell

empty stress test (P , .000) was found. The supine empty stress test had a sensitivity of 79%
and a specificity of 62.5% for the detection of a low leak point pressure. The negative
predictive value was high at 90%.
Hsu et al. (20) reported on their experience with a supine stress test performed at a bladder
volume of 200 mL. Cough and Valsalva maneuvers were performed after bladder filling to
200 mL with sterile normal saline solution by gravity. Efflux of the bladder solution from the
meatus coinciding with the cough or Valsalva maneuver was defined as a positive clinical test.
ISD was defined as an ALPP of ,100 cmH2O, and the supine stress test had 93.5% sensitivity,
90.0% specificity, 96.7% positive predictive value, and 81.8% negative predictive value for
detecting ISD. It was concluded that the supine stress test is easy, quick, and inexpensive, and a
positive test is a reliable predictor of ISD.

IV. CLINICAL APPLICATION

A. Female Stress Urinary Incontinence
Urethral pressure measurements, such as maximal urethral closing pressure, have been
frequently and extensively used to assess urethral sphincteric deficiency (21 – 23). Despite a
great deal of evidence to the contrary, maximal urethral pressure measurements have been
considered by many to be closely related to continence function. This theory was challenged by
McGuire et al. (2), who in 1993 reported on results comparing MUCP with ALPP. One hundred
twenty-five women were divided into three types of stress urinary incontinence according to
their proximal urethral closing pressure and the degree of rotational descent of the urethra (no
rotation, 458 rotation, and .458 rotation). Patients with low abdominal leak point pressure
(,60 cmH2O) had more severe incontinence, with 75% of them having type 3 incontinence (low
urethral pressure, no urethral hypermobility). Patients with high ALPP (.90 cmH2O) showed a
lesser degree of incontinence and were classified as having only types 1 or 2 of incontinence
(high urethral pressure and minimal or gross hypermobility, respectively). The middle group
(ALPP 60– 89 cmH2O) had either type 2 or type 3 stress urinary incontinence. ALPPs were
therefore correlated with the type of incontinence. However, abdominal pressures required to
cause stress incontinence were unrelated to maximum urethral pressure, which indicates that
maximum urethral pressure has little relationship with urethral resistance to abdominal pressure.
This correlation between low ALPP values and ISD has been confirmed by others (24 – 26).
The value of distinguishing between ISD and anatomical incontinence is based primarily
on different treatment modalities allocated for different types of incontinence. Traditionally,
sling procedures, injectable bulking agents, and artificial urinary sphincters have been used for
the treatment of ISD, while other treatment modalities, such as suspension procedures, have
been used for the treatment of anatomical incontinence. This concept has recently been
challenged. A considerable overlap exists between these entities (27,28). Moreover, treatments
such as sling procedures, which were traditionally used for the treatment for ISD, are reported to
be as effective for anatomical incontinence (29). In light of these facts, the true value of ALPP
determinations and the categorization of patients into anatomic and ISD types of incontinence
are still to be determined.

B. Postprostatectomy Incontinence
VLPP has been extensively used as a research tool in studies on the pathophysiology of
postprostatectomy incontinence. Desautel et al. (30) report their findings in 39 (35 radical, 4
TURP and radiation) patients referred for evaluation of incontinence after prostatectomy.
 Leak Point Pressures 161

Sphincteric damage was found to be the sole cause of urinary incontinence in 23 patients (59%)
and a major contributor in 14 others (36%). Twenty-seven patients (69%) had VLPP
,103 cmH2O (mean ¼ 55) with a urethral urodynamic catheter in place. An additional 10
(26%) had VLPP ,150 cmH2O (mean ¼ 63) upon removal of the catheter. VLPP is suggested
as an indication of the severity of sphincteric damage. The importance of removing the
urodynamic catheter during measurement of the VLPP was emphasized. Bladder dysfunction
characterized by detrusor instability and/or decreased bladder compliance was seen in 15
patients (39%). Thus, in this group of patients, incontinence was mainly due to sphincteric
damage. The severity of incontinence was correlated with VLPP values.
Winters et al. (31) reported similar results in 92 patients with incontinence at least 1 year
after prostatectomy (65 patients [71%] after radical prostatectomy [RP] and 27 patients [29%]
after transurethral resection of the prostate or TURP). Valsalva leak point pressures (VLPP)
were measured in the absence of a bladder contraction at a 150-mL volume and at 50-mL
increments thereafter until maximum functional capacity was reached. The predominant
urodynamic finding was sphincteric incompetence, as VLPPs were obtained in 85 patients (92%)
and ranged from 12 to 120 cmH2O. Detrusor overactivity was a common finding and occurred in
34 patients (37%); however, it was found to be the sole cause of incontinence in only three
patients (3.3%). There was no statistically significant difference in the incidence of sphincteric
incompetence after RP or TURP; however, TURP patients had a higher incidence of detrusor
overactivity, which was statistically significant (P ¼ .019). No correlation was found between
the severity of incontinence (measured by preoperative pad usage) and VLPP. It was concluded
that, although bladder dysfunction may be contributing problem in patients with post-
prostatectomy incontinence, it is rarely the only mechanism for this disorder. Since bladder
dysfunction may coexist or be the sole cause of postprostatectomy incontinence, urodynamic
studies are important to define the exact cause(s) of incontinence after prostatectomy.
Gudziak et al. (32) examined the relationship between maximum urethral pressure, which
was measured at the level of the membranous urethra, or extrinsic urethral sphincter function,
and abdominal leak point pressure in 27 men with postprostatectomy incontinence. No
correlation was found between maximum urethral and abdominal leak point pressures. Extrinsic
urethral sphincter function was normal in all patients, while all patients but one had evidence of
ISD. It is suggested that postprostatectomy stress incontinence is caused by sphincter
dysfunction due to ISD and is not correlated with extrinsic sphincteric function, or maximal
urethral pressure.

C. Urinary Diversion
Leak point pressure was used as part of the evaluation of bilateral hydroureteronephrosis
following ileal conduit urinary diversion by Knapp et al. (33) A conduit urodynamic study was
used to evaluate conduit function with a triple-lumen urodynamic catheter to simultaneously
measure conduit pressure proximal and distal to the fascia during filling under fluoroscopy. In
four control patients with normal upper tracts, conduit leak point pressures ranged from 5 to
20 cmH2O. Abnormalities were found in five of six patients with bilateral hydroureterone-
phrosis. These included functional stomal stenosis in two patients, an atonic loop in one patient,
segmental obstruction in one patient, and a high-pressure, noncompliant distal segment in one
patient. It is concluded that loop urodynamics can serve as a useful tool in the evaluation
of postoperative bilateral hydronephrosis. Leak point pressures were also used to evaluate the
postoperative continence status in women who had undergone modified nerve sparing radical
cystectomy and creation of an ileal orthotopic neobladder (34).
162 Madjar and Appell

Intraoperative use of LPP measurements have been attempted to adjust the continence
mechanism and thus insure adequate continence after cutaneous urinary diversion (35).
Intraoperative LPP was measured before detubularization using a simple standing column
manometer and arterial line tubing. Whenever leakage occurred at pressure ,75 –80 cmH2O,
the continence mechanism was adjusted and LPP measurement was repeated to ensure adequate
continence. Seventy-seven patients participated in the study. Adjustment of the continence
mechanism was required in 32 of the 41 patients in whom the native appendicocolic junction
was used and in all 36 patients in whom the tapered ileum and ileocecal valve were used. After
adjustment, all patients attained leak pressures .80 cmH2O. With a follow-up period of 30– 100
months, all 77 patients were continent on an intermittent catheterization program and none has
required revision of the continence mechanism.
Leak point pressures have been also used to evaluate operative success of incontinent
ileovesicostomies in tetraplegic patients (36). Postoperative urodynamics demonstrated subjects
(n ¼ 7) to have a mean stomal leak point pressure of 7.7 cmH2O (range 5– 10). In follow-up
of 12– 15 months, no patient demonstrated calculus formation, hydronephrosis, autonomic
dysreflexia, or worsening renal function.

V. DETRUSOR LEAK POINT PRESSURE

A. Technique
For DLPP determination, the bladder is first emptied. Bladder filling is performed at 60 mL/min
in adults and at up to 20 mL/min in children. Bladder pressure is measured while the urethral
meatus is observed for leakage. The study is completed once a Pdet of 40 cmH2O is reached,
leakage is observed, a detrusor contraction occurs, or the maximum volume recovered at a few
episodes of intermittent catheterization is reached (37).

B. Clinical Application
In 1981 McGuire et al. (1) reported the clinical progress of 42 myelodysplastic patients studied
urodynamically and followed for a mean of 7.1 years. DLPP was 40 cmH2O or less in 20 patients
and .40 cmH2O in 22 patients. No patient in the low-pressure group had vesicoureteral reflux,
and only two patients showed ureteral dilatation on excretory urography. In contrast, of the
patients in the higher-pressure group 15 (68%) showed vesicoureteral reflux, and 18 (81%)
showed ureteral dilatation on excretory urography. Thus, a striking relationship between
intravesical pressure at the time of urethral leakage and the clinical course in this group of
myelodysplastic patients was demonstrated.
A new modification of the technique used to measure detrusor leak point pressure in
patients with myelodysplasia was later introduced by Combs and Horowitz (38). DLPP is
measured during standard multichannel urodynamics. Once leakage occurs, DLPP is recorded
and the catheter is removed. With the cessation of leakage, the catheter is reinserted and detrusor
pressure is again noted. This cycle is repeated several times, and the average difference is noted.
Fifty-four patients in whom leakage occurred were included in this study. Three groups of
patients were identified: (a) (20 patients)—detrusor leak point pressure .40 and ,40 cmH2O
with the catheter in and out, respectively; (b) (29 patients)—detrusor leak point pressure
consistently ,40 cmH2O with the catheter in and out; and (c) (five patients)—detrusor leak
point pressure consistently .40 cmH2O with the catheter in and out. All patients in group (b) had
normal upper tracts. Although detrusor leak point pressure was .40 cmH2O using standard
measurement techniques in both groups (a) and (c), upper-tract changes were demonstrated in
 Leak Point Pressures 163

40% of patients in group (c) but only in 5% of patients in group (a). This modification is
suggested as a more accurate measurement of DLPP and a better means of identifying patients at
increased risk for renal deterioration. The main critique of this study is the low number of
participants in group (c), making comparison between groups (a) and (c) difficult.
Kim et al. (39) have demonstrated that DLPP of 40 cmH2O is also useful in the case of
transurethral resection of the external sphincter in patients with spinal cord injury and detrusor-
external sphincter-dyssynergia (DSD). DLPP was retrospectively analyzed in 55 spinal cord
injury patients who had undergone transurethral resection of the external sphincter. Patients with
DLPP .40 cmH2O had a significantly higher incidence of upper-tract damage (P ¼ .021) and
persistent DSD (P ¼ .00008). DLPP .40 cmH2O is therefore suggested as a valid indicator of
failure of transurethral resection of the external sphincter procedure.
DLPP has been widely used in other instances as a outcome measure of various operative
procedures to treat neurogenic bladder such as external sphincterotomy (40), external sphincter
dilatation (41), and combination therapy of intermittent catheterization and oral anticholinergic
medications (42).

VI. CONCLUSIONS

Both ALPP and DLPP have been extensively studied. DLPP is a valuable tool in identifying
patients at increased risk for upper-tract deterioration. ALPP is used to determine the severity of
stress urinary incontinence and to categorize patients with stress urinary incontinence into
anatomical and ISD types of incontinence. The clinical value of ALPP will be determined by
standardization of technique and interpretation. Future determination of the need to categorize
patients into ISD and anatomical types of stress urinary incontinence will also have an impact on
the clinical value of ALPP.

REFERENCES

1. McGuire EJ, Woodside JR, Borden TA, Weiss RM. Prognostic value of urodynamic testing in
myelodysplastic patients. J Urol 1981; 126:205.
2. McGuire EJ, Fitzpatrick CC, Wan J, Bloom D, Sanvordenker J, Ritchey M, Gormley EA. Clinical
assessment of urethral sphincter function. J Urol 1993; 150:1452.
3. Stohrer M, Goepel M, Kondo A, Kramer G, Madersbacher H, Millard R, Rossier A, Wyndaele JJ. The
standardization of terminology in neurogenic lower urinary tract dysfunction: with suggestions for
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Urodyn 1999; 18:139.
4. Bump RC, Elser DM, Theofrastous JP, McClish DK. Valsalva leak point pressures in women with
genuine stress incontinence: reproducibility, effect of catheter caliber, and correlations with other
measures of urethral resistance. Continence Program for Women Research Group. Am J Obstet
Gynecol 1995; 173:551.
5. Sultana CJ. Urethral closure pressure and leak-point pressure in incontinent women. Obstet Gynecol
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6. Van Venrooij GE, Blok C, van Riel MP, Coolsaet BL. Relative urethral leakage pressure versus
maximum urethral closure pressure. The reliability of the measurement of urethral competence with
the new tube-foil sleeve catheter in patients. J Urol 1985; 134:592.
7. Hernandez RD, Hurwitz RS, Foote JE, Zimmern PE, Leach GE. Nonsurgical management of
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9. Plevnik S, Vrtacnik P, Janez J. Detection of fluid entry into the urethra by electric impedance
measurement: electric fluid bridge test. Clin Phys Physiol Meas 1983; 4:309.
10. Plevnik S, Brown M, Sutherst JR, Vrtacnik P. Tracking of fluid in urethra by simultaneous electric
impedance measurement at three sites. Urol Int 1983; 38:29.
11. Sutherst J, Brown M. The fluid bridge test for urethral incompetence. A comparison of results in women
with incontinence and women with normal urinary control. Acta Obstet Gynaecol Scand 1983; 62:271.
12. Payne CK, Raz S, Babiarz JW. The Valsalva leak point pressure in evaluation of stress urinary
incontinence. Technical aspects of measurements. J Urol 1994; 151:478 [Abstract].
13. Decter RM, Harpster L. Pitfalls in determination of leak point pressure. J Urol 1992; 148:588.
14. Theofrastous JP, Cundiff GW, Harris RL, Bump RC. The effect of vesical volume on Valsalva leak-
point pressures in women with genuine stress urinary incontinence. Obstet Gynecol 1996; 87:711.
15. Faerber GJ, Vashi AR. Variations in Valsalva leak point pressure with increasing vesical volume.
J Urol 1998; 159:1909.
16. Petrou SP, Kollmorgen TA. Valsalva leak point pressure and bladder volume. Neurourol Urodyn
1998; 17:3.
17. Peschers UM, Jundt K, Dimpfl T. Differences between cough and Valsalva leak-point pressure in
stress incontinent women. Neurourol Urodyn 2000; 19:677.
18. Madjar S, Balzarro M, Appell RA, Tchetgen MB, Nelson D. Baseline abdominal pressure and
Valsalva leak point pressures—correlation with clinical and urodynamic data. Neurourol Urodyn
2003; 22:2–6.
19. McLennan MT, Bent AE. Supine empty stress test as a predictor of low Valsalva leak point pressure.
Neurourol Urodyn 1998; 17:121.
20. Hsu TH, Rackley RR, Appell RA. The supine stress test: a simple method to detect intrinsic urethral
sphincter dysfunction. J Urol 1999; 162:460.
21. Awad SA, Bryniak SR, Lowe PJ, Bruce AW, Twiddy DA. Urethral pressure profile in female stress
incontinence. J Urol 1978; 120:475.
22. Brown M, Wickham JE. The urethral pressure profile. Br J Urol 1969; 41:211.
23. Hilton P, Stanton SL. Urethral pressure measurement by microtransducer: the results in symptom-free
women and in those with genuine stress incontinence. Br J Obstet Gynaecol 1983; 90:919.
24. Bump RC, Coates KW, Cundiff GW, Harris RL, Weidner AC. Diagnosing intrinsic sphincteric
deficiency: comparing urethral closure pressure, urethral axis, and Valsalva leak point pressures. Am J
Obstet Gynaecol 1997; 177:303.
25. Haab F, Zimmern PE, Leach GE. Female stress urinary incontinence due to intrinsic sphincteric
deficiency: recognition and management. J Urol 1996; 156:3.
26. Nitti VW, Combs AJ. Correlation of Valsalva leak point pressure with subjective degree of stress
urinary incontinence in women. J Urol 1996; 155:281.
27. Dietz HP, Herbison P, Clarke B. The predictive value of hypermobility and urethral closure pressure
in the diagnosis of female stress urinary incontinence. Neurourol Urodyn 2001; 20:490.
28. Madjar S, Balzarro M, Appell RA. Urethral hypermobility and intrinsic sphincteric deficiency—
separate entities or coexisting factors in women with stress urinary incontinence. J Urol 2002
[Abstract].
29. Zaragoza MR. Expanded indications for the pubovaginal sling: treatment of type 2 or 3 stress
incontinence. J Urol 1996; 156:1620.
30. Desautel MG, Kapoor R, Badlani GH. Sphincteric incontinence: the primary cause of post-
prostatectomy incontinence in patients with prostate cancer. Neurourol Urodyn 1997; 16:153.
31. Winters JC, Appell RA, Rackley RR. Urodynamic findings in postprostatectomy incontinence.
Neurourol Urodyn 1998; 17:493.
32. Gudziak MR, McGuire EJ, Gormley EA. Urodynamic assessment of urethral sphincter function in
post-prostatectomy incontinence. J Urol 1996; 156:1131.
33. Knapp PM Jr, Konnak JW, McGuire EJ, Savastano JA. Urodynamic evaluation of ileal conduit
function. J Urol 1987; 137:929.
34. Aboseif SR, Borirakchanyavat S, Lue TF, Carroll PR. Continence mechanism of the ileal neobladder
in women: a urodynamics study. World J Urol 1998; 16:400.
 Leak Point Pressures 165

35. Bissada NK, Marshall I. Leak point pressure use for intraoperative adjustment of the continence
mechanism in patients undergoing continent cutaneous urinary diversion. Urology 1998; 52:790.
36. Mutchnik SE, Hinson JL, Nickell KG, Boone TB. Ileovesicostomy as an alternative form of bladder
management in tetraplegic patients. Urology 1997; 49:353.
37. McGuire EJ, Cespedes RD, O’Connell HE. Leak-point pressures. Urol Clin North Am 1996; 23:253.
38. Combs AJ, Horowitz M. A new technique for assessing detrusor leak point pressure in patients with
spina bifida. J Urol 1996; 156:757.
39. Kim YH, Kattan MW, Boone TB. Bladder leak point pressure: the measure for sphincterotomy
success in spinal cord injured patients with external detrusor-sphincter dyssynergia. J Urol 1998;
159:493.
40. Juma S, Mostafavi M, Joseph A. Sphincterotomy: long-term complications and warning signs.
Neurourol Urodyn 1995; 14:33.
41. Park JM, McGuire EJ, Koo HP, Schwartz AC, Garwood CK, Bloom DA. External urethral sphincter
dilation for the management of high risk myelomeningocele: 15-year experience. J Urol 2001;
165:2383.
42. Pannek J, Diederichs W, Botel U. Urodynamically controlled management of spinal cord injury in
children. Neurourol Urodyn 1997; 16:285.
11
Videourodynamics

Jennifer Gruenenfelder and Edward J. McGuire

University of Michigan, Ann Arbor, Michigan, U.S.A.

I. INTRODUCTION

The patient with complaints of urinary incontinence or urinary retention cannot be diagnosed
reliably on the basis of history and physical alone. Urodynamics is an attempt to measure bladder
and urethral function objectively. Videourodynamics adds anatomic detail to these
measurements with the addition of a fluoroscopy unit, which allows real time imaging of
the bladder and urethra during filling and voiding. The information obtained is useful for both
the diagnosis and prognosis of urologic disease.
Urologic disease may result from a number of different etiologies. Neurologic diseases are
associated with bladder and urethral dysfunction, and generalizations can be made about the type
of dysfunction based upon the type of disease and the level of the lesion. These inferences are not
reliable. For example, among patients with spinal cord injury, we assume the following: Cervical
injury is associated with detrusor external sphincter dyssynergia (DESD); thoracic injury is
associated with detrusor hyperreflexia (DH) and DESD; and lumbar and sacral injuries are
associated with detrusor areflexia (DA). Kaplan et al. (1) showed that although these
generalizations are largely true. There are statistically significant numbers of patients with
cervical injury who have DA and patients with sacral injury with DESD. Patients with thoracic
and lumbar lesions had even greater variation in their urodynamic findings in the same study.
This study shows clearly why individual patients require urodynamic testing rather than making
treatment plans based on assumptions about dysfunction from the level of the lesion. Chancellor
et al. (2) showed that even patients with incomplete injuries to the thoracolumbar spine often
have occult neurogenic bladder dysfunction, including 41% of patients with ASIA E impairment
(otherwise completely neurologically intact).
Similarly, one cannot infer bladder dysfunction based on MRI findings of the anatomical
lesion of multiple sclerosis (3). The patterns of dysfunction in patients with neurogenic bladder
dysfunction caused by MS change over time, which means that urodynamics has a role not only
in initial diagnosis but also in managing patients with multiple sclerosis as it progresses (4).
Clearly, urodynamic monitoring is also important for diagnosis and prognosis of the neurogenic
bladder associated with myelodysplasia (5 – 7). It is from this patient population that we have
drawn many of our assumptions about the long-term prognosis of patients with poorly managed
neurogenic bladders.
167
168 Gruenenfelder and McGuire

The use of urodynamics is not limited to investigating the urologic manifestations of

neurologic disease. Its role has been delineated in the diagnosis of diseases of otherwise healthy
patients such as stress incontinence (8,9), benign prostatic hyperplasia (10,11), diabetic
cystopathy (12), vesicoureteral reflux (13,14), and incontinence resulting from surgical or
radiation injury (15 – 18). Thus, videourodynamics is an important tool in the diagnosis and
treatment of patients with a wide range of urological complaints. This chapter will describe the
basics of videourodynamics with some clinical applications to demonstrate its utility.

II. CYSTOMETROGRAM

The cystometrogram (CMG) is a measurement of bladder pressure during filling. A catheter with
a pressure transducer in its tip is placed into the bladder. There are a number of catheters
available. We prefer a triple-lumen catheter with pressure transducers placed to measure the
bladder and urethral pressure simultaneously (19 – 21). A rectal balloon with a pressure
transducer is also placed. The bladder is filled with saline, contrast dye, or carbon dioxide at
variable fill rates. We prefer a liquid infusion because leakage is more obvious and because the
gas can be irritating to the bladder wall (22). Pves is the measure of the bladder pressure during
filling. Pabd is the abdominal pressure measured by the rectal catheter. Pdet is the difference,
Pves –Pabd, and it is thought to be a measure of pure detrusor pressure. Although the subtracted
difference may give a more accurate measurement of pure detrusor function, many investigators
feel that Pves is sufficient clinical information, particularly in patients with high spinal cord
lesions who are unlikely to generate high abdominal pressures (23,24). We fill at a flow rate of
50 cc/min. The rate of filling should be slower in patients with detrusor hyperactivity and in
children.
The patients are asked to note the first sensation and the point at which they would
normally void. Sensation is thus a tool in measuring bladder function. First sensation, first desire
to void, and strong desire to void are reproducible, and there is a normal pattern to them that
likely corresponds with physiology (25). Delayed sensation can be seen in many disease
processes (12,17,26,27). Early sensation may indicate sensory urgency or interstitial cystitis,
although it often occurs simply as an artifact of filling the bladder with solution colder than body
temperature.
Capacity is the volume the patient is able to tolerate before he needs to void. This is
partially a subjective measurement as it also reflects bladder sensation. Typically the awake
bladder capacity is measured, although CMG can also be performed on patients receiving
general anesthesia. Functional bladder capacity is more accurately measured with a careful
voiding diary. Bladder capacity should be estimated prior to performing urodynamics,
particularly in children (28).
Compliance is a measure of the change in pressure as the volume changes, which is
expressed by the equation C ¼ DV/DPdet. Normal bladders have a high compliance; in other
words, they allow storage of a large volume of fluid with minimal changes in pressure. Low-
compliance bladders, in contrast, register large changes in Pdet over small changes in volume.
The expression of a ratio does not give an accurate picture of the change over time, and other
methods such as calculating the slope of the compliance curve or integrating the area under the
curve have been proposed as more methodical means of making the calculation (29). In practice,
most clinicians look at the slope of the detrusor pressure curve during filling (flat vs. steep)
without making formal calculations. Figure 1 demonstrates a study of a patient with low bladder
compliance which was improved with treatment. Low compliance is a marker of disease, and it
prognosticates deterioration of upper tract morphology and diminished renal function (30,31).
 Videourodynamics 169

Figure 1 This study demonstrates changes in compliance. A 60-year-old female with a history of a
radical hysterectomy and radiation for cervical cancer presented to the hospital with bilateral
hydronephrosis and elevated creatinine. A Foley catheter was placed. Her creatinine returned to baseline
values, and the hydronephrosis resolved. (A) Abnormal compliance. She was placed on ditropan,
imipramine, and intermittent self-catheterization. (B) The study done 2 months later; the abnormal
compliance has resolved.

Leak point pressures are another important variable in the CMG. There are two leak point
pressures of clinical significance: detrusor leak point pressure (DLPP), and abdominal leak point
pressure (ALPP). DLPP is the measure of Pdet required to induce leakage across the urethra when
the bladder is the main expulsive force, and it is an important measurement in patients with
neurogenic bladders. ALPP, in contrast, measures the resistance of the urethra to short increases
in Pabd induced by cough or Valsalva maneuvers.
DLPP is an important prognosticator of kidney function. Studies conducted on
myelodysplastic children correlated DLPP with the probability of upper tract damage. It was
shown that patients with DLPP . 40 cmH2O will develop upper tract damage (5,7,31). Thus,
compliance is an important factor, but outlet resistance also contributes to safe bladder function.
170 Gruenenfelder and McGuire

An abnormally compliant bladder that leaks at low pressures is not a dangerous bladder.
Conversely, in patients with poor compliance but high outlet resistance, damage will occur
(5,32). Figure 2 illustrates two examples of patients with neurogenic bladders and different
detrusor leak point pressures. Children who are maintained at low bladder pressures do not
develop upper tract damage, but they may not be continent. Efforts to lower outlet resistance will

Figure 2 These examples compare patients with abnormal compliance and different outlet resistance.
(A, B) A 61-year-old male with a T4 spinal cord injury (SCI) who underwent an ileal loop 38 years prior to
this imaging who sought an undiversion. (A) The image obtained on fluoroscopy. Note the small bladder
size and the open bladder neck. (B) Shows the tracing, which demonstrates a low capacity bladder and
markedly abnormal compliance. His DLPP is 43 cmH2O. In contrast, (C) shows a 46-year-old with a T12
SCI (Asia D) who presented to a urologist complaining of leakage of urine. Initial urodynamics revealed
ISD felt to be of neurological origin. The patient was treated with an artificial urinary sphincter (AUS), and
the reservoir is visible. He subsequently complained of persistent leakage, and this urodynamics study
shows a low volume, poorly compliant bladder with a high DLPP. (D) The tracing.
 Videourodynamics 171

Figure 2 Continued.

result in an improvement in compliance in this neurogenic population (33). These clinical

discoveries are corroborated by laboratory investigations documenting the effects of hydrostatic
pressure in bladder smooth muscle cells (34). Treatments in the neurogenic population should be
aimed at lowering DLPP by increasing capacity, improving compliance, and lowering outlet
resistance.
ALPP is the leak point pressure that measures resistance of the urethra to short increases in
abdominal pressure induced by cough or Valsalva maneuvers. This is the more important
variable in the patient complaining of leakage who does not have underlying neurological
disease. The standardized measurement is obtained by filling the bladder at a medium fill rate to
200 cc. The transducer is placed at a level even with the symphysis, and the patient is asked to
172 Gruenenfelder and McGuire

strain or cough repetitively until leakage is induced (33). ALPPs ,65 cmH2O are indicative of
intrinsic sphincter deficiency. Leakage at pressures 100– 150 cmH2O is more characteristic
of urethral hypermobility, although it helps to verify this with videourodynamics (33). Figure 3
demonstrates each of these conditions. These variables are less helpful in the presence of genital
prolapse, which tends to dissipate the pressure (35). ALPP is also useful to determine the
etiology of postprostatectomy incontinence (16). Figure 4 shows patients with incontinence
following treatment for prostate cancer.
During the course of filling short increases in Pves that may or may not be associated with
leakage are evidence of detrusor instability, also called detrusor hyperreflexia in patients
with known neurological diagnoses. Figure 5 illustrates this condition. Detrusor instability is
the urodynamic manifestation of urge incontinence, although many patients with urge
incontinence will not have urodynamic evidence of detrusor instability (36 – 38). Urge and stress
incontinence cannot be reliably distinguished by history and physical alone (8,39). Patients with
a history of urge incontinence with demonstrable detrusor instability are said to have motor urge
incontinence. If patients are symptomatic but have no evidence of bladder contraction on the
CMG, they are said to have sensory urgency (36).
The patient is asked to void when he feels full. Voiding pressure is measured, and the
flow is recorded in cc/sec. Qmax denotes the highest flow rate recorded in the study. The
normal values for men and women are 20 –25 cc/sec and 25 –30 cc/sec, respectively.
Because bladder pressure and abdominal pressure can be measured simultaneously, it is

Figure 3 These are two examples of the uses of ALPP. (A) Study of a 47-year-old female who complains
of incontinence. The photograph depicts urethral hypermobility and a cystocele. (B) The tracing, and she
does not leak until she reaches a pressure of 144 cmH2O during a cough. In contrast, (C) shows the
videourodynamics of a 55-year-old female who had a bladder suspension 6 years prior subsequently treated
with collagen and carbon particle injections. This photograph illustrates intrinsic sphincter deficiency. She
has an open bladder neck at rest. The carbon particles can still be seen lateral to the urethra. (D) The tracing;
and Pves is 39 cmH2O when she leaks.
 Videourodynamics 173

Figure 3 Continued.

possible to differentiate patients with poor flow caused by bladder outlet obstruction from
patients with poor flow caused by poorly contracting bladders. Free flow studies and
symptomatology are not as reliable measures of BOO. Figure 6 illustrates the urodynamics of
a patient with bladder outlet obstruction (BOO). The most widely used measurement of BOO
is the Abrams-Griffiths nomogram, which plots maximal flow rate against detrusor pressure at
the time of flow. The resulting plot can divide patients into obstructed, nonobstructed, and
equivocal (40). Nomograms for obstruction in women have been published but are not as
widely used or as well validated (41). This discrepancy reflects that women have fewer
174 Gruenenfelder and McGuire

Figure 3 Continued.

pathological conditions that cause obstruction, and indeed prior anti-incontinence surgery is
now the leading cause (42).
The electromyogram (EMG) is recorded during the filling and voiding phases of the
urodynamics procedure. This is a measurement of depolarization of the sphincter muscle
membrane. It can be recorded using either needle electrodes or surface electrodes (anal plug,
vaginal, catheter mounted, or skin patch). The needle electrode perhaps gives more accurate
measurements as it can measure individual motor units; however, needle electrodes are
considerably more uncomfortable for the patient. A baseline measurement of spontaneous
potentials should be recorded. The patient should then be asked to contract the perineal
muscles to record maximal firing potential. EMGs can be used to measure integrity of
perineal innervation, but they are more commonly used to measure the coordination of
voiding (43).
The first phase of voiding should be cessation of the electrical activity of the sphincter.
If the EMG shows an increase in perineal muscle activity at the onset of voiding, the patient
is diagnosed with DESD. These patients are at an increased risk of upper-tract damage from
high voiding pressures (44). Figure 7 illustrates the typical videourodynamics appearance of
DESD. Learned voiding dysfunction (nonneurogenic neurogenic bladder, or Hinman’s
syndrome) is diagnosed when this pattern is seen in a patient with no other neurological
findings (45 –47). DESD patients historically were treated with sphincterotomy, but it has
been shown that they have similar outcomes when treated with intermittent self-
catheterization (ISC) for management of their bladder dysfunction (44). More recently,
urodynamic data following sphincterotomy revealed that these patients often have incomplete
surgeries resulting in persistently elevated bladder pressures, and these elevations can cause
upper-tract damage (48). Patients with learned voiding dysfunction can be treated with ISC or
bladder retraining combined with medications (49).

III. VIDEOURODYNAMICS

Videourodynamics improves upon the information obtained from a CMG with the addition of
fluoroscopy. The bladder is filled with contrast dye during the CMG, and thus information about
 Videourodynamics 175

Figure 4 These are two examples of incontinence following a radical prostatectomy. (A) The first has
the typical open bladder neck of postprostatectomy incontinence, and his leak point pressure is 39 cmH2O.
(B) The second patient has the typical open bladder neck, but a much higher pressure was reached before he
leaked. The image shows that he had a urethral stricture that needed to be treated prior to treatment of his
incontinence from the prostatectomy.
176 Gruenenfelder and McGuire

Figure 5 This is the study of a 37-year-old female recently diagnosed with multiple sclerosis who
complains of urge incontinence and difficulty voiding. (A) Her bladder during filling. The wire above her
bladder in this photograph is a nerve stimulator. The bladder neck opens slightly with each contraction.
(B) The typical tracing of detrusor hyperreflexia.

structure and function can be gleaned during the test. It is important prior to the initiation of the
study, which is more expensive than conventional CMG, to determine if this imaging will yield
additional information. It does have the advantage of minimizing some of the artifacts of
conventional CMG. Anatomic images can be captured on videotape and correlated specifically
with the CMG during filling and voiding. The addition of video is most useful for the assessment
of incontinence, neurogenic bladder, and bladder outlet obstruction. It can also be used in
preparation for reconstructive procedures and to assess reservoirs or augmented bladders. We
 Videourodynamics 177

Figure 6 This 60-year-old male with atrial fibrillation and diabetes presented in urinary retention.
Physical exam revealed a large prostate estimated at 110 g by subsequent ultrasound. Because of the
possibility of diabetic cystopathy causing his retention, urodynamics was performed. (A) A trabeculated
bladder with several diverticula. (B) A maximum pressure of 191 cmH2O when the patient attempted to
void, although no urine flowed from his bladder. He was subsequently treated with an open prostatectomy,
and he now voids to completion.
178 Gruenenfelder and McGuire

Figure 7 This 57-year-old male with multiple sclerosis presented with an inability to void. In this
photograph of the voiding phase, his bladder neck is open, but the contraction of the external sphincter
keeps the urine from passing through the urethra. He has a trabeculated bladder. Voiding pressure is high.

further use videourodynamics to assess ureters prior to reconstruction. What follows is a

description of the methods and uses of videourodynamics.

A. Equipment and Technique

The typical videourodynamics unit consists of a fluoroscopic unit, a television monitor with
videotape capabilities, a multichannel recorder, a system for filling the bladder, and transducers.
Almost any type of fluoroscopy unit can be used, and generally the patient is exposed to less than
a minute of fluoroscopy. Although we have a dedicated fluoroscopic unit in our clinic, the same
information could be obtained from bringing standard CMG equipment to the fluoroscopy suite
of any hospital.
We favor a triple lumen 10F catheter. The most distal port is the largest, and it is used for
infusion of contrast. The next most distal port measures the intravesical pressure, and the third
port measures the pressure at the uretha. The catheter position is checked by fluoroscopy and
verified when the port measuring urethral pressure gives a pressure tracing that is not identical to
the bladder pressure measurements. We then infuse at a fill rate of 50 cc/min.
We do not routinely use a rectal balloon to monitor rectal pressure. We feel that the
addition of this measurement is not helpful. It adds to the stress of the overall test. Rectal
pressure measurements have been advocated as a way of separating increases in abdominal
pressure from detrusor instability, but we feel that the same information can be obtained from
watching the urethral pressure measurements, which are continuous, and from noting if the
bladder neck opens or remains closed and if there is leakage during increases in vesical pressure.
It has also been argued that the use of a rectal catheter allows the clinician to distinguish between
obstructed and unobstructed flow. We feel that the combination of flow rate, the appearance of
 Videourodynamics 179

the bladder neck on video, and the measurement of total pressure is sufficient to make that
diagnosis, as flow characteristics are determined more by urethral resistance than by the source
of pressure, whether it is abdominal straining or elevated detrusor pressure. Similarly, we do not
perform EMG during videourodynamics. It is most useful in the diagnosis of DESD, but we feel
that the appearance of DESD on video combined with the expected elevations of vesical pressure
are sufficient to make this diagnosis.

B. Stress Incontinence
Stress incontinence is a diagnosis clearly aided by the use of videourodynamics. The
classification of incontinence historically relied upon radiographic findings (50,51). Stress
urinary incontinence is currently defined as type 1, 2, or 3, depending on the presence or absence
and degree of urethral and bladder descent (52). Figures 8 –11 illustrate each of these types of
incontinence. Figure 12 illustrates how videourodynamics may help clarify the type of leakage
in an incontinent patient. Fluoroscopy allows for better visualization of a hypermobile urethra
during strain compared to physical exam alone. Patients with significant cystocele and uterine
descensus may have falsely elevated ALPP, which makes a diagnosis of the type of incontinence
by CMG alone more difficult. Reduction of the prolapse manually or with a pessary is helpful to
obtain a more accurate diagnosis, and this is helpful in planning treatment (35). Lack of stress
incontinence symptoms in patients with cystoceles is an unreliable indicator of what their
voiding may be like after surgical repair of the cystocele. It is therefore helpful to characterize
their anatomy with videourodynamics (53). At this point it is unclear what percentage of patients
with no symptoms of stress incontinence will be symptomatic following a repair of the prolapse,
and it is also unclear if performing the videourodynamics with a pessary helps predict that
population. The CARE study is addressing that question, and it is hoped that they will have some
early data by 2004.

C. Vesicoureteral Reflux
Videourodynamics is useful for the determination of vesicoureteral reflux. This has several
implications. The first is in the treatment of children with vesicoureteral reflux and no underlying
neuropathy. Dysfunctional voiding has been implicated both as a cause of vesicoureteral reflux
and a reason that surgery fails to correct it (54). Prospective videourodynamic studies have
shown that patients with bladder instability and reflux managed nonoperatively with
anticholinergics do as well as patients who are treated surgically (14). Thus, determination of
the cause of reflux is important in deciding upon a course of therapy. The second use is in
patients with neurogenic bladders. The presence of reflux has been shown to alter the reliability
of the CMG in examining compliance and capacity (13), which clearly influences treatment
decisions. Figure 13 shows an example of a patient with a neurogenic bladder and reflux. The
elimination of reflux in patients being treated to alter their capacity and compliance has been
shown to be a reliable marker of improvement (55,56).

D. Ureteral Obstruction
Videourodynamics can also be helpful in the measurement of ureteral obstruction. When a
patient presents with hydronephrosis, it must be ascertained if the collecting system is merely
dilated or truly obstructed. Diuresis scintigraphy and the Whitaker test are the two commonest
methods of answering this question. The Whitaker test is performed by through a percutaneous
nephrostomy tube. A pressure transducer is placed in the percutaneous nephrostomy tube and in
180 Gruenenfelder and McGuire

Figure 8 This is an example of type 1 incontinence. (A) The vesical neck closed at rest. (B) The descent,
not more than 2 cm, during stress. She had an ALPP of 125 cmH2O.

the bladder. The renal pelvis is then infused at a rate of 10 cc/min. The difference in pressure
between the bladder and the renal pelvis is calculated. If the difference in pressure is
,13 cmH2O, the system is considered normal. Higher values are consistent with obstruction,
and some investigators differentiate mild, moderate, and severe obstruction based on those
values (57). Although diuresis scintigraphy has the advantage of being less invasive and is thus
 Videourodynamics 181

Figure 9 This figure demonstrates type 2A stress incontinence. (A) The bladder at rest, with the vesical
neck closed and above the inferior margin of the pubic symphysis. (B) During stress the vesical neck and
proximal urethra open and descend .2 cm.
182 Gruenenfelder and McGuire

Figure 10 This patient illustrates type 2B incontinence. (A) A vesical neck closed at rest but located
below the margin of the pubic symphysis. (B) When she coughs or Valsalvas, there is significant descent,
although there does not have to be any descent be classified as type 2B. Pves was 91 cmH2O when she
leaked.
 Videourodynamics 183

Figure 11 This is an examples of type 3 incontinence or intrinsic sphincter deficiency. (A) The bladder
neck open at rest. (B) Leakage during at a leak point pressure ,45 cmH2O.

the preferred first test (58 –61), the Whitaker test offers the advantage of imaging the anatomic
point of obstruction when done with fluoroscopy in addition to giving functional information
about the kidney. Figure 14 illustrates the use of the test. It has also been observed that positional
changes can influence the results of the Whitaker test. Because such positional variations may be
relevant clinically, it is important to consider the Whitaker test in diagnosis for patients with
abnormal anatomy or intermittent symptoms (62).
184 Gruenenfelder and McGuire

Figure 12 A 49-year-old female underwent a total vaginal hysterectomy 2 months prior to this study.
She complained of incontinence. Fluoroscopy revealed extravasation of contrast into the vagina consistent
with a vesicovaginal fistula. The patient had normal compliance and no evidence of urethral hypermobility
or leakage.

Figure 13 This is the bladder of a 22-year-old patient with myelodysplasia who had a small capacity,
trabeculated bladder with poor compliance, reflux, and an open bladder neck at rest. Although the initiation
of anticholinergic therapy corrected the compliance and the reflux, she subsequently required a pubovaginal
sling for her intrinsic sphincter deficiency.
 Videourodynamics 185

Figure 14 (A) The Whitaker test of a 17-year-old male who presented initially with a ureteropelvic
junction obstruction diagnosed after a CT was done for abdominal trauma. He was treated with a
ureterocalicostomy. His hydronephrosis did not improve. Contrast 50 cc was instilled through his
percutaneous nephrostomy tube. Neither the bladder pressure nor the renal pelvis pressure exceeded
10 cmH2O. (B) The Whitaker test of a 34-year-old female patient with myelodysplasia treated initially with
a vesicostomy at birth, followed by an ileal loop at puberty. She subsequently had an undiversion with a
neobladder and an AUS. She was referred because of bilateral hydronephrosis, and her renal scan was
inconclusive. Whitaker test showed rapid appearance of contrast in the bladder; the highest pressure
difference between the bladder and the renal pelvis was 2 cmH2O.
186 Gruenenfelder and McGuire

Figure 15 (A) Study of a 68-year-old female who complained of leakage from her stoma following a
cystectomy with Indiana pouch. Fluoroscopic urodynamics showed that her compliance is normal, but she
has phasic contraction of the bowel segments, during which time she leaked. (B, C) Fluoroscopy images of
a 57-year-old male with a neobladder who presented in urinary retention. Videourodynamics revealed
bilateral reflux, high voiding pressures, and a stricture at the anastamotic ring.
 Videourodynamics 187

Figure 15 Continued.

E. Urinary Diversions
Videourodynamics is useful in the evaluation of patients who have had urinary diversions for
malignancy and for neurogenic bladders. Ileal conduits are the most common incontinent urinary
diversions. It is not unusual to have bilateral hydronephrosis following this procedure, but the
etiology of the dilatation needs to be elucidated. Patients with refluxing ureteral anastamoses
may get chronic dilatation of the urinary tract, but hydronephrosis may also arise from stomal
stenosis, ureteroileal anastamosis, or a poorly compliant loop. Knapp et al. used urodynamics to
study patients with ileal loops and bilateral hydronephrosis compared to patients with normal
upper tracts and ileal loops, and they found significant differences in these patient groups (63).
Urodynamics is also helpful in patients with neobladders performed for diversions in
patients with bladder cancer or neurogenic bladder. It has been used as an investigative tool to
compare the methods of bladder substitution. Lin et al. (64) compared patients with gastric
neobladders to patients with small-bowel or ileocecal substitution. They found greater
incontinence with lower capacity and worse compliance in the gastric neobladders. Thus, we see
that the use of videourodynamics offers a means of comparing new procedures to accepted
standards of care for urinary diversion. Santucci (59) compared orthotopic neobladders to stomal
urinary reservoirs with urodynamics, and this type of comparative analysis is certainly useful in
the preoperative counseling of patients.
Videourodynamics also allows for the post operative assessment of patients who complain
of incontinence or enuresis following diversion, as illustrated in Figure 15. Ordorica (60)
investigated patients with continent colonic urinary reservoirs. Urodynamics allowed the
diagnosis of incompetent outlet or high-pressure intestinal contraction of the reservoir as
treatable causes of intractable incontinence and showed the causes of difficult catheterization
(66,67). El Bahnasawy (62) showed that enuretic patient with orthotopic neobladders had higher
188 Gruenenfelder and McGuire

pressure and postvoid residuals and lower maximum flow and compliance in patients with
incontinence (68). Porru and Usai similarly used urodynamics to evaluate incontinence in their
neobladder patients (69,70). Similarly, videourodynamics enables monitoring of patients with
ileovesicostomy to show that the reservoirs continue to leak at low pressures that are safe for the
upper tracts (71 –73). These studies show that videourodynamics is essential in the diagnosis of
the incontinent or enuretic patient following urinary diversion.

IV. CONCLUSIONS

Videourodynamics combines the functional information obtained with the CMG and flow
studies with the anatomical information that can only be obtained using fluoroscopy. The use of
urodynamics is clearly essential in the diagnosis and long-term follow-up of patients who have
neurogenic bladders. It is also important in the treatment of patients who present with
incontinence either initially or as the consequence of another surgical procedure. A primer of
urodynamics is beyond the scope of this chapter, but we have attempted to show some of the uses
of this valuable tool.

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55. Jakobsen H. Sensitivity of 131I-hippuran diuresis renography and pressure flow study (Whitaker test)
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57. Knapp PM Jr. Urodynamic evaluation of ileal conduit function. J Urol 1987; 137(5):929 –932.
58. Lin DW. Urodynamic evaluation and long-term results of the orthotopic gastric neobladder in men.
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59. Santucci RA. Continence and urodynamic parameters of continent urinary reservoirs:
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65. Rivas DA, Karasick S, Chancellor MB. Cutaneous ileocystostomy (a bladder chimney) for the
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12
Pharmacologic and Surgical Management of
Detrusor Instability
H. Henry Lai, Michael Gross, Timothy B. Boone, and Rodney A. Appell
Baylor College of Medicine, Houston, Texas, U.S.A.

I. INTRODUCTION

Overactive bladder (OAB) is characterized by the urinary symptoms of frequency, urgency, and
urge incontinence as a result of involuntary detrusor contractions during bladder filling. Such
contractions are predominantly under the control of the parasympathetic nervous system.
Acetylcholine released from the parasympathetic nerve endings activates the M3 muscarinic
receptors on the detrusor smooth muscles and modulates bladder contractility. Antimuscarinic
agents inhibit the binding of acetylcholine to the muscarinic receptors and suppress involuntary
detrusor contraction (1). Immediate-release oxybutynin was the gold standard in pharmacologic
treatment of OAB for almost three decades. Its antimuscarinic (M3) activity is nonselective for
the urinary bladder, resulting in significant systemic side effects, particularly dry mouth, that
limit its clinical utility (2,3). Even though alternative routes of administration of oxybutynin,
such as intravesical instillation (4 – 6), intravesical implant (7), and rectal suppository (8), are
available, oral agents remain the mainstay in treatment of OAB. Newer pharmacologic agents,
e.g., tolterodine, and modified drug delivery mechanisms for oxybutynin (e.g., extended-release
oxybutynin) have revolutionized the treatment of OAB (4,5).
New drugs are always compared not only to placebo but also to immediate-release
oxybutynin, because of its long history and established efficacy (6). Originally identified in
the 1960s as a potential treatment for gastrointestinal hypermobility, oxybutynin was found
to be effective in inhibiting involuntary bladder contractions. It is a receptor subtype – specific
antagonist that binds with higher affinity to the M3 muscarinic receptors than to the other
receptor subtypes (M1, M2, M4, and M5). Oxybutynin also has direct spasmolytic (musculo-
tropic) and local anesthetic effects on the detrusor.
Even though the clinical efficacy of immediate-release oxybutynin is well documented,
dose-related antimuscarinic side effects are frequent. Dry mouth is the most common and
bothersome complaint, followed by constipation, blurred vision, dry eyes, urinary retention,
and drowsiness. These systemic side effects occur because oxybutynin is not targeted
specifically to the lower urinary tract. It also inhibits M3 receptors in the salivary glands, which
mediate salivary secretion, and M3 receptors in the intestines, which regulate bowel peristalsis.
Clinically, immediate-release oxybutynin appears more potent in causing dry mouth than in
inhibiting detrusor instability. This adverse effect is often severe enough to cause poor patient
191
192 Lai et al.

compliance, suboptimal dosing, and even drug discontinuation. Only 18 –22% of patients treated
with immediate-release oxybutynin remained on the medication after 6 months due to
intolerable side effects (9,10). Since OAB is a chronic debilitating condition requiring long-term
treatment, it is important that pharmacologic therapy be not only effective but also well
tolerated. The challenge has been to develop antimuscarinic agents that are as effective as
immediate-release oxybutynin but without the side effect loads.

II. TOLTERODINE

Tolterodine (Detrol) was the first drug developed specifically for the treatment of OAB. It is a
competitive muscarinic antagonist that exhibits similar affinities for muscarinic receptor
subtypes M1 –M5. Unlike immediate-release oxybutynin, which is a receptor subtype – specific
agent (for M3), tolterodine may be a more target-specific drug that possesses stronger selectivity
for the urinary bladder than for the salivary glands. In an anesthetized cat model (but only six
cats), tolterodine appeared more potent in inhibiting detrusor instability than salivation. This is
in contrast to immediate-release oxybutynin, which exhibited the opposite tissue-selective
profile (11,12). In a pilot study with healthy volunteers, tolterodine was well tolerated and
exhibited greater objective and subjective antimuscarinic effects on detrusor function than on
salivation (13). However, in another study on the effects on salivary volume, at 2 h following
tolterodine (2 mg) or immediate-release oxybutynin in healthy volunteers, there was less
suppression of salivary volume with immediate-release oxybutynin. However, there was a
complete return to normal by 10 h in the volunteers taking tolterodine, and those taking
immediate-release oxybutynin took longer to regain their respective salivary volume. In
addition, another group taking extended-release oxybutynin (10 mg) had a constant salivary
volume that was only slightly below that of those who were given placebo (14). The precise
mechanism responsible for any bladder-selective property of tolterodine remains to be
elucidated. Whether this is related to the differential affinities of the muscarinic receptors in
salivary glands and those in detrusor muscles for tolterodine and for immediate-release
oxybutynin or its metabolites remains to be confirmed in the human (4).
The recommended dosage of tolterodine is 2 mg BID based on Phase II dose-ranging
studies. No dose adjustment is necessary on the basis of metabolic phenotype (cytochrome P450
“extensive” vs. “poor” metabolizers) (15). Obviously, as the dosage of tolterodine increases,
clinical response improves, but tolerability declines. At a dosage of 2 mg BID, the incidence of
adverse effects, including dry mouth, is similar to that found with placebo, but clinical efficacy is
comparable to that of immediate-release oxybutynin. A lower dose (1 mg BID) results in less
favorable improvements in maximum cystometric capacity and volume at first contraction in
urodynamic tests. A higher dose (4 mg BID) quadruples postvoid residual volume (from 48 mL
to 163 mL) and may increase the risk of urinary retention (15,16). The rate of dry mouth also
approaches 56% at the higher dose (12). Ultimately, the recommended dosage of tolterodine was
set at 2 mg BID with the aim of achieving efficacy similar to that of immediate-release
oxybutynin but without the same side-effect burden. The half-life of tolterodine is 4 h.
Progression to peak therapeutic action is rapid. In Phase I clinical trials with healthy volunteers,
tolterodine exerted a marked inhibitory effect on bladder function within 2 h after a single oral
dose (13,17). However, clinically noticeable decreases in voiding frequency and incontinence
episodes do not occur immediately when behavioral aspects of patients are taken into account.
Modification of voiding habits is a gradual process, and it takes a period of time for the patient to
trust the enhanced control that he or she begins to experience from the medication. Patients
achieve 70% of the maximum effects within 2 weeks of treatment initiation (18,19). Optimal
 Management of Detrusor Instability 193

relief of OAB symptoms is achieved after 8 weeks of treatment (6,18,20). Clinical response
is sustained for at least a year in patients who are compliant and continue to take the medication (8).

A. Tolerability of Tolterodine over Immediate-Release Oxybutynin

The tolerability of tolterodine over immediate-release oxybutynin has been demonstrated by
numerous Phase III clinical trials. Most of these were prospective, randomized, multicenter,
placebo-controlled, parallel-group, double-blind studies that directly compared tolterodine to
immediate-release oxybutynin and placebo in patients who had urodynamically confirmed and/
or clinically significant bladder overactivity (18,21,22). Many of these trials were 12 weeks in
duration and virtually identical in study design, a feature that permitted data pooling and meta-
analysis to include over 1000 patients, increasing statistical power (23,24).
Phase III randomized trials have consistently demonstrated comparable objective and
subjective efficacy between tolterodine and immediate-release oxybutynin. Tolterodine reduced
the micturition frequency by 17 –21%, reduced urge incontinence episodes by 47%, and
increased mean volume per micturition (which is a surrogate measurement of bladder capacity)
by 21– 27% (18,21). Improvements in voiding diary variables were comparable between
patients who were randomized to receive 2 mg BID of tolterodine and those receiving 5 mg
TID a day of immediate-release oxybutynin (see Table 1), with the exception that immediate-
release oxybutynin appeared to more effective in relieving urge urinary incontinence than
tolterodine in one study 71% vs. 47%, respectively (18). These objective improvements in
voiding diary parameters were clinically relevant to the patient, as they translated into subjective
improvements in the patient’s perception of bladder symptoms. When asked to rate their
symptoms on an analog scale, 52% of tolterodine patients reported an improvement in symptom
scores after 12 weeks of treatment, compared with 50% and 39% of patients taking oxybutynin
and placebo, respectively (23).
Despite comparable efficacy at their recommended doses, tolterodine was better tolerated
than immediate-release oxybutynin. Dry mouth was still the most common adverse effect
(18,21,23). However, with tolterodine, there was a lower incidence of dry mouth, and, as
assessed by patients on an analog scale, there was a lower intensity of dry mouth when it
occurred. Half as many patients experienced dry mouth in the tolterodine arm (30 – 50%) as in
the oxybutynin group (69 – 87%). Most patients with dry mouth in the tolterodine arm reported
it to be mild, whereas most patients in the immediate-release oxybutynin group reported it
as moderate or severe (see Table 1). In studies that permitted dose reduction to prevent drug
discontinuation, the frequency and intensity of dry mouth remained higher among patients who
reduced their oxybutynin dosage from 5 mg TID to 2.5 mg TID (due to adverse effects),
compared with those who remained on the regular dose of tolterodine (2 mg BID) (18).
Fewer patients in the tolterodine arm withdrew from the study (6 – 8% vs. 17– 21% in the
oxybutynin arm) or reduced their dosage (7 – 8% vs. 23 –32% in oxybutynin) as a result of
adverse effects (18,21,23). The equivalent clinical efficacy and superior tolerability of
tolterodine compared to immediate-release oxybutynin translate into higher patient compliance
and fewer treatment withdrawals or dosage reductions. Tolterodine overcomes the current
limitations of immediate-release oxybutynin and offers a therapeutic advantage in terms of
improved tolerability. There are suggestions that tolterodine improves overall quality of life
(QOL) as measured by the Medical Outcomes Study 36 (MOS-36) 36-item short-form (SF-36)
instrument of OAB patients to a greater extent than oxybutynin or placebo, even though at this
time, no disease-specific QOL tool has been developed for patients with OAB (25).
In clinical practice, immediate-release oxybutynin is commonly started at a lower initial
dose of 2.5 mg TID and then titrated up to 5 mg TID to achieve a balance between efficacy and
194 Lai et al.

Table 1 Tolterodine (Detrol) Versus Immediate-Release Oxybutynin

Outcome Study Tolterodine Oxybutynin Placebo Comments

Frequency of Abrams et al. (18) 221% 219.5% 210.5% Tolterodine and

micturition Drutz et al. (21) 217% 217% 29% immediate-
Number of urge Abrams et al. 247% 271% 219% release
incontinence Drutz et al. 246% 252% 227% oxybutynin
episodes demonstrated
Volume per Abrams et al. þ27% þ31% þ7% comparable
micturition Drutz et al. þ21% þ34% þ8% efficacy.
Percent of Abrams et al. 89% 97% 81% Tolterodine
patients with Drutz et al. 78% 90% 75% exhibited
side effects Appell et al. (23) 75% 93% 78% tolerability
Percent of Abrams et al. 50% 86% 21% superior to that
patients with Drutz et al. 30% 69% 15% of immediate-
dry mouth Appell et al. 40% 78% 40% release
Percent of Abrams et al. 14% 51% (not reported) oxybutynin.
patients with Drutz et al. 9% 44% (not reported)
moderate to Appell et al. 17% 60% 6%
severe dry
mouth
Percent of Abrams et al. 8% 17% 12%
patients who Drutz et al. 6% 21% 7%
withdrew due Appell et al. 8% 20% 5%
to side effects
Percent of Abrams et al. 8% 32% 2%
patients who Drutz et al. 7% 23% 4%
reduced dosage Appell et al. 9% 32% 4%
due to side
effects

tolerability (26 – 28). A study was therefore performed to compare tolterodine with immediate-
release oxybutynin using an upward titration protocol (started at 2.5 mg, then increased to 5 mg
TID after 2 weeks) in patients .50 years of age to determine whether tolterodine was better
tolerated than immediate-release oxybutynin in that clinical scenario. Not surprisingly, despite
the upward titration strategy, tolterodine still exhibited comparable efficacy and superior
tolerability to those of immediate-release oxybutynin (20).
The long-term tolerability of tolterodine was demonstrated by open-label studies, even
though randomized trials that directly compare long-term adverse effects of tolterodine to those
of immediate-release oxybutynin are lacking. Only 9% and 15% of tolterodine patients withdrew
from open-label studies owing to side effects at 9 months and 12 months, respectively. Another
13% and 23% opted for dose reduction at the end of 9 months and 12 months, respectively
(29,30). This is in contrast to immediate-release oxybutynin; only 18% of OAB patients
remained on this therapy after 6 months owing to intolerable side effects (2,10). Retrospective
analysis of a filled prescription pharmacy database also confirmed that more OAB patients
remained on tolterodine therapy than on immediate-release oxybutynin after 6 months of
treatment (9). A poor response to oxybutynin in the past does not preclude patients from being
able to tolerate long-term treatment with tolterodine. In fact, tolterodine was well tolerated in
 Management of Detrusor Instability 195

89% of patients who had previously found oxybutynin to be unacceptable. There is no evidence
that antimuscarinic side effects worsened over time with long-term use (29).

B. Safety
When clinical trials of tolterodine first began, there was concern over the cardiac safety of the
medication, since it is closely related to terodiline, a drug that was removed from the market in
the 1980s because of concerns over arrhythmias and acute cardiac events. In almost every
tolterodine study, patients were very closely monitored and evaluated with respect to EKG
changes and potential adverse cardiac events. Other than a slight dose-dependent increase in
heart rate (3 –12 beats per minute) (15,31,32), and a corresponding shortening in uncorrected QT
interval, which one would expect from the antimuscarinic activity of tolterodine, no clinically
relevant changes in corrected QT intervals or EKG morphology were apparent (32). No serious
adverse cardiac event attributed directly to tolterodine use has been documented in any of more
than a few dozen well-conducted clinical trials.
Overall, CNS side effects are rare (19,33). Unlike immediate-release oxybutynin and its
major metabolite (N-desethyloxybutynin), which cross the blood-brain barrier and theoretically
may cause CNS adverse effects such as somnolence and cognitive impairment (34), tolterodine
has lower lipophilicity and therefore probably less penetration into the CNS (35,36), but it
must be remembered that tertiary amines all pass through the blood-brain barrier and both
oxybutynin and tolterodine are tertiary amines. Although tolterodine caused fewer disturbances
on quantitative-topographic EEG than oxybutynin in healthy volunteers (37) and the reported
incidence of somnolence in patients treated with immediate-release oxybutynin was 11.9%, in
patients on tolterodine, it was 3.0% (38). This must be taken in the context that clinical problems
have not been demonstrated in patients on extended-release oxybutynin, which may, again,
mean that CNS problems, if any, on oxybutynin may relate to metabolites of oxybutynin and not
the parent compound.
Tolterodine has no deleterious effects on blood pressure or on hematologic or biochemical
laboratory values during long-term treatment (29). It is safe and well tolerated in the elderly over
65 years of age (20,39). No cardiac arrhythmias were noted in a study that exclusively recruited
patients over 65 years of age (39). Although based on limited numbers of subjects, with short
follow-ups, another study found that tolterodine (0.1 mg/kg/d in two divided doses) appeared to
be safe in pediatric meningomyelocele patients with detrusor hyperreflexia (40).

III. EXTENDED-RELEASE OXYBUTYNIN

An extended-release formulation of oxybutynin (Ditropan XL) was released in 1999 (38). This
once-a-day formulation uses a patented oral osmotic (OROS) drug delivery system to slowly
release a controlled amount of oxybutynin into the gastrointestinal tract over a 24-h period.
Physically, extended-release oxybutynin resembles a conventional tablet, but it consists of two
core compartments: a drug layer containing the active ingredient (oxybutynin), and a push layer
containing osmotically active compounds. Both are wholly surrounded by a semipermeable
membrane with a laser-drilled hole on the drug side. Water in the gastrointestinal tract enters
the tablet and mixes with the oxybutynin to form a suspension. Water also enters the push layer
through the semipermeable membrane via osmosis. The push layer expands and pushes the
suspended drug out of the orifice into the gastrointestinal tract for absorption.
Aside from the convenience of once-daily administration, extended-release oxybutynin
eliminates the three times daily peak-to-trough serum concentration fluctuation associated with
196 Lai et al.

immediate-release oxybutynin. Such marked variation in oxybutynin level is thought to contribute

to the intolerable dose-dependent side effects of the drug. Studies with adult volunteers have shown
a smoother peak-to-trough fluctuation of plasma concentration with each dosing of extended-
release oxybutynin. Plasma level rises slowly over 4–6 h and remains fairly constant over the
24-h dosing interval (41,42). Steady-state concentration is reached by day 3 of administration.
In addition, the peak serum concentration of oxybutynin in the extended-release formulation is
2.5 times lower than that of the conventional formulation (41). Lower peak value and more stable
serum concentration are the pharmacokinetic hallmarks of extended-release oxybutynin.
Oxybutynin is metabolized by the cytochrome P450 enzyme system in the liver and the
small intestinal wall (“first-pass” metabolism). The primary metabolite, N-desethyloxybutynin,
is largely responsible for systemic side effects, particularly dry mouth and CNS effects (41 –43).
There is evidence that although oxybutynin and N-desethyloxybutynin have similar effects
on the detrusor, N-desethyloxybutynin is more potent in the salivary glands and causes more
severe dry mouth than the parent compound. Immediate-release oxybutynin, like most other
oral medications, is absorbed primarily in the small intestine and drains into the portal system. It
undergoes extensive first-pass metabolism in the upper gastrointestinal tract, producing high
serum levels of N-desethyloxybutynin, which causes intolerable side effects. In contrast,
extended-release oxybutynin is protected inside a nondisintegrating OROS capsule. It is released
at a steady rate for 24 h, spending only 3 –5 h in the upper gastrointestinal tract. Most of it is
released in the colon, where first-pass metabolism is much less extensive than in the small bowel
(44,45). As a result, first-pass metabolism is proportionally reduced, the serum ratio of
N-desethyloxybutynin to oxybutynin is reduced, and less severe dry mouth may be experienced
(42). This hypothesis is supported by a pilot study that showed that mean bioavailability was
higher for oxybutynin (153%) and lower for N-desethyloxybutynin (69%) in extended-release
oxybutynin than with immediate-release oxybutynin (41).

A. Improved Tolerability over Immediate-Release Oxybutynin

More stable serum concentration together with less first-pass metabolism may explain the
improved tolerability of extended-release oxybutynin over immediate-release oxybutynin.
Extended-release oxybutynin caused less suppression of saliva output and less severe dry mouth
than immediate-release oxybutynin in healthy adult volunteers (41,42). Whereas patients taking
extended-release oxybutynin and immediate-release oxybutynin had similar reductions in urge
incontinence (83% and 76– 87%, respectively) and total incontinence episodes (80 –81% and
75 –86%, respectively), indicating equivalent clinical efficacy (43,46), the incidence and
severity of dry mouth were lower in the extended-release oxybutynin group (see Table 2). Dry
mouth of any severity was reported by 68% and 87% of patients in the extended-release
oxybutynin and immediate-release oxybutynin groups, respectively (P ¼ .04) (43). Moderate or
severe dry mouth occurred in 25% and 46%, respectively (P ¼ .03). Dry mouth was still the
most common side effect of the extended-release formulation (68%), followed by somnolence
(38%), constipation (30%), and blurred vision (28%). With the exception of dry mouth,
extended-release oxybutynin and immediate-release oxybutynin were comparable in terms of
the rates of systemic side effects.
In one open-label study, 7.8% of OAB patients discontinued extended-release oxybutynin
at the end of 12 weeks because of adverse effects (47). Notably, neither the comparative (43,46)
nor the open-label studies (47) had a placebo arm, so the extent of placebo effects cannot be
ascertained. Whether the more favorable side-effect profile of extended-release oxybutynin
translates into higher patient compliance and fewer treatment withdrawals or dosage reductions
remains to be studied in placebo-controlled trials. For patients whose bladder symptoms have
 Management of Detrusor Instability 197

Table 2 Extended-Release Oxybutynin Versus Immediate-Release Oxybutynin

Extended-release Immediate-release
Outcome Study oxybutynin oxybutynin Comments

Number of urge Anderson et al.(43)a 284% 288% Extended-release

incontinence Versi et al.(46) 283% 276% and immediate-
episodes release
Percent of patients Anderson et al. 41% 40% oxybutynin
achieving total demonstrated
continence equivalent
efficacy.
Percent of patients Anderson et al. 87% 94% Extended-release
with side effects oxybutynin is
Percent of patients Anderson et al. 68% 87% better tolerated
with dry mouth Versi et al. 48% 59% than immediate-
Percent of patients Anderson et al. 25% 46% release
with moderate to Versi et al. 4% (at 5 mg/d) 7% (at 5 mg/d) oxybutynin.
severe dry mouth 9% (at 10 mg/d) 26% (at 10 mg/d)
19% (at 15 mg/d) 39% (at 15 mg/d)
40% (at 20 mg/d) 45% (at 20 mg/d)
Percent of patients Anderson et al. 15% 13%
who withdrew Versi et al. 3% 6%
due to side
effects
a
Dosage up to 30 mg/d was allowed in the extended-release randomized arm.

been stabilized on immediate-release oxybutynin, switching to extended-release oxybutynin

reduces the side effects without compromising clinical efficacy (48).
Maximum clinical benefit is achieved by week 4 and is sustained through 12 weeks of
maintenance therapy. The optimal dosage appears to be between 5 and 15 mg daily. In one trial, 70.8%
of participants chose a maintenance dose of 5–15 mg, while 17% used a dose of 25–30 mg daily.
Although the latter doses are higher than the maximum recommended dose, only 5.4% of these patients
discontinued treatment owing to antimuscarinic side effects (47). Up to 30 mg/d of extended-release
oxybutynin has been used safely in controlled studies (43). Extended-release oxybutynin may provide
important therapeutic options for motivated patients who require a higher dose to achieve optimal relief
of OAB symptoms without experiencing excessive side effects (e.g., neurogenic bladder).

B. Safety and Efficacy in the Elderly

Extended-release oxybutynin appears to be safe in the elderly. In a long-term, open-label,
community-based study, there was a very low incidence of CNS side effects, including changes
in mental acuity and memory (49). Over 50% of patients in that community-based study were
over 65 years of age. The drug demonstrated comparable efficacy across all age groups. In a
different open-label study evaluating urge incontinence, nearly equal numbers of patients older
and younger than 65 years achieved complete urinary continence (46). In addition, the rates of
dry mouth were similar. These results are important, since urge urinary incontinence is not only
prevalent among the elderly (affecting 12 –38% over age 60)(50) but is also the second leading
cause of patient admissions to nursing homes (51).
198 Lai et al.

C. Long-Term Tolerability and Compliance

Historically, only 18 – 22% of patients remained on long-term (.6 months) treatment with
immediate-release oxybutynin (9,10), in contrast to the case with extended-release oxybutynin;
60% of patients remained on the latter drug at 12 months, at doses of 15 mg or less (49). Overall
QOL is improved with long-term treatment of extended-release oxybutynin, as sleep disturbance
is reduced and incontinence impact questionnaire scores are lowered. Of patients taking
extended-release oxybutynin, 80% reported that the medication worked well or very well, and
88% were pleased or extremely pleased with the results. Only 16% of patients discontinued
therapy owing to adverse effects over the 12-month study period; the majority of these did so by
3 months.
One prospective, randomized, double-blind, parallel-controlled study directly compared
extended-release oxybutynin (10 mg/d) to tolterodine (2 mg BID) (52). Extended-release
oxybutynin appeared to be more effective than tolterodine in reducing voiding frequency (26.9%
vs. 21.9%), urge incontinence episodes (76.2% vs. 67.6%), and total incontinence episodes
(75.2% vs. 65.6%). The incidence of dry mouth (28.1% with extended-release oxybutynin vs.
33.2% with tolterodine), the severity of dry mouth (moderate to severe: 10.2% vs. 10.9%), and
rates of treatment discontinuation due to side effects (7.6% vs. 7.8%) showed no statistically
significant difference.

IV. EXTENDED-RELEASE TOLTERODINE

An extended-release, once-daily formulation of tolterodine (Detrol LA) is now available (53). It

uses a different extended-release technology from the OROS system. It has been found that
gastric pH may affect the bioavailability of the drug and that if extended-release tolterodine
is taken with antacids, the drug is released too soon, and the effective time of the medication
may be shortened and the tolerability reduced (6). In contrast, the drug metabolism and
bioavailability of extended-release oxybutynin are not affected by dietary intake of antacids.
Pharmacokinetic studies in healthy volunteers suggested that the extended-release formulation
of tolterodine has a smoother peak-to-trough concentration profile than immediate-release
tolterodine (54).
In the largest placebo-controlled study ever conducted in patients with OAB (more than
1500 patients), extended-release tolterodine (4 mg/d) demonstrated efficacy and tolerability
superior to those of immediate-release tolterodine (2 mg BID). Both extended-release and
immediate-release tolterodine significantly reduced number of incontinence episodes, voiding
frequency, and pad use compared to placebo (55). Notably, the extended-release formulation
was reported to be 18% more effective than regular tolterodine in reducing the median number of
incontinence episodes (P , .05). The physiological explanation for improved efficacy is not
clear; the difference may be related to statistical variations induced in the performance of the
analysis. For example, when the same statistics are based on the means rather than the median
reduction of overactive bladder symptoms, there is no statistical difference between extended-
release tolterodine (4 mg/d) and immediate-release tolterodine (2 mg BID).
The most common adverse effect was dry mouth. Aside from this, all other systemic side
effects were seen with similar frequency in the treatment groups and the placebo group. In the
extended-release arm, 23% of patients experienced dry mouth, of whom 1.8% reported severity
that interfered significantly with patient’s usual functioning (55). Patients taking extended-
release tolterodine had a 23% lower incidence of dry mouth than those taking regular tolterodine
(P , .02), even though the rates of drug withdrawal (5%) were similar between the two groups
 Management of Detrusor Instability 199

at the end of 12 weeks. Extended-release tolterodine was reported to be more effective in

reducing urge incontinence and better tolerated than the immediate-release formulation.
Head-to-head comparative studies between extended-release tolterodine and extended-
release oxybutynin are under way but have yet to be published. Both extended-release
tolterodine and extended-release oxybutynin offer therapeutic advantages over immediate-
release forms of these drugs, but it remains uncertain if either drug is better than the other in
terms of efficacy, tolerability, and compliance.

V. SURGICAL MANAGEMENT FOR DETRUSOR INSTABILITY

When medical therapy fails, surgical intervention from electrical stimulation done as an office
procedure to extensive procedures like augmentation or urinary diversion may be needed.
Any surgical intervention should be tailored to the patient with consideration of the degree of
his/her discomfort, underlying pathology, general health, and, obviously, the patient’s own
motivation.

A. Hydrodistension
Hydrodistension for irritative bladder symptoms was introduced in 1930 and was shown to
reduce pain, urgency, frequency, and to increase bladder capacity (56,57). The mechanism of
action is unclear. It has been suggested that hydrodistension leads to ischemic or mechanical
damage to submucosal nerve plexuses and stretch receptors thus leading to attenuation of pain,
frequency, and increase in bladder volume (58). This theory has been supported by axonal
degeneration seen in animal bladders after hydrodistension (59). Other suggested theories are
reduced proliferation rate of urothelial cells, reduced epidermal growth factors, and increased
urinary antiproliferative growth factor (59,60). A defect in bladder surface mucin may exist in
patients with interstitial cystitis in comparison to controls (61). In vitro and in vivo studies have
demonstrated that hydrodistension leads to increased urothelial excretion of substances such as
heparin-binding epidermal growth factor and glycoprotein-51 component of bladder surface
mucin and decreased excretion of antiproliferative growth factors (62).
Even though hydrodistension is a commonly used procedure, the best regimen and the
optimal frequency of treatments are still unknown. Two techniques that are used are the simple
hydraulic filling and the Helmstein intravesical balloon hydrodistension (63). In most cases
hydrodistension is done under regional or general anesthesia. In the simple hydraulic procedure
the bladder is filled with either sterile water or saline at 80 cmH2O until filling stops or until there
is leakage around the cystoscope. The bladder is drained after a few minutes. Some physicians
drain the bladder and refill it two or three times (62). For the Helmstein intravesical balloon
hydrodistension, the patient is under regional anesthesia. A catheter with a pressure transducer is
inserted into the bladder and the patient is taken to the recovery room. The intravesical pressure
is monitored for 3 h, and whenever the pressure goes below the midsystolic diastolic pressure,
more saline is applied to the catheter’s balloon. This procedure is especially useful for low-
capacity bladders. Most patients will require repeated procedures. The method of treatment and
the definitions of response are not standardized, and the therapeutic efficacy of hydrodistension
is therefore difficult to evaluate, but the reported success rates range from 18% to 77%.
Complications range from 5% to 10% with hematuria, dysuria, urinary retention, and bladder
perforation being the most common (62,64 –66). The degree and duration of relief that will be
obtained in a given patient are unpredictable, but in most cases the procedure offers only a
temporary relief.
200 Lai et al.

B. Ingelman-Sundberg Bladder Denervation Technique

Ingelman-Sunderg reported his transvaginal peripheral bladder denervation in 1959 (67). In his
preliminary series he studied 32 women with detrusor instability, and reported an 88% success
rate and a 70% cure rate. The procedure is considered to be most efficacious for patients with
detrusor instability. Patients with neurogenic bladders, poor compliance, and interstitial cystitis
gain less from the procedure. The assumption is that the procedure causes partial sensory
denervation of the trigonal area. The original procedure required extensive dissection of the
cervix and the bladder pedicals bilaterally with dissection of terminal pelvic nerve branches.
Since then the procedure has been modified with dissection limited to the bladder neck and the
subtrigonal area. Use of transvaginal local anesthesia in order to predict therapeutic outcome has
achieved favorable results (68). Transvaginal local anesthesia may be achieved with 5– 15 cc of
0.25% bupivacaine injected in the undersurface of the trigone. Resolution of symptoms for
several hours indicates that the patient may benefit from the procedure.
The procedure is performed under local or regional anesthesia. The patient is put in
lithotomy position, and a Foley catheter is inserted. The subtrigonal area is infiltrated with
normal saline, and an inverted U-shaped incision is made over the anterior vaginal wall with the
apex slightly proximal to the bladder neck. The vaginal mucosa and the pubocervical fascia are
transected off the underlying surface of the bladder. The transection at this level causes partial
denervation of the bladder. The vaginal flap is closed, and a vaginal pack is left for a few hours.
The operation can be performed in 15– 30 min and may be done in an outpatient setting. Other
studies that employed the Ingelman-Sundberg technique showed long-term success rates of
50 –72% (69,70). Cespedes et al., selecting patients according to their response to transvaginal
local anesthesia, demonstrated a cure rate of 64% (68). Cure was regarded as complete resolu-
tion of urge incontinence (UI). About 70% of these women still required some medications
after the procedure. In 34% there was only temporary or no response. The most frequent
complication after the procedure was urinary retention that was self-limited.

C. Transvesical Phenol Injections

Subtrigonal injections of 6% phenol for the treatment of bladder instability were reported in
1969 (71). Injection of these materials causes neurolysis of terminal pelvic nerve branches as
they enter the trigone. Approximately 10 – 20 cc of the material is injected through a cystoscope
in the submucosal level, bilaterally half-way between the bladder neck and each ureteral orifice.
The procedure requires either general or regional anesthesia. This treatment modality has
yielded mixed results, with some investigators reporting success rates as high as 82 –90%
(72,73) while others report poor success rates of 14 – 19% (74 – 76). Some studies attempted to
identify subcategories of patients who were most likely to benefit from this procedure. Blackford
et al. reported a success rate of 82% in women over the age of 55 years and ,14% in women
younger than that (72). In other studies patients with multiple sclerosis appeared to benefit most
from this procedure (72,77). To improve patient selection Madjar et al. used a transvaginal
bupivacaine injection (0.25%) on the assumption that patients who respond to the local
anesthetic will later respond to the subtrigonal phenol injection. In their study 23 of 42 patients
(54.7%) responded to the bupivacaine injection. Of all the patients who responded to the phenol
injections, 26% had symptomatic relief that lasted .3 months. In most cases relief of symptoms
is temporary and lasts from a few weeks to several months. Severe complications, such as
vesicovaginal fistulas, excoriation of the vaginal wall, and even the need for urinary diversion,
were reported in 25– 40% in two series (73,78). However, in these patients the phenol was mixed
in a nonaqueous, glycerol solution which retained the phenol in the perivesical fat for a longer
 Management of Detrusor Instability 201

period of time. Because of the high complication rate, many physicians consider previous pelvic
surgery or pelvic irradiation to be contraindications for this treatment. The high risk for
impotence in males is also a relative contraindication for injection.

D. Cystolysis
The theory underlying cystolysis is that adverse effects can be avoided by affecting only the
terminal nerve fibers entering the bladder. The technique of cystolysis is to divide the superior
vesical vessels and the ascending branches of the inferior vesical vessels in the posterior aspect
of the bladder. The dissection is made down to the level of the trigone. Hunner in 1918 described
a procedure of freeing the bladder from its surrounding tissue in order to alleviate irritative
symptoms. He reported long-term success of 73% in 19 patients who underwent the procedure.
These results were not reproduced in other studies that followed. Worth et al. reported that of
10 patients who had cystolysis, three were cured while the other seven had partial or no
improvement (79). A 7-year follow-up showed that the three patients who were cured had no
further symptoms (80). The procedure has been performed laparoscopically with similar results
(81). Albers et al. reported long-term follow-up in 11 patients of whom one was cured, four had a
partial response, and seven did not respond at all (82). Because there is disruption of sensory and
motor fibers during the procedure, most patients lose some of their detrusor contraction ability,
and in the Freiha report all patients augmented their detrusor contraction by straining after the
procedure (83). Because of the inconsistent results, cystolysis is rarely employed at this time.

E. Percutaneous Neuromodulation
Electrical stimulation (ES) for the treatment of urinary incontinence has evolved over the past 40
years. In 1963 Caldwell experimented with implantation of an electrode in the periurethral area
with the result that 50% of patients were cured or improved of their incontinence (84,85). Since
then, various techniques have emerged but the response rate has not changed significantly.
Although the mechanism of action of ES has been investigated in animal models, the mechanism
of action remains unclear in humans. Several theories have been proposed to explain the effect
of ES.
1. More than 100 years ago Griffith demonstrated relaxation of detrusor muscle in response
to activation of the pudendal nerve (86). In humans it was shown that sensory input through the
pudendal nerve inhibits detrusor activity (87). Thus, pudendal nerve stimulation and enhancement
of external sphincter tone may serve to control bladder overactivity and facilitate urine storage.
2. Stimulation of afferent sacral nerves in either the pelvis or lower extremities increases
the inhibitory stimuli to the efferent pelvic nerve and reduces detrusor contractility (88). The
assumption is that at low bladder volumes there is stimulation of the hypogastric nerve through
activation of sympathetic fibers, and at maximal bladder volume direct stimulation of the
pudendal nerve nuclei in the spinal cord. Another theory is that there is supraspinal inhibition of
the detrusor (89 –91).
3. The bladder responds to neural stimulation initially with rapid contraction followed by
slow, longer-lasting relaxation. With recurrent, repetitive stimuli there are decay and
downregulation of the bladder’s response, thus reducing the detrusor’s over activity.

F. The Stoller Afferent Nerve Stimulator

The Stoller afferent nerve stimulator (SANS; UroSurge, Coralville, IA) utilizes the peroneal
nerve for transcutaneous access to the S3 spinal cord region. Originally, McGuire reported the
202 Lai et al.

first study with ES of the posterior tibial nerve on 1983 (92). Of 22 patients with UI, 55% were
cured and 32% improved.
Peripheral nerve stimulation is performed by insertion of a 34-gauge needle three
fingerbreadths (4 cm) cephalad to the medial malleolus. The needle is advanced at a 308 angle
toward the ankle. A ground electrogram pad is placed on the same side, and the needle is
connected to the SANS device, a 9-V AC monopolar generator. Pudendal nerve reflex
stimulation at the frequency of 35– 40 Hz improves reinnervation and conversion of fast-twitch
into slow-twitch fibers. Stimulation of the detrusor muscle by 2 –10 Hz leads to reflex inhibition.
The SANS device is programmed to utilize both of these effects by generating a stimulus at the
frequency of 20 Hz. The stimulation is 0.5 –10 mA with a fixed pulse length of 200 msec. Proper
stimulation is recognized by great toe flexion or by fanning or flexion of the other digits.
In most cases the stimulation is applied for 30 min with repeated sessions that vary in
different protocols. Klingler et al. (93) with a protocol of treatments four times a week for 12
weeks in a group of 15 patients (11 women, four men) with a mean follow-up of 10.9 months
demonstrated reduction in pelvic discomfort in all patients. On the basis of patient complaints of
urgency and frequency, 46.7% of patients were defined as cured, 20% as improved, and 33.3%
as nonresponders. Urodynamic evidence of bladder instability was eliminated in 76.9%. In all
patients maximal capacity of the bladder was increased, and there was an increase in the volume
associated with first sensation and first desire to void. There was a statistically significant
difference in the daytime and nighttime frequencies before and after the treatment (P ¼ .002).
Patients with prolonged a history of interstitial cystitis and those with a structural abnormality in
the bladder wall did not seem to benefit from the treatment. No side effects or complications
were observed except transient hematomas at the puncture site.
Govier et al. (94) used the same SANS device on a group of 53 patients. More than 90% of
the patients were women. Needle placement, amperage, stimulus frequency, and stimulus
duration were the same as in the previous study. The treatment protocol was for 12 weekly
sessions of 30 min duration each. Eighty-nine percent of participants completed the 12-week
study. Of the 53 patients, 71% were either cured or improved and were started on a long-term
treatment. The patients had on average a 25% reduction in mean daytime and 21% reduction of
mean nighttime frequency, with a 35% reduction of average UI events. There was a statistically
significant improvement in the QOL and pain measurement indexes. Three adverse events were
noted: throbbing pain in the puncture site, right foot pain, and stomach discomfort. During the
study one patient was found to have cardiomyopathy, but it was not believed to be related to
the percutaneous procedure. The effect of the SANS device lasted after cessation of the initial
stimulation session. Proper selection of the stimulation site is very simple, and some suggest that
the patients themselves can perform future stimulations. The SANS was approved by the FDA in
February 2001.

G. Sacral Neuromodulation
Sacral nerve stimulation stemmed from research focusing on the effect of the voiding reflex, the
influence of sacral nerves on the voiding pattern, and central inhibitory control on micturition
(95,96). It is thought that sacral nerve stimulation induces a reflex inhibitory effect on the
detrusor through afferent and efferent fibers in the sacral nerves (97). As previously stated the
first attempt of neuromodulation through sacral ES was carried out in the 1960s by Caldwell
(95). About two decades later the technique has gained popularity for various lower urinary
tract dysfunctions, and especially for uninhibited bladder contractions (98–101). All candidates
are evaluated for response to sacral nerve stimulation. The goal of the first stage is to identify
a percutaneous localization of the sacral nerve, which provides the best neuroanatomical response.
 Management of Detrusor Instability 203

To localize the S3 foramen the sacral area needs to be sterilely prepared and draped. The
sciatic notches can be palpated either uni- or bilaterally. The S3 foramen can be found one finger
off the midline at the level of the sciatic notch. Local anesthetic is injected into the skin and the
subcutaneous fat with a 2-inch 22-gauge needle all the way down to the sacrum. Injection of the
local anesthetic to the foramina canal does not cause loss of motor response. Probing the relevant
area with a 21-gauge needle identifies the foramen. Once the foramen is identified, the margins
of the opening needs to be outlined. The nerve passes at the superior medial aspect of the
foramen (97). The response is indicated by flexion of the ipsilateral great toe and contraction of
the levator ani muscles. To facilitate the recognition of the stimulatory effect, two electrodes can
be positioned in the urethra and the anal canal. These electrodes record excitation of the external
urethral sphincter and the pelvic floor, respectively. Later, the electrode is firmly secured and a
trial of continuous stimulation is undertaken for a period of 3– 7 days. During this time the
stimuli are 210 msec, frequency 10 Hz, and amplitude ranging from 0.5 to 10 V, self-managed
and adjusted by the patient. Patients who respond favorably and demonstrate a 50% reduction in
their incontinent episodes are candidates for surgical implantation of the stimulator.
A prospective multicenter randomized study was carried out from December 1993 to
September 1999 utilizing the InterStim System (Medtronic Inc., Minneapolis, MN) (102). A
group of 96 patients (85 females, 11 males) were evaluated with an average follow-up time of
30.8 months. Baseline assessment included (a) medical and urological history, (b) urodynamic
testing, and (c) a 3-day voiding diary. Patients’ voiding diaries served as the primary outcome
measure. Seventeen of the 96 patients did not benefit from the device, and in 11 of them the
device was explanted. Twenty-six patients were defined as cured and had no episodes of UI.
Thirty-six had a significant improvement. With the average follow-up of 30.8 months, there
were a statistically significant reduction of leaking episodes, a decrease in the severity of the
leaking episodes, and a decrease in use of diapers or other absorbent pads (P , .0001).
Concomitantly, statistically significant effects were an increase in average volume per
void, an increase in maximal voided volume, improved urine stream, improved sensation of
“emptying” postvoid, decreased number of voids per day, and reduced pelvic discomfort. The
majority of patients who had a successful clinical outcome at 6 months demonstrated a sustained
beneficial effect later on. Adverse effects were pain at the pulse generator site that in most cases
was because of interference with a bony structure or belt line, infection, pain at lead site, and
lead migration. Baseline demographic parameters including age and gender were not predictive
of clinical outcome. While these results are encouraging, it should be emphasized that 50% of
patients do not respond to the test stimulation. Seventeen percent to 20% of those who initially
have a favorable response will proceed with implantation later, but will not benefit from the
device, and some of them will require an additional procedure to remove the stimulator. All in
all, about one-third of patients will have a long-term response to the treatment.

H. Detrusor Myectomy
Spontaneously formed bladder diverticuli are seen frequently in patients with neurogenic bladders
and in patients with long standing bladder outlet obstruction. The observation of this phenomenon
led Cartwright and Snow in 1989 to suggest deliberate removal of the detrusor muscle in order to
create a wide-mouthed iatrogenic diverticulum (103,104). The goal of the procedure is to increase
bladder capacity, reduce bladder storage pressure, attenuate the amplitude of the uninhibited
bladder contractions, and thus reduce episodes of urinary urgency, urge incontinence, and
frequency. The procedure was termed “autoaugmentation” in contrast to “augmentation,” which
applied to use of gastrointestinal tissue to augment the bladder. Autoaugmentation was designed to
avoid the inherent problems encountered when applying small or large bowel to the genitourinary
204 Lai et al.

tract. The procedure is performed under general or regional anesthesia, and the bladder is
exposed extraperitoneally after filling by gravity via a transurethral catheter. Indigo Carmine or
Methylene Blue mixed with saline may improve the view and aid in defining the dissection
level. The peritoneum is displaced cephalad, and 25% of the detrusor muscle at the bladder’s
dome is removed by blunt and sharp dissection, exposing the underlying bulging urothelium.
Cartwright recommends doing this part of the dissection with a two-channel urodynamic catheter
to ensure a 30–50% increase in the bladder’s volume under 20–40 cmH2O. Mucosal tears may be
repaired by figure of eight 6/0 absorbable sutures. The raised detrusor flaps may be anchored to the
psoas muscle, although they are more often than not resected (105–108).
Swami et al. (107) recommended making a small peritoneal incision so that the great
omentum may be pulled over and attached to the bladder’s anterior wall to prevent inflammatory
reaction and fibrosis. In their experience, patients who had an omental flap had less perivesical
fibrosis if another intervention was required, whereas patients who had no omental flap were
found to have the mucosa firmly adherent to the retropubic area when undergoing a subsequent
procedure. Other techniques employ demucosalized, colonic, gastric, and sigmoid tissue to cover
the urothelial diverticulum (109–111). Some physicians prefer not to cover the myectomized area,
assuming the procedure will reduce overall compliance (106). After the procedure a catheter is left
in place for 2–7 days. Before removal of the catheter a cystogram is performed. Cartwright (103)
recommends periodically distending the bladder 1 week after the procedure in order to prevent
contraction. However, most recent studies have not employed this technique. After removal of
the catheter the patient is instructed to do timed voiding, and postvoid residuals are checked. If
the patient is unable to void, he or she is instructed to perform clean intermittent catheterization
(CIC) q3h during the day and q4h at night. Although satisfactory results have been achieved with
laparoscopic autoaugmentation, only a limited number of patients have undergone the procedure
(112–114). Autoaugmentation may be appropriate for patients with moderately reduced bladder
capacity in need of a bladder augmentation no more than 50% of their original volume. The
reported success rates of the procedure reach 80% (105,107,115). Swami et al. (107) reported an
overall success rate of 63%, with a 70% success rate for patients with idiopathic instability and a
50% success rate for those with neuropathic instability. These results are inferior to the results
obtained by enterocystoplasty; however, the morbidity and complication rates are lower. Leng et al.
(108) compared the outcomes of two groups, 32 who had enterocystoplasty and 37 who had
detrusor myectomy, and concluded that these two techniques offered comparable results.
However, the enterocystoplasty group had a better outcome and needed fewer revisions than
the myectomy group. The complications rate in the enterocystoplasty group and the detrusor
myectomy group were 20% and 3%, respectively. Leng et al. (108) emphasized that detrusor
myectomy had minimal morbidity and did not preclude subsequent bowel augmentation if
subsequently required. Complications reported after autoaugmentation are urinary retention and
bladder perforation. Urinary retention requiring CIC is observed in ,15% of patients with no
underlying urological deficit (107). The risk for bladder perforation is higher in patients who are
required to perform CIC, especially in the early postoperative period.

I. Enterocystoplasty
The favorite, and still most commonly used technique for increasing bladder capacity and
compliance is the enterocystoplasty. Goodwin introduced enterocystoplasty in 1958 (116). The
goal of enterocystoplasty is to create a reservoir that will maintain low pressure and thus
prevent upper urinary tract deterioration. The low-pressure compliant system buffers the increase
in intravesical pressure secondary to uninhibited contractions and ameliorates the sensation of
urgency. Comorbidities such as vesicoureteral reflux and bladder outlet incompetence may be
 Management of Detrusor Instability 205

treated concomitantly. The augmented bladder should hold sufficient volume to be comfor-
table for at least 4 h. On the other hand, the augmentation should be to a volume that will enable
adequate drainage of the bladder. The augmentation creates a spherical shape, so the bladder’s
volume is determined by its radius according to the formula V ¼ 4/3R3. This formula can be
employed when calculating the additional volume that is needed for augmenting the bladder and
the length of bowel that is required (117). Various segments of bowel may be used for entero-
cystoplasty. Each segment of bowel has its own advantages and disadvantages. No matter which
segment of bowel is chosen for the enterocystoplasty, several key points need to be remembered:
1. The chosen segment of bowel needs to be detubularized.
2. No nonabsorbable sutures should be applied to the intraluminal surface of the augment.
3. The segment of bowel chosen needs to have a sufficient mesentery to reach the true
pelvis and be sewn to the bladder which has been divided either sagitally or
transversely (118,119).
4. When the procedure is concluded, a cystostomy tube should be left through the wall of
the native bladder and a drain should be left near the anastomotic site.

1. Choice of Bowel Segments

a. Ileum. When ileum is chosen, a segment 15 cm proximal to the ileocecal valve is
isolated. The total segment needs to be 20– 40 cm long and may be formed into a U-shaped
patch after it is detubularized. If a larger augmentation is needed the patch can be formed into
an “S” or W-shaped patch. The configuration of the ileum to the desired shape may be achieved
by a running 3-0 absorbable suture or by using absorbable staples. The patch is anastamosed
to the bladder with a 3-0 running absorbable suture.
b. Cecum. Cecocystoplasties have been performed since the early 1950s. In the last
decade they were replaced by either ileocystoplasty or ileocecocystoplasty. In ileocecocysto-
plasty a segment of ileum and cecum of equivalent length are mobilized and transected. After
detubularization through the ileocecal valve, the bowel is anastamosed to itself and then as a
patch on the bivalved bladder. In the Mainz ileocecocystoplasty a segment of ileum twice the
length of the cecum is isolated and anastamosed to itself in a U-shape and later to the cecum to
create a bigger patch. If needed, a tubularized segment of ileum may be kept as a chimney
serving for reanastomosis of the ureters.
c. Sigmoid. Sigmoidcystoplasty is employed most often in cases in which the
mesentery of the small bowel is too short and makes the anastomosis to the bivalved bladder
impossible. A 15 to 20-cm length of sigmoid colon is mobilized and resected. The sigmoid is
opened on its antimesenteric side and is formed to either a U-shape or an S-shape. Another
technique is to close the two ends of the resected sigmoid and to open the antimesenteric side and
then anastomose it to the bivalved bladder (120).
d. Stomach. Two techniques are available for performing gastrocystoplasty. The first is
to use the antrum with the blood supply of the left gastroepiploic artery. The gastric pedicle is
passed through a window in the transverse mesocolon and mesentery of the distal ileum. The
stomach is reanstomosed by a Billroth I gastroduodenostomy. The second technique is to use the
gastric body which is mobilized on either the right or left gastroepiploic vessels. A segment of
10 –20 cm of the greater curvature is mobilized and transected in a wedge shape that should not
reach the lesser curvature in order to avoid injury to the vagus nerve. Because of the abundance
of acid-secreting cells in the stomach, patients who undergo a gastrocystoplasty are more likely
to suffer later with dysuria and other irritative symptoms.
In most cases the bowel patch can be anastamosed to a bivalved bladder. In certain
instances, when the major complaint is pelvic pain associated with interstitial cystitis, some
206 Lai et al.

physicians perform a supratrigonal cystectomy. It has been reported that leaving the trigone
results in persistent complaints of pelvic discomfort (121). It should be noted, however, that
in some patients, complaints persisted even after complete cystectomy (122). Success rates of
enterocystoplasty vary considerably and range from 25% to 95% (118,119,122– 127). The wide
range reflects the fact in many series a number of the patients who were treated had interstitial
cystitis. These patients, as a rule, gained less from the procedure. Another reason for the wide
discrepancy is the inconsistency in defining and measuring success. In some of the studies
success rates vary considerably depending on the authors’ definitions of success and the patients’
view of the outcome (126). The complication rate after enterocystoplasty may be considerable.
Flood et al. (127) report of 116 patients with early and late complication rates of 22% and
44%, respectively, and found the following:

2. Early Complications
Bowel obstruction—prolonged ileus after entercystoplasty—is infrequent and occurs in 3% of
patients. In other reports in which prolonged ileus was regarded as .5 days, 10% of the patients
had prolonged ileus. However, at least some of these patients had some neurologic deficiency
(128). The segment of bowel that is used does not impact the duration of the ileus.
Fistula—may occur in 15% of patients. The most common site for leakage is the
anastomotic suture line between the bladder and the augment. Other possible sites may be the
suprapubic tube puncture site and the urethra in cases of concomitant sphincteric weakness. In
most cases the leakage ceases by itself with proper drainage. Only 1– 2% require an additional
procedure to obliterate the fistula (127).
Wound infection—as with other clean contaminated procedures, the wound infection rate
is 3 –5%.

3. Late Complications
Diarrhea and bowel dysfunction may develop in 10– 16% of patients after enterocystoplasty.
Patients may complain of increased bowel frequency and fecal incontinence. The removal of the
ileocecal valve is likely to cause diarrhea and may decrease transit time along the
gastrointestinal tract and cause bacterial backflow into the ileum and malabsorbtion of fat, B12,
and bile salts (129,130). Because vitamin B12 is absorbed exclusively in the ileum, resection of
the distal ileum may result in B12 deficiency, and subsequent megaloblastic anemia and
neurologic impairment. Therefore, the use of the distal 10– 20 cm of the ileum should be
avoided, if possible. Because body stores of B12 are significant, deficiency may not be apparent
for as long as 5 years. B12 levels should be monitored, and supplements should be given to
ileocystoplasty patients if levels decline.
Bladder compliance following augmentation should be monitored because even
detubularized segments of colon and ileum may cause peristaltic contractions and raise the
bladder pressure to .40 cmH2O (131). Colonic segments are more prone than small bowel to
cause significant contractions (132).
Other metabolic alterations may also occur. In patients who undergo enterocystoplasty,
acid is reabsorbed from the urine by the intestinal segments, which results in increased
chloride and decreased bicarbonate in the serum (133). In patients with normal renal function,
frank acidosis does not occur, but a continuous loss of bony buffers may lead to bone
demineralization (134). Bicarbonate supplementions may be required. Use of gastric segments
may cause hypokalemic hypochloremic metabolic alkalosis but may be the only option for
patients with renal deficiency (135). Another unique side effect associated with use of gastric
mucosa is the hematuria dysuria syndrome. The syndrome may affect up to 35% of the patients.
H2 blockers and hydrogen ion pump blockers may attenuate such symptoms.
 Management of Detrusor Instability 207

Increased risk of adenocarcinoma in the urinary tract was observed in ureterosigmoido-

stomies. The teratogenic compound is thought to be made up of nitrosocompounds that
result from the mixture of feces and urine. Nitrosocompounds are also observed in bladder
substitutions and bladder augmentations. Another factor that can increase production of nitro-
socompounds is the inflammatory reaction at the anastomotic site that produces cellular
proliferation and increased formation of free radicals. Tumor development occurs regardless of
the segment of bowel utilized (136 –138). There is a latency period until bladder neoplasms
develop; therefore annual surveillance with cytology and/or cystoscopy should start 5– 10 years
after formation of the augmentation.
Bladder and kidney calculi formation of bladder stones occurs in 8–50% (137,138). Most
stones are struvite and are the result of inadequate bladder drainage, retention of mucus, and
infection associated with urea-splitting organisms. Struvite stones have not been noted in
gastrocystoplasties. Formation of stones may be decreased by proper bladder emptying, adequate
bladder irrigation, and eradication of urea-splitting bacteria. About 6% of the patients form
kidney stones as result of reflux of contaminated urine and mucus to the upper collecting system.
Bacteruria is a common phenomenon after bladder augmentation, especially if there is a need for
CIC. Treatment of the isolated bacteria should be applied only if the patient is symptomatic or
when positive cultures show urea splitting organisms that may predispose the patient to bladder
calculi. The incidence of post augmentation UTIs is 4–13% (127,139). The gastrointestinal
segment used for augmentation continues to produce mucus, which may impede the bladder’s
drainage and may be a nidus for stone formation. Colonic segments produce the largest amount of
mucus, and gastric segments produce the least. Inflammatory responses to UTI in the augmented
bladder increase mucus formation. To prevent mucus buildup, routine bladder irrigation is
recommended. Instillation of N-acetylcysteine into the bladder may help dissolve the mucus (140).
N-acetylcysteine is not approved for this purpose by the Food and Drug Administration.
Bladder perforations have been reported in numerous studies with an incidence of 3–9%
(127,139,141). Some of the perforations were attributed to improper technique or noncompliance
with CIC. However, some of the perforations were regarded as “spontaneous” in patients who
were not catheterizing at all. Spontaneous perforations may be the result of a chronic inflammatory
process in the bladder, intestinal ischemia, or uncontrolled increased intravesical pressure. Any
patient with an enterocystoplasty who exhibits signs of peritonitis should be suspected to have a
bladder perforation. Urinary retention that necessitates CIC occurs in as many as 50% of patients
(123,127,142). The rate of retention correlates with the underlying pathology and the ratio of the
bowel’s surface area to the entire augmented bladder. All patients need to be informed that they
might need to do CIC after the operation and to learn how to perform it prior to the operation.

J. Urinary Diversion
There is almost no indication for performing urinary diversion in patients with OAB, in the
absence of a neurogenic cause. In case of unremitting pain such as in IC or irradiated bladders a
supratrigonal cystectomy should suffice. Diversion may be justified in a subcategory of patients
with “end-stage” bladders combined with severe sphincteric damage or pelvic pain. Description
of the various diversion options is beyond the scope of this chapter.

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13
Pharmacologic Management of
Urinary Incontinence
Alan J. Wein and Eric S. Rovner
University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania, U.S.A.

I. INTRODUCTION

There are multiple mechanisms, some proven in concept but others more theoretical, through
which a pharmacologic effect could facilitate bladder filling/urine storage. These include peri-
pheral and central motor (efferent) and sensory (afferent) sites of action. Clinical uropharmaco-
logy of the lower urinary tract is based primarily on an appreciation of the innervation and
receptor content of the bladder, the bladder outlet, and their related anatomic structures. The
drugs or classes of drugs used for therapy of lower urinary dysfunctions were, in general,
developed originally for their actions on other organ systems whose functions are controlled or
affected by innervation or drug receptor interaction. The targets of pharmacologic intervention
in the bladder body, base, or outlet include specific nerve terminals that alter the release a variety
of neurotransmitters, receptors and receptor subtypes, cellular second-messenger systems, and
ion channels. Peripheral nerves and ganglia, spinal cord, and supraspinal areas are also sites of
action of some agents to be discussed.
Despite disagreements on various details of neurophysiology, neuropharmacology, and
neuromorphology, all “experts” undoubtedly would agree that, for the purposes of explanation
and teaching, normal bladder filling and urine storage can be categorized as requiring the
following: (a) accommodation of increasing volumes of urine at a low intravesical pressure and
with appropriate sensation; (b) a bladder outlet that is closed at rest and remains so during
increases in intraabdominal pressure; and (c) absence of involuntary bladder contractions. All
types of therapy for storage disorders, regardless of whether the etiology is neurogenic or
nonneurogenic, can be classified within a functional scheme derived from this simple concept.
Using this classification, this presentation will summarize current thought regarding the efficacy
of various types of drug therapy for incontinence in the female, borrowing liberally from similar
prior presentations (1 – 8). As an apology to others in the field whose works are not specifically
cited, it should be noted that references have generally been chosen because of their
informational or review content and not because of originality or initial publication on a
particular subject.
215
216 Wein and Rovner

II. UROSELECTIVITY

Because autonomic innervation and receptor content are ubiquitous throughout the human
body’s organ systems, there are no agents in clinical use that are purely selective for action on
the lower urinary tract. Thus, the majority of side effects attributed to drugs facilitating bladder
storage or emptying are the collateral effects on organ systems that share some of the same
neurophysiologic or neuropharmacologic characteristics as the lower urinary tract. In general,
drug therapy for all lower urinary tract dysfunction is hindered by a lack of uroselectivity (9).
This concept describes a lack of selectivity of a drug for the lower urinary tract and is responsible
for a given agent’s systemic side effects. Many of the drugs described in this chapter are highly
effective agents in treating voiding dysfunction provided that the drug is administered in
sufficient quantity. However, dose dependent systemic adverse effects can often limit the
physician’s ability to maximally exploit a given drug’s therapeutic effects. Escalating dosages
often lead to increasing collateral effects on other organ systems. This often impairs reaching the
optimal dosage of the agent with resultant implications for an individual patient’s quality of life.
Nevertheless, improvements in uroselectivity can be approached in a number of ways: receptor
selectivity; organ selectivity; and alterations in drug delivery, metabolism, and distribution.
Receptor selectivity may be of little use unless the receptor is not expressed or operative in other
organs or pathways or unless a receptor subtype exists that is specific for the organ being treated
or its neurologic connections. Organ specificity, however, is indeed the Holy Grail of drug
therapy. The ideal organ-selective drug for the lower urinary tract would exert its desirable
effects only on the bladder and/or urethra, thus eliminating collateral effects elsewhere in the
body. Theoretically, the concept of organ specificity is very attractive but practically and
clinically it is very difficult to achieve. Alternate drug delivery systems may be helpful by
increasing the target concentration of an agent (intravesical therapy, e.g.) or by changing the
metabolism of a drug to lower the concentration of a metabolite particularly productive of side
effects. Certain drugs or their metabolites may be prevented from gaining access to a potentially
troublesome site of activity (through the blood brain barrier, e.g.) either by virtue of their innate
characteristics or by alteration. Given our current state of imperfection in this area, it is
important to distinguish potential laboratory from real clinical effects, both beneficial and
adverse, and it would be especially useful to construct a “therapeutic index” for each agent in
clinical use, one that integrates its therapeutic and undesirable effects and requirements.

III. THERAPY TO DECREASE DETRUSOR CONTRACTILITY OR

INCREASE BLADDER CAPACITY
A. Relatively Pure Anticholinergic Agents
Most of the neurohumoral stimulus for physiologic bladder contraction is from acetylcholine
(ACh)-induced stimulation of postganglionic parasympathetic muscarinic cholinergic receptor
sites on bladder smooth muscle. Atropine and atropinelike agents inhibit normal and involuntary
bladder contractions (IVC) of any etiology (10,11). Generally, volume to the first IVC increases,
the amplitude of the IVC decreases, and the total bladder capacity increases (12). However,
although the volume and pressure thresholds at which IVC is elicited may increase, the “war-
ning time” (the time between the perception that an IVC is about to occur and its occurrence) and
the ability to suppress the IVC do not increase. Therefore, to optimally suppress urgency and
incontinence, pharmacologic therapy must be combined with behavioral modification. Anti-
cholinergic agents do not significantly alter bladder compliance in normal individuals or in those
with detrusor overactivity in whom the initial slope of the filling curve on cystometry is normal
 Pharmacologic Management of Incontinence 217

prior to the IVC (5). The effect of pure antimuscarinics in patients who exhibit only decreased
compliance has not been well studied.
Andersson points out that, while it is widely accepted that there is no sacral para-
sympathetic outflow to the bladder during filling, antimuscarinic drugs increase and anti-
cholinesterase inhibitors decrease bladder capacity (13). Antimuscarinic drugs seem to affect the
sensation of urgency during filling, suggesting ongoing ACh-mediated stimulation of detrusor
tone. If this is the case, agents that inhibit ACh release or activity should contribute to bladder
relaxation or maintenance of low bladder tone during filling, with a consequent decrease in
filling and storage symptomatology unrelated to the occurrence of an IVC. Outlet resistance does
not seem to be clinically affected by anticholinergic agents.
The designations M1 through M5 are used to describe the pharmacologic and molecular
subtypes of muscarinic ACh receptors (14). Human urinary bladder smooth muscle contains a
mixed population of M2 and M3 subtypes, with a predominance of M2 receptors (80% of the total
muscarinic receptor population) (15). While the minor population of M3 receptors is believed to
be primarily responsible for mediating bladder contraction, experimental evidence suggests
that M2 receptors are also involved in bladder contractility in some species and in certain types
of LUT dysfunction (7,15 – 17). As alluded to earlier, the clinical utility of available antimu-
scarinic agents is limited by a lack of selectivity that is responsible for the classic peripheral
anticholinergic side effects. Although M3-selective agents have the potential to eliminate some
of these side effects, the M3 receptors in lower urinary tract tissues appear identical to those
elsewhere in the body (14). There may, however, be some heterogeneity among M3 receptors,
prompting many pharmaceutical companies to search for the “ideal” antimuscarinic that would
be relatively specific for the muscarinic receptors that regulate bladder contractility.
The potential side effects of all antimuscarinic agents include inhibition of salivary
secretions, blockade of the sphincter muscles of the iris and the ciliary muscle of the lens to
cholinergic stimulation, tachycardia, drowsiness, cognitive dysfunction, inhibition of gut
motility, and inhibition of sweat gland activity. Agents that possess ganglionic blocking activity
may also cause orthostatic hypotension and erectile dysfunction at the high doses generally
required for manifestation of nicotinic activity. In general, antimuscarinic agents are contra-
indicated in patients with narrow-angle glaucoma and should be used with caution in patients
with significant bladder outlet obstruction. Detailed efficacy and tolerability data for several
antimuscarinics are reviewed below.

1. Atropine sulfate (DL-hyoscyamine)

This agent is rarely used to treat OAB because of its adverse systemic effects (7). The
pharmacologically active portion of the racemic mixture of atropine is L-hyoscyamine. This
agent and hyoscyamine sulfate are reported to produce anticholinergic actions and side effects
similar to other belladonna alkaloids. Hyoscyamine sulfate is also available in a sublingual
formulation. The formulation offers a theoretical advantage, but controlled studies of its effects
on bladder hyperactivity are lacking (7).

2. Propantheline Bromide
This is a nonselective antimuscarinic that, as a quaternary ammonium compound, has a low
and varying biological availability (11). The usual adult dose is 15 –30 mg every 4 –6 h, but
often titration is necessary and higher doses are required. Few evaluable data on the drug’s
effectiveness in treating bladder overactivity are available. The Agency for Health Care Policy
and Research (AHCPR) Urinary Incontinence Guideline Panel reviewed five randomized
controlled trials (RCTs) of propantheline (18). Of the total number of patients enrolled, 82%
218 Wein and Rovner

were female. Reports of cure ranged from 0% to 5% (all figures refer to percent effect on drug
minus percent effect on placebo), reductions in urge incontinence ranged from 0% to 53%, side
effects ranged from 0% to 50%, and dropouts ranged from 0% to 9%. Controlled randomized
trials were also reviewed by Thüroff et al. (19) who reported a positive but variable response.

3. Tolterodine Tartrate
This agent was developed specifically for treatment of overactive bladder. It is not receptor
specific, but it and its primary metabolite have selectivity for the bladder over salivary gland
selectivity in some experimental models (20,21). Clinically it seems to have a favorable side
effect-profile not only with respect to dry mouth but with bowel and CNS effects as well (15).
A number of clinical trials have evaluated the efficacy and tolerability of tolterodine. Stahl
and colleagues first studied the effect of a single 6.4-mg dose on bladder and salivary function
and found that its inhibitory effect on bladder function persisted up to 5 h (22). Stimulated
salivation, however, was inhibited only near the time of peak serum levels. At 5 h after
administration, the effects on the bladder were maintained, but no significant effects on
salivation were detected. Appell reported on a pooled analysis of 1120 patients in whom
tolterodine (1 or 2 mg BID) was compared with immediate release oxybutynin (5 mg 3 TID) or
placebo (23). Compared with placebo, both active drugs significantly decreased the number
of incontinent episodes and micturitions occurring in 24 h and increased the volume voided per
micturition. Mean episodes of urge urinary incontinence decreased from 40% to 60% compared
to baseline, and frequency of urination decreased by 20%. The 2-mg dose of tolterodine and
the 5 mg (TID) dose of oxybutynin were equally efficacious, but tolerance was significantly
better with tolterodine when adverse events such as dry mouth (frequency and intensity), dose
reductions, and patient withdrawals were considered.
Chancellor and associates conducted a large double-blind study comparing tolterodine
(2 mg BID) with placebo (24). Tolterodine reduced urge incontinence episodes and also
produced significant reductions in micturition frequency and pad use compared with placebo. Of
tolterodine treated patients, 2% reported severe dry mouth and 10% reported moderate dry
mouth compared with 0% and 2%, respectively, of placebo patients. Mild dry mouth was
reported by 18% of drug-treated patients and by 6% of placebo-treated patients. Constipation
was reported by 7% of tolterodine recipients and 4% of placebo recipients. The profile and
frequency of other adverse events in the two treatment groups were similar. CNS adverse events
were not significantly different between the tolterodine and placebo groups. Several other
studies have reported similar findings with respect to tolterodine’s efficacy and tolerability
(25,26).
Tolterodine is now available in a once-daily formulation. The approval of this formulation
was based on a large-scale trial that compared the effects of this agent with placebo and the
twice-daily formulation (27). In this study, the median number of urge incontinence episodes in
patients receiving the once-daily formulation, the twice-daily formulation, and placebo were
reduced by 71%, 60%, and 33% respectively. Both preparations were statistically superior to
placebo, and the once-daily was statistically more effective than the twice-daily using this
outcome indicator. Statistically significant improvement in all other micturition diary variables
was recorded for both formulations over placebo. The incidence of dry mouth was 23% for once-
daily tolterodine, 30% for twice-daily tolterodine, and 8% for placebo.

4. Trospium Chloride
This is a quaternary ammonium non-receptor-selective antimuscarinic with low biologic
availability (19) and with minimal CNS penetration (28). In one study, trospium was as effective
 Pharmacologic Management of Incontinence 219

as oxybutynin in patients with hyperreflexia due to spinal cord injury, but had fewer adverse
effects (29). Summarized data from published and unpublished RCTs showed an average of 43%
(range 33 –54%) of 113 patients reported systemic anticholinergic side effects, described as
“generally mild” (29). This agent is currently undergoing trials in the United States.

5. Darifenacin
Darifenacin is a highly selective M3 receptor antagonist with selectivity in some animal models
for the urinary bladder over the salivary gland (30), but the clinical importance of this finding has
not been established (7). In a small placebo-controlled study, published only in abstract form, a
single 10-mg dose showed improvement in urodynamic parameters in patients with overactive
bladder, although significant reductions in salivary flow were also apparent (31). No effects on
salivation occurred at a dose of 2.5 mg, but this dose was no more effective than placebo as
measured by urodynamic parameters. In a randomized, double-blind trial of 25 patients with
detrusor instability, the effects of darifenacin 15 mg and 30 mg OD and oxybutynin 5 mg TID on
ambulatory urodynamic monitoring and salivary flow were compared (32). The two drugs had
similar urodynamic efficacy, but oxybutynin reduced salivary flow significantly more than
darifenacin. Darifenacin is currently in Phase III evaluation in the United States and elsewhere.

B. Anticholinergic Agents with “Mixed” Actions

In addition to their antimuscarinic properties, this group of drugs induce multiple in vitro
actions, including an independent “musculotropic” or “antispasmodic” action directly on smooth
muscle. This effect occurs at a site that is metabolically distal to the cholinergic or other
contractile receptor mechanism and is possibly related to calcium channel blockade. These drugs
may also possess some local anesthetic properties, which, like the direct musculotropic relaxant
effects, may only be relevant when given intravesically. When administered orally, the clinical
relevance of these actions as compared to their well-recognized antimuscarinic properties is
unclear, as these other effects only become apparent at much higher concentrations than their
antimuscarinic actions (11,15). Thus their clinical effects when administered orally, likely occur
solely through muscarinic blockade. If, however, any of these agents exerted a clinically
significant direct inhibitory effect independent of their antimuscarinic action, there would be a
therapeutic rationale for combination therapy with a relatively pure anticholinergic agent.

1. Oxybutynin Chloride
This agent is a potent muscarinic receptor antagonist, with some degree of selectivity for M3 and
M1 receptors. In human tissues, it has a higher affinity for muscarinic receptors in the parotid
gland than it does for those in the bladder (15).
Oxybutynin was originally developed to treat gastrointestinal hypermotility disorders.
In vitro, its direct, smooth muscle relaxant effects are 500 times weaker than its antimuscarinic
effects (11). This agent is a well-absorbed tertiary amine that undergoes an extensive first-pass
(liver) metabolism (19). The pharmacologic properties of its active metabolite (N-desethyl
oxybutynin) are similar to those of the parent compound, but the active metabolite occurs at
concentrations six times higher. The major metabolite is also thought to cause the majority of
adverse effects seen with this agent. Reducing the extent of first-pass metabolism by intravesical
administration, GI absorption outside the portal system, transdermal, or rectal administration are
potential avenues to improve tolerability.
Initial reports documented the agent’s success in depressing detrusor overactivity in
patients with neurogenic bladder dysfunction; subsequent reports have documented its success
220 Wein and Rovner

in inhibiting other types of bladder hyperactivity as well (10). Oxybutynin’s side effects
are antimuscarinic and are dose related. An additional theoretical consideration is its
physiochemical composition that might permit relatively greater penetration into the CNS
through the blood-brain barrier. This may account for some of the reports of adverse CNS effects
seen with this agent, especially in the geriatric population (33,34). The recommended oral adult
dose of the immediate release formulation is 5 mg three or four times daily.
The AHCPR Urinary Incontinence Guideline Panel reviewed six randomized clinical
trials (RCTs); 90% of the patients were female (18). Reports of cure ranged from 28% to 44%,
reductions in urge incontinence from 9% to 56%, side effects from 2% to 66%, and dropouts
from 3% to 45%. In a review of 15 RCTs of 476 patients treated with oxybutynin, Thüroff et al.
(19) reported a mean decrease in incontinence of 52% and a mean reduction in frequency of
micturitions for 24 hours of 33%. The overall “subjective improvement” rate was 74% (range
61 –100%). Side effects were reported by a mean of 70% (range 17 –93%) of patients.
Once-daily formulations of oxybutynin have been developed. Oxybutynin ER or XL uses
an innovative osmotic drug delivery system to release the drug at a controlled rate over 24 h.
This formulation overcomes the marked peak-to-trough fluctuations in plasma levels of both the
drug and its major metabolite, which occurs with immediate-release oxybutynin (35). A trend
toward a lower incidence of dry mouth with XL was attributed to reduced first pass metabolism
and to the maintenance of lower and less-fluctuating plasma levels of drugs. Clinical trials on XL
have concentrated primarily on comparing this drug with immediate-release oxybutynin.
Anderson et al. reported on a multicenter, randomized, double-blind study on 105 patients with
urge incontinence, or mixed incontinence with a clinically significant urge component. All had
been prior positive responders to IR oxybutynin (36). Urge urinary incontinence episodes were
the primary efficacy parameter. The number of weekly urge incontinence episodes decreased
from 27.4 to 4.8 after XL and from 23.4 to 3.1 after IR oxybutynin, and total incontinence
episodes decreased from a mean of 29.3 to 6 and from 26.3 to 3.8, respectively. Since only
patients who had previously responded to treatment with oxybutynin were selected for
treatment, these figures are not likely representative of what can be expected in clinical practice
in an untreated, naive patient population. Dry mouth of any severity was reported by 68% and
87% of the controlled and immediate-release groups, respectively, and moderate or severe dry
mouth occurred in 25% and 46%, respectively. Curiously, as voiding frequency was measured in
both groups, a statistically greater percent increase was seen in the XL patients (54%) than in the
IR patients (17%). The reason for the increase in urinary frequency seen in this study is unclear
and is at odds with nearly all other antimuscarinic studies in which urinary frequency was
measured as an outcome parameter. Another controlled study comparing efficacy and safety of
controlled-release oxybutynin with conventional immediate-release oxybutynin included 226
patients with urge incontinence (37). They were known to respond to anticholinergic therapy
and had seven or more urge incontinence episodes per week. Reductions in urge urinary
incontinence episodes from baseline to the end of treatment were 18.6 to 2.9 per week (83%
mean decrease) and 19.8 to 4.4 per week (76% mean decrease) in the XL and IR oxybutynin
groups (difference nonsignificant), respectively. The incidence of dry mouth increased with dose
in both groups, but there was no statistically significant difference in dry mouth rates between the
groups: 47.7% and 59.1% for the XL and IR, respectively. However, a significantly lower
proportion of patients taking XL had moderate to severe dry mouth or any dry mouth compared
with those taking IR oxybutynin.
Other administration forms of oxybutynin have been introduced. Rectal administration
(38,39) was reported to have fewer adverse effects than the conventional tablets, as was a
transdermal preparation (40). Intravesical administration has also been successful in reducing
systemic adverse effects while maintaining clinical improvement (41,42).
 Pharmacologic Management of Incontinence 221

2. Comparing Oxybutynin and Tolterodine

A comparison of the efficacy and tolerability profiles of the two once-daily preparations would
be of interest. To date, however, there have been no reported head-to-head studies, and
inferences from existing studies are complicated by differences in enrolled patient populations
and methodologies. Both tolterodine IR and oxybutynin XL have been compared to oxybutynin
IR. Oxybutynin XL was shown to have equivalent efficacy to IR. Tolterodine IR and oxybutynin
IR have also demonstrated equivalent efficacy. Tolterodine LA has not yet been directly
compared to any of the oxybutynin formulations in a clinical study, but has been shown to be
18% more effective than tolterodine IR using median episodes of urge incontinence as an
outcome indicator (27).
One study has been completed that compared oxybutynin XL with tolterodine IR (43). Of
378 patients enrolled, 332 completed the 12-week study. Compared to baseline, weekly urge
incontinence episodes per week were reduced (25.6 to 6.1 vs. 24.1 to 7.8, oxybutynin XL and
tolterodine IR groups, respectively) as was urinary frequency (91.8 to 67.1 vs. 91.6 to 71.5
episodes per week). Although there was a statistically significant difference between the two
drugs favoring oxybutynin in both of these outcome parameters, the overall clinical significance
of these differences (e.g., a difference of 1.7 urge incontinent episodes per week) is unclear.
Furthermore, like other oxybutynin XL controlled studies (36,37,43,44), there are some potential
issues regarding the study design. Results were analyzed on a completer basis, which assesses
the response rate in only those patients who completed the study. Secondly, statistical methods
employed for analysis of the final data employed parametric analysis when the assumption
of a normal distribution was unclear. Notably, however, adverse events including overall dry
mouth (28.1% vs. 33.2% for oxybutynin XL vs. tolterodine IR, respectively) and constipation
(7% vs. 6.2%, respectively) were not significantly different between the two groups. One small
pharmacological study has been conducted which compared once daily tolterodine and
oxybutynin (45). A double-blind, randomized, four-way crossover study compared oxybutynin
XL 15 and 25 mg versus tolterodine LA 6 mg. XL treatment resulted in a linear dose-dependent
increase in bladder capacity and a linear dose-dependent decrease in salivation. By extra-
polation, LA 6 mg had the same effect on bladder capacity as a 20-mg dose of XL and the same
effect on salivation as a 10-mg dosage.

3. Dicyclomine Hydrochloride
This agent is reported to possess a direct relaxant effect on smooth muscle in addition to an
antimuscarinic action. However, it is not widely used to treat OAB. The International
Consultation on Incontinence (Committee on Pharmacology) (7) rated this drug as effective
based on pharmacologic and physiologic evidence, but clinical evidence from good-quality
randomized control trials was lacking (15). The ICI failed to recommend dicyclomine for use.

4. Flavoxate Hydrochloride
This compound was originally thought to be a weak anticholinergic agent but, in addition, to
possess a direct inhibitory action. Andersson and colleagues (7) cite references showing it has no
anticholinergic effect but does have moderate calcium antagonist activity, local anesthetic
properties, and the ability to inhibit phosphodiesterase (15). Overall, favorable clinical effects
have been reported in some series of patients with frequency, urgency, and incontinence and in
patients with urodynamically documented detrusor hyperreflexia (46). However, Briggs and
colleagues reported essentially no effect on neurogenic detrusor overactivity in an elderly
population (47). A similar conclusion was reached by Chapple and associates in a double-blind,
222 Wein and Rovner

placebo controlled, crossover study of idiopathic detrusor overactivity (48). Reported side
effects are few. The drug failed to achieve a “recommended” assessment by the ICI, which noted
that cogent evidence of pharmacologic or physiologic efficacy (or both) was lacking for this
agent as well as evidence for its efficacy from good quality randomized controlled trials (48).

C. Potassium Channel Openers

These agents efficiently relax various types of smooth muscle (including detrusor smooth
muscle) by increasing potassium efflux, which results in membrane hyperpolarization. This
hyperpolarization reduces the probability that ion channels (primarily calcium) involved in
membrane depolarization will open, with subsequent relaxation or inhibition of contraction
(7,49). Potassium channel openers reduce spontaneous contractions as well as contractions
induced by carbachol and electrical stimulation.
Pinacidil and cromakalim, first-generation adenosine triphosphate (ATP)-sensitive
potassium channel openers, have been used clinically. Evidence from preliminary trials did
not support further efforts to pursue these drugs as treatment for detrusor overactivity (50,51),
perhaps because they were found to be up to 200 times more potent as inhibitors of vascular
smooth muscle preparations than detrusor muscle (7). However, attempts continue to develop a
bladder-selective potassium channel opener.

D. Calcium Antagonists
The role of calcium as a messenger in linking extracellular stimuli to the intracellular
environment is well established, including its involvement in excitation-contraction coupling
in striated, cardiac, and smooth muscle (7,49,52). The dependence of contractile activity on
changes in cytosolic calcium varies from tissue to tissue, as do the characteristics of the calcium
channels involved. However, interference with calcium inflow or intracellular release is
potentially a very potent mechanism for inducing bladder smooth muscle relaxation. These
results have prompted support for the view that combined muscarinic receptor and calcium
channel blockade might offer a more effective way to treat bladder overactivity than using either
type of agent alone.
Andersson conclude that available information does not currently support the use of oral
calcium antagonists as an effective treatment for detrusor overactivity (49). A bladder-specific
membrane calcium channel is not known to exist, and no agent blocks intracellular calcium
release only in bladder smooth muscle cells. Intravesical therapy could theoretically prove
useful, however.

E. Prostaglandin Antagonists
Prostaglandins are ubiquitous compounds that may potentially have a role in excitatory
neurotransmission to the bladder, in the development of bladder contractility or tension
occurring during filling, in the emptying contractile response of bladder smooth muscle to neural
stimulation, and even in the maintenance of urethral tone during the storage phase of micturition,
as well as in the release of this tone during the emptying phase (52 –54). Multiple mechanisms
exist whereby prostaglandin synthesis inhibitors might decrease bladder contractility in response
to various stimuli. However, no compelling clinical evidence supports their use in the treatment
of detrusor overactivity (52).
 Pharmacologic Management of Incontinence 223

F. b-Adrenergic Agonists
Because b-adrenergic receptors are present in human bladder muscle, researchers have
attempted to increase bladder capacity with b-adrenergic stimulation. Such stimulation can
cause significant increases in the capacity of animal bladders, which contain a moderate density
of b-adrenergic receptors (54,55). However, the International Consultation on Incontinence
Committee on Pharmacology did not recommend this group of agents because there was no
evidence of clinical effectiveness (54).
Recently, a b3-adrenergic receptor was identified and was shown to exist in human
detrusor smooth muscle (56,57). The presence of this receptor may explain the b-adrenergic
responses of detrusor muscle heretofore labeled atypical. Work is ongoing in this area.

G. a-Adrenergic Antagonists
At first glance, there seems to be no role for a-adrenergic antagonists to decrease detrusor
contractility or increase bladder capacity since these have minimal, of any, contractile effects
on human detrusor smooth muscle from normal individuals (7). However, the peripheral
contribution of such receptors to bladder overactivity can change in neurologic disease or injury
and as a result of bladder outlet obstruction or other causes. It is also possible that certain
excitatory aspects of the micturition reflex may involve central a1-adrenergic receptors (49).
a-Adrenergic blocking agents have been used to treat bladder and outlet abnormalities in
patients with so-called autonomous bladders (58). These include voiding dysfunction resulting
from myelodysplasia, sacral spinal cord or infrasacral neural injury, and radical pelvic surgery.
Decreased bladder compliance is often a clinical problem in such patients, and this, along with
a fixed urethral sphincter tone, results in the paradoxical occurrence of both storage and
emptying failure. Norlen summarized the evidence for the success of a-adrenolytic treatment in
these patients (58). Most would agree that the success has been moderate at best. Whether the
effects on detrusor overactivity are central or peripheral (or both) have yet to be definitively to be
definitively settled.

H. Tricyclic Antidepressants
Many clinicians believe that tricyclic antidepressants (particularly imipramine hydrochloride)
are useful agents for facilitating urine storage because they decrease bladder contractility and
increase outlet resistance (59). These agents have been the subject of numerous pharmacologic
investigations to determine the mechanisms of action responsible for their varied effects (60,61).
Most data are from attempts to explain the antidepressant properties of these agents and
therefore are primarily from CNS tissue. The results, conclusions, and speculations inferred
from the data are extremely interesting, but it is unknown whether they have relevance for the
lower urinary tract.
All of these agents possess varying degrees of at least three major pharmacologic actions:
they have central and peripheral anticholinergic effects at some, but not all, sites; they block the
active transport system in the presynaptic nerve ending, which is responsible for the reuptake of
the released amine neurotransmitters norepinephrine and serotonin; and they are sedatives, an
action that occurs presumably on a central basis, but may be related to antihistaminic properties.
Imipramine and doxepin are the most commonly prescribed tricyclics for detrusor overactivity;
data on their efficacy and tolerability for this indication are reviewed below.
224 Wein and Rovner

1. Imipramine
While this agent has prominent systemic anticholinergic effects, it has only A weak anti-
muscarinic effect on bladder smooth muscle (62). It does, however, exert a strong direct
inhibitory effect—which is neither anticholinergic nor adrenergic—on bladder smooth muscle
(63,64). The exact mechanism by which imipramine inhibits bladder activity is unknown.
Recently, it has been postulated that these effects may be due to increased serotonin activity (due
to reuptake blockade) in the central nervous system. This may involve a direct inhibition of
normal excitatory pathways or a depression of afferent ascending neural activity (49,65).
Clinically, imipramine has been shown to be effective in decreasing bladder contractility
and in increasing outlet resistance (66,67). The AHCPR combined results for imipramine and
doxepin, citing only three randomized clinical trials and an unknown percentage of female
patients (18). Percent cures were listed as 31%, percent reduction in urge incontinence as 20–
77%, and percent side effects as 0 –70%.
Our usual daily adult dosage for voiding dysfunction is 25 –75 mg once daily (possible
because of the drug’s long half-life). We begin with the lowest dose and increase it by 25-mg
increments every 7– 10 days if necessary, exercising extra caution in the elderly with respect to
any dose .50 mg. In our own experience, the effects of imipramine on the lower urinary tract
are often additive to those of the atropinelike agents. Consequently, combining imipramine with
an antimuscarinic or an antispasmodic is sometimes especially useful for decreasing bladder
contractility. When imipramine is used in conjunction with an atropinelike agent, the anti-
cholinergic side effects of the drugs may also be additive. When used in the larger doses emp-
loyed for antidepressant effect, the most frequent side effects of imipramine are anticholinergic.
However, though uncommon, serious other side effects can occur, including CNS effects,
postural hypotension, cardiac toxicity, weakness, and fatigue (60,61).
Consultation with the internist or cardiologist is always helpful in questionable situations.
Use is definitely contraindicated in patients receiving monamine oxidase inhibitors. All those
contemplating the use of imipramine or other tricyclics (doxepin, e.g.) should be thoroughly
familiar with the potential side effects and relative precautions.

I. Decreasing Sensory Input

Decreasing afferent input would be an ideal treatment for sensory disorders and for overactivity
in a bladder with relatively normal elastic and viscoelastic properties in which the sensory
afferents constitute the first limb in an abnormal micturition reflex. Maggi has written
extensively about this type of treatment, specifically with reference to the properties of capsaicin
(68,69).

Capsaicin
An irritant and algesiogenic compound obtained from hot red peppers, capsaicin has highly
selective effects on a subset of mammalian sensory neurons, including polymodal receptors and
warm thermoreceptors (70). It activates polymodal nociceptive neurons by opening a cation-
selective ion channel, allowing an influx of calcium and sodium ions that depolarize neuronal
pain fibers (71,72). This ion channel is known as vanilloid-receptor subtype 1 (VR1). Repeated
administration of capsaicin desensitizes and inactivates sensory neurons by several mechanisms.
Systemic and topical capsaicin produces a reversible antinociceptive and anti-inflammatory
action after an initially undesirable algesic effect. Local or topical application blocks C-fiber
conduction and inactivates neuropeptide release from peripheral nerve endings, accounting
for local antinociception and reduction of neurogenic inflammation. With local administration
 Pharmacologic Management of Incontinence 225

(intravesical), the obvious potential advantage of capsaicin is a lack of systemic side effects. The
actions are highly specific when the drug is applied locally, the compound affects primarily
small-diameter nociceptive afferents, leaving the sensations of touch and pressure unchanged,
although heat (not cold) perception may be reduced. Motor fibers are not affected. The effects
are reversible, although it is not known whether initial levels of sensitivity are regained.
DeRidder and Baert, in an excellent review article (73), summarized trials to that date as
detailed by DeSeze and colleagues (74). Eighty-four percent had “some improvement” in their
symptoms. The largest single series had been reported by DeRidder et al. (75); of 49 patients
with multiple sclerosis, in 27% results were termed excellent, and in 55%, improved. DeRidder
and Baert (73) also cite double blind trials using either placebo or the vehicle (30% ethanol in
saline), showing clearly that it is indeed the capsaicin that produces the positive result.

2. Resiniferatoxin (RTX)
This is the principal active ingredient in the drug euphorbium, the air-dried latex of the cactuslike
plant Euphorbia resinifera, which is chemically related to the phorbol esters (73,76). RTX is
likewise a vanilloid, and is, in fact, an ultrapotent (1000X) analog of capsaicin, but with minimal
initial excitatory effect. RTX may induce desensitization in concentrations that are so low that no
noxious effects are elicited (76). A summary of trials with resiniferatoxin is reported by DeRitter
and Baert (73). These trials used concentrations ranging anywhere from 0.01 mmol/L to 1 mmol/
L, dissolved in either 10% ethanol or saline. The largest open study comprised 27 patients with
multiple sclerosis and involuntary bladder contractions. A concentration of 0.5 –1 mmol/L in
10% ethanol was used. Twenty-one of 27 patients responded positively, mean bladder capacity
increasing after 1 month from 208 to 467 mL and the mean urine loss for 24 h decreasing from
163 to 23 mL. Further randomized placebo controlled studies are ongoing.
Neither capsaicin nor RTX is approved for clinical use in the United States. However, the
intravesical use of such agents has the potential to significantly contribute to the treatment
of bladder overactivity in patients with neurogenic and other types of lower urinary tract
dysfunction. Theoretically, activities affected by these agents should include only those
subserved by small unmyelinated afferent C fibers. A micturition reflex stimulated via
myelinated Ad afferent fibers should not, theoretically, be affected by capsaicinlike agents.

IV. THERAPY TO INCREASE OUTLET RESISTANCE

A. a-Adrenergic Agonists
The bladder neck and proximal urethra contain a preponderance of a1-receptor sites, which,
when stimulated, produce smooth muscle contraction. The static infusion urethral pressure
profile is altered by such stimulation, which produces an increase in maximum urethral pressure
(MUP) and maximum urethral closure pressure (MUCP). Various orally administered
pharmacologic agents are available that produce a-adrenergic stimulation. Generally, outlet
resistance is increased to a variable degree by such an action. Potential side effects of all of
these agents include blood pressure elevation, anxiety, and insomnia from stimulation of
the CNS; headache; tremor; weakness; palpitations; cardiac arrhythmias; and respiratory
difficulties. They should be used with caution in patients with hypertension, cardiovascular
disease, or hyperthyroidism (5).
226 Wein and Rovner

B. Ephedrine, Pseudoephedrine
Ephedrine is a noncatecholamine sympathomimetic agent that enhances release of nor-
epinephrine from sympathetic neurons and directly stimulates both a- and b-adrenergic
receptors. The oral adult dosage is 25– 50 mg QID. Some tachyphylaxis develops to its
peripheral actions, probably as a result of depletion of norepinephrine stores. Pseudoephedrine, a
stereoisomer of ephedrine, is used for similar indications with similar precautions. The adult
dosage is 30– 60 mg QID, and the 30-mg dose form is available in the United States without
prescription (Sudafed, others). Diokno and Taub (77) reported a “good to excellent” result in
27 of 38 patients with sphincteric incontinence treated with ephedrine sulfate. Beneficial effects
were most often achieved in those with minimal to moderate wetting, and little benefit was
achieved in patients with severe stress incontinence. In past years similar results had been
reported in the literature with the use of these agents; however, in retrospect, these results are
somewhat inconsistent with current opinion and show the value of accurate objective outcome
indicators and double-blind placebo-controlled studies.

C. Phenylpropanolamine (PPA)
PPA has classically been reported to share the pharmacologic properties of ephedrine and be
approximately equal in peripheral potency while causing less central stimulation. It is available
in 25- and 50-mg tablets and 75-mg time-release capsules and is a component of numerous
proprietary mixtures, some marketed for the treatment of nasal and sinus congestion (usually in
combination with an H1 antihistamine) and some marketed as appetite suppressants. Using doses
of 50 mg TID, Awad and associates (78) claimed that 11 of 13 females and 6 of 7 males with
stress incontinence were significantly improved after 4 weeks of therapy. MUCP increased from
a mean of 47 cmH2O to 72 cmH2O in patients with an empty bladder and from 43 cmH2O
to 58 cmH2O in patients with a full bladder. Using a capsule (Ornade) that then contained
50 mg of PPA, 8 mg of chlorpheniramine (an antihistamine), and 2 mg of isopropamide
(an antimuscarinic), Stewart and associates (79) reported that, of 77 women with stress urinary
incontinence, 18 were completely cured with one sustained release capsule taken BID. Twenty-
eight patients were “much better,” six were “slightly better,” and 25 were no better. In 11 men
with postprostatectomy stress incontinence, the numbers in the corresponding categories were 1,
2, 1, and 7. The formulation of Ornade has now been changed, and each capsule of drug contains
75 mg PPA and 12 mg chlorpheniramine.
The AHCPR Guideline (18) reports eight randomized controlled trials with PPA, 50 mg
BID, for stress urinary incontinence in females. Percent cures (all figures refer to percent effect
on drug minus percent effect on placebo) are listed as 0 – 14, percent reduction in incontinence as
19 –60, and percent side effects and percent dropouts as 5– 33 and 0 – 4.3, respectively.
There are potential complications of PPA, especially hypertension. Most recently the FDA
has asked manufacturers to voluntarily stop selling PPA-containing drugs and replace the
ingredient with a safer alternative (80). This request, which, it was hinted, may be replaced by a
ban, was based on a study reported by Kernan and coworkers (81) in the New England Journal
of Medicine. They compared 702 adults younger than 50 years old with subarachnoid or
intracerebral hemorrhage to 1376 controls, reporting the risk of hemorrhagic stroke to be 16
times higher in women who had been taking PPA as an appetite suppressant and three times
higher in women who had taken the drug for ,24 h as a cold remedy. This last finding was not
statistically significant. PPA was reported not to be associated with an increased risk of stroke
in men. In commenting on this article, Abramowicz and Zuccotti (82) writing in the Medical
Letter, noted that no case control studies were available on the safety of phenylephrine,
 Pharmacologic Management of Incontinence 227

ephedrine, or pseudoephedrine but did relate that case reports have associated ephedra alkaloids
with hypertension, stroke, seizures, and death. Their article concluded, “Phenylpropanolamine
may not be the only alpha-adrenergic agonist that can cause serious adverse effects when taken
systemically in over-the-counter products marketed for nasal congestion or weight loss.” Thus,
extreme caution must be exercised in choosing patients, especially women, for a-adrenergic
agonist therapy. We currently do not recommend this.

D. Imipramine; Duloxetine
The actions of imipramine have already been discussed in the section on inhibiting bladder
contractility. On a theoretical basis, an increase in urethral resistance might be expected if
indeed an enhanced a-adrenergic effect is produced at this level because of an inhibition of
norepinephrine reuptake. Many clinicians have noted improvement in patients who were treated
with imipramine primarily for reasons related to bladder hyperactivity, but who had, in addition,
some component of sphincteric incontinence. Gilja and coworkers (83) reported a study of
30 women with stress incontinence treated with 75 mg imipramine daily for 4 weeks. Twenty-
one women subjectively reported continence. Mean MUCP for the group increased from
34.06 mmHg to 48.23 mmHg. In an open study Lin and colleagues (84) reported that 25 mg
imipramine TID for 3 months resulted in a 35% cure rate by pad test in 40 women with stress
incontinence. In an additional 25%, there was a 50% or more improvement. Success seemed to
correlate with a higher urethral closure pressure.
Duloxetine, a combined serotonin and norepinephrine reuptake inhibitor, under conditions
of “bladder irritation,” enhances external urethral sphincter activity in the cat through
serotonergic and a1-adrenergic mechanisms, probably at a central level. It also produces a
centrally mediated increase in bladder capacity through a serotonergic mechanism (85).
Duloxetine is currently undergoing clinical trials in the United States.

E. Summary
Although some clinicians have reported spectacular cure and improvement rates with
a-adrenergic agonists and agents that produce an a-adrenergic effect in the outlet of patients
with sphincteric urinary incontinence, our own experience coincides with those who report
that treatment with such agents often produces satisfactory or some improvement in mild cases,
but rarely total dryness in cases of severe or even moderate stress incontinence. Such therapy,
when utilized, should always be employed in conjunction with pelvic floor physiotherapy/
biofeedback to achieve optimal results.

V. ESTROGENS FOR URINARY INCONTINENCE

In the postmenopausal female, on a statistical basis, the prevalence of lower urinary tract
symptoms, including incontinence, and urinary tract infection are increased. Estrogen levels
have obviously declined. The question is whether these phenomena are causally related. If so,
estrogen supplementation would be a rational therapy for incontinence. The role of estrogen
therapy in the treatment of bladder overactivity and stress incontinence has remained
controversial. Unfortunately, most reported studies are observational and not randomized,
blinded, or controlled. The situation is further complicated by the fact that a number of different
types of estrogen have been used with varying doses, routes of administration, and treatment
duration—some with progestational agents and some without. Some authorities even seem to
228 Wein and Rovner

advocate opposite positions on this question in different articles. If estrogen has a role in treating
LUTS in the postmenopausal female, it is most likely through one or more of the following
mechanisms: (a) raising the sensory threshold of the bladder and/or urethra; (b) increasing the
a-adrenoceptor sensitivity in urethral smooth muscle; (c) increasing urethral resistance by (b) or
by another mechanism; (d) correcting underlying urogenital atrophy.
Both Hextall (86) and Andersson (28) have carefully reviewed the relevant literature on
this subject and offered what we feel are valid summaries. Our inferences from their reports
regarding the success of estrogen usage in the treatment of various LUTS in the postmenopausal
female is as follows: stress incontinence—probably not; urge incontinence—probably not;
urgency and frequency—maybe; urinary tract infections—yes, especially with a vaginal
preparation.

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14
Behavioral Treatments

Diane K. Newman
University of Pennsylvania Medical Center, Philadelphia, U.S.A

I. INTRODUCTION

Behavior modification is an accepted treatment option for persons with urinary lower urinary
tract symptoms (LUTS) which include urinary incontinence (UI) and overactive bladder (OAB),
which include urgency, frequency, with or without urge UI and nocturia. These interventions
improve symptoms through identification of lifestyle habits and changing a person’s behavior,
environment or activity that are contributing factors or triggers (1). Interventions such as bladder
retraining and pelvic floor muscle rehabilitation attempt to decrease incontinence and OAB
symptoms through increasing awareness of the function and coordination of the bladder and
pelvic floor muscle so as to gain muscle identification, control, and strength and to decrease
bladder overactivity. These interventions are often referred to as behavioral treatments, and
involve learning new skills through extensive one-on-one patient instruction on techniques for
preventing urine loss, urgency, and other symptoms.
These treatments have a growing body of clinical research. The Agency for Health Care
Policy and Research (AHCPR) clinical practice guideline on urinary incontinence in adults
recommended these treatments as first line interventions (2,3). AHCPR is now known as the
Agency for Healthcare Research and Quality (AHRQ). These guidelines defined behavioral
interventions as a group of therapies used to modify stress, urge, or mixed urinary incontinence by
changing the person’s bladder habits or by teaching new skills. They have been defined to include
lifestyle changes (e.g., cessation of smoking, weight reduction, elimination of dietary bladder
irritants, adequate fluid intake, bowel regulation, moderation of physical activities, and exercises),
toileting programs (e.g., habit training and prompted voiding), bladder training, pelvic floor muscle
training or rehabilitation utilizing methods such as biofeedback, vaginal weights, and pelvic muscle
electrical stimulation. This chapter outlines the current research as well as clinical practice on
the use of behavioral treatment, specifically lifestyle or self-care practices, scheduled toileting
programs, bladder training and pelvic muscle rehabilitation. Despite the high level of evidence
supporting the effectiveness of behavioral therapy, there are few demonstrations of outcomes
obtained when this research is translated into clinical practice. A common complaint of behavioral
treatments is that the outcome reflects the combination of these treatments as opposed to a single
intervention. More research on clinical effectiveness is needed to encourage health care clinicians,
specifically doctors and nurses, to incorporate behavioral therapy instruction into standard
treatment care protocols.
233
234 Newman

II. LIFESTLE CHANGES/BEHAVIOR MODIFICATION

In many instances, lifestyle practices can be the contributing cause of LUTS, especially in
women. The following is the current summary of these practices.

A. Smoking
Conditions exist in which increased intra-abdominal pressure may promote the development of
UI and urinary urgency, particularly in women. These conditions include pulmonary diseases
such as asthma, emphysema, and chronic coughing such as seen in persons who smoke. Smoking
increases the risk of developing all forms of UI, and stress UI in particular, depending on the
number of cigarettes smoked. There may be several causes of the increased risk of stress UI in
smokers. Smokers have stronger, more frequent, and more violent coughing, which may lead to
earlier development of anatomic and pressure damage of the urethral sphincteric mechanism and
of vaginal supports (4). Violent and frequent, prolonged coughing can increase downward
pressure on the pelvic floor, causing repeated stretch injury to the pudendal and pelvic nerves.
Smoking is also the most important etiological factor in bladder cancer. There is felt to be
antiestrogenic hormonal effects of products found in tobacco products. These effects are felt to
affect the production of collagen synthesis. Nicotine has been shown to contribute to large phasic
bladder contractions in animal studies through the activation of purinergic receptors and has
been postulated to similarly affect the human bladder (5,6). There may also be an association
between nicotine and increased detrusor contractions.
Bump and McClish (7) demonstrated that women who previously smoked had a 2.2-fold
increase and those who currently smoked have a 2.5-fold increase in stress UI. One case control
study of 80 incontinent and 80 continent women established a strong statistical relationship
between cigarette smoking and urinary incontinence (8). Nuotio et al. (9) showed a correlation
between smoking and urinary urgency in a population based survey of 1059 women and men
aged 60– 89 years. A large cross-sectional study evaluated multiple risk factors for incontinence,
including smoking in women attending antenatal care (10). Smokers were more likely to report
incontinence than nonsmokers. The previous research was concentrated in women, but
Koskimaki et al. (11) showed an increased risk of LUTS in a survey of 2128 middle-aged and
elderly men who smoked currently or formerly. LUTS symptoms included incomplete bladder
empting and hesitancy, daily frequency, nocturia, urgency, and urge incontinence. The effects of
smoking on LUTS are probably mediated through the development of BPH. In men, tobacco
products may increase accumulation of androgens in the prostate gland. The study also found
that in men, the risk of LUTS decreased, disappearing 40 years after cessation of smoking. No
data have been reported examining whether smoking cessation in women resolves incontinence.
However, in clinical practice, women who smoke are educated on the relationship between
smoking and UI, and strategies designed to discourage women from smoking are often
suggested; however, no evidence supports their effectiveness (12).

B. Obesity
Obesity has been identified as an independent risk factor for the development of stress and mixed
UI in women (13 –16). Research looking at the relationship between obesity and incontinence
used body mass index (BMI). A BMI of
29 is considered normal or low weight, and a BMI of
30 a high weight or obese. The stress UI seen in obesity may be secondary to increases in intra-
abdominal pressure on the bladder and greater urethral mobility. Also, obesity may impair blood
flow or nerve innervation to the bladder. Elia et al. (13) reported on 540 women who responded
 Behavioral Treatments 235

to a questionnaire of which BMI status was attained. The association between BMI and UI was
statistically significant. Mommsen and Foldspang (16) reported on 2589 women in Denmark
who responded to a mailed questionnaire. BMI was found to correlate with urge UI in women
who reported having one or more episodes of cystitis. It was hypothesized that poor personal
hygiene in obese women may lead to an infectious process. Mommsen also found a relationship
between stress UI and an increased BMI. Dwyer et al. (17) found women with genuine stress UI
or with detrusor instability to have a higher mean BMI than the general population of the same
age. Roe and Doll (18) reported on 6139 (53% response rate) respondents to a British postal
survey on incontinence status. Significantly more obese respondents have UI than continent
respondents. This association was more prevalent in obese women than men. Brown et al. (19)
studied 2763 women who completed questionnaires on prevalence and type of incontinence as
part of a randomized trial of estrogen hormone therapy. A higher BMI and higher waist-to-hip
ratio were found to be predictors of stress UI and also of mixed UI when the major component
was stress. This study found that the prevalence of at least weekly stress UI increased by 10% per
5 units BMI. Højberg et al. (10) found that BMI . 30 and smoking were possible risk factors for
women attending antenatal care who were 16 at weeks’ gestation.
Weight loss is an acceptable treatment option for morbidly obese women. Research has
shown that stress UI symptoms decrease in morbidly obese women who undergo extreme weight
loss after gastric bypass surgery (20). At this time, there is little information on whether weight
loss resolves incontinence in women who are moderately obese. Subak et al. (21,22) showed that
improvement in UI was seen when participants lost as little as 5% from baseline weight so
weight loss is recommended in clinical practice to all women who have a BMI . 30. Clinicians
might suggest self-weight programs such as Weight Watchers or depending on the BMI refer the
women to a physician-monitored weight loss program or possibly weight reduction surgery.

C. Dietary Habits
There are components of everyday diet and bodily functions that can “trigger” LUTS which if
eliminated through modification can also decrease their effects. These components include
amount of fluid intake; the ingestion of certain beverages, foods, and medications; and
maintaining normal bowel regulation (23).

1. Fluid Management
Individuals may subscribe to either a restrictive or excessive fluid intake behavior. Adequate
fluid intake is needed to eliminate irritants from the bladder. Underhydration may play a role in
the development of urinary tract infections (UTIs) and decreases the functional capacity of the
bladder (24). Surveys of community-residing elders report self-care practices to include the self-
imposed restrictions of fluids, as they fear UI, urinary urgency, and frequency (25,26). Adequate
fluid intake is very important for older adults, who already have a decrease in their total body
weight and are at increased risk for dehydration.
However, the research showing the relationship of quantity of fluid intake to urinary
symptoms is inconclusive. In a geriatric population, there appears to be a strong relationship
between evening fluid intake, nocturia, and nocturnal voided volume (27). Nygaard and Linder
(28) surveyed teachers and questioned their voiding habits at work, allotted breaks, bladder
complaints including UTIs, and incontinence. Teachers who drank less while working to
decrease their voiding frequency had a twofold higher risk of UTI than those who did not report
self-imposed fluid restriction. There was no association between UTI and either voiding
infrequently at work or the mean number of voids at work. Fitzgerald et al. (29) surveyed
236 Newman

women who worked for a large academic center. Of the 1113 women surveyed, 21% (n ¼ 232)
reported UI at least monthly. Incontinent women were significantly older and had a higher BMI
than continent women. One of the strategies women in this study used to avoid urinary
symptoms was limiting fluids and avoiding caffeinated beverages.
Wyman et al. (30) reported a positive relationship between fluid intake and severity of UI
in women with stress UI over age 55 years. However, in this same study there was no correlation
in women with detrusor instability. In a randomized trial, Dowd (31) assigned 32 women to one
of three groups: group 1 increased fluid intake by 500 cc over baseline; group 2 decreased by
same amount; and group 3 maintained baseline level. The authors reported that 20 women who
had fewer incontinent episodes at the end of the trial attributed this to drinking more fluids.
Women in this study noted that it was easier to limit daily intake than to increase it. The
recommended daily fluid intake is 1500 mL, but many feel that a more appropriate intake is
1800 –2400 mL/d. To be adequately hydrated, it is felt that older patients must consume at
least 1500 –2000 mL/d of liquids (32). Many patients, especially women who are dieting or who
actively exercise, may drink excessive fluids that may total more than 4000 mL/d. If they are
experiencing UI, they should be encouraged to decrease the amount.
The timing of fluid may be important in persons who have problems with nocturia. Aging
causes an increase in nocturia, defined as the number of voids recorded from the time the
individual goes to bed with the intention of going to sleep, to the time the individual wakes with
the intention of rising. Nocturia is an average of greater than 2 nocturnal voids per night.
Nocturia can be diagnosed as nocturnal polyuria (NP), which causes the largest amount of urine
production to occur at rest while the person is supine. Chronic medical conditions such as
congestive heart failure, venous stasis with peripheral edema, hypoglycemia, excess urine
output, obstructive sleep apnea, and diuretics as well as evening/nighttime fluid consumption
are causes of NP. During the night, there is a lower level of physical activity, and body fluid
moves more quickly from one part of the body to another, causing an increase in the amount of
urine in the bladder. To decrease nocturia precipitated by drinking fluids primarily in the
evening or with dinner, the person should be instructed to reduce fluid intake after 7 PM and shift
intake toward the morning and afternoon.

2. Influence of Bladder Irritants

The type of fluid or food is felt to be important (33). Caffeine is an ingredient found in certain
beverages, foods, and medications and is felt to impact LUTS by causing a significant rise in
detrusor pressure (34). Caffeine has been shown to have an excitatory effect on detrusor muscle
contraction (35).
The consumption of caffeinated beverages, foods, and medications should not be
underestimated. In the United States, .80% of the adult population consumes caffeine in the
form of coffee, tea, or soft drinks on a daily basis. It is estimated to average 200 mg d, which is
equivalent to two 7.5-oz cups of brewed coffee (36). Additionally, the U.S. Food and Drug
Administration (FDA) has listed .300 drugs that are bought off over the counter (OTC) in
pharmacies and retail drug stores that contain caffeine. Caffeine is usually listed on the label of
the products.
In addition to caffeine, alcohol is also felt to have a diuretic effect that can lead to
increased frequency. Alcohol causes a release of antidiuretic hormone (ADH) from the posterior
pituitary (34). Alcohol with dinner may be a contributing factor for nocturia. Anecdotal evidence
suggests that eliminating dietary factors such as artificial sweeteners (aspartame) and certain
foods (e.g., highly spiced foods, citrus juices, and tomato-based products) may play a role in
continence (37).
 Behavioral Treatments 237

Research has shown that urine leakage decreased (63%) when caffeine consumption was
reduced from 23 to 14 g (38). Arya et al. (39) found that women (N ¼ 20) with higher caffeine
intake (484 + 123 mg/d) had a 2.4-fold increased risk for detrusor instability than women
(N ¼ 10) with a low caffeine intake (194 + 84 mg/d). There was also a correlation between
current smoking and caffeine intake. Bryant et al. (40) conducted a prospective randomized
controlled trial of persons with symptoms of urgency, frequency, and urge UI who routinely
ingested 100 mg or more of caffeine per day. Both groups were taught bladder training, but
the intervention group was also instructed to reduce caffeine intake. Significant improvement in
urine loss was seen in the intervention group. Results in this study appeared to affect the OAB
symptom of urgency. A 37% reduction was found among low users (100 – 200 mg of caffeine), a
5% reduction was found among medium users (201 – 300 mg) and a 4% increase was found
among the high users (.301 mg). Tomlinson et al. (38) showed in 34 women with symptoms of
UI (mostly mixed) who decreased caffeine intake (from 900 mL/d to 480 mL/d), episodes of
daily urine loss also decreased (from 2.33 to 1.0 mg/d).
Even though current research is not conclusive, clinicians should assess all patients with
LUTS for amount of daily caffeine intake. Patients should be advised about the possible adverse
effects caffeine may have on the detrusor muscle and the possible benefits of reduction of
caffeine intake (41). The patient should be instructed to switch to caffeine-free beverages and
foods or eliminate them and see if symptoms decrease or resolve. Patient Guide #1 lists the
caffeine intake of common products. Patients need to read product labels. Herbal teas that are felt
to be more “natural” usually contain caffeine unless stated otherwise. Patients seem to think that
iced tea has less caffeine than hot tea. In many patients who ingest large quantities, total
elimination may be unrealistic. It is recommended that patients with incontinence and
OAB avoid excessive caffeine intake (e.g., no more than 200 mg/d; 2 cups).

D. Bowel Regularity
Chronic constipation and straining during defecation can contribute to LUTS and pelvic organ
prolapse. The close proximity of the bladder and urethra to the rectum and their similar nerve
innervations make it likely that there are reciprocal effects between them (42). Constipation is
defined as having fewer than three stools per week. Usually a patient’s definition of constipation
is considerably broader, however, and includes straining during defecation, painful defecation,
dry hard stools, small stools, and incomplete or infrequent stool evacuation. Studies of severely
constipated women who have strained during defecation over a prolonged period have
demonstrated changes in pelvic floor neurological function (43).
Lubowski et al. (44) reported that denervation of the external anal sphincter and pelvic
floor muscles may occur in association with a history of excessive straining on defecation. Many
believe that if these are lifetime habits, they may have a cumulative effect on pelvic floor and
bladder function. Spence-Jones et al. (45) found that straining excessively at stool was
significantly more common in women with stress UI and in women with prolapse. Moller et al.
(46) reported an almost uniform positive association between straining at stool and constipation
and LUTS in women (N ¼ 487) 40 years of age. Moller postulated that chronic constipation and
repeated straining efforts induced progressive neuropathy in the pelvic floor. Charach et al. (47)
examined the effect of alleviating constipation on LUTS in 52 patients aged 65– 89. After
constipation treatment with laxatives (e.g., Senokot, lactulose) subjects reported fewer episodes
of urgency and frequency.
As there are data to suggest that chronic constipation and straining may be risk factors
for the development of LUTS, self-care practices that promote bowel regularity should be
an integral part of any treatment care plan. Suggestions to reduce constipation include the
238 Newman

addition of fiber to the diet, increased fluid intake, regular exercise, digital stimulation, and
establishment of a routine defecation schedule (see Patient Guide #2). Improved bowel function
can also be achieved by determining a timetable for bowel evacuation so that the patient can take
advantage of the urge to defecate. The schedule should be determined by the patient’s bowel
elimination pattern and previous time pattern for defecation. The patient should be taught never
to ignore the “call to stool,” the feeling that the bowel needs to be emptied.
Combining fluid management, elimination of bladder irritants, and regulation of bowels
may be the yield the maximum benefit. Dougherty et al. (48) conducted a randomized, controlled
trial in women (N ¼ 218) aged 55 years and older that incorporated reduction of caffeine
consumption, adjusting the amount and timing of intake, and making dietary changes to promote
bowel regularity, which were termed “self-monitoring activities.” Women in the intervention
group also received bladder training and biofeedback-assisted pelvic muscle exercises. Two
hundred eighteen women with stress, urge, or mixed UI were randomized, and 178 completed
one or more follow-ups. At 2 years the intervention group UI severity decreased by 61%. Self-
monitoring activities and bladder training accounted for most of the improvement.

III. TOILETING PROGRAMS

The Cochrane Collaboration has published systematic reviews for toileting programs which
include prompted voiding, habit training, and timed or schedule voiding (49 – 51). Each of these
toileting programs are caregiver dependent, which is defined as the need of a professional or
family caregiver to assist with toileting. These programs can be utilized to improve continence,
and the choice of which program is needed is determined by the cognitive status of the
individual, the variability of the voiding pattern, and the need for psychological reinforcement
for adherence to the regimen (52).

A. Dependent Scheduled Toileting Programs

A caregiver-dependent program that provides toileting on a scheduled time basis may be the
simplest initial approach. If residents in institutions like nursing homes or patients living at home
have an available and willing caregiver, a timed toileting program should be established, as at
least 60% of care-dependent patients can benefit. The premise of these programs is that if
the person is toileted on a preplanned schedule, the bladder will be emptied before incontinence
occurs. These patients may have mobility or cognitive impairment and may need assistance
(e.g., one-person assist), but may be able to cooperate with toileting. Studies suggest that
while fewer than 20% of frail elders become completely dry, 30– 50% of incontinent elders
improve with reduction in the number and amount of incontinence episodes.

B. Habit Training
Habit training, first described in England as “bladder drill,” is toileting a person on a rigid, fixed
schedule. Toileting takes place whether or not a sensation to void is present but is usually only
followed during waking hours. The goal is to keep the person dry, and no effort is made to
motivate the person to resist urgency and to delay urination. Prefixed times such as every 2 h
have been adopted for toileting programs in institutions such as nursing homes. However, a more
realistic schedule may be related to certain daily routines such as upon awakening, mid-morning
before or after meals, and at bedtime.
 Behavioral Treatments 239

C. Prompted Voiding
Prompted voiding (PV) is a type of scheduled toileting program that employs behavior
modification to reinforce both appropriate toileting behaviors and the individuals’ desire to stay
dry. PV is used for patients who are able to recognize urine leakage and are able to respond (will
void) when prompted. PV stresses active communication and interaction between a caregiver
and patient allowing the patient to take an active part in their incontinence and toileting
behavior. Characteristics of “high responders” (53,54) or those who were more likely to make
the greatest improvement in their incontinence include:
Has a bladder capacity of at least 200 cc and , 600 cc
Maximum voided volume . 150 cc
Postvoid residual , 200 cc
Has a small number (,4 times/12 h) of incontinent episodes per day
Responds to caregivers if prompted (asked and taken to the toilet) to void
Ability to ambulate independently or with assistance of one person
There are five major steps of a prompted voiding program that includes scheduled
checking to allow the patient to request toileting, discussing with the patient the incontinence
problem, prompting the patient to void, providing positive reinforcement to the patient for
making an effort to use the toilet, and if incontinent, indicate to the patient that the expectation is
that they stay dry.
Like habit training, this program is for frailer, older patients who require assistance from
family members and/or professional caregivers. At least 25 –40% of patients respond well to PV
while approximately 38% cannot successfully toilet even when provided assistance by
caregivers (53,55).
Another caregiver-dependent PV program involves toileting residents and other care-
dependent patients at times when they are most likely need to void, which are determined by
tracking voiding and UI and determining patterns using computerized recordings of wetness
(56,57).
Despite documented research and positive outcomes, PV interventions have not been
adopted by the staff in institutionalized settings such as nursing homes. There is a wide gap
between what is known and what is actually used. Research has documented the success of a
program called Behavioral Supervision Model, which defines responsibilities of staff members
for the prompted voiding intervention, staff feedback regarding performance, and consequences
based on staff performance evaluation (58). A novel staffing model that employed a “designated”
versus an “integrated” role in nursing homes of the certified nursing assistant (CNA) in the
delivery of a restorative care (walking program, exercise therapy) may have application to
delivery of continence care (59).

D. Independent Bladder Training

Bladder training is also commonly referred to as bladder retraining, as well as bladder
discipline, bladder drill, and bladder reeducation and is an education program that involves
learning and independent micturition behavior by the patient.

E. Bladder Training
Bladder training (BT) requires patients to resist the sensation of urgency, to postpone voiding,
and to urinate by the clock rather than in response to an urge. Mechanisms of action are not well
240 Newman

understood, but it is felt that bladder retraining improves cortical inhibition over detrusor
contractions, facilitates cortical ability over urethral closure during bladder filling, strengthens
pelvic striated muscles, and alters behaviors that affect continence (e.g., frequent response to
urgency). The goals of a BT program are to:
Improve bladder overactivity by controlling urgency and decreasing frequency
Increase bladder capacity
Reduce urge incontinence episodes
Jeffcoate and Francis (60) originally introduced bladder training that was called “bladder
drill” by implementing the program in hospitalized patients with bladder dysfunction secondary
to psychological disorders. At that time, it was prescribed for functional disorders of the bladder
for which surgical intervention was not expected to be successful. The management regimen
included education followed by a strict schedule of voluntary voiding with specific instructions
to avoid responding prematurely to urinary urgency. This type of bladder training was the basis
of a randomized controlled clinical trial of 123 women with detrusor instability, stress, and
mixed UI. Results on the group taught BT reduced number of incontinent episodes by 57% and
quantity of urine loss was reduced by 54% (61). In addition, BT significantly improved the
quality of life, specifically in the ability to carry out activities and relationships, to tolerate and
control symptoms and in improved ability to cope (62).
In the behavioral intervention research that focuses on persons with urge or mixed
incontinence, BT is an integral component. The Cochrane database includes a systematic review
of bladder training (63). BT is most appropriate for patients who have:
Stress, urge, or mixed incontinence
Cognition; are mentally intact
Ability to sense the urinary urge sensation
Comprehension; can read and follow instructions
Motivation; willing to comply with a structured education program
Prior to beginning a BT program, the patient should be educated about the lower urinary
tract, causes of urinary incontinence, and concepts of bladder urgency using easy-to-
understand visual aids such as “the urinary urge” (see Patient Guide #3). Education should
include the fact that “continence” is a learned behavior and the importance of the brain’s
control over lower urinary tract function. The clinician initiates the program by assigning a
voluntary voiding schedule, which includes voiding every 30 –60 min (64). The voiding
intervals are based on the baseline micturition frequency as determined by the bladder diary.
The initiation of BT with very short voiding intervals is particularly important for patients who
are experiencing urgency, as the shorter intervals will decrease or eliminate these symptoms
(61,65). The goal is for the patient to void “before” the urge sensation of bladder fullness.
Depending on the patient’s ability to keep the schedule and/or evidence of reduction of
incontinence episodes and/or urinary urgency and frequency, the scheduled intervals between
voiding is increased by 30 min until the patient can achieve a goal of voiding every 3 – 4 hr. In
many cases, patients find this schedule difficult. Therefore the patient should be told to adhere
to this schedule at least 75% of the day, and it is not realistic to expect patients to maintain this
voiding schedule during the night. The use of reminders such as a kitchen timer or stop watch
can be beneficial to helping the patient keep on a schedule (66). Self-monitoring through the
use of bladder diaries is used to evaluate adherence and to determine the next weekly voiding
interval.
Another essential part of BT patient education focuses on the cortical ability to delay
voiding and strategies for distraction. Concentration on an attentional task is useful in distracting
 Behavioral Treatments 241

the individual from the sensation of urgency (65). The patient is taught methods to resist or
inhibit the urge sensation so that an expanded voiding interval can be adopted. Improving the
ability to suppress the urge sensation and eventually diminish urgency will enable the patient to
adopt a more normal voiding pattern. There are several bladder control strategies or techniques
used to inhibit the urge sensation (67). They include:
Slow, deep breathing to consciously relax the bladder to combat a stressful rush to the
toilet
Performing five or six rapid, deliberate, and intense pelvic muscle contractions, or “quick
flicks” which are 2 – 3 sec in duration
As with most behavioral interventions, the relationship between the clinician and patient is
very important to the success of the retraining. The clinician must monitor the patient’s progress
and provide praise and encouragement where appropriate. The use of a signed patient agreement
or “contract” with the patient stating personal outcome goals can be helpful in motivating the
patient to adhere to the program and outlines expectations. It has been shown that women with
incontinence have diverse goals for incontinence treatment, which in some cases may be
improvement in urine leakage and not continence (68).
It is felt by most experts that combining behavioral interventions with treatments such as
drug therapy would increase symptom reduction. Mattiasson et al. (69) reported on a
multicenter, single-blind Scandinavian study of 505 subjects, predominantly women (mean age
63) with symptoms of OAB with and without urge incontinence that were either treated with
tolterodine 2 mg BID or tolterodine 2 mg BID and bladder retraining (BT). Subjects in the BT
group were provided with a written information sheet that outlined the principles of BT and
explained simple techniques that could be used to help improve bladder control. Both groups
received bladder diaries to track outcomes. Seventy-eight percent of subjects completed 24
weeks of treatment. The median percent reduction of voiding frequency for those receiving drug
therapy plus BT was 33% compared with 25% reduction in those subjects on drug therapy alone.
There was no significant difference between the groups in relation to reduction in incontinence
episodes or urgency. The authors term this approach as a “minimalist” approach, as there was no
physician or other professional. They feel this negates the need for an extensive personal
interaction between the patient and clinician; however, this is the only study that has shown this
technique. Other such programs have not been successful (70).

IV. PELVIC MUSCLE REHABILITATION

A. Pelvic Muscle Exercises
Dr. Arnold Kegel, an obstetrician-gynecologist, introduced pelvic muscle exercises in the late
1940s by implementing a comprehensive program of progressive contractions of the levator
ani muscle that incorporated biofeedback technology and was under direct supervision of a
trained nurse. Dr. Kegel demonstrated in several clinical trials that practicing these exercises
decreased stress urinary incontinence in childbearing women (71,72). These Kegel exercises,
or as they have become know as pelvic muscle exercises (PMEs) or pelvic floor muscle
training (PFMT), have been shown to decrease LUTS of incontinence, urgency, and fre-
quency (3).
The actual effects of PMEs on lower urinary tract function is not completely understood;
some studies show a relationship between changes in various measures of pelvic floor strength,
such as anal sphincter strength or increased urethral closure pressure and resistance, all of
242 Newman

which will prevent urine leakage (73 –77). The proposed mechanisms of action for PMEs are
that:
1. A strong and fast pelvic muscle contraction closes the urethra and increases urethral
pressure to prevent leakage during sudden increase in intra-abdominal pressure (e.g., during
a cough) (78,79). Urethral compression can be maximized by timing the muscle contraction at
the exact moment of intra-abdominal force (called the “knack”) (80 –83).
2. Rising intra-abdominal pressure (e.g., during coughing, laughing, sneezing) exerts a
downward (caudal) pressure or force on the bladder and urethra (84). Contraction of the levator
ani exerts a counterbalancing upward (cephalic) force by lifting the endopelvic fascia upon
which the urethra rests and pressing it upward toward the pubic symphysis, creating a
mechanical pressure rise (85,86).
3. Muscle contraction causes a pelvic muscle “reflex” contraction that precedes increased
bladder pressure and may inhibit bladder overactivity. The aim is to acquire learned reflex
activity.
As part of a rehabilitation program, PMEs increases support to the urethral sphincter and
detrusor muscle, thus preventing stress, urge, and mixed UI and is most appropriate in patients:
Who do not have cognitive impairments
Have the motivation to comply with the program
Have a pelvic floor that is neurologically intact
The goal of PFMT is to isolate the pelvic floor muscle, specifically the levator ani
(80,87 – 89). The PFMs are a striated, skeletal muscle group under voluntary control. PMEs
consist of repeated, high-intensity pelvic floor muscle contractions of two types of muscle fibers:
type I, slow-twitch muscle fibers, and type II, fast-twitch muscle fibers. At least 80% of the
levator ani muscle is type 1 muscle fibers. These fibers produce less force on contraction and
assist in improving muscle endurance by generating a slower, more sustained, but less intense,
contraction. Over time the continuous, though lower-intensity contraction of these muscle fibers
maintains a general level of support and urethral closure pressure. Type I muscle fibers are also
fatigue resistant. The second group is type II, or fast-twitch, fibers, which aid in strong and
forceful contractions. These fibers come into play during sudden increases in intra-abdominal
pressure by contributing to urethral closure. By exercising these fibers, pelvic muscle strength
will increase. Muscle inactivity, aging, and innervation damage can contribute to a decrease in
the proportion of type II fibers. As type II fibers fatigue easily, patients are taught to perform
rapid, repeated contractions in exercising them (75,76).
The functional demands on the fibers of PFM include sustaining force over time,
especially during increases in intra-abdominal pressure, developing force quickly and
contracting and relaxing voluntarily (90). During voiding, the person must relax the PFM to
open the external urethral sphincter to allow voiding. When these muscles do not function
properly, women in particular may develop stress UI, fecal incontinence, and pelvic organ
prolapse.
Dr. Kegel described four phases in the performance of PMEs (91):
1. Awareness of the function and coordination of the PFM muscle. For older adults and
persons whose pelvic muscle is severely relaxed, this may take several weeks.
2. Gains over muscle identification, control, and strength. Muscle strength is the maximal
force that can be generated by the PFM. Although the PFM is not flexible, the muscle must adapt
to different or changing requirements so the PFM must have contractibility and build force
quickly when contracting.
3. Firmness, thickening, broadening, and bulking of the muscles to increase muscle
endurance. Muscle endurance is a performance characteristic of the ability of the PFM to
 Behavioral Treatments 243

execute repeated contractions to and initial level of strength often called a “submaximum”
contraction.
4. Improvements of the symptoms indicate that the muscles are strengthening. At this
point some patients feel that their LUTS are so improved that regular exercising is no longer
needed.
For muscle contractility to improve, the initial muscle strength, power, endurance, repetitions,
and fatigue must be considered together with the principles of muscle training (92). The
following are the definitions for determining pelvic muscle contractility:
Strength—the maximum force or contraction that a muscle can generate.
Power—the ability for the muscle to “contract-relax” as quickly and strongly as possible,
until the muscle fatigues. These are often called “quick flicks.”
Endurance—this is the time, up to 10 sec, that the maximum muscle contraction can be
maintained or repeated, before a reduction in power of 50% or more is detected. In
other words, the muscle contraction is timed until the muscle fatigues.
Repetitions—the number of repetitions (up to 10) of the muscle contraction of equal force
that can be repeated. Use at least a 5-sec muscle relaxation between each two
contraction; easily fatigable muscles need a chance to recover, without permitting
excessive rest periods for strong muscles.
Fatigue—failure to maintain the required or expected force of the pelvic muscle
contraction for more than one or two times in succession.
The following definitions can be applied to pelvic floor muscle dysfunction:
1. Low-tone is the clinical finding of an impaired ability to isolate and contract the pelvic
floor muscles in the presence of a weak and atrophic PFM. Ideally, the patient will gain the
ability to recognize the difference between relaxation and contraction.
2. High-tone refers to the clinical condition of hypertonic, spastic PFM with resultant
impairment of muscle isolation, contraction and relaxation. A high resting baseline with high
variability and occasional spasms may be seen in patients with chronic pelvic pain syndromes. In
some cases, this excessive, elevated resting tone may be created unconsciously. Therapeutic
exercise is important in the management of pelvic pain as the patient often has a reduced level of
activity related to the prolonged nature of their pain. Rehabilitating the pelvic muscle can be
central in resolving pain when muscle spasm is present. Using PMEs on patients with high-tone to
enhance muscle relaxation is referred to as “downtraining.” Teaching a muscle to relax is often
more difficult than teaching it how to contract (uptraining), as the feeling of relaxation is small.
The patient should be cautioned not to:
1. Perform these exercises during voiding and not to stop and start urine flow as a form of
exercising. This exercise has good face validity for effectiveness because many patients initially
report an inability to stop the urine flow when it begins. However, there is some controversy over
this practice because it is nonphysiological and can be harmful (93).
2. Over-exercise the pelvic muscle. Women can develop levator ani myalgia by performing
excessive PFM exercises to reduce incontinence (94). Start slowly, building gradually.
Patients should be instructed on the correct technique of pelvic muscle exercises. Patients
have a difficult time identifying and isolating this muscle. Without sufficient information,
women may mistakenly bear down or exercise ineffectively. Specifically, women are told to
“draw in” and “lift up” of the perivaginal and anal sphincter muscles. Once patients are able to
identify the muscle, they are instructed to perform a series of “quick flicks,” or 2-sec
contractions, followed by sustained (endurance contractions) contractions of 5 sec and longer as
part of a daily exercise regimen (see Patient Guide #4). At least 10 sec of relaxation is
244 Newman

recommended between contractions. Encourage the patient to aim for a high level of
concentrated effort with each pelvic muscle contraction, as greater contraction intensity is
associated with improvement in pelvic muscle strength (74,76).
Patients are given verbal and written instructions for a daily exercise program based on the
baseline assessment of the patient’s PFMs strength, contraction, and endurance during the initial
assessment session. Visual aids are helpful (see Figs. 1, 2). Patients should be encouraged to aim
for a high level of concentrated effort with each pelvic muscle contraction, as greater contraction
intensity is associated with improvement in pelvic muscle strength (74,76). Patients are
instructed to exercise at least twice daily and to perform the exercises in three positions—lying,
sitting, and standing. A minimum of 30 – 45 PMEs per day is recommended (95). A gradual
increase in number of contractions over a period of PME practice has been shown to increase
muscle strength significantly and decrease urine loss. The patient should be instructed to contract
the muscle at the time of the UI episode (81,95). Contracting it before sneezing, coughing,
lifting, standing or swinging a golf club can prevent stress UI from occurring (see Patient Guide
#4). The muscle also can be contracted when a strong urge to void occurs. Results may not occur
until after 6 –8 weeks of exercise, and optimal results usually take longer. Self-monitoring
practice through the use of a calendar record, audio, and video taped material that review the
exercises can improve protocol compliance (37,96).
Most clinicians in this field have relied on the use of verbal and written instructions for
patients to use for home practice of PMEs, not the use of a home biofeedback device. There is a
paucity of research on the use of a home biofeedback device to aid in performing these exercises
at home while providing information to the clinician and patient about the success of the muscle
contraction (97,98).
Teaching women to strengthen the pelvic floor muscle as part of a comprehensive
behavioral program has been demonstrated to be effective in 50– 60% of women with SUI.
However, even after they have learned to do that, there is the additional problem that many find
too burdensome—the daily exercises necessary to increase muscle strength and control. As a
result, the noncompliance rate for this therapy can be high, varying from 10% to 40%. This can

Figure 1 Pelvic floor muscle in men. # 1995 Diane K Newman

 Behavioral Treatments 245

Figure 2 Pelvic floor muscle in women. # 1995 Diane K Newman

be frustrating to clinicians who provide these treatments, as poor outcome may be secondary to
noncompliance and out of their control.
Research in the area of PMEs is extensive but long-term results have been reported only
rarely (99). Cammu et al. (100) found that in women who had been successful with PMEs
initially, two-thirds maintained their success 10 years later. Practice of PMEs in primiparas
results in fewer UI symptoms during late pregnancy and postpartum (101).
Subak and colleagues (22,23) conducted a randomized trial for community dwelling women
who at least reported one UI episode per week. Women were randomly assigned to the behavioral
therapy (n ¼ 77) and control (n ¼ 75) group. Women in the behavioral therapy were asked to keep
urinary diaries and attend six weekly 20-min group instructional sessions with three to five
participants on bladder retraining and written and verbal instructions on PMEs, which was termed a
“low-intensity” behavioral therapy. Women in the control group did not receive any instructions
but were asked to keep urinary diaries for 6 weeks. At 6 weeks, the treatment group had a 50%
reduction in mean number of incontinence episodes compared with a 15% reduction or the control
group. They also experienced improved diurnal and total incontinence frequencies.
The Association of Women’s Health Obstetric and Neonatal Nurses (AWHONN) tested
the efficacy of a bladder and pelvic floor muscle training program in real-world ambulatory care
settings (88,102,103). Twenty-one clinical sites participated yielding a sample of 132 women
with a mean age of 51 years that originally screened positive for incontinence, received
instruction in bladder and pelvic floor muscle training, and persisted to a point of follow-up 4
months posttreatment. Significant reductions were noted between pre- and posttreatment in the
frequency of incontinent episodes, the volume of leakage per episode, the cost of self-
management, and the frequency of nocturia. Simultaneously, significant improvements were
reported in indices reflecting quality of life. Specifically, women indicated that the incontinence
was less bothersome and that they were avoiding fewer activities because of their incontinence.
These results demonstrate the effectiveness of an evidence-based protocol in actual clinical
settings and warrant the implementation of the protocol by nurses in general ambulatory
women’s health care settings across the United States (104).
246 Newman

B. Use of EMG or Manometric Measurement

Pelvic floor muscle strength is either measured by electromyography (EMG) or manometric
pressure. Most clinicians who specialize in this field prefer EMG measurements. EMG is the
graph of the electrical activity of a muscle and as a practical indicator of muscle activity has been
defined as:
The study of electrical potentials generated by the depolarization of muscle
A monitor of bioelectrical activity correlating to motor unit activity; it does not measure
the muscle contractility itself but the electrical correlate of the muscle contraction
An indicator of the physiological activity
The advantage of EMG over manometric pressure is that, provided the machinery is of sufficient
sophistication with adequate filtering, EMG apparatus can engage the use of the newer types of
electrodes that are lightweight and designed to stay in place, hence allowing more functional
positions during assessment and treatment (92). An added benefit is that EMG can be
multichannel, which allows the simultaneous reinforcement of contractions of the pelvic floor
muscles and inhibition of accessory muscles (e.g., abdominal muscle contractions). A common
error in contracting the PFM is to simultaneously contract the abdominal, gluteal, or adductor
muscles. This may mask the strength of the PFM contraction. Abdominal contraction increases
intra-abdominal pressure, which mechanically elevates bladder pressure, so it is important to
measure concurrent use of abdominal contraction (105). For the PMR treatment to be successful,
it is essential that the patient be able to isolate the pelvic floor muscles. When an additional
muscle group is contracting at the same time of the pelvic floor, it is called “recruitment.”
Monitoring for accessory muscle recruitment during initial EMG and subsequent visits are
necessary until recruitment stops and should be considered on all patients.
The use of multichannel EMG can be especially helpful in patients who are having
difficulty identifying and isolating the correct muscle. Four methods of EMG measurements
have been used in the investigation of lower urinary tract dysfunction (106):
Vaginal sensor
Anal sensor or plug electrode (anorectal)
Surface skin electrodes
Needle electrodes
Vaginal and anal sensors are designed to provide accurate detection of EMG muscle activity.
The accuracy of longitudinal sensing electrodes has been shown to be virtually identical to the
gold standard, inserted needle electrodes. The use of vaginal or rectal sensors is contraindicated
in the following:
Active vaginal infection or genital disease
Severe pelvic pain where insertion of the sensor causes vaginal or rectal discomfort
Pregnancy
Recent (within last 6 months) pelvic or rectal surgery
Untreated atrophic vaginitis
Dyspareunia
Menstrual period
In these cases consider the use of skin surface electrodes. Surface skin electrodes are relatively
non-invasive and well tolerated. They give quantitative information about muscle activity rather
than data for qualitative analysis. The first choice of electrode placement is at the 10 and
4 o’clock or 9 and 3 o’clock position on either side of the anus (see Fig. 3). Electrodes should be
 Behavioral Treatments 247

Figure 3 Surface skin electrode placement

placed close to the anus without touching the other sensor or without sensors overlapping.
Needle electrodes are primarily used during urodynamic testing. The EMG data are measured in
microvolts. The actual threshold of pelvic muscle strength required for maintaining continence
is unknown at this time as is unknown the normal values for pelvic muscle strength. The baseline
and all follow-up EMG recordings should include two set of measurements of:

First Set:
Maximum or “short/quick” muscle contractions of 2-sec duration
Resting muscle activity of 2-sec duration

Second set:
Sustained or “long” muscle contractions (5, 10, or 30 sec); the clinician should not go directly from
3- to 10-sec muscle contractions but increase in increments of 5 sec as patient’s ability
warrants
Resting muscle activity of 5-sec duration or for the same length of time as muscle contraction

The ability to relax one’s pelvic muscle following a contraction is of most importance if one is to
gain control and coordination of these muscles.
Manometry is the use of an instrument to detect, assess, and record pressure. A pressure
perineometer consists of a vaginal or rectal probe with a connector tube to a manometer.
Dr. Arnold Kegel first used the term “perineometer” for a vaginal pressure gauge specific to the
PFM. He developed this instrument for both diagnosis and nonsurgical treatment for women
with stress UI and pelvic muscle relaxation. Perineometers aim to show changes in pressure
caused by the contraction of the perivaginal musculature, to be observed on a manometer gauge.
The pressure changes can be measured in centimeters of water (cmH2O) or millimeters of
mercury (mm Hg). Depending on the sophistication of the equipment, the pressure changes may
be shown on a dial, a digital readout, a bar chart, or a graphical representation. Different types
of probes—air-filled, water-filled, individually made, and mass produced—have been reported
and can be performed by inserting sensors into the vagina or rectum. Although manometry and
pressure sensors are available with certain clinical systems and have been used in several clinical
trials, they are primarily used for treatment of rectal dysfunction (e.g. constipation, fecal
incontinence), not for treatment with LUTS. Theofrastous, Wyman et al. (107) used two water-
filled balloon manometric devices to measure vaginal and abdominal pressures. The group who
248 Newman

received a pelvic floor muscle training regimen demonstrated a 15– 23% improvement in pelvic
muscle strength.

C. Application of Biofeedback Therapy

The use of biofeedback therapy is a method of assessment and treatment of pelvic floor
dysfunction. Biofeedback relayed using EMG, when used as part of a pelvic muscle
rehabilitation program, is a method by which the patient is immediately made aware of the
physiologic state of the PFM. Feedback to the patient is in the form of tactile, verbal, visual, or
auditory methods. Biofeedback treatment may assist muscles that have increased tension even
when the patient or clinician cannot detect it. This is particularly true of the pelvic floor muscles,
as denervation damage may lead to impaired sensation. High levels of resting activity and
fleeting muscle spasms may be only visualized using EMG biofeedback instruments. Muscle
training that utilizes EMG biofeedback may improve the effectiveness of the muscle relaxation
efforts while strengthening weak pelvic muscles. A biofeedback-assisted exercise program
that stabilizes the pelvic floor muscles can reduce and eliminate symptoms of pelvic floor
dysfunction as seen in chronic pelvic pain syndromes.
Generally, visual, auditory, or verbal feedback techniques are used for neuromuscular
conditioning. These methods help to reinforce a particular task being performed. For example,
the display on a monitor screen of the pressure, or the EMG changes of the anal sphincter,
provide instant visual feedback to the patient regarding their performance. Similarly, during
muscle contraction the intensity (pitch of the electrical activity) of the sphincter muscle provides
corresponding auditory feedback to the patient regarding their performance. To determine PFM
strength, two indices recommended as outcome of muscle strength tests that can be recorded on
the EMG are the peak muscle contraction value and the average score. EMG or manometry can
record the following variables of the PFM:
Strength—recorded as the peak or maximum contraction that has the highest waveforms
indicating ability to sustain the muscle contraction
Endurance—average muscle contraction measured across the waveform
Contractibility—the rate of the original rise of the muscle contraction
Throughout the treatment session, the clinician reinforces the patient’s behavior and provides
compliments and other appropriate advice. This constitutes verbal feedback to the patient and is
an essential part of a behavioral treatment program. All three maneuvers are complimentary.
Motivation and active participation play a big part in the success of biofeedback therapy.
For incontinence and other LUTS, biofeedback therapy uses computer graphs or lights as a
teaching tool to help the patient identify and learn to control the correct muscles. Biofeedback
helps the patient locate the pelvic muscles by changing the graph or light when the patient
contracts or tightens the correct muscle.
Different biofeedback methods can be used in pelvic floor muscle (PFM) reeducation,
including proprioception and verbal encouragement during:
1. Digital (e.g., vaginal or rectal) PFM assessment of the levator ani muscle is a form of
biofeedback and is an important component of teaching correct pelvic muscle contraction and
muscle awareness (108). Verbal feedback of a voluntary contraction can also encourage and assist
in enhancing patient effort. A digital measure of pelvic muscle strength can be performed based on
pressure, duration of contraction, and displacement of the examiner’s finger. Palpation of muscular
attachments along the pubic arch and the insertion of the levator ani and coccygeus muscles are part
of the assessment. The levator ani can be palpated just superior to the hymeneal ring. Palpate the
levators at the 4 and 8 o’clock positions to determine if that reproduces any discomfort or
 Behavioral Treatments 249

tenderness. There are several different grading systems (examples are found in Tables 1 and 2) that
can be used to assess and document pelvic muscle strength in women. Using the scale described in
Table 1, a scale, assess pressure, which is defined as the strength of contraction on the finger. Scores
range from 0 for no pressure felt to 5 for strong compression, where the examiner’s finger(s) are
gripped. Ask the patient to squeeze hard and count in seconds to determine the duration of the
contraction, which is recorded in seconds. Note the displacement in plane by the amount of
movement of your finger(s) when the patient contracts her muscle. The rating scale starts with 1,
which is no displacement, to 5 when the examiners finger are moved upward and drawn in by the
contraction of the pelvic muscle. It may be helpful to perform a digital PMA pre- and posttreatment
to determine the increase in muscle strength, strength, and ability to isolate the levators.
2. Manometric and EMG biofeedback helps in PFM awareness, but also provides interest,
challenge, and reward for effort, a greater feeling of control, and progress in monitoring (109).
Research is extensive detailing the efficacy of the use of biofeedback-assisted behavioral
therapy for PFMT (110 –116). The 1996 guideline on Urinary Incontinence in Adults (3)
outlined the research that demonstrated that PMEs are indicated for patients with stress
incontinence and can reduce urgency and prevent urge UI. Pelvic floor reeducation has proven to
be effective in women with sphincter deficiency and detrusor instability. More recent research
has supported this claim (101,117,118). Behavioral modifications, pelvic muscle rehabilitation,
and bladder retraining programs have successfully decreased UI in homebound elders (119,120).
A study of men with urinary incontinence following radical prostate surgery showed that 88%
of the treatment group achieved continence in 3 months compared to 56% of the control
group (121).
Wyman and colleagues (122) randomized 204 women into three groups. Group 1 was
encouraged to use bladder training with the voiding interval set at 30 or 60 min and increased by
30 min each week. Group 2 received pelvic muscle instruction that included four office
biofeedback sessions; women were instructed to perform five fast and 10 sustained contractions
twice a day and work up to a total of 50 contractions by the third week. Participants were also
instructed to use pelvic muscle contractions for urge inhibition and preventive contractions
with exertional events. Group 3 received a combination of the two therapies. There were no
significant differences found pretreatment in any of the outcome variables. At the short-term
follow-up 2 weeks after treatment, the combination therapy group had significantly fewer
incontinent episodes, better quality of life, and greater satisfaction with treatment. However, by
3 months posttreatment, all three treatment groups had improved relative to baseline status. The
absence of differences among the three groups led the investigators to conclude that the type of
therapy (bladder or pelvic floor muscle training) may be less important than participation in a
structured intervention program.
Dougherty and colleagues (48) randomized 218 women, aged 55 and older who were
provided treatment in their home by a trained nurse practitioner. Group 1 was a control group.
Group 2 received a behavioral management for continence (BMC) program that consisted of
sequenced phases: (a) self-monitoring, (b) bladder training, and (c) biofeedback-assisted pelvic
muscle exercises. The BMC treatment was not found to have a significant impact on either urinary
frequency or voiding intervals. Amount of urine loss decreased in 61% of the BMC over the 2 years
of follow-up, whereas the control group’s urine loss worsened by 184%. However, both the BMC
and control groups’ episodes of urine loss decreased (70% and 16%, respectively).
Burgio and associates (123) compared the effectiveness of anorectal biofeedback-assisted
behavioral therapy for PFMT with drug therapy and placebo control and showed that the
behavioral intervention was more effective with 80% of those receiving behavioral experienced
a reduction in incontinence episodes compares with 68.5% if those receiving drug therapy and
only 39.4% of those receiving placebo.
 250
Newman

Table 1 Pelvic Muscle Rating Scale

Grade

0 1 2 3 4 5

Pressure None Flick, more than Felt at more than one Loose hold (full Snug (full Strong compression of
one point, but not point but not a full circumference) circumference) fingers
a full circumference
circumference (instant, mild
(instant, mild pressure)
pressure)
Displacement None Base lifting Base to midfinger Base to fingertip; lifting, Base to fingertip; lifting, Vigorous drawing up
gentle lift at tip strong lift at tip and in
Duration Seconds maintained

Source: Brink et al. (124).

 Behavioral Treatments 251

Table 2 Modified Oxford Scale for Pelvic Muscle Assessment

Grade Description

Nil 0 No discernible PFM contraction

Flicker 1 Feels like a flicker or a pulsation and
represents a very weak contraction
Weak 2 Weak contraction, is detected as an
increase in muscle tension, without
any discernible lift or tightening
Moderate 3 A moderate contraction characterized
by a degree of lifting of the posterior
vaginal wall, tightening of the
examiner’s finger (pubovisceralis)
and drawing in of the perineum. A
grade 3 as well as a grade 4 and 5
contraction is generally discernible
on visual perineal inspection.
Good 4 Produces elevation of the posterior
vaginal wall against resistance
(applied as pressure to the posterior
vaginal wall) and drawing in of the
perineum. If two fingers (index and
middle) are placed laterally in the
vagina and separated, a grade 4
contraction can squeeze them
together against resistance.
Strong 5 Strong resistance can be given against
elevation of the posterior vaginal
wall and approximation of the index
and middle fingers.

Clinician-supervised PME with biofeedback is felt to provide the most favorable long-
term results and many multidisciplinary pelvic floor dysfunction or “continence” centers provide
these services (37). Berghmans et al. (125,126) reviewed the literature regarding biofeedback-
assisted PMEs in women with stress and urge UI and felt there was a need for more research to
support these more intensive therapy regimens.
The most recent study was conducted by Burgio and colleagues (127) in women (n ¼ 222)
who had urge UI. Women were randomized to three treatment groups:
Group 1 received behavioral training that consisted of bladder retraining and PMEs with
anorectal biofeedback. They had four clinic visits with nurse practitioners at 2-week
intervals with a home program of PMEs.
Group 2 received behavioral training without biofeedback but digital pelvic muscle
assessment with information on muscle isolation and correct identification and was
given a home program of PMEs.
Group 3 were given a 20-page self-administered booklet that included an 8-week step-by-
step, self-help instructions on bladder retraining, and PMEs.
Results indicated that the outcomes of the three groups were not significantly different. Group 1
had 63.1% reduction in frequency of UI episodes, group 2 had 69.4% reduction in frequency of
252 Newman

UI episodes, and group 3 58.6% reduction in frequency of UI episodes. However, patients’

perceptions of treatment were significantly better for groups 1 and 2.

D. Combining Behavioral Treatments with Drug Therapy

In addition, a more recent study (128) examined the effects of combining behavioral treatment
and drug treatment for urge UI in ambulatory women. Subject’s reduction of incontinence went
from a mean 57.5% with behavioral therapy to a mean 88.5% overall reduction with combined
behavioral and drug (anticholinergic) treatment. The majority of the PME research used
biofeedback therapy to teach and train the PFM.

E. Use of Vaginal Weights

Vaginal weights are another example of a biofeedback technique, which educates women on
contraction of the PFMs. They have been most successful in woman with stress incontinence,
and can be used by the patient as part of a structured resistive pelvic muscle exercise program.
The weights are made of plastic and shaped like cones and are of increasing weights. The user
is instructed to insert the lightest weight into the vagina, in the position of a tampon. It should
be inserted so that it cannot be felt protruding from the opening of the vagina. The user then
walks around for up to 15 min. If the weight is retained during this time, the next-heaviest
weight is introduced and the procedure is repeated until a weight of a certain weight slips out.
The woman uses that weight to practice holding it in, by contracting the pelvic muscles, for up
to 15 min BID. When the woman can successfully hold one weight, she is told to switch to a
heavier one. To increase the exercise value of these weights, the woman is instructed to
practice retaining the weight during coughing, jumping, or any stress-provoking act that causes
incontinence. Theoretically, when the weight is placed in the vagina, it provides sensory
feedback and prompts a pelvic floor muscle contraction to keep it from slipping out. The
perceived advantages of vaginal weight training are that it involves less teaching time, can be
self-taught, may be motivational, and can be used with minimal supervision. There is strong
evidence that indicates it is an effective treatment for stress UI in pre- and postmenopausal
women (12), However, the evidence is inconclusive regarding the superiority of vaginal weight
training over PMEs alone or electrical stimulation; further there appears to be no added benefit
to use of vaginal weight training with PMEs (129,130). Although vaginal weight training may
take less instructional time in terms of office practice, it may be less acceptable to some
women than PFME alone as noted by higher attrition rates in some clinical trials (131).
Reasons given for their nonuse were aesthetic dislike, unpleasantness, discomfort, difficulty of
insertion, or bleeding (132).

F. Pelvic Floor Electrical Stimulation

Pelvic floor electrical stimulation (PFES) is the application of a low grade of electrical
stimulation to the pelvic floor muscles (PFMs) to stimulate the muscle to contract. PFES has a
twofold action: contraction of pelvic floor muscles, and inhibition of unwanted detrusor
contractions. PFES for stress UI is the result of stimulation of afferent fibers of the pudendal
nerve activating both the pelvic floor and periurethral muscles. For urge UI bladder inhibition
occurs through pudendal (afferent) to pelvic (efferent) nerve reflex and a pudendal to hypogastric
 Behavioral Treatments 253

reflex. The application of electric current to the pelvic floor muscles produces a reflex
muscle contraction without any effort on the part of the patient. Pelvic muscle electrical
stimulation combined with biofeedback may prove useful in that the electrical stimulation
provides a passive contraction with increased awareness of pelvic muscle contractions.
The parameters of most stimulation units include the waveform, the current intensity, the
pulse frequency, the ramping of impulses, and the on/off timing. The muscle contraction, called
neuromuscular stimulation, is a useful addition to pelvic floor exercises in the rehabilitation of
weakened pelvic muscles and is very beneficial for both men and women who are unable to
contract these muscles on command, as it leads to an improved comprehension of the activity of
the muscles and subsequently better active contraction. Also, PFES is used with patients as an
adjunct treatment to:
Assist with identification and isolation of pelvic muscle
Increase pelvic muscle strength
Decrease unwanted or uninhibited detrusor (bladder) muscle contraction
Assist with normalizing pelvic muscle relaxation
There are no documented side effects to electrical stimulation of the pelvic floor, but PFES
is contraindicated in the following:
Complete denervation of the pelvic floor (will not respond)
Dementia
Demand cardiac pacemaker
Unstable or serious cardiac arrhythmia
Pregnancy or planning/attempting pregnancy
Rectal bleeding
Active infection (UTI/vaginal)
Unstable seizure disorder
Swollen, painful hemorrhoids
Presence of vaginal vault prolapse
Pelvic surgery in past 6 months
Electrical stimulation is usually performed initially in the clinician’s office than prescribed as a
home program using a battery-operated home unit. The delivery of the electrical current to the
tissues is via a sensor, which may be on the surface of the skin (skin electrodes around the anus)
or by vaginal or rectal sensors and is used in conjunction with biofeedback. The home program
consists of using the stimulator for 15 min BID for several weeks to months, although the length
of time and number of treatments is highly variable. However, with the wide variations in
stimulation parameters including time, intensity, and frequency of sessions, it is difficult to make
comparisons across studies. Given the equivocal results, the benefit of electrical stimulation in
stress, urge, and mixed UI in women remains controversial (12).
There does not appear to be any consistency to PFES protocols used in clinical practice
to treat patients with stress, urge and mixed incontinence. The research in this area is
confusing because information is lacking on detail of stimulation parameters (intensity, pulse
duration), time PFES is used by the patient, devices used and methods of delivery (133 –138).
The Cochrane Database did not find any significant differences between the addition of PFES to
a PME program for self-reported cure (139).
Goode et al. (140) conducted a RCT of the effect of PFES to a behavioral intervention
program in women with stress only or mixed UI. This study was similar to their previous
research (127) except that PFES was added. Women (N ¼ 200) underwent an 8-week treatment
254 Newman

program and were asked to complete a daily bladder diary. Women were randomized to three
groups:
. Group 1 received behavioral training that consisted of anorectal biofeedback-assisted
PMEs, home exercises, and bladder control strategies.
. Group 2 received same program as Group 1 with PFES (performing both office and
home stimulation) using a vaginal sensor.
. Group 3 or control condition consisting of a self-administered self-help book on
behavioral treatments.
Results indicated that the addition of PFES did not seem to enhance the results of behavioral
training alone however, behavioral training with or without PFES were significantly more
effective than the self-help book. Actual results showed that behavioral training resulted in a
mean 68.6% reduction in frequency of UI episodes, behavioral training with PFES resulted in a
71.9% mean reduction and treatment with the self-help book a 52.5% reduction. The authors felt
that the two treatments of PMEs and PFES may overlap. This reinforces other research noted in
this chapter on behavioral interventions that suggest that this treatment is optimally implemented
in a clinical practice setting with trained professionals (doctors, nurse practitioners or nurses) to
ensure that patients are exercising the correct muscle. Also, a stepped approach in which
biofeedback and PFES are added to a less invasive program such as PMEs and lifestyle changes
is the preferred clinical approach and is supported by current reimbursement (141).

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258 Newman

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in older women with urinary incontinence. Nurs Res 1989; 38:196 – 197.
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Review). In: The Cochrane Library, Issue 1, 2002. Oxford: Update Software.
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of persistent postnatal urinary and faecal incontinence: randomised controlled trial. Br Med J 2001;
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133. Bent AF, Sand PK, Ostergard DR, Brubaker L. Transvaginal electrical stimulation in the treatment
of genuine stress incontinence and detrusor instability. Int Urogynecol J 1993; 14:9– 13.
134. Brubaker L, Benson JT, Bent A, et al. Transvaginal electrical stimulation for female urinary
incontinence. Am J Obstet Gynecol 1997; 177:536 – 540.
135. Luber KM, Wolde-Tsadik G. Efficacy of functional electrical stimulation in treating genuine
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of behavioral training with or without pelvic floor electrical stimulation on stress incontinence in
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143. Brubaker L, Benson JT, Bent A, Clark A, Shott S. Transvaginal electrical stimulation for female
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Geriatr Soc 1990; 38:338– 340.
145. Burns P, Pranikoss K, Nochajski T, Desotelle P, Harwood M. Treatment of stress incontinence with
pelvic floor exercises and biofeedback. J Am Geriatr Soc 1990; 38:341– 344.
146. Cammu H, Van Nylen M, Derde M-P, DeBruyne R, Amy JJ. Pelvic physiotherapy in genuine stress
incontinence. Urology 1991; 38(4):332– 337.
147. Dietz H, Wilson P, Clarke B. The use of perineal ultrasound to quantify levator activity and teach
pelvic floor muscle exercises. Int Urogynecol J 2001; 12:166– 169.
148. Engberg SJ, McDowell BJ, Weber E, Brodak I, Donovan N, Engberg R. Assessment and
management of urinary incontinence among homebound older adults: a clinical trial protocol. Adv
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Br J Urol 1984; 56:482 – 484.
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vaginal cones. Acta Obstet Gynaecol Scand 1997; 76: 455– 460.
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floor reeducation for stress incontinence: comparing three methods. Br J Community Nurs 2001;
6(5):230 – 237.
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long term care: promoting sustainability of prompted voiding. Unpublished manuscript, 2002.
153. Luber KM, Wolde-Tsadik G. Efficacy of functional electrical stimulation in treating genuine stress
incontinence: a multicenter, clinical trial. Physiotherapy 1997; 79:553 – 540.
154. Nygaard I, Kreder K, Lepic M, Fountain K, Rhomberg A. Efficacy of pelvic floor muscle exercises
in women with stress, urge, and mixed urinary incontinence. Am J Obstet Gynecol 1995; 174(1):
120– 125.
 Behavioral Treatments 261

155. Palmer MH, Fitzgerald S, Berry SJ, Hart K. Urinary incontinence in working women: an exploratory
study. Women Health. 1999; 29(3):67 – 80.
156. Theofrastous JP, Wyman JF, Bump RC, et al. Effects of pelvic floor muscle training on strength and
predictors of response in the treatment of urinary incontinence in women. Neurourol Urodyn 2002;
21:486– 490.

Patient Guide #1: Caffeine Chart

Source of caffeine Serving Size Caffeine (mg)
Coffee: Brewed, drip 8 oz. 100– 164
Brewed, percolated 8 oz. 80– 135
Instant 8 oz. 50– 75
Decaffeinated 5 oz. 2– 4
Tea (black or green) 1-min brew 5 oz. 20– 34
3-min brew 5 oz. 35– 46
5-min brew 5 oz. 39– 50
Instant tea 5 oz 30
Iced tea 12 oz. 67– 76
Hot chocolate 5 oz. 2– 15
Soft drinks Jolt Cola 12 oz. 71
Mountain Dew 12 oz. 54
Coca-Cola 12 oz. 60
Diet Coke 12 oz. 46
Tab 12 oz. 49
Pepsi-Cola 12 oz. 43
Diet Pepsi 12 oz. 36
Dr. Pepper 12 oz. 60
Red Bull 12 oz. 106
Chocolate desserts Brownie (with nut) 1.25 oz. 8
Cake 1/16 of 900 14
Ice cream 2/3 cup 5
Pudding 2 cup 6
Chocolate candy Milk chocolate 1 oz. 1– 15
Sweet, dark chocolate 1 oz. 20
Baking chocolate 1 oz. 25– 35
Painkillers Anacin 2 tablets 64
Excedrin 2 tablets 130
Vanquish 2 tablets 66
Midol 2 tablets 64
Darvon compound 2 tablets 65
Fiorinal 2 tablets 80
Norgesic 2 tablets 30
Cold/allergy Dristan 2 tablets 32
Sinarest 1 tablet 30
Stimulants No-Doz 2 tablets 200
Vivarin 1 tablet 200
# 1997 Diane K. Newman
262 Newman

Patient Guide #2: Maintaining Bowel Regularity

Sometimes urinary incontinence, urgency, and frequency may be aggravated by increased
pressure on the bladder from the pressure related to constipation or stool (hard) impaction.
Eating foods that have a lot of fiber helps overcome this problem. Fiber-rich foods include
whole-grain breads, brown or wild rice, cereals, nuts, and raw fruits and vegetables. Apricot
juice has more fiber content than prune juice. Another way to increase your fiber is by using a
special bran recipe.

How to make “Special Bran Recipe”

Mix together:
1 cup applesauce You can buy unprocessed wheat bran in the
1 cup coarse unprocessed wheat bran grocery or health food stores. This type of bran
3
4 cup prune juice is different from bran cereal.

Refrigerate mixture and take 2 tablespoons of the mixture every day. Take the mixture in the
evening for a morning bowel movement. Increase the bran mixture by one tablespoon until your
bowel movements become regular. If the amount exceeds 4 tablespoons, take the mixture in
divided doses in the morning and evening. Always drink one large glass of water with the mixture.

What if I don’t like the “Special Bran Recipe”?

Add unprocessed wheat bran to your diet. Start by using 1– 2 tablespoons every day. If necessary
for regulation, increase bran slowly over several weeks to approximately 6 tablespoons every
day. Mix bran in foods like applesauce, cereals, or sauces, or use it as a spice in gravies or
puddings. Sprinkle bran on ice cream, vegetable and fruit salads, or cottage cheese. Add to
muffins, breads, and cookies when baking.

When will I notice a change?

You may notice effects on bowel function 3– 5 days after starting bran or other natural remedies.
You should continue to use these remedies.

Will bran and other natural remedies harm me?

No! The normal reaction to bran is stomach bloating and increased gas. These symptoms usually
last for only the 1st week. If symptoms last longer, contact your nurse or doctor.
# 2001 Diane K. Newman

Patient Guide #3: Bladder Retraining—Controlling Urgency and Frequency

Frequency is voiding often, usually eight times or more in a 24-h period. Frequency can worsen
if you get into the habit of voiding “just in case,” which means that the bladder never fills
completely and holds only a small amount of urine. It is better to wait until the bladder is full.

Urgency is a sudden need to void immediately that can cause urine leakage on the way to
the bathroom. Urgency follows a wave pattern; it starts, grows, peaks and then subsides until
it stops.
 Behavioral Treatments 263

The key to controlling the urinary urge is not to respond by rushing to the bathroom. Rushing
causes movement, which jiggles your bladder, which in turn increases the feeling of urge.

Controlling the urge

The goal is for you to be voiding no more than every ___ hours. If you get the urge to void and it
is not yet your scheduled voiding time, stop all activity and sit down if possible. Then try one or
more of the following techniques that may help the urge to subside allowing the bladder to relax
and give you more time to get to the bathroom:
Take some slow, deep breaths through your mouth, concentrating on your breathing, or
Tighten your pelvic muscle quickly and hard several times in a row.
Use mental distraction strategies such as concentrating on an activity, such as
counting backward from 100 by sevens, or reciting the words of a favorite song or
nursery rhyme.
# 2001 Diane K. Newman

Patient Guide #4: Pelvic Muscle Exercises & the “KNACK”

WHAT IS THE PELVIC MUSCLE ? – Your pelvic muscle provides support to your bladder, and
rectum and, in women, the vagina and the uterus. If it weakens or is damaged, it cannot support
these organs and their position can change. This can cause problems with the organs normal
function. Keeping the muscle strong can help prevent bladder control problems and unwanted
urine leakage.

FINDING THE PELVIC MUSCLE – Without tensing the muscles of your leg, buttocks or abdomen,
imagine that you are trying to control the passing of gas or pinching off a stool. Or imagine you
264 Newman

are in an elevator full of people and you feel the urge to pass gas. What do you do? You tighten or
pull in the ring of muscle around your rectum – your pelvic muscle. You should feel a lifting
sensation in the area around the vagina or a pulling in of your rectum.

EXERCISE REGIMEN – There are two types of muscle contractions you will need to practice –
Short (2 second) or Quick contractions and Slow (3 or 5 or 10 second) or long contractions. To
do the short or quick muscle contractions, contract or tighten your pelvic muscle quickly and
hard and immediately relax it. For the slow or long (sustained) contractions, contract or tighten
your pelvic muscle and hold for a count of (3 or 5 or 10 as prescribed) seconds, then relax the
muscle completely for the same amount of time. It is equally important to control when your
muscle tightens and relaxes. Be sure to relax completely between each muscle tightening.

WHERE TO PRACTICE – You should do the exercises in these positions:

Lying Down – Lie on your back with your head on a pillow, knees bent and feet slightly
apart.
Sitting – Sit upright in a firm seat and straight-back chair, knees slightly apart, feet flat on
the floor or legs stretched out in front and crossed at the ankles.
Standing – Stand and lean on a back of a chair, knees slightly bent with feet shoulder
width apart and toes slightly pointed outward. You can also lean on the kitchen
counter with your hips flexed.

PERFORMING THE “KNACK” – In addition to doing your prescribed set of pelvic muscle
exercises, you should start contracting your pelvic muscle at the time your incontinence occurs.
Timing your pelvic muscle contraction to when your incontinence is most likely to occur is
called the “KNACK.” This is the skill of consciously timing an intentional contraction of the
pelvic muscles just before and throughout the activity that causes an increase in your urine
leakage (incontinence) or bladder control problem such as urgency.

HOW TO DO THE “KNACK” – The “KNACK” is an acquired motor skill that requires you to
anticipate your urine leakage. Any activity, which increases pressure in your abdomen, may
cause you to lose urine. Examples of such activities are: coughing, sneezing, laughing, bending/
lifting, carrying objects, sitting down, standing up, and going up/down stairs. During these
activities, pressure is placed on the bladder, forcing urine to leak out. You should practice the
“KNACK” by contracting the pelvic floor muscles:
† Immediately before initiating a hard cough and maintaining the contraction throughout
the cough
† Do 5 quick pelvic muscle contractions when you get a strong urge that you cannot control.
† Tighten your muscle on the way to the bathroom. Remember, the more exercising
you do:
– The stronger your pelvic muscles will get.
– The faster they will get stronger.
– The easier it will be to maintain muscle strength.

REMEMBER – It may take some time to translate the “KNACK” successfully into daily life.

MAKING THE EXERCISES PART OF YOUR DAILY ACTIVITY – Once your muscles are stronger and
you incontinence and urgency are better, you should do these exercises as part of your daily
routine (activities you do on a daily basis). This means you do both types of exercises, short and
long muscle contractions. You do not have to keep a formal count of the number of
 Behavioral Treatments 265

times you do each exercise. Just do them several times in a row and often enough to make them a
habit. Do your exercises when you are:
† Standing at the sink and brushing your teeth
† Sitting in the car at a stop light.
† Reading a book in bed.
† Going for a walk.
† Talking on the phone.

YOU MUST PRACTICE SO THAT EXERCISING BECOMES A HABIT.

ALMOST LIKE A REFLEX ACTION!!
# 2002 Diane K Newman
15
Pessaries and Vaginal Devices for
Stress Incontinence
G. Willy Davila and Minda Neimark
Cleveland Clinic Florida, Weston, Florida, U.S.A.

I. INTRODUCTION

Pessaries and other intravaginal devices have long been used for the treatment of pelvic floor
dysfunction in women. Initial descriptions of vaginal device use entailed intravaginal place-
ment of objects to support genital prolapse and/or administer therapeutic chemicals. Specific
applications of pessaries for women with stress urinary incontinence (SUI) are rather recent.
Owing to the high coexistence of genital prolapse and urinary incontinence, it is likely that
many women who were fit with a pessary for genital prolapse noted an improvement in their
urinary incontinence. Alternatively, women with exteriorized prolapse may have occult
stress incontinence which is uncovered upon being fit with a vaginal pessary for reduction of
the prolapse.
The concept of intravaginal device use as an option for SUI treatment is very useful for
the practicing clinician. As our population ages, with an increased incidence of pelvic floor
dysfunction, alternatives to surgery become more desirable. There are many urogynecologic
indications for pessary usage (Table 1). In addition, technological developments have led
to innovative designs of intravaginal devices with specific purposes such as elevation of the
urethrovesical junction (UVJ) (Fig. 1). To achieve continence, a device should provide elevation

Table 1 Indications for Pessary Use

Vaginal and uterine prolapse

Stress incontinence
Patient unable to safely undergo pelvic reconstructive surgery
Desire to delay surgery
Evaluation of continence mechanism in moderate to severe vaginal prolapse
Preoperatively demonstrate effectiveness of urethropexy for SUI
Pregnant patient with incompetent cervix/premature delivery/multiple gestation
Genital prolapse in the neonate
Low back/pelvic pain secondary to genital prolapse
Postoperative usage following pelvic reconstructive surgery to prevent recurrence

267
268 Davila and Neimark

Figure 1 Intravaginal devices specifically useful for enhancing bladder neck support: (a) Smith-Hodge
pessary; (continued)

and support of the urethrovesical junction and/or extrinsically enhance urethral sphincteric
function by compression. While doing this, outflow obstruction should be avoided to prevent
significant urinary retention and its consequences.

II. PESSARIES AND STRESS INCONTINENCE

Voiding difficulty, bladder outlet obstruction, and occult stress incontinence may coexist in a
patient with severe prolapse. The initial descriptions of vaginal pessary use for stress urinary
incontinence were not in its therapy, but rather in the uncovering of occult stress incontinence in
women with advanced degrees of prolapse (1). It was suggested that the mechanism of
continence in women with severe prolapse is urethral obstruction, which increases maximum
urethral closure pressure and pressure transmission ratio. It has been demonstrated that up to
70% of women with moderate to severe pelvic organ prolapse will demonstrate stress
incontinence once the prolapse has been reduced (2 –5). Subsequently, Bhatia and colleagues
described the impact of a Smith-Hodge pessary on urodynamic parameters in women with
stress urinary incontinence (6). A pessary’s effect on urethral mobility and urodynamic
parameters were described and noted to be similar to those of a successful bladder neck
 Pessaries and Vaginal Devices 269

Figure 1 (b) Introl Bladder Neck Support Prosthesis; (continued)

suspension (Table 2). No evidence of urinary outflow obstruction was found. The use of Smith-
Hodge pessaries for stress incontinence was popularized as a result of these data.
A “pessary test” was suggested for identification of occult stress incontinence in women
with advanced degrees of genital prolapse, and as a prognostic test for success of anti-
incontinence surgery—similar to a Bonney or Marshall test (7,8). Similarity in changes in
continence mechanism with improvements in functional urethral length, urethral pressure
profiles, and cough profiles was demonstrated in those who became asymptomatic with a pessary
and those who underwent a Burch urethropexy. Smith-Hodge, Ring, and Gellhorn pessaries are
most frequently used for this evaluation (2 –4,9). When using this test, care must be taken to
avoid compressing the urethra and causing outflow obstruction. Smith-Hodge pessaries are
especially useful for this purpose owing to the notched nature of the retropubic square end
(Fig. 1a). Another practical feature of the Hodge pessary is the ability to modify its shape by
folding it into a better-fitting device for an individual patient. The curvature of the pessary
frequently requires shape adjustment in order to achieve a snug retropubic fit.
Other intravaginal devices have also been studied for the nonsurgical treatment of SUI.
Contraceptive diaphragms, owing to their retropubic placement, may result in improved bladder
neck support. In one study, complete resolution of SUI was reported in 91% of women fit with a
diaphragm (10). Discomfort with the device in place led to discontinuation by 16% of the
women. In addition, contraceptive diaphragms have been associated with the occurrence of
urinary tract infections due to their effect on urethral outflow (11). Diaphragm fitting rings can
also be effective in treating SUI in some women (12). Diaphragms and fitting rings may be
useful in the patient with mild SUI and minimal prolapse. However, if significant prolapse is
present or urine loss occurs with minimal exertion, diaphragms may not be strong enough to
provide sufficient urethrovesical junction (UVJ) support.
Vaginal tampons have also been used for SUI. Many women have reported that SUI
is improved during menses when a tampon is in place. Tampons have been listed as effective
270 Davila and Neimark

Figure 1 (c) Continence Guard; (continued)

conservative options for the management of SUI (13). When compared to a Hodge pessary, a
super tampon was found to be equally effective in reducing urine loss during an exercise session
(14). In this study, the devices were used only during exercise sessions, and urodynamics was not
performed. Thus, the author’s conclusions may not be applicable to many women with SUI.
However, the wide availability and low cost of tampons make them an attractive first-line
intravaginal therapy for SUI. Importantly, extra-absorbent tampons should not be left in place
for more than 6 h at a time in order to avoid the risk of toxic shock syndrome.
Innovative devices specifically designed to elevate the bladder neck in a manner similar to
a bladder neck suspension have recently been studied. The Introl Bladder Neck Support
Prosthesis (BNSP) (Uromed Corp., Needham, MA) is available in the Far East but not widely
used in the United States, despite approval by the FDA (Fig. 1b). It is a silicone ring-shaped
device with two prongs at one end. Upon insertion, the prongs fit retropubically to provide
 Pessaries and Vaginal Devices 271

Figure 1 (d) Continence Ring.

bladder neck support (Fig. 2). It was shown to reduce urine loss by 80% in most users with stress
incontinence, with urodynamic effects similar to a bladder neck suspension (15). A multicenter
study evaluating women with stress and mixed incontinence confirmed these findings (16).
Fluoroscopic evaluation of a woman with a BNSP in place helps us understand the effect of a
vaginal device in enhancing bladder neck and proximal urethral support (Fig. 3). Its widespread
use was limited by its cost and by the difficulties encountered in individualized fitting. Women
who used the BNSP only during specific physical activities (i.e., jogging, tennis, etc.) were noted
to be the most successful subgroup of users.
A disposable intravaginal device specifically designed to provide urethral support during
exertion has been available in Europe. The Continence Guard is a single-use polyurethane
foldable device (Fig. 1c). Thyssen and Lose showed that 95% of their study population
were either dry or improved with the Continence Guard in place (17). Significant reduction in
urine loss on a 24-h pad test, without alteration in uroflowmetry parameters, was noted (18).
A multicenter study of this device revealed objective improvement in 75% of the study
population, with 46% being dry on a pad test (19).
Most recently, in the United Kingdom, a cylindrical vaginal device designed to provide
bladder neck support in women with stress incontinence has been marketed (Contiform, Bard
Limited Forest House, West Sussex, U.K.). Its cylindrical design prevents its collapse during
272 Davila and Neimark

Table 2 Urodynamic Effects of Pessaries

1. Enhance bladder neck support—normalize Q-tip angle

2. Lengthen urethra—increase functional urethral length
3. Enhance urethral sphincteric mechanism—increase urethral closure
pressure
4. Enhance urethral dynamic function—increase pressure transmission ratio
5. Allow normal voiding—no effect on uroflow parameters

strenuous activities. It is reported to not cause outflow obstruction and results in continence in
85% of users (Bard Limited Forest House, data on file).
Multiple other devices are being marketed for intravaginal treatment of SUI. However,
most have not undergone scientific study. Many commonly available pessaries have been
modified by adding a “cushion” at one end to enhance urethral compression (Fig. 1d). Care must
be taken to avoid urethral obstruction during usage.

Figure 2 Effect of intravaginal device in bladder neck support—lateral view.

 Pessaries and Vaginal Devices 273

Figure 3 Fluoroscopic appearance of intravaginal device enhancing proximal urethral support.

III. HISTORICAL PESSARY APPLICATIONS

In the 1800s, Hugh Lenox Hodge designed the lever pessary to treat uterine retroversion thought
to be a cause of pelvic pain (20). As modifications of the lever pessary were made, other
indications were proposed for its use. In 1961, Vitsky suggested that cervical incompetence was
due to a lack of central uterine support. Uterine retroversion has also been associated with
infertility and pelvic pain. Placing a lever pessary would displace the cervix posteriorly, thus
lifting the weight of the uterus off of the incompetent cervix (21). Women diagnosed with an
incompetent cervix were treated during pregnancy with a Hodge pessary from 14 to 38 weeks’
gestation, with an 83% successful pregnancy rate (22). Currently, cervical cerclage is the
treatment of choice for women with cervical incompetence. There is great controversy regard-
ing the possible causative role of uterine retroversion in many gynecologic conditions including
pelvic pain, infertility, and sexual dysfunction.

IV. PESSARIES FOR GENITAL PROLAPSE

Use of vaginal devices for prolapse reduction and administration of chemicals is documented as
far back as during the early Egyptian civilization. Written documentation of efforts to reduce
genital prolapse with vaginal objects dates back as far back as the fifth century. Modernization
of the pessary came with the discovery of vulcanization of rubber and a better understanding of
female anatomy. Since then, multiple modifications in pessary design and material selection for
manufacture have been made (23).
Advances in gynecologic surgery and anesthesia over the last several decades have
reduced the need for pessary usage in the treatment of prolapse and incontinence. However,
the recent increase in the elderly population requiring conservative treatment of prolapse
and incontinence has led to a resurgence of pessary use (24). In addition, there remains a very
acceptable role for therapeutic use of a vaginal pessary in the premenopausal patient. In a
recent survey administered to members of the American Urogynecologic Society, 77% of the
274 Davila and Neimark

respondents used pessaries as a first-line therapy for prolapse, and only 12% reserved pessaries
for women who were not surgical candidates. In addition, 92% of the physicians surveyed
believed that pessaries relieved symptoms associated with pelvic organ prolapse, and 48% felt
they had a therapeutic benefit in addition to relieving the symptoms (25).
In a simple prospective protocol for pessary management, patients with symptomatic
pelvic prolapse were given the option of pessary use versus surgery or expectant management. If
the vaginal pessary was chosen as the method of treatment, the patient was fitted with a ring
pessary or a pessary that could be retained without difficulty. The patient then followed up at
scheduled intervals to evaluate pessary effectiveness. Sixty-six percent of those who used a
pessary for .1 month remained users after 12 months. Fifty-three percent of the patients
continued to wear the pessary after 36 months (26). A retrospective series of 107 patients who
were fit with a Gellhorn, cube, or ring pessary for symptomatic vaginal prolapse for various
indications including medically unfit for surgery, awaiting surgery, or desired conservative
management, confirmed that at least 50% of the women continued use of their pessary without
complications at follow-up (27). Of those who continued pessary use, 20% were patients who
initially desired surgery but later declined because of their satisfaction with the vaginal pessary.
At our center, pessaries are frequently used as first-line therapy for prolapse and
incontinence. Review of our usage trends reveals rather equivalent use of the Smith-Hodge
and Continence Ring pessaries for SUI. For advanced degrees of prolapse, our most commonly
used pessary is the Gelhorn. Cube pessaries should only be used with extreme caution in women
who will be compliant with follow-up, as the suctioned adherence to the vaginal sidewalls may
lead to significant mucosal erosions and ulcerations. A significant number of women who wear
pessaries for SUI or prolapse eventually become frustrated with the efforts required for safe
pessary use, and opt for surgical management.

V. PESSARY TYPES

Many different types of pessaries are available, most made of medical-grade silicone or rubber.
Although the majority were designed for specific types of prolapse, clinical use is typically based
on a “best fit” choice (Table 3). Whichever pessary is chosen, it must fit snugly without causing
discomfort to the patient, allowing her to void easily. The health care provider must be prepared to
try several different types and sizes until the correct pessary is found for each individual patient.

VI. PERCEIVED DRAWBACKS TO PESSARY USE

Clinicians may be hesitant to recommend pessary use by women with SUI. Various factors
account for this reluctance. Owing to variations in pelvic anatomy, optimal fitting of a pessary
may be challenging. In addition, the large number of pessary types, each with various sizes,
further complicates the process. Because pessary fitting is a trial- and error-process, a clinician
must have a large inventory of pessaries of varying sizes in order to accomplish appropriate
fitting of patients. An appropriately fit pessary is comfortable, remains in place with ambulation,
and allows for normal voiding.
Pessary care recommendations should be followed closely for safe long-term use (Table 4).
The patient who cannot self-care for the pessary must be seen by the clinician on a regular basis.
We recommend scheduled office visits for pessary care every 6 weeks. Patients must be
encouraged to use intravaginal estrogen cream regularly. Some patients may be able to perform
pessary self-care if removal is facilitated by attaching a string (dental floss or suture) to the pessary.
Table 3 Pessary Types and Indications

Indications

Cystocele
Stress
Pessary Sizes Small Large Enterocele Rectocele Vault prolapse incontinence

Smith-Hodge 0–9 3  
Risser 0–9   
Marland 2–8  
Incontinence Dish (mm) 55 – 85  
Incontinence Ring 0 – 10  
Ring (with or without support) 0–9    
Gerhrung (with or without knob) 0–9   
Gellhorn (inches) 112 – 312     
Schaatz (inches) 112 – 312    
Doughnut (inches) 2 – 334     
Inflatable (inches) 2 – 334     
Cube 0–7     

Source: Ref. 23.

Pessaries and Vaginal Devices
275
276 Davila and Neimark

Table 4 Pessary Care Recommendations

Remove at least two nights per week

Leave out overnight
Insert 1 – 2 g estrogen cream during night while pessary is out
Wash pessary with soap and water
Reinsert using water-soluble lubricant
Report any unusual discharge, bleeding, or discomfort
Report any changes in bladder or bowel function
Have pelvic examination every 6 – 12 months

Source: Ref. 23.

Cost issues must also be considered. In many cases, reimbursement by insurance

companies does not cover the entire cost of a pessary. Additionally, no optimal distribution
systems through pharmacies or durable medical supply houses exist. The physician is thus
typically at financial risk when fitting pessaries.
Patients themselves may be hesitant to accept pessaries for SUI treatment. The common
notion that pessaries are used solely by elderly women with prolapse and contraindications to
surgical intervention frequently dissuades younger women from considering their use. Nevertheless,
young women of reproductive age are often ideal candidates for pessary treatment of SUI (Table 5).

VII. THE PATIENT WHO CANNOT BE FIT WITH A PESSARY

Not all female candidates can be successfully fit with a pessary. Typical reasons for inability to
be fit include vaginal scarring with loss of vaginal caliber or length from previous surgery,
severe urogenital atrophy, vaginal pain, and markedly restricted or enlarged vaginal introitus.
In women with restricted caliber, use of a vaginal tampon may reduce stress incontinence. In
those with significantly increased vaginal caliber, performing a perineoplasty and subsequent
refitting with a pessary should be considered. For elderly women with severe genital prolapse
who are not, and will not become, sexually active, and cannot be fit with a pessary, consideration
should be given to a colpocleisis performed under regional or local anesthesia.

VIII. CONTRAINDICATIONS TO PESSARY USE

Although the pessary can be a valuable tool in the treatment of stress incontinence and genital
prolapse, there are certain patients for whom pessary use may be considered contraindicated (Table 6).

Table 5 Ideal Candidate for Pessary Usage for SUI

Reproductive age
Comfortable with genital contact (i.e., tampon user)
Adequate manual dexterity
Usage primarily for specific activities (i.e., running)
Compliant with safe usage recommendations
Urethral hypermobility
Well-estrogenized vagina
Unscarred vagina
 Pessaries and Vaginal Devices 277

Table 6 Contraindications to Pessary Use

Severe atrophic tissues

Erosive or ulcerative changes in the vaginal mucosa
Inability to remove pessary on a regular basis
Undiagnosed vaginal bleeding
Undiagnosed vaginal discharge
Vaginal or cervical cancer
Noncompliance in follow-up
Impaired mental capacity

IX. SUMMARY

The concept of using an intravaginal device for treatment of stress incontinence is attractive to
many women suffering from stress urinary incontinence. Various devices specifically designed
to provide bladder neck support during exertional activities have been developed and proven to be
effective. Motivated patients who wish to avoid surgical therapy are the optimal candidates for
vaginal pessary use. Although several limiting factors may arise, including difficulty with insertion
and removal, interference with sexual activity, pelvic discomfort, and associated vaginal discharge,
vaginal devices are a valuable conservative option for the treatment of stress incontinence.

REFERENCES

1. Richardson DA, Bent AE, Ostergard DR. The effect of uterovaginal prolapse on urethrovesical
pressure dynamics. Am J Obstet Gynecol 1983; 146:901– 905.
2. Bergman A, Koonings PP, Ballard CA. Predicting postoperative urinary incontinence development
in women undergoing operation for genitourinary prolapse. Am J Obstet Gynecol 1988;
158:1171– 1175.
3. Veronikis DK, Nichols DH, Wakamatsu MM. The incidence of low-pressure 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 1997; 177:1305 –1314.
4. Rosenzweig BA, Pushkin S, Blumenfeld D, Bhatia NN. Prevalence of abnormal urodynamic test
results in continent women with severe genitourinary prolapse. Obstet Gynecol 1992; 79:539 – 542.
5. Chaikin DC, Groutz A, Blaivas JG. Predicting the need for anti-incontinence surgery in continent
women undergoing repair of severe urogenital prolapse. J Urol 2000; 163:531 – 534.
6. Bhatia NN, Bergman A, Gunning JE. Urodynamic effects of a vaginal pessary in women with stress
urinary incontinence. Am J Obstet Gynecol 1983; 147:876– 884.
7. Bhatia NN, Bergman A. Pessary test in women with urinary incontinence. Obstet Gynecol 1985;
65:220– 226.
8. Bergman A, Bhatia NN. Pessary test: simple prognostic test in women with stress urinary
incontinence. Urology 1984; 24:109 – 110.
9. Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. Urology 1999;
161:581– 586.
10. Suarez GM, Baum NH, Jacobs J. Use of standard contraceptive diaphragm in the management of
stress urinary incontinence. Urology 1991; 37:119 – 122.
11. Fihn SD, Johnson C, Pinkstaff C, Stamm WE. Diaphragm use and urinary tract infections: analysis
of urodynamic and microbiological factors. J Urol 1986; 136:853– 856.
12. Realini JP, Walters MD. Vaginal diaphragm rings in the treatment of stress urinary incontinence.
J Am Board Fam Pract 1990; 3:99 – 103.
278 Davila and Neimark

13. Marshall S. Conservative management of stress urinary incontinence [letter]. Urology 1991; 38:294.
14. Nygaard I. Prevention of exercise incontinence with mechanical devices. J Reprod Med 1995;
40:89– 94.
15. Davila GW, Ostermann KV. The bladder neck support prosthesis: a nonsurgical approach to stress
incontinence in adult women. Am J Obstet Gynecol 1994; 171:206 – 211.
16. Davila GW, Neal D, Horbach N, Preacher J, Doughtie JD, Karram M. A bladder neck support
prosthesis for women with stress and mixed incontinence. Obstet Gynecol 1999; 93:938 –942.
17. Thyssen HH, Lose G. Long term efficacy and safety of a disposable vaginal device (Continence
Guard) in the treatment of female stress incontinence. Int Urogyn J Pelvic Floor Dysfunct 1997;
8:130– 133.
18. Thyssen H, Lose G. New disposable vaginal device (Continence Guard) in the treatment of female
stress incontinence. Design, efficacy and short-term safety. Acta Obstet Gynaecol Scand 1996;
75:170– 173.
19. Hahn I, Milsom I. Treatment of female stress urinary incontinence with a new anatomically shaped
vaginal device (Conveen Continence Guard). Br J Urol 1996; 77:711 – 715.
20. Miller DS. Contemporary use of the pessary. In: Sciarra JJ, ed. Gynecology and Obstetrics.
Vol 1. Philadelphia: Lippencott-Raven, 1992:1– 12.
21. Vitsky M. Simple treatment of the incompetent cervical os. Am J Obstet Gynecol 1961;
81:1194– 1197.
22. Oster S, Javert CT. Treatment of the incompetent cervix with the Hodge pessary. Obstet Gynecol
1966; 28:206 –208.
23. Davila GW. Vaginal prolapse: management with nonsurgical techniques. Postgrad Med 1996;
99:171– 176, 181, 184–185.
24. Poma PA. Nonsurgical management of genital prolapse: a review and recommendations for clinical
practice. J Reprod Med 2000; 45:789 – 797.
25. Cundiff GW, Weidner AC, Visco AG, Bump RC, Addison WA. A survey of pessary use by members
of the American Urogynecologic Society. Obstet Gynecol 2000; 95:931 – 935.
26. Wu V, Farrell SA, Baskett TF, Flowerdew G. A simplified protocol for pessary management.
Obstet Gynecol 1997; 90:990 – 994.
27. Sulak PJ, Kuehl TJ, Shull BL. Vaginal pessaries and their use in pelvic relaxation. J Reprod Med
1993; 38:919 –923.
16
Current Role of Transvaginal Needle
Suspensions
Firouz Daneshgari
The Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

The modern era of surgical treatment of stress urinary incontinence (SUI) began in 1892 when
Poussan (1) proposed the concept of urethral meatus advancement, and it followed an amazing
and sometimes convoluted path through the 20th century. Transvaginal needle suspension
(TVNS) was introduced in the 1950s as a simpler and less invasive treatment for SUI in women.

II. DEVELOPMENT AND EVOLUTION OF TRANSVAGINAL NEEDLE

SUSPENSIONS

In 1959, Armand Pereyra (2) introduced a novel approach to surgical treatment of the
patient with genuine SUI. His decision on switching from the traditional Marshall-
Marchetti-Krants procedure was based on the failure of cases he observed, which he
attributed to “strands of fibrous material between the relaxed tissues and the posterior
aspects of the symphysis.” Therefore, he postulated that if the tissues could be suspended
from the rectus fascia, traction from coughing and Valsalva maneuver would not encourage
disruption of the repair. Pereyra devised the principle of the needle suspension with the
design of a ligature carrier. His first published results reported 28 successful procedures and
two failures.
In 1973, Thomas Stamey (3) from California described several modifications of the needle
suspension. The main revision was the use of cystoscopy to determine the position of the bladder
neck with accuracy and hence to place the sutures in close proximity to this point.
In 1979, Shlomo Raz (4), from the University of California at Los Angeles, reported
a modification of the Pereyra procedure using a curvilinear incision and including the
paravaginal tissues within the helical suture. Cobb and Radge (5), in 1978, suggested the use of a
double-pronged needle passer in order to reduce the number of passages of a needle through the
tissue. In 1989, Raz et al. (6) also described the “four-corner suspension”—a TVNS operation
that repairs anterior vaginal wall prolapse in addition to producing an anti-incontinence effect
due to its ability to place the bladder neck in the high retropubic position.
279
280 Daneshgari

III. SURGICAL TECHNIQUES

Regardless of the specific modifications, the general principles of the needle suspension remain
the same. These include suspension/elevation of the bladder neck and of the proximal urethra
(by vaginal wall or synthetic material) by use of a nonabsorbable suture. The details of surgical
techniques of various TVNS are discussed in another chapter.

IV. LEVEL OF EVIDENCE

No discussion on the assessment of a treatment option for UI could be complete without a

discussion on the issue of level of evidence. The evidence required in the medical literature is
limited to data reported in clinical trials, specifically excluding expert opinion. This is similar to
that required to determine the final judgment of a jury in a legal proceeding, which must be based
on the material evidence presented during the trial. The judgment (opinion) of the jury is not
evidence. Evidence is factual information presented.
Attempts to find such evidence have led several national and international organizations to
conduct exhaustive searches of the literature with the aim of providing some guidelines to
clinicians for UI management. In this regard, four documents have been released over the past
decade:
1. AHCPR’s Clinical Practice Guideline reports on UI in adults in 1992 and 1996 (7).
2. The report of the AUA Clinical Guidelines Panel on surgical management of female
SUI (8).
3. The report of the World Health Organization First and Second International
Consultations on Incontinence (ICI) (9,10).
All these documents were based on a review of the existing literature by panels of experts
who subsequently formulated the recommendations.
The AHCPR Report and ICI addressed the issue of data quality by dividing the level of
evidence into High (or A) Best: where the recommendation is supported by scientific evidence
from properly designed and implemented controlled trials providing statistical results that
consistently support the panel’s recommendation; Intermediate (or B) Acceptable: where the
recommendations are supported by scientific evidence from properly designed and implemented
clinical series that support the guideline statement; and Low (or C) Marginal: the
recommendation is supported by expert opinion.

V. REPORTED OUTCOMES

In 1997, the AUA Female Stress Urinary Incontinence Clinical Guidelines Panel published
guidelines for the surgical treatment of stress incontinence (8). The AUA report on surgical
management of female SUI was based on a final review of 282 articles by a selected panel of
experts that included treatment outcome reports in clinical trials including nonrandomized
controlled trials. Four major surgical techniques were studied: retropubic suspensions,
transvaginal suspensions, anterior repairs, and sling procedures. The following criteria were
reviewed in these trials: cure/dry, cure/dry/improved postoperative urgency, retention,
hospital days, resumption of normal activities, transfusion, general conservative complica-
tions, intraoperative complications, preoperative complications, subjective complications, and
complications requiring surgery. Based on this review, the panel concluded that (a) retropubic
 Transvaginal Needle Suspensions 281

suspensions and slings are the most efficacious procedures for long-term success on the basis of
cure/dry rates, but (b) retropubic suspensions and sling procedures are associated with slightly
higher complication rates (including postvoiding dysfunction) and with a longer convalescence,
and (c) anterior repairs are the least likely to be efficacious over time.
The level of evidence for the AUA guidelines recommendation was “Low (or C)
Marginal” by ICI’s and AHCPR’s guidelines. Despite that, however, these recommendations
have encouraged many urologists in the United States to use the sling as the primary procedure
for stress incontinence. This trend is illustrated clearly by comparing the results of two surveys
in which American urologists were asked what procedure they used for stress incontinence
related to urethral hypermobility. In the 1996 report, 71% of urologists used needle suspensions
and 25% used retropubic suspensions (11). In the 2001 report, 38% of urologists used needle
suspensions, 16% used retropubic suspensions, and 44% used slings for type I stress
incontinence; for type II stress incontinence, the corresponding numbers were 14%, 17%, and
68%, respectively (12).

VI. COMPLICATIONS

The reported incidence of de novo detrusor instability following needle suspensions has varied
between zero and 20%, with a mean incidence in the region of 5.8%. Voiding disorders may also
follow this procedure, with a mean of 5.8% and a range of 1 – 24% (13).

VII. CURRENT STATUS

One of the historical attractions of the TVNS was the minimally invasive advantage they had
over the alternatives of retropubic suspensions and pubovaginal slings. In addition, urologists
and gynecologists were originally taught to use retropubic or needle suspensions if the patient
had urethral hypermobility or anatomical incontinence. Sling operations were reserved for
cases of intrinsic urethral sphincter deficiency because they had higher morbidity. However,
with the improved understanding of the pathophysiology of SUI, we now believe that it is the
hammock support of the bladder neck or the urethra and not the intrapelvic position of the
urethra that helps the SUI. The surgical consequence of this enhanced understanding is that
the surgeons no longer pull the slings with tension. Moreover, with improved techniques,
suture material, and availability of allograft fascia, the morbidity of sling procedures
has decreased significantly (14,15). The combination of a low rate of long-term cure by
TVNS, decreased morbidity, and the ease of performing pubovaginal sling procedures has
increasingly created a situation where the use of TVNS as a primary treatment option for even
simple SUI is rapidly decreasing.

REFERENCES

1. Poussan. Arch Clin Bord 1892; 1.

2. Pereyra AJ. A simplified surgical procedure for the correction of stress urinary incontinence in
women. West J Obstet Gynecol 1959; 67:223 – 226.
3. Stamey TA. Cystoscopic suspension of the vesical neck for urinary incontinence. Surg Gynecol
Obstet 1973; 136:547– 554.
4. Raz S. Modified bladder neck suspension for female stress incontinence. Urology 1981; 17:82 –85.
282 Daneshgari

5. Cobb OE, Radge H. Simplified correction of female stress incontinence. J Urol 1978; 141:38 – 42.
6. Raz S, Klutke CG, Golomb J. Four-corner bladder and urethral suspension for moderate cystocele.
J Urol 1989; 142(3):712– 715.
7. Clinical Practice Guideline: Urinary Incontinence in Adults: Acute and Chronic Management. U.S.
Department of Health and Human Services. Public Health Service, Rockville, MD. Agency for Health
Care Policy and Research, 1996; AHCPR publication No. 96-0682.
8. Leach GE, Dmochowski RR, Appell RA, Blaivas JG, Hadley HR, Luber KM, Mostwin JL,
O’Donnell PD, Roehrborn CG. Female Stress Urinary Incontinence Clinical Guidelines Panel.
Summary report on surgical management of female stress urinary incontinence. J Urol 1997;
158(3 Pt 1):875 – 880.
9. Abrams P, Khoury S, Wein A, eds. Incontinence. First International Consultation on Incontinence,
Monaco, July 28 –July 1, 1988.
10. Abrams P, Carduzo L, Khoury S, Wein A, eds. Incontinence. 2nd International Consultation on
Incontinence, Paris, July 1 – 3, 2001.
11. Gee WF, Holtgrewe HL, Albertsen PC. Practice trends of American urologists in the treatment of
impotence, incontinence and infertility. J Urol 1996; 156:1778 – 1782.
12. Kim HL, Gerber GS, Patel RV. Practice patterns in the treatment of female urinary incontinence:
a postal and Internet survey. Urology 2001; 57:45– 48.
13. Jarvis FJ. Surgery for genuine stress incontinence. Br J Obstet Gynaecol 1994; 101:371 –373.
14. Chaikin DC, Rosenthal J, Blaivas JG. Pubovaginal fascial sling for all types of stress urinary
incontinence: long-term analysis. J Urol 1998; 160:1312– 1316.
15. Barnes NM, Dmochowski RR, Park R, Nitti VW. Pubovaginal sling and pelvic prolapse repair in
women with occult stress urinary incontinence: effect on postoperative emptying and voiding
symptoms. Urology 2002; 59(6):856– 860.
17
Anterior Vaginal Wall Suspension

Tracey Small Wilson and Philippe E. Zimmern

University of Texas Southwestern Medical Center, Dallas, Texas, U.S.A.

I. EVOLUTION

Raz described the first four-corner bladder and urethral suspension procedure in 1989 (1). He
recognized that many anti-incontinence procedures failed because they addressed anterior
vaginal wall prolapse or urethral hypermobility rather than addressing the two together. For
example, the Kelly-type plication corrected the cystocele by reapproximation of the
pubocervical fascia, but it was associated with a high failure rate for stress urinary incontinence
(SUI) (50 –80%) (2) partly because it did not support the proximal urethra and bladder neck.
Conversely, the Marshall-Marchetti-Krantz (MMK) bladder neck suspension corrected urethral
hypermobility but not the cystocele. Raz believed that bladder base descent and urethral
hypermobility must be corrected at the time of cystocele repair regardless of whether
incontinence existed. At that time, the only procedure accomplishing this combined goal was the
retropubic Burch cystourethropexy. Raz therefore drew from his experience with the modified
Peyrera needle suspension procedure to develop a vaginal technique that would simultaneously
address urethral hypermobility and anterior vaginal wall prolapse.
Raz’s original modification of the Pereyra suspension procedure incorporated the
urethropelvic ligament, pubocervical fascia, and vaginal wall (without its epithelium) into
helical suspensory sutures (3). He further modified this procedure to develop the four-corner
bladder neck suspension (1). By combining this initial set of helical sutures (placed at the
bladder neck) with a second set (placed at the level of the cystocele base), Raz created four sites,
or “corners,” from which the proximal urethra and bladder base were suspended. Via an
inverted U-shaped incision, these nonabsorbable sutures were placed very lateral (as with the
Burch suspension) to minimize the risk of outflow obstruction. They were then transferred
suprapubically by a ligature carrier and secured to the anterior rectus fascia. This procedure
essentially resuspended the anterior vaginal wall without repairing the fascial defect.
In his initial series of 120 patients with grade 2 or 3 cystocele Raz reported a 94% and 98%
subjective correction of incontinence and cystocele, respectively. Obstruction was relieved in
84% of patients, preoperative detrusor instability improved in 54%, and de novo urge occurred
in 5% (1). Despite these successes, patients continued to experience a significant amount of
suprapubic discomfort and cystocele recurrence.
Bruskewitz et al. compared several different anchoring materials and their rate of tissue pull
through and local tissue reaction in the rabbit abdominal wall (4). He concluded that loops of suture
283
284 Wilson and Zimmern

material had a lower incidence of tissue pull-through and tension loss over time. He believed this
was due to a lower initial tension and a greater cross-sectional area of the anchor material.
Using Bruskewitz’s findings, Leach and Zimmern modified the Raz four-corner
suspension to obtain a broader anterior vaginal wall anchor (5). They believed that broader
support of the upper vagina would protect the bladder neck repair and distribute pressure
more evenly during stress maneuvers. Their distal sutures were placed in the vaginal wall at
the bladder neck level and did not incorporate the urethropelvic ligaments. Proximal sutures
were placed in a helical fashion at the cystocele base to provide broader and stronger support of
the upper anterior vaginal wall. If the uterus was present, these helical sutures incorporated the
cardinal ligaments; if absent, they incorporated the scar of the vaginal cuff.
Long-term results of the four-corner procedure were reported in 1997 (6). Using both
subjective and objective outcomes, Dmochowski et al. (6) evaluated 47 patients after a mean of
37 months (range 15– 80 months) and found an 87% subjective cure or improvement rate.
Standing voiding cystourethrogram revealed recurrent cystocele, grade I or II (Baden-Walker
classification) (7), in 57%. This moderate recurrence rate was attributed to possible suture pull-
through from the cardinal ligament complex or apical cuff. Upon more careful evaluation of those
patients with recurrent cystoceles, the recurrent fascial defect was found to be centrally located.
Further modifications were therefore imposed. The current procedure, described below, is
referred to as an anterior vaginal wall suspension (AVWS).

II. INDICATIONS

The AVWS is indicated in patients diagnosed with SUI due to urethral hypermobility and a small
to moderate cystocele (grade I or II) with no midline fascial defect, as seen on voiding cystogram
(VCUG). Upper vaginal suspension sutures support and elevate the cystocele base, while the
distal sutures support the bladder neck, thereby correcting urethral hypermobility. Patients with
large cystoceles (grade III or IV) due to a central defect are best served with an anterior
colporrhaphy or an abdominal sacrocolpopexy along with support of the bladder neck (8).
The AVWS is not indicated in patients with SUI due to intrinsic sphincteric deficiency
(ISD) alone, and no urethral hypermobility. This procedure does not provide sufficient urethral
coaptation to ensure dryness in this population. If the patient has a cystocele in association with
ISD (as diagnosed by physical examination and urodynamics), a pubovaginal sling along with
support of the upper anterior vagina or an anterior colporrhaphy is indicated depending, on the
extent of the cystocele. Simultaneous correction of the cystocele is indicated to avoid excessive
angulation at the urethrovesical junction, which could produce outflow obstruction.

III. OPERATIVE TECHNIQUE

After induction of general anesthesia, the patient is placed in the high dorsal lithotomy position
using candy-cane stirrups. The lower abdomen, perineum, and vagina are properly prepped and
draped, and a ring retractor is positioned to aid visualization. A urethral catheter is inserted, and
the balloon is palpated to identify and mark the bladder neck. Marking sutures are now placed
at the vaginal apex—one in the midline and one 1.5 cm lateral to the midline on each side.
Beginning 1.5 cm lateral to the bladder neck, an incision is made in the anterior vaginal wall
and extended proximally to the level of the marking sutures—lateral to the cervix or to the
vaginal apex. The same procedure is repeated on the opposite side (Fig. 1). The area of anterior
vaginal wall between the incision lines will serve as the elevating vaginal wall plate and is
 Anterior Vaginal Wall Suspension 285

Figure 1 Initial setup of AVWS. Three marking sutures are placed at vaginal apex. Bilateral anterior
vaginal incisions are made extending from the level of the bladder neck to the vaginal cervix or cuff.

usually 3 cm in width and 4 –8 cm in length depending upon the length of the anterior vaginal
wall (average 6 cm). In the presence of a moderate cystocele, the redundant vaginal wall lateral
to these incisions should be excised lengthwise, preserving 0.5 –1 cm of tissue laterally in order
to recreate the lateral sulcuses upon closure of the vaginal wall.
The 3  4 –8 cm in situ anterior vaginal wall plate is now divided into equal quadrants
using a marking pen. The first of four No. 1 polypropylene sutures is placed into the scar of
the vaginal cuff or cardinal ligament and run distally in a helical fashion to the level of the
midvagina (half the length of the vaginal plate). The helical bites should traverse medially to the
middle of the vaginal plate and should incorporate the vaginal wall, excluding the epithelium.
The second suture is then placed at the level of the midvagina and run distally by two to three
helical passes to the bladder neck area (Fig. 2). The third and fourth sutures are placed similarly
on the opposite side.
A 3 – 4 cm transverse suprapubic incision is then made two fingerbreadths above the level
of the pubic symphysis and carried down to the level of the rectus fascia. This incision should
be as close to midline as possible to avoid genitofemoral nerve involvement. Owing to the risk
of bleeding, placement of the four suspension sutures and suprapubic incision are done before
entering the retropubic space. Blunt or sharp dissection at the level of the bladder neck is now
performed to develop the plane laterally between the endopelvic fascia and the pubic bone. Once
this space is cleared of all adherent tissue, the deep endopelvic fascia is perforated, which allows
entrance into the retropubic space. The retropubic space is then developed anteriorly using a
sweeping motion of the finger along the inside surface of the pubic bone. It is critical to keep the
catheter on gravity drainage to ensure bladder emptiness during this maneuver.
In a virgin case, there is little to no resistance entering the retropubic space at the site of the
lateral defect. However, after a Burch or MMK procedure, there may be a significant amount of
286 Wilson and Zimmern

Figure 2 Placement of suspension sutures. Note division of vaginal plate into quadrants. PS, proximal
sutures; DS, distal sutures.

retropubic scarring, which increases the risk of bladder injury during finger dissection or needle
passage. Once it is felt that only rectus fascia and muscle remain between a finger in the
suprapubic incision and one in the retropubic space, each of the four suspension sutures is
transferred to the suprapubic position using a ligature carrier. We use a double-pronged ligature
carrier; however, a single pronged instrument may be necessary in obese patients or in those
with significant abdominal wall and/or retropubic scarring. When possible, the proximal
suspension sutures (adjacent to cervix) are placed more lateral and cephalad than the distal
suspension sutures (Fig. 3).
After intravenous indigo carmine is given, cystoscopy with a 708 lens is performed to
exclude intravesical suture placement and/or bladder perforation and to confirm ureteral
integrity. If sutures are present in the bladder, they should be removed via the vaginal side and
repositioned. A large bladder perforation should be closed in multiple layers immediately with
possible interposition of a fat graft (9) (in this instance, the anti-incontinence procedure may
need to be aborted). The vaginal wall incisions are now closed with running 2-0 absorbable
suture. Using a rubber-shod right-angle clamp, each suture is grasped 1.5 –2 cm above the
rectus fascia and tied above the clamp as an assistant supports the vaginal plate in a position
parallel to the floor. This maneuver provides adequate support without over correction. An
antibiotic-soaked vaginal pack is inserted, and the suprapubic incision is closed.

IV. OUTCOMES

Both subjective and objective outcome measures have been used to assess effectiveness of the
AVWS. Lemack and Zimmern reported midterm results of the AVWS in 61 of 102 women who
 Anterior Vaginal Wall Suspension 287

Figure 3 Final appearance of suspension sutures. Note that sutures cover the entire vaginal plate.
Proximal sutures (PS) are placed more lateral and cephalad than distal sutures (DS).

had responded to questionnaires at a mean of 25 months following AVWS (10). Seventy-seven

percent of patients were subjectively cured or improved of their stress incontinence. Using a
visual analog scale and the quality-of-life question—“If you were to spend the rest of your life
with your urinary condition just the way it is now, how would you feel about that?”—the median
preoperative score was 6.7 (0, pleased; 10, terrible), and declined postoperatively to a median
response of 2. Eight percent experienced de novo urge incontinence, and diuretic use was the
only poor prognostic indicator. The standing voiding cystourethrogram (VCUG) has been used
as an objective outcome tool for anti-incontinence procedures (11). Showalter et al. (12)
compared the VCUG of 76 continent control patients to two surgical groups: group 1, 52 patients
who underwent an AVWS for urethral hypermobility and grade I or II cystocele; group 2, 36
patients with grade III or greater cystocele who underwent formal anterior colporrhaphy. After
3 –6 months, there was no difference in the urethral angle in patients who had undergone the
AVWS compared to controls. There was also a significant reduction in the lateral height of the
cystocele following AVWS and anterior colporrhaphy (Figs. 4, 5).
288 Wilson and Zimmern

Figure 4 Preoperative lateral VCUG demonstrating urethral hypermobility (urethral angle of 60 – 708)
associated with a mild cystocele.

Sexual function following AVWS has also been assessed. Lemack and Zimmern
subjectively evaluated 93 women at least 1 year following an AVWS alone or in combination
with a posterior colporrhaphy (13). Sixty percent of patients responded to a mailed
questionnaire. The same percentage of patients was sexually active postoperatively as
preoperatively; however, only 20% noted dyspareunia postoperatively, compared to 29%
preoperatively. Eighteen percent of patients reported intercourse to be worse postoperatively,
but these were not the same patients who reported dyspareunia. Thus, the etiology of this finding
remains unclear. Only one of 29 patients who had undergone an AVWS alone reported sexual
inactivity due to loss of libido or inability to have intercourse. The AVWS did not seem to
adversely affect the majority of women who were sexually active, and the incidence of
symptomatic vaginal narrowing was rare.
Other investigators have also utilized the anterior vaginal wall in anti-incontinence
procedures. Appell described the in situ vaginal wall sling, which utilizes the anterior vaginal
wall for support of the proximal urethra and bladder neck (14). This vaginal wall support is
 Anterior Vaginal Wall Suspension 289

Figure 5 Postoperative lateral VCUG demonstrating a normal urethral angle and a well-supported
bladder base.

anchored to the pubic bone, thereby limiting the amount of retropubic dissection. Kaplan also
described his long-term results with the vaginal wall sling (15). The AVWS is not a sling
procedure but does utilize the vaginal wall as a supporting structure.
There are many advantages to using the anterior vaginal wall in anti-incontinence
procedures. Namely, it does not require a separate harvesting incision (as is necessary for
autologous fascia); one avoids the risk of tissue contamination and disease transmission that is a
small but potential risk with allograft and xenograft materials; and there is less risk of infection
and erosion than is seen with synthetic materials.
The AVWS most resembles the Burch bladder neck suspension, which has recognized
durability and effectiveness in correcting stress urinary incontinence due to urethral
hypermobility. A recent meta-analysis found the Burch procedure to be 85% successful after
4 years (16). Like the Burch procedure, support of the AVWS is based on a broad vaginal anchor.
The retropubic dissection common to both procedures promotes scarring in this region, which
further enhances the vaginal support. The vaginal support in the Burch procedure is anchored to
290 Wilson and Zimmern

Cooper’s ligament, whereas the anchoring point for the AVWS is the rectus muscle tendon as it
inserts into the back of the pubic symphysis. The transvaginal approach for the AVWS allows
repair of concomitant pelvic prolapses through the same incision. In addition, lack of a
Pfannenstiel incision reduces postoperative incisional pain and allows for a shorter
convalescence following the AVWS.

V. CONCLUSION

The AVWS procedure is a reliable surgical option for the patient with stress urinary
incontinence due to urethral hypermobility in the presence of a small to moderate cystocele. It is
favorable to the patient due to its shortened convalescence and reduced postoperative morbidity.
From a surgeon’s perspective, it is easy to teach and reproducible. Midterm results of the AVWS
are respectable, and its long-term results are forthcoming.

REFERENCES

1. Raz S, Klutke C, Golomb J. Four-corner bladder and urethral suspension for moderate cystocele.
J Urol 1989; 142:712– 715.
2. 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 Gynaecol 1982;
89:459– 463.
3. Raz S. Modified bladder neck suspension for female stress incontinence. Urology 1981; 17:82 –85.
4. Bruskewitz RC, Nielsen KT, Graversen PH, Saville WD, Gasser TC. Bladder neck suspension
material investigated in a rabbit model. J Urol 1989; 142:1361– 1363.
5. Zimmern PE, Leach GE, Sirls L. Four-corner bladder neck suspension. In: Leach GE, ed. Atlas of the
Urologic Clinics of North America. Philadelphia: W.B. Saunders, 1994:29– 36.
6. Dmochowski RR, Zimmern PE, Ganabathi K, Sirls GL, Leach GE. Role of the four-corner bladder
neck suspension to correct stress incontinence with a mild to moderate cystocele. Urology 1997;
49:35– 40.
7. Baden WF, Walker TA. Surgical Repair of Vaginal Defects. Philadelphia: J.B. Lippincott, 1992.
8. Miyazaki FS, Miyazaki DW. Raz four corner suspension for severe cystocele: poor results. Int
Urogynecol J Pelvic Floor Dysfunc 1994; 5:94– 97.
9. Hernandez RD, Himsl K, Zimmern PE. Transvaginal repair of bladder injury during vaginal
hysterectomy. J Urol 1994; 152:2061– 2062.
10. Lemack GE, Zimmern PE. Questionnaire-based outcome after anterior vaginal wall suspension for
stress urinary incontinence (abstract). J Urol 2000; 163(4):73.
11. Zimmern PE. The role of voiding cystourethrography in the evaluation of the female lower urinary
tract. Prob Urol 1991; 5:23 – 41.
12. Showalter PR, Zimmern PE, Roehrborn CG, Lemack GE. Standing cystourethrogram: an outcome
measure after anti-incontinence procedures and cystocele repair in women. Urology 2001; 58:33– 37.
13. Lemack GE, Zimmern PE. Sexual function after vaginal surgery for stress incontinence: results of a
mailed questionnaire. Urology 2000; 56:223 –227.
14. Appell RA. In situ vaginal wall sling. Urology 2000; 56:499 – 503.
15. Kaplan SA, Te AE, Young GP, Andrade A, Cabelin MA, Ikeguchi EF. Prospective analysis of 373
consecutive women with stress urinary incontinence treated with a vaginal wall sling: the Columbia –
Cornell University experience. J Urol 2000; 164:1623 –1627.
16. Leach GE, Dmochowski RR, Appell RA, Blaivas JG, Hadley HR, Luber KM, Mostwin JL,
O’Donnell PD. Report on the Surgical Management of Female Stress Urinary Incontinence Clinical
Practice Guidelines. Baltimore: American Urological Association, 1997.
18
Retropubic Urethropexy

Jeffrey L. Cornella
Mayo Clinic Scottsdale, Scottsdale, Arizona, U.S.A.

I. INTRODUCTION

The suprapubic approach to anterior segment or urethrovaginal stabilization is known

as retropubic urethropexy. Retropubic urethropexy (RPU) procedures have a long and
important history in pelvic surgery. They remain an essential contribution to the surgical
armamentarium for the management of female urinary incontinence. This chapter will review
the history, techniques, and pertinent literature of the retropubic urethropexies—open and
laparoscopic.

II. RETROPUBIC URETHROPEXY VERSUS PUBOVAGINAL SLING

The past several years have seen an increasing trend for selection of the pubovaginal sling as
a primary incontinence procedure in the United States. There were two phenomena that
accelerated this trend. The first was accumulating data on the poor outcomes of needle-
suspension procedures. The second was the development of a less invasive pubovaginal sling,
in the form of the transvaginal tape procedure (TVT) (1). Additionally, the misconception of
intrinsic sphincteric deficiency as an entity with a possible laboratory diagnosis further resulted
in increased numbers of patients receiving slings. Practice trends may reach the point where the
majority of patients are simply relegated to a TVT procedure, with little clinical evaluation or
attention to paravaginal anatomy.
Caution should be exhibited prior to relegating all patients to TVT-like procedures. First
of all, the strong objective data on TVT procedures only extends 5–7 years (2). The Burch
urethropexy has 10- to 20-year objective data in several studies showing a high cure rate for
stress urinary incontinence (3 – 5). It is unclear how the TVT will perform at 10 years plus
compared to other procedures, especially if stretching of the sling material occurs.
Additionally, the TVT only supports the urethra, and if the patient has a paravaginal
defect, which is often the case, the patient would be best served with a site-specific repair of the
paravaginal area and retropubic urethropexy. If this is not done, the patient may continue to
show anterior wall descent and additional symptoms.

291
292 Cornella

The majority of patients with low urethral pressures or low Valsalva leak-point pressures
are candidates for urethropexy, as the subsequent section on patient selection in this chapter will
emphasize.

III. HISTORY OF RETROPUBIC URETHROPEXY

In many respects the retropubic urethropexy was introduced in the United States by the work of
George Reaves White (6). White studied anatomy under Josef Halban in Vienna, just after the
turn of the 20th century. The 1909 and 1912 articles regarding a radical cure for cystocele by
White documented both a vaginal and an abdominal approach to the anterior segment (6,7).
The anterior approach was a retropubic vaginopexy in the form of a paravaginal defect repair
(PVDR). The anterior sulcus of the vaginal was reattached to the appropriate anatomic site, the
arcus tendineus fascia pelvis (ATFP). This technique was lost for decades until its resurrection
by the work of A. Cullen Richardson in the late 1970s.
In the interim, 30 years before the articles of Richardson, a different procedure for fixation
of the urethra was described. This procedure was not a site-specific repair, but rather fixed the
urethra to the posterior symphysis and disregarded the anterior lateral sulcus. Marshall et al.
reported their female incontinence procedure in 1949 (8). Thousands of women have since
received the Marshall-Marchetti-Krantz (MMK) procedure and its modifications for the control
of urinary stress incontinence. It consists of fixation of the urethra and bladder by a bilateral
series of three chromic sutures to the periosteum of the symphysis.

Figure 1 Tied paravaginal sutures attaching anterior lateral sulcus of vagina to obturator internis muscle
along the white line (ATFP). (Used with permission of John Miklos.)
 Retropubic Urethropexy 293

A patient who did not receive this intended procedure because of a weak periosteum was
responsible for precipitating a new point of attachment and thus a different retropubic
urethropexy. The operating surgeon was John Christopher Burch, and he chose as a new site
of attachment, the iliopectineal ligament of Cooper (9). This procedure, performed in 1958,
eventually became known as the Burch procedure. It would become the gold standard of the
retropubic urethropexies. It has the largest literature and greatest long-term follow-up of any
operation for female urinary incontinence. It is often the Burch procedure that other techniques
for urinary incontinence are compared to in randomized studies. It will be the main procedure
emphasized in this chapter, given the strong foundation of underlying literature.

IV. TECHNIQUES AND EFFICACY OF OPEN PROCEDURES

A. Paravaginal Defect Repair
The anterior lateral sulcus of the vagina is normally attached to the arcus tendineus fascia pelvis
and portions of the levator musculature. The majority of anterior compartment defects, which
are often referred to as cystoceles, are related to detachment and separation of this anatomic site
(10). Restoration of the anatomy via the abdomen offers a symmetrical and complete repair
without potentially inducing neuropathy by penetration of the urogenital diaphragm. It is a
site-specific repair that often results in the cure of female urinary stress incontinence. A series
of sutures attach the anterior lateral sulcus to the ATFP or white line of the obturator internis
muscle.
It is not considered a standalone incontinence operation used by the majority of surgeons
who treat female urinary stress incontinence, owing to a lack of prospective studies documenting
its efficacy. The single prospective study that compared the PVDR to the Burch procedure for the
treatment of female urinary incontinence showed a significantly higher failure rate in those
patients receiving the paravaginal defect repair (11). Enrollment in this study by Mario Colombo
was discontinued after 36 patients owing to the high failure rate of the PVDR for incontinence.
Colombo reported the cure as 61% (P , .004) in the PVDR group and 100% (P , .02) 18 of 18
in the Burch group.
This failure may be secondary to persistent or recurrent urethrovesical junction descent
from relaxation of the anterior vaginal wall in the midline, despite the restoration of paravaginal
anatomy. The may be evidenced by the fact that in Colombo’s study all of the postoperative
Burch patients had a negative urethral angle on cotton swab testing, but only 33% of the PVDR
patients. Patients who continued to have midline urethral descent despite paravaginal support
demonstrated high rates of failure. Thus, patient selection in the office by documenting lack of
urethral descent during instrumental support of the anterior lateral sulci may be beneficial in
increasing the cure rate in PVDR patients.
Concomitant PVDR at the time of urethrolysis for the management of voiding dysfunction
secondary to urethropexy is a consideration. Webster et al. reported 15 women with voiding
dysfunction following cystourethropexy who underwent takedown and substitution with a
PVDR (12). All 13 women who had symptoms of bladder instability experienced resolution of
their symptoms, and of seven patients who required intermittent self-catheterization preopera-
tively, only one required catheterization postoperatively. A successful outcome was achieved in
14 of 15 patients. The article underscores the anatomic correction of the PVDR technique, which
does not result in elevation of the urethrovesical junction beyond its normal anatomic position.
To treat patients receiving a Burch or MMK procedure adequately who have a
concomitant paravaginal defect, a PVDR may be accomplished simultaneously. This is often
referred to as a paravaginal-plus or MMK-plus procedure. In this setting the Burch procedure
294 Cornella

would be seen as the primary incontinence operation, and the PVDR corrects a defect and further
supports the anterior vaginal wall.

1. Technique of Outpatient Mini-Incision Paravaginal Defect Repair

Long-acting local anesthetic is infiltrated into the fascia prior to closing the fascia and skin. A
4-cm transverse suprapubic incision is made followed by a 4-cm fascial incision. The fascia is
mobilized off the underlying rectus muscle followed by lateral dissection into the space of
Retzius. A mini-Bookwalter retractor is placed followed by entry into the bladder dome. The
surgeon’s left hand is placed within the vagina and fiberoptic light facilitates visualization. The
surgeon begins on the left side with identification and delineation of the full length of the anterior
lateral sulcus. A gauze stick facilitates additional retraction of the bladder, and the anterior
lateral sulcus is elevated with the vaginal hand. Vessels will be noted coursing in a longitudinal
course along the sulcus. The obturator foramen is palpated, and care is taken to avoid the nerve
and vessels including the aberrant branch of the obturator vein. Sutures are placed initially into
the obturator internis when operating on the patient’s left side and in the anterior lateral sulcus
when operating on the patient’s right side. A single bite is taken into the obturator internis at the
level of the ATFP, and double bites are taken into the vaginal sulcus. Two to five sutures are
placed along the sulcus from an area just inferior to the ischial spine to the symphysis pubis. In
elderly patients, the arcuate line may not be visible and the attachment of the vagina is along a
course 1 –1.5 to 2 cm below the obturator foramen. Bites into the obturator internis as 3– 4 mm
deep and 1 cm long, avoiding vital structures that are 7.5 mm deep. The ureter courses 2.5 – 3 cm
medial to the superior aspect of the anterior lateral sulcus. Delineation of the ureter is possible by
use of the vaginal finger palpating the structure against the abdominal finger. The sutures are tied
on the left side of the patient prior to placing sutures on the right. If a concomitant Burch
urethropexy is done, the paravaginal sutures are tied first to establish the proper length of the
Burch sutures as they course up to Cooper’s ligament.

B. Marshall-Marchetti-Krantz
The MMK procedure was first accomplished in a female on June 8, 1944 (13). Modifications of
the MMK must involve suturing of the periurethral tissues to the midline cartilage or periosteum
of the symphysis pubis in order to maintain this designation. Mainprize and Drutz in a review of
56 articles through the year 1988 stated that the overall success rate was 86.1% in 2712 cases
(13). They noted that even in repeat procedures, the cure rate was high at 84.5%. Lee et al. noted
in a series of 549 patients followed 2 – 16 years a 91% subjective cure rate in 227 primary
patients and a 90% subjective cure rate in 322 repeat procedures (14).
Colombo et al. reported a randomized comparison between the MMK and the Burch
procedure (15). A full urodynamic investigation was done 6 months after surgery. The cure rate
for the MMK was noted be 65% on urodynamic testing and a subjective cure rate of 85% at mean
3.5 years. The Burch procedure was found to have an objective cure rate of 80%.
The MMK is effective in patients with low urethral pressures if they have hypermobility of
the urethra. Quadri et al. did a prospective, randomized comparison of the MMK and the Burch
urethropexy in patients with low urethral pressures who demonstrated urethral descent (16).
Only 15 patients were studied in each group. At 1 year, stress tests were negative in 93% of
women who underwent the MMK procedure and 53% of those who underwent the Burch
procedure.
In their review, Mainprize and Drutz (13) reported the overall complication rate was
21.1% with 5% wound complication rate, a 3.8% urinary tract infection rate, and a 2.5%
 Retropubic Urethropexy 295

Figure 2 Completed paravaginal defect repair and Burch urethropexy. The paravaginal sutures are
tied first and determine length of the Burch sutures. The latter are tied without additional tension. This
stabilizes, but does not elevate the anterior vagina. (Used with permission of John Miklos.)

incidence of osteitis pubis. Kammerer reported 15 cases of osteitis pubis diagnosed after 2030
MMK procedures at the Mayo Clinic (17).

1. Technique of the Outpatient Mini-Incision MMK Procedure

Long-acting local anesthetic is infiltrated into the fascia prior to closing the fascia and skin.
A 4-cm transverse suprapubic incision is made followed by a 4-cm fascial incision. The fascia is
mobilized off the underlying rectus muscle followed by lateral dissection into the space of
Retzius. A mini-Bookwalter retractor is placed followed by entry into the bladder dome. The
surgeon’s left hand is placed within the vagina, and fiberoptic light facilitates visualization. The
bladder dome is opened to facilitate precise suture placement. The urethrovesical junction is
palpated with one finger in the bladder and two fingers of the vaginal hand separated by the
catheter. The vaginal hand is positioned with each finger on the urethrovesical junction, and
the abdomen hand retracts fat medially, allowing visualization of the white periurethral tissue.
Permanent sutures are placed with the needle initially entering closest to the urethra and then
coursing lateral in a perpendicular direction for a distance of 1 cm. The sutures are check after
placement by palpating with a finger in the bladder to determine distance lateral to the urethra
and position relative to the urethrovesical junction. A total of four sutures are placed, two on
each side of the urethra with the secondary sutures just distal to the initial urethrovesical junction
sutures. All sutures are passed through the midline cartilage of the symphysis taking care to
ensure that they are in the inferior aspect of the cartilage, thus avoiding overelevation. The
cartilage of the symphysis has less blood supply than surrounding tissues and an aseptic
technique is essential. Needles passing through the vagina should be cut and replaced with a
296 Cornella

Figure 3 A small cystotomy allows precise suture placement, ability to check the bladder for suture
material and ureteral efflux, and placement of a suprapubic catheter. (Used with permission of the Mayo
Foundation.)

clean free-Mayo needle prior to passing through cartilage. The sutures are tied and the bladder
is examined to ensure that it is free of suture material and the ureters are examined for efflux.
The bladder is then closed in a double layer closure with 2-0 Chromic with incorporation of
a 16-gauge catheter into the apex of the incision. The catheter is placed through a right lower
quadrant stab incision.

C. Burch
In 1961 Burch reported a series 53 retropubic urethropexies (9). In seven of these patients the
ATFP served as the area of attachment for the periurethral sutures. In 46 cases the iliopectineal
ligament was used. In 1968 Burch reported a 9-year experience with the operation resulting in
a 93% cure rate with only 12.5% of the 143 patients having a 5-year follow-up (18). Only 12
patients in the series had undergone a previous incontinence operation. The operative technique
was described in detail and included three sutures of 2-0 Chromic attaching the periurethral
tissues directly to Cooper’s ligament. Postoperative enterocele occurred in 7.6% of patients
despite cul-de-sac reinforcement being added to the procedure early in the series.
The majority of Burch procedures performed today are similar to the modification reported
by Emil A. Tanagho (19). The article, which did not describe Tanagho’s results, was presented
at the Western section meeting of the American Urologic Association in Coronado in 1976.
Tanagho placed his sutures in a far-lateral position, used two sutures bilaterally (No. 1 Dexon),
and emphasized avoidance of undue tension on the anterior vaginal wall. He commented that
two fingers could be placed between the symphysis and urethra, stressing that the vagina did not
have to be contiguous with Cooper’s ligament.
 Retropubic Urethropexy 297

Figure 4 The surgeon’s vaginal hand supports the urethrovesical junction, with one finger on each side
of the catheter. Combined intravesical palpation and vaginal palpation allows precise delineation of the
bladder neck and lateral distance of sutures from the urethra. (Used with permission of the Mayo
Foundation.)

The concept of not overelevating the vaginal wall at the time of retropubic urethropexy
was an important one and it presaged the hammock hypothesis of John O.L. DeLancey (20).
Patients could experience cure with less risk of urinary retention and bladder overactivity
secondary to obstruction. It is consistent with the concepts of the hammock hypothesis that
Burch procedures should stabilize and not elevate the anterior vaginal wall. Tanagho’s
modification by its lateral placement of sutures, reduced compression, and overelevation of
the urethra. It is important when reviewing articles describing Burch results to note the
technique utilized and to what degree the anterior vaginal wall was elevated. Articles that
298 Cornella

Figure 5 Sutures are placed 3 – 4 mm lateral to the urethra. A 22-guage catheter is in the urethra. The
surgeon’s two fingers straddle the urethra. (Used with permission of the Mayo Foundation.)

describe apposition of the wall to Cooper’s ligament or significant elevation will have a higher
incidence of prolonged voiding dysfunction and enterocele formation.
There are several studies that document long-term results of the Burch urethropexy.
Herbertsson and Iosif studied 72 women who underwent Burch colposuspension with pre-
operative and postoperative urodynamics (21). Objective follow-up occurred a mean of 9.4 years
later. The objective surgical cure rate was 90.3% (a negative stress test with at least 300 cc
within the bladder. The enterocele formation rate in this study was 4%.
Feyereisl et al. reported urodynamic outcome in 87 patients, 5 – 10 years after Burch
urethropexy (3). Patients with greater than grade I prolapse or cystocele were excluded.
Inclusion criteria included objective stress leakage in the absence of detrusor instability and
documented hypermobility of the urethra. Stress incontinence was objectively cured in 81.6% of
patients. Cure was defined as a dry, symptom-free patient, without objective loss during
coughing in the standing position with 400 cc of bladder volume.
Alcalay et al. reported a 10- to 20-year follow-up of the Burch colposuspension (4). This
was a longitudinal retrospective study with a long-term follow-up including symptom review,
uroflowmetry, and an extended pad test. Objective cure was defined as inability to demonstrate
 Retropubic Urethropexy 299

stress incontinence during clinical examination and provocative urodynamics. The authors
stated that cure on incontinence is time dependent, with a decline for 10 –12 years when a
plateau of 69% is reached.
Langer et al. reported a long-term (10 – 15 years) follow-up after Burch colposuspension in
127 patients (5). An additional postoperative urodynamic examination was accomplished at least
10 years after surgery in 109 patients. The cure rate was 93.7%, with cure defined as subjective
and objective dryness. Following surgery there was an improvement in symptoms of frequency
(P , .001), urgency (P , .01), and urge incontinence (P , .001).

1. Prospective, Randomized Studies Comparing Burch Urethropexy and

Anterior Colporrhaphy
Anterior colporrhaphy or the Kelly procedure was utilized in the management of female urinary
incontinence for decades. It became popular after the concepts of the paravaginal defect were
lost to common awareness and before creation of other retropubic urethropexies. There remain
proponents of the procedure for incontinence correction to date, despite a preponderance of
objective evidence supporting retropubic urethropexy for this indication. There are now several
prospective, randomized studies comparing Burch urethropexy to anterior colporrhaphy.
In 1995 Bergman and Elia reported a 5-year objective follow-up of a surgical comparison
between three procedures for the treatment of urinary incontinence (22). The series consisted of
127 patients without a history of previous incontinence surgery. Multichannel urodynamics were
performed preoperatively and at 3 months, 12 months, and 5 years postoperatively. Patients were
randomized to the anterior colporrhaphy with Kelly plication, Pereyra procedure, and the Burch
urethropexy. Ninety-three subjects were available for the 5-year objective follow-up. The
success rates were 37% for the anterior colporrhaphy, 43% for the Pereyra procedure, and
82% for the Burch urethropexy. Seventy percent of the colporrhaphy patients had a urethroves-
ical junction descent at 5 years, compared with 7% of the Burch patients. Many patients who
had cure at 1 year but demonstrated a positive cotton swab test, were noted to be failures at
5 years.
Kammerer-Doak performed a randomized trial comparing the Burch urethropexy to the
modified anterior colporrhaphy (23). Thirty-five patients were randomized with preoperative
and postoperative urodynamic testing as a component of the study. Objective cures 1 year
after surgery showed 16 of 18 (89%) of Burch patients were cured compared to five of 16 (31%)
of colporrhaphy patients. Subjective and objective ratings of incontinence severity by
questionnaires and pad testing were significantly lower for the Burch patients than for the
colporrhaphy patients. Mobility of the urethrovesical junction was lower for the Burch patients.
Liapis et al. reported a randomized study of three operations for stress incontinence, the
MMK, Burch, and anterior colporrhaphy (24). The patients were examined clinically and
urodynamically preoperatively and 60 months after surgery. There was a significant difference
in results between the procedures at 5 years. The cure rate was 89% for the Burch procedure and
56% and 67% for the AC and MMK, respectively (P , .001).

2. Technique of Mini-Incision Outpatient Modification of the

Burch Urethropexy
Long-acting local anesthetic is infiltrated into the fascia prior to closing the fascia and skin.
A 4-cm transverse suprapubic incision is made followed by a 4-cm fascial incision. The fascia is
mobilized off the underlying rectus muscle in the usual fashion followed by lateral dissection
into the space of Retzius. A mini-Bookwalter retractor is placed followed by entry into the
300 Cornella

bladder dome. A suture tag is placed at the superior aspect of the bladder incision. The surgeon’s
left hand is placed within the vagina, and fiberoptic light facilitates visualization. Two sutures of
No. 1 Ethibond are placed on each side of the urethra, taking double bites with each suture
through almost full-thickness vagina. The initial suture is at the urethrovesical junction, and
the second suture is 1 cm inferiorly. All sutures are at least 4 mm lateral to the urethra. Precise
placement of each suture is confirmed by subsequent palpation via the cystotomy. The lateral
distance from the urethra, the position relative to the urethrovesical junction, the affect on the
urethra with suture elevation, and the distance of the lower suture from the urethral meatus are
noted. The retractor is removed from each side during placement of sutures through Cooper’s
ligament. The rectus muscle on the side of placement is retracted with Greene retractors. Each
strand of the suture pairs is placed through the ligament, with the second strand of each pair
taking a second bite into the ligament. Needles, which have passed through the vagina, are
removed and replaced with free-Mayo needles prior to passage through Cooper’s ligament. The
interior of the bladder is then examined for absence of suture material and bilateral efflux of
urine via the ureters. The Foley catheter is removed and a cotton swab test is performed with the
table and patient’s back parallel to the floor. A zero to 2108 angle to the horizontal is established
by elevating or loosening the sutures. The goal of the procedure is stabilization rather then
elevation. The sutures are then tied with precise square knots, maintaining equal and opposite
tension on the strands while tying. The bladder is then closed in a double layer closure with 2-0
Chromic with incorporation of a 16-gauge catheter into the apex of the incision. The catheter is
placed through a right lower quadrant stab incision.

Figure 6 The Marshall-Marchetti-Krantz sutures are placed into the vagina and cartilage of the
symphysis. After placing a double bite into the vagina, the needle is removed and replaced with a new free-
Mayo needle prior to placement into the cartilage. This decreases risk of infection. A total of four sutures
are placed. (Used with permission of the Mayo Foundation.)
 Retropubic Urethropexy 301

Figure 7 The bladder is closed in a double-layer closure incorporating the catheter into the incision.
(Used with permission of the Mayo Foundation.)

V. PATIENT SELECTION FOR SURGERY

Patients with genuine stress urinary incontinence and hypermobility of the urethra in the absence
of severe bladder overactivity are candidates for Burch urethropexy. This includes patients with
low urethral closure pressures or low Valsalva leak-point pressures if they also demonstrate
urethral hypermobility.
The best definition of intrinsic sphincteric deficiency is functional: stress urinary
incontinence despite complete support of the urethra in the absence of uninhibited bladder
contractions. These patients are not candidates for urethropexy because they lack urethral
mobility.
Bergman et al. performed a study showing that patients who have ,308 of urethral descent
with urinary stress incontinence have a 55% failure rate associated with Burch urethropexy (25).
Data on the transvaginal tape (TVT) procedure show that individuals with a nonmobile urethra
and stress incontinence are also at increased risk of failure with TVT surgery (2).
Patients with low urethral pressures who have urethral junction rotation are not at
increased risk of failure following Burch urethropexy. Sand et al. performed a prospective
randomized comparison of the pubovaginal sling procedure and the Burch urethropexy in
patients with low urethral pressures (26). The cure rate was comparable in the two procedures.
Hsieh et al. confirmed this in a separate study (27). The aim of their study was to determine
whether an isolated low Valsalva leak-point pressure could be an independent risk factor for
Burch failure in patients with a normal maximum urethral closure pressure. Twenty-four women
with objectively proven stress incontinence, Valsalva leak-point pressures ,60 cmH2O and
302 Cornella

MUCP values .20 cmH2O were evaluated preoperatively and postoperatively. At .1-year
follow-up, 22 of the 24 (91.7%) patients were objectively continent.
Patients with preoperative hypermobility of the urethra who demonstrate stress
incontinence postoperatively, despite restoration of urethral support, have intrinsic sphincteric
deficiency. This may occur after any operation for stress incontinence, including on occasion the
pubovaginal sling procedure. This failure must be secondary to occult deficiency in nerve,
muscle, and connective tissue that could not be diagnosed preoperatively. This occult deficiency
results in deficient urethral resistance despite restored urethral support after surgery. We have
no urodynamic parameters that predict which preoperative patients will fall into this group. The
future may hold promise in diagnosing this tendency through laboratory assessment of deficient
muscle, nerve, and connective tissue.
As an example of such assessment, Kenton et al. reported on the role of urethral
electromyography in predicting patients who have preoperative urethral hypermobility, but fail
to have their stress leakage repaired with Burch urethropexy (28). Eighty-nine women who
underwent preoperative testing with urethral EMG and cystometrograms were also assessed
postoperatively. Fifty-nine of 74 women (80%) were objectively cured, and 15 women had
persistent urinary stress incontinence at 3 months. Women who were cured did not differ from
those who failed in age, parity, menopausal status, maximum urethral closure pressure, Valsalva
leak-point pressure, maximum cystometric capacity, and detrusor instability or prolapse stage.
Electrical activity of the urethra was calculated in these patients during rest, voluntary urethral
squeezing, repetitive coughing, and bladder filling. There was no difference in any EMG
parameters between the two groups when measured at rest, with urethral squeezing, or during
bladder filling. Women who were cured did demonstrate better motor unit action potential
activation with repetitive coughing than those with persistent leakage.

VI. LAPAROSCOPIC BURCH PROCEDURES

Vancaille and Schuessler reported the first laparoscopic colposuspension (MMK) case series in
1991 (29). The literature reflects a lack of standardization and precise outcome measurements.
Prospective, randomized comparisons of laparoscopic to open technique include the studies by
Summitt et al. and Fatthy et al. (30,31). Comparable rates of stress incontinence cure were noted
between the two groups in each of the studies. Prospective, randomized studies that show
increased cure by open technique include Burton et al. (32) and Su et al. (33). Su examined
success at 1 year and showed an 84% cure with the laparoscopic approach and a 95.6% cure with
the open technique. The randomized study by Burton included a 3-year follow-up with a 40%
failure rate in the laparoscopic group compared with a 15% failure rate in the open group.
Several authors have reported an increased complication rate with the laparoscopic
approach. Speights et al. reported on frequency of lower urinary tract injury at laparoscopic
Burch and PVDR (34). There were no ureteral injuries, and four patients of 171 had cystotomies.
Walter et al. compared morbidity and costs of laparoscopic versus open Burch when
performed with concomitant vaginal prolapse repairs (35). A retrospective review of 76
laparoscopic and 143 open Burch procedures with at least one concomitant vaginal repair for
symptomatic prolapse was accomplished. The group with open urethropexy had an older age,
greater degree of prolapse, fewer concurrent hysterectomies, and a greater number of vaginal
procedures than the group with the laparoscopic Burch procedures. There were minimal
differences in complications. There were no differences in estimated blood loss, operative time,
hemoglobin change, hospitalization, or hospital charges between the two groups. Considering
that a significant percentage of incontinent patients require some type of concomitant prolapse
 Retropubic Urethropexy 303

repair, the benefits of laparoscopy in this setting is less evident. Kholi et al. showed that despite
shorter hospital stay, the direct costs of laparoscopic Burch were higher than those of the open
technique (36).
Persson et al. showed the benefit of two sutures on each side of the urethra in comparison
to one (37). Objective cure rate was 83% in the women with two sutures, compared to the 58% of
patients with one suture.
The current literature would indicate additional large prospective, randomized studies
with adequate power are needed.

VII. LONG-TERM BLADDER COMPLICATIONS OF

RETROPUBIC URETHROPEXY

Symptoms of voiding dysfunction and de novo detrusor instability are most likely increased by
excessive elevation of the vagina and secondarily the bladder trigone at urethropexy. Greater
elevation may result in obstruction and secondary effects on bladder muscle. The benefit of
stabilization and not elevation may be an important factor to consider in decreasing
postoperative complications of voiding dysfunction.
Alcalay et al. noted that the most frequent complication in their series was de novo
detrusor instability (DI) (14.7%) (4). The rate of de novo DI was commensurate between those
having primary or secondary operations. The authors noted that the development of de novo DI
is a bad prognostic factor for long-term objective cure. Women who developed postoperative DI
continued to have symptoms of urgency and urgency incontinence for .10 years. In addition,
Alcalay et al. noted that 22% of patients still complained of voiding dysfunction 10 years or
more after surgery, and four of these patients underwent urethrotomy. The authors found that
preoperative factors had poor predictive value for postoperative voiding dysfunction.
In an earlier study, Stanton’s group had followed 92 patients with no evidence of preoperative
DI on urodynamics who had undergone Burch urethropexy. Postoperative urodynamics showed
that 75 (81.5%) had stable bladders and 17 (18.5%) had unstable bladders (38).
In Langer et al.’s 10-year follow-up objective study, the incidence of de novo DI was
16.6% and 18.7% of postoperative patients developed anatomical defects (5). De novo DI
appeared in 12 of 17 patients during the first year of follow-up. It took longer for the majority of
anatomical defects to become manifest.
In the study by Feyereisl et al., the prevalence of postoperative DI was noted to be 14.9%
and the prevalence of late voiding difficulties was 4.6% (3). In the study by Kammerer et al., the
complication rate was no different in the Burch group compared to the anterior colporrhaphy
group (23).
De novo DI complicated the postoperative course in two of 40 (5%) patients in the
prospective study of Colombo et al. (this was half the amount noted in the MMK group) (11).
Vierhout et al. reviewed six studies totaling 396 patients who had undergone urethropexy.
Sixty-eight (17%) developed de novo DI (39). The prevalence varied from 5% to 27% in the
different studies.
Current knowledge indicates that patients with mixed incontinence who demonstrate DI at
low bladder volumes are at higher risk of failure from retropubic urethropexy. This does not mean
that patients with detrusor instability demonstrated at higher volumes are not candidates for
urethropexy. The majority of female incontinent patients over the age of 60 probably have mixed
incontinence. Colombo, in a retrospective study, showed that in a group of mixed-incontinence
patients, the objective stress incontinence cure rate 2 years after urethropexy was 75% (40). To be
considered cured, patients had to be subjectively free of any incontinence symptoms.
304 Cornella

Figure 8 The completed Marshall-Marchetti-Krantz procedure. The sutures are in the lower one-half of
the symphysis avoiding excessive elevation. (Used with permission of the Mayo Foundation.)

The incidence of long-term urinary retention and its adverse sequelae after urethropexy is
more difficult to estimate. The studies have not reported specific residual urine amounts at 5– 10
years of follow-up. It is unclear in Alcalay et al.’s study how many patients had persistently high
residual urine values in the group of voiding dysfunction patients (4). Four of 366 patients had
subsequent urethrotomy. Residual urine values were not reported in the 10- to 20-year follow-up
category. Feyereisl et al. in their 5- to 10-year follow-up of Burch urethropexy patients noted a
residual urine value .60 mL in 16% of patients (3). The number of patients demonstrating long-
term residual urine determinations .150 mL or 200 mL is not reported.
The risk of enterocele or rectocele formation after colposuspension may also be decreased
by avoidance of excessive elevation of the vagina. Some series show up to a 26.7% risk of
prolapse following colposuspension (41).
Demirci and Petri have documented a review of perioperative complications in the
Burch literature (42). Wiskind et al. reported a need for blood transfusion in 0.7– 2.3% of
cases (41).
 Retropubic Urethropexy 305

Figure 9 The Burch sutures are placed with each strand of the suture pair going through Cooper’s ligament.
Stabilization and not elevation of the anterior wall is achieved in order to decrease the risks of voiding
dysfunction and bladder overactivity. (Used with permission of John Miklos. Copyright John Miklos.)

VIII. CONCOMITANT GYNECOLOGIC SURGERY AND

RETROPUBIC URETHROPEXY

Objective studies of hysterectomy at the time of urethropexy show no effect on incontinence

cure or longevity of cure. Meltomaa et al. in a recent prospective study looked at morbidity
and long-term subjective outcome between Burch colposuspension alone and Burch with
concomitant abdominal hysterectomy (43). There was no difference in subjective short- and
long-term (5 years) outcome. Complications related to operation occurred in 29.2% of the Burch
group and 46.2% of the Burch/hysterectomy group. Complications were mainly related to
infection and postoperative anemia. The reoperation rate was 1.5% for the Burch group and
2.6% for the Burch/hysterectomy group.
Sze et al. compared the surgical morbidity, postoperative course, and hospital charges of
Burch colposuspension performed in conjunction with abdominal versus vaginal hysterectomy
(44). The abdominal route had significantly longer hospital stays and higher hospital charges
than the vaginal group.

IX. CONCLUSION

The retropubic urethropexy remains an important procedure in the surgical management of

female urinary incontinence. Burch urethropexy has a replete literature with some of the longest
objective follow-up series of any incontinence procedure. It is effective in patients with low
306 Cornella

urethral pressure who have hypermobility of the urethra. It can be accomplished with a mini-
incision allowing precise placement of sutures, and allows performance of a concomitant PVDR
with site-specific correction of paravaginal defects.

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anesthesia for treatment of female urinary incontinence. Int Urogynecol J 1996; 7:81– 86.
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vaginal tape (TVT) procedure for surgical treatment of female stress urinary incontinence. Int
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3. Feyereisl J, Dreher E, Haenggi W, Zikmund J, Schneider H. Long-term results after Burch
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6. White GR. A radical cure by suturing lateral sulci of vagina to white line of pelvic fascia. JAMA
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7. White GR. An anatomical operation for the cure of cystocele. Am J Dis Wom Child 1912;
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8. Marshall VF, Marchetti AA, Krantz KE. The correction of stress incontinence by simple
urethrovesical suspension. Surg Gynecol Obstet 1949; 88:509.
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colposuspension and abdominal paravaginal defect repair for female stress urinary incontinence.
Am J Obstet Gynecol 1996; 175:78 – 84.
12. Webster GD, Kreder KJ. Voiding dysfunction following cystourethropexy. J Urol 1990;
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13. Mainprize TC, Drutz HP. The Marshall-Marchetti-Krantz procedure: a critical review. Obstet
Gynecol Surv 1988; 43:724 –729.
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prospective, randomized trial. Am J Obstet Gynecol 1994; 171:1573 – 1579.
16. Quadri G, Magatti F, Belloni C, Barisani D, Nicola N. Marshall-Marchetti-Krantz urethropexy and
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of the urethra: early results of a prospective randomized clinical trial. Am J Obstet Gynecol 1999;
181:12– 18.
17. Kammerer-Doak DN, Cornella JL, Magrina JF, Stanhope CR, Smilack J. Osteitis pubis after
Marshall-Marchetti-Krantz urethropexy: a pubic osteomyelitis. Am J Obstet Gynecol 1998;
179:586– 590.
18. Burch JC. Cooper’s ligament urethrovesical suspension for stress urinary incontinence. Am J Obstet
Gynaecol 1968; 6:764 – 774.
19. Tanagho EA. Colpocystourethropexy: the way we do it. J Urol 1976; 116:751– 753.
20. DeLancey JOL. Structural support of the urethra as it relates to stress urinary incontinence: the
hammock hypothesis. Am J Obstet Gynecol 1994; 170:1713– 1720.
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21. Herbertsson G, Iosif GS. Surgical results and urodynamic studies ten years after retropubic
urethropexy. Acta Obstet Gynaecol Scand 1993; 72:299– 301.
22. Bergman A, Elia G. Three surgical procedures for genuine stress incontinence: five-year follow-up of
a prospective randomized study. Am J Obstet Gynecol 1995; 173:66– 71.
23. Kammerer-Doak DN, Dorin MH, Rogers RG, Cousin MO. A randomized trial of Burch urethropexy
and anterior colporrhaphy for stress urinary incontinence. Obstet Gynecol 1999; 93:75 – 78.
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three operative methods for genuine stress incontinence. J Gynecol Surg 1996; 12:7– 13.
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incontinence with low-pressure urethra. Am J Obstet Gynecol 2000; 182:30 –34.
27. Hsieh GC, Klutke JJ, Kobak WH. Low Valsalva-leak point pressure and success of retropubic
urethropexy. Int Urogynecol J 2001; 12:46 – 50.
28. Kenton K, Fitzgerald MP, Shott S, Brubaker L. Role of urethral electromyography in predicting
outcome of Burch retropubic urethropexy. Am J Obstet Gynecol 2001; 185:51 –55.
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1:169– 173.
30. Summitt RL, Lucente V, Karram MM. Randomized comparison of laparoscopic and transabdominal
Burch urethropexy for the treatment of genuine stress incontinence. Obstet Gynecol 2000; 95(Suppl):2.
31. Fatthy H, El Hoa M, Samaha I, Abdallah K. Modified Burch colposuspension: laparoscopy versus
laparotomy. J Am Assoc Gynecol Laparosc 2001; 8:99 – 106.
32. Burton G. A three year randomized urodynamic study comparing open and laparoscopic
colposuspension. Neurourol Urodyn 1993; 16:353 –354.
33. Su TH, Wang KG, Hsu CY. Prospective comparison of laparoscopic and traditional colposuspension
in the treatment of genuine stress incontinence. Acta Obstet Gynecol 1997; 76:576 – 582.
34. Speight SE, Moore RD, Miklos JR. Frequency of lower urinary tract injury at laparoscopic Burch and
paravaginal repair. J Am Assoc Gynecol Laparosc 2000; 7:515 – 518.
35. Walter AJ, Morse AN, Hammer RH, Hentz JG, Magrina JF, Cornella JL, Magtibay PM. Laparoscopic
versus open Burch retropubic urethropexy: comparison of morbidity and costs when performed with
concurrent vaginal prolapse repairs. Am J Obstet Gynecol 2002; 186:723 – 728.
36. Kholi N, Jacobs PA, Sze EHM, Roat TW, Karram MM. Open compared with laparoscopic approach
to Burch colposuspension: a cost analysis. Obstet Gynecol 1997; 90:411 – 415.
37. Persson J, Wolner-Hanssen, P. Laparoscopic Burch colposuspension for stress urinary incontinence: a
randomized comparison of one to two sutures on each side of the urethra. Obstet Gynecol 2000;
95:151– 155.
38. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress
urinary incontinence. Br J Urol 1979; 51:204– 207.
39. Vierhout ME, Mulder AFP. De novo detrusor instability after Burch colposuspension. Acta Obstet
Gynaecol Scand 1992; 71:414– 416.
40. Colombo M, Zanetta G, Vitobello D, Milani R. The Burch colposuspension for women with and
without detrusor overactivity. Br J Obstet Gynaecol 1996; 103:255 – 260.
41. Wiskind AK, Creighton SM, Stanton SL. The incidence of genital prolapse after the Burch
colposuspension. Am J Obstet Gynecol 1992; 167:399 – 405.
42. Demirci F, Pertri E. Perioperative complications of Burch colposuspension. Int Urogynecol J 2000;
11:170– 175.
43. Meltomaa SS, Haarala MA, Taalikka MO, Kiiholma PJA, Alanen A, Makinen JI. Outcome of Burch
retropubic urethropexy and the effect of concomitant abdominal hysterectomy: a prospective long-
term follow-up study. Int Urogynecol J 2001; 12:3– 8.
44. Sze EHM, Kohli N, Miklos JR, Roat TW, Karram MM. Comparative morbidity and charges asso-
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90:42– 45.
19
Laparoscopic Treatment of Urinary
Stress Incontinence
Thomas L. Lyons
Center for Women’s Care and Reproductive Surgery, Atlanta, Georgia, U.S.A.

I. INTRODUCTION

The treatment of urinary incontinence is a costly endeavor in the United States with over billion
dollars spent each year when all forms of management are considered, including the sale of adult
diapers and the cost of medical and surgical care. Incontinence remains the most common cause
for tertiary admission for long-term custodial care in the older patient.
Since urinary stress incontinence (USI) is the most common type of incontinence and the
numbers of this diagnosis are increasing owing to the active postreproductive years population,
the incidence of this already common disorder is becoming more frequent. Stress incontinence
occurs almost exclusively in women and is stated to occur, at least to some degree, in 85% of
women over the age of 18. The majority of women with USI are multiparous, and pregnancy or
parturition, with its accompanying hormonal effects, pelvic floor, and pelvic neurological
damage, is at the basis for the problem. In a majority of cases, patients are able to manage their
symptoms using one or a combination of medical therapies, behavior modification, and pelvic
floor conditioning. These therapies include Kegel exercises, behavior modification, electrical or
ultrasonic stimulation of pelvic musculature, and a number of pharmacologic agents that act in a
neuroleptic manner to improve urethral sphincter tone. However, if these alternatives have been
exhausted, then surgery is the appropriate solution. The goal of surgery in this and every instance
is to provide an effective solution with minimal medical and economic morbidity.
Because of the pandemic nature of USI and the difficulty of reliably correcting the problem
with existing surgical techniques, over 300 surgical procedures have been developed over the
years to deal with the problem (1 –11). Similarly, as minimally invasive techniques have been
applied in this area, a multitude of variations and new procedures have been proposed, many of
which have “borrowed” names from traditional procedures whether the laparoscopic procedure
resembled the old procedure or not. This means that some “laparoscopic Burch” procedures are
not Burch procedures in the real sense of the word. The purpose of this chapter is to present some
of the variations which have been proposed and what available data are present on these
modifications. In addition, we will attempt to carefully describe the procedure that we currently
perform and present the data and rationale that supports this approach.
Most gynecologists will agree that the gold standard surgically speaking in the treatment
of USI is retropubic culposuspension (Burch procedure) (2,3). The Marshall, Marchetti, Krantz
309
310 Lyons

(MMK) procedure is also included in this discussion (1). We also include the paravaginal repair,
which was described by Richardson in the mid-1970s, as a component of this type of repair
that is referred to as “site-specific defect repair of the pelvic floor” (4). The other type
of surgical treatment recommended for USI is the suburethral sling procedure (11). This is the
preferred method by most urologists, and although we have performed these procedures
with laparoscopic assistance, we do not suggest that this should be the norm. It is important to
apply a global approach to pelvic floor reconstruction, as rarely do the defects described here exist
in absence of corresponding defects of the posterior compartment. Therefore, when the treatment
of USI is considered, all defects are approached and treated at the same time. This invariably
improves outcomes not only in the short term, but also extended follow-up is improved.

II. HISTORICAL CONTEXT

Originally, vaginal approaches to this USI problem were considered the only alternative to
pessaries and nonsurgical methods of improving continence. In fact, the problem was rarely
discussed and the initial descriptions of anterior colporraphy with the Kelley Kennedy plication in
1913 were rapidly accepted over the existing techniques, which had greater morbidity with
uniformly poor outcomes (5). The subsequent development of vaginal approaches progressed under
the auspices of proficient surgeons such as Nichols and Richardson into the latter half of the 20th
century (4,6). Still, however, there were treatment failures particularly, over long-term follow-up.
Midcentury, a retropubic approach to the problem was suggested by Marshall, Marchetti,
and Krantz (MMK) (1). This retropubic urethropexy seemed to improve outcomes but also
brought new morbidity of osteitis pubis and urinary retention. A decade later the Burch
modification was proposed and later modified by Tanangho and others into the procedure that is
currently being used by most gynecologists and urologists (12). The clinical success rates quoted
short term are in the high 80% range for this procedure.
Despite the excellent clinical outcomes, there was concern regarding the morbidity
associated with the need for laparotomy to perform these procedures which gave rise to a number
of new procedures. One group of these procedures were called the “needle procedures.” Most
notable among these proposed procedures were those described by Raz (7), Pereyra (8), Stamey
(9), and Gittes (10). In further investigations these procedures have yielded relatively
disappointing success rates of 50– 70% (13).
The sling procedures which were first applied in the 1970s have produced good clinical
outcomes, particularly in those patients with intrinsic sphincter deficiency (ISD) and mixed
incontinence (11). These procedures also have morbidities that include the need for laparotomy
in some cases and the potential for rejection/infection of the sling material itself. Although
many of these problems have been obviated, very few gynecologists perform sling procedures
routinely, and most urologists who use them do not approach the posterior and/or concomitant
anterior compartment defects.
The late 1980s and the 1990s brought the replacement of a number of laparotomy-based
gynecologic procedures with laparoscopic alternatives. In most instances, the laparoscopic
approaches have produced similar clinical results with significant reductions in overall costs and
morbidity. Logically, applications of minimally invasive techniques to USI and defects of the
anterior compartment were the next step in this area. A Medline search of information on this
application in 2002 reveals a wealth of papers on the laparoscopic applications to USI. However,
standardization of these papers is difficult to assess but will be presented in the next segment of
this discussion.
 Laparoscopic Treatment of USI 311

The first report of laparoscopic retropubic treatment of USI was by Vancaille and
Shuessler, a gynecologist and an urologist, respectively, in 1991 (14). Vancaille has
subsequently developed his techniques after Zacharin, the well-known Australian surgeon (15),
while other gynecologists in the United States, including Lui, Lyons, and others, have pursued
a site-specific approach to retropubic repairs (16 – 19). Table 1 summarizes the results of a
Medline search on laparoscopic applications to USI.

III. TECHNIQUE

The technique that will be described here is the favored technique in our institution and this
technique is similar to that of Lui, Miklos, and Wattiez. There are differences, but those

Table 1 Laparoscopic Urinary Stress Incontinence Procedures—Clinical Out-

comesa

Patients Follow-up Cure rate

Reference (n) (months) (%)

Vancaillie et al. (14) 9 3 100

Liu et al. (18) 107 3 – 27 97.2
Liu (19) 58 24 94.8
Burton (20) 30 12 73
Gunn et al. (21) 15 4–9 100
Liu (22) 132 24 96.2
Nezhat (23) 62 8 – 30 91.9
Lam et al. (24) 15 9 98
Langebrekke et al. (25) 8 3 88
Lyons et al. (26) 20 12 92
Lyons (27) 38 18 90
Polascik et al. (28) 12 21 – 36 83
Von Theobald et al. (29) 37 42 86
Cooper et al. (30) 113 1 – 28 87
Kung et al. (31) 31 14 – 30 97
Nieves (32) 35 4 – 30 90
Radomski (33) 34 12 – 26 85
Shwayder (34) 20 12 – 54 100
Burton (35) 30 36 60
Lobel et al. (36) 35 1 – 51 68.6
Papasakelariou et al. (37) 32 24 90.6
Su et al. (38) 46 12 80.4
Das (39) 10 36 90
Lee et al. (40) 48 26 93.8
Miannay et al. (41) 36 17 79
Ross (42) 48 30 – 41 89
Saidi et al. (43) 70 5 – 27 91.4
Fatthy et al. (44) 34 18 87.9
Lee et al. (45) 150 36 90.7
Zullo et al. (46) 30 12 89
a
Patient reports no loss of urine with Valsalva.
312 Lyons

differences are predominately typical surgeon-specific idiosyncrasies. After an accurate

diagnosis is made, the patient is prepped for surgery with a magnesium citrate bowel prep and is
consented for pelvic floor reconstruction. If there are indications for hysterectomy, then
hysterectomy is performed with laparoscopic supracervical hysterectomy (LSH), the preferred
procedure. This allows excellent ability to reconstruct the pericervical ring of fascia and also
facilitates the repair of the posterior compartment and vault support.
The patient is positioned as shown in Figure 1. Dual monitors placed at the patient’s feet
are at or above eye levels for surgeon comfort. The trocar placement is as shown in Figure 2. The
midline trocars are 10/12 mm in diameter and allow for passage of the laparoscope in the
subumbilical site and the introduction and extraction of curved needles of adequate size through
the suprapubic site. The lateral trocars are 5 mm in diameter and are placed well lateral to the
rectus muscles and as high as the suprapubic midline trocar at least four fingerbreadths above the
symphysis. This allows an adequate angle to access both the space of Retzius and the posterior
cul-de-sac. A 20-cc bulb Foley catheter is placed in the bladder.
After completion of the hysterectomy, posterior compartment repair is accomplished
which usually includes a high McCall’s culdoplasty and vault suspension. This is performed
with #0 Ethibond (Ethicon Inc., New Brunswick, NJ) suture in an ipsilateral fashion. A relaxing
incision is made medial to the ureter on each side to identify and avoid kinking of the ureter with
this suspension procedure.
The space of Retzius is entered by making an incision in the anterior wall peritoneum
1 inch above the symphysis pubis. This incision is extended bilaterally to the obliterated
umbilical ligaments. Blunt and sharp dissection is used to identify first the symphysis and
Cooper’s ligaments and then the lateral pelvic sidewall, obturator neurovascular canal,
neurovascular bundle, the ischial spine, the arcus tendinius (White’s line of the pelvis), the arcus
of the levator ani, and the paravaginal fascia (Fig. 3). The entire area is cleared or fat and areolar

Figure 1
 Laparoscopic Treatment of USI 313

Figure 2

tissue (Tanangho modification) (12). Then the endopelvic fascia of the vagina is then sutured
using #2-0 Ethibond (Ethicon Inc., New Brunswick, NJ) to the corresponding arcus tendinius
fascia pelvis, thus correcting the lateral cystocele defect. This suture can be placed as an
interrupted suture or in a running fashion. After both paravaginal defects have been repaired in

Figure 3
314 Lyons

Table 2 Follow-up Laparoscopic Burch Urethropexya

Suture Success % (N) Failure % (N)

Vicryl 50% (14) 50% (14)

Ethibond 76% (60) 24% (19)
a
Based on 80.7% response rate.

this fashion then the Burch sutures are placed. Ethibond #0 suture is placed in an interrupted
figure of eight fashion through the endopelvic fascia 1 – 2 cm lateral to the urethra with one
suture at the midurethral level and one at the urethrovesical junction. These sutures are
then taken through Cooper’s ligament and tied, stabilizing the urethra and the U/V junction.
This repair corresponds to the paravaginal-plus repair described by Shull in the late 1980s
and constitutes completion of the repair of the anterior compartment. The anterior peritoneal
defect is closed using #2-0 Vicryl (Ethicon Inc., New Brunswick, NJ) in a running purse-string
manner.
Cystoscopy is performed 5 min after 5 cc of indigo carmine is injected intravenously
documenting ureteral patency and the absence of suture material in the bladder. A 17 or 19 Fr
cystoscope with 708 lens is helpful in this portion of the procedure. Absence of ureteral effluent
requires investigation of ureteral patency. The catheter is removed as soon as the patient is
ambulatory and the patient is allowed to void. Voiding abnormalities are common in the first few
days but resolve rapidly. In the patient who is unable to void 5 h after the catheter is removed, the
catheter is replaced and left overnight. Virtually all patients are able to void by morning.
However, all patients are counseled about voiding difficulties postprocedure and are taught self-
catheterization for this instance. Patients are discharged from the facility when discharge criteria
are met and they wish to leave. This means that all patients are discharged within 23 h, and the
average discharge is accomplished in 11 h. Patients are encouraged to resume most normal
activity as soon as they feel comfortable but are restricted from intercourse and repetitive
straining or heavy lifting for 4 – 6 weeks.
It is important to note at this time in the technical segment of this chapter that the use of
permanent suture material is significant when treating support type defects. The present author’s
experience confirms this need. Table 2 summarizes the early experience in laparoscopic Burch
procedures when first absorbable, and then permanent materials were used. Success rates have
been maintained since that time when using permanent suture material.
Other described techniques involve the use of Prolene or other mesh materials and stapling
or tacking devices to attach the mesh to Cooper’s ligament and the paravaginal fascia,
respectively (47), the use of the laparoscope to facilitate the performance of a “needle” or a sling
procedure (36), and the placement of sclerotic materials into the space of Retzius under
laparoscopic guidance all being described as a laparoscopic Burch procedure. Representative
data from these techniques are included in Table 1. Conclusions regarding the efficacy of these
procedures are left to the reader.

IV. DISCUSSION

Ultimately, there are a number of factors that will eventually contribute to the adoption of
laparoscopically directed pelvic floor reconstruction. These are the same factors that should
 Laparoscopic Treatment of USI 315

govern the adoption of any surgical or medical procedure. First and foremost, the procedure
must accomplish the task that it is proposed to do. There seems to be ample evidence that this
goal can be achieved with laparoscopic retropubic culposuspension. In the data generated to
date, although little level I evidence is available, it appears that in competent hands results
should be equivalent at worst.
Secondly, morbidity should be improved or no worse than existing techniques. Again, the
evidence appears convincing that laparoscopic procedures definitely reduce short-term
morbidity and mortality when compared to laparotomy procedures. There are some who
argue that laparoscopy has a morbidity in and of itself, but the arguments for this position thus
far have remained unconvincing. Medicolegally speaking, entry into the abdomen has a
definable morbidity whether that entry is made laparoscopically or via laparotomy.
Thirdly, there is the question of cost. There certainly is no question that cost is and
should be an issue in the performance of surgery. We must look, therefore, at cost and not
at “charges,” which some would have us believe are the actual costs of surgery. Charges
are what the hospital or facility charges the patient or the patient’s insurer for the procedure
and almost always bear only a vague resemblance to the actual cost of the procedure.
Operating-room time is an issue, and, early in the learning curve, any new procedure will
take more time, but it is our observation that this is no longer an issue once proficiency is
gained. No special materials or devices are needed for this procedure, although some have
been suggested. Intangible costs of more rapid return to work have not been addressed in
the literature to date but based on information derived from work done with laparoscopic
cholecystectomy and laparoscopic hysterectomy the cost savings from these procedures
could be substantial (48,49).
Finally, there is the question of technical training and credentialing. The procedures
described are not new procedures as such but only different modes of access to perform “tried-
and-true” procedures. Certainly, suturing laparoscopically is one of the more difficult skills to
learn by the novice laparoscopist, but it does not represent a barrier that is in any way
unreachable by a surgeon who is willing to practice this technique and apply it in his or her
practice. The potential reduction in morbidity for that surgeon’s patients is well worth the extra
efforts involved. There have also been concerns that somehow adoption of these procedures
would signal an end to vaginal surgery and its attendant discipline. It is this author’s belief that
the further anatomic knowledge that is attainable with laparoscopic surgery can serve to improve
the vaginal skills of the operator and potentially open more vaginal opportunities for possible
success in correcting these defects.
Pelvic floor reconstruction is a discipline that, in reality, has only one century of history. In
that period of time, great strides have been made and many solutions have been found to these
problems that affect women in their day-to-day lives. At the same time, advances have been
made in surgery that have made surgical procedures safer and more effective for our patients. At
the end of the 20th century, operative laparoscopy entered the scene and has made an impact on
numerous gynecologic and general surgical procedures (50). Owing to the technical difficulty of
some of these procedures, assimilation into the mainstream of therapeutic options has been less
rapid (51). Lack of level I evidence has been suggested as the reason for this slow uptake, but
since there is a dearth of such evidence for existing procedures, it is doubtful that this is the case.
How best to perform pelvic floor reconstruction, and what are the anatomic and what are the
physiologic explanations for these disorders and their attendant symptomologies are questions
for which answers remain lacking. This is truly a surgical field that is a “work in progress.” It is
felt that if laparoscopically directed approaches can further any of this knowledge, anatomically
or surgically, then the effort was well spent.
316 Lyons

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vesicourethral suspension. Surg Gynecol Obstet 1949; 88:590.
2. Burch JC. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence,
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3. Burch JC. Cooper’s ligament urethrovesical suspension for stress urinary incontinence. Am J Obstet
Gynecol 1968; 100:764 – 771.
4. Richardson AC, Edmonds PB, Williams N. Treatment of stress urinary incontinence due to
paravaginal fascial defect. Obstet Gynecol 1982; 57:357 – 360.
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7. Raz S, Sussman FM, Erickson DB, Bugg KS, Nitti VW. The Raz bladder neck suspension results in
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9. Stamey TA. Endoscopic suspension of the vesicle neck for urinary incontinence in females: a report
on 203 consecutive patients. Am Surg 1980; 192:465 – 471.
10. Gittes RF. No incision pubovaginal suspension for stress incontinence. J Urol 1987; 138:568 – 574.
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12. Tanagho EA. Culpocystourethropexy: The way we do it. J Urol 1976; 116:751 – 753.
13. Bergman A, Ballard CA, Konings PP. Comparison of three different surgical procedures for
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160:1102– 1107.
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1:169– 173.
15. Zacharin RF. The anatomic supports of the female urethra. Obstet Gynecol 1968; 32:754 – 759.
16. Miklos JR, Kohli N. Laparoscopic paravaginal repair plus Burch urethropexy: review and descriptive
technique. Urology 2000; 56:64 – 69.
17. Wattiez A, Boughizane S, Alexandre F, Canis M, Mage G, Pouly JL. Laparoscopic procedures for
stress incontinence and prolapse. Curr Opin Obstet Gynecol 1995; 7:317 – 321.
18. Liu CY, Paek W. Laparoscopic retropubic colposuspension (Burch procedure). J Am Assoc Gynecol
Laparosc 1993; 1:31– 35.
19. Liu CY. Laparoscopic retropubic colposuspension (Burch procedure). A review of 58 cases. J Reprod
Med 1993; 38:526 – 530.
20. Burton GA. A randomized comparison of laparoscopic and open colposuspension. Neurourol Urodyn
1994; 13:487 –498.
21. Gunn GC, Cooper RP, Gordon NS, Gagnon L. Use of a new device for endoscopic suturing in the
laparoscopic Burch procedure. J Am Assoc Gynecol Laparosc 1994; 2:65 – 70.
22. Liu CY. Laparoscopic treatment of genuine urinary stress incontinence. Baillieres Clin Obstet
Gynaecol 1994; 8:789 – 798.
23. Nezhat CH, Nezhat F, Nezhat CR, Rottenberg H. Laparoscopic retropubic cystourethropexy. J Am
Assoc Gynecol Laparosc 1994; 1:339 – 349.
24. Lam AM, Jenkins GJ, Hyslop RS. Laparoscopic Burch colposuspension for stress incontinence:
preliminary results. Med J Aust 1995; 162:18 – 21.
25. Langebrekke A, Dahlstrom B, Eraker R, Urnes A. The laparoscopic Burch procedure. A preliminary
report. Acta Obstet Gynaecol Scand 1995; 74:153– 155.
26. Lyons TL, Winer WK. Clinical outcomes with laparoscopic approaches and open Burch procedures
for urinary stress incontinence. J Am Assoc Gynaecol Laparosc 1995; 2:193– 198.
27. Lyons TL. Minimally invasive retropubic colposuspension. Gynaecol Endosc 1995; 4:189– 194.
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28. Polascik TJ, Moore RG, Rosenberg MT, Kavoussi LR. Comparison of laparoscopic and open
retropubic urethropexy for treatment of stress urinary incontinence. Urology 1995; 45:647 – 652.
29. Von Theobald P, Guillaumin D, Levy G. Laparoscopic preperitoneal colposuspension for
stress incontinence in women. Technique and results of 37 procedures. Surg Endosc 1995; 9:1189–1192.
30. Cooper MJW, Cario G, Lam A, Carlton M. A review of results in a series of 113 laparoscopic
colposuspensions. Aust NZ J Obstet Gynaecol 1996; 36:44 – 48.
31. Kung RC, Lie K, Lee P, Drutz HP. The cost effectiveness of laparoscopic versus abdominal Burch in
women with urinary stress incontinence. J Am Assoc Gynecol Laparosc 1996; 3:537 – 544.
32. Nieves A. Long-term results of laparoscopic Burch. J Am Assoc Gynecol Laparosc 1996; 3:S35.
33. Radomski SB, Herschorn S. Laparoscopic Burch bladder neck suspension: early results. J Urol 1996;
155:515– 518.
34. Shwayder JM. Laparoscopic Burch cystourethropexy compared with the transperitoneal and
extraperitoneal approaches. J Am Assoc Gynecol Laparosc 1996; 3:S46 – S47.
35. Burton GA. A three-year randomized urodynamic study comparing open and laparoscopic
colposuspension. Neurourol Urodynam 1997; 16:353 – 354.
36. Lobel RW, Davis GD. Long-term results of laparoscopic Burch urethropexy. J Am Assoc Gynecol
Laparosc 1997; 4:341– 345.
37. Papasakelariou C, Papasakelariou B. Laparoscopic bladder neck suspension. J Am Assoc Gynecol
Laparosc 1997; 4:185– 189.
38. Su TH, Wang KG, Hsu CY, Wei HJ, Hong BK. Prospective comparison of laparoscopic and
traditional colposuspensions in the treatment of genuine stress incontinence. Acta Obstet Gynecol
Scand 1997; 76:576 – 582.
39. Das S. Comparative outcome analysis of laparoscopic colposuspension, abdominal colposuspension
and vaginal needle suspension for female urinary incontinence. J Urol 1998; 160:368– 371.
40. Lee CL, Yen CF, Wang CJ, Huang KG, Soong YK. Extraperitoneal colposuspension using CO2
distension method. Int Surg 1998; 83:262 – 264.
41. Miannay E, Cosson M, Lanvin D, Querleu D, Crepin G. Comparison of open retropubic and
laparoscopic colposuspension for treatment of stress urinary incontinence. Eur J Obstet Gynecol
Reprod Biol 1998; 79:159 – 166.
42. Ross JW. Multichannel urodynamic evaluation of laparoscopic Burch colposuspension for genuine
stress incontinence. Obstet Gynecol 1998; 91:55– 59.
43. Saidi MH, Sadler RK, Saidi JA. Extraperitoneal laparoscopic colposuspension for genuine urinary
stress incontinence. J Am Assoc Gynecol Laparosc 1998; 5:247 – 252.
44. Fatthy H, El Hao M, Samaha I, Abdallah K. Modified Burch colposuspension: laparoscopy versus
laparotomy. J Am Assoc Gynecol Laparosc 2001; 8:99 – 106.
45. Lee CL, Yen CF, Wang CJ, Jain S, Soong YK. Extraperitoneal approach to laparoscopic Burch
colposuspension. J Am Assoc Gynecol Laparosc 2001; 8:374 –377.
46. Zullo F, Palomba S, Piccione F, Morelli M, Arduino B, Mastrantonio P. Laparoscopic Burch
colposuspension: a randomized controlled trial comparing two transperitoneal surgical techniques.
Obstet Gynecol 2001; 98:783 – 788.
47. Ou CS, Presthus J, Beadle E. Laparoscopic bladder neck suspension using hernia mesh and surgical
staples. J Laparoendosc Surg 1993; 3:563 – 566.
48. Demco L. Hysterectomy panel discussion. J Am Assoc Gynecol Laparosc 1994; 13:287 – 295.
49. Bass EB, Pitt HA, Lillemoe KD. Cost-effectiveness of laparoscopic cholecystectomy versus open
cholecystectomy. Am J Surg 1993; 165:466 –471.
50. Soper, NJ, Brunt LM, Kerbl K. Laparoscopic general surgery. N Engl J Med 1994; 330:409– 419.
51. Levy BS, Hulka JS, Peterson HB. Operative laparoscopy: AAGL membership survey. J Am Assoc
Gynecol Laparosc 1994; 14:301 – 314.
20
Insertion of Artificial Urinary Sphincter in
Women
H. Roger Hadley
Loma Linda University, Loma Linda, California, U.S.A.

I. INTRODUCTION

The artificial urinary sphincter (AUS) is an effective alternative to the urethral sling or periurethral
injection therapy for the treatment of urinary incontinence in women as a result of intrinsic sphincteric
deficiency (ISD) or type III stress urinary incontinence (1,2). In women with anatomic (type II)
urinary incontinence associated with poor bladder neck support (hypermobility), the AUS is rarely
inserted in deference to the more commonly used urethral sling or standard bladder neck suspension.
Intrinsic sphincter deficiency in women may be associated with or due to scarring
following multiple prior anti-incontinence operations, neurologic disorders (myelomeningocele,
sacral cord tumor, or peripheral neuropathy), radical pelvic operations (abdominoperineal
resection or radical hysterectomy), pelvic radiation therapy, and estrogen deficiency, or senile
changes of the urethra and vagina. Because intrinsic sphincter deficiency leads to inadequate
urethral closure, a standard bladder neck suspension is unlikely to alleviate the patient’s stress
urinary incontinence. Operative management, therefore, is directed toward improving urethral
closure with a suburethral sling, periurethral bulking agents, or insertion of the AUS.
The AUS is a manufactured device that includes a pump, a reservoir to store and regulate
the pressure of the hydraulic fluid, and a cuff designed to provide a uniform circumferential
compression on the urethra and bladder neck (Fig. 1). To empty her bladder the patient cycles the
pump component of the AUS which is placed in the subcutaneous tissue of the labia majora. The
American Medical System AS-800 is the only artificial sphincter currently commercially
available and can be implanted using either a transvaginal or transabdominal approach.
This chapter describes the technique of transvaginal implantation of the artificial urinary
sphincter in the treatment of incontinence due to intrinsic sphincter deficiency (type III stress
urinary incontinence).

II. URINARY INCONTINENCE DUE TO SUSPECTED INTRINSIC

SPHINCTER DEFICIENCY

Evaluation of the incontinent female patient should include a history, physical examination,
radiographic evaluation, and urodynamic studies. The patient with genuine stress urinary
319
320 Hadley

Figure 1 The AS-800 AUS in a woman. The cuff is placed around the bladder neck, the pressure-
regulating balloon in the prevesical space, and the pump in the labia majora. (From Ref. 14.)

incontinence due to intrinsic sphincter deficiency will report loss of urine with abdominal
straining that may or may not be associated with urgency. Previous anti-incontinence
procedures, radical pelvic operations, history of orthopedic or neurologic disorders, and
currently used medications (including replacement hormones) constitute important historical
information.
Physical examination includes measurement of postvoid residual volume and an
assessment of vaginal wall integrity and pelvic floor support. With the bladder filled to near
capacity, the patient is assessed for stress urinary incontinence in the supine and/or upright
position. Not only is it imperative to witness the loss of urine simultaneous to abdominal
straining, but it is also important to make note of the severity of incontinence—i.e., losses of
large volumes of fluid with minimal provocation. The Q-tip deflection test is used to assess
urethral mobility. Neurologic examination of the lower extremities and perineum is performed
to evaluate the lower lumbar and sacral cord segments. Cystourethroscopy is done to assess
urethral coaptation, bladder trabeculation, and the unlikely presence of a fistula.
Radiographic evaluations may include a standing voiding cystourethrogram with resting
and straining views. A well-supported urethra with an open bladder neck not associated with a
bladder contraction is consistent with primary urethral insufficiency.
Urodynamic studies include a filling cystometrogram and measurement of urethral leak
point pressure. Leakage of urine associated with a leak point pressure of ,80 –100 cmH2O in
the absence of a detrusor contraction supports the diagnosis of intrinsic sphincter deficiency.
Women with severe leakage (e.g., ,40 –50 cmH2O) may need to be identified in a separate
category, since these patients do not respond as well to traditional treatments as compared to
their counterparts with higher pre-treatment leak point pressures.
 Artificial Urinary Sphincter 321

Video urodynamics, if available, provides a concurrent fluoroscopic and urodynamic

assessment that allows a simultaneous and perhaps a more accurate evaluation of the cause and
type of urinary incontinence.

A. Patient Selection
Implantation of an AUS is reserved for those who have genuine stress urinary incontinence
despite a well-supported bladder neck and no significant bladder instability. If the incontinent
patient has concomitant vesical instability, simultaneous pharmacologic or operative
management may be required to achieve urinary continence.
In the patient with urinary incontinence due to primary urethral insufficiency, conservative
measures should be tried before operative intervention. These nonoperative measures include
timed voiding, fluid restriction, pelvic floor exercises, systemic or topical estrogens, a-receptor
agonists, and anticholinergic medications. If the patient continues to be incontinent despite
conservative treatment, placement of the artificial urinary sphincter may be considered.
Because the more commonly used modes of therapy—urethral sling and periurethral
bulking agents—have not been as successful in patients with severe incontinence and low leak
point pressures, the AUS should be seriously considered and, indeed, may be best suited in
these patients since it is designed to provide a uniform circumferential compression on the
incompetent bladder neck.

B. Technique
The artificial urinary sphincter is composed of three parts: the inflatable cuff, the pressure-
regulating balloon, and the pump (Fig. 1). The cuff is placed circumferentially around the
bladder neck, the pressure-regulating balloon is positioned in the prevesical space, and the pump
is put in the labia majora. When the pump is squeezed, fluid moves from the cuff to the balloon
reservoir. This decompression of the cuff opens the bladder neck and allows the patient to void.
After 1 – 2 min the pressure-regulating balloon automatically reinflates the cuff, which then
reestablishes urethral coaptation and continence.
Three different techniques have been described for the transvaginal placement of the
artificial urinary sphincter (1,3,4). The inherent advantage of the transvaginal approach is the
possibility of dissection of the urethrovaginal plane, which is often obliterated after previous
anti-incontinence procedures. The transvaginal technique allows dissection of the urethrova-
ginal plane under direct vision.
A vertical incision is made in the anterior vaginal wall (Fig. 2). The incision extends from a
point midway between the bladder neck and the external meatus to the proximal bladder neck. A
plane under the vaginal wall is created on each side of the incision with sharp dissection. The
dissecting scissors are first pointed laterally to the pubis ramus and then upward toward the
ipsilateral shoulder of the patient (Fig. 3). Sufficiently thick vaginal flaps are created in anticipation
of closure of the vagina over the soon-to-be-placed cuff of the artificial urinary sphincter. If the
patient has not had a previous bladder neck operation, blunt finger dissection may be performed to
separate the endopelvic fascia from its lateral attachments to the pubic rim. The finger should
sweep from lateral to medial, creating a window into the retropubic space. In the patient with dense
scar tissue, sharp dissection will be required to enter the retropubic space. The urethra and bladder
neck can then be separated posteriorly and laterally from the vagina and the pelvic side wall with
sharp and blunt dissection. A similar procedure is followed on the opposite side.
The posterior aspect of the bladder neck is dissected free from the underlying anterior
vaginal wall. It is important to mobilize the bladder from the vaginal wall without extending the
322 Hadley

Figure 2 With the patient in the modified dorsolithotomy position, a vertical incision is made in the
anterior vaginal wall. (From Ref. 14.)

vaginal incision toward the apex of the vagina. Leaving an intact thick vaginal wall underneath
the bladder neck will lessen the likelihood of cuff erosion into the vagina.
Attention is next directed to the anterior aspect of the proximal urethra or bladder neck to
free its attachments from the overlying symphysis pubis. If possible, blunt finger dissection
should be used to perform this part of the procedure. However, in the patient who has had a
previous retropubic operation, dense scarring may be encountered in the anterior portion of the
urethra. Overly aggressive dissection may lead to unintentional bladder opening or urethral tear.
The dissection on the anterior side of the urethra may be particularly difficult because of its
relative inaccessibility through the transvaginal approach. To facilitate exposure of the top side
of the urethra a separate suprameatal incision may be used. The previously placed Foley catheter
is retracted downward, and a small (1 – 2 cm), crescent-shaped incision is made above the
external meatus (Fig. 4A). Sharp dissection is then done in the midline below the symphysis
pubis (Fig. 4B). After the bladder is allowed to drop away from its attachments to the symphysis,
lateral blunt dissection can be easily performed to complete the dissection to the retropubic
space previously opened through the vaginal incision. Thus, a circumferential dissection is
completed around the bladder neck. However, if one is readily able to free the urethra from its
anterior attachments through the vaginal incision alone, this suprameatal dissection is not
necessary.
After the proximal urethra has been freed circumferentially, a broken-back small vascular
clamp (Dale femoral-popliteal anastomosis clamp, Pilling 35-3543) is passed around the urethra
from the left to right. The cuff-measuring tape is grasped and passed around the urethra (Fig. 5),
and the circumference of the urethra is measured. If the circumference is equivocal, it is best to
err in favor of a slightly larger cuff size. Using a curved clamp, the appropriate-size cuff of the
 Artificial Urinary Sphincter 323

Figure 3 Using a combination of sharp and blunt dissection, the retropubic space is entered lateral to the
bladder neck. (From Ref. 14.)

artificial urinary sphincter is placed around the proximal urethra (Fig. 6). If the pump of the
artificial urinary sphincter is to be inserted into the right labium majus, the cuff is withdrawn
from right to left. If, however, the pump is to be placed in the left labia majora, the cuff should be
withdrawn from left to right. The cuff is then locked in place (see Fig. 6) and rotated 1808 so that
the hard-locking button lies on the anterior aspect of the urethra, away from the anterior vaginal
wall (Fig. 7).
A 4-cm transverse suprapubic incision is made on the side that the pressure-regulating
balloon and pump mechanism will be implanted. The tubing passer is passed antegrade under
fingertip guidance from the suprapubic incision lateral to the midline and down to the vaginal
incision on the ipsilateral side of the bladder neck. (This operative step is similar to passing a
needle carrier under fingertip guidance during a Pereyra-type bladder neck suspension.) The cuff
tubing is attached to the tubing passer and then withdrawn up to the suprapubic incision. The
anterior rectus sheath is incised transversely, and the prevesical space is developed adjacent to
the bladder. The pressure-regulating balloon is then inserted in the prevesical space. In women,
the 51 –60 cmH2O pressure balloon reservoir is routinely used.
From the suprapubic incision a subcutaneous tunnel is created through which the pump
will be inserted into the labia majora. The pump is passed into the labia majora to the level of the
urethra with the deactivation button facing anteriorly.
Filling of the cuff and reservoir is performed according to the instructions specified by the
manufacturer. The tubings are trimmed to the appropriate lengths and then irrigated to remove
any air or debris from the system.
The suprapubic and vaginal wounds are irrigated with copious amount of antibiotic
solution. The wounds are then closed in multiple layers with absorbable sutures to ensure good
324 Hadley

Figure 4 (A) If dense scarring is encountered anterior to the urethra, a separate incision is made above
the urethral meatus. (B) The suprameatal dissection is done in the midline just below the symphysis pubis.
(From Ref. 14.)
 Artificial Urinary Sphincter 325

Figure 5 A Penrose drain is placed around the bladder neck to demonstrate the completed
circumferential dissection. (From Ref. 14.)

coverage of the prosthesis with healthy overlying tissue. If the integrity of the vaginal wall
appears to be compromised, an interposition of a vascularized flap (e.g., Martius flap) should be
considered. The pump is left in the deactivated mode for 6 weeks.
A vaginal gauze pack is placed and removed on the first postoperative day. The Foley
catheter is removed on the third postoperative day.

III. DISCUSSION

Favorable outcomes of transvaginal placement of the AUS have been published. Appell reported
a series of 34 patients in whom the artificial urinary sphincter was placed through simultaneous
vaginal and abdominal incisions (1). Nineteen patients underwent follow-up of 3 years. The
overall continence rate was 100%. Three patients, however, required revisionary operations for
inadequate cuff compression and connector leak. Abbassian described the implantation of the
artificial urinary sphincter in four patients utilizing the vaginal incision alone (4). At mean
follow-up of 14 months, all patients were dry.
The potential advantage of the artificial urinary sphincter over the urethral sling is the
capability to place a known circumferential compressive force around the entire urethra rather
than a single force on the posterior surface of the urethra. Women with severe leakage (e.g.,
,40 – 50 cmH2O) do not respond as well to traditional treatments as compared to their
counterparts with higher pretreatment leak point pressures. The AUS may therefore be the
preferred treatment in those patients with severe symptoms of stress incontinence associated
with very low leak-point pressures.
326 Hadley

Figure 6 The cuff of the artificial urinary sphincter is passed around the bladder neck and then locked in
place. (From Ref. 14.)

In addition, a decreased likelihood of urinary retention and bladder instability may be

associated with the artificial urinary sphincter. The incidence of prolonged postoperative urinary
retention after the urethral sling operation has been reported to be up to 10%, especially in
patients with a preoperative hypotonic bladder (5). Persistent postoperative frequency and
urgency due to bladder instability has been demonstrated in 6 – 18% of patients after placement
of the pubovaginal sling in the treatment of type III stress urinary incontinence (6,7). In our
experience of 25 patients who underwent transvaginal placement of the AS-800 artificial urinary
sphincter for primary urethral insufficiency, seven patients had preoperative hypotonic bladder
documented on urodynamic studies. Follow-up lasted from 3 to 16 months (mean, 7.3 months).
None of the patients developed clinically significant postoperative frequency or urgency. All
seven patients were dry and able to void spontaneously with or without abdominal straining.
Prolonged (i.e., .1 month) urinary retention requiring intermittent catheterization was not
demonstrated by any of the patients who had hypocontractile bladders preoperatively (8).
The continence rate of the AUS successfully implanted either by the transvaginal or
transabdominal approach in women who have not had an erosion in either the bladder or vagina
has been very good. A recent series of more than 200 women undergoing a transabdominal
placement of the AUS reported a continence rate of .90% with a mean follow-up of 3.9 years.
In this same series the explantation rate was 6% (12).
Long-term reliability of the artificial sphincter, regardless of the technique of implantation,
is reported sparingly in the urological literature. Our experience from the artificial sphincter in
both men and women indicates that the revision rate from all causes is 50% at 5 years and
.90% at 10 years. Similar 10-year revision rates have been reported from Fulford et al. (13).
 Artificial Urinary Sphincter 327

Figure 7 The cuff is rotated 1808 clockwise so that the hard-locking button lies anterior to the urethra,
away from the anterior vaginal wall. (From Ref. 14.)

Erosion of the AUS, like all nonhuman implantable devices, is a risk that cannot be
completely avoided. Extrusion may occur if the pump erodes through the skin of the labium or
the cuff erodes into the urethra or the vagina. Device erosion has been attributed to poor
circulation, low-grade infection, technical difficulties, and shifting of the cuff (4). Cuff erosion
commonly occurs in patients who have undergone prior pelvic irradiation (9). Our earlier
experience included two patients who had been previously irradiated for cervical carcinoma.
Both patients developed repeated cuff erosion into the vagina despite multiple revisionary
operations. With the use of a low-pressure-regulating balloon (51 – 60 cmH2O pressure), delayed
primary activation of the cuff, and exclusion of the patient with prior pelvic radiotherapy, the
incidence of device erosion may be much reduced (1,9). In the past, mechanical malfunction of
the artificial urinary sphincter has been common, revision occurring in 31 – 43% of women with
the device (10,11). However, since the introduction of the newly improved cuff design and the in
situ activation-deactivation control assembly of the AS-800 model in 1983, the incidence of
mechanical malfunction has dramatically decreased (2).

IV. SUMMARY

Intrinsic urethral deficiency in women with stress urinary incontinence associated with a
nonmobile, well-supported urethra and bladder neck is certainly a challenge in management
to the urinary incontinence specialist. Many of these patients have undergone previous
328 Hadley

unsuccessful anti-incontinence operations. The artificial urinary sphincter is a viable alternative

treatment modality to the urethral sling or periurethral injection therapy for these difficult
patients. It may be the most appropriate mode of treatment for those patients with severe stress
incontinence since these patients have not responded well to the customary urethral slings and
periurethral bulking agents.
The advantage of the transvaginal approach in the placement of the artificial urinary
sphincter is that it offers the surgeon the ability to dissect through the difficult urethrovaginal
plane under direct vision. In the patient with abundant scar tissue, the addition of a suprameatal
incision reduces the likelihood of an inadvertent cystotomy or urethral injury during the anterior
dissection of the urethra.
With familiarization of the implantation technique, the use of a low-pressure-regulating
balloon reservoir (51 –60 cmH2O pressure), delayed primary activation of the cuff, and selective
patient criteria (e.g., exclusion of patients with prior pelvic irradiation), the artificial urinary
sphincter can result in reasonable long-term social continence in patients with urinary
incontinence due to intrinsic urethral insufficiency. In the subgroup of patients with a
combination of hypotonic bladder and intrinsic sphincteric incompetence, the artificial urinary
sphincter may be the initial treatment of choice over the urethral sling because of its lower
incidence of prolonged postoperative urinary retention and vesical instability.

REFERENCES

1. Appell RA. Techniques and results in the implantation of the artificial urinary sphincter in women
with type III stress urinary incontinence by a vaginal approach. Neurourol Urodyn 1988; 7:613– 619.
2. Webster GD, Perez LM, Khoury JM. Management of type III stress urinary incontinence using
artificial urinary sphincter. Urology 1992; 39(6):499– 503.
3. Hadley R. Transvaginal placement of the artificial urinary sphincter in women. Neurourol Urodyn
1988; 7:292– 293.
4. Abbassian A. A new operation for insertion of the artificial urinary sphincter. J Urol 1988; 140:512 –
513.
5. Blaivas JG, Jacobs BZ. Pubovaginal fascial sling for the treatment of complicated stress urinary
incontinence. J Urol 1991; 145:1214– 1218.
6. Blaivas JG, Olsson CA. Stress incontinence: classification and surgical approach. J Urol 1988;
139:727.
7. McGuire EJ, Bennett CJ, Konnak JA. Experience with pubovaginal slings for urinary incontinence at
the University of Michigan. J Urol 1987; 138:525.
8. Wang Y, Hadley HR. Artificial urinary sphincter in the female: is it procedure of choice for the patient
with type III urinary incontinence associated with an acontractile bladder?. J Urol 1992; 147(4):377A.
9. Duncan HJ, Nurse DE, Mundy AR. Role of the artificial urinary sphincter in the treatment of stress
incontinence in women. Br J Urol 1992; 69:141.
10. Donovan MG, Barrett DM, Furlow WL. Use of the artificial urinary sphincter in the management of
severe incontinence in females. Surg Gynecol Obstet 1985; 161:17.
11. Light JK, Scott FB. Management of urinary incontinence in women with the artificial urinary
sphincter. J Urol 1985; 134:476 – 478.
12. Costa P. The use of an artificial urinary sphincter in women with type III incontinence and a negative
Marshall test. J Urol 2001; 165(4):1172– 1176.
13. Fulford SCV, Sutton C, Bales G. The fate of the “modern” artificial urinary sphincter with a follow-up
more than 10 years. Br J Urol 1997; 79:713– 716.
14. Wang Y, Hadley R. Artificial sphincter: transvaginal approach. In: Raz, S, ed. Female Urology. 2nd
ed. Philadelphia: W.B. Saunders, 1996.
21
Urethral Injectables in the Management of
SUI and Hypermobility
Sender Herschorn and Adonis Hijaz
University of Toronto and Sunnybrook and Women’s Health Sciences Centre,
Toronto, Ontario, Canada

I. INTRODUCTION

Murless, in 1938, first reported on injection of sodium morrhuate around the urethra by (1), and
since then various materials have been injected for urinary incontinence as an alternative to
surgery. Quackels (2) reported paraffin wax in 1955, and Sachse (3) used sclerosing agents in
1963. The initial results were poor, and significant complications such as pulmonary emboli and
urethral sloughing were seen. Polytetrafluoroethylene (Teflon) paste, was first introduced by
Berg (4) and then popularized by Politano (5) in the 1970s. Shortliffe et al. (6) published the first
report on glutaraldehyde cross-linked collagen, and more recently autologous fat injection
(7) has been described. Newer agents, such as silicone microparticles (8) and injectable
microballoons, have also been reported (9).
Despite a tremendous growth in interest recently in injectable agents, there have been few
published prospective randomized trials comparing different agents or injectables to other
treatments for SUI. Outcome measures have not been standardized. This article will summarize
the properties, published results, and complications of the various agents as well as examine
some of the controversies.

II. MECHANISM OF ACTION OF INJECTABLES

It is generally agreed that these agents improve intrinsic sphincter function. Collagen
injections have been reported (10,11) to augment urethral mucosa and to improve coaptation
and intrinsic sphincter function as evidenced by an increase in posttreatment abdominal leak
pressure (12 –14). Initial investigators with collagen (15,16) postulated obstruction as a
mechanism of action, but Monga et al. (11) showed that successfully treated patients have an
increased area and pressure transmission ratio in the first quarter of the urethra. They
suggested that placement of the injectable at the bladder neck or proximal urethra prevents
bladder neck opening under stress. Proper placement of the injectable, possibly just below the
bladder neck, rather than actual quantity (17) of the agent improves intrinsic sphincter
deficiency (ISD).
329
330 Herschorn and Hijaz

The ideal injectable agent (18) should be easily injectable and conserve its volume over
time. If unsuccessful, it should not interfere with subsequent surgical intervention. It should also
be biocompatible, nonantigenic, noncarcinogenic, and nonmigratory. To date, no substance has
met all of these requirements.

III. PATIENT SELECTION

Patients with ISD and normal detrusor function are candidates for injectable agents (19).
McGuire et al. (20) identified these patients with the use of abdominal leak pressures to measure
the strength of the intrinsic sphincter. Low leak pressures (,65 cmH2O) correlate well with type
3 videourodynamic findings, i.e., a poorly functioning bladder neck and proximal urethra (ISD),
and higher leak pressures correlated with types 1 or 2 hypermobility.
The presence of ISD is the primary indication for the use of injectable agents in patients
with stress incontinence (10). Since ISD can coexist with hypermobility (21), injectables have
been administered to patients with hypermobility to improve the ISD component of their
incontinence. Furthermore, elderly women with hypermobility, who are poor operative risks,
have also been injected (22).

IV. INJECTION TECHNIQUES

The materials can be administered under local anaesthesia with cystoscopic control as an
outpatient procedure. Both the periurethral and transurethral methods are done to implant the
agent within the urethral wall, preferably into the submucosa or lamina propria. It is thought that
the implant should be positioned at the bladder neck or proximal urethra. Different sites can
be chosen such as 3 and 9 o’clock or 4 and 8 o’clock positions. The needle size depends on the
viscosity of the injectable. Pre- and postoperative antibiotics are usually administered. The
technique of injection is seen in Figures 1 and 2.
With the periurethral approach, perimeatal blebs are raised with 1% or 2% lidocaine at the 3
and 9 o’clock or 4 and 8 o’clock positions 3–4 mm lateral to the urethral meatus. A 20F
urethroscope with a 308 telescope is inserted into the urethra after instillation of topical urethral
lidocaine. The periurethral needle is introduced and advanced parallel to endoscope sheath until its
position can be seen cystoscopically just below the bladder neck within the mucosa. Care must be
taken to prevent the needle from getting to close to or entering the urethral lumen as rupture of the
mucosa and extravasation will occur. Rocking the needle will confirm the position of the tip. If
penetration of the mucosa occurs, the needle should removed and repositioned. The substance is
injected either unilaterally or bilaterally to create the appearance of “prostatic” lobes. The patient
is asked to cough or strain in the supine and then upright position. If leakage still occurs, more
agent may be given. If no leakage is seen, the procedure may be terminated. The patient then voids
and can be discharged. Acute retention can be treated by insertion of a fine 8F catheter.
The implant can also be injected transurethrally through the cystoscope with specially
designed needles. Teflon, silicone microparticles, and fat, owing to their high viscosity, may
require the use of injection guns.

A. Collagen
Glutaraldehyde cross-linked collagen or Gax-collagen is a highly purified suspension of
bovine collagen in normal saline containing at least 95% type I collagen and 1– 5% type III
 Urethral Injectables for SUI 331

Figure 1 Periurethral collagen injection. The 20F cystoscope with a 308 lens is positioned in the urethra
while the substance is injected into the bladder neck region.

collagen (23). This cross-linking makes the Gax-collagen resistant to the fibroblast-secreted
collagenase. As a result of this, the Gax-collagen is only very slightly resorbed. The implant
causes no inflammatory reaction or granuloma formation and is colonized by host fibroblasts and
blood vessels. It is not known to migrate. However, it does degrade over time and is replaced by
host collagen, to explain its persistence (23).
Since 2 –5% of patients (24) are sensitized to collagen through dietary exposure, all
patients must undergo a skin test into the volar aspect of the forearm 30 days prior to treatment.
Positive responders should be excluded.

1. Collagen Results
Numerous reports of its efficacy, safety, ease of administration, and relative lack of morbidity
have appeared since the first description of collagen injections for urinary incontinence. Our
original report, with short-term follow-up of 6 months (12), showed a cured and improved rate of
90.3%. With longer follow-up the success rate decreased, but there were still long-term cures.
Table 1 lists various reported series.
332 Herschorn and Hijaz

Figure 2 (a) Cystoscopic view of the open bladder neck region prior to injection. (b) Collagen has
been injected via the periurethral route on the patient’s left side. Note the intraluminal bulking effect of
the agent.

Persistence of the implant itself has been demonstrated with magnetic resonance
imaging of the urethra at intervals of up to 22 months after injection although the measured
volume was less than that injected (25). Early results are generally good with success rates
of 72– 100% (Table 1). Maintenance of good results in the long term may be from durability
of the initial procedure itself or from reinjections with additional collagen. It is important
for authors to differentiate the durability of the original procedure(s) from reinjections or
top-ups by reporting the follow-up period starting from after the last injection.
Table 1 Comparison of Collagen Parameters and Results

No. pts.
Study No. pts. Type of incontinence Follow-up (mo.) No. pts. dry (%) No. pts. improved (%) failed (%)

Stricker and Haylen (26) 50 ISD Mean: 11 21 (42) 20 (40) 7 (14)

Range: 1 –21
Kieswetter et al. (27) 16 Not specified 9 7 (44) 7 (44) 2 (12)
Eckford and Abrams (15) 25 Not specified 3 16 (64) 4 (16) 5 (20)
O’Connell et al. (28) 44 42 with ISD 1 –2(longest 7) 20 (45) 8 (18) 16 (37)
2 hypermobile

Moore et al. (29) 11 Types 1 and 3 2 1 (9) 7 (63) 2 (18)

Winters and Appell (13) 50 ISD .12 48 (96) dry or socially continent 2 (4)
McGuire and Appell (10) 17 Mobile .12 8 (47) 3 (17) 6 (35)
137 ISD .12 63 (46) 47 (34) 29 (19)
Faerber (22) 12 Type 1 10.3 (Range 3 – 24) 10 (83) 2 (17) 0
Monga et al. (11) 60 Some hypermobile 3 (N ¼ 59) 27 (46) 24 (40)
12 (N ¼ 54) 22 (40) 20 (37)
24 (N ¼ 29) 14 (48) 6 (20)
Richardson et al. (14) 42 ISD 46 (10– 66 after 1st 17 (40) 18 (43) 7 (17)
injection)

(continued )
Urethral Injectables for SUI
333
 334

Table 1 Continued

No. pts.
Herschorn and Hijaz

Study No. pts. Type of incontinence Follow-up (mo.) No. pts. dry (%) No. pts. improved (%) failed (%)

Herschorn et al. (30) 181 Type 1: 54 Mean: 22 (Range 4 – 69) 42 (23) 94 (52) 45 (25)
Type 2: 67 .¼24 (N ¼ 62) 27 (43.5) 29 (46.8) 6 (9.7)
Type 3: 60 .¼36 (N ¼ 25) 13 (52) 8 (32) 4 (16)
Smith et al. (31) 94 Type 3 Median: 14 36 (38.3) 27 (28.7) 31 (33)
Khullar et al. (17) 21 Not specified 24 (minimum) 10 (48) 2 (9) 9 (43)
Swami et al. (32) 107 Some hypermobile 24 (minimum) 27 (25) 43 (40) 37 (35)
Cross et al. (33) 103 Type 3 Median: 18 (Range 6 – 36) Substantially 29 (20) 7 (6)
improved 103 (74)
Groutz et al. (34) 63 Type 3 Mean 6.4 þ 4.9 13% 10% good 18%
17% fair
42% poor
Bent et al. (35) 90 Type 1&2 12 19 (21%) 19 (21%) 62 (58%)
Corcos and Fournier (36) 40 Type 1 (8) Av 52; 12 (30%) 16 (40%) 12 (30%)
Type 2 (20) 47 – 55
Type 3 (12)
 Urethral Injectables for SUI 335

Longer-term results of more than 1 –2 years vary from 57%, cure and improved (17), to
94% (36). Most patients need one or two treatment sessions with means of 5.6 – 15 cc collagen.
Since patients are treated at different times and durations of follow-up vary, the Kaplan-Meier
curve can be useful to display the persistence of a good result. In our series (30), the probability
of remaining dry was 72% at 1 year, 57% at 2 years, and 45% at 3 years (Fig. 3). Winters and
Appell (13) also reported a similar 50% rate of complete continence in the multicentre trial after
2 years. Corcos and Fournier reported a 4-year follow-up with 40% improvement and 30% cure
rates (36). Additional administration of collagen usually resulted in restoration of continence,
and this has to be factored into the reporting.
Berman and Kreder (37) analyzed the cost effectiveness of collagen versus sling
cystourethropexy for type 3 incontinence. They concluded that surgery was more cost effective
than collagen.

2. Collagen and Hypermobility

The use of collagen for patients with hypermobility has been reported. Moore et al. (29) included
patients with both type 1 and type 3 abnormalities. Faerber (22) treated elderly patients with type
1 abnormality. In the report by McGuire and Appell (10), the results at .1 year in women with
ISD were similar to those in women with hypermobility, although there were far more women
with ISD. However, Appell (19) subsequently reported that these patients with hypermobility
all required bladder neck surgery within 2 years. Monga et al. (11) included patients with
hypermobility and found that cure rates were not reduced for women with up to 2.5 cm of
movement. In our series of 181 patients there was no significant difference in outcome in patients
with or without hypermobility (30). Steele et al. (38) found that urethral mobility did not
significantly affect the success rate. As a matter of fact, four of six patients with urethral
hypermobility were dry at the 6-month follow-up examinations; however, among the 19 women

Figure 3 Durability: Kaplan-Meier curve showing durability of cure of incontinence after the last
collagen injection in 78 patients. (From Ref. 30.)
336 Herschorn and Hijaz

without hypermobility, only a 32% remained dry. Corcos and Fournier found no difference
between patients with and without bladder neck hypermobility in their 4-year follow-up on 40
patients (36).

3. Collagen Complications
Treatment-related morbidity has been minimal. Urinary retention ranges from 1% to 21%
(12,13,19) and can be managed with intermittent catheterization or short-term foley. Urinary
tract infection occurs in 1– 25% (12,13,19). Extravasation resolves quickly with flushing away
of the dilute collagen suspension and sealing over of the small needle site. Hematuria can occur
in 2% of patients (19). Another rare complication is periurethral abscess formation (39).
Other complications include de novo instability, seen in 11 of 28 elderly women (39%)
treated by Khullar et al. (17). Stothers et al. reported de novo urgency with urgency incontinence
in 43 of 337 patients (12.9%), 21% of whom did not respond to anticholinergics (40).
Another rare complication is a reaction in the previously negative skin test site following a
urethral collagen injection (24). This occurred in three patients (1.9%) and was associated with
arthralgias in two. This reaction has been reported before in the dermatologic literature (41), and two
negative pretreatment skin tests have been suggested to prevent it. The potential for hypersentivity
reactions is present since antibody production is stimulated by collagen injection (42).

B. Polytetrafluoroetylene Paste (PTFE, Teflon, Urethrin)

Polytetrafluoroetylene Paste (Teflon) is composed of equal parts Teflon paste and glycerine with
polysorbate 20 (43). Teflon is a resin polymer with a very high molecular weight and high
viscosity, and is composed of small particles (40 mm in diameter). It is inert and stable, and does
not induce an allergic response. However, it does cause a local inflammatory response with
histiocytes phagocytizing the particles and coalescing to form foreign body giant cells and a
granuloma. There is also fibrous tissue ingrowth that adds to the bulk formed by the Teflon.
Owing to the small particle size, Malizia et al. (44) also showed distant migration of teflon
particles to pelvic nodes, lung, brain, and kidneys of experimental animals.
Teflon paste has been used to treat urinary incontinence since 1964, but it was not reported
until 1975, by Berg (4). Since that time, numerous reports relating to its use in treating
incontinence have appeared in the literature. Although not approved in the United States, Teflon
has been approved in Canada and in other countries.
It may be injected via the periurethral route and volumes of up to 10 –20 cc are reported.
The procedure is done under local or spinal anesthesia, and repeats may be done after 6 months.
We have modified the procedure by injecting small amounts (2.5 cc) via the periurethral
approach under local anesthetic (45). Heating the Teflon reduces its viscosity and allows
injection without a gun.

1. Teflon Results
Table 2 lists various series. There are wide-ranging outcomes with longer-term series showing
poorer results (33 –76% cure and improved) than those of short-term series (57 – 86%) (46 –54).

2. Teflon Complications
Since relatively large volumes of Teflon have been injected with the patient under general
anesthesia, the incidence of urinary retention at 25% (46) is higher than that of collagen.
Irritative voiding symptoms have also been seen transiently in 20% (48). Urinary infection is
 Urethral Injectables for SUI 337

Table 2 Teflon Results for Female Stress Incontinence

No. Follow-up Pts. dry Pts. improved Pts. failed

Study pts. (mo.) (%) (%) (%)

Politano et al. (46) 51 6 26 (51) 10 (20) 15 (29)

Lim et al. (47) 28 — 6 (21) 9 (33) 13 (46)
Schulman et al. (48) 56 3 39 (70) 9 (16) 8 (4)
Deane et al. (49) 28 3 – 24 9 (32) 8 (28) 11 (40)
Beckingham et al. (50) 26 36 2 (7) 7 (27) 17 (66)
Harrison et al. (51) 36 61 4 (11) 8 (22) 24 (67)
Lotenfoe et al. (52) 21 11 8 (38) 4 (19) 9 (43)
Lopez et al. (53) 74 31 41 (56) 15 (20) 18 (24)
Vesey et al. (54) 36 9 (3 – 36) 20 (56) 4 (11) 12 (33)
Herschorn and Glazer (45) 46 12 14 (31) 19 (41) 13 (28)

rare at 2% (47). Perineal discomfort may occur in 5% (46), and transient fever in 10– 15% of
patients. Perforation and extravasation can occur and, if recognized at the time of injection, the
Teflon should be removed.
Although Teflon particles can migrate (44), only one case of clinical significance has been
reported in the literature in humans. Claes et al. (55) described a woman previously treated with
large volumes of periurethral Teflon for urinary incontinence who later presented with
lymphocytic alveolitis and fever. Light microscopy showed Teflon particles in the lungs. She
was treated successfully with steroids. Mittleman and Marraccini (56) reported an incidental
finding of postmortem interstitial pulmonary granulomas in a previously asymptomatic man who
had received Teflon. Kiilhoma et al. (57) reported three complications out of 22 women—a
sterile periurethral abscess, a urethral diverticulum, and a urethral granuloma—that all required
surgical intervention. In another case, the material migrated into the bulbar corpus spongiosum
causing perineal pain for 3 months necessitating medication for pain relief (58).
Although neoplastic transformation was hypothesized (44), there has never been a clinical
occurrence reported. Furthermore, in a long-term rat study, Dewan et al. (59) demonstrated no
increase in tumor risk and no tumors found at the injection site.
Despite the potential for complications with Teflon the actual rate of reported problems is
low. However, Teflon is rarely used as an injectable now.

C. Autologous Fat
Autologous fat has been used for aesthetic and defect reconstruction since the 1980s (60).
Although fat is biocompatible and readily available, 50–90% of the transferred adipose tissue graft
may not survive (61). Graft survival depends on minimal handling, low suction pressure during
liposuction, and the use of large-bore needles. Smaller grafts survive better than larger ones (62).
The procedure involves harvesting abdominal wall fat by liposuction either under local
(63) or general anesthesia (64). The injection is usually carried out via the periurethral route with
a 16- or 18-gauge needle. Postprocedure care may involve intermittent catheterization or even a
suprapubic tube (64).

1. Autologous Fat Results

A number of reports of urethral fat injections have been published and appear in Table 3. Most of
the series report short-term results with success apparently lower than that of other injectables,
338 Herschorn and Hijaz

Table 3 Results of Autologous Fat Injection

No. pts. No. pts.

No. Follow-up No. pts. improved failed
Study pts. (mo.) dry (%) (%) (%)

Cervigni and Panei (7) 14 9.7 8 (57) 4 (29) 2 (14)

Santarosa and Blaivas (65) 12 11 7 (58) 5 (42)
Trockman and Leach (63) 32 6 4 (12) 14 (44) 14 (44)
Haab et al. (66) 45 7 6 (13) 13 (29) 26 (58)
Su et al. (64) 26 Mean 17.4; 13 (50) 4 (15) 9 (35)
range 12 – 30
Palma et al. (67) 30 12 1 injection: 4/13 (34)
2 injections:11/17 (67)

apart from the study of Su et al. (64) with a follow-up of more than 12 months. Palma et al. (67)
showed that repeat injections improved the cure rate from 31% to 64%. Haab et al. (66) reported
a comparative study with collagen. After a mean of 7 months, 13% of the women with fat
injection were cured versus 24% of the women with collagen injections. The subjective
improvement rate was also higher with the collagen. Lee and colleagues reported a randomized
double-blind study of autologous fat versus saline injection (68). At 3 months, six of 27 (22.2%)
and six of 29 (20.7%) women were cured or improved in the fat and saline groups, respectively.
In this study periurethral fat injection did not appear to be more efficacious than placebo in
treating stress urinary incontinence.

2. Autologous Fat Complications

Reported complications are similar to other injectables with urinary infection, retention,
hematuria, and extravasation. Additional problems, such as pain, with donor site, the abdominal
wall, hematomas, and infection may also be seen. Other noteworthy complications are urethral
pseudolipoma (69) and fat embolism (39), one of which was fatal (70).

D. Silicone Microimplants
Silicone microimplants (8) are solid polydimethylsiloxane (silicone rubber) particles suspended
in a nonsilicone carrier gel that is absorbed by the reticuloendothelial system and excreted
unchanged in the urine. Since 99% of the particles are between 100 and 450 mm in diameter, the
likelihood of migration is low. Henly et al. (71) demonstrated distant migration of small
particles, ,70 mm, but no migration of particles .100 mm in diameter. Although there was a
typical histiocytic and giant cell reaction within the injection site, there was no granuloma
formation in response to the larger particles. Since the substance is quite viscous, it must be
injected with an injection gun and a 16-gauge tip transurethral needle.

1. Silicone Microimplant Results

Hariss et al. (8) reported on 40 patients followed for a minimum of 3 years at which time 16
(40%) were dry, 7 (18%) were improved, and 17 (42%) failed. Twelve of the 16 required one
injection, and four needed two injections to become dry. Sheriff et al. (72) reported an overall
success of 48% in 34 patients after unsuccessful stress incontinence surgery, and Koelbl et al. (73)
 Urethral Injectables for SUI 339

reported a 60% success rate in 32 women after 12 months but noted a time-dependent decrease in
success. Radley et al. (74) reported a success rate of 61% (19.6% cured and 41.1% improved) in
60 women after a mean of 19 months. Barranger et al. (75), in a group of 21 patients, reported a
dry rate of 19%, improved rate of 38%, and failure rate of 52% at a median follow-up of 31
months. Interestingly, they did not observe a time-dependent decrease in results.

2. Silicone Microimplant Complications

Self-limited side effects of hematuria, dysuria, frequency, and retention have been reported in a
minority of patients. The lack of a granulomatous reaction and migration of the large silicone
particles may provide some benefit over Teflon, although no long-term data are available.
Despite the laboratory and clinical evidence of safety with the large particles concerns still exist
about the small silicone particle migration and long-term tissue response to the injection (71).

E. Other New Injectables

Calcium hydroxylapatite, which is a normal constituent of bone, can be manufactured into
particles of a spherical mean diameter of 100 mm. There is one report of its use in 10 women
with ISD and limited hypermobility (76). After 1 year, seven reported substantial improvement,
two improved, and one had no change. No significant complications were reported.
Another new synthetic agent, Durasphere, is composed of nonabsorbable pyrolytic
zirconium oxide beads suspended in a carrier gel. The nonreactive beads range in size from 251
to 300 mm. Lightner et al. (77) reported results of a randomized trial compared to bovine
collagen. At 1 year after the last treatment, 49 (80.3%) of 61 women in the Durasphere group had
an improvement in Stamey continence grade of 1 or more, compared with 47 (69.1%) of 68
women in the collagen group. The difference was not statistically significant. There was also no
difference in number of injections or pad weight test. However, the injected initial and repeat
injection volume of Durasphere was significantly less than those of collagen. Adverse events
were similar, but more women had posttreatment urgency and acute retention with Durasphere.
Pelvic x-rays taken at 1 and 2 years after injection showed stability of the bulking agents at the
injection site. This suggests potential durability. In another, small series of 13 women, Pannek
and colleagues (78) reported a decline in success from 76.9% at 6 months to 33% at 12 months.
In contast to the previous study, they demonstrated particle migration locally and to distant sites
on follow-up plain x-rays.

V. IMPLANTABLE MICROBALLOONS

To obviate the degradation and movement of injectable materials, Atala and coworkers (79)
developed a self-detachable implantable balloon system. The balloon is a silicone elastomer
with a check valve that prevents escape of the solution that is injected at the time of implant. The
filling solution is a biocompatible cross-linked hydrogel that maintains its volume within the
silicone shell. The balloons are inserted into the submucosal area, usually periurethrally, with
cystoscopic control.
Pycha et al. (9) reported that eight (42%) of 19 women were dry and seven (36.8%) were
improved after a mean of 14.4 months. The patients with hypermobility had a poor outcome.
Rare complications included bladder instability and balloon extrusion.
340 Herschorn and Hijaz

VI. CONCLUSIONS

Considerable progress has been made since the introduction of collagen injections. Injectable
agents are used for buttressing the ISD component of the incontinence, but patients with
concomitant hypermobility may benefit as well. They have also been administered to elderly
patients who were not surgical candidates. However, there are still a number of areas in which
further study is needed.
Durability is a concern. Although long-term successes have been reported with collagen
and Teflon, the results of both deteriorate over time. Similarly autologous fat and silicone
microimplants yield poorer long-term than short-term results. Comparisons of injectables and
injectables to surgery have been done to a limited degree and prospective studies have yet to be
reported. Despite the ease of the technique and the attractiveness to patients of an outpatient
procedure that can be repeated if necessary, the cost-effectiveness of injectable agents relative to
other treatments, such as newer, minimally invasive surgical procedures, still has to be
addressed.
Safety of the material is also a concern. All of the injectables have excellent safety profiles,
although the risk of migration and granuloma formation with Teflon has prevented its
widespread use. Rare but serious complications have also been reported with collagen and
autologous fat. The long-term risks of silicone microparticles, carbon beads, and balloons are
unknown. Longer-term and comparative studies may settle these issues.
An exciting experimental model of using injected muscle derived cells into the bladder
and urethra has been reported (80). There was persistence of the injected muscle cells compared
to injected collagen. This may ultimately lead to additional treatments for stress incontinence.
Despite the shortcomings of the technology, the lack of long-term data, and the continuing
need for an ideal agent, injectables are a viable minimally invasive alternative. Furthermore,
since they do work in patients with hypermobility, this has lead to an increase our knowledge of
the pathophysiology of stress incontinence. The two major components in stress incontinence,
ISD, and hypermobility can be considered as interdependent and not separate entities. The
relative importance of each component in any patient is variable, so the result of bulking in one
patient with hypermobility may not the same as that in another. Other than the challenges
mentioned above, it would be beneficial to identify factors in patients with hypermobility that
would predict for success with injectables. More work also needs to be done to find out whether
results can be improved by injecting the agent at sites other than the bladder neck.

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22
Vaginal Sling Surgery: Overview, History, and
Sling Material
Keith J. O’Reilly*
Tripler Army Medical Center, Honolulu, Hawaii, U.S.A.

Kathleen C. Kobashi
Virginia Mason Medical Center, Seattle, Washington, U.S.A.

I. INTRODUCTION

The pubovaginal sling (PVS) is considered the gold standard for the treatment of female stress
urinary incontinence (SUI). Originally described for the treatment of intrinsic sphincter deficiency
(ISD), PVSs have been utilized to treat other types of SUI. There have been many modifications
to the technique over the years, but the principles behind the PVS still hold today. The sling is
placed beneath the proximal urethra and bladder neck to provide support and compression and to
prevent proximal urethral descent during increased intra-abdominal pressure. Numerous materials
have been utilized over the years to construct slings, and newer materials continue to be
introduced in an attempt to decrease morbidity and improve durability of the procedure and
patient satisfaction. This chapter will discuss the history of the PVS and examine the various
materials used to construct slings as well as the different fixation techniques available.

II. HISTORY

The PVS was first described in 1907 by Van Giordano (1). The sling was constructed using
gracilis muscle. Goebell, in 1910, described a sling constructed from the pyramidalis muscle (2).
This was later modified by Frangenheim in 1914, who incorporated the overlying rectus fascia in
a flap (3). Stoeckel then added a plication of muscular structures around the bladder neck via a
vaginal approach (4). Common to all these operations was the belief that muscle placed around
the bladder neck would acquire a sphincterlike function. Later, in 1933, Price described the first
sling constructed from fascia lata (5). In this procedure, the fascia lata was passed beneath the
urethra from a suprapubic approach, and the ends of the fascia were secured to the rectus muscle.
In 1942, Aldridge described the use of a fascial sling that compressed the urethra during times of
increased intra-abdominal pressure (6). Rectus fascia without muscle was passed through the
retropubic space, and the ends were sutured beneath the urethra. This became a classic technique

*Current affiliation: Madigan Army Hospital, Tacoma, Washington, U.S.A.

345
346 O’Reilly and Kobashi

and was used for many years. In 1962, Narik and Palmrich modified the Aldridge technique by
leaving the external oblique aponeurosis attached to the pubic tubercle and then suturing the
ends beneath the proximal urethra (7). Complications associated with these procedures included
urethrovaginal fistulas, urethral slough, outlet obstruction, and retropubic abscess. Given the
high complication rates, slings fell out of favor for several years.
McGuire and Lytton revived the pubovaginal sling procedure for type III SUI in 1978
using autologous rectus fascia (8). They described a combined abdominal and vaginal approach
and reported an 80% success rate for ISD. Blaivas and Jacobs then modified the procedure by
penetrating the endopelvic fascia and by completely detaching the rectus fascia from the
abdominal wall (9). Subsequent studies have confirmed that there is no difference in efficacy
between free and pedicled fascial flaps for sling surgery (10). The results obtained by McGuire
and Lytton have been further corroborated by other reports and therefore confirm the success and
durability of the autologous fascia pubovaginal sling procedure for stress urinary incontinence
(11 – 15). In 1996, the American Urological Association Clinical Guidelines Panel performed a
meta-analysis of the literature regarding anti-incontinence procedures (16). The panel reported
an overall success rate with slings of 82 –84% at 48 months, regardless of sling material or
anchoring technique employed.

III. CHOICE OF SLING MATERIALS

A. Autologous Fascia/Tissue
Numerous materials such as autologous fascia, cadaveric fascia, and synthetics have been used
for pubovaginal slings with varying results. The choice of sling material ultimately depends on
the preferences of the patient and the surgeon. Each material has its own advantages, dis-
advantages, and inherent complications.
Autologous fascia has been the gold standard material for the pubovaginal sling. Table 1
summarizes several authors’ results with autologous fascia. Complications related to the sling
material are extremely rare, primarily consisting of de novo detrusor instability or urinary
retention.
Rectus fascia has been the most commonly used fascia and has proven long-term results.
The fascia is harvested via a Pfannenstiel incision. In most cases, an adequate piece of fascia can
be harvested despite prior lower abdominal surgery. One advantage of using rectus fascia is that
following the harvesting of the fascia, no repositioning of the patient is necessary. Disadvantages
include a limitation in the maximum length of fascia attainable, increased patient morbidity
secondary to pain at the incision site, potential for abdominal wall hernia, and a theoretical

Table 1 Contemporary Results of the Pubovaginal Sling Using Autologous Fascia

Type of Success Follow-up Postop De novo Sling

Author n fascia (%) (mos.) retention urgency erosion

Morgan (17) 247 Rectus 88 52 2.4 7 0

Chaikin (18) 251 Rectus 92 36 2 3 0
Govier (14) 32 Fascia lata 87 14 3 9 0
Beck (19) 170 Fascia lata 92 NR “High” ,1 0
Haab (20) 40 13 Rectus; 86 48 2.7 10 0
27 fascia lata
 Vaginal Sling Surgery 347

concern of poorer tissue quality if there has been prior lower abdominal surgery or radiation
therapy to the area. The tensile strength of rectus fascia has been found to be approximately four
times less than that of fascia lata (21).
Conversely, autologous fascia lata has been favored over rectus fascia by some authors
because of improved tensile strength and better length, which can make adjustment of the sling
tension easier. Fascia lata is also thought to provide long segments of unscarred fascia, which
translates into more equal distribution of pressure on the urethra and more uniform urethral
closure. There are also fewer postoperative activity restrictions than with the use of rectus fascia.
Disadvantages include the time to harvest and reposition the patient, pain at the harvest site,
muscle herniation at the harvest site, and cosmetic issues (22). In one study, 38% of patients
were unhappy with the appearance of the leg scars (23).
Another source of autologous tissue that has been utilized as a sling material is an in situ
vascularized island of anterior vaginal wall. In 1996, Kaplan et al. compared the safety and
efficacy of an autologous rectus fascial sling versus a modified vaginal wall sling for ISD (24).
Both procedures were effective in treating incontinence, but the authors were able to demonstrate
that the vaginal wall sling was associated with a significantly shorter hospital stay, decreased
catheter time, decreased pain, and fewer days lost from work. In a follow-up report, Kaplan et al.
demonstrated durable results of the vaginal wall sling at a mean of 39 months (25). Subjectively,
93% of women were either satisfied or very satisfied. Recurrent stress incontinence occurred in
4%, and there was an 8% incidence of de novo instability and/or urge incontinence. Concerns
with regard to the use of vaginal wall slings include the development of suburethral inclusion
cysts reported by Su and Woodman (26,27). Additionally, the harvesting of vaginal mucosa from
the anterior wall may affect pelvic support as demonstrated by the 7% incidence of new pelvic
prolapse associated with this procedure. Lastly, vaginal tissue quality may vary depending on the
estrogen status of the patient, exposure to radiation, and prior surgeries.

B. Allograft Fascia
Allografts are tissue harvested from human donors, usually cadavers, and transplanted into a
human recipient. Soft tissue allografts have been used in clinical practice for more than 20 years.
Orthopedic surgeons have used fascia lata allografts in the reconstruction of the anterior cruciate
ligament, and ophthalmologists have used it in orbital floor repair. However, cadaveric fascia
was not widely used in incontinence surgery until 1996 (28).
An important issue concerning the use of cadaveric fascia lata is the potential of
transmitting infectious disease, such as HIV and other viruses. The risk of HIV transmission
from soft tissue allografts is one in 1.7 million to one in 8 million, which is lower than the risk of
HIV infection from a blood transfusion (29,30). Simmonds et al. documented the only case of
HIV transmission due to tissue transplantation, which developed in a woman who received a
bone allograft in 1985 from a seronegative donor (31). Since 1985, not only have all donors have
been screened for HIV and other viruses, but more than 60,000 organ transplants and 1 million
tissue plants have been performed without an increase in disease transmission (30).
Another potential risk of transplantation of cadaveric fascia is the transmission of prions.
Prions are proteinacious particles that are the causative agents of spongiform encephalopathy, of
which the most common is Creutzfeldt-Jakob disease. Prions are very resistant to treatments that
target nucleic acids such as radiation (32). However, prions may be destroyed by denaturing
agents. One manufacturer (Mentor Corporation, Santa Barbara, CA) has designed a treatment
process that addresses the risk of prion disease without affecting the tensile strength of the
graft (33). The patented processing technique involves gamma irradiation followed by
solvent dehydration. Despite the theoretical risk and heightened worldwide awareness of
348 O’Reilly and Kobashi

prion-transmitted diseases, there are no cases of a transmissible spongiform encephalopathy

associated with cadaveric fascia lata (32).
The Food and Drug Administration (FDA) regulates licensed tissue banks that process
cadaveric fascia. Tissue banks are required to perform an extensive process of donor selection,
donor testing, and a multistep tissue processing in order to remove tissue antigenicity and the
risk of disease transmission. Prior to harvesting, donors are screened for a history of carrying
hepatitis and other viruses. Serologic tests for HIV, hepatitis B, hepatitis C, HTLV-1, and
syphilis are then performed.
The tissue is processed by one of several techniques: freeze-drying alone, gamma
irradiation with freeze-drying, or solvent dehydration. There is some concern that different
processing techniques may alter the tensile strength of the allograft. Lemer et al. demonstrated
that the tensile strength and tissue consistency was decreased in freeze-dried fascia as compared
to solvent-dehydrated fascia, acellular dermal grafts, and autologous fascia (35). Conversely,
Sutaria and Staskin found no statistical difference in the tensile strengths of freeze-dried,
gamma-irradiated and freeze-dried, or solvent-dehydrated gamma-irradiated fascia (36).
Allograft fascia lata is an attractive alternative to autologous fascia lata because it avoids
foreign body reactions associated with synthetic grafts. Early reports have demonstrated that
operative time, hospital stay, and postoperative time may be decreased with the use of allograft
fascia (37,38). With respect to effectiveness, early results with cadaveric fascia lata have been
promising. Amundsen et al. reported on the results of 104 patients who underwent a pubovaginal
sling using a 2  15 cm strip of freeze-dried, nonirradiated cadaveric fascia lata. With a follow-
up of 19.5 months, 87% were significantly improved (37). They also reported no adverse events
related to the fascia. Brown and Govier compared 121 consecutive women who underwent a
pubovaginal sling using cadaveric fascia with a group of 46 women who underwent a
pubovaginal sling using autologous fascia (34). With a mean follow-up of 12 months in the
cadaveric fascia lata group, 85% were cured of their SUI. These results were very similar to
those achieved with autologous fascia. Cadaveric fascia lata has also been used to address not
only SUI, but also pelvic organ prolapse. Kobashi and Leach reported on a new technique using
solvent dehydrated cadaveric fascia lata to perform simultaneous transvaginal sling and
cystocele repair. The authors reported that no recurrent cystoceles occurred and that 72% of
patients were completely dry at a follow-up of 6 months (39).
The results attained with cadaveric fascia have been promising, and there have been
minimal complications secondary to the cadaveric fascia. However, the follow-up has been
short, and there is question regarding the durability of fascia lata. Chaikin and Blaivas described
a case of an early failure of a cadaveric fascial sling in which the holding sutures had pulled
through (40). Fitzgerald and Brubaker reported on 35 patients who underwent a pubovaginal
sling with freeze-dried and irradiated cadaveric fascia (41). They reported a 69% cure rate, but
eight patients (23%) were considered to be failures. Of these, seven (20%) were initially cured of
their stress incontinence but went on to develop subjective and objective failure by 6 months. At
reoperation, there were either remnants of the fascia or no evidence of fascia at all. Carbone et al.
recently reported on their series of cadaveric fascial slings, which demonstrated a 40%
failure rate along with a reoperative rate of 16.9% (42). At the time of reoperation, the fascial
sling was noted to be attenuated or fragmented. The fascia used in this series was obtained from
several tissue banks and processed by irradiation. It is becoming apparent that processing
techniques, in addition to surgical technique employed, play a role in the short- and, presumably,
long-term success of a procedure.
The fate of fascial allografts is well documented in the orthopedic literature, but there is
little data in the urological literature, and there has been no good animal model studied. The
process of incorporation is multifactorial and is heavily dependent on tissue, donor, and recipient
 Vaginal Sling Surgery 349

factors. The process of incorporating fascial allografts involves initial donor fibrocyte death
followed by neovascularization, fibroblast migration, remodeling, and maturation (41). Varia-
tions in harvesting site and processing techniques affect the quality of the tissue. It has been shown
that solvent-dehydrated cadaveric fascia lata and cadaveric dermal allografts have signifi-
cantly higher tensile strength and less tissue variability than does freeze-dried cadaveric fascia
lata (35).
Though cadaveric fascia lata is FDA approved, there are no regulations regarding the
quality or thickness of the fascia that is harvested, a fact that may be reflected in the variable
results from one center to another (34,37,38,41,42). This concern can be addressed by using a
commercially available solvent dehydrated product in which the tissue consistency and strength
may be more similar to that of autologous fascia. Also, the characteristics of the donor, including
age and comorbidities, must be considered. Little is known about what role the recipient plays in
graft incorporation and the healing process. Will surgical outcome vary with the recipient’s
ability to incorporate the allograft? What role do recipient comorbidities and immune reaction
play? Does the existence of scarring from prior surgery inhibit neovascularization of the graft
and fibroblast proliferation? Although graft antigenicity is lessened after processing, an immune
reaction still occurs. What patient characteristics will facilitate or hinder the fibroblast pro-
liferation and remodeling along the graft? Still another unresolved issue is the ideal length of
fascial strip to be used and the method of fixation. The lengths of fascia used by Amundsen et al.
(37) and Govier et al. (34) (2  15 cm and 2  24 cm, respectively) were longer than those used
by Fitzgerald (41) and Carbone (42) (2  10 cm and 2  7 cm, respectively), and different
methods of fixation were used by each group. So it may be that the technique, not the fascia, is
the cause for varying success. More than likely, it is both.
In summary, the use of cadaveric fascia lata as sling material for a PVS is safe and
effective. It is associated with a shorter operative time and decreased postoperative pain. How-
ever, controversy does exist with regard to its durability. Studies with longer follow-up will be
needed to further clarify its role as a sling material.

C. Synthetic Materials
In recent years there has been interest in using synthetic materials as an alternative to autologous
fascia in the pubovaginal sling procedure in order to decrease operative time, postoperative pain,
and need for hospitalization, and, in theory, to improve the durability of the results. There is no
question that autologous slings have good long-term cure rates, and failures are usually apparent
within the first 3 months. However, autologous fascia is subject to the same cellular degeneration
and fascial tears experienced by host tissues that contributed to the original problem of SUI. In
theory, the ideal sling material should last the lifetime of a patient and should not be at risk for
degradation. It is believed that the biomechanical properties of synthetic material are superior to
those of autologous tissue. The question is whether this will translate into improved long-term
durability with synthetic slings. The first synthetic sling, which utilized nylon, was described
in 1965 (43). Since that time a number of different synthetic materials, such as polytetra-
fluoroethylene (Gore-Tex), polypropylene (Marlex), polyethylene (Mersilene, Silastic), and non-
absorbable polyester impregnated with bovine collagen matrix (ProteGen), have been used as
sling material. SUI cure rates using synthetic slings have been reported to be 77– 90% at a mean
follow-up of 4 –8 years (44 – 47). Despite apparent long-term durability, synthetic slings are
more prone to infection and erosion. In their review of the literature, the AUA Clinical
Guidelines Panel found reports of only 12 of 1715 patients (.007%) with vaginal or urethral
erosion of autologous fascial slings. In contrast, 41 of 1515 patients (.027%) with synthetic
slings had erosion of the material into the vagina or urethra (16). The incidence of erosion and
350 O’Reilly and Kobashi

infection has varied with the type of material utilized. Polymeric silicone, polytetrafluoro-
ethylene, and polyester have the highest incidence of erosion ranging from 11% to 55% (48,49).
Owing to the problems with erosions and infections, the woven polyester slings were withdrawn
from the U.S. market.
Kobashi et al. reported a multicenter review of 34 patients who required removal of the
woven polyester sling secondary to erosion, infection, or pain (48). The most common
presenting complaints were delayed vaginal discharge (62%), vaginal pain (62%), suprapubic
pain (32%), and recurrent urinary tract infection (15%). Other symptoms included recurrent
stress incontinence, vaginal bleeding, and irritative voiding symptoms. The mean time interval
from sling insertion to removal was 7.95 months (range 1– 22 months). Vaginal erosions alone
occurred in 50%, urethral erosions occurred in 20%, and urethrovaginal fistulas occurred in 17%.
Treatment was surgical removal of all the foreign material, following which only 20% of patients
were dry.
The mechanism behind the erosion of the synthetic slings through the vagina and urethra
appears to be multifactorial. Possible mechanisms of erosion may be considered according to
the site of erosion and the material used. Vaginal erosions may occur as a result of delayed
infection of the synthetic sling which leads to separation of the vaginal incision, vaginal erosion
of the sling material, and subsequent onset of vaginal discharge (48). Urethral erosion may occur
secondary to excessive tension of the sling on the urethra or unrecognized urethral injury at
the time of insertion. The weave properties of different sling materials and tissue reaction to
the synthetic material are also important factors. It is important that the material be able to be
incorporated by the host tissue. Smooth-surfaced materials are poorly incorporated and may be
prone to complications (49). Tissue reaction to the material may create inflammation
and subsequent wound breakdown and erosion. Efforts to decrease inflammation have included
extensive irrigation with antibiotic solutions, impregnating the mesh with antibiotics, and
covering the mesh in a plastic sheath at the time of implantation to prevent contamination.
One of the new and promising synthetic slings used today is composed if a polypropylene
(Prolene) mesh. The mesh tape is placed around the midurethra without tension. The mesh
can be placed via either the tension-free vaginal tape (TVT) technique (Gynecare, Falls
Church, VA), first described in 1996 by Ulmsten et al. (50), or the new SPARC procedure,
recently introduced by American Medical Systems (Minnetonka, MN). Regardless of the
approach used, this procedure can be carried out under local anesthesia in 30 min in an
outpatient setting. A small vaginal incision is made along the anterior wall of the vagina, and the
dissection carried laterally on either side of the midurethra. With the TVT technique, trocars
with the tape attached are passed through the urethropelvic ligament, behind the symphysis,
and out through the lower abdomen. Conversely, the SPARC procedure involves passage of
thin trocars under finger guidance from two small suprapubic incisions to the vaginal incision,
similar to the technique of needle passage in the traditional bladder neck suspensions.
Theoretically, SPARC allows a more controlled passage of the trocars between the suprapubic
and vaginal incisions.
Minuscule “spikes” along the edges of the polypropylene mesh anchor the sling to the
patient’s tissue, securing it in place in a tension-free fashion. Regardless of which of the two
techniques is used to place and position the tape, the theories behind the mechanism of anti-
incontinence are similar. One theory is that the narrow ribbon at the midurethra attempts to
re-create the normal urethral support mechanisms and kink the urethra with increased
abdominal pressure. This mechanism requires hypermobility and is therefore not suitable for
the fixed urethra. A second theory is that, as increased intra-abdominal pressure causes
urethral mobility, the tape also migrates distally and anteriorly, resulting in compression of the
urethra between the tape and pubic bone (51).
 Vaginal Sling Surgery 351

Early results with the TVT revealed a cure rate of 80%, and local tolerance of the tape has
been high. Haab et al. reported on 62 patients with a minimum of 1-year follow-up. They
reported a cure rate of 87%, with another 9.6% who were improved and 3.3% in whom the
procedure failed. De novo detrusor instability was noted in 6.4%; 59 of 63 patients (93.7%)
were able to void immediately; and all patients voided spontaneously within 4 days. There was
no evidence of outlet obstruction, infections, or erosions; however, there were six bladder
perforations (52). Ulmsten et al. recently reported on the 3-year results of the TVT in 50
consecutive patients followed prospectively. They reported a cure rate of 86% with an additional
11% who were significantly improved. There were no cases of retention or major intra- or
postoperative complications. There were no signs of deterioration of the results over the 3 years,
nor were there any erosions or rejection of the tape (53).
The concept of using a synthetic sling material is appealing because it does not have the
morbidity of harvesting the graft. The material is permanent, and the results of the procedure
should therefore be durable. There is also no risk of transmissible disease. In the past, synthetics
have been associated with higher complication rates mainly due to erosions and infections.
However, it appears that the composition of the synthetic material used is of utmost importance.
This is exemplified by a report from Ulmsten and Petros, who performed a procedure using
polytetrafluoroethylene versus polyethylene terephthalate as the sling material. They reported a
10% rate of erosion at one year (54). This is in contrast to the polypropylene mesh now used.
The polypropylene mesh has large interstices that allow in-growth of fibroblasts and hence,
incorporation by the host tissue. TVT is gaining popularity in the United States, and there have
been over 100,000 cases performed worldwide. Erosions have been rare. Both the TVT and
SPARC using the polypropylene mesh are promising techniques, but, as with all procedures,
further studies with adequate follow-up are imperative to properly establish their role in the
armamentarium of treatment of female SUI.

D. Sling Fixation Techniques

With the evolution of the pubovaginal sling, there has been a shift in the fixation techniques
employed. Originally, the rectus fascia was left attached to the pubic tubercle. Further modi-
fications involved detaching the fascia from the bone and fixing it to or over the rectus fascia.
These forms of fixation necessitate a suprapubic incision that may be prone to infection and hernia.
Injury to the urethra and bladder may occur with passing the fascial strip from the vaginal incision
to the abdominal incision. Also, persistent pain secondary to nerve entrapment may occur
when suprapubic fixation is used. Nevertheless, the suprapubic fixation of a pubovaginal sling is fast
and inexpensive, and has proven durable and effective over the long term.
Since the goal of the pubovaginal sling is to recreate a hammocklike support beneath the
urethra, the type of material used as well as the point of fixation for this material is important to
the success of the procedure. The previous transvaginal needle suspensions that were fixed to
the rectus fascia were prone to failure over time. One theory for the cause of failure was that
the sutures pulled through the periurethral tissue. As the rectus muscles move with Valsalva
maneuver, so may the sutures supporting the sling. This change in tension may predispose
sutures to pull through the periurethral tissue or the sling material. In the animal model, this has
been found to be dependent on the amount of tension and the characteristics of the tissue being
fixed (55). The Burch bladder neck suspension involves secure fixation to Cooper’s ligament and
has demonstrated durable results (16). This procedure requires an abdominal incision and hence
has the potential of increased patient morbidity.
Newer techniques of fixation have moved toward a completely transvaginal approach.
Bone anchors placed transvaginally to the underside of the pubic bone have recently gained
352 O’Reilly and Kobashi

tremendous popularity. Bone anchor suture fixation in a cadaveric model has been found to be
more stable than fixation to the rectus fascia but no better than fixation to Cooper’s ligament
(56,57). Several bone anchor systems are now commercially available. Several early reports
utilizing bone anchors to perform a transvaginal sling have been promising (58). The
pubovaginal sling procedure using allograft fascia and bone anchors can be performed with
minimal morbidity and on an ambulatory basis. There are increased costs associated with the
anchoring systems, but this cost must be weighed against decreased operative time, decreased
hospital stay, and decreased patient convalescence. Long-term data on the efficacy of these
procedures are necessary, and follow-up is ongoing.
One of the major concerns associated with the use of bone anchors is the potential for the
development of osseous complications in the form of osteomyelitis or osteitis pubis. Osteitis
pubis is a noninfectious inflammatory condition that causes pain in the pubic bone.
Osteomyelitis is a pyogenic infection of the bone and marrow. Both conditions present with
similar symptoms but vary with regard to treatment. Osteitis pubis represents an inflammation
of the pubic bone secondary to periosteal trauma. It may also present with suprapubic pain,
leukocytosis and radiographic changes such as irregular bone margins and widening of the
symphysis. This condition is generally not progressive and responds to conservative measures
such as non steroidal anti-inflammatory medications and physical therapy.
Osteomyelitis may present with suprapubic pain, difficult ambulation, and/or a wide-
based gate. A key point in the history is that the pain is progressive. Patients may also describe
fevers, chills, or erythema of the suprapubic skin. There may be an associated leukocytosis and
an elevation in the erythrocyte sedimentation rate (ESR). Radiographic evaluation can be
performed with plain anteroposterior radiography, CT scan, MRI, or bone scan. The findings
may vary from irregular bony margins, widening of the pubic symphysis, and superficial bone
destruction early in the disease to localized bone destruction and sequestration later in
the process. While a bone scan may be positive in both osteomyelitis and osteitis pubis, a
negative bone scan generally indicates that there is no osteomyelitis. Cultures are obtained via
needle aspiration prior to instituting treatment. Osteomyelitis is treated with a 4- to 6-week
course of antibiotics. However, if there is evidence of necrosis, surgical debridement is needed in
addition to antibiotics.
Historically, the risk of infectious osseous complications associated with all forms of
pelvic surgery is 1 –3% (59). More specific to anti-incontinence procedures is a 0.76% risk of
osseous infection associated with the Marshall-Marchetti-Krantz retropubic urethropexy (60).
Leach reported five cases of infected bone anchors requiring removal following implantation of
7000 anchors (61). In an extensive Medline review, Rackley et al. found six reported cases of
osteomyelitis involving bone anchors in 1018 procedures (0.6%) (59). Interestingly, all of the
infections reported occurred in cases in which the bone anchors were placed from a suprapubic
approach. There have been no formally reported cases of infectious complications associated
with the transvaginal placement of the bone anchors. The reason for this is unclear and may
represent a reporting bias given that there have been twice as many reported cases of suprapubic
versus transvaginal anchor placement (62). Also, the technique, type of anchor used, and the
amount of dissection required are different between the two types of bone anchors.
The organisms isolated from the reported cases of osteomyelitis included Pseudomonas,
Staphylococcus aureus, Entercoccus, and Citrobacter. Coincidentally, these are the same
organisms that have been isolated from infections complicating pelvic surgery that does not
require bone anchors (59). Prophylaxis is of the utmost importance in preventing this
dreaded complication. First, the urinary tract should be sterile prior to the procedure.
Second, prophylactic antibiotics with a broad range of coverage against gram-positive, gram-
negative, and anaerobic organisms should be given prior to the procedure. At the authors’
 Vaginal Sling Surgery 353

institution, intravenous cefazolin and gentamycin are administered preoperatively followed by

an oral fluoroquinolone postoperatively for 1 week. In patients who are allergic to penicillin,
vancomycin is substituted perioperatively. With this regimen there have been no infectious
complications in over 250 cases involving transvaginal bone anchor placement (58).
In summary, bone anchor technology offers a secure form of fixation for the pubovaginal
sling. It is technically easier to perform and is associated with decreased operative time and
postoperative pain. It allows the procedure to be performed transvaginally, which may be of
benefit to patients who are morbidly obese or who have had prior lower abdominal surgery. Also,
the incidence of voiding dysfunction and de novo urgency after these procedures is minimal
(62). The infectious risks as reported in the literature are no greater than what is historically
reported for other pelvic procedures not using bone anchors. Patients must be counseled
carefully on the potential risks of this technology. In addition, as with any new technique, long-
term follow-up is necessary to further define its role in the treatment of SUI.
In an attempt to offer the same secure fixation as bone anchors but avoid the osseous
complications, there are new reports of performing transvaginal fixation to Cooper’s ligament
using commercially available needle devices (63). The new techniques are promising; however,
they may be difficult in patients who have undergone prior anti-incontinence procedures
secondary to scarring, but appropriate follow-up of new procedures will continue to advance the
techniques available.

IV. CONCLUSION

The field of female urology is expanding and undergoing rapid advances. New techniques and
materials are being introduced into the market every year. This makes it difficult for the clinician
to decide which material and technique is safe and effective. Currently, the pubovaginal sling
procedure using autologous fascia is the gold standard for the treatment of female SUI.
Autologous fascia has the longest follow-up, most durable results, and a favorable risk-benefit
ratio with regard to potential complications. The results obtained with cadaveric fascia,
polypropylene mesh, and bone anchors are promising, but the follow-up is still immature.
Ultimately it is the decision of the patient and the surgeon as to what material is to be used for the
transvaginal or pubovaginal sling, and both parties must be aware of the risks and benefits of the
material and anchoring technique chosen.

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incontinence with minimal alteration in proximal urethral mobility. Urology 2000; 55:512 – 514.
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of 1 year. J Urol 2001; 165:159– 162.
53. Ulmsten U, Johnson P, Rezapour M. A three-year follow-up of tension free vaginal tape proce-
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54. Ulmsten U, Petros P. Intravaginal slingplasty (IVS): an ambulatory surgical procedure for treatment
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60. Kammerer-Doak DN, Cornella JL, Magrina JF. Osteitis pubis after Marshall-Marchetti-Krantz
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56(suppl 6A):15– 22.
63. Koduri S, Goldberg RP, Sand PK. Transvaginal therapy of genuine stress incontinence. Urology
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23
Use of Cadaveric Fascia Lata Allograft for
Pubovaginal Slings
Matthew B. Gretzer and E. James Wright
The Johns Hopkins Medical Institutions, Baltimore, Maryland, U.S.A.

I. INTRODUCTION

The pubovaginal sling has become a favored treatment option for stress urinary incontinence
(SUI). While initially indicated for treating SUI secondary to intrinsic sphincter deficiency, it
has proven versatile for the management of urethral hypermobility (type 2 incontinence)
(1). Originally introduced by Giordano (2) in 1907, the concept of suburethral support was
reintroduced in 1978 by McGuire and Lytton (3). This work described successful results using
autologous rectus fascia for sling construction and set the stage for ongoing exploration into
sling materials and techniques to minimize morbidity, operative time, and time of recovery.
Many options are available, and the quest for a gold standard continues.
Autologous fascia has endured the test of time as a safe and effective material; however,
the added morbidity and time associated with procurement propel the search for alternative sling
materials. Current options for pubovaginal sling materials include allografts (cadaveric fascia
lata and dermis), xenografts (porcine dermis and small intestinal submucosa, bioengineered
collagen matrices, and a host of synthetic materials including Marlex, Gore-Tex, and polypro-
pylene. While synthetic materials have exhibited durable results without the time and morbidity
of harvest, concern over the potential for urethral erosion and other complications has often
overshadowed their successful application (4 –6). Cadaveric fascia lata allografts (CFLA) have
been available for more than 20 years and are well described in the orthopedic (7,8) and
ophthalmologic (9) literature. This experience of safety and stability over time has extended to
new applications in urologic and urogynecologic reconstructive surgery. This chapter describes
the technical and material aspects of CFLA sling and justifies its role in effective incontinence
therapy.

II. PREOPERATIVE EVALUATION

Selection of patients for pubovaginal sling is well described elsewhere in this volume. All
patients should have an accurate urogynecologic history and physical exam. The presence and
symptoms of pelvic organ prolapse should be evaluated for consideration of concomitant repair.
A voiding diary, pad test, and urodynamic evaluation are helpful in the overall assessment of
357
358 Gretzer and Wright

symptoms and outcome from intervention. After urine studies have excluded infectious
processes, those with a history of prior pelvic surgery may undergo cystoscopy to evaluate for
the presence of foreign body or other intravesical pathology.

III. SURGICAL TECHINIQUE

Numerous techniques are described for pubovaginal sling placement. Among these are
variations in the choice of incision, extent of urethropelvic ligament perforation, degree of
urethrolysis, sling dimensions, and choice of fixation. While refinements continue, an
evidenced-based, universally accepted approach remains to be established. Ultimately, the
chosen method should allow easy reproducibility and achieve an outcome that approximates
published standards. The technique described below satisfies these requirements and offers the
surgeon a method for sling placement associated with minimal morbidity, surgical efficiency,
and favorable outcome.
Two factors associated with successful pubovaginal sling surgery are accurate placement
at the urethrovesical junction and correct tension. Inappropriate sling placement or excessive
tension risks postoperative voiding dysfunction or urinary retention. Undue laxity may result in
continued incontinence.

A. Anesthesia/Position
Regional or general anesthesia may be used without particular advantage to either technique for
sling surgery. Preoperative antibiotics should be administered. The patient is placed in the
modified lithotomy position with the knee and hip at 908 flexion so as to minimize neural stretch.
Following suprapubic, vaginal and perineal preparation, a 16Fr Foley catheter is placed into the
bladder and the balloon filled with 10 cc of fluid.

B. Allograft Preparation
As there are different sources for allograft material, specific tissue bank recommendations for
preparation prior to the start of the operation should be followed. A 2  13 cm strip of fascia is
created, and the ends are bound through and through with O-PGA suture to prevent dissection
along the fiber planes (Fig. 1A). While debate continues as to optimal sling dimensions, we
believe the technique descried provides a sling long enough for fixation in the retropubic
space without reliance on suspension sutures or bone fixation, yet not so long as to require
passage through the rectus fascia for proper tensioning. Two delayed absorbable or monofilament
sutures of equal length are placed through the bound ends of the sling in a helical fashion to
provide temporary suspension. The ends of these sutures are made even to allow symmetric sling
placement (Fig. 1B).

C. Vaginal Dissection
The urethrovesical junction is identified by palpation of the Foley balloon through the anterior
vaginal wall and labeled with a skin marker (Fig. 2). The anterior vaginal wall has no reliable
landmarks to identify this position. Estimation of the bladder neck “by eye” is discouraged, as
this may result in placement of the sling too distal from the bladder neck. Two longitudinal
incisions are made on either side of the vesicle neck mark, forming an H configuration (Fig. 2).
A subepithelial tunnel is made at the vesical neck. Potts scissors angled “on the flat” at a 458
 Cadaveric Fascia Lata Allograft 359

Figure 1 (A) A 2  13 cm strip of fascia is created with the ends bound through and through with
O-PGA suture. (B) Two delayed absorbable or monofilament sutures of equal length are placed through the
bound ends of the sling in a helical fashion to provide temporary suspension.

angle can aid this dissection (Fig. 3). This tunnel ensures accurate placement of the sling
preventing cephalad or caudad displacement, and eliminating the need for additional fixation.
Flaps are raised laterally from the vaginal wall incisions. Dissection of the vaginal
epithelium from the underlying urethropelvic ligament laterally on each side is extended to the
urethropelvic ligament. With the bladder empty, the urethropelvic ligament is perforated using
scissors pointed somewhat superiorly and laterally. This allows entry into the retropubic space.
360 Gretzer and Wright

Figure 2 Location of the urethrovesical junction is marked, and two longitudinal incisions are made on
either side of the vesical neck mark, forming an H configuration.

The space is dissected digitally, freeing the bladder from the symphysis pubis to create a space
for the sling to traverse the retropubic space through the endopelvic fascia.
A 1- to 2-cm midline suprapubic incision is made and a ligature carrier passed through the
rectus fascia and guided through the retropubic space to emerge in the vaginal introitus. Lateral

Figure 3 A subepithelial tunnel is made under the vesical neck using Potts scissors.
 Cadaveric Fascia Lata Allograft 361

extension of this incision is avoided in order to reduce damage to cutaneous nerves and the
possible risk of postoperative pain. One should also avoid placing the abdominal incision
directly over the pubis, as this may cause discomfort during intercourse after the suspending
sutures are tied.

D. Sling Placement
The suspension suture is passed on the ligature carrier and transferred to the suprapubic incision.
The opposite end of the sling is passed through the subepithelial tunnel (Fig. 4) and process
repeated. Following sling placement, Indigo Carmine is administered intravenously, and
cystoscopy is performed to inspect bladder or ureteral injury. A 708 lens simplifies evaluation of
the anterior wall and superior bladder neck, where most injuries occur as the ligature carrier is
passed. The position of the sling at the bladder neck can be examined on exiting the bladder by
gently pulling on the suspension sutures. Following bladder inspection, the suspending sutures
are tied.
As stated above, proper sling tension is imperative to successful outcome. One method to
ensure a tension-free position of the sling is to place the arms of a forceps on either side of the
sling as it exits the subepithelial tunnel (Fig. 5A). Tying the sutures over the rectus fascia in this
manner limits both sling redundancy and excessive tension (Fig. 5B). A cystoscope with
downward traction on the urethra can accomplish the same goal. Repeat cystoscopy can be done
to check the urethra for undue cephalad angulation and confirm proper laxity. The course of the
urethra should be unimpeded, and suprapubic pressure should allow for crede voiding.
The suprapubic and vaginal incisions are closed with absorbable suture. The vagina can
be packed with gauze soaked with either povidine iodine (Betadine) or estrogen cream accord-
ing to preference. The vaginal pack is removed the morning following surgery. A cystotomy or
Foley catheter can be used for 24 h or longer, after which time a voiding trial can be initiated.

Figure 4 The opposite end of the sling is passed through the subepithelial tunnel.
362 Gretzer and Wright

Figure 5 (A) Placing arms of forceps on either side of the sling as it exits the tunnel to ensure a tension-
free position of the sling. (B) Tension-free sling position after tying sutures over rectus muscle.

IV. OUTCOMES

Enthusiasm for cadaveric fascial slings has increased with increasing availability of allograft
tissue, awareness of savings in time and morbidity, and published efficacy. Since 1996, reports
continue to emerge supporting favorable outcomes using fascial allografts (10 –15). These
results, described in Table 1, appear comparable to studies examining fascial autografts using
 Cadaveric Fascia Lata Allograft 363

Table 1 Results of Pubovaginal Sling Using Fascial Allografts

% Improved % “Cure”
Author Processing method #Pts. F/u(mean) (0 – 2 pads/d) (0 pads/d)

Elliot (14) Solvent-dried, þIRa 26 15 mo. 92 77

Amundsen (13) Freeze-dried, 2IR 104 19 mo. 84 63
Wright (10) Freeze-dried, 2IR 59 12 mo. 98 N.A.
Handa (12) Freeze-dried, 2IR 16 12 mo. 85 79
Brown (11) Freeze-dried, ?IR 121 12 mo. 83 74
Fitzgerald (15) Freeze-dried, þIR 35 6 mo. 83 69
a
IR, gamma irradiation.

rectus fascia and fascia lata (11,16 – 20). The latter are shown in Table 2. The most notable
difference in assessing these outcomes is a shorter follow-up available for the allograft cohorts.
These comparisons are perhaps hindered by variability in methods used to evaluate outcomes,
which include validated postal survey questionnaires, third-party telephone interviews, and
clinical examination. In most of these critiques, patients using less than one pad per day without
significant urge symptoms or retention were designated as having a favorable outcome.
Better standardization of outcome measures is necessary to improve direct comparison, and
future studies should strive to adhere to ICS recommendations for outcome evaluation. Never-
theless, outcomes measured in a variety of ways appear to be fairly consistent between allograft
and autograft fascial slings.
Given a shorter evaluation horizon for cadaveric allograft slings, questions remain about
their long-term effectiveness, durability, and potential for autolysis (21 –23). Allograft and
autograft fascia exhibit significant histologic variability in vivo, ranging from minimal change
to neovascularization to complete replacement (24). While yielding an overall success rate of
83%, Fitzgerald et al. (15,21) observed a 17% failure rate of cadaveric fascial slings within 5
months after surgery. At reoperation in seven of 35 patients, no consistent histologic pattern
emerged in the grafts to explain a lack of efficacy. Similarly, Blander et al. described histologic
findings in five “failed” slings (22). The adverse outcomes in this series included de novo
retention as well as recurrent SUI. No distinct histologic pattern emerged for either outcome.
Curiously, absence of allograft and presumed autolysis did not preclude persistent urinary
retention.

Table 2 Results of Pubovaginal Sling Using Fascial Autografts

Processing % Improved % “Cure”

Author method #Pts. F/U (mean) (0 – 2 pads/d) (0 pads/d)

Haab (16) RFAa 40 4 yr. 86 46

Iglesia (17) RFA 50 3 mo. 94 73
Chaikin (18) RFA 251 3 yr. 92 73
Morgan (19) RFA 247 4 yr. 88 82
Brown (11) FLAb 46 3.5 yr. 85 73
Breen (20) FLA 72 2 yr. 90 N.A.
a
RFA, rectus fascia lata.
b
FLA, fascia lata.
364 Gretzer and Wright

It appears that both autograft and allograft fascial slings have a high success rate as well as
a demonstrable failure rate (25,26). Most overt failures occur early, within the first 6 – 12 months,
irrespective of the material used (11,15,19). With lengthening follow-up, fewer failures due to
recurrent SUI are seen after 1 year, with most studies reporting a “cure” rate approaching 15%
lower than the rate of improvement and overall patient satisfaction. The source of these
differences is not well studied. Whether due to unrecognized host vs. graft reactions or other
specific patient characteristics remains a focus for further investigation.
Another area of continuing concern in the use of allograft fascia is a potential for disease
transmission. In an attempt to minimize risk from tissue transplantation, the FDA established
standards for donor screening (27) which currently include HIV, hepatitis, and history of cancer,
neurodegenerative conditions, syphilis, and rabies. Following the introduction of PCR and DNA
probing techniques, identification of these diseases has nearly eliminated any risk of donor
transmission. In more than 60,000 organ transplants and 1 million of tissue transplants, only one
case has been reported of HIV transmission. This case was identified from a bone graft. Since the
introduction of strict guidelines in 1985, no cases of HIV transmission have been reported (28) in
organ or soft tissue transplants. Further review of the literature does not identify a single case of
disease originating from transplanted allograft fascia (29).
Beyond concern for identifiable pathogens is concern regarding potential risk of prion
transmission. In proteinacious substances implicated in various forms of spongiform
encephalopathy including Creutzfeld-Jacob disease, scrapie, and mad and cow disease (30 –
32), prions defy culture and characterization. While prions are resistant to methods aimed at
destroying nucleic acids, they may be inactivated by denaturing detergents or chemotropic ions
(31,32). These processes must be weighed against damage to the tissue rendering it unsuitable
for transplant. To date, no case of prion infection has been described in a patient who had not
received tissue with origin in or proximity to brain, dura mater, cornea, pituitary extracts, or
brain stimulation electrodes. More than 200,000 soft tissue transplants are done annually,
while fewer than 200 cases of prion related encephalopathy have been documented since their
classification. It is unlikely that cadaveric fascia lata represents a prion reservoir.
In addition to donor screening, tissue preparation methods strive to eliminate disease
transmission risk. Allograft processing involves combinations of bactericidal and antiviral
solutions, flash freezing, freeze-drying, solvent dehydration, and gamma irradiation. These
methods render the material sterile and virtually free of cellular elements to the extent that it will
not impair its suitability for transplantation. Beyond specific requirements, processing methods
are proprietary. Lack of standardization may account for variability in allograft tissue, although
studies suggest ex vivo durability is independent of processing technique (33,34). Cellular
elements and nucleic acid can persist in allograft fascia (35,36), but the degree to which this
contributes to outcome or risk is uncertain.
In comparing the performance of allograft fascia to autografts and synthetics, questions
about strength arise. This is especially true in the face of variations in tissue processing. That such
processing may affect the strength and durability of allograft tissue is speculative. While studies
(33,34,36) from both orthopedic and urologic literature reveal maximum load to failure values of
315 Newtons and 250 Newtons for solvent-dried and freeze-dried cadaveric tissue, respectively,
these forces (500–700 lb) likely exceed those generated physiologically at the bladder neck and
proximal urethra. Consequently, it is not clear that the ex vivo strength of fascial allografts is
related to in vivo success of pubovaginal sling. Data are not available reporting the tensile
strength necessary for success of the pubovaginal sling in vivo. A single study by Kim et al.
evaluated an in vivo model of cadaveric allograft application in an animal model (37). Using the
“trouser tear test,” these authors found similar decreases in durability of both autologous and
allograft fascia over time. The clinical implications of their findings are unclear.
 Cadaveric Fascia Lata Allograft 365

V. CONCLUSION

Cadaveric fascia allografts offer decreases in operative time and morbidity relative to autografts
(39). Current evidence supports this material as a safe and viable option among the vast array
of available options (40). There is a measurable failure rate of allograft fascia which seems to
manifest in the first 6 –12 months of application. This rate does not appear to be significantly
different from the failure rate of autograft fascia. Therefore, the search for a conclusive gold
standard continues. Consistent “cure” rates of 80 – 86% can be obtained with most sling
procedures, while patient “satisfaction” rates remain between 92% and 96%.

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seronegative organ tissue donors. N Engl J Med 1992; 326:726.
29. Parizek J, Mericka P, Husek P. Detailed evaluation of 2959 allogenic and zenogenic dense connective
tissue grafts (fascia lata, pericardium, and dura mater) used in the course of 20 years for duraplasty in
neurosurgery. Acta Neurochir 1997; 139:827 – 838.
30. Prusiner SB. Novel proteinaceous infectious particles cause scrapie. Science 1982; 216(4542):136–144.
31. Prusiner SB. Prions. Proc Natl Acad Sci USA 1998; 95(23):13363– 13383.
32. Cashman NR. A prion primer. Can Med Assoc J 1997; 157(10):1381– 1385.
33. Hinton R. A biomechanical analysis of solvent-dehydrated and freeze-dried human fascia lata
allografts. A preliminary report. Am J Sports Med 1992; 20(5):607 –612.
34. Sutaria PM, Staskin DR. Tensile strength of cadaveric fascia lata allograft is not affected by current
methods of tissue preparation (abstract). J Urol 1999; 161:1194.
35. Sadhukhan P, Rackley RR, Bandyopadhyay S. Extraction of celluar genetic material from human
fascia lata allografts. In: AUA Annual Meeting, Dallas, 1999.
36. Fitzgerald MP, Mollenhauer J, Brubaker L. The antigenicity of fascia lata allografts. BJU Int 2000;
86(7):826– 828.
37. Lemer ML, Chaikin DC, Blaivas JG. Tissue strength analysis of autologous and cadaveric allografts
for the pubovaginal sling. Neurourol Urodyn 1999; 18(5):497– 503.
38. Kim HL, LaBarbera MC, Patel RV. Comparison of cadaveric and autologous fascia using an in vivo
model. Urology 2001; 58:800.
39. Labasky RF, Soper T. Reduction of patient morbidity and cost using frayed cadaveric fascia lata for
pubovaginal sling. J Urol 1997; 154(Abstract 1794):459.
40. Wright EJ. Current status of fascia lata allograft slings treating urinary incontinence: effective or
ephemeral? Tech Urol 2001; 7(2):81 – 86.
24
Autologous Fascia Lata Sling
Cystourethropexy
Karl J. Kreder
University of Iowa, Iowa City, Iowa, U.S.A.

I. INTRODUCTION

Pubovaginal sling cystourethropexy has recently become one of the primary surgical treatment
options for women with urinary incontinence. The procedure has evolved over time with regard
to clinical indications, patient selection criteria, surgical techniques, and sling materials. This
chapter reviews the historical development of pubovaginal sling cystourethropexy using fascia
lata. The selection of graft materials is considered and the utility of fascia lata emphasized.

II. HISTORY

The idea of using autologous graft material as a sling behind or around the urethra for treatment
of urinary incontinence is not actually a new concept. In 1907 Giordano (1) described mobilizing
the distal end of the gracilis muscle and wrapping it around the urethra. In 1910 Goebell (2)
introduced the use of a sling of pyramidalis muscle sutured behind the urethra. This technique
was subsequently modified by Frangenheim (3) and Stoeckel (4). Squire (5) described the use of
the levator ani muscles, and Martius (6) advocated use of the bulbocavernosus muscles as
pedicled flap grafts to support the urethra. In 1942, Aldridge (7) described the use of bilateral
strips of rectus fascia, passed through the rectus abdominis muscles and sutured together
posterior to the urethra. Narik and Palmrich (8) described the creation of a sling from the fascia
of the inguinal aponeurosis of the external oblique muscles. They advocated preserving the
attachment of the fascia at the level of the pubic tubercle. These techniques eventually fell out of
favor because of a significant complication rate, including prolonged urinary retention, sling
erosion, iatrogenic bladder and urethral injuries, and recurrent incontinence.
Price first reported using a fascia lata sling in a female with sacral agenesis (9). Beck and
colleagues described the use of fascia lata for the creation of a suburethral sling for the treatment
of recurrent urinary incontinence (10 – 12). Originally, the procedure was considered a secondary
procedure to be used in cases of failed prior surgical repair, or in patients who lacked substantial
pubovaginal tissues. Beck’s group reported a 92% overall cure rate in 170 women treated with
fascia lata pubovaginal sling cystourethropexy for recurrent stress urinary incontinence (SUI)
(12). Others have demonstrated similar results using this technique (Table 1).
367
368 Kreder

Table 1 Fascia Lata Sling Results

Authors No. of patients Dry (%) Improved (%) Failed (%)

Griebling et al. (35) 30 26 (87) 4 (13) 0 (0)

Govier et al. (36) 30 21 (70) 6 (20) 3 (10)
Handa et al. (59) 14 11 (79) 1 (7) 2 (14)
Ogundipe et al. (57) 8 7 (88) 0 (0) 1 (11)
Karram et al. (58) 10 9 (90) 1 (10) 0 (0)
Beck et al. (12)b 170 157 (92) 4 (2) 9 (5)
Addison et al. (56) 97 84 (87) 8 (8) 5 (5)
Low et al. (55) 43 37 (86) 4 (9) 2 (5)
Ridley (50) 36 30 (86) 4 (11) 2 (6)
Total 438 382 (87) 32 (7) 24 (5)
a
UDS: urodynamic studies.
b
Cumulative data include patients previously reported in Ref. 10 and 11.
Source: Ref. 64.

III. INDICATIONS
A. Intrinsic Sphincter Deficiency
For many years, the primary indication for fascia lata sling cystourethropexy has been the
management of women with SUI who demonstrate a significant component of intrinsic sphincter
deficiency (ISD). ISD has multiple etiologies, including neurologic, anatomic, and primary
causes (13 – 15). Neurologic factors include disruption of the sacral nerve roots S2 – S4 during
major pelvic surgery, loss of autonomic neural control associated with myelodysplasisa,
radiation therapy, lumbosacral spinal cord injuries, or anterior spinal artery syndrome. Anatomic
causes of ISD include congenital defects such as spinal dysraphism, periurethral scarring
from prior anti-incontinence surgery, or urethral atrophy due to estrogen deficiency in postmeno-
pausal women. Although idiopathic ISD has been described, the etiology of ISD can usually be
identified (16).
Several diagnostic modalities have been used to identify ISD, including cystourethro-
scopy, cystography, multichannel urodynamics with measurement of abdominal leak-point
pressure, urethral pressure profilometry, and videourodynamics. ISD is classically diagnosed by
an open bladder neck at rest on erect cystography and a low Valsalva leak-point pressure
(VLPP) (15). The VLPP is a reasonably simple test that generally correlates with the degree of
urethral dysfunction (17,18).

B. Urethral Hypermobility (Type II Incontinence)

SUI caused by urethral hypermobility has traditionally been treated surgically with vaginal or
abdominal-urethral suspension procedures. Recently, however, it has been recognized that
pubovaginal sling cystourethropexy may be used for the management of patients with isolated
type II or combined ISD and type II stress urinary incontinence (19 – 23). Specifically, the overall
success rates for slings appear to be greater than those for needle suspension procedures and
comparable to the Burch procedure. As shown in Table 1, a review of the published literature
on pubovaginal slings reveals that 87% of patients overall are dry postoperatively, with an
additional 7% significantly improved. In comparison, several recent studies of the long-term
results for needle suspension procedures revealed that 20 –47% of patients were dry, with
 Autologous Fascia Lata Sling Cystourethropexy 369

29 –71% categorized as improved (24 –26). Although more long-term data are necessary, it
also appears that the results of pubovaginal sling cystourethropexy are durable. Finally, the
procedure could potentially prevent some of the treatment failures associated with traditional
urethral suspension procedures. The incidence of ISD appears to be higher in older women, and,
as patients age, many may develop ISD. This anatomic change is not addressed by standard
cystourethropexy procedures, which may explain why some patients develop recurrent
incontinence over time. Theoretically, a sling cystourethropexy performed initially for stress
incontinence caused by urethral hypermobility may prevent recurrent incontinence caused by
the subsequent development of ISD.
In the author’s early experience with pubovaginal sling cystourethropexy for the treatment
of patients with combined urethral hypermobility and ISD (20), 11 patients with isolated ISD
and 16 with combined ISD and urethral hypermobility who underwent pubovaginal sling
cystourethropexy were evaluated. The preoperative diagnoses were confirmed in all patients
with multichannel urodynamics; mean follow-up in this study was 22 months. Of the 11 patients
with isolated ISD, six (55%) were dry, two (18%) had continued urge with incontinence,
two (18%) developed de novo urge with incontinence, and one (9%) had continued stress
incontinence. In comparison, 13 of the 16 patients (81%) with combined ISD and urethral
hypermobility were dry, three (19%) had continued urge with incontinence, and none had de
novo urge or continued stress incontinence.
Others have also shown pubovaginal sling cystourethropexy to have promising results
in women with urethral hypermobility, both with and without concomitant ISD. O’Donnell
reported the utility of creation of a pubovaginal sling and simultaneous retropubic bladder neck
suspension in patients with combined type II and type III incontinence (21). Cross et al. reported
the results of pubovaginal sling cystourethropexy in 124 patients treated for SUI (22): 50% of the
patients in this series had ISD, 35.4% had type II incontinence, and 14% had both diagnoses. The
overall cure rate for SUI was 90% at a mean follow-up of 19 months. Zaragoza (23) reported
complete continence after a mean follow-up of 25 months in 95% of 38 women with type II
incontinence and 96% of 22 women with type III incontinence.
These early data support the use of pubovaginal sling procedures as a primary surgical
treatment in women with SUI due to either type II, type III, or combined incontinence.

C. Other Indications
Pubovaginal sling cystourethropexy has been utilized to treat incontinence in a variety of
complex patient populations. Woodside reported that two women with incontinence after pelvic
trauma and urethral injury were continent at 6 and 15 months, respectively, after pubovaginal
sling cystourethropexy (27). Chancellor et al. described the use of pubovaginal sling cysto-
urethropexy in the management of women with urethral dysfunction secondary to long-term
indwelling catheter drainage (28). Ghoniem and Monga reported the combined use of a
pubovaginal sling and a Martius flap graft for patients with vesicovaginal fistula involving the
internal sphincter (29). Swierzewski and McGuire reported the simultaneous performance of
urethral diverticulectomy and pubovaginal sling cystourethropexy (30).
Gormley et al. (31) reported an overall continence rate of 92% in 15 adolescent females
after pubovaginal sling cystourethropexy. Mean follow-up was 54 months. Ten of the patients in
this series had spinal dysraphism, three were incontinent after pelvic trauma, and two underwent
concomitant augmentation cystoplasty for poor bladder compliance. Secondary procedures were
required in three patients, including repeat sling in two, and repeat bladder augmentation in one.
Pérez et al. reported a continence rate of 58.3% in 24 girls who underwent rectus fascia sling
cystourethropexy (32). The majority of these patients had neurogenic bladder secondary to
370 Kreder

spinal dysraphism, and the highest success rates were identified in those who underwent
combined pubovaginal sling and augmentation cystoplasty. Walker et al. (33) successfully used
a modification of the rectus fascia sling for both male and female patients with incontinence
associated with neurogenic bladder. In this case the fascia was wrapped around the urethra to
cause luminal apposition.
Pubovaginal sling cystourethropexy has also been used successfully in elderly women.
Carr et al. (34) reported resolution of stress incontinence symptoms in all 19 geriatric women
(median age 72 years) treated with rectus fascia sling cystourethropexy. Mean follow-up was 22
months. Similar results were reported by Griebling et al. in a cohort analysis of our older and
younger pubovaginal sling patients (35). At a mean follow-up of 10.5 months, 65% of 26 older
women (mean age 67.6 years) were dry, and 27% significantly improved. Of the 28 younger
women (mean age 48.9 years), 82% were dry and 18% were significantly improved.

IV. SURGICAL TECHNIQUE

A. Fascia Lata Graft Harvest
Fascia lata grafts can be harvested by a variety of methods. In one technique, the skin and
subcutaneous tissues overlying the fascia lata of the lateral thigh and upper leg are incised along
the entire length of the planned graft. However, several modifications have been described to
obviate the need for such a long incision. Govier (36) described making three small incisions
perpendicular to the planned graft. Dissection is then carried down to the fascia lata along the
entire length of the graft beneath the skin and subcutaneous tissues. A strip of fascia lata
24  2.5 cm is harvested, cleared of fat, and tailored to a 2-cm width.
Beck et al. (10) described the use of a fascial stripper to obtain the fascia lata graft. A
modification of Beck’s technique is described below (37). A line is drawn from the anterior
superior iliac spine to the lateral epicondyle of the knee. A 3-cm-long longitudinal incision is
then created just proximal to the distal mark (Fig. 1A), and dissection is carried down to the level
of the fascia lata. Two small parallel incisions are made longitudinally in the distal fascia lata.
The tissue is then raised off the underlying muscle, and a suture of 0-Prolene is secured in the
distal end of the fascia. A Crawford fascial stripper (Fig. 1B; Karl Stortz Medical Instruments,
St Louis, MO) is then used to harvest a strip of fascia lata which is 20  2 cm in dimension
(Fig. 1C). A second 0-Prolene suture is secured in the proximal end of the graft, which is placed
in saline for future use. The subcutaneous tissues and skin are closed with absorbable sutures.
A compressive elastic bandage is wrapped around the thigh and proximal leg to provide
hemostasis. The bandage is usually removed 8 h postoperatively, and early ambulation is
encouraged.

B. Sling Placement
The sling placement procedure we utilize is a modification of the techniques described by Beck
et al. (10–12) and McGuire and Lytton (38). The patient is placed in the dorsal lithotomy position,
and the lower abdomen and vagina are prepared and draped. A small transverse lower abdominal
incision is made, and dissection is carried down to the rectus abdominis fascia just superior to the
symphysis pubis. A Foley catheter and a weighted vaginal speculum are placed. The vaginal
mucosa is incised longitudinally on either side of the urethra at the level of the bladder neck. A
tunnel is then created in the retropubic space on either side of the urethra, using sharp and blunt
dissection. This tunnel is dissected to the level of the posterior rectus abdominis fascia (Fig. 2). A
space is created between the urethra and the vaginal mucosa, and the fascia lata graft is placed in
 Autologous Fascia Lata Sling Cystourethropexy 371

Figure 1 (A) Location of the 3-cm incision over the underlying fascia lata. (B) The Crawford fascial
stripper (Karl Stortz Medical Instruments, St Louis, MO). (C) Harvest of the 20  2 cm section of fascia
lata using the Crawford fascial stripper.

position posterior to the urethra. A tonsil clamp is then used to pierce the rectus abdominis fascia
just lateral to the midline. The clamp is passed by fingertip guidance through the previously created
retropubic tunnel to the vagina. The ends of the 0-Prolene sutures at one end of the sling are then
grasped with the clamp and brought out through the abdominal incision. The procedure is repeated
on the contralateral side (Fig. 3). The sling is tied without any tension on the graft. Cystoscopy is
performed to ensure that no iatrogenic bladder or ureteral injuries have occurred. The abdominal
and vaginal incisions are closed and a vaginal pack is placed. A new Foley catheter is placed to
provide postoperative bladder drainage. The vaginal pack is removed on postoperative day 1, and
the catheter is removed on day 7. The patient is instructed to perform postvoid self-catheterization
until residual urine volumes are consistently below 100 mL.
372 Kreder

Figure 2 Retropubic dissection prior to placement of the fascia lata sling.

C. Suture Techniques
A number of different techniques have been described to secure the sling. Initially, the fascial
sling was secured directly to the rectus fascia on each side. Subsequently, the technique was
modified to that described by Govier et al. (36), whereby the two ends of the sling are tied over
the rectus fascia without anchoring the sling directly to the rectus fascia. Pérez et al. (32)
described securing the ends of the fascial graft to Cooper’s ligament with or without crossing the
ends of the graft across the midline to improve urethral coaptation. Ghoniem (38) described
wrapping the sling around the urethra at the level of the bladder neck.
Various techniques have been advocated to secure the sling at the level of the bladder
neck. Gormley et al. (31) described suturing the midportion of the sling to the periurethral fascia.
Govier et al. (36) used three interrupted absorbable sutures to tack the sling to the bladder and
urethra. It is likely not necessary to secure the sling at the urethra, provided a submucosal tunnel
is created for placement of the sling.

D. Sling Tension
Most authors now agree that proper sling placement using a tension-free technique is critical for
a satisfactory surgical outcome. Excessive sling tension has been identified as a significant risk
factor for persistent postoperative urinary retention. We prefer a technique in which the ends of
the graft are brought up to the rectus abdominis fascia, allowed to settle into position by gentle
traction on the Foley catheter, and secured to the rectus abdominis fascia as previously
described. The urethra is carefully inspected after this procedure to ensure that it is in an
anatomic position without evidence of overcorrection.
 Autologous Fascia Lata Sling Cystourethropexy 373

Figure 3 Fascia lata sling in place, just prior to tying the sutures.

Other authors have utilized different techniques for adjusting sling tension intraoperatively.
Beck et al. (12) used intraoperative urethral manometry to create an intraurethral pressure of
50–90 cmH2O at the sling site. MeGuire et al. (39) described adjusting sling tension by endoscopic
observation with direct visualization of mucosal “soft” coaptation. Govier (36) described adjusting
the sling tension until one finger could be placed between the suture and the anterior abdominal
wall. Rovner et al. (40) have described using a cystoscope sheath placed transurethrally to stabilize
the urethral angulation when the sling is secured to the rectus abdominis fascia.

E. Selection of Graft Material

A wide variety of materials have been used as grafts for pubovaginal sling cystourethropexy.
Currently, the most common include autologous rectus fascia or fascia lata, or allogenic fascia.
Permanent and absorbable synthetic materials have also been used (41 – 44), but these do present
a higher risk of infection and erosion. The reported rates of urethral erosion and need for graft
explantation with synthetic materials have ranged from 14% to 23% (43 –48).
Autologous materials have the advantage of low erosion rates and no potential for
transmission of viral disease or infection. Theoretically, fascia lata offers several advantages
over rectus fascia. It generally has greater tensile strength than rectus fascia and is less affected
by the patient’s nutritional status or prior abdominal surgery (14). The use of fascia lata also
minimizes the risk of developing an abdominal wall hernia, which may occur after rectus fascia
harvest. The disadvantage of using autologous fascia is the time required for harvest and
additional morbidity associated with the harvest site (i.e., pain, hematoma).
Synthetic graft materials do offer the advantage of decreased overall surgical time because
the graft harvesting step is eliminated. Cadaveric allogrant fascia lata has been used by a number
374 Kreder

of authors (49 – 54). However, there is some concern about possible transmission of viral or
infectious disease, as well as the possibility of graft autolysis.

V. CLINICAL RESULTS

A review of the literature regarding fascia lata pubovaginal sling cystourethropexy revealed
an overall success rate of 87% in 438 reported patients. An additional 7% of patients had
improvement of incontinence symptoms, and only 5% experienced no improvement over base-
line. These data are summarized in Table 1. It should be noted that these studies represent a
compilation of several variations in surgical technique and patient selection.
Early reports by both Ridley (50) and Low (55) suggested that pubovaginal sling procedures
with fascia lata were effective for the management of SUI. More recent studies have confirmed
these findings. At a mean follow-up of 10 months, Griebling et al. (35) reported that 26 of 30
patients (87%) who had undergone a pubovaginal sling cystourethropexy with a fascia lata graft for
treatment of SUI were dry, and four (13%) were improved. In comparison, 11 of 21 patients (52%)
who had undergone pubovaginal sling with a rectus fascia graft were dry, eight (38%) were
improved, and two (l0%) were unchanged from preoperative baseline. Govier et al. treated 32
females for ISD with fascia lata sling cystourethropexy (36). At a median follow-up of 14 months,
87% required no pads (chart review), and 70% required no pads (independent patient survey).
Eighty percent of the patients claimed they would choose to undergo the procedure again.
In 1988, Beck et al. (12) reported their 22-year experience of 170 patients treated for SUI
with fascia lata pubovaginal sling cystourethropexy. The overall symptomatic cure rate was
92.4%. At that time they recommended the procedure be reserved for patients with recurrent SUI
or those not amenable to other therapy. Similarly, Addison et al. (56) reported the results of
pubovaginal sling procedures performed for recurrent SUI over a 25-year period. The overall
cure rate for these 97 patients was 87%, with an additional 8% improved after surgery. They
recommended that the procedure be used primarily for recurrent incontinence. Only three
patients in this series underwent pubovaginal sling placement as the initial surgical treatment for
incontinence. The authors also recommended that the procedure should usually be performed in
conjunction with anterior colporrhaphy.
Ogundipe et al. (57) compared the use of fascia lata and synthetic graft material in a small
prospective study. The found 100% cure in the eight patients treated with a synthetic graft, and 87.5%
in the eight patients treated with a fascia lata graft at 6 months follow-up. Postoperative urodynamic
evaluation revealed no significant differences between the two groups. Although not statistically
significant, there was a slightly higher complication rate in the group treated with the synthetic slings.
Karram and Bhatia (58) described the use of a patch of fascia lata as a suburethral support.
The 5  7 cm patch was secured under the urethra with nonabsorbable helical sutures placed
laterally and brought up to the rectus abdominis fascia.
Handa et al. (59) recently reported the use of banked fascia lata grafts taken from cadaveric
donors. They reported an overall subjective cure rate of 86% and an objective cure rate of 79%.
One patient in this series experienced persistent urinary retention, which has required continued
clean intermittent self-catheterization.

VI. COMPLICATIONS

Prolonged urinary retention, urgency, and urge incontinence are the most commonly reported
complications after pubovaginal sling cystourethropexy. Anatomic or functional obstruction
 Autologous Fascia Lata Sling Cystourethropexy 375

may occur if the sling is tied with excessive tension. Significant postoperative bladder outlet
obstruction usually occurs in ,5% of patients (14). Beck reported a mean interval of 59.6 days
between surgery and the return of consistent voiding function (12). In this author’s experience,
however, most patients are able to void spontaneously within 2 weeks of surgery.
Several different surgical techniques have been described to release the sling tension in
cases of prolonged obstruction (60 –62). In a recent series of 54 women treated at our institution
with pubovaginal sling cystourethropexy (30 fascia lata sling, 21 rectus fascia sling, three
vaginal wall sling), the overall complication rate was 37% (32). However, the majority of these
complications were minor and self-limited. Only two women experience prolonged urinary
retention, which has required intermittent self-catheterization.
De novo detrusor instability is a troubling complication of pubovaginal sling cys-
tourethropexy, reported to occur in up to 15 – 20% of patients. These symptoms may severely
affect a patient’s overall quality of life, and often require treatment with anticholinergic
medication.
Other complications are less common. Brodak et al. (63) reported the development of a
levator hernia through the pelvic floor 18 months after sling cystourethropexy performed in
combination with transvaginal vesicovaginal fistula repair. Govier et al. (36) reported that
one patient needed physical therapy for prolonged leg pain after the fascia lata graft harvest.
Addison et al. (56) reported eight bladder lacerations in a series of 97 patients who underwent

Table 2 Complications of Fascia Lata Sling Cystourethropexy

Authors No. of patients Complications

Griebling et al. (35)a 30 (54 total) 10, urinary tract infection

2, wound infection
1, vaginal hemorrhage, incisional hernia,
thigh hematoma, thrombophlebitis,
allergic reaction, hypotension, death
Govier et al. (36) 30 1, leg pain, sling revision
Handa et al. (59) 14 2, wound infection
1, persistent retention
Ogundipe et al. (57) 8 none reported
Karram et al. (58) 10 none reported
Beck et al. (12)b 170 26, pyrexia
14, pyuria
9, pulmonary atelectasis
8, wound infection
6, wound seroma
5, sling revision
Addison et al. (56) 97 8, bladder perforation
6, persistent retention
5, enterocele
2, wound infection
1, pulmonary embolus, thrombophlebitis
Low et al. (55) 43 3, genitourinary fistula (deemed not from
sling), wound infections (number not cited)
Ridley (50) 36 8, pyruria
a
Includes complications from 24 additional patients (21 rectus fascia sling, 3 vaginal wall sling).
b
Cumulative data include patients previously reported in Refs. 10 and 11.
376 Kreder

pubovaginal sling over a 25-year period. In all cases the injury was identified intraoperatively
and repaired immediately. No long-term sequelae were reported in these cases. In addition,
five patients in their series developed enteroceles, of which three required subsequent surgical
repair. The complications listed in the published reports on fascia lata sling cystourethropexy
are summarized in Table 2.
Pubovaginal sling cystourethropexy using autologous fascia lata as the graft material is an
appealing surgical option for the treatment of urinary incontinence in women. It has shown its
usefulness as both a primary operation and a secondary procedure in cases of prior failed surgical
repair. A review of the reported literature on fascia lata pubovaginal slings reveals an overall
cure rate of 87%, with an additional 7% reporting symptomatic improvement over baseline. The
selection of fascia lata as the graft material offers several advantages: it is durable and readily
available in most patients, it can be harvested in a minimally invasive fashion, and the risks of
postoperative complications such as abdominal hernia are minimized. The technique has shown
promise in the management of complex patient populations, including adolescents, the elderly,
and patients with neurologic causes of incontinence, particularly when combined with augmen-
tation cystoplasty. In addition, the procedure has been used successfully to treat incontinence
caused by pure ISD, urethral hypermobility, or combined etiologies.

REFERENCES

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1910; 2:187– 191.
3. Frangenheim P. Zur operativen behandlung der inkontinenz der mannlichen hamrohre. Verhandl
Deutsch Gesellsch Chir 1914; 43:149– 152.
4. Stoeckel W. Aber die Verwendung der Musculi pyramidales bie der operativen behandlung der
incontinentia urinae. Zentralbl Gyniiko 1917; 41:11 – 19.
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7. Aldridge AH. Transplantation of fascia for relief of urinary stress incontinence. Am J Obstet Gynecol
1942; 44:398 –411.
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9. Price PB. Plastic operation for incontinence of urine and of feces. Arch Surg 1933; 26:1043.
10. Beck RP, Grove D, Arnusch D, Harvey J. Recurrent urinary stress incontinence treated by the fascia
lata sling procedure. Am J Obstet Gynecol 1974; 120:613 –621.
11. Beck RP, Lai AR. Results in treating 88 cases of recurrent urinary stress incontinence with the
Oxford fascia alata sling procedure. Am J Obstet Gynecol 1982; 142:649 – 651.
12. Beck RP, McCormick S, Nordstrom L. The fascia lata sling procedure for treating recurrent genuine
stress incontinence of urine. Obstet Gynecol 1988; 72:699 – 703.
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deficiency: recognition and management. J Urol 1996; 156:3– 17.
14. Haab F, Zimmern PE, Leach GE. Diagnosis and treatment of intrinsic sphincter dysfunction in
females. AUA Update Series. Lesson 35, Vol. XV. American Urological Association: Baltimore,
MD, 1996:282 – 287.
15. Blaivas JG. Intrinsic shpincter deficiency. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED,
Wein AJ, eds. Campbell’s Urology, Update 17. Philadelphia: W.B. Saunders, 1996:1– 11.
16. Horbach NS, Ostergard DR. Predicting intrinsic urethral sphincter dysfunction in women with stress
urinary incontinence. Obstet Gynecol 1994; 84:188– 192.
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17. McGuire EJ, Fitzpatrick CC, Wan J, Bloom D, Sanvordenker J, Ritchey M, Gormley EA. Clinical
assessment of urethral sphincter function. J Urol 1993; 150:1452 –1457.
18. McGuire EJ, Cespedes RD, O’Connoll HE. Leak-point pressures. Urol Clin North Am 1996;
23:253– 262.
19. Leach GE, Dmochowski RR, Appell RA, Blaivas JG, Hadley HR, Luber KM, Mostwin JL,
O’Donnell PD, Roehborn CG. Female stress urinary incontinence clinical guidelines panel summary
report on surgical management of female stress urinary incontinence. J Urol 1997; 158:875 – 880.
20. Kreder KJ, Austin CJ. Treatment of stress urinary incontinence in women with urethral hypermobility
and intrinsic sphincter deficiency. J Urol 1996; 156:1995 – 1998.
21. O’Donnell PD. Combined Raz urethral suspension and McGuire pubovaginal sling for treatment
of complicated stress urinary incontinence. J Ark Med Soc 1992; 88:389 –392.
22. Cross CA, McGuire EJ, Cespedes RD. Our experience with pubovaginal slings in patients with stress
urinary incontinence. J Urol 1997; 157:460A, abstract 1797.
23. Zarazoga MR. Expanded indications for the pubovaginal sling: treatment of type 2 or 3 stress
incontinence. J Urol 1996; 156:1620– 1622.
24. Christensen H, Laybourne C, Eickhoff JH, Fromdt-Moller C. Long-term results of the Stamey bladder-
neck suspension procedure and of the Burch colposuspension. Scand J Urol Nephrol 1997; 31:349–353.
25. Trockman BA, Leach GE, Hamilton J, Sakamoto M, Santiago L, Zimmern PE. Modified Pereyra
bladder neck suspension: 10-year mean followup using outcomes analysis in 125 patients. J Urol
1995; 154:1841 – 1847.
26. Korman HJ, Sirls LT, Kirkemo AK. Success rate of modified Pereyra bladder neck suspension
determined by outcomes analysis. J Urol 1994; 152:1453 – 1457.
27. Woodside JR. Pubovaginal sling procedure for the management of urinary incontinence after urethral
trauma in women. J Urol 1987; 138:527– 528.
28. Chancellor MB, Erhard MJ, Kilholma PJ, Karasick S, Rivas DA. Functional urethral closure with
pubovaginal sling for destroyed female urethral after long-term urethral catheterization. Urology
1994; 43:499 –505.
29. Ghoniem GM, Monga M. Modified pubovaginal sling and Martius graft for repair of the recurrent
vesicovaginal fistula involving the internal urinary sphincter. Eur Urol 1995; 27:241– 245.
30. Swierzeski SJ III, McGuire EJ. Pubovaginal sling for treatment of female stress urinary incontinence
complicated by urethral diverticulum. J Urol 1993; 149:1012– 1014.
31. Gormley EA, Bloom DA, McGuire EJ, Ritchey ML. Pubovaginal slings for the treatment of urinary
incontinence in female adolescents. J Urol 1994; 152:822 – 825.
32. Pérez LM, Smith EA, Broecker BH, Massad CA, Parrott TS, Woodward JR. Outcome of sling
cystourethropexy in the pediatric population: a critical review. J Urol 1996; 156:642 – 646.
33. Walker RD III, Flack CE, Hawkins-Lee B, Kim DJ, Parramore H, Hackett RL. Rectus fascial wrap:
early results of a modification of the rectus fascial sling. J Urol 1995; 154:771 –774.
34. Carr LK, Walsh PJ, Abraham VE, Webster GD. Favourable outcome of pubovaginal slings for
geriatric women with stress incontinence. J Urol 1997; 157:125 – 128.
35. Griebling TL, Schrepferman CG, Nygaard IE, Kreder KJ. Sling cystourethropexy for treatment
of women with stress urinary incontinence: comparison of older and younger patients. J Am Geriatr
Soc 1997; 45:S42, abstract P125.
36. Govier FE, Gibbons RP, Correa RJ, Weismann RM, Pritchett TR, Hefty TR. Pubovaginal slings using
fascia lata for the treatment of intrinsic sphincter deficiency. J Urol 1997; 157:117 – 121.
37. Kreder KJ, Nygaard IE. Fascia lata sling cystourethropexy. J Urol 1995; 153:205A, abstract V-7.
38. Ghoniem GM. Bladder neck wrap: a modified fascial sling in treatment of incontinence in
myelomeningocele patients. Eur Urol 1994; 25:340 – 342.
39. McGuire EJ, Bennett CJ, Konnak JA, Sonda LP, Savastano JA. Experience with pubovaginal slings
for urinary incontinence at the University of Michigan. J Urol 1987; 138:525 – 526.
40. Rovner ES, Ginsberg DA, Raz S. A method for intrtoperative adjustment of sling tension: prevention
of outlet obstruction during vaginal wall sling. Urology 1997; 50:273 – 276.
41. Fianu S, Söderberg G. Absorbable polyglactin mesh for retropubic sling operations in female urinary
stress incontinence. Gynecol Obstet Invest 1983; 16:45 –50.
378 Kreder

42. Morgan JE, Heritz DM, Stewart FE, Connolly JC, Farow GA. The polypropylene pubovaginal
sling for the treatment of recurrent stress urinary incontinence. J Urol 1995; 154:1013 – 1014.
43. Errando C, Batista JE, Artano P. Polytetrafluorethylene sling for failure in female stress incontinence
surgery. Worl J Urol 1996; 14(suppl 1):S48– S50.
44. Norris JP, Breslin DS, Staskin DR. Use of synthetic material in sling surgery: a minimally invasive
approach. J Endourol 1996; 10:227– 230.
45. Ghoniem GM, Shaaban A. Suburethral slings for treatment of stress urinary incontinence. Int
Urogynecol J 1994; 5:228– 239.
46. Bent AE, Ostergard DR, Zwick-Zafutto M. Tissue reaction to expanded polytetrafluorethylene
suburethral sling for urinary incontinence: clinical and histologic study. Am J Obstet Gynecol 1993;
169:1189– 1204.
47. Weinberger MW, Ostergard DR. Long-term clinical and urodynamic evaluation of the poly-
tetrafluorethylene suburethral sling for treatment of genuine stress incontinence. Obstet Gynecol
1995; 86:92– 96.
48. Weinberger MW, Ostergard DR. Postoperative catheterization, urinary retention, and permanent
voiding dysfunction after polytetrafluorethylene suburethral sling placement. Obstet Gynecol 1996;
87:50– 54.
49. Labasky RF, Soper T. Reduction of patient morbidity and cost using frozen cadaveric fascia lata
for the pubovaginal sling. J Urol 1997; 157:459, abstract 1794.
50. Ridley JH. Appraisal of the Goebell-Frangenheim-Stoeckel sling procedure. Am J Obstet Gynecol
1966; 95:714 –721.
51. Carbone JM. Pubovaginal sling using cadaveric fascia and bone anchors: disappointing early results.
J Urol 2001; 165:1605– 1611.
52. Amundsen CL. Outcome in 104 pubovaginal slings using freeze-dried allograft fascia lata from a
single tissue bank. Urology 2000; 56(suppl 6A):2 –8.
53. Fitzgerald MP, Mollenhauer J, Bitterman P, Brubaker L. Functional failure of fascia lata allografts.
Am J Obstet Gynecol 1999; 181:1339 – 1346.
54. Singla AK. The use of cadaveric fascia in the treatment of stress urinary incontinence in women.
BJU Int 2000; 85:264 – 269.
55. Low JA. Management of severe anatomic deficiencies of urethral sphincter function by a combined
procedure with a fascia lata sling. Am J Obstet Gynecol 1969; 105:149 – 155.
56. Addison WA, Haygood V, Parker RT. Recurrent stress urinary incontinence. Obstet Gynecol Annu
1985; 14:254 –265.
57. Ogundipe A, Rosenzweig BA, Karram MM, Blumenfeld D, Bhatia NN. Modified suburethral sling
procedure for treatment of recurrent or severe stress urinary incontinence. Surg Gynecol Obstet
1992; 175:173 –176.
58. Karram MM, Bhatia NN. Patch procedure: modified transvaginal fascia lata sling for recurrent or
severe stress urinary incontinence. Obstet Gynecol 1990; 75:461– 463.
59. Handa VL, Jensen JK, Germain MM, Ostergard DR. Banked human fascia lata for the suburethral
sling procedure: a preliminary report. Obstet Gynecol 1996; 88:1045– 1049.
60. Carr LK, Webster GD. Voiding dysfunction following incontinence surgery: diagnosis and treat-
ment with retropubic or vaginal urethrolysis. J Urol 1997; 157:821 – 823.
61. Ghoneim GM, Elgamasy A-N. Simplified surgical approach to bladder outlet obstruction following
pubovaginal sling. J Urol 1995; 154:181 – 183.
62. Raz S. Atlas of Transvaginal Surgery. Philadelphia: W.B. Saunders, 1992.
63. Brodak PP, Juma S, Raz S. Levator hernia. J Urol 1992; 148:872 – 873.
64. Griebling TL, Berman CJ, Krader KJ. Fascia lata sling cyfousethropexy for the management of
female urinary incontinence. Int Urogynecol 1998; 9:165– 173.
25
The In Situ Anterior Vaginal Wall Sling

Howard B. Goldman
University Hospitals of Cleveland, CASE School of Medicine, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

Over the past decade the surgical treatment of woman with stress urinary incontinence has
undergone tremendous evolution. A number of studies evaluating urologists’ practice patterns
have demonstrated a clear shift from bladder neck suspensions, either retropubic or transvaginal,
to slings (1,2). While much of this may be due to a better understanding of the mechanisms of
stress urinary incontinence (SUI), in all likelihood the development of “minimally invasive”
sling procedures with less patient morbidity and which are easier for surgeons to perform has
significantly contributed to this shift in preferences as well.
Initially, autologous fascia, either rectus fascia or fascia lata, was the most common
material used for pubovaginal slings. It remains the gold standard. In an effort to reduce the
morbidity and discomfort associated with fascial harvest, other materials have been used for
sling formation. Synthetic materials offer ease of availability, but they may have a higher rate of
infection and erosion, and they can be costly. Cadaveric and other biologic tissues are easily
obtainable, but they too can be costly, have at least a theoretic risk of transmission of infection,
and may not offer comparable uniform strength and durability. On the other hand, the in situ
anterior vaginal wall sling (AVWS) avoids the morbidity of autologous fascial harvest, does not
have an increased rate of infection or erosion, is available at no cost, and avoids any risk of
infectious disease transmission.
Raz first introduced the AVWS in 1989 (3). This technique uses in situ vaginal wall over
the bladder neck and proximal urethra as the sling material, thus making fascial harvest
unnecessary. Various modification of Raz’s original technique have been introduced, but the
concept of an in situ patch of tissue functioning as a backboard beneath the bladder neck and
proximal urethra remains the same.

II. PATIENT SELECTION

Most women with documented SUI are candidates for an AVWS. However, patients with a
history of prior vaginal surgery who have significant scarring of the anterior vaginal wall may
not be suitable. In addition, postmenopausal women with very thin or significantly irritated
vaginal skin may not be ideal candidates for an AVWS. In these cases a 6- to 8-week course of
379
380 Goldman

hormone replacement via vaginal cream may restore some of the suppleness of the vaginal wall.
Other women with severe vaginal stenosis either secondary to previous surgery or postmeno-
pausal changes may not be best served with an AVWS.
Furthermore, women with significant intrinsic sphincteric deficiency may not be ideal
candidate for an AVWS. A number of studies that reviewed outcomes in women after an AVWS
showed a trend toward higher failure rates in those patients with lower Valsalva leak-point
pressures (VLPP). Studies by Raz, Litwiller, Su, and Goldman note this and based on these
findings women with a VLPP ,50 cm H2O may do better with a fascial or other type of sling
(3 – 6).

III. SURGICAL TECHNIQUE

After appropriate anesthesia has been achieved, the patient is placed in a modified
dorsolithotomy position, the hair over the pubic bone is shaved, and the vagina and lower
abdomen are prepped and draped in the usual fashion. A single dose of a broad-spectrum
intravenous antibiotic is administered. Labial retraction sutures, a weighted vaginal speculum,
and a Foley catheter are placed.
The bladder neck is identified by placing gentle traction on the Foley catheter and
palpating the Foley balloon through the vaginal wall. A “Block A” is marked on the anterior
vaginal wall (AVW), with the top of the “A” at a point halfway between the bladder neck and the
urethral meatus and the proximal transverse marking of the “A” just proximal to the bladder
neck. The legs of the “A” connect both transverse markings laterally and continue proximally
along the anterior vaginal wall for a distance just greater than the distance between the two
transverse markings.
Using a No. 15 blade on a long-handled scalpel, incisions are made along the markings.
(Some find that infiltration of saline or lidocaine with epinephrine into the AVW facilitates
dissection.) It is easiest to start at the proximal AVW along one leg of the “A” and incise to the
midpoint of the top of the “A” and then repeat that incision on the other side. Then the transverse
incision near the bladder neck can be made. The box between the transverse incisions will
become the sling, while the area between the legs of the “A” will become a flap of AVW that will
cover the sling. Of note, some surgeons incise only around the sling (not forming a flap) or just
make the lateral sling incisions and do not cover the sling with a flap of AVW.
At this point, the vaginal skin between the legs of the “A” is dissected from the underlying
pubocervical fascia but left attached proximally (Fig. 1). The rectangle of skin that will be used
as the sling is freed distally and laterally from any attachments but left completely in situ. Using
first sharp and then blunt dissection, the lateral spaces are opened along the periurethral fascia
until the underside of the pubis is easily palpated. (Some prefer to continue the dissection further
and perforate the endopelvic fascia.)
A 3-cm transverse incision is made one fingerbreadth above the pubis. A Stamey needle is
passed from each lateral edge of the incision through the rectus fascia and under finger guidance
into the vagina. Cystoscopy is performed to ensure no bladder perforation. If perforation is
noted, the needle is removed and replaced. A No. 1 polypropylene suture is passed in a
horizontal mattress configuration incorporating the pubocervical fascia and vaginal wall through
each lateral edge of the sling. (Helical or other types of suture attachment through the sling edges
can be done instead.) Both ends of each suture are passed through the corresponding Stamey eye
and brought up to a prepubic position (Fig. 2). The previously formed flap is advanced over
the sling and the vaginal wall is closed with a running, locking 2-0 polyglactin suture (Fig. 3).
The weighted vaginal speculum is removed. (Some prefer to place transvaginal bone anchors
 Anterior Vaginal Wall Sling 381

Figure 1 Incisions of “Block A” and preparations of flap. (Courtesy of R.A. Appell.)

and sutures transvaginally, thus avoiding the prepubic incision. Long-term success rates of this
modification are unknown.)
At this point, the prepubic sutures can be stabilized or tied according to the surgeon’s
preference. One technique is to pass one end of each set of sutures through periosteum or rectus
fascia with a Mayo needle and then loosely tie the two ends of the suture together on each side.
Others prefer to tie both sets of suture ends across the midline in one large knot. Still others use
bone anchors or have another system for tying the sutures down with the appropriate minimal
tension.
Scarpa’s fascia is approximated with a 3-0 chromic suture, and the skin is closed with a
running 4-0 polyglactin subcuticular suture. Steri-Strips and a dressing are applied to the
prepubic wound and a vaginal packing impregnated with either hormonal cream or antibiotic
ointment is placed. The labial retraction sutures are removed and the procedure is completed.
(For bladder drainage, a urethral or suprapubic catheter can be left in place for a few days or
the patient can be given an opportunity to void postoperatively. If she cannot, intermittent
catheterization can be instituted.)
Patients are discharged on oral analgesics and instructed to avoid heavy lifting or
strenuous activity for 4 – 6 weeks.
382 Goldman

Figure 2 Placement of sutures through the anterior vaginal wall sling. (Courtesy of R.A. Appell.)

IV. RESULTS

The reported success rates for the AVWS range from a high of 100% to a low of 61% (subjective
cure) (7,5). The majority of authors report success in 70 –95% of patients (Table 1). Some of the
differences in the reported outcomes may be due to variations in the definition of success.
There are three studies of note that have a documented average follow-up longer than 2
years. Litwiller et al. reported on a series of 42 evaluable patients followed for an average of 31
months. They noted resolution of SUI in 71% (4). Lobel and Sand reported an 80% success rate
in a series of 90 patients followed for an average of 26 months (8). The largest series, which

Figure 3 Closure of the anterior vaginal wall flap over the sling. (Courtesy of R.A. Appell.)
 Anterior Vaginal Wall Sling 383

Table 1 Reports of Efficacy of AVWS

No. of patients Percent with Length of follow-up

Author with follow-up prior procedure (months) Successful outcome

Raz (3) 26 100 10 – 28 85% (excellent 77%, very

good 8%)
Juma (11) 54 89 23.9 94.4% (excellent 90.7,
very good 3.7%)
Couillard (7) 18 100 18 100% (all dry)
Pidutti (12) 12 100 17.3 92% (excellent 67%,
improved 25%)
Lessans (13) 29 25 7 82% (dry 41%, improved
41%)
Raz (10) 160 54 1 93% (SUI resolved)
Kaplan (9) 36 100 ? (likely 16) 97% (SUI resolved)
Liwiller (4) 42 72 31 71% (SUI resolved) (92%
in those with
LPP . 60)
Lobel (8) 90 33 26 80% (70% complete or
almost complete cure;
10% somewhat
improved)
Masoudi (14) 23 17 13 85% (SUI cured or
improved)
Cummings 16 ? 8.1 88% (75% dry; 13%
(15) improved but using
pads)
Su (5) 23 100 15 60.9% (subjective cure)
34.8% (objective cure)
Kaplan (9) 335 ? 39.8 96% (SUI resolved)
Goldman (6) 39 51 19 79.5% (SUI resolved)
(93% in those with
VLPP . 50)

consisted of a combination of patients treated at three different centers, was reported by Kaplan
et al. (9), who noted a 96% success rate in a group of 373 patients followed for an average of 40
months. Importantly, the success rate for patients with follow-up exceeding 5 years was 94%. It
should be noted that Raz et al. (10), in another large study of 160 patients followed for an average of
only 17 months, reported a 93% success rate, which is similar to the result of Kaplan et al.
Various authors evaluated possible patient factors that may predict a successful outcome.
Goldman et al. noted an overall 80% success rate (6). However, they noted that the majority of
their failures were in those with lower Valsalva leak-point pressures (VLPP). After using
receiver operator characteristic curves to identify a VLPP that predicted a successful outcome,
they found that those with a VLPP of 50 cmH2O or higher had a success rate of 93%, whereas
those with a VLPP less than 50 cmH2O had a success rate of 40% (4). Similarly, Litwiller et al.
noted a success rate of 92% in their patients with isolated hypermobility, whereas those with
pure ISD and a mixed problem had success rates of 72% and 62%, respectively. In addition,
Su et al.(5) found that patients with an objective cure had higher maximal urethral closure
pressures than those who failed. Finally, Raz et al. noted a trend toward late recurrence of stress
384 Goldman

incontinence in their group of patients with intrinsic sphincter deficiency (ISD) (10). Thus, a
number of reports support the concept that patients with a lower VLPP (VLPP ,50 cmH2O per
Goldman et al.) and more significant ISD have a worse outcome than those with a higher VLPP.
In contrast, Kaplan et al. found no difference in outcome between patients with ISD (VLPP
,60 cmH2O) and those with anatomic incontinence (VLPP . 60 cmH2O) (9). Their findings
are clearly different from those of the aforementioned groups, and this difference is difficult to
explain.

V. COMPLICATIONS

Significant intraoperative hemorrhage is rare, and its rate of occurrence is similar to that seen in
other sling procedures. Infection, usually a urinary tract infection or a prepubic or suprapubic
wound infection, occurs in ,5% of patients. Rare cases of inclusion cyst formation in the buried
piece of AVW have been reported (16). Delayed spontaneous voiding or chronic retention
occurs in ,5%, whereas de novo detrusor instability and/or obstructive voiding complaints may
occur in as many as 15% of cases. Urethrolysis may be necessary on occasion. Significant
failure—persistent SUI—occurs in 5– 25% of patients.

VI. CONCLUSIONS

The in situ AVWS is a technically straightforward, minimally invasive procedure for treatment
of female SUI. It minimizes patient morbidity and avoids some of the potential problems
associated with use of synthetic or biologic materials. Reported success rates range from 70% to
95%, with the largest series reporting successful outcomes in .90% of patients. Some authors
report that success rates are lower in patients with lower VLPP values, but not all studies support
that concept.

REFERENCES

1. Kim HL, Gerber GS, Patel RV, Hollowell CM, Bales GT. Practice patterns in the treatment of female
urinary incontinence. A postal and internet survey. Urology 2001; 57:45.
2. Leach GE, Dmochowski RR, Appell RA, Blaivas JG, Hadley HR, Luber KM, Mostwin JL, O’Donnell
PD, Roehrborn CG. Female stress urinary incontinence clinical guidelines panel summary report on
surgical management of female stress urinary incontinence. J Urol 1997; 158:875.
3. Raz S, Siegel AL, Short JL, Synder JA. Vaginal wall sling. J Urol 1989; 141:43.
4. Litwiller SE, Nelson RS, Fone PD, Kim KB, Stone AR. Vaginal wall sling: long-term outcome
analysis of factors contributing to patient satisfaction and surgical success. J Urol 1977; 157:1279.
5. Su T, Huang J, Wang Y, Yang J, Wei H, Huang C. Is modified in-situ vaginal wall sling operation the
treatment of choice for recurrent genuine stress incontinence? J Urol 1999; 162:2073.
6. Goldman HB, Rackley RR, Appell RA. The in situ anterior vaginal wall sling: predictors of success.
J Urol 2001; 166:2559.
7. Couillard DR, Deckard-Janatpour KA, Stone AR. The vaginal wall sling: a compressive suspension
procedure for recurrent incontinence in elderly patients. Urology 1994; 43:203.
8. Lobel RW, Sand PK. Long-term results of vaginal wall suburethral sling. J Urol 1997; 157:459A.
9. Kaplan SA, Te AE, Young GPH Andrade A, Cabelin MA, Ikeguchi EF. Prospective analysis of 373
consecutive women with stress urinary incontinence treated with a vaginal wall sling: The
Columbia– Cornell University experience. J Urol 2000; 164:1623.
 Anterior Vaginal Wall Sling 385

10. Raz S, Stothers L, Young GPH, Short J, Marks B, Chopra A, Wahle GR. Vaginal wall sling for
anatomical incontinence and intrinsic sphincter dysfunction: efficacy and outcome analysis. J Urol
1996; 156:166.
11. Juma S, Little NA, Raz S. Vaginal wall sling: four years later. Urology 1992; 39:424.
12. Piduitti RW, George SW, Morales A. Correction of recurrent stress urinary incontinence by needle
urethropexy with a vaginal wall sling. Br J Urol 1994; 73:418.
13. Lessans KD, Gordon DA, Despradel V, Witmore KE. Modified vaginal wall sling with pubic bone
anchors for the treatment of stress urinary incontinence. J Urol 1996; 155:699A.
14. Masoudi JF, Whitmore KE, Gordon DA, Lessans KD, Campion MJ. Modified vaginal wall sling with
bone anchors for the treatment of urinary incontinence and cystocele. J Urol 1997; 157:460A.
15. Cummings JM, Parra RO, Boulher JA. Comparison of vaginal wall sling with pubovaginal sling for
stress incontinence from intrinsic sphincteric deficiency. J Urol 1997; 157:461A.
16. Woodham PJ, Davis GD. The relationship of the in situ anterior vaginal wall sling to a vaginal
epithelial cyst. Int Urogynecol J Pelvic Floor Dysfunct 2000; 11:124.
26
CATS: Cadaveric Transvaginal Sling

Dawn M. Bodell
Tower Urology Institute for Continence, Los Angeles, California, U.S.A.
Gary E. Leach
Tower Urology Institute for Continence, Los Angeles, California, U.S.A.

I. INTRODUCTION

Pubovaginal/transvaginal slings have become the gold standard for the treatment of all types of
female stress urinary incontinence, whether the stress urinary incontinence (SUI) is secondary to
intrinsic sphincter deficiency (ISD) or hypermobility of the urethra (1). The author’s sling
procedure of choice is the cadaveric transvaginal sling procedure (CATS).

II. INDICATIONS AND PATIENT SELECTION

A successful sling procedure requires an appropriate preoperative evaluation, starting with the
history and physical exam. The key components of the history should include the impact the
incontinence has on the patient’s quality of life. The SEAPI incontinence score facilitates a
subjective assessment of the patient’s symptoms (Appendix A). The physical examination
should document urethral hypermobility or a fixed urethra and provide documentation of pelvic
relaxation. Patients with pelvic prolapse should have the prolapse repaired simultaneously with
the sling procedure (2). Patients with stress urinary incontinence and a fixed or extremely
elevated urethra should also have urethrolysis performed in order to release the urethra from
the surrounding scar tissue and fixation, and thus allow the sling to apply adequate urethral
compression (3). Prior to performing a sling procedure, a urodynamic evaluation should be
completed to confirm stress urinary incontinence, exclude detrusor instability at low bladder
volumes, and evaluate the patient’s ability to empty the bladder.

III. FASCIA

The choices of fascia for the sling can be autologous or allograft fascia. Cadaveric fascia has
become a more popular choice of material than autologous material for a multitude of reason,
including shortening of operative time and hospital stay, while decreasing postoperative pain
and shortening the recuperation period.
387
388 Bodell and Leach

Tutoplast, produced by Mentor Corporation, is a solvent-dehydrated, gamma-irradiated

fascia, which is our fascia of choice. The Tutoplast processing includes a five-step process:

1. Screening: The U.S. Food and Drug Administration serologically screens donor
candidates and the fascia. The fascia is inspected for cleanliness, quality, structure,
and size. Donor tissue will be rejected if there is an adverse medical or social history
that might be suspicious for any infectious disease or malignancy.
2. Processing: The fascia is cleaned in a saline solution and then osmotically treated.
This treatment destroys any bacteria or viruses.
3. Denaturization: NaOH and H2O2 treatment inactivates any prions, destroys any
remaining viruses, and removes all antigens. Exposure time to NaOH is limited in this
step to avoid any significant weakening of the collagen.
4. Preservation: Water is extracted from the tissues via organic solvents, to preserve
the dense collagenous fiber structure.
5. Gamma irradiation: The fascia is cut to the appropriate size and treated with gamma
irradiation to sterilize the tissue. The amount of radiation is limited to ,2.5 Mrad, to
limit weakening of the fascia.

Testing of the solvent-dehydrated fascia revealed significantly higher stiffness, higher

maximum load to failure, and higher maximum load per unit width of graft with the solvent-
dehydrated fascia (4). Boone reviewed 26 stress urinary incontinent patients who underwent
a pubovaginal sling with cadaveric fascia lata (Tutoplast), with a minimum follow-up of
12 months (5). The outcome results reported 25 of 26 (96%) patients to be “significantly”
improved postoperatively. Twenty-four of 26 (92%) of the patients wore no more than one pad
daily, and 77% of the patients were completely dry. Only two patients required more than one
pad: one of the patients went from four pads to two pads. Two patients experienced de novo
urgency, which was controlled with anticholinergics. No patient underwent a second operation.
This study supports the longer-term sling results obtained with solvent dehydrated cadaveric
fascia lata.
Conversely, Raz et al. performed 154 consecutive bone-anchored cadaveric fascia
pubovaginal slings with a follow-up of 10.6 months (6). The type of fascia used in theses cases
was freez-dried fascia from a California tissue bank. Of the 154 patients, 58 (37.6%) had
recurrent incontinence (grades 2 –3), with 26 (16.9%) patients having undergone a second
pubovaginal sling procedure. Average time to reoperation was 9 months. Attenuated, frag-
mented, or absent fascia was noted at the time of reoperation. This study demonstrated that all
cadaveric fascia is not “created equally.” Lemer et al. (7) compared autologous rectus fascia,
dermal graft, solvent-dehydrated cadaveric fascia lata, and freeze-dried cadaveric fascia lata.
The cadaveric freeze-dried fascia lata had the weakest tensile strength of all the tissues studied.
Also, the freeze-dried cadaveric fascia had the most inconsistencies in the tissues among the
other fascias compared. Solvent-dehydrated cadaveric fascia and dermal grafts were identical
to native autologous rectus fascia with regard to tensile strength and tissue stiffness. Thus, the
use of the tissue bank “frozen” fascia was a significant factor accounting for the poor sling
results obtained by Raz. Also, the authors avoid the use of synthetic sling materials because
allograft fascia has a significantly lower infection and erosion rate, when compared to synthetic
materials (8 – 11).
In conclusion, the choice of the appropriate sling material is extremely important. For the
transvaginal sling procedure, the authors use the 2  7 cm strip of cadaveric solvent dehydrated
allograft fascia lata.
 Cadaveric Transvaginal Sling 389

IV. BONE ANCHORS

In 1949, the Marshall-Marchetti-Krantz vesicourethropexy was one of the first procedures to

use bone fixation as part of a suspension procedure for the correction of female stress urinary
incontinence (12). In 1988, Leach described a suprapubic bone fixation technique for needle
suspension procedures (13). This technique fixed the suspension sutures directly into the pubic
tubercle, utilizing a strong Mayo needle, as opposed to securing the suspension suture to the rectus
fascia. This bone fixation technique alleviated the complication of ilioinguinal nerve entrapment
caused by the sutures being placed laterally in the rectus fascia, thereby decreasing postoperative
pain from nerve entrapment. Benderev developed his modification of needle suspension using bone
anchors with the Vesica procedure (14). Nativ further modified the placement of bone anchors by
using an entirely transvaginal approach to complete the cystourethropexy which was further
developed into a sling procedure (15). The technique employed a drill and transvaginal bone anchor
system. This entirely transvaginal technique revolutionized the sling procedure.
Advantages of this transvaginal bone anchor fixation include minimal postoperative pain
and bleeding. Since no needles or sutures are passed through the retropubic space, the risk of
bladder perforation is significantly decreased. Also, utilizing the author’s transvaginal sling
technique outlined below, the endopelvic fascia is not routinely perforated during the proce-
dure. Thus, it is possible that the risk for postoperative vaginal prolapse and recurrent stress
incontinence may be reduced when the endopelvic fascia remains intact (16).
There is also a decreased rate of bone infection with the transvaginal bone anchors when
compared to suprapubic anchor placement. Rackley et al. (17) found no pubic bone infections in
314 patients who had undergone a transvaginal sling with bone anchor placement compared to a
.86% osseous complication rate associated with suprapubic bone anchors. The reported rate of
osseous infections from a Marshall-Marchetti-Krantz retropubic urethropexy was .76%, with
an overall incidence of an infectious bone bone anchor complications in female pelvic
reconstructive procedures was found to be .6% (18).

V. SURGICAL TECHNIQUE
A. Preoperative Preparation
Prior to performing a sling procedure, the urine is confirmed to be sterile. Patients are taught how
to do self-catheterization preoperatively, or a suprapubic catheter may be placed at the time
of the procedure for those patients with documented incomplete bladder emptying and inability
to perform self-catheterization. A providone iodine vaginal douche is performed the night
before surgery. Perioperative antibiotics are given, preferably a first-generation cephalosporin,
ampicillin, or vancomycin (if a penicillin allergic), combined with an aminoglycoside. When
timing allows, patients with vaginal wall atrophy are instructed to use an estrogen vaginal cream
three times a week for 4 – 6 weeks preoperatively.

B. Operative Procedure
Patients are placed in the dorsal lithotomy position. A Foley catheter is inserted, and a Scott
retractor (Lonestar, Houston, TX) is secured to the medial buttocks with towel clamps. Palpation
of the foley balloon identifies the bladder neck. The anterior vaginal epithelium is injected with
plain saline and an inverted “U” shaped incision is made from the mid-urethra to the bladder
neck. (Fig. 1). The inverted “U” flap is mobilized to the bladder neck. Stopping the vaginal wall
flap dissection at the level of the bladder neck prevents the sling from migrating above the
390 Bodell and Leach

Figure 1 An inverted “U” incision is made in the anterior vaginal wall.

bladder neck. Sharp lateral dissection at the level of the bladder neck cleans off the undersurface
of the pubic bone for accurate placement of the bone anchors. As previously mentioned, the
endopelvic fascia is not routinely perforated, to minimize the chance of significant bleeding in
the space of Retzius and to maintain the integrity of the endopelvic fascia.
Prior to placing the bone anchors, suspension sutures and anchors need to be chosen. Two
types of bone anchors are available: an anchor with polypropolene (prolene) suture attached to
the bone screw, and a “loop”-type anchor through which a suture of the surgeon’s choice
can be placed (Fig. 2). The choice of suture depends on the patient. A suture is threaded through
the loop screw.
Once the pubic bone is cleared of tissue posteriorly, the transvaginal bone anchor is
placed. Before placing the anchor, the bladder is drained to minimize the risk of bladder
perforation. To avoid injury to the bladder or bladder neck during the bone anchor placement,
the backside of a forceps is used to retract the bladder medially away from the anchor placement
site. The drill is positioned on the underside of the pubic bone so that the anchor is flush with
the bone (Fig. 3). Once the drill is activated, a change in tone of the drill motor confirms that the
anchor is firmly placed into the bone. Once the anchor is seated, the drill is removed and
the attached suture is vigorously pulled upon to confirm secure anchor placement. This same
bone anchor insertion process is completed on the contralateral side.
A 2  7 cm piece of Tutoplast fascia is soaked in antibiotic solution. The edge of the
fascia is folded over to minimize the risk of suture “pull-through” by cross-hatching the fascial
fibers (Fig. 4). An 18-gauge needle facilitates atraumatic passage of the suture through the
overlapping end of the sling (Fig. 5). The bladder neck suture is placed more medially through
fascia than the distal suture, to keep the fascial strip tight against the bladder neck. Once both
 Cadaveric Transvaginal Sling 391

Figure 2 Drill and loop screw with suture attached to the screw.

ends of the suture attached to the bone anchor are brought through the end of the sling, the suture
is tied flush to the bone anchor. A 2-0 Vicryl suture secures the distal edge of the sling to the
periurethral tissues to prevent “rolling” of the sling toward the bladder neck. The correct suture
tension, while tying the sling in place, is determined by folding over the fascial strip and placing
an Allis clamp on the folded portion of the fascia and then stretching the fascia to the
contralateral bone anchor site (Fig. 6). Once the proper tension is determined, the suspension

Figure 3 The bone anchor drill is positioned on the underside of the pubic bone.
392 Bodell and Leach

Figure 4 The edge of the fascial sling is folded over to minimize the risk of suture “pull through.”

sutures are passed through the free end of the sling in the same fashion as the other side. The
sutures are tied snugly (without any clamp between the urethra and the sling), to create a well
supportive “backstop” for the urethra. To eliminate the stress incontinence, it is critical that the
sling not be tied too loosely.
A 2-0 Vicryl suture secures the distal edge of the sling to the periurethral tissue.
Cystoscopy with a 308 lens confirms the absence of bladder or urethral injury from the bone
anchor placement. Antibiotic solution is used to irrigate the vaginal incision throughout
the procedure. The Foley catheter is placed to drainage and the vaginal incision is closed with
a running 2-0 Vicryl suture. An antibiotic-soaked vaginal packing is placed.

Figure 5 The sutures attached to the bone anchor are placed atraumatically through the fascial strip with
the more proximal suture placed more medially.
 Cadaveric Transvaginal Sling 393

Figure 6 Folding over an adequate amount of the sling ensures proper sling tension.

C. Postoperative Care
The vaginal packing and Foley catheter are removed on the first postoperative day. Patients
are given a voiding trial and the postvoid residual urine volume is checked. When postvoid
residuals are .100 mL, patients are reinstructed in self-catheterization. When patients have a
suprapubic catheter (SPT), postvoid residuals can be checked via the SPT. Intravenous
antibiotics are discontinued on the first postoperative day, and patients are started on an oral
antibiotic (cephalosporin or a fluoroquinolone). Oral antibiotics are continued for 1 week to
minimize the risk of osteitis pubis or wound infection. Most patients have minimal post-
operative pain that is controlled with acetominophen. For 6 weeks, patients are instructed to
comply with complete pelvic rest (i.e., nothing in the vagina: no tampons or intercourse) and
to avoid heavy lifting.

VI. RESULTS
A. The AUA Guidelines Panel
The American Urological Association Guidelines Panel did an in depth data analysis, reviewing
over 5000 articles, related to the surgical treatment of female stress urinary incontinence.
Practice recommendations were formulated based on reported surgical outcomes obtained with
the different types of anti-incontinence procedures. The panel compared four general groupings
of procedures: transvaginal suspensions, anterior repairs, retropubic suspensions, and slings.
“Cure/dry” rate and “cure/improved” rates were tabulated with this meta-analysis with 3
follow-up periods: 12 – 23 months, 24 – 47 months, and 48 months or longer. There was no
statistical difference in outcomes within each group of procedures at any time interval. Among
394 Bodell and Leach

the different anti-incontinence procedures, there was a statistical difference in outcomes only at a
follow-up period of .48 months.
Slings and retropubic suspensions had the best long-term success rate of 83% and 84%,
respectively. The panel concluded that the most effective surgical procedures (at .48-month
follow up) were obtained with slings and retropubic suspensions (Fig. 7).
The panel also examined complication rates for synthetic slings. Based on the literature
reviewed, synthetic slings had a higher erosion and infection rate than the “nonsynthetic” slings.
The risk of vaginal erosion for synthetic slings was .7%, compared to .01% for autologous slings.
The risk of urethral erosion with synthetic slings was 2%, compared to only .3% with autologous
slings (Table 1).
A more global assessment of the “success rates” should also include patient satisfaction
and a patient generated confidential questionnaire. Sirls et al. did an outcome analysis of 151
patients, with a 25-month follow up, who had undergone a modified Pereyra bladder neck
suspension (19). The study consisted of a retrospective chart review and a simultaneous,
confidential patient questionnaire, which was reviewed by a second party. The confidential
questionnaire results revealed a cure in 47% of the patients and improvement of SUI in 65% of
the patients. In contrast, the results with the simultaneous retrospective chart review revealed a
cure in 72% of the patients and 89% of the patients were improved. Sirls concluded that the way
postoperative data was obtained greatly impacted outcome results. Although the surgical results
are significantly less “optimistic” with subjective questionnaires than with chart review, clearly,
subjective questionnaires most accurately assess patient satisfaction and surgical outcomes.
Thus, the authors have evaluated their transvaginal sling results utilizing a confidential
questionnaire completed by the patients and reviewed by an independent party at 6-month
intervals following the sling procedure.
Since there are no standardized definitions for surgical outcomes following anti-
incontinence surgery, Groutz et al. (20) conducted a study to develop an outcome instrument
incorporating multiple noninvasive outcome measures including a 24-h voiding diary, a 24-h
pad test, uroflowmetry, postvoid residual urine, and a postoperative patient questionnaire (20).
Ninety-four pubovaginal sling patients were studied, with a minimum follow-up of 1 year (mean
3.4 years). The outcome data were formulated into an incontinence score, which is the sum of

Figure 7 AUA outcomes data of 4 categories surgical procedures at .48 months follow-up. (# 1994,
1995, 1996, 1997 American Urological Association, Inc. All rights reserved.)
 Cadaveric Transvaginal Sling 395

Table 1 Comparative Complication Rates for Sling Materials

Autologous materials Homologous materials Synthetic materials

Complications (1715 pts) (414 pts) (1515 pts)

Vaginal erosion 1 pt (0.0001) 0 10 pts (0.0007)

Urethral erosion 5 pts (0.003) 0 27 pts (0.02)
Fistula 6 pts (0.0003) 0 4 pts (0.002)
Wound sinus 3 pts (0.0002) 0 11 pts (0.007)
Wound infection 11 pts (0.006) 9 pts (0.02) 15 pts (0.009)
Seroma 6 pts (0.003) 0 1 pt (0.0007)

three categories: a 24-h voiding diary, 24-h pad test, and a patient questionnaire (Appendix B).
Cure is classified as a score of 0 and failure as a score of 6. With this new response score, only
47% were defined as totally cured (zero score following the sling). These results more accurately
represent realistic outcomes following the sling procedure.

B. Cadaveric Transvaginal Sling (CATS) Results

The CATS procedure has been performed on 229 patients with 186 patients followed for more than
1 year. The age range was from 23 to 90 years (mean 63 years). Patients are followed closely with
follow-up visits and confidential questionnaires competed every 6 months after the sling to obtain
accurate long-term outcome data. The longest follow-up has been 43 months with a mean follow up
of 21.2 months. On the confidential questionnaire, 50/186 (27%) of the patients reported 100%
improvement, 105/186 (54%) were .80% improved, and 118 (69%) were .50% improved.
Persistent urgency was noted in 32 (17%), and de novo urgency in 20 (11%). Mean SEAPI scores
were 6.2 preoperatively and 2.4 postoperatively, representing a significant decrease (P , .0001).
Overall, 109/186 (56%) of patients were .80% satisfied with the procedure on a visual analog
scale (with a mean satisfaction score of 67%), and 69% would recommend the surgery to a friend.
Fifty-eight (31%) reported ,50% improvement. Of these, 18 (9.7%) had stress urinary
incontinence, 23 (12.3%) had mixed incontinence, five (2.7%) had urge incontinence, and four
(2.1%) patients were not clear regarding the cause of their dissatisfaction. Eight of 58 (35%)
patients had no incontinence but based their dissatisfaction on urinary urgency. Few late failures at
.1 year were reported (6/58; 10.3%). The majority of failures (40/58; 65%) experienced recurrent
incontinence within 3 months following surgery. No unexpected postoperative urinary retention
occurred. Complications included osteitis pubis (without osteomyelitis), managed in two patients
with nonsteroidal medication, and wound separation in three patients, which healed secondarily.

VII. CONCLUSIONS

The AUA guidelines panel recommendations support the use of the sling as a first-line treatment
for female stress urinary incontinence. Patient selection and appropriate preoperative evaluation
are critical to the success of the sling procedure. Utilizing nonfrozen cadaveric fascia lata
(Tutoplast) obviates the need for tissue harvesting and decreases postoperative pain. Also, the
complications associated with the use of synthetic sling materials are avoided. Results with the
transvaginal sling, incorporating the use of transvaginal bone anchors and Tutoplast cadaveric
fascia, are encouraging.
396 Bodell and Leach

REFERENCES

1. Leach GE, Dmochowski RR, Appell RA. Female stress urinary incontinence clinical guidelines panel
summary report on surgical management of female stress urinary incontinence. J Urol 1997;
158:875– 880.
2. Kobashi KC, Mee SL, Leach GE. A new technique for cystocele repair and transvaginal sling: the
cadaveric prolapse repair and sling (CaPs). Urology 2000; 56:9– 14.
3. Leach GE. Urethrolysis. Urole Clin North Am 1994; 2:23 – 27.
4. 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 1992; 20(5):
607– 612.
5. Elliot DS, Boone TB. Is fascia lata allograft material trustworthy for pubovaginal sling repair?
Urology 2000; 56:772 – 776.
6. Carbone JM, Kavaler E, Raz S. Pubovaginal sling using cadaveric fascia and bone anchors:
disappointing early results. J Urol 2001; 165:1605 – 1611.
7. Lemer ML, Chaikin DC, Blaivas JG. Tissue strength analysis of autologous and cadaveric allografts
for the pubovaginal sling. Neurourol Urodyn 1999; 18:497 – 503.
8. Bent AE, Ostergard DR, Zwick-Zaffuto M. Tissue reaction to expanded polytetrafluoroethylene
suburethral sling for urinary incontinence: clinical and histology study. Am J Obstet Gynecol 1993;
169:1198– 1207.
9. Choe JM, Kothandapani R, James L. Autologous, cadaveric, and synthetic materials used in sling
surgery: comparative biomechanical analysis. Urology 2001; 58:482 – 486.
10. Leach GE, Kobashi KC, Mee SL. Erosion of woven polyester synthetic (ProteGen) pubovaginal sling.
J Urol 1999; 161:106.
11. Duckett JR, Constantine G. Complications of silicone sling insertion for stress urinary incontinence.
J Urol 2000; 163:1835– 1837.
12. Marshall VF, Marchetti AA, Krantz DE. The correction of stress incontinence by simple vesico-
urethral suspension. Surg Gynecol Obstet 1949; 88:509.
13. Leach GE. Bone fixation technique for transvaginal needle suspension. Urology 1988; 31:388– 390.
14. Benderev T. Anchor fixation and other modifications of endoscopic bladder neck suspension. Urology
1992; 40:409 –418.
15. Nativ O, Levine S, Madjar S. Incisionless per vaginal bone anchor cystourethropexy for the treatment
of female stress incontinence: experience with the first 50 patients. J Urol 1997; 158:1742 – 1744.
16. Kohle N, Sze EHM, Roat TW. Incidence of recurrent cystocele after transvaginal needle suspension
procedures with and without concomitant anterior colporrhaphy. Am J Obstet Gynecol 1996;
175:1476– 1480.
17. Rackley RR, Abdelmalak JB, Madjar S. Bone anchor infections in female pelvic reconstructive
procedures: a literature review of series and case reports. J Urol 2001; 165:1975– 1978.
18. Kammerer-Doak DN, Cornella JL, Magrina JF. Osteitis pubis after Marshll-Marchetti-Krantz
urethropexy: a pubic osteomyelitis. Am J Obstet Gynecol 1998; 179:586.
19. Sirls LT, Keoleian CM, Korman HJ, Kirkemo AK. The effect of study methodology on reported
success rates of the modified Pereyra bladder neck suspension. J Urol 1995; 154:1732 – 1735.
20. Groutz A, Blaivas JG, Rosenthal VE. A simplified urinary incontinence score for the evaluation of
treatment outcomes. Neurourol Urodyn 2000; 19:127– 135.
 Cadaveric Transvaginal Sling 397

Appendix A SEAPI Incontinence Score (Subjective)

S Stress related 0 ¼ no urine loss

1 ¼ loss with strenuous activity
2 ¼ loss with moderate activity
3 ¼ loss with minimal activity, or gravitational incontinence
E Empting ability 0 ¼ no obstructive symptoms
1 ¼ minimal symptoms
2 ¼ significant symptoms
3 ¼ voiding only in dribbles, or urinary retention
A Anatomy 0 ¼ no descent during strain
1 ¼ descent, not to introitus
2 ¼ descent though introitus with strain
3 ¼ Through introitus without strain
P Protection 0 ¼ never used
1 ¼ used only for certain occasions
2 ¼ used daily for occasional accidents
3 ¼ used continually for frequent accidents or constant leaking
I Inhibition 0 ¼ no urgency incontinence
1 ¼ rare urgency incontinence
2 ¼ urgency incontinence once a week
3 ¼ urgency incontinence at least once a day

Source: Ref. 1.

Appendix B Groutz and Blaivas Response Score for

Assessment of Surgical Outcomes of Anti-Incontinence
Procedures

1. 24-h voiding diary

a. No urinary incontinence (urge or stress) episodes: 0 points
b. 1 –2 incontinence episodes: 1 point
c. 3 incontinence episodes: 2 points
2. 24-h pad test
a. Total weight gain of the pads 8 g: 0 points
b. Total weight gain of the pads 9 – 20 g: 1 point
c. Total weight gain of the pads .20 g: 2 points
3. Patient questionnaire
a. Patient considers herself as cured: 0 points
b. Patient considers herself as improved: 1 point
c. Patient considers the operation to have failed: 2 points
The response scores the sum of the above subscores and is classified as:
Cure: total score 0
Good response: total score 1 – 2
Fair response: total score 3 – 4
Poor response: total score 5
Failure: total score 6

Source: Ref. 20.

27
Tension-Free Vaginal Tape: An Innovative,
Minimally Invasive Pubovaginal Sling
for Female Stress Urinary
Incontinence
Vincent R. Lucente*
Pennsylvania State University, College of Medicine, Hersey, Pennsylvania, U.S.A.

Marisa A. Mastropietro†
Lehigh Valley Hospital, Allentown, Pennsylvania, U.S.A.

I. INTRODUCTION

The first surgical approach for the treatment of female stress urinary incontinence (SUI)
was published in 1914 by Howard Kelly, describing his technique of urethral plication (1).
Since then, over 100 surgical procedures and various modifications have been described in
the literature. The fact that our knowledge of the functional anatomy of the urethra and the
physiology of the normal continence mechanism continues to evolve is no doubt interrelated
to why such a plethora of surgical procedures has been reported.
Despite the growing body of comparative studies, a systematic review of the literature in
1996 by Black and Downs could not determine the “best procedure” for surgical treatment of
female SUI based on scientific evidence (2). More recently, however, an expert clinical panel of
the American Urological Association concluded that retropubic suspensions and slings provide
the most effective long-term cure rate. The sling operation, however, was associated with
significant complications (3). The higher incidence of postoperative voiding dysfunction and the
potential for sling erosion is often cited as the rationale against sling procedures as the primary
surgery of choice for correcting female SUI (4). Improved techniques and new sling materials
have contributed to a gradual lowering of these complication rates (5,6). Another advantage of
sling procedures is that they are more effective in women with intrinsic sphincter deficiency
(ISD), which has been identified as a significant risk factor in reducing long-term surgical
success.
As with all other surgeries, the traditional sling procedure, despite its success to date, is
faced with today’s challenge, if not the defined trend of modern surgery, that is to be performed
less invasively with consistent results and fewer complications. In 1995 Ulmsten and Petros

*Current affiliation: Institute for Female Pelvic Medicine and Reconstructive Surgery, Allentown,
Pennsylvania, U.S.A.
†
Current affiliation: Lincoln Hospital, Bronx, New York, U.S.A.

399
400 Lucente and Mastropietro

responded to this challenge by introducing an innovative minimally invasive pubovaginal sling

procedure—the tension-free vaginal tape (TVT) (7).

II. HISTORICAL BACKGROUND

The TVT procedure was developed based on a theory regarding the urethral continence
mechanism postulated by Ulmsten. His hypothesis was a significant shift from widely held
previous views: Enhorning’s theory of abdominal pressure transmission, which required proper
elevation of the bladder neck into the abdominal pressure zone (8), and DeLancey’s theory of a
vaginal hammock providing active (muscular) and passive (connective tissue) support to the
urethra (9). Ulmsten’s theory is based on the concept that the urethral continence mechanism is
controlled by the interplay of three anatomical structures and their associated function: the
tension of the pubourethral ligaments, the muscular activity of the pubococcygeus and levator
ani, and the condition of the suburethral vaginal hammock (10,11). These three structures are
thought by Ulmsten to be connected to each other via the vagina and surrounding connective
tissue “glue.” Ulmsten considers these structures to be closely integrated in a complicated
coordination to close, as well as open the bladder neck and urethra. Although defects in any one
of these structures or in their interplay may result in urinary incontinence and/or voiding
dysfunction, it is the tension in the pubourethral ligaments that is most essential for the correct
interplay between the muscular component and the vaginal hammock (Fig. 1). If tension within
the pubourethral ligaments is inadequate, forward contraction of the pubococcygeus muscle
and backward-downward contraction of the remaining levator muscles will be ineffective in
“kinking” the urethra during stress. Ulmsten refers to this kink in the urethra as the urethral
“knee,” demonstrated on lateral urethrocystography and located just distal to the maximum
urethral closing pressure zone, which corresponds to the location of the insertion of pubourethral
ligaments (Fig. 2).
Based on his integral theory, Ulmsten introduced the first TVT procedure as a simple
ambulatory surgical procedure referred to as the intravaginal slingplasty (IVS) (7). This initial
TVT procedure varied slightly from the current technique. The IVS procedure involved a single
2-cm vertical suprapubic incision and a concomitant “double-breast” vaginal plasty in cases
where there was excessive vaginal tissue noted. In addition, the sling material itself was not
made of the current unique TVT prolene, but rather a variety of materials including Mersilene,
Gortex, Teflon, and Lyodura. In 1996, Ulmsten reported on an improved surgical technique and
instrumentation for the IVS procedure, establishing the TVT procedure as it is known today (12).
This modification also included the sling material being solely of a prolene mesh, 40-cm-long
and 10-mm-wide covered by a plastic sheath swedged on two stainless steel needles. A recent
study examining the initial stiffness and peak breaking load of commonly used sling materials
demonstrated that the TVT prolene has by far the lowest initial stiffness (Fig. 3). The TVT
elastic limit is only reached at an elongation of almost 50% of its initial length although at
relatively low forces. Its fracture point is reached at very high elongation and on exertion of a
relatively high force. It may be that the unique biomechanical properties of the TVT prolene
have contributed to the fact that the material seems unusually biocompatible in its current use as
a suburethral sling (13). Additional instrumentation consists of a reusable stainless steel
introducer handle along with a reusable rigid Mandarin (catheter guide) (Fig. 4).

III. SURGICAL TECHNIQUE

The TVT procedure is most often performed under local anesthesia with intravenous sedation.
This approach allows the patient to participate in the “cough test,” an important step for correctly
 Tension-Free Vaginal Tape 401

Figure 1 Opening and closure of inner urethra and bladder neck is mainly controlled by three anatomical
structures; the tension of the pubourethral ligaments (PUL), the activity of the pubococcygeus muscles
(PCM) and levator muscles (LP ¼ levator plate; LMA ¼ longitudinal muscle of the anus), and the
condition of the suburethral vaginal hammock, i.e., the vaginal wall on which urethra and bladder neck are
lying. All structures are connected to each other via the vagina and connective tissue “glue.” The tension in
the pubourethral ligaments is essential for correct interplay between the muscles and the vaginal hammock.
Opening of the urethra and bladder neck occurs when PCM stop their forward contraction, when PUL has
an adequate tension securing bladder neck in correct anatomical position and when there is backward-
downward contraction of the levator muscles. Hereby the suburethral vaginal hammock is loosened allowing
the inner urethra and bladder neck to funnel. Forward contraction of PCM and backward contraction via
levator muscles actively closes (kinks) the inner urethra and bladder neck provided there is adequate
tension in PUL. In the lower panel the forces acting on the inner part of the urethra and bladder neck (BN)
are simplified. The importance of the interplay among PUL, PCM, vaginal hammock, and levator plate on
closing and opening of inner urethra and bladder neck is obvious. USL, uterosacral ligaments; N, free nerve
terminals or stretch receptors in the bladder base and inner part of urethra; X, the site where vagina is fixed
to the bladder base. (From Ref. 7.)

placing the Prolene tape. For patients undergoing concomitant pelvic reconstructive or
obliterative vaginal surgery, regional anesthesia may be required. For this clinical scenario at
least one study has suggested that epidural regional anesthesia is preferable to a spinal block
(14). If general anesthesia is indeed necessary, reproducing the cough test by simulating the
abdominal forces of a cough via a brisk and vigorous credé maneuver is recommended. The
credé maneuver, however, is not analogous to a cough in the awake patient. Therefore, caution
should be exercised when using this maneuver to adjust the TVT under general anesthesia, as
it has been suggested in at least one study to be associated with a potential for increased
postoperative voiding dysfunction and/or retention as well as de novo detrusor instability (15).
402 Lucente and Mastropietro

Figure 2 Urethral pressure profile measurement and lateral urethrocystography in a continent female. As
seen the “urethral knee” indicating the main position/fixation of the pubourethral ligament is located just
distal to the high pressure zone of the urethra. It is important that the sling is positioned at the urethral knee.
FUL, functional urethral length; MUP, maximum urethral pressure. (From Ref. 7.)

The procedure is performed with the patient in the dorsal lithotomy position with the lower
extremities supported in adjustable Allen-type stirrups. The degree of Trendelenburg is
important, as this will affect the angle or tilt of the pubic symphysis, which can affect the
technical aspects of navigating the TVT needles safely through the retropubic space with
constant and direct contact with the posterior aspect of the pubic symphysis. An 18 Fr Foley
catheter is inserted into the urethra, and the bladder is emptied. A local anesthetic is applied
suprapubically at two points, 1 – 2 cm above the pubic symphysis and 2 – 3 cm lateral to midline.

Figure 3 Typical load-deformation curves for the seven tested permanent materials. (From Ref. 13.)
 Tension-Free Vaginal Tape 403

Figure 4 Tension-free vaginal tape system (Gynecare, Somerville, NJ) consists of (clockwise from top)
rigid catheter guide, stainless-steel needle introducer, and TVT device with polypropylene mesh attached to
stainless-steel needles. (From Ref. 61.)

The abdominal skin, underlying rectus muscle and fascia, and the posterior aspect of the pubic
bone are infiltrated bilaterally. Two small abdominal skin incisions (0.5 – 1.0 cm) are then made
at these points. No further abdominal dissection is necessary. A Sims speculum is then inserted
into the vagina to allow visualization of the anterior vaginal wall. The external urethral meatus is
easily visualized, and the indwelling Foley bulb is utilized to identify the location of the internal
urethral egress. Using these two anatomical landmarks, the region of the midurethra is easily
identified. The same local anesthetic solution is then injected into the vaginal submucosa at the
level of the midurethra along the midline and slightly lateral to each side of the urethra. Allis
clamps are then placed on the vaginal wall at the level of midurethra bilaterally for counter-
traction as a small sagittal incision (1.5 cm) is made in the midline. The incision should begin
0.5– 1 cm proximal to the external urethral meatus.
Following the midline scalpel incision, Allis clamps are replaced on the cut edges of the
vaginal wall, and Metzenbaum scissors are utilized to minimally dissect the vaginal wall
bilaterally, freeing it from the underlying periurethral tissue and developing a small tunnel
bilaterally. This dissection should be limited to a depth of only 1 –1.5 cm. The surgeon should
take great care to avoid puncturing through the pubocervical fascia or injuring the urethra. After
the vaginal incision and periurethral dissection are completed, additional local anesthetic
solution should be administered bilaterally. Using a long spinal needle and an examination finger
within the vaginal canal for guidance, the needle is placed through the vaginal incision
periurethrally until the bevel of the needle reaches the inferior and posterior aspect of the pubic
symphysis. Approximately 15– 20 cc additional local anesthetic solution is placed at this
location bilaterally.
The bladder is then drained via the Foley catheter, and a rigid catheter guide (Mandarin) is
inserted into the catheter. The handle of the rigid catheter guide is then deviated to the ipsilateral
side of the anticipated passage of the forthcoming TVT device. Gentle pressure inward or
cephalad will further encourage retraction of the ventral aspect of the bladder dome away from
the posterior aspect of the pubic symphysis. (Figs. 5,6) With the aid of introducer handle, the
surgeon places the tip of the needle into the previously developed periurethral tunnel, utilizing
both hands to correctly and safely pass the needle. The needle is directed only slightly lateral,
most often in direct alignment with the patient’s ipsilateral axilla. An additional reference point
is the previously made ipsilateral suprapubic incision. The TVT needle is steadily and gradually
404 Lucente and Mastropietro

Figure 5 Paraurethral dissection is performed after an initial midline incision on the anterior vaginal
mucosa at the level of the midurethra. Note the small suprapubic abdominal stab incisions bilaterally.
(From Ref. 61.)

advanced by applying gentle pressure with the palm of the vaginal hand and continued with
vaginal finger guidance and slight pressure from the second hand placed on the introducer
handle. As the needle tip passes through the pubocervical fascia, a distinct drop in resistance can
be appreciated.

Figure 6 After bilateral dissection of the paraurethral space, the rigid catheter guide is inserted into the
urinary catheter. The handle of the guide is deflected to the ipsilateral side and the needle is inserted into the
paraurethral space. (From Ref. 61.)
 Tension-Free Vaginal Tape 405

At this point, with downward deflection of the introducer handle the surgeon guides the
needle superiorly through the space of Retzius with the needle being immediately opposed to the
backside of the pubic symphysis. (Figs. 7,8) As the needle opposes the underside of the rectus
muscle and fascial sheath, significant resistance is again appreciated. The introducer handle is
then utilized to apply pressure directly anterior, advancing the needle up through the previously
made abdominal incision. The surgeon’s nondominant hand is placed suprapubically to further
guide the needle tip up through the abdominal incision (Fig. 9).
The rigid catheter guide and Foley catheter are removed, and diagnostic urethrocystoscopy
is performed to evaluate for any unintentional injury of the urethra or bladder. Once correct
needle placement is confirmed, the needle is passed completely up through the abdominal
incision. The steps of the procedure are then repeated on the opposite side. Care should be taken
to ensure the tape is not twisted under the urethra (Fig. 10).
After correct placement of the TVT device and before removal of the protective sheath, a
cough test is performed to identify the correct positioning of the tape. The cough test is
conducted with a full bladder (250 –300 mL saline) (Fig. 11). Once the proper positioning of the
tape is obtained, the plastic sheath is removed and the prolene mesh is left in place without
tension under the midurethra. The abdominal ends of the tape are cut just below the skin’s
surface. The procedure is completed with closure of the abdominal and vaginal incisions
(Fig. 12).

IV. MECHANISM OF ACTION

Since its inception the TVT procedure has generated much debate as to its mechanism of action.
With that in mind, researchers have examined a wide range of outcomes from its effect on
voiding and urodynamic parameters to radiologic and connective tissue changes.

Figure 7 The tip of the needle is angulated laterally and the endopelvic fascia is perforated just behind
the inferior surface of the pubic symphysis. (From Ref. 61.)
406 Lucente and Mastropietro

Figure 8 After perforation of the endopelvic fascia, the tip of the needle is guided through the retropubic
space along the backside of the pubic symphysis. (From Ref. 61.)

Historically, GSI patients have been examined for urethral hypermobility as a contributing
factor to their symptoms, and anti-incontinence procedures have long been directed toward the
resolution of hypermobility as a way to restore the urethra back to its abdominal position,
thereby improving the pressure transmission ratio. Recent studies have demonstrated that despite

Figure 9 After perforation of the rectus fascia, a hand is used to palpate the needle tip suprapubically and
guide the needle to the abdominal incision. (From Ref. 61.)
 Tension-Free Vaginal Tape 407

Figure 10 After the technique is repeated on the other side, the TVT sling is in place with the tape lying
flat against the posterior surface of the midurethra. (From Ref. 61.)

postoperative persistence of urethral hypermobility, cure rates for the TVT procedure have
been maintained and equal to the Burch colposuspension (16 – 18).
In one recent study, further evaluation of urodynamic indices revealed a decrease in
resting maximum urethral closing pressure along with an increase in dynamic maximum urethral
closing pressure and in resting and dynamic functional urethral length, although statistical
significance was not reached (19). Another study, however, demonstrated no change in

Figure 11 The needles are detached and an instrument is placed between the tape and the urethra. Gentle
traction on each end brings the tape in contact with the urethra and correct tension is adjusted with an
intraoperative cough stress test. (From Ref. 61.)
408 Lucente and Mastropietro

Figure 12 The incisions are closed. The completed procedure allows fixation of the tape below the
midurethra with the ends just below the skin level. (From Ref. 61.)

maximum urethral closing pressure while revealing an increase in the pressure transmission
ratio, which has been demonstrated with other anti-incontinence procedures, such as the Burch
colposuspension and needle suspension procedure (18).
Other researchers have questioned whether the TVT’s success is contingent upon an
outflow obstruction at the urethral “knee.” A few early reports have suggested this as a possible
mechanism based on an increased urethral resistance and elevated postvoid residual volumes
along with decreased maximum flow rates as seen on pressure flow studies during follow-up at
less than 1 year (20,21).
In an attempt to explain the TVT mechanism on an anatomic basis, both radiologic and
histologic studies have been initiated. Initial studies utilizing ultrasound and magnetic resonance
imaging revealed that the tape remained in either the middle or distal urethra and demonstrated
convexity toward the urethra. The tape maintained its position at the abdominal wall in all
patients evaluated (22). Biochemical analyses from paraurethral connective tissue biopsies up to
2 years postoperatively demonstrated no change in the amount of collagen present, although
registering increased collagen metabolism (23).

V. PROCEDURAL OUTCOMES
A. Clinical Results
With the initial introduction of the intravaginal slingplasty (IVS), 50 patients were surgically
treated for pure genuine stress incontinence (GSI) or mixed incontinence with predominant
stress incontinence symptoms. Seventy-eight percent of patients were cured of stress
incontinence symptoms while 12% demonstrated significant improvement (7). Expanding on
this initial report, a case series using only a Prolene sling in patients with primary SUI
demonstrated 84% cure with 8% improvement at 2 years follow-up (12). In 1999, Ulmsten and
colleagues reported on the surgical outcome of TVT at 3 years including an 86% cure rate with
12% significantly improved (24). Other authors reported similar success rates (19,25 – 30). With
time, additional clinical research continued to demonstrate the high success rates associated
 Tension-Free Vaginal Tape 409

with the TVT procedure. Nilsson and colleagues reported a sustained objective cure rate of
84.7% along with 10.6% significantly improved after 5 years. All patients in this multicenter
trial demonstrated preoperative SUI. Complications were few in number: 3.3% retropubic
hematoma, 1.1% bladder perforation, and 3.3% intraoperative bleeding of .200 mL. No
surgical intervention was required. Transient voiding dysfunction (,4 days postoperatively)
was present in 4.4%. Interestingly, of the patients with preoperative urgency symptoms, 56%
were relieved of their symptoms. Six percent of patients reported de novo urge symptoms
postoperatively, but no urodynamic proven detrusor instability was demonstrated (31).

B. Subpopulation Studies
In addition to the sustained high cure rates of the TVT in the patient with primary GSI, similar
success rates have been reported in subgroups of GSI patients. Azam and colleagues reported
on a cohort of patients with recurrent SUI without ISD after multiple procedures including
needle suspension procedures, Burch and MMK colposuspensions, urethral bulking agents,
anterior colporrhaphy, with Kelly plications and vaginal sling procedures. At the 1-year
follow-up after TVT, a cure rate of 81% along with a success rate of 87% was demonstrated
in a patient population of 67 women with a median of two prior surgical procedures (32).
This was reproduced at a mean follow-up of 4 years with 82% cured and 9% significantly
improved (33).
Early reports of the TVT procedure in patients with ISD as defined by a low urethral
closure pressure (MUCP , 20 cmH2O) demonstrated a high patient satisfaction rate of 85%,
equal to that of patients with normal urethral closure pressure, despite a significantly lower
objective cure rate of only 37% at a follow-up of only 1 year (34,35).
One study has specifically examined TVT outcomes in ISD patients refractory to
periurethral collagen injection. No significant difference with regard to success or complication
rates was demonstrated (36). A long-term study of patients with ISD demonstrated a sustained
cure rate after TVT of 74% with an additional 12% significantly improved after 4 years (37).
Furthermore, in patients experiencing mixed urinary incontinence, the TVT procedure resulted
in a cure rate of 85% and 4% improvement for both stress and urge symptoms at a mean follow-
up of 4 years (38).
There have been a few recent reports specifically examining the safety and efficacy of
performing the TVT procedure in obese patients. These studies have shown no difference in
success or complication rates when compared to normal-weight patients (39,40).
The low procedural morbidity and the opportunity to use local anesthesia would seem to
make the TVT procedure well suited for the elderly patient population. We performed a
retrospective review of 83 women age  70 years (advanced elderly), who underwent a TVT
procedure for GSI, comparing the outcomes to 179 patients with age , 70 years (41). Several
differences were noted between the groups. The advanced elderly patients presented with a
higher rate of overactive bladder symptoms; a greater percentage (19%) had also undergone
prior periurethral collagen injections, and they experienced an increase in combined prolapse
surgery with the anticipated findings of increased operative time and increased estimated blood
loss. The success rate, defined as subjective cure, was similar with a 95.2% for the advanced
elderly patients and a 98.9% cure rate for the control group. Two smaller studies reporting on 45
women and 18 women, respectively, have also demonstrated the safety and efficacy of TVT
when performed in the advanced elderly (42,43). It appears from these preliminary studies that
age alone does not appear to decrease the success rate of the TVT procedure as a treatment for
female GSI.
410 Lucente and Mastropietro

VI. POTENTIAL COMPLICATIONS

In general, the complications associated with a TVT procedure occur far less frequently than
similar pubovaginal sling-type procedures. Table 1 demonstrates the reported incidence of such
minor and major complications according to data gathered and reported by Gynecare in over
200,000 worldwide cases. The more minor complications include transient voiding dysfunction,
urinary retention, retropubic bleeding and/or hematoma formation, perforation of the bladder,
and localized infection. Complications more typically associated with the use of synthetic
materials with sling procedures, such as complete graft erosion, rejection, sinus tract formation,
or development of a fistula, have not been reported. There have been cases of localized erosion
or vaginal extrusion, as well as obturator nerve irritation, retained plastic sheath, and vaginal
wall laceration, however, these appear to be extremely rare occurrences.
Most concerning to surgeons performing the TVT procedure are the rare but nonetheless
significant vascular injuries that have been reported during tape placement. These injuries have
involved the obturator, external iliac, femoral, and inferior epigastric vessels. Additionally,
significant hemorrhage has been reported from venous bleeding in the retropubic space, possibly
from the inferior vesical veins or, alternatively, disruption of the venous supply along the
posterior aspect of the pubic symphysis (44,45). To avoid vascular injury it is imperative that the
operating surgeon maintain the curved TVT tunneler (trocar) in direct contact with the posterior
aspect of the pubic bone medial to the pubic tubercle. Any inadvertent lateral or cephalad
migration of the tunneler could potentially result in vascular injury. One recent study described
the proximity of the major vessels in the retropubic space and anterior abdominal wall to the
TVT needle (46). The study was performed on 10 fresh frozen cadavers, during which
measurements from the lateral aspect of the needle to the medial aspects of the vessels were
obtained and recorded. All vessels measured were lateral to the TVT needle. The vessels studied
included a superficial epigastric, inferior epigastric, external iliac, and obturator (Table 2). Based
on this study, the authors concluded that the TVT needle, if laterally directed or externally
rotated during the course of insertion, could result in major vascular injury. Venous bleeding
that is not readily controlled by direct pressure or vaginal packing can be managed with the
placement of a 30-cc Foley balloon inflated to a 50-cc volume, upon which significant traction is
placed, taping the Foley to the medial aspect of the thigh. This will effectively tamponade most
venous bleeding in the retropubic space, which will encourage effective coagulation and clot
formation (47). Hematomas usually present within the first 12 h of surgery. The presentation
is that of significant pressurelike discomfort in the suprapubic or vaginal area. The diagnosis
can be obtained by a careful bimanual exam and confirmed by ultrasound investigation. Most
hematomas will resolve spontaneously without intervention; however, ultrasound-guided

Table 1 Gynecare TVT Tension-free Support for Incontinence: Statement

Regarding Complications

Complication U.S. Non-U.S. Total %

Vascular injury 3 25 28 0.01

Vaginal mesh exposure 13 2 15 0.008
Urethral erosion 8 0 8 0.004
Bowel perforation 4 6 10 0.005

Source: Gynecare, Somerville, NJ.

 Tension-Free Vaginal Tape 411

Table 2 Vessel Distance from TVT Needle

TVT needle Midpubic bone

Vessel Mean cm (range) Mean cm (range)

Superficial epigastric 3.9 (0.9– 6.7) 7.2 (4.4– 9.3)

Inferior epigastric 3.9 (1.9– 6.6) 7.4 (4.8– 10.0)
External iliac 4.9 (2.9– 6.2) 8.3 (6.5– 10.9)
Obturator 3.2 (1.6– 4.3) 6.9 (5.2– 8.4)

Source: Ref. 46.

drainage should be considered for larger hematomas (.8 cm), as the likelihood of potential
infection is increased.
The most common procedure associated infection is that of an acute bacterial cystitis. One
must remember this is a nosocomial infection when prescribing antibiotic therapy. True wound
infections following a TVT procedure are rare. This may be a result of the protective nature of
the plastic tape, which minimizes the likelihood of bacterial inoculation or contamination during
placement, passage, and subsequent tape adjustment. Additionally, Prolene as a graft material
has been associated with less risk of infection than other synthetic materials (48). The liberal use
of preoperative topical estrogen, in either cream or suppository form, may help reduce the
incidence of vaginal atrophy or mucosal irritation, which may contribute to wound infection.
Treatment of wound infection includes broad-spectrum antibiotics and pelvic rest. Surgical
debridement or intervention is most often not required.
Bladder perforation during the TVT procedure has been reported in most all clinical
studies. It is the most frequently reported complication occurring on average 6% of the time. It
is more commonly seen in patients who have undergone a previous retropubic suspension. The
perforation rate tends to vary, depending on surgeon experience and patient population from as
low as 0% to as high as 23.1%. The surgeon should avoid the tendency to place the TVT needle
more laterally after encountering a bladder perforation. Ideally, one should assess the location of
the inadvertent puncture and readjust placement accordingly. In general, perforations occur at
the 10 and 2 o’clock positions, safely away from the trigone and ureteral orifices. If such
perforation occurs, the TVT tunneler is withdrawn and redirected with closer adherence to the
posterior aspect of the pubic symphysis in conjunction with perhaps improved deviation of the
bladder with gentle inward pressure (cephalad) of the indwelling rigid catheter, helping to
elongate the bladder to a more elliptical shape rather than a bulbous contour, thus increasing the
distance between the bladder and the posterior aspect of the pubic symphysis. For more midline
perforations, some lateral correction may be warranted—however, never beyond the pubic
tubercle. These patients should have continuous bladder drainage via an indwelling Foley
catheter for 24 –48 h.
A variable incidence of voiding dysfunction including urinary retention has been reported
after the TVT procedure. Contributing factors include preoperative detrusor hypocontractility,
patient age, anesthesia type, and failure to adhere to the standardized technique of tape
adjustment including utilization of an intraoperative cough test. For patients who are unable to
initiate a void postoperatively, conservative management can be employed with an indwelling
catheter for 24 – 48 h. The possibility of a hematoma should also be entertained and an
appropriate evaluation performed. If the patient continues to be unable to void beyond 72 h,
surgical intervention can be employed via a simple opening of the vaginal incision under local
412 Lucente and Mastropietro

anesthesia with bilateral downward pulling of the mesh lateral to the urethra on both sides for a
limited distance (5 – 6 mm). After 10 days, this “loosening” of the mesh is often not possible.
These patients should be instructed on intermittent self-catheterization and scheduled for a
potential surgical release in 4 – 6 weeks. This time frame will allow the tissue to heal and the
mesh to become fixed laterally at the level of the pubocervical fascia. Persistent retention or
refractory voiding dysfunction is relatively uncommon—however, one that can be successfully
managed with a fairly simple surgical midline release of the Prolene tape. Rardin and colleagues
recently described a collective series of 848 women over a 2-year period who underwent a TVT
procedure. Among these patients, 19 (2.2%) had severe voiding dysfunction, described as either
urinary retention, significant incomplete bladder emptying, or severe urgency or urge-related
incontinence, refractory to conservative management. These patients underwent a vaginal TVT
surgical release: 15 by midline tape transection, and four by midline tape excision of a 2- to
11-mm segment. All patients had at least partial resolution of voiding dysfunction immediately
following the takedown procedure. Ten of the 19 women had complete resolution of symptoms.
Twelve of the 19 patients (63%) remained completely continent after the release, three (60%)
had only mild incontinence described as still being significantly improved or baseline, and only
four patients (21%) had recurrence of their stress urinary incontinence (49).

VII. TVT WITH CONCOMITANT SURGERY

It has been well recognized that proper identification and correction of pelvic support defects
in addition to performing surgery for incontinence improves patient outcomes (50 –52). The
incidence of pelvic organ prolapse requiring concomitant reconstructive pelvic surgery at
the time of surgery for SUI has been reported to be as high as 42% (53). Several reports on
the clinical outcomes of patients undergoing the TVT procedure have included patients
receiving concomitant surgery for pelvic organ prolapse (30,54). Only a few studies have
specifically examined the safety and efficacy of the TVT in combination with reconstructive
pelvic surgery.
Jomaa was the first to report on combining the TVT procedure with an anterior and/or
posterior colporrhaphy in 32 patients under local anesthesia. Ninety-three patients were cured
with a mean hospital stay of 2 days (55). We performed a retrospective review comparing 47
patients who underwent TVT with concomitant vaginal surgery (TVT þ) to 133 patients who
underwent TVT alone (TVT) (56). Concomitant vaginal surgery consisted of one or more of the
following procedures: sacrospinous ligament fixation (one), vaginal hysterectomy (one),
enterocele repair (4), anterior colporrhaphy (eight), posterior colporrhaphy (13), LeFort
colpocleisis (14), or perineorrhaphy (15). The mean operative time and estimated blood loss was
appropriately increased as anticipated in the TVT þ group. The hospital stay was also
marginally increased; however, most often remained ,24 h. The only operative complication
was that of bladder perforation, which was similar in the two groups, occurring in 6.4% of the
TVT þ patients and 6.8% of the TVT patients; no patients developed any wound infection or
tape rejection. Twenty-four-hour spontaneous micturition rates were also similar in the two
groups. One hundred thirty-one patients (98.5%) of the TVT group reported a subjective cure
versus 47 (100%) of the TVT þ group. Lastly, 41% of the TVT þ had local anesthesia with
sedation, 58% had regional anesthesia, and only 2% (one patient) received general anesthesia,
whereas 96% of the TVT group had local anesthesia, 4% had regional, and 0.8% (one patient)
underwent general. In conclusion, we have found that the TVT pubovaginal sling can be safely
and effectively performed with concomitant vaginal surgery without significant increase in
morbidity.
 Tension-Free Vaginal Tape 413

VIII. COMPARATIVE STUDIES

Although there are several ongoing studies comparing the clinical outcome of the TVT
procedure to that of the Burch colposuspension, only a few have reported on preliminary
findings or conclusions. One of the earlier studies involves comparing the open Burch
colposuspension to the TVT. In this study the Burch procedure was found to have a significantly
greater blood loss and increased hospital stay, yet a similar success rate at 6 months (57).
Vassallo and colleagues reported on a retrospective analysis among women who underwent
either a TVT or laparoscopic Burch procedure for treatment of SUI. Seventy-four women were
identified and followed for at least 1 year. The overall objective cure rates were comparable with
88% for the laparoscopic Burch and 92% for the TVT procedure. There were no significant
differences in time to resumption of normal voiding or related irritative bladder symptoms
such as urgency, frequency, and/or urge incontinence. There was a trend toward increasing
intraoperative complications among the TVT group; however, this did not reach statistical
significance. The TVT patients were noted to have a shorter operative time as well as a shorter
hospital stay (58). In terms of cure and improvement rates, Fotte reported the opposite finding,
with a higher rate among patients undergoing laparoscopic colposuspension (59). The
laparoscopic colposuspension group had a cure or improved rate of 94%, versus 82% for the
TVT group. The laparoscopic group did require a significantly longer operative time, but had
less intraoperative and post-operative complications. Voiding difficulty was significantly less
in the laparoscopic group, 0% versus 18%.

A. TVT-OBTURATOR

The worldwide adaptation of retropubic TVT has been associated with a number of
intraoperative complications including bladder perforations, urethral injuries, retropubic
hematoma formation, and rarely, complications with significant consequences such as injury to
bowel, major blood vessels and nerves. Consistent with the spirit of improving procedural safety,
recent modifications in the method of placement of the tension free mid urethral sling have taken
place. To avoid blind passage of introducers into the retropubic space, a unique approach using
the obturator foramina has been developed.
The transobturator approach was first described by Dr. Emmanuel DeLorme in France in
September of 2001 (62). DeLorme used an Emmet needle the path of which carried it through a
skin incision in the thigh fold, through the inferior-medial aspect of the obturator foramen, the
anterior recess of the ishiorectal fossa under the levator muscles, and through the pubocervical
fibromuscular tissue to exit a suburethral incision. The tape was then withdrawn through the
same path. The same procedure was performed on the opposite side to form the midurethral
sling. Initial data have demonstrated similar cure rates when compared to traditional retropublic
placement with a lower incidence of bladder injury (63). As the obturator approach was adopted
by others however, lower urinary tract injuries were experienced. Vaginal tears and groin
hematomas have also since been reported (64–66).
In an attempt to further improve upon the intraoperative safety profile of a obturator
approach, Dr. Jean de Leval more recently described a transobtuator technique of tape placement
with a helical passer that begins at the vaginal incision, follows the same path and exists the skin
2 cm lateral to the thigh fold thus earning it the “inside-out” designation. Initial reports are
encouraging suggesting a similar efficacy with no reported adverse events thus far reported (67).
Long term data demonstrating sustained efficacy of the TVT-Obturator approach are eagerly
awaited.
414 Lucente and Mastropietro

IX. CONCLUSION

The TVT procedure has been proven to be an effective minimally invasive approach to the
surgical management of female stress urinary incontinence. The TVT-obturator system will
most likely result in additional patient safety. With TVT’s widespread use, both clinical success
and patient safety will only be achieved through continued close adherence to the technical
aspects of the procedure as originally described. It has been referred to as perhaps the most
exciting and most innovative procedure for stress incontinence in the last 40 years (60).

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surgical treatment of urinary stress incontinence. Br J Obstet Gynaecol 2001; 108:414 – 419.
28. Soulie M, Cuvillier X, Benaissa A. The TVT procedure in the treatment of female urinary stress
incontinence: a French prospective multicentre study. Eur Urol 2001; 39:709– 715.
29. Haab F, Sananes S, Amarenco G. Results of the TVT procedure for the treatment of type II SUI at
a minimum follow-up of 1 yr. J Urol 2001; 165(1):159– 162.
30. Meschia M, Pifarotti P, Bernasconi F, Guercio E. TVT: analysis of outcomes of complications in 404
stress incontinent women. Int Urogynecol J 2001; 12(suppl 2):S24– S27.
31. Nilsson CG, Kuuva N, Falconer C. Long-term results of the tension-free vaginal tape (TVT)
procedure for surgical treatment of female stress urinary incontinence. Int Urogynecol J 2001;
12(suppl 2):S5– S8.
32. Azam U, Frazer MI, Kozman EL. The tension-free vaginal tape procedure in women with previous
failed stress incontinence surgery. J Urol 2001; 166(2):554– 556.
33. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in women with recurrent stress urinary
incontinence—a long-term follow-up. Int Urogynecol J 2001; 12(suppl 2):S9 – S11.
34. Kulseng-Hanssen S. Success of TVT operation in patients with low urethral pressure. 31st Annual
Meeting of the International Continence Society, Seoul, South Korea, Sept 18 – 21, 2001.
35. Ohkawa A, Kondo A, Baba S. TVT operation is it effective for those patients suffered from type III
incontinence? 31st Annual Meeting of the International Continence Society, Seoul, South Korea, Sept
18 – 21, 2001.
36. Murphy M, Horton TR, Druckenmiller J, Lucente V. Tension free vaginal tape for the treatment of
ISD refractory to periurethral collagen injection. 22nd Annual Scientific Meeting of the American
Urogynecologic Society, Chicago, Oct 25– 27, 2001.
37. 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 2001;
12(suppl 2):S12– S14.
38. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in women with mixed urinary
incontinence—a long-term follow-up. Int Urogynecol J 2001; 12(suppl 2):S15 – S18.
39. Chung MK, Bradley AF, Chung RP. TVT for treatment of urinary incontinence in obese women. 21st
Annual Scientific Meeting of the American Urogynecologic Society, Hilton Head, SC, Oct 25 – 28,
2000.
40. Rufford I J, Toozs-Hobson P, Cardozo LD. Where surgeons dare; the effect of body weight on TVT
success rates. 31st Annual Meeting of the International Continence Society, Seoul, South Korea, Sept
18 – 21, 2001.
41. Horton TR, Druckenmiller J, Lucente V. Pubovaginal sling use and tension-free vaginal tape in
advanced elderly women. 22nd Annual Scientific Meeting of the American Urogynecologic Society,
Chicago, Oct 25 – 27, 2001.
42. Nilsson C. The effect of age and time on the outcome of TVT surgery. 31st Annual Meeting of
the International Continence Society, Seoul, South Korea, Sept 18 – 21, 2001.
43. Fischer M. Tension-free vaginal tape (TVT) in the elderly. 31st Annual Meeting of the International
Continence Society, Seoul, South Korea, Sept 18 –21, 2001.
416 Lucente and Mastropietro

44. Walters MD, Tulikangas PK, Lasala C, Muir T. Vascular injury during tension-free vaginal tape
procedure for stress urinary incontinence. Obstet Gynecol 2001; 98(5)Part 2:957– 959.
45. Tim K, Kim H, Lee S. Vascular injury following tension-free vaginal tape (TVT and stress
incontinence). 31st Annual Meeting of the International Continence Society, Seoul, South Korea,
Sept 18 – 21, 2001.
46. Muir T, Tulikangas PK, Paraiso MF, Walters MD. The relationship of tension-free vaginal tape
insertion to the vascular anatomy of the retropubic space and the anterior abdominal wall. 22nd
Annual Scientific Meeting of the American Urogynecologic Society, Chicago, Oct 25 – 27, 2001.
47. Katske FA, Raz S. Use of a Foley catheter to obtain transvaginal tamponade. Urol 1983; 21:627.
48. Iglesia CB, Fenner DE, Brubaker L. The use of mesh in gynecological surgery. Int Urogynecol J
Pelvic Floor Dysfunct 1997; 8:105– 115.
49. Rardin C, Lucente V, Miklos J. Takedown of tension-free vaginal tape for the treatment of refractory
postoperative voiding dysfunction. 22nd Annual Scientific Meeting of the American Urogynecologic
Society, Chicago, Oct 25 – 27, 2001.
50. Drutz HP, Alnaif B. Surgical management of pelvic organ prolapse and stress urinary incontinence.
Clin Obstet Gynecol 1998; 41:786 – 793.
51. Bruce RG, El-galley RE, Galloway NT. Paravaginal defect repair in the treatment of female urinary
incontinence and cystocele. Urology 1999; 54:647– 651.
52. Serels SR, Rackley RR, Appell RA. In situ slings with concurrent cystocele repair. Tech Urol 1999;
5:129– 132.
53. Ng CS, Rackley RR, Appell RA. Incidence of concomitant procedures for pelvic organ prolapse and
reconstruction in women who undergo surgery for stress urinary incontinence. Urology 2001;
57(5):911– 914.
54. Tamussino K, Hanzal E, Kolle D. The Austrian tension-free vaginal tape registry. Int Urogynecol J
2001; 12(suppl 2):S28– S29.
55. Jomaa M. Combined tension-free vaginal tape and prolapse repair under local anesthesia in patients
with symptoms of both urinary incontinence and prolapse. Gynecol Obstet Invest 2001; 51:184– 186.
56. Horton TR, Druckenmiller J, Lucente V. Concomitant vaginal surgery with tension-free vaginal tape
pubovaginal sling for treatment of female stress urinary incontinence and pelvic support defects. 27th
Scientific Meeting of the Society of Gynecologic Surgeons, Lake Buena Vista, FL, March 5 –7, 2001.
57. Ward KL, Hilton P, Browning J. A randomised trial of colposuspension and tension-free vaginal tape
(TVT) for primary genuine stress incontinence. 30th Annual Meeting of the International Continence
Society, Tampere, Finland, Aug 28 – 31, 2000.
58. Vassallo B, Murphy M, Lucente V, Karram M. TVT versus laparoscopic burch: a retrospective
review at 1 – 4 years. 27th Scientific Meeting of the Society of Gynecologic Surgeons, Lake Buena
Vista, FL, March 5 – 7, 2001.
59. Fotte A. Which is the best minimally invasive procedure? TVT versus laparoscopic colposuspension.
31st Annual Meeting of the International Continence Society, Seoul, South Korea, Sept 18 –21, 2001.
60. Stanton SL. Some reflections on tension-free vaginal tape—a new surgical procedure for treatment of
female urinary incontinence. Int Urogynecol J 2001; 12 (suppl 2):S1– S2.
61. Kohli N, Miklos JR, Lucente V. Tension-free Vaginal Tape: a minimally invasive technique for
treating female SUI. Contemp Ob/Gyn May 1999.
62. De Lorme E. Prog. Urol. 2001; 11:1306–1313 La bandelette trans-obturatrice: un procede mini-
invasif pour traiter l’incontinence urinair d’effort de la femme.
63. Droupy et al. Abstract #779 EUA March 2003 Trans-obturator urethral support for female stress
urinary incontinence: 1 year outcome of a new surgical procedure.
64. Dargent D, Bretones S, George P, Mellier G. Gynécol Obstét Fertil 2002; 30:576–82 Insertion of a
suburethral sling through the obturator membrane in the treatment of female urinary incontinence.
65. Costa et al. Abstract #334 ICS October 2003 Trans-obturator tape (TOT) for female stress urinary
incontinence: Preliminary results of a prospective multicenter register.
66. Hermieu JF, et al. Progres en Urologie 2003; 13:115–117 Plaie vesicale apres bandelette trans-
obturatrice.
67. Leval J de, European Urology. 2003; 44:724–730 Novel surgical technique for the treatment of
female stress urinary incontinence: Transobturator vaginal Tape inside-out.
28
Distal Urethral Polypropylene Sling

Larissa V. Rodrı́guez
University of California Los Angeles, Los Angeles, California, U.S.A.

I. INTRODUCTION

The etiology of stress urinary incontinence is not completely understood. In the past, bladder
neck suspensions were performed in order to correct anatomic abnormalities, and bladder
neck and urethral hypermobility. These procedures were attractive because of their simplicity,
low morbidity, and excellent early success. With time, the successes seen with these procedures
have not proven to be durable, and alternative surgical procedures have been developed.
Sling procedures for the treatment of female stress urinary incontinence have been used for
almost 100 years. The first sling, described in 1907 by Von Giordano, used gracilis muscle
wrapped around the urethra (1). The procedure was reintroduced in 1978 by McGuire and Lytton,
who suspended a piece of rectus fascia under the bladder neck for the treatment of intrinsic
sphincter deficiency (2). Because of the initial relatively high incidence of complications
associated with pubovaginal slings, such as sling erosion and urinary retention, these procedures
did not achieve popularity until the last decade. Since then, multiple variations in surgical
technique have been reported using new sling materials and anchoring techniques to increase
both durability and ease of placement, and decrease surgical morbidity.
Until recently, the indications for bladder neck suspensions were type I and II stress
incontinence, and slings were reserved for only type III incontinence. With the poor long-term
durability of needle suspension procedures, interest has been renewed in sling procedures (3 –6).
A meta-analysis of various surgical techniques for the treatment of stress incontinence showed
pubovaginal slings to have superior durability to needle suspension procedures, and similar
durability to retropubic suspension (4). Slings have been shown to be as effective as and more
durable than bladder neck suspensions for the treatment of all types of stress incontinence, and
their popularity has therefore spread. Many new procedures and materials have emerged. Recent
studies have focused on new materials, innovative ways to anchor the sling, changes in location
of the sling, and broadening the application of slings for multiple types of incontinence. This
plethora of procedures has led to an increased need for well-controlled, objective outcome
studies in order to understand the impact of these surgeries on our patients.
The success of new techniques for the treatment of stress urinary incontinence has
broadened our understanding of the pathophysiology of the disease and has led to new theories
to explain the anatomic and physiologic processes that lead to incontinence in the female.
417
418 Rodrı́guez

For example, the success of distal urethral slings suggests that, contrary to previous thinking, the
correction of anatomic hypermobility is not necessary to correct stress incontinence (7).
Most sling procedures can be categorized by location of the sling: (1) the proximal urethra
and bladder neck; (2) mid to distal urethra (Table 1), and the choice of sling material (Table 2).
This chapter will discuss the technique and mechanism of cure of distal urethral slings and
describe our current technique and results.

II. PATHOPHYSIOLOGY

Female stress incontinence has been categorized as occurring with or without urethral
hypermobility (8,9). Classically, sling procedures have been reserved for the treatment of
individuals with stress incontinence without urethral hypermobility (2). The AUA guidelines for
the treatment of stress urinary incontinence (SUI) demonstrated excellent long-term durability
of these procedures, and subsequent authors have demonstrated excellent cure rates for
pubovaginal slings performed on patients with urethral hypermobility as well (4,10,11).
Several recent investigations have called into question the mechanism by which sling
procedures correct stress incontinence. Theories ranging from a backboard that improves
coaptation to frank urethral kinking leading to mild obstruction have been reported. Fulford and
coworkers demonstrated significant increases in both postvoid residual and voiding pressures,
with a concomitant decrease in peak flow rates in individuals treated with pubovaginal slings
(12). Similarly, Klutke and coworkers demonstrated a tendency toward obstructed voiding
patterns in patients who had undergone successful anti-incontinence procedures (13). These
results have not been supported by several other studies, which have shown no evidence
of obstruction on postoperative urodynamics in patients treated with slings (14). Ongoing efforts
to define outflow obstruction in women may be helpful in studying the mechanism of success of
sling procedure (7,15). At this time it is impossible to tell how these procedures correct urinary
incontinence.
The use of distal urethral slings has broadened our understanding of urethral support and
the mechanism of continence. Using the tension-free vaginal tape procedure Klutke and
coworkers have demonstrated high rates of cure of stress incontinence without correcting
urethral hypermobility (16). Thus, it seems that the anatomic correction of bladder neck
hypermobility is not as important as previously thought in the prevention of stress urinary
incontinence.
The proximal urethra and bladder neck are supported by the urethropelvic ligament. This
is the primary mechanism of continence in women, responsible for passive continence. A defect
in this support leads to bladder neck hypermobility and opening of the bladder neck. Since up to

Table 1 Variables Between Sling Procedures

Location Anchoring method Sling length

Bladder neck/proximal urethra None (TVT) Anterior vaginal wall only

Mid and distal urethra Absorbable sutures Vaginal wall þ retropubic space
Nonabsorbable sutures Vaginal wall þ retropubic
space þ suprapubic
Bone anchors
 Distal Urethral Polypropylene Sling 419

Table 2 Currently Utilized Sling Materials

Material

Autologous Cadaveric Synthetic Other

Vaginal wall Fascia lata PTFE/Gore-Tex Cadaveric fascia

Rectus fascia Polypropylene (Prolene) Pelvicol
Fascia lata Polypropylene (Marlex) DuraDerm
Polyester (Prote-Gen) Repliform
Polyethylene (Mersilene) DermMatrix
AlloDerm
Stratasis
SABRE

50% of women with hypermobility do not suffer from urinary incontinence, we know that a
defect to this area alone is not sufficient to cause urinary incontinence.
Unlike bladder neck suspensions and the pubovaginal sling, distal urethral slings do not
cure SUI by correcting hypermobility. The distal urethral complex is composed of the
pubourethral ligaments, the intrinsic sphincteric mechanism of the urethra, the extrinsic
sphincter, and the levator muscle located immediately distal to the pubourethral ligament. All
these elements interact and have a role in providing resting tonicity to the middistal urethra,
induce urethral coaptation, and respond protectively at the time of increased intra-abdominal
pressures by increasing urethral resistance. They not only provide anatomic support but also
contribute to the normal function of the urethra. For simplicity, we refer to everything proximal
to the pubourethral ligaments as proximal urethra and everything distal as distal urethra. Past
surgical procedures have targeted the proximal urethra and bladder neck by elevating the bladder
neck to an intra-abdominal position, fixing the proximal urethra to the pubic bone, or increasing
the resistance of the proximal urethra. Newer procedures supporting the distal urethra work by a
different mechanism. Anatomically, the distal suburethral slings both bring the urethra closer to
the pubic bone and provide support posteriorly. The distal slings leave the bladder neck and
urethra intact and hypermobile. The distal urethral function is altered, allowing for increased
segmental distal urethral resistance and better urethral coaptation. The proximity of the urethra
to the symphysis pubis allows for a more efficient impact of the levator musculature on the
urethra at the time of increased intra-abdominal pressures. In addition, the sling itself may also
provide support posteriorly to provide a “distal backboard,” which also contributes to better
urethral coaptation.
Thus continence can be achieved by correcting the proximal urethral sphincter (proximal
urethra and bladder neck) in procedures such as bladder neck and retropubic suspensions or
proximal urethral slings, correcting the distal urethral sphincter as with the transvaginal tape
procedure (TVT; Ethicon) and other distal suburethral slings, or addressing the intrinsic
mechanism of the urethra with the use of injectables.

III. MID TO DISTAL SUBURETHRAL SLINGS

The TVT procedure was introduced by Ulmsten et al. in 1996 (17). It has been shown to be an
effective therapy for the treatment of stress incontinence (7,13,17 –29). Based on similar
anatomic location and mechanisms of cure as the TVT, other procedures have been described.
Such procedures include SPARC (American Medical Systems), Safyre (Promedon, Argentina),
420 Rodrı́guez

and SABRE (Mentor) among others. Since some of these procedures will be discussed in other
sections of this book, we will not focus on them in this chapter. Although a significant body of
literature exists regarding outcomes of surgery and complications from the TVT, very few data
are available on these newer procedures. All these techniques involve placement of a synthetic
sling at the level of the mid to distal urethra, and all are commercial product that include
placement needles or passers and prefabricated slings. As such, they can be costly. They differ
primarily in the approach to placement (from suprapubic area to vagina or vice versa, from
vagina to the suprapubic area) and in the particular hardware necessary for their placement.
Although simple to perform, these procedures require special instrumentation, and their
price is prohibitive in many parts of the world. In addition, for some of these procedures, the
technique for placement is blind without finger guidance, and this has lead to high rates of bladder
perforations, rare cases of injuries to the bowel or major vessels, and even death (30 – 32).
We have described the placement of a mid to distal urethral polypropylene sling (DUPS)
for the treatment of SU (33,34). Unlike other distal urethral slings, our procedure is inexpensive
with an approximate cost of $15 for the mesh, does not require special instrumentation, and is
placed only within the retropubic space. The procedure is simple and quick, with an average
operating room time of 28 min. The rest of this chapter will focus on the surgical technique and
outcomes of the DUPS.

IV. DUPS: AN INEXPENSIVE ALTERNATIVE TO COMMERCIALLY

AVAILABLE PRODUCTS
A. Surgical Technique
A 1  10 cm thinly woven polypropylene (Ethicon, Inc.) mesh is prepared and 0 polyglactin
(Vicryl) suture is placed at each end. The patient is placed in high dorsal lithotomy position. The
lower abdomen and genitalia are prepped and draped in a sterile fashion. The labia are retracted
laterally with stay sutures. A Lowsley retractor is used to place a suprapubic tube. A 16F Foley
catheter is inserted per urethra, and the bladder is emptied. A weighted vaginal speculum is used
for exposure. An Allis clamp is used to grasp the anterior vaginal wall just proximal to the
meatus. Two oblique lateral incisions are made in the anterior vaginal wall (Fig. 1). One
additional Allis clamp is placed at the distal portion of each of the oblique incisions to aid
in the exposure. The dissection is carried out laterally over the glistening periurethral fascia
toward the ipsilateral shoulder. A small window into the retropubic space is made at the level of
the mid to distal urethra (Fig. 2).
A suburethral tunnel is created in the anterior vaginal wall 1.5 cm from the urethral
meatus, using a fine, right-angle clamp (Fig. 3). The sling is transferred underneath the
suburethral tunnel (Fig. 4). A suprapubic puncture is made just above the symphysis. A double-
pronged needle (Cook Urological, Inc., Spencer, IN) is passed under finger control through the
fascia and retropubic space to the level of the oblique vaginal incision, and the previously placed
polyglactin sutures from the polypropylene mesh are transferred to the suprapubic incision.
A similar maneuver is done on the other side. Cystoscopy is performed to rule out bladder or
urethral perforation.
To guarantee tying of the sling under no tension, one Allis clamp is placed through each
vaginal incision to firmly hold the sling in the horizontal position while the assistant ties the
polyglactin sutures suprapubically (Fig. 5). The suture knots are located 3 mm bellow the skin
and are not immediately above the fascia. The retropubic space is irrigated with betadine
solution. The vaginal incisions are closed with 3.0 polyglactin. A subcuticular stitch with 4.0
polyglactin is used to close the suprapubic incision. A vaginal pack and dressing are applied.
 Distal Urethral Polypropylene Sling 421

Figure 1 Vaginal exposure and lateral incisions.

Postoperatively, the vaginal pack is removed in the recovery room, 2 h after the procedure.
The suprapubic tube is capped and the patient is instructed to void every 3 h and record her
postvoid residual. The patient is discharged home. The suprapubic tube is removed once
postvoid residuals are ,50 cc.

Figure 2 Entering the retropubic space.

422 Rodrı́guez

Figure 3 Suburethral vaginal tunnel.

B. Surgical Outcomes
From November 1999 to February 2002, 301 patients underwent the polypropylene sling for the
treatment of SUI. The average age was 59.3 years (41 – 83). Our series consists of a complex SUI
population. Of the 301 patients, 62% suffered from mixed incontinence and 139 (46%) of the
patients had failed an average of 1.6 (1 – 5) prior anti-incontinence procedures. In addition, 55%
of the patients had concomitant prolapse surgery with 33% of patients undergoing a concomitant
rectocele repair, 7% a cystocele repair, and 10% a vaginal hysterectomy among others.
When reporting perioperative complications we evaluated all patients who underwent the
polypropylene sling procedure. In this group, there were 301 patients with an average follow up
of 10.3 months (1–23 months). Complications occurred in ,0.3% of patients except development
of cystocele, which occurred in 2% of patients. Of these seven patients, none had cystocele repair at
the time of the sling surgery. Four of these patients had symptomatic cystoceles that required
surgical repair. No patients developed urethral erosion or permanent retention. Three patients had
prolonged voiding dysfunction requiring intermittent catheterization for a maximum of 3 months.
This resolved, and they are voiding spontaneously without residual. One patient developed a
vaginal erosion of the polypropylene mesh. This patient originally had urethral erosion from a
cadaveric fascial sling with abscess formation. At the time of her procedure, the cadaveric fascial
sling was removed, the urethra was reconstructed, and the polypropylene sling was placed. To date,
no other patients have required removal of the sling because of pain, infection, or erosion.
The surgical failure rate for this procedure is 2.3%, with seven patients in our series
requiring further intervention. Of these patients, four were treated successfully with durasphere
injections, two were treated with repeat polypropylene sling, and one, with severe urethral
incompetence, was treated with a spiral sling. The de novo urge incontinence rate was 6.8%.
 Distal Urethral Polypropylene Sling 423

Figure 4 The sling is placed under the vaginal tunnel.

It is always difficult to report success and failure rates in anti-incontinence surgery since
how these terms are defined can change these rates by up to 50%. Although the Urodynamic
Society and the American Urologic Association have made genuine attempts to standardize the
evaluation of treatment outcomes in urinary incontinence, most of these recommendations are
not being followed, and there are no specific recommendations as to how to assess patient
quality of life (QOL) or how to gather this information (35,36). Although a number of
validated questionnaires are available to assess QOL issues in the incontinent population, the
means for conducting this assessment is still nonstandardized (37). One thing is known;
numerous studies have demonstrated lower cure rates when patients subjective outcomes are
compared to physician assessment and objective cure rates on physical exam, pad tests, or
UDS (3,38,39). In addition, clinical outcomes do not always translate into patient satisfaction
(40). Examples of this phenomenon include diverging success rates reported for particular
procedures. One such procedure is the pubovaginal sling where physicians report success rates
of 70– 100% compared to subjective cure rates of 46 –55% (10,41 – 44). These discrepancies
are seen across the board with abdominal urethropexy having objective cure rates of 93%
versus subjective cure rates of 54% (45). Sirls et al. compared retrospective chart reviews
following modified Pereyra bladder neck suspension and found disparate success rates of 72%
cure rates using chart reviews versus 47% using patient questionnaires (39). In a recent
randomized study comparing the TVT to colposuspension, the objective cure rated defined as a
negative pad test and a negative cystometry was 66% in the TVT group versus 57% in the
colposuspension group (46). More interesting, when patients filled out validated question-
naires, only 59% and 53% of patients reported cure of SUI, respectively. In addition, only 36%
and 28% reported no leakage of urine under any circumstance.
424 Rodrı́guez

Figure 5 Adjusting sling tension using two Allis clamps.

In light of the biases present when members of the medical staff are involved in gathering
outcome data, we chose to evaluate our patients with patient self-assessment. Of the 301 patients
there were 92 patients with a minimum follow-up of 12 months (mean 16; range 12 –23).
Patients were evaluated by self-reported questionnaires looking at the presence, absence, and
frequency of symptoms, bother from symptoms (short form of the urogenital distress inventory,
UDI-6), and global quality of life question related to urinary symptoms. Self-assessment
questionnaires were available on 76 (83%) of the 92 patients with a minimum 1-year follow-up
Eighty-four percent of patients reported symptoms of SUT never or less than once a week, with
69% never experiencing SUI. On the UDI-6, 86% of the patients reported either never or rarely
being bothered by symptoms of SUI. The postoperative mean QOL related to urinary symptoms
was 1.5 (scale of 0– 6), between pleased and mostly satisfied.
Patients were asked to list the number of pads used per day regardless of the indication
(SUI, UI, protection, hygiene, etc.). The mean number of pads used before surgery was 2.5 and
postoperatively 0.8 (P , .05). Postoperatively, 61% of patients reported never wearing pads.
There was no statistically significant difference between maximum flow rates and postvoid
residuals obtained before and after surgery. In addition, patients were asked to rate their percent
improvement in a scale of 0– 100%. The patients reported an average improvement of 86% after
surgery.
Combining all the available data, we defined failures as patients who reported being
,50% improved, had a positive Marshall’s test on physical exam, or reported severe symptoms
of or bother from SUI on questionnaires. With this definition, the failure rate was 11%, and the
cure or improved rate 89%. Objective cure rate, defined as a negative stress test on physical
exam with the patient in the standing and lithotomy positions, was 92%.
 Distal Urethral Polypropylene Sling 425

V. CONCLUSIONS

The etiology of female SUI appears to be more complex than previously understood. Although
the proximal urethra is the primary continence mechanism, the distal urethra appears to play an
essential role as a compensatory mechanism. Repairs directed at either the bladder neck or the
distal urethra appear to be effective. The middistal suburethral polypropylene sling offers an
inexpensive, safe, and simple alternative treatment for patients with SUI. The procedure offers
high objective but lower patient-determined, subjective cure rates.
Although numerous sling procedures have been described, their efficacies are highly
variable. It is clear that variations in how authors measure success, and the lack of objective
outcome analysis, have made it very difficult to evaluate all these procedures. There is a need
for well-controlled, randomized outcome studies before definite determinations regarding the
efficacy and durability of these procedures can be made.

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17. Ulmsten U, Henriksson L, Johnson P, Varhos G. An ambulatory surgical procedure under local anesthesia
for treatment of female urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 1996; 7:81.
426 Rodrı́guez

18. Lebret T, Lugagne PM, Herve JM, Barre P, Orsoni JL, Yonneau L. Evaluation of tension-free vaginal
tape procedure. Its safety and efficacy in the treatment of female stress urinary incontinence during the
learning phase. Eur Urol 2001; 40:543.
19. Jeffry L, Deval B, Birsan A, Soriano D, Darai E. Objective and subjective cure rates after tension-free
vaginal tape for treatment of urinary incontinence. Urology 2001; 58:702.
20. Haab F, Sananes S, Amarenco G, Ciofu C, Uzan S, Gattegno B. Results of the tension-free vaginal
tape procedure for the treatment of type II stress urinary incontinence at a minimum followup of 1
year. J Urol 2001; 165:159.
21. Brophy MM, Klutke JJ, Klutke CG. A review of the tension-free vaginal tape procedure: outcomes,
complications, and theories. Curr Urol Rep 2001; 2:364.
22. Carlin BI, Klutke JJ, Klutke CG. The tension-free vaginal tape procedure for the treatment of stress
incontinence in the female patient. Urology 2000; 56:28.
23. Azam U, Frazer MI, Kozman EL, Ward K, Hilton P, Rane A. The tension-free vaginal tape procedure
in women with previous failed stress incontinence surgery. J Urol 2001; 166:554.
24. 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 2001; 12(suppl 2):S12.
25. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in women with recurrent stress urinary
incontinence—a long-term follow up. Int Urogynecol J Pelvic Floor Dysfunct 2001; 12(suppl 2):S9.
26. Nilsson CG, Kuuva N, Falconer C, Rezapour M, Ulmsten U. Long-term results of the tension-free
vaginal tape (TVT) procedure for surgical treatment of female stress urinary incontinence. Int
Urogynecol J Pelvic Floor Dysfunct 2001; 12(suppl 2):S5.
27. 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 2001; 108:414.
28. Niemczyk P, Klutke JJ, Carlin BI, Klutke CG. United States experience with tension-free vaginal tape
procedure for urinary stress incontinence: assessment of safety and tolerability. Tech Urol 2001;
7:261.
29. Moran PA, Ward KL, Johnson D, Smirni WE, Hilton P, Bibby J. Tension-free vaginal tape for
primary genuine stress incontinence: a two-centre follow-up study. BJU Int 2000; 86:39.
30. Kuuva N, Nilsson CG. A nationwide analysis of complications associated with the tension-
free vaginal tape (TVT) procedure. Acta Obstet Gynecol Scand 2002; 81:72.
31. Madjar S, Tchetgen MB, Van Antwerp A, Abdelmalak J, Rackley RR. Urethral erosion of tension-
free vaginal tape. Urology 2002; 59:601.
32. Klutke C, Siegel S, Carlin B, Paszkiewicz E, Kirkemo A, Klutke J. Urinary retention after tension-
free vaginal tape procedure: incidence and treatment. Urology 2001; 58:697.
33. Rodriguez LV, Raz S. Polypropylene sling for the treatment of stress urinary incontinence. Urology
2001; 58:783.
34. Rodriguez LV, Berman J, Raz S. Polypropylene sling for treatment of stress urinary incontinence: an
alternative to tension-free vaginal tape. Tech Urol 2001; 7:87.
35. Lee RS, DeAntoni E, Daneshgari F. Compliance with recommendations of the urodynamic society for
standards of efficacy for evaluation of treatment outcomes in urinary incontinence. Neurourol Urodyn
2002; 21:482.
36. Blaivas JG, Appell RA, Fantl JA, Leach G, McGuire EJ, Resnick NM. Standards of efficacy for
evaluation of treatment outcomes m urinary incontinence: recommendations of the urodynamic
society. Neurourol Urodyn 1997; 16:145.
37. Corcos J, Beaulieu S, Donovan J, Naughton M, Gotoh M. Quality of life assessment in men and
women with urinary incontinence. J Urol 2002; 168:896.
38. Deval B, Jeffry L, Al Najjar F, Soriano D, Darai E. Determinants of patient dissatisfaction after a
tension-free vaginal tape procedure for urinary incontinence. J Urol 2002; 167:2093.
39. Sirls LT, Keoleian CM, Korman HJ, Kirkemo AK. The effect of study methodology on reported
success rates of the modified Pereyra bladder neck suspension. J Urol 1995; 154:1732.
40. Eisen SV. Assessment of subjective distress by patients’ self-report versus structured interview.
Psychol Rep 1995; 76:35.
 Distal Urethral Polypropylene Sling 427

41. Chaikin DC, Blaivas JG. Weakened cadaveric fascial sling: an unexpected cause of failure. J Urol
1998; 160:2151.
42. Morgan TO Jr, Westney OL, McGuire EJ. Pubovaginal sling: 4-year outcome analysis and quality of
life assessment. J Urol 2000; 163:1845.
43. Haab F, Trockman BA, Zimmern PE, Leach GE. Results of pubovaginal sling for the treatment of
intrinsic sphincteric deficiency determined by questionnaire analysis. J Urol 1997; 158:1738.
44. Hassouna ME, Ghoniem GM. Long-term outcome and quality of life after modified pubovaginal sling
for intrinsic sphincteric deficiency. Urology 1999; 53:287.
45. Tegerstedt G, Sjoberg B, Hammarstrom M. Clinical outcome or abdominal urethropexy-
colposuspension: a long-term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 2001; 12:161.
46. Ward K, Hilton P. Prospective multicentre randomised trial of tension-free vaginal tape and
colposuspension as primary treatment for stress incontinence. BMJ 2002; 325:67.
29
Transvaginal Cooper’s Ligament Sling for the
Treatment of Stress Urinary Incontinence and
Low-Pressure Urethra

Sanjay Gandhi and Peter K. Sand

Evanston Continence Center, Northwestern University, Evanston, Illinois, U.S.A.

I. INTRODUCTION

Many consider retropubic urethropexies and bladder neck slings to be the standard of care
surgeries for the surgical treatment of stress urinary incontinence (SUI). Although the increased
enthusiasm for midurethral tape procedures has shifted some focus from these traditional
operations, they still enjoy the best long-term results.
In women with intrinsic sphincteric deficiency and urethral hypermobility, surgical treatment
focuses on increasing urethral resistance. Standard colposuspensions, such as the Burch or
Marshall-Marchetti-Krantz retropubic urethropexies, improve the support of the sphincteric unit
without obstruction. Most reports suggest that these procedures are less successful in patients with
intrinsic sphincteric deficiency (1–4). McGuire first suggested that failure of multiple incontinence
procedures was associated with the presence of low resting urethral pressure (,20 cmH2O) with or
without urethral hypermobility (1). Hilton and Stanton reported that patients whose surgery failed
had relatively lower proximal or maximal urethral closure pressures postoperatively than those with
a successful surgery (2). Sand and colleagues reported a 54% failure rate for Burch colposuspension
in patients with a maximum urethral closure pressure 20 cmH2O, compared with 18% in women
with “normal” urethral pressures (4). Other studies (3,5) have confirmed these findings and have
been used to justify the use of sling procedures for the treatment of intrinsic sphincteric deficiency.
Since the introduction of the laparoscopic retropubic urethropexy (6), there has been signi-
ficant enthusiasm for minimal-access techniques. Minimally invasive vaginal sling procedures
along with the availability of allografts and xenografts enable the surgeon to recreate the bladder
neck support offered by slings, but without the morbidity of an abdominal incision and a graft
harvest. In response to this trend, we developed an entirely transvaginal sling procedure with the
graft tied to Cooper’s ligament with no intervening suture bridges (7).

II. PROCEDURE

Cooper’s ligament—as opposed to rectus fascia-is utilized as the anchoring structure for this sling
to allow for an immobile suspension point to remove anterior mobility as a variable while tensioning
429
430 Gandhi and Sand

the sling. Cooper’s ligament has been proven a strong structure for supporting the bladder neck
abdominally and has been used for abdominal-vaginal slings. The Capio CL device (Boston Scientific,
Natick, MA) is used to place sutures into Cooper’s ligament (Fig. 1). The sling material is tied such that
it directly apposes the ligament without intervening suture bridges. In theory, this technique creates a
sling that is independent of abdominal-wall activity and changes in rectus muscle tone.
A Foley catheter is inserted to drain the bladder and identify the urethrovesical junction.
Dilute vasopressin solution is injected beneath the epithelium of the anterior vaginal wall. An
inverted midline T-incision is made on the anterior wall of the vagina extending from the base of
the bladder to approximately 2 cm proximal to the external urethral meatus. The vaginal epithelium
is sharply dissected from the underlying endopelvic connective tissue bilaterally to the level of the
descending pubic rami. Metzenbaum scissors are used to perforate right against the rami at the level
of the bladder neck to avoid bladder injury and to assure proper entrance into the retropubic space
(Fig. 2). On entry into the retropubic space, Cooper’s ligament is palpated and cleared of any fatty
tissue. This may be challenging in women with prior retropubic operations, but it does not prevent
us from placing sutures in Cooper’s ligament. Especially in patients with prior incontinence
operations, lysis of any urethral attachments to the pubis allows mobility of the urethrovesical
segment and facilitates proper positioning of the sling at the bladder neck.
The Capio CL device is used to deliver permanent monofilament sutures bilaterally into
Cooper’s ligament (Figs. 3, 4). A laminated tape measure is backloaded onto one suture and used
to measure the distance from the suture insertion in the ligament to the bladder neck. Doubling of

Figure 1 Capio CL device.

 Transvaginal Cooper’s Ligament Sling 431

Figure 2 Entry into retropubic space.

this length defines the sling length required. Anterior colporrhaphy, if needed, is performed prior
to measuring the length of the sling. If cadaveric fascia is to be used, the ends are airplane-folded
to prevent suture pull through as previously described (8). Both suture ends are passed through
the ends of the sling graft previously pierced with 16-gauge angiocaths. The sling is then tied in
place bilaterally to Cooper’s ligament with no suture bridges between the sling and the ligament.
Other surgeons have used a similar technique to place a suture suspended sling (Fig. 5).
Although some authors have suggested avoiding straightening a folded sling (9), we prefer
anchoring the anterior and posterior edges of the sling periurethrally to prevent the sling from
rolling up when fascia is used. The vagina is then closed.

III. MATERIAL

The choice of sling material has generated much controversy in the literature. Although many
case series have described success rates for sling procedures, only a handful have described the
in vivo tissue changes that occur and might affect operative success. Because of significant local
complications associated with synthetic materials, many surgeons have used autologous fascia,
but it is associated with increased operative time, convalescence, and pain. Cadaveric allograft
fascia might offer decreased operating-room time and patient morbidity, but there has been
controversy as to their durability (10 – 12). Different tissue processing techniques may affect the
432 Gandhi and Sand

Figure 3 Inserting device behind pubic bone.

durability of allografts; solvent dehydration may provide an advantage over freeze-dried tissues
as it preserves the tensile strengths of collagen in in vitro studies (13,14).
We initially used freeze-dried cadaveric fascia in 68% of our cohort. We are currently
using porcine dermis for our slings: it is easier to manipulate, remains intact in vivo for at least
2 years, and does not require airplane-folding the ends to prevent suture pullout as described
with fascial allografts (14,15). In the absence of a randomized trial comparing sling materials,
we cannot be sure which is best (16).

IV. OUTCOMES

In our initial case series, we operated on 105 women with SUI, low urethral closure pressure, and
urethral hypermobility. These women all had a transvaginal Cooper’s ligament anchored sling.
Subjective stress and urge incontinence symptoms were assessed, and patients underwent
urodynamic testing preoperatively and at 14 weeks postoperatively. Objective assessment at 1
year included a standing stress test at 250 mL and structured pelvic examination.
Women in the cohort had an average age of 70 years and an average mean body mass
index of 26.8 kg/m (2). On preoperative questionnaires 71% of women had symptoms of stress
 Transvaginal Cooper’s Ligament Sling 433

Figure 4 Retropubic view of device in proper position over Cooper’s ligament.

incontinence while 77% had urge incontinence. On preoperative urodynamic testing, the mean
preoperative closure pressure was 12.3 cm H2O, and 78% of our cohort had concomitant
detrusor overactivity on urethrocystometry. All women had SUI and a low-pressure urethra on
urodynamic testing with and without support of concomitant prolapse.
At 14 weeks follow-up, 64 of 91 women (70%) had objective cure of their stress
incontinence, while 20 women (22%) developed type III stress incontinence with operative
correction of their urethral hypermobility. Seven women (8%) had recurrent stress incontinence
with urethral hypermobility. Sixty-seven percent of women with objective failures at 14 weeks
were asymptomatic of stress incontinence. Overall, 16 of 91 women were symptomatic of stress
incontinence postoperatively. Of those women with preoperative detrusor overactivity, 90% had
persistent detrusor overactivity on urodynamic testing, and 48% of women without preoperative
detrusor overactivity developed de novo detrusor overactivity.
At 1-year follow-up, 84% of women had subjective cure of their stress incontinence
while 42% had a subjective cure of their urge incontinence. Eighty-eight percent of those
tested had a negative stress test and an objective cure of their preoperative stress incontinence.
Voiding dysfunction was similar to other sling procedures that have been documented in
previous studies (17 – 19). The median time to normal voiding for the cohort was 10 days.
The majority of patients used clean intermittent self-catheterization. Ninety percent of women
were voiding with normal residuals (,50 mL) by 6 weeks. Frequently, patients who
underwent the sling procedure described a delay in initiation of voiding and a less forceful
stream. We had two women who underwent urethrolysis for prolonged retention and who are
currently voiding well.
434 Gandhi and Sand

Figure 5 Tying sling into place from Cooper’s ligament to Cooper’s ligament.

V. COMPLICATIONS

There were no intraoperative complications directly related to the sling procedure. One woman
had a stroke in the evening after surgery; one woman developed a retropubic hematoma that was
drained percutaneously; and there were two fascial erosions into the vagina that were managed
in the office. Fewer than 5% of women had significant long-term voiding dysfunction requiring
self-catheterization beyond 12 months. Two women underwent urethrolysis to address post-
operative retention and did well.

VI. CONCLUSION

Women in this cohort, who on average were older, were mildly overweight, had detrusor
overactivity, and had low closure pressures, have had good resolution of their stress incontinence
with the transvaginal Cooper’s ligament sling. The procedure is minimally invasive and pro-
vides the additional supportive benefits of a sling in preventing recurrent anterior vaginal wall
 Transvaginal Cooper’s Ligament Sling 435

prolapse. Because of anterior anchoring to Cooper’s ligament which is immobile, retention and
pareuresis are less common than we have seen with pubovaginal slings. These Capio CL
transvaginal slings are also associated with far less pain and offer the cosmetic advantage of no
abdominal incision. This also makes them ideal outpatient procedures. This operation has
become our standard for women with intrinsic sphincter insufficiency, replacing the need for
pubovaginal or transvaginal bone-anchored slings.

REFERENCES

1. McGuire EJ. Urodynamic findings in patients after failure of stress incontinence operations. Prog Clin
Biol Res 1981; 78:351.
2. Hilton P, Stanton SL. Urethral pressure measurement by microtransducer: the results in symptom-free
women and in those with genuine stress incontinence. Br J Obstet Gynaecol 1983; 90:919 – 933.
3. Bowen LW, Sand PK, Ostergard DR, Franti CE. Unsuccessful Burch retropubic urethropexy: a case-
controlled urodynamic study. Am J Obstet Gynecol 1989; 160:452 – 458.
4. Sand PK, Bowen LW, Panganiban R, Ostergard DR. The low pressure urethra as a factor in failed
retropubic urethropexy. Obstet Gynecol 1987; 69:399– 402.
5. Koonings PP, Bergman A, Ballard CA. Low urethral pressure and stress urinary incontinence in
women: risk factor for failed retropubic surgical procedure. Urology 1990; 36:245– 248.
6. Vancaillie TG, Schuessler W. Laparoscopic bladderneck suspension. J Laparoendosc Surg 1991;
1:169– 173.
7. Koduri S, Goldberg RP, Sand PK. Transvaginal therapy of genuine stress incontinence. Urology
2000; 56:23– 27.
8. Sutaria PM, Staskin DR. Cadaveric allograft strength: an assessment of the effects of preservation
techniques and the methods of suture fixation using two separate experimental models. Neurourol
Urodyn 1999; 18:324 –325.
9. Wright EJ. Current status of fascia lata allograft slings treating urinary incontinence: effective or
ephemeral? Tech Urol 2001; 7:81– 86.
10. Carbone JM, Kavaler E, Hu JC, Raz S. Pubovaginal sling using cadaveric fascia and bone anchors:
disappointing early results. J Urol 2001; 165:1605 – 1611.
11. Fitzgerald MP, Mollenhauer J, Brubaker L. Failure of allograft suburethral slings. BJU Int 1999;
84:785– 788.
12. Elliott DS, Boone TB. Is fascia lata allograft material trustworthy for pubovaginal sling repair?
Urology 2000; 56:772 – 776.
13. Kobayashi T, Takei T, Yagi R. Reconstruction of the four major ligaments in an unstable knee joint
after dislocation by solvent-preserved human fascia lata transplantation. Arch Orthop Trauma Surg
1989; 108:246 –249.
14. Lemer ML, Chaikin DC, Blaivas JG. Tissue strength analysis of autologous and cadaveric allografts
for the pubovaginal sling. Neurourol Urodyn 1999; 18:497 – 503.
15. Chaikin DC, Blaivas JG. Weakened cadaveric fascial sling: an unexpected cause of failure. J Urol
1998; 160:2151.
16. Choe JM, Kothandapani R, James L, Bowling D. Autologous, cadaveric, and synthetic materials used
in sling surgery: comparative biomechanical analysis. Urology 2001; 58:482– 486.
17. McLennan MT, Melick CF, Bent AE. Clinical and urodynamic predictors of delayed voiding after
fascia lata suburethral sling. Obstet Gynecol 1998; 92:608 –612.
18. Richter HE, Varner RE, Sanders E, Holley RL, Northen A, Cliver SP. Effects of pubovaginal sling
procedure on patients with urethral hypermobility and intrinsic sphincteric deficiency: would they do
it again? Am J Obstet Gynecol 2001; 184:14 – 19.
19. Beck RP, McCormick S, Nordstrom L. The fascia lata sling procedure for treating recurrent genuine
stress incontinence of urine. Obstet Gynecol 1988; 72:699 – 703.
30
Management of Postoperative Detrusor
Instability and Voiding Dysfunction
Peter O. Kwong and O. Lenaine Westney
University of Texas Health Science Center, Houston, Texas, U.S.A.

I. INTRODUCTION

Stress urinary incontinence (SUI) is frequently encountered in urology and urogynecology.

Today there are multiple surgical procedures, each with several variations for correcting SUI.
The selected surgery depends on the etiology (urethral hypermobility vs. intrinsic sphincter
deficiency) of the incontinence, and surgeon preference.
Anti-incontinence procedures have reported very good outcomes, with success rates
ranging from 80% to 95% initially (1). The Female Stress Urinary Incontinence Clinical
Guidelines Panel summary reported 48-month cure rates of 84% and 83% for retropubic
suspensions and suburethral slings, respectively (2).
Although the surgical procedures to correct SUI have been reasonably successful, there are
potential complications including persistent stress urinary incontinence, urethral erosion, de
novo detrusor instability, and urethral obstruction (3). Iatrogenic urethral obstruction occurs in
5 –20% following anti-incontinence procedures (4,5). With the Marshall-Marchetti-Krantz
retropubic suspension, urethral obstruction rates range from 5% to 20% (6,7). Holschneider et al.
reported a 5– 7% obstruction rate with transvaginal needle suspensions (8). With respect to
pubovaginal slings, there is a 2 –12% prolonged urinary retention rate (beyond 4 weeks) and a
3 –24% de novo urgency rate (9). The Female Stress Urinary Incontinence Clinical Guidelines
Panel noted a prolonged retention rate and de novo urgency rate of 6– 11% and 3 –11% in sling
procedures, 3 –7% and 8– 16% in retropubic suspensions, and 4– 8% and 3– 10% in transvaginal
needle suspensions (2).
Tension-free vaginal tape (TVT), which is supposed not to cause obstruction because it
ideally is placed tension free, is not immune from inducing iatrogenic urethral obstruction
requiring tape division (10,11). Carlin et al.’s TVT series of more than 100 patients had 3%
de novo urgency and ,1% prolonged urinary retention (12). Even the minimally invasive
transurethral injection of collagen has a 13% incidence of de novo detrusor instability and a 2%
incidence of urinary retention (13).
Postoperative urgency and urge incontinence may be due to urethral obstruction or due to
detrusor instability, which may be de novo or preexisting. Detrusor instability has been defined
urodynamically as an involuntary detrusor contraction of any magnitude with an urge or increased
detrusor pressure of 15 cmH2O or greater without urge (14). Forty percent to 55% of patients
437
438 Kwong and Westney

with SUI also have coexisting urge incontinence and urgency that are not demonstrated
urodynamically. Hence, the distinction between motor urgency (with involuntary detrusor
contractions) and sensory urgency (without involuntary detrusor contractions) has been identified
to describe symptomatology that fails to correlate with urodynamic findings. In patients with urge
incontinence, urodynamic evidence of detrusor instability is present in 50–90% (15). Preexisting
urge incontinence resolves in 50–80% after correction of the SUI (9,15). While many series have
failed to reveal any preoperative parameter to predict whose urge incontinence will resolve
postoperatively, a recent study by Schrepferman et al. showed that patients with SUI and
preoperative low-pressure (detrusor contractions ,15 cmH2O) motor urgency were much more
likely (92% cure) to have resolution of urgency symptoms postoperatively, in contrast to those
with high-pressure motor urgency (27.8% cure) or with sensory urgency (39.3% cure) (15).
In lieu of detrusor instability (persistent or de novo), the post-operative development of
voiding dysfunction may be due to iatrogenic urethral obstruction. The cause of the obstruction
is usually secondary to over-correction of the urethrovesical angle (urethral hypersuspension) by
excess tension of the suspension sutures (retropubic or sling), urethral distortion by a suture
placed to close to the urethra or by buckling of the sling material (3,16). The obstruction then
leads to obstructive and/or irritative voiding symptoms or urge incontinence. These symptoms
can be very distressing to the patient, as she has now traded stress urinary incontinence for what
many consider more problematic and unpredictable-urge incontinence. Thus, the patient should
be informed preoperatively about the possible post-operative complications and the plan to treat
them if the complications arise (3).

II. PRESENTATION OF POSTOPERATIVE VOIDING DYSFUNCTION

Urethral obstruction following anti-incontinence surgery often presents as urinary retention or

obstructive voiding symptoms (hesitancy, incomplete bladder emptying, weak urinary stream,
urinary straining), but many patients present primarily with irritative voiding symptoms
(urgency, frequency, nocturia) and urge incontinence. Recurrent urinary tract infections may
also point to occult outlet obstruction. Upon further evaluation, these patients usually
demonstrate elevated postvoid residuals (3). In studies of patients who developed urethral
obstruction after anti-incontinence surgery, 60 –84% presented with obstructive symptoms, and
55 –75% presented with irritative symptoms (1,3,16). Therefore, one must suspect iatrogenic
urethral obstruction in any patient who presents with obstructive and/or irritative voiding
symptoms or recurrent urinary tract infections (UTIs) following an anti-incontinence procedure.
It is not unusual to see a brief period of voiding dysfunction and poor bladder emptying
during the immediate postoperative period. This may be explained by a local inflammatory
reaction in the area of the surgical dissection. These symptoms are usually transient and normal
voiding returns when the response resolves (usually within 2–4 weeks). During this period, the
patient is instructed to perform self-catheterization after voiding until postvoid residuals are
,60 mL, which indicates return of efficient bladder emptying (9). If voiding dysfunction persists
beyond 6–12 weeks or if urinary retention persists beyond 4 weeks, then one should begin to be
concerned about urethral obstruction and initiate a formal workup for the voiding dysfunction.

III. EVALUATION OF VOIDING DYSFUNCTION

The evaluation of prolonged voiding dysfunction following anti-incontinence surgery includes

a complete history and physical, a postvoid residual, and full urodynamic study (filling and
 Postoperative Detrusor Instability 439

voiding phases). The history includes a voiding diary, current voiding pattern (daily number
of episodes of frequency/urgency/nocturia, amount of incontinence, obstructive symptoms),
type and date of the anti-incontinence surgery, and prior surgeries or treatments that may affect
urination and voiding pattern prior to the anti-incontinence procedure. The physical examination
should be thorough—abdominal, pelvic, and neurological. One should note the position of the
urethra and whether it is mobile or fixed against the retropubis with Valsalva, urine leakage
with Valsalva or cough, and presence of any pelvic organ prolapse. With frank urethral
hypersuspension, the urethra is fixed in a high retropubic position, at times creating a relative
anterior vaginal wall prolapse (4).
A post-void residual urine volume should also be obtained in all patients regardless of
specific symptomatology. A large postvoid residual in the patient with frequency suggests that
an underlying obstruction may be the cause of the irritative voiding symptoms (3).
Cystoscopy may also be performed, looking for urethral distortions or suture/sling
erosion. Careful examination may document severe anterior deviation due to excessive suture or
sling tension. Additionally, irritative symptoms and/or UTIs may herald exposure of synthetic
material to the urinary stream.
The urodynamic evaluation includes a free-flow measurement, a multichannel
fluoroscopic urodynamic study with provocative maneuvers to evaluate bladder compliance,
instability, and persistent SUI. A pressure-flow voiding study is performed to evaluate maximum
detrusor pressure during voiding, looking for evidence of obstruction. Fluoroscopic cysto-
urethrography is helpful in identifying the specific site of obstruction. However, in females,
definitive evidence of voiding dysfunction (especially obstruction) on urodynamic studies has
proven to be very difficult, with no consistent findings.
The diagnosis of bladder outlet obstruction (BOO) in females has gradually evolved as it
has become apparent that the criteria classically used to diagnose obstruction in males do not
apply in females. Women normally have significantly lower voiding detrusor pressures than
males. Many women void by relaxing the pelvic floor muscles or by abdominal straining with
very low or no detrusor pressure. This has led several investigators to redefine the criteria for
diagnosing BOO obstruction in females (17).
Farrar et al. diagnosed obstruction primarily by flow rates, using Qmax , 15 mL/sec with
a voided volume of at least 200 mL as criteria for obstruction. They believed that relative BOO
with low Qmax may exist even with normal or low detrusor pressure (18). Massey and Abrams
defined female BOO if two or more of four parameters were present, including Qmax , 12 mL/
sec, detrusor pressure at Qmax . 50 cmH2O, urethral resistance (Pdet Qmax =Q2max ) . 0.2, or
significant postvoid residual (PVR) with high pressure or resistance (19). Axelrod and Blaivas
proposed the BOO criteria of Pdet Qmax . 20 cmH2O and Qmax , 12 mL/sec (20). Later, Nitti
et al. recommended video fluorourodynamics during voiding to diagnose BOO by radiographic
evidence of obstruction (closed or narrow bladder neck or discrete area of urethral narrowing
with proximal dilatation), not using any strict pressure-flow criteria. However, they did note that
patients with radiographic evidence of BOO had lower mean Qmax, higher mean Pdet Qmax, and
higher mean PVR than patients with no obstruction. As with all of the other studies, there was
wide variability in the urodynamic parameters (17).
Chassagne et al. analyzed clinically obstructed women to define a set of cutoff urodynamic
parameters to diagnose BOO in women. The parameters of Qmax , 15 mL/sec and Pdet
Qmax . 20 cmH2O were used (21). However, Qmax was obtained with a transurethral catheter in
place during the pressure-flow study. The transurethral catheter can lead to test-induced BOO
due to urethral irritation and/or relative mechanical obstruction of the urethra. Therefore, Groutz
et al. compared the “free” Qmax from the uroflow study and the Qmax from the pressure-flow
study, finding that “free” Qmax was significantly higher than Qmax, while the voided volume was
440 Kwong and Westney

the same (22). However, Lemack and Zimmern’s study did not reveal any significant
difference (23).
Most recently, Blaivas and Groutz compared 50 unobstructed female controls with 50
women with obstruction as defined by the presence of one or more of three parameters, including
(a) free Qmax  or 12 mL/sec in repeated flow studies with a sustained detrusor contraction and
with Pdet Qmax  20 cmH2O; (b) radiographic evidence of BOO during a sustained detrusor
contraction of at least 20 cmH2O and low Qmax; and (c) sustained detrusor contraction of at least
20 cmH2O but unable to void. From their study, they constructed a nomogram that used the two
parameters of free Qmax and Pdet max to diagnose BOO in females. The nomogram was able to
separate obstructed from unobstructed women and also distinguished three zones of BOO
severity (mild, moderate, and severe). The three zones also correlated with symptom scores from
the AUA symptom index scale. They further emphasized that the nomogram should be used only
to help in the diagnosis of BOO in female, not to direct treatment (24).
There are no standardized criteria for obstruction in this patient population. Normally,
obstruction is characterized on pressure-flow study by elevated detrusor pressure (.30–
50 cmH2O) with low flow rate (,12 – 15 mL/sec). However, in the female with obstruction, this
finding is often absent. Nitti and Raz demonstrated urodynamic evidence of obstruction in only
56% of their patients who underwent and responded well to urethrolysis, while Carr and Webster
reported urodynamic evidence of obstruction in only 22% (16,25). One subset of patients who
responded well to urethrolysis despite documented low detrusor pressure and low flow rate or
urinary retention may be explained by the fact that some women void by urethral relaxation
without obvious detrusor activity. These patients likely had a relative urethral obstruction (16).
Evidence of uninhibited bladder contractions (motor urgency) may also be absent despite
subjective symptoms of urgency and urge incontinence (sensory urgency). In Cross et al.’s study,
only 30% with urge incontinence demonstrated urodynamic evidence of detrusor instability. Other
authors note that there are no preoperative factors, including urodynamic parameters and type of
and time from anti-incontinence surgery, that predicted success of the urethrolysis (3,4,16,26).
Even those with no detrusor contraction by urodynamic study responded well to urethrolysis.
However, there is a trend toward a lower success rate in patients with preexisting low bladder
contractility, large postvoid residual, or detrusor instability (1,25,27).
Owing to the variability of urodynamic findings in females with voiding dysfunction
after anti-incontinence surgery and no consistent urodynamic parameter that predicts outcome
of urethrolysis, many physicians do not base their decision to perform urethrolysis on the
urodynamic study alone. According to Carr and Webster, the best indicators of obstruction after
anti-incontinence surgery are new irritative or obstructive voiding symptoms or urge incon-
tinence in addition to a physical exam that reveals urethral hypersuspension. The absolute
criterion for urethrolysis is the correlation between the time of onset voiding dysfunction and the
anti-incontinence surgery (16,28). Goldman et al. further report that the urodynamic study is not
required in a patient who had documented normal voiding pattern prior to the anti-incontinence
surgery, a clear temporal relationship between the anti-incontinence surgery and the onset of
voiding dysfunction, and a large postvoid residual (3). They had seven patients who fit these
criteria, five (75%) of whom responded well to urethrolysis.

IV. TREATMENT
A. Conservative Management
Conservative measures can be tried initially with the hope that the voiding dysfunction will
improve or resolve spontaneously. Intermittent self-catheterization can be employed if urinary
 Postoperative Detrusor Instability 441

retention or inefficient bladder emptying is the main problem. The decision to pursue a non-
operative course should also be based on knowledge regarding the material of the suspension
sutures and sling material. For example, synthetic sling and suture materials are less likely to change
with respect to urethral compression than an absorbable suture and organic sling combination.
For irritative voiding symptoms and detrusor instability, anticholinergic agents may be used
to give relief, but using anticholinergics in the face of obstruction may exacerbate poor bladder
emptying. The exact time course of the irritative symptom resolution is not well documented in
most incontinence procedure series. However, Cross et al. reported that 22 of 26 (85%) of patients
with de novo urge incontinence/urgency treated with anticholinergics and timed voiding were
symptom free within 3 months (29). In addition to pharmaceutical treatment, other conservative
therapeutic options including behavioral therapy, pelvic floor exercises, biofeedback, and
electrical stimulation, all of which are covered in other chapters, should be utilized.
The likelihood of spontaneous resolution or improvement of voiding dysfunction due to
obstruction is small if it has not occurred after 6 – 12 weeks postoperatively because the
periurethral scarring has fixed the proximal urethra and bladder neck to the retropubis. Thus,
surgical mobilization via urethrolysis is often required to correct the iatrogenic urethral
obstruction produced by hypersuspension of the urethra and bladder neck.

B. Surgical Management
1. Urethrolysis
The primary surgical approach to urethral obstruction is urethrolysis—transvaginal, retropubic,
or infrapubic (30 – 32). As previously stated, the timing of intervention is generally related to the

Figure 1 Inferior hypogastric innervation to the bladder.

442 Kwong and Westney

Figure 2 Injection of subtrigonal local anesthetic.

severity of the obstruction and the material used for the procedure. The selection of urethrolysis
technique is based on the number of prior attempt at urethrolysis, the type of anti-incontinece
procedure, and surgical experience. The individual techniques will be discussed in the following
chapter.

2. Other Surgical Procedures

If the symptoms are primarily those of detrusor instability and if urethrolysis fails to improve the
problem, other surgical options may be entertained, assuming that mechanical obstruction has
been eliminated. These procedures include partial bladder denervation (the Ingelman-Sundberg
procedure), detrusor myectomy, sacral nerve stimulation, and augmentation cystoplasty.
Detrusor myectomy, sacral nerve stimulation, and augmentation cystoplasty are covered in other
sections of this text.
In the 1950s, Ingelman-Sundberg originally described the bladder denervation procedure,
which relieved detrusor instability by disrupting the inferior hypogastric innervation to the
 Postoperative Detrusor Instability 443

Figure 3 Inverted-U incision for subtrigonal dissection.

bladder (33) (Fig. 1). It was believed that the sensory input from the trigone was decreased
while normal voiding and bladder sensation continued. Later modifications led to less extensive
dissection in the transvaginal approach to the partial bladder denervation procedure for the
treatment of refractory detrusor instability.
To determine who will most likely benefit from the partial bladder denervation procedure,
patients are initially screened by transvaginally injecting approximately 10 mL of 0.25%
bupivacaine into the subtrigonal area using a 22-gauge spinal needle to temporarily block the
nerves that would be transected by the denervation procedure (Fig. 2) Patients who experienced
significant relief of symptoms during the following 24 h would then be offered the partial
bladder denervation procedure (34).
The patient is placed in a dorsal lithotomy position, and a 16F Foley catheter is placed
into the bladder. A weighted vaginal speculum is placed for retraction. An inverted-U incision
centered over the trigone is made on the anterior vaginal wall. With plane of dissection super-
ficial the bladder serosa, the vaginal epithelium and perivesical fascia are sharply dissected
444 Kwong and Westney

off of the trigone, thus disrupting the innervation to this area (Fig. 3). The limits of the
dissection are extended laterally and posteriorly to the terminal branches of the pelvic nerves.
The vaginal mucosa incision is closed with locked running or interrupted 2-0 chromic suture; a
betadine-soaked or estrogen cream – impregnated vaginal pack is placed. The procedure takes
15– 20 min. The vaginal pack and Foley catheter are removed the next day, checking the
postvoid residual to confirm adequate bladder emptying.
Response rates have been demonstrated to be durable with a long-term positive response
(median follow-up of 44.1 months) of 68%, with complete response in 54% and partial response
in 14% (35). Thus, the Ingelman-Sundberg partial-bladder denervation procedure offers a
minimally invasive option in those determined to be responders by pretest injection.

V. CONCLUSION

The surgical correction of SUI is commonly performed with very high rates of cure of the SUI.
However, postoperative voiding dysfunction can decrease the patient’s satisfaction with
the procedure. The signs of obstruction may be UTIs, irritative symptoms, or obstructive
symptoms. While the irritative symptoms may resolve spontaneously or respond to conservative
measures, patients having persistent symptoms require further workup including a urodynamic
evaluation. Often the only indication for additional surgery (i.e., urethrolysis) may be a temporal
relationship of onset of symptoms to the anti-incontinence surgery. For those who fail to
improve after urethrolysis and continue to have primarily severe irritative voiding symptoms
without evidence of obstruction, the Ingelman-Sundberg partial bladder denervation, detrusor
myectomy, sacral nerve stimulator, or augmentation cystoplasty are options.

REFERENCES

1. Foster HE, McGuire EJ. Management of urethral obstruction with transvaginal urethrolysis. J Urol
1993; 150:1448 – 1451.
2. Leach, GE, Dmochowski RR, Appell RA, Blaivas JG, Hadley HR, Luber KM, Mostwin JL,
O’Donnell PD, Roehrborn CG. Female stress urinary incontinence clinical guidelines panel summary
report on surgical management of female stress urinary incontinence. J Urol 1997; 158:875 – 880.
3. Goldman HB, Rackley RR, Appell RA. The efficacy of urethrolysis without resuspension for
iatrogenic outlet obstruction. J Urol 1999; 161:196 – 198.
4. Cross CA, Cespedes RD, English SF, McGuire EJ. Transvaginal urethrolysis for urethral obstruction
after anti-incontinence surgery. J Urol 1998; 159(4):1199– 1201.
5. Appell RA. Editorial: urinary incontinence. J Urol 1994; 152:103– 104.
6. Zimmern PE, Hadley HR, Leach GE, Raz S. Female urethral obstruction after Marshall – Marchetti –
Krantz operation. J Urol 1987; 138:517 – 520.
7. McDuffie RW Jr, Litin RB, Blundin, KE. Urethrovesical suspension (Marshall – Marchetti – Krantz):
experience with 204 cases. Am J Surg 1981; 141:297– 298.
8. Holschneider CH, Solh S, Lebhertz TB, Montz FJ. The modified Pereyra procedure in recurrent stress
urinary incontinence: a 15-Year review. Obst Gynecol 1994; 83:573 – 578.
9. Westney OL, McGuire EJ. Pubovaginal sling. Atlas Urol Clin North Am 2000; 8(1):23 – 39.
10. Romanzi LJ, Blaivas JG. Protracted urinary retention necessitating urethrolysis following tension-
free vaginal tape surgery. J Urol 2000; 164:2022 – 2023.
11. Choe JM. Tension-free vaginal tape: is it truly tension-free? J Urol 2001; 166:1003.
12. Carlin BI, Klutke JJ, Klutke CG. The tension-free vaginal tape procedure for the treatment of stress
incontinence in the female patient. Urol 2000; 56(6)(suppl 1):28– 31.
 Postoperative Detrusor Instability 445

13. Dmochowski RR, Appell RA. Injectable agents in the treatment of stress urinary incontinence in
women: where are we now? Urol 2000; 56(6)(suppl 1): 32 – 40.
14. Carlson KV, Rome S, Nitti VW. Dysfunctional voiding in women. J Urol 2001; 165:143 –148.
15. Schrepferman CG, Griebling TL, Nygaard IE, Kreder KJ. Resolution of urge symptoms following
sling cystourethropexy. J Urol 2000; 164:1628 – 1631.
16. Carr LK, Webster GD. Voiding dysfunction following incontinence surgery: diagnosis and treatment
with retropubic or vaginal urethrolysis. J Urol 1997; 157:821– 823.
17. Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999;
161:1535– 1540.
18. Farrar DJ, Osborne JL, Stephenson TP, Whiteside CG, Weir J, Berry J, Milroy EJG, Turner
Warwick R. A urodynamic view of bladder outflow obstruction in the female: factors influencing the
results of treatment. Br J Urol 1975; 47:815– 822.
19. Massey, JA, Abrams PA. Obstructed voiding in the female. Br J Urol 1988; 61:36– 39.
20. Axelrod SL, Blaivas JG. Bladder neck obstruction in women. J Urol 1987; 137:497 – 499.
21. Chassagne S, Bernier PA, Haab F, Roehrborn CG, Reisch JS, Zimmern PE. Proposed cutoff values to
define bladder outlet obstruction in women. Urology 1998; 51:408 – 411.
22. Groutz A, Blaivas JG, Chaiken DC. Bladder outlet obstruction in women: definition and
characteristics. Neurourol Urodyn 2000; 19:213 – 220.
23. Lemack GE, Zimmern PE. Pressure flow analysis may aid in identifying women with outflow
obstruction. J Urol 2000; 163: 1823– 1828.
24. Blaivas JG, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract
symptomatology. Neurourol Urodynam 2000; 19:553 – 564.
25. Nitti VW, Raz S. Obstruction following anti-incontinence procedures: diagnosis and treatment with
transvaginal urethrolysis. J Urol 1994; 152:93– 98.
26. Dmochowski RR, Leach GE, Zimmern PE, Roskamp DA, Ganabathi K. Urethrolysis to relieve outlet
obstruction after prior incontinence surgery. J Urol 1997; 151:420. Abstract.
27. Austin P, Spyropoulos E, Lotenfoe R, Helal M, Hoffman M, Lockhart JL. Urethral obstruction after
anti-incontinence surgery in women: evaluation, methodology, and surgical results. Urology 1996;
47(6):890– 894.
28. Carr LK, Webster GD. Bladder outlet obstruction in women (Urodynamics II). Urol Clin North Am
1996; 23(3):385– 392.
29. Cross CA, Cespedes RD, McGuire EJ. Our experience with pubovaginal slings in patients with stress
urinary incontinence. J Urol 1998; 159:1195 – 1198.
30. McGuire EJ, Letson W, Wang S. Transvaginal urethrolysis after obstructive urethral suspension
procedures. J Urol 1989; 142:1037– 1039.
31. Webster GD, Kreder KJ. Voiding dysfunction following cystourethropexy: its evaluation and
management. J Urol 1990; 144:670– 673.
32. Petrou SP, Brown JA, Blaivas JG. Suprameatal transvaginal urethrolysis. J Urol 1999;
161:1268– 1271.
33. Westney OL, McGuire EJ. Surgical procedures for the treatment of urge incontinence. Tech Urol
2001; 7(2):126 – 132.
34. Cespedes RD, Cross CA, McGuire EJ. Modified Ingelman– Sundberg bladder denervation procedure
for intractable urge incontinence. J Urol 1996; 156:1744 – 1747.
35. Westney OL, Lee JT, McGuire EJ, Palmer JL, Cespedes DA, Amundsen CL. Long-term results of
Ingelman– Sundberg denervation procedure for urge incontinence refractory to medical therapy.
J Urol 1999; 161:77. Abstract.
31
Postoperative Complications of Sling Surgery

Elizabeth A. Miller and George D. Webster

Duke University Medical Center, Durham, North Carolina, U.S.A.

I. INTRODUCTION

The sling procedure for the treatment of urinary incontinence in women was described by
Goebell in 1910 using gracilis muscle (1) and was later modified by Aldrigde in 1942 (2), who
first described using abdominus rectus fascia for urethral compression. Since its inception in the
early part of the 20th century, the sling procedure had been modified and ultimately replaced by
other forms of anti-incontinence surgery, such as the retropubic and transvaginal bladder neck
suspensions. The concept of using a fascial strip to provide compression of the urethra was
revitalized in 1978, when McGuire et al. (3) described its use in the treatment of type III stress
urinary incontinence (SUI), or incontinence secondary to intrinsic sphincter deficiency (ISD).
Until very recently, the sling procedure was thought to only be effective in the treatment of ISD,
and anatomic descent was best treated with bladder neck suspension procedures. However, it is
now widely accepted as an effective treatment for type II SUI, or incontinence resulting from
urethral hypermobility/anatomic descent. The sling procedure has now gained widespread use
by both urologists and gynecologists. Cure rates for both types II and III incontinence range from
75% to 93%, with 95– 98% of women reporting significant improvement in symptoms (4,5).
However, along with its success and expanded utility has come a greater knowledge of the
complication profile. We are now aware of several well-described complications of the sling
procedure: urethral obstruction, de novo urgency, urethral/vaginal erosion, and infection.
This chapter will review the diagnosis and management of the most commonly described
complications of the sling procedure.

II. URETHRAL OBSTRUCTION

A. Clinical Presentation
Urethral obstruction is an uncommon but very disturbing complication of sling surgery. The
incidence of unintended urethral obstruction following the sling procedure varies and is reported
to be between 1% and 4% (4,5). Common presenting symptoms of urethral obstruction other
than urinary retention include new-onset urgency or urge incontinence and incomplete bladder
emptying. Fifty-five percent to 93% of women complain of irritative symptoms immedi-
ately following surgery (7,8). A similarly high percentage (64 –81%) either are performing
447
448 Miller and Webster

intermittent catheterization for incomplete emptying or are in urinary retention (68). Not all
women display obstructive symptoms, yet have urethral obstruction. In a series of women with
urethral obstruction resulting from bladder neck suspension and sling procedures, one-third
complained exclusively of irritative symptoms without other signs of obstruction such as
retention or high postvoid residual urine volumes (9). Identification of women with urethral
obstruction resulting in obstructive or irritative symptoms can be problematic, since detrusor
hypocontractility and de novo urge, respectively, share this symptomatology. Urodynamic
assessment, cystoscopy, and vaginal examination can help identify urethral obstruction.

B. Diagnosis: Urodynamics
Urodynamic evaluation can aid in the identification of functional obstruction following a sling
procedure. The urodynamic definition of urethral obstruction in women has not been agreed
upon; however, several definitions have been offered (Table 1). Nitti et al. (10) suggest that the
use of video fluoroscopy may be the most sensitive tool for the detection of obstruction. Using
video to identify obstruction, they found that obstructed women had higher detrusor pressures at
peak flow (42.8 vs. 22.1 cmH2O) and lower peak flow rates (9 vs. 20 cmH2O) than unobstructed
women.
Using the criteria of PDET .30– 40 cmH2O and PFR ,15 cc/sec, Amundsen (7), Carr
(11), and Nitti and Raz (12) show that only 33%, 22%, and 56%, respectively, showed no signs
of obstruction, but were likely obstructed based on the temporal relationship between onset of
symptoms and anti-incontinence surgery. In all three series, urethrolysis was at least 75%
successful. Additionally, urodynamic evidence of obstruction does not predict favorable surgical
outcomes following urethrolysis. Cross et al. (9) showed that in a comparison of those with and
without urodynamics signs of obstruction, the two groups did equally well after urethrolysis.
Amundsen et al. (7), in a study of 32 women, showed that of the 93.5% who had good
outcomes, 41% showed no evidence of obstruction on urodynamics. In Goldman’s study of
31 women, seven did not have preoperative urodynamics, and five of these (75%) had good
results following takedown, a success rate similar to that of those who had had urodynamics.
Based on this information, it has been concluded that urodynamic evaluation may not be
necessary in the evaluation of urethral obstruction following sling procedures. These authors feel
that sufficient valuable information is obtained from the study despite these reports to justify its
continued use, but certainly that equivocal studies should not be used to exclude women from a
sling takedown. The most important information in making the diagnosis of urethral obstruction
is the temporal relationship of the onset of symptoms to the sling procedure.

Table 1 Urodynamic Criteria for Urethral Obstruction

Author PDETa (cmH2O) PFRb (cc/sec)

Axelrod et al. (34) .20 ,15

Massey et al. (35) .50 ,12
Petrou et al. (15) .20 ,12
Amundsen et al. (7) ,15 ,12
Nitti et al. (10) Flouroscopically
a
PDET: detrusor pressure at peak flow rate.
b
PFR: peak flow rate.
 Postoperative Complications of Sling Surgery 449

C. Diagnosis: Cystoscopy and Vaginal Examination

Cystoscopy has also proven to be of benefit in diagnosing urethral obstruction in women after a
sling procedure. Cystoscopy provides information on the urethral axis, the presence of urethral
erosion, and loss of urethral mobility as identified by loss of the ability to sagitally rotate the
urethra, all of which are important elements in diagnosing urethral obstruction. Additionally, the
site of sling obstruction can often be seen as a posterior “knucle” in the urethra while viewing
the lumen with a 08 or 308 lens. An estimate of the urethrovesical angle is obtained by measuring
the angle of the cystoscope from horizontal that is required to maintain the urethral lumen in the
center of the cystoscopic field during urethroscopy. A normal urethrovesical angle with the
patient in the dorsal lithotomy position ranges from 08 to 308, where the horizontal axis is zero.
An obstructed urethra following a sling procedure often demonstrates negative (the eyepiece of
the cystoscope deflecting toward the floor) angulations, up to 608 or more. This negative
angulation is the result of excessive elevation of the mid to proximal urethra by a sling which is
too tight. Obstruction may also be suspected if rotation of the cystoscope in the sagittal plain is
restricted. Finally, sling erosion at the mid to proximal urethral is usually easily identified with
urethroscopy. Complete inspection of the bladder ensures that there is no suture or sling material
inside the bladder, causing irritative symptoms.
Vaginal examination in obstructed women following a pubovaginal sling procedure often
demonstrates retropubic angulation of the anterior vaginal wall at the level of the mid to
proximal urethra. The vaginal examination is also important in identifying other vaginal patho-
logy that may or may not be related to sling obstruction, such as vaginal erosions and prolapse.
Concurrent pathologies should be treated at the time of incision of the obstructing sling.

D. Treatment
Obstruction following a pubovaginal sling procedure can be treated by incising the sling or by
performing urethrolysis. Several approaches to sling incision or takedown have been described
(7,8). Our preferred technique is to incise the sling in the midline direcely beneath the urethra.
The sling is approached through a midline anterior vaginal wall incision, the incision being
carefully deepened until the often pristine and usually easily identifiable transversely oriented
fibers of the sling are encountered. The sling is often deeply located and the bladder may fold
over the sling, making the dissection quite intimidating. Repeated palpation of the sling over the
shaft of the cystoscope will help direct the dissection (6). The sling is circumferentially isolated
(Fig. 1) and incised in the midline and generally the urethra immediately sags between the
separated sling ends, confirming the release. Occasionally, more urethral mobility is needed and
the sling ends may be further dissected off of the urethra laterally (Fig. 2). Intraoperatively, the
success of the procedure may be determined by creding the full bladder and observing the
resulting urinary stream and by confirming restoration of adequate sagittal mobility using
the cystoscope. Amundsen et al. reported that 93.5% achieved efficient voiding within 1 week of
the procedure. Sixty-seven percent with urge incontinence had resolution of their symptoms.
Only three of 32 women in this study reported SUI symptoms following sling takedown; one of
these went on to receive periurethral collagen injection therapy.
Others have reported that urethrolysis can be performed for sling obstruction with equally
effective results. Vaginal urethrolysis for obstruction following abdominal and transvaginal
bladder neck suspension procedures was described by Zimmern (13) and Kreder (14) and
applied by several others in the treatment of sling and bladder neck suspension obstruction. Its
use in the treatment of sling obstruction has never been evaluated exclusively, since most
reported series include both sling and bladder neck suspensions without stratifying by procedure.
However, according to recent reports (8,9), the technique has been found to be effective for both,
450 Miller and Webster

Figure 1 Circumferential dissection of the sling in preparation for incision.

but it requires considerably more dissection than simple midline sling incision. We feel the
formal urethrolysis should be reserved for those in whom sling incision fails.
A variety of vaginal incisions can be employed for urethrolysis, including inverted
U-shaped, midline, paramedian, or suprameatal (15). The vaginal epithelium is elevated on
either side of the urethra, at the level of the obstruction (usually mid to proximal urethra). The
vesicopelvic and endopelvic fascial layers are incised sharply, and the retropubic attachments of
the urethra to symphysis are released. The endpoint of dissection is marked by achieving
sufficient urethral mobility as demonstrated by posterior rotation of the urethra while applying
pressure on the Foley catheter or a transurethral instrument (9) or complete circumferential
mobilization of the urethra from the undersurface of the symphysis (8). Although outcome
measures vary by study, 84 – 87% of women have significant improvement in voiding efficiency
(8,9), with a similar improvement in irritative symptoms (85%) and an overall cure rate of 72%
for both irritative and obstructive symptoms (9). Application of a Martius labial fat pad flap is
often necessary to prevent recurrence of urethral-symphyseal attachment with recurrent
obstruction in cases of secondary urethrolysis.
Recurrent incontinence following surgery to relieve sling obstruction ranges from 0% to
23%. The variation likey depends on the degree to which the urethra is mobilized. The
suprameatal approach is a unique approach to urethrolysis that limits lateral dissection and is
said to prevent recurrent incontinence (15). This technique uses an inverted U-shaped incision
from 9 to 3 o’clock 1 cm anterior to the urethral meatus. The plane between the urethra and
undersurface of the symphysis is developed, allowing direct visualization of the sling. This
technique differs from the previously described transvaginal urethrolysis in that the tethering
 Postoperative Complications of Sling Surgery 451

Figure 2 Clamped incised ends of the sling in preparation for further mobilization.

attachments can be released under direct vision, while the lateral vesicopelvic ligament is left
intact. Petrou et al. believe that by maintaining continuity of the vesicopelvic ligament, recurrent
incontinence can be prevented. There were no patients in their series of 12 women who
complained of posturethrolysis incontinence, compared with 2.5 –19% in other transvaginal
urethrolysis series (8,9). However, resolution of retention was not as good in this series
compared to others (Table 2).
Outcomes of urethrolysis or sling takedown may be dependent on the degree to which the
urethra is mobilized, or the presling anatomy is restored. Most women find the symptoms of
obstructions to be more bothersome than those of recurrent incontinence, and therefore are more
willing to trade the latter for resolution of irritative and obstructive symptoms. Therefore, the
goal of sling takedown or urethrolysis should be restoration of normal and efficient voiding.

E. Prevention of Urethral Obstruction

To our knowledge, there have been no practically useful and proven techniques to prevent
urethral obstruction during sling placement. However, most agree that there should be no tension

Table 2 Outcomes of Urethrolysis or Sling Incision for Treatment of Sling Obstruction

Resolution of retention Resolution of urgency Recurrent incontinent

Author (%) (%) (%)

Amundsen et al. (5) 93.5 67 9

Cross et al. (13) 87 85 2.5
Goldman et al. (8) 84 NA 19
Petrou et al. (15) 65 67 0
452 Miller and Webster

on the sling and therefore no visible compression of the urethra once the sling is secured in place
with the patient in the dorsal lithotomy position. Urethral compression by the sling is activated
during rises in intraabdominal pressure, as shown flouroscopically by Ghoneim et al. (16) They
showed flouroscopically that during straining the sling moves upward and cephalad, while the
bladder base moves downward and caudad. Appropriate tension, therefore, allows for urethral
compression during rises in intra-abdominal pressure only.
Several ideas have been proposed to identify the appropriate tension intraoperatively.
Measuring urethral pressure during the sling placement has been proposed but has not been
proven technically practical (3). Yamada et al. proposed ultrasounding the urethra-vesical angle
to identify inappropriate angulation of the urethra during sling placement. Finally, Blaivas and
Jacobs recommend placing downward tension on a cystoscope placed in the urethra while
securing the sling. The authors prefer to hold the sling several millimeters from the urethra,
while the assistant ties the suspending prolene sutures suprapubically. In this way, the sling is
positioned loosely beneath the urethra.
It is certainly true to say that sling tension probably needs to vary from patient to patient
depending on the degree of urethral hypermobility, the rigidity of the urethra, and perhaps even
the magnitude of the intrinsic sphincter deficiency. This is an evolving science, and at present we
have no objective way by which to determine the individual patient’s needs. Indeed, it is also
evident to all who perform pubovaginal sling surgery that sling tension seen at surgery may be
very different from what is seen several weeks later. We believe that it may be possible that the
sling, in some cases, shrinks during the remodeling process, or that the tension in the surgical
position may not translate into that which exists in the upright, ambulatory position, so that
despite appropriate tension placed at the time of surgery, urethral obstruction develops.

III. DE NOVO URGE

The etiology of new urge symptoms (de novo urge) after pubovaginal sling procedure is not
known. The incidence is reported to range from 7% to 17.5% (5,17,19). This incidence is
somewhat lower (0 – 15.6%) in recent outcome studies of the polypropylene mesh midurethral
sling (TVT or SPARC systems) (22,23). Often a thorough evaluation including vaginal exami-
nation, cystoscopy, and urodynamics in a patient with new-onset urgency after a sling procedure
will reveal obstruction. Irritative symptoms will resolve in up to 67– 85% following incision of
the obstruction sling, or urethrolysis without additional treatments, as was discussed in the
previous section. When obstruction has been definitively ruled out, de novo urge is present by
exclusion.
De novo urge may resolve within several months of the sling procedure. Kaplan et al. (19)
report one of the largest prospective analysis of the pubovaginal sling procedure. In this series,
30 of 373 women developed de novo urge, and eight of these (26%) had resolution of their
symptoms by the average 40-month follow-up interval. In a similar series of women undergoing
fascial sling, Juma et al. (24) found that 50% of those who reported initial de novo urge had
persistent urge several months after the sling procedure. Although most long-term studies have
not identified rates of de novo urge resolution, from our experience, most urge incontinence that
is seen in the early postoperative period, without coexistence of obstruction, will resolve. In the
interim, symptoms can be managed with a combination of behavioral therapy, pelvic floor
reeducation and strengthening, and anticholinergic medication such as tolterodine (Detrol) or
oxybutynin (Ditropan) with excellent results. If conservative management is not effective in
controlling irritative symptoms, the diagnosis of urethral obstruction should be readdressed.
 Postoperative Complications of Sling Surgery 453

IV. URETHRAL EROSION OR VAGINAL EXTRUSION

A. Clinical Presentation
Erosion of sling material either into the urethra or through the vaginal epithelium is rare and is
seen most commonly when synthetic sling material is used. The incidence of synthetic sling
erosion ranges widely, from 0% to 23% (25,26,28). However, more contemporary series have
reported lower erosion rates. The Female Stress Urinary Incontinence Clinical Guidelines Panel
of 1997 performed a rigorously selected meta-analysis of the incontinence literature dating from
1994 to 1997, and found the incidence of vaginal and urethral erosions with synthetic material
was 0.007% and 0.02%, respectively (29). In one of the largest and most recently reported
synthetic sling experiences to date, Choe and Staskin (25) report that five of 141 (4%)
consecutive Gortex patch slings developed vaginal erosions, and there were no urethral erosions.
Vaginal erosion rates with polypropylene mesh slings using the TVT system are similarly low,
0.4%, with no reported urethral erosions (22). Kobashi et al. (30) found the prevalence of vaginal
erosions to be more common than urethral extrusion. Their study reviewed 34 women who
presented with woven polyester sling erosion: 50% vaginal, 20% urethral, and 17% concurrent
urethrovaginal. Erosion using autologous or allogenic fascial slings is reported to be 0.007%
according to the Female Stress Urinary Incontinence Clinical Guidelines Panel, and reported
only in case series (31,32). Autologous and allogenic fascial erosions more commonly involve
the urethra as the result of excessive sling tension during initial placement. Amundsen and
Webster (33) recently reported a series of nine patients who developed urethral erosion and sling
obstruction. The nine slings involved included: allograft fascia lata (5), autologous rectus (1),
woven polyester treated with bovine collagen (2), and Prolene mesh (1).
We feel that it is important to differentiate between urethral and vaginal erosion of sling
material. In the former, the sling material is surgically removed from the urethral lumen, and the
urethra is closed, while vaginal expulsion of sling material can be treated more conservatively
(see Sec. IV.C below).

B. Diagnosis
Chronic vaginal discharge and vaginal pain or pressure are the most common presenting
symptoms of vaginal erosion. Vaginal examination may reveal granulation tissue, without overt
evidence of erosion. However, careful examination will uncover sling material beneath the
granulation tissue in most cases. Symptoms of urethral erosion include dysuria and urethral
pain, irritative voiding symptoms, recurrent incontinence or urinary retention, and macro- or
microscopic hematuria. In Amundsen’s recent report of sling urethral erosions (33), 50%
presented with retention, while the remaining had urge incontinence requiring at least three pads
per day. Urethral erosion should also be suspected when a patient complains of persistent
dysuria, without evidence of urinary tract infection. The diagnosis is made by urethroscopy,
which reveals the sling as a glistening white material within the urethral lumen or at the 6
o’clock position. Erosions of either type have been reported to occur up to 4 years from the time
of the initial surgery. Golomb et al. (32) report a case of an autologous fascial sling in which the
patient developed an acute UTI and urinary retention. The catheterization was traumatic, and
shortly thereafter the patient developed severe irritative symptoms. Barbalias and Barbalias (28)
similarly report two patients in which their Gortex sling erosion presented 3.5 years after initial
placement. Therefore, the index of suspicion for a vaginal or urethral erosion should remain
high when women present with classic symptoms of erosion, despite the time interval between
placement and presentation.
454 Miller and Webster

C. Treatment
Treatment of urethral or vaginal erosion requires sling removal. Synthetic sling material must be
removed completely. Autologous and allogenic material should be removed at the site of
erosion, but residual material located lateral to the urethra and within the retropubic space may
be left in situ (32,33). Suspending sutures for both synthetic and autologous/allogenic may also
remain in place. Synthetic slings are associated with a variable degree of scar. Some are encased
in a pseudosheath and are easily removed (30). Others are heavily embedded in dense fibrosis.
Autologous and allogenic slings are usually found with very little reactive tissue and well
preserved (7). After removing sling material, the urethra may be primarily closed with
absorbable suture, or left open to heal with catheter stenting. We prefer primary closure of the
urethra. Martius labial fat flaps may be used to cover the urethra in the event that urethral
damage is significant, or vaginal and urethral erosions have occurred concurrently and where
fistula development is feared. Extensive vaginal erosion may be covered with a Martius skin
island pedicle flap. When treating urethral erosions, a urethral catheter is usually left in place for
7 days, or alternatively, the urine may be diverted with a suprapubic catheter for a similar
amount of time. Some recommend a voiding cystourethrogram prior to suprapubic tube removal
to ensure urethral integrity.
Vaginal erosions of autologous or allogenic sling material very often epithelialize over and
do not need surgical revision. This process can be aided with the use of topical estrogen cream.
When synthetic material has eroded through the vaginal epithelium, it can be locally excised
with good success.

V. CONCLUSION

In summary, the sling procedure for stress urinary incontinence is a safe and effective procedure.
The most common complications, urethral obstruction, de novo urge, and sling erosion, are
uncommon and can usually be managed effectively.

REFERENCES

1. Goebell R. Zur operativen beseitigung der angebornen inctoninentia vesicae. Ztschr Gynak 1910;
2:187– 190.
2. Aldridge A. Transplantation of fascia for relief of urinary stress incontinence. Am J Obstet Gynecol
1942; 44:398 –342.
3. McGuire E, Lytton B. Pubovaginal sling procedure for stress incontinence. J Urol 1978; 1191:82 –84.
4. Wright JE, Carr LK, Webster GD. Pubovaginal sling using cadaveric allograft fascia for the treatment
of intrinsic sphincter deficiency. J Urol 1998; 160:759 – 762.
5. Cross CA, McGuire EJ. Our experience with pubovaginal slings in patients with stress urinary
incontinence. J Urol 1998; 159:1195– 1198.
6. Webster GD. Cadaveric fascia slings. Atlas of the Urol Clinics of North America 2000; 81:41 – 49.
7. Amundsen CL, Webster GD. Variations in strategy for the treatment of urethral obstruction after a
pubovaginal sling procedure. J Urol 2000; 164:434– 437.
8. Goldman HB, Rackley RR, Appell RA. The efficacy of urethrolysis without re-suspension for
iatrogenic urethral obstruction. J Urol 1999; 1611:196– 198; discussion 198– 199.
9. Cross CA, Cespedes RD, English SF, McGuire EJ. Transvaginal urethrolysis for urethral obstruction
after anti-incontinence surgery. J Urol 1998; 1594:199 – 1201.
10. Nitti VW, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999; 161:535 – 1540.
 Postoperative Complications of Sling Surgery 455

11. Carr LK, Webster GD. Voiding dysfunction following incontinence surgery: diagnosis and treatment
with retropubic or vaginal urethrolysis. J Urol 1997; 1573:821– 823.
12. Nitti VW, Raz S. Obstruction following anti-incontinence procedures: diagnosis and treatment with
transvaginal urethrolysis. J Urol 1994; 1521:93– 98.
13. Zimmern PE, Hadley HR, Leach, GE, Raz S. Female urethral obstruction after Marshall-Marchetti-
Krantz operation. J Urol 1987; 138:517.
14. Webster GD, Kreber KJ. Voiding dysfunction following cystourethropexy: its evaluation and
management. J Urol 1990; 144:670– 673.
15. Petrou SP, Brown JA, Blaivas JG. Suprameatal transvaginal urethrolysis. J Urol 1999;
1614:1268 –1271.
16. Ghoniem GM, Kapoor DS. Nonautologous sling material. J Urol 2001; 2(5):357–363.
17. Kuo H. Anatomical and functional results of pubovaginal sling procedure using polyproplyene mesh
for the treatment of stress urinary incontinence. J Urol 2001; 166:152 –157.
18. McGuire EJ, O. C. H. Surgical treatment of intrinsic urethral dysfunction. Urologic Clinics of North
America 1995; 223:657 – 664.
19. Kaplan SA, Te AE, Young GP, Andrade A, Cabelin MA, Ikeguchi EF. Prospective analysis of 373
consecutive women with stress urinary incontinence treated with a vaginal wall sling: the Columbia –
Cornell University experience. J Urol 2000; 1645:1623 –1627.
20. Morgan T, O Jr, Westney OL, McGuire EJ. Pubovaginal sling: 4-Year outcome analysis and quality
of life assessment. J Urol 2000; 1636:1845 – 1848.
21. Chaikin DC, Rosenthal J, Blaivas JG. Pubovaginal fascial sling for all types of stress urinary
incontinence: long-term analysis. J Urol 1998; 1604:1312– 1316.
22. Abouassaly R, Corcos J. Complications of tension-free vaginal tape surgery: a multi-institutional
review of 242 cases. AUA Annual Meeting 2002.
23. White M, Katz D, Stone AR. Tension free vaginal tape versus pubovaginal sling: is there a difference
in quality of life? AUA Annual Meeting 2002.
24. Juma S, Little NA, Raz S. Vaginal wall sling: four years later. Urology 1992; 395:424– 428.
25. Choe JM, Staskin DR. Gore-Tex patch sling: 7 years later. Urology 1999; 544:641– 646.
26. Hom D, Desautel MG, Lumerman JH, Feraren RE, Badlani GH. Pubovaginal sling using
polypropylene mesh and vesica bone anchors. Urology 1998; 515:708 – 713.
27. Bent AE, Ostergard DR, Zwick-Zaffuto M. Tissue reaction to expanded polytetrafluoroethylene
suburethral sling for urinary incontinence: clinical and histologic study. Am J Obstet Gynecol 1993;
1695:1198 –1204.
28. Barbalias G, Barbalias D. Use of slings made of indigenous and allogenic material (Gortex) in type III
urinary incontinence and comparison between them. Eur Urol 1997; 31:394 –396.
29. Leach GE, Appell RA. Female Stress Urinary Incontinence Clinical Guidelines Panel summary report
on surgical management of female stress urinary incontinence. J Urol 1997; 157:875.
30. Kobashi KC, Dmochowski R, Mee SL, Mostwin J, Nitti VW, Zimmern PE, Leach GE. Erosion of
woven polyester pubovaginal sling. J Urol 1999; 1626:2070 – 2072.
31. Handa VL, Stone A. Erosion of a fascial sling into the urethra. Urology 1999; 545:923.
32. Golomb J, Groutz A, Mor Y, Leibovitch I, Ramon J. Leibovitch J. Management of urethral erosion
caused by pubovaginal fascial sling. Urology 2001; 571:159 – 160.
33. Amundsen CL, Webster GD. Continence outcome and management following urethral erosion of the
pubovaginal sling. AUA Annual Meeting 2002.
34. Axelrod SL. Bladder neck obstruction in women. J Urol 1987; 137:497.
35. Massey JA. Obstructed voiding in the female. B J Urol 1988; 61:36.
32
Detrusor Myomectomy

Patrick J. Shenot
Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A.

I. INTRODUCTION

The efficacy of enterocystoplasty has been demonstrated in numerous studies. Clinical

success, measured by improved patient quality of life and decreased upper urinary tract
complications, has been clearly established. The requirement of bowel segment isolation and
reanastomosis, however, has a significant risk of early complications, such anastomotic leakage or
intestinal obstruction.
Potential long-term sequelae of enterocystoplasty include bowel dysfunction, metabolic
derangements, and spontaneous perforation of the intestinal segment. Urinary retention
requiring intermittent catheterization may be required for at least 15% of patients following
enterocystoplasty (1). Enterocystoplasty may also predispose to the subsequent development of
malignancy. A growing number of malignancies have been reported in the world literature in
patients who have undergone enterocystoplasty (2 – 4).
Detrusor myomectomy, also termed bladder autoaugmentation, is a technique that increases
bladder capacity and lowers intravesical storage pressures without the use of intestinal segments.
By utilizing only autologous bladder tissue, it is hoped that low-pressure bladder storage will be
assured while also minimizing the risk of complications by eliminating involvement of the
gastrointestinal system in this urologic reconstruction procedure.
Autoaugmentation of the urinary bladder is accomplished by disruption of the detrusor
musculature to an extent significant to permit the eventual formation of a large bladder
diverticulum, which can effectively reduce abnormal contractility and improve the functional
capacity of the bladder. The disruption of the detrusor can be accomplished using a simple
incision, referred to as a myomyotomy, although greater success has been achieved with
myomectomy, where a patch of detrusor muscle is actually removed from the anterior surface
of the bladder.

II. HISTORY OF ENTEROCYSTOPLASTY AND DETRUSOR MYOMECTOMY

Anticholinergic and other pharmacological agents are often effective in decreasing uninhibited
detrusor contractions. These medications also represent the first line of treatment for the high-
pressure, noncompliant, small-capacity bladder, although patients usually require an intermittent
catheterization program once satisfactory storage pressure is achieved. When medical therapy
457
458 Shenot

fails to improve continence and bladder storage parameters, surgical bladder augmentation is
often employed.
Tizzoni and Foggi reported the first use of small intestine as a tissue graft for bladder
augmentation, enterocystoplasty, in dogs in 1888 (5). Ten years later, the first human ileo-
cystoplasty was performed by Mikulicz (6). Currently, enterocystoplasty remains the standard
treatment for the surgical correction of the small-capacity, poorly compliant bladder that is
unresponsive to medical therapy. This technique is also useful in patients with intractable urge
incontinence who have failed less invasive therapies.
Although generally effective, potential problems may be associated with the use of
gastrointestinal segments for bladder augmentation. In the case of intestinal segments, these
structures tend to retain at least some of their absorptive function. The reabsorption of urinary
solutes may result in the development of electrolyte abnormalities, especially during periods of
dehydration or in patients with renal insufficiency (7). In the creation of intestino-intestinal and
intestino-vesical anastomoses, one must be aware of the potential for anastomotic leakage,
fistula formation, and possibly intestinal obstruction to occur postoperatively.
Several other concerns have arisen with the development of bladder augmentation
techniques. Mucus, produced by the intestinal segment, has proved bothersome and may
partially occlude drainage catheters, requiring intermittent irrigation of the bladder. In some
patients, bowel peristalsis has contributed to episodic urinary leakage after intestinal bladder
augmentation. Deficiency of vitamin B12 may result in pernicious anemia in those with isolation
of the terminal ileum from the fecal stream, while adenocarcinoma has developed in some
patients in the bowel segments used for bladder augmentation. These problems, as well as
the direct complications of a bowel segment isolation, have encouraged the development of
alternative methods to improve urinary storage without involvement of the gastrointestinal
system.
During the past 30 years, various nonintestinal materials have been studied for potential
application during bladder augmentation. Many investigators have tried a variety of natural
or synthetic tissues including free fascial grafts, lyophilized dura, pericardium, and placental
membranes. In addition, the use of synthetic materials such as polytetrafluoroethylene (Teflon),
felt, and a gelatin sponge material has been attempted (8 –12). None of these materials have
proven to be suitable for bladder augmentation because of the development of infections,
rejection, scarring and graft contracture, metaplastic bone and/or calculus stone formation, or
urinary fistula formation.
Cartwright and Snow in 1989 reported a technique which they named bladder auto-
augmentation (13,14). The principle of this surgical technique is that the detrusor muscle
over the dome of the bladder is excised leaving the underlying bladder urothelium intact.
A large bladder diverticulum results in augmented bladder capacity and permits the low-pressure
storage of urine. Since no other tissue is used, the term autoaugmentation was coined. Both
myomyotomy and myomectomy have been advocated for bladder autoaugmentation. Most
experienced investigators recommend the more extensive myomectomy rather than a simply
myomyotomy because of improved success rates. There is little evidence to support the routine
use of detrusor myomyotomy.
Detrusor myomectomy in adults may offer many advantages over enterocystoplasty.
Because intestinal manipulation is avoided, anastomotic complications and electrolyte problems
should not occur. The entire procedure may be performed extraperitoneally, which also will
minimize effects on the intestine. It is possible that autoaugmentation is ideal for the patient who
has undergone previous abdominal surgery and is left with significant intraperitoneal scarring, or
who could be at risk for the short bowel syndrome if an intestinal segment was isolated for use
in enterocystoplasty.
 Detrusor Myomectomy 459

III. TECHNIQUES OF DETRUSOR MYOMECTOMY

A. Preoperative Preparation
Preoperatively, all patients should undergo a thorough medical evaluation including
videourodynamics to determine the functional status of the bladder and sphincter. Surgical
intervention is appropriate if alternative therapies have failed to improve symptoms of frequency,
urgency, and incontinence. Although intermittent catheterization is not required in all patients,
the ability and willingness of patients to perform this postoperatively should be confirmed
before contemplating this procedure. Clean intermittent catheterization technique should ideally
be taught before the procedure as part of routine preoperative teaching. We routinely utilize both
mechanical and antibiotic bowel preparation prior to surgery. If detrusorectomy is found to
be technically impossible intraoperatively, conventional enterocystoplasty can be accomplished
if the bowel preparation has been performed. Intravenous antibiotics are administered pre-
operatively.

B. Operative Technique
The urethral meatus is prepped into the operative field to allow placement of an indwelling
urethral catheter with self-retaining balloon. The retropubic space may be exposed using either a
Pfannensteil or low midline abdominal incision. The bladder is exposed and filled with saline.
The catheter may be connected with a Y connector to both a normal saline reservoir for irrigation
and a drainage bag to facilitate distension and emptying of the bladder during dissection. The
anterior wall of the bladder is identified, with gentle blunt and sharp dissection used to free
the peritoneum from the bladder surface (Fig. 1). Detrusor myomectomy may be performed
using either the intraperitoneal or extraperitoneal approach. At the present time, most surgeons
experienced in this technique strongly recommend an extraperitoneal approach so that the
peritoneum can act to reinforce to bladder diverticulum created by the myomectomy, preventing

Figure 1 Extraperitoneal exposure of the anterior wall and dome of the bladder. The detrusor is scored
with electrocautery in the midline.
460 Shenot

intraperitoneal leak and decreasing the risk of rupture. Once adequate exposure is achieved, the
detrusor muscle is scored in the midline using needle-tip electrocautery.
The incision is extended from anterior to posterior over the entire dome of the bladder.
After the detrusor has been divided through three-fourths of its thickness, the muscle is separated
from the urothelium using a fine hemostat or a Kitner dissector. The remaining detrusor fibers
overlying the epithelium are gently spread apart with a hemostat until they are disrupted. Thus,
the bladder epithelium becomes exposed along the entire length of detrusor incision (Fig. 2).
Although not technically demanding, this dissection can be tedious, especially in highly
trabeculated bladders. It is imperative to minimize inadvertant tears of the bladder epithilium
as these can prevent adequate bladder distension and make the subsequent dissection much
more difficult.
The detrusor margin on one side of the incision is then grasped with Allis clamps while the
bladder is fully distended. A plane is developed using blunt dissection between the detrusor
muscle and the intact bladder epithelium, proceeding laterally. This plane of dissection is
maintained while keeping the epithelium intact. The dissection progresses laterally in each
direction up to the entire dome until at least one-half to two-thirds of the detrusor muscle of the
entire bladder is stripped away from the epithelium.
During the myomectomy, the bladder is repeatedly emptied and filled with saline through
the urethral catheter to facilitate the dissection. Small openings in the epithelium are repaired
with the application of a right-angle clamp to the opening which is then secured with a 4-0
chromic ligature. After the detrusor is freed from the mucosal epithelium, the redundant detrusor

Figure 2 Epithelium bulging through detrusor myomotomy.

 Detrusor Myomectomy 461

flaps are excised. We attempt to remove the detrusor from the entire anterior and lateral surfaces
of the bladder (Fig. 3). To achieve this extensive myomectomy, the superior vascular bladder
pedicles must be sacrificed, with the dissection extending laterally and inferiorly to the level of
the inferior bladder pedicle. Bilateral psoas hitches may be performed using absorbable suture to
prevent reannealment of the cut detrusor edges, although this is usually unnecessary. At the
completion of the procedure, the prevesical space should be drained.

C. Postoperative Care
The surgical result of myomectomy is that of a thin, quite large diverticular patch of bladder
epithelium, bulging from the bladder as it is filled. An exposed segment of very thin mucosa may
be at increased risk of rupture because of increased wall tension at large capacity. The mucosal
diverticulum, however, may become protected by a layer of peritoneum and omentum of
adequate thickness to reduce the risk of rupture. Postoperatively, a urethral catheter is left
indwelling. Cyclic distension and drainage of the bladder with saline irrigant may help avoid
scarring of the autoaugmentation in the contracted position. Alternatively, the catheter may be
put to 20 cm of back pressure by draping it over the bedrail. Cystography is performed 3– 5 days
postoperatively. If no extravasation is evident, the indwelling catheter is removed, and, if
necessary, the patient may begin an intermittent catheterization program. Initially, intermittent
catheterization is performed every 3– 4 h. As the diverticulum created by the autoaugmentation
matures, the interval between catheterizations can be lengthened. Patients are maintained on a
prophylactic regimen of antimicrobial therapy at least until the indwelling catheter is removed.
Postoperatively, patients are evaluated with a videourodynamic evaluation 3 months following
surgery (Fig. 4). Urodynamic follow-up is most important in patients with poor compliance who
are at risk for upper urinary tract compromise. Anticholinergic agents may be administered to

Figure 3 Completed detrusor myomectomy. Note the Foley catheter balloon visible through the thin
translucent bladder epithelium.
462 Shenot

Figure 4 Cystogram obtained from videourodynamic study 3 months following detrusor myomectomy.
The large augmented segment is clearly seen arising from the bladder dome.

assure low-pressure urinary storage. The anticholinegic regimen can eventually be tapered and
ultimately discontinued.

IV. CLINICAL RESULTS OF DETRUSOR MYOMECTOMY

Following initial success with an animal model, Cartwright and Snow (13,14) utilized this
technique in seven pediatric patients with both neurogenic and nonneurogenic voiding dysfunction.
This procedure resulted in marked clinical improvement in five patients, although one showed only
modest improvement and one eventually required enterocystoplasty. Bladder capacity improved
in three of the five patients studied urodynamically, while compliance improved in four.
After performing this procedure on 19 patients, Cartwright and Snow have noted that
although bladder capacity did not consistently increase after autoaugmentation, most patients
developed improvement in their urinary storage pressure. Thus, urinary storage occurs under
lower pressure postoperatively, accompanied not only by improved continence but also by
improvement in upper urinary tract dilatation.
Stohrer and associates in Germany performed the first autoaugmentation on an
adult bladder in 1989. Since then, Stohrer et al. have reported their experience in 29 patients with
neurogenic and nonneurogenic voiding dysfunction (15). In this report, the majority of patients
were able to void spontaneously postoperatively. Preoperatively, three patients required
intermittent catheterization for urinary drainage, while postoperatively, an intermittent
catheterization program was used by 12 patients. Preoperatively, five patients demonstrated
vesicoureteral reflux radiographically, while reflux resolved in two patients and was reduced
from bilateral to unilateral in two additional patients. No complications occurred as a result of
autoaugmentation. Subjective success was reported as excellent in 16 patients and as good
 Detrusor Myomectomy 463

in eight cases. A later study by the same investigators confirmed the efficacy of this procedure in
50 patients treated with this technique. (16).
In 1994, Kennelly and associates reported on the treatment of a small capacity, poorly
compliant bladder with autoaugmentation in five patients, 18 –73 years old (17). Operative
time averaged only 106 min, and the hospital stay was only 6 days for this patient group.
No postoperative complications occurred. In follow-up ranging from 12 to 82 weeks, bladder
capacity increased from 75 mL to 310 mL, or from 40% to 310%. Compliance improved in all
patients. While three patients demonstrated reflux preoperatively, this resolved in one patient and
improved in two patients. Of four patients who were incontinent preoperatively, three became
continent and extended the interval between catheterizations. Upper tract function remained
stable, and no patient required enterocystoplasty to control elevated intravesical pressure.
Leng and colleagues reported on a heterogeneous group of 61 patients who had undergone
37 primary detrusor myomectomies and compared their outcomes to 32 enterocystoplasties (18).
Eight patients with detrusor instability underwent detrusor myomectomy. All eight demonstrated
urodynamic improvement, with all but one patient spontaneously voiding postoperatively. One
patient reported persistent urge incontinence and subsequently underwent enterocystoplasty.
Leng et al. also noted clinical and urodynamic improvement in three of six patients with radiation
cystitis who underwent this procedure. They report an overall 73% success rate in this diverse
group of patients treated with primary detrusor myomectomy. Of note, the rate of serious
complications was 22% in patients undergoing enterocystoplasty but only 3% in those treated
with primary detrusor myomectomy.
Given that autoaugmentation is successful in improving urinary storage, refinement of the
technique could reduce operative time, hospital stay, and the rate of complications. The recent trend
in minimally invasive surgery has spurred several investigators to employ laparoscopy to achieve
bladder autoaugmentation (19–21). This alternative surgical approach has been reported in very
small numbers of patients with limited follow-up. To date, this approach has not been widely utilized.

V. APPLICATION OF DETRUSOR MYOMECTOMY

Although detrusor myomectomy offers definite advantages when compared to traditional

techniques, it is clear that the results of this procedure with regard to increases in bladder capacity
and reduced detrusor overactivity indicate that this technique is inferior to conventional
enterocystoplasty. With any novel technique, enthusiastic preliminary reports are often made
before the potential complications have been realized. The number of cases reported is small with
relatively short follow-up. Currently, detrusor myomectomy should be offered only to highly
selected patients who would otherwise be candidates for conventional enterocystoplasty. The
ability to improve urinary storage capacity in patients with intractable urge incontinence without
disturbance of the gastrointestinal system may greatly reduce the rate of serious complications.
Since this is an extraperitoneal procedure, it may be ideal for patients with previous
intraperitoneal surgery. Lastly, the laparoscopic approach to detrusor myomectomy may evolve
into viable minimally invasive procedure for the treatment of refractory detrusor overactivity.

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464 Shenot

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autoaugmentation. J Urol 1994; 152:303 –306.
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16:758– 763.
19. Ehrlich RM, Gershman A. Laparoscopic seromyotomy (autoaugmentation) for nonneurogenic
bladder in a child: initial case report. Urology 1993; 42:175 – 178.
20. McDougal EM, Clayman RV, Figenshau RS, Pearle MS. Laparoscopic retropubic autoaugmentation
of the bladder. J Urol 1995; 153:123– 126.
21. Braren V, Bishop MR. Laparoscopic bladder autoaugmentation in children. Urol Clin North Am
1998; 25:533 –540.
33
Management of Refractory Detrusor
Instability: Anterior Flap Extraperitoneal
Cystoplasty

Eric S. Rovner
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.
David A. Ginsberg
University of Southern California School of Medicine, Los Angeles, California, U.S.A.
Shlomo Raz
David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.

I. INTRODUCTION

Enlargement or augmentation cystoplasty may be useful in a number of clinical situations,

including the treatment of decreased functional or organic bladder capacity. In general,
conservative therapy including behavioral modification, intermittent catheterization, anti-
cholinergic medication, and/or electrical stimulation is successful in treating the majority of
these patients. However, a number of patients will be refractory to these conservative measures
and will continue to have unacceptable symptoms of frequency, urgency, urge incontinence,
and perhaps even upper urinary tract deterioration due to high-pressure storage of urine. It is
this group of patients in whom augmentation cystoplasty may have a therapeutic role.
Neuromodulation is a promising new alternative therapy in a subset of this patient population,
but long-term data are still lacking.
Many methods and approaches exist for bladder augmentation using varying segments of
bowel (ileum, colon, etc.) (1 – 3), or urothelium (4) including autoaugmentation (5). All of these
procedures have the common goals of providing drainage of the upper urinary tract into a low-
pressure, high-capacity urinary reservoir. The use of bowel for enlargement cystoplasty has
many well-documented disadvantages and has historically been associated with morbidity (6).
Among the problems associated with enterocystoplasty are a large abdominal incision and
intraperitoneal exploration with subsequent disruption of the gastrointestinal tract in order to
harvest the bowel segment. This often results in a prolonged postoperative ileus requiring
nasogastric tube decompression, especially in the neurogenic population who have neurogenic
bowel in addition to their neurogenic bladder. Devastating complications associated with
standard enterocystoplasty include intraperitoneal abscess, fistula, bowel obstruction, and
prolonged ileus. The anterior flap extraperitoneal cystoplasty (AFEC) is a modification of the
465
466 Rovner et al.

standard enterocystoplasty intended to minimize the preoperative, intraoperative, and

postoperative complications historically associated with this procedure.
The AFEC is a variation of the standard cup-patch technique popularized by Goodwin and
associates at UCLA (7). AFEC is performed through an extraperitoneal approach to the bladder
with retrieval and then harvest of an ileal segment through a small peritoneal window. Care is
taken to avoid significant manipulation of the intraperitoneal contents by working through a small
peritoneotomy. Reconstitution of the GI tract (ileoileostomy) is performed extraperitoneally and
then the anastomosed bowel is returned into the peritoneal cavity through the small peritoneal
window. The peritoneal window is closed against the base of the mesentery of the harvested
bowel segment, sealing the vesicointestinal anastomosis from the peritoneal cavity and placing
the harvested segment in an extraperitoneal location adjacent to the bladder. A broad-based
anterior bladder flap is fashioned and reflected cephalad where a wide vesicointestinal anastomosis
is performed extraperitoneally. We feel this modified technique of augmentation cystoplasty may
be associated with a faster return to bowel function and a shorter hospital stay.
We do not perform AFEC in the presence of multiple previous abdominal and pelvic
surgeries where scar or adhesions may limit the ability to remain extraperitoneal or may limit the
mobility of the bowel segment. We also do not perform AFEC if concomitant intra-abdominal or
ureteric surgery is to be performed. Patients with renal insufficiency may not be candidates
for AFEC, as the interposition of bowel in the urinary tract may lead to the provocation or
aggravation of metabolic complications due to the reabsorption of certain urinary constituents.
Patients with significant urethral disease (stricture, etc.), which may limit the ability to perform
clean intermittent catheterization (CIC), or those who are unable or unwilling to perform CIC
are likewise not good candidates for AFEC. Finally, patients with Crohn’s disease, short gut
syndrome, or other bowel conditions potentially affecting GI function and viability are not
offered AFEC.

II. TECHNIQUE

Preoperative evaluation includes a thorough medical history with special attention toward
previous abdominal surgery and the presence of GI disease which would limit use of the
ileum (Crohn’s disease, etc.), physical examination, upper urinary tract imaging, determination
of renal function (serum creatinine), and videourodynamics—including an assessment of
sphincteric function. Finally, an assessment is made of the patient’s willingness and ability to
perform clean intermittent catheterization, as this is critical to both long-term success and patient
satisfaction.
Bowel preparation begins at home 2 days preoperatively and consists of a clear liquid diet
and mild laxatives. The patient is brought into the hospital on the day of surgery, and intravenous
antibiotics are administered preoperatively. The patient is placed in the supine position
maintaining access to the urethra. A nasogastric tube is not routinely placed. A Foley catheter is
placed per urethra.
Through a Pfannenstiel or lower midline incision the retropubic space is entered. The
dome of the bladder is visualized and the unopened peritoneum is swept off the posterior bladder
(Fig. 1). A small peritoneotomy (Fig. 2) is performed and a segment of ileum is grasped and
brought into the extraperitoneal space through the peritoneal window. The operative field is
isolated to prevent gross contamination and a 15- to 20-cm segment of ileum is selected based on
an adequate vascular supply. This segment is isolated on its mesentery, using hemostats and the
GIA stapling device. The gastrointestinal (GI) tract is then reconstituted with a side-to-side,
functional end-to-end stapled anastomosis reinforced with nonabsorbable suture. The GI
 Refractory Detrusor Instability 467

Figure 1 The retropubic space is entered and the peritoneum is swept off the posterior bladder. (Drawing
courtesy of Shlomo Raz.)

Figure 2 A small peritoneal window is made to gain access to the intraperitoneal contents. (Photograph
courtesy of Shlomo Raz.)
468 Rovner et al.

anastomosis is placed back into the peritoneal cavity, and the peritoneum is circumferentially
closed about the base of the mesentery of the isolated ileal segment leaving this portion
extraperitoneal (Fig. 3). It is important that the peritoneotomy not be closed too tightly, resulting
in compression of the mesenteric blood supply to the augment segment. If this occurs, the bowel
segment may appear ischemic or have an appearance of vascular congestion secondary to poor
venous return, and the peritoneal closure should be loosened.
The isolated ileal segment is opened, irrigated with an antibiotic solution, folded into a
“U” configuration (Fig. 4) and detubularized eccentrically using the electrocautery (Fig. 5). The
medial aspects of the detubularized bowel are now anastomosed, forming a patch (Fig. 6).
An anterior bladder flap is now created by incising on the posterior bladder wall in the shape
of an inverted “U” (Fig. 7). This flap is raised as caudally as possible in order to create maximum
mobility of the anterior flap. The anterior bladder flap has four advantages: (a) a wide based flap
avoids an hourglass configuration of the augmented bladder; (b) the posterior placement of the
flap puts the mesentery in a position where internal herniation is unlikely; (c) the bladder can be
additionally incised in the anterior midline to obtain more bladder edge for the anastomosis if
necessary; and (d) the anterior bladder flap may be advanced cephalad towards the ileal segment,
which may be helpful in patients with a short or relatively immobile mesentery (8).
The ileal segment is anastomosed to the bladder and bladder flap using two layers of
absorbable suture (Fig. 8). Prior to closure of the augmented bladder a suprapubic tube is placed
to allow dual drainage of the augmented bladder. A Penrose drain is left in the retropubic space.
Beginning postoperative day 1, the augmented bladder is irrigated twice daily with saline
to prevent the formation of inspissated mucous plugs. The Foley catheter is removed 2– 3
weeks postoperatively after a radiograph confirms a well-healed augment without extravasation,
and the patient is instructed to void and check postvoid residuals through the suprapubic tube.

Figure 3 The peritoneal window is closed around the base of the mesentery of the ileal segment.
(Drawing courtesy of Shlomo Raz.)
 Refractory Detrusor Instability 469

Figure 4 The ileal segment is placed into a “U” configuration. (Photograph courtesy of Shlomo Raz.)

Figure 5 The ileal segment is debularized eccentrically. (Photograph courtesy of Shlomo Raz.)
470 Rovner et al.

Figure 6 After detubularization the medial walls of the ileal patch are anastomosed, forming a patch.
(Photograph courtesy of Shlomo Raz.)

Figure 7 An anterior based bladder flap is created by incising as caudally as possible on the posterior
bladder wall in the shape of an inverted “U.”
 Refractory Detrusor Instability 471

Figure 8 (a) Diagram of anastomosis of the ileal patch to the bladder. (b) Intraoperative photograph of
the anastomosis of the ileal patch to the bladder. (Courtesy of Shlomo Raz.)

If the residuals remain high, the patient is reinstructed on the technique of clean intermittent
catheterization, and the suprapubic tube is removed.

III. RESULTS

In 1997, Albo and coworkers reported their initial experience with AFEC (9). There were 23 women
and four men. Fourteen patients were noted to have a defined neurologic condition and detrusor
hyperreflexia, and 13 were considered to have nonneurogenic voiding dysfunction. All patients had
failed conservative therapy. Of the 27 patients, 25 had an “uneventful” postoperative convalescence
from AFEC without requiring nasogastric decompression. In these 25 patients the mean time to oral
472 Rovner et al.

(enteral) nutrition was 3.5 days and mean hospitalization was 5.5 days. Complications included one
patient with a prolonged ileus and one patient with clostridium difficile enterocolitis. An additional
patient required emergent laparotomy 3 months postoperatively for a bladder perforation after
failing to catheterize as instructed. Overall, at a mean follow-up of 9 months, 92% of patients were
cured or experienced marked improvement in voiding symptoms. Forty-four percent of patients still
required anticholinergic therapy postoperatively, and 60% of patients were on CIC. There was no
difference in success between neurogenic and nonneurogenic groups.
Subsequently, Rovner and colleagues reported on an update of this series (10). Forty-two
patients (24 nonneurogenic and 18 neurogenic) were followed for a mean of .15 months
following AFEC. Overall, 90% of patients were tolerating a regular diet by postoperative day 5.
Range of inpatient hospital stay was 3 –22 days, with .80% discharged by postoperative
day 6. At a mean follow-up of over 15 months .80% of patients were cured or significantly
improved from symptoms of urinary urgency and frequency, and almost 90% were cured or
significantly improved with regard to preoperative symptoms of urge incontinence. There have
been no cases of fistula or small bowel obstruction. Other than the complications noted above,
two additional patients had a postoperative GI hemorrhage requiring transfusion.

IV. CONCLUSIONS

We have found AFEC to be a simple and effective method of augmentation cystoplasty in select
patients. Theoretically, extraperitoneal performance of the procedure and minimal handling of the
bowel and peritoneal contents should reduce perioperative morbidity and complications. Isolation of
the vesicointestinal anastomosis from the peritoneum minimizes risks of urinary fistula formation,
uncontrolled urinary extravasation, and intraperitoneal abscess formation and infection. In addition,
the risk of postoperative intraperitoneal adhesions and subsequent bowel obstruction is potentially
reduced owing to the minimal disruption of the peritoneum. Principles of AFEC include minimal
intraperitoneal bowel manipulation, an extraperitoneal bowel resection, and vesicointestinal
anastomosis performed and isolated outside the peritoneal cavity. Limited bowel manipulation and
isolation of the peritoneal contents from the vesicointestinal anastomosis may allow an earlier return
of bowel function, shorter hospital stay, and reduced perioperative morbidity.

REFERENCES

1. Gil-Vernet JM Jr. The ileocolic segment in urologic surgery. J Urol 1965; 94:418.
2. Smith RB. Use of ileocystoplasty in the hypertonic neurogenic bladder. J Urol 1975; 113:125.
3. Luangkhot R, Peng BCH, Blaivas JG. Ileocystoplasty for the management of refractory neurogenic
bladder: surgical technique and urodynamic findings. J Urol 1991; 146:1340.
4. Churchill BM, Aliabadi H, Landau EH. Ureteral bladder augmentation. J Urol 1993; 150:716– 720.
5. Cartwright PC, Snow BW. Bladder autoaugmentation: early clinical experience. J Urol 1989;
142(2 Pt 2):505 – 508.
6. Khoury JM, Timmons SL, Corbel L, Webster GD. Complications of enterocystoplasty. Urology
1992; 40:9.
7. Goodwin WE, Winter CC, Barker UF. Cup-patch technique of ileocystoplasty for bladder
enlargement or partial substitution. Surg Gynecol Obstet 1959; 108:240.
8. Chopra A, Stothers L, Raz S. Bladder augmentation. Urol Clin North Am 1995; 3(2):81 – 93.
9. Albo M, Raz S, Dupont MC. Anterior flap extraperitoneal cystoplasty. J Urol 1997; 57(6):2095–2098.
10. Rovner ES, Ginsberg DA, Albo ME, Raz S. Anterior flap extraperitoneal cystoplasty (AFEC):
a simplified method of ileal augmentation cystoplasty. J Urol 1997; 157(4):397A.
34
Laparoscopic Enterocystoplasty

Raymond R. Rackley and Joseph B. Abdelmalak

Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A

I. INTRODUCTION

When a patient with bladder dysfunction due to noncompliance or reduced functional capacity
does not benefit from conventional therapies, one choice for treatment is augmentation
cystoplasty. This procedure involves anastomosing a segment of bowel to the urinary bladder in
order to create a large, fully functional storage container that can be emptied at the patient’s will.
The procedure is typically performed using an open laparotomy incision and can utilize several
different portions of bowel, as long as the segments have good blood supplies and are of
adequate size (1). Each segment of bowel has its own advantages and disadvantages, and the
decision as to which portion to use is based on the history and current and future needs of
the patient, and the preference of the surgeon. This highly effective reconstructive technique
protects the upper urinary tract while allowing the patient to regain continence (2 – 5). First
performed in a dog in 1888, enterocystoplasty was later shown to be successful in human
subjects (6), and is currently the most widely accepted method of treating refractory bladder
dysfunction.
Although this procedure has a high success rate, many patients opt not to seek treatment
owing to the stigmas of open surgery namely complications, pain, and morbidity. Additional
consequences of open surgery include delayed postoperative recoveries, increased metabolic
needs for wound healing, and prolonged hospital stays. These consequences are most prolific in
the elderly and in patients with previously diagnosed neurologic and other comorbid conditions,
and can be potentially avoided by the use of a laparoscopic approach. Patients who have
undergone enterocystoplasty using this technique report less postoperative pain and morbidity,
improved comesis, and shorter hospital stays and recuperation times than those who have
received the surgery through conventional open methods. In addition, it has been shown that
laparoscopy notably reduces the number and severity of intra-abdominal adhesions associated
with open surgery (7).
Laparoscopic bladder augmentation is a technically complex procedure in which the main
goal is to achieve the benefits of open surgery while avoiding its detriments. However, the
mechanical difficulties associated with laparoscopic bladder augmentation have greatly limited
its use, despite the prevalence of similar techniques in other routine urological surgeries. In this
article, the authors illustrate their method of reconstructive laparoscopic enterocystoplasty as it
has developed through their experience with 17 patients.
473
474 Rackley and Abdelmalak

II. INDICATIONS AND PATIENT SELECTION

Laparoscopic augmentation cystoplasty provides a surgical solution for those patients with
noncompliant small bladders that have not responded to more traditional therapies. Using a
minimally invasive approach, the procedure involves making an incision of the bladder wall
for anastomosis of a segment of bowel. Patients with ventriculoperitoneal shunts (such as those
with a myelomingocele) are likely to have intra-abdominal adhesions that may interfere with
laparoscopic techniques. For patients with neurogenic bladder dysfunction, they will need to
perform clean intermittent catheterization for extended periods of time following the operation
in order to effectively empty their bladders. Lastly, a continent catheterizable abdominal stoma
(in addition to bladder augmentation) may be necessary for patients who are not able to
catheterize themselves via the urethra.
Before the operation, upper and lower urinary tract studies are valuable for establishing a
baseline evaluation. Urodynamics and cystoscopy are also helpful; they provide information
regarding the competence of the urinary sphincter. Additionally, one may obtain routine
laboratory studies, including: renal function and serum electrolytes, a whole blood cell count,
urinalysis, and a urine culture (when appropriate).

III. PATIENT PREPARATION

Two days prior to surgery, the patient should be placed on a clear liquid diet; on the day
preceding the operation, a bowel preparation must be performed. Preoperative antibiotics are
recommended for bowel and urinary tract surgical prophylaxis, as are antifungal medications
when appropriate. Owing to chronic constipation, patients with neurological diseases may
require more time for an adequate bowel preparation.
The procedure begins with the patient fitted in pneumatic compression stockings and
situated in the supine position. Padded shoulder braces are used to prevent patient sliding during
extreme excursions in the head-down or Trendelenberg position. Next, he/she is anesthetized
and intubated, followed by the insertion of an oral gastric tube. The patient is then moved to the
low-lithotomy position where he/she remains for the rest of the operation. The patient’s arms are
tucked and protected along the sides so as to facilitate the surgical team’s ability to direct their
operative movements deep into the pelvis.
During the first few procedures, cystoscopy was used to aid in the insertion of internal-
external ureteral stents (7F, 90 cm; Circon Surgitek, Santa Barbara, CA) into the renal pelvis,
which provided both intraoperative and postoperative drainage. Maximal intraoperative
drainage of urine was obtained by leaving the straight ends of the stents outside the external
urethral meatus and securing them to a 20– 24F urethral catheter. However, the use of these
internal-external ureteral stents prevented effective bladder irrigation by interfering with the
formation of an adequate seal of the urethra around the urethral catheter. It was later found that
ureteral stents were unnecessary, as it is possible to provide effective intraoperative urine and
pelvic fluid drainage by intermittently opening the 20– 24F urethral catheter without losing the
pneumoperitoneum during the procedure.

IV. SURGICAL TECHNIQUE (9)

There are many features essential to a successful bladder augmentation. First, a segment of
bowel must be chosen based on a broad, well-vascularized mesenteric pedicle. This portion must
 Laparoscopic Enterocystoplasty 475

then be excised, and the remaining segments of bowel joined together. Next, the bowel segment
must be detubularized and reconfigured while avoiding peritoneal soiling of bowel contents.
After this has been accomplished, the bladder should be mobilized, and an adequate-size
cystotomy performed. Lastly, the bowel segment should be anastomosed to the bladder, creating
a tension-free, watertight, full-thickness seal, and the surgeon should confirm adequate post-
operative urinary drainage.
Several ports are useful for the manipulation of laparoscopic tools. The first, a disposable
10- to 12-mm port with occluding balloon and cuff, is introduced through an incision made at
the umbilical crease and is guided into the peritoneal cavity under direct vision. A 10-mm 108
laparoscope can later be inserted through this port. Next, two ports are introduced
paraumbilically in order to facilitate suturing. These ports are 10 and 5 mm and are located
bilaterally at the lateral borders of the rectus muscle at the level of the umbilicus (Fig. 1). One
last 5-mm port should be placed medially to the left anterior superior iliac spine. The
introduction of additional ports may be beneficial; their location will depend on the segment
of bowel being used and the surgeon’s preference.

Figure 1 Options for selection of port sizes and location in laparoscopic enterocystoplasty procedures.
(Courtesy Cleveland Clinic Foundation.)
476 Rackley and Abdelmalak

V. BOWEL SELECTION AND MOBILIZATION

While many segments of bowel may be used for laparoscopic enterocystoplasty, a chosen
section must meet the following requirements: (a) a length of 15– 20 cm ensures that an adequate
augmented bladder capacity will be obtained; (b) the bowel segment should reach the area of the
bladder neck without tension; and (c) the bowel mesentery must contain an adequate blood
supply. These criteria are the same as for open enterocystoplasty, and the selection of a portion
of bowel is based on the clinical requirements of the patient.
When ileum is to be used for augmentation, ileocystoplasty, the surgeon must first identify
the ileocaecal junction. The section of bowel to be used for augmentation must be located at least
15 cm proximal to the ileocaecal junction in order to preserve absorptive bowel functions
after the segment is removed. The portion selected is then clamped off using small, 5-mm
laparoscopic bowel clamps. Inserting a 5-mm laparoscope into the lower left port and
illuminating the area will help to identify the vascular mesenteric pedicle associated with this
segment of bowel. Portions of the mesentery adjacent to the proximal and distal ends of the
selected section of bowel are then scored with laparoscopic electrosurgical scissors, which
facilitates subsequent extracorporeal identification.
The use of sigmoid colon, sigmoidocystoplasty, is suggested for patients who meet the
following criteria: (a) neurogenic bladder dysfunction accompanied by defecating dysfunction
with a resultant redundant sigmoid colon; (b) ability to perform intermittent catheterization
via the urethra; and (c) do not require a continent catheterizable stoma. Removing this
segment of bowel can be done in a similar manner as above, with the additional insertion of a
10-mm port medial to the level of the right anterior iliac spine. This aids in mobilization of
the bowel segment so that it may be manipulated via the extension of the lower left abdominal
port (Fig. 2).
For patients who do require a continent catheterizable stoma, the right colon and terminal
ileum should be used. The peritoneum lateral to the cecum and ascending colon, and the
peritoneum of the terminal aspect of the Z line are incised, and the entire right colon and terminal
ileum are mobilized for extracorporeal manipulation via the extended incision of the umbilical
port. This is facilitated by making certain that the patient’s thighs are kept in a low position with
low lithotomy. Once incised, the cecum and ascending colon are anastomosed to the bladder,
while the 10 –12 cm of terminal ileum is used to create a catheterizable channel and stoma at the
umbilicus.

VI. EXCLUSION AND REANASTOMOSIS OF THE BOWEL

The umbilical port is removed after exsufflation of the pneumoperitoneum. Next, the umbilical
incision is enlarged circumumbilically (it may also need to be extended an extra 2 cm in obese
cases) in order to allow for delivery of the preselected bowel segment. Care must be taken
to ensure proper proximal-distal orientation of the loop and to avoid twisting of the mesenteric
pedicle. Using traditional open surgical techniques, the selected portion of bowel and its
mesenteric pedicle is then divided between clamps and isolated as described above in ileo-
cystoplasty (Fig. 3). Bowel anastomosis is performed cephaled to the excluded segment of bowel
using traditional open surgical techniques, and the mesenteric defect is repaired. The bowel
is then immediately returned to the abdomen via the umbilical port, which ensures that
the umbilical incision will not need to be enlarged should the reanastomosed bowel or the
reconfigured bowel segment for augmentation become edematous.
 Laparoscopic Enterocystoplasty 477

Figure 2 Selection of port sizes and location for laparoscopic sigmoidocystoplasty. (Courtesy Cleveland
Clinic Foundation.)

VII. REFASHIONING OF THE ISOLATED BOWEL SEGMENT

The isolated bowel segment should be draped in moist warm sponges and irrigated with normal
saline until the returning irrigation is clear. Next, an incision is made along the border of the
bowel, opposite the side of the mesentery. A U-shaped plate is created by a side-to-side
anastomosis with 2-0 Vicryl sutures (Fig. 4) when using the small bowel or sigmoid colon. The
refashioned bowel segment is then reintroduced to the peritoneal cavity. Ports are replaced
in order to reestablish the pneumoperitoneum. In ileocystoplasty, this involves inserting
a disposable 10- to 12-mm blunt-tip port with a fascial retention balloon and foam cuff to
minimize gas leakage. In sigmoidocystoplasty, it involves reducing the lower left incision to
accommodate a 10-mm port. A laparoscope can then be inserted, and the isolated bowel segment
can be oriented and inspected to exclude torsion of the pedicle.
When the right colon and terminal ileum are to be used, as in patients who require a
catheterizable stoma, the cecum and proximal colon must be detubularized, and the appendix
removed. The terminal ileum is then plicated over a 16F red rubber catheter using a
gastrointestinal anastomosis stapling device (GIA stapler), and the ileocecal junction is
imbricated and intussuscepted to augment the continence mechanism of the ileocecal valve
using 2-0 silk sutures (Fig. 5). To facilitate intracorporeal laparoscopic identification and
manipulation, orientation sutures are placed at the cephalic end (undyed, 2-0 Vicryl on a CT-1
needle) and the caudal end (dyed, 2-0 Vicryl on a CT-1 needle) of the bowel patch. The 16F red
rubber catheter is then secured to the terminal end of the catheterizable segment of the ileum with
478 Rackley and Abdelmalak

Figure 3 Extracorporeal isolation and manipulation of the small bowel via the umbilical port site.
(Courtesy Cleveland Clinic Foundation.)

a 2-0 silk suture for atraumatic intracorporeal manipulation and for delivering this terminal
segment to the umbilicus for stoma maturation at the end of the procedure. The isolated bowel
patch is then returned to the abdominal cavity and the infraumbilical incision is closed over a 10-
to 12-mm blunt-tip port with a fascial retention balloon and foam cuff, which minimizes gas
leakage for the remainder of the operation. As in ileo- and sigmoidocystoplasty, once the
pneumoperitoneum has been reestablished, the laparoscope is inserted and the bowel segment is
oriented and inspected to rule out torsion of the pedicle.
While both isolation of the bowel section for augmentation and reestablishing bowel
continuity can be done laparoscopically, we prefer to perform them extracorporeally by
delivering the bowel outside the abdomen through the umbilical or lower port sites. This offers
many advantages: (a) it makes it easier to obtain a precise measurement of the bowel segment;
(b) the vascularity of the mesentery can be ensured before an incision is made; (c) if the
mesentery is long enough to be delivered outside the body without evidence of ischemia, then it
should be an adequate length to reach the bladder neck without tension; (d) the reanastomosis
of the bowel can be performed with increased confidence using open surgical techniques;
(e) likewise, the detubularization and modification of the bowel segment can be performed
quickly by open suturing techniques; (f) irrigation of the excluded loop can be performed
without peritoneal spillage, which minimizes the chance of pelvic abscess formation; and (g) this
approach yields significant savings in overall operative time and cost.
 Laparoscopic Enterocystoplasty 479

Figure 4 Detubularization and reconfiguration of the isolated bowel segment. (Courtesy Cleveland
Clinic Foundation.)

VIII. BLADDER MOBILIZATION AND CYSTOTOMY

For the remainder of the operation, the patient should be placed in the Trendelenberg
position. This ensures that the bowel loops do not encroach upon the pelvic cavity, and aids
in the subsequent steps of the procedure. The next step in mobilization of the bladder is
distension of the bladder with saline via the urethral catheter. Finally, an incision is made
through the peritoneum surrounding the bladder. It originates at the medial border of the left
medial umbilical ligament and continues linearly to the right medial umbilical ligament. The
median umbilical ligament is taken down during the procedure using electrosurgical scissors,

Figure 5 Detubularization and reconfiguration of the right colon and ileum for cecocolocystoplasty in
preparation for formation of a catheterizable stoma. (Courtesy Cleveland Clinic Foundation.)
480 Rackley and Abdelmalak

and when needed, the lateral peritoneum incisions can be extended along the medial umbilical
ligaments to increase exposure. Another means for increasing exposure is dissection of the
loose areolar tissue surrounding the bladder; this allows for greater access to the bladder neck
and perivesical spaces.
The cystostomy begins with a curvilinear incision through the bladder wall. The apex
of the incision is at the bladder neck, and the base extends posteriorly past the midcoronal plane
of the bladder dome (Figs. 2, 3). This type of incision greatly disrupts the musculature of the
bladder, facilitates the anastomosis of bowel, and is particularly useful in patients in whom the
presence of a uterus may prevent an adequate cystostomy incision.

IX. ENTEROVESICAL ANASTOMOSIS

There are many possible methods of securing the bowel to the bladder. However, to ensure a
watertight anastomosis, we prefer to begin by attaching the “posterior” wall of the reconfigured
bowel patch to the apical portion of the bladder flap and continue suturing in a medial (point A)
to lateral (points B and C) direction on each side (Fig. 6). Beginning the anastomosis at the
“anterior” wall of the bowel segment may impede the closing of the posterior segment, as this
portion will be difficult to visualize owing to the constraints of the pelvic anatomy.
Using laparoscopic suturing (5-mm needle holder and a 5-mm grasper) and intracorporeal
knot-tying techniques, we finish the anastomosis by securing the anterior portion of the bowel
segment to the bladder. The bladder is then distended with saline to confirm a watertight
anastomosis (Fig. 7), and a Jackson-Pratt drain is inserted into the pelvic cavity through the
lower lateral five port sites. In female patients, bladder drainage is maintained with a 20 – 24F

Figure 6 Intracorporeal suturing of the isolated bowel segment to the bladder. Point A is at the apical
aspect of the newly formed bladder flap that was derived from the anterior aspect of the bladder wall near
the bladder neck when the cystotomy incision was made. (Courtesy Cleveland Clinic Foundation.)
 Laparoscopic Enterocystoplasty 481

Figure 7 Completed view of the bowel to bladder anastomosis in preparation for maturation of the
catheterizable stoma to the umbilicus. (Courtesy Cleveland Clinic Foundation.)

urethral catheter. A smaller urethral catheter is preferred for males; therefore, a suprapubic tube
is placed through the bladder wall and extends to the outside of the body through the lower port
site. Any 10-mm port sites, as well as the umbilical incision, are closed in layers.
When patients require a catheterizable stoma, the isolated ileal segment is positioned with
the attached red rubber catheter is secured with an endoclamp via the umbilical port. Once the
pneumoperitoneum has been decompressed, the terminal end of the ileal segment is delivered
to the umbilicus and secured to the anterior rectus fascia and skin; 4-0 chromic sutures are used
to perform a Y-V flap maturation of the stoma to the skin of the umbilicus. In obese patients, the
use of the umbilicus as the site of stoma formation decreases the amount of ileum needed to
mature the stoma to the skin. Finally, to optimize bladder drainage and healing of the newly
created channel, a 16F catheter is isolated through the stoma and into the bladder.

X. POSTOPERATIVE MANAGEMENT

The oral-gastric decompression tube is removed, the patient is extubated, and the Jackson-Pratt
drain is taken out once drainage is ,25 mL or fluid chemistries indicate peritoneal fluid. The
patient is allowed to leave the hospital if afebrile and has completed three consecutive meals,
the first tending to be consumed the first postoperative day. Patients are discharged with the
indwelling urethral catheter for drainage and are instructed to perform daily bladder
irrigation using 100 mL sterile saline via the uretheral catheter, they are also given daily low-
dose antibiotics for prophylaxis. At 3 weeks postoperative, the urinary catheter is removed and
intermittent catheterization is begun. While the catheter at the umbilical stoma is usually capped
482 Rackley and Abdelmalak

at the time of hospital discharge, it may be used to flush out the bladder during daily irrigation
practices in the weeks following surgery.

XI. RESULTS (TABLE 1)

Seventeen laparoscopic enterocystoplasties were performed in patients with neurogenic bladder

dysfunction between June 1999 and November 2001, including five ileocystoplasties, three
sigmoidocystoplasties, one colocystoplasty, and eight cecocolocystoplasties with a continent
catheterizable ileal stoma. Blood loss for all procedures was minimal, averaging 175 mL and not
exceeding 250 mL. The entire operation lasted an average of 7.0 h (range 5.3– 8 h), with
laparoscopic suturing taking a mean 2.4 h (range 1.7– 3.1 h). Sixteen of 17 patients were able to
resume eating 24 h postsurgery, and patients were ready to be discharged from the hospital an
average of 5.7 days (range 3– 7 days) after the procedure. This, along with the fact that patients
did not need long-term care, was remarkable considering that most of the patients suffered from
underlying neurological conditions. The only complications that accompanied these procedures
were a trocar-induced rectus sheath hematoma during a sigmoidocystoplasty and a self-limited
paralytic ileus. The former was controlled laparoscopically, and the latter through conservative
treatment.
Each patient consented to participate in our follow-up study that consisted of filling out
validated surveys about their bladder control (BLCS) and bowel control (BWCS) before and
after the surgery. Two male (14.4%) and 12 female (85.6%) patients with an average age of 40
years (range 18 –62) were able to complete at least the 6th month postoperative questionnaires

Table 1 Laparoscopic Enterocystoplasty Cases

Age Primary Op. T Bl. L H. S

ID (yr) Sex disease (h) (mL) (d) Bowel used

1 27 M Sensory 6.15 300 10 Ileum

urgency
2 49 F MS 7 350 9 Sigmoid colon
3 30 F SCI 7 200 5 Cecum and rt colon and ileum
4 48 F TM 3.15 60 6 Ileum
5 36 F MS 8 150 6 Cecum and rt colon and ileum
6 62 M MS 5 300 4 Ileum
7 18 F SCI 8 110 6 Cecum and rt colon and ileum
8 46 F MS 8 125 6 Cecum and rt colon and ileum
9 52 F MS 5.15 200 5 Sigmoid colon
10 23 F Spina bifida 8 200 6 Rt colon
11 38 F MS 7 350 7 Cecum and rt colon and ileum
12 45 F SCI 9.15 550 5 Cecum and rt colon and ileum
13 31 F SCI 9 300 4 Cecum and rt colon and ileum
14 58 F MS 4 150 4 Ileum
15 27 F SCI 7 200 3 Sigmoid colon
16 39 M MS 8 200 4 Cecum and rt colon and ileum
17 49 F DI 8 200 3 Ileum

Op. T (h), operative time (h); H. S (d), hospital stay; Bl. L (mL), blood loss (mL); MS, multiple sclerosis; SCI,
spinal cord injury; TM, transversmyelitis; DI, detrusor instability.
 Laparoscopic Enterocystoplasty 483

based on a mean follow-up of 17 months (range 7– 27). Significant improvement in bladder

control was seen with a decline in average score on the BLCS from 14.9 + 5.0 to 1.6 + 1.8,
P ¼ .0002. However, there was no significant change in bowel function, with an average
preoperative BWCS score of 6.4 + 6.5 and a mean postoperative score of 5.3 + 6.0, P ¼ .30.
It is important to emphasize that bowel function control score did not decrease despite the
removal of a segment of bowel for bladder augmentation.

XII. SUMMARY

As in open enterocystoplasty, laparoscopic bladder augmentation uses various segments of

bowel to enlarge the bladder and to restore compliance. While benefits of laparoscopic surgery
include decreased pain, morbidity, and recovery time (an attractive option to those with complex
comorbid illnesses), a major drawback of this type of surgery is cost. However, as surgeons
become more familiar with laparoscopic techniques, reusable equipment is implemented, cost-
saving strategies are employed, and surgical time and length of hospital stay decrease, a decline
in overall cost become apparent (4).
For those who undergo laparoscopic augmentation cystoplasty owing to neurogenic
bladder dysfunction, a significant improvement in bladder control without impairment of bowel
control has been documented. Our experience demonstrates that laparoscopic augmentation
cystoplasty technique may be a practical alternative to traditional open enterocystoplasty in
improving the quality of life of our patients.

REFERENCES

1. Novick AC. Augmentation cystoplasty. In: Operative Urology. Baltimore: Williams and Wilkins,
1982:98.
2. Hasan ST, Marshall C, Robson WA, Neal DE. Clinical outcome and quality of life following
enterocystoplasty for idiopathic detrusor instability and neurogenic bladder dysfunction. Br J Urol
1995; 76:551– 557.
3. Mundy AR, Stephenson TP. Clam: ileocystoplasty for the treatment of refractory urge incontinence.
Br J Urol 1985; 57:641 – 646.
4. Rink RC, Adams MC. Augmentation cystoplasty. In: Marshal F, ed. Textbook of Operative Urology.
Philadephia: W.B. Saunders, 1990:914– 926.
5. Smith JJ, Swierzewewski SJ. Augmentation cystoplasty. Urol Clin North Am 1997; 24:745 – 754.
6. Mikulicz J. Zur Operation der angeborenen Blasenspalte. Zentralbl Chir 1899; 26:641.
7. Garrard CL, Clements RH, Nanney L, Davidson JM, Richards WO. Adhesion formation after
laparoscopic surgery. Surg Endosc 1999; 13:10 –13.
8. Hobart MG, Gill IS, Schweizer D, Schweizer D, Bravo EL. Financial analysis of needlescopic versus
open adrenalectomy. J Urol 1999; 162(4):1264– 1267.
9. Rackley RR, Abdelmalak BJ. Laparoscopic augmentation cystoplasty: surgical technique. Urol Clin
North Am 2001; 28:663– 670.
35
Management of Refractory Detrusor
Instability: Sacral Nerve Root Stimulation
Patrick J. Shenot
Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A.

I. INTRODUCTION

Clinical manifestations of urinary voiding dysfunction include urge incontinence, urgency-

frequency, and urinary retention. Patients with nonobstructive urinary retention have few
treatment options except intermittent catheterization. The treatment of refractory detrusor
overactivity represents one of the most challenging problems in urology. Conservative treatment
rarely results in a durable cure of patients with urge incontinence and bladder overactivity.
Pharmacologic and behavioral techniques result in total cure in ,50% of patients (1). Once
behavioral and pharmaceutical options have failed, these patients have been traditionally been
offered more invasive treatments such as bladder augmentation. While effective, this technique
is highly invasive and irreversible, and it carries significant complication rates. Other minimally
invasive surgical treatments for refractory detrusor overactivity, such as transvaginal detrusor
denervation, produce unreliable results. Detrusor myomectomy represents a potential treatment
option, but this technique has not been widely studied. Sacral neuromodulation offers an
alternative, reversible minimally invasive treatment for patients with urge incontinence, urinary
urgency-frequency syndrome, and nonobstructive, nonneurogenic urinary retention refractory to
conservative therapy.

II. HISTORY

Although neurostimulation techniques for urinary incontinence were first applied in the 1960s,
the foundation for sacral neuromodulation arose out the neurostimulation program at the
University of California, San Francisco. Following extensive animal studies, a clinical program
at this institution was initiated that laid the foundation for the clinical application of this
therapy. Tanagho and Schmidt reported on a diverse group of patients who benefited from
neuromodulation of sacral the nerve roots (1,2). It was demonstrated that electrical stimulation
of the sacral nerve root could reduce inappropriate neural activity to inhibit the overactive
detrusor. Promising results at this and other centers led to the commercial development of
the InterStim device (Medtronic Inc, Minneapolis, MN), large-scale clinical trials, and FDA
485
486 Shenot

approval for the treatment of refractory urge incontinence in 1997. Further testing and clinical
trials resulted in subsequent approval of the device (April 1999) for significant symptoms of
urgency-frequency and nonobstructive urinary retention. This implantable sacral neurostimulation
system comprises a neurostimulator, an extension cable, and a quadripolar stimulating electrode
that is implanted in one of the sacral foramen, most commonly S3. Although other stimulation
systems have been studied, this is the only device that has gained widespread acceptance.
Despite recent advances in the clinical application of sacral nerve stimulation, the exact
mechanism by which it works is not understood. The finding that sacral neuromodulation can
be used to treat both detrusor overactivity and urinary retention suggests that in patients with
voiding dysfunctions it has a conditioning effect on neural excitability and can restore neural
equilibrium between facilatory and inhibitory influences although the exact mechanism of
action in each of these conditions may be different (4). The basic principles of neuromodulation
are that electrical stimulation is intrinsically inhibitory and that activity in one neural pathway
can influence activity in other pathways. It is generally assumed that sacral nerve stimulation
results in afferent inhibition of sensory processing in the spinal cord. Evidence suggests that
this occurs via a polysynaptic reflex mechanism, but it is unclear whether such a reflex is at a
segmental level within the sacral cord or involves spinobulbospinal pathways (5). Proposed
mechanisms of afferent stimulation include direct activation of afferents fibers in the sacral
nerve root or perhaps activation of the pelvic floor with subsequent amplification of afferent
impulses (6).

III. PATIENT SELECTION

Sacral neuromodulation may be considered for patients with urge incontinence, urinary urgency-
frequency syndrome, and nonobstructive urinary retention who have failed more conservative
forms of management. These patients should have undergone a comprehensive evaluation,
including a thorough medical history; general, neurologic, and pelvic examinations; urinalysis;
culture; voiding diary; and postvoid residual (PVR) urine determination. Diagnostic testing,
such as cystoscopy, urine cytology, and urodynamics, should be considered to rule out any
treatable conditions. An accurate, complete voiding diary is critical to document baseline
voiding behaviors and judge the patient’s response to therapy. Patients being evaluated for this
therapy should be willing and competent to completely and accurately fill out voiding diaries at
various time points during evaluation.
Attempts at conservative management should be made using some combination of altered
fluid intake, medication, pelvic floor exercises (with or without biofeedback), and bladder
interval training. Only after a patient fails a diligent attempt at conservative therapy should SNS
be considered. Patients with neurologic disorders, such as multiple sclerosis, are potential
beneficiaries of this therapy, but experience is limited and it is unknown how the progressive
nature of these conditions will impact on long-term results of this treatment (7). In addition,
the foreseeable need for magnetic resonance imaging (MRI) studies represents a relative
contraindication to this procedure.

IV. TEST PROCEDURE

A. Acute Nerve Stimulation Testing
Acute nerve stimulation testing is done with the patient in the prone position. Pillows may be
placed under the lower abdomen to achieve slight flexion of the hips to position the sacrum
 Refractory Detrusor Instability 487

horizontally. The sacral area is prepared with povidone-iodine and sterile drapes are placed to
allow visual observation of the motor responses of the pelvic floor, calves, and feet. Using
palpation of bony landmarks or fluoroscopy, the approximate location of the S3 foramina are
located at the level of the greater sciatic notch about one finger width from the midline (Fig. 1)
Local anesthesia is then achieved by infiltrating the subcutaneous tissue and periostium taking
care not to infiltrate the foramen itself. An insulated foramen needle is placed in the appropriate
foramen at an angle of approximately 608 relative to the skin (Fig. 2). The needle is stimulated
using an external stimulator at a set frequency and pulse width while the voltage is gradually
increased. The sensory and motor responses to stimulation are recorded (Table 1). Sensory
responses to S3 stimulation typically include a pulling sensation in the rectum which extends
forward to the scrotum or labia. Motor responses to S3 stimulation include contraction of the

Figure 1 Sacral anatomy. The S3 foramen lies at the level of the sciatic notch one finger breadth from the
midline. This is a valuable radio graphic landmark that aides the in locating the S3 foramen. The S4
foramen lies at the sacral crest, where the sacrum flattens out and serves as a useful topographic landmark.
(Courtesy of Medtronic, Inc.)
488 Shenot

Figure 2 The insulated foramen needle is advanced at an angle of 608 to the skin and perpendicular to
the bony surface of the sacrum. (Courtesy of Medtronic, Inc.)

levators (“bellows” response of the perineum) and plantar flexion of the great toe. S2 stimulation
leads to “clamp” response of the anal sphincter and lateral leg rotation. S4 stimulation results in a
perineal bellows response but no lower extremity motor response. Occasionally, stimulation at
S4 will produce a better response owing to variations in neural anatomy. In difficult cases, it is
sometimes helpful to map the sacral responses during acute nerve stimulation testing to
determine the appropriate foramen in which the temporary or permanent lead should be placed
(Fig. 3). Fluoroscopy may be invaluable in locating and placing the foramen needle, but
radiographic information should only serve to confirm the impressions derived from stimulation
responses.

Table 1 Important Responses to Acute Sacral Nerve Root Stimulation

Response to acute stimulation

Ipsilateral lower
Nerve root Pelvic floor extremity Sensation

S2. Primary somatic Contraction (“clamp”) Lateral leg/hip Contraction of base

contributor of pudendal of anal sphincter rotation, plantar of penis or vagina
nerve for external flexion of entire foot,
sphincter, leg, foot contraction of calf
S3. Virtually all pelvic Pelvic floor bellows Plantar flexion of great Pulling in rectum,
autonomic functions toe; other toes show extending to
and striated muscle variable response scrotum or labia
(levator ani)
S4. Pelvic autonomic and Pelvic floor bellows No lower-extremity Pulling in rectum
somatic; no leg or foot motor stimulation only
 Refractory Detrusor Instability 489

Figure 3 Intraoperative fluoroscopic “map” showing foramen needles in S2, S3, and S4 in a patient
under general anesthesia during permanent implantation. The characteristic leg rotation noted upon
stimulation of S2 indicates that the S3 foramen is located one segment lower.

B. Subchronic Phase: Peripheral Nerve Evaluation (PNE)

Once the desired responses are obtained, the test stimulation lead is inserted through the needle,
and the needle is removed. The lead is securely taped to the skin and attached to the external
stimulator. The patient is able to adjust the voltage amplitude so that he/she maintains the
maximum comfortable level of stimulation. Sacral radiographs are obtained to document lead
placement. These may aid in placing the permanent lead in the same position in those patients
who proceed to permanent implantation. Voiding diaries are kept for 3– 7 days before the leads
are removed. PNE is considered successful if there is significant (.50%) objective improvement
in the particular parameter being evaluated. A voiding diary is then repeated when the patient’s
symptoms return to baseline to exclude the rare patient who derives long-term benefit from
subchronic stimulation. Repeat testing may be considered in patients who had a suboptimal
response to PNE. In one series, 65% of patients with a positive test stimulation were identified
during the first test stimulation, 21.5% during a second stimulation, and 13.5% during additional
testing (unpublished data from Medtronic to the FDA). Patients with a positive response are
offered permanent neurostimulator implantation.

V. PERMANENT NEUROSTIMULATOR IMPLANTATION

Permanent implantation may be performed either under general anesthesia with nonparalytic
agents or using a combination of local anesthetics and intravenous sedation. Broad-spectrum
antibiotics are administered perioperatively, and the patient is positioned as previously
described. Acute nerve stimulation testing is performed to locate the desired motor response,
which should correspond to that noted during earlier testing. Once the desired foramen and
490 Shenot

responses are noted, a paramedian incision is made directly over the needle. The incision is
carried down to the level where the foramen needle enters the lumbodorsal fascia. The fascia is
clean of overlying fat using a Kitner dissector, the hub of the foramen needle is cut off, and a
14-gauge angiocatheter sheath is placed over the needle and through the foramen. A quadripolar
lead is placed through the angiocatheter, and the catheter is removed. The lead tested to assure
desired motor responses in at least three of the four levels, and the locking collar is placed at the
location where the lead perforates the lumbodorsal fascia. The collar is secured to the fascia
using nonabsorbable sutures to prevent lead migration. A second incision is made over the
upper buttock 3– 5 cm below the iliac crest, and a subcutaneous pocket is created for the
neurostimulator. A tunneling device is utilized to transfer the free end of the lead to the buttock
incision. A connecting lead is secured between the quadripolar stimulating lead and the
neurostimulator. The neurostimulator is placed in the subcutaneous pocket, and both incisions
are closed in layers with absorbable suture. A radiograph is obtained to document placement
(Fig. 4). Alternatively, the neurostimulator may be placed subcutaneously in the anterior
abdominal wall using a longer connecting lead, but this technique has fallen out of favor owing
to the need to reposition the patient and excellent patient tolerance for buttock placement (8).
The patient is discharged within 23 h and returns 1 week later for initial activation of the
neurostimulator.

A. Two-Stage Implantation
Two-stage sacral neurostimulator implantation is an alternative method that may increase the
number of patients who may benefit from this therapy (9). The technique involves acute
stimulation testing as previously described. Instead of placing a temporary lead, the permanent

Figure 4 Intra-operative fluoroscopic view following placement of quadripolar electrode and permanent
neurostimulator. AP and lateral pelvic radiographs are taken immediately following implantation to
document lead placement.
 Refractory Detrusor Instability 491

quadripolar electrode lead is placed in the desired foramen and tunneled to the proposed site for
permanent neurostimulator placement in the upper buttock. A small incision is made and the
permanent lead is connected to a percutaneous extension wire, which is then tunneled to the
contralateral side and brought through a small skin puncture. The extension wire is connected to
an external neurostimulator. In the next 5 – 7 days voiding diaries are obtained. If the desired
objective and subjective improvement is noted, the percutaneous extension is removed and the
permanent neurostimulator is placed as the second stage procedure. If the trial is unsuccessful,
the leads are removed using local anesthesia. Future developments may include the development
of a permanent electrode that can be placed percutaneously without fear of lead migration.
The two-stage technique offers several advantages. Because the lead is fixed to the
lumbodorsal fascia with sutures, the problems encountered with early lead displacement
inherent to PNE are obviated. The use of a quadripolar lead for test stimulation allows greater
flexibility in the setting of stimulation parameters that should increase the percentage of
responders who will then qualify for permanent neurostimulator implantation.
Although there are some concerns about infection, the long subcutaneous tunnel through
which the percutaneous extension is placed minimizes this risk. This technique, which received
FDA approval in 2001, is commonly utilized in patients who have failed a percutaneous trial. It
is rapidly gaining favor as the initial technique (in lieu of PNE) for the initial testing of this form
of therapy. Bilateral sacral nerve root stimulation has been utilized in select cases, but to date
there is no convincing evidence that this will significantly improve clinical efficacy (10). An
alternative approach involves the bilateral implantation of cuff electrodes following sacral
laminectomy. This technique may improve the efficacy of chronic sacral neuromodulation by
preventing lead migration, but the procedure is much more invasive and the necessity for sacral
laminectomy may limit patient acceptance.

B. Postimplantation Activation and Programming

Within 1 week of implantation, the neurostimulator is activated. A console programmer allows
transcutaneous adjustment of stimulation parameters including amplitude, rate of stimulation,
pulse width, and either continuous or cycling mode. After basic parameters are set, the patient
can easily adjust the amplitude of stimulation within limits set by the treating physician by using
a small handheld programmer. The patient is instructed to turn the stimulator up to the maximum
comfortable level. Patients with urinary retention are instructed to turn the device off to void.
The neurostimulator battery has an estimated lifespan of 7 – 10 years.

VI. EFFICACY OF SACRAL NERVE STIMULATION

During the 1980s and 1990s, a number of centers in Europe and the United States reported on
their experience with SNS for various urinary voiding dysfunctions (11 –15). These were case
series that lacked control groups and simply compared the clinical symptoms of patients before
and after neurostimulator implantation. The most convincing evidence for the efficacy of sacral
neuromodulation was derived from a prospective, randomized study (MDT-103) conducted at
16 centers in North America and Europe. This study included patients with urge incontinence,
urinary urgency-frequency, and urinary retention who had failed standard medical therapy and
who demonstrated at least a 50% improvement from baseline during test stimulation. These
patients were randomized to either the treatment (immediate implantation) group or control
(delayed implantation) group (Fig. 5).
492 Shenot

Figure 5 Design of MDT-103, a multicenter, prospective randomized controlled trial of 581 patients
with urge incontinence, significant urgency-frequency, or urinary retention who failed standard treatment
or standard treatment was deemed medically inappropriate. (From Refs. 16 – 19.)

A. Results of the Multicenter Randomized Controlled Trial (MDT-103)

1. Urge Incontinence
It is clear that sacral neuromodulation decreases both the frequency and the severity of leakage
in patients with refractory urge incontinence (16). After 6 months, 77% of patients who were
randomized to neurostimulator implantation experienced no heavy leaking episodes compared
to 8% in the control (no implant) group. Forty-seven percent of those treated achieved complete
continence at 6 months compared to none in the control arm. Clinical efficacy was sustained for
18 months with 52% of patients being completely dry and 24% showing .50% improvement. The
same group later reported that sacral nerve stimulation is a durable and effective treatment for
refractory urge incontinence with sustained long-term benefit through an average of 30.8 months.

2. Urinary Frequency
Hassouna and associates studied 51 patients with refractory urgency-frequency who successfully
completed test stimulation in a randomized controlled study (18). Compared to the control
 Refractory Detrusor Instability 493

group, the treatment group demonstrated significantly improvements in the number of voids
daily, volume voided per void, and degree of urgency before void. Symptoms returned to
baseline when the neurostimulators were turned off 6 months following implantation.
Approximately half of the patients (48%) reported either a 50% or greater decrease in urinary
frequency or complete resolution of urinary frequency (fewer than eight voids per day).
Improvement in urinary urgency was reported by 83%. These responses remained essentially
unchanged through the 18-month follow-up period. Favorable urodynamic responses were seen
in those patients with detrusor instability noted during initial evaluation.

3. Urinary Retention
Sacral neuromodulation has proven effective in selected patients with nonobstructive retention
(19). Compared to the control group, the treatment group had statistically and clinically
significant reductions in the catheter volume per catheterization. Of the patients treated with
implants, 69% eliminated catheterization at 6 months and an additional 14% had a 50% or
greater reduction in catheter volume per catheterization. Successful results were achieved in
83% of the implant group with retention compared to 9% of the control group at 6 months.
Temporary inactivation of sacral nerve stimulation therapy resulted in a significant increase in
residual volumes. The efficacy of sacral nerve stimulation was sustained through 18 months after
implantation.

B. Complications
Percutaneous test stimulation has been proven to be exceedingly safe. The most common
adverse event in 914 test stimulations in MDT-103 was lead migration which occurred in 11.8%
of procedures (Medtronic Inc., unpublished data to FDA). Technical problems and pain were
the two next most common events, occurring in ,3% of patients. The rate of complications
requiring surgical intervention associated with test stimulation was noted in one patient (0.1% of
procedures). This involved a test stimulation electrode that became dislodged during routine
removal requiring surgical removal.
There is a relatively high incidence of adverse events associated with sacral nerve
stimulator implants. Evaluation of the safety of sacral nerve stimulation was established by
pooling safety data in a population of 219 patients with implants for urge incontinence, urgency-
frequency, and retention. Pooling of safety data from these three indications was justified based
on the identical study protocol, devices, efficacy results, and safety profile (18). The probability
of postimplant adverse events that exceeded 5% at 12 months included pain at neurostimulator
site (15.3%), new pain (9.0%), suspected lead migration (8.4%), infection (6.1%), transient
sensation of electrical shock (5.5%), and pain at the lead site (5.4%). Surgical revision of the
implanted neurostimulator or lead system was performed in 33.3% of cases patients to resolve an
adverse event. There were no reports of serious adverse device effects or of permanent injury
associated with the devices or use of sacral nerve stimulation. It is expected that as implanting
physicians gain experience in this technique and technical improvements in this device are
introduced, the moderately high complication rates should fall.

VII. CONCLUSION

The management of voiding dysfunction remains one of the most challenging problems faced by
the practicing urologist. Although the mode of action of sacral neuromodulation is poorly
494 Shenot

understood, controlled studies have clearly shown the superiority of this treatment to
conservative therapy. Implantation and testing techniques are easily learned by surgeons with
particular interest in voiding dysfunction. The use of sacral nerve modulation via an implantable
system is an effective, minimally invasive, potentially reversible tool for the management of
refractory voiding dysfunction. Improvements in the technical design of the neurostimulation
system promise to simplify the techniques of testing and implantation and reduce the significant
complication rate of this therapy.
The field of neurostimulation is rapidly evolving. Since the completion of earlier studies
on sacral nerve stimulation, procedural advances including new, less invasive technology and
surgical techniques have led to greater acceptance among the patient and physicians. A tined
quadripolar stimulation lead and introducer system, approved by the FDA in 2002, has
significantly decreased the invasiveness of sacral nerve stimulation using the Interstim system.
Tined leads offer sacral nerve stimulation through a sutureless anchoring procedure. This
procedure can be conducted under local anesthesia. This allows for the evaluation of patient
sensory response during the implant procedure ensuring optimal lead placement. This improved
technique results in faster patient recovery times as a result of a minimized surgical incision.
Electrical stimulation of the pudendal nerve has been demonstrated to inhibit detrusor
activity. Chronic neurostimulation of pudendal afferents may provide effective treatment for
disorders of detrusor overactivity. There are significant technical challenges inherent to placing
and maintaining an electrode near the pudendal nerve in humans. The development of new
implantable microstimulators has made chronic implantation or pudendal neurostimulators
feasible. The bionw (Advanced Bionics, Sylmar, California) is a new generation generic
implantable microstimulator implanted using minimally invasive techniques. The bionw
microstimulator contains a rechargeable battery, sophisticated electronics, and stimulating
electrodes in a 3 mm  28 mm cylinder and weighing only 0.75 grams. It is implanted through
the use of a needle-like instrument. The bionw has received CE Mark approval for use in urinary
urge incontinence in the European Union and is currently in a U.S. Phase II clinical study for this
indication.
Future technology breakthroughs in the field may include “closed-loop system”
neurostimulators that continually monitor and stimulate the nervous system to preemptively
detect and treat the underlying disorder, as well as integrated treatment methods in which drugs
help to target neurostimulation to specific cells.

REFERENCES

1. Urinary Incontinence Guideline Panel. Urinary Incontinence in Adults: Clinical Practice Guidelines.
Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S.
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2. Schmidt RA, Tanagho EA. Clinical use of neurostimulation. Urologe 1990; 29:191 – 195.
3. Tanagho EA. Principles and indications of electrostimulation of the urinary bladder. Urologe 1990;
29:185– 190.
4. Schmidt RA, Doggweiler R. Neurostimulation and neuromodulation: a guide to selecting the right
urologic patient. Eur Urol 1998; 34(suppl):23 – 26.
5. Fowler CJ, Swinn MJ, Goodwin RJ, Oliver S, Craggs M. Studies of the latency of pelvic floor
contraction during peripheral nerve evaluation show that the muscle response is reflexly mediated.
J Urol 2000; 163:881– 883.
6. Dijkema HE, Weil EHJ, Mijs PT, Janknegt RA. Neuromodulation of sacral nerves for incontinence
and voiding dysfunctions. Clinical results and complications. Eur Urol 1993; 24:72 – 76.
 Refractory Detrusor Instability 495

7. Bosch JLHR, Groen J. Treatment of refractory urge urinary incontinence with sacral spinal nerve
stimulation in multiple sclerosis patients. Lancet 1996; 348:717 – 719.
8. Scheepens WA, Weil EH, Van Koeveringe GA, Rohrmann D, Hedlund HE, Schurch B, Ostardo E,
Pastorello M, Ratto C, Nordling J, Van Kerrebroeck PE. Buttock placement of the implantable pulse
generator: a new implantation technique for sacral neuromodulation-a multicenter study. Eur Urol
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9. Janknegt RA, Weil EHJ, Eerdmans PH. Improving neuromodulation: technique for refractory
voiding dysfunctions: two-stage implant. Urology 1997; 358– 362.
10. Hohenfellner M, Schultz-Lampel D, Dahms S, Matzel K, Thuroff JW. Bilateral chronic sacral
neuromodulation for treatment of lower urinary tract dysfunction. J Urol 1998; 160:821– 824.
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and pelvic pain. World J Urol 1991; 9:138 – 141.
12. Dijkema HE, Weil EH, Mijs PT, Janknegt RA. Neuromodulation of sacral nerves for incontinence
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13. Koldewijn EL, Rosier PF, Meuleman EJ, Koster AM, Debruyne FM, Van Kerrebroeck PE.
Predictors of success with neuromodulation in lower urinary tract dysfunction: results of trial
stimulation in 100 patients. J Urol 1994; 152:2071– 2075.
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urge incontinence. J Urol 1998; 159(5):1516– 1519.
15. Weil EH, Ruiz-Cerda JL, Eerdmans PH. Clinical results of sacral neuromodulation for chronic
voiding dysfunction using unilateral sacral foramen electrodes. World J Urol 1998; 16:313 – 321.
16. Schmidt RA, Jonas U, Oleson KA, Janknegt RA, Hassouna MM, Siegel SW, Van Kerrebroeck PE.
Sacral nerve stimulation for treatment of refractory urinary urge incontinence. Sacral Nerve
Stimulation Study Group. J Urol 1999; 162:352 – 357.
17. Janknegt RA, Hassouna MM, Siegel SW, Schmidt RA, Gajewski JB, Rivas DA, Elhilali MM,
Milam DC, Van Kerrebroeck PE, Dijkema HE, Lycklama a Nyeholt AA, Fall M, Jonas U,
Catanzaro F, Fowler CJ, Oleson KA. Long-term effectiveness of sacral nerve stimulation for
refractory urge incontinence. Eur Urol 2001; 39:101 – 106.
18. Hassouna MM, Siegel SW, Nyeholt AA, Elhilali MM, Van Kerrebroeck PE, Das AK, Gajewski JB,
Janknegt RA, Rivas DA, Dijkema H, Milam DF, Oleson KA, Schmidt RA. Sacral neuromodulation in
the treatment of urgency-frequency symptoms: a multicenter study on efficacy and safety. J Urol
2000; 163:1849 – 1854.
19. Jonas U, Fowler CJ, Chancellor MB, Elhilali MM, Fall M, Gajewski JB, Grunewald V,
Hassouna MM, Hombergh U, Janknegt R, van Kerrebroeck PE, Lycklama a Nijeholt AA, Siegel SW,
Schmidt RA. Efficacy of sacral nerve stimulation for urinary retention: results 18 months after
implantation. J Urol 2001; 165:15 – 19.
36
Physical Exam and Assessment of Pelvic
Support Defects
Steven Swift
Medical University of South Carolina, Charleston, South Carolina, U.S.A.

I. INTRODUCTION

Prior to examining and describing pelvic organ support defects in the female, all clinicians should
have several tools in mind that will aid in providing a comprehensive and accurate diagnosis. These
tools should include an understanding of what represents normal pelvic organ support versus
pathologic prolapse, an inventory of symptoms that can be attributed to pelvic organ prolapse, and a
reliable method of describing the physical findings during the exam. While the first two tools may
seem unnecessary in the subject who has an obvious vaginal bulge that protrudes 4–5 cm beyond
the vaginal opening and complaints of inability to completely empty her bowels or bladder, they are
crucial in evaluating the subject who has a cystocele and no or minimal symptoms.
Until recently these tools were not readily available, and it is only within the past decade
that investigators have begun to study these aspects of pelvic organ support defects. Three
articles, all published in the past 5 years, have attempted to describe the normal distribution of
pelvic organ support, but despite this, there remains a lack of consensus as to what is normal
support versus pathologic prolapse. The recent development of quality of life (QOL) tools,
specific to pelvic organ prolapse, are providing us with a reliable inventory of symptoms
attributable to this condition, but there are still some misconceptions regarding symptoms of
milder forms of prolapse. Finally, there has also been significant progress in standardizing the
description of pelvic organ support. The publication of the Pelvic Organ Prolapse Quantification
(POPQ) system in 1996 provided the first universally recognized and reliable system to codify
pelvic organ support and prolapse.
This chapter will discuss how to approach the physical assessment of a patient with pelvic organ
support defects from the standpoint of investigating symptoms and physical findings. This should
allow the clinician to better manage and appreciate the subtleties of pelvic organ support defects.

II. NORMAL SUPPORT VERSUS PATHOLOGIC

PELVIC ORGAN PROLAPSE

Pelvic organ prolapse is something that when present or absent is obvious, but the point at which
an individual goes from normal support to pathologic prolapse cannot be defined. When the
497
498 Swift

leading edge of the prolapse extends well beyond the limits of the introitus, there is obvious
pathology that all clinicians recognize. When there is little to no movement of any vaginal walls
with Valsalva, the absence of pelvic organ prolapse is apparent, but the patient with pelvic organ
support somewhere in between these extremes often presents a dilemma. Distinguishing age
appropriate normal pelvic support from abnormal prolapse is often a very subjective clinical
decision. This stems from the paucity of data in the literature regarding the normal distribution of
pelvic organ support in women. Several recent studies have begun to explore this, but the
findings are not consistent. One thing that is apparent is that as the patient ages, her pelvic organs
begin to relax into the vaginal canal. What is normal support in 55-year-old women may be early
signs of impending pelvic organ prolapse in 19-year-old women.
There are three studies in the literature that reported the normal distribution of pelvic organ
support in populations of women. The first looked at all women between the ages of 18 and 59
in a small Swedish city (1). They found that only 2% of women had pelvic organ prolapse
described as the leading edge of the prolapse being at or beyond the vaginal introitus. These
women with prolapse were all in the top quartile of the age range investigated. In the second
study, a group of perimenopausal women taking soy supplements for hormone replacement
therapy were investigated and they found very few women with any degree of pelvic relaxation
(2). In contrast, another study of women between the ages of 18 and 81 presenting for annual
exams found a wide range of pelvic organ support with a much greater degree of pelvic
relaxation than noted in previous studies (3). These authors demonstrated that as women age the
leading edge of their pelvic organs descends into the vaginal canal such that by the time they
reach the sixth decade of life the leading edge of their pelvic organs is often at the level of the
introitus (Fig. 1). These studies give some information on the normal distribution of pelvic organ
support; however, they do not define what is normal and what is pathologic pelvic organ support.
One of the drawbacks to these studies is that subjects examined were not always questioned
regarding their symptoms to determine at what level of support women begin experiencing
symptoms of pelvic organ prolapse. Since pelvic organ prolapse is often a QOL issue,
determining the degree of symptoms experienced by subjects with varying degrees of support
would help us understand what represents symptomatic pelvic organ prolapse.
Every patient should serve as her own control. If a patient is asymptomatic and has some
evidence of a pelvic organ support defect on physical exam, then the clinician may want to
follow that patient over time to see if her support worsens. Alternatively, if the subject has new
symptoms attributable to prolapse, then she should be thoroughly investigated and treated
regardless of her degree of support. What is an asymptomatic degree of support in one subject
may lead to symptoms in another. The data presented above on the normal distribution of pelvic
organ support can aid in counseling subjects with minor degrees of relaxation who have
concerns. This information may reassure some patients that they have age-appropriate support.
The definition of pelvic organ prolapse seems obvious but is often extremely complicated.
Instead of relying on any one physical finding or stage of support as a definition, the clinician
should put the physical findings in the context of a patient’s symptoms and the distribution of
normal support for her age. The clinician should be able to provide relief for their symptomatic
patients without being overly aggressive in asymptomatic individuals.

III. SYMPTOMS OF PELVIC ORGAN PROLAPSE

The vaginal vault is surrounded by the bladder and urethra anteriorly, the uterus and small
intestines superiorly, and the rectum and lower sigmoid posteriorly. Therefore, it is not
surprising that when the vaginal support is abnormal, the function of these surrounding
 Pelvic Support Defects 499

Figure 1 Distribution of pelvic organ support by POPQ stage in 487 women presenting for annual
gynecologic healthcare. Note how the peak of the age range curves shifts to the right as the age increases.

structures is compromised. The symptoms commonly attributed to pelvic organ prolapse are a
vaginal bulge, low back pain, sense of pelvic pressure and fullness, constipation, urinary and/or
fecal incontinence, and the inability to empty the bladder and/or rectum (4). While it appears
that this list is complete and all of these symptoms could be anticipated in subjects with pelvic
organ prolapse, the only symptom that is consistently acknowledged by patients with severe
prolapse is the presence of a vaginal bulge that can be seen or felt (5). This is often accompanied
by a sense of pelvic pressure and fullness that is worse late in the day, with any prolonged
standing or during physically demanding activities. However, the sense of pelvic fullness or
pressure can also be a result of vaginal irritation from atrophy or vaginitis in a patient with
otherwise excellent pelvic organ support. In postmenopausal women, complaints of pelvic
pressure and a sense of something “wanting to fall out” of the vagina are often a symptom of
severe urogenital atrophy particularly if the subject denies the presence of a vaginal bulge. In the
only study to compare symptoms in subjects with and without objective pelvic organ prolapse,
the symptom of heaviness in the lower abdomen was reported in 9.7% of subjects with any
degree of prolapse and in 7.5% of subjects with no prolapse (1).
While it seems counterintuitive, the presence of urinary or fecal incontinence is generally
not encountered in subjects with more severe degrees of pelvic organ prolapse. It has long been
noted that urinary incontinence often improves as a patient’s prolapse worsens and subjects with
more severe degrees of prolapse register complaints more obstructive in nature. Therefore, it is
not surprising from organ prolapse QOL questionnaires that the symptoms of urinary and fecal
incontinence play a minor role in pelvic organ prolapse. The King’s College Prolapse Quality of
Life tool (P-QOL) leaves out any reference to stress urinary or fecal incontinence but has
multiple questions regarding difficulty emptying the bladder and rectum (6). There are a few
questions regarding urge incontinence and irritative voiding symptoms. The common lower
urinary and intestinal tract symptoms involve the patient having to manually reduce her vaginal
prolapse or bulge in order to fully empty either her rectum or her bladder. This symptom is much
more prevalent than incontinence in women with genital prolapse.
Stress urinary incontinence can commonly become symptomatic when severe prolapse is
reduced either surgically or with a pessary. This is often referred to as potential, latent, or occult
stress incontinence and occurs in anywhere from 15% to 80% of subjects (7,8). It should be sought
out during physical exam, particularly if contemplating surgical correction of the prolapse.
500 Swift

The symptoms of pelvic pain and or pressure are fairly nonspecific and do not specifically point
to a diagnosis of pelvic organ prolapse. The symptom of low back pain is common to a multitude of
conditions, and while often present in women with pelvic organ prolapse, it is not specific.
When identifying and discussing signs and symptoms of pelvic organ prolapse, the
practitioner should focus on the patient’s report of a vaginal bulge along with obstructive urinary
and fecal symptoms. These are the more common symptoms that can be relieved when the
prolapse is reduced. While symptoms of urinary and fecal incontinence are uncommon, if
present, they should be explored.

IV. PELVIC ORGAN SUPPORT DEFECTS

There are countless systems for codifying pelvic organ support in the literature that date back to
the late 1800s. They have been proposed by some of the fathers of modern gynecology
(Professor Scanzoni, Dr. Keustner, and Dr. Howard Kelley), and while all have gained regional
notoriety, no one system attained universal acceptance. In addition, none of these early systems
were studied to determine their intra- or interexaminer reliability (9 – 11). The extent of this
problem was documented in a review of over 100 articles and 15 textbooks that used or
described various classification systems for pelvic organ prolapse (12). They found no consensus
in how pelvic organ support defects were classified and in all but a few instances found no
detailed description of any system being used.
The first system to gain widespread acceptance in the United States was the Baden and
Walker “half-way” system that was introduced in 1972 and updated in 1992 (13,14). In this
system, the vagina is divided up into six areas that are described separately, the anterior wall or
urethrocele and cystocele, the posterior vaginal wall or rectocele, the apex or enterocele, the
cervix, and the perineal body. The system then describes support for each of these segments
based on the concept of half-way. If the segment being described descends no more than half-
way to the introitus, it is said to be stage 1. If the segment descends into the lower half of the
vagina but not through the introitus, it is stage 2. If it descends through the introitus but is less
than half-way to completely prolapsed, then it is stage 3, and any prolapse greater than this is
stage 4. This system was recently studied and demonstrated good intra-examiner reliability.
As described, the system is somewhat difficult to understand. For example, the anterior
and posterior vaginal walls are continuous structures that begin at the introitus and extend up to
the cervix and posterior fornix, respectively, or the cuff scar in the hysterectomized woman.
Therefore, it can be difficult to decide what portion or aspect of the anterior and posterior walls to
describe as descending into the lower half of the vaginal canal, as the lower half of each wall is
already part of the lower half of the vaginal canal. Despite this, most clinicians find this system
simple to use and it has demonstrated good interexaminer reliability (13).
In 1996, the International Continence Society’s Committee on Terminology devised a
classification system to recommend for international use (15). Out of this meeting came the
Pelvic Organ Prolapse Quantification (POPQ) system. Similar to the “half-way” system, it
divides the vagina up into several points that are each described independently. There are a total
of nine points (eight if the women has had a hysterectomy) that are measured and reported in a
3  3 grid (Fig. 2). Instead of using vague terms to describe which aspect of the prolapsing organ
or vaginal wall is to be judged, the POPQ requires that specific points on the vaginal walls and
cervix be measured in 0.5-cm increments. In addition, the measurements are made around the
fixed point of the hymenal remnants instead of the more vague introitus. If the point being
described remains above the hymen, its position is recorded, in centimeters, as a negative
number. If the point being described descends to the level of the hymen, its position is recorded
 Pelvic Support Defects 501

Figure 2 Diagrammatic representation of the nine points of the POPQ and the 3  3 grid used for
reporting.

as 0. If the point passes beyond the hymen, its position is recorded, in centimeters, as a positive
number. One overall stage is assigned for the patient as the most dependent or the most prolapsed
point. The anterior, posterior, apical vaginal walls and cervix are not assigned individual stages.
The POPQ is a relatively complex system, and the document describing the technique for
obtaining the nine measured points is seven pages in length, requiring a very thorough reading to
understand how certain measures are derived. The A points of the anterior (Aa) and posterior
(Ap) vaginal wall are determined by measuring 3 cm proximal to the urethral meatus for the Aa
and 3 cm proximal to the hymenal remnent at the posterior fourchette for Ap (Fig. 4). Point B
anterior (Ba) and posterior (Bp) are usually the most difficult to appreciate. They are the only
points that are not fixed. They are used to designate the most dependant segments of the anterior
and posterior vaginal walls that are between point Aa and point C anteriorly and point Ap and
point D posteriorly (or point C posteriorly if the patient has had a prior hysterectomy). Point C
represents the cervix or cuff scar (after hysterectomy). Point D represents the posterior fornix or
apex of the vagina and is not measured if the patient has had a hysterectomy. These points on the
vaginal wall are then observed as the patient performs either a cough or Valsalva. Where they

Figure 3 Diagrammatic representation of the four point of the simplified POPQ.

502 Swift

Figure 4 Diagrammatic representation of a stage 3 anterior vaginal wall prolapse identifying both the
POPQ points and the simplified POPQ points. The POPQ points Aa, Ba, C, D, Ap, and Bp are all associated
with lines ending with an arrowhead. The simplified POPQ points are represented by lines ending in x’s.

descend in relation to the hymen is recorded in centimeters as either zero, a positive number, or a
negative number, as described above. The genital hiatus (GH) is a measurement from the urethral
meatus to the hymenal remnant at the posterior fourchette. This may be a misleading terms as the
genital hiatus is actually the opening in the levator ani muscle that the vagina perforates. The
perineal body (PB) is a measurement from the hymenal remnant at the posterior fourchette to the
middle of the anus. The total vaginal length (TVL) is a measure of the total vaginal length from
the hymeneal remnant to the vaginal apex. This is the only number recorded with the patient at
rest. Once all of the numbers are obtained, a stage is assigned and a vaginal profile can be drawn.
The staging system is described in Table 1. The easiest way to remember the staging system is to

Table 1 Ordinal Staging System of the POPQ

Stage Leading edge of points Aa, Ba, Ap, Bp Leading edge of point C and/or D

0 All 4 points are 3 cm above the hymenal Points C and D are at a position above the
remnants (value ¼ 23) hymenal remnants that is equal to or
within 2 cm of the total vaginal length
(values  2(tvla 2 2))
1 All points are .1 cm above the hymenal remnants (value  21)
2 Leading edge of the prolapse protrudes to a point to or above 1 cm above the hymenal remnants
but no more than 1 cm beyond the hymenal remnants (value  21 to  þ1)
3 Maximal prolapse protrudes at least 1 cm beyond the hymenal remnants but ,2 cm the total
vaginal length (value  þ1 to þ(tvl 2 2))
4 Maximal prolapse protrudes to within 2 cm of the total length of the vaginal tube (value 
(tvl 2 2))
a
tvl ¼ total vaginal length.
 Pelvic Support Defects 503

focus on the limits of stage 2 support. If the prolapsing organ being described comes to within
1 cm of the hymenal remnants, either above or through, then it is stage 2. If there is some
movement of the vaginal wall but it does not descend to the limits of stage 2, then it is stage 1. If the
prolapsing vaginal wall is .1 cm past the hymenal remnants, then it is stage 3. If there is no
movement of the vaginal points, then it is stage 0, and complete uterovaginal prolapse is stage 4.
The POPQ, while difficult to learn initially, has several advantages over the other systems
that rely on stages instead of specific measures. This is particularly apparent in following a
patient over time to determine if the patient’s pelvic support is changing or is stable. Instead of
using stages, which are relatively gross descriptions of support that encompass a wide range of
possible positions, the POPQ gives specific measures to within 0.5 cm. For example:

A subject presents in referral for evaluation of an anterior vaginal wall defect that is relatively
assymptomatic. On exam her point Aa and Ba are at 21 cm (1 cm above the hymenal
remnants) with Valsalva. She has stage 2 support. She is followed for 6 months and on return
her point Aa and Ba are now at þ1 cm (1 cm past the hymenal remnants). She still has stage 2
support but has obviously progressed, and the clinician may now consider an intervention. If
she were followed by the gross description of stage, then her progression would be less
apparent.
Alternatively, a patient presents with a mild anterior vaginal wall defect such that her point
Aa and Ba are at 21.5 cm (1.5 cm above the introitus). She has stage 1 support. On
reevaluation 6 months later, her point Aa and Ba are at 21 cm and she is now stage 2. This
patient has had almost no progression, but without the specific measures of the POPQ it would
appear she has had a one full stage progression.

The use of stages is adequate for describing populations, but a more descriptive system
like the POPQ has more clinical applicability for evaluating and following individual patients. In

Figure 5 Diagrammatic representation of a stage 4 prolapse identified both the POPQ points and the
simplified POPQ points. The POPQ points Aa, Ba, C, D, Ap, and Bp are all associated with lines ending
with an arrowhead. The simplified POPQ points are represented by lines ending in x’s.
504 Swift

addition, the POPQ system was the first to undergo extensive testing and was shown to have
excellent intra- and interexaminer reliability (16 –19).
The International Federation of Gynecologists and Obstetricians (FIGO) in 1998 became
interested in endorsing a pelvic organ prolapse classification system for worldwide use. It
initially considered the POPQ but found the system to be too complex to endorse for worldwide
use by nonspecialists. Therefore a simplified version of the POPQ was developed with the
International Urogynecological Association (IUGA) (20). This simplified version retained the
staging system of the POPQ but eliminated stage 0 (Fig. 4). Stages 1– 4 remained essentially
identical to the POPQ. If the simplified version is adopted by FIGO, it will allow for crossover so
that research employing the POPQ system can be translated into clinically useful information
that doctors could use in their practice.
In the simplified version there are only four points measured instead of nine as with the
POPQ; anterior vaginal wall, posterior vaginal wall, the cervix (if present), and posterior fornix.
In describing the anterior vaginal wall, a point half-way between the hymenal remnants or
urethral meatus and the cervix or cuff is identified. This is done by gently retracting the posterior
vaginal wall with a Sims speculum, disarticulated Graves speculum, or two fingers to fully
expose the anterior vaginal wall. The subject is then asked to Valsalva, and where that point on
the vaginal wall descends to, in relation to the hymenal remnants, is documented as the stage for
the anterior vaginal wall. A similar technique is employed to describe the stage of the posterior
vaginal wall except that a point is chosen half-way between the hymenal remnants and the
posterior fornix or cuff scar. Practitioners should be able to identify when the leading edge of the
prolapse is .1 cm above or past the hymenal remnants with close inspection. Therefore, no
specific measuring device is necessary. In addition, while the use of the descriptors of anterior
vaginal wall, posterior vaginal wall, and apical vaginal segments is encouraged, the older terms
of cystocele, rectocele, and enterocele are deemed acceptable. In the POPQ system these terms
are disallowed.
This system was studied at one institution and its interexaminer reliability was deemed
excellent (21). The modified IUGA/FIGO system was compared to the POPQ, and there was
excellent agreement between the two systems for staging the various segments as well as for the
overall stage. The simplified POPQ is still undergoing testing at various centers throughout the
world to further study its inter- and intraexaminer reliability as well as to document its
agreement with the POPQ. Prior to its adoption by FIGO it must also prove to be a simple and
easy-to-use tool in clinical practice.
The three systems for describing and codifying pelvic organ support have their own
advantages and disadvantages. The Baden and Walker “half-way” system and the simplified

Table 2 Ordinal Staging System for the Simplified POPQ

Leading edge of anterior and posterior vaginal wall, cervix, apex or posterior fornix (or cuff scar
in the hysterectomized women). Each of the four segments (three in the hysterectomized
Stage women) is graded independently.

1 Prolapse that remains at least 1 cm above of the hymenal remnants.

2 Prolapse that descends to the introitus, defined as 1 cm above or below the hymenal remnants.
3 Prolapse that descends past the introitus, but does not represent complete vaginal vault eversion
or complete procidentia uteri.
4 Complete vaginal vault eversion or complete procidentia uteri. (If one segment is stage 4 then
all segments are stage 4.)
 Pelvic Support Defects 505

POPQ appear to be easy to use but lack specificity for describing subtle changes. The POPQ,
while excellent at describing the detail of all aspects of pelvic organ support, can be cumbersome
to employ in a busy clinical setting and requires practice and continued use to become
comfortable using.

V. CONDITIONS FOR PERFORMING THE EXAM

There are many opinions regarding how to exam the subject with suspected pelvic organ
prolapse. Some authors advocate always examining subjects in the standing position; others state
that subjects should be examined with an empty bladder or only late in the afternoon, after they
have been on their feet for several hours. While all of these recommendations seem appropriate,
few have been studied to determine if they really allow the clinician to better determine the full
extent of the subjects prolapse. Only patient positioning during the exam has been investigated.
It has been demonstrated that exams in the dorsal lithotomy and standing position are equivalent
(22). The authors concluded that patient positioning was not important, and they suggested the
physician allow the patient to confirm her exam. This can be done by having the patient feel
the bulge during the exam or use a mirror to visually confirm your findings. If you cannot
reproduce the subjects complaints, then examining the subject more upright or having her come
back late in the day for a follow-up exam may be indicated.
Another area, which is somewhat controversial, involves examining for the presence of
occult or potential stress urinary incontinence. This involves reducing the prolapse during the
exam and testing for the presence of stress incontinence. As previously mentioned, it is
uncommon for subjects with severe anterior vaginal prolapse to have complaints of stress
urinary incontinence. However, when the prolapse is corrected, either surgically or with a
pessary, stress incontinence is unmasked in up to 80% of patients. It is felt that the anterior
vaginal wall prolapse “kinks” the urethra leading to obstruction. Correcting this “kink” then
reveals stress incontinence. This can be assessed during the examination by doing provocative
testing with the patient’s prolapse reduced. The provocative testing can range from a simple
cough stress test with the bladder symptomatically full to stress testing during a multichannel
urodynamic exam. Several techniques have been advocated for reducing the prolapse. This can
be done with a pessary, disarticulated speculum directed into the sacrum, a vaginal pack, large
cotton swab stick or two fingers placed in the vagina to support the apex. Regardless of the
technique, it is important not to obstruct the urethra by compressing it against the posterior
aspect of the pubic bone. If stress incontinence is only demonstrated with the prolapse reduced,
then potential or occult stress incontinence is diagnosed. There are many ways to address this at
the time of intervention but those will be discussed elsewhere.

VI. SUMMARY

Defining and describing pelvic organ prolapse is often more difficult than clinicians think.
Obvious severe prolapse can be recognized by even the most junior health care provider as
pathology. It is the more subtle forms of support defects that require a thorough understanding.
By understanding the variations of normal support, the symptoms attributable to pelvic organ
support defects, and the systems used to describe the prolapse, the practicing clinician will be
better able to determine appropriate and well-timed interventions.
506 Swift

REFERENCES

1. Samuelsson EU, Victor FTA, Tibblin G, Svardsudd KF. Signs of genital prolapse in a Swedish
population of women 20 to 59 years of age and possible related factors. Am J Obstet Gynecol 1999;
180:299– 305.
2. Bland DR, Earle BB, Vitolins MZ, Burke G. Use of the pelvic organ prolapse staging system of the
International Continence Society, American Urogynecologic Society, and the Society of Gynecologic
Surgeons in perimenopausal women. Am J Obstet Gynecol 1999; 181:1324 – 1328.
3. Swift SE. The distribution of pelvic organ support in a population of women presenting for routine
gynecologic healthcare. Am J Obstet Gynecol 2000; 183:277–285.
4. American College of Obstetricians and Gynecologists. Pelvic Organ Prolapse. ACOG Technical
Bulletin 214. Washington, DC: ACOG, 1995.
5. Elkermann RM, Cundiff GW, Bent AE, Nihira MA, Melick C. Correlation of symptoms with location
and severity of pelvic organ prolapse. Abstract presented at the 25th Annual Meeting of the
International Urogynecology Association, Rome, Italy, Oct 22 – 25, 2000.
6. Digesu GA, Khullar V, Cardozo L, Robinson D, Salvatore S. P-QOL: a validated quality of
life questionnaire for symptomatic assessment of women with uterovaginal prolapse. Abstract
presented at the 25th Annual Meeting of the International Urogynecology Association, Rome, Italy,
Oct 22 – 25, 2000.
7. Weil A, Gianoni A, Rottenberg RD, Krauer F. The risk of postoperative urinary incontinence after
surgical treatment of genital prolapse. Int Urogynecol J 1993; 4:74– 79.
8. Zivkovic F, Taumissimo K, Michelitsch L, Haas J. Urethral profilemetry in women with uterovaginal
prolapse. Int Urogynecol J 1995; 6:10 – 13.
9. Kelly HA. Operative Gynecology. New York: Appleton & Co., 1898.
10. Scanzoni FW. Senkung und Vorfall des uterus und der scheide. In: Scanzoni FW, ed. Lehrbuch der
Krankheiten der weiblichen geschlechstorgane. 5th ed. Vienna: Braumueller, 1875:654 – 664.
11. Kuestner O. Prolapsus uteri et vaginea. In: Kuestner O, Bumm E, Doederlein A, Kroenig B, Menge C,
eds. Kurzes Lehrbuch der Gynaekologie. Jena: G Fischers, 1912:159 – 181.
12. Brubaker L, Norton P. Current clinical nomenclature for description of pelvic organ prolapse. J Pelvic
Surg 1996; 2:257– 259.
13. Baden WF, Walker TA. Genesis of the vaginal profile: a correlated classification of vaginal
relaxation. Clin Obstet Gynecol 1972; 15:1048 –1054.
14. Baden WF, Walker TA. Physical diagnosis in the evaluation of vaginal relaxation. Clin Obstet
Gynecol 1972; 15:1055 – 1069.
15. Bump RC, Mattiasson A, Bo K. The standardization of terminology of female pelvic organ prolapse
and pelvic organ dysfunction. Am J Obstet Gynecol 1996; 175:10– 17.
16. Kobak WH, Rosenberger K, Walters MD. Interobserver variation in the assessment of pelvic organ
prolapse. Int J Urogynecol Pelvic Floor Dysfunc 1996; 7:121 – 124.
17. Hall AF, Theofrastous JP, Cundiff GC, Harris RL, Hamilton LF, Swift SE, Bump RC. 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 1996; 175:1467 – 1469.
18. Athanasiou S, Hill S, Gleeson C, Anders K, Cardozo L. Validation of the ICS proposed pelvic
prolapse descriptive system. Neurourol Urodyn 1995; 14:414 – 415. Abstract.
19. Schussler B, Peschers U. Standardisation of terminology of female genital prolapse according to the
new ICS criteria: inter-examiner reliability. Neurourol Urodyn 1995; 14:437– 438. Abstract.
20. Swift SE, Freeman R, Petri E, Scotti R, Dwyer P, Ulmsten U. Proposal for a world-wide, user-friendly
classification system for pelvic organ prolapse. 16th FIGO World Conference, Washington DC,
September 4, 2000.
21. Swift SE, Morris SA. Inter-examiner reliability of a simplified pelvic organ prolapse quantification
system. Abstract presented at the 26th Annual Scientific Meeting of the International Urogynecologic
Society, Melbourne, Australia, 2001.
37
Radiographic Evaluation of Pelvic Organ
Prolapse
Craig V. Comiter
University of Arizona Health Sciences Center, Tucson, Arizona, U.S.A.

I. INTRODUCTION

Pelvic organ prolapse and pelvic floor relaxation are common problems in older multiparous
women, affecting 16% of women aged 40– 56 (1). A detailed knowledge of pelvic anatomy is
paramount for the proper evaluation and management of such patients. Pelvic support defects
result from both neurophysiologic and anatomic changes (2) and often occur as a constellation
of abnormal findings. Although a thorough pelvic examination is always indicated, 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, strength of Valsalva maneuver, and modesty of the patient, the
surgeon may be limited in his or her ability to accurately diagnose the components of pelvic
prolapse. Furthermore, with uterine prolapse, the cervix and uterus may fill the entire introitus,
making the diagnosis of concomitant pelvic 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. Accurate preoperative staging should
reduce the risk of recurrent prolapse. Radiographic evaluation plays an important role in the
identification of these defects, and should be used as an extension of the physical examination.

II. ANATOMY

The female pelvis can be divided into three compartments: anterior, middle, and posterior. No
longer are these compartments the domains of the urologist, gynecologist, and coloproctologist,
respectively. On the contrary, urologists and gynecologists are increasingly working together in
treating pelvic prolapse, and many specialized “female urologists” and “urogynecologists” are
now quite adept at taking care of all aspects of pelvic prolapse and the often associated voiding
dysfunction.

A. Bony and Musculofascial Support

The bony pelvis is a scaffold from which the intrapelvic structures draw their support. The
tendinous arc, a linear fascial condensation arising from the obturator internus muscle, extends
507
508 Comiter

from the ischial spine to the lower portion of the pubic symphysis, and represents the insertion
point for the levator muscles, providing the musculofascial support for a large portion of the
anterior pelvis (3). The sacrospinous ligaments arise from the posterior aspect of the ischial
spines and insert onto the anterolateral sacrum and coccyx, providing a broad support for the
posterior pelvis.
The pelvic diaphragm is the superior layer of striated muscle and fascia, which provides
the inferior support for the pelvic viscera. The levator ani muscle group, composed of the
pubococcygeus and iliococcygeus, forms a hammock upon which the bladder, proximal vagina,
and intrapelvic rectum lie. The vagina, rectum, and urethra traverse the pubococcygeus through
a funneled hiatus. The anterior muscular decussation forms the external sphincter of the urethra.
The medial fibers of the pubococcygeus (puborectalis), which travel posteriorly along the
urethra, vagina, and rectum, fuse anterior to the rectum, forming part of the perineal support
deep to the perineal body. Reflex contraction of this levator sling elevates and compresses the
urethra, vagina, and rectum during straining maneuvers.
The “fascial” covering of the levator muscles provides a major part of the normal pelvic
visceral support. The levator fascia consists of two leaves—the endopelvic fascia (abdominal
side), and the pubocervical fascia (vaginal side). The urethra, bladder, vagina, and uterus are all
enveloped within these two layers. The two leaves are made of a fibrofatty connective tissue
which fuses laterally, inserting in the tendinous arc of the obturator internus. Specialized
condensations of this levator fascia in the areas of the midurethra, bladder neck, bladder body,
and cervix play a major role in pelvic organ support.

B. Anterior Vaginal Wall Support

The pubourethral ligaments span from the midportion of the female urethra to the inferior pubis.
Laxity of theses structures permit posterior and inferior movement of the midurethra, con-
tributing to stress incontinence (4). The urethropelvic ligaments support the urethra and bladder
neck to the tendinous arc. The vesicopelvic ligaments support the bladder base and anterior
vaginal wall by attaching laterally to the tendinous arc of the obturator fascia. Tears in these
ligaments lead to a lateral defect cystocele, and weakness of the midline pubocervical fascia
leads to a central defect cystocele.

C. Uterine Support
The cardinal ligaments are the most posterior condensations of the levator fascia, attaching the
lateral aspects of the cervix to the ischial spines, thereby supporting the cervix and upper vagina.
By supporting the vaginal vault, they form the base of the levator fascial rectangle responsible
for bladder support as well (5). The uterosacral ligaments run from the posterolateral cervix
and vaginal fornices to the insert at the second, third, and fourth sacral vertebrae (S2 –S4) (4).
Weakness of these ligamentous structures contributes to uterine prolapse or, in the absence of a
uterus, can lead to vault prolapse, enterocele, and apical cystocele formation.

D. Posterior Vaginal Support

The rectovaginal septum, a fibrous continuation of the cul-de-sac, is composed of the fused
posterior vaginal connective tissue and prerectal connective tissue, which insert into the perineal
body caudally (5). This rectovaginal septum acts to prevent anterior herniation of the rectum into
the posterior vagina. The proximal relation of the rectovaginal septum to the sacrouterine-
cardinal complex also contributes to vaginal apical support.
 Radiographic Evaluation 509

Normally, the distal vagina forms an angle of inclination of 458 from the vertical, while the
proximal vagina lies more horizontally over the levator plate, pointing toward S2-S3 (6). The
upper vagina is held over the levator plate by the cardinal and uterosacral ligaments, and this
angulation is maintained by a strong levator plate and anterior traction of the levator sling.
Normally intra-abdominal pressure may be displaced, and the downward pressure of the uterus
and cervix is directed toward the posterior vaginal wall and levator plate. However, when the
normal proximal vaginal orientation is altered and the vaginal axis becomes more vertical
(pelvic floor relaxation), rectocele formation is likely. Moreover, with levator laxity and anterior
proximal vaginal rotation, the cul-de-sac assumes a dependent position, open to the direct impact
of intra-abdominal forces, potentially predisposing to enterocele formation and vault prolapse.

E. Perineal Support
The bulbocavernosus muscles, superficial and deep transverse perinealmuscles, external anal
sphincter, and central perineal tendon comprise the urogenital diaphragm. This muscular sheet,
which lies caudal to the levator ani, provides additional pelvic support.

III. PHYSIOLOGIC EVALUATION

One in three patients presenting with prolapse also suffer from urinary or fecal incontinence (7).
Multichannel urodynamics is clearly the gold standard for assessing voiding dysfunction and
complex incontinence, which often accompany pelvic prolapse. A detailed urodynamic evalua-
tion includes measurement of postvoid residual volume and bladder compliance, as well as
documentation of the presence or absence of unstable detrusor contractions, bladder outlet
obstruction, and the degree of sphincteric function/dysfunction. By combining radiographic
imaging and direct cystoscopic visualization of the bladder, a comprehensive evaluation of the
incontinent patient will often lead to a precise diagnosis with logical treatment options.
Anorectal physiologic testing is often used for assessment of anorectal neural integrity,
nerve conduction, and muscular performance. Rectal manometry may detect abnormalities
in rectal and anal pressures, while pudendal nerve terminal motor latency dysfunction is often
related to stretch-induced injury following childbirth (8). Needle electromyography (EMG), by
measuring electrical activity and quality, can reveal denervation and reinnervation injuries. Prior
to endoanal ultrasonography, EMG was the only reliable method to preoperatively identify
external sphincter tears (9). While few of these tests are absolutely diagnostic, these techniques
provide valuable complementary information when considered together with symptoms, clinical
findings, and imaging results (10).

IV. IMAGING TECHNIQUES

Radiographic imaging plays an important adjunctive role to the physical examination in the
evaluation of pelvic organ prolapse and pelvic floor relaxation.

A. Intravenous Urography
An intravenous urogram (IVU) is often utilized for the evaluation of hematuria, for the purpose
of identifying a renal mass, renal or ureteral stone, upper tract urothelial filling defect, and
510 Comiter

hydroureteronephrosis. Furthermore, the functional nature of the IVU often allows the physician
to distinguish between obstructive and nonobstructive hydronephrosis.
The most common reasons for obtaining an IVU in a woman with pelvic organ prolapse
are to detect hydronephrosis and to evaluate for ureteral obstruction from previous pelvic
surgeries (11). Hydronephrosis secondary to uterine prolapse was first reported nearly a century
ago (12), and, depending on the series presented, the prevalence of hydronephrosis with uterine
prolapse varies from 0% to 100% (13,14). Moreover, while ureteral injuries during hysterectomy
occur in 0.1– 2.5% of cases (15), it has never been shown that routine preoperative IVU in
patients with pelvic prolapse reduces the incidence of ureteral injury (16). In two contemporary
series of patients with pelvic organ prolapse and no known malignancy, the prevalence of
hydronephrosis on routine preoperative IVU was 7% (11,16), with 1% of patients rated as having
severe dilatation. While the incidence of hydroureteronephrosis was low, it did increase with
worsening pelvic prolapse and was more common with uterine prolapse than with vault prolapse.
Serum creatinine levels were neither sensitive nor specific for predicting hydronephrosis,
and knowledge of preoperative anatomy did not change the incidence of ureteral injury during
surgery (11,16).
Approximately 3% of patients will have a significant adverse reaction to the IVU (16). At
the University of Arizona Division of Urology, we do not routinely utilize any radiographic
study to image the upper tracts in patients with normal renal function and pelvic prolapse. With
the routine use of intravenous indigo carmine for determination of ureteral patency, there have
been no instances of ureteral injury in more than 300 cases of transvaginal repair of pelvic organ
prolapse over a 3-year period.

B. Fluoroscopy
Fluoroscopy is an excellent and time-tested technique for investigating pelvic organ prolapse.
By instilling contrast material into the bladder (anterior compartment), vagina (middle compart-
ment), or rectum (posterior compartment), the dynamic relationships among the pelvic organs
may be viewed in real time.

1. 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
(17), this technique permits the preoperative visualization of the position and supportive role of
these muscle groups. Widening of the levator or genital hiatus, which often follows traumatic
childbirth and predisposes to pelvic floor relaxation and visceral prolapse, can be demonstrated
with levator myography. Today, this information may be obtained noninvasively with computed
tomography (CT) (18) and magnetic resonance imaging (MRI) (19,20).

2. Cystography
Lateral cystography allows for a static view of the bladder and bladder outlet in relation to the
pubic bony structures. Early investigators utilized a bead chain cystourethrogram to aid with the
analysis of the posterior urethrovesical angle (2,21,22). Voiding cystourethrography (VCUG) is
mainly utilized for demonstrating a cystocele, evaluating bladder neck hypermobility, and
demonstrating an open bladder neck at rest (sphincteric incompetence). Dynamic lateral fluoro-
scopy at rest and during straining is an important adjunct to the urodynamic evaluation, useful
for demonstrating the presence of and degree of urethrovesical hypermobility and cystocele
 Radiographic Evaluation 511

Figure 1 Cystogram demonstrating bladder neck descent and funneling in a patient with stress urinary
incontinence.

formation (Fig. 1). While the radiographic findings do not always correlate well with
urodynamic findings (23,24), in the incontinent patient with cystographic and/or cystoscopic
evidence of an open bladder neck at rest and a low leak point pressure, the diagnosis of
sphincteric incompetence is more certain (Fig. 2). Other pathologic conditions detected by
VCUG include vesicoureteral reflux, vesicovaginal fistula, and urethral diverticular disease.

Figure 2 (A) Cystogram demonstrating open bladder neck, consistent with intrinsic sphincter
dysfunction. (B) Cystoscopic view confirms radiographic findings.
512 Comiter

3. Defacography
Defacography, or evacuation proctography, is used for evaluating the posterior (anorectal)
compartment. Commonly measured variables include rectal volume, rectal emptying, perineal
and pelvic floor muscle function, and anal sphincter function (2,18,25 – 27). Although the
clinical value of defacography in the evaluation and management of constipation is not well
proven (2,28), the presence of an obvious anatomic abnormality in a fecally incontinent patient
such as a large rectocele, severe intussusception, or prolapse, supports surgical intervention.
Evacuation proctography relies on opacification of the rectal vault with barium paste (25 –
27,29) Instilling the paste is quite cumbersome, requiring a large-caliber enema similar to a
caulking gun. Typically, 80– 300 cc of paste is instilled, often confounded by reflux into the
sigmoid colon (30,31). Fluoroscopic images are recorded with the patient relaxed and while
performing active contraction of the pelvic floor; this should result in elevation of the pelvic
floor musculature. The patient is then examined during cough and during a maximal straining
maneuver, noting any pelvic floor descent or fecal incontinence. Finally, defecation is accom-
plished, and note is made of any rectocele, incomplete emptying, or need for digital assistance
with evacuation.
In the cooperative patient, dynamic proctography 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 (31). Intussusception may be visible as a circumferential
invagination of the rectal wall, presenting as mucosal prolapse through the anus in its most
severe form. Limitations of this examination are the cumbersome and potentially painful
instillation of rectal barium paste, lack of correlation between the viscosity of the paste and the
individual patient’s stool, and the inability of many patients to defecate on command. Modesty
makes this a difficult technique for many individuals. Additionally, the presence of a rectocele in
and of itself may be of limited concern, as previous studies have shown that an anterior rectal
bulge is commonly demonstrated in nulliparous asymptomatic patients (31). Furthermore, the
presence of or size of a rectocele does not correlate well with the completeness of barium
evacuation (32).

4. Colpocystourethrography
First introduced in France in 1965, the colpocystourethrogram combines opacification of the
bladder, urethra, and vagina (33). Modified and made popular in the mid-1970s, the colpo-
cystourethrogram is a dynamic study of pelvic support and function (34). The anatomical
relationships among the bladder, urethra, and vagina may be demonstrated, and when combined
with proctography may be even more useful in outlining the anatomy of the normal pelvis and of
complex pelvic organ prolapse.
Any insult that alters the normal anatomic relationships, such as hysterectomy, pelvic floor
relaxation, or bladder neck suspension, may predispose to enterocele formation. In the case of
pelvic floor relaxation, as often occurs in the multiparous woman, widening of the levator hiatus
leads to a diminution in the pubococcygeal contraction in response to straining. This results in
insufficient vaginal angulation, with the proximal vagina becoming more vertically oriented.
Similarly, bladder neck suspension without proper repair of concomitant pelvic floor relaxation
results in anterior displacement of the vagina. The cul-de-sac is left unprotected and exposed to
increases in intra-abdominal pressure, predisposing to enterocele formation. An enterocele,
defined as herniation of the peritoneum and its contents at the level of the vaginal apex, may be
appreciated during straining or defecation during colpocystoproctography, seen as widening of
the rectovaginal space (35). Dynamic fluoroscopy has been shown to be more accurate than
physical examination in demonstrating an enterocele (32,36).
 Radiographic Evaluation 513

The accuracy of dynamic colpocystoproctography is even further enhanced by opacifying

the small bowel. The patient drinks oral barium 2 h prior to the examination. With the vagina,
bladder, small intestine, and rectum opacified, the vaginal axis may be measured at rest and with
straining, and any prolapse of the anterior, middle, or posterior vaginal compartment is evident.
Moreover, the examiner should be able to distinguish among various organs that may prolapse
into a widened rectovaginal space, differentiating enterocele from sigmoidocele, further refining
the operative approach.
Some investigators have advocated the use of positive-contrast peritoneography (37,38).
By instilling water-soluble contrast medium directly into the peritoneal cavity, the pelvic
peritoneal recesses may be imaged during relaxation, straining, voiding, and defecation.
However, it is the author’s opinion that this practice is unnecessarily invasive, risking peritonitis.

C. Ultrasound
Sonography offers a convenient, inexpensive, and radiation-free technique. Anorectal
endosonography is a standard method for staging and following anal and rectal cancers, and
for evaluating benign anorectal conditions such as anal sphincter defects, perianal abscesses, and
fistulae (39). The integrity of the anal sphincter muscles may be assessed with a high-frequency
(.7 MHz) transducer that produces a panoramic image (40,41). Defects in the internal sphincter
generally appear as an echogenic discontinuity in the hypoechoic muscle between the vagina and
rectum. On the other hand, external sphincteric injuries appear as hypoechoic lesions in a
normally echogenic structure (40,41). Sonographic findings predict intraoperative diagnosis
with a 95% accuracy (42 –44). The recent advent of 3D sonography promises to further increase
our understanding of anal sphincteric dysfunction (45). Moreover, a thickened sonographic
appearance is indicative of sphincteric spasm or hypertrophy, which is often observed with
obstructed defection (46).
Similar to fluoroscopy, a dynamic component may be added to sonography. In particular,
dynamic ultrasound allows identification of an enterocele. A sagittal view probe is positioned
in the rectum and directed against the ventral rectal wall. A 7.5-MHz radial rotating axial
endoprobe is recommended (47). During a straining maneuver, widening of the rectovaginal
septum, diminution of the peritoneal-anal distance, and herniation of bowel contents into the cul-
de-sac may be observed (47). This technique can also accurately distinguish between small
intestine and sigmoid colon loops which may enter the cul-de-sac.
Ultrasound is also useful for demonstrating vesicourethral anatomy (48) via abdominal,
rectal, vaginal, or perineal transducer (49 – 51). Abdominal sonography has the advantage of
being the least invasive, but has the disadvantage of potential interference from bony structures.
Transabdominal ultrasound with a lower-frequency probe (,5.0 MHz) allows adequate
resolution without pubic bone shadowing (52). Bladder neck descent may be measured during
straining maneuvers (53). Vaginal ultrasound is the most commonly used and best-studied
approach (54,55). Careful technique permits the examiner to avoid elevating the bladder neck
with the probe, and the measurement of bladder neck hypermobility has been shown to be
reproducible in experienced hands (54). While a urethral catheter is useful for identifying
the bladder neck, it is not necessary (56). Transperineal sagittal sonography provides a
reproducible method for measuring resting and straining angles of the vesicourethral junction
and for identifying cystoceles (57).
“Contrast” sonography utilizes echogenic material that can settle into the bladder neck
region with gravity, and can demonstrate bladder neck funneling with straining (58). This
dynamic method of ultrasonic visualization offers two distinct advantages over the bead chain
cystourethrogram: minimizing invasiveness, and eliminating the use of ionizing radiation.
514 Comiter

Ostrzenski et al. have introduced a novel method for diagnosing paravaginal defects using
contrast ultrasonography (59). A water-filled condom is placed intravaginally, and trans-
abdominal pelvic ultrasound is performed with attention directed at the paravaginal spaces. In
their study, paravaginal defects were identified in women with cystoceles and stress urinary
incontinence with 100% accuracy (confirmed by laparoscopy). Furthermore, follow-up
ultrasound revealed resolution of the defects in all patients postoperatively. This innovative
technique should prove useful in the preoperative assessment of anterior vaginal prolapse, and
may be used as an objective method for determining the success of surgical repair (59). Contrast
ultrasonography is a safe, noninvasive, and simple office-based technique.
Overall, the information obtained from sonography is comparable to that from cysto-
graphy, but avoids the ionizing radiation and the need for urethral catheterization (60). Both
techniques provide the surgeon with reproducible information with either static or dynamic
examination. With the use of vaginal, rectal, abdominal, and perineal probes, dynamic ultra-
sonography may be a reasonable substitute for dynamic fluoroscopy, obviating the need for
opacification of the bladder, small bowel, and large bowel, and avoiding the radiation exposure.

D. Computed Tomography
Computerized axial tomography (CT) has not been shown to be particularly useful in the
evaluation of pelvic organ prolapse. This radiological method has the disadvantage of imaging
structures which lie in the axial plane via an axial imaging technique. The components of the
levator plate and urogenital diaphragm are better seen in the coronal plane or sagittal view.
While CT images can be reconstructed into a coronal view using cumbersome and expensive
computer software, poor image quality and distorted special resolution have limited the utility of
this presentation technique (18).
Various groups have demonstrated the accuracy of CT pelvimetry (61,62). While debate
remains over the utility of pelvimetry with regard to the risk of pelvic organ prolapse, this
technique has been shown to be a simple, reproducible, and accurate method to measure pelvic
dimensions and the capacity of the birth canal, with acceptably low-dose radiation exposure.

E. Magnetic Resonance Imaging

The development of fast-scanning MRI techniques has improved our ability to describe and
quantify anatomical changes that may cause pelvic floor relaxation. Fast-scan Valsalva imaging
formated in a pseudokinematic cine-loop, provides a dynamic way to study the anatomical
changes that occur with prolapse. MRI offers a method to noninvasively evaluate the female
pelvis without ionizing radiation. Organ descent may be simultaneously evaluated in all three
pelvic compartments. Kelvin’s group has utilized “triphasic” dynamic MRI, consisting of a
cystographic, proctographic, and posttoilet phase to facilitate the recognition of prolapsed
organs that may be obscured by other organs that remain unemptied (32). Additionally, MRI has
been shown to be useful for measuring levator muscle thickness (63) (Fig. 3), urethral length,
and the thickness and integrity of periurethral muscle ring (19). The addition of 3D imaging has
the advantage of quantification of muscle volume, which may give a more accurate represen-
tation of the relationships among pelvic floor structures, thereby potentially improving surgical
planning (63).
Yang et al. were the first to popularize dynamic fast magnetic resonance imaging for the
evaluation of pelvic organ prolapse (19). Since then, other investigators have shown that MRI is
more sensitive than physical examination for defining pelvic prolapse (20,64,65). While some
advocate the use of contrast opacification of the bladder, vagina, and rectum (32,66), others have
 Radiographic Evaluation 515

Figure 3 MRI demonstrating asymmetry of levator muscles. Note that atrophied right-sided
pubococcygeus (dashed arrow) is thinner than normal left-sided muscle (solid arrow).

shown that the vagina, rectum, bladder, urethra, and peritoneum are adequately visualized
without any contrast administration (64,65) (Fig. 4). By avoiding instrumentation of the vagina
or urethra, iatrogenic alteration of the anatomy is minimized (20).
The group from UCLA recently published their experience using 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-shot fast spin echo (SSFSE, General
Electric) for evaluating the female pelvis (64,65). 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. Images were looped for viewing on a
digital station as a cine stack and for measuring the relationship of pelvic organs to fixed
anatomical landmarks. The first set of images are volumetric sagittal cuts from left to right, used
to locate the midsagittal plane and to survey the pelvic anatomy. The second set of images are
obtained with four cycles of repeated relaxation and Valsalva maneuver (64,65). Total image
acquisition time is 2.5 min, and total room time is 10 min per study. The charge for each study
(including interpretation) is only $540.
This dynamic MRI technique has been shown to be useful for grading pelvic organ
prolapse and pelvic floor relaxation in a simple and objective manner (65). The size of the
levator hiatus and 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
516 Comiter

Figure 4 Midsagittal MRI demonstrating normal female anatomic structures.

anal canal. The “M-line” (muscular pelvic floor relaxation) measures the descent of the levator
plate from the fixed pubosacral line. The pubosacral line spans the distance from the pubis to the
sacrococcygeal joint (Fig. 5). The “O” classification (organ prolapse) describes the degree of
visceral prolapse beyond the H-line. The degree of cystocele, rectocele, enterocele, and uterine
descent were graded as 0, 1, 2, or 3 (none, mild moderate, severe; Fig. 6).
In a group of women with symptomatic prolapse, the H-line was significantly wider than in
a control group (7.5 + 1.5 cm vs. 5.2 + 1.1 cm, P , .001). Similarly, the levator muscular
descent (M-line) was greater in the prolapse groups than in the control group (4.1 + 1.5 cm vs.
1.9 + 1.2 cm, P , .001) (65). These objective findings fit well with our knowledge of the

Figure 5 MRI, sagittal view in a patient with pelvic prolapse. 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 pubosacral line (PSL).
 Radiographic Evaluation 517

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 (67). 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

Figure 6 (A) Cystogram demonstrates cystocele only. (B) MRI demonstrates cystocele, enterocele, and
vault prolapse. (C) Enterocele with minimal pelvic floor relaxation. (D) Combined cystocele, enterocele,
rectocele, and significant pelvic floor relaxation.
518 Comiter

Figure 6 Continued.

both increase with pelvic floor relaxation 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 (Fig. 6).

Figure 7 (A) Sagittal MRI. (B) MR urogram. Large cystocele and uterine prolapse, causing bilateral
ureteral obstruction, with resulting hydroureteronephrosis.
 Radiographic Evaluation 519

MRI findings were compared to physical examination and intraoperative findings.

HASTE-sequence MRI was more accurate than physical examination in identifying cystoceles,
enteroceles, vault prolapse, and pelvic organ pathology such as uterine fibroids, urethral
diverticula, ovarian cysts, and Nabothian and Barholin’s gland cysts (64). Comiter et al. found
that with dynamic MRI, surgical planning was altered in .30% of cases, most often because of
occult enterocele not appreciated on physical examination (68).

Figure 8 (A) Dynamic MRI (relaxed and straining) demonstrates bladder neck funneling and stress
urinary incontinence. (B) Similar demonstration with lateral cystogram.
520 Comiter

In patients with severe prolapse, especially with renal insufficiency, the surgeon must rule
out obstructive hydroureteronephrosis. This may be accomplished by MR urogram, adding only
30 sec of examination time and no additional morbidity (Fig. 7). MRI may also be useful for the
radiographic evaluation of stress incontinence. Hypermobility of the proximal urethra and
bladder neck descent are important pathological features in the diagnosis of genuine stress
urinary incontinence (69,70). Measurement data on dynamic MRI for the bladder neck position
and the extension of cystocele at maximal pelvic strain are comparable with lateral cysto-
urethrogram data (71) (Fig. 8).
The disadvantage of MRI is that the study must be performed supine, as no upright MRI
machines are currently available. However, dynamic MRI with relaxing and straining views has
been shown to adequately demonstrate organ prolapse during straining in the supine position
(68,72,73). 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 (64). 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 pelvic
organ prolapse and pelvic floor relaxation.

V. SUMMARY

A detailed working knowledge of normal and abnormal female pelvic anatomy is necessary for
the proper evaluation of pelvic organ prolapse. However, even the most experienced gyne-
cologist 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. Radiographic evaluation of the woman with pelvic organ prolapse and
pelvic floor relaxation should be viewed as a valuable extension of the physical examination.
Urography, voiding cystography, dynamic colpocystodefacography, sonography, and MRI are
each useful for the evaluation of pelvic prolapse and pelvic floor relaxation. MRI will continue to
play an increasingly important role owing to its superior visualization of fluid-filled viscera and
soft tissues, and the ability to simultaneously visualize all important pelvic organs without the
need for patient preparation, instrumentation, or exposure to ionizing radiation.

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38
Surgical Therapy of Uterine Prolapse

Karyn Schlunt Eilber,* Nirit Rosenblum,† and Shlomo Raz

University of California, Los Angeles, California, U.S.A.

I. INTRODUCTION

Uterine prolapse is a relatively common, disabling condition and often requires surgical
intervention. Hysterectomy is the second most commonly performed gynecological surgery in
the United States after cesarean section with 600,000 procedures done each year (1). In a
review by the National Center for Health Statistics for the years 1988 – 1990, 16.3% of
hysterectomies were performed for pelvic prolapse (2). Thus, almost 100,000 hysterectomies
are performed each year for prolapse. Although over 70% of hysterectomies are performed
transabdominally, the transvaginal approach is preferred when there is associated vaginal
prolapse (3). By understanding the female pelvic anatomy and maintaining control of the uterine
vascular pedicles, a transvaginal hysterectomy can effectively be performed with minimal
morbidity.

II. UTERINE ANATOMY

The uterus is a viscous muscular organ located between the bladder and rectum and is usually in
an anteverted position. The superior portion of the uterus, the fundus, is covered anteriorly and
posteriorly by the peritoneum. Uterine support is mainly provided by the pelvic floor
musculature and two sets of ligaments: the uterosacral and the cardinal (Mackenrodt’s)
ligaments. The body of the uterus is enclosed between the double-layered broad ligaments. Each
broad ligament extends from the lateral aspect of the body of the uterus and contains a Fallopian
tube, the round and ovarian ligaments, and the uterine and ovarian vessels (4 – 6). The broad
ligaments do not contribute greatly to uterine support.
The uterosacral and cardinal ligaments pass from the cervix to the sacrum and arcus
tendineus, respectively. These ligaments are localized thickenings of the endopelvic fascia and
fuse at the cervix to provide the major uterine and apical vaginal support (6 – 8). Anterior to the
vagina the endopelvic fascia is referred to as the pubocervical fascia and posteriorly is termed
the rectovaginal fascia, or Denonvillier’s fascia (7). These layers consist of fibrofatty tissue and
do not represent a true fascia. The fusion of the cardinal and uterosacral ligaments becomes

*Current affiliation: Memorial Sloan-Kettering Cancer Center, New York, New York, U.S.A.
†
Current affiliation: NYU School of Medicine, New York, New York, U.S.A.

525
526 Eilber et al.

clinically significant when performing a transvaginal hysterectomy, as will become apparent in

the subsequent description of the technique.
The pelvic floor musculature that provides significant uterine support includes the levator
ani muscle group (pubococcygeus, iliococcygeus, puborectalis) and the coccygeal muscles (5).
Other anatomic structures that contribute uterine and vaginal support include the bony pelvis, the
urogenital diaphragm, and the perineal body (6).

III. PATHOPHYSIOLOGY OF PROLAPSE

The pathophysiology of uterine prolapse can be more easily understood when considering the
interactions of the ligamentous support of the uterus and the pelvic floor. DeLancey described
pelvic support in terms of levels (9): Level I support refers to support of the upper vagina and
cervix by the cardinal-uterosacral complex; level II support is that of the midportion of the
vagina to the arcus tendineus; and level III support involves the fusion of the anterior, lateral, and
posterior vagina to the urethra, levator ani, and perineal body, respectively.
Uterine prolapse is the result of a defect in level I support. Some theorize that attenuation
of the cardinal-uterosacral ligament complex may occur because of trauma (childbirth), chronic
elevations in abdominal pressure or, possibly atrophy, allowing the cervix to descend and move
anteriorly. The uterus then begins to rotate posteriorly such that the intraabdominal pressure is
directed on the anterior surface of the uterus. The uterus becomes progressively more retroverted
until the axis of the uterus is in an essentially vertical position at which time prolapse occurs
(7,10,11).
The exact etiology of pelvic prolapse is still unclear. Abnormalities in sacral nerve
function or collagen have been suggested. Predisposing factors for the development of prolapse
include increasing age, multiparity, maximal infant birth weight, postmenopausal status, chronic
constipation, prior surgery for prolapse, and decreased pelvic floor muscle strength (9,12,13).

IV. CLINICAL EVALUATION

The clinical evaluation of the patient with uterine prolapse includes a complete history and
physical examination as well as a limited number of ancillary tests. Considerations such as
symptomatology, associated prolapse, pathology of other pelvic organs, urinary incontinence,
reproductive status, and sexual function all influence the choice of management.

A. History
The most common presentation of uterine prolapse is a patient complaining of a mass or bulge at
the introitus. Other presenting complaints include perineal pressure, dyspareunia, or difficulty
walking (14 – 16). When concomitant prolapse of other organs is present, urinary retention,
urinary incontinence, or constipation may also occur. Less commonly, a patient presents simply
because uterine prolapse was incidentally found on routine physical examination. Symptoms are
classically aggravated by standing and may improve when the patient resumes a recumbent
position.
It is important to determine whether the patient has had a previous hysterectomy.
Occasionally what is assumed to be uterine descent is only cervical descent after a prior
supracervical hysterectomy. Also of importance is any known history of uterine disease such as
fibroids or endometriosis, symptoms of urinary incontinence, sexual function, bowel function,
and the overall health status of the patient.
 Surgical Therapy of Uterine Prolapse 527

B. Physical Examination
Physical examination should be performed both in the supine and standing positions, as the
severity of prolapse is not always evident in the recumbent position. When in the supine position,
the patient needs to perform a Valsalva maneuver in order to fully appreciate the prolapse.
Uterine examination includes determination of the level of cervical descent, uterine size,
uterine mobility, and any abnormal gross pathology. The anterior, posterior, and apical vaginal
walls are examined separately with the aid of a half-speculum. Speculum examination is useful
to assess the remainder of the pelvic floor for other prolapse such as cystocele, rectocele, or
enterocele and also to assess the presence of urethral hypermobility. The size of the introitus and
vaginal canal should also be noted as this may limit transvaginal delivery of an enlarged uterus.
Rectal and pelvic floor tone are also assessed. At the time of surgery the physical examination
should be repeated. The degree of uterine descent and other prolapse may become more
pronounced with the patient under general anesthesia.

C. Diagnostic Tests
A urinalysis and postvoid residual urine volume are obtained for all patients. For patients with
uterine prolapse and no history of stress or urge incontinence and normal residual urine, we do
not routinely perform a urodynamic evaluation. However, for patients with the above symptoms
or with elevated residual urine, we recommend assessment of the lower urinary tract with
urodynamic studies and cystoscopy. Stress incontinence that is masked by the prolapse may
manifest itself after correction of the prolapse (16,17). Furthermore, as many patients with
prolapse are elderly, detrusor instability associated with obstruction versus hyperreflexia sec-
ondary to an occult neurologic condition must be identified. Cystoscopy is useful to rule out any
intrinsic urethral or bladder abnormalities that may be causing lower urinary tract symptoms.
Imaging of the upper urinary tracts is also recommended as patients with uterine prolapse
are more likely to have associated hydronephrosis as compared to other vaginal prolapse and
may be severe enough as to cause renal failure (18,19). Our preferred imaging test to assess the
presence of hydronephrosis as well as other pathology is the dynamic magnetic resonance
imaging (MRI). A dynamic MRI of the pelvis not only identifies the presence of hydronephrosis,
but it also allows for evaluation of the uterus and adnexa for abnormal pathology that might
preclude a vaginal hysterectomy. The dynamic MRI is a relatively simple, noninvasive test that
takes only minutes to complete. There is no need for intravesical contrast as the bladder is quite
distinct on the MRI. Sagittal images are taken of the pelvis with the patient at rest and then with a
Valsalva maneuver. Pelvic organ prolapse and other pathology are readily identified with this
imaging modality (Fig. 1). Advantages include its ability to accurately determine uterine and
ovarian pathology as well as the presence and degree of associated prolapse.

V. CLASSIFICATION

The pelvic organ prolapse quantification (POP-Q) is a validated staging system for defining
vaginal prolapse. This staging system separately addresses the vaginal compartments (anterior,
posterior, apical) and defines the extent of prolapse in relation to the hymen. Stage 0 indicates no
prolapse, stage 1 implies that the most distal portion of the prolapsed organ is .1 cm above the
hymenal ring, stage 2 defines prolapse within 1 cm of the hymen (proximal or distal), stage 3
denotes prolapse .1 cm distal to the hymen, and stage 4 implies complete vaginal eversion (20).
528 Eilber et al.

Figure 1 MRI of the pelvis. Dynamic MRI of the pelvis demonstrating uterine prolapse.

As we routinely obtain a dynamic pelvic MRI for patients with uterine prolapse, we classify
uterine prolapse based on this study. Prolapse is classified in reference to the puborectalis hiatus
(sling) which is formed by the puborectalis muscle (the most inferior part of levator ani) and
includes the urethra, vagina, and rectum. The degree of prolapse is based on 2-cm increments:
mild uterine prolapse is between 0 and 2 cm below the hiatus, moderate prolapse is 2 –4 cm, and
severe prolapse is .4 cm below the hiatus (21).

VI. THERAPEUTIC OPTIONS

When choosing the type of treatment for uterine prolapse, several considerations must be made.
The degree of prolapse and the patient’s symptomatology are the main considerations. Patients
with minimal prolapse and/or mild symptoms often require no therapy. For patients in their
reproductive years, it is of paramount importance to determine whether childbearing is desired.
Current and expected sexual function must be discussed. The size of the uterus and uterine
pathology must also be taken into account as well as associated prolapse of other organs. Lastly,
but not least important, the overall health status of the patient must be considered.

A. Conservative Treatment
The primary nonsurgical treatment for uterine prolapse involves the use of a pessary. This option
is reserved mainly for patients who are not surgical candidates or who do not wish surgical
intervention. Efficacy of this treatment relies on the adequacy of perineal outlet support, which is
often lacking in this patient population.
 Surgical Therapy of Uterine Prolapse 529

Complications secondary to pessary use include mechanical irritation or ulceration of

the vaginal mucosa. Topical estrogen cream may alleviate these symptoms. In extreme cases the
pessary may become embedded or erode into the vaginal wall, requiring surgical intervention
for removal. Erosion of a pessary through the anterior vaginal and bladder walls has been
reported (22).
Another use of a pessary is for diagnostic purposes. Patients with symptoms that do not
necessarily correlate with the degree of prolapse may wear a pessary for a few weeks to
determine whether the symptoms are indeed secondary to prolapse.

B. Surgical Treatment
The basic tenet of surgical repair of uterine prolapse is that the defect is not with the uterus itself
but with the pelvic support. Thus, hysterectomy alone is not sufficient to treat pelvic prolapse.
Every effort must be made to restore normal pelvic anatomy with adequate support and create a
functional vaginal vault.

1. Uterine Sparing Procedures

Many women choose to avoid hysterectomy because of a delay in childbearing to a later age, a
belief that the uterus plays a role in sexual satisfaction, or more effective medical treatment of
menorrhagia (23 – 25). For women desiring uterine preservation, the more commonly performed
procedures include the Manchester operation, the Gilliam suspension, sacrospinous hysteropexy
(cervix to the sacrospinous ligament), and sacral hysteropexy (cervix to sacrum) (11,26 –28).
More recently a laparoscopic approach to hysteropexy has been described (29). For the rare
cases of patients who are not sexually active and who might otherwise use a pessary, colpocleisis
is another alternative.
a. Manchester Operation. The Manchester operation is a transvaginal uterine
suspension reserved for the patient with combined uterine prolapse and cystocele. The goal of
this surgery is to bring the cardinal and uterosacral ligaments anterior to the lower uterine
segment in order to restore the uterus to an anteverted position (30). In this procedure the cervix
is amputated and the cardinal and uterosacral ligaments are sutured to the anterior, lower
uterine segment (30,31). This repair is followed by a standard anterior repair and/or Kelly
plication (30). The problems with this repair include a .20% prolapse recurrence within months
of surgery, a decrease in fertility, and difficulty with future cervical sampling for cytologic
analysis (32,33).
b. Gilliam Suspension. The Gilliam suspension is another technique when attempting
to preserve childbearing potential. In this procedure the round ligaments are sutured to the rectus
sheath via the internal inguinal ring (11). This may be performed either through a lower
abdominal incision or laparoscopically. There are no adverse sequelae for subsequent
pregnancies, although some patients report transient round ligament pain (11). Gordon reported
a 93% success rate with this procedure (34). However, this procedure is not effective in the
long run as it does not address the basic condition of weakness of the pelvic floor and the
cardinal-uterosacral ligament complex.
c. Hysteropexy. Sacrospinous hysteropexy and sacral hysteropexy involve fixation of
the cervix to the sacrospinous ligament or sacrum, respectively. Sacrospinous vaginal fixation
has been found to be effective in 64– 97% of cases while sacral colpopexy has an 84 –98%
success rate (35,36). Unfortunately, these repairs rely on nonphysiologic support of the upper
vagina and may result in prolapse of other organs (29). Potential complications include bleeding,
sciatic nerve injury, and rectal laceration (36,37). Furthermore, dissection to remove the cervix
530 Eilber et al.

from the sacrospinous ligament or sacrum is difficult if a hysterectomy is required subsequent to

one of these procedures.
d. Laparoscopic Hysteropexy. Recently a laparoscopic suture hysteropexy has been
described which involves plication of the uterosacral ligaments which are then reattached to the
cervix. The reported success rate in 43 women was 81%, and two women subsequently
completed term pregnancies without recurrence of prolapse (29). Complications included a
uterine artery laceration in one patient that required a laparotomy and ureteral kinking in two
patients which required only a relaxing incision in the peritoneum.
e. Colpocleisis. Colpocleisis as described by LeFort involves excision of anterior and
posterior vaginal flaps proximal to the prolapsed cervix to the level of the introitus. The denuded
areas are then approximated (31). Disadvantages of this procedure are loss of sexual function,
inability to perform cytologic cervical analysis, and urinary incontinence in up to 24% of patients
(38). However, Ahranjani et al. reported no recurrence of prolapse in a series of 30 patients (39).

2. Hysterectomy
A multitude of approaches to hysterectomy have been described such that it is impossible to
include a description of them all. This chapter will focus on the technique of vaginal hysterec-
tomy and provide a brief overview of other approaches to hysterectomy.
a. Subtotal Hysterectomy. Subtotal or supracervical hysterectomy is a procedure that
was largely discarded in the past but has recently made a slight resurgence. Advocates of the
subtotal hysterectomy propose that it preserves posthysterectomy bladder and sexual function
(40 – 43). The procedure involves separation of the uterine body from the cervix, and the cervical
stump is left remaining.
The most common short-term complications are infection (1.0 – 5.0%), hemorrhage
(0.7 – 4.0%), and adjacent organ injury (0.6 –1.0%) (44). These rates are comparable to those for
total hysterectomy. Ewies and Olah reported that the most common long-term complication
following subtotal hysterectomy was regular menstruation (45). No study has proven any
superiority of subtotal hysterectomy over total hysterectomy in terms of operative complications
or sexual function, and thus total hysterectomy remains the procedure of choice for most women.
b. Abdominal Hysterectomy. The great majority of hysterectomies performed in
the United States are abdominal. Indications for using the abdominal approach include
surgeon preference, known or suspected pelvic adhesions or endometriosis, leiomyoma,
adnexal pathology, the need to remove adnexal structures and the absence of pelvic relaxation.
The possibility of oophorectomy should be determined preoperatively.
The operation is performed through either a low midline or Pfannenstiel incision. Although
many techniques for abdominal hysterectomy have been described, typically the round ligament
on one side of the uterus is ligated then transected and the leaves of the broad ligament are
separated. The infundibulopelvic or utero-ovarian ligaments are then mobilized above the ureter,
ligated and cut. Care should be taken to clearly disect out the ureter on the medial leaf of the broad
ligament. After the bladder is dissected off the lower uterine segment, the uterine vessels are
clamped and suture is ligated. The ipsilateral cardinal ligament and uterosacral ligament are also
clamped and the suture ligated. The uterus is then dissected from the vaginal wall, and, depending
on surgeon preference, the vaginal cuff is left open or closed after bleeders are controlled (30,46).
Bladder and ureteral injury occur in 0.5% and 0.5 –1.0% of cases, respectively (47).
A multicenter, prospective, nonrandomized study of 1851 patients reported a perioperative death
rate of 0.1% after abdominal hysterectomy (48).
c. Laparoscopic Hysterectomy. With the increasing popularity of minimally invasive
surgical techniques, descriptions for the technique of laparoscopic hysterectomy have emerged.
 Surgical Therapy of Uterine Prolapse 531

The terms “laparoscopic hysterectomy” and “laparoscopic-assisted vaginal hysterectomy” both

refer to a variety of procedures that include a portion of the operation performed vaginally.
Compared to the traditional abdominal approach, the laparoscopic approach has the benefits of
shorter hospital stay and decreased convalescence. However, no benefit has been found for the
laparoscopic approach compared to the vaginal approach (49). When added anesthesia time and
the cost of disposable instruments are considered, the cost of laparoscopic surgery is $3000
more when compared to the vaginal approach (50).
Laparoscopic hysterectomy has been classified into four types: a type I procedure includes
dissection up to but not including the uterine arteries, a type II procedure involves division of the
uterine artery pedicle, a type III procedure is performed when the cardinal-uterosacral ligament
complex is partially dissected, and complete division of this complex constitutes a type IV
procedure (51). A Finnish report on 3928 women who underwent a laparoscopic hysterectomy
from 1995 to 1996 reported major complications in 2.2% and one death secondary to a massive
pulmonary embolus (52). The complications of ureteral injury, vesicovaginal fistula, intestinal
injury, and cystotomy occurred in 1.2%, 0.4%, 0.4%, and 0.18% of cases respectively.
d. Vaginal Hysterectomy. Vaginal hysterectomy has the advantage of avoiding the
morbidity associated with an abdominal incision, but several important relative and absolute
contraindications to vaginal hysterectomy exist: size disproportion (enlarged uterus and vaginal
stenosis), obliteration of the cul-de-sac, adnexal tumor, pelvic tumor, pelvic inflammatory
disease, and malignancy of the uterus or ovaries (10). A history of endometriosis of unknown
extent is also considered a contraindication (53).

C. Technique
Prophylactic quinolone antibiotics are administered preoperatively. Following administration of
adequate anesthesia, the patient is placed in the dorsal lithotomy position. If no contraindication
exists, we prefer the use of spinal anesthesia. The suprapubic area, vagina, and external genitalia
are prepped with an iodine-based solution. Sutures are used to retract the labia laterally. A
weighted speculum is inserted for vault exposure. If a bladder neck suspension or cystocele
repair is planned, a Lowsley retractor may be used to place a suprapubic catheter. The bladder is
emptied via a catheter. A ring retractor with elastic stays is placed for exposure, and two Lahey
clamps are used to grasp the cervix. Using electrocautery, a circumferential incision is made
approximately 1 cm from the cervical os (Fig. 2). Sharp dissection is used to dissect the uterus
from the bladder and develop the vesicoperitoneal space (Fig. 3). This dissection is facilitated
by placing gentle traction on the tenacula and pointing the scissors toward the uterus. A Heaney
retractor is used to retract the bladder anteriorly. Maneuvers to avoid an inadvertent cystotomy
include dissection in the midline of the uterus and remaining parallel to the glistening white
surface of the uterus.
At this point attention is turned toward the posterior dissection. The posterior peritoneal
fold is exposed in a similar fashion to the vesicoperitoneal fold, and the posterior peritoneum is
opened sharply. The cul-de-sac is inspected for adhesions or other pathology. A Heaney retractor
is placed in the posterior peritoneum. If difficulty is encountered when attempting to expose the
cul-de-sac, the hysterectomy may be initiated in an extraperitoneal fashion by severing the
uterosacral ligament and caudal portions of the cardinal ligament close to the cervix. This
maneuver allows descent of the uterus to provide better visualization.
Division of the ligamentous attachments is now performed. With the cervix under
slight traction, a right-angle clamp is introduced into the cul-de-sac alongside the cervix. The
cardinal and uterosacral ligaments are sequentially isolated first with a large right-angle then
with a Phaneuf clamp and divided with electrocautery (Figs. 4,5). The stumps are ligated with
532 Eilber et al.

Figure 2 Incision. A circumferential incision is made 1 cm from the cervical os with electrocautery.

Figure 3 Exposure of anterior uterus. Sharp dissection is used to expose the anterior uterus and
develop the vesicoperitoneal space.
 Surgical Therapy of Uterine Prolapse 533

Figure 4 Isolation of cardinal-uterosacral ligaments. Right-angle and Phaneuf clamps are used in
succession to better delineate the cardinal-uterosacral complex.

Figure 5 Transection of cardinal-uterosacral ligaments. The cardinal-uterosacral ligaments are

transected using electrocautery.
534 Eilber et al.

figure-of-eight suture ligatures (of a delayed absorbable suture). These sutures are left long and
placed in the grooves of the retractor ring. Anterior retraction of the bladder exposes the
vesicoperitoneal fold (Fig. 6). At this point the uterus can be everted and brought outside the
introitus (Fig. 7). Safe entry into the anterior peritoneum can be made by placing a finger through
the cul-de-sac and up over the fundus to tent the peritoneum. Electrocautery can then be used to
incise the peritoneum overlying the surgeon’s finger. Now the broad ligament is exposed and
ligated as above (Fig. 8). If the adnexae are not removed, their attachments are also now divided.
The utero-ovarian ligament, Fallopian tube, and round ligament are visible from anterior to
posterior and are sequentially divided and ligated. The uterus is finally removed. A circular
arrangement of the six ligated pedicles and their attached sutures remains (Fig. 9).
Two methods are used to provide vault support and vaginal depth: perivesical and
prerectal fascia are approximated in order to close the cul de sac; and a modified McCall
culdoplasty is performed. The culdoplasty sutures are placed first. Starting outside the vaginal
wall toward the peritoneal cavity (in the area of the ligated cardinal-uterosacral complex),
bilateral figure-of-eight sutures of 0-Vicryl are used to incorporate the area lateral to the rectum
and the uterosacral ligaments as they cross the iliococcygeus muscle in the posterolateral pelvic
wall (Figs. 10,11). These sutures are 8 – 10 cm from the vaginal cuff. They are tagged at this
time and will not be tied until after the cuff is closed. Exposure is facilitated by packing the
peritoneal cavity with moist laparotomy sponges.
Two pursestring sutures of 0-Vicryl are now placed to close the cul-de-sac. These sutures
incorporate the prerectal fascia, the cardinal-uterosacral ligament complex, the broad ligaments,

Figure 6 Exposure of vesicoperitoneal fold. Anterior retraction of the bladder exposes the peritoneal
cavity.
 Surgical Therapy of Uterine Prolapse 535

Figure 7 Eversion of uterus. After the bilateral cardinal-uterosacral ligaments have been ligated, the
uterus is manually everted (note leiomyoma).

and the perivesical fascia (Fig. 12A, B). It is extremely important to stay in the midline when
incorporating the perivesical fascia as sutures placed too lateral may cause ureteral injury. The
purse-string sutures are also tagged and not tied at this time. The sutures of the previously ligated
pedicles of the broad ligaments and the cardinal-uterosacral ligament complex are identified on
each side and approximated in the midline. The purse-string sutures are now tied. If
simultaneous repair of other prolapse or bladder neck suspension is planned, it is now performed.
Finally, the culdoplasty sutures are tied. Vaginal depth is restored with tying of the culdoplasty
sutures (Fig. 13). Excess vaginal wall is excised before closure with a running absorbable suture
(Figs. 14 and 15).
536 Eilber et al.

Figure 8 Division of broad ligament. The surgeon’s index finger is inserted into the peritoneal cavity
and hooked around the uterine vessels (broad ligament), which are ligated in the same fashion as the
cardinal-uterosacral ligaments.

D. Complications
Short-term complications common to both the abdominal and vaginal approaches include
hemorrhage, infection, and adjacent organ injury, although these complications occur less
frequently with the vaginal technique (44,48,54). Ileus may also occur with the abdominal
approach but responds well to conservative treatment. Interestingly, bladder and ureteral
injury occurs less commonly during vaginal hysterectomy than during abdominal hys-
terectomy. It has been proposed that traction applied to the cervix in combination with
anterior retraction of the vesicouterine peritoneal fold provides sufficient displacement of the
ureters (55). An important point to remember is that as long as the uterus is freely mobile,
the technical difficulty of hysterectomy increases with increasing degrees of prolapse owing
to the inconsistent anatomy (10). In a recent 10-year review by Varol et al., the overall
complication rate was 44% for abdominal hysterectomy compared to 27.3% for vaginal
hysterectomy (3). Furthermore, the abdominal hysterectomy group was four times more likely
 Surgical Therapy of Uterine Prolapse 537

Figure 9 Transected uterine pedicles. Arrangement of the transected pedicles of the cardinal, uterosacral,
and broad ligaments before approximation.

Figure 10 Origin of culdoplasty sutures. The culdoplasty sutures are initiated outside the vaginal wall
and brought into the peritoneal cavity.
538 Eilber et al.

Figure 11 Placement of culdoplasty sutures. Inside the peritoneal cavity, a figure-of-eight culdoplasty
suture approximates the area lateral to the rectum and the uterosacral ligaments as they cross the
iliococcygeus muscle.

Figure 12 Placement of purse-string suture. The purse-string suture is shown incorporating the
transected cardinal-uterosacral complex (a) and the perivesical fascia (b).
 Surgical Therapy of Uterine Prolapse 539

Figure 12 Continued.

Figure 13 Restoration of vaginal depth. Vaginal depth is restored when the culdoplasty sutures are tied.
540 Eilber et al.

Figure 14 Postoperative result. Postoperative result following transvaginal hysterectomy.

to require surgical intervention at readmission and had a higher febrile morbidity and minor
complication rate.
Long-term complications include recurrent prolapse and urinary fistula. The majority of
vault prolapse involves only the upper vagina and is asymptomatic. More significant prolapse is
uncommon. Prolapse that develops following hysterectomy may be an enterocele that occurred
because of insufficient closure and/or support of the cuff. Enterocele may also develop
postoperatively if concurrent pelvic floor relaxation was not repaired. Absence of the normal
posterior vaginal axis may promote further prolapse of the cuff.
Ureterovaginal and vesicovaginal fistulas occur in 0.09 –0.5% and 0.6% of cases,
respectively (10). With adequate anterior retraction of the bladder, ligation of the pedicles close
to the cervix and avoidance of lateral placement of the purse-string sutures in the perivesical
fascia, bladder, and ureteral injury can be avoided. In regard to overall lower urinary tract
function, Vierhout concluded that there is minimal to no effect of nonradical hysterectomy on
lower urinary tract function (56).
Sexual function has always been a concern following hysterectomy; however, recent data
indicate that hysterectomy actually improves sexual functioning and overall quality of life.
 Surgical Therapy of Uterine Prolapse 541

Figure 15 Pathologic specimen. The uterus is removed intact with surgical margins in close proximity
to the uterus, which facilitates avoidance of ureteral injury.

Rhodes and associates found that after hysterectomy, the occurrence of sexual relations and
orgasm increased and the rates of dyspareunia and low libido decreased (57). Similarly,
researchers from the Maine Medical Assessment Foundation concluded that hysterectomy
relieved pelvic pain, fatigue, depression, and sexual dysfunction and improved quality of life 1
year postoperatively (58).

VII. CONCLUSION

Uterine prolapse is a condition that, depending on severity of prolapse and symptoms, can be
treated conservatively or surgically. Surgical treatment includes uterine sparing procedures and
hysterectomy. Hysterectomy can be performed by the traditional abdominal approach, laparo-
scopically, or vaginally. Considerations such as surgeon preference, uterine size, uterine and/or
adnexal pathology, and fertility must be taken into account before choosing therapy.
542 Eilber et al.

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39
Vaginal Hysterectomy and Other Operations
for Uterine Prolapse
Paul M. Fine and Dallas Johnson
Baylor College of Medicine, Houston, Texas, U.S.A.

I. HISTORICAL PERSPECTIVE
A. Prolapse
Uterine prolapse was an ancient affliction. It was described by the Egyptians 2000 years BC . The
uterus had been described by Aristotle as “the seat of womanhood” and was considered an
indispensable and vital organ that somehow embodied the spirit of the woman. It is therefore not
surprising that ancient practitioners tried or suggested multiple therapies of every imaginable
type to correct prolapse without removing this vital organ of womanhood (1). Succession
therapy and vaginal pessaries were two popular nonsurgical treatments for genital prolapse.
Succussion therapy, described by Hippocrates (460 – 377 BC .), involved securing the patient to a
frame with ropes then inverting her to a head-down position. The entire frame was then moved
up and down in a shaking motion to allow gravity to return the uterus to its normal pelvic
position. This was followed by placement of an object in the vaginal canal to prevent recurrence
of the prolapse. A widely used object was half of a pomegranate soaked in vinegar as
recommended by Diocles of Carystos in the 4th century BC (2).
Over the centuries many objects of various sizes and shapes were utilized as pessaries. There
are many ancient writings describing pelvic discomfort, foul-smelling vaginal discharge, and
bleeding. There were sporadic reports of vaginal amputation of the prolapsed part from as early as
100 AD by Soranos (3) through the early 19th century. The prolapsed part was ligated as high as
possible, followed by excision with the knife or cautery, or allowing the ligated organ to slough over
a period of weeks (4). Genital prolapse was the first recorded indication for hysterectomy (5).

B. Anesthesia
The discovery of general anesthesia using chloroform and ether was a medical milestone. There
is debate as to who was the first to use chloroform as an anesthetic. The German chemist Justus
von Liebig discovered chloroform in 1831 (6). Simpson used chloroform fumes to lessen the
pain of labor in 1847 (7). The subsequent discovery of ether as a general anesthetic agent was an
important American contribution to medicine. Crawford Long, a practitioner in rural Georgia,
first used ether as a general anesthetic in 1842 and published his results in 1849. Oliver Wendell
Holmes first suggested the name “anesthesia” (6).
545
546 Fine and Johnson

C. Antisepsis and Asepsis

The discovery of general anesthesia opened the door to the rapid progress in pelvic surgery, but
the discovery of antisepsis and asepsis was equally important. Semmelweis proved the
contagiousness of puerperal fever at the Vienna Krankenhaus and published it in 1845. His
insistence of asepsis by thoroughly scrubbing of the hands in the delivery room caused him to
be ridiculed and persecuted by his colleagues, eventually forcing him into an insane asylum,
where he died at the age of 47 (8). Joseph Lord Lister devised a method of antisepsis by
sterilizing of the operating room and operating field with carbolic spray in 1865 (9).

D. Hysterectomy
Oslander reported eight partial vaginal hysterectomies in 1808. His first such procedure in 1801
for cervical cancer required traction on a nonprolapsed uterus. He used a speculum to aid in
visualization then, with traction, sharply excised the cancerous cervix with a knife and curved
scissors (10). In 1842, Charles Clay of Manchester removed a fibroid uterus. He had opened the
abdomen to remove an ovarian tumor and encountered a large fibroid uterus. He then performed
a supracervical hysterectomy. Unfortunately, the patient died on postop day 15. The first
successful removal of a fibroid uterus occurred in 1853 by Dr. Walter Burnham of Lowell, MA.
He was forced to remove the uterus without intending to do so. The abdomen had been opened to
remove what was thought to be an ovarian cyst when the patient suddenly vomited and extruded
the fibroid uterus through the incision. He was unable to replace it and was forced to perform the
hysterectomy. He was encouraged by colleagues to attempt further hysterectomies. Of his next
15 attempted hysterectomies, only three survived. Gilman Kimball, also of Lowell, was the first
to correctly diagnose uterine fibroids preoperatively, and performed an abdominal hysterectomy
for that indication in September 1853 (11).
Between 1800 and 1875, cervical cancer provided the impetus in vaginal surgery. In
1810, Wrisberg delivered a prize-winning essay to the Vienna Royal Academy of Medicine
advocating vaginal hysterectomy for cervical cancer. Paleta, an Italian surgeon, in 1812
reported the removal of the entire uterus vaginally, although he had intended to remove only the
cancerous cervix and lower uterine segment (12). Conrad Langenbeck of Gottingen, Germany,
performed the first planned successful vaginal hysterectomy in 1818 and reported it in 1819.
The patient had cervical cancer and prolapse. She was 50 years of age at the time of surgery and
lived until the age of 76. It is remarkable that Langenbeck performed this successful surgery
without an assistant, anesthesia, antisepsis, hemostatic clamps, and blood transfusion and
without opening the peritoneum (13). The first reported American vaginal hysterectomy was
by J.F. Warren in 1829 (14). This was not a complete hysterectomy, as the fundus was not
removed.
Blood loss and infection were the major causes of death from early hysterectomy. By
1880, the operative mortality from vaginal hysterectomy was under 40% compared to a 70%
mortality following abdominal hysterectomy. Wilhelm Freund in Breslau, Germany (1881),
developed the technique of placing hemostatic clamps (“compression forceps”) on the broad
ligament rather than ligation or cautery during abdominal hysterectomy. He left them in place
for several days prior to removing them (15). Pean, a French surgeon, reported in 1889 the
technique of combined clamping and suturing. His mortality rate was only 2% for vaginal
hysterectomy. Pean also first described the morcellation technique for vaginal removal of fibroid
uterus in 1886 (16).
 Vaginal Hysterectomy 547

II. HISTORICAL OPERATIONS FOR UTERINE PROLAPSE

The Manchester-Fothergill operation, first performed by Duncan of Manchester in 1879 (17),

consists of cystocele and rectocele repairs, if necessary, amputation of the cervix and suture of
the cervical ligaments in front of the cervix to draw the cervix up into the vagina. The Watkins
transposition operation was first performed by Thomas J. Watkins in 1898. It was used to correct
cystocele and uterine prolapse with generally satisfactory results. It has also been referred to as
the interposition operation. The technique involved repositioning or interposing the uterine
fundus between the anterior vaginal wall and urethra/bladder (18). The Spalding-Richardson
procedure was described in 1937 by Edward H. Richardson (19). Spalding had independently
described a nearly identical procedure earlier in 1919 (20). The procedure consists of removal of
the cervix and corpus of the uterus and utilization of the isthmic portion of the uterus with its
broad and uterosacral ligament attachments into which the cystocele repair may be anchored.
This procedure allowed for the removal of the diseased vaginal portion of the cervix, removal of
the uterine corpus with the tubes and ovaries if indicated, destruction or excision of the
remaining endocervical canal, retention and use of a well vascularized uterine isthmus with
proven supporting structures, and the pubocervical and rectovaginal fascial attachments. This
procedure is more difficult to perform than a vaginal hysterectomy. Should disease develop in
the retained portion of the uterus, surgery to remove it may be complicated. The LeFort
colpocleisis was first described by Leon LeFort in 1877 for the treatment of total procidentia
(21). It is still used today in selected patients. It has the advantage of high success rates (.95%)
in the cure of advanced procidentia combined with relatively quick operating time and
avoidance of general anesthesia in often medically compromised patients. It is described in
detail below.

A. LeFort Colpocleisis
There are various modifications of the original technique described. The basic technique is to
denude a rectangular area of anterior and posterior vaginal mucosa from the level of the cervix to
the urethrovesical crease and then to suture these “mirror image” denuded areas together
anteroposteriorly, creating a permanent internal pessary. Care is taken to leave sufficient vaginal
mucosa bilaterally to allow formation of bilateral canals for drainage of cervical secretions. Care
is also taken to remove only the vaginal epithelium, preserving the underlying fibromuscular or
“fascial” layer. This allows for better vaginal support, better vascularity, and deeper placement
of sutures with less risk of bowel or bladder injury. Injection with a dilute pitressin solution may
facilitate this dissection. Scoring with the knife or marking with a pen outlines the rectangular
areas on the anterior and posterior vaginal mucosa to be excised. Smith-Pratt clamps are useful
in grasping the vaginal mucosa for counter traction during this dissection.
The epithelial edges below the cervix are reapproximated with interrupted absorbable
sutures (0 or 00 Vicryl or Dexon). Beginning at the top (near the cervix), interrupted rows of
sutures (also 0 or 00 Vicryl or Dexon) are placed between the anterior and posterior denuded
vaginal wall. The prolapse is gradually reduced by these rows of sutures. Generally, these rows
are placed 1– 1.5 cm apart with the interrupted sutures of each row 1.0 cm apart laterally. Once
the prolapse has been reduced, the outer vaginal epithelial edges are reapproximated with
interrupted sutures (0 or 00 Vicryl or Dexon). Perineorraphy should then be performed with
midline plication to reduce the genital hiatus and increase the thickness of the perineal body.
Obviously, the LeFort colpocleisis is intended for use in the elderly and frail woman whose
future sexual activity is not a concern. It is advisable to perform a dilatation and curettage prior
to LeFort colpocleisis to rule out occult endometrial malignancy. Preoperative testing for occult
548 Fine and Johnson

stress urinary incontinence can be performed with prolapse reduction stress testing (pessary
stress test). Minimally invasive anti-incontinence procedures such as tension-free vaginal tape
(TVT) can be performed concurrently in patients with preoperative complaints of stress urinary
incontinence, or demonstration of urinary stress incontinence with the prolapse reduction stress
test. The LeForte colpocleisis can also be performed for posthysterectomy vaginal vault prolapse
with similar indications for patient selection. Creation of bilateral vaginal tunnels is less
important in these patients since there will not be any uterine or cervical secretions to drain.

B. Gilliam Uterine Suspension

First described by D.T. Gilliam in 1900, the Gilliam uterine suspension is still occasionally used.
This procedure involves exteriorizing a knuckle of round ligament transperitoneally and lateral
to the rectus muscle bilaterally. This exteriorized knuckle of round ligament is then attached to
the anterior rectus fascia using permanent sutures. This procedure converts a prolapsed or
retroverted uterine fundus to an anteflexed and more well-supported position (22). The
procedure can be done by open laparotomy or by laparoscopic technique. It was often done
concurrently with infertility surgical procedures in order to elevate the adnexae out of the cul-de-
sac in the hope of reducing future adnexal adhesions. High recurrence rates of uterine prolapse
have been reported following Gilliam suspension. This is due to restretching of the round
ligament. In addition, fewer fertility surgeries are performed today because of higher pregnancy
rates with assisted reproductive technology. Enhancement of fertility or reduction of adnexal
adhesions with concurrent Gilliam suspension was also never demonstrated.

III. HYSTERECTOMY
A. Contemporary Practice and Incidence
Generally, women today with symptomatic uterine and pelvic organ prolapse are advised to
complete childbearing prior to undergoing reconstructive pelvic surgery. Although the addition
of hysterectomy does not enhance the success of operations for stress urinary incontinence,
hysterectomy is frequently performed for standard gynecological indications. Gynecological
indications for hysterectomy include severe dysmenorrhea (painful menses), menorrhagia
(heavy menses), menometrorrhagia (frequent and heavy menses), endometriosis, high-grade
cervical intraepithelial neoplasia (dysplasia), and atypical adenomatous hyperplasia of the endo-
metrium. Fibroids and uterine prolapse remain the most common indication for hysterectomy in
the United States. Hysterectomy is currently the second most common surgical procedure
performed in the United States (cesarean section is first), with almost 600,000 performed in
1997. Of these 63% were done abdominally and only 37% vaginally or with the laparoscopic
approaches (23). As the population ages, the estimated number of hysterectomies will increase.
Using 1987 age-specific hysterectomy rates and population projections from the Census Bureau,
over 823,000 hysterectomies will be performed in 2005 (24). Vaginal or abdominal hysterec-
tomy is frequently performed in combination with other pelvic reconstructive procedures.

B. Vaginal or Abdominal?
The choice of a vaginal or abdominal approach for hysterectomy will depend on several fac-
tors. Uterine enlargement greater than a 12- to 14-week pregnancy may require an abdom-
inal approach. Morcellation techniques are currently a “dying art,” but in trained hands allow
for vaginal removal of an 18- to 20-week-size uterus (to the umbilicus). Many younger
 Vaginal Hysterectomy 549

gynecologists are unfamiliar or uncomfortable with this technique. The presence of adnexal
pathology including large pelvic masses, suspected pelvic malignancy, or probable pelvic
adhesions such as those following myomectomy or pelvic abscess, may favor an abdominal
approach. Desired removal of tubes and ovaries is not generally an indication for abdominal
approach since bilateral salpingo-oophorectomy can be safely accomplished vaginally in .90%
of cases. The requirement of an abdominal incision for a concurrently planned Burch
urethropexy or abdominal sacrocolpopexy may also favor an abdominal approach for
hysterectomy. Some would argue that the need for an abdominal incision in a Burch would
justify an abdominal approach to hysterectomy. Others would argue that the Burch urethropexy
following vaginal hysterectomy requires a smaller incision with less invasion of the peritoneal
cavity and no bowel packing. Prior cesarean section was once considered a relative
contraindication for vaginal hysterectomy. Several recent studies, including one from our
institution, have demonstrated the safety and efficacy of vaginal hysterectomy in patients with
one or multiple prior cesarean sections (25). Benson compared the abdominal approach for
pelvic reconstructive surgery to the vaginal approach and found less evidence of neuropathy, as
measured by pudendal nerve terminal motor latency studies, than with the abdominal approach
(26). Pudendal terminal motor latency measurements do not necessarily correlate with
denervation of the pelvic floor and a definitive answer to this question awaits more randomized
controlled clinical trials.
Obviously, the decision regarding the route of hysterectomy will depend on the above
factors as well as surgeon preference. Vaginal hysterectomy has been performed in the same-day
surgery setting in selected patients, and has been shown to be less expensive in direct costs than
either abdominal or laparoscopic hysterectomy. Discussion of laparoscopic hysterectomy is
beyond the scope of this chapter. Obviously there is a steep learning curve to become proficient
in laparoscopic assisted or total laparoscopic hysterectomy. Concurrent repair of pelvic organ
prolapse of anterior, posterior, or apical vaginal defects can also be accomplished vaginally.
Obesity may favor the choice of the vaginal route.
A nulliparous patient may also be a candidate for a vaginal hysterectomy. However,
a nulliparous and obese patient with little uterine descent, a narrow pubic arch, and upper thigh
and gluteal obesity may prove a challenge, even to the most experienced vaginal surgeon.
These patients are also technically difficult from an abdominal perspective owing to the thick
abdominal wall, and a deep and narrow bony pelvis. Finally, any orthopedic condition
preventing positioning in the dorsal lithotomy position would contraindicate a vaginal approach.

C. Risks: Vaginal Versus Abdominal Hysterectomy

There is an incidence of complications following hysterectomy in the range of 15%. This is more
easily understood by considering the anatomy and technical details. Opening the vaginal cuff
contaminates the peritoneal cavity with upper vaginal flora. The bowel, bladder, and ureters are
close to the lines of incision, clamping, and suturing. Pelvic surgery also predisposes to
thromboembolism. Obviously many factors influence risk including patient’s age and general
health, the indication for hysterectomy, the urgency (emergency or planned), the use of suction
drainage and prophylactic antibiotics, the experience and training of the surgeon, and the choice
of vaginal versus abdominal approach.
Comparative risks of vaginal and abdominal hysterectomy were assessed by the
Collaborative Review of Sterilization (CREST) study conducted by the Centers for Disease
Control (CDC) between 1978 and 1981. This study included women aged 15 –44 who had
nonemergency, nonradical hysterectomies at nine institutions for all indications excluding
pregnancy and cancer. One thousand eight hundred fifty-one patients were analyzed for 568
550 Fine and Johnson

vaginal and 1283 abdominal procedures. The overall complication rate was 24.5 per 100 women
who had vaginal hysterectomy and 42.8 per 100 women who underwent abdominal
hysterectomy. Thus, the risk for one or more complications was 70% higher in the abdominal
hysterectomy group than in the vaginal hysterectomy group (relative risk of 1.7). The risk of
infection was 2.1 times higher and the risk of transfusion was 1.9 times higher for the abdominal
hysterectomy patients (27). A smaller but more recent study has shown similar trends but
significantly lower complication rates. The complications following vaginal hysterectomy were
10.4% versus 13.6% for abdominal hysterectomy. The decrease in hematocrit was 5.7% for
vaginal and 6.5% for abdominal hysterectomy. Hospital stay was 2.1 days for vaginal and 2.7
days for abdominal hysterectomy (28).

IV. VAGINAL HYSTERECTOMY

A. Technique
There are numerous classical descriptions and illustrations of the technique of vaginal
hysterectomy. Most are derived from the technique described by Heaney. We will emphasize
modifications of technique especially as it relates to prevention of future pelvic floor
dysfunction. The decision to inject vasoconstrictors diluted with saline into the pericervical
tissues is optional. The author prefers to use a solution of 20 units of pitressin diluted with 20 cc
saline injected 3608 around the cervical/vaginal tissues. A short Auvard weighted speculum is
placed in the vagina, and the bladder is drained with a red rubber catheter. The cervix is grasped
on the anterior and posterior lip with Lahey thyroid or “Massachusetts” traction forceps. Care
must be taken to grasp only the outer (more distal) cervix, as the bladder may be relatively lower
on the cervix in elderly patients with anterior wall prolapse or prior cesarean section. The choice
of a sharp knife or angled Bovie tip is optional, but we prefer sharp knife dissection to better
identify the proper tissue planes and to minimize tissue necrosis. Classically, a circumferential
incision is made at the cervicovaginal junction. This incision transects the full thickness of the
vaginal epithelium. However, since the posterior cul-de-sac is entered first, we prefer a U-shaped
incision starting from three and continuing to the 9 o’clock position. In this manner, the cul-de-
sac peritoneum can be entered and the uterosacral ligaments divided before any anterior
cervicovaginal incision is needed. There is no reason to start potential bleeding in the anterior
area until dissection into the vesicouterine space is necessary as the blood only runs downward
obscuring the posterior operative field. In addition, initial division of the uterosacral ligaments
allows for better mobilization of the uterus downward with traction and, therefore, better
visualization and access.
With countertraction and a gauze-wrapped forefinger, the cul-de-sac peritoneum is
identified and entered by sharp dissection with the curved Metzanbaum or Harrington scissors.
In patients with uterine prolapse, this peritoneal reflection is often more distal from the cervix,
and the posterior vaginal incision is therefore made lower into the cul-de-sac. A rectal finger may
aid in clarifying this altered anatomy. Once the posterior cul-de-sac peritoneum is entered, the
uterine fundus and adnexae are palpated to exclude unexpected uterine or adnexal pathology. A
decision can then be finalized regarding the technical feasibility of continuing with the vaginal
approach if any doubt had existed.
Conversion to an abdominal approach at this point can easily be accomplished. In the
event of excessive bleeding from the posterior colpotomy, a running locking suture can be
placed. Prior injection of vasoconstrictors eliminates the need for this. At this point, the short-
bladed Auvard weighted speculum is replaced with the long-bladed weighted speculum with the
 Vaginal Hysterectomy 551

blade inserted into the peritoneal cavity through the posterior colpotomy. This facilitates the
visualization of the posterior compartment and pelvic sidewall.
Attention is now given to the anterior dissection. Using the scalpel or angled Bovie tip, an
inverted “U” incision is made on the anterior cervix, from 9 to 3 o’clock, with care being taken to
stay on the distal cervix in patients with anterior wall prolapse or prior cesarean. Traction on the
cervix with countertraction with an anterior right-angled retractor will aid in identifying the
correct tissue plane because the vagina will retract when cut to the correct full-thickness depth. If
this does not occur, the cut anterior vaginal wall may be grasped with Allis tissue forceps and
pulled anteriorly under tension. Sharp dissection with curved Metzanbaum scissors, tip down
and staying close to the cervix, will facilitate entry into the vesicouterine space. Once the
cleavage plane of the vesicocervical space is reached, gentle dissection with the finger will lift
the bladder off the cervix. If the bladder pillars are prominent, they can be cross-clamped close to
the cervix, transected, and ligated to provide better lateral exposure. The location of the
peritoneal reflection is palpable as the two slippery mesotheleal surfaces sliding on one another.
The peritoneum can then be elevated with a Sarot artery forceps and transected. The forefinger is
placed through the peritoneal opening, and a Haney right-angle retractor is placed below this
forefinger to guide its placement into the peritoneal cavity.
Visualization of bowel and omentum confirms correct intraperitoneal entry. An opposing
right-angle retractor may facilitate visualization of bowel and/or omentum. In cases with an
enlarged and well-supported uterus or prior cesarean section, this peritoneal reflection may be
higher up and technically difficult to enter. In this case, the transverse cervical (“cardinal” or
“Mackenrodt”) ligament may be safely divided first to allow further descent of the uterus and
better visualization of the anterior peritoneal reflection. A curved uterine sound can also be
passed from the cul-de-sac around the uterus anteriorly to help identify the proper tissue plane.
In cases where difficulty has been encountered in entering the anterior peritoneum, the bladder
integrity can be tested by transurethral instillation of methylene blue or sterile milk into the
bladder.
Once the anterior and posterior peritonea have been entered, the ureter can often be
palpated to determine its position prior to shortening and transecting the uterosacral and cardinal
ligaments. Shortening of these ligaments prior to reattachment is important for apical cuff
support. Only if the ligaments are shortened will the vaginal cuff be held at a level higher than
that of the prolapsed cervix, unless some other type of apical cuff suspension is planned such as a
sacrospinous ligament fixation. To palpate the ureter, a retractor is placed in the lateral
vaginal fornix and a finger in the anterior cul-de-sac. Because the ureter must pass under the
uterine artery and enter the bladder anterior to the examining finger, it can be palpated against
the retractor blade. The characteristic snap of the ureter permits its identification. It can be
followed for some distance by moving the retractor and examining finger anteriorly and
posteriorly.
At this point, the uterosacral ligaments are palpated and cross-clamped with Heaney-type
hysterectomy forceps if not already divided as described above. If significant shortening of the
uterosacral ligament is planned, this step is done after the anterior peritoneum is opened in order
to palpate the ureter first. Placement of this clamp more laterally and more distal from the uterus
will shorten the uterosacral pedicle and assist in better apical support of the vaginal cuff later
when reattached to the vaginal cuff. The uterosacral pedicles are not cut flush with the clamp.
Instead, an extra 2 mm of tissue is left to aid in future identification and to facilitate later
resuturing of these pedicles to the angles of the vaginal cuff. In addition, transfixion suturing is
used to avoid the tie coming loose when traction is placed on this pedicle later. These pedicles
are tagged with a curved hemostat. We use 0 Dexon or Vicryl synthetic absorbable suture
throughout the hysterectomy utilizing “popoff ” CT-1 size tapered needles. The transverse
552 Fine and Johnson

cervical (cardinal or Mackenrodt) ligaments are similarly grasped by swinging the Heaney
forceps out laterally to shorten this pedicle, and a transfixion suture is placed. These pedicles are
also not cut flush with the clamp as described above; rather they are rather tagged with a straight
hemostat. If a long cervix makes visualization or access to the uterine fundus difficult, all or part
of the cervix may now be amputated (Fig. 1A) and the remaining lower uterine segment
regrasped (Fig. 1B) prior to division of the uterine arteries. The uterine artery is bilaterally cross-
clamped with the Heaney forceps placed perpendicular to the lateral uterus, making sure that the
pedicle includes the peritoneum anteriorly and posteriorly. This assures the complete purchase
of the uterine vessels. These vascular pedicles are not transixed to avoid hematoma or held with
tags that might cause slippage. The lower broad ligament is then bilaterally clamped and
divided.
At this point, the uterine fundus can usually be delivered through the posterior colpotomy
site by grasping it with a single toothed tenaculum and using gentle traction. This exposes the
remaining connections between the uterus and adnexal structures (round ligament, Fallopian
tube, and utero-ovarian vessels). These uteroadnexal structures are then divided using a variety
of techniques. We prefer to first place a free ligature with the digital flip placement (Fig. 2)
followed by clamping with Heaney forceps distal to the free tie. A transfixion suture distal to
the free tie is then placed (Fig. 3). This allows for a double tie on this rather large pedicle and
the benefit of a transfixion suture without risk of hematoma (29). The uterus is thus
removed. These utero-ovarian pedicles are then tagged until hemostasis of all pedicles has been
confirmed.
When the uterus is enlarged by fibroids, delivery of the fundus may not be possible. At the
point where the uterine arteries have been successfully divided and ligated, various morcellation
techniques can be utilized with minimal blood loss. The uterus may be divided sagitally and one-
half of the uterus pushed cephalad while the other half is now accesssable for division of the
uteroadnexal structures. Then, the remaining hemiuterus is brought down to complete the
hysterectomy. Myomectomy can be utilized to reduce the size of the bulky fundus. The fundus
may also be “cored” sequentially to facilitate lateral access for clamping. If, however, the uterine
arteries are unable to be divided because of anatomical or technical difficulty, the vaginal
approach should be abandoned in favor of an abdominal approach. Attempted morcellation prior
to division and ligation of the uterine arteries will result in excessive blood loss, poor
visualization, and “blind clamping.”
Following removal of the uterus, all pedicles are examined for hemostasis with gentle
traction on the tagged ligatures as needed. A moistened sponge stick is useful as both a bowel
retractor and blotting instrument. If necessary, two 4  4 gauzes can be placed in the ring
forceps to create a “double sponge stick” where more deflection of bowel is required.
The adnexae are now visualized and palpated. If adnexectomy is planned or indicated by
unexpected pathology it is now performed. The adnexa is better mobilized by first dissecting it free
from the remaining round ligament. The tissues under the proximal remaining round ligament are
serially cross-clamped and ligated with 00 synthetic absorbable suture. The adnexa is then grasped
with Babcock forceps and gently pulled medially exposing the infundibulopelvic ligament and
vessels (Fig. 4). The prior separation of the round ligament from the adnexa greatly facilitates this,
especially when the adnexae are relatively high in the pelvis. The infundibulopelvic structures are
clamped, usually with a Sarot or Mixter right-angled forceps, divided, and ligated. Transfixion
sutures are not used because of the risk of hematoma. This pedicle may, however, be doubly
ligated by flashing the clamp or by placement of two sandwiched clamps if space permits. The
pelvic sidewalls are carefully examined for hemostasis. Several large series have demonstrated the
efficacy (.90% success) and safety in performing transvaginal bilateral salpingo-oophorectomy.
In our opinion, however, because of the potentially increased risk of postoperative ovarian abscess
 Vaginal Hysterectomy 553

Figure 1 (A) Amputation of long cervix. (B) Regrasping of cervical stump.

554 Fine and Johnson

Figure 2 (A, B, C, D) Digital flip placement of utero-ovarian tie.

Figure 3 (E, F, G) Transfixion suture placed distal to digital flip free tie.
 Vaginal Hysterectomy 555

Figure 4 Separation of round ligament facilitating adnexal removal.

due to contamination from the vaginal field, an ovary with a ruptured functional cyst should be
removed. This complication may occur despite the use of prophylactic antibiotics.
Culdoplasty, if indicated, may now be performed by a variety of techniques that are
described elsewhere in this textbook. Although the need for closure of the pelvic peritoneum is
controversial, it is our opinion that it should be closed when the adnexae are conserved in
premenopausal women. This avoids prolapse of the distal tube through the vaginal cuff. Once
hemostasis of the pedicles has been confirmed, this peritoneal closure is begun. The anterior
peritoneum is grasped with a long Allis forceps. Sweeping a SpongeStick downward on the
anterior peritoneum will bring the anterior peritoneal edge into plain view. The long-bladed
Auvard weighted speculum is replaced with the short-bladed Auvard. The posterior vaginal wall
is grasped with another long Allis forceps. Utilizing a non-pop-off synthetic absorbable 0 or 00
suture, the pelvic peritoneum is closed with a purse-string suture taking care not to place the
suture too deep anteriorly avoiding the bladder, and to avoid the uterine artery pedicles laterally.
The peritoneum is closed as high as possible. Care should be taken to not incorporate the adnexal
pedicle into this suture. Such incorporation would bring the adnexa into opposition with the
vaginal cuff and potentially cause later deep thrust dyspareunia. The patient is placed in
Trendelenberg position and the assistant’s forefinger is placed into the peritoneal cavity
while the purse-string suture is tied. This avoids trapping of intra-abdominal contents in the
suture. The finger is withdrawn as the suture is snugged down. Irrigation of the vagina is then
performed.
Now the shortened uterosacral ligament and transverse cervical ligament pedicles are
reattached to the lateral vaginal cuff bilaterally. This is an important step in reestablishing proper
apical support of the post-hysterectomy vaginal vault. These pedicles had been tagged and
purposefully cut to leave a large and easily identifiable pedicle. There are numerous techniques
to reattach these pedicles directly with interrupted sutures. We prefer the “lasso” technique
where the uterosacral and transverse cervical pedicles are placed under tension by gentle
traction, and a suture of 0 Vicryl or Dexon is placed in the vaginal mucosa from outside to inside
entering just below these ligaments. This suture is then brought around both of these pedicles
(“lassoing” them), and then brought from inside to outside (Fig. 5). The lateral vagina is grasped
556 Fine and Johnson

Figure 5 Fixation of uterosacral and transverse cervical ligament pedicles to lateral vaginal cuff for
apical support.

with an Allis forceps and brought downward during tying of this suture above the Allis. With this
technique, the angle sutures are placed more cephalad on the vaginal cuff, maximizing apical
support. This lasso technique is more effective in controlling bleeding that might occur between
the uterosacral and transverse cervical pedicles or for bleeding that might result from direct
suture placement through the pedicle itself.
At this point the vaginal cuff is closed with either interrupted or a continuous locking
suture. One or two layers may be utilized. The proper closure of the full thickness of anterior and
posterior vagina reapproximates the anterior pubocervical fascia with the posterior rectovaginal
fascia. This is an important step in minimizing the potential for later enterocele formation.
Nonclosure of the vaginal cuff, as might occur with “whip-stitching” of the vaginal cuff, leaves
an apical transverse “fascial” defect through which the bowel can later herniate to form an
enterocele. With the use of prophylactic preoperative antibiotics and careful hemostatic
technique, there are few indications to whip-stitch the vaginal cuff for drainage in our opinion.
There is also no need to leave the vaginal cuff open to start the incision for colporraphy if one is
planned. To do so results in a “T”-type incision at the vaginal cuff that is inherently weaker.
Additional bleeding from the vaginal cuff during colporraphy is also avoided.
The bladder is now drained with a red rubber catheter if anterior colporraphy is planned;
otherwise, a Foley to gravity drainage is placed. The presence of clear urine without hematuria is
reassuring. It is debatable whether cystoscopy and ureteral evaluation with IV dye is required
routinely following vaginal hysterectomy. However, we would recommend it be performed in
cases of advanced uterine prolapse, concurrent culdoplasty, high uterosacral suspension of the
vaginal cuff, difficult entry into the anterior peritoneum including prior cesarean section, and
difficult morcellation cases. It should also be performed where bleeding has occurred following
adnexectomy, and additional suture placement in the pelvic sidewall was required to secure
 Vaginal Hysterectomy 557

hemostasis. Obviously, cystoscopy can be performed earlier following any of the above stages in
the procedure rather than waiting until the end.
Once the weighted speculum is removed, adequate vaginal cuff support will be evidenced
by visualization of lateral dimples where the uterosacral and transverse cervical ligaments had
been reattached. Additionally, the vaginal length will be equal to or greater than the surgeon’s
finger (generally .7 cm). If vaginal cuff support is inadequate at this point, additional cuff
suspension may be indicated including vaginal or abdominal techniques including sacrospinous
ligament fixation or abdominal sacral colpopexy. Patients with significant preoperative uterine
prolapse to or beyond the hymeneal ring should always be consented for these possible
procedures.

B. Complications
Although performed occasionally in an outpatient surgical setting, vaginal hysterectomy should
be considered a major surgical procedure with the risks usually associated with such procedures.
The complications unique to vaginal hysterectomy are discussed in this section.

1. Intraoperative Complications
Cystotomy may occur during attempt to enter the vesicouterine peritoneal space. This occurs
more frequently in patients with prior cesarean section with scarring in this area. These
cystotomies are at the base of the bladder and generally above the trigone. Because the
dependant portion of the bladder is involved, care must be taken to close the cystotomy in
several layers and test for a watertight repair with sterile milk or Methylene Blue dye instilled
transurethrally. Cystoscopy with IV Indigo Carmine dye should also be performed to confirm
bilateral ureteral patency following such repair. The bladder should be drained for 7 –10 days
postoperatively.
Ureteral injury may occur during any hysterectomy. Patients with prolapse have distorted
anatomy and the ureter may lie ,0.5 cm lateral to the cervix (15). Care should be taken to place
the clamps close to the uterus. Cystoscopic evaluation with IV Indigo Carmine dye may be
helpful to confirm bilateral ureteral integrity and should be performed in cases of advanced
pelvic organ prolapse.
GI injury may occur as a laceration of the rectum. Small defects may be repaired with a
simple two-layer closure with synthetic absorbable suture while large lacerations may require a
diverting colostomy following repair.

2. Postoperative Complications
Vaginal cuff cellulitis or abscess can occur following either abdominal or vaginal hysterectomy.
The vagina is a bacterially contaminated area despite preoperative douching or prolonged
prepping in the OR. Cuff cellulitis generally presents on the second or third postoperative day
with fever in the 1018 range with excessive tenderness and induration of the vaginal cuff.
Spiking fevers may be indicative of a vaginal cuff abscess. A palpable, fluctuant, and tender
mass in the vaginal cuff may be palpated. The formation of a vaginal cuff hematoma may
predispose to abscess formation. Ultrasonic evaluation is helpful in delineating the size and
location since pelvic exam is limited owing to tenderness. Transvaginal drainage in the operating
room is performed for palpable cuff abscesses. Radiology-guided needle drainage may be
required for nonpalpable pelvic abscesses. These infections are polymicrobial, and intravenous
broad-spectrum antibiotics covering gram-positive, gram-negative, and anaerobic bacteria are
needed.
558 Fine and Johnson

Urinary retention. The Foley catheter is normally removed on the morning of the first
postoperative day, and most patients have no difficulty in resumption of voiding. However,
occasionally, patients may require Foley drainage for an extra day or two. This is more common
in patients with multiple prior cesarean sections where separation of the bladder off the uterus
was more difficult. It may also be more common with prolonged anterior vaginal retraction in
technically difficult cases.
Vesicovaginal fistula. This relatively rare complication may occur days to several weeks
postoperatively. The patient generally complains of continuous vaginal leakage of urine.
Diagnosis may be confirmed by transurethral installation of Methylene Blue dye in the bladder
with a tampon placed into the vagina. Transvaginal leakage of the dye through the fistula will
result in blue staining of the inner portion of the tampon. These fistulas are more common
following recognized cystotomy with repair, or may occur following undiagnosed cystotomy or
inadvertent passage of a suture into the bladder during closure of the pelvic peritoneum or
vaginal cuff. Generally, the vesicovaginal fistula repair is delayed for 3 months to allow
complete resolution of induration and swelling. Occasionally a small fistula may spontaneously
heal during this prolonged catheter drainage. A vaginal repair can be accomplished by the
Latzko procedure, which is essentially an upper vaginal colpocleisis without excision of the
fistulous tract (30). Other surgeons, and most urologists, prefer the abdominal approach.
Vaginal prolapse is a rare complication of hysterectomy that may be avoided if proper
attention is paid to vaginal vault support during the procedure (31,32). Suspension of the vault
from the uterosacral-cardinal ligament complex provided they are of adequate strength, or
colpopexy should prevent this complication.

C. Recuperation
Patients generally have a faster recovery following vaginal compared to abdominal
hysterectomy. Lack of an abdominal incision facilitates early ambulation and fewer respiratory
complications. Without the need for bowel packing, there is quicker return of normal bowel
function, typically on the first postoperative day. It should be remembered that the synthetic
absorbable sutures used, typically Dexon or Vicryl, are hydrolyzed and predictably lose .70%
of their strength within 4 weeks. Patients are often relatively pain-free at 3 weeks postop and,
accordingly, return to full activity. Studies have shown that wound tensile strength at 3 weeks
postoperatively is only 25% as compared to preoperatively and rarely more than 50% at 6 weeks
postoperative (33). Patients therefore must be cautioned to refrain from heavy lifting (.20–
30 lb) and refrain from intercourse until after the 6-week postoperative visit. Proper healing of
the vaginal cuff, including the newly reattached apical lateral ligamentous support (transverse
cervical and uterosacral ligaments) and the midline fascial suture line (pubocervical and peri-
rectal), requires 6 –8 weeks at a minimum. As the synthetic absorbable sutures hydrolyze, the
patient may notice a vaginal discharge, possibly blood tinged. She may even notice pieces of
suture passed transvaginally. This is normal. She should refrain from tampon use during the
6-week post-operative period. Physiological estrogen replacement therapy may be begun or
restarted upon full ambulation. Patients previously on combined estrogen-progestagen regimens
may be switched to an estrogen only formulation.

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J 1899; 15:420 – 423.
19. Richardson EH. An efficient composite operation for uterine prolapse and associated pathology. Am J
Obstet Gynecol 1937; 34:814 – 827.
20. Spalding AB. A study of frozen sections of the pelvis with description of an operation for pelvic
prolapse. Surg Gynecol Obstet 1919; 29:529– 536.
21. Le Fort L. Nouveau procede pour la guerison du prolapsus uterin. Bull Gen Therap 1877;
92:337– 344.
22. Gilliam DT. Round-ligament ventrosuspension of the uterus: a new method. Am J Obstet Gynecol
1900; 41:299.
23. Farquhar CM, Steiner CA. Hysterectomy rates in the United States 1990– 1997. Obstet Gynecol 2002;
99:229– 234.
24. Pokras R. Hysterectomy: past, present and future. Stat Bull Metrop Insur Co 1989; 70:12.
25. Poindexter YM, Sangi-Haghpeykar H, Poindexter AN, Young RL, Fine PM, Miller HJ. Previous
cesarean section: a contraindication to vaginal hysterectomy? J Reprod Med 2001; 46:840 –844.
26. Benson JT, McClellan E. The effect of vaginal dissection on the pudendal nerve. Obstet Gynecol
1993; 82:387 –390.
27. Dicker RC, Scally MJ, Greenspan JR. Hysterectomy among women of reproductive age: trends in the
United States, 1970– 1978. JAMA 1982; 248:323.
28. Doucette RC, Sharp HT, Alder SC. Challenging generally accepted contraindications to vaginal
hysterectomy. Am J Obstet Gynecol 2001; 184(7):1386– 1391.
29. Fine PM, Thomakos N, Young RL. Digital flip placement of free ligatures in hysterectomy. J Gynecol
Tech 1998; 4:51 – 53.
30. Gershenson DM, DeCherney AH, Curry SL, Brubaker L. Operative Gynecology. Philadelphia:
W.B. Saunders, 2001:404.
31. Symmonds RE, Williams TJ, Lee RA, Webb MJ. Posthysterectomy enterocele and vaginal vault
prolapse. Am J Obstet Gynecol 1981; 140:852.
32. Webb MJ, Aronson MP, Ferguson LK, Lee RA. Posthysterectomy vaginal vault prolapse: primary
repair in 693 patients. Obstet Gynecol 1998; 92:10.
33. Orr JA, Shingleton JM. Complications in Gynecologic Surgery: Prevention, Recognition, and
Management. Philadelphia: J.B. Lippincott, 1994:171 – 178.
34. Hurd WW, Chee SS, Gallagher KL, Ohl DA, Hurteau JA. Location of the ureters in relation to the
uterine cervix by computed tomography. Am J Obstet Gynecol 2001; 184:336 – 339.
40
Advanced Anterior Vaginal Wall Prolapse
(Stage III and IV)
Christina H. Kwon and Peter K. Sand
Evanston Continence Center, Evanston, Illinois, U.S.A.

I. INTRODUCTION

Anterior vaginal wall prolapse is a common finding, especially in parous women. While often
secondary to a cystocele (loss of support of the posterior wall of the bladder), anterior
vaginal wall prolapse may also be secondary to an enterocele (herniation of the peritoneum
through the endopelvic connective tissue). Anterior vaginal wall prolapse is best defined as a
relaxation of the anterior vaginal wall supports. Histologic studies have determined that the
vagina is made up of three layers: the epithelium, muscularis, and adventitia (1). The
frequently used term “endopelvic fascia” is a misnomer and should be abandoned, as there is
no vaginal “fascia.” Support for the vagina is supplied by the levator ani muscles and the
lateral attachments of the endopelvic connective tissue layers to the arcus tendineus fasciae
pelvis (“white line”).
White proposed three theories in 1912, derived from his historic cadaveric dissections on
the etiology of these support defects (2). The first was that support defects occurred from
overstretching of the vaginal wall and thinning of the supporting tissue. The second theory
attributed this to stretching of the attachment of the bladder to the uterus. Finally, he proposed
that stretching of the ligamentous suspension of the bladder led to prolapse. In 1976, Richardson
proposed the concept of site-specific defect repair, with lateral, transverse, and midline defects in
the pubocervical connective tissue (3). Historically it has been difficult to surgically obtain
optimal repair of the anterior compartment prolapse. In a review of his surgical outcomes after
sacrospinous ligament suspension, Shull et al. declared that “the anterior segment provides the
greatest challenge to restoration of normal anatomy” (4).
In 1995, the International Continence Society, the American Urogynecologic Society, and
the Society of Gynecologic Surgeons formally adopted a standardized system of terminology for
the description of female pelvic organ prolapse and pelvic floor dysfunction (5). This system
uses the hymen as a fixed point of reference for a quantitative prolapse description. In stage III,
the most distal portion of the prolapse is .1 cm beyond the plane of the hymen but protrudes no
farther than 2 cm less than the total vaginal length. Stage IV is reserved for essentially complete
eversion of the lower genital tract or complete procidentia. This chapter focuses on stage III and
IV anterior vaginal wall prolapse.
561
562 Kwon and Sand

II. PATHOPHYSIOLOGY OF SEVERE ANTERIOR VAGINAL

WALL PROLAPSE
A. Anatomic Supports and Histology
As mentioned previously, the vagina histologically is composed of three layers: the epithelium
(often referred to as the mucosa, despite the absence of mucous secretory glands); muscularis;
and adventitia. The vaginal epithelium is composed of a nonkeratinizing squamous epithelium
overlying a thin connective tissue layer, the lamina propria. The vaginal muscularis is primarily
composed of smooth muscle with smaller amounts of collagen and elastin. The adventitia is a
connective tissue layer of collagen and elastin that lies between the vaginal muscularis and the
bladder. At the level of the urethra, this adventitial layer is less distinct, with fusion of the
muscular layers of the vagina and urethra.
Laterally the anterior vagina is attached by fibrous connections to the parietal fascia
overlying the levators, which forms the arcus tendineus fasciae pelvis. The arcus tendineus
extends from the inferior aspect of the pubis at the level of the pubic tubercle to the ischial spine.
These lateral fibrous attachments, in conjunction with the levator ani, protect the anterior vaginal
wall from downward forces generated intra-abdominally. The top one-third of the vagina is also
supported by the uterosacral-cardinal ligament complex by its suspension bilaterally to the fascia
overlying the sacrum.
The top two-thirds of the vagina are supported by the levator ani, which is composed of
three muscles: the puborectalis, the ischiococcygeus, and the iliococcygeus. These muscles work
in conjunction with the coccygeus muscle to form the pelvic diaphragm. The levator ani muscles
separate in the midline anteriorly to form the urogenital hiatus that allows passage of the urethra,
vagina, and rectum. The levator ani maintain a constant basal tone that keeps this potential space
almost completely closed. Posterior to the rectum, the levator ani muscles meet in the midline to
form the levator plate. The levator plate is responsible for absorbing and responding to sudden
increases in intra-abdominal pressure, often likened to a trampoline-type effect (6). The tonic
contraction of the pelvic diaphragm is normally reflexively increased in response to increased
intra-abdominal pressure in a fraction of a second (7).
The endopelvic connective tissue also plays a major role in the support of the vagina. This
connective tissue contains fibrous elements such as collagen, and elastin, a viscoelastic matrix
made up of proteoglycans. The inherent strength of a tissue is dependent on its collagen content.
More than 19 different types of collagen have been identified, but two types of fibers
predominate in determining tensile strength. Type I collagen, the most abundant type, is
composed of two chains of a1(I) and one a2(I) chain. These are cross-striated fibrils that are
found in a large variety of tissues. Type III collagen fibers are smaller and more randomly
organized than type I. They are composed of three identical chains called a1(III). Type III
collagen is found in large amounts in blood vessels and in small amounts in tissues containing
type I collagen (8).
With increasing age, collagen turnover becomes slower (9). Following menopause this
decrease in the turnover rate leads to tissue with a higher collagen content with changes in cross-
linking (10). In women with genital prolapse, this change in collagen metabolism leads to a
significant reduction in the type I : III collagen ratio (11). The result is tissue that has increased
load-bearing potential, but with decreased elasticity (12).
After surgical repair, collagen is essential for wound healing. Although the exact
mechanisms underlying wound healing are still being explored, fibroblasts synthesize and
secrete collagen. The more flexible type III collagen is the primary type found during the early
healing phase. As the scar matures, the stronger type I collagen gradually replaces the type III
collagen. Tissue can approach but will never reach its original strength. Other factors in tissue
 Advanced Anterior Vaginal Wall Prolapse 563

healing certainly seem to have an effect but have not been fully elucidated. For example,
cigarette smoking has been shown to impair collagen production in wound-healing pro-
cesses (13).

B. Predisposing Factors
It is generally accepted that vaginal delivery is a predisposing factor toward the development of
prolapse, although the exact etiology is unclear. During childbirth, downward expulsive efforts
of the mother as well as compression from the presenting part of the fetus combine, exposing the
pelvic floor to great amounts of potential compression injury. This can cause direct damage to
the endopelvic connective tissue and the vaginal walls as well as indirect injury to the pelvic
musculature by potential nerve compromise, either caused by direct compression or by a
neuropathic stretch injury. EMG studies have shown that vaginal delivery causes partial
denervation of the pelvic floor (14). Invesigators have found an association between weakening
of the pelvic floor postpartum and the degree of lacerations and incisions of the perineum during
vaginal delivery (15,16).
Although the exact mechanism is unclear, vaginal delivery clearly has a significant effect
on the pelvic floor muscles. When the pelvic diaphragm does not maintain an adequate basal
resting tone, the genital hiatus widens. The pelvic viscera become increasingly reliant on their
ligamentous supports and their inherent tissue strength as the support from the levator plate
lessens. Repetitive stress and tension from increases in intra-abdominal pressure can eventually
cause separation or attenuation of these connective tissue supports. Denervation injury from
vaginal childbirth can contribute to this loss of tone. Conditions such as muscular dystrophy,
myelodysplasia, and trauma, which affect spinal cord pathways and pelvic nerve roots, are
associated with pelvic organ prolapse resulting from flaccid paralysis of the pelvic floor
musculature (17).
Connective tissue also plays a major role in the support of the pelvic viscera. Collagen
deficiency or imbalance can contribute to pelvic organ prolapse. Women undergoing surgery for
pelvic organ prolapse have significant changes in their endopelvic connective tissue with a
decreased number of fibroblasts and an increase in the amount of abnormal collagen when
compared to samples taken from women having hysterectomy without pelvic organ prolapse
(18). Women with joint hypermobility have also been found to be at increased risk for the
development of pelvic organ prolapse as a result of their underlying connective tissue disorder
(19). As mentioned earlier, cigarette smokers have been found to have impaired collagen
production in wound healing (13), which may also be compounded by repetitive and chronic
coughing. This may explain the increased rate of stress urinary incontinence in current and
former smokers (20).

III. CONSERVATIVE THERAPIES FOR ADVANCED PELVIC

ORGAN PROLAPSE

Pessaries are the most common nonsurgical way to support pelvic organ prolapse. A pessary is
an object that is placed into the vagina to support the anterior, posterior, and apical vaginal walls.
There is evidence that pessaries have been used as early as the 5th century BC (21). A wide
variety of items and materials have all been used as pessaries in the past, such as wood, rags, and
even various fruits. Today pessaries are most commonly made of latex rubber, silicone, or
acrylic. Pessaries come in multiple shapes and sizes. They are available by prescription after
examination and fitting by a health care provider. Pessaries are very useful in those patients who
564 Kwon and Sand

cannot or choose not to undergo surgery. They can also play a vital role in delaying surgery to a
more favorable time, such as in a young woman who has not yet completed her childbearing.
Fitting a pessary is an educated trial and error process. Various types of pessaries are
available for use (Fig. 1). A digital vaginal examination allows one to have a general idea of the
length and depth of the vagina. It is often easiest to begin with the largest pessary that can be
accommodated in the vaginal introitus but does not protrude from the orifice. If a woman has
signs of urogenital atrophy, using a local estrogen cream nightly for a 2-week period prior to
attempting a pessary fitting may improve her comfort level during the fitting. The pessary should
be moistened with water or a small amount of lubricant to decrease the friction on insertion.
Once it has been inserted into the vagina, the pessary should not cause discomfort to the patient
and should not be extruded on Valsalva. If this is successful, the patient should stand and walk
around the exam room. She should cough, Valsalva, and bend down with the pessary in place. If
the pessary is not expelled by these efforts and is not uncomfortable for the patient, then the
fitting is successful. If the pessary falls out, it is either too small or of an improper shape to
maintain support in the vagina. If the pessary causes discomfort or irritation, it is too large. If the
pessary causes urinary obstruction or retention, it is also too large. A different size or an
alternative shape can be tried.

Figure 1 Various types of pessaries. A, Hodge with knob (silicone); B, Risser (silicone); C Smith
(silicone); D Hodge with support (silicone); E Hodge (silicone); F Tandem cube (silicone); G Cube
(silicone); H Hodge with support knob (silicone); I Regula (silicone); J Gehrung (silicone); K Gehrung
with knob (silicone); L Gellhorn 95% rigid (silicone); M Gellhorn flexible (silicone); N Gellhorn rigid
(acrylic); O Ring with support (silicone); P Ring with knob (silicone); Q Ring with support þ knob
(silicone); R Shaatz (silicone); S Incontinence dish with support (silicone); T Ring incontinence (silicone);
U Ring (silicone); V Incontinence dish (silicone); W Inflatoball (latex); X Donut (silicone).
 Advanced Anterior Vaginal Wall Prolapse 565

Ideally, the patient should be able to remove and insert the pessary on the daily basis. If she
is unable to do this herself, she should come back to the office at 2- to 3-month intervals for
removal and cleansing, although this interval should be tailored for the individual patient and the
pessary type. The vagina should be systematically inspected for any abrasions or pressure ulcers.
The pessary should be cleansed with regular soap and water. Regular use of a vaginal estrogen
cream is advocated if there is no contraindication in the postmenopausal patient, especially if the
pessary is not removed on a daily basis. If estrogen is contraindicated in the patient, Trimo-San
(Milex Products, Inc., Chicago, IL) vaginal gel is helpful in maintaining proper vaginal pH to
prevent bacterial vaginosis.
Pessaries can be associated with complications as well. Abrasions or ulcers of the vagina
can cause vaginal bleeding. The pessary should be removed and the vagina carefully inspected.
Application of silver nitrate can help stop vaginal bleeding in ulcerated areas. The pessary
should not be replaced into the vagina until the ulcer has healed. Vaginal estrogen cream can be
used to help heal and prevent future ulcerations. Vaginal discharge and odor may come from
bacterial overgrowth. More frequent removal and cleansing usually resolves the problem.
Recurrent ulceration and persistent discharge are common reasons why patients discontinue
pessary use. Pessaries may also become less supportive as prolapse worsens, or the patient may
develop urinary incontinence, recurrent infections, vaginal pain, or rectal pressure.
Incarceration of the pessary may also occur, usually because of neglect and failure to have
removal performed for a prolonged period of time. Using topical estrogen cream regularly prior
to attempted removal can often be helpful. In some cases, patients may need regional or general
anesthesia to allow for adequate pelvic relaxation to permit removal. In rare cases, a fistula can
result, usually in cases of extreme neglect with a rigid pessary.
Poor posterior introital support usually requires the use of a Gellhorn or cube pessary.
Specially designed pessaries may also be useful for concurrent stress incontinence. Although it is
truly a trial-and-error process, finding a correctly fitting pessary provides an alternative to
surgical correction for some patients with vaginal prolapse, and can have great impact on their
quality of life. With an increasingly aging population, pessaries will continue to be useful in
managing pelvic organ prolapse.

IV. SURGICAL REPAIR TECHNIQUES

Two different surgical approaches to anterior vaginal support defects are available. The anterior
colporrhaphy aims to excise or plicate weakened or redundant endopelvic connective tissue via a
vaginal approach. Vaginal tissue can also be excised abdominally to repair a cystocele (22). An
alternative procedure is the paravaginal repair. This procedure aims to reattach isolated lateral
defects between the endopelvic connective tissue and smooth muscle of the anterior lateral
vaginal wall to the arcus tendineus fasciae pelvis.

A. Anterior Colporrhaphy
The anterior colporrhaphy aims to plicate the vaginal muscularis and adventitia underlying the
bladder to reduce redundancy and protrusion of the bladder and vaginal wall into the vagina and
beyond (Fig. 2A – G). The patient is placed in the dorsal lithotomy position. The vagina and
perineum should be sterilely prepped and draped. A Foley catheter should be inserted to drain
the bladder as well as to assist in identification of the bladder neck. Hydrodissection using sterile
saline with or without vasopressin can facilitate identification of the plane of dissection and
decrease bleeding.
Figure 2 Technique of anterior colporrhaphy. (A) Dissection of the vaginal epithelium from the
underlying endopelvic connective tissue. (B) Cutting epithelium in the midline to expose endopelvic
connective tissue overlying bladder. (C) Sharp dissection of the endopelvic connective tissue off of the
vaginal epithelium flaps. Care should be taken to preserve the endopelvic connective tissue overlying
the bladder by dissecting this tissue deep enough off of the vaginal flaps to reach the relatively avascular
plane just beneath the vaginal epithelium. Bracing the tissue behind the scissor tips helps prevent cutting
through the vaginal epithelium. (D) Once a plane has been established, blunt dissection can also be
performed using a gauze sponge. Again, bracing the tissue behind the traction point can help prevent
tearing. (continued )
 Advanced Anterior Vaginal Wall Prolapse 567

Figure 2 (continued ) (E) Plication of redundant endopelvic connective tissue using no. 0 delayed-
absorbable vertical mattress suture at the lateral borders of the mobilized endopelvic connective tissue.
(F) Tying the sutures in the midline corrects the redundancy, repairing the cystocele. The excess vaginal
epithelium is trimmed. (G) The trimmed vaginal epithelium edges are approximated in the midline using
interrupted or a running locked suture of no. 2-0 delayed-absorbable suture to complete the anterior
colporrhaphy.
568 Kwon and Sand

If the anterior colporrhaphy is being performed concomitantly with a vaginal hyst-

erectomy, the anterior cut edge of the vaginal apex should be grasped to the right and left of
midline with Allis clamps, Kocher clamps or the hooks of a self-retaining vulvar retractor. If the
patient has previously had a hysterectomy or is preserving her uterus, the most inferior edge of
the anterior vagina or the anterior fornix should be grasped with Allis clamps lateral to the
midline. A horizontal incision should be made between these clamps. Using Metzenbaum
scissors, a vertical T-shaped incision should then be extended from the midline of the vagina up
to the level of the urethrovesical junction. Allis clamps, Kocher clamps, or hooks should be
placed along these cut vertical edges and held out laterally. The endopelvic connective tissue is
then sharply and bluntly dissected off of these vaginal flaps out laterally, taking care to preserve
as much endopelvic connective tissue on the bladder. The lateral extent of the dissection should
be the medial borders of the descending pubic rami bilaterally.
Vertical mattress sutures of delayed absorbable or permanent sutures are placed along the
lateral edges of the endopelvic connective tissue and tied to plicate the tissues in the midline. The
importance of preserving as much endopelvic connective tissue upon the bladder becomes
apparent during this step, as having adequate tissue prevents intravesical sutures and adds to the
strength of the repair. These sutures also should not be placed on the vaginal tissue.
Alternatively, specific defects in the endopelvic connective tissue may be identified during
the initial dissection. These may be directly repaired in a site-specific fashion in the
midline, laterally, or transversely with interrupted or running delayed absorbable sutures. When
the anterior endopelvic connective tissue has been supported, the vaginal epithelium should be
trimmed and closed using a running, locked, absorbable suture.

B. Paravaginal Defect Repair

Richardson et al. popularized the idea of the site-specific defect repair for the anterior
compartment (3). Using careful physical examination, isolated defects in the connective tissue
supports of the anterior quadrant of the pelvis can be identified. Lateral defects were most
commonly detected, and are described as unilateral or bilateral defects in the fascia laterally or
near its attachment to the levator insertion at the lower margin of the superior pubic ramus. The
fibrous connections forming the lateral attachment of the vagina to the arcus tendineous fasciae
pelvis (ATFP) may have torn, leading to a left, right, or bilateral paravaginal defect. Classically
these are described as maintaining the ruggae in the anterior vaginal wall, as stretching or
thinning of the tissue is not the etiology for the relaxation. In theory, if the lateral attachments are
torn, plication of redundant tissue in the midline could actually exacerbate the problem by
placing greater medial tension on the already compromised paravaginal separation from the
arcus tendineus. For these deficiencies, a paravaginal repair is advocated. From the level of
the urethrovesical junction to near the vaginal apex, the vaginal muscularis and adventitia are
reapproximated to the ATFP. This repair can be performed via a retropubic abdominal or a
vaginal approach (23). One must also be cautious not to neglect a concurrent central defect as
this may be worsened by paravaginal lateral tensioning of the anterior vaginal wall. This is often
missed at the time of surgery when paravaginal sutures may be placed medial to the anterior
lateral vaginal sulcus, hiding this defect by stretching out the anterior vaginal wall without
correcting the central defect in the endopelvic connective tissue.

C. Abdominal Paravaginal Repair

Abdominally, a Pfannensteil skin incision can be used to access the retropubic space. After the
rectus fascia is incised sharply, the rectus muscles are separated laterally. The space of Retzius is
 Advanced Anterior Vaginal Wall Prolapse 569

then accessed medial to the pubic ramus on both sides. The loose areolar tissue should be cleared
from the pubic bone using blunt dissection. The arcus tendineous fasciae pelvis extends from the
posterior aspect of the pubis (at the level of the pubic tubercle) to the ischial spine. The bladder
and the urethra may be gently retracted medially using a “daisy sponge,” made of several folded
4
4 sponges placed in a ring forcep. Care should be taken not to reflect the bladder off the
anterior vaginal surface, as this may disrupt its venous supply from the inferior vesical plexus
and cause exuberant bleeding. The ATFP is easiest to identify at its insertion at the back of the
pubic bone. Its course should be followed as it extends to the ischial spine.
Similar to performing an abdominal retropubic urethropexy, the operator’s nondominant
hand is placed into the vagina and used to elevate the periurethral and perivesical tissue. Using
nonabsorbable sutures, a series of interrupted or “figure of eight” sutures are placed along the
length of the ATFP to the detached vaginal muscularis and adventitia at the anterior lateral
vaginal sulcus from the level of the urethrovesical junction to the ischial spine. Three to six
sutures per side will likely be needed to reapproximate the length of the defect. Fewer sutures are
needed if a Burch retropubic urethropexy is performed concomitantly. Bleeding that may be
encountered from the venous plexuses of the vagina is usually controlled after tying the sutures.

D. Vaginal Paravaginal Repair

When using the vaginal approach to this repair, the goal continues to be reapproximation of the
detached vaginal muscularis and adventitia laterally to the arcus tendineous. A vaginal approach
requires more technical skill than the open retropubic approach. Patient selection is important in
choosing this procedure, as a narrow pubic arch will limit exposure to the retropubic space,
making an open retropubic approach a better choice in these patients.
The patient should be placed in dorsal lithotomy position and the bladder drained prior to
starting the procedure. Marking sutures are placed through the vaginal epithelium at the level of
the urethrovesical junction 1 cm to the right and left of midline. If the patient has had a
previous hysterectomy, marking sutures are placed at the vaginal apices. If a concomitant
vaginal hysterectomy and culdoplasty are performed, the culdoplasty sutures should be left
untied until all paravaginal sutures have been placed. Allis clamps should be placed at the lateral
edges of the vaginal apex. If a concomitant central defect is to be repaired or a sling placed, a
midline incision should be made in the vaginal epithelium up to the level of the urethrovesical
junction. The endopelvic connective tissue should be dissected off of the vaginal epithelium
sharply to the medial border of the descending pubic ramus laterally. Metzenbaum scissors
are placed against the pubic ramus at the level of the urethrovesical junction, and the scissors are
pushed toward the ipsilateral shoulder to enter the space of Retzius. The index finger can then be
used to extend this space along the inferior pubic ramus toward the ischial spine. Alternatively, if
only a paravaginal or bilateral paravaginal defect exists, the initial incision may be made in the
anterior lateral vaginal sulci. This allows for the vaginal sutures to be placed in an undissected
vaginal wall and limits blood loss. The arcus tendineous fascia pelvis can then be followed from
the back of the pubic ramus to the ischial spine by retracting the bladder and urethra medially
using a Briesky-Navratil retractor. Allis clamps or retractor hooks can be placed laterally to
retract the vaginal epithelium. Using permanent suture, the first stitch should be placed just
anterior to the ischial spine through the arcus tendineous (or through the obturator internus fascia
if the arcus tendineous is too attenuated). The suture line is started here, as traction on this first
stitch can facilitate placement of the subsequent sutures. A series of three to six sutures should
be placed and tagged sequentially, starting from the ischial spine and moving anteriorly along
the arcus tendineous to the level of the urethrovesical junction, leaving the needles intact on the
570 Kwon and Sand

sutures. It is helpful to have a marking system on the series of tagging clamps (such as small
pieces of tape or placing sutures into a horse’s comb) so the sutures do not become disordered.
Beginning with the most distal suture, the needle is placed through the endopelvic
connective tissue at the level of the urethrovesical junction and then through the undersurface of
the vaginal epithelium at the level of the previously placed distal marking suture. This sequence
is continued posteriorly, with the most proximal suture anterior to the ischial spine being placed
through the undersurface of the vaginal epithelium at the level of the apex marking sutures. Care
should be taken when placing the sutures through the medial vaginal edge that an adequate
margin is left on the cut medial edge to allow for subsequent vaginal closure. The sutures should
be left untied. The process is repeated on the other side. The stitches are then tied sequentially in
a distal to proximal direction, alternating from one side to the other. If a central defect exists,
traditional anterior colporrhaphy sutures can then be placed to plicate the redundant endopelvic
connective tissue. The vaginal epithelial flaps can be trimmed once all sutures have been placed
and tied, and can be closed using a running suture of a delayed absorbable suture.

E. Adjunctive Materials to Enhance Long-Term Success of the Repair

The ideal biomaterial, natural or man-made, would be able to perform, augment, or replace a
natural function (24). The ideal adjunctive material must be mechanically strong, cause no
inflammatory reaction, be sterilizable, be resistant to modification by the body tissue, and be
convenient to use. There currently exists no adjunctive material that meets all of these criteria.
General surgeons first popularized the use of synthetic biomaterials by applying them to the
repair of abdominal wall hernias. This approach has also been used in the repair of anterior
vaginal wall prolapse, although there is a lack of data that prove their efficacy. In 1996, Julian
published results on using Marlex polypropylene mesh in the repair of recurrent vaginal prolapse
(25). A trapezoidal piece of synthetic mesh was sewn from the urethrovesical junction anteriorly
to the vaginal apex posteriorly and to the levator fascia laterally. None of the patients who
received the mesh had recurrence of anterior vaginal wall prolapse, although 25% of these
patients had mesh-related complications postoperatively. This approach was not advocated as a
primary procedure for the repair of anterior vaginal wall prolapse; rather, it was recommended
only for those patients with two or more reparative failures.
Other observational studies have subsequently been published in the literature describing
the usually successful experience of using a synthetic mesh, most often Marlex polypropylene,
in reducing recurrence of anterior vaginal wall prolapse (26 –29). These studies are most often
limited by their small numbers of patients and lack of long-term follow-up.
Many physicians have begun using xenografts and allografts to enhance outcomes
following anterior vaginal wall repairs. Theoretically these materials have the advantage of
possibly being better tolerated by the vagina than synthetic material, although they too have been
associated with minor erosions. These materials are quite expensive, however, and there is no
published literature proving their benefits or efficacy.
One prospective randomized controlled trial was performed using polyglactin 910 mesh to
prevent recurrent anterior vaginal wall prolapse by Sand et al. (30). This mesh is absorbable, and
instead of being used as an overlay, it was used as a bulking material folded into the anterior
colporrhaphy stitches. The approach is thought to enhance scarring just anterior to the suture
line, providing greater protection to an area potentially more vulnerable to direct intra-
abdominal downward forces. Patients with anterior vaginal wall prolapse to or beyond the
hymenal ring were eligible for the study. At 1 year postoperatively, 30 of 70 (43%) women who
did not receive mesh had recurrent anterior vaginal wall prolapse to the midvaginal plane versus
18 of 73 (25%) women who did receive polyglactin 910 mesh (P ¼ 0.02). Prolapse to the
 Advanced Anterior Vaginal Wall Prolapse 571

hymenal ring occurred in 8 of 70 (11.4%) controls and in 2 of 73 (2.7%) women with mesh
(P ¼ 0.04). No patients had recurrent prolapse past the hymenal ring.
One randomized study of three different treatments of anterior vaginal wall prolapse
has been performed. Weber et al. compared the effects of “standard anterior colporrhaphy”
(muscularis plication in the midline without tension), versus “ultralateral anterior colporrhaphy”
(dissection laterally to the limits of the pubic rami with plication of the muscularis in the midline
under tension), versus “standard anterior colporrhaphy plus mesh” (polyglactin 910 mesh placed
over the plication and anchored at the lateral limits of the dissection). Over 50% of the women
enrolled in their study had stage III anterior vaginal wall prolapse or greater. At 1 year, 10 of 33
patients (30%) of the standard anterior colporrhaphy group had satisfactory or optimal anatomic
outcome, versus 11 of 26 (42%) of the standard plus mesh group, versus 11 of 24 (46%) of the
ultralateral anterior colporrhaphy group. No significant differences among the three different
techniques were detected, although the sample sizes for each group were small, allowing for the
possibility of type II error in the conclusions. The authors acknowledged that although the
percentages for “successful” anatomic outcomes were relatively low, all three techniques
provided excellent symptomatic relief from vaginal protrusion with no clinically significant
differences among the groups (31).

F. Effect of Concomitant Operations on Anterior Compartment Prolapse

There also exists evidence that concomitant procedures at the time of anterior vaginal wall prolapse
repair may affect long-term outcomes. Kohli et al. reported a significantly higher incidence of
recurrent anterior prolapse if concomitant needle bladder neck suspension was performed with an
anterior colporrhaphy (32). This effect was also seen in a randomized, prospective comparison of
needle colposuspension versus endopelvic fascia plication in women undergoing vaginal
reconstruction for stage III or IV pelvic organ prolapse (33). Especially when combined with a
sacrospinous vaginal vault suspension, those patients randomized to receive concomitant needle
suspension developed a relatively high incidence of early, advanced, recurrent, anterior vaginal
prolapse. The needle suspension also increased the short-term complications without providing
additional protection from the development of de novo genuine stress incontinence.
Sacrospinous vaginal vault suspension has also been associated with recurrent anterior
segment prolapse theoretically because of the exposure of the anterior segment to increased
pressure caused by the fixed retroversion of the vagina (34,35). Conversely, concomitant
suburethral slings at the time of reconstructive vaginal surgery have been shown to significantly
reduce the recurrence of anterior vaginal wall prolapse. The presence of any type of suburethral
sling was associated with a 54.8% reduction in anterior prolapse recurrence (36). This finding
should be taken into consideration when planning a surgical repair for the woman with
concurrent prolapse and genuine stress incontinence. The same group also showed a
significantly higher long-term risk of anterior vaginal wall prolapse associated with a traditional
posterior approach to the sacrospinous vaginal vault suspension, whereas an anterior approach to
the sacrospinous vaginal vault suspension (37) was associated with no such risk.
The available literature on repair of the anterior vaginal wall is surprisingly sparse, with
the majority of these publications usually being descriptive outcome studies. Our ability to
surgically correct this condition can be enhanced if we can predict those for whom progression
or recurrence of their prolapse is most likely. As our understanding of the etiology of pelvic
organ prolapse improves, we will improve our treatment of the condition and may ultimately be
better able to prevent its occurrence.
572 Kwon and Sand

REFERENCES

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repair. Obstet Gynecol 1997; 89:311– 318.
2. White GR. An anatomic operation for the cure of cystocele. Am J Obstet Dis Women Child 1912;
65:286– 290.
3. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;
126:568– 573.
4. 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 1992; 166(6 Pt 1):1764 – 1768.
5. Bump RC, Mattiasson A, Bo K, Brubraker LP, DeLancey JO, Klarskov P, Shull BL, Smith AR. The
standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J
Obstet Gynecol 1996; 175:10 – 17.
6. Gill EJ, Hurt WG. Pathophysiology of pelvic organ prolapse. Obstet Gynecol Clin North Am 1998;
25(4):757– 769.
7. Rosenzweig BA, Bhatia NN. Temporal separation of cough-induced urethral and bladder pressure
spikes in women with urinary incontinence. Urology 1992; 39(2):165– 168.
8. Prockop DJ, Kuivaniemi H, Tromp G. Inherited disorders of connective tissue. In: Fauci A,
Braunwald E, Isselbach K, Wilson J, Martin J, Kasper D, et al. Harrison’s Principles of Internal
Medicine. New York: McGraw-Hill, 1998.
9. Mays PK, McAnilty RJ, Campa JS, Laurent GJ. Age-related changes in collagen synthesis and
degradation in rat tissue. Importance of degradation of newly synthesized collagen in regulation of
collagen production. Biochem J 1991; 276:307 –313.
10. Falconer C, Ekman-Ordeberg G, Ulmsten U. Changes in paraurethral connective tissue at menopause
are counteracted by estrogen. Maturitas 1996; 24:197 –204.
11. Norton P, Boyd C, Deak S. Collagen synthesis in women with genital prolapse or stress urinary
incontinence. Neurourol Urodyn 1992; 11:300 – 301.
12. Vogel KG, Paulsson M, Heinegard D. Specific inhibition of type I and type II collagen fibrillogenesis
by the small proteoglycan of tendon. Biochem J 1984; 223:587– 597.
13. Jorgensen LN, Kallehave F, Christensen E, Siana JE, Gottrup F. Less collagen production in smokers.
Surgery 1998; 123:450 – 455.
14. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: a
neurophysiological study. Br J Obstet Gynaecol. 1990; 97(9):770– 779.
15. Rockner G, Jonasson A, Olund A. The effect of mediolateral episiotomy at delivery on pelvic floor
muscle strength evaluated with vaginal cones. Acta Obstet Gynecol Scand 1991; 70:51 – 54.
16. Klein MC, Gauthier RJ, Robbins JM, Kaczoroswki J, Jorgensen SH, Franco ED, Johnson B,
Waghorn K, Gelfand MM, Guralnick MS. Relationship of episiotomy to perineal trauma
and morbidity, sexual dysfunction, and pelvic floor relaxation. Am J Obstet Gynecol 1994;
171:591– 598.
17. Loret de Mola JR, Carpenter SE. Management of genital prolapse in neonates and young women.
Obstet Gynecol Surv 1996; 51:253– 260.
18. Makinen J, Soderstrom KO, Kiilholma P, Hirvonen T. Histological changes in the vaginal con-
nective tissue of patients with and without uterine prolapse. Arch Gynecol 1986; 239(1):
17 – 20.
19. Norton PA, Baker JE, Sharp HC, Warenski JC. Genitourinary prolapse and joint hypermobility in
women. Obstet Gynecol 1995; 85(2):225– 228.
20. Bump RC, McClish DK. Cigarette smoking and urinary incontinence in women. Am J Obstet
Gynecol 1992; 167:1213 – 1218.
21. Miller DS. Contemporary use of the pessary. In: Sciarra JJ, ed. Gynecology and Obstetrics. Vol. 1.
Philadelphia: J.B. Lippincott, 1995:1– 12.
22. Macer GA. Transabdominal repair of cystocele, a 20 year experience, compared with the traditional
vaginal approach. Am J Obstet Gynecol 1978; 131:203 –207.
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23. 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 Obstet Gynecol 1994;
171:1429– 1439.
24. Cervigni M, Natale F. The use of synthetics in the treatment of pelvic organ prolapse. Curr Opin Urol
2001; 11:429 –435.
25. Julian TM. The efficacy of Marlex mesh in the repair of severe, recurrent vaginal prolapse of the
anterior midvaginal wall. Am J Obstet Gynecol 1996; 175:1472– 1475.
26. Nicita G. A new operation for genitourinary prolapse. J Urol 1998; 160:741– 745.
27. Flood CG, Drutz HP, Waja L. Anterior colporrhaphy reinforced with Marlex mesh for the treatment
of cystoceles. Int Urogynecol J 1998; 9:200– 204.
28. Migliara R, De Angelis M, Madeddu G, Verdacchi T. Tension-free vaginal mesh repair for anterior
vaginal wall prolapse. Eur Urol 2000; 38:151– 155.
29. Canepa G, Ricciotti G, Introini C, Vigliercio G, Puppo P. Horseshoe-shaped Marlex mesh for the
treatment of pelvic floor prolapse. Eur Urol 2000; 39(suppl 2):23– 26.
30. Sand PK, Koduri S, Lobel RW, Winkler HA, Tomezsko J, Culligan PJ, Goldberg R. Prospective
randomized trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Obstet
Gynecol 2001; 184:1357 – 1364.
31. Weber AM, Walters MD, Piedmont MR, Ballard LA. Anterior colporrhaphy: a randomized trial of
three surgical techniques. Am J Obstet Gynecol 2001; 185:1299 – 1306.
32. Kohli N, Sze EHM, Roat TW, Karram MM. Incidence of recurrent cystocele after anterior
colporrhaphy with and without concomitant transvaginal needle suspension. Am J Obstet Gynecol
1996; 175:1476 – 1482.
33. Bump RC, Hurt WG, Theofrastous JP, Addison WA, Fantl JA, Wyman JF, McClish DK. Randomized
prospective comparison of needle colposuspension versus endopelvic fascia plication for potential
stress incontinence prophylaxis in women undergoing vaginal reconstruction for stage II or IV pelvic
organ prolapse. Am J Obstet Gynecol 1996; 175:326 – 333.
34. Bonney V. The principles that should underlie all operations for prolapse. J Obstet Gynaecol Br
Commonw 1934; 41:669– 683.
35. Holley RL, Varner RE, Gleason BP, Apffel LA, Scott S. Recurrent pelvic support defects after
sacrospinous ligament fixation for vaginal vault prolapse. J Am Coll Surg 1995; 180:444 – 448.
36. Goldberg RP, Koduri S, Lobel RW, Culligan PJ, Tomezsko JE, Winkler HA, Sand PK. Protective
effect of suburethral slings on postoperative cystocele recurrence after reconstructive pelvic
operation. Am J Obstet Gynecol 2001; 185:1307 –1313.
37. Winkler HA, Tomeszko JE, Sand PK. Anterior sacrospinous vaginal vault suspension for prolapse.
Obstet Gynecol 2000; 95:612 – 615.
41
Anterior Vaginal Wall Prolapse:
Mild/Moderate Cystoceles
Harriette M. Scarpero and Victor W. Nitti
New York University School of Medicine, New York, U.S.A.

I. INTRODUCTION

Pelvic organ prolapse is a common disorder affecting millions of women worldwide. The
lifetime risk of undergoing surgery for prolapse by age 80 is 11.1% (1). Correction of anterior
compartment relaxation, specifically cystocele and cystourethrocele, comprises a significant
proportion of the procedures done for prolapse. Within a large cohort of HMO participants,
384 patients underwent one or more surgeries for correction of prolapse. Of these, 154
(40.1%) were performed on the anterior compartment. Another 60 (15.6%) procedures were
done for correction of combined anterior and posterior compartment prolapse.
Anterior vaginal wall prolapse may involve the urethra, manifesting as urethral hypermo-
bility and/or the bladder, cystocele. In many cases, small and moderate degrees of anterior vagi-
nal wall prolapse are asymptomatic and do not require treatment. However, cystoceles may be
associated with pelvic discomfort, sexual dysfunction, recurrent urinary tract infections, diffi-
culty voiding, difficulty defecating, or incontinence. Stress urinary incontinence may occur as
part of the clinical condition of prolapse associated with urethral hypermobility and lack of ure-
thral support. It may also be associated with intrinsic sphincter deficiency. Patients with cysto-
cele can also experience urinary incontinence secondary to detrusor instability which may, or
may not, be related to the cystocele itself (2). Anterior vaginal wall prolapse is often associated
with prolapse of other vaginal compartments: apical (uterine or enterocele) and posterior (rec-
tocele or posterior enterocele).
The annual direct cost to society of pelvic organ prolapse procedures is significant. In
1997 the direct costs were $1012 million, with $74.2 million (7%) spent on the correction
of cystoceles (3). An additional $279 million (28%) were spent on combined cystocele and
rectocele repair. As the population ages and life expectancy increases, the number of cases
performed for pelvic organ prolapse will certainly increase, translating into an even greater
cost burden on society. A better understanding of the condition, its causes, and how to diagnose
it accurately will improve the cost-effectiveness of our treatment and hopefully patient
satisfaction.
575
576 Scarpero and Nitti

II. ANATOMY

The anterior compartment of the female pelvis is composed of the bladder and urethra. Prolapse
of this compartment may manifest as varying degrees of cystocele, urethral hypermobility, or
intrinsic sphincteric deficiency (4). These defects may be seen alone or, more commonly, in
combination with each other or with defects of the apical compartment (enterocele, uterine pro-
lapse) or posterior compartment (rectocele, posterior enterocele). Any discussion of anterior
compartment prolapse requires a basic understanding of its supporting anatomy.
The pelvic organs are suspended over the pelvic floor by the endopelvic fascia (EPF). This
fascia is not like the tough ligamentous fascia of the rectus abdominous. Rather, it is a thinner
condensation of smooth muscle fibers, blood vessels, connective tissue, and nerves; yet it is
important to the stability of the pelvic organs and support of the vagina in particular (5). It is
the first mechanism of defense against forces causing genital prolapse. Also of paramount
importance to pelvic support are the levator ani muscles, which constrict the lumen of the vagina
to prevent prolapse and produce a solid support on which the organs can rest. The levators are
intimately connected to the EPF by virtue of their fascial covering, which merges into the adja-
cent EPF. A third source of support is a flap valve mechanism which results from the first two
anatomic arrangements (6). In the flap valve mechanism, as abdominal pressure is placed on the
suspended upper vagina, which has a horizontal axis in its natural state, the force pins the vagina
against the levator muscles rather than everting it (6).
Delancey described three levels of vaginal support (Fig. 1) (6). The upper vagina, level 1,
is supported by the parametrium, a term given to the EPF that attaches the vagina to the pelvic

Figure 1 Levels of pelvic organ support as described by DeLancey. In level I the paracolpium suspends
the vagina from the lateral pelvic walls. Fibers from level I extend vertically and posteriorly towards the
sacrum. In level II the vagina is attached to the arcus tendineus fasciae pelvis and support fascia of the
levator ani. [From Ref. (6).]
 Anterior Vaginal Wall Prolapse 577

sidewall in that region. The cardinal and uterosacral ligaments are contained within the parame-
trium and support the uterus, cervix, and upper vagina. The cardinal ligaments, which primarily
support the cervix, also provide support for the bladder base as it fuses with the EPF in
that region, known as the pubocervical fascia. In cases of uterine prolapse, the cardinal ligament
is lax, displacing the pubocervical fascia laterally and predisposing to cystocele formation. At
midvagina, level 2, the EPF attaches to the vagina more laterally and stretches it transversely
between the bladder and rectum. Level 2 EPF is termed the paracolpium. As the EPF approaches
the bladder and urethra, it splits into two sheaths and envelops both the abdominal side and vagi-
nal side of these structures. The abdominal side is still referred to as endopelvic fascia while the
vaginal side is termed the periurethral or pubocervical fascia. Other names for condensations of
EPF may be found in the literature. For example, the band or hammock of fascial support that
extends from the arcus tendineus has been described as the pubovesical ligament (7) and the ure-
thropelvic ligament in the urological literature (7,8). More proximally, where it supports the
bladder, this condensation has been called the vesicopelvic ligament. Anteriorly, a condensation
of (levator fascia/EPF) forms the pubourethral ligament, which is a pair of dense connective tis-
sue bands. The pubourethral ligament arises from the vaginal wall and periurethral tissue and is
attached to the undersurface of the symphysis pubis (6,9). The distal vagina, level III, is securely
fixed by direct attachment to adjacent structures. It is not subject to the same risk of laxity as
levels I and II.
The support of the anterior vaginal compartment (bladder and urethra) is dependent on the
integrity of the EPF and its attachments to the pelvic sidewall at the arcus tendineus (Fig. 2).
Breaks in the integrity of these structures produce defects that result in particular forms of cysto-
cele: central and lateral (Fig. 3) (10). A central defect occurs by an attenuation or tear in the
enveloping pubocervical fascia between bladder and vaginal wall. A lateral defect occurs
when the EPF separates from its side wall attachment at the arcus tendinevs (11). Lateral defects

Figure 2 Retropubic view of bladder neck and urethral support drawn from cadaver dissections
according to DeLancey. The pubovesical muscle (PVM) can be seen going from the vesical neck (VN)
to the arcus tendineus fasciae pelvis (ATFP) and running over the paraurethral vascular plexus (PVP).
ATLA, arcus tendineus levator ani; b, bladder; IS, ischial spine; LA, levator ani muscles; OIM&F,
obturator internus muscle and fascia; PS, pubic symphysis; U, urethra. [From Ref. (7).]
578 Scarpero and Nitti

Figure 3 (A) Central defect cystocele. Note the break in the pubocervical fascia causing central
herniation (Normal support shown in inset). (B) Lateral defect cystocele. Note the laxity or break in the
attachment of the endopelvic fascia to the arcus tendineus fasciae. [From Ref. (10).]

are not thought to be caused by attenuation of the EPF at this area, only true separation (12).
Separation may occur on one or both sides. Isolated lateral defects are fairly common while
isolated central defects comprise ,10% of cystoceles (13). Combinations of central and lateral
fascial defects are very common especially in larger symptomatic cystoceles.

III. GRADING SYSTEMS

This chapter addresses mild to moderate cystoceles specifically. The designation of mild or
moderate is subjective and must be translated into an accepted grading scale. Several grading
systems have been used for cystocele and prolapse in general. One common system is the half-
way system described by Baden and Walker, which uses the hymen as a reference point (Table 1)
(14). Although this system is widely used, it has been criticized for lacking reproducibility and
specificity (15).
An attempt to standardize the terminology of female pelvic organ prolapse was adopted by
the International Continence Society (ICS) and other groups in 1995 (16). They recommended
 Anterior Vaginal Wall Prolapse 579

Table 1 Baden and Walker Grading System

Grade Definition

0 Normal position for bladder

I Descent halfway to the hymen
II Descent to the hymen
III Descent halfway past the hymen
IV Maximum possible descent for bladder

that terms such as cystocele, rectocele, enterocele, or urethrovesical junction be avoided because
these terms imply an unrealistic certainty as to what structures inhabit the vaginal bulge. This
concern is particularly appropriate in women who have undergone prior prolapse surgery. In
the ICS grading system, Pelvic Organ Prolapse Quantification (POP-Q), the hymenal ring is
the fixed anatomic landmark of reference. Six sites of the vagina and perineal body are measured
in centimeters from the hymen. Two points of reference are given to the anterior aspect, pos-
terior, and apical vagina. Measurement of the genital hiatus, perineal body, and total vaginal
length are also included (Fig. 4). The intraobserver and interobserver reliability of this system
has been shown to be very good, and it allows for a very accurate measurement of distances
(17). The disadvantage of this system is that it is cumbersome and better suited for evaluating
radiographic images of the pelvic floor than performing in vivo measurements. In clinical prac-
tice this system seems particularly useful when describing surgical outcomes. For example, it is
much more informative to describe the leading edge of a prolapse as 2 cm inside the hymenal
ring as compared to a preoperative finding of 0.5 cm outside the hymenal ring, instead of
describing the same situation as a prolapse reduction from grade 3 to grade 1.

IV. PREOPERATIVE EVALUATION

It is difficult to determine whether a patient’s symptoms are directly caused by the cystocele
alone. Shull has advocated pelvic organ support must be related to pelvic organ function, and
thus every specific defect should be repaired to give the best opportunity for resolution of symp-
toms and reduction of the risk of new defects (18). If this is true, and this can only be determined
by defining a clear set of outcome parameters that would include certain visceral functions, then
it would be argued that any degree of prolapse, even small or asymptomatic, is clinically signifi-
cant and should be corrected. Additionally, in patients with a cystocele, symptoms of stress urin-
ary incontinence cannot be attributed solely to it. Urethral dysfunction from intrinsic sphincteric
incontinence may coexist (2,4).
A careful physical examination is necessary in evaluating patients with pelvic prolapse.
We prefer to examine the patient with a full bladder in the dorsal lithotomy position. The vaginal
mucosa is first inspected for any signs of mucosal atrophy. Spreading the labia for better
visualization of the urethral meatus, the patient is asked to cough and Valsalva to test for stress
incontinence, urethral mobility, and anterior vaginal wall prolapse. The lower blade of a Graves
speculum is used to retract the posterior vaginal wall and gain better visualization of the anterior
vaginal wall. The patient is asked to Valsalva and any descensus of the anterior vaginal wall is
graded. Although not pathognomonic, central defects classically produce a bulge in the anterior
vaginal wall that causes disappearance of the normal vaginal rugae. In postmenopausal women
with significant atrophy of the vaginal tissues, the rugae may be absent from lack of
 580
Scarpero and Nitti

Figure 4 (A) Six sites (points Aa, Ba, C, D, Bp, and Ap), genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) used for pelvic organ support
quantification. Point Aa ¼ point located in the midline of the anterior vaginal wall 3 cm proximal to the external urethral meatus. Point Ba ¼ point that
represents the most distal (dependent) position on any part of the upper anterior vaginal wall. Point C ¼ point that represents either the most distal (dependent)
edge of the cervix or leading edge of the vaginal cuff after hysterectomy. Point D ¼ point that represents the location of the posterior fornix in a woman with a
cervix. It is omitted if patient has had a hysterectomy. Point Bp ¼ point that represents the most distal (dependent) postion of any part of the upper posterior
vaginal wall from the vaginal cuff or posterior vaginal fornix to point Ap. (23 cm by definition if no prolapse). Point Ap ¼ point located in the midline of the
posterior vaginal wall 3 cm proximal to the hymen. (range of position of point Ap relative to hymen is 23 to þ3 cm by definition). Genital
hiatus ¼ measurement of distance in cm from middle of the external urethral meatus to the posterior midline hymen. Perineal body ¼ measurement of distance
in cm from the posterior margin of the genital hiatus to the midanal opening. Total vaginal length ¼ greatest depth of the vagina in cm when point C or D is
reduced to its full normal position (eccentric elongation of prolapsed vaginal wall should not be included in the measurement of total vaginal length).
(B) (a) Grid and line diagram of complete eversion of vagina. The most distal point of anterior wall (point Ba), vaginal cuff scar (point C), and most distal
point of the posterior wall (point Bp) are all at the same position (þ8) and points Aa and Ap are maximally distal (both at þ3). 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 23 because there is no anterior or
posterior wall descent. Lowest point of the cervix is 8 cm above the hymen (28) and posterior fornix is 2 cm above this (210). Vaginal length is 10 cm and
genital hiatus and perineal body measure 2 and 3 cm, respectively. This represents stage 0 support. [From Ref. (15).]
 Anterior Vaginal Wall Prolapse 581

estrogen instead. Lateral defects have been detected on exam by palpating the break in the
EPF on bimanual exam and by identifying movement of the lateral sulcus. It has also been
described that using a ring forceps to elevate the lateral sulcus, the lateral defect cystocele is
corrected (19). The sensitivity and negative predictive value of this method of clinical assess-
ment of paravaginal defects are good. Specificity and positive predictive value of this diagnostic
pearl are poor (20).
If the patient has not undergone a hysterectomy, the uterus should be evaluated for pro-
lapse and movement. In posthysterectomy patients, support of the vaginal vault must be
assessed. An enterocele may appear as a high continuation of the rectocele bulge in the posterior
vaginal wall. They can be differentiated by palpation of the rectovaginal septum. The examiner’s
index finger is placed in the rectum and his/her thumb in the vagina. The patient is then
instructed to cough or bear down. An increased thickness in the rectovaginal septum may indi-
cate a loop of small bowel insinuating itself between the vagina and rectum (enterocele).
If stress urinary incontinence with cough or Valsalva is not seen initially, the prolapse is
reduced with either the speculum blade, a pessary, or packing. The patient is asked to cough and
Valsalva again. Occult stress incontinence is diagnosed if leakage is seen with the prolapse
reduced. It may be necessary to evaluate the patient in the standing position to demonstrate leak-
age. We routinely examine women in the standing position in addition to in lithotomy because it
provides a more realistic impression of the degree of prolapse experienced during daily activity.
The patient is asked to elevate one foot on a step, which separates the legs and provides better
visualization of the perineum and vagina. The vagina is examined for any prolapsing mass at rest
and with Valsalva. If there is any question of the degree of uterine descensus or from which
compartment the prolapse originates, the same maneuver is performed with two of the exami-
ner’s fingers within the vagina.
It is important to assess bladder emptying preoperatively, which can be done at the time of
physical examination with bladder ultrasound or catheterization. We routinely perform preoperative
urodynamics on patients to assess for any bladder dysfunction or voiding abnormality that may not
have been suggested in the patient’s history. It also provides a baseline for comparison should the
patient develop any new lower urinary tract symptoms postoperatively. Women with occult stress
incontinence can be identified with careful preoperative examination and urodynamic evaluation
with reduction of the prolapse. We routinely perform simultaneous anti-incontinence surgery in
all patients with clinical or occult stress incontinence. We have found no significant added morbid-
ity from the addition of a pubovaginal sling to transvaginal prolapse repair.
In the case of mild to moderate cystoceles (grades 1, 2, and 3), the addition of radiographic
studies to the preoperative evaluation is likely of less yield than in cases of severe prolapse. In
significant prolapse, even that of the anterior vaginal wall, it may be harder to tell what structures
are actually included in the bulging mass. A voiding cystourethrogram (VCUG) in the antero-
posterior view can define a cystocele well and demonstrate how far the bladder base descends
below the inferior margin of the pubic symphysis during straining (21). Lateral views are
required to assess the urethra and bladder neck descent fully (22). Fluoroscopy during videouro-
dynamic studies may also be used to obtain a VCUG. The benefits of preoperative urodynamics
in the detection of occult stress urinary incontinence or other voiding dysfunction has been
espoused elsewhere in this chapter. When one has the capabilities of fluoroscopy during the
urodynamic study, there is the added benefit of being able to elucidate the anterior vaginal
wall anatomy. It also provides objective evidence of stress incontinence, an estimation of
residual volume, and an assessment of any urethral pathology such as diverticulum.
Magnetic resonance imaging (MRI) of the pelvis is another method of detecting the
components of prolapse. It offers the advantage of being noninvasive, rapid, and free of ionizing
radiation, and it provides superior soft-tissue differentiation. Structures can also be evaluated in
582 Scarpero and Nitti

multiple planes without any distortion of image quality as in reconstructing computed tomo-
graphy images. Arguably, however, it is expensive, and its utility may be greater in cases of
enterocele and vault prolapse than in anterior vaginal wall prolapse. In complicated cases of
severe prolapse, MRI is ideal for objective radiographic evaluation. It lends itself well to simple
objective grading for quantifying pelvic floor prolapse (23).
Preoperative cystoscopy is helpful to evaluate the bladder for trabeculation, foreign body, or
other pathology. In the absence of an abnormal urinalysis however, the yield of cystoscopy may be
low. We typically perform a quick cystoscopic inspection of the bladder at the start of surgery.

V. NONSURGICAL MANAGEMENT

Cystoceles may be treated nonsurgically with pelvic floor exercises or pessaries and surgically
with a variety of procedures depending on the specific defect involved. When comparing
nonsurgical to surgical treatment or comparing methods of surgical repair, it is important to
realize that the outcome parameters used in evaluation of these options differ considerably.
There are no established guidelines for what outcome parameters to use in evaluating results,
nor are the definitions of terms such as cured, improved, or failed standardized (Table 2).

Table 2 Reported Surgical Outcomes of Anterior Vaginal Wall Prolapse Repair

Results at F/U (%)

Type of No. of Mean (refers only to cure Type of
procedure Lead author patients F/U of cystocele) graft used

Anterior Walter (48) 86 14 m Cured (100) N

colporrhaphy Porges (49) 299 31 m Cured (97) N
Colombo (32) 33 60 m
Gr I (97) N
Gardy (2) 45a 24 m Cured (95) N
Kohli (50)b 27 13 m Cured (93) N
40 13 m Cured (67) N
Vaginal Chesson (30) 32 9m Cured (97) AFL/CFL
Paravaginal Shull (51) 62 1.6 y Cured (73) N
Benson (52) 48 2.5 y Cured (29) N
Four-corner Raz (38) 120 24 m Cured (98) N
bladder neck Dmochowski (53) 47 37 m Cured (43) N
suspension
Other vaginal Raz (40) 51 34 m Cured (88) N
procedures Julian (54) 24 2y Cured (66) vs. (100) N vs. S
Migliari (41) 15 23 m Cured (93) S
Kobashi (42) 50 6m Cured (100) CFL
Nicita (43) 44 13.9 mc Cured (100) S
Retropubic Bruce (33) 52 17 m Cured/improved (85) N
paravaginal Shull (31) 149 6 – 48 m Cured (95) N
Richardson (12) 213 2–8 y Cured (92) N
Benson (52) 40 2.5 y Cured (58) N
a
17 patients subtracted from total number of patients because they had urethral suspension alone for mild cystocele.
b
Divided into those that underwent anterior colporrhaphy alone (27) and those that underwent anterior colporrhaphy and
transvaginal needle bladder neck suspension (40).
c
Median rather than mean. m, months; y, years; N, none; S, synthetic; AFL, autologous fascia lata; CFL, cadaveric
fascia lata.
 Anterior Vaginal Wall Prolapse 583

Not all studies include quality-of-life (QOL) evaluations, and when used there is no uniformity
in which QOL instrument is employed. These differences make comparison of various studies
difficult.
This section will highlight the treatment options and techniques that are recognized and
reported in the literature. The descriptions of various surgical techniques are not meant to be
as detailed as could be obtained from a surgical atlas or from the original article. When learning
the technique, the original source should be consulted for a detailed description.
“Watchful waiting” is an option with any form of prolapse except the most severe that is
causing such serious complications as erosion of vaginal skin, threatened eviseration, or hydro-
nephrosis. However, if the mild to moderate cystocele is not repaired surgically, there is cer-
tainly a chance of progression and the risk of developing other associated pelvic floor defects.
Patients should be apprised of these risks when considering watchful waiting. In asymptomatic
cases, patients may reasonably choose not to intervene, yet they may also inquire as to whether
there is anything they can do to help lower the risk of progression of their prolapse.
Pelvic floor exercises have been studied as a treatment for rehabilitation of the pelvic floor
musculature. As originally described by Kegel in 1948, the exercises could help strengthen the
pelvic support after childbirth (24). Most recent studies have focused exclusively on its efficacy
in the treatment of urinary incontinence, not prolapse, and there are no good data in the literature
to suggest that the exercises slow or arrest the progression of pelvic organ prolapse.
Pessaries used most commonly for more severe pelvic organ prolapse can also be used for
the symptomatic moderate cystocele. In most cases pessaries are reserved for patients who either
do not want surgery or who are not surgical candidates; however, no strict indication for pessary
exists. In a survey of the American Urogynecologic Society, 77% used pessaries as first-line
therapy for prolapse, whereas 12% reserved pessaries for women who were not surgical candi-
dates (25). A pessary was used more commonly for anterior defect (89%) than any other specific
defect (posterior, apical, or complete procidentia).
No strict contraindications to pessary use exist, either. Some conditions that place a
woman at higher risk for complication with pessary include vaginal mucosal atrophy that results
from low estrogen status and radiation, as well as the inability to independently change and clean
the pessary (26). Reported complications include vaginal wall ulceration, fistula formation, and
bowel herniation (27,28). In order to avoid complication it is necessary to choose a pessary that
fits well without excessive pressure on the vaginal mucosa. In women with vaginal mucosal atro-
phy, the use of estrogen either topically or systemically should be encouraged. Patients should
also be taught to remove and clean the pessary frequently. No consensus exists as to how fre-
quently to change the pessary, usually every 1 – 2 months. Some physicians have the patient
return to the office for frequent pessary changes. Each time the pessary is changed, the vagina
should be inspected closely with a full speculum to determine if any vaginal erosion is occurring.
The pessary should be discontinued at any sign of such erosion.
Not all women are able to use a pessary successfully. Some patient characteristics and
habits make pessary use more difficult. A patient with a large introitus may not be able to retain
a pessary. In the patient with occult stress urinary incontinence, the use of a pessary will render
them incontinent and thus may worsen their quality of life. Sexual activity does not preclude
pessary use, but the patient must be able to remove it herself.

VI. SURGICAL MANAGEMENT

All cystocele repairs revise the pubocervical fascia in some manner. They may be performed
vaginally (e.g., anterior colporraphy) or retropubically (e.g., paravaginal repair). Combined
584 Scarpero and Nitti

central and lateral defects may require a combination of methods. The advent of minimally inva-
sive surgery had led to the application of laparoscopy in retropubic repair.
Whether to repair an asymptomatic mild or moderate cystocele is controversial. Some
advocate surgical repair only if performing other vaginal surgery such as hysterectomy or an
anti-incontinence procedure. If undergoing surgery for incontinence such as a pubovaginal
sling or urethropexy, it is reasonable to repair an asymptomatic small to moderate cystocele
since fixation of the urethra and bladder neck may promote progression of the remainder of
the anterior vaginal wall. Others suggest repair any detected prolapse. Most patients with a
grade 3 or higher cystocele will require treatment.

VII. REPAIR OF CENTRAL DEFECTS

Anterior colporrhaphy consists of plication of the pubocervical fascia and is the most common
method of central defect repair. This approach alone is not recommended in combined central
and lateral defects because it does not correct the lateral component. When performing an
anterior colporrhaphy, the patient is placed in the dorsal lithotomy position. Exposure of the
anterior vaginal wall is facilitated by using an Allis clamp to grasp the prolapsing wall and
stretch it cephalad. A weighted vaginal speculum in the vagina helps to reduce the posterior
wall. A midline incision is made in the vaginal wall from the area of the cardinal ligament attach-
ment to just distal to the bladder neck. The vaginal wall is then dissected off the bladder and
underlying attenuated pubocervical fascia so the entire cystocele can be exposed. When full
exposure is accomplished, the bladder is reduced with a finger or small packing of polyglycolic
acid (PGA) mesh, so that the pubocervical fascia can be visualized clearly and reapproximated
in the midline. The PGA mesh packing does not add strength to the repair, but we have found it
useful to keep the bladder reduced.
After successful plication, it is not necessary to remove the mesh. Plication sutures used
are 2-0 PGA and extend from the bladder neck to the cardinal ligaments (Fig. 5). The addition

Figure 5 Anterior colporrhaphy. The vaginal wall is dissected off of the bladder and pubocervical fascia
via a midline incision. The pubocervical fascia is reapproximated with 2-0 absorbable suture from the
bladder neck to the cardinal ligaments, avoiding vaginal wall. [From Ref. (40).]
 Anterior Vaginal Wall Prolapse 585

of a Kelly plication stitch to narrow the urethrovesical junction in cases of stress incontinence
has been advocated by some authors. The Kelly plication was originally described as an anti-
incontinence procedure. The pubocervical fascia at the bladder neck is plicated in order to
reduce the diameter of the urethra at the site of funneling (29). We prefer to perform a formal
anti-incontinence procedure, e.g., pubovaginal sling, when overt or occult stress incontinence
is present. In cases in which the pubocervical fascia is too attenuated for adequate repair, a
piece of synthetic mesh or allographic material may be employed to strengthen the repair and
prevent suture pull-through (30). The graft is interposed between the pubocervical fascia and
vaginal wall on one side, securing it to the inner side of one vaginal wall and pubocervical fascia
laterally on each side. It is trimmed and stretched beneath the bladder to be interposed between
the structures on the opposite side. After completion of the colporrhaphy, the vaginal wall is
trimmed and closed with interrupted absorbable sutures.
Keeping in mind the discrepancies of technique, time to follow-up, definitions of cure and
failure, and the incidence of concomitant procedures, the anterior colporraphy has a published
failure rate of 0 –20% (5).

VIII. REPAIR OF LATERAL DEFECTS

Lateral defects may be repaired retropubically or vaginally. The most anatomical repair is a
paravaginal defect repair. The goal of paravaginal repair is to reattach the pubocervical fascia
to the arcus tendineus, thus restoring support to the bladder, urethra, and anterior vaginal
wall. The paravaginal repair was originally described as a retropubic route, which is ideal for
isolated lateral defects. A vaginal paravaginal repair can easily be combined with a central defect
repair for combined central and lateral defects.
Abdominal retropubic paravaginal repair can be accomplished via a low midline or trans-
verse incision. The retropubic space is developed so that the bladder neck, symphysis pubis,
endopelvic fascia, arcus tendineus, and obturator fascia can be clearly identified. Avulsion of
the pubocervical fascia can be seen easily by placing two fingers of the nondominant hand in
the vagina to elevate the vaginal wall and paravaginal fascia. This maneuver also facilitates
correct placement of the sutures. The defect is repaired with multiple permanent sutures such
as 0-Ethibond placed 1 cm apart along the superior lateral angle of the vagina to the arcus
tendineus that runs from the lower edge of the symphysis to the ischial spine (12,31). The sutures
should be placed through the paravaginal fascia, vaginal wall (excluding the epithelium), and the
arcus tendineus (Fig. 6). In cases where the arcus cannot be clearly identified, sutures may be
placed in the obturator fascia. The sutures are not tied until all have been placed. Some authors
have recommended that a set of sutures be placed through Cooper’s ligament, thus performing a
combined Burch and paravaginal repair. We also perform this routinely and feel it should always
be done in cases with concomitant type II stress incontinence.
Richardson, who is responsible for the popularization of the paravaginal defect repair,
stated that the procedure was not intended as an operation for incontinence. As an incontinence
procedure, the paravaginal defect repair falls short of Burch colposuspension. In a randomized
comparison of the two procedures for the correction of stress urinary incontinence, Burch out
performed paravaginal defect repair with a cure rate of 100% versus 72% (32). Bruce et al.
found a 72% cure of incontinence at 17 months in patients who underwent paravaginal defect
repair for type 2 stress urinary incontinence (33). The paravaginal repair distributes the
weight-bearing suture line along a much greater length of vaginal wall. When Burch reported
his urethrovaginal fixation to Cooper’s ligament for stress incontinence, he described placing
an additional three sutures from paravaginal fascia to the white line. He found that
these additional sutures not only restored the normal anatomy of the bladder neck but also
586 Scarpero and Nitti

Figure 6 A finger is placed in vagina to help demonstrate the paravaginal defect. None of the sutures are
tied until all have been placed. [From Ref. (31).]

resulted in “surprising correction of most of the cystocele” (34). In a group of 147 patients, Shull
et al. reported a 95% cure rate of cystoceles after paravaginal defect repair (31). Five percent
developed an enterocele postoperatively. Richardson reported his long-term results with the pro-
cedure in 1980. Of 233 repairs with a minimum of 2 years follow-up, 223 were cured of anterior
wall prolapse, for a failure rate of 4.7% (12). A total of 188 were cured of incontinence. Others
have reported a 3– 14% failure rate with paravaginal defect repair (5).
Paravaginal repair performed through a vaginal approach is more technically challenging,
but allows one to also perform a central defect repair in cases of combined defects. The goal of
restoring vaginal and urethral support to the arcus remains the same. A midline incision is made
in the vaginal wall then separated from the attenuated pubocervical fascia and bladder, all the
way to the pubic bone bilaterally. It is important that the most distal portion of the cystocele
be mobilized so that the entire bladder can be reduced to its normal anatomic position. The retro-
pubic space is entered by sharply perforating the endopelvic fascia with Metzenbaum scissors at
the level of the pubic bone. The lateral attachment of the endopelvic fascia is then completely
taken down using blunt dissection. The bladder is retracted medially and the paravaginal space is
identified. The arcus tendineus should be palpated and seen running between the ischial spine
and the symphysis pubis. Care should be exercised to remain posterior and inferior the obturator
nerve and vessels to prevent damage to them. Also of anatomic relevance are the internal puden-
dal vessels that run posterior and medial to the ischial spine. Knowledge of these anatomic
relationships can help avoid complications from an errant suture. Permanent sutures are then
placed through the arcus tendineus (or obturator fascia) and the pubocervical fascia, plus full
thickness of vaginal wall, excluding the epithelium (Figs. 7, 8). Sutures should be placed
 Anterior Vaginal Wall Prolapse 587

Figure 7 Technique of vaginal paravaginal defect repair. (a) The vagina is opened through a midline
incision. (b) The opened vagina reveals bilateral paravaginal defects. (c) The bladder is retracted
medially to expose the arcus tendineus. Permanent sutures are placed into the arcus tendineus or
obturator fascia (see Fig. 8 below). Four to five sutures are placed from ischial spine to the pubic bone.
(d) Each suture is then passed through the detached edge of the endopelvic fascia and in inside of the
vaginal epithelium forming a three point closure. [From Ref. (36).]

laterally in the vaginal wall, although not so lateral as to preclude midline reapproximation (35).
No sutures should be tied until all are placed on both sides. This procedure can be combined with
a sacrospinous ligament fixation or other vault suspension, pubovaginal sling, anterior colpor-
rhaphy, or pubovaginal sling. It may also be combined with graft interposition to correct both
central and lateral defect (36).
Needle suspensions are another method of restoring lateral support based on the principles
of the Raz bladder neck suspension (37). The four-corner bladder neck suspension was described
for the treatment of moderate (grades 2 and 3) cystocele due to lateral defect only (38). In this
procedure, an extra set of polypropylene suspension sutures is placed in the vaginal wall and
pubocervial fascia, proximal to the bladder neck suspension sutures. Early results of this pro-
cedure were encouraging but unfortunately, this procedure, like needle suspensions for stress
incontinence, did have a significant number of late failures. However, the principles developed
were applied to other more durable procedures.

IX. LAPAROSCOPIC REPAIR OF THE ANTERIOR VAGINAL WALL

A variety of procedures for pelvic reconstruction can be performed laparoscopically but require pro-
ficiency in laparoscopic techniques and have a steep learning curve. The advantages of laparoscopy
cited include better visualization deep in the pelvis due to the magnified view, smaller incisions, and
possible reduced morbidity and reduced blood loss. These improvements generally lead to the
588 Scarpero and Nitti

Figure 8 Vaginal paravaginal repair; placement of sutures in the arcus tendineus. Sutures placed through
the arcus tendineus fascia pelvis and the anterior vaginal wall, excluding the squamous epithelium. [From
Ref. (35).]

expectation of faster patient recovery, shorter hospital stay, a decreased analgesia requirement, and
quicker return to normal activities for the patient. Currently the majority of these procedures use
laparoscopy as a mode of access and do not modify the conventional surgical approach (39).
Laparoscopic paravaginal repair is performed under general anesthesia in the dorsal litho-
tomy position. The vagina and perineum are prepped into the field, and a Foley catheter is
placed. The first trocar (10 mm) is inserted through the umbilicus. Two other trocars (5 mm
and 10 mm) are placed in the lower abdomen on left and right, respectively. Before dissection
into the retropubic space is begun, the bladder is filled with 300 cc of normal saline to identify
the bladder dome and thus facilitate the dissection. The parietal peritoneum is incised transver-
sely 2 cm above the bladder dome. Dissection is then carried out bluntly toward the top of the
pubic bone. Once in the retropubic space, the bladder is retracted medially to expose the arcus
tendineus. If present, paravaginal defects can be seen clearly with this maneuver. If any Burch
sutures are to be placed concomitantly, the paravaginal defect should be closed first. Just as in
the open approach, the urethrovesical junction and vaginal wall adjacent to it are identified.
Correct placement of the sutures can be aided by putting two fingers of the surgeon’s nondomi-
nant hand into the vagina to elevate the lateral vagina and help sweep the urethra medially, away
from the repair. A permanent suture on a CT 1 needle is used for intracorporeal suturing.
Prospective randomized trials comparing the laparoscopic method to the classic open methods
remain to be done before recommending it in place of traditional methods.

X. COMBINED CENTRAL AND LATERAL DEFECT REPAIRS

Based on the four-corner repair described above, Raz et al. later described a procedure utilizing
the principals of needle suspension to fix larger cystoceles with combined central and lateral
defects (Fig. 9) (40). A vertical incision is made in the anterior vaginal wall extending from
 Anterior Vaginal Wall Prolapse 589

Figure 9 Grade IV cystocele repair. A midline incision is made in the anterior vaginal wall from the
midurethra to base of bladder where anterior extensions of cardinal ligaments insert. The pubocervical
fascia is identified laterally. After perforation of the endopelvic fascia into the retropubic space, two sets
of No. 1 polypropylene suspension sutures are placed as described in the text. After transfer to the
anterior abdominal wall, the central defect repair is performed as shown in Figure 3. [From Ref. (40).]

the midurethra to the posterior edge of the cystocele. Dissection is performed laterally in the
avascular plane between the bladder and vaginal wall. The pubocervical fascia is exposed on
both sides. Posteriorly, the dissection reaches the cervix or peritoneal fold, exposing the attenu-
ated cardinal ligaments. If indicated, a hysterectomy or enterocele repair may be performed.
At the level of the bladder neck, the retropubic space is entered sharply. The medial edges of
the urethropelvic ligaments are exposed.
As described above for the four-corner bladder and bladder neck suspension, suspension
sutures of No. 1 polypropylene are placed. However, the proximal sutures are placed under
direct vision. These sutures are then transferred to the suprapubic region by needle suspension
technique. Following transfer, a central defect repair is performed by plicating the pubocervical
fascia across the midline using 2-0 PGA sutures as in Figure 3. The vaginal wall is trimmed
and closed. Raz et al. reported excellent or good results in 88% with a mean follow-up of 34
months (40).
We have used the grade IV cystocele repair using an autologous fascial pubovaginal sling
in place of the distal suspension sutures in cases where there is concomitant stress incontinence.
Migilari and Usai described another similar procedure where a 5  5 cm synthetic mesh (60%
polyglactin 910 and 40% polyester) is tailored to create an enclosure anteriorly to accommodate
the urethra and the bladder base (41). The suspension sutures are then incorporated into the
mesh’s four corners. The sutures were then passed suprapubically and tied. Fourteen of
15 women (93%) who underwent this procedure for grade 4 cystocele were cured at a mean
follow-up of 23 months.
Because of reported long-term recurrences of anterior vaginal prolapse, several new
techniques using allographic and synthetic repairs have been described to improve long-term
590 Scarpero and Nitti

success rates. These procedures seem to make sense anatomically but await long-term results.
Kobashi and Leach described a technique using allograft fascia lata (42). A midline anterior
vaginal wall incision is made, extending from the distal urethra to the cystocele’s apex. The blad-
der and urethra are dissected off of the anterior vaginal wall and the underside of the pubic bone is
cleared. The bladder is mobilized medially away from the pubic bone, and the endopelvic fascia
is perforated. A 6  8 cm segment of cadaveric fascia lata is incised into a T-shaped configura-
tion with the top portion serving as the 2-cm sling. The corners of the sling portion are folded in
triangular fashion to cross the fascial fibers, decreasing the risk of sutures pulling through the
fascia. Bone anchors placed transvaginally anchor the sling to the pubic bone. The remainder
of the fascial patch is secured to the medial edge of the levator muscles bilaterally with No. 0
polydioxanone suture and at the vaginal cuff or cervix with absorbable sutures to reduce the
cystocele. Nicita described a similar procedure using polypropylene mesh sutured directly to
the arcus tendineus bilaterally with polypropylene sutures (Fig. 10) (43).
As in the procedure described by Kobashi and Leach, the mesh is fashioned in such a way as
to provide urethral support. We have recently started using a similar technique using allographic
fascia because of the risk of erosion of synthetic material. A piece of fascia is sutured to the arcus

Figure 10 (A) Shape of mesh. a and b, anterior posterior edge. c and d, lateral wings. Distance between a
and b is equal to anteroposterior dimension of cystocele. (B) Suture a fixes mesh to bladder neck. Suture b
to cervix or cardinal ligaments, and sutures c and d to openings through pubic bone insertions of arcus
tendineus of endopelvic fascia. [From Ref. (43).]
 Anterior Vaginal Wall Prolapse 591

tendentious bilaterally, while a separate piece (or a single piece fashioned into a T-shape) is used
as a pubovaginal sling. We prefer to secure the sling in the standard fashion (the pubovaginal sling
extends into the retropubic space and is tied over the midline rectus fascia). The bladder sling
portion of the fascia (or mesh) should also repair the central defect as the bladder is packed
into its normal anatomic position. However, we prefer to also plicate the pubocervical fascia in
the midline if possible as in an anterior colporrhaphy. These procedures should theoretically
correct central and lateral defects as well as urethral hypermobility and intrinsic sphincter
deficiency. The potential problem with such procedures involves the foreign material that must
be used. Synthetic material is durable, but there is a risk of infection and erosion. Recent literature
suggests that cadaveric fascia used as a pubovaginal sling may not have the durability of auto-
logous fascia (44). Unfortunately, the amount of fascia required to perform a prolapse repair is
too large to harvest easily from the rectus fascia or fascia lata. Therefore, until long-term data
are available, such procedures should be done in select patients with informed consent.

XI. COMPLICATIONS

Paying careful attention to detail during surgery can minimize complications. In the absence of
any bleeding diathesis, significant bleeding with cystocele repair is unusual. In one study of 52
retropubic paravaginal repairs, the mean estimated blood loss was 350 mL. Three patients
required blood transfusion (33). Most bleeding in the retropubic space is due to the high vascu-
larity of the vagina and the venous complex beneath the inferior pubic bone. During transvaginal
procedures, bleeding may occur if dissection is carried out in the wrong plane. The vaginal wall
should be taken off of the pubovesical fascia directly on its white shiny surface. Adherence to
this principle may be difficult in cases of previous surgery and scarring, so bleeding is a higher
risk in these patients. Perforation of the endopelvic fascia required in a vaginal paravaginal
repair is another potential source of bleeding. The vessels responsible are usually difficult to
visualize, but with the wider dissection and opening of EPF in this procedure, the bleeding
site may be seen and can be overseen with a 2-0 PGA figure-of-eight stitch.
Bladder or ureteral injuries are rare, but can be discovered intraoperatively with the aid of
cystoscopy and the administration of indigo carmine. Failure to see efflux of blue-stained
urine after placement of sutures may signify kinking or ligation of a ureter. Before taking down
the sutures, consider performing a retrograde pyelogram. In some cases the ureter is patent and
the ipsilateral kidney is poorly functioning instead. If ureteral kinking or ligation is confirmed,
the offending suture must be removed and replaced. The ureter may be prophylactically stented.
Bladder injuries should be closed in two layers. In retropubic procedures bladder injuries
are easily closed in two layers with absorbable sutures. In transvaginal procedures injuries to the
bladder most commonly occur when perforating into the retropubic space. The risk of this can be
reduced by ensuring that the bladder is empty prior to perforation. Should inadvertent injury to
the bladder occur, two-layer closure can usually be accomplished transvaginally. If the patient
has a history of pelvic irradiation, an omental flap of labial fat pad interposition is recommended
to prevent fistula formation (45,46). If a bladder injury is not detected until after surgery, a trial
of conservative management with a Foley catheter may be tried.
Early postoperative complications of surgery for cystocele include wound infection,
immediate postoperative retention, and irritative voiding symptoms. Retention is most likely
in cases in which an anti-incontinence procedure has also been performed. In the study of results
of retropubic paravaginal repair, Bruce et al. found that 32% of patients required clean intermit-
tent catheterization (CIC) for 2 weeks after repair, whereas 70% of patients who underwent
paravaginal defect repair and sling required CIC for this length of time (33).
592 Scarpero and Nitti

Long-term complications include postoperative voiding dysfunction such as stress incon-

tinence, detrusor instability (frequency, urgency, urge incontinence), and incomplete voiding.
Stress incontinence can be minimized with proper preoperative evaluation and performance
of simultaneous anti-incontinence procedure, when indicated. De novo detrusor instability is
a known complication of all bladder surgery and occurs in 5 – 7% of patients (38,40). However
preexisting urge incontinence secondary to detrusor instability has been reported to resolve in
63% of cases (47). Incomplete emptying secondary to urethral obstruction (1% of cases)
may also occur and may require urethrolysis. When impaired emptying is due to poor contrac-
tility, this a condition that likely existed preoperatively and may require clean intermittent cathe-
terization. Other complications include chronic pain, vaginal shortening or stenosis, and
dyspareunia. Care should be taken not to aggressively excise excessive vaginal wall causing
vaginal shortening. Finally, a missed or “potential” prolapse of other organs can result in clinical
postoperative prolapse—for example, apical prolapse or enterocele.

XII. CONCLUSION

A number of surgical techniques have been described for repair of anterior vaginal prolapse.
These techniques continue to evolve as our understanding of the anatomy and pathophysiology
of prolapse improves. The mere evolution of new techniques is a sign that one “perfect” or stan-
dard technique does not exist, and no procedure is completely satisfactory for all patients. What
has been established is that it is important to correct all identifiable defects both with relationship
to the cystocele and to other areas of prolapse. Procedures will likely continue to be developed
that emphasize a more minimally invasive approach with optimal long-term results and
improvement in patient quality of life.

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42
Diagnosis and Treatment of the
Stage IV Cystocele
Nancy B. Itano,* Fernando Almeida,*
Larissa V. Rodrı́guez, and Shlomo Raz
University of California, Los Angeles, California, U.S.A.

I. STAGE IV CYSTOCELE

A cystocele is defined as anterior vaginal wall (bladder) prolapse into the vagina, with or
without urethral hypermobility. Cystoceles have been described by several different classifi-
cation systems, and most commonly categorized by the degree of bladder descent and ana-
tomic defect as in the Baden and Walker classification (1) (Table 1). More recently the
International Continence Society (ICS) has accepted standardization of the terminology for
pelvic organ prolapse quantification (POP-Q) (2). Using POP-Q, both the stages III (Ba)
and IV (C, D) would be classified as grade IV cystoceles, according to the traditional nomen-
clature (Table 2). However, it is rare to see an isolated stage III or IV cystocele without
concurrent pelvic organ prolapse. The focus of this chapter is the pathophysiology, diagnosis,
and surgical treatment of severe bladder prolapse, which for simplicity will be referred to as
stage IV cystocele.
The goals of surgery in patients with severe prolapse are correction of all anatomic defects
and restoration of bowel and bladder function. Anatomic considerations include vaginal depth,
restoration of vaginal axis, urethral hypermobility, and closure of the widened urogenital
diaphragm and levator hiatus. Creating normal anatomy, however, does not ensure a return to
normal bladder, bowel, and sexual function.
The natural history of a cystocele is a continuous progression from mild to severe prolapse
(correlating to stages 0 to IV), 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 (stage I and II) are asymptomatic, except when accompanied by urinary incontinence.
Pelvic prolapse does not spontaneously regress and, often, does not become symptomatic until
the descent reaches the introitus (3).

*Current affiliation: Mayo Clinic Scottsdale, Scottsdale, Arizona, U.S.A.

595
596 Itano et al.

Table 1 Cystocele Classifications

By degree of bladder descent

Grade 0 No prolapse
Grade I Prolapse to proximal vagina with straining
Grade II Prolapse to midvagina with straining
Grade III Prolapse to introitus with straining
Grade IV Prolapse to introitus at rest
By anatomic defect
Central Attenuation of midline pubocervical
fascia; loss of rugae
Lateral Loss of paravaginal support; rugae present

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.

II. ANATOMIC CONSIDERATIONS

To treat pelvic organ relaxation, one must gain an understanding of pelvic floor support. We
will focus on the anterior compartment, in which laxity will present as a cystocele. In the treat-
ment of vaginal prolapse, however, all levels of support must be addressed in order to produce a
successful outcome.
Normally, in the standing position, the vagina forms a “banana” 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 vagina forms a 458 angle from the vertical
plane. The proximal vagina then lies almost horizontally over the posterior levator plate creating
a 1108 angle, which is maintained by the anterior pull of the pubococcygeus muscle (anterior
segment of the levator plate).
This support is due to the connective tissue and muscular components of the pelvic floor.
Superiorly, and adjacent to the pelvic organs, is the pelvic diaphragm. Inferiorly, and more
superficial, is the urogenital (UG) diaphragm. The pelvic diaphragm, and its investing connec-
tive tissue, is the primary source of pelvic organ support (4 – 8). The UG diaphragm consists of
the bulbocavernosus muscle on either side of the introitus and the external anal sphincter sur-
rounding the anus. The transverse perinei (superficial and deep) inserts on the ischial tuberosities
and fuses in the midline on the central tendon. The superior and inferior perineal fascia
reinforces these muscles. Both muscle and fascia must be incorporated in a repair of the
perineum.

Table 2 Standardized Pelvic Organ Prolapse (POP) Staging for Anterior Vaginal Wall Relaxation

Stage Findings

0 No prolapse is demonstrated. (Aa, Ba are 23 cm.)

I Most distal portion of the prolapse is .1 cm above the level of the hymen.
II Most distal portion of the prolapse is
1 cm proximal to the hymen or distal to the hymen.
(Aa and Ba are between 21 cm and þ1 cm.)
III Most distal portion of the prolapse is .1 cm below the hymen but protrudes no more than
2 cm less than the total vaginal length (cm).
IV Complete eversion of the total length of the lower genital tract.
 Diagnosis and Treatment of the Stage IV Cystocele 597

The pelvic diaphragm muscles consist of the levator ani and coccygeus. The levator ani
can be subdivided into the pubococcygeus and the iliococcygeus. The pubococcygeus muscle
is a thick, U-shaped muscle that arises from the pubic symphysis and fuses around the urethra,
vagina, and anus, as the organs exit through the diaphragm. It creates a sling like hammock, pull-
ing the organs anteriorly. The pubococcygeus (also referred to as the pubovisceralis) contracts to
create anterior angulation of these organs, serving to prevent prolapse. The iliococcygeus creates
a horizontal sheet that attaches laterally, creating the fibrous band arcus tendineus levator ani
(ATLA) where the levator ani attaches to the pelvic sidewall and obturator internus muscle.
The insertion of the ATLA to the sidewall divides the obturator internus into supralevator
and infralevator segments. The levator plate (and ATLA) extends anteriorly to attach to the
underside of the midpubic bone. The opening in the levators, in which the urethra, vagina,
and rectum exit, is called the urogenital (UG) hiatus. The arcus tendineus fascia pelvis
(ATFP) is the medially based fascia that directly envelops the organs as they pass through the
pelvic diaphragm. The ATFP is an extension from the levators to the pelvic organs as they
cross the levator hiatus. The ATFP attaches anteriorly to the pubic rami and expands to the
ischial spines bilaterally. This fascial layer lies on the cephalad surface of the levator plate.
The pelvic diaphragm has investing connective tissue, which is less organized and distinct
than traditional fascia. The top layer of connective tissue overlying the pelvic diaphragm is
referred to as endopelvic fascia. The paracolpium is the connective tissue that attaches to the
vagina, and the parametrium attaches to the uterus. Prominent folds of the paracolpium
and parametrium are clinically referred to as the cardinal ligaments, which attach laterally to
the pelvic sidewall and ischial spine, and the uterosacral ligaments, which attach posteriorly
on the sacrum. DeLancey has described three levels of support (9) from this viscerofascial
layer. Level I suspends the top two-thirds of the vagina to the posterior sidewall. These fibers
include the uterosacral-cardinal ligament complex, which extend toward the sacrum. Level II
attaches the midvagina to the sidewalls, ATFP, and ATLA. Most distally, level III, is local
support as the “fascia” attaches the urethra to the pubic bone and vagina to the perineal body.
To better understand the surgical anatomy, we describe four areas of interest in the anterior
compartment. When we describe ligaments, we are referring to the condensations of connective
tissue that provide pelvic organ support: (a) The pubourethral ligaments support the midurethra
to the inferior rami of the symphysis, and are analogous to the puboprostatic ligaments in the
male. (b) The urethropelvic ligaments provide support of the proximal urethra to the lateral
pelvic sidewall. They consist of both the periurethral and endopelvic fascia, as each envelops
the proximal urethra. (c) The vesicopelvic ligaments provide support of the bladder to the
ATFP. This includes the perivesical connective tissue, as seen in the vaginal exposure of the
bladder, and the endopelvic fascia. (d) The cardinal-sacrouterine ligament complex attaches
to the bladder base and cervix (or vaginal vault, if reapproximated during the hysterectomy).
Microscopic studies suggest that these fascial layers encountered during vaginal surgery may
be histologically indistinct from the deep vaginal wall, and not a separate “fascia” (10).

III. ETIOLOGY AND PATHOPHYSIOLOGY

Pelvic organ prolapse is prevented by several mechanisms. The pelvic floor musculature has
basal resting tone, an involuntary reflex, and voluntary activity. At rest, there is static tone of
the levator plate and UG diaphragm that creates the anorectal angle (normal range, 60– 1208)
and narrows the UG hiatus. This banana shape of the vagina is very important in preventing
future prolapse. After surgery, the vaginal axis must recreate this alignment, so that increased
abdominal pressures causes coaptation of the proximal vagina against the levator shelf. If the
vaginal vault is not secured posteriorly, increases in abdominal pressure will cause the pelvic
598 Itano et al.

contents to be pushed out (telescoped) of the vagina (11). Increases in intra-abdominal pressure
causes a reflexive arc that contracts the pelvic floor to further angulate the rectum anteriorly and
narrow the levator hiatus. Similarly, there is a coordinated involuntary reflex to relax the pelvic
floor, which occurs during defecation. This widens the UG hiatus and straightens the distal
rectum to allow for evacuation of stool. The pelvic floor musculature is also under somatic
control, so that the pelvic floor can be voluntarily contracted or relaxed. Pelvic floor muscles
exercises (PFME) are an application of this capability. Loss of levator function will cause
loss of normal support and the vaginal axis, making pelvic organ prolapse more likely.
Normal function of the levator ani requires functioning muscle fibers (primarily slow-
twitch, type I fibers) and intact neural connections. Innervation of the muscles is primarily
derived from the ventral roots of the second, third, and fourth sacral nerve roots via the pudendal
nerve. There also may be direct innervation to the cranial surface of the levators through the third
and fourth sacral motor nerve roots (8). The investing connective tissue layers provide static
support.
Because of the complexity of pelvic organ support, vaginal prolapse is likely multifactorial.
A cystocele results when there is damage to the level II supports and/or pelvic floor dysfunction.
Traditionally, cystoceles have been categorized into central and lateral (paravaginal) defects.
A central defect presents as midline weakness. This may be due to stretching of vaginal
tissue beyond its capacity to recover, so that the vesicopelvic fascia covering the levator
hiatus becomes attenuated and the vaginal wall thins (12). A lateral defect occurs when there
is weakness or disruption of lateral attachments of the vagina (and ATFP) to the ATLA. Cysto-
celes with an isolated central defect represent only 5– 15% of all cystoceles, whereas a lateral
paravaginal defect is present in 70– 80% of patients. Stage IV cystoceles usually present with
both defects.
Poor function of the levator ani muscles may be due to direct myopathic injury or from an
abnormality of innervation. Loss of pelvic floor function will cause the UG hiatus to widen,
increasing the risk of organ prolapse. Relaxation of the pubococcygeus will similarly decrease
the angulation of the midvagina, so that the upper vagina does not lie flat against the pelvic floor
plate. Instead of a banana configuration, the vagina would be vertically oriented, allowing for the
pelvic contents to be pushed out of the vagina.
The reason for a 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 child-
birth creates transient neurological damage to the pelvic floor that is restored after 2 months (13).
The pelvic floor neuropraxia related to vaginal delivery is associated with multiple births,
prolonged labor, high birth weigh, and traumatic deliveries. Other risk factors for neurological
damage are congenital abnormalities, loss of neuronal mass, aging, chronic constipation
(abdominal straining), and perineal laxity (5,7). In a study of 50 women with prolapse, Sharf
performed electromyography on the levator ani and found evidence of denervation in half of
the patients (13). Other studies have confirmed evidence of neurological damage to the UG
muscles in pelvic prolapse (14,15).
The connective tissue of the pelvic floor (“endopelvic fascia”) can be described as a group
of collagen fibers interlaced with elastin, smooth muscle cells, fibroblasts, and vascular struc-
tures. These structures may be weakened due to pregnancy and parturition, lack of estrogen,
aging, diet, chronic straining, and certain connective tissue disorders (Ehlers-Danlos and
Marfan’s syndrome) (6). Patients with vaginal prolapse have fewer fibroblasts and more
collagen fibers in the pubocervical fascia than do controls (16). It has also been shown there
may be a difference in collagen metabolism, with a reduction in type I : III collagen ratio.
Type I collagen is less flexible than type III collagen, but has increased tensile strength (17).
Intrinsic collagen abnormalities and other individual predisposition factors (genetics, differences
 Diagnosis and Treatment of the Stage IV Cystocele 599

in pelvic architecture, inherent quality of the pelvic musculature, and tissue response to injury)
might also explain why patients with known risk factors do not develop prolapse and why many
patients without any known risk factor do.
Risk factors for anterior vaginal wall prolapse include: neuropathy, myopathy, aging,
hormonal, surgical trauma (especially previous vaginal hysterectomy), vaginal childbirth, and
increased abdominal pressures (obesity, constipation, chronic cough).
Correction of a cystocele alone, without reconstructing the entire pelvic floor, may further
alter the vaginal axis and increase the likelihood of uterine prolapse, enterocele and rectocele
formation (18). Additionally, a severe cystocele rarely occurs in isolation. Michael et al. (19)
observed a simultaneous enterocele in 35%, rectocele in 63%, and uterine prolapse in 38% of
patients with grade IV cystoceles. Urethral hypermobility, coaptation, and function should
also be addressed at the same time.

IV. CLINICAL PRESENTATION

A. Symptoms
Cystoceles are often asymptomatic until pelvic organ prolapse is severe. The most common
complaint due to anterior compartment prolapse is vaginal bulging, with or without suprapubic
pressure and pain. Other possible coexisting symptoms include urgency, frequency, urge incon-
tinence, stress incontinence, recurrent urinary tract infections, back pain, renal failure, and
urinary retention. Obstructive voiding symptoms are due to urethral kinking when the bladder
descends beyond the pubic ramus but the urethra remains fixed. This is commonly seen in the
setting of previous surgery (i.e., bladder neck suspension, urethropexy, sling) (19). Patients
may describe using unusual positions to void, such as pelvic tilting, squatting, and standing.
In contrast, patients with concomitant urethral dysfunction may present with stress urinary
incontinence, especially when the cystocele is manually reduced.

B. Clinical Evaluation
There are some critical points in the evaluation of a stage IV cystocele that must be answered
before treatment. The degree of cystocele and concurrent voiding dysfunction such as stress
incontinence, detrusor overactivity, and ability to empty to completion should be investigated.
Surgical planning is also affected by the need to preserve sexual function and vaginal depth. The
overall health of the patient is considered as well as the impact of the symptoms on the patient’s
quality of life.
Preoperative planning demands an assessment of which pelvic organs are prolapsing and
to what degree. Associated abnormalities of the perineum and levator hiatus should also be
noted. It must be decided what should be done with the urethra, in the face of such severe pelvic
floor relaxation. If the quality of the vaginal tissue is poor, it must be decided whether local
estrogen replacement is needed.

C. Physical Examination
A thorough physical examination must be done with a full bladder, at rest, and with straining, in
both the standing and supine positions. The goal of examination is to determine the degree
of prolapse, the specific anatomic defects, and the presence of concomitant organ prolapse.
Straining and standing should accentuate the degree of descent. In the supine position, we try
to determine the origin of prolapse. Using a half-speculum blade we retract the posterior vaginal
wall and ask the patient to strain, to evaluate the anterior defect. An isolated central defect is
600 Itano et al.

identified as bulging in the central region of the vagina (midline) with the lateral sulci high and
well supported. Loss of vaginal rugae is due to smooth muscle atrophy of the vaginal wall, as is
commonly seen in older patients, and is a nonspecific finding. A lateral defect is identified when
there is loss of the lateral vaginal sulci, as the vesicopelvic fascia attenuates from the ATFP.
There will be loss of the “M” vaginal profile (coronal view) and sliding herniation of the bladder
into the vagina. After characterizing the anatomic defects, it is important to reduce the cystocele
to elicit occult stress urinary incontinence and urethral hypermobility. Similarly, we retract the
anterior vaginal wall to determine the presence of a posterior defect. A digital rectal exam
assesses rectal tone, presence of impacted stools, attenuation of the prerectal fascia, and perineal
laxity. Using both blades of speculum, the vaginal vault or cervix can be examined for uterine
descent, vault prolapse, and enterocele.
To ensure consistency, examiners must note the conditions of the exam findings, such as
rest, strain, or supine positioning. Using the POP-Q classification, stage III (Ba) is the most
severe form of isolated anterior compartment prolapse. This is when the point that represents
the most dependent position of the anterior vaginal wall descends .1 cm below the hymen
but protrudes no further than 2 cm less than the total vaginal length (TVL-2). Stage IV is
total vaginal eversion, with the most distal portion of prolapse descending a minimum of 2 cm
less than the total vaginal length, and in most instances, the entire vaginal length. The cervix (C)
or vaginal cuff is most commonly the leading point (2).

D. Imaging Studies
In the setting of a large introital bulge, it may be difficult to differentiate a severe cystocele from
an enterocele by only physical exam (20). Imaging studies can be helpful in assessing severe
organ prolapse, especially when one compartment has such significant bulging that it acts as
a space-occupying lesion.
An ideal imaging study should provide precise information about which structures are
prolapsed, the presence of urinary retention and obstruction, urethral hypermobility and urinary
incontinence.

1. Cystourethrography
The patient should be upright and have a full bladder. Films should be taken during both rest and
strain. This exam provides information about bladder position, bladder neck funneling, urethral
mobility, stress incontinence, and postvoid residual. The presence of a rectocele can also be
inferred when bowel gas is identified below the pubic symphysis. This exam is static and
does not provide information about other pelvic organs or soft tissues of the pelvic floor.

2. Dynamic Fluoroscopy (Colpocystodefecography, Vaginography)

This study relies on making the organs of interest radiopaque (bladder, vagina, rectum) and
studying their positional changes with straining under fluoroscopy. This is a dynamic exam
done with the patient upright. Standing recreates the setting in which the patient experiences
maximal vaginal bulging. Unfortunately, contrast paste must be placed into the vagina and
rectum, which can be uncomfortable.

3. Ultrasonography
Ultrasound (US) is an attractive imaging modality because it is easy to perform, is minimally
invasive, and avoids radiation exposure. Tubo-ovarian and renal disease can also be assessed
 Diagnosis and Treatment of the Stage IV Cystocele 601

during the same exam. There is evidence that US is useful in evaluating bladder neck
hypermobility, but transvaginal imaging for pelvic prolapse does not provide adequate visualiza-
tion of the soft tissues (21). Translabial ultrasound can be used to quantify prolapse, although
it appears to be better for the anterior compartment and uterine descent than the posterior
compartment (22).

4. Dynamic Magnetic Resonance Imaging

Recently, MRI has been used to evaluate pelvic prolapse. It is performed quickly, without
contrast or ionizing radiation, and permits visualization of the soft tissues as well as the
upper urinary tract. Gousse and colleagues have shown that in comparison with findings at
surgery, MRI has a 100% sensitivity, 83% specificity and a positive predictive value of 97%
when assessing cystoceles. When compared to colpocystodefecography, MRI does not require
intravesical catheterization, does not require contrast, and is fast (5 min) and noninvasive.
MRI may be less sensitive, underestimating the extent of apical and posterior compartment
defects (23,24). Unfortunately, MRIs must be performed in the supine position, which
diminishes the downward forces that can be generated with abdominal straining.
At our institution, pelvic MRI is done without endorectal or endovaginal coils, with the
intention of being as noninvasive as possible (Fig. 1). The diagnostic value would be increased
with the addition of water-soluble lubricant in the vagina and/or rectum.

Figure 1 Midsaggital MRI (HASTE sequence) demonstrating a large cystocele herniating below the
pubic symphysis.
602 Itano et al.

E. Video Urodynamic Study

A urodynamic study (UDS) can be done with or without video assistance. Both methods provide
information about bladder compliance, capacity, sensation of filling, detrusor instability,
and contractility. An advantage in performing video urodynamics is the capability to correlate
standing cystography (anatomic information) with simultaneous pressure-flow studies.
Choosing to use fluoroscopy should be based on cost, availability, and familiarity with this
method.
The importance of documenting the presence of urinary incontinence among patients with
large cystoceles is controversial. The incidence of occult stress urinary incontinence is felt to be
as high as 22 –80% among patients with high stage vaginal vault prolapse (25). Owing to the
masked urinary incontinence and the high incidence of postoperative de novo stress inconti-
nence, many authors routinely perform a concomitant anti-incontinence surgery in all anterior
vaginal reconstruction independent of continence status.
A recent study by Barnes et al. (26) retrospectively reviewed the charts of 38 women with
grade 3 –4 prolapse who did not have significant symptoms of stress incontinence. None of the
patients demonstrated stress incontinence during physical exam or video urodynamic studies,
until the prolapse was mechanically reduced. All patients subsequently had documented stress
incontinence with a mean abdominal leak point pressure of 86 cmH2O. All patients then under-
went surgical repair of the prolapse and a pubovaginal sling. None of the patients developed
permanent retention. Recurrent stress incontinence occurred in 5% of the patients. Conversely,
Chaikin and colleges (27) evaluated 24 “continent” women with severe cystoceles. They used a
pessary to reduce the cystocele during UDS and documented incontinence in only 58% of
patients. The patients with overt incontinence received an anti-incontinence procedure, and
the others did not. With a mean follow-up of 47 months, no patients treated only by colporrhaphy
developed incontinence. They recommend concomitant anti-incontinence procedures in patients
with overt leakage. In order to improve the sensitivity of the urodynamic test to reveal urinary
incontinence, the use of a pessary or a vaginal pack can be used to reduce the cystocele (28,29).
Complete reduction of the vaginal prolapse is not always possible with a pessary if the
prolapse is severe. Additionally, there has been no proven correlation between pessary reduction
and the reduction obtained by surgery. Vaginal packing and pessaries can also artificially
obstruct the urethra. It is our feeling that a nonobstructive anti-incontinence procedure to support
the urethra should be done to restore urethral function and prevent incontinence.
Determining the presence of bladder instability is important in preoperative counseling
because it can affect the postoperative result. In the majority of cases (60 –80%), urgency
may resolve after surgery (30). Some patients may have no change in urgency or even see
their urgency exacerbated by sling placement and/or bladder neck elevation. UDS may also
indicate urinary obstruction preoperatively with an elevated voiding pressure, low urinary
flow, or radiologic evidence of urethral kinking.

F. Cystourethroscopy
This exam is performed to rule out concurrent pathology in the bladder and urethra, such as blad-
der carcinoma, urethral diverticulum, stones, or foreign bodies (such as suture material) from
previous surgery. Cystoscopic illumination can also be used to differentiate an enterocele
from a cystocele (31). A pelvic exam is performed with the cystoscope in the bladder. The blad-
der transilluminates through the anterior vaginal wall, so that the extent of the bladder prolapse is
demarcated (Fig. 2).
 Diagnosis and Treatment of the Stage IV Cystocele 603

Figure 2 Cystoscopic transillumination of the cystocele. The illumination ends at the most proximal
extent of the cystocele, demarcating the border between the cystocele and enterocele.

We assess bladder neck competence both at rest and during straining. It can also be used
as a bedside urodynamic exam, assessing filling sensation, postvoid residual, and visual cysto-
metrics for bladder contractions. With a full bladder, a supine Valsalva stress test can be
performed to look for urethral leakage.

G. Upper Urinary Tract Evaluation

Patients with a stage IV cystocele should have upper tract imaging because there is a 4– 7%
incidence of moderate hydroureteronephrosis amongst patients with severe vaginal prolapse
(32,33). This risk is greater in patients with procidentia. Ultrasound, excretory urography,
computed tomography, or MRI can be used. An advantage of MRI is the ability to simul-
taneously evaluate the upper urinary tract, tubo-ovarian disease, and pelvic organ prolapse
simultaneously.

H. Laboratory Evaluations
Patients must have sterile urine prior to proceeding with an operative procedure. In preparation
for surgery, we routinely obtain a complete blood count, basic metabolic panel, and coagulation
profile in addition to the urine culture.
604 Itano et al.

V. TREATMENT

Treatment of the stage IV cystocele cannot be addressed in isolation but rather as a component of
the entire pelvic floor, including restoration of vaginal depth and axis. Obviously, the superior
and posterior compartments must be reconstructed, in addition to the UG hiatus and perineum.
There are several approaches to surgery, including abdominal, laparoscopic, and/or vaginal
repair.

A. Abdominal Approach
There are two classic abdominal techniques that have been used together in the treatment of
anterior vaginal wall prolapse: the paravaginal defect repair (PVDR) by Richardson (34), and
the Burch colposuspension (35). Most abdominal approaches are made with the patient in
a low lithotomy position with a Pfannenstiel incision. A 16 –18F urethral catheter is useful to
isolate the bladder neck.
In Richardson’s surgery, after the retropubic space has been dissected, the bladder
neck, urethra, anterior vaginal wall, and ATLA are identified. The operator then inserts his
nondominant hand into the vagina and using his finger, elevates the lateral sulcus of the vagina
to the level of the bladder neck. The first permanent suture placed attaches the lateral vagina wall
to the levator fascia and ATLA. Three additional sutures are passed anterior and posterior to the
first stitch at intervals of 1– 2 cm. Sutures are held, being tied only after the last suture has been
placed.
Richardson (34), who first described the anatomic surgical repair for cystocele,
emphasized that his technique was designed solely to correct the paravaginal defect and did
not address the urethra. In fact, this procedure only repairs the level II lateral support, and
does not address the vaginal axis, central defects, sacrouterine-cardinal ligament weakness, or
urethral dysfunction.
In a follow-up of 2– 8 years using this approach in properly selected patients, the overall
success was 95% (34). Recently Bruce et al. (36), using the same technique, with a mean follow-
up of 17 months showed an 80% cystocele cure rate and 72% cure of urinary incontinence.
Colposuspensions are well known among physicians that treat urinary incontinence. The
difference between the Burch colposuspension and a PVDR is that the lateral vaginal wall is sus-
pended to Cooper’s ligament instead of the ATLA. Excessive tension must be avoided to prevent
postoperative urinary retention. Although the Burch procedure has been initially described to
treat anterior wall descent, it is used more commonly to treat urinary incontinence. Thus,
there are limited data showing its success as solely a cystocele repair.
Modifications have been made, including various suture materials, location of suture
placement, use of anchoring devices, and different graft materials. A recent randomized trial
compared three anterior colporrhaphy techniques (37): standard plication colporrhaphy,
standard colporrhaphy with polyglactin mesh, and an ultralateral anterior colporrhaphy.
Preoperative and postoperative exams were standardized with the POP-Q staging system, as
recommended by the International Continence Society. At a mean follow-up of 23 months,
patients in all three groups had similar anatomic cure rates (standard, 30%; standard with
mesh, 42%; ultralateral 46%). Symptomatology related to the prolapse also resolved without
significant difference among the three groups.
Sullivan et al. (38), reported results with a modified sacrocolpopexy to treat complete
pelvic organ prolapse. This group used several pieces of Marlex mesh (CR Bard Inc, Charlotte,
NC) as a scaffold for support. The peritoneal sac is dissected off the vaginal apex in the treatment
of the enterocele, and mesh is placed behind the vagina reinforcing the rectovaginal septum. It is
 Diagnosis and Treatment of the Stage IV Cystocele 605

attached to the perineal body with a two-pronged Cobb-Ragde needle passer. Polypropylene
(Prolene: Johnson & Johnson, Cincinnati) is used to fix the mesh superiorly to the S1– 2 perios-
teum. Lateral support is created with two additional strips of mesh, attached to the posterior
mesh on either side of the vagina, and then suspended to Cooper’s ligament bilaterally. If
there is a prominent cystocele, an additional piece of bridging mesh is placed anterior to the
vagina, sutured to the lateral mesh strips. There was a 5% mesh erosion rate and 4% rate of
reoperation for small bowel obstruction. Specific outcomes of vault prolapse were not included
in the outcome reporting, but 36% underwent corrective surgery for bladder-related symptoms
and 28% underwent subsequent repair of anorectal mucosal prolapse or rectocele. Mean follow-
up was .5 years. Because of the need for additional corrective surgery for bladder symptoma-
tology and low posterior compartment defects, the authors feel that their total mesh repair is
only a foundation for pelvic support. Rectocele repair and/or urethral support should be done
concomitantly if needed, presumably through a vaginal and/or rectal approach. The widened
levator hiatus itself is not repaired with this approach.
Despite good results with the abdominal approaches, it is not clear if these procedures
should be used in all stages of cystocele. There have been a limited number of studies evaluating
the anatomic result (prolapse) as the primary outcome measure. Abdominal procedures are an
excellent option for patients with cystoceles who may require concurrent abdominal surgery
(such as transabdominal hysterectomy or oophorectomy), have a isolated lateral defect, or
have a narrow vagina that does not allow adequate surgical exposure. Besides the increased
morbidity, a major disadvantage of any abdominal approach is that low posterior compartment
abnormalities (rectocele or rectal mucosal prolapse), a widened levator hiatus, and urethral
dysfunction are not corrected.

B. Laparoscopic Approach
The laparoscopic retropubic bladder neck suspension was first described in 1991 (39). Reported
advantages include a shorter hospital stay, faster recovery, improved visualization, and
decreased blood loss. With the increased training in laparoscopy and classic teaching from
traditional abdominal approaches, some surgeons have begun treating urinary incontinence
and anterior vaginal wall relaxation with a laparoscopic paravaginal repair. Because results
with a paravaginal defect repair alone were less successful than with the Burch procedure,
some authors began to repair the paravaginal defect together with the Burch bladder neck
suspension with good results. The laparoscopic route can be transperitoneal or extraperitoneal
(retropubic). The surgical procedure starts with the placement of the trocars, usually consisting
of a 10-mm trocar at the umbilicus, which is used to house the camera. An additional two or three
5-mm trocars are placed in lower quadrants of abdomen. The dissection of the retropubic space
is made, and after the anatomic structures have been visualized, sutures are placed as previously
described.
There have been variations in suture placement, number of sutures, suture material, use
of allograft or synthetic materials, and anchoring devices (40). In a retrospective study by
El-Toukhy and Davies (41), patients with genuine stress incontinence underwent either an
open Burch or a laparoscopic modified Burch colposuspension. The bladder neck was elevated
using polypropylene mesh (2.5  5 cm) and titanium tacks. Two titanium coils were placed into
the paravaginal tissue with the strip of mesh, and then the other end of the mesh was adhered to
Cooper’s ligament with two additional coils. This was then repeated on the contralateral side.
Early results show that the laparoscopic route is equivalent to the open procedure for treatment
of stress incontinence, but that with time, the laparoscopic approach is less durable (“cure” at .2
years, laparoscopic 62% versus open 79%, P , 0.05). Outcome of prolapse is not quantified.
606 Itano et al.

Because laparoscopy allows the performance of similar procedures with minimal invasive-
ness, adherence to strict anatomic principles must remain. Sutures can be difficult to place and
time-consuming to tie, so some laparoscopic surgeons have modified the technique to use fewer
sutures. With each modification, there is a mandatory time lag to see if the results remain durable.
However, if the laparoscopic approach is performed the same as open surgery, it would allow a
more confident extrapolation of previously published outcomes to more contemporary series.
There is a lack of published data available regarding the success of laparoscopic surgery
for the treatment of severe anterior vaginal prolapse. The majority of studies using a laparo-
scopic approach on the anterior vaginal wall are related to the treatment of urinary incontinence.
The laparoscopic approach, as with the open abdominal approach, may be an option in patients
whose prolapse can be addressed without vaginal reconstruction and who need concomitant
abdominal surgery.

C. Vaginal Approach
Historically, in 1914, Kelly and Drum first described the anterior colporrhaphy as a treatment for
stress incontinence (47). The continence results were disappointing, but repair of the anterior
vaginal prolapse was successful, and this became a widely popularized treatment for cystoceles.
The central pubocervical fascia defect is corrected by plicating the “fascia,” imbricating the
detrusor, and approximating the tissue in the midline. Because the goal of the initial “Kelly” pli-
cation was continence, the sutures were placed at the level of the proximal urethra and urethro-
vesical junction. Variations of the anterior colporrhaphy include the shape of the vaginal
incision, extent of dissection, and which layers are plicated (4).
There have been numerous modifications to the anterior colporrhaphy, including the use of
synthetic or allograft materials, suture placement, and anchoring techniques. Synthetic materials
have been used to correct anterior vaginal wall prolapse since 1996, when Julian described
the use of Marlex mesh to treat severe anterior prolapse (42). Currently, several materials are
available for use, but the ideal biocompatible material should be chemically and physically
inert, noncarcinogenic, durable, sterile, readily available, noninflammatory, and inexpensive.
Vaginal paravaginal repairs have also been popularized, either alone or in conjunction
with an anterior colporrhaphy. The anatomic goal of the traditional abdominal approach
(PVDR) is a reapproximation of the ATFP to the ATLA. From a vaginal approach, the objective
is to reattach the anterolateral vaginal sulcus (ATFP) to the pubococcygeus muscle and fascia.
Bone anchoring devices can also be used to place hardware to the underside of the pubic bone
and/or Cooper’s ligaments.
There have been successful reports of stage IV cystocele repair with cadaveric dermis (43)
and cadaveric fascia lata (Tutoplast; Mentor Corp., Santa Barbara, CA) (44). These repairs
address both the central and paravaginal defects, and incorporate allograft materials.
It would be ideal to use nonattenuated autologous fascia, but the size needed for complete
vaginal reconstruction is prohibitive owing to the morbidity of harvest. One day genetic engineering
may allow for the production of autologous materials for surgical use. We currently use polypropy-
lene because it is nonabsorbable, macroporous, monofilamentous, flexible, and sterile. The large
pore size (.75 mm) allows for the ingrowth of macrophages, fibroblasts, collagen, and blood
vessels. This aids in rebuilding autologous tissue within the mesh and allows for the chemotaxis
of macrophages in battling infection. Another theoretical advantage of monofilament mesh is that
bacteria cannot infiltrate as they can with a multifilament composition (45). Stiffness is another
important property that is related to pore size. A larger pore size confers greater flexibility, so
that polypropylene (1500 mm) is more flexible than Marlex (600 mm). It is postulated that erosion
is less likely with a larger pore size, because of the host tissue ingrowth and material flexibility.
 Diagnosis and Treatment of the Stage IV Cystocele 607

VI. OUR TECHNIQUE

In the anterior compartment, we specifically address four defects: urethral hypermobility, lateral
bladder support (paravaginal), perivesical fascia (central) support, and separation of sacrouterine
ligaments. Options for surgical treatment include abdominal, laparoscopic, or vaginal approaches.

Four-Defect Repair of Stage IV Cystocele

1. Urethral hypermobility
2. Central defect (attenuation of perivesical fascia)
3. Paravaginal defect (attenuation of lateral vesicopelvic
fascia)
4. Separation of the sacrouterine ligament complex

With the patient in dorsal high-lithotomy position a 16F urethral catheter is placed to drain
urine from the bladder. Exposure is maximized with a weighted vaginal speculum and a Scott
ring retractor with six hooks (placed at the odd-numbered hands of a clock).
If there is significant uterine prolapse, we proceed with hysterectomy and complete
vault prolapse suspension prior to cystocele repair. The cuff is secured to the inferior edge of

Figure 3 Metzenbaum scissors in the retropubic space. The urethropelvic ligament can be seen medially.
608 Itano et al.

the uterosacral ligament complex bilaterally. If an enterocele is identified, we repair it prior to

the cystocele repair, because these obliterative sutures will be used as the base of the cystocele
repair. We close the cul-de-sac in purse-string configuration. These sutures distally incorporate
the pararectal fascia, prerectal fascia, cardinal ligaments, and bladder wall within the
peritoneum.
We initially perform a distal urethral prolene sling (DUPS) in all patients with stage IV
cystoceles, as previously described (46). An Allis clamp is used to retract the urethra superiorly.
Two oblique incisions are made in the distal vagina, carefully avoiding the inner labia. Metzen-
baum scissors are used to expose the periurethral fascia. A small window is made in the
retropubic space with the aid of a curved Mayo scissors directed to the patient’s ipsilateral
shoulder bilaterally. The medial edges of the urethropelvic ligaments are seen (Fig. 3). A tunnel
between the vaginal wall and periurethral fascia is made at the level of the distal urethra with a
fine right angle, 1.5 cm cephalad from the urethral meatus. A soft Prolene mesh sling, measuring
1  10 cm, is passed in through the superficial tunnel (Fig. 4). On each end there is a 0-polyglactin
suture. The sling is positioned using the Raz double-pronged ligature carrier (Cook Urological,
Spencer, IN) through a 1-cm midline transverse puncture. An Allis clamp is placed on each arm
of the sling, on either side of the urethra, and held in a horizontal plane while tying down the
sutures, to prevent tying the sling with too much tension. Additionally, the ties are only secured
at the level of the superficial subcutaneous fat 3-mm below the skin. Incisions are closed with a
running locking 3-0 polyglactin suture.
An Allis clamp is used to grasp the anterior vaginal wall at the point of greatest cystocele
descent (about midway between the urethra and vaginal cuff) (Fig. 5). A vertical midline

Figure 4 Superficial tunnel in the anterior vaginal wall for the distal urethral Prolene sling (DUPS).
 Diagnosis and Treatment of the Stage IV Cystocele 609

Figure 5 (A) Two Allis clamps are placed on the most distal anterior wall prolapse (correlating to
point Ba). (B) A vertical incision will be made, extending proximally to the vaginal cuff.

Figure 6 Exposure of the bladder and perivesical fascia utilizing the midline vertical incision.
610 Itano et al.

Figure 7 (A) Anterior colporrhaphy: interrupted sutures placed in the lateral perivesical fascia.
(B) Horizontal mattress sutures imbricating the attenuated central defect (perivesical fascia).
 Diagnosis and Treatment of the Stage IV Cystocele 611

Figure 8 Vaginal paravaginal defect repair: lateral sutures placed in the infralevator obturator fascia just
proximal to the descending pubic ramus.

incision is made in the anterior vaginal wall extending from the bladder neck to the vaginal cuff.
The dissection is made laterally in the avascular plane between the vaginal wall and perivesical
connective tissue. At the level of bladder, the lateral dissection exposes the vesicopelvic fascia to
free the herniated bladder from the anterior vaginal wall (Fig. 6). The dissection is carried
laterally until the descending ramus of the pubic bone is palpable bilaterally. This allows access
to infralevator obturator “fascia” as it condenses on the pubic bone. This will be the basis of our
vaginal paravaginal defect repair, as an immobile structure to secure the mesh. The vesicopelvic
fascia can be identified and is noted to be thin medially, becoming thicker laterally toward the
levator ani muscles. Posteriorly, the dissection will reach the peritoneal fold, exposing the atten-
uated and pathologically separated cardinal ligaments as they fuse with the pubocervical fascia.
Sutures are placed through the cardinal ligaments and brought midline, to form the most prox-
imal support of the bladder. If a hysterectomy or enterocele repair was done, we use the purse-
string suture to mark the bladder base (sacrouterine ligaments).
The reconstruction starts with a central defect repair. Horizontal mattress sutures are
placed in the lateral aspects of the perivesical fascia (3-0 polyglactin) from the bladder neck
to the vaginal cuff (Fig. 7). Once all sutures have been placed, they can be tied in the
anterior-to-posterior direction, after cystoscopy is done to ensure ureteral efflux and that the
bladder is without injury. To correct the lateral defect, we place a 0-polyglactin suture through
612 Itano et al.

Figure 9 5  5 cm polypropylene mesh disk to be used in the four-defect cystocele repair. It will be
secured to the plicated sacrouterine ligaments, obturator fascia, and vesicopelvic fascia at the level of
the urethrovesical junction with 2-0 polyglactin.

the previously dissected infralevator obturator connective tissue (Fig. 8). After that, a circular
soft Prolene mesh is cut in the shape of a disc (5  5 cm) (Fig. 9). This is secured to the pre-
viously plicated cardinal ligaments posteriorly and then the obturator fascias laterally. Two
additional sutures are placed anteriorly, one on each side of the proximal urethra/bladder
neck, to complete the fixation of the mesh.
If there was a vault repair, the colposuspension sutures (to the sacrouterine ligaments) are
tied prior to trimming the excess vaginal wall. The vaginal incision is closed with a running 3-0
polyglactin suture. If a rectocele is present, we restore the rectovaginal “fascia,” levator hiatus,
and perineal defects. An antibiotic soaked vaginal pack is placed for 2 – 3 h. Most patients go
home after 24 h of observation. The suprapubic tube is clamped and attempts at voiding are insti-
tuted prior to discharge.
The majority of patients void within 72 h, so placement of a suprapubic tube or urethral cath-
eter (and possible preoperative teaching of intermittent catheterization) is the surgeon’s preference.
Because many of our patients are not local residents, we currently place a suprapubic tube and teach
the patient how to remove it once postvoid residuals are ,60 cc. We do keep the catheter for a
minimum of 1 week to minimize possible urinary extravasation with its removal.
We have reported our promising results with the Prolene sling in treating stress urinary
incontinence (46). We have had similar success in the treatment of prolapse and, importantly,
have not had any cases of urinary obstruction or mesh erosion.
 Diagnosis and Treatment of the Stage IV Cystocele 613

VII. CONCLUSION

The diagnosis and treatment of stage IV cystoceles is challenging, even to the most experienced
pelvic surgeons. The etiology is multifactorial and most patients present with concomitant pelvic
organ prolapse. A thorough preoperative evaluation allows one to address all pelvic floor ana-
tomic defects at the time of surgery.

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43
Surgical Correction of Paravaginal Defects

Matthew D. Barber
Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

The durable surgical correction of pelvic organ prolapse remains a significant challenge for
pelvic reconstructive surgeons. Prolapse of the anterior vaginal wall, usually in the form of a
cystocele, is the most common form of pelvic organ prolapse (1). Recent studies suggest
that, of the various segments of the vagina which may be involved in prolapse (anterior,
posterior, or apical), the anterior vaginal wall is the segment most likely to demonstrate recur-
rent prolapse after reconstructive surgery (2). Additionally, normal anterior vaginal support
plays an important role in supporting the urethra and loss of this support can contribute to
the development of stress urinary incontinence (3). It is therefore important that the pelvic
reconstructive surgeon understand the normal support mechanisms of the anterior vaginal
wall and the full spectrum of techniques for correction of anterior vaginal prolapse and
cystoceles.
In 1909, George R. White described a method of cystocele repair that consisted of “sutur-
ing the lateral sulci of the vagina to the white line of pelvic fascia” through a vaginal approach
(4). His was the first known description of the paravaginal defect as a cause of anterior vaginal
wall prolapse. As fortune would have it, Howard Kelly described his method of cystocele repair
4 years later and, perhaps owing to Kelly’s renown and/or the relative simplicity of his oper-
ation, the Kelly plication and its modifications became the primary technique of cystocele repair
for the next 70 years and White’s concepts were largely forgotten (5). In 1976, Richardson et al.
reintroduced the paravaginal defect repair, but described a technique of repair using an abdomi-
nal approach (6). They described isolated defects of the pubocervical “fascia” as the cause of
anterior vaginal wall prolapse and, based on cadaveric dissections, concluded that the majority
of cystoceles resulted from a detachment of the pubocervical fascia at or near its lateral attach-
ment to the arcus tendineus fasciae pelvis (ATFP). Since this report, the paravaginal defect
repair has become a widely used procedure for correcting anterior vaginal prolapse. Vaginal
and laparoscopic techniques have also been described. This chapter will discuss the current
understanding of anterior vaginal support and review the current concepts in diagnosis and sur-
gical correction of paravaginal defects. Specifically, abdominal and vaginal paravaginal defect
repairs will be discussed. Correcting paravaginal defects using the laparospcopic approach will
be discussed in Chapter 44.

615
616 Barber

II. ANATOMY OF ANTERIOR VAGINAL SUPPORT

The vagina is a hollow, flattened fibromuscular tube lined with nonkeritinized stratified squa-
mous epithelium. The longitudinal shape of the vagina resembles a trapezoid, being narrowest
at the introitus and becoming progressively wider as you approach the vaginal apex and cervix.
In the transverse dimension, the vagina is H-shaped at its distal end (toward the introitus) and
flattened proximally (Figs. 1, 2). Underlying the vaginal epithelium is the vaginal muscularis,
a well-developed layer made up primarily of smooth muscle along with collagen and elastin
(7). Some have labeled this layer of the anterior vaginal wall pubocervical fascia. Although
this term is widely used, the use of the term “fascia” is a misnomer, as it does not accurately
reflect the histology of the vagina (7).
Normal, vaginal support is maintained by intact pelvic floor muscles and connective tissue
supports. DeLancey described three levels of connective tissue support for the vagina (Fig. 2)
(8). The cervix and top one-fourth of the vagina are suspended by the cardinal/uterosacral liga-
ment complex (level I). The distal one-fourth is supported by fusion of the lower vagina to the
urogenital diaphragm and perineal body (level III). The middle half (level II) is attached to the
pelvic sidewall bilaterally. The lateral vagina attaches to the levator ani muscle on each side
along a line from the anterior pubic rami to the ischial spine known as the “white line,” or
arcus tendineus fasciae pelvis (ATFP). The ATFP is formed from a condensation of the obturator
internus and levator ani fascia and is composed primarily of organized fibrous collagen (9),
making the lateral connective tissue attachment of the vagina more dense than the superior/
apical connective tissue support of the cardinal and uterosacral complex (8). The distal aspect
of the ATFP as it inserts into the inferior pubis can be found 35 – 55 mm below the pectineal
line. The midportion of the ATFP is 25 – 50 mm directly below the obturator foramen, and its

Figure 1 Vagina and supporting structure in a woman after hysterectomy. Bladder has been removed
above vesical neck. ( ) indicates location of ischial spine. Note the lateral attachment of the vagina to
the arcus tendinious fasica pelvis. (From Ref. (8).)
 Surgical Correction of Paravaginal Defects 617

Figure 2 Levels of vaginal support: level I, apical support from the cardinal/uterosacral ligament
complex; level II, vagina is attached to arcus tendineus fascia pelvis (ATFP) laterally; level III, distal
perineal fusion. Note that in the distal vagina, the vaginal cross section is H-shaped and in the proximal
vagina, the vaginal cross section resembles a flattened tube. [From Ref. (8).]

proximal end predictably terminates at the ischial spine (10). DeLancey demonstrated, through
careful cadaveric dissections, that transecting level I support results in apical prolapse, while
detaching level II support results in anterior vaginal prolapse and cystoceles (8). The loss of
lateral, or level II, support is often referred to as a paravaginal defect.
Strobehn and DeLancey conceptualized the paravaginal defect as similar to a semiadhe-
sive note being peeled off a wall as described in Figure 3 (11). Shull has noted that paravaginal
defects may occur in three forms: the entire arcus may remain attached to the pelvic sidewall
with the lateral vagina breaking away from the arcus; the ATFP may pull away from the side
of the pelvis but remain attached to the lateral vagina; or the ATFP may split with a portion
of it remaining attached to the levator ani and a portion attached to the lateral vagina (12).
The anterior vaginal wall provides support to the urethra and may play an important role in
urinary continence. The urethra lies on a hammocklike supportive layer composed of endopelvic
connective tissue and anterior vaginal wall. DeLancey hypothesized that increased intra-
abdominal pressure, as with a cough or sneeze, causes compression of the urethra against this
hammocklike layer, thereby compressing the urethral lumen closed (3). The stability of the sub-
urethral layer depends on the intact connection of the anterior vaginal wall and its connective
tissue attachments to the ATFP and levator ani muscles. Detachment of the anterior vaginal
wall from the pelvic sidewall, or relaxation of the anterior vaginal wall itself, can result in ure-
thral hypermobility and genuine stress incontinence. With this in mind, some have advocated
reattachment of the anterior vaginal wall to its lateral attachments (a paravaginal defect repair)
as a treatment for genuine stress incontinence. Urethral support is not the only factor involved
in urinary continence; competence of the urethral sphincter itself plays an important role. This
may partially explain why paravaginal defect repair has had only modest success as an anti-
incontinence procedure.
Anterior vaginal prolapse can result from loss of midline, lateral, and/or superior support.
In Richardson’s original study he reported loss of lateral support (paravaginal defects) in 67% of
618 Barber

Figure 3 A semiadhesive note is an example of paravaginal defect of the vagina (A). Imagine a creased
note pasted at a right angle to the wall, so that its free edge, representing the anterior vaginal wall, projects
obliquely toward the floor (B). The crease of the note represents the pubocervical fascia that normally
inserts at the arcus tendineus fascia pelvis overlying the fascia of the levator ani muscle, represented by
the wall (C). As traction is applied to the note (the anterior vaginal wall), the note peels away from the
wall (levator ani muscle) (D). [From Ref. (9).]

his 93 patients with “symptomatic anterior quadrant relaxation” (6). Three-quarters of his
patients with paravaginal defects had unilateral loss of support, with the majority being right-
sided. In contrast to this early study, some authors have found that in women with advanced
anterior vaginal prolapse (ICS stage III or IV), paravaginal defects occur in fewer than half
and that when they do occur, bilateral, rather than unilateral, loss of support is found most
often (13,14).

III. DIAGNOSIS OF PARAVAGINAL DEFECTS

A. Physical Examination
A method for clinically identifying paravaginal defects in women with prolapse was originally
described by Richardson in 1976 and utilized two tongue blades to mimic lateral vaginal support
(6). Shull, using the original ideas of Richardson and subsequent work by Baden and Walker,
later described a more standardized method to clinically evaluate anterior wall support defects
(15). A curved ring forceps is placed in the lateral vaginal sulci and directed toward the ischial
spines along the course of the ATFP to reproduce the lateral support of the vagina. A Sims spec-
ulum is placed posteriorly to expose the anterior vaginal wall and reduce any posterior prolapse.
The patient is asked to strain maximally, and, if complete reduction of the anterior prolapse
 Surgical Correction of Paravaginal Defects 619

occurs with the ring forceps in this position, she is thought to have paravaginal defects. If, when
she strains, the anterior vagina continues to bulge between the arms of the ring forceps without
any evidence of reduction, this suggests a midline loss of support. If supporting the lateral vagina
results in partial reduction of the prolapse, she is thought to have lost both midline and lateral
support. Unilateral elevation of each vaginal sulcus allows differentiation of bilateral and unilat-
eral paravaginal defects.
Current evidence suggests that this technique of physically assessing anterior vaginal sup-
port may not accurately reflect findings at the time of surgery, however. A study of 117 women
found a discrepancy between the prevalence of paravaginal defects noted at a standardized pre-
operative clinical examination (63%) and the prevalence of discrete paravaginal detachment
noted at surgery (42%) (13). The clinical finding of paravaginal defects in this study was sensi-
tive (sensitivity 92%) but not specific (specificity 52%) and had an adequate negative predictive
value (91%), but low positive predictive value (61%). Subjects in whom normal paravaginal
support was found at physical examination usually had intact paravaginal support confirmed
at surgery, but fewer than two-thirds of women who were thought to have paravaginal defects
based on physical examination actually had them at the time of surgery. Accuracy of the clinical
examination was not affected by previous anterior colphorraphy, previous hysterectomy, or
stage of prolapse, but a significant decrease in examination accuracy was noted in patients
who had undergone previous retropubic urethropexy (13).

B. Radiology
Several authors have used magnetic resonance imaging (MRI) to evaluate lateral vaginal sup-
port. Aronson et al. used a vaginally placed endoluminal coil coupled to a pelvic phased-
array coil to image periurethral and paravaginal anatomy in four continent and four incontinent
women (16). Lateral vaginal attachment was seen in all four of the continent women (Fig. 4). In
two of the four incontinent women, paravaginal defects were suspected on clinical examination,
and lateral detachment of the vagina from the levator ani muscles was clearly seen in both of
these women. In another study, Huddleston et al. demonstrated bilateral paravaginal defects
using MRI and a standard body coil in 12 women with genuine stress incontinence and clinically
suspected paravaginal defects (17). The preoperative MRI findings were confirmed intraopera-
tively, and postoperative MRI revealed intact paravaginal attachment in 10 of 12 women after
retropubic paravaginal defect repair. Although MRI appears promising for preoperative detec-
tion of paravaginal defects, it is expensive and not universally available. It is therefore unlikely
that MRI will replace clinical examination as the preoperative assessment of choice for pelvic
organ prolapse.
Ultrasonography is less expensive than MRI, more widely available, and commonly used
to image pelvic organs. Unfortunately, studies investigating the use of ultrasound to diagnose
paravaginal defects have shown mixed results. Ostrzenski et al. investigated the use of transab-
dominal ultrasonography for the detection of paravaginal defects (18,19). They placed a water-
filled condom into the vagina as a contrast medium and made the ultrasound diagnosis of para-
vaginal detachment if the bladder appeared to sag on either side of the water-filled vagina. Using
this technique, they found that paravaginal defects were present in all of 16 women with genuine
stress incontinence and in two of the three primiparous continent women in their study. None of
the five nulliparous continent patients in their study demonstrated paravaginal defects clinically
or ultrasonographically (19). Surgery confirmed paravaginal defects in all of the patients with
genuine stress incontinence. In contrast, Nguyen et al. found that the ultrasound appearance
of paravaginal defects could be demonstrated in both patients with and without clinically appa-
rent prolapse and that the size of the apparent defect directly correlated with the amount of water
620 Barber

Figure 4 Axial T1-weighted image from a 57-year-old woman with genuine stress urinary incontinence,
showing full field of view of paravaginal detachment (arrow) at level of urethrovesical junction. p, pubic
symphysis; u, urethra; o, obturator internus muscle; v, vaginal wall; c, endovaginal coil; l, levator ani
muscle; r, rectum. [From Ref. (16).]

in the vaginal balloon (20). They concluded that the appearance of lateral bladder sagging that
suggested paravaginal detachment was actually an artifact created by the intravaginal water-
filled balloon. Based on these findings, it appears that ultrasonography is not a useful tool for
detecting paravaginal defects, at least using the only technique that has been described in the
literature thus far.
It is important to understand the limitations of the clinical and radiographic assessment of
pelvic relaxation. The preoperative evaluation for specific defects in pelvic support is important
in planning the surgical repair of pelvic organ prolapse, but until better techniques are available,
neither physical examination nor radiology can substitute for a careful intraoperative assessment
of vaginal support defects.

IV. SURGICAL TECHNIQUES

The goal of the paravaginal defect repair is to correct anterior vaginal wall prolapse that results
from loss of lateral support by reattaching the lateral vaginal sulcus to its normal attachment site
along the ATFP. This can be performed abdominally (retropubically), vaginally, or laparosco-
pically. As many patients may have loss of midline and/or superior (level I) support in addition
 Surgical Correction of Paravaginal Defects 621

to loss of lateral support (paravaginal defects), the reconstructive pelvic surgeon may need to
combine the paravaginal defect repair with an anterior colporraphy and/or a vaginal vault sus-
pension in order to completely correct a patient’s anterior vaginal prolapse.

A. Abdominal (Retropubic) Approach

The patient is placed in modified lithotomy position using low leg holders such as Allen stirrups,
and is draped to allow both abdominal and vaginal access. The bladder is drained with a Foley
catheter. The abdomen may be entered through either a transverse or vertical abdominal
incision. While this procedure may be performed entirely retroperitoneally, entering the perito-
neal cavity and packing the bowel out of the pelvis often provides better visualization of the
retropubic space. Entering the peritoneal cavity also allows for concurrent hysterectomy or
additional abdominal prolapse repairs that may be necessary. The retropubic space is entered,
and the bladder is retracted medially to expose the lateral aspect of the retropubic space. The
pubic bone, obturator muscle, obturator fossa, and neurovascular bundle identified. Blunt dissec-
tion is used to identify the lateral vagina, urethra, and ischial spine. A fluffed-up gauze and a
medium malleable retractor can be useful to retract the bladder medially to expose these lateral
structures. The normal site of lateral vaginal attachment on the pelvic sidewall from the interior
aspect of the superior pubic ramus to the ischial spine is then identified. If the lateral vagina is
avulsed from this attachment site, then a paravaginal defect is present. As physical examination
is less than perfect in identifying paravaginal detachment, a bilateral assessment of paravaginal
support should be made in all patients in whom paravaginal defects are suspected.
The surgeon’s nondominant hand is the placed into the vagina and used to elevate the lat-
eral superior vaginal sulcus to its site of normal attachment along the course of the ATFP. Typi-
cally, four to six simple interrupted stitches of nonabsorbable suture (No. 0 or 2-0) are used to
reattach the lateral vagina to the ATFP. The first suture is placed through the full thickness
(excluding the vaginal epithelium) of the lateral vaginal apex and then through the ATFP and
the aponeurosis of the levator ani muscle just distal to the ischial spine. This suture is tied
and cut. Additional sutures are placed at 1-cm intervals through the lateral vaginal wall and
into the levator ani aponeurosis along the entire course of the ATFP. In patients with a cystocele
and genuine stress incontinence, many surgeons combine an abdominal paravaginal repair with a
Burch colposuspension (Fig. 5). At the end of the procedure, cystoscopy should be performed to
document ureteral patency and the absence of intravesical sutures. Closed-suction drainage of
the retropubic space is rarely indicated. Postoperatively, the bladder is drained with either a
transurethral or suprapubic catheter until normal voiding occurs.

B. Vaginal Approach
Paravaginal defect repair using the transvaginal approach can be more challenging than the ret-
ropubic approach, but offers the advantage of avoiding an abdominal incision and facilitating a
concurrent anterior colporrhaphy for those women with loss of midline as well as lateral anterior
vaginal support. The technique begins similar to that of an anterior colporraphy. Patients are
placed in dorsal lithotomy position. A Foley catheter is used to drain the bladder. A weighted
speculum is placed into the vagina. A midline vertical incision is made through the vaginal
epithelium from the midurethra to the vaginal apex. The vaginal epithelium is then sharply
dissected off the underlying vaginal muscularis, and the dissection is continued laterally to
the pelvic sidewall from immediately behind the pubic rami to the level of the ischial spine.
Visualization of the adipose tissue of the retropubic space from this transvaginal approach con-
firms the presence of a paravaginal defect, as normal lateral attachment of the anterior vaginal
622 Barber

Figure 5 (A) Retropubic approach to the paravaginal defect repair. The avulsed vaginal sulcus has been
sutured to the arcus tendineus fascia pelvis bilaterally. (B) The paravaginal repair has been combined with a
Burch colposuspension to provide preferential support to the urethrovesical junction. [From Ref. (34).]

wall would preclude this. If visualization is limited, gentle palpation of the lateral attachment
site can be used. The ability of the examining finger to enter the retropubic space indicates a
paravaginal defect. Every precaution should be taken to avoid iatrogenic creation of paravaginal
defects with dissection, palpation, or retractors.
Once a paravaginal defect is identified, the normal site of lateral attachment of the vagina
should be clearly visualized. This can be facilitated by placing a gauze sponge through the para-
vaginal defect into the retropubic space and using a narrow deaver retractor to retract the sponge,
underlying adipose tissue, and lateral bladder anteriorly. A Briesky-Navratil retractor can then
be used to retract the remainder of the bladder medially, clearly exposing the levator ani muscle
and the course of the ATFP from the ischial spine to the inferior aspect of the pubic ramus. Five
to seven interrupted nonabsorbable sutures (No. 0 or 2-0) are placed at 1-cm intervals through
the ATFP and the aponeurosis of the levator ani muscle from the level of the ischial spine to the
pubic symphysis at 1-cm intervals and their needles left on. Once all of the stitches are placed
through the ATFP, the sponge in the retropubic space is removed. Each stitch is then placed
through the lateral edge of the detached vaginal muscularis ( pubocervical “fascia”) at their cor-
responding level and then tied. Once paravaginal support has been assessed and, if necessary,
restored on both sides, a midline plication of pubocervical “fasica” (anterior colporrhaphy),
 Surgical Correction of Paravaginal Defects 623

a bladder neck plication, or sling can be performed, as necessary. The vaginal epithelium is then
trimmed and closed. If a vaginal hysterectomy is needed, this should be performed prior to the
paravaginal defect repair. If a vaginal vault suspension or culdeplasty is necessary, these sutures
should be placed prior to the paravaginal defect repair, but not tied until the paravaginal defect
repair has been completed. As with the retropubic approach, cystoscopy should be performed at
the end of the procedure to confirm ureteral patency and the absence of intravesical sutures.
Transurethral or suprapubic bladder drainage should continue until normal voiding occurs
(Figs. 6 –9).

V. SURGICAL OUTCOMES
A. Genuine Stress Incontinence
Richardson et al. introduced the retropubic paravaginal defect repair in 1976 as an operation for
correction of defects of lateral vaginal support that resulted in cystourethroceles and stress urin-
ary incontinence (6). In this initial report, they described their experience treating 60 women
with both anterior vaginal prolapse and “significant” stress urinary incontinence that resulted

Figure 6 Vaginal paravaginal repair. Marking sutures placed at urethrovesical junction and vaginal
apices. [From Ref. (32).]
624 Barber

Figure 7 Vaginal paravaginal repair. A right-angle retractor is in the retropubic space, retracting the
bladder medially. The suture is through the arcus tendineus fasciae pelvis 2 cm ventral to the ischial
spine. [From Ref. (32).]

from paravaginal defects. After an average of follow-up of 20 months, 86% of their patients were
subjectively cured of their stress incontinence, and an additional 6% were improved. Addition-
ally, all but two patients had satisfactory correction of their anterior vaginal prolapse. Over the
next 15 years, a number of authors published the results of case series that demonstrated similar
encouraging results with cure rates from 86% to 97%. Table 1 summarizes the results of studies
in which the retropubic paravaginal defect repair was used as the sole anti-incontinence
operation.
In spite of these encouraging early results, evidence suggests that paravaginal defect repair
is not as effective as other standard anti-incontinence procedures such as the Burch or MMK
retropubic urethropexies or the suburethral sling. In 1996, Colombo et al. published the results
of a randomized trial comparing Burch colposuspension to paravaginal defect repair for treat-
ment of genuine stress incontinence (21). This is the only randomized trial evaluating paravagi-
nal defect repair as an anti-incontinence operation. They found that paravaginal defect repair
was inferior to Burch colposuspension for treatment of genuine stress incontinence. The subjec-
tive cure rate for the Burch procedure in this trial was 100%, compared with 72% for paravaginal
defect repair. Similarly, the objective (urodynamic) cure rates in this trial were 100% for Burch
and 61% for paravaginal defect repair. These authors concluded that paravaginal defect repair
should not be recommended for treatment of stress incontinence (21).
One reason why the paravaginal defect repair may be inferior to other anti-incontinence
procedures is that it does not preferentially support the urethra or bladder neck, but rather pro-
vides equal support along the entire length of the anterior vaginal wall. In the Columbo et al.
study, Burch urethropexy significantly increased the functional urethral length and pressure
 Surgical Correction of Paravaginal Defects 625

Figure 8 Vaginal paravaginal repair. A series of sutures has been placed in the arcus tendineus fasciae
pelvis from a point ventral to the ischial spine to the back of the pubic bone. [From Ref. (32).]

transmission ratio measured in the proximal two-thirds of the urethra, whereas the paravaginal
defect repair did not (21). Because of this, some surgeons have opted to combine the paravaginal
defect repair with a retropubic urethropexy in order to gain the advantages of both operations.
Thompson et al. refer to this combination as a “paravaginal plus,” and found in a retrospective
review of 454 patients that the combination of the paravaginal defect repair with a MMK pro-
cedure provided a higher cure rate for stress urinary incontinence than either urethropexy alone
or paravaginal defect repair alone (22). In addition to its retrospective design, a weakness of this
report is that the group who received the paravaginal defect repair alone was followed for over a
year longer than the other two groups.
Paravaginal defect repair using the transvaginal approach has been used infrequently as an
isolated procedure for treatment stress urinary incontinence. Current evidence suggests that it
has less than satisfactory results when used in this capacity (Table 2). In a recent report by
Mallipeddi et al., 57% of subjects with anterior vaginal prolapse and genuine stress incontinence
treated with a vaginal paravaginal repair and a bladder neck plication had persistent urinary
incontinence after an average of 1.6 years of follow-up (23). These authors concluded that
while the vaginal paravaginal repair is safe and effective for correction of anterior vaginal pro-
lapse, it has limited applicability in the surgical correction of genuine stress incontinence.

B. Anterior Vaginal Prolapse

The paravaginal defect repair has been widely used for correction of anterior vaginal prolapse
thought to result from lateral vaginal detachment. Current evaluation of the success rate of this
procedure for treatment of anterior vaginal prolapse is limited to case series and retrospective
626 Barber

Figure 9 Vaginal paravaginal repair. The suture in the arcus tendineus faciae pelvis near the pubic bone
is also sewn into the lateral margin of the pubocervical fascia periurethrally at the site of the marking suture
at the urethrovesical junction. (From Ref. (32).)

reviews. Reports of retropubic paravaginal repair demonstrate anatomic success rates ranging
from 92% to 97% (Table 3), and reports of vaginal paravaginal repair demonstrate success
rates of 76– 100% (Table 4) after variable lengths of follow-up. Failure or recurrence of anterior
vaginal prolapse after paravaginal defect may occur laterally, centrally, or both. Elkins et al.
reported a 8% lateral recurrence rate and a 22% central recurrence rate after transvaginal para-
vaginal defect repair in 25 patients with grade III or greater pelvic organ prolapse (24). At the
time of the initial surgery, bulging of the midline bladder wall that was present after paravaginal
repair was repaired with purse-string or imbricating sutures. Young et al. retrospectively eval-
uated 100 subjects who underwent vaginal paravaginal repair along with other reconstructive
procedures for symptomatic pelvic organ prolapse (25). Subjects received an anterior colpor-
raphy and a vaginal paravaginal repair if a midline cystocele was thought to be present in
addition to paravaginal defects. They found a lateral anterior wall recurrence rate of 2% and
a central anterior recurrence rate of 22% after an average of 11 months of follow-up (25).
Other studies do not provide separate results of lateral versus central recurrence. To date
there are no studies comparing paravaginal defect repair with or without midline anterior repair
to traditional anterior colporraphy alone.

C. Complications
Complications after paravaginal defect repair are, for the most part, infrequent. Febrile morbid-
ity occurs in 6 –20% of patients and is most often self-limited. Lower urinary tract injury occurs
in 0 –4%, similar to other pelvic reconstructive procedures (26). In the randomized trial
 Surgical Correction of Paravaginal Defects 627

Table 1 Outcomes of Abdominal Paravaginal Repair for Treatment of Genuine Stress Incontinence

Follow-up
No. of Improved Failed
Study (year) patients Study design Mean Range Dry (%) (%) (%)

Richardson et al. 60 Retrospective 20 mo 3 – 48 mo 86 6 8

(1976) (6) cohort
Richardson et al. 233 Retrospective NR 2 – 8 yr 88 7 5
(1981) (29) cohort
Baden 215 Retrospective NR 2– 15 yr 85 NR 15
and Walker cohort
(1987) (30)
Shull and Baden 149 Retrospective 48 mo 0.5– 6 yr 97 0 3
(1989) (14) cohort
Colombo et al. 18 Randomized 2.2 yr 1 – 3 yr 72 5 22
(1996) (21)a trial
Thompson et al. 130 Retrospective 39.5 mo NR 49 31 20
(1998) (22)b cohort with
controls
Bruce et al. 25 Retrospective 17 mo NR 72 12 16
(1999) (28)c cohort with
control

NR, not reported.

a
Randomized trial of Burch colposuspension (n ¼ 18) versus abdominal paravaginal repair (n ¼ 18). Subjective cure rate
for Burch group (100%) was significantly higher than that of the paravaginal group (72%) (P ¼ 0.02)
b
Study retrospectively compared cure rates of paravaginal repair (n ¼ 130; dry, 49%; improved, 31%; failure, 20%),
retropubic urethropexy (n ¼ 194; dry, 64%; improved, 20%; failure, 16%) and paravaginal repair combined with retro-
pubic urethropexy (n ¼ 130; dry, 78%; improved, 14%; failure, 8%).
c
Study retrospectively reported cure rates of paravaginal repair for stress urinary incontinence with bladder neck hyper-
mobility (n ¼ 25; dry, 72%, improved, 12%; failure, 16%) and of paravaginal repair with rectus muscle sling for stress
urinary incontinence due to intrinsic sphincteric deficiency (n ¼ 27; dry, 85%, improved, 8%, failure, 7%).

performed by Columbo et al., paravaginal defect repair resulted in a quicker return to normal
voiding and a lower long-term catheterization rate than the Burch cystourethropexy (11% vs.
17%, respectively). The rate of irritable bladder symptoms postoperatively was low in both
groups (0% and 5%, respectively) (21). While paravaginal repair through the vaginal approach

Table 2 Outcomes of Vaginal Paravaginal Repair for Treatment of Genuine Stress Incontinence

Follow-up
No. of
Study (year) patients Study design Mean Range Cure (%) Failed (%)

Baden and Walker 47 Retrospective NR 2– 15 yr 77 33

(1987) (30) cohort
Farrel and Ling 27 Retrospective 8 mo NR 96 4
(1997) (31) cohort
Mallipeddi et al. 21 Retrospective 20 mo 0.8– 35 mo 43 57
(2001) (23) cohort

NR, not reported.

628 Barber

Table 3 Outcomes of Abdominal Paravaginal Repair for Treatment of Anterior Vaginal Prolapse

Follow-up
No. of
Study (year) patients Study design Mean Range Cure (%) Failed (%)

Richardson et al. 60 Retrospective 20 mo 3 – 48 mo 97 3

(1976) (6) cohort
Richardson et al. 233 Retrospective NR 2 – 8 yr 95 5
(1981) (29) cohort
Shull and Baden 149 Retrospective 48 mo 0.5– 6 yr 95 5
(1989) (14) cohort
Bruce et al. (1999) 52 Retrospective 17 mo NR 92 8
(28) cohort
Scotti et al. (1998) 40 Prospective 39 mo 7 – 52 mo 97 3
(27)a cohort

NR, not reported.

a
Paravaginal attachment site included ischial periosteum and obturator membrane in addition to arcus tendinius fasciae
pelvis.

offers some potential advantages over the retropubic approach including shorter recovery time,
the ability to simultaneously correct midline anterior defects and the avoidance of an abdominal
incision, it may have a higher rate of intraoperative hemorrhage and blood transfusion. Young
et al. reported a 9% blood transfusion rate in their series of 100 vaginal paravaginal repairs, and
three patients required intraoperative vascular surgery consultation (25). Similarly, 12% of
patients received a blood transfusion in the Elkins et al. series of 25 patients who received a
vaginal paravaginal repair (26). This is in contrast to a transfusion rate of 0 –4% in series of

Table 4 Outcomes of Vaginal Paravaginal Repair for Treatment of Anterior Vaginal Prolapse

Follow-up
No. of
Study (year) patients Study design Mean Range Cure (%) Failed (%)

White 19 Retrospective NR Up to 3 yr 100 0

(1909) (4) cohort
Shull et al. 62 Retrospective 1.6 yr 0.1– 5.6 yr 76 24
(1994) (32) cohort
Farrell and Ling 27 Retrospective 8 mo NR 80 20
(1997) (31) cohort
Nguyen and Bhatia 10 Retrospective 1 yr NR 100 0
(1999) (33) cohort
Elkins et al. 25 Retrospective NR 0.5 – 3 yr 76 24
(2000) (24) cohort
Mallipeddi et al. 35 Retrospective 20 mo 8– 35 mo 97 3
(2001) (23) cohort
Young 100 Retrospective 11 mo 1– 36 mo 78 22
(2001) (25) cohort

NR, not reported.

 Surgical Correction of Paravaginal Defects 629

abdominal paravaginal defect repair (6,14,21,27,28). The limited exposure and technical chal-
lenge of the vaginal approach likely explain this difference.

VI. CONCLUSION

Anterior vaginal prolapse commonly results from loss of lateral vaginal support. Paravaginal
defect repairs appear to be effective in correcting this loss of lateral support and can be
performed from abdominal, vaginal, or laparoscopic approaches. Although initially advocated
as a treatment for genuine stress urinary incontinence, current evidence suggests that it is less
effective than other standard anti-incontinence procedures. Studies evaluating the long-term effi-
cacy of the paravaginal defect repair and studies comparing paravaginal defect repair with other
procedures for treating anterior vaginal prolapse are necessary.

REFERENCES

1. Samuelsson EC, Victor FTA, Tibblin G, Svardsud KF. Signs of genital prolapse in a Swedish popu-
lation of women 20 to 59 years of age and possible related factors. Am J Obstet Gynecol 1999;
180:299– 305.
2. Shull BL, Bachofen C, Coates KW, Kuehl TJ. A transvaginal approach to repair of apical and other
associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 2000;
183:1365– 1373.
3. DeLancey JOL. Structural support of the urethra as it relates to stress urinary incontinence: the ham-
mock hypothesis. Am J Obstet Gynecol 1994; 170:1713 – 1723.
4. White GR. Cystocele. JAMA 1909; 21:1707– 1710.
5. Kelly HA. Incontinence of urine in women. Urol Cutaneous Rev 1913; 17:291 – 293.
6. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;
126:568– 571.
7. Weber AM, Walters MD. Anterior vaginal prolapse: review of anatomy and techniques of surgical
repair. Am J Obstet Gynecol 1997; 89:311– 318.
8. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;
166:1717– 1724.
9. Strohbehn K. Normal pelvic floor anatomy. Obstet Gynecol Clin North Am 1998; 25:683 – 705.
10. Mauroy B, Goullet E, Stefaniak X. Bonnal JL, Amara N. Tendinous arch of the pelvic fascia: appli-
cation to the technique of paravaginal colposuspension. Surg Radiol Anat 2000; 22:73– 79.
11. Strohbehn K, DeLancey JOL. The anatomy of stress incontinence. Oper Tech Gynecol Surg 1997;
2:5– 16.
12. Shull BL. How I do the abdominal paravaginal repair. J Pelvic Surg 1995; 1:43 –46.
13. Barber MD, Cundiff GW, Weidner AC, Coates KW, Bump RC, Addison WA. Accuracy of clinical
assessment of paravaginal defects in women with anterior vaginal wall prolapse. Am J Obstet
Gynecol 1999; 181:87 – 90.
14. Shull BL, Baden WF. A six-year experience with paravaginal defect repair for stress urinary incon-
tinence. Am J Obstet Gynecol 1989; 160:1432– 1439.
15. Shull BL. Clinical evaluation of women with pelvic support defects. Clin Obstet Gynecol 1993;
36:939– 951.
16. Aronson MP, Bates SM, Jacoby AF, Chelmow D, Sant GR. Periurethral and paravaginal anatomy: an
endovaginal magnetic resonance imaging study. Am J Obstet Gynecol 1995; 173:1702 – 1708.
17. Huddleston HT, Dunnihoo DR, Huddleston PM, Meyers PC. Magnetic resonance imaging of defects
in DeLancy’s vaginal support levels I, II, III. Am J Obstet Gynecol 1995; 172:1778 – 1782.
630 Barber

18. Ostrzenski A, Osborne NG, Ostrenska K. Method for diagnosing paravaginal defects using contrast
ultrasonograpic technique. J Ultrasound Med 1997; 16:673 – 677.
19. Ostrzenski A, Osborne NG. Ultrasonography as a screening tool for paravaginal defects in women
with stress incontinence: a pilot study. Int Urogynecol J 1998; 9:195– 199.
20. Nguyen JK, Hall CD, Bhatia NN. Sonographic diagnosis of paravaginal defects: A standardization of
technique. Int Urogynecol J 2000; 11:341-345.
21. Colombo M, Milani R, Vitobello D, Maggioni A. A randomized comparison of Burch colposuspen-
sion and abdominal paravaginal defect repair for female stress urinary incontinence. Am J Obstet
Gynecol 1996; 175:78 – 84.
22. Thompson PK, Mooney RJ, Plummer A, Bahar VT. Paravaginal plus: a better incontinence oper-
ation? J Pelvic Surg 1998; 4:157 – 162.
23. Mallipeddi PK, Steele AC, Kohli N, Karram MM. Anatomic and functional outcome of vaginal para-
vaginal repair in the correction of anterior vaginal prolapse. Int Urogynecol J 2001; 12:83– 88.
24. Elkins TE, Chesson RR, Videla F, Menefee S, Yordan R, Barksdale PA. Transvaginal paravaginal
repair: a useful adjunctive procedure in pelvic relaxation surgery. J Pelvic Surg 2000; 1:11– 15.
25. Young SB, Daman JJ, Bony LG. Vaginal paravaginal repair: one-year outcomes. Am J Obstet
Gynecol 2001; 185:1360 – 1367.
26. Harris RL, Cundiff GW, Theofrastous JP, Yoon H, Bump RC, Addison WA. The value of intraopera-
tive cystoscopy in urogynecologic and reconstructive pelvic surgery. Am J Obstet Gynecol 1997;
177:1367– 1369.
27. Scotti RJ, Garely AD, Greston WM, Flora RF, Olson TR. Paravaginal repair of lateral vaginal wall
defects by fixation to the ischial periosteum and obturator membrane. Am J Obstet Gynecol 1998;
179:1436– 1445.
28. Bruce GR, El-Galley RES, Galloway NTM. Paravaginal defect repair in the treatment of female stress
urinary incontinence and cystocle. Urology 1999; 54:647 – 651.
29. Richardson AC, Edmonds PB, Williams NL. Treatment of stress urinary incontinence due to parava-
ginal fascial defects. Obstet Gyencol 1981; 57:357– 362.
30. Baden WF, Walker T. Urinary stress incontinence: evolution of paravaginal repair. Female Patient
1987; 12:89– 105.
31. Farrell SA, Ling C. Currycombs for the vaginal paravaginal defect repair. Obstet Gynecol 1997;
90:845– 847.
32. Shull BL, Benn SJ, Kuehl TJ. Surgical management of prolapse of the anterior vaginal segment: an
analysis of support defects, operative morbidity and anatomic outcomes. Am J Obstet Gynecol 1994;
171:1429– 1439.
33. Nguyen JK, Bhatia NN. Transvaginal repair of paravaginal defects using the Capio suturing device: a
preliminary experience. J Gynecol Tech 1999; 5:51 – 54.
34. Cundiff GW, Addison WA. Management of pelvic organ prolapse. Obstet Gynecol Clin North
America 1998; 25:914.
44
Paravaginal Repair: A Laparoscopic Approach

John R. Miklos and Robert Moore

Atlanta Urogynecology Associates, Atlanta, Georgia, U.S.A.
Neeraj Kohli
Harvard University, Boston, Massachusetts, U.S.A.

I. INTRODUCTION

The support of the anterior vaginal wall, with its overlying bladder and urethra, is dependent
upon the inherent strength of the pubocervical fascia and its lateral attachment to the pelvic
sidewalls. Specifically, the pubocervical fascia is attached to the arcus tendineus fascia pelvis
(also termed “the white line”). The arcus tendineus fascia pelvis is a condensation of intervening
connective tissue overlying the obturator internus muscle (Fig. 1). Upon vaginal inspection the
anterior lateral vaginal sulcus shows excellent support when the pubocervical fascia and the
arcus tendineus are intact (Fig. 2). Loss of the lateral vaginal attachment to the pelvic sidewall
is called a paravaginal defect and usually results in a cystourethrocele, urethral hypermobility,
and/or stress urinary incontinence (Fig. 3). Vaginal inspection in patients with bilateral para-
vaginal defects reveals loss of anterior vaginal wall support with detachment of the
lateral sulci, resulting in a displacement cystocele (Fig. 4). White (1) first described the para-
vaginal repair in 1909, but it did not gain popularity until decades later, when Richardson
(2,3) and Shull (4,5) described their abdominal and vaginal approaches to this type of anterior
wall repair. Paravaginal defect repair has been described using not only vaginal and open
abdominal approaches but also, more recently, via a laparoscopic approach (6 – 8).

II. OPERATIVE INDICATIONS

Laparoscopy should be considered as only a mode of abdominal access and not a change in the
operative technique. The surgical repair of paravaginal defects should not be different whether
the approach is vaginal, abdominal, or laparoscopic. Ideally, the indications for a laparoscopic
approach to paravaginal defect repair should be the same as an open abdominal approach. The
laparoscopic approach to paravaginal defect repair can be substituted for an open paravaginal
repair in the majority of cases. Factors that might influence this decision include previous
abdominal, pelvic or anti-incontinence surgery, the patient’s weight, the need for concomitant
surgery, and the surgeon’s experience. The surgeon’s decision to proceed with a laparoscopic
paravaginal repair should be based on an objective clinical assessment that is consistent with
a paravaginal defect cystocele or cystourethrocele, as well as the surgeon’s own surgical skills.
The paravaginal repair can be performed alone or in combination with a urethropexy procedure
in patients with concomitant stress urinary incontinence.
631
632 Miklos et al.

Figure 1 Normal anterior vaginal wall support (aerial view). The space of Retzius and normal anterior
vaginal wall support.

III. PREOPERATIVE CONSIDERATIONS

A bowel preparation should be considered in any patient undergoing advanced reconstructive

pelvic surgery. The authors recommend a full liquid diet 48 h prior to surgery, and a clear liquid
diet and one bottle of magnesium citrate 24 h before surgery. This regimen appears to improve
operative field visualization by bowel decompression and reduces the chance of contamination in
case of accidental bowel injury. A single dose of prophylactic intravenous antibiotics is adminis-
tered 30 min before surgery. Antiembolic compression stockings are routinely used. The patient
is intubated, given general anesthesia, and placed in dorsal lithotomy position with both arms
tucked to her side. A 16F three-way Foley catheter with a 5-mL balloon tip is inserted into the
bladder and attached to continuous drainage. The authors find that a 30-cc balloon tip filled to
capacity actually will hinder visualization and suture placement, especially paraurethrally.

IV. SURGICAL TECHNIQUE

The technique of abdominal entry and insufflation is a matter of surgeon’s preference.

The authors routinely perform open laparosocopy at the inferior margin of the umbilicus.
A 10-mm access port is inserted to introduce the laparoscope. The abdomen is insufflated
 Paravaginal Repair: A Laparoscopic Approach 633

Figure 2 Normal anterior vaginal wall support (vaginal exam). The anterior vaginal wall is well
supported with normal lateral fornix attachment.

with CO2 to 15 mm Hg intra-abdominal pressure. Three additional ports are placed under direct
vision (Fig. 5). The type of port, choice of port size, and placement depend upon the planned
concomitant surgery as well as the surgeon’s preference.
The bladder is filled in a retrograde fashion with 200– 300 mL of sterile water, allow-
ing identification of the superior border of the bladder edge. A harmonic scalpel is used to incise
the peritoneum 3 cm anterior to the bladder reflection, between the obliterated umbilical
ligaments (Fig. 6). Identification of loose areolar tissue confirms a proper plane of dissection.
After the space of Retzius has been entered and the pubic ramus visualized, the bladder
is drained to prevent injury. Using blunt dissection the retropubic space is developed by separ-
ating the loose areolar and fatty layers. Blunt dissection is continued until the retropubic anat-
omy is visualized. The pubic symphysis and bladder neck are identified in the midline and the
obturator neurovascular bundle, Cooper’s ligament, and the arcus tendineus fascia pelvis (white
line) are visualized bilaterally along the pelvic sidewall (Fig. 1). The anterior vaginal wall and its
point of lateral attachment from its origin at the pubic symphysis to its insertion at the ischial
spine are identified. If paravaginal wall defects are present, the lateral margins of the pubocer-
vical fascia will be detached from the pelvic sidewall at the arcus tendineus fascia pelvis. The
lateral margins of the detached pubocervical fascia and the broken edge of the white line can
usually be clearly visualized confirming the paravaginal defect. Unilateral or bilateral defects
may be present (Fig. 3).
After identification of the defect, the repair is begun by inserting the surgeon’s nondomi-
nant hand into the vagina to elevate the anterior vaginal wall and the pubocervical fascia to their
normal attachment along the arcus tendineus fascia pelvis. A 2-0 nonabsorbable suture
with attached needle is introduced through the 12-mm port and the needle is grasped using a
laparoscopic needle driver.
634 Miklos et al.

Figure 3 Paravaginal defects (aerial view). Loss of lateral vaginal attachment at the arcus tendineus,
resulting in a cystourethrocele.

The first suture is placed near the apex of the vagina through the paravesical portion of
the pubocervical fascia. The needle is then passed through the ipsilateral obturator internus
muscle and fascia around the arcus tendineus fascia at its origin 1 – 2 cm distal to the ischial
spine. The suture is secured using an extracorporeal knot-tying technique. Good tissue approxi-
mation is accomplished without a suture bridge. Sutures are placed and tied sequentially along
the paravaginal defects from the ischial spine toward the urethra. Usually a series of four to six
sutures are required to repair the paravaginal defect unilaterally. The surgical procedure is then
repeated on the opposite side if a bilateral paravaginal defect is present. Paravaginal defect
repairs restore anterior vaginal wall lateral attachment and support (Fig. 6). However, paravagi-
nal defect repair has little support in the literature for treatment of stress urinary incontinence. If
a patient has concomitant stress urinary incontinence, a laparoscopic urethropexy procedure can
be performed after the paravaginal repair.
The urethropexy will focus on the distal aspect of the anterior vaginal wall and the para-
vaginal repair will anatomically restore and support the proximal (bladder) portion of the
anterior vaginal wall. Instead of placing four to six paravaginal sutures on each side as
previously described, the proximal paravaginal repair, between the ischial spine and the urethro-
vesical junction, usually only requires two or three sutures on each side. This portion of the
surgery should repair the cystocele but will do nothing to support the urethra and its coexisting
stress urinary incontinence. The authors recommend coupling a Burch urethropexy with the
 Paravaginal Repair: A Laparoscopic Approach 635

Figure 4 Paravaginal defects (vaginal exam). Loss of lateral vaginal attachment at the arcus tendineus,
resulting in a cystourethrocele.

paravaginal repair to address the incontinence. A total of four sutures should be placed to
complete the Burch urethropexy: two sutures bilaterally, one paraurethrally at the midurethra,
and the other at the urethral vesical junction (Fig. 8). By coupling the Burch urethropexy
with the paravaginal repair, the surgeon can address both the proximal cystocele and the distal
urethral hypermobility and its coexisting stress urinary incontinence.
Upon completion of the Burch and/or paravaginal repair the intra-abdominal pressure is
reduced to 10– 12 mm Hg, and the retropubic space is inspected for hemostasis. Cystoscopy is
performed to rule out urinary tract injury. The patient is given 5 mL of Indigo Carmine and
10 mL of furosemide intravenously, and a 708 cystoscope is used to the visualize the bladder
mucosa, assess for unintentional stitch penetration and bladder injury, and confirm ureteral
patency. After cystoscopy, attention is returned to laparoscopy. The authors recommend routine
closure of the anterior peritoneal defect using an absorbable suture or a multifire hernia stapler.
All ancillary trocar sheaths are removed under direct vision to ensure hemostasis and exclude
iatrogenic bowel herniation. Excess gas is expelled and fascial defects of 10 mm or more are
closed using delayed absorbable suture. Skin edges are closed using an absorbable suture. Post-
operative bladder drainage and voiding trials are accomplished using a transurethral catheter,
suprapubic tube, or intermittent self-catheterization.
636 Miklos et al.

Figure 5 Laparoscopic incision sites. Port size and placement are illustrated.

Figure 6 Peritoneal incision. Using a harmonic scalpel to incise the peritoneum between the obliterated
umbilical ligaments and anterior to the bladder.
 Paravaginal Repair: A Laparoscopic Approach 637

Figure 7 Paravaginal repair: conventional repair of paravaginal defects. Nonabsorbable suture is used to
reapproximate the pubocervical fascia (i.e., anterior vaginal wall) back to its original point of lateral
attachment, known as the arcus tendineus fascia pelvis (i.e., “white line”).

V. CLINICAL RESULTS

Most studies reporting the efficacy of paravaginal repair in the treatment of genuine stress incon-
tinence, whether performed vaginally or abdominally, lack appropriate outcome data and control
groups. In a randomized prospective trial, Colombo et al. (12) performed Burch colposuspension
on 18 patients and abdominal paravaginal repair on 18 patients with genuine stress incontinence.
Patients undergoing Burch colposuspension had a significantly higher subjective (100% vs.
72%; P ¼ 0.2) and objective (100% vs. 61%; P ¼ 0.04) cure rates compared with patients
undergoing paravaginal repair. The study was discontinued early because the authors no longer
regarded it as ethical to propose paravaginal repair for the treatment of stress urinary inconti-
nence (13). Specifically, data regarding the efficacy of laparoscopic paravaginal repair are
also limited. Ostrzenski (14) performed laparoscopic paravaginal repair in 28 women with stress
urinary incontinence. The subjective cure rate was 93% with follow-up ranging from 1 to 4.5
years. Pre- and postoperative urodynamic testing were not utilized. Given a patient has conco-
mitant stress urinary incontinence with anterior vaginal wall prolapse due to paravaginal
defects, the authors recommend coupling the paravaginal repair with a proven anti-incontinence
operation such as a Burch urethropexy or a transvaginal sling.
Most surgeons utilize the paravaginal repair for the correction of anterior vaginal wall
prolapse and do not rely on this operation for the treatment of stress urinary incontinence.
638 Miklos et al.

Figure 8 Paravaginal plus Burch urethropexy. The paravaginal sutures are placed to restore anatomy
and correct the proximal cystocele, and four additional paraurethral suspension sutures (i.e., Burch
urethropexy) are placed in patients diagnosed with stress urinary incontinence.

Paravaginal repair is an anatomically correct operation for the treatment of anterior vaginal
wall prolapse due to paravaginal defects. As described above, the objective of the paravaginal
repair is to reattach the anterolateral vaginal sulcus to the obturator internus muscles and
fascia at the level of the white line. Anterior vaginal wall prolapse cure rates .95%
have been reported utilizing the abdominal approach (2 – 4), and .90% utilizing the vaginal
(5,9 – 11) approach to paravaginal repair. Literature concerning the efficacy of the laparo-
scopic paravaginal repair for the cure of anterior vaginal wall prolapse is lacking. A recent
review of our experience (15) revealed that 130 of 171 patients had a Burch urethropexy
and paravaginal repair, 23 of 171 patients a Burch urethropexy alone, and 18 of 171 patients
a paravaginal repair alone. Of the authors’ 171 patients, four (2.3%) had injury to the lower
urinary tract during laparoscopic Burch urethropexy or paravaginal repair. All four injuries
were cystotomies, two in patients with previous open retropubic urethropexies. No ureteral
ligations or intravesical placement of suture was diagnosed. Other surgical parameters for
the laparoscopic Burch urethropexy and paravaginal repair include an estimated blood loss
of 50 mL, average hospital stay of ,23 h, and an average operative time of 70 min. All
patients had their surgery completed via laparoscopy.
Assuming that the paravaginal repair technique is not compromised by the
abdominal approach utilized (laparoscopic vs. laparotomy), one should expect equal surgical
efficacy.
 Paravaginal Repair: A Laparoscopic Approach 639

VI. CONCLUSION

Defects in the lateral attachment of the pubocervical fascia to the arcus tendineus fasciae pelvis
results in anterior vaginal wall prolapse and subsequent cystocele. The literature supports the use
of paravaginal repair in the treatment of anterior vaginal wall prolapse but does not support its
use for the treatment of stress urinary incontinence.
The authors support the use of the laparoscopic paravaginal repair in the treatment of
cystocele or cystourethroceles in patients with lateral anterior vaginal wall defects. The laparo-
scopic approach to paravaginal defect repair can be substituted for an abdominal or transvaginal
paravaginal repair in the majority of cases. Factors that might influence this decision include
previous abdominal, pelvic or anti-incontinence surgery, patient’s weight, the need for concomi-
tant surgery, and the surgeon’s experience. The paravaginal repair can be performed alone or
in combination with a urethropexy procedure in patients with concomitant stress urinary
incontinence.

REFERENCES

1. White GR. Cystocele, a radical cure by suturing lateral sulci of vagina to white line of pelvic fascia.
JAMA 1909; 65:286– 290.
2. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;
126:568– 573.
3. Richardson AC, Edmonds PB, Williams NL. Treatment of stress urinary incontinence due to para-
vaginal fascial defects. Obstet Gynecol 1981; 57:357– 361.
4. Shull BL, Baden WF. A six year experience with paravaginal defect repairs for stress urinary incon-
tinence. Am J Obstet Gynecol 1989; 160:1432– 1437.
5. Shull BL, Benn SJ, Kuehl TJ. Surgical management of prolapse of the anterior vaginal sement: an
analysis of support defects, operative morbidity and anatomic outcome. Am J Obstet Gynecol.
1994; 171:1429 – 1439.
6. Miklos JR, Kohli N. Paravaginal plus Burch procedure: a laparoscopic approach. J Pelvic Surg 1998;
4:297– 302.
7. Miklos JR, Kohli N. Laparaoscopic paravaginal repair plus Burch colposuspension: review and
descriptive technique. Urology 2000; 56:64 – 69.
8. Ross JW. Techniques of laparoscopic repair of total vault eversion after hysterectomy. J Am Assoc
Gynecol Laparosc 1997; 4(2):173 – 183.
9. Elkins TE, Chesson RR, Videla F, Menefee S, Yordan R, Barksdale PA. Transvaginal paravaginal
repair: a useful adjunctive procedure in pelvic relaxation surgery. J Pelvic Surg 2000; 6:11– 15.
10. Young SB, Daman JJ, Bony LG. Vaginal paravaginal repair: one-year outcomes. Am J Obstet Gyne-
col 2001; 185:1360– 1367.
11. Mallipeddi PK, Steele AC, Kohli N, Karram MM. Anatomic and functional outcome of vaginal para-
vaginal repair in the correction of anterior vaginal wall prolapse. Int Urogynecol J 2001; 12:83–88.
12. Colombo M, Milani R, Vitobello D. A randomized comparison of Burch colposuspension and
abdominal paravaginal defect repair for female stress urinary incontinence. Am J Obstet Gynecol
1996; 175:78 –84.
13. Nguyen JK. Current concepts in the diagnosis and surgical repair of anterior vaginal prolapse due to
paravaginal defects. Obstet Gynecol Surv 2001; 56:239 – 246.
14. Ostrzenski A. Genuine stress urinary incontinence in women: new laparoscopic paravaginal recon-
struction. J Reprod Med 1998; 43:466 – 482.
15. Speights SE, Moore RD, Miklos JR. Frequency of lower urinary tract injury at laparoscopic Burch
and paravaginal repair. J Am Assoc Gyencol Laparosc 2000; 7(4):515 – 518.
45
Transvaginal Levator Myorraphy for Vaginal
Vault Prolapse
Gary E. Lemack and Philippe E. Zimmern
University of Texas, Southwestern Medical Center, Dallas, Texas, U.S.A.

I. INTRODUCTION

The progressive development of vaginal pain or pressure in women with vaginal vault prolapse
and the frequent presence of accompanying lower urinary tract symptoms or bowel symptoms
often ultimately result in the desire for treatment. Proper repair of vault prolapse will not
only restore vaginal position and function, but also result in an improvement of pelvic symp-
toms. Though conservative measures such as colpocleisis or pessaries may be appropriate to
consider in a subset of women who are less fit for surgery, most active women desire an inter-
vention that will not preclude or interfere with intercourse. Surgical procedures offer the best
hope of a permanent correction, and several techniques have been described, including both
abdominal (1,2) and vaginal approaches (3,4).
Both approaches for repairing vault prolapse appear to be equally efficacious. However,
using vaginal approaches, recovery is expedited, and the morbidity occasionally associated
with open abdominal procedures is minimized. While for years several authors have advocated
sacrospinous fixation as a means of treating vaginal vault prolapse (5,6), the inherent dangers
associated with possible damage to the adjacent vascular and neural structures make it a less
favored approach for some. Additionally, vaginal axis often becomes altered with a unilateral
fixation, and there may be an increased risk of secondary cystocele formation following
traditional vaginal approaches (7). Therefore, an alternative vaginal approach was developed
over 10 years ago, using the levator shelf to both recreate the pelvic floor and to anchor
the upper vagina. The principles of this repair are based on an understanding of defects in the
pelvic floor that have been addressed in previously described abdominal levator repairs for
incontinence (8).

II. TECHNIQUE
A. Preoperative Evaluation
After performing a thorough history (with particular attention to previous attempts at repair), a
physical examination is performed. Care is taken to assess each vaginal compartment so as
to detect laxity posteriorly, anteriorly, and from the vault. Often, examination in the standing
641
642 Lemack and Zimmern

position may help to distinguish a rectocele from an enterocele associated with vault prolapse. If
the patient is noted to have an atrophic or ulcerated vagina, she is given vaginal estrogen cream
to administer topically, which may enhance wound healing postoperatively.
Since supine physical examination may underestimate the degree of prolapse present, we
normally obtain a standing voiding cystourethrogram (VCUG) prior to proceeding with surgical
correction. This study is performed largely from a lateral view with and without straining, both
with a Foley catheter and then during voiding (9). The VCUG gives information about the pre-
sence and extent (central and/or lateral defects) of cystocele, degree of urethral hypermobility,
presence of bladder wall trabeculations, urethral configuration during voiding, amount of post-
void residual, and presence or absence of vesicoureteral reflux. Determining the severity of the
anterior vaginal prolapse may impact on the type of surgical repair recommended in conjunction
with the vault fixation, and impact the need for further renal imaging preoperatively. Currently,
we obtain upper tract imaging in women who have grade 3 or 4 cystoceles (Baden classification)
in order to evaluate for hydronephrosis and for the possible need for intraoperative ureteral
stenting.
It is our practice to perform urodynamics both with and then without a vaginal pack to
reduce the associated cystocele, which is frequently present. While still controversial, recent
evidence suggests that correction of the prolapse during urodynamics may affect both pressure
flow relationship during voiding and may unmask incontinence during testing (10). These find-
ings, in turn, may influence the nature of the surgical repair, and play a role in preoperative coun-
seling. If a hysterectomy is being considered, pelvic ultrasound is obtained to assess uterine size
and endometrial lining, as well as to evaluate for ovarian abnormalities, since they are not
always easily removed from a vaginal approach.
The overall goals of the procedure depend on the clinical scenario. When uterine prolapse
is present, the levator myorraphy to fix the vault is coupled with vaginal hysterectomy, entero-
cele repair, and possible posterior repair. When an associated mild to moderate cystocele is
present, an anterior vaginal wall suspension, which anchors the upper vagina to the cardinal liga-
ments bilaterally, is also performed. Larger cystoceles will normally require both central and
lateral support. If the uterus has already been removed and an enterocele is present, vault fixation
and enterocele repair are carried out. By closing the enterocele sac, recreating a strong levator
plate and anchoring the upper vagina to that plate, a normal vaginal cavity with an adequate
posterior axis is restored. Other times, the enterocele sac can be identified and purposefully
not entered, but instead dissected proximally. Vault fixation and enterocele repair can still be
carried out after a levator myorraphy is accomplished, though in this instance, the dissection
remains extraperitoneal.

B. Technique of Vault Prolapse Repair After Hysterectomy

Patients are normally administered general anesthesia and given intravenous antibiotics at the
start of the procedure. Pneumatic compression stockings are applied and the patient is placed
in the dorsal lithotomy position. While the legs should be positioned fairly high, care should
be taken not to overextend or overabduct the hips, overflex the knees, and to be sure that all joints
are well padded. The perineum and suprapubic areas are completely trimmed and prepped since
an associated bladder neck suspension is often also required. A critical step is the placement of a
rectal pack (vaginal pack soaked with povidone iodine and surgical lubricant), which is inserted
after the vagina, perineum, and lower abdomen have been prepped.
After placing the patient in Trendelenburg position, a Lone Star retractor (Lone Star, Inc.,
Houston, TX) is placed, exposing the vaginal bulge over the prolapsed vault (Fig. 1), which nor-
mally represents the position of the enterocele. Generally, panendoscopy is carried out, noting
 Transvaginal Levator Myorraphy 643

Figure 1 Vault prolapse. E, enterocele sac. This can be confirmed by simultaneous placement of rectal
pack (to establish extent of rectocele), and catheter or cystoscope (to establish extent of cystocele).

the position of the ureters, and examining for bladder wall changes (trabeculations, diverticuli).
For large prolapses, it is our practice to place a suprapubic tube at this point. Ureteral stents can
be useful in case of hydronephrosis or in reoperations when trigonal anatomy has been distorted.
A urethral catheter is then placed, leaving the bladder on drainage during the entire case. Two
sutures are placed at the fornices of the vaginal vault for identification at the conclusion of the
case, and the dimensions of the reduced vagina are measured. We normally place a weighted
speculum at this point, but, owing to foreshortening associated with the exteriorization of the
prolapse, it may not be able to be placed until later in the case.
After infiltrating the incision line with sterile saline, a midline incision is made overlying
the area of prolapse extending from the vaginal apex as far distally as the associated rectocele is
appreciated. Occasionally, if a large ulcerated area on the vaginal wall is present, this area will
be excised superficially at the beginning of the procedure to ensure it is not incorporated in the
closure. If there is any suspicion of its appearance, it is sent to pathology for frozen section
analysis. Vaginal flaps are developed on both sides of the original incision, reapplying the
hooks of the Lone Star retractor periodically to provide enhanced exposure. Often, a Deaver
will be required to retract the bladder superiorly during this dissection.
After the vaginal flaps have been created and the dissection continued to the vaginal apex,
the enterocele sac may be identified. It may be difficult to differentiate the enterocele sac from a
large cystocele, and in these cases either a Van Buren sound or cystoscope placed into the blad-
der may aid in differentiating between the two. The peritoneal cavity is entered and small lapar-
otomy pads are positioned to displace the bowels superiorly. Placing the patient in a more
644 Lemack and Zimmern

exaggerated Trendelenburg position may enhance exposure by allowing the peritoneal contents
to gravitate away from the operative field. The levator musculature can then be identified bilat-
erally along the pelvic sidewall, just lateral to the rectum, which can easily be appreciated by the
presence of the preplaced rectal pack (demonstrated from intraabdominal view in Fig. 2). A No.
1 absorbable suture is then placed into the levator musculature (which is covered by a thin layer
of peritoneum), 3 cm above the junction of the levator with the rectum, coming out just above
the rectum within the body of the levator. This suture should be placed fairly deep into the body
of the muscle, and then the same suture is used to secure the levator muscle on the contralateral
side. This suture will later be tied across the midline to accomplish the levator myorraphy which
is shown postplacement from a cephalad view within the pelvis in Figure 3. The entire pelvis
should then be able to be rocked by tugging firmly on this suture. Another suture, similarly posi-
tioned into the body of the levator, is then placed 1 cm proximal to the last suture. Both are left
on stay clamps until the next step, the closure of the enterocele sac, is accomplished.
Prior to securing these sutures each across the midline and completing the levator myor-
raphy, a purse-string suture is placed circumferentially to close the peritoneal cavity, taking care
to remain superficial particularly along the peritoneal surface of the posterior bladder. The land-
marks used for enterocele closure are prerectal fascia posteriorly, pelvic sidewall laterally
(taking care to avoid the ovarian vessels which loom very close below the peritoneal surface),
and peritoneal surface over the posterior bladder wall anteriorly (Fig. 4). One should take care to
leave the ovaries within the peritoneal cavity if present, normal appearing, and not easily
reached to be removed during hysterectomy. This purse-string suture is placed above the levator
sutures, so as not to include them into the peritoneal cavity closure. After the peritoneal packs are
removed and the purse-string suture cinched down, Indigo Carmine is administered intrave-
nously and cystoscopy is carried out to insure ureteral patency. Any redundant portion of the
enterocele sac is excised.
The two preplaced levator sutures are then tied sequentially across the midline, and final
cystoscopic examination is performed. A strong, gushing efflux should be seen from both
ureters. If there is any doubt as to their patency, the levator suture may need to be cut and
replaced. If there is persistent decreased flow (no flow or very sluggish), then retrograde pyelo-
grams and/or stenting may be required to assure ureteral patency. The levator sutures (proximal
and distal) are then tagged with a hemostat. If the patient is sexually active, one should ensure
at this point that there is not excessive tightening of the upper vaginal segment by inserting two
or three fingers into the vaginal cavity. If this is the case, usually the more distal of the levator
sutures can be removed without jeopardizing the strength of the repair. If an anterior repair or
anti-incontinence procedure is required, it can now be carried out, followed by a rectocele repair
with perineorraphy, if indicated.
Prior to closing the epithelial edges at the vaginal apex, one end of each of the proximal
and distal levator myorraphy sutures from one side is threaded on a No. 6 curved Mayo
needle and transfixed at the new vaginal apex from the inside out, separated by 1 cm from
each other. The ideal placement of these sutures is at the vaginal fornix, which had been marked
by a stay suture at the start of the procedure. The same is carried out on the contralateral side,
with one end taken from the more proximal of the levator sutures, and one from the more distal
of the two. The former proximal and distal levator sutures are then secured to one another
thereby firmly anchoring the upper vagina to the newly created levator plate. Figure 5 demon-
strates the levator myorraphy sutures transfixed to the apex of the vagina, and Figure 6 shows the
final appearance of the recreated vaginal floor with direct apposition of the vaginal apex to the
rebuilt levator plate.
In some instances, entry into the enterocele sac may be unnecessary, particularly if the sac
is located proximally, high at the vaginal vault. In these cases, it can often be dissected cranially,
 Transvaginal Levator Myorraphy 645

Figure 2 Classic abdominal approach to enterocele/prolapse repair during hysterectomy. Note the
uterosacral ligaments, adjacent to the rectum, used for vaginal vault fixation and/or enterocele closure.

Figure 3 Placement of levator sutures, view from pelvis. Two No. 1 absorbable sutures are placed
intraperitoneally into the body of the levator muscles bilaterally, and they are drawn together in the
midline after being tied vaginally. L, levator muscles; R, rectum.
646 Lemack and Zimmern

Figure 4 Extraperitoneal levator myorraphy. Levator muscles have been tied across the midline, while
enterocele sac has not been entered. It has been dissected proximally and is now secured behind the midline
myorraphy.

away from the rectocele, while leaving the sac intact. However, failure to repair an enterocele
may lead to recurrent prolapse. The levator sutures can still be placed, tied, and secured to
the vaginal vault, but they remain entirely extraperitoneal (Fig. 4).
After completion, an antibiotic-soaked vaginal pack is placed, and a Foley urethral cath-
eter (and suprapubic tube if placed earlier) is left to drainage. The vaginal pack and urethral cath-
eter are left in place for 24 – 48 h and then removed. Residuals are checked by ultrasound or
suprapubic tube. If residuals are .100 mL, clean catheterization is performed, or, if a supra-
pubic tube has been placed, the tube is opened and residuals recorded until ,100 mL. This
occurs in generally less than 5 days.

III. RESULTS AND COMPLICATIONS

Postoperatively, most patients are hospitalized for 24 – 48 h. In our experience, no patients have
experienced anesthetic complications. As with most vaginal procedures, there is very little need
for postoperative analgesics, and all patients are ambulatory by the first postoperative day.
Patients are advised to avoid sexual intercourse for at least 3 months postoperatively, to give
the repair time to heal, and to allow time for all vaginal sutures to resorb.
A multicenter review of results using the levator myorraphy for repair of vaginal vault pro-
lapse or for vaginal vault fixation in the setting of vaginal hysterectomy is under way. We
 Transvaginal Levator Myorraphy 647

Figure 5 Vaginal vault has been fixed to levator myorraphy (lm) sutures (one on each side passed for this
photo). Note closure of vaginal vault (sutures) just superior to the levator myorraphy sutures, with direct
apposition of the vaginal vault to the rebuilt levator muscle complex beneath.

recently reported on 36 women who underwent levator myorraphy and vaginal vault fixation at
the University of Texas Southwestern Medical Center over the last 4 years and who had at least 1-
year follow-up and who completed a five-question telephone interview (mean follow-up 27.9
months, range 12 – 45 months) (11). Five patients required reoperation (four vaginal and one
abdominal). One had a symptomatic cystocele, two had anterior enteroceles, and two had recur-
rent vault prolapse. Occasional urge urinary incontinence was reported in 20 of 36 women,
though pad usage was rarely required, while stress urinary incontinence was noted by four
women (present in eight preoperatively). On examination, mild to moderate cystoceles were
noted in seven asymptomatic women.
Sexual function, while not a priority in many elderly patients undergoing prolapse surgery (12),
may be important to younger women (13). Among the women answering the telephone questionnaire,
14 were sexually active with three (21%) reporting discomfort with intercourse. Among these 14
were three women unable to have intercourse preoperatively because of the extent of prolapse. In
most women, there appeared to be no deleterious affect on sexual function, similar to our findings
in women undergoing anterior vaginal wall suspension surgery for stress incontinence (14). Overall,
when asked how satisfied they were with the results of the surgery, six women (17%) were dissatisfied
with the results of their operation (,50% satisfied) and 17 were extremely satisfied (.90%).
The major complications associated with any repair of vaginal prolapse include hemor-
rhage requiring transfusion, ureteral injury, rectal injury, rectal pain upon defecation, vaginal
narrowing affecting sexual function, and prolapse recurrence. In our hands, the risk of significant
648 Lemack and Zimmern

Figure 6 Final appearance of the posterior vaginal wall after completion of levator myorraphy. Vault
fixed in high location. Posterior suture line extends from vault toward perineum. Vagina is capacious,
with the natural 1308 posterior axis preserved.

bleeding has been minimal, with only two patients requiring transfusion over a 10-year period of
performing this procedure in over 120 patients. One patient with bilateral ureteral obstruction
was noted to be anuric in the recovery room, and required reexploration with removal of
one of the levator myorraphy sutures. One patient was noted to have flank pain and unilateral
hydronephosis after repair, which permanently resolved after 3 months of ureteral stenting.
We have had five cases where ureteral drainage was noted to decrease intraoperatively after
tying one of the levator myorraphy sutures. Prompt return of urine flow was observed after
removing one of the sutures, and we suspect that medial traction on the distal ureters resulted
from tying the levator myorraphy stitch. Secondary anterior enterocele formation has been
noted in two asymptomatic patients postoperatively, neither of whom has required revision or
sacrocolpopexy as yet. Rectal pain is uncommon, but when present usually subsides within
4 –6 weeks after the procedure and is best treated with stool softeners and warm Sitz baths.

IV. CONCLUSION

The levator myorraphy repair for vaginal vault prolapse is minimally invasive, is well tolerated,
requires no specific instrumentation, and is successful in the great majority of cases. Since no
intra-abdominal exploration is required, postoperative hospital stay is minimized. Risks to the
pudendal nerve and vessels are avoided using this technique, and therefore any pelvic surgeon
comfortable with vaginal surgery should be able to complete this repair without difficulty. As
 Transvaginal Levator Myorraphy 649

with any enterocele and vault repair, ureteral injury is always a risk, and precautions should be
taken throughout the procedure to guard against this possibility.

REFERENCES

1. Lane FF. Repair of posthysterectomy vaginal vault prolapse. Obstet Gynecol 1962; 126:590– 596.
2. Timmons MC, Addison WA, Addison SB, Cavenar MG. Abdominal sacral colpopexy in 163 women
with posthysterectomy vaginal vault prolapse and enterocele. J Reprod Med 1992; 37:322– 327.
3. Winkler HA, Tomeszko JE, Sand PK. Anterior sacrospinous vaginal vault suspension for prolapse.
Obstet Gynecol 2000; 95(4):612– 615.
4. Goldberg RP, Tomezsko JE, Winkler HA, Koduri S, Culligan PJ, Sand PK. Anterior or posterior
sacrospinous vaginal vault suspension: long-term anatomic and functional evaluation. Obstet Gynecol
2001; 98(2):199– 204.
5. Nichols DH. Sacrospinous fixations for massive eversion of the vagina. Am J Obstet Gynecol 1982;
142:901– 904.
6. Morley GW, DeLancey JOL. Sacrospinous ligament fixation for eversion of the vagina. Am J Obstet
Gynecol 1988; 158:872 – 881.
7. Sze EH, Kohli N, Miklos JR, Roat T, Karram MM. A retrospective comparison of abdominal sacro-
colpopexy with Burch colposuspension versus sacrospinous fixation with transvaginal needle suspen-
sion for the management of vaginal vault prolapse and coexisting stress incontinence. Int Urogynecol
J 1999; 10(6):390– 393.
8. Mouritsen L, Hansen PT, Kielmann J, Nielsen EL. Results of abdominal levator-muscle repair in urin-
ary stress incontinence. Scand J Urol Nephrol 1987; 21:281– 284.
9. Lemack GE, Zimmern PE. Voiding cystourethrography and magnetic resonance imaging of the lower
urinary tract. In: Corcos J, Schick E, eds. The Urinary Sphincter. NY: Marcel Dekker, 2001:407– 422.
10. Romanzi LJ, Chaikin DC, Blaivas JG. Effect of genital prolapse on voiding. J Urol 1997;
161:581– 586.
11. Lemack G, Blander DS, Margulis V, Zimmern PE. Vaginal vault fixation and prevention of enterocele
recurrence by high midline levator myorraphy (HMLM): physical examination and questionnaire-
based follow-up. Eur Urol 2001; 40:648 – 651.
12. Holley RL, Varner RE, Gleason BP, Apfell LA, Scott S. Sexual function after sacrospinous ligament
fixation for vaginal vault prolapse. J Reprod Med 1996; 41:355 – 358.
13. Weber AM, Walters MD, Schover LR, Mitchinson A. Sexual function in women with uterovaginal
prolapse and urinary incontinence. Obstet Gynecol 1995; 85:483 – 487.
14. Lemack GE, Zimmern PE. Sexual function after vaginal surgery for stress incontinence: results of a
mailed questionnaire. Urology 2000; 56:223 –227.
46
Sacrospinous Ligament Suspension for
Vaginal Vault Prolapse
Roger P. Goldberg and Peter K. Sand
Northwestern University Medical School, Evanston, Illinois, U.S.A.

I. INTRODUCTION

Sacrospinous vaginal vault suspension has been utilized for the repair of vaginal vault prolapse
for several decades—first described in Europe in 1958 (1), and later introduced to the United
States in 1971 (2). Long-term support of the vaginal apex can be achieved in 81 –100% of
cases (3 –6) even in the presence of severely attenuated pelvic supports, with anatomic and
sexual function effectively maintained in the vast majority of cases. Maintaining familiarity
with variations of surgical technique, and key anatomical landmarks, will help the reconstructive
surgeon to maximize the efficacy and safety of this operation.

II. INDICATIONS
A. Posthysterectomy Vault Prolapse
The most common indication for sacrospinous ligament suspension is resuspending a prolapsed
posthysterectomy vaginal apex. For women with pelvic ligaments and connective tissue supports
that are severely attenuated or absent, the sacrospinous ligament provides a consistently strong
site for apical fixation. Sacrospinous ligament suspension carries the advantages of the trans-
vaginal approach performed within the retroperitoneal rather than intra-abdominal space, invol-
ving relatively limited dissection beyond that which is performed for transvaginal enterocele,
rectocele, and cystocele repair. After sacrospinous suspension, the vaginal apex is suspended
posterolaterally to the ligament on either side or both sides.

B. Accompanying Vaginal Hysterectomy

Whereas the role of sacrospinous ligament suspension for posthysterectomy vault prolapse is
widely accepted, its use as a “prophylactic” measure to prevent future apical prolapse—at
the time of vaginal hysterectomy—has been a subject of debate. Some surgeons have advoca-
ted sacrospinous suspension as an adjunct to vaginal hysterectomy only when pelvic con-
nective tissues are markedly weakened, as demonstrated either by advanced uterine prolapse
651
652 Goldberg and Sand

preoperatively or absent uterosacral ligaments intraoperatively (7). Cruikshank and Cox (8) per-
formed sacrospinous ligament suspension on 48 of 135 such patients with lax or absent utero-
sacral ligaments at the time of vaginal hysterectomy; only one case of recurrent vaginal vault
prolapse was noted postoperatively, with no apparent excess morbidity. The authors concluded
that sacrospinous fixation is an appropriate adjunct to vaginal hysterectomy for cases involving
significant connective tissue weakness. Smilen and Porges (9) reported a trend indicating that
for severe uterine prolapse, adding that sacrospinous suspension to vaginal hysterectomy and
colporrhaphy may reduce the odds of recurrent apical prolapse.
Other retrospective studies, however, have indicated that even in the presence of utero-
vaginal prolapse, sacrospinous ligament suspension at the time of hysterectomy is not routinely
indicated (4,10,11). The use of McCall culdoplasty following vaginal hysterectomy, even in the
presence of markedly attenuated uterosacral ligaments, has been supported by retrospective ana-
lyses (12,13), including Colombo et al., who evaluated 62 matched pairs of women undergoing
hysterectomy with either sacrospinous ligament suspension or McCall culdoplasty (14). Oper-
ative time and average blood loss were greater in the sacrospinous group, and recurrent cysto-
celes were more likely at follow-up ranging from 4 to 9 years. No differences were found with
respect to the rates of recurrent prolapse of the vaginal apex (5 – 8%), overall prolapse at any site,
or sexual function (14). However, the potential for bias within a retrospective study design—due
to the assignment of subjects to their “strongest available ligament” at the time of surgery—
limits the conclusions that can be drawn. In actual practice, sacrospinous ligament suspension
may occasionally represent the most reliable alternative for apical fixation at the time of vaginal
hysterectomy, if no palpable uterosacral ligaments exist.

C. For Uterine Suspension

Finally, sacrospinous ligament suspension has been successfully utilized for women with symp-
tomatic uterovaginal prolapse who wish to preserve their uterus and reproductive capacity.
Kovac and Cruikshank (15) evaluated 19 women (average age 27) who underwent uterine-spar-
ing sacrospinous ligament suspension, and reported that four of five of them who subsequently
underwent a successful pregnancy and vaginal delivery did not have recurrent apical prolapse.
The procedure entails fixation of the distal uterosacral ligaments to the sacrospinous ligament,
often combined with uterosacral plication to reduce the risk of enterocele formation. Bilateral
rather than unilateral suspension was performed in 15 of the 19 subjects in this series, to
avoid lateral deviation of the uterus and any adverse effect it might have on reproductive
capacity.

III. TECHNIQUES
A. Exposing the Ligament
Access to the sacrospinous ligament and coccygeus muscle can be achieved by several means.
The most common approach, as described by Nichols (16), involves a posterior vaginal incision
and posterior colporrhaphy dissection, facilitating perforation of the rectal pillar near the ischial
spine. With blunt dissection of the pararectal space medial to the ligament, the coccygeus muscle
and sacrospinous ligament are exposed. The “anterior” sacrospinous suspension technique (17),
on the other hand, involves perforation into the retropubic space through an anterior colpor-
rhaphy incision, and dissection of the ipsilateral paravesical and paravaginal area from the
level of the bladder neck to the ischial spine. For cases involving mainly anterior compartment
defects with no rectocele, the anterior approach facilitates suspension of the vaginal apex
 Sacrospinous Ligament Suspension 653

without a posterior vaginal incision. Finally, some surgeons approach the sacrospinous ligament
by resecting a circumferential patch of excess epithelium at the most advanced portion of the
prolapsed vaginal cuff—a region of the vaginal skin that overlies an enterocele in most cases.
After repair of the enterocele, the ligament is exposed with posterolateral dissection within
the retroperitoneal plane. Because this apical approach exposes both the anterior vaginal epi-
thelium with underlying pubocervical fascia, and the posterior vaginal epithelium with rectova-
ginal fascia, sutures can be anchored through either or both of these cuff edges. Briesky-Navratil
retractors are well suited for exposing the coccygeus muscle and sacrospinous ligament without
obstructing the surgical field; some surgeons find retractors or suction devices mounted with a
fiberoptic light source to be particularly useful for identifying the retroperitoneal anatomy.

B. Suture Placement
Various devices have been specifically designed for placing sutures into the sacrospinous liga-
ment—including the Deschamps ligature carrier, Miya hook (18), and in-line “push and catch”
suturing devices (19). With proper assistance, some surgeons find a standard long curved needle
holder to be sufficient. The use of a “minimally invasive” device for transvaginal fixation of the
vaginal apex to the sacrospinous ligament, without an incision, has been recently described (20).
Among 12 women, the procedure appeared to be safe and well tolerated, with one case of recur-
rent vault prolapse reported at a mean follow-up of 16 months. Prospective, longer-term studies
will be necessary to determine its safety and efficacy.
Suturing into the sacrospinous ligament should be performed with key anatomic land-
marks in mind. The lateral suspension suture is placed through the ligament 1– 2 fingerbreadths
medial to the ischial spine to safeguard against injury to the pudendal vessels, though the risk of
this particular complication may be commonly overestimated (44). Care must be taken to place
sutures through the superficial portion of the ligament, rather than deep into or around it.
Medially, the rectum represents the anatomic boundary for suture placement. During this
stage of the operation, the primary surgeon must ensure that all retractors maintain their proper
position. The traumatic insertion of retractors beyond the ligament, or excessive medial traction
against the rectum and presacral area, is a potential source of operative complications. Medial
rather than lateral placement of sutures in the ligament also allows for a more cephalad suspen-
sion of the vaginal vault.
Fixation of the vaginal wall at the apex is most commonly performed with permanent
monofilament sutures; other surgeons prefer synthetic absorbable material to reduce the theor-
etical risk of suture erosion and granulation tissue formation. Preparation of the vaginal apex for
fixation can involve either full cuff closure, or a circumferential “whip stitch” for securing
hemostasis followed by apposition of the open cuff against the ligament. Medial and lateral
anchoring sutures are secured to the undersurface of the posterior vaginal cuff epithelium (for
the posterior approach), or anterior vaginal cuff epithelium (for the anterior approach), or
both (for the apical approach). Although scarring and fibrosis at the interface of the ligament
and new vaginal apex may theoretically eliminate the need for sutures after the initial healing
phase, the relative advantages of permanent versus absorbable sutures have not been scientifi-
cally evaluated.
Regardless of the type of suture used or anatomic approach to the ligament, a few prin-
ciples for suture placement appear to be universally important. First, the surgeon should take
care to avoid the creation of a “suture bridge” between the vagina and ligament; the use of pulley
stitches, which attach one end of each suture to the vaginal cuff epithelium, may help in apply-
ing the vagina directly against the ligament. Secondly, maintaining a width of at least two
654 Goldberg and Sand

centimeters between the medial and lateral fixation sutures will minimize the risk of constriction
at the vaginal apex.

C. Unilateral Versus Bilateral

Sacrospinous ligament suspension is most commonly performed as a unilateral procedure on
the patient’s right side owing to the mechanical advantage afforded to right-hand-dominant
surgeons, and the anatomic advantage resulting from the absence of the sigmoid colon on
the right. Bilateral suspension was emphasized in early reports (21) and even recently has
been advocated by some experienced surgeons (22). Pohl and Frattarelli (23) reported no
recurrent apical prolapse among 40 women treated with bilateral sacrospinous ligament sus-
pension after 6– 40 months follow-up. Cespedes (24) reported good success following bilat-
eral sacrospinous fixation by the anterior vaginal approach; at 17 months, no recurrent
vault prolapse was seen in 27 of 28 women with grade 3 –4 prolapse. However, there is little
evidence to suggest that bilateral suspension improves outcomes compared with the unilateral
approach (4). Moreover, in comparison to the unilateral sacrospinous ligament suspension, the
bilateral procedure entails more extensive dissection and requires generous width at the vagi-
nal apex to avoid causing tension between fixation points. Because of these additional chal-
lenges and its lack of clear advantage, the bilateral technique is utilized far less often than
unilateral fixation.

D. Pre- and Perioperative Considerations

The decision to proceed with sacrospinous ligament suspension may be influenced by a patient’s
specific anatomic features or medical history. For women with prior intra-abdominal surgery,
pelvic adhesions, or other contraindications to abdominal surgery, the fully retroperitoneal
nature of sacrospinous ligament suspension may confer advantages with respect to surgical
risk, operative time, and speed of recovery. Preoperative evaluation should also include assessment
of bony and soft tissue pelvic anatomy. Markedly foreshortened bony pelvic dimensions—such
as a true “platypoid” pelvis—may limit the surgeon’s ability to preserve adequate vaginal length,
and weigh against the choice of sacrospinous suspension for sexually active patients. With
respect to soft tissue, the length of the vaginal vault should be sufficient to avoid tension follow-
ing sacrospinous fixation, which may predispose to suture pullout, anatomic distortion, and poss-
ibly even an “unmasking” of potential urinary incontinence due to posterior displacement of the
urethra from the pubic bone (9). In the absence of adequate length, operative revision of the cuff,
or suspension to a more anterior or distal structure such as iliococcygeus fascia (25), may be
performed. Consideration of concomitant sacrospinous vaginal suspension on the right, with
an iliococcygeal suspension on the left at a slightly more distal point, may lead to improved api-
cal support and diameter.
Preoperative planning should include assessment of estrogen status for postmenopausal
women, and consideration of systemic or local estrogen therapy before surgery if the vaginal
cuff epithelium appears thin or poorly vascularized. Estrogen improves vaginal vascularization
and supports an improved epithelium and connective tissue. A well-estrogenized vaginal
epithelium should therefore facilitate healing at the site of suture fixation and reduce the likeli-
hood of subsequent surgical failure resulting from suture “pullout” from the vaginal side.
At the time of surgery, coexisting pelvic floor support defects need to be recognized and
repaired. An unrecognized enterocele, in particular, is often to blame for the rare case of recur-
rent apical prolapse following sacrospinous suspension. As with all reconstructive operations,
 Sacrospinous Ligament Suspension 655

appropriate patient selection and flexibility in the operating room will maximize the odds of
success.

IV. ANATOMIC OUTCOMES

A. Support of the Vaginal Apex
The long-term efficacy of sacrospinous ligament suspension for resuspending a prolapsed vagi-
nal cuff has been borne out by several clinical series. The success rates of the larger reports, with
mean follow-up intervals, are listed in Table 1. Although the majority of outcomes reported for
the sacrospinous ligament suspension have referred to either the posterior or apical approach,
recent reports evaluating the anterior sacrospinous ligament suspension have found similar
rates of success. Furthermore, based on one retrospective analysis of 168 women following
either anterior (n ¼ 76) or posterior (n ¼ 92) sacrospinous vault suspension, no measurable
differences appeared to exist with respect to apical support, vaginal caliber according to
maximum dilator size, or angle of the vaginal vault (26).
Following sacrospinous ligament suspension, the apex of the vagina is retroverted and
laterally positioned—anatomic changes that appear to have no functional consequences. Morley
and DeLancey proposed that this asymmetry might even confer a functional benefit postopera-
tively by positioning the vaginal vault away from the urogenital hiatus and over the levator
muscles, lessening the intra-abdominal pressures applied to the vaginal apex. Narrowing of
the vaginal apex into a cylindrical shape, due to the excision of excess anterior and/or posterior
vaginal epithelium, is felt by some to be a desired anatomic consequence of unilateral sacrospi-
nous suspension (27). Following bilateral suspension, a T-shaped or Y-shaped (with concomi-
tant enterocele repair) vaginal apex will often be appreciable by examination, but appears to
confer no functional disadvantage.
One matched case control study compared sacrospinous suspension to iliococcygeus
fixation for prolapse of the vaginal apex, and reported higher “patient satisfaction” scores
among the sacrospinous group at a mean follow-up of 20 months. Nonsignificant trends

Table 1 Suspension of the Vaginal Apex: Sacrospinous Ligament Suspension

Mean follow-up Success: apical

Study No. of subjects (months) support (%)

Richter and Albrich, 1981 (47) 81 not reported 100

Nichols, 1982 (48) 163 24 97
Morley and DeLancey, 1988 (4) 71 12 96
Shull et al., 1992 (25) 41 48 98
Pasley, 1995 (30) 156 35 94.4
Hardiman and Drutz, 1996 (5) 125 6 – 60a 97.6
Paraiso et al., 1996 (35) 243 73.6 93
Meschia et al., 1999 (51) 91 12 85
Winkler et al., 2000 (17) 75 8.5 93
(anterior approach)
Cespedes, 2000 (37) 28 17 96.4
(anterior bilateral approach)
Lantzsch et al., 2001 (41) 123 57 96.7
a
Follow-up reported as range; mean interval not specified.
656 Goldberg and Sand

indicated better support after the sacrospinous approach, according to both subjective and
objective outcomes (28).

B. Anterior Vaginal Wall Support

The anterior vaginal compartment appears to represent a particularly vulnerable site following
sacrospinous vaginal vault suspension, perhaps a consequence of vaginal retroversion predis-
posing to a compensatory abnormality. Several clinical series, but not all (29), have demon-
strated an elevated risk of cystocele formation following sacrospinous ligament suspension.
Recurrent cystoceles have been reported in 7.6 – 92% (4,30,36,47) of women after sacrospinous
ligament suspension, depending on the other specific procedures performed concurrently.
Although early series found recurrent cystoceles in 6% of women who had satisfactory
support at the apex (4), Paraiso (35) reported significant anterior wall defects in 26.7% of
women after sacrospinous ligament suspension. Another retrospective series, comparing 122
sacrospinous suspensions to a variety of other reconstructive procedures performed by a single
surgeon, reported that sacrospinous suspension had no association with subsequent anterior
compartment defects.
Sze et al. (3) reported on 96 women who had pelvic organ prolapse to or beyond the
hymen, and compared women who underwent sacrospinous ligament suspension with and with-
out concomitant transvaginal needle suspension. An overall 33% rate of recurrent prolapse was
observed when the two procedures were performed in tandem, compared with 19% in women
who underwent sacrospinous suspension only. The difference, however, did not reach statistical
significance. Barber et al. (50) reported a 21% incidence of stage III cystoceles following sacro-
spinous ligament suspension, at a mean follow-up interval of 19 months. The incidence rose to
36% when sacrospinous suspension was performed in tandem with needle bladder neck suspen-
sion. Although the precise mechanisms leading to recurrent anterior vaginal wall prolapse have
yet to be outlined, it has been proposed that posterior deflection of the vaginal vault after sacro-
spinous ligament suspension leads to increased “exposure” of the anterior compartment to intra-
peritoneal forces (31,32). Shull et al. (25) suggested that underestimation of the severity of
anterior prolapse on preoperative examination—or overreliance on the apical suspension for
compensation of anterior support defects—may also play a role. In their series, 16% of patients
with anterior vaginal wall prolapse before surgery had no repair of the anterior vaginal wall per-
formed during their initial surgery. Accurately identifying all areas of prolapse and tailoring the
pelvic reconstruction according to intraoperative findings, represent key ingredients for a
successful outcome.

C. Vaginal Anatomy and Sexual Function

Most studies of sacrospinous ligament suspension have focused on anatomic outcomes—specifi-
cally, the rates of recurrent apical and anterior vaginal prolapse. Fewer studies have addressed
outcomes more directly relevant to function, such as vaginal length, caliber, axis, and sexual satis-
faction. Morley and DeLancey reported vaginal stenosis in four of 78 women evaluated at least 1
year after sacrospinous ligament suspension, and one patient with vaginal foreshortening requir-
ing subsequent vaginaplasty. Elkins et al. (33) and Given et al. (34) quantified postoperative
vaginal anatomy in more detail, reporting an average vaginal length following sacrospinous liga-
ment suspension of 8.3 cm, and 8.2 cm, respectively. Paraiso et al. (35) evaluated an even wider
variety of outcomes following sacrospinous suspension at a mean interval of 98.8 months.
Vaginal length averaged 8.0 cm, and vaginal caliber measured as less than two fingerbreadths
in 17%; new-onset vaginal constriction was reported in 7.4%.
 Sacrospinous Ligament Suspension 657

Sexual dysfunction following pelvic reconstruction with sacrospinous suspension was

reported in 14% by Paraiso et al. (35); however, less than half represented de novo cases. Surpri-
singly, vaginal length and caliber, and the presence of specific support defects, were not
associated with reported sexual activity in this series. Holley et al. (36), on the other hand,
concluded that postoperative vaginal narrowing was a significant predictor of sexual activity
following sacrospinous suspension and vaginal reconstruction, with 25% of patients reporting
postoperative sexual dysfunction. When vaginal narrowing did not occur, sexually active part-
ners reported either unchanged or improved sexual function. These authors, in agreement with
other reports (14,36), concluded that vaginal narrowing and sexual dysfunction after sacrospi-
nous ligament suspension is most often the result of anterior colporrhaphy and the repair of
other concomitant defects rather than the sacrospinous suspension itself. Retroversion of the
vaginal apex, and deviation after unilateral sacrospinous suspension, appear to have no adverse
effects on coital function postoperatively.
Another retrospective analysis addressed sexual outcomes in 133 women following
sacrospinous ligament suspension: 76 following posterior sacrospinous suspension, and 57 follo-
wing anterior suspension, at a median interval of 41.3 months. Before surgery, 19 (33%) were
sexually active in the anterior vault suspension group, and 0% reported dyspareunia; 28 (37%)
were sexually active in the posterior vault suspension group, with nine (13%) reporting dyspar-
eunia. At long-term follow-up, two subjects in the anterior vault suspension group and two in the
posterior vault suspension group reported new onset dyspareunia; three of these four cases of de
novo dyspareunia were referable to either severe atrophy or recurrent grade 3 prolapse, and none
were attributed to vaginal narrowing or shortening. Sacrospinous ligament suspension itself thus
appears to have minimal if any impact on sexual function postoperatively, and the choice of
anterior or posterior technique has no discernable impact on sexual outcomes. Perhaps most
encouragingly, five women in this series reported dyspareunia at their preoperative baseline
visit, which resolved after vaginal reconstruction with sacrospinous ligament suspension.

D. Predictors of Success
The long-term success of sacrospinous ligament suspension depends on a multitude of factors,
including the quality of endopelvic connective tissues, postoperative convalescence, lifestyle
factors, and the repair of all coexisting pelvic floor support defects at the time of surgery.
Clearly, over the years after vaginal reconstructive surgery, new risk factors may emerge
along with changes in hormonal status and activity patterns; physical stresses, such as a chronic
cough or constipation, may accumulate over time. Regardless of the multiple factors deter-
mining surgical success, it appears that a successful healing process in the short term may reflect
strong odds for success over the long run. Shull et al. (25) reported that among 81 women treated
with sacrospinous ligament suspension and pelvic reconstruction, the absence of any pelvic
support defect at the 6-week postoperative visit was associated with only 3% likelihood that
the patient would require subsequent reconstructive surgery within 2 –5 years.

V. SAFETY AND COMPLICATIONS

Aside from the general risks accompanying transvaginal reconstructive surgery, specific poten-
tial risks associated with the sacrospinous should be addressed. Local neurological compli-
cations may include sacral neuropathy (11). Pudendal nerve entrapment may result in pain
localizing in the buttocks or perineum, and may improve following replacement of lateral
fixation sutures more medially (37). Gluteal pain or paresthesias may occur after sacrospinous
658 Goldberg and Sand

suspension (3,38,39), possibly due to peripheral nerve trauma. Though these symptoms are
nearly always transient and self-limited, they may persist for a period of weeks or even
months postoperatively. Cruikshank found that 20 of 135 women experienced buttock pain
after sacrospinous ligament suspension, with all cases resolving spontaneously by 6 weeks.
Even in the absence of direct pudendal nerve injury, pain may still occur due to the wide distri-
bution of nerve tissue throughout the ligament and apparently most concentrated in its medial
portion (40). Sciatic nerve irritation after sacrospinous suspension has been described as a
new-onset problem (41) and as an exacerbation of previous symptoms (4).
Serious vascular injury is a rare complication of sacrospinous ligament suspension, but can
be life-threatening. Morley and DeLancey (4) reported a transfusion rate of only 4%, and one
infected hematoma resulting in sepsis. Various other series have reported transfusion rates
ranging from 2% to 28% (30,42). To effectively manage pelvic hemorrhage, familiarity with the
surrounding anatomic landmarks is essential. Verdeja et al. (43) demonstrated that the pudendal
neurovascular bundle ranges in location from 0.90 to 1.30 cm medial to the ischial spine; the sciatic
nerve is located 3.10–3.30 cm medial to the spine. Based on these anatomical relationships, the
sacrospinous ligament would appear to be most vulnerable along its lateral third. Yet another series
of cadaver dissections, performed by Barksdale et al. (44), showed the pudendal neurovascular bun-
dle to be relatively shielded from injury by the ischial spine and sacrospinous ligament. The inferior
gluteal artery—with a more perpendicular course relative to the ligament—was the vascular struc-
ture whose location appeared most vulnerable to injury. The authors referred to three elements of
the operation that may carry particular risk: suture placement along the posterior ligament, retractor
placement beyond the ligament, and overly aggressive denuding of the ligament surface.
For the vast majority of cases involving significant bleeding, ligation with either sutures or
surgical clips can be achieved under direct exposure with simple retraction; a rectal examining finger
can be particularly useful for both tamponade and exposure of medial vessels. Systematic inspection
of the superior, inferior, and lateral surfaces of the dissected space should be performed—with par-
ticular focus on the ligament and adjacent coccygeus muscle, right medial rectal surface, and endo-
pelvic connective tissue adjacent to the perforation of the rectal pillar. Throughout a 16-year
experience performing sacrospinous ligament suspension procedures at our center, hemorrhage
from the ligament or coccygeus muscle has been observed as an exceedingly rare event. Far
more commonly, bleeding encountered during the sacrospinous dissection results from the shearing
of small vessels along the medial aspect of the rectum (3,45) due to overzealous medial retraction;
less commonly, deeper vessels in the presacral area can be disrupted by the medial retractor. In this
latter case, if an individual vessel cannot be visualized with adequate retraction and lighting, the use
of prolonged pressure packing may become necessary. Selective arterial embolization may be con-
sidered in hemodynamically stable patients if a defect or injured vessel cannot be localized (44).
Although Hardiman and Drutz (5) reported a 10% incidence of febrile morbidity following
vaginal reconstructive surgery that included sacrospinous ligament suspension, the risk of clini-
cally significant infection resulting from the apical suspension itself appears to be low. The lack
of a tissue graft eliminates the risk of foreign body infection, but suture abscesses can develop on
rare occasion (46,47). Proctotomy has been reported (30,48); however, significant injuries to the
bowel are rare. In contrast to uterosacral vault suspension techniques, ureteral injuries are also
exceedingly rare, though bladder laceration has been reported (47).

VI. CONCLUSIONS

The “best” choice of operation for advanced prolapse of the vaginal apex remains a subject of
debate. According to some surgeons, the correction of all anatomic defects and restoration of
 Sacrospinous Ligament Suspension 659

“normal anatomy” should be the overarching goal. Others regard a “compensatory” postoperative
anatomy as acceptable and perhaps even preferable in certain cases, for achieving maximizing
long-term function and minimizing the risk of recurrent or de novo prolapse. Whatever operation
is chosen, its success should be evaluated according to how effectively it relieves symptoms and
restores normal bladder, bowel, and sexual function. In experienced hands, it appears that a var-
iety of suspension techniques for the vaginal apex—through both vaginal and abdominal
routes—can restore a normal anatomy while preserving sexual function. Ideally, to achieve
the optimal outcomes for each patient, given the specific strengths and limitations characterizing
their pelvic floor anatomy, the reconstructive surgeon should maintain a high level of skill with
several techniques.
Sacrospinous vaginal vault fixation offers a generally short operative time and recovery
period, lack of an abdominal incision, avoidance of a graft, reliable strength even in the presence
of severely weakened pelvic supports, and excellent postoperative function despite a new poster-
olateral position for the vaginal apex. Long-term support of the prolapsed vaginal apex appears
comparable to abdominal colpopexy, with shorter operative time and avoidance of intraabdom-
inal surgery. Advocates of abdominal sacral colpopexy, on the other hand, highlight a longer
postoperative vagina on average (49), with a midline orientation. Suspension of the vaginal
apex to the proximal uterosacral ligaments has been favored by some recently, and can indeed
achieve an excellent anatomic and functional outcome. However, the uterosacral tissues
will occasionally lack sufficient tensile strength for an effective vault suspension, and the
risk of ureteral injury may be as high as 11% when multiple fixation sutures are placed into
the uterosacral ligament (50). Based on the existing literature it appears that each of these
operations, in experienced hands, can provide excellent long-term outcomes. Prospective com-
parison between sacrospinous ligament suspension and its alternatives will hopefully be the
subject of future research.
For the surgical management of advanced prolapse of the vaginal apex, sacrospinous
ligament suspension represents a highly reliable transvaginal alternative. Familiarity with the
various methods for approaching the ligament and anchoring the vaginal apex will allow the sur-
geon to easily combine this operation with a variety of other vaginal reconstructive procedures.
Adherence to fundamental anatomic and surgical principles will ensure that a functional vaginal
anatomy is maintained, and that complications are minimized.

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19. Lind LR, Shoe J, Bhatia NN. An in-line suturing device to simplify sacrospinous vaginal vault
suspension. Obstet Gynecol 1997; 89(1):129– 132.
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heilkd 1968; 28:321 – 327.
22. Nichols DH. Transvaginal sacrospinous colpopexy. J Pelvic Surg 1996; 2:87 – 91.
23. Pohl JF, Frattarelli JL. Bilateral transvaginal sacrospinous colpopexy: preliminary experience. Am J
Obstet Gynecol 1997; 177:1356 – 1362.
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25. Shull BL, Capen CV, Riggs MW, Kuehl TJ. Preoperative and postoperative analysis of site-specific
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struction. Am J Obstet Gynecol 1992; 166:1764 – 1767.
26. Goldberg RP, Tomezsko JE, Winkler HA, Koduri S, Culligan PJ, Sand PK. Anterior or posterior
sacrospinous vaginal vault suspension: long-term anatomic and functional evaluation. Obstet Gynecol
2001; 98:199 –204.
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Williams & Wilkins; 1989:328– 357.
28. Maher CF, Murray CJ, Carey MP, Dwyer PL, Ugoni AM. Iliococcygeus or sacrospinous fixation for
vaginal vault prolapse. Obstet Gynecol 2001; 98(1):40 – 44.
29. Smilen SW, Saini J, Sallach SJ, Porges RF. The risk of cystocele after sacrospinous suspension. Am J
Obstet Gynecol 1998; 179:1465 – 1471.
30. Pasley WW. Sacrospinous suspension: a local practitioner’s experience. Am J Obstet Gynecol 1995;
173:440– 448.
31. Elkins TE, Hopper JB, Goodfellow K, Gasser R, Nolan TE, Schexnayder MC. Initial report of
anatomic and clinical comparison of the sacrospinous ligament fixation to the high McCall
culdoplasty for vaginal cuff fixation at hysterectomy for uterine prolapse. J Pelvic Surg 1995;
1:12– 17.
32. Shull BL. Pelvic organ prolapse: anterior, superior, and posterior vaginal segment defects. Am J
Obstet Gynecol 1999; 181:6 – 11.
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33. Elkins TE, Hopper JB, Goodfellow K, Gasser R, Nolan TE, Schexnayder MC. Initial report of ana-
tomic and clinical comparison of the sacrospinous ligament fixation to the high McCall culdeplasty
for vaginal cuff fixation at hysterectomy for uterine prolapse. J Pelvic Surg 1995; 1:12 –17.
34. Given FT, Muhlendorf IK, Browning GM. Vaginal length and sexual function after colpopexy for
complete uterovaginal eversion. Am J Obstet Gynecol 1993; 169:284 – 287.
35. Paraiso MF, Ballard LA, Walters MD, Chi Lee J, Mitchinson AR. Pelvic support defects and visceral
and sexual function in women treated with sacrospinous ligament suspension and pelvic reconstruc-
tion. Am J Obstet Gynecol 1996; 175:1423 – 1431.
36. Holley RL, Varner RE, Gleason BP, Apffel LA, Scott S. Sexual function after sacrospinous ligament
fixation for vaginal vault prolapse. J Reprod Med 1996; 41:355 – 358.
37. Alevizon SJ, Finan MA. Sacrospinous colpopexy: management of postoperative pudendal nerve
entrapment. Obstet Gynecol 1996; 88:713 – 715.
38. Guner H, Noyan V, Tiras MB, Yildiz A, Yildirim M. Transvaginal sacrospinous colpopexy for
marked uterovaginal and vault prolapse. Int J Gynaecol Obstet 2001; 74(2):165– 170.
39. Cespedes RD. Anterior approach bilateral sacrospinous ligament fixation for vaginal vault prolapse.
Urology 2000; 56:70 – 75.
40. Barksdale PA, Gasser RF, Gauthier CM, Elkins TE, Wall LL. Intraligamentous nerves as a potential
source of pain after sacrospinous ligament fixation of the vaginal apex. Int Urogynecol J Pelvic Floor
Dysfunct 1997; 8(3):121 – 125.
41. Lantzsch T, Geopel C, Wolters M, Koelbl H, Methfessel HD. Sacrospinous ligament fixation for
vaginal vault prolapse. Arch Gynecol Obstet 2001; 265(1):21 –25.
42. Heinonen PK. Transvaginal sacrospinous colpopexy for vaginal vault and complete genital prolapse
in aged women. Acta Obstet Gynecol Scand 1992; 71:377 – 381.
43. Verdeja AM, Elkins TE, Odoi A, Gasser R, Lamoutte C. Transvaginal sacrospinous colpopexy:
anatomic landmarks to be aware of to minimize complications. Am J Obstet Gynecol 1995;
173:1468– 1469.
44. Barksdale PA, Elkins TE, Sanders CK, Jaramillo FE, Gasser RF. An anatomic approach to pelvic
hemorrhage during sacrospinous ligament fixation of the vaginal vault. Obstet Gynecol 1998;
91:715– 718.
45. Morley GW. Discussion of: Cruikshank SH, Cox DW. Sacrospinous ligament fixation at the time of
transvaginal hysterectomy. Am J Obstet Gynecol 1990; 162:1611 – 1619.
46. Porges RF, Smilen SW. Long-term analysis of the surgical management of pelvic support defects. Am
J Obstet Gynecol 1994; 171:1518– 1528.
47. Richter K, Albrich W. Long-term results following fixation of the vagina on the sacrospinous liga-
ment by the vaginal route (vaginaefixatio sacrospinous vaginalis). Am J Obstet Gynecol 1981;
1412:811– 816.
48. Nichols DH. Sacrospinous fixation for massive eversion of the vagina. Am J Obstet Gynecol 1982;
142:901– 904.
49. Given FT, Muhlendorf IK, Browning GM. Vaginal length and sexual function after colpopexy for
complete uterovaginal eversion. Am J Obstet Gynecol 1993; 169:284 – 287.
50. Barber MD, Visco AG, Weidner AC, Amundsen CL, Bump RC. Bilateral uterosacral ligament
vaginal vault suspension with site-specific endopelvic fascia defect repair for treatment of pelvic
organ prolapse. Am J Obstet Gynecol 2000; 183:1402 – 1411.
51. Meschia M, Bruschi F, Amicarelli F, Pifarotti P, Marchini M, Crosignani PG. The sacrospinous
vaginal vault suspension: critical analysis of outcomes. Int Urogynecol J 1999; 10:155– 159.
47
Surgical Treatment of Vaginal Apex Prolapse:
Transvaginal Approaches
Mark D. Walters
Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

Tristi W. Muir
Brooke Army Medical Center, Fort Sam Houston, Texas, U.S.A.

I. INTRODUCTION

In recent years, the problem of pelvic organ prolapse has been given much more attention. Many
women are living longer, and there is more interest in maintaining self-image of femininity and
the capacity of sexual activity beyond menopause. Although few data on the incidence or preva-
lence of various forms of pelvic organ prolapse exist, the incidence appears to be rising based on
increased longevity of women.
The management of pelvic organ prolapse can be difficult. Several support defects often
coexist, and simple anatomic correction of the various defects does not always result in normal
function of the vagina and surrounding organs. To accomplish the goals of pelvic reconstruction,
the surgeon must thoroughly understand normal anatomical support and physiological function
of the vagina, bladder, and rectum. These goals are to restore anatomy, maintain or restore
normal bowel and bladder function, and maintain vaginal capacity for sexual intercourse.
This chapter discusses the pathology and surgical correction of posthysterectomy apical
prolapse via the vaginal route. Obliterative procedures, such as colpectomy, and the transabdom-
inal and laparoscopic support procedures are described elsewhere in this text.

II. PATHOLOGY OF PELVIC ORGAN PROLAPSE

DeLancey (1) described the anatomy of vaginal vault eversion and divided vaginal support into
levels I, II, and III. In level I, the cervix (in a woman who has her uterus in place) or the vagi-
nal apex (in a woman who has previously had a hysterectomy) is suspended to the cardinal and
uterosacral ligaments. In level II, the areas along the base of the bladder anteriorly and along
the rectum posteriorly are attached to the arcus tendineus fasciae pelvis or to the fascia over the
levator ani muscle. Level III, the area along the base of the hymen and perineum, is derived
from the urogenital sinus and is an area of fusion to the perineal body. Richardson (2) believed
that the connective tissue around the vaginal tube, generally called endopelvic “fascia,” does
not stretch or attenuate but rather breaks at specific definable points. By integrating the con-
cepts of suspension of level I with breaks in pelvic connective tissue, one can conclude that
enterocele and vaginal apex prolapse result from specific defects of the presacral endopelvic
663
664 Walters and Muir

fascia (cardinal-uterosacral ligaments), where they connect to the apex of the vagina. The vagi-
nal epithelium covering the connective tissue is not important in maintaining normal support.
Pelvic organ prolapse can result when normal pelvic organ supports are subjected chroni-
cally to increases in intra-abdominal pressure or when defective genital support responds to
normal intraabdominal pressure. Individual organs that pass through the levator ani can lose
support singly or in combination, resulting in various degrees and combinations of pelvic
organ prolapse. This loss of support occurs as a result of damage to any of the pelvic supportive
systems. These systems include the bony pelvis, to which the soft tissues ultimately attach; the
pelvic diaphragm, with the levator ani muscles and their fibromuscular attachments to the pelvic
organs; the subperitoneal retinaculum and smooth muscle component of the endopelvic fascia
(the cardinal and uterosacral ligament complex); and the perineal membrane. The perineal
body and the walls of the vagina can lose tone and weaken from pathologic stretching from
childbirth and attenuating changes of aging and menopause.
Loss of support or integrity of the anterior and posterior vaginal walls results in cystocele
and rectocele, respectively. Uterovaginal prolapse occurs with damage or attenuation of endo-
pelvic fascia that supports the uterus and upper vagina over the pelvic diaphragm. Furthermore,
when the muscles of the pelvic diaphragm weaken as a result of congenital factors, childbirth
injury, pelvic neuropathy, and/or aging, the levator ani lose resting tone and fail to contract
quickly and strongly with increases in intra-abdominal pressure. Muscle atrophy and a wider
levator hiatus result; weak and less rapid muscle contractions with rises in intra-abdominal
pressure contribute to related symptoms of urinary and fecal incontinence.
Apical enterocele is a common defect seen in women with prior hysterectomy. In this case,
the anterior vaginal wall muscularis (pubocervical “fascia”), the rectovaginal “fascia” poster-
iorly, or both, have separated from the supportive endopelvic fascia (uterosacral ligaments)
at the apex of the vagina. With apical and posterior enterocele a defect occurs at the superior
or transverse portion of rectovaginal “fascia” allowing a peritoneal sac with intra-abdominal
contents to herniate between the rectum and apex of the vagina. A poorly supported vaginal
apex and/or posterior vaginal wall often prolapses with the enterocele, leading to concurrent
apical prolapse and rectocele.
Etiologic factors for the development of pelvic organ prolapse are incompletely under-
stood. In their case control study, Swift et al. (3) found that advancing age, increasing weight
of infants delivered vaginally, a history of hysterectomy, and previous prolapse surgery were
the strongest etiologic predictors of severe pelvic organ prolapse. Conditions and life situations
that chronically increase intra-abdominal pressure also appear to increase the risk of uterine
and vaginal prolapse. These factors include obesity (4), heavy lifting at work (5), and bowel
dysfunction (6).
The normal vaginal axis of a nulliparous woman in the standing position is nearly horizon-
tal and is directed toward S3 and S4 (7). Distortion of the normal vaginal axis during reconstruc-
tive pelvic surgery may predispose women to the development of pelvic organ prolapse at an
anatomic site opposite to where the repair was performed. Examples of this are the development
of posterior vaginal wall prolapse after colposuspension procedures for stress incontinence and
the development of anterior vaginal wall prolapse after suspension of the vaginal apex to the
sacrospinous ligament.
The true incidence and prevalence of vaginal prolapse are unknown. In a cross-sectional
study of over 21,000 women attending a menopause clinic in Italy, uterine prolapse was found in
5.5%, the frequency increasing with age, number of vaginal births, and increased weight (4).
Olsen et al. (8) determined that women have a 11% lifetime risk of undergoing a single operation
for pelvic organ prolapse and urinary incontinence, and reoperation for these conditions was
common.
 Surgical Treatment of Vaginal Apex Prolapse 665

III. GENERAL CONCEPTS OF SURGICAL REPAIR

When mild forms of isolated uterovaginal prolapse (descent of the cervix not beyond the mid-
portion of the vagina) are present, vaginal hysterectomy and culdeplasty with anterior and pos-
terior colporrhaphy are usually sufficient to relieve the patient’s symptoms or restore normal
vaginal function. Prophylactic measures performed at the time of hysterectomy (vaginal or
abdominal) probably decrease the incidence of future vaginal vault prolapse and enterocele.
These measures include routine reattachment of endopelvic fascia—cardinal and uterosacral
ligaments—to the vaginal vault and routine use of culdeplasty sutures, cul-de-sac obliteration,
or enterocele excision after removal of the uterus.
During the preoperative assessment of patients with prolapse, certain decisions must be
made:
1. If the uterus is still present, should hysterectomy be part of the surgical correction?
The majority of patients require removal of the uterus. The techniques of vaginal and abdominal
hysterectomy are sufficiently discussed in other texts and will not be mentioned further. If hys-
terectomy is not desired, then pessary use or LeForte partial colpocleisis should be considered. If
surgical correction is needed and the patient desires fertility potential (or simply chooses to not
have her uterus removed), the preferred surgical approach is controversial because few data
exist. A review of the subject has been published by Nichols (9). Abdominal (or laparoscopic)
approaches to such patients via modified sacral uterocolpopexy probably provide the most
durable repair. Abdominal, laparoscopic, or vaginal uterosacral ligament uterine suspension
are innovative and potentially effective approaches, but cure rates are unknown. Sacrospinous
fixation with preservation of the uterus also has been shown to be effective in a small selected
group of patients (10).
2. Is the surgical correction intended to preserve a functional vagina? The operations dis-
cussed in this chapter are aimed at preservation of vaginal and coital function. For patients in
whom future sexual function is not a goal or operative time and morbidity are best kept at a mini-
mum, colpectomy with partial or complete colpocleisis may be indicated.
3. Should the surgical correction be approached via a vaginal or abdominal route?
Factors such as the patient’s general medical condition and weight, the need for concurrent
surgical procedures, and the preference and expertise of the surgeon influence this decision.
A prospective randomized trial by Benson et al. (11) seems to indicate that an abdominal
approach to prolapse provides a better anatomic and functional outcome when compared with
a vaginal approach, although more studies are clearly needed.
4. Does the patient have occult or potential stress urinary or fecal incontinence? When
choosing the route of surgical correction, the surgeon always must consider the correction of
lower urinary tract and lower gastrointestinal dysfunction. Preoperative reduction of the pro-
lapse followed by urodynamic or rectal manometric tests will help the physician to answer
this question and to determine which concurrent operations are required.
As previously mentioned, any reconstructive surgery should return the upper vagina
to the normal near-horizontal axis. Failure to recognize an enterocele or failure to recon-
struct a widened levator hiatus may predispose to postoperative recurrent vaginal prolapse.
The length of the vagina is also an important factor for surgical success. The upper 3 –4 cm
of the vagina lies horizontally over the levator plate. Operations that shorten the vagina do
not allow the upper vagina to lie over the levator plate and may predispose to recurrent vaginal
prolapse.
Although many different techniques have been described to suspend the vagina, only the
most popular techniques done via the vaginal route will be discussed.
666 Walters and Muir

IV. VAGINAL PROCEDURES THAT SUSPEND THE VAGINAL APEX

A. Sacrospinous Ligament Suspension: Surgical Anatomy
To perform this procedure correctly and safely, the surgeon must be familiar with pararectal
anatomy as well as the anatomy of the sacrospinous ligament and its surrounding structures
(Fig. 1) (12). The sacrospinous ligaments extend from the ischial spines on each side to the
lower portion of the sacrum and coccyx. Nichols and Randall (13) described the sacrospinous
ligament as a cordlike structure lying within the substance of the coccygeus muscle. However,
the fibromuscular coccygeus muscle and sacrospinous ligament are basically the same structure
and thus are called the coccygeus-sacrospinous ligament (C-SSL). The coccygeus muscle has a
large fibrous component that is present throughout the body of the muscle and on the anterior
surface, where it appears as white ridges. The C-SSL can be identified by palpating the ischial
spine and tracing the flat triangular thickening posteriomedially to the sacrum. The fibromuscu-
lar coccygeus is attached directly to the underlying sacrotuberous ligament.
Posterior to the C-SSL and sacrotuberous ligament are the gluteus maximus muscle and
the fat of the ischiorectal fossa. The pudendal nerves and vessels lie directly posterior to the
ischial spine. The sciatic nerve lies superior and lateral to the C-SSL. Also superiorly lies an
abundant vascular supply that include superior gluteal vessels and a hypogastric venous plexus
(Fig. 1).

Figure 1 Anatomy of the coccygeus-sacrospinous ligament (C-SSL) complex and surrounding

structures. Note close proximity of pudendal vessels, hypogastric plexus, inferior gluteal vessels, and
sciatic nerve to C-SSL. (From Ref. 12.)
 Surgical Treatment of Vaginal Apex Prolapse 667

B. Sacrospinous Ligament Suspension: Surgical Technique

Before this operation is initiated, one should have preoperatively recognized the ischial spine
and C-SSL on pelvic examination. Preoperative estrogen replacement therapy should be
given liberally, if appropriate. We prefer to use a vaginal estrogen cream for 4 – 6 weeks
preoperatively.
Performance of this operation almost always requires simultaneous correction of the
anterior and posterior vaginal walls and enterocele repair. Displacing the prolapsed vaginal
apex to the sacrospinous ligament to see whether the anterior and posterior vaginal wall prolapse
disappears, helps to determine whether cystocele and rectocele repairs are needed. The patient
should be routinely consented for these repairs because many times it is difficult to discern the
extent of the various defects preoperatively.
The technique of unilateral sacrospinous ligament fixation is as follows:
1. The patient is placed in dorsal lithotomy position and the bladder is drained before the
first incision. Prophylactic antibiotics are given routinely before the operation.
2. The apex of the vagina is grasped with two Allis clamps, and downward traction is
used to determine the extent of the vaginal prolapse and associated pelvic support defects.
The vaginal apex is reduced to the sacrospinous ligament intended to be used, usually on the
right. The apex is tagged with two sutures for its later identification.
3. If the patient has complete eversion of the vagina and requires anterior vaginal wall
repair and/or bladder neck suspension, we prefer doing this portion of the operation first. During
this procedure one should dissect the bladder base away from the vaginal apex, thus lowering the
risk of cystotomy. An anterior colporrhaphy with suburethral plication and/or sling is com-
pleted. The anterior vaginal wall epithelium is closed with a continuous running suture.
4. The posterior vaginal wall is then incised. After a transverse perineal incision, a mid-
line posterior vaginal wall incision is made just short of the apex of the vagina, leaving a small
vaginal bridge 3– 4 cm wide. In the majority of cases, an enterocele sac is present. This sac
should be dissected off the posterior vaginal wall and closed with a high purse-string suture.
Once the enterocele has been incised and ligated, one is ready to begin the sacrospinous ligament
fixation.
5. The first step is entry into the perirectal space. The rectal pillar separates the recto-
vaginal space from the perirectal space. The rectal pillar is areolar tissue that may contain a
few small muscle fibers and blood vessels. In the majority of cases, entry into the perirectal
space is best achieved by breaking through the fibroareolar tissue just lateral to the enterocele
sac at the level of the ischial spine. This maneuver can usually be accomplished bluntly by mobi-
lizing the rectum medially. The use of gauze on the index finger or a tonsil clamp may aide in
breaking through into this space.
6. Once the perirectal space is entered, usually on the right, the ischial spine is identified
and, with dorsal and medial movement of the fingers, the C-SSL is palpated. Blunt dissection is
used to further remove tissue from this area. The surgeon should take great care to ensure that
the rectum is adequately retracted medially. At this time we recommend performing a rectal
examination to ensure that no inadvertent rectal injury has occurred.
7. Two techniques have been popularized for the actual passage of sutures through the
ligament (Fig. 2). The first technique uses a long-handled Deschamps ligature carrier and
nerve hook (Fig. 2A). Long straight retractors are used to expose the coccygeus muscle. Heaney
retractors or Breisky-Navratil retractors are preferred. One must take great care not to let the tip
of the medial retractor be pushed across the anterior surface of the sacrum, risking potential
damage to nerves and vessels. If the right sacrospinous ligament is to be used, the middle and
index fingers of the left hand are placed on the medial surface of the ischial spine and, under
668 Walters and Muir

direct vision, the tip of the ligature carrier penetrates the C-SSL at a point two fingerbreadths
medial to the ischial spine. When pushing the ligature carrier through the body of the C-SSL,
considerable resistance should be encountered; this must be overcomed by forceful yet con-
trolled rotation of the handle of the ligature carrier. If visualization of the C-SSL is difficult,
the muscle and the ligament can be grasped in a long Babcock or Allis clamp, which helps to
isolate the tissue to be sutured. After suture passage, the fingers of the left hand are withdrawn.
The retractor is suitably repositioned and the tip of the ligature carrier is visualized. Alterna-
tively, sutures may be delivered under direct investigation without the placement of the left
hand in the space and with use of lateral and medial Breisky-Navratil retractors and a posterior
retractor. The suture is then grasped with a nerve hook (Fig. 2A). A second suture is similarly
placed 1 cm medial to the first. To ensure that an appropriate amount of tissue has been obtained,
one should be able to gently move the patient with traction of the sutures.
A second technique that has been popularized for passing the sutures through the C-SSL is
the technique of Miyazaki (14) using a Miya hook ligature carrier (Fig. 2B). Several disposable
instruments have since been developed to imitate this technique. The proposed advantage is that
it is safer and easier to direct the ligature carrier into the C-SSL with palpation and then pull
it down into the safe perirectal space below. In this modification, the surgeon uses the middle
finger of one hand to palpate the C-SSL approximately two fingerbreadths medial to the ischial
spine. The Miya hook with a suture attached is slid along the palmer surface of the hand that has
palpated the ligament and the hook point pushed through the C-SSL from above downward
(Fig. 2B). The handle of the instrument is closed and elevated and the posterior notched retractor
is placed to visualize the posterior tip of the instrument. A nerve hook is used to retrieve the
suture (Fig. 2B, inset). Again, this procedure can be performed with retractors, under direct
vision as an alternative to the use of the operator’s left hand.

Figure 2 (A) Passage of Deschamps ligature carrier with suture through C-SSL. Note that needletip is
passed in superior direction. Retrieval of suture is with nerve hook. (B) Passage of Miya hook through
C-SSL. Note that needletip is passed inferiorly. Retrieval of suture is facilitated by using notched
speculum. (From Ref. 12.)
 Surgical Treatment of Vaginal Apex Prolapse 669

8. The surgeon is now ready to bring these stitches out to the apex of the vagina. If
nonabsorbable sutures are used, then the sutures should be placed through the full-thickness
fibromuscularis of the undersurface of the vaginal apex but not through the epithelium. The
suture is placed and tied by a single half-hitch, while the free end of the suture is held long. Trac-
tion of the free end of the suture pulls the vagina directly onto the C-SSL. A square knot fixes it
in place. Some surgeons prefer to use delayed absorbable suture and, in this case, the free end of
the suspending sutures can be passed through the vaginal apex and tied. It is important that the
vagina come into direct contact with the coccygeus muscle to facilitate scarring and to ensure
that no suture bridge exists. While tying these sutures, it may be useful to perform a rectal exam-
ination to detect any suture bridges.
9. After these sutures are tied, the posterior colpoperinorrhaphy is completed, as needed,
and the vagina is packed with a moist gauze overnight.
The results of sacrospinous fixation are difficult to evaluate because few studies report
long-term follow-up, and prospective randomized surgical trials utilizing this technique are
rare. Karram et al. (12) reviewed the literature on cure rates for studies reported from 1981 to
1997. After 2 or more years of follow-up, objective cure rates ranged from 70% to 94%. Recur-
rent vaginal apex prolapse is relatively uncommon. The most common site for recurrent prolapse
in nearly every series is the anterior vaginal wall, perhaps because the vagina is pulled in an
exaggerated posterior direction, possibly exposing the anterior vaginal wall to excessive intra-
abdominal forces.
One of the largest studies on surgical outcomes after sacrospinous ligament suspension
and pelvic reconstruction was reported by Paraiso et al. (15). This study followed 243 patients
for an average of 74 months. Recurrent vaginal support defects were found in the anterior,
posterior, and apical segments in 37%, 14%, and 8% of patients, respectively. Defect-free sur-
vival rates at 5 and 10 years were 80% and 52%, respectively. In this study only 4.5% of patients
underwent subsequent pelvic reconstructive surgery.
Although infrequent, serious intraoperative complications can occur with sacrospinous
ligament fixation. Potential complications of the procedure include hemorrhage from the
veins around the C-SSL complex, buttock pain, pudendal nerve injury, rectal injury, stress urin-
ary incontinence, and vaginal stenosis (15).

C. Endopelvic Fascia Repair (Modified McCall Culdeplasty)

Webb et al. (16) reported on 660 women who underwent primary endopelvic fascia repair for
posthysterectomy vault prolapse between 1976 and 1987. The technique of this repair is as
follows:
1. An elliptical wedge of vaginal epithelium is excised initially from the anterior and
posterior walls of the prolapsed vagina to narrow the vault and to allow access to the lateral
apical supports of the vagina and rectum. The width and length of the excised wedge are
determined by the desired dimensions of the reconstructed vagina.
2. The enterocele sac is isolated and excised, and the ureters are identified by palpation
or dissection.
3. Up to three modified McCall stitches are placed. Each suture incorporates a full thick-
ness of the posterior vaginal wall, the cul-de-sac peritoneum, the remnants of the uterosacral-
cardinal ligament complex laterally, and the fascial tissue lateral and posterior to the upper
vagina and rectum.
4. Sutures are then tied, resulting in fixation of the prolapsed vaginal vault to the upper-
most portion of the endopelvic fascia as well as high closure of the cul-de-sac peritoneum.
670 Walters and Muir

Webb et al. (16) reported results of 660 women, most of whom were followed up with
a questionnaire. Information about recurrent prolapse was available on 504 women (76%).
Fifty-eight patients (9%) complained of a “bulge” or “protrusion” at the time of questioning.
The question about satisfaction with the operation was answered by 385 patients, and 82% indi-
cated that they were satisfied. Forty-two (22%) of 189 sexually active women complained of
dyspareunia.

D. Iliococcygeus Fascia Suspension

In 1963, Inmon (17) described bilateral fixation of the everted vaginal apex to the iliococcygeus
fascia just distal to the ischial spines in three patients with atrophied uterosacral ligaments. The
technique of this repair is as follows:
1. The posterior vaginal wall is opened in the midline as for a posterior colporrhaphy,
and the rectovaginal spaces are dissected widely to the levator ani muscles bilaterally. The dis-
section is extended bluntly toward the ischial spines.
2. With the surgeon’s nondominant hand pressing the rectum downward and medial, an
area 1– 2 cm caudad and posterior to the ischial spine in the iliococcygeus muscle and fascia is
exposed (Fig. 3). A single No. 0 delayed absorbable suture is placed deeply into the levator
muscle and fascia. Both ends of the suture are passed through the ipsilateral posterior section
of vaginal apex and held with a hemostat. This is repeated on the opposite side.

Figure 3 Iliococcygeus fascia suspension. (A) With the surgeon’s finger pressing the rectum downward,
the right iliococcygeus fascia suture is placed. Inset: view of the dissected vagina. (B) Abdominal view of
the endopelvic fascia. Plus marks show the approximate location of the iliococcygeus fascia sutures. (From
Ref. 19.)
 Surgical Treatment of Vaginal Apex Prolapse 671

3. The posterior colporrhaphy is completed and the vagina closed. Both sutures are tied,
elevating the posterior vaginal apices. This repair is probably most effective when done in con-
junction with a culdeplasty or uterosacral ligament suspension.
From 1981 to 1993, Shull et al. (18) and Meeks et al. (19) used the Inmon technique to treat
152 patients with posthysterectomy vault prolapse or total uterine procidentia. There were four
intraoperative complications, including one rectal and one bladder laceration and two cases of
hemorrhage requiring transfusion. Thirteen (8%) patients developed recurrent pelvic support
defects at various sites 6 weeks to 5 years after the initial procedure; two had vault prolapse,
eight had anterior vaginal wall relaxation, and three had posterior wall defects.
In a more recent retrospective study, Maher et al. (20) compared the results of ilioco-
coccygeus fascia suspension to sacrospinous ligament suspension in 128 patients. Objective
cure (defined as no vaginal prolapse beyond the halfway point of the vagina) was found
in 53% of patients after iliococcygeus fascia suspension, and in 67% after sacrospinous liga-
ment suspension. As with other studies, most recurrences of prolapse were in the anterior
vaginal wall.

E. High Uterosacral Ligament Suspension With Fascial Reconstruction

A technique for vaginal apex prolapse and enterocele repair—high uterosacral ligament suspen-
sion with fascial reconstruction—can be performed either transvaginally, transabdominally, or
laparoscopically. The approach is not as important as are the concepts involved. This operation
closely follows the principles of hernia surgery used in the management of umbilical, ventral,
and inguinal hernias: the identification of a “fascial” defect, reduction of intraabdominal con-
tents, closure and reinforcement of the defect. The enterocele must be closed and both the
anterior and posterior vaginal walls must be reliably suspended at the apex. In a woman
with normal support, the vaginal apex is suspended by the cardinal and uterosacral ligaments;
these same structures are used in most operations for prolapse and enterocele repair. The
technique of this repair is as follows:
1. The patient is placed in dorsal lithotomy positon, and the bladder is drained before the
first incision. Prophylactic antibiotics are given routinely before the operation.
2. We attempt to identify the limits of the enterocele by physical examination, look-
ing for demarcation of rugae along the anterior and posterior walls of the vagina near the
apex. The absence of rugae implies deficient or absent connective tissue and, by inference,
defines the borders of the enterocele itself. Occasionally, an enterocele is not present and
entry into the peritoneal cavity is not possible. In this case, an extraperitoneal suspension
to uterosacral ligaments or an iliococcygeus fascia suspension or sacrospinous ligament
suspension is done.
3. The vaginal epithelium at the apex is grasped with Allis clamps and a vasoconstricting
solution is injected submucosally. The vaginal epithelium is incised with a scalpel vertically or
in a diamond shape (Fig. 4), the enterocele is identified, and the edges of the vaginal epithelium
are dissected sharply away from the enterocele sac.
4. The enterocele sac is opened by sharp dissection, and the abdominal cavity is
inspected for the presence of adhesions or other pathology. A large, moist, soft pack is placed
in the posterior cul-de-sac and hollow of the sacrum. A wide Deaver or Breisky-Navratil retrac-
tor is used to elevate the pack and the intestines out of the operative field.
5. The ischial spines are palpated. The remnants of uterosacral ligaments are found pos-
terior and medial to the ischial spines. They can be identified more easily by using Allis or
Kocher clamps attached to the vaginal epithelium at approximately 4 o’clock and 8 o’clock
(at the old hysterectomy scar) to place tension on structures in the lateral wall of the pelvis
672 Walters and Muir

Figure 4 High uterosacral ligament vaginal suspension. To identify the enterocele sac, a diamond-
shaped incision is made at the vaginal apex, and the epithelium is dissected away to facilitate
identification of the enterocele.

(Fig. 5). The clamp is elevated and pulled straight upward; when tension is placed with the
clamp, the contralateral index finger is used to palpate the connective tissue condensations
along the side of the pelvis (uterosacral ligaments).
6. A series of interrupted nonabsorable (or delayed absorbable) sutures then are placed in
each uterosacral ligament beginning at approximately the level of, but posterior and medial to,
the ischial spine. The needle is driven from a lateral to medial position each time. Care should be
taken to avoid the ureter with these sutures. After the first suture has been placed, the second is
placed in a more cephalad and medial position (toward the sacrum). The third is placed cephalad
and medial to the second (Fig. 6).
7. After the suspensory sutures have been placed, the gauze pack and retractors are
removed, and the surgeon should perform any required cystocele repair and/or bladder neck sus-
pension or sling, as needed. The suspensory sutures in the uterosacral ligaments are then system-
atically placed into the most apical portions of the pubocervical and rectovaginal “fasciae.” The
most superior suspensory sutures (closest to the sacrum) are sewn to the most medial portions of
the pubocervical and rectovaginal fasciae, as shown in Figure 6. This suture can be nonabsorb-
able or delayed absorbable. The suture next to that one is placed more laterally into the
pubocervical and rectovaginal fasciae. The most caudal (delayed absorbable) suture then is
placed most laterally into the pubocervical and rectovaginal fasciae and passed out the vaginal
epithelium laterally at 3 o’clock and 9 o’clock.
8. The patient is given intravenous Indigo Carmine, and the suspensory sutures are
tied sequentially. Once the suspensory sutures have been tied properly, the apex of the vagina
 Surgical Treatment of Vaginal Apex Prolapse 673

Figure 5 High uterosacral ligament vaginal suspension. To identify the uterosacral ligament, an Allis
clamp is placed on the vaginal epithelium at the right apex and pulled straight upward (arrow). The
right uterosacral ligament, now on tension, is visible in the pelvis. Inset: A long Allis clamp is used to
grasp the right uterosacral ligament.

should be in the hollow of the sacrum and the connective tissue tube closed at the vaginal
apex.
9. Cystoscopy is performed to ensure ureteral patency. If no flow of urine is seen from
one of the ureters, the sutures are removed on that side one at a time from lateral to medial. This
usually restores ureteral patency. If not, then cul-de-sac exploration and ureteral stent placement
may be necessary.
10. The vaginal epithelium is assessed and tailored to the contour of the vagina by excis-
ing excess tissue. The epithelial incision is closed vertically or horizontally with an absorbable
suture.
This technique of vaginal vault suspension, and enterocele repair also can be done laparo-
scopically or transabdominally. Figure 7 shows the approximation of the vaginal cuff to utero-
sacral ligaments, in conjunction with an anterior colporrhaphy. In the case of a woman who has
vaginal apex prolapse and urodynamic stress incontinence, our preference would be to perform a
sling in conjunction with the procedure. When appropriate, a perineorrhaphy is performed at the
completion of the procedure.
Several studies have described outcomes of series of patients with vaginal prolapse after
uterosacral ligament vaginal suspension. No prospective trial comparing this operation with
others has been done. Shull et al. (21) described the results of 302 consecutive women who
underwent uterosacral ligament vaginal suspension. Eighty-seven percent of women had optimal
anatomic outcomes with no prolapse at any site in the vagina at follow-up examination. Only 5%
of patients had development of stage II or greater prolapse at any site and most recurrences were
674 Walters and Muir

Figure 6 High uterosacral ligament vaginal suspension. Three sutures are placed from lateral to medial
in each uterosacral ligament. The arms of the sutures are brought through the vaginal muscularis anteriorly
(pubocervical fascia) and posteriorly (rectovaginal fascia). The most lateral suture on each side is
absorbable, and is passed through the vaginal epithelium at the apex.

in the anterior wall. A 1% rate of intraoperative ureteral injury or obstruction and a 1% rate of
blood transfusion were reported (21).
Barber et al. (22) performed uterosacral ligament vaginal suspension on 46 women with
pelvic organ prolapse. At follow-up examination, 23% of patients had stage II prolapse, usually
a recurrent cystocele or rectocele. Two patients (5%) developed stage III apical prolapse with
enterocele and required another operation. Importantly, five of 46 patients (11%) were found
to have ureteral obstruction intraoperatively after the apex suspension sutures were tied. This
observation underscores the need to assess ureteral patency in every patient at the completion
of this procedure and to remove any offending sutures if a ureter is obstructed.

V. CONCLUSION

The prevalence of vaginal prolapse appears to be increasing. This may be because of the
increased longevity of women, but also is probably a result of inadequate recognition and repair
of pelvic organ support defects when pelvic surgery has been performed. The standard use of
 Surgical Treatment of Vaginal Apex Prolapse 675

Figure 7 Completed uterosacral vaginal vault suspension and anterior colporrhaphy.

cul-de-sac plication (McCall culdeplasty) at every hysterectomy and urethropexy would prob-
ably decrease the likelihood of iatrogenic enterocele. Finally, more education and research in
the principles of pelvic and vaginal reconstructive surgery are needed to improve care to all
affected women.

REFERENCES

1. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;
166:1717– 1724.
2. Richardson AC. The anatomic defects in rectocele and enterocele. J Pelvic Surg 1995; 1:215.
3. Swift SE, Pound T, Dias JK. Case-control study of etiologic factors in the development of severe
pelvic organ prolapse. Int Urogynecol J 2001; 12:187– 192.
4. Progetto Menopausa Italia Study Group. Risk factors for genital prolapse in non-hysterectomized
women around menopause. Results from a large cross-sectional study in menopausal clinics in
Italy. Eur J Obstet Gynecol Reprod Biol 2000; 93:135 –140.
5. Jorgensen S, Hein HO, Gyntelberg F. Heavy lifting at work and risk of genital prolapse and herniated
lumbar disc in assistant nurses. Occup Med (Oxf) 1994; 44:47 – 49.
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6. Spence-Jones C, Kumm MA, Henry MM, Hudson CN. Bowel dysfunction: a pathogenic factor in
uterovaginal prolapse and urinary stress incontinence. Br J Obstet Gynaecol 1994; 101:147 –152.
7. Funt MI, Thompson JD, Birch H. Normal vaginal axis. South Med J 1978; 71:1534 –1535.
8. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL. Epidemiology of surgically managed
pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997; 89:501– 506.
9. Nichols DH. Fertility retention in the patient with genital prolapse. Am J Obstet Gynecol 1991;
164:1155– 1158.
10. Kovac RS, Cruikshank SH. Successful pregnancies and vaginal deliveries after sacrospinous uterosa-
cral fixation in five of nineteen patients. Am J Obstet Gynecol 1993; 168:1778 – 1790.
11. Benson JT, Lucente V, McClellan E. Vaginal versus abdominal reconstructive surgery for the treat-
ment of pelvic support defects: a prospective randomized study with long-term outcome evaluation.
Am J Obstet Gynecol 1996; 175:1418 – 1421.
12. Karram MM, Sze E, Walters MD. Surgical correction of uterine and vaginal apex prolapse: vaginal,
abdominal and obliterative procedures. In: Walters MD, Karram MM, eds. Urogynecology and
Reconstructive Pelvic Surgery. 2nd ed. St. Louis: Mosby, 1999.
13. Nichols DH, Randall CL. In: Vaginal Surgery. 3rd ed. Baltimore: Williams & Wilkins, 1989.
14. Miyazaki FS. Miya hook ligature carrier for sacrospinous ligament suspension. Obstet Gynecol 1987;
70:286– 288.
15. Paraiso MFR, Ballard LA, Walters MD, Lee JC, Mitchinson AR. Pelvic support defects and visceral
and sexual function in women treated with sacrospinous ligament suspension and pelvic reconstruc-
tion. Am J Obstet Gynecol 1996; 175:1423 – 1431.
16. Webb MJ, Aronson MP, Ferguson LK, Lee RA. Posthysterectomy vaginal vault prolapse: primary
repair in 693 patients. Obstet Gynecol 1998; 92:281 – 285.
17. Inmon WB. Pelvic relaxation and repair including prolapse of vagina following hysterectomy. South
Med J 1963; 56:577– 582.
18. Shull BL, Capen CV, Riggs MW, Kuehl TJ. Bilateral attachment of the vaginal cuff to iliococcygeus
fascia: an effective method of cuff suspension. Am J Obstet Gynecol 1993; 168:1669– 1674.
19. Meeks GR, Washburne JF, McGehee RP, Wiser WL. Repair of vaginal vault prolapse by suspension
of the vagina to iliococcygeus (prespinous) fascia. Am J Obstet Gynecol 1994; 171:1444 – 1452.
20. Maher CF, Murray CJ, Carey MP, Dwyer PL, Ugoni AM. Iliococcygeus or sacrospinous fixation for
vaginal vault prolapse. Obstet Gynecol 2001; 98:40– 44.
21. Shull BL, Bachofen C, Coates KW, Kuehl TJ. A transvaginal approach to repair of apical and other
associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 2000;
183:1365– 1374.
22. Barber MD, Visco AG, Wiedner AC, Amundsen CL, Bump RC. Bilateral uterosacral ligament
vaginal vault suspension with site-specific endopelvic fascia defect repair for treatment of pelvic
organ prolapse. Am J Obstet Gynecol 2000; 183:1402–1410.
48
Abdominal Sacrocolpopexy for the Correction
of Vaginal Vault Prolapse
J. Christian Winters and Richard Vanlangendonck
Ochsner Clinic Foundation, New Orleans, Louisiana, U.S.A.

R. Duane Cespedes
Wilford Hall Medical Center, Lackland AFB, Texas, U.S.A.

I. INTRODUCTION

Prolapse of the vaginal vault is one of the most challenging conditions encountered by pelvic
surgeons. A comprehensive knowledge of the anatomy and function of female pelvic organs
is essential to achieve optimal outcome. Vaginal vault prolapse is reported to occur in 20%
of all women with prolapse (1). As the life expectancy of the population increases and aware-
ness of this condition improves, a greater number of patients with this condition will be
detected.
Vaginal vault prolapse occurs as a loss of apical support, which is a result of detach-
ment or excessive stretching of the cardinal and uterosacral ligaments from the vagina.
Factors predisposing to this form of pelvic floor relaxation include multiparity, enterocele,
trauma occurring during labor and delivery, postmenopausal atrophy, obesity, connective
tissue abnormalities, and strenuous physical activity. Vaginal vault prolapse is usually accom-
panied by a cystocele, rectocele, enterocele, or a combination of these defects (2). Richter
reported that 72% of patients with vault prolapse had a combination of other pelvic floor
defects (3).
Ideally, treatment of vaginal vault prolapse should recreate almost normal vaginal
anatomy by preserving vaginal depth and axis to create a functional vagina with durable pelvic
support. This should be performed utilizing procedures with minimal morbidity and a low
recurrence rate.
There are many procedures to correct vaginal vault prolapse, and several factors must be
considered when selecting therapy. Proper evaluation should encompass identification of all
anatomic defects, assessment of urethrovesical, anal sphincter and sexual function, and the
medical condition of the patient. Once these factors are considered, optimal selection of treat-
ment is possible for each individual. In this chapter we will describe how to diagnose vaginal
vault prolapse, and review the use of the most common abdominal approach to repair this pelvic
floor defect, the abdominal sacral colpopexy.
677
678 Winters et al.

II. EVALUATION OF VAGINAL VAULT PROLAPSE

A patient with vaginal vault prolapse often complains of vaginal protrusion and pressure, dys-
pareunia, difficulty walking, pelvic pain, and urinary or anal incontinence. Difficulty voiding,
recurrent urinary tract infections, and inability to empty the bladder are associated symptoms.
Some women present with isolated complaints of urinary incontinence and no local symptoms
related to the prolapsed vaginal vault. Patients with complete vaginal vault eversion or uterine
procidentia may develop hydronephrosis due to angulation of the ureters (4). The psychological
impact of this problem on females can be significant.
Meticulous examination is important not only to establish the diagnosis, but also to
uncover the other disorders of pelvic floor dysfunction that frequently occur with vaginal vault
prolapse. Support of the anterior vaginal wall, vaginal apex (or uterus), posterior vaginal
wall, and perineum should be separately evaluated. During examination of the anterior vaginal
wall, the urethral support should be assessed. In many cases, the lack of support and hyper-
mobility of the urethra are obvious with straining; however, a sterile cotton swab test may be
employed with a well-lubricated cotton swab placed at the level of the bladder neck in equivocal
exams. During straining, a deflection of the cotton swab .308 signifies urethral hypermobility
(5). If a cystocele is present, it should be determined if the loss of support is in the midline
(“central defect”) or paravaginal, caused by a “lateral defect” separation of the vagina from
its attachment to the pelvic side wall at the arcus tendineus. This is done simply by placing
sponge forceps into the lateral fornices of the vagina to reapproximate the lateral vaginal
walls to the arcus. If this completely reduces the prolapse, an isolated lateral defect exists. How-
ever, if prolapse of the anterior wall still occurs during support of the lateral vaginal wall, a cen-
tral defect exists. If apical support with the forceps completely reduces the cystocoele, a
transverse defect due to separation from the apical paracervical support of the anterior vaginal
wall may exist. With half the speculum displacing the anterior vaginal wall, the posterior wall of
the vagina is assessed. It is important to distinguish the etiology of prolapse high in the posterior
vaginal wall as either enterocele or high rectocele. This is accomplished by bimanual rectova-
ginal examination in the supine and/or standing position to detect an enterocele. If a sac
or bowel can be palpated during this exam, this indicates the presence of an enterocele. If no
enterocele sac or bowel is palpated between the rectum and vagina, this defect is most likely
a high rectocele. A high rectocele can be confirmed by transvaginal palpation of the examiner’s
finger in the rectum without intervening tissue between the rectum and the vaginal wall.
The assessment of apical support of the vagina is easiest when the cervix is present, as it is
a well-defined landmark of the vaginal apex. With straining, the descent of a well-supported
uterus should not occur, and is noted by an absence of cervical descent. The descent of the cervix
half-way to the hymenal ring indicates a moderate loss of uterine support. In posthysterectomy
patients, defining the true vaginal apex can be more difficult. This is a difficult aspect of the
pelvic examination that warrants attention to detail, as apical prolapse can be hidden by large
anterior or posterior compartment prolapse or partially reduced by the examining speculum.
The cuff scar will denote the apex, and “dimples” at the lateral aspects of the apex of the vagina
usually represent attachments of the uterosacral ligaments. When the cuff and apex of the vagina
extend half-way to the hymenal ring with straining, these patients have significant prolapse of
the vaginal vault. Many patients may need to be evaluated in the standing position with the
examiner’s fingers placed at the vaginal apex. If the examiner’s fingers descend half-way to
the hymenal ring or more with straining, significant vault prolapse exists. However, women
may be symptomatic with even lesser degree of apical prolapse. When it is difficult to identify
the exact pelvic floor defects present, dynamic evaluation of the pelvic floor can be accom-
plished with magnetic resonance imaging (6,7).
 Abdominal Sacrocolpopexy 679

It is essential for the clinician to also detect any functional abnormalities of the lower
urogenital tract by assessing lower urinary tract and colorectal function. Stress incontinence may
develop after correction of prolapse (8,9), most likely as a result of “unmasking” occult stress urin-
ary incontinence after the bladder support is restored. A stress test with reduction of the vaginal
prolapse by a pessary or vaginal packing should be performed. Care should be taken to not occlude
the urethra during packing, as a false-negative result may occur. Many of these women have con-
comitant urethral sphincteric deficiency, so the authors prefer urodynamics with vaginal packing to
assess abdominal leak-point pressures to evaluate urethral function. This is an accurate way to
assess abdominal leak-point pressures in patients with significant prolapse (10,11), and allows
selection of the most appropriate stress incontinence procedure. All patients should be
carefully screened for colorectal dysfunction. Although the vast majority of patients complain
of constipation, symptoms of fecal incontinence and/or rectal prolapse should be completely
evaluated. Rectal ultrasonography and/or sphincter manometry with electromyography testing
should be considered in patients complaining of fecal incontinence.
After evaluation of pelvic floor defects and pelvic organ function, treatment options can be
based on the patient’s age, medical condition, coexisting vaginal support defects, previous sur-
gical procedures, and the desire for sexual activity. There is not one procedure for vaginal vault
prolapse correction that is optimal for all patients. The patients should be individualized, and the
pelvic surgeon should be proficient in several procedures to achieve correction of vaginal vault
prolapse. In the young female who desires a fully active lifestyle and sexuality, or a patient who
has failed a transvaginal approach to vaginal vault suspension, the abdominal sacral colpopexy
is an excellent procedure to achieve durable support to the vaginal apex while restoring a
functional vagina.

III. ABDOMINAL SACRAL COLPOPEXY: SURGICAL TECHNIQUE

Pelvic surgeons should be familiar with many of the surgical principles to achieve a most
successful outcome. Important details to successfully complete this procedure are cul-de-sac
closure, fixation of the vaginal apex to the sacrum with graft interposition, and correction of
any paravaginal defects. To just suspend the apex of the vagina with mesh and not complete
these associated repairs, places a patient at significant risk for recurrent enterocele or cystocele.
Postmenopausal women with ovaries remaining are counseled about the risks and benefits
of oophorectomy at the time of surgical intervention. All patients are administered a mechanical
bowel preparation. Thromboembolic elimination stockings and sequential compression devices
are utilized. The patients are positioned in the low lithotomy position, providing both trans-
vaginal and transabdominal access. A low midline abdominal incision is preferred to allow
exposure of the sacral promontory. A Pfannenstiel incision may also be chosen in younger
patients, although exposure may be slightly more difficult. If anterior colporrhaphy or pubo-
vaginal sling is needed, these procedures should be performed initially as access may be
more difficult following colpopexy. When a sling is performed, the authors complete the vaginal
dissection but do not perforate the endopelvic fascia until after a paravaginal repair is performed.
Venous bleeding into the retropubic space can complicate exposure of the arcus tendineus on the
pelvic sidewall. We commonly perform the anterior repair and place sutures to secure the sling
into position initially. After the abdominal sacral colpopexy and abdominal enterocele repair are
completed, the paravaginal repair is performed. When the retropubic space is exposed, the endo-
pelvic fascia is perforated and the sling is positioned using the previously placed sutures.
The operation begins by entry into the peritoneal cavity and removal of adhesions within
the pelvis. Packing of the small intestine and sigmoid colon is performed above the level of the
680 Winters et al.

sacral promontory to complete exposure. An incision is made in the posterior peritoneum over
the sacral promontory, extending into the cul-de-sac along the right lateral aspect of the rectum.
Electrocautery is utilized when dividing the fatty tissue over the promontory. Excessive blunt
dissection is avoided in this area as shearing of presacral veins with severe bleeding may
occur. Care is taken to avoid the middle sacral vein traversing over the promontory. The anterior
sacral ligament is visualized. Two or three permanent sutures (authors use No. 1 Ethibond,
MO-7 needle [Ethicon Inc, Johnson & Johnson, Somerville, NJ]) are placed into the ligament
and periosteum over the sacral promontory (insert) (Fig. 1). These sutures are safely secured
for later placement into the graft. The peritoneum over the vaginal cuff is incised, and the per-
itoneum is dissected off of the apex of the vagina (Fig. 2). Large EEA (end-to-end anastomosis)
sizers are useful to provide exposure of the vaginal apex and facilitate suture placement. Spongesticks
are to be avoided as retained sponge material can occur during suture placement (12). A 2.0-cm-wide
segment of graft is sutured to the exposed vaginal cuff utilizing six permanent sutures (authors
use 2-0 Ethibond). The graft is secured to the vagina by folding it over the cuff of the vagina and
allowing the long end of the graft to exit posteriorly and extend to the sacrum (Fig. 3). After
placing an obturator in the vagina, the enterocele sac (if present) is identified and elevated
with an Allis clamp. Several permanent purse-string sutures are placed into the enterocele sac to
obliterate it (Fig. 4). A Halban culdeplasty is performed by placing linear sutures (2-0 Ethibond)
into the posterior peritoneum on the anterior surface of rectum up to the graft on the vaginal
cuff. The central sutures are placed through the obliterated enterocele sac to prevent recurrence
of enterocele (Fig. 5). Upward retraction of the graft will assist in exposing the cul-de-sac.
Usually four to six sutures are utilized to complete adequate cul-de-sac closure. After closure
of the cul-de-sac, the graft is secured to the sacral promontory with the preplaced permanent
sutures. The proper length of the graft is established by placing the obturator all the way into
the vagina, but not pushing the vagina upward. The graft is placed around the right lateral aspect
of the rectum. A space of two fingerwidths between the graft and the rectum prevents

Figure 1 An incision is made in the posterior peritoneum over the sacral promontory, and sutures of No. 1
Ethibond (MO-7 needle) are placed into the ligament and periosteum over the sacral promontory (insert).
 Abdominal Sacrocolpopexy 681

Figure 2 The peritoneum is dissected off the apex of the vagina. The peritoneum is preserved as a flap
for later placement over the graft. Dissection is facilitated by placing an EEA sizer in the vagina.

Figure 3 The graft is sutured to the exposed vaginal cuff utilizing six sutures of 2-0 Ethibond.
682 Winters et al.

Figure 4 Purse-string sutures of 2-0 Ethibond are placed into the enterocele sac to obliterate it.

compression of the rectum over the graft (Fig. 6). The excessive length of the graft is trimmed
after fixation to the sacrum. The graft is positioned in the retroperitoneal space by closing the
presacral peritoneum over the graft, and covering the graft on the vagina with the superior
edge of the peritoneum flap over the vagina. (Figure 7 demonstrates the completed repair in
sagittal view.) Note the completed culdeplasty obliterating the cul-de-sac and the vaginal cuff
supported by the suspensory graft. When properly performed, the reoccurrence of enterocele

Figure 5 Step 5. A Halban culdeplasty is performed by placing linear sutures (2-0 Ethibond) through the
posterior peritoneum and on the outer surface of rectum up to the vaginal cuff.
 Abdominal Sacrocolpopexy 683

Figure 6 The graft is secured to the promontory. Note two fingers between graft and rectum to prevent
excess tension.

and vault prolapse should be minimal. Paravaginal repair and stress incontinence procedure are
then performed if indicated. The patient is then examined to determine if posterior repair is
needed.

A. Results
The sacral colpopexy has been consistently documented as an excellent method to correct
vaginal vault prolapse with success rates of 85 –100%. Minimal failure rates are reported in
numerous series (Table 1).

Figure 7 Completed repair, sagittal view.

684 Winters et al.

Table 1 Failure (Recurrent Vaginal Vault Prolapse) Rates and Complications After Abdominal Sacral
Colpopexy

Complications
Mean and/or
No. of Mean follow-up Concomitant Failure Graft recurrent
Author patients age (months) surgery N (%) material prolapse

Addison (13) 54 58.4 39 6 A/P repairs 2 (3.7) Mersilene Hemorrhage 1

Fox (14) 29 57 14 N/A 0 (0) Teflon Mesh infect. 1
Cystotomy 1
Foot palsy 1
Patsner (15) 75 62 36 25 radical hyst 2 (2.7) Marlex Mesh erosion 1
Snyder (16) 116 62 43 N/A 8 (6.7) PTFE Mesh erosion 4
Dacron Cystocele and
rectocele 24
Diana (7) 15 57 20 N/A 0 (0) Prolene None
Virtanen (18) 30 60.7 36 N/A 4 (13.3) LyoDura Mesh erosion 1
Gore-Tex Cystocele
(18%)
Rectocele
(15%)
Benson (19) 40 66.2 30 12 anterior rep 1 (2.5) N/A Cystocele 4
20 posterior rep Enterocele 2
19 culdeplasty
Cowan (20) 39 54.5 30 N/A 1 (2.6) Mersilene Mesh erosion 2
Prolene
Winters (21) 20 67 11.3 Anterior rep 1 0 (0) Marlex Cystocele 3
Posterior rep 5 Rectocele 3
PV sling 9
Burch 7

B. Abdominal Sacral Colpoperineopexy

Cundiff and associates have described a technique to incorporate the correction of posterior
compartment defects and perineal descent associated with vaginal vault prolapse (22). The
rationale is to decrease the incidence of recurrent enterocele, rectocele, and perineal body
descent by incorporating the posterior vaginal fascia and perineal body into the suspensory
procedure. This is done by extending the mesh all the way down the posterior vaginal wall to
the perineal body or the portion of the posterior vaginal fascia that is contiguous with the peri-
neal body. In the initial 19 patients, excellent reduction in prolapse and perineal descent was
achieved. The procedure evolved into a combined abdominal and vaginal approach with either
perineal fixation sutures or mesh transferred abdominally through a vaginal incision (23).
Although excellent reduction in prolapse was achieved, the incidence of mesh erosion was
higher in the procedures that required transvaginal passage of suture or mesh. In the abdominal
sacral colpoperineopexy procedures done entirely abdominally, the incidence of mesh erosion
was low. Studies comparing the result of traditional sacral colpopexy and posterior repair
with colpoperineopexy are needed.
 Abdominal Sacrocolpopexy 685

C. Abdominal Sacral Colpopexy: Graft Material

When selecting appropriate graft interposition material for use in colpopexy procedures, one
should consider a graft with significant strength and durability. Additionally, this material
should elicit minimal inflammatory or foreign body reaction, and not serve as a nidus for
infection. The length of the segment needed varies depending on vaginal depth; often the
length is too long to consider the use of autologous fascia. Cadaveric fascia lata may be
used. Sizes are available to complete most colpopexy procedures, and the risk of erosion
appears low. Concern that a lack of strength of this material precipitated early failure of
pelvic reconstructive procedures (24,25) has prompted most pelvic surgeons to use synthetic
graft material. The most commonly utilized synthetic materials are: Marlex (26) (CR Bard,
Cranston RI), Mersilene (13) (Ethicon, Somerville, NJ), Prolene (27) (Ethicon, Somerville,
NJ), and Gore-Tex (28) (WR Gore, Flagstaff, AZ). All of these materials have been utilized
with excellent success rates.
The major concern when utilizing synthetic mesh material during pelvic reconstruction is
infection and/or erosion of the material into the vagina. In a review of the literature, Iglesia et al.
reported on the incidence of mesh erosion for abdominal sacral colpopexy. This review com-
prised procedures utilizing Marlex, Prolene, Mersilene, and Gor-Tex graft materials. Marlex
and Mersilene had minimal erosion complications, and Gore-Tex had the highest incidence of
erosion. The overall incidence of erosion of all types of graft materials in sacral colpopexy
procedures was 9% (29). The likelihood of encountering a mesh complication when utilizing
Marlex or Mersilene appears to be ,5%. If the mesh is exposed vaginally, the incidence of
erosion is much higher. This implies that bacterial contamination does have a role in promoting
mesh erosion. Additionally, avoiding excessive tension is an important step to reduce erosion.
Compression can decrease blood flow to the area of the vagina where the mesh is attached,
promoting ischemia and tissue breakdown.
In summary, the incidence of mesh erosion after colpopexy is very low, particularly if
using Marlex or Mersilene. Exposure of the mesh to the vaginal flora and excessive compression
of the mesh are factors that increase the risk of mesh complications. If one performs an abdomi-
nal sacral colpopexy with attention to detail, the use of synthetic material is durable providing
long-lasting support with minimal risk of infection or erosion.

IV. DISCUSSION

The first abdominal sacral colpopexy was reported by Lane in 1962 (30). He expressed concern
that many procedures to correct vaginal vault utilized the already weakened, tenuous supporting
“fascia” for reconstruction. The repairs mainly consisted of the reapproximation of weak tissue
to provide support. His modification of existing suspensory procedures included placement of a
supporting vascular graft on the vaginal apex and suspending it to the sacrum utilizing a stain-
less-steel staple. The use of the vascular graft arose out of concern over the amount of tension
frequently required to suture the vaginal apex directly to the promontory. Eventually the graft
was secured to the sacrum by permanent sutures, replacing the staple. He concluded, “The
advantages of this procedure are that vaginal function is maintained, difficult dissection is not
required, and an indestructible plastic replaces the inadequate supporting structures which
were factors in the production of the prolapse” (30). These principles described by Lane still
apply today.
The abdominal sacral colpopexy maintains a functional vagina; it restores maximum
vaginal length and durable support by securing the vaginal apex to the periosteum of the sacrum.
686 Winters et al.

This surgical approach demands excellent exposure of the pelvis, which facilitates more
complete reduction of the enterocele, and cul-de-sac obliteration. Several modifications in
technique have been described using autologous fascia (31,32) and synthetic mesh (33,34) in
different configurations, and results appear to be comparable. Timmons and Addison observed
only three recurrences in 250 patients treated with abdominal sacral colpopexy over 20 years
(35). Many reports demonstrate minimal failure rates (Table 1).
Most previous reports have defined treatment success after colpopexy as an absence of
prolapse to the hymen or lack of symptoms related to prolapse. The incidence of site-specific
pelvic defects occurring after colpopexy is not clearly reported. The incidence of “de novo”
anterior wall defects (anterior wall defects not diagnosed before or during the operation for
which no anterior colporraphy was performed) has been reported to be 18% after sacrospinous
fixation (36). In the authors’ experience, the incidence of recurrent central cystocele and recto-
cele after abdominal sacral colpopexy is not uncommon, and similar to the reported incidence of
recurrent defects after sacrospinous fixation. The completion of a colpopexy with a paravaginal
repair does not correct central cystocele or rectocele defects. Extension of the graft posteriorly
may help prevent rectocele formation. Careful examination should be carried out in an attempt to
determine if a significant anterior central defect exists. If present, one should consider anterior
colporraphy prior to colpopexy. More study is needed to identify site-specific defects occurring
after colpopexy and to determine the clinical significance of these defects.
The most significant complication of sacral colpopexy is life-threatening hemorrhage from
disruption of the presacral vessels. The risk of significant bleeding has been reported from 1.2–
2.6% and may be controlled with the use of stainless steel thumbtacks if encountered (37).
Addison described a modification of technique securing the mesh to the sacral promontory to
reduce the risk of bleeding from presacral vessels (38). Since employing this technique, he
has not encountered significant bleeding. The authors have not encountered significant blood
loss, utilizing fixation of the graft high on the sacral promontory. Mesh erosion into the sigmoid
colon has not been observed, and we believe this complication is prevented by assuring a space
between the mesh and sigmoid that will accept two fingers and by meticulous retroperitoneal
placement of the mesh. In addition, positioning of the mesh loosely around the bowel will
prevent postoperative bowel obstruction.
As in other major pelvic operations postoperative ileus can occur, and this is the most
common bowel dysfunction encountered postoperatively. Mesh infection and/or erosion into
the vagina has been reported to occur in 9% of all cases (29). However, Timmons et al.
(33), Hardimann et al. (39), and Benson and colleagues (19) had no mesh complications in a
combined 281 patients. Podratz and colleagues removed mesh in two out of 50 patients for
erosion or infection (40), and recurrent vaginal vault prolapse did not occur after mesh removal.
Simultaneous pubovaginal sling procedures and abdominal sacral colpopexy have been
performed by the authors. Although there is a concern about abdominal mesh infection occurring
with pubovaginal sling procedures, the authors have not encountered this problem.
Comparative studies of colpopexy to transvaginal vault suspension procedures are rare.
Benson et al. (19) reported the results of a randomized controlled trial comparing vaginal and
abdominal correction of vaginal vault prolapse. In the vaginal group, the surgical outcome
was optimal in 29%, satisfactory in 38%, and unsatisfactory in 33%. In the abdominal group,
surgical outcome was optimal in 58%, satisfactory in 26%, and unsatisfactory in 16%. There
was no significant difference between the groups in morbidity, complications, hemoglobin
change, dyspareunia, pain, or hospital stay. They concluded that the correction of vaginal
vault prolapse was more effective with an abdominal approach (19). By providing more normal
restoration of vaginal axis and preserving maximal depth, the sacral colpopexy restores a func-
tional vagina. These factors should be considered when planning operative correction in the
 Abdominal Sacrocolpopexy 687

sexually active patient. Given (41) found sacral colpopexy to be superior to sacrospinous fixation
in terms of vaginal length. After colpopexy an 11.3-cm length of functional vagina was
measured versus 8.2 cm in length after sacrospinous fixation. Angulo and Kligman (42)
observed normal return to sexual activity without recurrent prolapse with a follow-up period
of 36 months in 18 patients.
Since 1962, the correction of vaginal vault prolapse by abdominal sacral colpopexy
has undergone modifications. Consistently superior rates of success have been achieved largely
as a result of adhering to the basic principles described by Lane: closure of the cul-de-sac and
suspension of the vaginal vault by a strong mesh material. Laparoscopic transabdominal
sacral colpopexy has been performed in an effort to provide less invasive surgery and shorter
hospitalization (43). At present, limitations of this modality include a steep learning curve, cum-
bersome laparoscopic knot tying, and possibly longer operative times (44). Laparoscopic repair
of vaginal vault prolapse will become more widely used as technology develops better suturing
and anchoring devices. With continued adherance to the basic principles of the procedure, these
modifications should also provide durable support of the vaginal apex while decreasing the over-
all morbidity of the procedure.

V. CONCLUSION

Abdominal sacral colpopexy is an excellent procedure to correct vaginal vault prolapse. The pro-
cedure can be performed with minimal complications. Because of its durability and preservation
of a functional vagina, this procedure should be considered not only for those women who have
failed a previous transvaginal suspension procedure, but also as a primary approach in young
females with vaginal vault prolapse.
Pelvic surgeons are especially suited to master the techniques essential to perform a suc-
cessful colpopexy and incorporate this procedure into their armamentarium for pelvic floor
reconstruction.

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and complications. Am J Obstet Gynecol 1996; 175:612– 615.
40. Podratz K, Ferguson L, Hoverman V, Lee R, Symonds R. Abdominal sacral colpopexy for post-
hysterectomy vaginal vault descensus. J Pelvic Surg 1995; 1:18– 23.
41. Given FT. Vaginal length and sexual function after colpopexy for complete uterovaginal eversion.
Am J Obstet Gynecol 1993; 169:284 – 287.
42. Angulo A, Kligman I. Retroperitoneal sacrocolpopexy for correction of prolapse of the vaginal vault.
Surg Gynecol Obstet 1992; 169:319– 323.
43. Dorsey JH, Sharp HT. Laparoscopic sacral colpopexy and other procedures for prolapse. Baillieres
Clin Obstet Gynecol 1995; 9:749 – 756.
44. Liu CY, Reich H. Correction of genital prolapse. J Endourol 1996; 10:259 – 265.
49
Laparoscopic Abdominal Sacral Colpopexy

Marie Fidela R. Paraiso

Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

Laparoscopic treatment of vaginal apex prolapse has not become as popular as laparoscopic
hysterectomy and Burch colposuspension most likely owing to vaginal route preference by
many gynecologic surgeons and the technical difficulty of laparoscopic suturing. Since Nezhat
et al. (1) reported a small series of laparoscopic sacral colpopexies in 1994, there have been few
subsequent case series on surgical procedures for pelvic organ prolapse.
The reported advantages of laparoscopic prolapse surgery are: (a) the improved visual-
ization of the anatomy of the presacral space, rectovaginal space, and peritoneal cavity
due to laparoscopic magnification and improved hemostasis; (b) shortened hospitalization;
(c) decreased postoperative pain; (d) rapid recovery and return to work; and (e) cosmetic appear-
ance of smaller incisions. Disadvantages of laparoscopic abdominal sacral colpopexy include:
(a) technical difficulty in acquiring suturing skills; (b) increased operating time early in the
surgeon’s experience especially if concomitant procedures are performed; (c) necessity of a
highly skilled laparoscopic assistant; and (d) increased hospital cost secondary to increased
operating room time and the use of disposable surgical instruments (2).
When performing laparoscopic procedures for repair of vaginal apex prolapse, the laparo-
scopic operation must be identical to conventional pelvic reconstructive procedures, and cure
rates must be similar to those performed by other routes. The goals of the surgery to relieve
symptoms, correct anatomic defects, and restore or maintain urinary, bowel, and sexual function
should not be compromised when operating by the laparoscopic route.

II. INDICATIONS

The indications for laparoscopic sacral colpopexy are identical to those for the open abdominal
route. A patient should desire maintenance or restoration of sexual function or vaginal preser-
vation. Surgeon and patient preference and the laparoscopic skill of the surgeon determine
the choice of laparoscopic route. Additional factors that should be considered include history
of previous pelvic or anti-incontinence surgery, previous failed vaginal apex suspensions, a
small or foreshortened vagina, severe levator muscle weakness and atrophy, severe abdomino-
pelvic adhesions, advanced patient age and weight, chronically increased abdominal pressure,
691
692 Paraiso

need for concomitant pelvic surgery, and patient ability to undergo general anesthesia. Some sur-
geons choose to perform laparoscopic sacral colpopexy only in cases of isolated apical segment
defects because of the increased operative time.
Laparoscopic sacral colpoperineopexy (3) involves the attachment of a graft material that
spans from perineal body to the sacrum and incorporates the length of the posterior vaginal wall.
This extensive modification of the sacral colpopexy is indicated in patients who have vaginal
apex prolapse and concomitant perineal descent (4). This graft may be attached to the perineum
by the laparoscopic route or by the vaginal route prior to laparoscopic fixation to the sacrum.

III. ANATOMY

When considering the repair of pelvic organ support, a surgeon needs to keep in mind the three
levels of support of the vagina described by DeLancey in 1992 (5). The top fourth of the vagina
(level I) is suspended by the cardinal/uterosacral complex; the middle half (level II) is attached
laterally to the arcus tendineus fasciae pelvis and the medial aspect of the levator ani muscles;
and the bottom fourth (level III) is fused to the perineal body. The endopelvic connective tissue
(referred to as the pubocervical fascia anteriorly) contributes to the integrity of the anterior vagi-
nal wall. The rectovaginal “fascia” contributes to the support of the posterior wall of the vagina.
All pelvic support defects, whether anterior, apical, or posterior, usually represent a break in the
continuity of the endopelvic “fascia” and/or a loss of its suspension, attachment, or fusion to
adjacent structures. The goals of pelvic reconstructive surgery are to correct all defects, thus
reestablishing vaginal support at all three levels and to maintain and/or restore normal visceral
and sexual function.
The key anatomic landmarks of sacral colpopexy are the middle sacral artery and vein,
sacral promontory with anterior longitudinal ligament, the aortic bifurcation and vena cava at
the L4-5 level, the right common iliac vessels and right ureter at the right margin of the pre-
sacral space, and the sigmoid colon at the left margin. The left common iliac vein is medial to
the left common iliac artery and can be damaged during dissection or retraction as discussed
in Chapter 48.
Additional anatomic landmarks of laparoscopic sacral colpoperineopexy are the recto-
vaginal septum comprised of Denonvilliers’ “fascia” and its lateral attachment to the medial
aspect of the levator ani muscles and fusion to the perineal body. Denonvilliers’ “fascia” is
the endopelvic connective tissue which is attached to the uterosacral cardinal ligament complex
superiorly, the superior fascia of the levator ani muscles laterally, and the perineal body
inferiorly. The rectovaginal septum is the posterior point of attachment of the sacral colpopexy
mesh. Rectovaginal “fascia,” rectovaginal septum, and Denonvilliers’ “fascia” are synonymous
terms. The pubocervical “fascia” is the anterior point of mesh attachment during sacral
colpopexy.

IV. OPERATIVE TECHNIQUE OF LAPAROSCOPIC

SACRAL COLPOPEXY

In addition to the infraumbilical port for the laparoscope, one 10/12-mm trocar should be placed
in the lower quadrants bilaterally for suture introduction. Two 5-mm ports are placed at the level
of the umbilicus, lateral to the rectus muscle for retraction. After the ancillary ports are placed,
anterior dissection taking care to avoid damage to the bladder is performed (Fig. 1). The bladder
may be filled with 200– 300 cc of sterile water to aid the dissection. A vaginal obturator,
 Laparoscopic Abdominal Sacral Colpopexy 693

Figure 1 Dissection of the pubocervical and rectovaginal fasciae. Manipulators have been placed in the
vagina and rectum.

SpongeStick, or equivalent vaginal manipulator (EEA sizer by U.S. Surgical Corp., Norwalk,
CT, or the CDH by Ethicon Endo-Surgery Inc., Cincinnati, OH) is used for delineation of the
vaginal apex and/or rectum. In order to delineate the rectovaginal fascia, the vaginal EEA
sizer is directed anteriorly while the rectal EEA sizer is directed cephalad (Fig. 2). Dissection
of the peritoneum off the posterior vaginal apex and use of electrocautery are avoided to
decrease risk of vaginal erosion. Sharp dissection is performed with scissors into the avascular
space until the inferior point of mesh fixation is reached. In cases of laparoscopic sacral colpo-
perineopexy, dissection is carried down to the perineal body. Vaginal palpation or transillumi-
nation is helpful to ensure that the dissection to the perineum has been achieved.
The peritoneum overlying the sacral promontory is incised longitudinally and extended to
the cul-de-sac. A laparoscopic blunt tipped instrument or suction irrigator is used to expose the
periosteum of the sacral promontory (Fig. 3). If blood vessels are encountered during the dissec-
tion, coagulation or clip placement is used to achieve hemostasis. If exposure of the sacral pro-
montory and presacral space is not adequate, the patient should be tilted to her left and/or a
snake retractor (Genzyme Corporation, Cambridge, MA) placed through an ancillary port.
A 15  2.5 cm piece of autologous fascia lata, freeze-dried nonradiated cadaveric fascia
lata, polypropylene, Mersilene mesh, or xenograft (porcine dermis, porcine intestinal submu-
cosa, or bovine pericardium) is introduced through the 10/12-mm port. Use of synthetic
materials should be considered if the integrity of the pelvic floor muscles and their nerve supply
are poor. When a T-shaped mesh is used, a 52.5 cm mesh is sutured to the larger piece of mesh
with No. 0 nonabsorbable suture. In order to construct the T-shaped mesh in one piece, a surgeon
may fold a 15  5 cm piece of mesh in half, incise the mesh 10 cm longitudinally, and stitch it
with No. 0 polypropylene suture at the apex of the incision (Fig. 4). This technique results in
694 Paraiso

Figure 2 Delineation of the rectovaginal septum after placement of EAA sizers into the vagina and
rectum.

a doubled layer at the base of the T. The shortest arm of the mesh is sutured to the vaginal apex
anteriorly with two or three pairs of No. 0 nonabsorbable sutures (Fig. 5) and to the posterior
vaginal apex and rectovaginal septum with three or more similar rows of suture (Fig. 6).
When using a T-shaped mesh, it is easier to suture the anterior portion first so that the cephalad
portion of the mesh may be retracted anteriorly while the posterior rows of sutures are being
placed. The sutures are tied extracorporeally as they are placed.
The technique we currently use, involves suturing two pieces of mesh separately. I believe
that this modification places less tension on the anterior vaginal wall thus resulting in fewer
mesh erosions. The shorter piece of mesh (10  2.5 cm) is sutured to the anterior wall. A larger
piece (15  2.5 cm) is sutured to the posterior vaginal wall. Care is taken to place the stitches
through the entire thickness of the vaginal wall excluding the epithelium. The surgeon stitches
the mesh to the longitudinal ligament of the sacrum with two or three stitches of No. 0 non-
absorbable suture. Titanium tacks or hernia staples may also be utilized to attach the mesh to
the longitudinal ligament (Fig. 7). No undue tension is placed on the mesh. The redundant por-
tion of the mesh is excised. The peritoneum is re-approximated over the mesh with No. 2-0 poly-
glactin suture (Fig. 8). If the mesh remains exposed, sigmoid epiploic fat may be sutured over it.
If a graft is secured by vaginal route, an introital incision and dissection of the vaginal epi-
thelium off the underlying vaginal muscularis are performed. This dissection extends to the
medial aspect of the levator ani muscles and superiorly into the enterocele sac. The mesh is
stitched laterally to the iliococcygeus and pubococcygeus fasciae and muscles with three No.
2 braided polyester sutures. The stitch placed most cephalad is at the level of the ischial
spine. Use of an allograft or xenograft may result in less infection and erosion. Visco et al.
have reported a 40% rate of synthetic mesh erosion and shorter time to erosion when sutures
 Laparoscopic Abdominal Sacral Colpopexy 695

Figure 3 Incision of the peritoneum from sacral promontory to cul-de-sac and dissection of the presacral
space.

Figure 4 Configuration of the one-piece T-shaped Prolene mesh.

696 Paraiso

Figure 5 Attachment of the short arm of the T-shaped Prolene mesh to the anterior vagina.

Figure 6 Attachment of one of the long arms of the T-shaped mesh to the perineal body and posterior
vaginal wall.
 Laparoscopic Abdominal Sacral Colpopexy 697

Figure 7 Titanium tacks secure the mesh to the anterior longitudinal ligament of the sacrum with no
tension.

Figure 8 The peritoneum is reapproximated over the mesh.

698 Paraiso

or mesh were placed vaginally and brought into the abdominal field when comparing vaginal-
abdominal sacral colpoperineopexy with abdominal sacral colpopexy (6). We recommend
placement of a fascial graft, allograft, or xenograft vaginally and stitching a synthetic graft
over the proximal portion of the graft laparoscopically in order to complete the vaginal-laparo-
scopic sacral colpoperineopexy.
A concomitant laparoscopic colposuspension is performed if the patient has genuine stress
incontinence. A paravaginal defect repair may also be performed, if needed, to prevent compen-
satory anterior defects or repair coexisting paravaginal defects. If rectal prolapse is present,
a rectopexy may be performed laparoscopically. We perform these combined cases with our
colorectal surgery colleagues.
A concomitant culdeplasty may be performed prior to laparoscopic attachment of the
posterior mesh to the vagina and sacrum (Fig. 9). The Moschcowitz procedure is performed
laparoscopically exactly as during laparotomy. A No. 0 nonabsorbable 36-in suture is stitched
in the peritoneum around the cul-de-sac in a purse-string fashion and subsequently tied extra-
corporeally. Additional sutures are placed as needed. The ureters should be carefully examined
during and after the Moschcowitz procedure. The peritoneum medial to the ureters may be
incised in order to prevent ureteral kinking.
Alternatively, the Halban procedure may be performed by suturing No. 0 nonabsorbable
suture starting at the posterior vagina and proceeding longitudinally over the cul-de-sac perito-
neum and then over the anterior inferior sigmoid serosa. These sutures are tied as they are
placed. Sutures should be 1 cm apart. There is little risk of ureteral compromise with this pro-
cedure; however, it is important to visualize the ureters after all sutures are tied. Outcome data
for Moschcowitz and Halban procedures do not exist.

Figure 9 A culdeplasty incorporating the uterosacral ligaments has been performed after posterior
attachment of the graft.
 Laparoscopic Abdominal Sacral Colpopexy 699

V. CLINICAL OUTCOME OF LAPAROSCOPIC SACRAL COLPOPEXY

The current gynecologic literature for laparoscopic pelvic reconstruction is sparse and consists
of descriptive studies with short-term follow-up. Nezhat et al. (1) reported a series of 15 patients
who underwent laparoscopic sacral colpopexy in whom the mean operative time was 170 min
(range 105 –320 min) and mean blood loss was 226 mL (range 50– 800 mL). The mean hospital
stay was 2.3 days, excluding the case converted to laparotomy for presacral hemorrhage. The
cure rate for apical prolapse was 100% at 3 –40 months. Lyons (7) reported four laparoscopic
sacrospinous fixations and 10 laparoscopic sacral colpopexies with operative times comparable
to vaginal and abdominal approaches. He reported less intra- and postoperative morbidity with the
laparoscopic route, which was attributed to a superior anatomic approach and better visualization
of anatomic structures. Nezhat et al. (1) and Lyons (7) both used mesh and suture and at times
stapled the mesh into the longitudinal ligament of the anterior sacrum rather than suturing it.
Ross (8) evaluated 19 patients with posthysterectomy vaginal apex prolapse prospectively
with extensive preoperative and post-operative testing including multichannel urodynamics and
transperineal ultrasound. All patients underwent sacral colpopexy, Burch colposuspension, and
modified culdeplasty. Paravaginal defect repair and posterior colporrhaphy were added as indi-
cated. The author reported seven complications: three cystotomies, two urinary tract infections,
one seroma, and one inferior epigastric vessel laceration. Five patients had recurrent defects
which were all less than grade 2 (two paravaginal defects and three rectoceles). Vaginal length
ranged from 10.8 to 12.1 cm, and no sexually active patients reported sexual dysfunction. All but
four patients voided spontaneously, and no one required more than 4 days of catheterization. All
were discharged within 24 h. The cure rate at 1 year was 100% for vaginal apex prolapse and
93% for genuine stress incontinence, although two patients were lost to follow-up.
Cosson et al. in the French literature (9) have reported the largest series of 83 women
undergoing laparoscopic sacral colpopexy. Six cases required conversion to laparotomy; thus,
77 women underwent successful procedures with 60 of them having concomitant supracervical
hysterectomy. Two strips of synthetic mesh were placed. Operative time decreased from 292 to
180 min as the surgeon gained experience. Three patients required reoperation, one for recurrent
prolapse and two for recurrent stress incontinence.
Our first 18 patients who underwent laparoscopic sacral colpopexy had a 100% cure of the
apical vaginal prolapse, with 13% of patients having recurrent anterior vaginal prolapse and 13%
having posterior vaginal wall prolapse (10). One patient who was undergoing concomitant rec-
topexy required conversion to laparotomy. The majority of patients underwent concomitant
laparoscopic Burch and paravaginal defect repairs. I have noted that with increased experience,
time for sacral colpopexy alone has decreased to 90 min. To date we have performed over 80 of
these procedures.
There are several reports of laparoscopic rectopexy in the colorectal surgery literature,
which is beyond the scope of this chapter. We have performed seven combined laparoscopic
sacral colpopexy and rectopexy cases to date. One patient underwent laparoscopic sigmoid
resection. In that case, cadaveric fascia was used for sacral colpopexy to avoid infection of syn-
thetic mesh.

VI. CONCLUSION

The principles of laparoscopic reparative procedures for vaginal apex prolapse, enterocele, and
concomitant perineal descent are not new; it is the route by which they are performed that is
different. Laparoscopic sacral colpopexy and colpoperineopexy are feasible and safe. Adequate
700 Paraiso

laparoscopic suturing skills are essential when performing these procedures. The increase in
operative time may elevate the cost of the procedure early in a surgeon’s experience. The laparo-
scopic route offers many advantages to women who require abdominal sacral colpopexy. Pro-
spective clinical trials and long-term follow-up are warranted from experienced laparoscopic
surgeons prior to universal application of laparoscopy for the repair of pelvic organ prolapse.

REFERENCES

1. Nezhat CH, Nezhat F, Nezhat C. Laparoscopic sacral colpopexy for vaginal vault prolapse. Obstet
Gynecol 1994; 84:885 – 888.
2. Paraiso MR, Falcone T, Walters MD. Laparoscopic surgery for genuine stress incontinence and pelvic
organ prolapse. In: Walters MD, Karram MM, eds. Urogynecology and Reconstructive Pelvic
Surgery. 2d ed. Chicago: Mosby, 1998.
3. Paraiso MFR, Tulikangas PK. Laparoscopic sacral colpoperineopexy with control of a presacral
bleed. Proceedings of the 21st American Urogynecologic Society Conference 2000, Hilton Head,
SC, and the 24th American Association of Gynecologic Laparoscopists Conference 2000,
Orlando, FL.
4. Cundiff GW, Harris RL, Coates K, Low VH, Bump RC, Addison WA. Abdominal sacral colpoper-
ineopexy: a new approach for correction of posterior compartment defects and perineal descent
associated with vaginal vault prolapse. Am J Obstet Gynecol 1997; 177:1345– 1353.
5. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;
166:1717– 1728.
6. Visco AG, Weidner AC, Barber MD, Myers ER, Cundiff GW, Bump RC. Vaginal mesh erosion after
abdominal sacral colpopexy. Am J Obstet Gynecol 2001; 184:297– 302.
7. Lyons TL. Minimally invasive treatment of urinary stress incontinence and laparoscopically directed
repair of pelvic floor defects. Clin Obstet Gynecol 1995; 38:380– 391.
8. Ross JW. Apical vault repair, the cornerstone of pelvic vault reconstruction. Int Urogynecol J 1997;
8:146– 152.
9. Cosson M, Bogaert E, Narducci F, Querleu D, Crepin G. Laparoscopic sacral colpopexy: short-term
results and complications in 83 patients. J Gynecol Obstet Biol Reprod 2000; 29:746– 750.
10. Paraiso MFR, Margossian H, Tulikangas PK, Walters MD. Laparoscopic sacral colpopexy and pelvic
reconstruction. J Am Assoc Gynecol Laparosc 200; 7(3):S46. Abstract.
50
Colpocleisis for the Treatment of Severe
Vaginal Vault Prolapse
R. Duane Cespedes
Wilford Hall Medical Center, Lackland AFB, Texas, U.S.A.

J. Christian Winters
Ochsner Medical Foundation, New Orleans, Louisiana, U.S.A.

I. INTRODUCTION

Pelvic prolapse conditions have plagued women for thousands of years; however, it is only
recently that procedures have been developed that safely and effectively treat these conditions.
Even today, pelvic prolapse conditions remain a challenging problem, with vault prolapse
remaining the most difficult problem to treat because multiple support defects usually coexist.
A thorough understanding of pelvic anatomy, pathophysiology, and urodynamics and experi-
ence in selecting the appropriate surgical techniques are required to treat vault prolapse with
minimal morbidity or treatment failures. Although the goal of a vault prolapse procedure is to
restore normal anatomy and function in most cases, this is not always possible or necessary.
For the elderly, the medically unstable, and sexually inactive individual, it may be preferable
to simply “close off ” the vagina to maximize long-term results and minimize operative compli-
cations. These procedures, including colpocleisis and partial colpocleisis, are thought of
as “destructive” procedures and are currently unpopular; however, these procedures can be
extremely helpful in certain situations and should be in every reconstructive surgeon’s
armamentarium.
The traditional approach to colpocleisis has been to simply “invert” the vagina using
purse-string sutures after removing the vaginal epithelium. While simple to perform, after
repairing referred treatment failures who used this approach, we began to utilize a different
approach, which emphasizes the strength of an anterior repair and extensive posterior repair
which is then sutured together. This vaginal closure is then reinforced with a strong perineor-
rhaphy. The purpose of this chapter is to discuss the indications, procedural aspects, and results
of performing a multicompartment colpocleisis and partial colpocleisis for total vault prolapse in
elderly females.

The opinions contained herein are those of the authors and are not to be construed as reflecting the views
of the Air Force or the Department of Defense.

701
702 Cespedes and Winters

II. PATHOPHYSIOLOGY AND INDICATIONS

All pelvic prolapse conditions result from weakness or damage to the normal pelvic support
systems (1). Many etiologies have been proposed for pelvic floor relaxation including multi-
parity, advanced age, prior pelvic surgery, hormonal insufficiency, obesity, neurological
disorders, connective tissue disorders, and strenuous physical activity (2,3). Vaginal vault
prolapse, the most severe form of pelvic prolapse, can occur after a hysterectomy if the vault
is not adequately resuspended to the cardinal and uterosacral ligaments (4). The incidence of
vault prolapse after hysterectomy is reported to be as high as 18.2% and is accompanied by
significant prolapse in other areas in at least 72% of patients (5,6).
A complete vaginal colpocleisis is an appropriate option for the treatment of severe, symp-
tomatic vaginal vault prolapse in women who have been sexually inactive for many years and do
not desire continued sexual function. This procedure is especially useful in elderly women with
multiple medical problems in whom a definitive procedure with little risk of recurrence and
minimal associated morbidity is desired (7).
Partial colpocleisis is indicated when retention of a prolapsing uterus is desired. As
partial colpocleisis usually precludes future coital function and examination of the cervix is
virtually impossible, most women with a prolapsing uterus are probably better served by
vaginal hysterectomy followed by a colpocleisis or one of the standard vault suspensions.
As noted by Ridley, “Any operation less than a complete colpocleisis has an increased
incidence of failure,” and therefore we rarely utilize a partial colpocleisis (8). The ideal
candidate for partial colpocleisis is a frail, elderly female with a documented normal cervix
and uterus who has failed a trial with a pessary and is a poor surgical risk for a vaginal
hysterectomy. In many of these patients, the risk of hysterectomy outweighs the risk of
symptomatic prolapse recurrence because these patients are usually not physically active,
which reduces the risk of subsequent recurrence.

III. EVALUATION
A. History
Patients with high-grade vaginal vault prolapse commonly complain of a mass prolapsing
through the introitus with a feeling of vaginal fullness. When severe, the prolapse can
cause difficulty walking and low back pain that worsens with activity and are relieved by
lying flat. Patients frequently complain of associated voiding dysfunction. Stress urinary
incontinence can be caused by either urethral hypermobility (a sequela of pelvic relaxation)
or from intrinsic sphincter deficiency (ISD) (9). Most candidates for colpocleisis are elderly,
and ISD is much more common in this age group. It is important to distinguish between these
two causes of stress urinary incontinence (SUI) as suspension procedures are associated with
a higher failure rate in patients with ISD. Some patients complain of frequency and urgency
due to incomplete emptying from urethral obstruction, which may result from rotation of the
cystocele around a partially fixed urethra. Many patients do not complain of SUI due to this
urethral obstruction, and leak only when the prolapse is reduced while lying flat or upon
urodynamic testing. Recurrent urinary tract infections may also occur from the incomplete
emptying.
Bowel complaints, especially “constipation,” are common in this group of elderly patients;
however, constipation alone is not specific for a rectocele or pelvic prolapse. “Splinting”
(i.e., applying finger pressure to the posterior vaginal wall to effectively empty the bowels) is
relatively specific for a rectocele but may not always respond to surgical correction (10).
 Colpocleisis 703

B. Physical Examination and Studies

In the severe cases of prolapse for which colpocleisis is indicated, the diagnosis is generally
straightforward with a pelvic exam demonstrating total prolapse of the vaginal vault (Fig. 1).
Any associated conditions such as cystocele, enterocele, or rectocele will be repaired by the col-
pocleisis. In severe prolapse cases, radiographic studies should be considered to rule out possible
ureteral obstruction from the severe ureteral angulation that can occur. If ureteral obstruction is
demonstrated, a ureteral stent should be placed if the procedure cannot be performed expedi-
tiously (11).
We have found that it is easier to perform the vaginal exam at the same time as the uro-
dynamics evaluation. Urodynamics should be performed on all patients to unmask “occult” SUI.
Significant pelvic prolapse can cause urethral obstruction; therefore, the prolapse must be
reduced during the stress maneuvers to create the situation that will exist after the procedure.
The easiest way to reduce the prolapse and not alter the leak-point pressure measurement is
to pack the vagina with lubricated gauze and hold the vault in place with the lower blade of
a vaginal speculum taking care not to obstruct the urethra (12) (Fig. 2). A Pap smear and

Figure 1 Severe vaginal vault prolapse in an elderly patient.

704 Cespedes and Winters

Figure 2 (A) A patient with moderate-grade prolapse without stress incontinence demonstrates the
severe urethral hypermobility usually associated with vault prolapse. The urethra is noted to be directed
vertically with mild straining. (B) After packing of the vagina with gauze and supporting the vault with
a speculum, the urethra is now directed horizontally, and occult incontinence was demonstrable with
coughing. At the arrow, the bladder neck and urethra are shown to be unobstructed.

endometrial biopsy and/or dilatation and curettage should be performed if a partial colpocleisis
is considered, as access to the uterus will be impossible after the procedure (13).

C. Stress Incontinence: Techniques of Repair

Almost all women who require a colpocleisis will also have significant urethral hypermobility,
and some will complain of SUI. The choice of an anti-incontinence procedure is difficult in this
elderly population, who are more likely to suffer the adverse consequences of anti-incontinence
procedures than younger patients. The prevention of postoperative SUI must be balanced with
the avoidance of disabling detrusor instability or urinary retention, as medical therapy may
not improve symptoms, and a urethrolysis after colpocleisis can be quite difficult.
Incontinence associated with urethral hypermobility can be treated with a sling or one of
the suspension procedures; however, the authors do not perform transabdominal incontinence
procedures in these patients because of the additional morbidity and similar rates of voiding
 Colpocleisis 705

dysfunction as sling procedures. A Kelly plication of the bladder neck may be considered in two
patient groups (14). If SUI cannot be demonstrated with the prolapse reduced, a Kelly plication
can be used to provide additional support at the bladder neck. If an elderly, debilitated patient has
minimal SUI and cannot perform clean intermittent catheterization (CIC) then a Kelly bladder
neck plication or minimally invasive sling may be performed. Minimally invasive sling tech-
niques include a vaginal wall sling without perforation of the endopelvic fascia, or a paravaginal
sling secured bilaterally to the arcus tendineus using a Capio needle driver (Boston Scientific,
Natick, MA). These slings are minimally obstructive and CIC is rarely necessary (15). Transure-
thral collagen injections can be used if the patient develops significant SUI postoperatively (16).
If ISD is detected on urodynamic testing, a sling procedure or collagen injection is prefer-
entially used (17,18). Pubovaginal slings are ordinarily used in patients with ISD, and cadaveric
fascia or dermal grafts are utilized in most sling procedures to minimize the morbidity of auto-
logous fascia harvest (19,20). Transient retention is common in this elderly group of patients,
and all patients undergoing sling procedures should be instructed on CIC techniques preopera-
tively. Debilitated patients who cannot perform CIC may undergo a minimally invasive sling or
Kelly plication with collagen injections if the SUI is not adequately treated.

IV. SURGICAL TECHNIQUES

A. Total Colpocleisis
Colpocleisis is performed with the patient in standard lithotomy position. A 16F Foley catheter is
placed into the bladder for continuous drainage, and labial retraction sutures and a weighted
vaginal speculum provide the necessary exposure.
An anti-incontinence procedure and anterior colporrhaphy are performed first. A midline
vaginal incision is made on the anterior wall 1 –2 cm proximal to the urethral meatus and extend-
ing just beyond the site of the proposed new vaginal cuff. In most cases, the vagina will only be
2 –4 cm long when the colpocleisis is complete. The vaginal epithelium and smooth muscle are
dissected off the pubocervical “fascia” in the usual manner, and multiple interrupted absorbable
sutures are ordinarily used to perform the anterior repair (21,22). The extent of the anterior repair
depends on which anti-incontinence procedure is performed. The anti-incontinence procedure is
then performed and the epithelium closed.
The posterior vaginal wall and perineum are then repaired. A triangular perineoplasty
incision is made and the epithelium defined by this incision is excised. Injectable saline is infil-
trated into the posterior vaginal wall to aid dissection. Caudal retraction with an Allis clamp
placed on the edge of the perineoplasty incision greatly facilitates the dissection of the epi-
thelium from the posterior vaginal wall. The previously closed incision on the anterior vaginal
wall defines the proximal extent of the posterior vaginal wall dissection (Fig. 3). Lateral dissec-
tion is continued to the posterior lateral sulcus. Dissection of the epithelium from the enterocele
sac is usually slow and tedious, especially at the cuff; however, unlike a vault suspension, the
enterocele sac is not opened or ligated (23). A colpocleisis obliterates the vaginal canal, so an
enterocele has no place to recur (24). In addition, we have seen redundant bladder, small
bowel, and rectum misidentified as “the sac” and mistakenly opened. If the enterocele can be
manually reduced into the abdomen, the enterocele can be left alone. If the enterocele will not
remain reduced, purse-string absorbable sutures incorporating the sac and uterosacral remnants
can be used to reduce the sac. If these sutures are placed, cystoscopy should be performed after
intravenous administration of Indigo Carmine to ensure ureteral patency. The foundation of the
repair is the creation of multiple strong tissue layers which will resist the enterocele and pelvic
prolapse. Basically, an extensive posterior repair and perineoplasty are used to create this
706 Cespedes and Winters

Figure 3 The incontinence procedure and anterior repair have been completed. The gaping introitus and
severe apical and posterior wall defects can be clearly seen.

barrier. In most cases, two or three sequential layers of pararectal and levator fascia are brought
together in the midline using a combination of permanent and absorbable interrupted sutures
(Figs. 4 – 6). Two sequential purse-string sutures incorporating the completed anterior repair
and the extensive posterior repair ensures a permanent closure of the vagina. As seen in
Figure 7, after redundant posterior vaginal epithelium is excised, the lateral wall vaginal epi-
thelium is dissected free and “rolled” anteriorly to form the new posterior vaginal wall. Gener-
ally, the vagina is 2 –4 cm deep after the colpocleisis is completed. The remaining posterior
vaginal edges are brought together in the midline using a running chromic catgut suture. An
extensive perineoplasty is the final step in the procedure. This is performed by placing multiple
O-Vicryl sutures deeply into the central tendon and bulbocavernosus muscles using a horizontal
mattress sutures. The perineal skin is then closed with an absorbable suture. It is important that
the perineorrhaphy not be extended too far anteriorly or the urethral meatus will be obstructed.
The final result can be seen in Figure 8.

B. Our Results Using Total Colpocleisis

Our experience using this colpocleisis procedure in 44 patients (mean age 78, range 68 –91)
has been favorable (25). All 44 patients underwent a multicompartment vaginal colpocleisis
 Colpocleisis 707

Figure 4 The first layer has been closed on the posterior wall, and the lateral vaginal wall incisions later
used to form the new posterior vaginal wall have been made.

for either grade 3 or grade 4 vault prolapse accompanied by associated enteroceles, cysto-
celes, and rectoceles. Thirty-seven patients demonstrated SUI: seven patients underwent a
pubovaginal sling, four had a modified vaginal wall sling, and 26 had a paravaginal
sling. Seven had a Kelly plication as incontinence could not be demonstrated. At a mean
follow-up of 27 months (range 1– 62), all 44 patients are cured of vaginal vault prolapse,
and there have been no recurrences of rectoceles or enteroceles. Three patients who under-
went a Kelly plication and three who underwent a paravaginal sling have mild SUI, with
four successfully treated with collagen injections. The other two patients have not desired
further therapy. One patient who underwent a pubovaginal sling had large postvoid
residuals and urge incontinence requiring a urethrolysis. The mean estimated blood loss
for the entire procedure (including incontinence procedures) was 175 mL and operating
time 140 min. There were no significant complications, and all patients were satisfied
with the results of the colpocleisis; however, two patients remain unsatisfied with their con-
tinence status owing to persistent urge incontinence. No patient has regretted the loss of
sexual function.
708 Cespedes and Winters

Figure 5 An intraoperative photograph showing the second layer (held by the forceps) on the posterior
wall to be repaired. The strength of the posterior fascial layers used to close the vagina can be clearly seen.
The diminishing size of the vagina is also evident.

C. Partial Colpocleisis
Many surgeons have published variations of LeFort’s original description of partial colpocleisis
(26). The Goodall and Power modification of the LeFort operation limits the LeFort closure of
the medial vagina to the proximal third of the vagina (27). This modification was designed to
permit continued coital function. If preservation of sexual function is a goal, then a vaginal
hysterectomy with vault suspension is a better option. Miklos and Karram recently published
a paper demonstrating that the LeFort partial colpocleisis can be safely performed using a com-
bination of pudendal nerve block, local anesthetic infiltration, and intravenous sedation if
necessary (28).
The partial colpocleisis is initiated by excising a rectangular strip of epithelium from both
the anterior and posterior vaginal walls (Fig. 9). The distal extent of the anterior incision is
located 3– 4 cm from the urethral meatus and the proximal extent of the incision is 2 –3 cm
from the cervix. The cervix is pushed into the depths of the vagina as the exposed anterior
and posterior vaginal walls are sutured together using multiple interrupted O-Ethibond sutures.
We place a 14F Red-Robinson catheter along the vaginal sidewalls to assist in the formation of
 Colpocleisis 709

Figure 6 The last layer has been closed on the posterior wall. The three-layer closure can be seen with
the three separate layers marked by A, B, and C. The anterior repair and posterior repair will be
subsequently sutured together (not shown) to create a strong barrier, which will prevent future vault
prolapse and enterocele formation.

mucosal drainage canals (Figs. 10, 11). The vaginal epithelium overlying the supported cervix is
then closed, and a tight perineal body closure is performed to lend overall strength to the repair
(Fig. 12). The Robinson catheter is removed on postoperative day 4 in most cases.
As for the total colpocleisis, prevention of postoperative incontinence depends on a careful
preoperative urodynamic assessment. Many patients will require an anterior repair in addition to
an incontinence procedure. For ISD, a pubovaginal or paravaginal sling is used in most cases.
Transurethral collagen is used to treat any patients with postoperative incontinence.

V. OUTCOMES AND COMPLICATIONS

The long-term risk of prolapse recurrence following total colpocleisis is not well documented in
the recent literature (29). DeLancey and Morley, using a purse-string inversion technique,
reported one recurrence in 33 patients after a mean follow-up of 3 years (24). Over the past
710 Cespedes and Winters

Figure 7 The lateral vaginal wall epithelial flaps are dissected free from the side walls and “rolled”
anteriorly to form the new but much shorter posterior vaginal wall.

3 years, we have seen two of these inverted purse-string-type colpocleisis procedures performed
elsewhere present to us with recurrent prolapse and subcutaneous enteroceles. This led us to
develop a different approach that emphasizes the strength of an anterior and extensive posterior
repair which is then sutured together. This vaginal closure is then reinforced with a strong peri-
neorrhaphy to provide additional support. The authors noted that in the time it takes to perform
an inverted purse-string-type colpocleisis repair, an anterior and multilayer posterior repair can
be completed. The results of this modified colpocleisis have been very good, with no recurrences
in 44 patients with a mean follow-up of 27 months. The only other contemporary report is from
Ridley, who performed a modified LeFort colpocleisis in 41 patients. No postoperative failures
were noted in this 1971 series with a maximum follow-up of 6 years (8).
The morbidity associated with these procedures appears to be quite low, especially in light
of the advanced age and medical instability in most of these patients. This can probably be attrib-
uted to the shorter operating times and decreased blood loss associated with a partial colpocleisis
as compared to a definitive vault suspension. The loss of sexual function has not been a problem
in any of our patients or in DeLancey and Morley’s report; however, these patients must be care-
fully selected to avoid this potential problem (24).
Partial colpocleisis, while historically yielding good results, can be problematic in some
patients because the uterus and cervix are concealed from examination. With admittedly
 Colpocleisis 711

Figure 8 A postoperative photograph demonstrating the completed repair after the extensive perineal
body closure has been performed.

small numbers, we have not yet seen a patient return with vaginal bleeding following partial col-
pocleisis, and only four cases of cancer developing in these patients have ever been reported (8).
Therefore, we recommend that this procedure be reserved for high-risk patients and that a care-
ful preoperative assessment (including Pap smear and uterine biopsy if necessary) be performed
to prevent any problems.
Ureteral obstruction with resulting hydronephrosis occurs in 8% of patients undergoing
surgery for pelvic prolapse (30). Patients with severe prolapse have a higher incidence, with
up to 34% of patients demonstrating hydronephrosis on preoperative upper urinary tract ima-
ging. In almost all cases, mild to moderate hydronephrosis related to pelvic prolapse resolves
following surgical repair. In most cases in which surgical repair is imminent, preoperative ima-
ging rarely changes the surgical management; however, patients with severe pelvic prolapse in
which nonoperative therapy is pursued or surgical therapy will be delayed should undergo upper
urinary tract imaging with stenting if obstruction is found.
Stress urinary incontinence that develops after a prolapse repair is performed has been
called iatrogenic, latent, or, most commonly, occult incontinence. Reports have demonstrated
that up to 50% of women with vault prolapse who do not complain of SUI will have leakage
712 Cespedes and Winters

Figure 9 The first step in a LeFort partial colpocleisis. A rectangular segment of epithelium from the
anterior and posterior vaginal walls is incised and subsequently removed.

Figure 10 The anterior and posterior incised vaginal edges are sewn together using a catheter to help
form the drainage channels.
 Colpocleisis 713

Figure 11 The first layer of the anterior to posterior wall closure has been completed. Subsequent layers
are then closed until the cervix is deep within the vagina.

Figure 12 The final appearance of a LeFort partial colpocleisis after an extensive perineal body and
distal rectocele closure used to strengthen the repair.
714 Cespedes and Winters

with the prolapse reduced and up to 75% will have a component of ISD (31,32). Ridley noted a
11% incidence of occult incontinence in his 47 patients, whereas DeLancey and Morley did not
report any cases of occult incontinence (8,24). In our series, three patients who had incontinence
only when the prolapse was reduced declined a formal incontinence procedure, and they
required collagen injections postoperatively for SUI. Currently, the potential for postoperative
incontinence can be accurately predicted before the procedure by reducing the prolapse when
performing the pelvic exam and during urodynamics. This preoperative evaluation also allows
the incontinence procedure to be tailored to the patient’s specific problem and decreases the risk
of postoperative incontinence.

VI. SUMMARY

The goal of reconstructive pelvic surgery is to restore normal anatomy and function; however,
this is not always possible or necessary. For the elderly, medically unstable, and sexually inac-
tive individual with severe symptomatic vault prolapse, partial or total colpocleisis may be the
preferred procedure because of the low incidence of morbidity and consistently durable results.
Accordingly, these colpocleisis procedures should be in every reconstructive surgeon’s
armamentarium.

REFERENCES

1. DeLancy JOL. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;
166:1717– 1722.
2. Norton PA. Pelvic floor disorders: the role of fascia and ligaments. Clin Obstet Gynecol 1993;
36:926– 938.
3. Wall LL. The muscles of the pelvic floor. Clin Obstet Gynecol 1993; 166:910 – 914.
4. Berglass B, Rubin IC. Study of the supportive structures of the uterus by levator myography. Surg
Gynecol Obstet 1953; 97:677 – 692.
5. Herbst AL, Mishell DR, Stenchever MA, Droegemueller W. Disorders of the abdominal wall and
pelvic support. In: Stenchever MA, ed. Comprehensive Gynecology. 2d ed. Philadelphia: Mosby
Year Book, 1992:594.
6. Richter K. Massive eversion of the vagina: pathogenesis, diagnosis and therapy of the true prolapse of
the vaginal stump. Clin Obstet Gynecol 1982; 25:89 – 92.
7. Morley GW. Vaginal approach to treatment of vaginal vault prolapse. Clin Obstet Gynecol 1993;
36:984– 994.
8. Ridley JH. Evaluation of the colpocleisis operation: a report of fifty-eight cases. Am J Obstet Gynecol
1972; 113:1114 – 1119.
9. McGuire EJ, Cespedes RD, O’Connell HE. Leak-point pressures. Urol Clin North Am 1996;
23:253– 262.
10. Siproudhis L, Lucas RJ, Raoul JL. Defecatory disorders, anorectal disorders and pelvic floor dysfunc-
tion: a polygamy? Int J Colorectal Dis 1992; 7:102– 106.
11. Zimmern PE. The role of voiding cystourethrography in the evaluation of the female lower urinary
tract. Prob Urol 1991; 5:23 – 33.
12. Ghoniem GM, Walters F, Lewis V. The value of the vaginal pack test in large cystoceles. J Urol 1994;
152:931– 934.
13. Karram MM, Sze EHM, Walters MD. Surgical treatment of vaginal vault prolapse. In: Walters MD,
Karram MM, eds. Urogynecology and Reconstructive Pelvic Surgery. 2d ed. St. Louis: Mosby,
1999:235– 256.
 Colpocleisis 715

14. Pelusi G, Bacchi P, Demaria F, Rinaldi A. The use of the Kelly plication for the prevention and treat-
ment of genuine stress urinary incontinence in patients undergoing surgery for genital prolapse. Int
Urogynecol J 1990; 1:196– 200.
15. Couillard D, Deckard-Janatpour K, Stone A. The vaginal wall sling: a compressive suspension
procedure for recurrent incontinence in elderly patients. Urology 1994; 43:203 – 207.
16. O’Connell HE, McGuire EJ, Aboseif S. Transurethral collagen injection therapy in women. J Urol
1995; 154:1463 – 1466.
17. Haab F, Zimmern PE, Leach GE. Diagnosis and treatment of intrinsic sphincter dysfunction in
females. AUA 1996; Update Lesson 35 Vol 15.
18. O’Connell HM, McGuire EJ, Usui A. Pubovaginal slings in 1994. J Urol 1995; 153:525A, Abstract
1186.
19. Cespedes RD, Cross CA, McGuire EJ. Pubovaginal fascial slings. Tech Urol 1997; 3:195– 201.
20. Blaivas JG, Jacobs BZ. Pubovaginal sling in the treatment of complicated stress incontinence. J Urol
1991; 145:1214 – 1218.
21. Beck RP, McCormick S, Nordstrum L. A 25 year experience with 519 anterior colporrhaphy
procedures. Obstet Gynecol 1991; 78:1011 – 1015.
22. Kohli N, Sze EHM, Roat TW, Karram MM. Incidence of recurrent cystocele after anterior colpor-
rhaphy with and without concomitant transvaginal needle suspension. Am J Obstet Gynecol 1996;
175:1476– 1481.
23. Nichols DH, Randall CL. Enterocele. In: Nichols DH, Randal CL eds. Vaginal Surgery. 4th ed.
Baltimore: Williams & Wilkins, 1996:345.
24. DeLancy JOL, Morley GW. Total colpocleisis for vaginal eversion. Am J Obstet Gynecol 1997;
176:1228– 1235.
25. Cespedes RD, Winters JC, Ferguson KH. Colpocleisis for the treatment of vaginal vault prolapse.
Tech Urol 2001; 7:152– 160.
26. LeFort L. Nouveau procede pour la guerison du prolapsus uterin. Bull Gen Ther 1877; 92:337– 346.
27. Goodall JR, Power RM. A modification of the LeFort operation for increasing its scope. Am J Obstet
Gynecol 1937; 34: 968– 971.
28. Miklos JR, Sze EHM, Karram MM. Vaginal correction of pelvic organ relaxation using local anes-
thesia. Obstet Gynecol 1995; 86:922– 926.
29. Smale LE, Smale CL, Mundo NG, Rivera R. Vaginectomy: profile of success in treating vaginal
prolapse. Medscape Womens Health 1997; 2(3):5.
30. Beverley CM, Walters MD, Weber AM, Piedmonte MR, Ballard LA. Prevalence of hydronephrosis in
patients undergoing surgery for pelvic organ prolapse. Obstet Gynecol 1997; 90:37– 41.
31. Gallentine ML, Cespedes RD. Occult stress urinary incontinence and the effect of vaginal vault
prolapse on abdominal leak point presses. Urology 2001; 57:40– 44.
32. Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999;
161:581– 587.
51
Rectocele Repair/Posterior Colporrhaphy

Nirit Rosenblum,* Karyn S. Eilber,† and Larissa V. Rodrı́guez

University of California, Los Angeles, California, U.S.A.

I. INTRODUCTION

Damage to or anatomical changes in the posterior vaginal compartment may not be as clinically
apparent as anatomic alterations in the anterior vaginal compartment, yet these abnormalities in
pelvic floor support are clinically relevant in vaginal reconstructive surgery. Identification of
posterior vaginal wall defects during routine gynecologic or urologic evaluation is critical in
planning a definitive therapeutic approach to pelvic reconstruction. While the presence of pos-
terior vaginal wall relaxation, or rectocele, may not necessarily be symptomatic, restoration of
posterior vaginal wall support helps to restore both vaginal axis and function. The normal hori-
zontal position of the proximal half of the vagina is restored, recreating a posterior curvature to
the vaginal axis, thereby preventing progression of pelvic organ prolapse. Changes in intra-
abdominal pressure will allow coaptation and closure of the vaginal vault, providing restored
pelvic floor support for the pelvic organs. Thus, identification and repair of concomitant pos-
terior vaginal wall defects are important in the treatment of symptomatic patients with other
defects in pelvic floor support.

II. ANATOMY AND PATHOPHYSIOLOGY OF PELVIC FLOOR

RELAXATION

In a normal female, the levator plate functions as a broad horizontal support mechanism on
which the rectum and proximal vagina rest. This anatomic positioning is important during
increases in intra-abdominal pressure, allowing two compensatory mechanisms to take place.
First, there is reflex contraction of the levator musculature, pulling the midvagina forward
while pushing the proximal vagina posteriorly; these active mechanisms increase the midvaginal
angle and prevent pelvic organ prolapse. Secondly, the reflex contractions of the levator ani and
urogenital diaphragm muscles narrow both the genital hiatus in the levator muscle and the vaginal
introitus, further narrowing the defect through which pelvic organ prolapse occurs (1,2).
Many factors, including childbirth, aging, loss of estrogen stimulation, chronic abdominal
straining and heavy labor, weaken the pelvic floor and its associated support structures. Child-

*Current affiliation: NYU School of Medicine, New York, New York, U.S.A.
†
Current affiliation: Memorial Sloan-Kettering Cancer Center, New York, New York, U.S.A.

717
718 Rosenblum et al.

birth causes stretching of the prerectal and pararectal “fasciae,” with detachment of the prerectal
“fascia” from the perineal body, allowing rectocele formation (3). In addition, childbirth
damages and weakens the levator musculature and its fascia, attenuating the decussating
prerectal levator fibers and the attachment of the levator ani to the central tendon of the
perineum. The result is a convex sagging of the levator plate with a loss of the normal horizontal
vaginal axis (2) (Fig. 1). The vagina becomes rotated downward and posteriorly, no longer pro-
viding horizontal support. These anatomic changes allow downward herniation of the pelvic
organs along this new vaginal axis (4). Enterocele formation is caused by intra-abdominal press-
ure transmission to the pouch of Douglas. Widening of the anogenital hiatus and damage to the
urogenital diaphragm and central tendon further facilitates pelvic prolapse by preventing the
normal compensatory narrowing of the vaginal opening (Fig. 2). Varying degrees of perineal
tears contribute to widening of the vaginal introitus.
There are several critical components of pelvic floor relaxation that are associated with
rectocele formation. Loss of the normal horizontal axis of the levator plate and vagina, weakness
of the urogenital and pelvic floor diaphragms, detachment of the levator ani from the central
tendon of the perineum, and widening of the anogenital hiatus allow intra-abdominal forces
to be transmitted directly to pelvic organs without normal underlying compensatory mechan-
isms. In addition, the rectovaginal septum becomes attenuated, allowing anterior displacement
of the rectum (5). Isolated breaks in the rectovaginal septum facilitate rectocele formation.
Generally, there are several areas along the rectovaginal septum where breaks are com-
monly found. The most common site is a transverse separation immediately above the attach-
ment of this septum to the perineal body, resulting in a low rectocele (seen just inside the
introitus). A midline vertical defect is equally common, and apical transverse breaks have

Figure 1 (A) Schematic diagram of a normal levator ani muscular sling. (B) Schematic diagram of a
damaged and attenuated levator ani muscular sling, resulting in a convex sagging of the pelvic floor and
loss of the normal horizontal vaginal axis.
 Rectocele Repair/Posterior Colporrhaphy 719

Figure 2 Schematic diagram of a widened levator hiatus, including damage to both the genital hiatus
(A) and the central tendon of the perineum (B).

Figure 3 Schematic diagram of locations in the rectovaginal septum where segmental breaks commonly
occur, contributing to rectocele formation. The lines represent the most common locations of breaks in the
rectovaginal septum.
720 Rosenblum et al.

also been described, which may represent a poorly repaired or poorly healed episiotomy (Fig. 3).
Rarely, one can see lateral separation on one side (6). Therefore, each of these components of
pelvic floor relaxation must be addressed at the time of rectocele or posterior vaginal wall repair.
Identification of this pathophysiology is critical when evaluating female patients with symptoms
or signs of pelvic floor relaxation, including stress incontinence associated with urethral hyper-
mobility and/or intrinsic sphincter deficiency. Correction of anterior wall prolapse and bladder
neck hypermobility alone further predisposes the patient to subsequent uterine prolapse as well
as enterocele and rectocele formation. Maintenance of the normal horizontal vaginal axis is an
important goal of surgical repair of pelvic floor relaxation, in order to allow compensatory mech-
anisms to be re-established. Corrective surgery should include correction of the rectocele by
reinforcement of the prerectal and pararectal “fasciae,” repair of the levator muscle defect to
restore the levator hiatus, restoration of the horizontal supporting plate of the proximal vagina,
and repair of the perineum (5).

III. RECTOCELE CLASSIFICATION AND PREVALENCE

Classification of posterior vaginal wall prolapse is based on physical assessment, which has been
recently standardized by the International Continence Society. Using this system, vaginal and
perineal measurements are made at different sites, providing quantification of prolapse affecting
discrete vaginal components. All measurements are made in centimeters relative to the hymen as
the reference point. Negative values represent positions above the hymen; positive values rep-
resent points beyond or outside the hymen. Physical examination should include the staging of
prolapse as previously described, as well as a rectovaginal and anal sphincter examination, an
assessment of pelvic muscle contraction as well as a screening pelvic neurologic exam (7).
The grading of rectocele on physical examination was previously subjective and based on
the location and degree of posterior vaginal wall protrusion (Table 1) (8). The rectal examination
includes elevation of the rectum into the vagina to assess the degree of anterior rectal wall displa-
cement and to assess the thickness and integrity of the perineal body. Evaluation of the recto-
vaginal septum performed during a bimanual examination may identify the presence of a sac of
tissue in the rectovaginal septum (an enterocele), as well as attenuation of the rectovaginal septum
(9).
Perineal tears are graded on a scale of I to IV, based on the posterior extent of the injury
(Table 2) (10). Rectoceles are further classified based on their anatomic position: low, mid, or
high. Low rectoceles result from childbirth causing disruption of the prerectal “fascia” and leva-
tor musculature from their attachments to the central tendon. In addition, direct damage to the
central tendon itself will contribute to formation of a low rectocele. Midvaginal rectoceles are
the most common and result from attenuation and stretching of the perirectal and prerectal

Table 1 Classification of Rectocele Based on Physical Examination

Grade Physical examination findings

I Posterior vaginal wall protrusion, saccular in nature, at level of hymenal ring with associated
depression of perineum
II Posterior vaginal wall protrusion at the level of the levator hiatus (more proximal)
III Posterior vaginal wall protrusion outside or beyond the level of the introitus

Source: Ref. (8).

 Rectocele Repair/Posterior Colporrhaphy 721

Table 2 Classification of Perineal Tears

Grade Location of perineal tear

I Tear limited to hymenal ring

II Tear involving the perineal body but not the anal sphincter
III Tear involving the anal sphincter
IV Tear extending into the anal mucosa

Source: Ref. (10)

“fasciae.” High rectoceles are often associated with enteroceles due to weakening of the upper
portion of the rectovaginal septum or breaks in the prerectal “fascia.”
The prevalence of rectoceles depends on the population of women studied. The incidence
of rectoceles in the general population ranges between 20% and 80% (11). Clearly, there is a
high incidence of women with asymptomatic rectoceles. In a cohort of patients with stress urin-
ary incontinence, Raz et al. found a significant percentage of patients with rectocele and this
incidence increased with the degree of associated prolapse (12,13). Severe anterior vaginal
wall prolapse is often associated with significant posterior wall prolapse. In patients with defe-
catory dysfunction, the incidence of rectocele varies between 27% and 61%. A rectocele .2 cm
in size is more likely to correlate with the presence of symptoms, making it more clinically
significant (14).

IV. SYMPTOMATOLOGY

Posterior vaginal wall relaxation can lead to a variable degree of symptomatology, depending on
rectocele size and generalized bowel habits. Constipation is a common complaint, reportedly
found in 75– 100% of patients with rectoceles (11). Despite the correlation of constipation to
the presence of a rectocele, there are many other factors that can contribute to constipation.
Other rectal symptoms include incomplete emptying, a sensation of rectal pressure, a vaginal
bulge, and fecal straining. Furthermore, the need for either vaginal digitalization or manual peri-
neal pressure to facilitate defecation may be necessary (15 – 17). A variety of nonspecific symp-
toms such as rectal pain, bleeding, fecal or flatal incontinence, low back pain associated with the
upright position, and dyspareunia are also associated with rectoceles (9). On the other hand,
many patients with rectoceles will be completely asymptomatic. The relationship between
anatomic abnormalities and clinical symptoms is not clear, and often the correlation is poor (18).

V. EVALUATION
A. History
Questions pertaining to both bowel and sexual function symptoms associated with rectocele or
posterior vaginal wall defects should be addressed and subjectively quantified. Many middle-
aged and older women will complain of constipation that may or may not be related to the
presence of a rectocele. There are many factors involved in bowel function that must be
taken into consideration; if severe, referral to a gastroenterologist or colorectal surgeon may
be appropriate.
722 Rosenblum et al.

B. Physical Examination
Assessment of the posterior vaginal compartment should be a routine component of any patient
being examined for incontinence or pelvic organ prolapse. This includes inspection for the
presence of enterocele, rectocele, and perineal weakness. Generally, posterior compartment
evaluation is performed by placing half of a vaginal speculum to displace the anterior vaginal
wall and allow complete visualization of the posterior wall during straining. Digital examination
with one finger in the vagina and one finger in the rectum allows for assessment of the recto-
vaginal septum, which is often quite attenuated with large rectoceles, and may contain an
enterocele sac. Physical examination may not reliably distinguish an enterocele from a high
rectocele. Furthermore, inspection of the rectovaginal septum for isolated breaks, typically
found near its attachment to the perineal body or in the midline, is performed by placing a finger
in the rectum and lifting up the posterior vaginal wall. Finally, inspection of the perineal body is
performed to identify a defect associated with a widened introitus and a shortened perineum. In
cases of severe prolapse, combined defects of posterior vaginal wall support at the level of the
pelvic floor and the perineum often occur.
The assessment of vaginal axis is achieved by digital examination. In a nulliparous woman
with a well-supported pelvic floor, there will be a posterior curvature of the proximal vagina
(“banana-shaped”). In a patient with pelvic floor relaxation, the vaginal axis will be horizontal
in the lithotomy position. Restoration of this posterior vaginal axis helps prevent further devel-
opment or recurrence of pelvic organ prolapse. Increases in abdominal pressure will cause
vaginal coaptation when the normal banana-shaped axis has been restored.
The final portion of the posterior compartment examination involves assessment of the
anal sphincter, including resting tone, voluntary activity, and reflex activity. Defects in the exter-
nal anal sphincter may be associated with symptoms of fecal and flatal incontinence. Digital
examination is performed during rest, strain, cough, and voluntary contraction.

C. Radiographic Examination
The reported sensitivity of pelvic examination for the diagnosis of rectocele ranges from 31%
to 81% (19 – 23). In addition, physical examination cannot reliably distinguish an enterocele
from a high rectocele. For these reasons, imaging modalities have been used to aid in the
diagnosis of a rectocele. Plain upright pelvic radiography, often obtained prior to voiding
cystourethrography, may demonstrate an enterocele, a rectocele, or both. The hallmark is
the presence of radiolucent gas 3 –4 cm below the pubococcygeal line. Additional imaging
can be performed by use of evacuation proctography, or defecography. However, the corre-
lation between defecography and symptomatology in guiding patient selection for repair has
been limited (20,22 –25).
Magnetic resonance imaging (MRI) is a very useful tool in identifying and quantifying the
presence of a rectocele as well as associated pelvic floor dysfunction, pelvic organ pathology,
and pelvic organ prolapse. Static images are obtained in both sagittal and parasagittal planes
from left to right across the pelvis. These are followed by a set of dynamic images in the mid-
sagittal plane acquired during the resting and straining states. This particular set of dynamic
images is helpful in identifying pelvic floor descent and pelvic organ prolapse. The pubococcy-
geal line and posterior puborectalis muscle sling are fixed anatomic reference points, used to
quantify organ prolapse and pelvic floor dysfunction. Organ prolapse is defined as any protrusion
through the puborectalis hiatus. Specifically, a rectocele is easily identified when filled with gas,
fluid or gel (26,27) (Fig. 4). Although MRI without the use of a rectal contrast agent is relatively
poor in diagnosing rectoceles in comparison with the detection rates of other forms of prolapse,
 Rectocele Repair/Posterior Colporrhaphy 723

Figure 4 Magnetic resonance image of the pelvis in the sagittal plane during the straining state. A large,
gas-filled rectocele (R) is seen protruding beyond the puborectalis hiatus. Bladder (B), symphysis (S),
pubococcygeal line (PCL), puborectalis hiatus (H).

we currently rely primarily on MRI as a diagnostic tool in the evaluation of women with pelvic
floor relaxation and organ prolapse.

D. Identification of Perineal Laxity

In addition to posterior vaginal wall prolapse, the presence of perineal laxity is an important com-
ponent of pelvic floor dysfunction. The urogenital diaphragm, made up of bulbocavernosus,
superficial, and deep transverse perinei muscles and external anal sphincter musculature, joins
with the levator ani to form the central tendon of the perineum (28). Attenuation of these struc-
tures along with detachment from the central tendon results in perineal laxity. On physical exam-
ination, there is an outward convexity of the perineum with straining and an increased distance
between the posterior vaginal fourchette and the anus. Often, this defect will be present in associ-
ation with rectocele. Specific symptoms associated with perineal laxity include severe consti-
pation and the need to apply perineal pressure in order to evacuate the rectum. In addition, the
patient may notice a bulging of the perineum during straining, or increases in abdominal pressure.

VI. INDICATIONS FOR RECTOCELE REPAIR

In general, the repair of posterior vaginal wall prolapse is undertaken together with associated
pelvic floor relaxation and organ prolapse. Surgical correction of cystocele, uterine prolapse,
or enterocele often includes rectocele repair, as pelvic floor laxity usually affects all vaginal
compartments (20). Rectocele repair during prolapse surgery helps to restore normal vaginal
axis and introital diameter, thereby preventing future prolapse recurrence. Symptoms of a sig-
nificant rectocele include difficult evacuation, sensation of a vaginal bulge, constipation, the
724 Rosenblum et al.

need to splint the vagina in order to empty the rectum, fecal straining, and dyspareunia. These
complaints are considered relative indications for surgical treatment, although the indications for
repair of asymptomatic pelvic floor laxity at the time of incontinence surgery are less well
defined and accepted.
Surgical repair of anterior vaginal wall prolapse or of incontinence alone leaves a portion
of the vaginal hernia uncorrected, thereby exposing it to increased abdominal forces and facil-
itating further weakening of the pelvic floor with time (29). Repair of the posterior vaginal wall
restores the normal horizontal vaginal axis, decreasing the likelihood of recurrent prolapse post-
operatively (28). Furthermore, restoration of posterior vaginal wall support creates a backboard
against which the urethra and bladder neck can be compressed, possibly improving the outcome
of anti-incontinence surgery. Thus, we recommend simultaneous repair of asymptomatic mod-
erate or severe pelvic floor weakness with anti-incontinence surgery in order to achieve these
aforementioned goals.

VII. INDICATIONS FOR PERINEAL REPAIR

Generally, repair of the perineal body is performed at the time of rectocele repair to restore
vaginal axis, recreate the anchoring of the levator ani muscle to the central tendon of the
perineum, and restore the normal urogenital diaphragm. When there is specific herniation of
the perineum and an increased distance between posterior fourchette and anus, a formal peri-
neonhaphy should be undertaken. Indications for this type of repair are based on the patient’s
defecatory dysfunction, such as severe constipation and the need to provide manual perineal
pressure in order to defecate effectively.

VIII. SURGICAL TECHNIQUE OF RECTOCELE REPAIR

The surgical repair of a rectocele incorporates three goals: rectocele reduction by plication of
prerectal and pararectal “fascia,” or endopelvic connective tissue, reconstruction of the levator
hiatus by reapproximation of the prerectal levator fibers, and repair of the perineal body. These
steps result in reconstruction of the rectovaginal septum as well as restoration of the horizontal
levator plate. The perineal body repair reanchors the muscles of the lower vagina and perineum,
restoring the urogenital diaphragm. A variety of surgical techniques have been described for the
correction of posterior vaginal wall relaxation: posterior colporrhaphy with plication of the para-
rectal and prerectal “fascia”; traditional posterior colporrhaphy with levator ani approximation;
and segmental repair of the rectovaginal septal defects. Each of these techniques will be
described in addition to their associated complications and outcomes.
Preoperative preparation includes a lower bowel preparation with oral laxatives, such as
bisacodyl, taken the two nights prior to surgery. In addition, a clear-liquid diet is advised for
48 h prior to surgery. Broad-spectrum intravenous antibiotics are administered the day of sur-
gery to cover anaerobes, gram-negative bacilli, and group D enterococcus. We routinely utilize
a fluoroquinolone antibiotic, unless contraindicated.

A. Plication of Prerectal and Pararectal Fasciae with Levator Reconstruction

The patient is placed in the dorsal lithotomy position with thorough perineal and vaginal prep-
aration. A Betadine-soaked laparotomy pad is inserted as a rectal packing, followed by draping;
care is taken to isolate the rectum from the operative field by double draping with adherent
membranes. The drapes are then affixed to the perineum with sutures and the labia majora
are retracted superiorly and laterally with stay sutures. A Foley catheter is placed, and anti-
 Rectocele Repair/Posterior Colporrhaphy 725

Figure 5 Photograph of rectocele following intraoperative exposure of posterior vaginal wall.

incontinence surgery, cystocele repair, vaginal hysterectomy, or enterocele repair is performed

first. Surgical repair of the posterior vaginal wall is then performed.
A Scott ring retractor is utilized to provide lateral exposure of the vaginal vault (Fig. 5).
Upward retraction of the anterior vaginal wall with a Heaney retractor improves visualization
and prevents inadvertent narrowing of the vagina by excessive excision of vaginal wall tissue.
Two Allis clamps are placed along the posterior fourchette at the 5-o’clock and 7-o’clock pos-
itions (Fig. 6). A V-shaped incision is made, creating a triangular flap of skin that is subsequently
excised, exposing the attenuated perineal body (Figs. 7, 8). Two Allis clamps are then used to
grasp the posterior vaginal wall overlying the rectocele, approximately 3 cm apart. An inverted
V-shaped incision is made in the epithelium overlying the midportion of the rectocele, with its
apex at the proximal most portion of the rectocele (Figs. 9, 10). Sharp dissection with Metzen-
baum scissors aids in developing the plane between the posterior vaginal wall and the herniated
rectal wall, thereby exposing the attenuated prerectal “fascia” (Fig. 11). It is important to main-
tain dissection along the vaginal wall as to avoid injury to the rectum. The dissection extends
laterally to expose the pararectal “fascia” and is carried out along the midline to the level of
the apex of the vagina. The isolated triangle of vaginal wall overlying the rectocele is then
excised (Fig. 12).
Reconstruction of the posterior pelvic floor is performed next. A Heaney retractor is used
to retract the rectum downward, reducing the rectocele and facilitating reapproximation of the
pararectal and prerectal fascia. A running, interlocking 2-0 Vicryl suture begins at the apex of
the vagina and is continued to the level of the levator hiatus (Fig. 13A). The first apical suture
incorporates the uterosacral ligaments as well as the prerectal and pararectal “fascia.” The
running suture incorporates the edges of the vaginal epithelium with generous, deep bites of
the right and left pararectal “fascia” as well as prerectal “fascia” (Fig. 13B). The levator mus-
culature is incorporated in the distal one-third of the posterior vaginal wall closure with a
figure-of-eight suture, to the level of the perineal incision. This last suture results in reapproxi-
mation of the levator hiatus, restoring the normal caliber of the introitus. It is important to pay
726 Rosenblum et al.

Figure 6 Intraoperative photograph of posterior vaginal fourchette (PF), seen held by two Allis clamps,
with anterior vaginal wall retracted by Heaney retractor.

Figure 7 (A) Schematic diagram depicting inverted triangular incision of posterior fourchette during
rectocele repair. (B) Photograph of triangular incision of posterior fourchette.
 Rectocele Repair/Posterior Colporrhaphy 727

Figure 8 Photograph of excision of posterior fourchette epithelium and underlying tissue.

Figure 9 Schematic diagram of posterior vaginal wall dissection overlying rectocele, in a triangular
fashion, from the level of the levator ani musculature to the posterior fourchette incision.
728 Rosenblum et al.

Figure 10 Photograph of two Allis clamps grasping posterior vaginal wall overlying rectocele, with
proximal clamp at level of levator ani (LA) musculature. Line represents incision of vaginal epithelium
on either side of Allis clamps. Arrowhead at level of levator ani hiatus.

Figure 11 Photograph depicting dissection under posterior vaginal wall epithelium using Metzenbaum
scissors from posterior fourchette to vaginal cuff or cervix in the midline.
 Rectocele Repair/Posterior Colporrhaphy 729

Figure 12 Photograph depicting excision of posterior vaginal wall epithelium at the level of the levator
hiatus.

Figure 13 (A) Schematic diagram of rectocele repair suture line from level of vaginal cuff to posterior
fourchette. Absorbable suture material is used in a running, interlocking fashion with incorporation of
pararectal and prerectal fascia beneath vaginal epithelium. (B) Photograph depicting suture placement
incorporating posterior vaginal epithelium and underlying pararectal fascia.
730 Rosenblum et al.

close attention to the creation of a smooth posterior vaginal wall, without the creation of painful
ridges (28,30).
Repair of the perineum is then carried out by reapproximating the central tendon. Vertical
mattress sutures of 2-0 Vicryl are placed in the perineum to reapproximate the bulbocavernosus
muscles, the transverse perineal muscles and the levator complex. Finally, the overlying perineal
skin is reapproximated with a running suture of Vicryl. An antibiotic-impregnated vaginal
packing is placed at the completion of the procedure to aid in hemostasis. Patients are discharged
home on stool softeners for 1 month.
Vasavada et al. reviewed the outcomes of 380 patients who underwent this method of
rectocele repair with a mean follow-up of 22 months. Thirty-one percent of patients (117)
had symptomatic posterior pelvic floor relaxation while 69% (263) were asymptomatic, the
majority presenting with concomitant stress urinary incontinence, anterior vaginal wall prolapse,
or uterine prolapse. One of the primary complaints related to rectocele was constipation, in 26%.
Following posterior vaginal wall repair and levator reconstruction, 67% reported improvement
in constipation. Furthermore, 95.7% are free of recurrent rectocele on physical examination
at follow-up. Four percent exhibited recurrence of rectocele, grade II or higher, some with
associated symptoms (31).

B. Traditional Posterior Colporrhaphy

The patient is again placed in the dorsal lithotomy position, and the vagina and perineum
are prepped in the usual sterile fashion, as previously described. A triangular incision along
the posterior fourchette is performed, and an additional incision is made in the midline of the
posterior vaginal wall from the posterior fourchette to the apex of the rectocele. The vaginal
epithelium is dissected free from the underlying perirectal “fascia” to the level of the rectocele
apex. This dissection is also carried out laterally on either side of the incision line. A finger is
then used to retract the rectocele downward, allowing identification of the levator ani muscles
laterally. Heavy absorbable sutures are then placed through the levator ani margins in order
to reapproximate the muscular defect in the midline along the entire length of the exposed
rectum. The perirectal “fascia” is then closed with interrupted absorbable suture in the midline,
as a second layer of repair. Excess posterior vaginal wall epithelium is excised followed by
closure of the posterior vaginal wall with an uninterrupted, absorbable suture. A formal recon-
struction of the hymenal ring is then carried out in addition to closure of the perineal body (32).
This method of posterior colporrhaphy, as opposed to the aforementioned technique, involves
more extensive lateral dissection, entrance into the pararectal space, and exposure of the levator
musculature. Thus, the levator ani musculature is plicated along the entire length of the posterior
vaginal wall incision.
Kahn et al. retrospectively reviewed the outcomes of 231 women who underwent tra-
ditional posterior colporrhaphy in order to determine both anatomical cure and effects on
both bowel and sexual function. Mean follow-up was 42.5 months. Sixty-one percent of patients
underwent follow-up physical examination and interview, while 13% underwent a telephone
interview alone. The only symptom that was decreased postoperatively following posterior col-
porrhaphy was that of a lump or sensation of intravaginal pressure. The symptoms of incomplete
bowel emptying, constipation, fecal incontinence, and sexual dysfunction increased postopera-
tively. Sixty-two percent of women reported improvement in their bowel symptoms, while 12%
experienced more difficult defecation. A significant number of women in this study reported
de novo symptoms of incomplete bowel emptying (22%), constipation (23%), fecal incontinence
(8%), and sexual dysfunction (16%). The overall anatomical cure rate based on follow-up physi-
cal examination was 76% (35). The conclusions of this study are somewhat limited by its retro-
 Rectocele Repair/Posterior Colporrhaphy 731

spective nature and lack of a standardized postoperative questionnaire. However, this study con-
firms that constipation and bowel dysfunction are not always associated with the presence of a
rectocele. Despite anatomical correction of posterior wall prolapse, a significant number of these
women continued to experience bowel dysfunction in follow-up. This point emphasizes the mul-
tifactorial nature of bowel dysfunction that must be taken into consideration when counseling
patients prior to surgery for pelvic prolapse.

C. Defect-Specific Rectocele Repair

More recently, several authors have recommended a modified, discrete defect rectocele repair
with attention given to the rectovaginal “fascia” as a separate layer (6,18). Cadaveric and
surgical dissections confirmed the presence of this layer and its role in the development of a
rectocele (6). The rectovaginal septum begins at the cul-de-sac, superiorly, and extends to the
perineal body. This tissue layer consists of dense collagen fibers, smooth muscle, and dense
elastin. Overdistention during childbirth causes tearing and separation within this septum,
resulting in formation of a linear rectocele. This septum can become detached from the perineal
body as well as from the deep endopelvic connective tissue. Adequate assessment of this
defect is performed with one finger in the rectum and several fingers in the vagina, especially
with the patient in an erect posture during Valsalva maneuvers. A similar bimanual examination
is done intraoperatively to identify specific defects in the rectovaginal septum that will be
repaired (33).
Repair of discrete defects in the rectovaginal septum is carried out by placing the non-
dominant index finger in the rectum and bringing it forward to distinguish areas of uncovered
rectal muscularis from those covered by the semitransparent rectovaginal septum. Allis clamps
are placed on surrounding connective tissue to facilitate repair of specific defects. Interrupted 2-
0 sutures are used to plicate over the exposed rectal wall (11). Cundiff et al. (34) describe an
avascular plane between the vaginal epithelium and rectovaginal “fascia.” Thus, bleeding during
this dissection generally originates from the underlying rectal muscularis, providing further
clues to the areas of rectovaginal septum disruption. These authors do not routinely plicate
the levator ani muscles during defect-specific rectocele repair.
Porter et al. (36) reviewed the outcomes of 125 women who underwent defect-specific rec-
tocele repair, either alone or in conjunction with other pelvic procedures. Patients were exam-
ined postoperatively and given questionnaires addressing quality of life, sexual function and
bowel function. The site-specific method of rectocele repair was performed, without plication
of the levator ani musculature. In the majority of these cases (79 of 125), surgical correction
was performed for a symptomatic rectocele. Anatomic correction was achieved in 82% with a
mean follow-up of 18 months. Quality-of-life symptoms improved in all respects following
surgery. Furthermore, bowel symptoms improved significantly following repair; specifically,
55% reported improvements in deflection difficulties, 73% in pelvic pain or pressure, 74% in
sensation of a vaginal mass, and 65% in the need to splint. Fecal incontinence and constipation
were not significantly altered by surgical repair. Overall, 44% reported improvement or cure in
their constipation. Reported dyspareunia significantly improved or was cured postoperatively in
73%, worsened in 19%, and arose de novo in 3% (11).
Cundiff et al. (34) reported a similar series of 69 women who underwent discrete defect
rectocele repair and were followed with objective physical examination as well as subjective
symptom questionnaires. Preoperative symptoms related to rectocele included sexual dysfunc-
tion (36%) and defecatory dysfunction (71%). Postoperative questionnaires were given at a
median of 24 months following surgery, and revealed a statistically significant improvement
in rectocele symptoms. Dyspareunia in sexually active women improved from 29%
732 Rosenblum et al.

preoperatively to 19% at long-term follow-up. Constipation decreased significantly from 46%

preoperatively to 13% following surgery. The need for splinting was eliminated in 63% of
women, and fecal incontinence improved in 56% of women (34).

IX. OUTCOMES FOLLOWING RECTOCELE REPAIR

The main goals of posterior compartment reconstruction include restoration of bowel and sexual
function, repair of a widened vaginal hiatus, and restoration of the normal vaginal axis.
However, overcorrection can lead to significant vaginal narrowing and dyspareunia.
Outcomes following rectocele repair, whether it be traditional posterior colporrhaphy or
defect-specific repair of the rectovaginal septum, are not entirely conclusive based on current
studies. Bowel dysfunction is a complex, multifactorial process that may or may not be associ-
ated with the presence of a rectocele or perineal hernia. Rectocele repair helps to restore normal
vaginal anatomy and pelvic support, which may facilitate complete rectal evacuation with
appropriate transmission of intra-abdominal pressures. The effect of posterior colporrhaphy
on sexual dysfunction postoperatively has not been clearly demonstrated. Future studies with
validated sexual function questionnaires are needed to adequately assess any impact of rectocele
repair on sexual function, taking into consideration the impact of concomitant pelvic surgery.

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2. Berglas B, Rubin IC. Study of the supportive structures of the uterus by levator myography. Surg
Gynecol Obstet 1953; 97:677.
3. Kuhn RJ, Hollycock VE. Observations on the anatomy of the rectovaginal pouch and septum. Obstet
Gynecol 1982; 59:445.
4. Nichols DH, Milley PS, Randall CL. Significance of restoration of normal vaginal depth and axis.
Obstet Gynecol 1970; 36:251.
5. Raz S, Little NA, Juma S. Female urology. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED Jr, eds.
Campbell’s Urology. Philadelphia: W.B. Saunders, 1992:2782 – 2829.
6. Richardson AC. The rectovaginal septum revisited: its relationship to rectocele and its importance in
rectocele repair. Clin Obstet Gynecol 1993; 36:976 –983.
7. Weber AM, Abrams P, Brubaker L, Cundiff G, Davis G, Dmochowski RR, Fischer J, Hull T,
Nygaard I, Weidner AC. The standardization of terminology for researchers in female pelvic floor
disorders. Int Urogynecol J 2001; 12:178 – 186.
8. Beecham CT. Classification of vaginal relaxation. Am J Obstet Gynecol 1980; 136:957.
9. Walters MD. Pelvic organ prolapse: cystocele and rectocele. In: Walters MD, Karram MM, eds.
Clinical Urogynecology. St. Louis: Mosby, 1993:225– 235.
10. Baden WF, Walker TA, Lindsey JH. The vaginal profile. Tex Med 1968; 64:56.
11. Mollen RM, Van Larrhoven CJ, Kuijpers JH. Pathogenesis and management of rectoceles. Semin
Colon Rectal Surg 1996; 7:192 – 196.
12. Raz S, Sussman EM, Erickson DB, Bregg KJ, Nitti VW. The Raz bladder neck suspension: results in
206 patients. J Urol 1992; 148:845 – 850.
13. Raz S, Little NA, Juma S, Sussman EM. Repair of severe anterior vaginal wall prolapse (grade IV
cystourethrocele). J Urol 1991; 146:988– 992.
14. Mimura T, Roy AJ, Storrie JB, Kamm MA. Treatment of impaired defecation associated with recto-
cele by behavioral retraining (biofeedback). Dis Colon Rectum 2000; 43:1267– 1272.
15. Mellegren A, Anzen B, Nilsson BY, Johansson C, Dolk A, Gillgren P, Bremmer S, Holmstrom B.
Results of rectocele repair: a prospective study. Dis Colon Rectum 1995; 38:7– 13.
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16. Karlbom U, Graf W, Nilsson S, Pahlman L. Does surgical repair of a rectocele improve rectal empty-
ing? Dis Colon Rectum 1996; 39:1296 – 1302.
17. Murthy VK, Orkin BA, Smith LE, Glassman LM. Excellent outcome using selective criteria for rec-
tocele repair. Dis Colon Rectum 1996; 39:374 – 378.
18. Van Laarhoven CJ, Kamm MA, Bartram CI, Halligan S, Hawley PR, Phillips RK. Relationship
between anatomic and symptomatic long-term results after rectocele repair for impaired defecation.
Dis Colon Rectum 1999; 42:204– 211.
19. Kelvin FM, Maglinte DD. Dynamic cystoproctography of female pelvic floor defects and their inter-
relationships. AJR 1997; 169:769– 774.
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contribution of dynamic cystoproctography and comparison with physical examination. AJR 1999;
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21. Siproudhis L, Ropert A, Vilotte J, Bretagne JF, Heresbach D, Raoul JL, Gosselin M. How accurate is
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pelvic ‘floor-oscopy’. Dis Colon Rectum 1995; 38:695 –699.
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multidisciplinary symposium on defecatory disorders. Am J Obstet Gynecol 2000; 182:S1 – S10.
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Top Magn Res Imag 2001; 12:83 – 92.
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Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ, eds. Campbell’s Urology. Philadelphia: W.B.
Saunders, 1998:1059– 1094.
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contemporary approach to posterior pelvic floor relaxation: the UCLA experience. (Submitted for
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Gynecology. Philadelphia: Lippincott Williams and Wilkins, 1997:1044– 1059.
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ment of the discrete defect rectocele repair. Am J Obstet Gynecol 1998; 179:1451 – 1457.
35. Kahn MA, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. Br J Obstet
Gynaecol 1997; 104:82 – 86.
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52
Evaluation and Management of Rectoceles

Jeffrey L. Segal and Mickey M. Karram

Good Samaritan Hospital, Cincinnati, Ohio, U.S.A.

I. INTRODUCTION

Pelvic organ prolapse accounts for 10 –20% of all major gynecologic surgeries according
to one epidemiologic study (1). Approximately 11% of American women require surgery
for pelvic organ prolapse and/or urinary incontinence, and of these, about 25 – 30% require
a second procedure for recurrence (2). A rectocele is a form of pelvic organ prolapse in
which there is herniation or bulging of the posterior vaginal wall, with the anterior wall of
the rectum in direct apposition to the vaginal epithelium. Although the true prevalence of rec-
toceles is unknown, Olsen et al. noted that 76% of women with documented pelvic organ pro-
lapse had a rectocele (2).
In the past, the surgical repair of rectoceles was generally successful in “fixing” the vaginal
bulge. However, owing to a general lack of understanding of the correlation between anatomic
support and functional derangement, functional outcomes have not been thoroughly addressed.
Today, as the elderly population continues to grow and become more active, the outcome
measures of surgery should include not only the success of restoring anatomy, but also quality-
of-life issues, including the relief of symptoms related to prolapse and the maintenance or res-
toration of visceral and sexual function. The goals of this chapter are to review the anatomy
and pathophysiology of rectoceles as well as the recent developments in diagnosis and
management.

II. PELVIC ANATOMY

During the late 1800s it was believed that the main support of the uterus was the vagina, which
in turn was supported by the insertion of the levator muscles into the perineal body. Today,
based largely on the work of DeLancey, three basic levels of support for the vagina are
described: level 1 consists of support of the cervix and upper vagina over the levator plate
by the cardinal-uterosacral complex; level 2 reflects support of the mid-vagina by lateral con-
nections to the arcus tendinous fascia pelvis; and level 3 reflects support of the lower vagina by
connections to the perineal membrane anteriorly and the perineal body posteriorly (3,4). Defects
in these various levels of support can result in the formation of a rectocele at anatomic sites that
correspond to the level of the defect. High rectoceles, which are often due to stretching or
735
736 Segal and Karram

disruption of the top third of the vaginal wall and the cardinal-uterosacral ligament complexes,
are associated with loss of uterine support and genital descensus. Middle rectoceles, which are
often influenced by parturition, are associated with separation of the rectovaginal septum and
loss of pelvic floor support. Low rectoceles are associated with disruption of the perineal
body and are thought to be secondary to an inadequately repaired obstetric injury or overdisten-
sion during childbirth (5).
Despite earlier controversy regarding the existence of the rectovaginal septum, surgical
and cadaveric dissections (6) as well as histologic specimens (7) have confirmed a layer of
dense tissue between the rectum and the vagina, consisting of collagen, smooth muscle and
elastin fibers (6,7). This layer of fascia, which was first described in men by Denonvilliers
in 1839, is known as rectovaginal fascia, Denonvillier’s fascia, prerectal fascia, vaginal fascia,
and the rectogenital septum (7). It extends from the sacrum to the perineum and laterally
merges into the fascial covering of the iliococcygeus and pubococcygeus muscles. Richardson
(6) demonstrated five types of isolated tears in the rectovaginal septum in patients with a rec-
tocele. The most common was a transverse break above its attachment to the perineal body,
resulting in a low rectocele, followed by a midline vertical defect, resulting in a midvaginal
rectocele, and finally a lateral separation down one of the sides of the fascia. An L- or U-
shaped defect was also described, in which there is a combination of a lateral separation
down one side and a transverse separation from the perineal body (6). Figure 1 illustrates
the five types of defects (8). These contributions by DeLancey, Nichols, and Richardson
have resulted in a better understanding of the anatomy of rectoceles as well as a change in
the surgical approach used to repair them.

Figure 1 Five types of isolated tears in the rectovaginal septum in patients with a rectocele. (From
Ref. 8.)
 Evaluation and Management of Rectoceles 737

III. ETIOLOGY OF RECTOCELES

Although the true etiology of rectoceles is unclear, childbirth is a known risk factor. Childbirth
has been shown to result in stretching and distension of the pelvic floor as well as tearing of the
endopelvic fascia, including the rectovaginal septum. Prolonged straining during labor and des-
cent of the presenting part also can result in traction and pressure of the pudendal nerve as it
courses along the pelvic side wall causing partial denervation of the levator ani muscles.
These changes lead to widening of the genital hiatus, perineal laxity and descent, and pelvic
floor relaxation. During straining, because the vaginal opening can no longer completely
close, the posterior vaginal wall is subjected to a higher pressure gradient.
Additionally, defecation disorders, such as chronic constipation and nonrelaxing pubo-
rectalis syndrome, which are associated with excessive straining, can also cause peripheral neuro-
pathies as well as stretching and tearing of connective tissues. Chronic increased intra-abdominal
pressure related to straining, resulting in a pudendal neuropathy with associated denervation of the
pelvic diaphragm and external anal sphincter, can also lead to the development of fecal inconti-
nence (9). Fecal incontinence, however, when associated with a rectocele, can have a multifactor-
ial etiology, including occult rectoanal intussusception, complete rectal prolapse, physiologic
dysfunction, decreased anorectal sensation, and frank sphincter disruption or atrophy. In deter-
mining the cause-and-effect relationship between rectoceles and defecatory dysfunction, one
needs to better determine whether prolonged straining results in a rectocele or whether a rectocele
results in stool trapping and prolonged straining. It is likely that a combination of both of these
factors, and others, are causes (10). Table 1 lists coexisting causes of defecatory dysfunction (11).

Table 1 Coexisting Causes of Defecatory Dysfunction

1. Physiologic pelvic outlet obstruction (associated with contraction of the puborectalis and external anal
sphincter during attempted defecation)
Anismus
Paradoxical puborectalis contraction
Spastic pelvic floor
Puborectalis dyssnergia
2. Anatomic pelvic outlet obstruction
Rectoanal intussusception—infolding of the rectum into but not beyond the anal verge, which can
induce a sensation of incomplete evacuation
Solitary rectal ulcer syndrome—a benign condition caused by straining and associated with rectal
bleeding, mucous discharge, pain, and difficult evacuation
Rectal prolapse—full-thickness intussusception of the rectum toward or through the anal canal
associated with straining, constipation, mucous discharge, bleeding, and soiling
Rectocele—herniation or bulging of the posterior vaginal wall, with the anterior wall of the rectum
in direct apposition to the vaginal epithelium
Sigmoidocele—due to collapse of the rectal wall from extrinsic compression of the hernia contents
and stasis of the sigmoid loop
3. Colonic inertia (slow transit throughout the colon)
4. Combined outlet obstruction and colonic inertia
5. Other
Perineal descent—perineal descent below the ischial spines during rest and with straining, which
may be associated with a pudendal neuropathy secondary to persistent straining
Fecal incontinence—often associated with sphincter disruption or denervation, but may also be due
to reflex relaxation of the anal sphincter when a large rectocele is filled with feces

Source: Ref. 11.

738 Segal and Karram

Other predisposing factors include postmenopausal status, connective tissue disorders,

hysterectomy, and previous colposuspension and prolapse surgery. It has been suggested that
a hysterectomy results in pelvic denervation, which can contribute to the later development
of a rectocele (12). Retropubic colposuspension is felt to antevert the vagina and thus predispose
women to posterior vaginal wall defects. Abnormalities may also arise when the rectovaginal
fascia is not securely reattached to the perineal body during an episiotomy repair (13).

IV. SYMPTOMS

The majority of patients with an isolated rectocele are asymptomatic. In fact, Shorvon et al.
found that 76% of asymptomatic nulliparous volunteers had small rectoceles on defecography
studies (14). However, symptoms can gradually arise as a rectocele progresses due to the
bulge or mass that a patient may feel in the vagina, which can cause pelvic pain or pressure,
dyspareunia, and low back pain. These symptoms relating to pressure and a feeling of heaviness
are typically worse at the end of the day after a patient has spent a prolonged period of time on
her feet, and generally improve when the patient lies down. Symptoms are also often related to
stool becoming trapped within the rectal bulge. Other related symptoms, as listed in Table 2,
may include incomplete rectal emptying, difficulty with defecation requiring the need to splint,
aching after a bowel movement, and postevacuation fullness. Although there are no published
studies describing the natural history of rectoceles, current opinion suggests that they progress
slowly over the years, and that functional difficulties tend to wax and wane, but progress slowly
over time (13).
As noted in the previous section, constipation and other forms of defecatory dysfunction,
such as fecal incontinence and paradoxical sphincter reaction, may coexist with rectoceles. The
degree of posterior vaginal wall prolapse, however, does not correlate well with bowel dysfunc-
tion. Although they may frequently coexist, they do not necessarily have a causal relationship
(10). Therefore one should appropriately counsel a potential surgical candidate who, for
example, presents with a symptomatic rectocele and constipation, that repair of the rectocele
may relieve symptoms related to stool trapping, but may not effectively relieve constipation.
Because many of the symptoms of a rectocele overlap other pelvic floor disorders, it is impera-
tive to rule out other treatable causes of symptoms, such as rectal intussusception or prolapse,

Table 2 Symptoms Associated with a Rectocele

Symptoms that may be directly related to Symptoms that may overlap

rectocele other pelvic floor disorders

Feeling of vaginal mass/bulge Constipation

Pelvic or rectal pain/pressure Fecal incontinence
Dyspareunia Fecal urgency
Low back pain Stool clustering
Incomplete rectal emptying Outlet obstruction
Need to splint or insert fingers into vagina,
rectum, or perineal support to facilitate
defecation
Aching after a bowel movement
Postevacuation fullness
 Evaluation and Management of Rectoceles 739

perineal descent, and dyskinetic puborectalis syndrome (15) prior to surgically correcting
posterior vaginal wall prolapse.

V. EVALUATION AND DIAGNOSIS

A. Physical Exam
The patient is examined first in the lithotomy position. All segments of vaginal support should be
assessed in a site-specific fashion using the split blade of a Graves speculum or a Sims speculum.
To visualize the posterior vaginal wall best, the speculum is used to displace the anterior vaginal
wall. The patient is then asked to perform a Valsalva maneuver or cough vigorously, and if bul-
ging of the posterior vaginal wall is noted, then a rectocele should be suspected. To better assess
the extent of the prolapse, the patient should be reexamined in the standing position. A rectova-
ginal exam should be performed to assess the rectovaginal fascia as well as to rule out an enter-
ocele, which can often occur in conjunction with a rectocele. An enterocele can be identified as a
separate bulging sac arising from a higher point in the vagina. During the rectal exam the index
finger should push toward the posterior vaginal wall in order to better assess the integrity of the
rectovaginal fascia. A rectal exam may also be useful to assess the integrity of the external anal
sphincter, especially for patients with symptoms of fecal incontinence. It can also be helpful in
identifying other causes of defecatory dysfunction, such as a posterior rectocele, intussusception,
skin tags, and mucosal prolapse (16).
The severity of a rectocele can be quantified either using the Baden-Walker grading sys-
tem (17) or the Pelvic Organ Prolapse Quantification (POP-Q) system (18). Although it provides
more precise information than the halfway system and may be useful for comparing anatomical
changes following surgery, it does not identify structures behind the vaginal wall and does not
quantify the size of the rectocele from the rectal side (16).
One should also look for perineal body defects. Perineal body defects are associated with a
widened introitus with straining, and a decreased distance between the posterior margin of the
vaginal introitus and the anterior margin of the anus. Measurements of the perineal body and
genital hiatus are included as standard measurements in the POP-Q system. Routine evaluation
of pelvic floor muscle function should also be performed by asking the patient to selectively con-
tract and relax the pelvic floor muscles with the examiner’s fingers in the vagina.

B. Adjunctive Studies
Ancillary studies, which include both radiologic and physiologic investigations as listed in Table 3,
are being used to identify concomitant pathology, explain pathophysiology, provide objective out-
come criteria and predict patients who will benefit most from surgery (11,19). However, there is no
gold standard in diagnosing rectoceles, and the usefulness of these adjunctive studies in improving
functional outcome is limited owing to the complex neuromuscular, physiological, and mechanical
interactions that contribute to anorectal dysfunction (16). In general, rectoceles that are not associ-
ated with defecatory dysfunction do not require additional ancillary tests.

C. Defecating Proctography
For women with functional disorders of the pelvic floor, several recent studies have shown a lim-
ited role for proctography and dynamic MRI in characterizing posterior vaginal wall prolapse
prior to surgery (20 –22). The advantage of defecating proctography over physical examination
is that in addition to providing a two-dimensional quantification of rectal parameters to diagnose
 740

Table 3 Ancillary Studies for Women with Functional Disorders of the Pelvic Floor

Test Purpose Parameters Usefulness

Defecating To evaluate dynamics of evacuation by visualizing During resting/squeezing/straining Useful in detecting size of rectocele.
proctography the anorectum fluoroscopically after filling the phases, anorectal angle, anal canal Can detect other anatomic
rectum with liquid barium and barium paste. length, puborectalis length, and abnormalities that may cause
perineal descent are evaluated. overlapping pelvic symptoms,
Segal and Karram

To provide structural information. By measuring barium trapping, time including anorectal

and completeness of evacuation are intussusception, sigmoidoceles,
estimated. rectoceles, rectal prolapse, and
perineal descent.
Some use barium trapping as a
criterion for rectocele repairs, but
overall not a useful predictor of
clinical outcome after rectocele
repair.
Dynamic MRI Combines dynamic visualization of rectal evacuation NA Provides global view of all intrapelvic
and fast-sequence examination of the pelvis to compartments.
detect anatomic and functional abnormalities. Aids in the differentiation of complex
combined pelvic floor disorders.
Endoanal Provides morphologic assessment of the internal and NA Useful in detecting an anatomic
ultrasonography external anal sphincters, the puborectalis muscle, defect associated with fecal
and the rectovaginal septum. incontinence.
Anorectal manometry Sensory devices are used to quantitatively assess Resting and squeeze anal pressures, Useful in determining the physiologic
resistance to spontaneous evacuation by the including high-pressure zone, and components of fecal incontinence
anorectal mechanism. anal canal length. and constipation.
Using balloon distension, sensory capabilities of the Rectal sensory threshold, sensation of
rectum to provide a feeling of imminent emptying fullness, maximum tolerable
are also assessed. volume, and rectal capacity.
Rectoanal inhibitory reflex and
anocutaneous reflex.
Electromyography. To assess the neuromuscular integrity of the anal Electric activity in muscles of Useful in detecting muscular and
canal, using concentric needle electrodes or continence during anorectal neurogenic damage in fecal
cutaneous surface electrodes which record motor function. incontinence and inappropriate
unit action potentials generated by the EAS and Impaired recruitment or evidence of muscle activity in pelvic outlet
puborectalis muscles at rest and with contraction. denervation obstruction.
To assess the functional activity and presence Sphincter mapping Useful in determining degree of
of neurologic damage of the anal sphincter Fiber density and nerve latency denervation and conduction
and pelvic floor muscles. Measure striated muscle function defects.
Pudendal nerve terminal Provides evaluation of pelvic floor neuromuscular NA Useful in determining neurogenic
motor latency. integrity by measuring the length of time required cause of fecal incontinence
for a fixed electrical stimulus to travel along the Useful for predicting outcome after
pudendal nerve between the ipsilateral ischial anterior overlapping
spine and the anal verge. sphincteroplasty
Colonic transit study Radiopaque markers are ingested and the percentage NA Useful in determining pelvic outlet
that are passed within a specified time as well as obstruction and colonic inertia.
their distribution is measured. Slow colonic transit may be
predictive of poor outcome
of a rectocele repair.
Mucosal electro- Uses electrode to pass current or probes which NA Useful to detect sensory impairment
sensitivity and provide hot and cold stimuli to assess the sensory in patients with fecal incontinence.
thermal sensitivity function of the anorectum.
tests.

Source: Refs. 11,16,19.

Evaluation and Management of Rectoceles
741
742 Segal and Karram

a rectocele, it can detect other anatomic abnormalities such as enteroceles, sigmoidoceles,

perineal descent, and internal rectal prolapse. More importantly, defecating proctography also
provides functional information regarding the efficiency of rectal emptying by enabling patients
to mimic their defecating abnormalities in a physiologic manner.
However, the normal range of motion of the rectovaginal axis has not been determined,
and cut-off values for diagnosing a rectocele are merely arbitrary numbers (13). Many reports
define rectoceles 2.0 –3.0 cm as being significant and indicative of patients who may benefit
from operative repair (23,24), while others report that retention of contrast medium at defeco-
graphy should be part of the selection criteria in determining who should undergo surgery.
Preoperative size or grade of emptying, however, has not been shown to correlate well with
symptoms (25,26).
Some have also advocated defecography as means of better detecting unsuspected recto-
celes. Studies have shown, however, that physical examination alone has a 91 – 94% sensitivity
in detecting a rectocele compared with proctography (27). Overall, rectoceles and other ana-
tomic abnormalities may be easily and objectively diagnosed by defecating proctography, but
its usefulness in the clinical evaluation of a rectocele and its ability to predict clinical outcome
after a repair is limited (28).

D. Dynamic MRI Defecography

Dynamic MRI defecography has been considered superior compared to traditional defecating
proctography because it is noninvasive, does not require ionizing radiation, and can provide a
global view of all intrapelvic compartments (21). The study combines dynamic visualization
of rectal evacuation with fast-sequence MRI examination of the pelvis. It helps determine
complex, combined pelvic floor disorders such as rectoceles, enteroceles, rectal intussusception
or prolapse, descending perineum, and dyskinetic puborectalis syndrome in association with
defecation abnormalities, such as fecal incontinence, urgency, stool clustering, or outlet obstruc-
tion (22). Matsuoka et al. have shown, however, in comparing the two modalities, that despite
costing 10-fold more than videoproctography, dynamic pelvic MRI has not been shown to
change clinical decision making (29).

E. Physiologic Anorectal Studies

Anorectal studies can include anorectal manometry, electromyography, pudendal nerve terminal
latency studies, and colonic transit studies as described in Table 3. In reviewing anorectal
function tests, however, there are no physiologic findings that are specific for a rectocele
(28). Although pudendal nerve terminal motor latency times are often increased in patients
with perineal descent and chronic straining (31), prolonged latency is not consistently associated
with rectoceles (32), and is not a good predictor of outcome after a rectocele repair (33). Those
with an irritable rectum often feel an urge to defecate at small volumes and may experience
symptoms of incomplete emptying and fecal incontinence. It is thought that a rectocele repair
may worsen these symptoms by reducing rectal volume; anorectal manometry may prove help-
ful in this instance (16).
Van Dam et al., in a prospective study (34), evaluated the prognostic value of clinical and
physiologic tests, such as defecography, pelvic floor electromyography, anorectal manometry,
and balloon expulsion studies in women with obstructed defecation undergoing rectocele repair.
They found that slow colonic transit studies were the only useful predictors of poor outcome in
relieving obstructive symptoms after a combined posterior colporrhaphy and transanal repair.
They also showed that women without a daily urge to defecate or a stool frequency of less
 Evaluation and Management of Rectoceles 743

than once per week or both, also had a worse postoperative outcome. The usefulness of colonic
transit studies as part of the routine preoperative evaluation was later confirmed in separate
prospective studies by Lopez et al. and Mellgren et al. (35,36). Mellgren also found through elec-
trophysiologic analysis that two out of three patients with preoperative paradoxical sphincter
reaction did not improve after a rectocele repair (36). However, the sample size was small,
and a prospective study by Van Dam et al. found that paradoxical sphincter contraction did
not affect the outcome of a rectocele repair (37).

F. Operative Criteria
Owing to the large prevalence of small rectoceles among healthy women, the association of
rectoceles with defecatory dysfunction, and the varied results of rectocele repair reported
among different investigators, it has become a challenge to decide who will most benefit
from a surgical repair of a rectocele. As a result, various groups have tried to establish preopera-
tive criteria to predict surgical outcome (38,39). Because gynecologists have traditionally eval-
uated a rectocele repair by its effects on vaginal function and coloproctologists have traditionally
evaluated its effect on bowel function, different operative criteria and surgical techniques have
evolved.
Rosato (39) and Murthy et al. (38) each describe strict criteria in determining which
patients with a rectocele to select for surgery, as can be seen in Table 4. In accordance to his
selection process, Murthy et al. recommended a rectocele repair for only 25 out of 132 patients
with a confirmed rectocele who were evaluated for functional pelvic complaints. Besides defeco-
graphy, they did not find any physiologic studies useful for recommending a repair (38).
Watson et al. require for operation demonstration of a large rectocele on evacuation proc-
tography and a history of defecation aided by vaginal digitation (33). They, like others, believe
that the preoperative need for vaginal digitalization for complete rectal evacuation is a signifi-
cant test for predicting good outcomes of a rectocele repair. Other studies have also shown that
many women with rectoceles do not need to splint, while some women without rectoceles do use
manual pressure to assist in defecation (12,23,40). The feeling of incomplete emptying is not
specific for rectoceles and can be due to many other disorders of the pelvic floor, including

Table 4 Criteria of Patient Selection for Rectocele Repair

Rosato’s criteriaa
1. Rectocele 4 cm in diameter as measured during defecography
2. Nonemptying or partial emptying of rectocele during evacuation phase of defecography
3. Rectal or vaginal symptoms present for longer than 12 months
4. Persistence of rectal or vaginal symptoms for at least 4 weeks, despite increased dietary fiber (35 g/d)
5. Need of rectal or vaginal digitation or perineal support maneuver to facilitate rectal evacuation
Murthy’s criteriab
1. Sensation of a vaginal mass or bulge that required digital support and/or rectal digitizing for
evacuation that was confirmed to be a rectocele
2. Demonstration on defecography of contrast retention in the rectocele
3. The presence of a very large rectocele associated with anterior rectal wall prolapse
a
At least three of the five criteria should be present.
b
Only one criteria required.
744 Segal and Karram

irritable rectum, enterocele, sigmoidocele, rectal intussusception, descending perineum syn-

drome, and slow transit constipation.
Coexisting causes of constipation, such as those listed in Table 1, could be predictors of a
poor outcome following a rectocele repair due to the possibility that the rectocele is only a sec-
ondary condition. Paraiso et al. (41), in evaluating anatomic and functional outcomes utilizing a
traditional posterior colporrhaphy, compared pre- and postoperative symptoms in women with
successful versus unsuccessful outcome. Although not statistically significant, those with an
unsatisfactory outcome were more likely to have persistent straining after surgery.

VI. TREATMENT

It is generally agreed that only symptomatic rectoceles require treatment. However, for patients
with asymptomatic rectoceles who are undergoing reconstructive repair of other pelvic
organ defects, current expert opinion recommends concomitant surgical correction of the
rectocele (13).

A. Nonsurgical Approaches
Conservative therapy typically consists of pelvic floor rehabilitation for small degrees of pro-
lapse and the initiation of oral or topical estrogen for those whose vaginal tissue is noted to
be atrophic. A pessary can also be utilized as a temporizing measure for those with larger
degrees of prolapse who are high surgical risks, or it can also be used to simulate a surgical repair
to see if associated symptoms improve. Because surgical approaches have had mixed results in
their efforts to relieve rectal emptying, it is important to treat underlying defecation disorders
first. Biofeedback would be an appropriate first line of treatment for dyssnergic defecation,
and constipation can initially be treated with a fiber-enriched diet and bulk-forming agents
(28). The use of botulinum toxin has potential promise to inhibit paradoxical puborectalis con-
tractions based on a limited study of 14 patients with symptomatic anterior rectoceles and outlet
obstruction (42).

B. Surgical Approaches
There are several different procedures with many variations to surgically correct rectoceles,
which include transvaginal, transperineal, endorectal, transabdominal, and laparoscopic
approaches. All share similar goals: to relieve symptoms, to restore anatomy, and to maintain
or restore visceral and sexual function. To date there are no controlled studies comparing the
different types of repair.

C. Traditional Posterior Colporrhaphy

In 1867 Simon first described the term posterior colporrhaphy as a means to support the uterus
when it was prolapsed (43), and in 1870, Hegar introduced the colpoperineorrhaphy, which was
used to treat all forms of pelvic organ prolapse at that time (44). The traditional posterior
colpoporrhaphy consists principally of reinforcing the rectovaginal fascia with a side-to-side
plication, and oftentimes, the levator ani muscles are then plicated over the rectum in the mid-
line. A perineorrhaphy is typically then performed by placing deep sutures into the perineal
muscles and fascia to build up the perineal body. The incorporation of the levator plication
may have arisen from observations of widening of the levator hiatus in patients with uterine
 Evaluation and Management of Rectoceles 745

prolapse (16). Plication of the levator ani muscles strengthened uterine support because it was
believed that the levators supported the vagina, which in turn supported the uterus (44).
Using this approach the fascia is typically oversewn without ever identifying the defects.
Because the normal vaginal anatomy is not properly restored, symptoms related to defecatory
and sexual dysfunction are not adequately relieved. The traditional posterior colpoperineorrha-
phy combined with a levator ani plication often results in increased dyspareunia due to constric-
tion of the vaginal tube, partial closure of the genital hiatus, a transverse ridge created in the
posterior vaginal wall, and atrophy and scarring of the levator muscles.
Francis and Jeffcoate in 1961 reported a 50% rate of dyspareunia following posterior
colporrhaphy, which was thought to be secondary to overnarrowing of the introitus by means
of a tight levator ani plication (45). Kahn and Stanton reported an increase in sexual dysfunction
from 18% preoperatively to 27% postoperatively following a traditional posterior colporrhaphy,
which they attributed to levator muscle atrophy and scar formation (46). In a prospective obser-
vational study of 108 patients using a traditional approach, Paraiso et al. found significant
improvement in the severity of bowel symptoms and vaginal prolapse symptoms, but also
noted increased dyspareunia (41). Another prospective study by Mellgren et al. of 25 patients
showed similar findings. These authors, however, still support incorporating the levator ani
muscles as part of their repair, citing better restoration of a firm rectovaginal septum with
good functional results (36).

D. Defect-Specific Repair
Based largely on the findings of Richardson and Nichols, we prefer a defect-specific rectocele
repair, which entails reapproximation of fascial breaks without performing a levator plication.
Our technique for performing a defect specific repair is as follows:
The desired size of the introitus, which is typically three fingerbreadths, is first approxi-
mated by placing Allis clamps bilaterally on the labia minora and bringing them together
along the midline. A finger of the nondominant hand is then inserted in the rectum, and a
diamond-shaped wedge of perineal skin is removed, which again is tailored to the desired
size of the introitus. The width and length of the perineal incision is dependent on the epithelium
needed for restoration of the perineal body. Sharp dissection is utilized to make a plane in the
rectovaginal space and to completely mobilize the posterior vaginal wall away from the anterior
rectal wall up to the vaginal apex, laterally to the tendinous arch of the levator ani and inferiorly
to the perineal body (see Figs. 2, 3).
Care is taken to leave as much fascia as possible on the rectum. Any pararectal fascia
adherent to the posterior vaginal wall is mobilized, and redundant vaginal mucosa is trimmed
along the midline if deemed appropriate. The finger in the rectum is used to elevate the anterior
rectal wall to help delineate any fascial tears. Durable fascia is then plicated over the entire
anterior rectal wall with interrupted 2-0 delayed absorbable sutures to resupport any segments
that had been torn or attenuated. The following diagrams illustrate various defect-specific
closures: Figure 4 shows a low transverse defect between the perineum and the distal edge of
the rectovaginal fascia with a defect-specific closure using interrupted sutures, while Figure 5
illustrates a midline longitudinal defect. After reapproximating the vaginal mucosa along the
posterior vaginal wall with a layer of 3-0 delayed absorbable running suture, a perineorrhaphy
is performed if the perineal body is deficient or if the patient has a large genital hiatus. It is also
utilized to add posterior vaginal length for a patient with postoperative vaginal shortening.
Photographs delineating the surgical steps can be found in Appendix.
If at the completion of the defect-specific repair one cannot comfortably admit three
fingers in the vagina, relaxing incisions are made through the full thickness of the vagina.
746 Segal and Karram

Figure 2 The dashed line outlines the area of perineal skin and posterior vaginal wall to be excised.
(From Ref. 8.)

One should take into consideration that the levator ani and perineal muscles are relaxed from
general anesthesia and that they will contract postoperatively. Vaginal scarring and postmeno-
pausal atrophy could account for further narrowing in the future.
In three retrospective reviews of a defect-specific rectocele repair, recurrence rates varied
from 18% to 23% with a mean follow-up between 12 and 18 months (47–49). Bowel and sexual
function were subjectively improved. Cundiff et al., in a series of 69 patients undergoing a defect
specific repair, reported constipation improved in 84%, dyspareunia improved in 66%, and fecal
incontinence improved in 56% (48). This study noted the site-specific defect repair reestablishes
the integrity of the rectovaginal fascia and at the same time repairs perineal descent, which may
explain improved anorectal function. Outcomes, however, were not as good for fecal inconti-
nence and constipation in the other studies (47,49). In Kenton et al.’s series of 66 patients at
1-year follow-up after a site-specific repair, constipation was clinically unchanged, and 64%
returned to their preoperative practice of splinting (49). This study theorizes that perhaps
the need for manual evacuation represents a rectocele of advanced stage in which chronic
overdistension of the rectal wall results in physiologic abnormalities that are not amenable to
surgical repair (49).
 Evaluation and Management of Rectoceles 747

Figure 3 With a finger in the rectum, the posterior vaginal wall is sharply dissected from the anterior
vaginal wall. (From Ref. 8.)

In a prospective study evaluating the defect-specific repair on 67 patients with a follow-up

of only 3 months, Glavind et al. found no recurrences, an 85% cure for those with difficulties
evacuating the rectum, and resolution of dyspareunia in six of eight sexually active patients.
Two, however, developed de novo dyspareunia (50).

E. Transanal Repair
Low rectoceles with weakened rectovaginal septums are often repaired endorectally by colo-
rectal surgeons in an effort to simultaneously treat anorectal pathology, such as hemorrhoids,
fissures, papillae, and anal stenosis (51). This anorectal approach developed over time from
the perceived failure of a vaginal repair to correct a ballooning anterior rectal wall. In 1965
748 Segal and Karram

Figure 4 A low transverse defect between the perineum and the distal edge of the rectovaginal fascia,
closed in a defect-specific fashion with interrupted sutures. (From Ref. 8.)

Redding recognized that rectoceles could be a cause of anorectal symptoms (52), and in 1967,
Marks reported that only focusing on the vaginal deformity does not adequately relieve symp-
toms (53). Under the assumption that the loose inner lining of the rectocele following a posterior
colporrhaphy was associated with an urge to defecate, he recommended a combined vaginal
repair with a transanal resection of redundant rectal mucosa. This technique, however, resulted
in a large number of recurrences and rectovaginal fistulas.
Based on Sullivan et al.’s initial description of an endorectal repair of a rectocele (54),
today the colorectal surgeon’s approach typically involves an endorectal plication using oblit-
erative sutures to reduce the rectal luminal size. This may be indicated for patients with outlet
obstruction or rectal herniation associated with thinning of the rectal submucosa and increased
rectal reservoir size (55). It is inappropriate, however, for patients with high rectoceles and
associated enteroceles. As described by Nichols, the redundant mucosa and submucosa of the
weakened anterior rectal wall is first identified after inserting a rectal retractor. Two obliterative
layers are then placed incorporating the full thickness of the rectal wall starting at the muco-
cutaneous junction (9). Others have also described incising the rectal mucosa above the dentate
line in a transverse direction and then, depending on the size of the rectocele, excising a
rectangular portion of mucosa (28).
Overall, transanal repairs have been shown to reduce the size of rectoceles on procto-
graphy. Although having inconsistent effects on anal pressures, they tend to improve rectal sen-
sation, resulting in an urge to defecate at lower volumes and improving constipation and
incontinence (16). In a prospective evaluation utilizing a transanal approach, Murthy et al.
found improvements in constipation, incontinence, and symptoms of a vaginal mass (38). In a
retrospective comparison, however, Arnold et al. found no significant difference between a
 Evaluation and Management of Rectoceles 749

Figure 5 A midline longitudinal defect with a defect-specific closure using interrupted sutures. (From
Ref. 8.)

transanal approach and the traditional posterior colporrhaphy in regard to constipation, fecal
incontinence, and dyspareunia (56). The only difference was a greater frequency of postopera-
tive pain with the vaginal approach. A more recent prospective study confirmed these results
(57).

F. Laparoscopic Rectocele Repair

The indications for a laparoscopic rectocele repair are the same as those utilizing a vaginal or
transanal approach. Paraiso et al. suggests using electrocautery, harmonic scalpel, or laser to
open the rectovaginal septum (58). Blunt and/or sharp dissection is used to open the rectovagi-
nal space extending to the perineal body. The perineal body is sutured to the rectovaginal septum
and the rectovaginal fascial defects are closed with No. 0 nonabsorbable suture. If the recto-
vaginal fascia is detached from the iliococcygeus fascia, it is reattached with No. 0 nonabsorb-
able suture. The medial aspects of the levator ani muscles may also be plicated. Lyons and Winer
incorporate polyglactin mesh from the uterosacral ligament complex to the perineal body in their
laparoscopic rectocele repairs. They prospectively evaluated 20 patients who had this repair for
1 year and found a 95% rate of symptom relief (59). Larger prospective randomized trials
750 Segal and Karram

comparing a laparoscopic repair to a more traditional approach are needed, however, before any
conclusions can be drawn regarding its efficacy.

G. Incorporation of Mesh
For patients with high rectoceles, recurrence of posterior vaginal wall prolapse, or little or no
supportive tissue to use in a repair, the use of mesh has been suggested as a means to improve
the strength of the repair. Mesh, however, has historically been associated with vaginal erosion,
sinus formation, and infection (60). In 1981 Oster and Astrup incorporated a dermis graft in the
rectovaginal space as part of a posterior colporrhaphy for large rectoceles in 15 patients, and
reported good outcomes after a mean follow-up of 2.6 years (61).
Two recent studies, however, in which mesh was incorporated transabdominally have had
suboptimal results: Sullivan et al. (62) reported their experience using what they describe as a
total pelvic mesh repair on 236 patients who had failed previous reconstructive surgery or
had rectal procidentia combined with genitourinary prolapse. Utilizing a transabdominal
approach they incorporated a strip of Marlex mesh to reinforce the rectovaginal septum as
part of their repair. During a median follow-up of 5.3 years, 10% of patients required reoperation
secondary to complications specific to the repair, and 28% required postoperative surgical cor-
rection of anorectal mucosal prolapse or rectocele. Baessler and Schuessler (63), as part of an
abdominal sacrocolpopexy, used Gore-Tex mesh to support the posterior vaginal wall. During
a mean follow-up of 26 months, rectoceles recurred in 57% and the authors have since switched
to a site-specific defect rectocele repair.
Sand et al. (64) performed a prospective, randomized controlled trial using polyglactin 910
mesh during primary or recurrent anterior and posterior colporrhaphy in women with central cysto-
celes and found no effect of the mesh on the success of the rectocele repair. However, the power of
the study was limited owing to the low incidence of recurrent rectoceles. In a prospective study
Watson et al. (32) utilized a transperineal approach with the placement of Marlex mesh to replace
the rectovaginal septum in 9 patients requiring preoperative vaginal digitation. They found defeca-
tory dysfunction improved in 88% without recurrence over 29 months. As with laparoscopic recto-
cele repairs, more research is needed before a conclusion can be reached on the efficacy of mesh as
part of the rectocele repair. It does seem apparent, however, from the transabdominal studies, that in
addition to incorporation of mesh, repair of the fascial defects is required.
Table 5 compares the anatomic and functional outcomes following these various
approaches to a rectocele repair.

VII. COMPLICATIONS

Complications of vaginal surgery in general include bleeding, infection, vaginal shortening, and
vaginal wall inclusion cyst formation. Complications particular to a rectocele repair include inci-
dental proctotomy and subsequent development of a rectovaginal fistula, which has been
reported in up to 5% of patients. Urinary retention is a frequent but temporary complication,
occurring in 12.5% of patients. The incidence of dyspareunia, which had been reported to
occur in up to 30% of patients, has decreased in incidence in more recent studies (65). Early
recurrence is thought to be caused by a failure to identify and repair all support defects, while
late recurrence is probably caused by further weakening of supportive tissue related to aging,
chronic straining, neurologic deficits associated with pelvic floor injury, estrogen deficiency,
or significant alteration of the vaginal access.
Table 5 Summary of Anatomic and Functional Outcomes

Investigators Paraiso Mellgren Kahn and Glavind and

et al. (41) et al. (36) Stanton (46) Madsen (50)
Study type Retrospective Prospective Retrospective Prospective
Year 2001 1995 1997 2000
Type of repair Traditional Traditional Traditional Defect-specific
Sample size 108 25 231 67
Recurrence rate 12% 20% 24% 0%
Mean follow-up 9.9 12 42.5 3
(mos)
Symptoms Preop Postop Preop Postop Preop Postop Preop Postop
Constipation/ 76% 45% 96% 52% 22% 33% — —
straining
Splinting/manual 45% 8% 48% 0% — — — —
evacuation
Incomplete emptying — — — — 27% 38% 40% 15%
Fecal incontinence 10% 2% 8% 8% 4% 11% — —
Feeling lump/ — — — — 64% 31% — —
pressure
Dyspareunia 2% 12% 6% 18% 18% 27% 12% 6%

(continued )
Evaluation and Management of Rectoceles
751
 752

Table 5 Summary of Anatomic and Functional Outcomes

Investigators Porter et al. (47) Cundiff Kenton Watson Murthy

et al. (48) et al. (49) et al. (32) et al. (38)
Study type Retrospective Retrospective Retrospective Prospective Retrospective
Year 1999 1998 1999 1996 1996
Segal and Karram

Type of repair Defect-specific Defect-specific Defect-specific Transperineal Transanal

with Marlex
mesh
Sample size 125 69 66 9 33
Recurrence rate 18% 18% 23% 0 —
Mean follow-up 18 12 12 29 31
(mos)
Symptoms Preop Postop Preop Postop Preop Postop Preop Postop Preop Postop
Constipation/ 60% 50% 46% 13% 41% 23% — — 35% 16%
straining
Splinting/manual 24% 14% 39% 25% 30% 15% 100% 11% — —
evacuation
Incomplete emptying — — — — — — — — — —
Fecal incontinence 24% 21% 13% 8% 30% — — — 29% 12%
Feeling lump/ 38% 14% — — 86% 9% — — 61% 12%
pressure
Dyspareunia 67% 46% 29% 19% 28% 2% 33% — — —
 Evaluation and Management of Rectoceles 753

VIII. CONCLUSION

Over the past several decades, a better understanding of the anatomic relationships of the pelvic
floor and posterior vaginal wall has altered the way we approach rectoceles, which has resulted
in improved anatomic and functional postoperative outcomes. However, we have clearly been
less successful in treating defecatory disorders associated with rectoceles. Although a surgical
repair may reduce the dimensions of a rectocele, it does not alleviate rectal emptying difficulties
that may be caused by other factors. Future research should better address (a) the relationship
between defecatory dysfunction and rectoceles, and (b) preoperative studies that can be useful
predictors of outcome regarding defecatory dysfunction following a rectocele repair. Addition-
ally, prospective randomized trials are needed to compare the various surgical approaches to
repair rectoceles. Both objective and subjective findings need to be described pre- and post-
operatively in order to better determine surgical outcomes. Although the incidence of postopera-
tive dyspareunia has decreased, it still remains an associated complication. Routine levator ani
plication is no longer advocated, but dyspareunia may still result from vaginal scarring and
narrowing as well as from the development of a vaginal constriction ring. The goal of the
reconstructive pelvic surgeon should be to restore the normal vaginal axis and caliber as well
as to maintain vaginal length, and, at the same time, to maintain or restore visceral and sexual
function. To do so one must have a clear and thorough understanding of the pelvic anatomy as
well as mechanisms of pelvic support.

APPENDIX

Appendix A A distal rectocele with attenuated perineum.

754 Segal and Karram

Appendix B The initial wedge of perineal skin has been removed.

Appendix C The posterior vaginal wall is completely mobilized from the anterior rectal wall using
sharp dissection. Note that a narrow piece of vagina has been dissected in the midline. The width of
this segment of vagina is determined by estimating the amount of vagina that will need to be
trimmed.
 Evaluation and Management of Rectoceles 755

Appendix D Identification of fascia to be utilized for plication over the anterior rectal wall.

Appendix E Mobilization of the fascia off the posterior vaginal wall.

756 Segal and Karram

Appendix F The fascia has been completely mobilized off the right vaginal wall. Note that the midline
wedge of vaginal skin has no underlying fascia, confirming a midline-type defect.

Appendix G A high transverse defect is demonstrated. Note the fascia is present over the distal anterior
rectal wall.
 Evaluation and Management of Rectoceles 757

Appendix H Completed fascial defect repair. Durable fascia has been plicated over the entire anterior
wall (From Ref. 8.).

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53
Vesicovaginal Fistula: Complex Fistulae

Karyn Schlunt Eilber,* Nirit Rosenblum,† and Larissa V. Rodrı́guez

David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.

I. INTRODUCTION

In 1672, the first vesicovaginal fistula (VVF) repair was reported in which quills were used to
approximate wound edges with silk threads (1). Since then, techniques utilizing abdominal,
vaginal, and combined abdominal and vaginal approaches with and without tissue interposition
have been described. This chapter will discuss the current concepts in evaluation and manage-
ment of this potentially devastating condition.
The true incidence of vesicovaginal fistulae is unknown but has been estimated at 0.3 –2%
(1 – 3). The various etiologies of VVF are listed in Table 1. In developed countries, hysterectomy
is the main cause of VVF, while in some areas of Africa and Asia obstetric trauma is the
predominate cause (4,5). Obstetrical VVFs result from necrosis of the vaginal wall and bladder
secondary to pressure from the fetal head during prolonged labor, and usually involve a large
area of tissue damage. Associated injuries may include total urethral loss, urethrovaginal fistula,
cervical destruction, and rectovaginal fistula (6). The focus of this chapter will be on VVF
secondary to causes other than prolonged labor.
Vesicovaginal fistula after hysterectomy is most common after a laparoscopic approach
(2.2/1000) followed in decreasing order by total abdominal hysterectomy (1.0/1000) and vagi-
nal hysterectomy (0.2/1000) (3). The Mayo Clinic also reviewed causes of VVF and found that
82% were due to gynecologic surgery, 8% to obstetrical procedures, 6% to pelvic radiotherapy,
and 4% to trauma or fulguration (7). Because in developed nations the majority of VVFs are a
complication of hysterectomy, risk factors, and preventive measures need to be considered. Prior
pelvic surgery including cesarean section, cervical conization, radiation therapy, and endo-
metriosis may predispose patients to development of a VVF (8).

II. DIAGNOSIS
A. History
An individual with a VVF typically presents with continuous leakage of urine shortly after a
pelvic operation or procedure. The temporal relationship of the onset of symptoms and pelvic
trauma (surgery or vaginal delivery) must be ascertained. A history of radiation, prior treatments

*Current affiliation: Memorial Sloan-Kettering Cancer Center, New York, New York, U.S.A.
†
Current affiliation: NYU School of Medicine, New York, New York, U.S.A.

761
762 Eilber et al.

Table 1 Etiology of Vesicovaginal Fistula

Congenital (rare)
Acquired
Surgical
Gynecologic procedures
Hysterectomy
Bladder neck suspension
Anterior colporrhaphy
Colposuspension
Urologic procedures
Sling
Injectable bulking agents
Other pelvic surgery
Obstetric
Prolonged labor
Cesarean section
Radiation
Malignancy
Infection
Trauma
Foreign body

or attempts at repair, infection of the vaginal cuff, and the patient’s general state of health must
also be determined. Depending on the size and location of the fistula, leakage may range from
an occasional vaginal discharge between normal voiding per urethra to continuous leakage that
prevents the patient from storing a volume of urine adequate for volitional voiding. Radiation
therapy –induced VVF may present months to years following the treatment. A case has been
reported in which a large vesicovaginal fistula developed 38 years after a radical hysterectomy
and radiation (9).
When a patient presents with constant vaginal urinary leakage, the differential diagnosis
includes VVF, ureterovaginal fistula, urethrovaginal fistula, and uterovesical fistula. History,
physical examination, and selected diagnostic tests allow the diagnosis to be made with
certainty.

B. Physical Examination
During physical examination, the vagina needs to be evaluated for depth, diameter, mobility,
prolapse of other organs, and evidence of vaginal atrophy. When a fistula is detected, the
size, number (multiple/single), and location need to be noted. Finally, the patient needs to be
evaluated for urethral hypermobility and incontinence.
Meticulous inspection of the vagina using a speculum facilitates visualization of the fistu-
lous tract. The quality and quantity of the surrounding vaginal tissue should be assessed. Most
fistulae that develop after hysterectomy are located at the vaginal cuff. For fistulous tracts that
are not easily seen, the bladder can be filled with diluted Methylene Blue and the vagina
inspected for leakage of the blue fluid. If the fistula is still not demonstrated, the vagina can
be packed with gauze or a tampon. After the patient is allowed to ambulate for a short time,
the gauze or tampon can be inspected for blue staining. Another method of demonstrating the
presence of a VVF involves oral phenazopyridine, which causes orange discoloration of the
urine. Phenazopyridine is administered a few hours before packing the vagina. Orange staining
 Vesicovaginal Fistula 763

of the vaginal packing implies that the vaginal fluid is urine. A positive oral phenazopyridine
test in the presence of a negative Methylene Blue bladder instillation implies the presence of
a ureterovaginal fistula. Retrograde pyelography should be performed in anyone with a strong
suspicion of ureterovaginal fistula.
If the diagnosis of VVF is in doubt, the fluid draining from the vagina must first be proven
to be urine. The diagnosis can be confirmed if an adequate amount of fluid is collected and
analyzed for creatinine. The creatinine measurement should be manyfold that of serum creati-
nine. If the creatinine measurement is similar to or less than that of the serum creatinine
measurement, other sources of the fluid such as peritoneal fluid, lymphatic fluid, Fallopian
tube secretions, or vaginal discharge must be considered (10). The phenazopyridine test can
also be used to differentiate between urine and other secretions.

C. Diagnostic Tests
Cystoscopy must be performed in all patients in whom there is a suspicion or diagnosis of VVF.
Cystoscopy may identify the location of the fistula, and is necessary to identify the location of
the ureteral orifices in relation to the fistula, the size and number of fistulous tracts, to evaluate
the bladder capacity, and to rule out the presence of any foreign body within the bladder or
fistulous tract. Biopsy of the fistulous tract must be performed in any patient with a history
or suspicion of malignancy.
A voiding cystourethrogram (VCUG) should also be performed in all patients to objec-
tively demonstrate the fistula and evaluate for any evidence of prolapse or stress urinary incon-
tinence (Fig. 1). VCUG is also useful to image fistulae to the uterus or rectum. The reported
incidence of iatrogenic ureteral injuries following gynecologic surgical procedures ranges
from 0.05% to 1% (11,12). Vesicovaginal and ureterovaginal fistulae coexist in up to 25% of

Figure 1 VCUG demonstrating communication between bladder and vagina.

764 Eilber et al.

cases (13 –16). As such, routine examination of the upper urinary tract by means of intravenous
pyelography, retrograde pyelography, or computed tomography (CT) is essential when evaluat-
ing a patient with a VVF to rule out concomitant ureteral injury and/or obstruction. Retrograde
pyelography must be performed if there is a strong suspicion that a ureterovaginal fistula is
present that is not demonstrated by intravenous pyelography.

III. CONSERVATIVE MANAGEMENT

Conservative measures including prolonged catheter drainage of the bladder or fulguration of

the fistulous tract may be considered for small, well-vascularized, nonirradiated fistulae or for
patients who have a small tract following prior repair. Although spontaneous resolution of
VVF after prolonged catheter drainage (19 – 54 days) has been reported, this is a relatively
rare event (17 – 20). Surgical reconstruction must be considered if resolution is not seen after
4 weeks of catheterization (15). The degree of tissue atrophy secondary to hormone deficiency
or chronic infection may affect the rate of spontaneous closure. Therefore, in addition to catheter
drainage, the use of antibiotic therapy and estrogen replacement therapy may also facilitate
spontaneous closure (21,22).
Stovsky et al. reported a 73% success rate following electrocoagulation of vesicovaginal
fistulae ,3.5 mm in size (23). Successful ablation of small fistulous tracts by the use of the
Nd-YAG laser has also been reported (24). Although small VVFs may respond to these conser-
vative measures, there is little utility in delaying repair for a trial of conservative therapy for
larger, complex, or radiation-induced fistulae.

IV. OPERATIVE MANAGEMENT

General considerations for the management of vesicovaginal fistulae are listed in Table 2. Sev-
eral principles are essential to ensure a successful VVF closure. It is necessary to obtain adequate
exposure of the fistulous tract and have healthy tissues available for the repair. The closure
should be multilayered, watertight and tension free. Overlapping suture lines should be avoided.
Also, it is essential to have maximal urinary drainage during the healing process. In many cases,
tissue interposition is a useful adjunct to the above techniques.

A. Timing of Surgery
There has been much debate over the timing of surgical repair of vesicovaginal fistulae (Table 3).
Early interventions usually involve repairs done only a few weeks after injury while delayed
repairs refer to the traditionally described waiting period of 3– 6 months following the injury.
The rationale for delayed repair is to allow resolution of the acute inflammatory response and
tissue edema. Although there are no randomized studies comparing the outcomes, several
authors have described similar success rates of early and late repair (14,25 –32). Successful
fistula repair as early as 10 days after the injury has been reported (32).
Owing to the distressing nature of this condition, we advocate early (2 – 3 weeks) repair
following recognition of the injury. Contraindications to early repair include VVF resulting
from radiation injury or obstetrical trauma or prior failed repair, when associated tissue necrosis
requires several months to fully delineate the extent of the injury. We also advocate waiting
several months after a failed fistula repair to allow the postoperative inflammatory process to
 Vesicovaginal Fistula 765

Table 2 General Considerations in Management of VVF

Etiology of fistula
Timing of surgery
Abdominal vs. vaginal approach
Excision of fistulous tract
Postoperative drainage
Tissue interposition
Concomitant procedures
Treatment of stress urinary incontinence
Augmentation cystoplasty
Sexual function
Adjuvant treatment
Antibiotic therapy
Hormone replacement therapy
Anticholinergic therapy

subside. Each case should be considered on an individual basis so as not to compromise surgical
success for the sake of social convenience.
In developed nations, the majority of vesicovaginal fistulae are complications of clean
gynecologic procedures. For most of these cases immediate repair should be attempted unless
infection of the vaginal cuff or pelvic infection is present (23). When an abdominal approach
is planned and the fistula is the result of an abdominal hysterectomy, we recommend a delayed
repair. Aside from these circumstances, no additional risks or compromise of surgical success
have been documented when instituting a short waiting period (14,22,25– 31).

B. Abdominal Versus Vaginal Approach

The main consideration when choosing between the vaginal and abdominal approach to the
repair of vesicovaginal fistulae should be the surgeon’s level of comfort with each technique.

Table 3 Timing and Success of VVF Repair

Reference No. patients % Success Timing of repair Approach

Elkins et al. (26) 23 91 2 – 3 mos Vaginal

Wang and Hadley (27) 16 94 7 , 3 mos, 9 . 3 mos Vaginal
Collins et al. (31) 38 72 29 , 4 wks, Vaginal
9 , 8 wks
Blaivas et al. (30) 24 96 14 , 3 mos, 15 vaginal, 8 abdominal,
10 . 3 mos 1 spontaneous closure
Persky et al. (32) 7 86 ,10 wks 6 abdominal, 1 vaginal
Blandy et al. (28) 25 100 12 , 6 wks, Abdominal
13 . 6 wks
Diaz Calleja et al. (44) 6 100 .3 mos Abdominal
Motiwala et al. (39) 68 81 3 mos 58 transvesical,
10 abdominal
Nesrallah et al. (40) 29 100 6 wks to 48 mos O’Conor technique
(median 8 wks)
766 Eilber et al.

We support the adage that the best operation is the first operation, and thus the approach chosen
should be that with which the surgeon is most experienced and familiar.
We prefer the vaginal approach for the repair of most VVF because it avoids the morbidity
of an abdominal incision and cystotomy. A long or a narrow vagina is not a contraindication to
the vaginal approach. A relaxing episiotomy can be done to facilitate exposure in an individual
with a narrow introitus. The abdominal approach should be considered when concomitant
abdominal procedures need to be performed (augmentation cystoplasty for a noncompliant blad-
der or repair of associated ureteral injury or other abdominal pathology).

C. Excision of Fistulous Tract

Historically, VVF repair has included wide excision of the fistulous tract to ensure approxi-
mation of healthy tissue. A number of surgeons have advocated repairing vesicovaginal fistulae
without excision of the tract (23,27,29,30). A disadvantage of tract excision is that during
repair of a small fistula, excision of the fistulous tract may increase the size of the fistula and
make the repair more complex. Furthermore, hemorrhage encountered during an attempt to
excise the fistulous tract may require the use of coagulation and result in the creation of more
nonviable tissue, which could decrease the patient’s chance for cure. The fistulous tract need
not be excised, as it provides good anchoring tissue for the sutures of the first layer of the repair.
An additional advantage of not excising the tract occurs when the fistula is in close proximity to
the ureteral orifices. By not excising the fistula in this setting, ureteral stents may be used to
identify the ureteral orifices and the fistula simply closed, avoiding injury to the trigone and
ureters and the need for ureteral reimplantation.

D. Postoperative Drainage
Continuous, uninterrupted postoperative urinary drainage is essential to prevent bladder disten-
sion, which can create tension on suture lines and urinary extravasation. Urethral and suprapubic
catheters are used whether a vaginal or abdominal approach is used. Additional pelvic drainage
with a Penrose or Jackson-Pratt drain is recommended when a using a transvesical approach.
Anticholinergic therapy is also essential to help prevent involuntary detrusor contractions.

E. Tissue Interposition
All vesicovaginal fistulae are repaired with a multilayer approach. Fistulae secondary to radi-
ation or those with poor-quality tissue after a prior attempted repair have a higher rate of success
when tissue interposition is used (19,23,26,27,29,33). Recently, Evans et al. reported on the use
of interposition flaps in transabdominal repairs of VVF (34). The surgical success rate was 100%
when an interposition flap was used, compared to only 64% success rate without interposition.
Omentum is commonly used with the abdominal approach. Several options are available with
the transvaginal approach including the Martius flap, peritoneum, rotational labial flap, gluteal
flap, and gracilis flap.

F. Stress Incontinence
During the preoperative evaluation, the presence of stress urinary incontinence (SUI) prior to the
development of the fistula must be determined. The reported incidence of SUI occurring follow-
ing VVF repair ranges from 7% to 27% (35 –37). Simultaneous correction of stress incontinence
 Vesicovaginal Fistula 767

during fistula repair avoids the need for a separate surgical procedure and the psychologic
distress of incontinence following an otherwise successful fistula repair.

G. Sexual Function
Preoperative determination of the patient’s current and future expectation of sexual function is
of paramount importance. For patients who are sexually active, attempts at preservation of a
functional vagina must be made. Local or systemic estrogen replacement should be considered
in patients who show signs of vaginal atrophy. For patients who are not sexually active and
present with large fistulae, partial colpocleisis could be considered in order to maximize tissue
coverage of the repair (23).

V. SURGICAL APPROACHES

Prior to any repair, adequate time must be allowed for all evidence of infection to subside. All
fistula repairs should include the use of a broad-spectrum antibiotic prior to surgery. Preopera-
tive urine cultures may aid in the choice of antibiotic. Additionally, pre- and postoperative
hormone replacement may facilitate healing.

A. Vaginal Approach
The vaginal technique for uncomplicated vesicovaginal fistulae is a five-step process that results
in a three-layer fistula repair (23). Many modifications exist, the main variable being that of fis-
tula excision.

Step 1: Patient Preparation

Padded boots are placed on the patient before placing her in the high lithotomy position. The
suprapubic area and external genitalia are shaved and then prepped with an iodine-based wash.
Sutures are placed to retract the labia. Ureteral stents are placed at this time if preoperative cysto-
scopy indicated the fistulous tract to be in close proximity to the ureteral orifices. A urethral cath-
eter is used to fill the bladder with normal saline, and a curved Lowsley retractor is used to place a
suprapubic catheter via a small puncture wound in the suprapubic area. Vaginal packing may be
necessary to occlude the fistulous tract during filling of the bladder. A ring retractor with elastic
stays and a weighted speculum are used to gain exposure. Posterolateral episiotomies may need to
be performed for a narrow vagina in order to gain maximum exposure of the vaginal vault.

Step 2: Isolation of Fistula

The fistula is catheterized with an 8 or 10F Foley catheter (Fig. 2A). Before insertion of the cath-
eter, the tract may need to be dilated with metal sounds. Traction may be placed on the catheter
to bring the fistula closer to the surgeon. If the fistula cannot be catheterized, an abdominal
approach should be considered. To aid in catheterization, Methylene Blue is instilled into the
bladder, and the tract may be visualized and catheterized. In the rare case that catheterization
is still not possible, the repair can be performed under vision of Methylene Blue. After catheter-
ization, a circumferential incision in the vaginal mucosa around the fistulous tract is made
(Fig. 2B). The incision is then extended in an asymmetric “J” or inverted “J,” depending on
the location of the fistula. This allows for development of anterior or posterior vaginal flaps,
which later will be used to cover the repair (Fig. 2C).
768 Eilber et al.

Figure 2 (A) Catheterization of fistulous tract with Foley catheter. (B) A circumferential incision around
the fistulous tract with a margin of several millimeters is indicated. (C) Development of a vaginal wall flap.
(D) First layer of repair: transverse approximation of the edges of the fistulous tract. (E) Second layer of
repair: imbrication of first layer with perivesical fascia. (F) Third layer of repair: advancement of
vaginal flap.
 Vesicovaginal Fistula 769

Figure 2 Continued.
770 Eilber et al.

Figure 2 Continued.
 Vesicovaginal Fistula 771

Step 3: Creation of Flaps

Creation of anterior and posterior flaps is begun in healthy tissue away from the opening of the
fistulous tract. The tissue circumscribing the fistulous tract is left intact. This technique avoids
enlargement of the fistulous tract. Each flap is dissected for several centimeters from the fistula
to expose the perivesical fascia.

Step 4: Closure of Fistula

The first layer of the repair is created by approximating the edges of the fistulous tract and a few
millimeters of surrounding tissue with interrupted 3-0 absorbable sutures (Vicryl or Dexon) in a
transverse fashion (Fig. 2D). These sutures incorporate the bladder wall and the fistulous tract
itself. The second layer of perivesical fascia imbricates the prior layer also using interrupted,
absorbable sutures (Fig. 2E). Before proceeding to the next layer, the integrity of the repair is
tested by filling the bladder with Methylene Blue dyed saline. The third layer of the repair is
advancement of the vaginal flap at least 3 cm beyond the fistula closure (Fig. 2F). Excess tissue
from the flap is excised. The vaginal wall is then closed with a running, locking absorbable suture.

Step 5: Postoperative Care

The vagina is packed with a triple sulfa- or iodine-soaked gauze. The packing is removed 2 h
postoperatively and the patient is discharged home. The urethral and suprapubic catheters
drain to a single collection bag via a “Y” connector and are removed 2 –3 weeks postoperatively.
Oral antibiotics are continued until the catheters are removed, and anticholinergics are used as
needed. It is important to avoid bladder spasms during the healing phase to avoid tension on the
suture lines and urinary extravasation. Patients are instructed to avoid sexual intercourse for 3
months after surgery.

B. Abdominal Approach
The indications for an abdominal approach have been discussed previously and include the
surgeon’s preference and the need for concomitant abdominal procedures such as repair of uret-
eral injury or ureteral reimplantation. A previous failed vaginal approach does not preclude
another transvaginal attempt (27). The same preoperative considerations for the vaginal approach
must be taken into account, including the use of antibiotics, hormone replacement, and catheter
drainage as well as the need for bowel preparation when augmentation cystoplasty is planned.
The patient is positioned supine with the lower extremities slightly abducted in order
to provide access to the vagina. The vagina and lower abdomen are prepared and a suprapubic
catheter is placed using a Lowsley retractor. A urethral catheter is also placed. A Pfannenstiel
or low-midline incision is made, and the space of Retzius is developed. In general, efforts should
be made to remain extraperitoneal unless omentum will be needed for tissue interposition. In these
cases, a small peritoneal window can be made at the end of the repair, and the omentum mobilized.
The bladder is retracted cephalad with Allis clamps, and, starting laterally, the plane
between the bladder and vagina is developed. Identification of the fistula may be facilitated
by filling of the bladder with diluted Methylene Blue. After the bladder is completely dissected
free and the fistulous tract is identified, the fistula may be catheterized toward the vagina to
facilitate dissection of the bladder base. The bladder and vaginal defects are then each repaired
in two layers using interrupted, absorbable sutures. An omental or peritoneal flap is placed
between the bladder and vagina (Fig. 3). Urethral and suprapubic catheters are used for bladder
drainage. Pelvic drainage is unnecessary unless the transvesical approach is used.
772 Eilber et al.

Figure 3 Tissue interposition between bladder and vagina. (From Ref. 61.)

C. Transvesical Approach
O’Conor and Sokol originally described the transvesical approach for the repair of vesicovaginal
fistulae (38). This technique involves creating a cystotomy in the sagittal plane, both anterior and
posterior, until the fistula is reached. Once the fistula is identified, the plane between the vagina
and bladder is developed, and each is closed in two layers of absorbable sutures. Omentum is
usually interposed between the bladder and vagina. Success rates with this technique range
from 87% to 100% (39 – 42).

D. Success Rates
Multiple factors, including cure rate, patient morbidity, and patient satisfaction, must be con-
sidered when gauging the success of a procedure. A prospective, randomized study comparing
the outcome of the vaginal versus abdominal approach to VVF repair has not been reported;
however, there are multiple modern series reporting success rates from 90% to 100% with
both approaches (29,43 –45). As mentioned previously, the approach that is most successful
is the one with which the surgeon is most experienced.

E. Complications
For both the vaginal and abdominal approaches, the two most worrisome potential intraopera-
tive complications are hemorrhage and ureteral injury. Meticulous hemostasis should be
achieved as hematoma formation may result in disruption of the suture line and recurrent
fistula formation. The use of electrocautery should be minimized. Excessive bleeding encoun-
tered during dissection of the vaginal flaps should be controlled with absorbable sutures. When
ureteral injury is in question, Indigo Carmine should be administered intravenously and cysto-
scopy performed to identify efflux of urine from the ureteral orifices. Early postoperative com-
plications such as bleeding, infection, or bladder spasms should be treated aggressively, as any
of these may weaken the repair. Ileus is often encountered following the abdominal approach.
 Vesicovaginal Fistula 773

Late complications of any approach include unrecognized ureteral injury or fistula recur-
rence. In the immediate postoperative period, ureteral obstruction or extravasation should be
treated with percutaneous nephrostomy drainage. Retrograde procedures such as pyelography
or ureteroscopy should be avoided, as these may result in disruption of the repair. Fistula recur-
rence may be repaired transvaginally with the use of tissue interposition. A delayed complication
specific for the abdominal approach is bowel obstruction, which is usually successfully treated
with conservative measures. Finally, a potential late complication of the vaginal approach is
vaginal shortening or stenosis, which may require vaginoplasty.

VI. COMPLEX FISTULAE

We consider complex fistulae those that are the result of radiation therapy, large fistulae
(.1 cm), obstetrical fistulae associated with other injuries, recurrent fistulae, fistulae high in
the vaginal vault, and those associated with poor-tissue quality due to either hormone deficiency
or ischemia. Special surgical techniques to provide tissue interposition are required for the repair
of complex fistulae. The use of flaps increases the chance of surgical success by filling in dead
space and providing an added layer of well vascularized tissue to the repair.

A. Radiation Fistulae
Special consideration must be given when dealing with radiation fistulae. The incidence of VVF
after radiation therapy for cervical cancer ranges from 0.6% to 3% depending on disease stage
and dosimetry (46). Unfortunately, modifications in mode of delivery and dosimetry have not
decreased this incidence (47 – 49).
A fistula is usually the result of ischemic tissue injury secondary to obliterative endarteritis
(46). The site of fistula formation is typically the trigone because, unlike the rest of the bladder,
which changes position with filling and emptying, it is a relatively immobile area, making it
vulnerable to higher radiation exposure. Nevertheless, all surrounding tissue is susceptible to
radiation injury. Not uncommonly the bladder becomes a fibrotic, small-capacity, noncompliant
organ following radiation therapy. Thus, when dealing with radiation-induced VVF, it is impera-
tive to evaluate bladder capacity. Fistula repair is likely to fail if a high-pressure, noncompliant
bladder is not augmented owing to increased pressure on the suture line. If augmentation cysto-
plasty is necessary, a nonirradiated bowel segment should be used to minimize complications
with the vasculature to the augment or the bowel anastomosis.

B. Tissue Interposition
1. Martius Flap
The Martius flap is a fibrofatty labial flap first described by Heinrich Martius in 1928 (50). This
flap has been used for the repair of a variety of fistulae involving the pelvic floor: urethrovaginal,
peritoneovaginal, perianal, and vesicovaginal (51 – 53). Anatomical studies have demonstrated
that the flap is composed of fibroadipose tissue from the labia majora and receives its blood
supply anteriorly from the external pudendal artery and posteriorly from the internal pudendal
artery (26). Branches of the obturator artery and vein enter the lateral aspect of the flap adjacent
to the ischiopubic ramus but are sacrificed during harvest of the flap (23,26). The clinical import-
ance of the blood supply is that the flap may be divided at either the superior or inferior margin
and mobilized depending on the individual needs.
774 Eilber et al.

Preparation of the flap begins with a longitudinal incision over the labia majora. The
medial, lateral, and posterior borders of dissection are the labiocrural fold, the labia minora
and bulbocavernosus muscle, and the urogenital diaphragm, respectively (23,26). A Penrose
drain is used to encircle the entire thickness of the fibrofatty flap, and gentle downward traction
is applied as it is freed from the surrounding tissues (Fig. 4A). The superior or inferior portion is
then clamped and transected, and the free end is now transferred from the labial area to the fistula
site (Fig. 4B). Fixation of the flap is done with interrupted, absorbable sutures in a tension-free
manner (Fig. 4C). Finally the vaginal flap is advanced over the Martius flap, and the wound is
closed. Excellent hemostasis is important, and a small Penrose or Jackson-Pratt drain is left in
the labial incision as well as a light-pressure dressing. Ice packs placed on the labia during the
immediate postoperative period are also useful to prevent edema and hematoma formation.
The morbidity associated with the use of a Martius flap is minimal, but deep dissection into
the erectile tissue of the vestibular bulb can cause serious hemorrhage (26). Overall, success
rates have been good with most series reporting .90% success in fistula repairs utilizing a
Martius flap (26,33,51).

2. Peritoneal Flap
The ease of preparation and location makes the peritoneal flap well suited for fistulae high in the
vaginal vault. The posterior peritoneum, including the preperitoneal fat, is isolated using sharp
dissection (Fig. 5). The flap is then advanced over the first two layers of the fistula repair. Inter-
rupted, absorbable sutures are used to anchor the peritoneum without tension. The vaginal wall
flap is advanced as the final layer. In their original description of the use of a peritoneal flap for
the transvaginal repair of vesicovaginal fistulae, Raz and associates reported success in nine of
11 patients (82%) (54). Since then the success rate for 83 patients has improved to 96%, with
77% of those having failed a prior repair (55).

Figure 4 (A) Mobilization of Martius flap from superior attachments. (B) Transfer of Martius flap from
donor site to fistula repair. (C) Fixation of Martius flap.
 Vesicovaginal Fistula 775

Figure 4 Continued.
776 Eilber et al.

Figure 5 Development of peritoneal flap.

Inadvertent peritoneotomy is the most common complication of a peritoneal flap. A peri-

toneotomy can easily be repaired without compromise of the peritoneal flap. The use of a peri-
toneal flap is reserved for fistulae high in the vaginal canal, and we do not recommend its use in
reconstruction of distal defects.

3. Omental Interposition
The omentum is an ideal tissue for interposition because of its ability to establish neovascularity.
This makes it particularly useful for the repair of complex fistulae. It can be used in the abdomi-
nal approach for fistula repair or in the vaginal approach if it was mobilized into the pelvis during
a prior procedure. Cure rates of 93% have been reported when omental interposition is used
during complex fistula repair (60).
The blood supply to the omentum arises from the right and left gastroepiploic arteries.
These then give rise to the right and left omental arteries which extend inferiorly to form a
“U.” In approximately one-third of patients, no mobilization is required to bring the flap to
the pelvis. Another third require division of the left gastroepiploic artery and lateral splenorenal
ligaments. The remainder of patients require complete mobilization of the omentum by separ-
ating the attachments to the transverse colon and mesocolon and ligating the short gastric vessels
(56 – 59).
Omental interposition is used almost exclusively with the transabdominal approach to
vesicovaginal fistulae. Previous surgery and/or radiation therapy may affect the amount of
omentum available and its mobility.
 Vesicovaginal Fistula 777

4. Full-Thickness Labial (Martius) Flap

For situations in which there is insufficient vaginal epithelium to achieve primary closure, a
full-thickness labial (Martius) flap may be rotated to cover the defect. This flap provides a
well-vascularized fibrofatty layer as well as full-thickness skin coverage. Following closure
of the fistula, a “U” incision is made 1 cm lateral to the labia majora with the base at the level
of the posterior fourchette (Fig. 6). The flap is dissected from the fascia covering the pubic bone
and includes the labial skin and fibrofatty tissue. The flap is rotated to cover the repair, and the
edges are sutured in place with absorbable sutures (61).
Margolis et al. reported an initial 100% flap survival in four patients who had undergone
repair of VVF. One ultimately developed delayed recurrence (62). Carr and Webster also
reported excellent results in four patients (63). Potential complications include an undesirable
cosmetic result and reduced cutaneous sensation along the harvest site (61,63).

5. Gluteal Flap
Gluteal flaps are used mainly for patients with postradiation fistulae when there is paucity of
vaginal tissue and no other viable skin source is available to provide skin coverage. Following
closure of the first two layers as described for an uncomplicated VVF repair, an incision is made
in the vaginal wall and continued toward the midportion of the labia majora. This incision is then
extended toward the gluteal area (Fig. 7A). The skin is undermined and a flap is rotated and
advanced into the vaginal canal to cover the first two layers of the fistula repair (Fig. 7B).

Figure 6 Incision for a full-thickness labial flap.

778 Eilber et al.

Figure 7 (A) Incision for a gluteal skin flap. (B) Transfer of gluteal flap to cover defect.
 Vesicovaginal Fistula 779

The flap is secured in place with interrupted, absorbable sutures, and finally the vaginal flaps are
sutured to the edges of the flap (23). Potential complications of the gluteal flap are those common
to all flaps, including wound infection and sloughing of the flap due to poor blood supply. Injury
to the anal sphincter is a complication unique to the gluteal flap (64). Careful surgical technique
must be employed to prevent this complication.

6. Gracilis Myocutaneous Flap

Both labial and gluteal flaps provide tissue coverage but do not provide for vaginal depth or
restoration of sexual function. On the other hand, a myocutaneous flap is useful for complex,
postradiation fistulae or vaginal vault deficiencies in which vaginal reconstruction is required.
The gracilis muscle is a long, straplike muscle that extends from the inferior border of the
symphysis pubis to the medial condyle of the femur. It is an accessory muscle for thigh
adduction and knee flexion, and can be sacrificed without loss of function. The muscle
alone can be used as an interposition, or a myocutaneous flap can be used to fill a large vagi-
nal defect.
For gracilis flap harvest, an elliptical incision centered over the gracilis muscle is made on
the medial aspect of the thigh (Fig. 8). The maximum skin island is 8 cm wide by 22 cm long and
should not include the distal third of the muscle (59). The muscle is detached at its distal
tendinous insertion point, and the flap is dissected until the vascular pedicle is identified. A tun-
nel is developed from the donor site to the vaginal introitus in order to transfer the flap to the
vaginal area.
Although there are no large series reporting on the success of this flap, several
authors report good outcomes when using the gracilis flap for the repair of VVF (64 – 66).
The main complication is considerable scar formation, but there is usually no functional defect
(19,67).

Figure 8 Gracilis myocutaneous flap. (From Ref. 61.)

780 Eilber et al.

VII. CONCLUSION

Vesicovaginal fistula is a devastating complication resulting from various etiologies. With the
proper preoperative evaluation and planning, the great majority of vesicovaginal fistulae can
be repaired with the transvaginal approach. Complicated fistulae have a greater chance for suc-
cess with the use of tissue interposition. Adequate drainage, anticholinergic therapy, and prophy-
lactic antibiotic coverage postoperatively also increase the rate of surgical success.

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39. Motiwala HG, Amlani JC, Desai KD, Shah KN, Patel PC. Transvesical vesicovaginal fistula repair:
a revival. Eur Urol 1991; 19:24 – 28.
40. Nesrallah LJ, Srougi M, Gittes RF. The O’Conor technique: the gold standard for supratrigonal
vesicovaginal fistula repair. J Urol 1999; 161:566 – 568.
41. Cetin S, Yazicioglu A, Ozgur S, Ilker Y, Dalva I. Vesicovaginal fistula repair: a simple suprapubic
transvesical approach. Int Urol Nephrol 1988; 20:265– 268.
42. Udeh FN. Simple management of difficult vesicovaginal fistulas by anterior transvesical approach.
J Urol 1985; 133:591– 593.
43. Langkilde NC, Pless TK, Lundbeck F, Nerstrom B. Surgical repair of vesicovaginal fistulae: a ten-
year retrospective study. Scand J Urol Nephrol 1999; 33:100– 103.
44. Diaz Calleja E, Calatrava Gadea S, Caldentey Garcia M, Moreno Perez F, Lapuerta Torres E, Garcia
Victor F. Surgical repair of vesico-vaginal fistulae with abdominal-transvesical approach. Comments
on this technique with long-term results. Arch Esp Urol 1997; 50:55– 60.
45. Frohmuller H, Hofmockel G. Transvaginal closure of vesicovaginal fistulas. Urologe A 1998; 37:102.
46. Perez CA, Grigsby PW, Lockett MA, Chao KS, Williamson J. Radiation therapy morbidity in carci-
noma of the uterine cervix: dosimetric and clinical correlation. Int J Radiat Oncol Biol Phys 1999;
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48. Perez CA, Breaux S, Bedwinek JM, Madoc-Jones H, Camel HM, Purdy JA, Walz BJ. Radiation
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53. Kay AR. Labial fat pad grafts (modified Martius graft) in complex perianal fistulas. Ann R Coll Surg
Engl 1999; 81:143.
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flap. J Urol 1993; 150:56– 59.
55. Eilber KS, Rosenblum N, Rodrı́guez L, Raz S. 10-year experience of transvaginal vesicovaginal
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56. Woo HH, Rosario FJ, Chapple CR. The treatment of vesicovaginal fistulae. Eur Urol 1996; 29:1 –9.
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116:341– 347.
58. Turner-Warwick RT, Wynne EJC, Handley-Ashken M. The use of the omental pedicle graft in the
repair and reconstruction of the urinary tract. Br J Surg 1967; 54:849– 853.
59. Sirls LT, Leach GE. Repair of vesicovaginal fistula. In: Ehrlich RM, Alter GJ, eds. Reconstructive
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Med J 1985; 67:143– 144.
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62. Margolis T, Elkins TE, Seffah J, Oparo-Addo HS, Fort D. Full-thickness Martius grafts to preserve
vaginal depth as an adjunct in the repair of large obstetric fistulas. Obstet Gynecol 1994; 84:148– 152.
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65. Gerges DG, Mesfen W. Repair of a complex vesicovaginal fistula using a musculocutaneous flap of
the gracilis muscle. J Urol (Paris) 1984; 90:491 – 493.
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54
Vesicovaginal Fistula: Abdominal Approach

Martin B. Richman and Howard B. Goldman

Case Western Reserve University, University Hospitals of Cleveland, Cleveland, Ohio, U.S.A.

I. HISTORY

A vesicovaginal fistula (VVF) is an abnormal channel between the urinary bladder and the
vagina that results in urinary leakage. Most of these fistulas occur in otherwise healthy
women who undergo elective gynecologic surgery for benign disease, and as a result of the
fistula, are completely incontinent of urine. This incontinence can have physical implications
such as skin breakdown and infection as well as psychological sequelae such as depression
and avoidance of social situations as the woman with a VVF is constantly wetting pads and is
at risk of leaking onto her clothing and smelling from urine.
VVFs have been reported for hundreds of years, with the first description of repair by Van
Roonhuyse in 1672 (1). However, the first modern description of VVF repair was by Sims in
1852, which emphasized the general principles of fistula repair, including adequate operative
exposure, a tension-free closure, and adequate, continuous postoperative drainage to permit
healing (2).
Modern-day VVF repair is performed by either an abdominal or vaginal approach, each
with advantages and disadvantages. The next three chapters will describe the different tech-
niques and applications of the abdominal and vaginal approaches for the management of vesico-
vaginal fistulae.

II. ETIOLOGY

Approximately 90% of VVFs in developed countries are due to prior pelvic surgery, with
abdominal hysterectomy for benign disease accounting for 70% of these (3). The incidence of
fistulas secondary to iatrogenic surgical trauma is reported as being between 0.1% and 2%
(4,5). The remaining 10% of VVFs in developed countries are the result of radiation, infection,
foreign bodies, and pelvic malignancies, including cervical, vaginal, and endometrial carci-
nomas (3) (Table 1). Fistulas resulting from radiation injury tend to be accompanied by exten-
sive fibrosis and a compromised blood supply (4), making their management more complex and
outcomes often less predictable.
In underdeveloped countries, most VVFs are the result of obstetrical trauma (6), particu-
larly pressure necrosis of the bladder and vagina that occurs with compression of these structures
between the infant’s head and the pubic bone during prolonged labor (3). This mechanism results
783
784 Richman and Goldman

Table 1 Etiology of Vesicovaginal Fistula

Iatrogenic injury from pelvic surgery

Gynecologic surgery
Obstetric surgery
Urologic surgery
Radiation injury
Pelvic malignancy
Pelvic trauma
Obstetric trauma from prolonged labor
Vaginal or vesical foreign body

in morbidity for over 5 million women annually and is estimated to occur in three to four out of
every 1000 deliveries (4). Tissue loss from ischemic injury may continue into the early postpartum
period, and delay of repair must be considered until all sequelae of the trauma are evident. VVFs
from obstetric trauma rarely occur in developed countries owing to the superior obstetric care
available to the female population, including the use of early surgical delivery of the infant in
complicated labor.
Most VVFs become evident at approximately the 10th postoperative day after pelvic
surgery (7), although some are immediately evident in the first few postoperative hours or
even while still in the operating room. The vaginal component of the fistula occurs at the suture
line of the vaginal cuff. The bladder may become involved owing to a small posterior bladder
laceration that occurs intraoperatively. Often this injury is unrecognized in the operating
room. The bladder injury results in a pelvic urinoma that ultimately drains through the vaginal
cuff suture line. Other mechanisms of intraoperative injury that can result in a VVF are due to
ischemia from cautery use or injury due to an inadvertent suture placed in the bladder while
attempting to control intraoperative bleeding. Either of these can lead to delayed necrosis and
subsequent fistula formation. With any of these mechanisms of injury and ensuing fistula, the
patient reports vaginal drainage that may or may not be continuous depending on the size of
the fistula.
Radiation-induced necrosis causes 3% of all VVFs (8). Radiation therapy results in
chronic regional tissue damage. These fistulas can occur months to years after the conclusion
of therapy, and oftentimes repair is further complicated by the presence of prior abdominal
surgery for the malignancy. Prior to the repair of fistulas related to cancer or the treatment of
cancer, the recurrence of tumor should be ruled out with a biopsy of the fistula margin (6).

III. DIAGNOSIS

Though some fistulas may be easy to diagnose by a complete history and physical exam, many
others will need further tests, including dye tests and radiographic imaging. Evaluation of a
suspected VVF begins with a thorough medical history and physical examination. Past medical
history is important to elucidate previous pelvic surgeries and malignancies with or without radi-
ation therapy. Obtaining the underlying reason for fistula formation can be important in planning
an operative technique for repair. It is important to elicit from the patient whether incontinence
began immediately after pelvic surgery or whether it began days or weeks later. A woman with a
VVF that was initially missed may present to the office with a diagnosis of stress or urge incon-
tinence, and may have been having occasional leakage for months. Upon further evaluation, an
 VVF: Abdominal Approach 785

association can be made between the onset of incontinence and a relatively remote pelvic
surgery.
A pelvic exam is crucial in the evaluation of a potential fistula. The presence of urine in the
vaginal vault is highly suspicious for a urinary-genital fistula. Other findings indicative of a VVF
include observing a hole or an area of granulation tissue at the vaginal cuff or apex. With a large
fistula, a defect may even be palpated during a digital vaginal exam.
A urinary-vaginal fistula also can be diagnosed by placing a vaginal packing or tampon in
the vagina and giving the patient oral pyridium or intravenous Indigo Carmine. The presence of
orange or blue discoloration on the vaginal pack or tampon indicates a fistula. The fistula can be
further localized with the Double Dye Test (9,10). Classically, this test is performed by placing a
vaginal packing or tampon in the vagina while the patient is in the lithotomy position. A Foley
catheter is then placed and the bladder is filled with 1% carmine solution, a red dye. Next, 5 mL
of Indigo Carmine solution is injected intravenously. This is normally excreted by the kidneys as
a blue dye within 15 min (6). The vaginal packing is then examined for the presence of blue
staining indicating an ureterovaginal fistula or red staining indicating a vesicovaginal fistula,
or both. Red staining at the distal most part of the packing may indicate a urethral vaginal fistula.
Today, this test is most commonly done with oral pyridium, which colors the urine orange, given
for 24 h prior to the test, and then Indigo Carmine is instilled into the bladder during the test.
Radiographic imaging is also useful in the workup of a suspected urinary-vaginal fistula.
In the presence of a VVF, a cystogram will almost always demonstrate contrast flowing from the
bladder to the vagina (Fig. 1). On the other hand, a normal cystogram nearly rules out the possi-
bility of a VVF. Computed tomography can be another useful modality. The presence of
excreted contrast in the vaginal vault usually indicates a communication between the vagina
and the urinary system, and the fistula may even be visualized with thin-cut images through
the pelvis (Fig. 2). Intravenous or retrograde pyelography should be performed to exclude the
possibility of concurrent ureterovaginal fistula or ureteral injury. With all radiographic studies,
careful examination of the films is important, as the surgeon must have a complete understand-
ing of the extent of the injury before attempting repair.
Cystourethroscopy and vaginoscopy may be important for diagnosis and evaluation of a
VVF. During cystoscopy, the surgeon can look for one or more holes, which sometimes can be
quite large and obvious. In the absence of a clear defect, irregularities of the mucosa may be
suspicious for a fistula. Once a defect is found, cystoscopy can be useful for characterizing
the location and size of the fistula, and how far it is from the ureteral orifices. Proximity of
the fistula to one or both ureteral orifices may indicate the need for ureteral reimplantation during
fistula repair. With vaginoscopy, one should look for small holes or areas of granulation signify-
ing the location of a small fistula.

IV. TIMING OF REPAIR

The timing of repair of a VVF is controversial and has been debated extensively in the literature.
Classically, surgeons waited 3– 6 months after the injury to allow inflammation to decrease and
to let surrounding tissues heal. In the past quarter-century, however, early repair of iatrogenic
fistulas attributed to pelvic surgery has been advocated (11). Several authors report equivalent
success rates of fistula closure with early repair for fistulas resulting from recent pelvic surgery
(12,13). Most who advocate early repair mention the severe mental and physical distress a VVF
presents to the usually otherwise healthy woman.
VVFs that are recognized in the immediate postoperative period have the best chance at
successful repair if done as soon as the fistula is noted. However, early repair is not indicated
786 Richman and Goldman

Figure 1 AP and lateral cystogram demonstrating filling of vagina (asterisk) with contrast after
introduction of contrast into bladder. Diagnostic of a VVF.

in fistulas that result from obstetric trauma or from radiation therapy, since these injuries
often result in ischemic injury and severe inflammation and one must let these processes
stabilize prior to attempting a repair. A waiting period must also be considered in those
with pelvic infection or infection of the vaginal cuff. Once acute local inflammation has sub-
sided, either a vaginal or an abdominal approach can be utilized for successful early repair of
a VVF (13).
If a waiting period before repair is necessary, a Foley catheter may be placed to diminish
the amount of leakage and allow the patient a more normal lifestyle. Unfortunately, there may be
persistent leakage of urine even with Foley catheter decompression (7).
 VVF: Abdominal Approach 787

Figure 2 Computerized tomography image of contrast in both bladder and vagina suggestive of a VVF.

V. ABDOMINAL APPROACH TO VVF REPAIR

A. Indications for Abdominal Approach
There have been a few reports of successful resolution of VVF with conservative measures such
as long-term bladder drainage or with fulguration of the fistulous tract (14,15). However, most
fistulas require surgical repair. Many studies have shown that the best chance for successful
surgical repair of a VVF is at the first attempt, and regardless of the method used, the basic
principles of fistula repair must be followed (Table 2). These include a tension-free repair
with tissue that has an adequate blood supply and is free of infection and inflammation. Avoid-
ance of overlapping suture lines and the use of fine suture is recommended. Postoperative blad-
der drainage and decompression are essential for healing of the repair.
VVFs can be repaired by either a vaginal approach or an abdominal approach. Each
method has advantages and disadvantages for the patient. The route of repair that is most

Table 2 Principles for Successful Fistula Repair

Tension-free repair
Adequate tissue blood supply
Tissues free of infection and inflammation
Multiple-layer repair and/or interposition of other healthy
tissue
Avoidance of overlapping suture lines
Postoperative rest for the repair site (bladder drainage and
decompression)
788 Richman and Goldman

comfortable to the surgeon based on training and experience is also an important factor in plan-
ning the operative approach. The vaginal approach often leads to less morbidity and a quicker
recovery as the patient is spared an abdominal incision and bivalving of the bladder. This
approach will be discussed in the subsequent chapter.
The abdominal approach to repair of VVF, which can be performed by either a transverse
Pfannenstiel or a low-midline incision, affords the surgeon the opportunity to simultaneously
treat other intra-abdominal pathology, including the repair of coexisting ureteral injury or fistula
and bowel injury or fistula. This approach also permits augmentation cystoplasty for radiation-
induced cystitis with a contracted bladder. Laparotomy also allows the opportunity to easily
interpose omentum to reinforce a large or recurrent fistula. The abdominal approach to repair
can also be done with an extraperitoneal technique if the above are not needed but the patient
has vaginal stenosis or has comorbid musculoskeletal abnormalities that would prohibit posi-
tioning or adequate exposure with the vaginal approach. Finally, many surgeons may be more
comfortable with an abdominal approach based on their personal training and experience.

B. Standard “O’Conor” Approach (Fig. 3)

The standard technique for abdominal approach of VVF repair was first described by O’Conor
(16), and is the most common method of abdominal repair used today. The patient is placed in
either the low lithotomy position or supine with the legs slightly separated and the knees
abducted to allow intraoperative access to the vagina. A urethral Foley catheter is placed and
a lower-midline or Pfannenstiel incision is made. If possible, the repair is performed from an
extraperitoneal approach unless access to intraperitoneal structures is desired, in which case
the peritoneum is opened and retracted from the dome of the bladder, packing the small
bowel out of the way. Either way, the bladder is opened over the dome, and stay sutures are
placed bilaterally. Surgeon choice and fistula location dictate the need for insertion of ureteral
catheters.
The bladder wall is then bisected down to the edge of the fistula, and the fistula is excised
from the bladder. Bladder exposure is improved by the placement of a self-retaining retractor
with the lateral blades holding the lateral bladder walls. Mobilization of the bladder and vagina
on either side of the fistula is performed to allow for proper closure of both structures in separate
planes. We have found that placement of a metallic rectal dilator within the vagina allows for
easier identification of the proper planes, and facilitates closure of the vaginal defect. The vaginal
component of the fistula is completely excised as it becomes exposed. The vagina is then closed
vertically or transversely with inverting interrupted synthetic absorbable sutures, taking care to
avoid tension. More recently, the necessity of excising the fistulous tract has been questioned,
and many surgeons just close the separate tissue layers without removal of the fistula tract.
The bladder epithelium and subepithelium are closed with 3-0 running chromic suture, and
the muscularis and adventitia are reapproximated from the outside with 2-0 synthetic absorbable
sutures. It is frequently easiest to begin the bladder closure by first closing the detrusor poster-
iorly and then closing the mucosa. Once the closure gets to the area of the dome, the mucosa can
then be closed first and the detrusor second. Care must be taken to assure that the closure is
tension free as the success of the repair is more dependent on the effectiveness of the bladder
approximation than on the vaginal closure. Prior to bladder closure, the ureteral catheters are
removed, or, if they were not placed, ureteral patency is assured by carefully watching for bilat-
eral efflux of urine (this may be easier to see after intravenous injection of Indigo Carmine).
If a transperitoneal approach was undertaken, a peritoneal flap or omental graft can be
mobilized and placed between the vagina and bladder and tacked into place. A large fistula or
one resulting from radiation necrosis may be best managed with a myofascial flap such as
 VVF: Abdominal Approach 789

Figure 3 (A) The bladder is incised sagittally to the level of the fistula. (B) The fistulous tract is
circumscribed and excised from surrounding tissue. (C) The vagina and bladder are closed separately.
(D) Omentum is sutured down between the vagina and bladder.
790 Richman and Goldman

Figure 3 Continued.

one mobilized from the rectus abdominis muscle (8). Some recommend omental interposition
for all fistula repairs (17), while others report excellent results with simple transvesical repair
without the use of interposition grafts (18). Interposition of tissue is usually easy, and we recom-
mend it for all cases. This is especially important with ischemic or recurrent fistulas. Our
technique for omental interposition is to first place three 2-0 synthetic absorbable sutures into
 VVF: Abdominal Approach 791

healthy tissue at the deep apex of the repair and then draw the needle through the omentum and
use these sutures to seat the omentum into the pelvis to cover the repair.
Regardless of whether an interposition flap was utilized, the bladder must be adequately
drained postoperatively with a urethral Foley catheter and/or a suprapubic catheter. At the
time of repair, it is our practice to place a 24F Malecot suprapubic tube with two of the flanges
excised to allow unobstructed drainage. We leave the urethral Foley catheter in as well and it is
removed as soon as the urine clears.

C. Vesical Autoplasty
In addition to the classic suprapubic transvesical repair described above, other methods of
abdominal repair have been reported. Gil-Vernet and colleagues described a technique of vesical
autoplasty in recurrent VVFs to cover a large defect after excision of the fistulous tract (19). This
modification can be used through a transperitoneal or extraperitoneal transvesical approach, and
they reported a 100% success rate in a series of 42 patients with complex fistulas.
This technique involves mobilizing a full-thickness flap off the dome of the bladder to use
for closure of the posterior bladder defect. The bladder is first incised transversely through the
dome, and ureteral catheters are inserted. Stay sutures are then placed in the fistulous orifice and
the surrounding fibrous tissues to simplify excision of a wider margin of affected tissue. The
fistula and surrounding tissue are then excised until the well-vascularized, healthy bladder wall
is encountered. After dissection and development of the tissue plane between the bladder and
the vagina, a one-layer interrupted suture closure of the vaginal wall is completed. A flap of bladder
wall is then formed through a bilateral, symmetrical incision of the superior edge of the resected
defect toward the dome of the bladder until there is sufficient tissue to fill the defect. The flap is
then approximated to the resection edges in one layer with interrupted 3-0 catgut sutures.

D. Free Mucosal Graft (Fig. 4)

Ostad and colleagues presented a technique of a free bladder mucosal graft during simple extra-
peritoneal repair of VVF (20). This modification eliminates any loss of bladder capacity as no
detrusor muscle is excised, and success was 100% in their small study of six patients.

Figure 4 Free mucosal graft. (From Ref. 20.)

792 Richman and Goldman

With an extraperitoneal approach, the bladder is opened through a small midline cystotomy,
and the bladder mucosa surrounding the fistula is excised for a circumferential distance of 1 cm
and discarded. No attempt is made to excise the fistulous tract from either the bladder or the
vagina. Next, a free bladder mucosal graft is taken from the edge of the cystotomy line. This
graft is placed over the fistula opening, replacing the excised surrounding mucosa, and sutured
in place with interrupted 4-0 chromic catgut sutures. The mucosal harvest site is expected to
reepithelialize in 4 –6 weeks.

E. Laparoscopy
A laparoscopic approach to abdominal repair was described by von Theobald and colleagues
(21). They presented a case where, via laparoscopic guidance, the bladder was dissected
away from the vagina and the fistula was excised from the bladder. The bladder was closed
in a single layer and an omental flap was dissected and placed between the bladder and vagina,
with endostapling of the flap to the vagina. This procedure was successful at 6-month follow-up.

F. Interposition of Tissue
The interposition of translocated tissue between the bladder and the vagina in conjunction with
the repair of a VVF is often recommended for complex and recurrent fistulas. Tissue that is used
in VVF repair serves the purposes of a mechanical barrier to fistula recurrence and as a source of
reperfusion of previously poorly vascularized tissue. This tissue must be highly vascular and
easily mobilized with its blood supply.
The transperitoneal abdominal approach grants the surgeon the opportunity to use the
omentum for this purpose. Walters first recommended the use of an omental flap in the repair
of recurrent VVFs (22). He proposed suturing omentum between the vaginal and bladder
closures to prevent the suture lines from overlapping. As described above, we do this by first
placing three 2-0 synthetic absorbable sutures into healthy tissue at the deep apex of the repair
and then placing the needles through the omentum and using these sutures to draw the omentum
into the pelvis and cover the repair (Fig. 3D).
The omentum is usually sufficient to reach the pelvis with no or minimal alteration. How-
ever, if there is insufficient pelvic extension of the omentum, Turner-Warwick and colleagues
described a method for creating and utilizing an omental pedicle graft (23). To extend the omen-
tum to the pelvis, it must be mobilized with care to preserve an adequate blood supply. Since the
left gastroepiploic artery is usually smaller than the right, it is often best to mobilize and divide
the left side of the omentum along the greater curvature of the stomach and extend it to the pelvis
based on the right gastroepiploic blood supply.
Eisen and colleagues described the use of a peritoneal flap interposition graft in VVF
repair (24). Via a transperitoneal, transvesical approach, they formed a peritoneal flap from
the lateral parietal pelvic peritoneum at the time the bladder was opened. The flap was then inter-
posed between the vagina and bladder after fistula excision and primary closure of both
components.
Brandt and colleagues proposed a technique of bladder mucosa autografting for interposi-
tion between the bladder and the vagina (25). After excision of the fistula tract and closure of
both the bladder and the vagina, a free mucosal graft is taken from the dome of the bladder.
The donor bed is fulgurated and left to reepithelialize. The graft is then placed between the blad-
der and vagina at the site of the repaired fistula with the mucosal surface facing the vagina, and
both the vaginal serosa and posterior bladder wall are sutured to the graft. With this technique,
 VVF: Abdominal Approach 793

they reported a 96% success rate in 80 women with VVFs that resulted from gynecologic
surgery.
For large postradiation fistulas, Salup and colleagues proposed interposition of a rectus
abdominis myofascial flap (8). They used a split right rectus abdominis flap based on the
right deep inferior epigastric vessels. The muscle is divided from the pubis, placing the distal
end of the myofascial flap in the pelvis for interposition.
We have found that any of these tissues serve as viable options and highly recommend
interposition of tissue, as there is no downside and the benefit is significant reinforcement of
the repair.

G. Postop Care
Postoperative bladder decompression is essential to permit adequate healing of the VVF repair.
A urethral Foley catheter may or may not be placed. For low fistulas, the Foley balloon could
place pressure on the repair site, leading to failure. A suprapubic drainage tube from the bladder
should be placed in all cases. If both urethral and suprapubic catheters are placed, the urethral
catheter may be removed as soon as the urine clears and the suprapubic tube should be kept to
gravity drainage for at least 2– 3 weeks. Smaller, simple fistula repairs heal quicker than large
defects that contain ischemic tissues, and duration of bladder decompression should be based on
the complexity of the fistula.
Low dose-prophylactic antibiotics may be used until the catheters are removed. Anticholi-
nergic medications should be used to prevent bladder spasms that could cause suture line
breakdown.
Routine cystography before removal of the suprapubic tube is probably unnecessary, as a
persistent fistula will be readily noticeable when the tube is clamped prior to its removal. Never-
theless, many surgeons feel more comfortable obtaining a cystogram that shows no leak prior to
removing the catheter.

H. Results (Table 3)
Success rates for abdominal repair of VVFs are reported as 88 –100% by all authors. The great-
est successes are reported in patients with simple fistulas such as the 40 patients reported by
Landes with a 100% success rate (18). Eisen and colleagues reported a 93% success rate in
their series with a peritoneal flap interposition (24). O’Conor’s cumulative results from three
different studies showed a 91% success rate with a total of 77 patients (16,26). Bissada and
McDonald reported a 100% success rate in seven patients with giant VVFs, which included radi-
ation-induced and obstetrical fistulas (27). Wein and colleagues reported 88% success with
34 patients, although two of their patients who failed had fistulas related to the surgical treatment
of malignancies and recurrent tumor was found at the site of fistula recurrence (28). Gil-Vernet
and colleagues reported a 100% success in their study with vesical autoplasty in 42 patients with
complex fistulas (19). Blandy and colleagues reported 100% success in their series of 25 patients
with the same outcome in early or late repair (12). More recent studies reveal similar findings
with success rates of 90%, 100%, and 92% with 11, 29, and 25 patients, respectively (29 –31).

VI. CONCLUSIONS

Vesicovaginal fistulas can develop as a complication of pelvic surgery, radiation necrosis, or

obstetric trauma, and can be extremely debilitating to the affected woman. VVFs can be repaired
794 Richman and Goldman

Table 3 Success Rates for Abdominal Repair of Vesicovaginal Fistula

Number of
Author Year patients Success rate Comments

Landes (18) 1979 40 40/40 (100%) Simple transvesical fistula

repair
Eisen et al. (24) 1974 29 27/29 (93%) Peritoneal flap interposition
O’Conor (16) 1973 77 70/77 (91%)
1980
Bissada et al. (27) 1983 7 7/7 (100%) “Giant” fistulas from
radiation and obstetrics
Wein et al. (28) 1980 34 30/34 (88%) Recurrent tumor found with
2 of 4 failures
Gil-Vernet et al. (19) 1988 42 42/42 (100%) Vesicle autoplasty for
complex fistulas
Blandy et al. (11) 1991 25 25/25 (100%) Compared early vs. late
repair
Leng et al. (29) 1998 11 10/11 (90%) Compared to 30% success
with vaginal repair in
similar complexity of
fistula
Nesrallah et al. (30) 1999 29 29/29 (100%)
Langkilde et al. (31) 1999 25 23/25 (92%) Compared to 42% success
with vaginal repair in
similar complexity of
fistula

by either a vaginal approach or an abdominal approach. The abdominal approach to repair of

VVF affords the surgeon the opportunity to simultaneously treat other intra-abdominal pathol-
ogy and allows one the opportunity to interpose omentum to reinforce a large or recurrent fistula.
It is also important to use the method of repair most comfortable to the surgeon, and often this is
the abdominal approach.
Many studies have shown that the best chance for successful surgical repair of a VVF is the
first attempt, and regardless of the timing of repair or method used, the basic principles of fistula
repair must be followed. With good technique, one should expect a success rate of at least 90%
when using an abdominal approach for vesicovaginal fistula repair.

REFERENCES

1. Zacharin RF. Grafting as a principle in the surgical management of vesicovaginal and rectovaginal
fistulae. Aust N Z J Obstet Gynecol 1980; 20(1):10 – 17.
2. Sims JM. On the treatment of vesico-vagina fistula. Am J Med Sci 1852; 23:59– 82.
3. Stothers L, Chopra A, Raz S. Vesicovaginal fistula. In: Raz S, ed. Female Urology. Philadelphia:
W.B. Saunders, 1996:490 – 506.
4. Kreder K. The current trend in vesicovaginal fistula repair. Contemp Urol 1999; 34 – 43.
5. Thomas K, William G. Medicolegal aspects of vesicovaginal fistulae. Br J Urol 2000; 86:354– 359.
6. Rackley RR, Appell RA. Vesicovaginal fistula: current approach. In: AUA Update Series. Houston:
AUA Office of Education, 1998:162 – 167.
 VVF: Abdominal Approach 795

7. Carr L, Webster G. Abdominal repair of vesicovaginal fistula. Urology 1996; 48(1):10 – 11.
8. Salup RR, Julian TB, Liung MD, Narayanan K, Finegold R. Closure of large post-radiation vesico-
vaginal fistula with rectus abdominis myofascial flap. Urology 1994; 44(1):130– 131.
9. Raghavaiah NV. Double-dye test to diagnose various types of fistulas. J Urol 1974; 112(6):811– 812.
10. O’Brien WM, Lynch JH. Simplification of the double-dye test to diagnose various types of vaginal
fistulas. Urology 1990; 36(5):456.
11. Persky L, Herman G, Guerrier K. Nondelay in vesicovaginal fistula repair. Urology 1979; 13(3):273–275.
12. Blandy JP, Badenoch DF, Fowler CG, Jenkins BJ, Thomas NWM. Early repair of iatrogenic injury to
the ureter or bladder after gynecological surgery. J Urol 1991; 146(3):761– 765.
13. Blaivas JG, Heritz DM, Romanzi LJ. Early versus late repair of vesicovaginal fistulas: vaginal and
abdominal approaches. J Urol 1995; 153(4):1110– 1113.
14. Falk HC, Orkin LA. Nonsurgical closure of vesicovaginal fistulas. Obstet Gynecol 1957; 9(5):538–541.
15. Stovsky MD, Ignatoff JM, Blum MD, Nanninga JB, O’Conor VJ, Kursh ED. Use of electrocoagula-
tion in the treatment of vesicovaginal fistulas. J Urol 1994; 152(5):1443 –1444.
16. O’Conor VJ, Sokol JK, Bulkley GJ, Nanninga JB. Suprapubic closure of vesicovaginal fistula. J Urol
1973; 109(1):51– 54.
17. Evans DH, Madjar S, Politano VA, Bejany DE, Lynne CM, Grousse AE. Interposition flaps in trans-
abdominal vesicovaginal fistula repairs: are they really necessary? Urology 2001; 57(4):670– 674.
18. Landes RR. Simple transvesical repair of vesicovaginal fistula. J Urol 1979; 122(5):604– 606.
19. Gil-Vernet JM, Gil-Vernet A, Campos JA. New surgical technique for treatment of complex vesico-
vaginal fistula. J Urol 1989; 141(3):513– 516.
20. Ostad M, Uzzo RG, Coleman J, Young GPH. Use of a free bladder mucosal graft for simple repair of
vesicovaginal fistulae. Urology 1998; 52(1):123– 126.
21. Von Theobald P, Hamel P, Febbraro W. Laparoscopic repair of a vesicovaginal fistula using an omen-
tal J flap. Br J Obstet Gynaecol 1998; 105:1216 –1218.
22. Walters W. An omental flap in transperitoneal repair of recurring vesicovaginal fistulas. Surg Gynecol
Obstet 1937; 64:74– 75.
23. Turner-Warwick RT, Wynne EJC, Handley-Ashken M. The use of the omental pedicle graft in the
repair and reconstruction of the urinary tract. Br J Surg 1967; 54(10):849– 853.
24. Eisen M, Jurkovic K, Altwein J-E, Schreiter F, Hohenfellner R. Management of vesicovaginal fistulas
with peritoneal flap interposition. J Urol 1974; 112(2):195– 198.
25. Brandt FT, Lorenzato FR, Albuquerque CD. Treatment of vesicovaginal fistula by bladder mucosa
autograft technique. J Am Coll Surg 1998; 186(6):645– 648.
26. O’Conor VJ. Review of experience with vesicovaginal fistula repair. J Urol 1980; 123(3):367– 369.
27. Bissada NK, McDonald D. Management of giant vesicovaginal and urethrovaginal fistulas. J Urol
1983; 130:1073.
28. Wein AJ, Malloy TR, Carpiniello VL, Greenberg SH, Murphy JJ. Repair of vesicovaginal fistula by a
suprapubic transvesical approach. Surg Gynecol Obstet 980; 150:57– 60.
29. Leng WW, Amundsen CL, McGuire EJ. Management of female genitourinary fistulas: transvesical or
transvaginal approach? J Urol 1998; 160(6):1995– 1999.
30. Nesrallah LJ, Srougi M, Gittes RF. The O’Conor technique: the gold standard for supratrigonal
vesicovaginal fistula repair. J Urol 1999; 161(2):566– 568.
31. Langkilde NC, Pless TK, Lundbeck F, Nerstrom B. Surgical repair of vesicovaginal fistulae: a ten-
year retrospective study. Scand J Nephrol 1999; 33:100 – 103.
55
Urethrovaginal Fistula

John B. Gebhart and Raymond A. Lee

Mayo Clinic and Mayo Clinic College of Medicine, Rochester, Minnesota, U.S.A.

I. INTRODUCTION

The female urethra, because of its well-protected location, is rarely involved in injury. When
injury does occur, it is usually related to childbirth or operation (1). Occasionally, the urethra
sustains injury from penetrating trauma or undergoes avulsion from pelvic trauma resulting
from a motor vehicle accident (2 – 5). When childbirth results in urethral injury, it is often caused
by instrumentation or laceration. Obstructed birth or neglect of the second stage of labor,
although not common in developed countries, continues to be a common cause of urethral
and vaginal injury in underdeveloped countries (6).
The diagnosis of urethral injury can generally be made on careful inspection, which on
occasion may require anesthesia. The integrity of the urethra and bladder neck can be assessed
by physical examination and be greatly aided by cystourethroscopy or voiding cystourethro-
graphy. If trauma is detected but the urethra is intact, a urethral catheter can be inserted to ensure
adequate drainage of the bladder. If a defect is noted, immediate operative repair can be accom-
plished by reconstructing the urethra, its supporting tissues, and the anterior vaginal wall with
interrupted 4-0 delayed absorbable sutures. If there is a delay in diagnosis or there is significant
edema, operative repair may be delayed.

II. ETIOLOGY

Prolonged labor continues to be a common cause of destruction of the urethra and the base of the
bladder in patients in medically deprived countries (6 – 9), whereas anterior colporrhaphy and
diverticulectomy are leading causes of urethrovaginal fistulas in the United States (10 –13).
The excision of friable, infected urethral diverticulum can be tedious and inexact (14,15).
Despite meticulous efforts to reconstruct the urethral floor accurately, infection and edema
may lead to imperfect healing and fistula formation. Overzealous plication of the urethra,
inadvertent intramural placement of a suture (vaginal or retropubic needle suspension), or a
suburethral sling placed under tension may produce a fistula of the urethra or a greater
calamity—actual slough of the entire urethral floor and bladder neck (11). In addition, coital
injury, malignancy, and radiation therapy may lead to urethral fistula.
797
798 Gebhart and Lee

III. CLINICAL PRESENTATION

Patients who experience trauma to the urethra from forceps or vacuum delivery or from auto-
mobile accidents have leakage immediately or within the first 24 h after damage. If a urethral
catheter was in place temporarily, after either delivery or trauma, catheter removal is generally
followed promptly by leakage of urine. In our experience, most urethrovaginal fistulas occur
after an operation for diverticulum or a procedure for cystocele or stress urinary incontinence
(SUI), such as an anterior colporrhaphy or pubovaginal sling. Patients who have undergone
these operations generally have a catheter in place for 2– 7 days. Some of these patients may
have an unrecognized suture through the wall of the urethra, which generally results in necrosis
of the tissue and possibly associated hematoma formation or some degree of infection, the com-
bination of which results in fistula formation and leakage of urine. The patient may initially be
continent, only to experience leakage 1– 2 weeks postoperatively.
Patients who have had irradiation generally note the leakage sometime after the treatment,
generally within 2 – 4 months. Occasionally, a fistula develops as the result of long-term pressure
beneath the urethra that results in erosion. This is more likely to occur with synthetic sling
material, but it may occur with any graft material, especially if placed under too great a
tension (16).
Simple urethrovaginal fistula, depending on its location relative to the bladder neck, may
not produce urinary incontinence and may not necessitate operative repair. Fistulas located near
the bladder neck may be technically more difficult to repair. Even after what appears to be a
successful repair, the patient may experience stress urinary incontinence related to fibrosis, fix-
ation, and poor contractility of the urethral musculature. One can consider performing an anti-
incontinence procedure at the time of fistula repair if SUI is also part of the symptom complex
(17). This decision should be individualized, and the consideration of additional procedures
should in no way compromise the success of the primary goal, which is resolution of the fistula.
A more complex problem is presented by patients who had a major slough resulting in a linear
loss of the floor of the urethra and frequently involving the bladder neck and base of the
bladder.

IV. OPERATIVE REPAIR

The basic phases of operative reconstruction consist of a linear incision, much like that for an
anterior colporrhaphy, and mobilization of the vaginal epithelium laterally off the underlying
pubocervical fascia (Fig. 1). This procedure must be accomplished in the proper bloodless tissue
plane sufficiently lateral to establish mobility so that a tension-free closure of the urethra can be
accomplished.
Once the fistula is completely mobilized and the scar tissue (fistula tract) is removed, the
fistula itself is closed with fine 4-0 delayed absorbable sutures placed extramucosally, and the
tissue edges are approximated free of tension and with excellent hemostasis (Fig. 2A). The pre-
sence of a small-caliber catheter within the urethra frequently assists in accurate placement of
the sutures to close the fistulous tract. This initial suture line is imbricated with a second set
of sutures, the most distal suture being just distal to the original suture line (Fig. 2B). Snug pli-
cation of the bladder neck by approximation, under the urethra, of the tissue (pubocervical
fascia) lateral to the urethra to create a tension-free second layer of sutures is mandatory for
a successful repair. A tension-free closure of the vaginal wall as a third layer (Fig. 3), or
when necessary for the obliteration of dead space and actual replacement of the anterior wall
 Urethrovaginal Fistula 799

Figure 1 Incision and mobilization of fistula. (From Ref. 18. By permission of Mayo Foundation.)

Figure 2 Multilayer closure of incised fistula. (From Ref. 18. By permission of Mayo Foundation.)
800 Gebhart and Lee

Figure 3 Enclosed vaginal suture line with Foley catheter in place. (From Ref. 18. By permission of
Mayo Foundation.)

of the vagina with a pedicled skin, fibrofatty labial graft or Martius labial fat pad graft, may be
indicated.
A second-stage retropubic urethrovesical suspension for patients who have a good ana-
tomical result with an apparently intact urethra but who nevertheless remain incontinent (intact
urethra with stress incontinence) may be necessary at a later date. Continence often cannot be
predicted at the time of closure of the urethral fistula.

V. TRAUMATIC DISRUPTION OF URETHRA

Trauma is an infrequent cause of severe injury to the urethra. When it does occur, surgical repair
usually can be undertaken once the patient is stabilized. In Figure 4, the urethra was traumati-
cally disrupted from the bladder during operative vacuum extraction delivery. When catheteri-
zation was attempted, the catheter passed through the intact urethral meatus up the intact distal
urethra, where it escaped into the vagina. Once the disrupted site was identified, the catheter
could be passed through the bladder neck into the bladder. Reconstruction was begun by devel-
oping a flap of vaginal wall hinged posteriorly (Fig. 5). The reconstruction of the urethra begins
with reanastomosis of the disrupted urethra to the bladder neck, with the initial suture placed in
the 12 o’clock position. Each fine delayed absorbable suture is placed in an extramucosal pos-
ition, reanastomosing the urethra to the bladder neck (Fig. 6). Once the urethra is reconstructed,
the vaginal flap is placed in such a way that it avoids overlying suture lines (Fig. 7). A small
urethral catheter (10F) is left in place for 5 – 7 days, after which it is removed and spontaneous
voiding occurs.
 Urethrovaginal Fistula 801

Figure 4 Traumatic disruption of the urethra. (From Ref. 19. By permission of Mayo Foundation.)

Figure 5 Vaginal flap exposing disrupted urethra at bladder neck. (From Ref. 19. By permission of
Mayo Foundation.)
802 Gebhart and Lee

Figure 6 Reconstruction of urethra beginning with first suture at the 12 o’clock position. (From Ref. 19.
By permission of Mayo Foundation.)

Figure 7 Closed vaginal flap with underlying closed urethra. (From Ref. 19. By permission of Mayo
Foundation.)
 Urethrovaginal Fistula 803

VI. LINEAR URETHROVAGINAL FISTULA

In patients who have a linear urethrovaginal fistula, urethral reconstruction may be more diffi-
cult, and urinary continence, even in what appears to be a well-constructed urethral tube, may
not be predictable. The basic principles of the repair are the same as those for simple urethro-
vaginal fistula. An incision is made in the anterior vaginal mucosa adjacent to the margin of
the defect, with wide mobilization of the vaginal wall laterally to, or past, the descending
pubic ramus (Fig. 8). The anatomical defect may appear to be rather extensive; however, the
actual loss of urethral tissue and muscle may be minimal. The injury results in retraction of
the uninvolved musculature into the urethral roof, which is usually intact in affected patients.
After the vaginal mucosa is mobilized laterally, a small portion of the roof of the remaining ure-
thra is mobilized in preparation for reconstruction of a new urethral tube (Fig. 9). The remaining
urethral roof should provide the patient with a continent (albeit narrow) urethra.
Usually, a No. 8 or No. 10 urethral catheter is placed in the bed of the roof of the urethra;
this permits accurate approximation of the freed edges of the roof of the urethra in reconstruction
of the tube (Fig. 10A). The sutures are placed in an interrupted fashion with 4-0 delayed absorb-
able suture positioned extramucosally. This initial suture line reconstructing the urethra is
inverted with a second layer approximating the periurethral tissues to aid in support of the initial
suture line (Fig. 10B). The third layer of sutures is placed in the cervicopubic fascia to plicate the

Figure 8 Proposed line of incision about fistula and anterior vaginal wall. (From Ref. 18. By permission
of Mayo Foundation.)
804 Gebhart and Lee

Figure 9 Mobilization of vaginal wall. (From Ref. 18. By permission of Mayo Foundation.)

Figure 10 Multilayered reconstruction of urethra and suburethral tissues. (From Ref. 18. By permission
of Mayo Foundation.)
 Urethrovaginal Fistula 805

urethra and bladder neck areas further (Fig. 10C). Figure 11A shows the third layer tied and
closure of the vaginal wall, which in this case was approximated free of tension (Fig. 11B).

VII. SLOUGH OF URETHRAL FLOOR

In patients who have a slough of the entire floor of the urethra, including the bladder neck and the
base of the bladder, reconstruction of a continent urethra may be more difficult. The surgical
repair is initiated with a vertical incision in the anterior vaginal wall extending close to either
edge of the defect, after which the vaginal mucosa is separated from the underlying cervicopubic
fascia far laterally to provide for the possibility of reconstruction of a tension-free urethral tube
(Fig. 12).
What later will be the second row of sutures is initially placed under direct vision to permit
large, more secure portions of the supporting tissue to be obtained without fear of entering the
urethra. The insertion of a finger into the open bladder neck ensures accurate identification and
location of the ureters during the snug plication of the bladder neck (Fig. 13). Once these sutures
are placed in the supporting tissues, they are tagged laterally.
The urethral tube is reconstructed in the manner already described, and care is taken to
approximate the edges of the urethral mucosa accurately without entering the future urethral
lumen. These sutures are then tied with a No. 4-0 delayed absorbable suture, after which the pre-
viously placed sutures are tied to result in a second layer of closure of the urethra (Fig. 14). If
further supporting sutures of the cervicopubic fascia can be placed, this step is also accomplished
at this time (Fig. 15).

Figure 11 Result with closure of vaginal mucosa. (From Ref. 18. By permission of Mayo Foundation.)
806 Gebhart and Lee

Figure 12 Proposed incision. (From Ref. 18. By permission of Mayo Foundation.)

Figure 13 Placement of second (deep) layer of sutures. (From Ref. 18. By permission of Mayo
Foundation.)
 Urethrovaginal Fistula 807

Figure 14 Primary reconstruction of urethral tube. (From Ref. 18. By permission of Mayo Foundation.)

Figure 15 Closure of fascia and proposed site of flap. (From Ref. 18. By permission of Mayo
Foundation.)
808 Gebhart and Lee

Occasionally, patients with linear loss of the urethral floor have loss of a significant
portion of the anterior vaginal wall, and thus approximation of the wall of the vagina cannot
be accomplished without undue tension (Fig. 15). In these cases, the size of the defect is accu-
rately evaluated, and an appropriate tongue of tissue from the labium majus is identified to be
incised and swung into the vagina to replace the anterior vaginal wall. This fibrofatty,
bulbocavernous flap is usually hinged anteriorly, but it may be hinged posteriorly depending
on the nature of the defect. The flap is developed, and the small venous bleeders in the sub-
cutaneous tissues are suture-ligated or cauterized as necessary. The most distal portion of
the flap (that deepest into the vagina) is secured initially with full-thickness interrupted 3-0
delayed absorbable sutures (Fig. 16). Care is taken to suture the labial flap to the edge of
the vagina in an accurate way to promote primary healing. At the point at which the flap
approximates the urethral meatus, it has a tendency to “hide” the meatus and may need to
be tailored accordingly.
The site of the graft is closed with an initial layer of subcutaneous sutures, which permits
closure of the skin edges of the labium with a No. 4-0 delayed absorbable suture in a tension-free
fashion (Fig. 17). A small suction catheter has been placed under the reconstructed urethra. This
is brought out through a stab wound laterally and usually is removed in 3 – 4 days. Despite
adequate vesical neck plication and satisfactory elevation and support of the reconstructed
urethra, what appears to be an anatomically sound urethra may not provide satisfactory urinary

Figure 16 Mobilization of bulbocavernous flap. (From Ref. 18. By permission of Mayo Foundation.)
 Urethrovaginal Fistula 809

Figure 17 Flap closure. (From Ref. 18. By permission of Mayo Foundation.)

control. In approximately 50% of patients, a delayed second-stage modified Marshall-Marchetti-

Krantz type of bladder neck elevation may be required for urinary control.

REFERENCES

1. Lee RA, Symmonds RE, Williams TJ. Current status of genitourinary fistula. Obstet Gynecol 1988;
72:313– 319.
2. Hemal AK, Dorairajan LN, Gupta NP. Posttraumatic complete and partial loss of urethra with pelvic
fracture in girls: an appraisal of management. J Urol 2000; 163:282 – 287.
3. Turner-Warwick R. Prevention of complications resulting from pelvic fracture urethral injuries—and
from their surgical management. Urol Clin North Am 1989; 16:335 – 358.
4. Parkhurst JD, Coker JE, Halverstadt DB. Traumatic avulsion of the lower urinary tract in the female
child. J Urol 1981; 126:265– 267.
5. Podesta ML, Jordan GH. Pelvic fracture urethral injuries in girls. J Urol 2001; 165:1660 –1665.
6. Arrowsmith S, Hamlin EC, Wall LL. Obstructed labor injury complex: obstetric fistula formation and
the multifaceted morbidity of maternal birth trauma in the developing world. Obstet Gynecol Surv
1996; 51:568 –574.
7. Shigui F, Qinge S. Operative treatment of female urinary fistulas. Report of 405 cases. Chin Med J
(Engl) 1979; 92:263– 268.
8. Vanderputte SR. Obstetric vesicovaginal fistulae. Experience with 89 cases. Ann Soc Belg Med Trop
1985; 65:303 –309.
810 Gebhart and Lee

9. Hamlin RH, Nicholson EC. Reconstruction of urethra totally destroyed in labour. BMJ 1969; 1:147–150.
10. Gray LA. Urethrovaginal fistulas. Am J Obstet Gynecol 1968; 101:28 – 36.
11. Symmonds RE, Hill LM. Loss of the urethra: a report on 50 patients. Am J Obstet Gynecol 1978;
130:130– 138.
12. Carlin BI, Klutke CG. Development of urethrovaginal fistula following periurethral collagen injec-
tion. J Urol 2000; 164:124.
13. Guerriero WG. Operative injury to the lower urinary tract. Urol Clin North Am 1985; 12:339– 348.
14. Lee RA. Diverticulum of the female urethra: postoperative complications and results. Obstet Gynecol
1983; 61:52– 58.
15. Ganabathi K, Leach GE, Zimmern PE, Dmochowski R. Experience with the management of urethral
diverticulum in 63 women. J Urol 1994; 152:1445 –1452.
16. Kobashi KC, Dmochowski R, Mee SL, Mostwin J, Nitti VW, Zimmern PE, Leach GE. Erosion of
woven polyester pubovaginal sling. J Urol 1999; 162:2070 – 2072.
17. Blaivas JG. Treatment of female incontinence secondary to urethral damage or loss. Urol Clin North
Am 1991; 18:355– 363.
18. Lee RA. Atlas of Gynecologic Surgery. Philadelphia: W.B. Saunders, 1992: 273–279.
19. Lee RA. Management of genitourinary fistulas. In: Hurt WG, ed. Urogynecologic Surgery. 2nd ed.
Philadelphia: Lippincott Williams & Wilkins, 2000:141 – 148.
56
Female Urethral Diverticula

Sandip P. Vasavada and Raymond R. Rackley

Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

The first description of a diverticulum of the female urethra was in 1805, and in the subsequent
years only sporadic reports were noted (1). In the 1950s there was an increase in the incidence of
diagnosis. Davis and Cian noted that as clinicians become more aware of the condition, the
frequency of diagnosis increases (2). In one report, the compilation of 121 cases of urethral
diverticula was the largest of its time, where 71 cases were diagnosed over 60 years, then a
further 50 cases in the following 12 months (3). From this report the notion developed that in
order to diagnose female urethral diverticula one must first suspect it. Investigators who
described their experience with urethral diverticula stated that in order to identify patients
with urethral diverticula, more general awareness of this condition must prevail (4).
Urethral diverticula can be difficult to diagnose; they are often overlooked as a source of
recurrent urinary tract infections, chronic pelvic pain, and voiding dysfunction. These patients
can be diagnostic challenges. The standard evaluation for all patients with acute and chronic
pelvic disorders should include urethral diverticula in the differential diagnosis, so that the diag-
nosis and ultimate therapy will not be prolonged. Most patients present with a constellation of
nonspecific irritative and obstructive voiding symptoms, making the correct diagnosis more
challenging to identify; however, suspecting female urethral diverticula may ultimately lead
to the correct diagnosis and treatment. It has been shown that there is often a significant
delay in the diagnosis of female urethral diverticula in the majority of patients (5 –8). Even
now, there are likely many women who have had this diagnosis overlooked as a cause for
their pelvic disorders, and many of these patients have seen more than one pelvic specialist,
either urology or gynecology, for their symptoms. Changes in the standard evaluation of
women with complaints of pelvic pain disorders should be instituted, so that with a thorough
history, physical exam and appropriately selected radiologic imaging, an exact diagnosis of
the correct urethral pathology can be made.

II. INCIDENCE

The true incidence of urethral diverticulum is unknown and the reported incidence varies.
The incidence of urethral diverticula was examined in 1967; Andersen showed that of 300
women examined for cervical cancer nine patients were diagnosed with urethral diverticula,
811
812 Vasavada and Rackley

an incidence of 3% (9). The estimated incidence in the literature shows that urethral diverticula
have been identified in 0.6– 6% of women (6,10,11).

III. IDENTIFICATION AND EVALUATION

A. Etiology
The female urethra is a short tubular structure that is surrounded by multiple periurethral ducts
and glands, the largest being the Skene’s glands that are adjacent to the distal urethra and drain
into the meatus (12). Congenital anomalies of the female urethra are quite rare. Infrequently
obstructing urethral valves have been identified; more often, an ectopic ureter is identified within
the urethra, which may masquerade as a urethral diverticular communication site (12). In one
report an ectopic ureter was identified draining into a urethral diverticulum (13).
It is exceptionally rare to identify congenital urethral diverticula; however, suburethral
cysts have been identified in the newborn (14). In those few instances, the urethral diverticula
have been shown to be remnants of Gartner’s ducts cysts, diverticula linked histologically to
cloacal rests, and even diverticula confused as a possible urethral duplication (11,15). Neverthe-
less, the incidence of childhood female urethral diverticula is exceedingly low, and as such
urethral diverticula are rarely diagnosed before the age of 20 years (2).
Female urethral diverticula are diagnosed most frequently in the third to fifth decades
(6,10,11). Most diverticula are acquired, and a favored hypothesis regarding the etiology of
female urethral diverticulum begins in the paraurethral glands. In accordance with anatomic
studies by Huffman of the periurethral ducts and glands, most diverticula of the female urethra
are located dorsally or laterally and distally (16). Female urethral diverticula are thought to arise
from repeated infection, subsequent destruction of the paraurethral glands, and then abscess for-
mation within the periurethral and urethral glands which lie in the mid to distal urethra along the
posterolateral wall near the 3 and 9 o’clock positions. These obstructed glands then rupture into
the urethral lumen and remain as outpouchings off the urethra, which eventually epithelialize
becoming a true urethral diverticulum as opposed to a urethrocele or pseudodiverticulum (7).
Other possibilities to the etiology of female urethral diverticula include the formation of
urethral diverticula resulting from obstetric trauma; however, there are significant numbers of
diverticula diagnosed in nulliparous women, and urethral diverticula are no more common in
women of high parity (2,15). Also cited as a possible source is trauma from urethral instrumen-
tation, and postoperative urethral and vaginal surgery. Another rare, iatrogenic cause for urethral
diverticulum has been described after collagen injection therapy for treatment of stress urinary
incontinence, resulting in a noncommunicating diverticulum with obstruction of a periurethral
gland and persistent accumulation of secretions (17). Noncommunicating urethral diverticula
result when the communication site from the urethra to the diverticulum closes off.
Urethral diverticula are urothelial mucosa lined sacs that lie outside the urethra within the
periurethral fascia which lack surrounding muscle. They are prone to urine stasis and repeated
infections. Inflammation and chronic irritation due to the presence of urine and debris may lead
to malignant degeneration into adenocarcinoma (18 – 24), transitional cell carcinoma (25), or
squamous cell carcinoma. More commonly, the stasis of urine causes repeated urinary tract
infection and possible calculus formation. Recurrent urinary tract infections are a frequent com-
plaint of women with urethral diverticula, positive urine cultures (.100,000 colony-forming
units per milliliter) will often grow strains of Escherichia coli, or other gram-negative bacilli,
as well as gram positive species, such as Streptococcus fecalis. Peters and Vaughn showed
that of the 32 women 19 (59%) had culture-proven urinary tract infections, and out of six asymp-
tomatic women with diverticula, four (60%) had significant bacteriuria (26). They also noted an
 Female Urethral Diverticula 813

association that urethral diverticula are more common in patients with previous gonococcal
infections, which in turn may contribute to its etiology in those women (26).
Urinary stasis may result in the formation of calculi. This has been clearly described before
with renal calculi formation in the face of ureteropelvic junction obstruction, bladder calculi sec-
ondary to benign prostatic hypertrophy, and now urethral diverticular calculi. Case reports of
urethral diverticulum with calculi have been found across all age ranges. A symptomatic preg-
nant woman was treated with incision and removal of the urethral diverticular calculi as an out-
patient (27). A case report of an elderly woman with a firm vaginal mass was due to the presence
of a large 5  6 cm stone in a urethral diverticulum (28). As such, calculi in diverticula are rare,
with stone formation occurring in about 1.5 – 10%, usually as a result of stagnate urine, salt depo-
sition, and mucus from the epithelial lining of the diverticula (28).
The location, number, and extent of urethral diverticula have an impact on the choice of
treatment. A classification system for female urethral diverticula has been described by Leach,
the LNSC3 (location, number, size, configuration, communication, and continence) (29).
Providing an accurate description of the diverticulum under evaluation will in turn facilitate
its subsequent treatment.

B. Presentation
Women will present to their physicians with a host of symptoms, and regrettably the patient’s
description of each complaint is not always textbook clear. Therefore, the task is left up to
the doctor to identify, evaluate, and treat the pathology. A history of recurrent urinary tract infec-
tions, stress urinary incontinence, and incomplete voiding are some of the most common pre-
senting symptoms in women with urethral diverticula (Table 1) (6,8,10,30 –35). According to
Hoffman, the single most important complaint is postmicturition-dribbling (30), and dysuria
and dyspareunia complete the classic triad (11). These are all nonspecific complaints, however
if the symptoms are also accompanied by urgency, urge incontinence, frequency, and a protrud-
ing vaginal mass, this is then more highly suggestive of a urethral diverticulum. If pus can be

Table 1 Most Common Initial Complaints in Women Who Present for Evaluation
and Are Ultimately Found to Have Urethral Diverticula from 1964 to 2000

Mean (%) St dev Range (%)

Recurrent urinary tract infections 47 +25 9– 83

Stress urinary incontinence 46 +28 28 – 100
Incomplete voiding 33 +7 28 – 38
Dysuria 29 +21 4– 58
Urgency 28 +11 18 – 47
Urge incontinence 27 +14 11 – 35
Frequency 26 +9 16 – 38
Postvoid dribbling 21 +22 4– 65
Lower abdominal pain 20 +25 1– 50
Pus per urethra 18 +28 3– 50
Protruding vaginal mass 18 +14 7– 17
Dyspareunia 13 +8 1– 24
Hematuria 10 +5 5– 18
Urine retention 10 +8 3– 21
Difficulty voiding 8 +6 2– 14
814 Vasavada and Rackley

expressed out the meatus with manual compression of the anterior vaginal wall, then this
strongly indicates the presence of a urethral diverticulum. Romanzi et al. reviewed their
experience with diverse presentations of urethral diverticula and decided that when symptoms
mimic other disorders and especially when they do not improve and respond with standard
therapy, it is important to entertain the possibility that the source of the pathology is a urethral
diverticulum (8).
Patients who have hematuria, difficulty voiding, and even frank urinary retention may
have urethral diverticula, as well as a malignancy. In the patient who goes into acute urinary
retention without any noted underlying neurologic, myopathic, pharmacologic, or pyschogenic
cause, malignancy should be considered until it is excluded. As vertebral disk disease, spinal
stenosis, spinal cord injury, transverse myelitis, radical pelvic surgery, postherpes zoster infec-
tion, and diabetes mellitus all can result in acute urinary retention in women, anatomic obstruc-
tion by carcinoma in a urethral diverticulum causing bladder outlet obstruction may also result in
the inability to void.
Commonly patients are given an initial diagnosis after their preliminary evaluation,
which is accompanied by the treatment of choice for that suspected condition (Table 2)
(5,8,36,37). Many patients receive a variety of treatments that include antibiotics, anticholiner-
gics, antidepressants, bladder hydrodistension, and urethral dilations for suspected pelvic
disorders. Some of the more common presumed diagnoses are chronic cystitis, trigonitis,
incontinence, vulvovestibulitis, sensory urgency, and psychosomatic disorders. We have
seen patients mislabeled as interstitial cystitis/chronic pelvic pain syndrome (38), which
carries the heavy burden of a chronic disease, when in fact these patients had true urethral
pathology. Hence, the patients may at times express degrees of frustration and lack of hope
because their symptoms have been longstanding. Therefore, a high index of suspicion is in
order, as several patients may also not be overtly symptomatic upon initial evaluation. In sum-
mary, in any case of persistent lower urinary tract symptoms unresponsive to therapy, one
should exclude a urethral diverticulum.

Table 2 Initial Diagnoses First Given to Patients and Their

Subsequent Treatments Before the Diagnosis of Female
Urethral Diverticulum

Diagnosis Treatment

Chronic cystitis Antibiotics

Trigonitis Antibiotics
Cystitis cystica Antibiotics
Stress urinary incontinence Anti-incontinence surgery
Urge incontinence Anticholinergic therapy
Interstitial cystitis Hydrodistension
Idiopathic pain syndrome DMSO instillation
Tricyclic antidepressant therapy
Urethral syndrome Urethral dilation
Vulvovestibulitis Vaginal creams
Antibiotic/antifungal
Cystocele Surgery
Sensory urgency Anticholinergics
Psychosomatic disorder Psychotherapy
Pharmacotherapy
 Female Urethral Diverticula 815

C. Diagnosis
To establish the correct diagnosis in women with a myriad of symptoms it is critical to perform a
thorough history and physical examination. Included in a standard history are questions relating
to urinary control for stress urinary incontinence, urgency and urge incontinence, and pad usage.
Irritative voiding symptoms such as, frequency, nocturia, urgency, dysuria, urinary tract infec-
tions, pyelonephritis, and hematuria should be noted. Obstructive voiding symptoms such as
poor urine stream, difficulty voiding, hesitancy, and double voiding should also be noted. A
complete obstetric history should be taken, noting the number of pregnancies, live births, and
methods of delivery. A neurologic history and bowel patterns should be included in the ques-
tions. A complete medication list with allergies, and past medical and surgical histories are
also important.
The physical exam should be performed in a warm room, with the patient in a hospital
gown. The general exam of neck, thorax, back, and abdomen can be accomplished completely
and quickly. A focused genitourinary exam is then performed with the patient in lithotomy pos-
ition. A warmed half-speculum is gently placed into the vagina to expose the anterior abdominal
wall. The urethra and bladder are well visualized, and the patient is asked to Valsalva and cough,
performing a supine stress test to evaluation for hypermobility, stress urinary incontinence, and
the presence of a cystocele. The cervix and posterior vaginal walls are then inspected, checking
for discharge, inflammation, and masses. At this point, palpation of the anterior and posterior
vaginal walls is performed. Careful attention is given to palpation of the urethra with attempts
to express purulent material via the meatus and evaluation for suburethral masses or tenderness.
Postvoid residuals can be accomplished with an office ultrasound, or with a red rubber catheter;
the catheterized urine specimen should be sent for urine culture. If the patient had complaints of
hematuria and irritative voiding symptoms, a urine cytology should be obtained.
Not all patients will present with a suburethral mass, and not all suburethral masses are
urethral diverticula. The differential diagnosis of periurethral masses is extensive and includes:
urethral diverticulum, urethrocele, Skene’s gland abscess, Gartner’s duct cyst, ectopic
ureterocele, vaginal wall inclusion cyst, and other, less frequent diagnoses (Table 3) (31,39).

Table 3 Differential Diagnosis

of Suburethral Masses

Urethral diverticulum
Urethrocele
Skene’s gland abscess
Gartner’s duct cyst
Ectopic ureterocele
Vaginal wall inclusion cyst
Urethral carcinoma
Vaginal carcinoma
Vaginal fibroma
Vaginal leiomyoma
Vaginal leiomyosarcoma
Hernangioma
Urethral varices
Endometriosis of the vagina
Sarcoma botryoides
Vaginal wall metastasis
816 Vasavada and Rackley

The urethra may be tender, and on occasion a large diverticulum is evident as an anterior wall
mass that may express pus and debris from the urethral meatus when compressed. Often, though,
the physical exam is normal. Again, suspicions of a urethral carcinoma or calculi arise if a firm
mass is palpated along the vaginal wall.
Urinary incontinence may be seen in patients suspected of having a urethral diverticulum.
Examination for urethral hypermobility, stress incontinence, and pelvic organ prolapse are docu-
mented during the physical examination. Evidence of stress urinary incontinence may require
urodynamic testing to assess the abdominal leak point pressure, and to determine a need for a
simultaneous sling with the excision of the diverticulum and reconstruction of the urethra (7,32).
One must clinically suspect a urethral diverticulum in order to select the most appropriate
procedures and imaging studies. Many patients with urethral diverticula will undergo urody-
namic testing to evaluate their complaints of voiding dysfunction. Urodynamics provide infor-
mation on bladder function, during both the storage and voiding phases, and electromyography
(EMG) is utilized during some examinations when there is a history of complex voiding patterns
and to assess for the presence of detrusor-sphincter dyssynergia. Not all patients will require uro-
dynamic testing; however, it should be used in patients who have had previous pelvic surgery,
recurrent stress urinary incontinence after bladder surgery, and urinary retention without any
other known reason.
Urodynamics was performed in a patient who was ultimately diagnosed with a urethral
diverticula-containing adenocarcinoma. Clearly, there is an obstructive pattern; from the
exam one sees there is very high voiding pressure, and extremely low flow, which is especially
noteworthy in a woman (Fig. 1). The bladder capacity was within normal limits with a maximal

Figure 1 Pressure flow study. Voiding phase: the patient received total infusion volume of 367 cc. The
maximum pressure (pDet) was 115 cmH2O. Urinary flow rates were Q maximum, 3 mL/sec, Q average,
2 mL/sec. Pressure flow report shows minimal urination, requiring 97 sec, with extremely high voiding
pressures. Cystometry phase of urodynamics not shown (there was no bladder instability).
 Female Urethral Diverticula 817

infused volume of 369 mL, bladder pressures during cystometry showed a low normal pDet of
7 cmH2O and a compliant bladder. The maximum pressure during voiding was 115 cmH2O with
a maximum flow rate of 3 mL/sec (Fig. 1).
Urethroscopy may help establish the diagnosis of urethral diverticula, as it is easily per-
formed, has minimal morbidity, and will often produce a high yield of the correct diagnosis
in experienced hands. Urethroscopy should be focused on the posterior wall in the 3 and 9
o’clock positions to try to identify the suspected communication sites. Properly performed ure-
throscopy under anesthesia was shown to be the best method to confirm the presence of a urethal
diverticulum (34). In a study by Ganabathi, they were able to identify 53 of the 57 communi-
cation sites to the diverticula by cystourethroscopy (31). To supplement the pertinent history,
a thorough physical examination, urodynamic testing, cystourethroscopy, and radiologic
imaging have clearly enhanced the female urethral diverticular detection rate.

D. Radiologic Imaging
With suspicion of a female urethral diverticulum, the judicious selection of imaging techniques
should correctly establish the diagnosis and provide details that aid in surgical excision.
Traditionally, the evaluation to confirm the diagnosis of female urethral diverticula was
performed with positive pressure urethrography (PPUG) and voiding cystourethrography
(VCUG). There are currently several modalities available to identify and characterize female
urethral diverticula: PPUG, VCUG, ultrasonography, and magnetic resonance imaging (MRI).
There continue to be ongoing controversies as to which modality is the most accurate, while
considering parameters such as cost, time, and patient comfort.

1. Positive Pressure Urethrography

In the female, a retrograde urethrogram is performed with a double balloon catheter (Trattner
catheter). After catheterizing the urethra, both balloons were inflated with fluid, one inside
the bladder, the other on the perineum (12). Contrast was then infused under pressure to fill
out the urethral communications, while there was constant traction on the bladder balloon to
occlude the bladder neck and prevent contrast from entering the bladder, thus leaving the con-
trast to exit through the side holes and fill the urethral cavity (12). When performing PPUG, the
urethral diverticula were best seen when varying the concentration of contrast in both the prox-
imal and distal balloon and then using undiluted contrast for the urethral injection (40). PPUG, in
one study, was found to have the highest accuracy and sensitivity in detecting urethral diverti-
cula when compared to all other imaging modalities (41). While there are diagnostic benefits to
PPUG, there is often hesitation in ordering this study secondary to patient discomfort, invasive-
ness, and infrequent performance in the radiology departments. In another study, MRI was
shown to be a more sensitive modality in detecting diverticula when compared to PPUG (42).
Out of six patients with urethral diverticula, MRI identified four; however, PPUG identified
only one diverticulum (42).

2. VCUG
Historically, voiding cystourethrography has been the radiologic study of choice, as it is easy to
perform, and may identify the number and the location of female urethral diverticula. The tech-
nique in acquiring the x-ray films is important during a VCUG, for if the initial KUB does not
show the inferior pubic rami, it is quite possible to miss the urethral pathology, as the urethra
usually falls quite low on the KUB (Fig. 2). To obtain the best study, both lateral and AP (ante-
roposterior) views of the pelvis during voiding delineate the position and number of diverticula
818 Vasavada and Rackley

Figure 2 Voiding cystourethrogram demonstrates urethral diverticula. Postvoid film demonstrates

urethral diverticula at the level of the pubic bone, as well as a moderate postvoid residual. No
abnormalities were noted within the bony structures of the pelvis.

in relation to the urethra. As shown in Figure 3A and 3B, at least three diverticula are observed in
the study, noting the position to be inferior to the urethra on the lateral view.
However, the success rates of VCUG vary when compared to PPUG and MRI. Wang
reviewed a 3-year experience comparing VCUG and PPUG to evaluate for female urethral diver-
ticula and found that the sensitivity for VCUG was 51.3%, which was significantly lower than
with PPUG, sensitivity 84.6% (35). A recent study showed that in 22 of 30 cases the VCUG
failed to demonstrate a female urethral diverticulum, but it was seen on PPUG (33). The
costs of both tests were noted in the study, and they were found to be quite comparable, within
only $5.00 of each other. A comparison between endoluminal MRI and VCUG demonstrated
that VCUG missed 7% of the diverticula, and it underestimated their size and complexity (43).

3. Ultrasonography
The sonographic appearance of urethral diverticula was first described using a transabdominal
approach (44). Transabdominal ultrasound is not considered an invasive test, and as an imaging
modality it is frequently well tolerated. The development of higher-frequency probes and
enhanced detection rates lead to the development of endovaginal, and the transperineal
approaches. The noninvasive nature of transperineal ultrasound was considered advantageous
in using this method as a screening technique for urethral diverticula (45).
 Female Urethral Diverticula 819

Figure 3 Voiding cystourethrogram demonstrates several urethral diverticula. (A) Anterior/posterior

voiding phase view shows three urethral diverticula. (B) Lateral voiding phase view clearly shows the urethral
communication to the diverticula and the inferior position of the diverticula in relation to the urethra.
820 Vasavada and Rackley

Translabial ultrasonography (46), by placing the transducer against the labia minora and
urethra, has also been described as a noninvasive approach to imaging the female urethra. An
endorectal 5-MHz transducer has clearly shown the presence of a urethral diverticulum,
which may differ from endovaginal transducers that will focus on the uterine neck not the
anterior vaginal wall (47). The transperineal approach will be able to view both the sagittal
and the coronal planes; however, there is often inadequate visualization of the urethra (47).
The transrectal approach may be superior to the others to identify calculi, debris, or filling
defects with diverticula. Evaluation of urethral diverticula can be done as a safe, accurate,
and relatively inexpensive imaging modality by using the transrectal approach (48). Ultrasono-
graphy (transvaginal, transperineal, and endourethral) of urethral diverticula was investigated by
Siegel in comparison to detection results with VCUG. Both ultrasound and VCUG identified 13
of the 15 urethral diverticula; however, ultrasonography provided more information on the
extent and location of the communication site within the urethra (49).
Intraoperative monitoring can be accomplished with an endoluminal catheter-based ultra-
sound transducer to provide improved identification of the size, orientation, and characteristics
of urethral diverticula and surrounding tissues (50). The endoluminal catheters used were 6F or
9F (12.5 or 20 MHz), and provided a 360-degree transaxial image, and were able to effectively
differentiate fluid and solid components (50). The main limitation of ultrasonography as an
imaging modality is that it is highly technician and operator dependent.

4. MRI
Magnetic resonance imaging (MRI) of the female urethra is very accurate. Over the previous
years MRI has developed several methods by which to image the female urethra. There have
been advances in the development of endoluminal (43), endovaginal (37), endorectal (5), and
external coils for MRI. All methods clearly distinguish urethral disorders; a standard protocol
used extensively requires an external coil, T2-weighted noncontrast study of the pelvis, which
does not require premedication, instrumentation, or contrast opacification (51). The urine within
the bladder has high signal intensity, bright white on T2-weighted images, and a fluid filled ure-
thral diverticulum will also show a high signal intensity sac, and the soft tissue of the urethra has
low signal intensity (52). Midsagittal and axial views (Fig. 4A and 4B) of the pelvis are
requested with each study; MRI clearly identifies urethral pathology, which provides a superior
examination for surgical planning by accurately delineating the extent of the diverticula (52).
Figure 4a demonstrates an example of a large 3-cm “saddlebag” urethral diverticulum with
an internal septation, from a MRI in the axial plane (53).
Urethral diverticula may contain debris, infected urine, calculi, and carcinoma. When
additional lesions are suspected, tumors show enhancement with intravenous gadolinium (20).
The multiplanar capability and excellent soft tissue contrast of MRI allow demonstration of peri-
urethral and diverticular anatomy (54). MRI of urethral diverticular adenocarcinoma is shown in
the midsagittal, and axial views of the pelvis (Fig. 5A and 5B) with an enhancing mass in the
urethral diverticulum is evident.
Hricak showed that urethral diverticula were identified in all patients with the diagnosis
(54). In a comparison of urethroscopy, PPUG and MRI of 20 women with voiding symptoms,
MRI was shown to have a better sensitivity, and both positive and negative predictive values
(55). Clearly, MRI of the female pelvis provides excellent visualization of urethral diverticula,
in addition to identifying other pelvic pathology—for example, pelvic organ prolapse (51).
Therefore, at present, MRI is often the procedure of choice for evaluation of suspected urethral
diverticula.
 Female Urethral Diverticula 821

Figure 4 Axial and midsagittal MRI T2-weighted images were obtained through the pelvis. There is a
large urethral diverticulum measuring approximately 3.0  2.0  2.5 cm. (A) Axial MRI shows portions
of the diverticulum are seen to surround the urethra (arrow), as a “saddlebag” urethral diverticulum. The
urethra has low intensity on MRI T2-weighted noncontrast images. (B) Midsagittal MRI T2-weighted
image demonstrates a large urethral diverticulum (arrow) with high signal intensity, and a partially filled
bladder with the same signal intensity as the diverticulum.

IV. URETHRAL AND URETHRAL DIVERTICULAR PATHOLOGY

A. Benign
Pathology reports of urethral diverticula most often reveal chronic inflammation within transitional
cell epithelium, however, there will be times when other lesions are discovered. Vaginal leio-
myoma are rare anterior vaginal wall masses that may mimic urethral diverticula (Table 3), and
they may be removed during a vaginal exploration for a presumed urethral diverticulum. Careful
histologic examination of the pathology specimen is needed to assure the benign nature of the entity
and to rule out leiomyosarcoma (39). Case reports of benign pathology findings within urethral
diverticula have shown calculi, Wegener’s granulomatosis, and nephrogenic adenoma (56–59).
Nephrogenic adenomas arise from chronic irritation and infection of the transitional cell
epithelium, creating a metaplastic response. These are more commonly reported from bladder biop-
sies in the trigone, posterior or lateral bladder walls, and the bladder dome (59). Histologically,
822 Vasavada and Rackley

Figure 4 Continued.

nephrogenic adenoma is a benign lesion with no malignant potential, consisting of tubular struc-
tures with a single layer of cuboidal and columnar epithelium resembling renal tubules. Nephro-
genic adenomas of the bladder will recur in a number of cases.

B. Malignant
Urethral diverticular malignancies are rare in women. Until 1993 only 53 cases had been
reported, first in 1951 (24). The histology of malignancy within a urethral diverticulum confirms
that adenocarcinoma is the most common (59%) followed by transitional cell carcinoma (30%),
and the least common is squamous cell carcinoma (11%) (24). This histological pattern differs
from malignancies of the urethra. The predominant cell type of malignancies of the urethra is
most commonly squamous cell carcinoma. The most common presenting symptoms of patients
with malignancy within a urethral diverticulum are dysuria, frequency, urethral bleeding, and
outflow obstruction (Fig. 1).
Imaging of the female urethra is very accurate using MRI. Imaging of urethral
adeno carcinoma is often best seen on pelvic MRI with and without intravenous gadolinium (20).
T2-weighted images after gadolinium display increased signal intensity and tumors demonstrate
enhancement (Fig. 5) (54).
 Female Urethral Diverticula 823

Figure 5 Axial and midsagittal MRI T2-weighted images were obtained through the pelvis. There is a
urethral diverticulum with enhancement after intravenous gadolinium. (A) Axial MRI shows a high signal
intensity urethral diverticulum (arrow) with an infiltrative central filling defect that enhances with
gadolinium. (B) Midsagittal MRI T2-weighted images show a urethral diverticulum with a central filling
defect (arrow).

Clear cell adenocarcinoma has been also called “mesonephric carcinoma” because of its
morphologic resemblance to clear cell carcinoma of the kidney. Three theories to the origin
of urethral diverticular carcinoma are periurethral gland changes, metaplastic changes of the
transitional cell epithelium, and embryonic remnants that undergo malignant change (24).
The predominance of adenocarcinoma as the most common malignancy in urethral diverticula
may best be explained by the diverticula arising from periurethral glands (24). The cells of origin
have been more recently studied. The female paraurethral ducts are thought to be embryologi-
cally homologous to the male prostate gland and are the likely origin for diverticular cancer of
the urethra (60). Immunohistochemical staining analysis of endocrine cells in female paraure-
thral ducts noted a strongly positive staining for carcinoembryonic antigen (CEA) and a negative
result for prostate-specific antigen (PSA). Further analysis revealed that the proximal and distal
parts of the paraurethral ducts have different histology and that the cancer cell of origin may be
from different parts within the paraurethral duct (61).
824 Vasavada and Rackley

Figure 5 Continued.

The therapy of choice for malignancy within a female urethral diverticulum has been to
perform an anterior pelvic exenteration (18,19,21 –23). It is necessary to remove the bladder,
urethra, anterior wall of the vagina, distal ureters, uterus, salpinx, ovaries, and pelvic lymph
nodes, as well as create a urinary diversion. The urinary diversion is most often either an
ileal conduit or a continent cutaneous diversion. Diverticulectomy alone is inadequate treatment
secondary to the high rate of recurrence.

V. MANAGEMENT OF FEMALE URETHRAL DIVERTICULA

A. Nonsurgical
A number of patients who do not have significant symptoms from the diverticulum may be
followed, treated with antibiotics and anticholinergics, and forego surgery if they remain
asymptomatic (31). These small diverticula may be followed with conservative methods,
which may include simple observation, manual postvoid decompression, aspiration, or even
older methods of diverticular packing or injection therapy (41).
Female urethral diverticula identified during pregnancy should be managed conservatively
during the antenatal period. Four cases of urethral diverticulum during pregnancy were all
 Female Urethral Diverticula 825

managed nonoperatively; three women underwent aspiration of their diverticulum for treatment
of urethral symptoms, and one woman was treated with antibiotics alone, with excision per-
formed postnatally (62). Aspiration can be performed easily using local anesthesia, gently insert-
ing an 18-gauge needle into the diverticulum, and slow aspiration of diverticular fluid with a
syringe (62).
Thus, nonsurgical management of urethral diverticula ought to be considered in all
patients in whom the risk of surgery might outweigh the benefits, as in pregnancy. Hemorrhage
and trauma of surgery in the vaginal and periurethral tissues could lead to wound breakdown,
infection, and possible development of urethrovaginal fistula. Surgical management of female
urethral diverticula might be best delayed until after the postnatal period, after antibiotic therapy
has reduced inflammation, or in patients who are at the greatest risk for postoperative
complications.

B. Surgical
1. Historical
The surgical techniques for the treatment of female urethral diverticulum have evolved as the
incidence of this diagnosis has increased. Over the years the treatment options for symptomatic
urethral diverticula have included incision and drainage with or without packing of the sac,
marsupialization into the vagina, endoscopic electrofulgaration of the diverticular sac, and for-
mal transvaginal open excision (10).
In an early technique, Ellik described draining and cleansing the diverticulum via a direct
stab incision through the vaginal mucosa, then packing the diverticulum with strips of oxycel
until it was a semisolid mass (63). The oxycel would obliterate the cavity and seal the urethral
communication by “fibrotic assimilation” (63). The benefits of the technique in 1957 were noted
to minimize surgical trauma and operating time, as well as expedite tissue healing and conva-
lescence (63).

2. Marsupialization
Spence and Duckett advocated a “generous meatotomy”(4) to be employed for distal diverticu-
lum, but could result in incontinence if performed in proximal to midurethral diverticula. This
treatment was felt to be an effective treatment only for distal urethral diverticula, and required
leaving the bladder neck area and proximal urethra completely untouched. The basic surgical
technique involved incising along the floor of the urethra from the meatus to the diverticular
ostia and trimming redundant tissue and saucerizing the sac into the vagina (4).

3. Endoscopic
Minimally invasive treatment options in the treatment of female urethral diverticula have
evolved from cauterization of the exposed urethral wall to transurethral electrocoagulation,
always using urethroscopy as an invaluable intraoperative aid to verify the location and number
of diverticular ostia. Lapides, using electrocautery for the transurethral incision of the diverticu-
lar ostia, was the first to describe endoscopic treatment of urethral diverticula (64). In continued
attempts to simplify the treatment of urethral diverticula, the transurethral incision of diverticula
using a cold urethrotome in a longitudinal fashion both proximally and distally to widely open
the roof of the diverticulum was employed (65). Transurethral diverticulotomy promotes drain-
age of diverticular contents into the urethra, noting that recurrent urethral diverticula may
develop, as this was not considered a definitive cure as transvaginal diverticulectomy.
826 Vasavada and Rackley

Transurethral electrocoagulation (34) was performed by insertion of the knife electrode

through the diverticular ostia and elevating the resectoscope to invert the diverticula sac; then
the tented roof was fulgarated as well as the wall of the diverticulum. This technique reminds
us of the endoscopic treatment of bladder diverticula, where the sac is pulled into the bladder
and then cauterized. Minimally invasive surgery for the treatment of urethral diverticula
using an endoscopic approach is considered safe and effective regardless of the location, and
in comparison to formal transvaginal diverticulectomy, has a shorter operative time and less
risk of postoperative incontinence and urethrovaginal fistula (64).

4. Excision of Urethral Diverticula

Patients want definitive treatment for their urethral diverticula in most instances, especially
patients with significant symptoms. A transvaginal formal excision of the urethral diverticula
is our treatment of choice for symptomatic women. During the evaluation of a patient if there
is a considerable amount of inflammation and infection, incision and drainage of an infected ure-
thral diverticulum may be needed prior to excision. Also, stress urinary incontinence often coex-
ists with urethral diverticula, and should be evaluated prior to surgery with urodynamics, in
order to determine the need for concomitant pubovaginal sling surgery. Urodynamics that reveal
detrusor instability may require anticholinergic therapy prior to surgery, to diminish the poten-
tial for high-pressure voiding, which could harm a new urethral reconstruction. Once a patient
with a urethral diverticulum selects surgical excision, we proceed.
After the patient is prepped and draped a 16F Foley catheter is inserted and the bladder is
filled with 200 cc normal saline. A suprapubic tube is placed using a Lowsley retractor through
the lower midline anterior abdominal wall, and then placed on gentle traction to avoid irrigation
extravasation. The urethral Foley is replaced once the Lowsley is removed, and a Scott ring with
hooks and a weighted vaginal speculum is used for retraction. Exposure of the anterior vaginal
wall reveals a cystic mass in the midurethra (Figs. 6, 7). An inverted U-incision is outlined with a
marking pen, up to near the distal aspect of the urethral diverticulum and just proximal to the
urethral meatus (Fig. 8). A prepared solution of 1 : 200,000 lidocaine with epinephrine is injected
into the anterior vaginal wall to facilitate dissection and hemostasis.
A flap of the anterior vaginal wall is prepared and carefully dissected with Metzenbaum
scissors (Fig. 9). Care should be taken to keep this dissection very superficial over the periure-
thral fascia, to avoid entrance into the urethral diverticula. The hooks are then advanced to
retract the edges of the anterior vaginal wall (Fig. 10). The periurethral fascia should be opened
transversally (Figs. 11, 12). It is imperative that the dissection be carried out precisely and that
each layer be identified and preserved to assist in later reconstruction of the periurethral fascia
and vaginal wall flaps (66). The periurethral fascia is dissected posteriorly, and the distal dissec-
tion of this fascia further exposes the wall of the diverticulum (Fig. 13). This dissection is easier
while the diverticulum is still full of fluid; a full diverticular sac aids in identification of the edge
of the sac and mobilization of the sac off the urethra and surrounding tissues. Another aid in the
surgical dissection of a friable urethral diverticulum can be accomplished by placing a pediatric
Foley into the diverticula, inflating the balloon, and distending a collapsed diverticula (40).
In an intact urethral diverticulum, the wall of the diverticulum is opened transversely, and
a collection of pus and fluid is drained. The lumen of the diverticular sac is seen, and the thick
wall of the sac is dissected free from the spongy tissue of the urethral wall (66). The diverticulum
is excised flush to the point of entrance of the urethral wall (Fig. 14). The Foley balloon is taken
down and the catheter is brought into the urethral lumen and irrigation of the urethra demon-
strates the point of communication, the diverticular ostium (Fig. 15). The urethral communi-
cation site is identified and closed with fine synthetic absorbable suture in a longitudinal
 Female Urethral Diverticula 827

Figure 6 Intraoperative photograph demonstrate a suburethral swelling with labial sutures and a vaginal
weighted speculum.

fashion and the periurethral fascia is reconstructed transversely and the sutures are applied in a
figure-of-eight fashion and tied individually (Fig. 16). The two flaps of the periurethral fascia
and muscular wall of the urethra are identified (Fig. 17). The defect in the periurethral fascia
is sutured adjacent to the urethra in a vertical manner to close the dead space and prevent a recur-
rence of the diverticulum (67,68) (Fig. 18). The periurethral fascia is closed to avoid any over-
lapping suture lines, which could lead to a dehiscence. The catheter is partially removed and the
urethra is irrigated to confirm a watertight closure. The transverse closure of the periurethral
fascia and urethral wall has been completed (Fig. 19). If a Martius flap or a vaginal sling is
necessary, it may be placed after the closure of the periurethral fascia, with the Martius fat
pad graft most superficial, prior to closure of the anterior vaginal wall flap (7,32,69). A Martius
labial fat pad graft can be used between the urethra and the vaginal wall when there is absence of
adequate periurethral fascia for a second layer or when operating on recurrent diverticula
(31,69).
The excess of vaginal wall is excised and the anterior vaginal wall is advanced forward in
order to cover the area of the reconstruction. Running a 2-0 synthetic absorbable suture is used to
complete the closure of the anterior vaginal wall (Fig. 20). An antibiotic or conjugated estrogen
based pack is placed into the vagina, and the urethral and suprapubic catheters are left to gravity
drainage.
When the urethral diverticulum is circumferential or a “saddlebag” (Fig. 4), it must
be completely excised anterior to the urethra and behind the pubic rami. This dissection can
be rather unwieldy, and visualization can be difficult. When a circumferential diverticulum is
828 Vasavada and Rackley

Figure 7 Anatomical representation demonstrates the vaginal exposure obtained with the Scott ring
retractor, hooks, weighted speculum, urethral Foley catheter, and the approximate position along the
Foley catheter of the urethral diverticulum.

encountered it may be necessary to completely divide the urethra, and excise a segment, in order
to expose the dorsal wall of the diverticulum (70). Reconstruction of the urethra requires a
tension-free end-to-end anastomosis; if the urethral ends will not meet the dorsal wall of the
diverticulum, it can be tubularized to construct a “neourethra.”
Surgical excision of female urethral diverticula is the standard therapy in symptomatic
patients. Outstanding surgical results require absolute adherence to surgical principles and an
understanding of the surgical anatomy of the layers of vaginal wall, periurethral fascia, and
urethra. The most important factors in urethral diverticula operative success and avoidance of
complications include a watertight anastomosis, precise dissection, anatomical closure of the
urethral layers, and nonoverlapping suture lines.

5. Excision of Urethral Diverticula and Concomitant Bladder Neck Suspension

Urethral diverticula may often present in women who have primary complaints of stress urin-
ary incontinence (71 BASS). Between 28% and 100% (Table 1) of patients may present with
bona fide stress urinary incontinence and a coexisting urethral diverticulum. Ganabathi per-
formed transvaginal needle suspension in 48% of patients to treat stress urinary incontinence
intraoperatively before proceeding with the urethral diverticular dissection; the needle sus-
pension was performed first to prevent manipulation and compression of the diverticular
sac (31). Continence rates from that study show that 45 of 56 (80%) of women were
 Female Urethral Diverticula 829

Figure 8 Intraoperative photograph demonstrates the placement of the inverted U-incision.

continent after surgery in those women who had a concomitant needle suspension and
urethral diverticulum excision (31). Also reported was that the incontinence cure rate with
needle suspension did not show long-lasting results; the recurrent stress incontinence rate
was 20% (11/56). A concomitant pubovaginal sling showed improved continence rates post-
operatively; Swierzewski showed that all patients were cured of their stress urinary inconti-
nence during follow-up of a mean 17 months (72). Faerber has shown that 16 women were
able to successfully perform simultaneous urethral diverticulectomy and pubovaginal sling
safely, without erosion and with excellent continence rates (32). Pubovaginal sling can be
successfully performed at the time of urethral diverticulectomy in patients with genuine stress
incontinence.

6. Postoperative Care
Patients who undergo surgery for urethal diverticula are discharged the same day as surgery or
within 23 h, with both a urethral Foley and a suprapubic tube to gravity drainage. Antibiotics and
anticholinergics are used while the catheters remain in place. A VCUG 2 weeks after surgery is
obtained to rule out extravasation. If a small amount of extravasation is seen, the urethral Foley
is removed and the suprapubic tube remains in place. A repeat VCUG is performed the following
week to demonstrate the resolution of extravasation. The suprapubic tube is then plugged and
voiding trials begin, until the patient can void with low postvoid residual urine volumes, at
which point the suprapubic tube is removed.
830 Vasavada and Rackley

Figure 9 Anatomical representation demonstrates preparation of the anterior vaginal wall flap carefully
dissected away from the periurethral fascia.

VI. COMPLICATIONS
A. Intraoperative Complications
During surgery it is always possible to encounter the unexpected complication. Most impor-
tantly, it is necessary to be prepared for the unexpected, recognize the error, and understand
the anatomy; this will help hasten the correction and completion of a successful surgery. Rarely
is excessive bleeding noted in vaginal surgery; however, this is usually controlled with judicious
use of electrocautery and timely wound closure with vaginal packing for a tamponade effect.
If the urethral diverticulum was large and a large defect is noted in the urethra, this can be
difficult to reapproximate. To close the urethral defect it may be necessary to expose more of the
urethral wall and suture the edges over a smaller 8F catheter. Incomplete excision of the sac (65)
should be noted intraoperatively; the sac would need to be completely excised to prevent recur-
rence of urethral diverticula or urethrovaginal fistula.
Patients with long-standing urinary tract infections often have diverticula that are signifi-
cantly inflamed and infected, even if they have been on antibiotic therapy. This often leaves
poor-quality tissue for the urethral reconstruction. A vascularized Martius fat pad graft placed
between the periurethral fascia and the vaginal wall adds a protective layer, helping to minimize
the occurrence of a urethrovaginal fistula (69). If a large periurethral abscess is seen on explora-
tion, a staged procedure may be required. First incision and drainage of the abscess is needed,
followed by the urethral diverticulum excision at a later date, after a period of healing.
 Female Urethral Diverticula 831

Figure 10 Intraoperative photograph demonstrates the anterior vaginal wall flap held by hooks and
exposure of the periurethral fascia overlying the urethral diverticulum (arrow).

Large proximal urethral diverticula may extend into the trigone and bladder neck, which
can be rather difficult to excise. The ureters lie in a position along the trigone and then out lat-
erally; it is essential to identify them ahead of periurethral fascial closure. Bladder and ureteral
injury can occur and should be recognized promptly and repaired. Intravenous injection of
Indigo Carmine will assess both ureteral and bladder integrity (68,73).

B. Postoperative Complications
The most-recognized complications after urethral diverticular surgery are urethrovaginal fistula,
urethral diverticula recurrence, and new-onset urinary incontinence. In a review of the literature
before 1995, Ganabathi showed the most common postoperative complications were urethro-
vaginal fistula (mean 4.2%), recurrent diverticulum (mean 12.2%), stress incontinence (mean
8.5%), recurrent urinary tract infections (mean 11.7%), and urethral strictures (mean 2.1%) (31).
The urethrovaginal fistula formation is the most difficult and most dreaded complication of
diverticular surgery, and should only be treated after a reasonable period of healing (66), usually
3 months. Inflammation must be reduced before attempted reconstruction to optimize the chance
for a successful repair. In revision cases of vaginal surgery a Martius fat pad graft is often used
over the repair to improve vascularity and postoperative healing.
Recurrent urethral diverticula have been shown in up to 12% of cases (31). Risk factors
include active urethral infection at the time of surgery, difficult dissection, and excessive suture
832 Vasavada and Rackley

Figure 11 Intraoperative photograph demonstrates the transverse location (arrow) to make the incision
of the periurethral fascia overlying the diverticulum.

Figure 12 Anatomical representation of the transverse incision using a No. 15 blade to cut one tissue
layer over the underlying urethral diverticulum.
 Female Urethral Diverticula 833

Figure 13 Anatomical representation of the diverticular dissection both proximally and distally with
fine Metzenbaum scissors, used to carefully dissect the periurethral fascia off the diverticulum without
entering it.

Figure 14 Anatomical representation of urethral diverticular excision flush with the urethral wall.
834 Vasavada and Rackley

Figure 15 Anatomical representation demonstrating the communication site of the urethral diverticulum
by taking down the Foley balloon, withdrawing the catheter into the lumen and flushing the catheter with
normal saline.

Figure 16 Anatomical representation demonstrates the urethral communication site is sutured using fine
absorbable suture in a longitudinal fashion with care to avoid the urethral catheter and closure of the dead
space in transverse figure of eight interrupted sutures.
 Female Urethral Diverticula 835

Figure 17 Intraoperative photograph demonstrates identification of the periurethral fascia (arrow)

within the forceps in preparation of dead space closure.

Figure 18 Intraoperative photograph shows Haney needle holder and suture vertically oriented and
parallel to the urethra in order to close the adjacent dead space (arrow).
836 Vasavada and Rackley

Figure 19 Intraoperative photograph demonstrates completion of the transverse periurethral fascia

closure (arrow).

Figure 20 Anatomical representation demonstrates final closure of the anterior vaginal wall flap using
running synthetic absorbable suture after excising excess vaginal wall tissue.
 Female Urethral Diverticula 837

line tension. Care must be taken during the primary repair to avoid these risk factors, even if
mobilization of the urethra is necessary.
Secondary stress urinary incontinence that was not present before surgery is rare, but may
develop in women because of dissection of the urethral support mechanisms. A nonfunctional
urethral sphincter mechanism may result in severe incontinence; extensive dissection of the ure-
thral wall causes this damage. Postoperative stress incontinence may require treatment with a
subsequent pubovaginal sling or periurethral injection therapy (66).
Once postoperative complications are recognized and identified, proper planning will lead
to a cure. It may be necessary to delay a repair in order for tissues to heal from the primary sur-
gery, and prevent subsequent failures. The curative strategy must be conveyed to the patient for
her to develop accurate expectations.

VII. SUMMARY

It has been 50 years since T.D. Moore stated, “There is convincing evidence that this lesion is
one of those conditions which is found in direct proportion to the avidity with which it is sought”
(74). This observation holds true today; the single most important diagnostic instrument for the
discovery of female urethral diverticula is a high index of suspicion (3). The key to successful
treatment of female urethral diverticula is not only in the surgical management, but also in the
identification and evaluation of the patients who present with a myriad of symptoms. Spence and
Duckett noted that “recognition of this disorder is particularly gratifying” (4). It is our respon-
sibility to include urethral diverticula in the differential diagnosis when evaluating women that
appear to have urethral syndrome, interstitial cystitis, and urgency-frequency syndrome, before
these labels are misplaced on these patients. The diagnosis may not be obvious, and the pathol-
ogy not easily seen on physical exam; however, if the index of suspicion is high and the proper
radiologic imaging studies are acquired, then the correct diagnosis will be made.
The evaluation of the female urethral diverticulum has evolved over the past 50 years, yet
once the accurate diagnosis is identified, the management is mostly straightforward. Strict adher-
ence to the principles of surgical reconstruction will eradicate the diverticulum and prevent com-
plications and recurrences. The method of identification, evaluation, and management for female
urethral diverticulum as well as some of the surgical technical points are described to help
accomplish a successful reconstruction and avoid complications.

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57
Urethral Reconstruction in Women

Jerry G. Blaivas and Adam J. Flisser

Joan and Sanford Weil College of Medicine, Cornell University, New York, New York, U.S.A.

I. INTRODUCTION

Disorders of the female urethra requiring reconstruction are rare. The most common conditions
requiring reconstruction are urethrovaginal fistula, urethral diverticulum, stricture, damage from
an indwelling catheter, and neoplasm. Surgical injury to the urethra is relatively rare, generally a
complication of urethral diverticulectomy or incontinence surgery (1), and considerably less
frequent than iatrogenic injury to the bladder or ureter. Urethrovaginal fistulae develop as a con-
sequence of obstetrical trauma, surgical injury during vaginal and pelvic surgical procedures,
erosion of synthetic materials placed near the urethra including synthetic pubovaginal slings
and vaginal grafts (2,3), neoplasm, and radiotherapy (4). The diagnosis of urethrovaginal fistula
is made by history and physical examination in the majority of cases, but in some instances,
particularly when there is erosion of a synthetic pubovaginal sling, it is appreciated only at
the time of cystoscopy.
Obstetric injuries are rare in industrial countries, but are not uncommon in the developing
world, where access to modern obstetric care is comparatively limited. The overwhelming
majority of genitourinary fistulae resulting from obstetric etiologies are due to prolonged
labor with compression of the fetal head against the undersurface of the pubis, causing pressure
necrosis of the bladder neck and urethra (5,6), and resulting in vesicovaginal, vesicouterine, or
ureteral fistulae; urethral fistula is relatively rare. Following this, surgical complications from
cesarean section for prolonged, obstructed labor, with or without hysterectomy, are the next
most common cause of fistula formation (5,7). Rare causes of fistula related to pregnancy
include complications from operative vaginal delivery (8) and suture erosions from Shirodkar
cerclage (9).
The most common causes of surgical injury to the urethra include urethral diverticulect-
omy, bladder neck suspension procedures, anterior colporrhaphy, and, much less commonly,
vaginal hysterectomy. In our experience, urethral diverticulectomy is a common cause of
urethral compromise (10). This most likely results from failure to obtain a tension-free closure
of the urethral defect created by excision of the diverticulum. During bladder neck suspension,
an unrecognized injury to the bladder or urethra may occur, or an errant suture may result in
tissue necrosis and subsequent fistula formation (11). We have also seen several patients who
sustained extensive tissue loss after a seemingly simple Kelly plication; pressure necrosis of
the urethra may have resulted from plication sutures that were tied too tightly around a urethral
841
842 Blaivas and Flisser

catheter. It is more common for long-term indwelling urethral catheters to cause pressure necro-
sis of the urethra, particularly in patients who are comatose or paralyzed (12,13).
Rarely, a large urethral diverticulum can cause pressure necrosis of the entire musculofas-
cial structure of the urethra, without any obvious signs or symptoms. MRI may reveal the
presence of this problem, but in most cases that we have seen the diagnosis was not apparent
until the time of surgery, after the diverticulum had been unroofed to expose a markedly attenu-
ated urethral wall; sometimes the urethral wall is composed of nothing more than mucosa.
Pelvic trauma may result in fracture or separation of the symphysis pubis and laceration of
the urethra and/or vesical neck (14 –16). There may be local invasion of the urethra or bladder
neck from carcinoma of vagina or cervix, or there can be extensive fibrosis of the urethra as a
consequence of radiation treatment of adjacent cancers (17). In some patients, urethral abnorm-
alities may not be manifest or apparent for months or even years after the precipitating event (4).
Regardless of the cause of urethral damage, the diagnostic and therapeutic challenges to the
surgeon are considerable. The goals of surgical correction are to create a continent urethra of appro-
priate length that permits the volitional, painless, and unobstructed passage of urine. In our experi-
ence, these goals can almost always be accomplished with a single operative procedure.

II. DIAGNOSIS

In most patients the diagnosis is apparent at the time of vaginal examination, yet we have been
surprised to see many patients in whom urinary leakage has been attributed to sphincteric incon-
tinence alone. This observation underscores the dictum that sphincteric incontinence should not
be definitively diagnosed unless an episode of incontinence is witnessed by the examiner.
A simple test to remove doubt that the urinary leakage is coming from the urethral meatus is
to occlude the meatus with a finger and have the patient cough or strain (with a comfortably
full bladder) while downward pressure is exerted on the posterior vaginal wall. This maneuver
usually allows visualization of vaginal urinary leakage even when the fistula itself cannot be
seen clearly.
Cystoscopy and pelvic examination are essential in order to evaluate (a) the extent of the
anatomic defect, (b) the possibility of unrecognized secondary fistulae, (c) the pliability of local
tissue, (d) the need for securing bulk-ensuring tissue pedicle flaps, (e) the need for concomitant
pelvic reconstructive surgery, and (f ) the timing of surgery. Coexisting vesicovaginal fistulae
are usually apparent at cystoscopic examination. If a vesicovaginal fistula is suspected but not
seen at the time of cystoscopy, a dye test can be performed by adding Methylene Blue to the
cystoscopy fluid. The vagina should then be inspected for signs of urinary leakage while the ure-
thra is occluded with a Foley balloon catheter.
In many patients, videourodynamic testing provides important information about urinary
incontinence, as well as the presence or absence of urethral obstruction, low bladder compliance,
and detrusor instability. Whenever there is surgical or obstetric damage to the urethra, one must
have a high index of suspicion that there are concomitant abnormalities such as vesicovaginal
or ureterovaginal fistula, ureteral obstruction, low bladder compliance, vesicoureteral reflux,
detrusor instability, or intrinsic sphincteric deficiency. In particular, neither a urethrovaginal fis-
tula nor a destroyed distal urethra causes urinary incontinence unless the proximal urethra and
vesical neck are also damaged. Sometimes, when the vesical neck remains intact, there may be
loss of the entire remaining portion of the distal urethra without any symptoms at all. These
lesions are generally discovered incidentally on physical examination and require no treatment
unless they are symptomatic. A careful, logically ordered evaluation is thus essential in all
patients to determine the underlying pathophysiology of their incontinence.
 Urethral Reconstruction in Women 843

Owing to the incidence of complicated occult fistulae in patients who have what appears to be
simple pathology, we recommend that intravenous pyelography be performed in all patients except
those in whom it is medically contraindicated. If ureteral injury is suspected, retrograde pyelogra-
phy should be performed, even in patients with a normal-appearing intravenous pyelogram.
Pelvic fractures may cause lower urinary tract symptoms in women due to sphincteric
damage, urethrovaginal fistula, or urethral stricture. The first two conditions are usually apparent
on physical examination with a full bladder; the last is suggested by a low flow rate and
confirmed by cystoscopy and videourodynamic testing.

III. INDICATIONS FOR SURGERY

The mere presence of extensive urethral damage is not an indication for surgery. The two main
relative indications for reconstruction are sphincteric incontinence and urethral obstruction. If
there is an associated condition, such as a vesicovaginal fistula, it should be repaired at the
same time. When sphincteric incontinence is present preoperatively, we believe that it should
be surgically corrected at the time of urethral reconstruction. In general, we prefer to
construct a fascial pubovaginal sling (18, Chaikin, 1998) with an interposed free graft of labial
fat (10,18 – 20) between the sling and the reconstructed vesical neck. Others have recommended
transvaginal bladder neck suspension in patients with less extensive anatomic damage and
incontinence due to urethral hypermobility (21).
Patients with urethral pathology who also suffer from disorders of detrusor function such
as impaired detrusor contractility, detrusor instability, or low bladder compliance, in our experi-
ence, have improved after successful surgical repair of their urethral pathology. Accordingly,
we do not recommend concomitant surgical intervention to treat these conditions at the time
of urethral reconstruction. One exception to this rule is low bladder compliance secondary to
radiation cystitis: in these patients, the effects of radiation on the bladder and urethra are usually
so severe that reconstructive surgery has a limited chance for success. It is usually best to
perform continent supravesical urinary diversion in lieu of urethrovesical reconstruction.

IV. TIMING OF SURGERY AND PREOPERATIVE MANAGEMENT

In the past, much controversy surrounded the timing of surgical repair. While for decades it had
been taught that surgery should be delayed for 3– 6 months or longer to allow adequate time for
tissue inflammation and edema to subside, there are abundant recent studies that suggest surgery
can be performed safely as soon as the vaginal wound is free of infection and inflammation and
the tissues are reasonably pliable (22 – 29). It is usually possible to perform the surgical repair
within 3– 6 weeks after the precipitating event; we have performed one reconstruction as
early as 7 days after obstetric trauma.
Management of incontinence during this interim period is often a difficult problem, and in
some patients Foley catheter drainage is insufficient. If significant leakage occurs with a Foley
catheter in place we generally recommend that the catheter be discontinued and the patient be
managed with superabsorbent incontinence pads.

V. GENERAL PRINCIPLES OF SURGICAL TECHNIQUE

Urethral reconstruction is technically demanding and requires a considerable degree of experi-

ence and skill. In inexperienced hands the risks may be prohibitive, and in some instances,
844 Blaivas and Flisser

when there is insufficient local tissue for reconstruction, it may be prudent to consider urinary
diversion rather than urethral reconstruction. The most important principles of surgical repair
include clear visualization and exposure of the operative site; creation of a tension-free, mul-
tiple-layered closure; assurance of an adequate blood supply; and adequate bladder drainage.
A tension-free closure can usually be accomplished by wide mobilization of surrounding tissue
but sometimes requires the use of local pedicle flaps or relaxing incisions in the anterior vaginal
wall. These are the same principles that should be employed to prevent urethral damage and fis-
tula formation after urethral diverticulectomy. We regard a urethral diverticulum as if it were a
urethrovaginal fistula that has not yet penetrated the vagina, and repair it accordingly.
In a woman with a damaged urethra, the vaginal tissue is often scarred, fibrotic, and
ischemic. Careful examination of the vagina is necessary prior to surgery to determine the actual
extent of urethral tissue loss and to assess the availability of local tissue for use in the reconstruc-
tion. In most instances sufficient anterior or lateral vaginal wall tissue can be mobilized and
rolled into a tube or patch graft for urethral reconstruction (6,10,18,20,21,30,31).
After reconstruction of the urethra it is usually advisable to interpose a well-vascularized
pedicle flap over the site of the repair. Various sources of tissue have been successfully used,
including the labia majora (18,21,32,33, Symmonds, 1928); rectus abdominus muscle
(30,34 – 38); gracilis myocutaneous (10); and perineal artery axial fasciocutaneous (Singapore)
flap (39).
To promote healing and prevent postoperative trauma to the repair site, bladder drainage is
best accomplished with a large suprapubic catheter placed at the beginning of the procedure. In
addition, we recommend the postoperative use of a urethral catheter as a stent. It is crucial that
the catheter be fixed to the anterior abdominal wall using adhesive dressings or sutures, in order
to prevent tension on the reconstruction while enabling the catheter to maintain urethral patency.

VI. SURGICAL APPROACH

There are three broad approaches to urethral reconstruction: anterior bladder flaps (21,40);
posterior bladder flaps (41); and vaginal wall flaps (6,10,20,30,31). These techniques appear
to have comparable success with respect to the creation of a neourethra, but continence is
achieved in only 50% of women who undergo anterior or posterior bladder flaps (21,40,41).
We believe that vaginal reconstruction with concomitant anti-incontinence surgery is consider-
ably easier, faster, and associated with much less morbidity than the bladder flap operations, and
for that reason we have of late found it unnecessary to employ these operations.

VII. RECONSTRUCTIVE TECHNIQUES

There are four basic techniques for urethral reconstruction: primary closure; lateral tube flaps;
advancement flaps; and labia minora pedicle grafts. In rare instances it may be necessary to
consider a myocutaneous flap, but this has never been necessary in our series.
The patient is placed in the dorsal lithotomy position, and cystourethroscopy is performed
to assess the relationship of the ureteral orifices to the damaged urethra. If the ureteral orifices
are in close proximity to the fistula, ureteral stents are placed and then removed at the end of the
case. A percutaneous suprapubic cystotomy tube (at least 14F) is placed and sewn to the anterior
abdominal wall unless a pubovaginal sling is planned, in which case this is deferred until the
sling has been harvested. A 16F Foley catheter is inserted into the bladder, and the balloon is
inflated with enough fluid to hold it securely at the vesical neck.
 Urethral Reconstruction in Women 845

The choice of incision depends on the amount of tissue loss and the local anatomy. Before
incising the vaginal wall for any concurrent procedures, such as pubovaginal sling, it is critical to
select the site and shape of the incisions that will be used for urethral reconstruction.
Any incisions will irreversibly determine the location and extent of vascularized vaginal tissue
available for the repair. For example, if an inverted U-shaped incision is made in the anterior
vaginal wall in anticipation of advancing it to cover the reconstruction, that tissue can no longer
be used as an advancement flap for urethral reconstruction should that prove necessary. Alter-
natively, if the surgeon chooses to make two parallel incisions alongside the intended site
of the urethra in order to create a tube graft, it is important to be sure that the distance between
the two incisions is sufficient so that the flaps can be closed over the entire circumference of the
catheter without any tension.

A. Primary Closure
Successful tension-free primary closure is possible for small urethral defects. The defect is
circumscribed widely enough so that the edges of the fistula tract can be approximated in the
midline without any tension (Fig. 1). We prefer to close the urethra with 3 : 0 or 4 : 0 chromic
catgut rather than longer-acting synthetic absorbable sutures because in our experience the latter
are subsequently associated with increased dysuria and pain during urethral instrumentation.
Since there is usually insufficient urethral wall tissue to allow approximation without narrowing
the urethra, it is rarely possible (or necessary) to excise the fistula tract. A second layer of
periurethral tissue is approximated as a horizontal layer whenever possible. Only after the repair
has been completed is the decision made regarding how to cover the wound. In some instances it
is possible to elevate lateral flaps and suture them in the midline over the wound. Alternatively,
an inverted U-shaped incision can be advanced. If a Martius labial fat pad graft is needed, it is
prepared prior to closure of the wound (Fig. 2). If a pubovaginal sling is necessary, the fat
pad graft is placed between the sling and urethra. The vaginal incision is closed with 2 : 0 or
3 : 0 chromic catgut.

B. Advancement Flap
If lateral flaps cannot be mobilized owing to insufficient vaginal tissue lateral to the urethral
pathology, it may be possible to repair the urethra and cover the repair with an advancement
flap from the vaginal wall cephalad to the damaged site. A U-incision is made in the anterior
vaginal wall long enough to be advanced and rotated to form the posterior and lateral walls
of a neourethra (Fig. 3). The flap is mobilized with a Metzenbaum scissors, reflected caudally,
and sutured in place over the urethral catheter. The resulting defect in the anterior vaginal wall
can sometimes be repaired by undermining the lateral and cranial wound edges, but in some
instances pedicle flaps may prove necessary.

C. Tube Graft (Fig. 4)

If there is extensive loss of the urethra and sufficient vaginal wall tissue, a rectangular incision
can be made wide enough to allow the vaginal wall to be rolled into a tube over a 16F catheter
and sewn in the midline without tension. A Martius flap (or other vascularized graft) and pub-
ovaginal sling are usually necessary to promote successful wound healing and continence. The
vaginal wall can be closed primarily, or, if there is insufficient tissue for primary closure, it is
usually possible to elevate another broad-based vaginal or labia minora pedicle graft to cover
the wound. We have found gracilis myocutaneous and rectus pedicle grafts to be unnecessary.
846 Blaivas and Flisser

Figure 1 Primary closure of small urethral defect. (A) The small urethral fistula is circumscribed and an
inverted “U” incision made. (B) Modified from Blaivas (10) The “U” incision is reflected cranially and
laterial flaps created. (C) The fistulae is closed with interrupted 3-0 or 4-0 chromic suture and the U flap
closed over the defect.

D. Labia Minora Pedicle Graft

When there is insufficient local vaginal wall tissue to use for the reconstruction, a labia minora pedi-
cle graft is the next choice. An oval-shaped incision is made in an adjacent hair-free portion of the
labia minora as close to the site of the urethra as possible (Fig. 5). The size of the incision should be
large enough to roll into a tube around a 16F catheter or to be used as a patch graft over the catheter
and allow loose approximation over the catheter. The incision is deepened around the labia and a
pedicle graft is raised on an anterior- or posterior-based blood supply. The graft is passed beneath
the vaginal wall and rotated so that the mucosal surface forms the inner wall of the reconstructed
urethra. In some patients it is not possible to create a tunnel for passage of the graft because of
 Urethral Reconstruction in Women 847

Figure 2 Martius graft. (A) An incision in the labia majora exposes the fat pad, which is freed from its
posterior attachments using sharp dissection. A vaginal incision is made in the lateral vaginal wall to provide
a passage for the graft. (B) The flap is mobilized through an incision in the lateral vaginal wall and sutured in
place over the reconstruction using absorbable suture. The vagina is then closed over the graft. Modified
from Rock (48).

extensive scarring, in which case an incision is made in the vaginal wall between the site of the new
urethra and the graft. It is usually possible to elevate flaps to cover the graft.
At the conclusion of the reconstructive procedure, the Foley catheter is fixed to the anterior
abdominal wall with a gentle loop to insure that undue tension is not placed on the urethra, preventing
both traumatic disruption of the repair and pressure necrosis. A Penrose drain should be placed for
drainage of the labial harvest sites for the Martius or labia minora flap, if one has been used.

VIII. POSTOPERATIVE CARE

The Penrose drain is removed as soon as there is minimal drainage, usually on the first
postoperative day. The urethral wound and catheter are checked frequently to be sure that
848 Blaivas and Flisser

Figure 3 Advancement flap. (A) A U-shaped incision is made in the anterior vaginal wall. (B) The U
shaped flap is rotated distally and sutured in place to form the posterior wall of the urethra. (C) The
vaginal wall is oversewn using interrupted sutures. (D) The completed repair. Modified from Rock (48).

there is no tension or pressure on the suture line. The urethral catheter is removed as soon as
feasible, usually within the first 2 –5 days, but always before the patient is discharged from
the hospital. A voiding cystourethrogram is performed though the suprapubic catheter on postop
day 14. If the patient voids successfully and there is no extravasation, the suprapubic tube is
removed. Otherwise, another voiding trial is undertaken 2 –4 weeks later.

IX. ANCILLARY PROCEDURES OFTEN USED WITH URETHRAL

RECONSTRUCTION
A. Pubovaginal Sling (Fig. 6)
A slightly curved transverse lower abdominal incision is made just below the pubic hairline and
carried down to the rectus fascia. The surface of the rectus fascia is dissected free of subcutaneous
tissue, and a suitable site is selected for excision of the fascial strip that will be used for the sling.
 Urethral Reconstruction in Women 849

Figure 4 Tube graft. (A) Following mobilization of the vaginal wall, a rectangular incision is made
around the urethral meatus. (B) The vaginal wall is rolled into a tubular neourethral over the urethral
catheter. (C) Martius graft interposition. (D) The vaginal wall is closed and a Penrose drain is placed in
the labial wound. Modified from Blaivas (10).

Two parallel horizontal incisions 2 – 3 cm apart are made in the midline of the rectus fascia. The
incisions are extended superolaterally for the entire width of the wound, following the direction
of the fascial fibers. The undersurface of the fascia is freed from muscle and scar. Prior to excising
the strip, each end of the fascia is secured with a long 2 : 0 monofilament nonabsorbable suture
using a running horizontal mattress stitch placed at right angles to the direction of the fascial
fibers. No attempt is made to mobilize the bladder or vesical neck from above.
850 Blaivas and Flisser

Figure 5 Labia minora flap. (A) An oval-shaped incision is made in the labia minora, which is then
reflected medially and sutured over the urethral catheter with chromic suture. (B) The closed labial and
urethral operative sites.

Once the appropriate incision for urethral reconstruction has been made in the anterior
vaginal wall, the lateral edges of the vaginal wound are grasped with Allis clamps and retracted
laterally. The dissection continues just beneath the vaginal epithelium with Metzenbaum scis-
sors pointed in the direction of the patient’s ipsilateral shoulder until the periosteum of the
pubis or ischium is palpated with the tip of the scissor. During this part of the dissection, it is
important to stay as far laterally as possible. This is best accomplished by dissecting with
the concavity of the scissors pointing laterally and by exerting constant lateral pressure with
the tips of the scissors against the undersurface of the vaginal epithelium. When the periosteum
is reached, the endopelvic fascia is perforated and the retropubic space entered. In most instances
this is easily accomplished by blunt dissection with the surgeon’s index finger. The tip of the
finger opposite the nail palpates the periosteum. The bladder and urethra are mobilized medially
as the finger advances and perforates the fascia, which frees the vesical neck and proximal ure-
thra from their vaginal attachments. In some instances this dissection must be performed sharply
with Metzenbaum scissors.
The surgeon’s left index finger is reinserted in the vaginal wound, retracting the vesical
neck and bladder medially. The inferior edge of the rectus fascia is grasped with a Kocher
clamp, and the right index finger is passed beneath the fascia and slides along the undersurface
of the pubis until the two fingers are touching. A long curved clamp (DeBakey) is inserted into
the incision and directed to the undersurface of the pubis. The tip of the clamp is pressed against
the periosteum and directed toward the index finger that is retracting the vesical neck and blad-
der medially. In this fashion, the clamp is guided into the vaginal wound. When the tip of the
clamp is visible, one end of the long suture, which is attached to the fascial graft, is grasped
and pulled into the abdominal wound. The procedure is repeated on the other side. An incision
is made in the rectus fascia just above the pubis lateral to the midline on either side just large
 Urethral Reconstruction in Women 851

Figure 6 Pubovaginal sling. (A) A Pfannenstiel incision is made exposing the rectus fascia. A 2 – 3-cm-
wide rectus fascial strip is harvested through a Pfannenstiel incision. (B) Prior to harvesting the sling, a 2-0
Prolene suture is placed at the sling margin, securing the end. (C) After the sling is secured with sutures at
both ends, the sling is removed. (D) Dissection with a Metzenbaum scissor into the retropubic space opens
the avascular plane beneath the vaginal epithelium. Modified from Blaivas (49). (Continued)

enough to accept the sling. The long ends of the suture attached to the sling are grasped and
pulled through the fascial incisions on either side. The rectus fascia is closed with a running
monofilament absorbable 2 : 0 suture. The fascial sling is now positioned from the abdominal
wall on one side around the undersurface of the vesical neck and back to the abdominal wall
on the other side. At the conclusion of the operation, the long ends of the sling are tied together
in the midline over the rectus fascia without any tension at all. The Martius flap is sewn in place
between the sling and the reconstructed urethra.
852 Blaivas and Flisser

Figure 6 (Continued) (E) Digital dissection perforates the retropubic space. (F) Using the vaginal index
finger to displace the urethra laterally, a long curved clamp is placed transabdominally onto the lateral
aspect of the vaginal finger. (G) The clamp is then threaded into the vagina. (H) The sling is then
secured with no tension by tying the sutures superficial to the closed rectus fascia. The sling is placed
superficial to the graft, and the vagina is closed directly over the sling.

B. Martius Flap (Fig. 2)

A vertical incision is made over the labia majora and carried down through Scarpa’s fascia. The
fat pad is mobilized being careful to preserve the pudendal artery, which arises from the pos-
terior portion of the wound. The fat pad is tunneled underneath the vaginal epithelium and
sewn in place over the suture lines of the neourethra. If a single labial fat pad graft does not pro-
 Urethral Reconstruction in Women 853

vide adequate coverage, a second graft may be obtained from the other side or a gracilis, peri-
neal, or rectus pedicle graft may be harvested; in practice, this will rarely be necessary. The pedi-
cle graft is placed between the sling and the reconstructed urethra. The vaginal wall is then
closed over the Martius flap.

C. Labia Minora Flap (Fig. 7)

A U-shaped incision is made in the hair-free portion of the labia minora being careful to preserve
the posterior and inferior labial blood supply. The fat pad is mobilized and the flap is rotated
medially. It may be rotated 1808 and used as a patch graft to reconstruct the urethra or left in
its anatomic position to cover the vaginal wound.

X. RESULTS

To date there have been few studies concerning reconstruction of the severely damaged urethra
(Table 1). Overall, successful anatomic reconstructions were reported in 67– 100% of women.
Most authors emphasized the need for well-vascularized pedicle flaps to ensure a successful out-
come. Continence was achieved in 55– 93% after a single operation, and postoperative urethral
obstruction was reported in 2 –41%. In the great majority of studies, the criteria for incontinence
and urethral obstruction were not specified, and, especially in view of lack of follow-up, the
results cited above should be considered optimistic. It does seem evident, however, that it is
important to perform an anti-incontinence procedure at the same time as the urethral reconstruc-
tion. Failure to do so resulted in incontinence rates varying from 50% to 84%. Most reports
indicated that secondary procedures to correct incontinence were successful in the majority of
patients.
Prior to this report, the largest series of urethral injuries was published by Hamlin and
Nicholson (20). All of the women suffered childbirth injuries, and all were quite extensive,
usually involving both the urethra and bladder. An excellent anatomic repair was achieved in

Figure 7 Labia minora flap. (A) A section of the labia minora is mobilized using sharp dissection, and
rotated into position to supply the posterior wall of the neourethra. (B) The flap is rotated and the vaginal
incisions closed with 3-0 chromic suture.
854 Blaivas and Flisser

Table 1 Studies Concerning Reconstruction of Severely Damaged Urethra

Author Number Continence (%) Cure/improved (%) Anatomic repair Obstruction (%)

Bruce (34) 6 83 100 100% 0%

Leng (23) 4 75 75 100% —
Blaivas (10) 49 90 92 96% 2
Tance (42) 34 — 82 82% —
Elkins (19) 20 50 55 90% 10
Mundy (43) 30 93 — 93% 41
Patel (44) 9 — 78 9/9 0
Morgan, 1978 9 56 89 100% 11
Elkins (30) 6 10 83 67% 17
Hamlin (20) 50 80 84 98% 12
Gray (6) 10 50 50 —
Symmonds (31) 20 65 90 85 —

49 of the 50 women, but eight (16%) had severe incontinence and many more had lesser degrees
of incontinence. Incontinence was usually cured after a second procedure.
Elkins et al. (19) reviewed the results of 36 vesicovaginal and/or urethrovaginal fistula
repairs performed by American visiting professors in West Africa. All of the vesical neck and
urethral fistulas resulted from obstructed labor. In this series, two of 13 proximal urethral fistulas
were complicated by “severe stress urinary incontinence” postoperatively. Bazeed et al. (7)
reviewed 86 cases of urovaginal fistulae in Egypt, including 13 cases of urethral fistula: two
patients had neourethras created, and 11 of 13 were corrected by simple repair, with three
failures.
We have operated on 98 women with extensive anatomic vesical neck and urethral defects.
The causes of the injury are listed in Table 2. All but one patient underwent a vaginal reconstruc-
tion (one patient had a Tanagho anterior bladder flap, which failed). Two patients with squamous
cell carcinoma of the distal third of the urethra underwent wide excision and urethral reconstruc-
tion with adjacent flaps. We used a Martius flap in all of the remaining patients except one who
had a gracilis flap. We have previously published the results of 49 of these women (10). Early in
our series, we did not routinely perform concomitant pubovaginal slings, and 50% of the women
who underwent a modified Pererya procedure had persistent sphincteric incontinence; all
were subsequently cured by a pubovaginal sling. Three of the remaining women developed
sphincteric incontinence; in one patient this was associated with necrosis of the reconstructed
urethra. Necrosis of the flap occurred in three patients, one had a previously unrecognized
vesicovaginal fistula, and one had urethral obstruction due to the pubovaginal sling. All but
one of the failures subsequently underwent reoperation, and all had a successful outcome. No
patient required intermittent catheterization, and at 1 year after their last surgery all were dry
(except for the one woman who refused reoperation).

XI. BLADDER FLAP TECHNIQUES

We believe that bladder flap reconstructions are almost never necessary in these patients, and the
single patient in whom we performed this procedure failed because of refractory detrusor
instability; however, these procedures can provide an alternative in patients in whom the extent
or location of the urethral pathology discourages a vaginal wall technique.
 Urethral Reconstruction in Women 855

Table 2 Causes of Urethral Damage in a Case Series of 98

Women

Cause Number

Transvaginal bladder neck suspension 27

Urethral diverticulectomy 26
Anterior colporraphy 13
Synthetic pubovaginal sling 9
Urethral diverticulum 9
Childbirth 5
Urogenital cancers 5
Trauma 2
Cesarean section 1
Vaginal hysterectomy 1
Total 98

Source: Blaivas, 1966.

The basic procedure is depicted in Figure 8 (40). In an extensive series, Elkins et al.
(19,21) reported their experience with a Tanagho-like procedure in 20 West African women
with extensive urethral damage due to obstructed labor. These patients all had large vesicova-
ginal fistulas, and because of extensive scarring, were not suitable for vaginal flap techniques.
The procedure was performed entirely via a vaginal approach: “The anterior and lateral fistula
edges are dissected sharply away from the pubic bone beneath the arch of the pubic ramus, thus
entering the retropubic space . . . from the vagina . . . the anterior bladder wall is dissected free of
surrounding tissues to the level of the peritoneal reflection” (21). The anterior bladder was mobi-
lized and a 3  3 cm flap was raised and rolled into a tube over a 16F catheter. The new urethra
was sutured either to the remaining distal urethra or at the site of the new meatus. The posterior
edges of the vesicovaginal fistula were approximated and “fixation sutures (were) placed through
the top portion of the neo-urethra to reattach the urethra to the base of the pubic periosteum.” In
the last three patients a modified Peyrera procedure was performed instead. A Martius fat pad
graft was then placed beneath the suture lines.
Eighteen of the 20 women so treated had a satisfactory anatomic repair of the fistula, but
four of the 18 had persistent stress incontinence that required further surgery. Two others had
refractory detrusor instability or low bladder compliance.

XII. CONCLUSION

Reconstruction of the severely damaged urethra is a technically challenging undertaking that

requires considerable surgical expertise. The vast majority of women with traumatic injuries
have sufficient vaginal tissue for a vaginal flap reconstruction, and we believe that the vaginal
approach offers the best chance for a successful outcome. However, in patients with extensive
vaginal scarring from childbirth injuries such as those reported by Elkins, bladder flap tech-
niques may be useful. The most important general principles are (a) adequate exposure of the
operative site; (b) careful selection of the vaginal incisions; (c) a tension-free, multiple-layered
closure; (d) assurance of an adequate blood supply, through a vascular graft; (e) concomitant
pubovaginal sling when anti-incontinence surgery is indicated; (f ) adequate bladder drainage;
and (g) meticulous attention to catheter care to prevent damage to the repair. Adherence to
856 Blaivas and Flisser

Figure 8 Tanagho procedure. (A) Anterior bladder wall flap is selected, mobilized, and held with
suspension sutures. (B) Urethra is transected at site of fistula. (C) The bladder flap is tubularized. (D)
The posterior bladder is closed. (E) The neourethra is sutured to the distal urethra.

these principles will substantially increase the chances for a successful reconstruction of the
urethra.

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 Urethral Reconstruction in Women 857

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17. Boronow RC, Rutledge F. Vesicovaginal fistula, radiation, and gynecologic cancer. Am J Obstet
Gynecol 1971; 111:85.
18. Blaivas JG. Female urethral reconstruction. In: Webster G, ed. Reconstructive Urology. Boston:
Blackwell Scientific Publications, 1993:873 – 886.
19. Elkins TE, DeLancey JO, McGuire EJ. The use of modified Martius graft as an adjunctive technique
in vesicovaginal and rectovaginal fistula repair. Obstet Gynecol 1990; 75:727 – 733.
20. Hamlin RHJ, Nicholson EC. Reconstruction of urethra totally destroyed in labor. BMJ 1969; 1:147.
21. Elkins TE, Ghosh TS, Tagoe GA, Stocker R. Transvaginal mobilization and utilization of the
anterior bladder wall to repair vesicovaginal fistulas involving the urethra. Obstet Gynecol 1992;
79(3):455– 460.
22. Blaivas JG, Heritz DM, Romanzi LJ. Early vs. late repair of vesicovaginal fistulas: vaginal and
abdominal approaches. J Urol 1995; 153:1110.
23. Leng WW, Amundsen CL, McGuire EJ. Management of female genitourinary fistulas: transvesical or
transvaginal approach? J Urol 1998; 160:1995.
24. Persky L, Herman G, Guerrier K. Nondelay in vesicovaginal fistula repair. Urology 1979; 13:273.
25. Wang Y, Hadley HR. Nondelayed transvaginal repair of high lying vesicovaginal fistulas. J Urol
1990; 144:34.
26. Badenoch DF, Tiptaft RC, Thakar DR, Fowler CG, Blandy JP. Early repair of accidental injury to the
ureter or bladder following gynaecological surgery. Br J Urol 1987; 59:516.
27. Cruikshank SH. Early closure of post-hysterectomy vesicovaginal fistulas. South Med J 1988;
81:1525.
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neal flap. J Urol 1993; 150:56.
29. O’Conor VJ Jr. Repair of vesicovaginal fistula with associated urethral loss. Surg Gynecol Obstet
1978; 146:251.
30. Ellis LR, Hodges CV. Experience with female urethral reconstruction. J Urol 1969; 102:214.
31. Symmonds RE. Loss of the urethral floor with total urinary incontinence: a technique for urethral
reconstruction. Am J Obstet Gynecol 1968; 103(3):665– 678.
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32. Carr LK, Webster GD. Full-thickness cutaneous Martius flaps: a useful technique in female recon-
structive urology. Urology 1996; 48:461.
33. Chassagne S, Haab F, Zimmern P. The Martius flap in vaginal surgery: technique and indications.
Prog Urol 1997; 7:120.
34. Bruce RG, El-Galley RES, Galloway NTM. Use of rectus abdominis muscle flap for the treatment of
complex and refractory urethrovaginal fistulas. J Urol 2000; 163:1212.
35. Fenner GC, Ahn CY, Shaw WW. The use of muscle flaps for coverage of perineal defects. In: Ehrlich RM,
Alter GJ, eds. Reconstructive and Plastic Surgery of the External Genitalia: Adult and Pediatric. Philadel-
phia: W.B. Saunders, 1998:423–435.
36. Tobin GR, Day TG. Vaginal and pelvic reconstruction with distally based rectus abdominis myocu-
taneous flaps. Plast Reconstr Surg 1988; 81:62.
37. Tobin FR. Pelvic, vaginal and perineal reconstruction in radical pelvic surgery. Surg Oncol Clin
North Am 1994; 3:397.
38. Wall LL, Copas P, Galloway NT. Use of pedicled rectus abdominis muscle flap sling in the treatment
of complicated stress urinary incontinence. Am J Obstet Gynecol 1996; 175:1460.
39. Zinman L. Use of myocutaneous and muscle interposition flaps in management of radiation-induced
vesicovaginal fistula. In: McDougal WS, ed. Difficult Problems in Urologic Surgery. Chicago: Year
Book, 1989:143 – 163.
40. Tanagho EA. Bladder neck reconstruction for total urinary incontinence: 10 years of experience.
J Urol 1981; 125:321.
41. Leadbetter GW Jr. Surgical correction of total urinary incontinence. J Urol 1964; 91:261.
42. Tancer ML. A report of thirty-four instances of urethrovaginal and bladder neck fistulas. Surg
Gynecol Obstet 1993; 177(1):77– 80.
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fistulas with modified Ingelman-Sundberg and Martius operations. J Urol 1980; 123:653.
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vesicovaginal fistula involving the internal urinary sphincter. Eur Urol 1995; 27:241.
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18:409.
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JB Lippincott Co., Philadelphia, 93–101, 1990.
58
Radical Cystectomy and Orthotopic
Neobladder Substitution in the Female
David A. Ginsberg and John P. Stein
University of Southern California, Los Angeles, California, U.S.A.

I. INTRODUCTION

The primary mode of therapy for muscle-invasive bladder cancer is radical cystectomy and
lower urinary tract reconstruction. Over the past several decades numerous advances in chemo-
therapy, intravesical immunotherapy, and bladder preservation protocols have been identified
in the treatment of bladder cancer. However, none of these treatment modalities are able to
achieve the survival rates of primary surgical management in the patient with invasive bladder
cancer. As we enter the 21st century, urinary diversion after radial cystectomy has reached a
new era. The ultimate goal of lower urinary tract reconstruction has become not only a means
to divert urine and protect the upper urinary tract, but also to provide patients a continent
means to store urine and allow for volitional voiding through the intact native urethra. These
advances in urinary diversion have been made in an effort to provide patients a more normal life-
style and positive self-image following cystectomy. In addition, these advances have lessened the
impact of surgery and allowed for a more aggressive approach in patients with higher grade (but
less invasive) lesions as well as patients with carcinoma in situ refractory to intravesical therapy.
Transitional cell carcinoma (TCC) of the bladder is the second most common malignancy
and cause of death of all genitourinary tumors. Although bladder cancer is more common in men
(ratio of 2.7 : 1), it continues to be a considerable source of morbidity and mortality in women.
Approximately 75 – 85% of patients with primary TCC of the bladder present with low grade
tumors, superficial tumors. Up to 75% of these superficial tumors recur, but the majority are
amenable to repeat transurethral resection and selected administration of intravesical immuno-
or chemotherapy as needed (1 –3).
However, 20 –40% of all patients with transitional cell carcinoma of the bladder will either
initially present with, or develop, an invasive carcinoma of the bladder. Invasive bladder cancer
includes a spectrum of tumors. Traditionally, tumor invasion of the bladder muscularis has been
the primary indication for aggressive surgical therapy. In addition, there is sufficient evidence to
suggest that high-grade tumors that invade the lamina propria (T1), superficial bladder tumors
with lymphovascular invasion (4,5), and lesions that are associated with carcinoma in situ
(6,7) in conjunction with a poor response to repeated transurethral resection and intravesical
therapy (8) are also at high risk for progression (3,4,8 – 13) and warrant an early aggressive
management.
859
860 Ginsberg and Stein

Radical cystectomy provides the optimal result with regard to accurate pathologic staging,
prevention of local recurrence, and overall survival in both male and female patients. Improve-
ments in medical, surgical, and anesthetic techniques over the past several decades have
dramatically decreased the morbidity and mortality associated with radical cystectomy. Prior
to 1970, the perioperative complication rate of radical cystectomy was reportedly close
to 35%, with a mortality rate of nearly 20%. This has dramatically diminished to a ,10%
complication rate and 2% mortality rate reported in contemporary series (2).
In addition, efforts have been made to provide an acceptable and functional form of urinary
diversion in women without compromise of a sound cancer operation. Two important criteria
must be fulfilled when considering any patient for orthotopic urinary diversion. First, under
no circumstance must the cancer operation be compromised by the reconstruction at the
urethroenteric anastomosis, retained urethra, or surgical margins. Second, the distal urethral
sphincteric mechanism must remain intact to provide a continent means of storing urine.
If these criteria can safely be maintained, the patient may then be considered an appropriate
candidate for orthotopic urinary diversion. We have pathologically demonstrated that the urethra
can be safely preserved in the majority of women with transitional cell carcinoma of the bladder
(14). Sound pathologic criteria in which to safely select appropriate female candidates for
orthotopic reconstruction following cystectomy and has been confirmed by others as well
(15). Currently, intraoperative frozen section of the proximal urethra is the most decisive method
to determine if a female patient may be an appropriate candidate for orthotopic diversion. It
should also be noted that the specific histopathological type of tumor did not preclude orthotopic
diversion as long as the aforementioned criteria for orthotopic reconstruction were maintained.
The initial clinical and functional results with this form of diversion in women have been
excellent (16 – 18). Orthotopic urinary diversion most closely resembles the original bladder in
both location and function, provides a continent means to store urine, and allows volitional void-
ing per urethra. This chapter will focus on the technique of radical cystectomy and orthotopic
diversion in the female patient with particular emphasis in the surgical preparation of the urethra
in women considering orthotopic diversion.

II. DEFINITION

Radical cystectomy (anterior exenteration) in women implies the en bloc removal of the pelvic
organs anterior to the rectum. This includes the bladder, urachus, ovaries, Fallopian tubes,
uterus, cervix, vaginal cuff, and the anterior pelvic peritoneum. The perivesical fat and pelvic
and iliac lymph nodes are also removed en bloc with the specimen. Certain issues regarding
the surgical technique of a radical cystectomy in women are critical in order to minimize
local recurrence and positive surgical margins, maximize cancer-specific survival, maintain
the remaining urethral sphincteric mechanism, and optimize postoperative urinary continence.

III. PREOPERATIVE EVALUATION

The complete evaluation, clinical staging, and decision-making process regarding bladder
cancer is beyond the scope of this chapter. Important points for the female patient in whom
you are considering orthotopic reconstruction at the time of radical cystectomy include exclu-
sion of tumor involving the anterior vaginal wall and bladder neck. If bimanual exam reveals
a deeply invasive posterior lesion with involvement of the anterior vaginal wall, the bladder
and tumor mass should be removed en bloc with the anterior vaginal wall. This may require
vaginal reconstruction if sexual function is desired postoperatively. In addition, women with
 Radical Cystectomy 861

tumor involving the anterior vaginal wall are at increased risk of urethral tumor involvement,
precluding orthotopic urinary diversion (14).
Furthermore, all women should undergo cystoscopic evaluation of the bladder neck (vesico-
urethral junction) as tumor involvement here may also preclude orthotopic reconstruction
(14,18). However, we do not recommend routine preoperative biopsy of this region unless
there is a significant suspicion for tumor because of the potential risk of injuring the continence
mechanism. With a confirmed method to reliably evaluate the proximal urethra (intraopera-
tively), we now rely on intraoperative frozen section analysis of the proximal urethra for proper
patient selection in women considering orthotopic lower urinary tract reconstruction.

IV. SURGICAL TECHNIQUE

A. Preoperative Preparation
Women undergoing radical cystectomy are admitted the morning prior to surgery for a mechan-
ical and antibacterial bowel preparation and intravenous hydration, and to be evaluated and
counseled by the enterostomal therapy nurse. A clear liquid diet may be consumed until mid-
night, at which time the patient takes nothing per mouth. A standard modified Nichols bowel
prep (19) is initiated the morning of admission: 120 mL of Neoloid per mouth at 9:00 AM ;
1 g of neomycin per mouth at 10:00 AM , 11:00 AM , 12:00 PM , 1:00 PM , 4:00 PM , 8:00 PM , and
12:00 AM ; and 1 g of erythromycin base per mouth at 12:00 PM , 4:00 PM , 8:00 PM , and 12:00 AM .
This regimen is well tolerated, obviates the need for enemas, and maintains nutritional and
hydrational support. Intravenous crystalloid fluid hydration is begun in the evening prior to
surgery, and maintained to ensure an adequate circulating volume as the patient enters the
operating room. Intravenous broad-spectrum antibiotics are administered en route to the
operating room, providing adequate tissue and circulating levels at the time of incision.
Preoperative evaluation and counseling by the enterostomal therapy nurse is a critical
component to the successful care of all patients undergoing cystectomy and urinary diversion.
Currently, .85% of female patients requiring cystectomy for bladder cancer undergo orthotopic
diversion at our institution (18). Women who are determined to be appropriate candidates for ortho-
topic reconstruction are instructed how to catheterize per urethra should it be necessary postopera-
tively. Furthermore, all patients are site marked for a cutaneous stoma, instructed in the care of a
cutaneous diversion (continent or incontinent form), and instructed in proper catheterization tech-
niques should medical or technical factors preclude orthotopic reconstruction. The cutaneous stoma
site is determined only after the patient is examined in the supine, sitting, and standing positions.

B. Patient Positioning
The patient is placed in the hyperextended supine position with the iliac crest located just below
the fulcrum of the operating table. All female patients considering orthotopic diversion should
have their legs placed in the modified frog-leg position, which allows easy access to the vagina
(Fig. 1). Care should be taken to ensure that all pressure points are well padded. Reverse
Trendelenberg position levels the abdomen parallel with the floor. The vagina is included in
the prep as to allow for intraoperative access. After the patient is draped, a 20F Foley catheter
is placed in the bladder, and left open to gravity.

C. Incision
A vertical midline incision is made extending from the pubic symphysis to the cephalad aspect
of the epigastrium. The incision should be carried lateral to the umbilicus on the contralateral
862 Ginsberg and Stein

Figure 1 Proper patient positioning for a women undergoing cystectomy. The iliac crest should be
located at the break of the table with the patient in the modified frog-leg position. (From Stein JP
Skinner DG. Radical cystectomy in women. Atlas Urol Clin 1997; 5(2):37–64.)

side of the marked cutaneous stoma site. The anterior rectus fascia is incised, the rectus muscles
are retracted laterally, and the posterior rectus sheath and peritoneum are entered in the superior
aspect of the incision. As the peritoneum and posterior fascia are incised inferiorly to the level of
the umbilicus, the urachal remnant (median umbilical ligament) is identified, circumscribed, and
removed en bloc with the cystectomy specimen (Fig. 2). This maneuver prevents early entry into
a high-riding bladder, and ensures complete removal of all bladder remnant tissue. Care is taken
to remain medial and avoid injury to the inferior epigastric vessels (lateral umbilical ligaments)
that course posterior to the rectus muscles. If the patient has had a previous cystotomy or
segmental cystectomy, the cystotomy tract and cutaneous incision should be circumscribed
full-thickness and excised en bloc with the bladder specimen. The medial insertion of the
rectus muscles attached to the pubic symphysis are then incised, maximizing pelvic exposure
throughout the operation.

D. Abdominal Exploration
A careful systematic intra-abdominal exploration is performed to determine the extent of
disease, evaluate for any hepatic metastases, and rule out evidence of gross retroperitoneal
adenopathy. The abdominal viscera are palpated to detect any unrelated, concomitant disease.
If no contraindications to proceed with surgery exist, all adhesions are incised and freed.
 Radical Cystectomy 863

Figure 2 Wide, en bloc excision of urachal remnant with cystectomy specimen. (From Stein JP, Skinner
DG. Radical cystectomy in women. Altas Urol Clin 1997; 5(2):37–64.)

E. Bowel Mobilization
Bowel mobilization starts with the right colon. A large right-angle Richardson retractor elevates
the right abdominal wall, and the cecum and ascending colon are then reflected medially to allow
incision of the lateral peritoneal reflection along the avascular white line of Toldt. The mesentery
to the small bowel is then mobilized off its retroperitoneal attachments cephalad (toward the
ligament of Treitz) until the retroperitoneal portion of the duodenum is exposed. Combined sharp
and blunt dissection facilitates mobilization of this mesentery along a characteristic avascular
fibroareolar plane. This mobilization is critical in setting up the operative field and facilitates
proper packing of the intra-abdominal contents into the epigastrium.
The left colon and sigmoid mesentery are then mobilized to the region of the lower pole of
the left kidney by incising the peritoneum lateral to the colon along the avascular white line of
Toldt. The sigmoid mesentery is then elevated off the sacrum, iliac vessels, and distal aorta up to
the origin of the inferior mesenteric artery. This provides a mesenteric window through which
the left ureter may pass (without angulation or tension) for later ureteroenteric anastomosis, and
also facilitates retraction of the sigmoid mesentery while performing the lymph node dissection.
864 Ginsberg and Stein

Care should be taken to dissect along the base of the mesentery, preventing potential injury to the
mesenteric blood supply to the colon.
Following mobilization of the bowel, a self-retaining retractor is placed. The right colon
and small intestine are carefully packed into the epigastrium with three moist lap pads, followed
by a moistened towel rolled to the width of the abdomen. The descending and sigmoid colon are
not packed and are left as free as possible, providing the necessary mobility required for the uret-
eral and pelvic lymph node dissection. Packing of the bowel begins by sweeping the right colon
and small bowel under the surgeon’s left hand along the right sidewall gutter. A moist open lap
pad is then swept with the right hand along the palm of the left hand, under the viscera along the
retroperitoneum and sidewall gutter. In similar fashion, the left sidewall gutter is packed. It is
often helpful to have the assistant provide counter traction on the descending or sigmoid
colon at this time to ensure it is left freely mobile. The central portion of the small bowel is
packed with a third lap pad. A moist rolled towel is then positioned horizontally below the
lap pads and cephalad to the bifurcation of the aorta. After the bowel has been packed, a
wide Deaver retractor is placed with gentle traction on the rolled towel to provide adequate
cephalad exposure.

F. Ureteral Dissection
The ureters are most easily identified in the retroperitoneum just cephalad to the common iliac
vessels. They are dissected into the deep pelvis several centimeters beyond the iliac vessels and
divided between two large hemoclips. A section of the proximal cut ureteral segment (distal to
the proximal hemoclip) is then sent for frozen section analysis to ensure the absence of carci-
noma in situ or overt tumor. The ureter is then mobilized cephalad and tucked under the rolled
towel to prevent inadvertent injury. Frequently, an arterial branch from the common iliac artery
or the aorta needs to be divided to provide adequate ureteral mobilization. In addition, the rich
vascular supply emanating from the ovarian vessels within the infundibulopelvic ligament
should also remain intact and undisturbed. These attachments are an important blood supply
to the ureter and help maintain an adequate vascular supply for the ureteroenteric anastomosis
at the time of reconstruction. Leaving the proximal hemoclip on the divided ureter during the
exenteration allows for hydrostatic ureteral dilation and facilitates the subsequent ureteroenteric
anastomosis.

G. Pelvic Lymphadenectomy
A meticulous pelvic lymph node dissection is routinely performed en bloc with radical cyst-
ectomy. When performing a salvage procedure following definitive radiation treatment
(.5000 rads), a pelvic lymphadenectomy is usually not performed because of the significant
risk of iliac vessel and obturator nerve injury (20).
The lymph node dissection is initiated 2 cm above the aortic bifurcation and extends over
the inferior vena cava to the genitofemoral nerve, the lateral limits of dissection. The cephalad
portions of the lymphatics are ligated with hemoclips to prevent lymphatic leak; the caudal
(specimen) side is ligated only when a vessel is encountered. A small anterior tributary vein
frequently originates from the vena cava, just above the bifurcation, and should be clipped
and divided if identified. At this time the infundibulopelvic ligament and corresponding ovarian
vessels are ligated and divided at the pelvic brim.
All fibroareolar and lymphatic tissues are dissected caudally off the aorta, vena cava, and
common iliac vessels over the sacral promontory into the deep pelvis. The initial dissection
along the common iliac vessels involves skeletonization of the arteries followed by dissection
 Radical Cystectomy 865

of the left common iliac veins. Lymphatic tissue is then brought medially onto to the sacral
promontory and then swept down onto the hollow sweep of the sacrum. At this point, with
the combined use of electrocautery and blunt dissection with a Sponge Stick, the lymphatic tis-
sue is pushed down to the presacral region. Significant bleeding from these presacral vessels can
occur if not properly controlled. Hemoclips are discouraged in this location as they can be easily
dislodged from the anterior surface of the sacrum and result in troublesome bleeding.
Once the proximal portion of the lymph node dissection is completed, a finger is passed
from the proximal aspect of dissection, under the pelvic peritoneum (anterior to the iliac
vessels), distally toward the femoral canal. The opposite hand can be used to strip the perito-
neum from the undersurface of the transversalis fascia. The peritoneum is then divided lateral
to the infundibulopelvic ligament. If performed properly, the only structure encountered is the
round ligament, which is clipped and divided.
A large right-angled rake retractor (Israel) is then used to elevate the lower abdominal wall
to aid in distal exposure in the area of the femoral canal. Tension on the retractor is directed
vertically toward the ceiling, with care taken to avoid injury to the inferior epigastric vessels.
The distal limits of the dissection are then identified: the circumflex iliac vein crossing anterior
to the external iliac artery distally, the genitofemoral nerve laterally, and Cooper’s ligament
medially. The lymphatics draining the leg, particularly medial to the external iliac vein, are care-
fully clipped and divided to prevent lymphatic leakage. This includes the lymph node of Cloquet
(also known as Rosenmuller), the distal limit of lymphatic dissection at this location. The distal
external iliac artery and vein are then circumferentially dissected. At this point in the dissection,
an accessory obturator vein (present in 40% of patients), originating from the inferiomedial
aspect of the external iliac vein, should be ligated, as inadvertent injury to the vessel can lead
to troublesome bleeding.
The subsequent maneuver is to join the proximal and distal dissections and complete the
dissection along the iliac vessels. The proximal external iliac artery and vein are skeletonized
circumferentially to the origin of the hypogastric artery (Fig. 3). Care should be taken to
clip and divide a commonly encountered vessel arising from the lateral aspect of the proximal

Figure 3 Technique of skeletonizing the external iliac artery and vein. (From Stein JP, Skinner DG.
Radical cystectomy in women. Altas Urol Clin 1997; 5(2):37–64.)
866 Ginsberg and Stein

external iliac vessels coursing to the psoas muscle. The external iliac vessels are then retracted
medially, and the fascia overlying the psoas muscle is incised medial to the genitofemoral nerve.
On the left side, branches of the genitofemoral nerve often pursue a more medial course and may
be intimately related to the iliac vessels, in which case they are excised.
At this point, the lymphatic tissue surrounding the iliac vessels is composed of a medial
and lateral component attached only at the base within the obturator fossa. The lateral lymphatic
compartment (freed medially from the vessels and laterally from the psoas) is bluntly swept into
the obturator fossa by retracting the iliac vessels medially and passing a small gauze sponge
lateral to the vessels along the psoas and pelvic sidewall (Fig. 4A). This sponge should be passed
anterior and distal to the hypogastric vein and directed caudally into the obturator fossa. The
external iliac vessels are then retracted anteriorly and laterally while the gauze sponge is care-
fully withdrawn from the obturator fossa with gentle traction using the left hand (Fig. 4B). This
maneuver sweeps all lymphatic tissue into the obturator fossa and facilitates identification of the
obturator nerve deep to the external iliac vein. The obturator nerve is best identified proximally
and carefully dissected free from all lymphatics. The obturator nerve is then retracted laterally
along with the iliac vessels (Fig. 5). At this point, the obturator artery and vein can be isolated as
they exit the pelvis through the obturator canal. They should be entrapped between the index
finger laterally (medial to the obturator nerve) and the middle finger medially of the left hand
and then carefully clipped and divided, ensuring that they stay medial to the obturator nerve.
The obturator lymph node packet is then swept medially toward the bladder, ligating small tribu-
tary vessels and lymphatics from the pelvic sidewall, and removed en bloc with the cystectomy
specimen.

H. Ligation of the Lateral Vascular Pedicle to the Bladder

Following dissection of the obturator fossa and division of the obturator vessels, the lateral
vascular pedicle to the bladder is isolated and divided. Isolation of the lateral vascular pedicle
is performed with the left hand. Traction is placed on the anterior branches of the hypogastric
artery with retraction of the bladder and toward the pelvis. The left index finger is then passed
medial to the hypogastric artery and posterior to the anterior visceral branches. The index finger
is directed caudally toward the endopelvic fascia, parallel to the sweep of the sacrum, and
defines the two major vascular pedicles to the anterior pelvic organs. The lateral pedicle, anterior
to the index finger, is composed of the visceral branches of the anterior hypogastric vessel. The
posterior pedicle, posterior to the index finger, is composed of the visceral branches between the
bladder/vagina, and the rectum.
The lateral pedicle is entrapped between the left index and middle fingers, and traction is
applied vertically and caudally. This facilitates skeletonization of the hypogastric artery. The
lateral pedicle is then divided between large hemoclips down to the endopelvic fascia, or as
far as is technically possible (Fig. 6). With blunt dissection the index finger of the left hand
helps identify the lateral pedicle and protects the vagina and rectum with medial displacement.
Large right-angle hemoclip appliers and each pair of hemoclips are positioned as far apart as
possible to ensure that 0.5– 1 cm of tissue projects beyond each clip when the pedicle is divided.
This prevents hemoclip dislodgment and unnecessary bleeding. Occasionally, in women with
an abundance of pelvic fat, the lateral pedicle may be thick and require division into two
manageable pedicles, which can also be suture ligated. The inferior vesicle vein serves as an
excellent landmark as the endopelvic fascia is just distal to this structure. It should be empha-
sized that no dissection be performed along the endopelvic fascia in female patients considering
orthotopic reconstruction, which could jeopardize the continence mechanism.
 Radical Cystectomy 867

Figure 4 (A) Technique of passing a small gauze sponge lateral to the external iliac vessels and medial
to the psoas muscle. (B) Technique of withdrawing the gauze sponge with the left hand. This aids in
dissecting the obturator fossa. (From Stein JP, Skinner DG. Radical cystectomy in women. Altas Urol
Clin 1997; 5(2):37–64.)
868 Ginsberg and Stein

Figure 5 Obturator fossa cleaned. This allows proper identification of the obturator nerve passing deep
to the external iliac vein. (From Stein JP, Skinner DG. Radical cystectomy in women. Altas Urol Clin 1997;
5(2):37–64.)

Figure 6 The left hand helps define the right lateral pedicle, extending from the bladder to the
hypogastric artery. This vascular pedicle is clipped and divided down to the endopelvic fascia. (From
Stein JP, Skinner DG. Radical cystectomy in women. Altas Urol Clin 1997; 5(2):37–64.)
 Radical Cystectomy 869

I. Ligation of the Posterior Pedicle to the Bladder

Following division of the lateral pedicles, the surgeon elevates the bladder anteriorly with a
small gauze sponge under the left hand while the assistant retracts on the peritoneum of the recto-
sigmoid colon in a cephalad direction, exposing the cul-de-sac (pouch of Douglas) (Fig. 7). This
provides excellent exposure to the recess of the cul-de-sac and the peritoneal reflection. The
peritoneum lateral to the rectum is incised with the incision extending anteriorly across the
cul-de-sac to join the incision on the contralateral side. The peritoneal incision in the cul-de-sac
should be made on the rectal side to allow for proper and safe development of Denonvilliers’
space between the anterior rectal wall and the posterior sheath of Denonvilliers’ fascia. The
rectum is swept off the posterior vaginal wall employing a posterior sweeping motion of the
fingers. This motion helps to thin and develop the posterior pedicle.

Figure 7 The bladder, uterus, ovaries, and Fallopian tubes are retracted in a caudal direction, exposing
the pouch of Douglas. (From Stein JP, Skinner DG. Radical cystectomy in women. Altas Urol Clin 1997;
5(2):37–64.)
870 Ginsberg and Stein

In the female patient, the posterior pedicles including the cardinal ligaments are divided
4 –5 cm beyond the cervix. All tissue is then swept off the lateral aspect of the vagina, and
the posterior vagina is incised at the apex just distal to the cervix. Cephalad pressure on a
previously placed sponge stick helps to identify the apex of the vagina (Fig. 8). This incision
is carried anteriorly along the lateral and anterior vaginal wall, forming a circumferential
incision (Fig. 9). The anteriorlateral vaginal wall is then grasped with a curved Kocher clamp
to provide traction. This facilitates dissection between the anterior vaginal wall and the bladder
specimen. Development of this posterior plane and vascular pedicle is best performed sharply
and carried just distal to the vesicourethral junction (Fig. 10). Palpation of the Foley catheter
balloon assists in identifying this region. At this point the specimen is only attached at the vesi-
courethral junction (Fig. 11). This dissection helps maintain a functional vagina which provides
pelvic support to the neobladder. The vagina is then closed at the apex and later suspended to the
sacrum to maintain adequate vaginal depth and prevent prolapse postoperatively.
Alternatively, in the case of a deeply invasive posterior bladder tumor, the anterior vaginal
wall should be removed en bloc with the cystectomy specimen to ensure adequate margins. After
dividing the posterior vaginal apex, the lateral vaginal wall subsequently serves as the posterior
pedicle, and the anterior vaginal wall remains attached to the posterior bladder specimen. The
Foley catheter balloon facilitates identification of the vesicourethral junction as the surgical
plane between the vesicourethral junction and the anterior vaginal wall is then developed distally
at this location. A 1-cm length of proximal urethra is mobilized while the remaining distal
urethra is left intact with the anterior vaginal wall. The vagina may be closed by a clam shell

Figure 8 Cephalad pressure on a previously placed sponge stick helps to identify the apex of the vagina
prior to making the initial vaginal incision.
 Radical Cystectomy 871

Figure 9 The vaginal incision is carried out circumferentially just distal to the cervix.

Figure 10 The plane between the anterior vaginal wall and the bladder specimen is sharply dissected.
The dissection is facilitated with traction placed at the vaginal wall with Kocher clamps and manually
on the bladder.
872 Ginsberg and Stein

Figure 11 Overhead view of the female pelvis. Palpation of the Foley catheter balloon assists in identi-
fying the distal aspect of the dissection; at this point the specimen is only attached at the vesicourethral
junction.

(horizontal) or side-to-side (vertical) technique. Other means of vaginal reconstruction may

include a rectus myocutaneous flap, detubularized cylinder of ileum, a peritoneal flap, or an
omental flap. We prefer to spare the anterior vaginal wall if orthotopic diversion is planned.
This eliminates the need for vaginal reconstruction and helps maintain the complex musculo-
fascial support system to the proximal urethra, which may be an important component to the
continence mechanism in these women.
An alternative to the standard antegrade approach to the posterior pedicle is a retrograde
approach. This should be considered when the proper anatomical plane between the anterior
vaginal wall and posterior bladder cannot be easily developed. The urethrovesical junction is
identified by palpation of the Foley balloon and the superficial branch of the deep dorsal vein
may be identified and ligated. The lateral aspect of the bladder neck and urethra is dissected
free to the point where it is easily identified sitting on the anterior aspect of the vagina. The
plane between the anterior vaginal wall and posterior bladder is then developed, the bladder
neck is elevated off the anterior vaginal wall, and a Satinsky clamp is placed across the bladder
neck, allowing division of the urethra just distal to the bladder neck and clamp. With cephalad
traction on the specimen, the plane between the bladder and vaginal may be developed, and dis-
section is continued sharply to the vaginal cuff with lateral attachments between the bladder and
vagina clipped as needed.
 Radical Cystectomy 873

J. Urethral Preparation
At the terminal stages of the cystectomy, careful preparation of the urethra is critical to avoid
injury to the continence mechanism. Minimal dissection should be performed in the region
anterior to the urethra. This helps prevents injury to the distal urethral sphincteric mechanism
and corresponding innervation, which studies have demonstrated arise from branches off the
pudendal nerve that course along the pelvic floor posterior to the levator muscles (21). In
addition, the pubourethral suspensory ligaments should be left intact. These ligaments provide
support and help maintain an intrapelvic neobladder position, which may also contribute to the
continence mechanism in women.
When the posterior dissection is completed (ensuring to dissect just distal to the vesico-
urethral junction), a Satinski vascular clamp is placed across the bladder neck. The proximal
urethra is divided anteriorly, distal to the bladder neck and clamp. Division of the anterior
two-thirds of the urethra exposes the urethral catheter. Six to eight 2-0 polyglycolic acid, ante-
riorly placed, urethral sutures are then placed equally under direct vision into the urethral
mucosa (Fig. 12). The rhabdosphincter, the edge of which acts as a hood overlying the dorsal
vein complex, is included in these sutures. This maneuver preserves urinary continence and
compresses the dorsal vein complex against the urethra for hemostatic purposes. The urethral
catheter is then drawn through the urethrotomy, clamped on the bladder side, and divided.
Cephalad traction of the clamped catheter on the bladder side occludes the bladder neck,
helps prevents tumor spill from the bladder, and provides exposure to the posterior urethra.
Two to four additional sutures are placed in the posterior urethra incorporating the rectourethralis
muscle or distal Denonvilliers’ fascia. The posterior urethra is then divided, and the specimen

Figure 12 Overhead view of the female pelvis. No anterior dissection has been performed and the initial
urethral sutures have been placed.
874 Ginsberg and Stein

removed. The urethral sutures are appropriately tagged to identify their location and placed
under a towel until the urethroenteric anastomosis is performed. Bleeding from the dorsal
vein is usually minimal at this point. If additional hemostasis is required, one or two anterior
urethral sutures can be tied to stop the bleeding. Frozen section analysis of the distal urethral
margin of the cystectomy specimen is then performed to exclude tumor involvement and confirm
appropriateness for orthotopic reconstruction.
Following removal of the cystectomy specimen, the pelvis is irrigated with warm sterile
water. The presacral nodal tissue previously swept off the common iliac vessels and sacral pro-
montory into the deep pelvis is collected and sent separately for pathologic evaluation. All nodal
tissue in the presciatic notch, anterior to the sciatic nerve, is also sent for histologic analysis.
Hemostasis is obtained and the pelvis is packed with a lap pad while attention is directed to
the urinary diversion. The pelvis is drained by a 1-inch Penrose drain for 3 weeks, and a
large suction hemovac drain for 24 h.

K. Lower Urinary Tract Reconstruction

The various reconstructive techniques (i.e., Kock ileal reservoir, T-pouch) have been described
previously and remains standard (22 – 24). Prior to briefly discussing our present method of
lower urinary tract reconstruction several important points need to be stressed for female patients
undergoing orthotopic diversion. Appropriate urethral preparation for the urethroenteric anasto-
mosis is essential, and is well described above. After the urethra has been prepared, a well-
vascularized omental pedicle graft, based on the left gastroepiploic arthery, is placed between
the reconstructed vagina and neobladder. This graft is secured to the levator ani muscles
and separates the suture lines of the vagina and neobladder, preventing fistulization (Fig. 13).

Figure 13 Sagittal section of the female pelvis. Note that a well-vascularized omental graft is placed
between the reconstructed vagina and neobladder. The omentum is secured to the levator ani muscles to
separate the suture lines and helps prevent fistulization.
 Radical Cystectomy 875

Lastly, once the urethroenteric anastomosis is complete the neobladder is secured with a 3-0
polyglycolic acid suture to the inferior aspect of the pubic symphysis. This helps maintains a
tension free urethroenteric anastomosis and ensures an intra-abdominal reservoir location.
The primary method by which we now perform lower urinary tract reconstruction is the
T-pouch; however, there is no “best” form of lower urinary tract reconstruction, and each
surgeon should use what he feels most comfortable with. The terminal portion of the ileum is
used to construct the orthotopic T-pouch ileal neobladder. The T-pouch is created from
44 cm of distal ileum placed in an inverted “V” configuration (each limb of the “V” measuring
22 cm), and a proximal 8 – 10 cm segment of ileum (afferent limb) is used to form the afferent
antireflux mechanism. A longer afferent ileal segment (proximal ileum) may be harvested if
needed to bridge the gap to a ureter whose length has been shortened/compromised.
The ileum is divided between the afferent ileal segment and the 44-cm segment that will
form the reservoir. The mesentery is incised for 2 –3 cm, and the segment of mesentery for each
piece of bowel is individually maintained. The proximal end of the isolated afferent ileal seg-
ment is closed with a running Parker-Kerr suture of 3-0 chromic and a third layer of interrupted
4-0 silk sutures. A standard small bowel anastomosis is performed to reestablish bowel continu-
ity and the mesenteric trap is closed.
The isolated 44-cm ileal segment is then laid out in an inverted “V” configuration (Fig. 14).
The antireflux mechanism works as a flap valve with the distal 3– 4 cm of the afferent ileal

Figure 14 The T-pouch is constructed from an isolated 44-cm ileal segment (laid out in an inverted “V”)
to form the reservoir and a proximal 8- to 10-cm segment of ileum to form the antireflux limb. (From
Ref. 24.)
876 Ginsberg and Stein

Figure 15 At the distal 3 – 4 cm of the isolated afferent ileal segment three to four mesenteric windows
of Deaver are opened (adjacent to the serosa of the ileum). Small Penrose drains placed through each
mesenteric window helps identify this space and facilitates suture passage (see insert with arrows). The
distal 3 – 4 cm of the afferent segment will be anchored into the serosal-lined ileal trough formed by the
base of the two adjacent 22-cm ileal segments. (From Ref. 24.)

segment anchored into the serosal-lined ileal trough formed by the base of the two adjacent 22-
cm ileal segments. Initially, mesenteric windows of Deaver are opened between the vascular
arcades for 3– 4 cm proximal to the distal most aspect of the isolated afferent ileal segment
(Fig. 15). A series of 3-0 silk sutures (usually two silks per window of Deaver) are then used
to approximate the serosa of the two adjacent 22-cm ileal segments at the base of the “V,”
with each suture passed through the previously opened window of Deaver. Preservation of
these arcades (blood vessels) maintains a well-vascularized afferent limb while allowing for
appropriate fixation of the afferent limb. Specifically, a silk suture is placed into the seromuscu-
lar portion of the bowel (adjacent to the mesentery) at the end of one of the 22-cm ileal segments
(Fig. 16A). The suture is then passed through the most proximal window of Deaver in the affer-

Figure 16 (A) A series of interrupted silk sutures are use to approximate the serosa of the base of the two
adjacent 22-cm ileal segments. (B) After passing the silk suture through the window of Deaver, it is placed
in a corresponding site on the adjacent 22-cm ileal segment. This suture will then be brought back through
the same window of Deaver and tied down. Maneuvering of the Penrose drains helps facilitate transfer of
the suture through the windows of Deaver. (From Ref. 24.)
 Radical Cystectomy 877

ent limb, placed in a corresponding seromuscular site of the bowel (next to mesentery) of the
adjacent 22-cm ileal segment, and then brought back through the same window of Deaver
and tied down (Fig. 16B). This process is repeated through each individual window of Deaver
until the distal 3– 4 cm of the afferent segment is permanently fixed in the serosal-lined ileal
trough. Placement of small (1/4 inch) Penrose drains through each window of Deaver facilitates
passage of the silk suture back and forth through the mesentery. The Penrose drains are systema-
tically removed as the afferent limb is fixed within the serosal-lined ileal trough.
Next, the previously anchored portion of the afferent ileal segment (distal 3– 4 cm) is
tapered on the antimesenteric (anterior) border over a 30F catheter (Fig. 17). Tapering of this
portion of the afferent ileal segment reduces the bulk and lumen of the afferent limb, facilitates
later coverage of the anchored afferent limb with ileal flaps, and increases the tunnel length-
to-lumen diameter ratio allowing for a more effective flap valve mechanism. The remaining
portion of the adjacent 22-cm ileal segments are then approximated together with a side-to-
side 3-0 polyglycolic acid suture (Fig. 18). Starting at the apex of the “V,” the bowel is then
opened adjacent to the serosal suture line using electrocautery. This incision is carried upward
toward the base where the afferent limb in anchored. At the level of the afferent ostium it is then
extended directly lateral to the antimesenteric border of the ileum, and carried upward (cepha-
lad) to the base of the ileal segment (Fig. 19). A similar incision is made on the contralateral 22-
cm ileal segment. This incision provides wide flaps of ileum that will ultimately be brought over
the tapered afferent ileal segment to create the antireflux mechanism in a flap valve manner
(Fig. 20).

Figure 17 The distal 3- to 4-cm afferent ileal segment, now anchored to the serosa of the base of the
adjacent 22-cm ileal segments, is tapered over a 30F catheter on the antimesenteric boarder. This can
usually be done with a GIA-55 stapler. (From Ref. 24.)
878 Ginsberg and Stein

Figure 18 The two 22-cm ileal segments are joined by a running 3-0 polyglycolic acid continuous
suture. The suture is placed adjacent to the mesentery and runs from the apex up to the ostium of the
afferent ileal segment. Note the formation of the “T” with the horizontal staple lines at the base of each
22-cm ileal segment and the vertical. (From Ref. 24.)

The previously incised ileal mucosa from the apex up to the ostium of the afferent limb is
then oversewn with two layers of a running 3-0 polyglycolic acid suture (Fig. 21). An interrupted
mucosa-to-mucosa anastomosis is then performed between the ostium of the afferent ileal limb
and the incised intestinal ileal flaps with 3-0 polyglycolic acid sutures (Fig. 22). The mucosal
edges of the ileal flaps, from both arms of the “V,” are then approximated over the tapered
portion of the afferent ileal limb (3 – 4 cm) with a running suture in two layers. This suture
line completes the posterior wall of the reservoir and creates the antireflux mechanism (Fig. 23).
The reservoir is then closed by folding the ileum in half in an opposite direction to which it
was opened (Fig. 24), and the anterior wall is closed with a running, two-layer 3-0 polyglycolic
acid suture (Fig. 25). This anterior suture line is stopped just prior to the end of the right side to
allow insertion of an index finger. This is the most mobile and dependent portion of the reservoir
and will later be anastomosed to the urethra (Fig. 26).
Once the pouch has been closed, each ureter is spatulated, and a standard, bilateral end-to-
side ureteroileal anastomosis is performed using interrupted 4-0 polyglycolic acid suture. These
anastomoses are stented with No. 8 infant feeding tubes. A 24F hematuria catheter is placed per
 Radical Cystectomy 879

Figure 19 The two 22-cm ileal segments are opened immediately adjacent to the serosal suture
line beginning at the apex and carried upward to the ostium of the afferent segment. At the ostium
the incision is directed lateral to the antimesenteric boarder and then cephalad to the base. The dashed
line depicts the incision line. (From Ref. 24.)

urethra, and the ureteral stents are secured to the end of the urethral catheter with a 3-0 nylon suture,
facilitating stent removal. A tension free mucosa-to-mucosa urethroileal anastomosis is performed.

V. POSTOPERATIVE CARE

All patients are monitored in a surgical intensive care unit for at least 24 h or until stable and safe for
transfer to the ward. Third-space fluid loss in these patients can be deceivingly large. A combination
of crystalloid and colloid fluid replacement is given through the first night after surgery and con-
verted to crystalloid on postoperative day 1. Prophylaxis against stress ulcer is initiated with an
H2 blocker. Intravenous broad-spectrum antibiotic are administered and converted to orals with
diet progression. Pain control is maintained with an epidural catheter, patient-controlled analgesic
system, or a combination of the two. Radiograph evaluation of the diversion is done 3 weeks after
surgery and, in the absence of contrast extravasation, results in removal of drainage catheters.
880 Ginsberg and Stein

Figure 20 Completing the incision of the bowel. Note the incision provides wide flaps of ileum that can
easily be brought over and cover the tapered distal afferent ileal segment to form the antireflux mechanism
in a flap-valve technique. (From Ref. 24.)

VI. RESULTS

Results are available in 88 women who have undergone orthotopic lower urinary tract recon-
struction with a median age of 67 years (range 31 –86 years) and follow-up of 30 months
(range 6– 117 months).

A. Continence/Voiding Pattern
Of the 88 patients in the study, 81 were evaluated by chart review, and 66 responded to a ques-
tionnaire. Results from the chart review revealed 61 (75%) patients dry (34 void spontaneously
and 27 intermittently catheterize) and 20 (25%) patients wet (defined as the use of two or more
pads a day) postoperatively. The questionnaire revealed similar results, with 52 (78%) patients
dry (22 spontaneously void and 30 catheterize) and 14 (22%) patients wet. Twelve patients have
undergone secondary procedures for urinary incontinence. Ten patients have undergone one to
 Radical Cystectomy 881

Figure 21 The incised ileal mucosa is oversewn in two layers from the apex to the ostium of the afferent
ileal segment. (From Ref. 24.)

Figure 22 A mucosa-to-mucosa, ileal-to-ileal anastomosis is performed between the ostium of the

afferent segment and the edges of the ileal flaps with interrupted 3-0 polyglycolic acid suture. (From Ref. 24.)
882 Ginsberg and Stein

Figure 23 The mucosal edges of the ileal flaps are brought over the tapered distal portion of the afferent
ileal segment. This suture line excludes the staple line form the reservoir, completes the posterior suture
line and creates the antireflux mechanism. (From Ref. 24.)

Figure 24 The reservoir is folded and closed in the opposite direction to which it was opened. (From
Ref. 24.)
 Radical Cystectomy 883

Figure 25 The anterior suture line is completed with two layers of a continuous 3-0 polyglycolic acid
suture. The anterior suture line is stopped just short of completion on the right side to the diameter of
an index finger, which will be the site of anastomosis to the urethral stump. (From Ref. 24.)

Figure 26 Completion of the T-pouch. The most mobile and dependent portion of the reservoir will be
anastomosed to the urethra following the ureteroileal anastomosis. (From Ref. 24.)
884 Ginsberg and Stein

four (average 2.8) collagen injections with significant improvement noted in three (30%) and no
change in the remaining seven patients. One patient with urinary incontinence underwent con-
version to a cutaneous reservoir for a pelvic recurrence and is now dry, and another patient
underwent fascial sling with resolution of her leakage.

B. Survival and Recurrence

As of August 1999 there were 75 evaluable patients who underwent cystectomy for TCC of
the bladder. Recurrent disease has been identified in 17 patients (23%): six patients with a
local/pelvic recurrence (8%), and 11 patients with distant recurrence (11%). There have been
13 deaths secondary to TCC. There have not been any urethral recurrences to date.

C. Complications
Advances in medical, surgical, and anesthetic techniques have reduced morbidity and mortality
associated with radical cystectomy. Early complications related to the radical cystectomy are
difficult, if not impossible, to separate from complications related to the urinary diversion.
Although complications related specifically to female patients requiring cystectomy have rarely
been reported (16 – 18), these complications are comparable to those seen in male patients under-
going the similar procedure.
A total of 21 patients (24%) suffered 24 early complications. Four of these complications
required operative management. Two patients returned to the operating room to remove a
retained portion of a broken Jackson-Pratt drain, one patient underwent evacuation of a clot
after a postoperative bleed 1 day after surgery, and one patient developed a urine leak requiring
bilateral percutaneous nephrostomy tube placement. There were two (2.2%) perioperative
deaths: one from a pulmonary embolus and one from sepsis.
Late complications were identified in 12 (14%) patients. Six patients were found to have
stones in their neobladder which were managed endoscopically. Five patients required operative
intervention: three for fistulae (one enterocutaneous, one pouch-bowel and one pouch-vagina),
one for a ureteroileal stricture, which ultimately required complete ileal substitution, and one
patient with a ventral incisional hernia.
In addition, we have found that age alone does not independently increase the risk of mor-
bidity or mortality from radical cystectomy and should not be a contraindication for definitive
surgical therapy for invasive bladder carcinoma (25,26).

VII. DISCUSSION

Although transitional cell carcinoma of the bladder is primarily thought of and seen in men,
women also suffer significant morbidity and mortality from this disease. The technique of en
bloc radical cystectomy with bilateral pelvic lymphadenectomy has provided superior survival
rates with lower pelvic recurrence rates compared to other forms of therapy for invasive bladder
cancer (27). Since radical cystectomy has become the primary form of therapy for invasive blad-
der cancer, emphasis has been directed to the quality-of-life issues, and reconstruction of the
genitourinary tract following the ablative surgery. Advances in lower urinary tract reconstruc-
tion (particularly women) have increased both patient and physician acceptance of radical
cystectomy. One recent report indicated that the option for orthotopic diversion led to an earlier
acceptance of cystectomy compared to those offered a cutaneous form of diversion, and that
 Radical Cystectomy 885

cystectomy improved survival (28). Modern urologic reconstructive techniques now allow for
creation of a urinary reservoir (orthotopic neobladder) with similar characteristics to the native
bladder: large-capacity, low-pressure, nonrefluxing, continent reservoir that allows volitional
voiding per urethra. This eliminates the need for a cutaneous stoma and the need for catheter-
ization, relying on the striated external sphincter for continence. We believe these advances,
which allow patients to return to a near normal lifestyle, with a positive self-image, will encou-
rage earlier treatment for invasive bladder tumors when the potential for cure is highest.
The progressive development of urinary diversion has been the result of persistent surgical
innovation to improve the treatment and quality of life of patients following cystectomy. This
evolution has developed along three distinct paths: an incontinent cutaneous form of diversion
(ileal conduit), a continent cutaneous form of diversion (Indiana and Kock pouch), and, most
recently, a form of diversion to the intact native urethra (orthotopic neobladder). We firmly
believe the orthotopic neobladder represents the most ideal form of urinary diversion available
in carefully selected male and female patients. The orthotopic neobladder most closely
resembles the original bladder in both location and function. Orthotopic diversion eliminates
the need for a cutaneous stoma and its often plagued continence mechanism. Patients retain a
more natural voiding pattern which provides a more normal lifestyle and an improved self-
image compared to other forms of diversion.
The excellent functional results in 88 women undergoing orthotopic neobladder diversion
confirms our initial experience with further follow-up. The majority of women are completely
continent (75%). By 6 months most women obtain the maximum degree of continence; however,
many of our patients achieve complete continence immediately following removal of their
urethral catheter 3 weeks after surgery. We attribute these results to the limited dissection
performed anterior to the urethra.
A precise understanding of the continence mechanism in women after orthotopic diversion
is still lacking. The multiple factors contributing to the continence mechanism in women under-
going orthotopic diversion likely include the distal urethral sphincteric mechanism and the
inherent fascial support of the urethra. Anatomic urethral support is primarily maintained by
the condensations of the levator fascia known as the urethropelvic (29) and the pubourethral
(30) ligament. The pubourethral ligament attaches at the level of the midurethra and helps main-
tain the urethra and neobladder in an intra-abdominal position.
The distal urethral sphincteric mechanism is composed of smooth muscle, striated muscle,
and spongy tissue. This mechanism is what is primarily responsible for continence in otherwise
normal patients with incompetent bladder necks and is identified at the level of the midurethra
(31,32). This level of continence has also been identified in fluorourodynamic evaluation of female
cystectomy patients with neobladders, and suggests that the distal urethral sphincteric mechanism
is the critical component in maintaining urinary continence in these female subjects (33). Passive
continence is secondary to the smooth muscle and spongy tissue component of the distal urethral
sphincteric mechanism. The striated portion of the sphincter is composed of “fast-twitch” (rapidly
contracting muscle responsible for active contraction of the sphincter as well as reflex contractions
which are seen with Valsalva-type maneuvers) and “slow-twitch” (responsible for basic urethral
tone) muscle, which are positioned extrinsic and intrinsic to the urethral wall, respectively.
Another controversial point in regard to female neobladders relates to the innervation to
the sphincteric mechanism in these patients. Although some authors have suggested that a sym-
pathetic nerve-sparing cystectomy is important in maintaining continence in women (16,28,34),
we make no attempt to perform a nerve-sparing cystectomy and remove all autonomic sympath-
etic innervation from just above the aortic bifurcation down to the proximal urethra. In addition,
we routinely sacrifice the sympathetic neurovascular bundle coursing along the lateral aspect of
the uterus and vagina. This primarily leaves somatic and parasympathetic innervation to the ure-
886 Ginsberg and Stein

thral sphincteric mechanism (or sympathetic via pathways that have yet to be identified), which
is apparently sufficient as evidenced by the high continence rate in our patients.
We present encouraging clinical and functional data with intermediate follow-up in
women undergoing orthotopic lower urinary tract reconstruction following cystectomy for a pel-
vic malignancy. Orthotopic diversion in women may be performed with few postoperative com-
plications, excellent continence results, a normal voiding pattern, and with high patient
acceptance. Although long-term follow-up will be required to define the true risk of urethral
recurrence in these women, we feel female subjects considering orthotopic diversion may be
safely and appropriately selected using strict pathologic criteria. We have found intraoperative
frozen section of the distal surgical margin (proximal urethra) to be the most accurate and
reliable method to determine if a woman is an appropriate candidate for orthotopic diversion.
Orthotopic reconstruction is a viable option in most male and female patients and signifies
another important step forward in the evolution of urinary diversion.

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neobladder incorporating a serosal lined ileal antireflux technique. J Urol 1998; 159(6):1836–1842.
25. Lerner SP, Skinner E, Skinner DG. Radical cystectomy in regionally advanced bladder cancer. Urol
Clin North Am 1992; 19:713– 723.
26. Figueroa AJ, Stein JP, Dickinson M, Skinner EC, Thangathurai D, Mikhail MS, Boyd SD, Lieskovsky G,
Skinner DG. Radical cystectomy for elderly patients with bladder carcinoma: an updated experience
with 404 patients. Cancer 1998; 83:141 –147.
27. Wishnow KI, Dmochowski R. Pelvic recurrence after radical cystectomy without preoperative radi-
ation. J Urol 1988; 140:42– 43.
28. Hautmann RE, Paiss T, Petriconi R. The ileal neobladder in women: 9 years of experience with 18
patients. J Urol 1996; 155:76– 81.
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ging of the female bladder neck and urethra. J Urol 1990; 143:563 – 566.
30. Zacharin RF. The anatomic support of the female urethra. Obstet Gynecol 1968; 21:754– 759.
31. Dupont MC, Albo ME, Raz S. A videourodynamic evaluation of bladder neck competence in females.
J Urol 1996; 153:abstract 536.
32. Chapple CR, Helm CW, Blease S, Milroy EJ, Rickards D, Osborne JL. Asymptomatic bladder neck
incompetence in nulliparous females. Br J Urol 1989; 64:357 – 359.
33. Grossfeld GD, Stein JP, Bennett CJ, Ginsberg DA, Boyd SD, Lieskovsky G, Skinner DG. Lower urin-
ary tract reconstruction in the female using the Kock ileal reservoir with bilateral ureteroileal ure-
throstomy: update of continence results and fluorourodynamic findings. Urology 1996; 48:383– 388.
34. Cancrini A, De Carli P, Fattahi H, Pompeo V, Cantiani R, Von Heland M. Orthotopic ileal neobladder
in female patients after radical cystectomy: 2-year experience. J Urol 1995; 153:956– 958.
59
Interstitial Cystitis

Marie-Blanche Tchetgen, Raymond R. Rackley, and Joseph B. Abdelmalak

Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

Interstitial cystitis (IC) is a poorly understood clinical syndrome characterized by urinary

frequency, urgency, and varying degrees of pelvic pain. Although Hunner (1) described bladder
ulcerations as early as 1915, and descriptions of submucosal hemorrhages and reduced bladder
capacity were attributed to Hand (2) in 1949, the etiology and pathophysiology of the disease
remain unclear. Significant research contributions have been made in recent years with the
support of the Interstitial Cystitis Association and NIH-NIDDK, but fundamental questions
remain.

II. EPIDEMIOLOGY

Epidemiological studies of IC have been scant, slowed by the low frequency of the disease and
the lack of a broad consensus regarding the definition of the disease. Criteria established for
research purposes by NIDDK have proven to be exceedingly restrictive as up to 60% of patients
clinically thought to have the disease would be excluded (3). Recent efforts aimed at better char-
acterizing the epidemiology of IC suggest that the disease may be more prevalent than pre-
viously thought (4). The first population-based study aimed at estimating the prevalence of IC
was published in 1999. IC-specific questionnaires were completed by participants in two
large population based long-term epidemiological studies, the Nurses Health Study (NHS) I
and II. A prevalence of confirmed IC cases of 52 per 100,000 in NHS I and 67 per 100,000
in NHS II were reported, much higher than previously reported rates of 18 – 36 per 100,000
(5,6). Other epidemiological characteristics such as age at onset of symptoms, age at diagnosis,
and delay in diagnosis were similar to previous published reports. Mean age at diagnosis was
54.4 in NHS I and 35.8 in NHS II. Mean time from onset of symptoms to diagnosis was 5.3
and 7.1 years, respectively.
The NHS cohorts were limited epidemiologically by the absence of men and children, as
well as the lack of racial and ethnic diversity. Current estimates indicate a male-female ratio of
approximately 1 : 9 (7), although there is increasing evidence that the disease may be underdiag-
nosed in men. In a study of 29 men diagnosed with IC over an 8-year period, 14 were initially
diagnosed with prostatitis and 11 with BPH, despite the fact that 21 of these men had the classic
889
890 Tchetgen et al.

form of the disease with associated Hunner’s ulcers (8). Similarly, the incidence of IC in children
may be higher than previously thought, with up to 50% of children with lower urinary tract
symptoms suggestive of IC satisfying NIDDK criteria modified for the pediatric population
(9). Further longitudinal epidemiological studies are needed in both the adult and pediatric popu-
lation in order to gain a more comprehensive understanding of the natural history of this disease
as well as its impact on quality of life. Evidence gathered so far is consistent with the charac-
terization of this disease as a chronic, often debilitating disease (10); however, little specific
information exists which addresses the variability observed in disease presentation. Recently,
investigators have proposed the use of a broadened clinical definition of IC, which includes
chronic pelvic pain of bladder origin, in an effort to facilitate a more accurate assessment of
the prevalence of these symptom complexes in the general population. However, the sensitivity
and specificity of such a classification would have to be established before undertaking any
longitudinal epidemiological studies (11).

III. ETIOLOGY

Although research advances in recent years suggest that a multifactorial process may be
involved in the development of the symptom complex of IC, the exact etiology of the disease
remains elusive (Fig. 1). Various theories have been proposed with varying degrees of support-
ing evidence; however, there is no unifying concept that allows a clear understanding of the
pathophysiology of the disease. The dominant theories include:
1. Alterations in urothelial permeability
2. Mastocytosis with release of pro-inflammatory mediators
3. Neural-immune mechanisms
4. Neural plasticity
5. Infectious agents
The hypothesis of increased urothelial permeability was first advanced by Parsons on the
basis of studies demonstrating that the glycosaminoglycans (GAG) layer of the bladder formed a

Figure 1 The etiology of interstitial cystitis.

 Interstitial Cystitis 891

protective barrier preventing urinary solutes from reaching the underlying cell membranes (12).
It is proposed that damage to this protective layer allows toxic substances such as urea, calcium,
and potassium into the bladder wall, resulting in nerve depolarization with subsequent develop-
ment of the characteristic symptoms of IC (13). It was further demonstrated that exogenous sul-
fated polysaccharides such as heparin, pentosan polysulfate, and hyaluronic acid can decrease
the movement of urea and potassium chloride across the bladder wall, and improve the symp-
toms of IC. The potassium chloride test was developed as a “leak test” for the bladder
epithelium, to be used in the diagnosis of IC. It is clear, however, that a leaky epithelium is
not the sine qua non of IC, as at least 25% patients who satisfy either the NIDDK or clinical
definition of the disease have a negative potassium sensitivity test.
Interestingly, patients with a positive test may be more likely to respond to sodium pen-
tosan polysulfate therapy (14). The “leaky” epithelium theory may constitute a piece of the IC
puzzle but research evidence to date does not support its consideration as the primary etiological
event leading to the clinical presentation of the disease.
Mastocytosis emerged as a potential etiological factor after the presence of mast cells
within the bladder wall of IC patients was described (15). Mast cells are found in only about
a third of IC patients, and although mast cell activation in this subgroup of IC patients correlates
with increased urinary levels of mast cell mediators such as histamine, histamine metabolites
(methylhistamines, 1,4-methylimidazole acetic acid), and tryptase (16 – 18), the diagnostic
importance of detrusor mastocytosis largely remains in question. Recent investigations suggest
that mast cell degranulation may in fact be one component of a sequence of events involving
neurogenic inflammation (19).
Maladaptive neurogenic inflammation has been recently proposed as a mechanism by
which the characteristic features of IC may be mediated. Indeed, IC shares many similarities
with other chronic visceral pain syndromes thought to be associated with neurogenic inflam-
mation: poor pain localization (pelvic), pain referred to adjacent areas (perineum, suprapubic
area, lower back, thighs), and evidence of inflammatory changes of unclear etiology. The evi-
dence suggesting the involvement of neurogenic inflammation in the pathophysiology of IC
includes the increased presence of substance P-containing nerve fibers in IC bladder biopsies
(20) and increased levels of immunoreactive substance P in the urine of IC patients (21).
Substance P is known to induce mast cell degranulation in a dose-dependent fashion (22)
and release of histamine, leading to increased vascular permeability and leukocyte migration
(23). More direct evidence of a neurogenic process possibly causing IC was presented by
Jasmine and colleagues in a model of neurogenic cystitis induced by viral infection of specific
neuronal circuits of the rat CNS (24). In these experiments, the abductor caudae dorsalis
(ACD) tail muscle was inoculated with the neurotropic pseudorabies virus (PRV), leading to
viral infection of the CNS motor neurons which innervate this muscle. Subsequent transsynap-
tic spread of PRV to the area of the lumbosacral spinal cord, where parasympathetic pregan-
glionic neurons innervating the bladder are located was demonstrated by immunostaining.
Approximately 96 h after inoculation, the rats manifested behavioral, macroscopic, and histo-
logic signs of cystitis. PVR immunostaining of the bladder wall was consistently negative, and
urine and bladder cultures were also negative for infectious virus. Spinal cord cultures from the
ACD-inoculated rats contained infectious virus. Total bladder denervation consistently pre-
vented bladder inflammation after ACD viral inoculation. Based on these observations, the
authors proposed that the immune response generated by PRV infection activated adjacent
somatic and autonomic central bladder neural circuits, resulting in neurogenically mediated
cystitis. Recent studies provide additional evidence supporting the role of mast cells in the
genesis of neurogenic cystitis (25): increase in urinary histamine levels precedes the onset
of inflammation, normalization of urinary histamine levels parallels a large reduction in the
892 Tchetgen et al.

density of granulated mast cells, and pre-emptive mast cell degranulation using a mast cell
degranulator compound prior to ACD viral inoculation prevents the development of neuro-
genic cystitis.
These observations serve as the backdrop for a model of the pathophysiology of IC charac-
terized by three defining stages: (a) centrally mediated neurogenic inflammation involving
primary sensory afferents to the bladder which release neuropeptides that in turn induce; (b)
mast cell degranulation leading to inflammatory response; and (c) the release of histamine
and other mast cell mediators that trigger inflammation (Fig. 2). Ultrastructural analysis of
the IC bladder by electron microscopy indicating the presence of mast cells in close proximity
to intrinsic nerves in the suburothelium lends further credence to this theoretical model (26).
However, the potential cause of such neurogenic inflammation remains unclear, and there is
no evidence that a viral infectious process is involved.

Figure 2 Proposed model of the pathogenesis of interstitial cystitis.

 Interstitial Cystitis 893

IV. DIAGNOSIS

The classic clinical presentation of IC is characterized by urinary frequency (8 times per day),
urgency, and pain on bladder filling relieved by voiding. On physical examination, patients may
display tenderness of the anterior vaginal wall and bladder base. The disease remains a diagnosis
of exclusion because the presenting symptoms are nonspecific and may vary in severity. The
diagnosis is based primarily on clinical suspicion, and based on the results of the Interstitial
Cystitis Database (ICDB) study, clinicians are discouraged from using the strict NIDDK criteria.
Routine urine culture and cytology are necessary to exclude infection or malignancy. Other diag-
noses to be ruled out include ureteral or bladder calculi, active genital herpes, urethral diverti-
culum, chemical cystitis (cyclophosphamide), radiation cystitis, and vaginitis (chalamydia,
ureaplasm). If IC is suspected, additional tests may be useful in establishing the diagnosis.
These include cystoscopy and hydrodistension under anesthesia, urodynamic evaluation, potass-
ium sensitivity test, urinary markers, and bladder biopsy.

A. Cystoscopy and Hydrodistension

Cystoscopy under anesthesia allows for comfortable and adequate bladder and urethral examin-
ation. Hydrodistension is performed by instilling fluid into the bladder under gravity at 80 –
100 cm of water pressure until the flow slows to a drip or stops altogether. Compression of
the urethra around the cystoscope sheath prevents efflux of fluid and ensures an accurate
measurement of bladder capacity. According to the NIDDK criteria, distension is held for
1 –2 min, although double distension or distension duration up to 10 min have been reported.
Upon decompression, the bladder is examined cystoscopically for the presence of glomerula-
tions, which are pinpoint petechial hemorrhages and constitute the most consistent cystoscopic
finding in patients with IC (Fig. 3). Glomerulations must be diffuse and present in at least three
quadrants of the bladder. Fissures and cracks that bleed after distension may be observed and are
suggestive of the classic or ulcer variety of IC. Although the presence of glomerulations has been
reported in normal women undergoing tubal ligation, it remains a helpful diagnostic tool in
symptomatic patients. Furthermore, hydrodistension may be therapeutic in 20 –30% of patients.

B. Urodynamic Evaluation
Urodynamic studies are not routinely recommended in the evaluation of the patient with IC,
although some findings make the diagnosis less likely. These include a bladder volume at the
first sensation to void .150 cc, maximum bladder capacity .350 cc, and the absence of
nocturia on pretesting baseline voiding log.
The presence of involuntary bladder contractions has been reported in 14% of IC
patients (ICDB) and does not exclude a clinical diagnosis of IC. A more stringent research defi-
nition of the disease as described by the NIDDK does, however, consider the presence of phasic
instability an exclusion criterion.

C. Potassium Sensitivity Test

The potassium chloride test (KCl test) is based on the premise that epithelial permeability dys-
function is the underlying factor which leads to the symptoms of IC. Increased urothelial per-
meability would allow diffusion of potassium into the submucosal and muscle layers of the
bladder, leading to nerve depolarization and possibly neurogenic inflammation. The KCl test
was proposed by Parsons as a provocative test aimed at identifying IC patients with epithelial
894 Tchetgen et al.

Figure 3 Diffuse glomerulations seen on cystoscopic evaluation of the bladder following

hydrodistension.

dysfunction. The test is conducted by instilling a dilute solution of potassium (40 mEq in
100 mL water) in the bladder for 5 min. The degree of urgency and pain is reported on a
scale of 0 (none) to 5 (severe), before and after the test. A change in score of 2 is considered
a positive test. The role of the KCl test in the diagnosis of IC remains controversial. It is limited
by a poor specificity as falsely positive tests are seen in patients with bladder overactivity, radi-
ation cystitis, and bacterial cystitis. In addition, false-negative tests have been reported in
patients with severe disease (13). Furthermore, when positive, the test may cause a significant
amount of discomfort and distress to the patient. Despite these limitations, there are data
suggesting that the KCl test may identify patients more likely to respond to therapies aimed
at restoring urothelial integrity such as sodium pentosan polysulfate and heparin. More studies
are needed to further clarify the role of the KCl test.

D. Urine Markers
A number of urine components are reported to be altered in IC patients and as such have been
evaluated as possible markers for the disease. The ideal marker should allow discrimination
between IC patients and healthy controls with minimal or no overlap and should be predictive
of the clinical presence of the disease and should normalize with successful treatment. Most
described alterations in IC urinary components relate to one or more of the possible etiologies
of IC and show significant overlap between IC and normal controls. Only two markers have
been identified that can clearly discriminate between IC patients and normal control groups:
glycoprotein-51 (GP-51), and antiproliferative factor (APF).
 Interstitial Cystitis 895

GP-51 is a glycoprotein produced and secreted by the bladder transitional epithelium of

humans and rabbits. Recent studies indicate that decreased levels of GP-51 are found in the blad-
der and urine of IC patients as compared to controls (27). However, GP-51 discriminates best
between IC patients and controls (no overlap in GP-51 urinary levels) when the former
meet all NIDDK criteria for the diagnosis of IC (28). Its clinical utility may therefore be as
limited as that of the NIDDK criteria.
APF inhibits the proliferation of cultured human bladder epithelial cells by inhibiting the
production of heparin-binding epidermal growth factor-like growth factor (HB-EGF). The
activity of APF is increased in the urine of IC patients and allows diagnosis of the disease
with a sensitivity of 91.4% and a specificity of 90.6%. Increased levels of APF correlate with
decreased levels of HB-EGF; therefore both have been evaluated as markers of IC. Urinary
levels of APF and HB-EGF have also been used to assess treatment outcome and were found
to normalize following cystoscopy and hydrodistension as well as sacral neuromodulation.
Importantly, normalization of the levels of these markers correlated with symptomatic relief.
These markers are promising but are not yet commercially available. Clearly, additional studies
are needed to better characterize the clinical utility of these markers and to understand how they
contribute to the pathophysiology of IC.

E. Bladder Biopsy
Bladder biopsy has traditionally played a minimal role in the diagnosis of IC, as the histopatho-
logic features were consistent with inflammation but were characteristically believed to be
relatively nonspecific (Fig. 4). Although useful to evaluate suspicious lesions and exclude

Figure 4 H&E staining revealing nonspecific inflammation of the urothelium and superficial muscle
layer.
896 Tchetgen et al.

carcinoma in situ, bladder biopsy is not required to establish the diagnosis of IC. Recent findings,
however, suggest that some histopathologic biopsy features may be predictive of specific IC
symptoms and in fact may underly the variability observed in IC symptomatology. Indeed,
the association between histopathologic features and IC symptoms was investigated using the
ICDB cohort population (29), which includes patients clinically diagnosed with IC even if
they do not meet the strict NIDDK criteria. Of the 637 patients in the ICDB, 211 consented
to bladder biopsy. According to the study protocol, two samples were obtained from the most
diseased area of the bladder in the following order of priority: Hunner’s ulcer if present;
glomerulations if present; normal-appearing posterior bladder wall if neither Hunner’s ulcer
nor glomerulations were present. In addition a third sample was obtained from the trigone
area of the bladder to serve as an internal control. Patients’ self-reported symptoms of urgency
and pain were recorded on a 10-point Likert scale, and daytime and nighttime frequency were
recorded in a 3-day voiding diary. As previously reported, cystoscopic pathology (presence or
severity of glomerulations and presence or absence of Hunner’s ulcer) was not statistically
associated with any specific IC symptom. Select biopsy features, however, were found to be
associated with symptoms of nighttime frequency, urinary frequency, and urinary pain when
separate multivariable predictive models adjusting for patient characteristics were used for
analysis. Specifically, complete loss of urothelium, mastocytosis in the lamina propria, and
the presence of granulation tissue in the lamina propria were independently strongly predictive
of increased nighttime frequency. Similarly, increasing vascular density in the lamina propria
correlated with progressively higher nocturnal frequency. An increase in the percentage of
submucosal granulation was associated with increased urgency as well as increased nighttime
frequency. Lastly, urinary pain was positively associated with the percentage of mucosa
denuded of urothelium and the percentage of submucosal hemorrhage present.
On the basis of these provocative findings, the authors suggest that three biologic
processes may be involved in the pathophysiology of IC: loss of the integrity of the urothelium,
vascular damage, and mucosal mastocytosis. These findings give credence to some of the exist-
ing theories regarding the pathophysiology of the disease and further illustrate the heterogeneity
that has made this disease so difficult to characterize. They do little, however, to elucidate the
sequence of events that ultimately lead to the development of IC. The relationship between
biopsy features and the natural history of the disease or treatment outcome also remains unclear
at this time, although long-term follow studies may provide additional insight.

V. TREATMENT

Treatment modalities used in the management of IC are generally directed at one or more of the
prevailing theories regarding the etiology of the disease. We propose a treatment algorithm that
allows a comprehensive, systematic, and practical approach to the clinical management of this
challenging condition (Table 1).

A. Oral Therapy
1. Sodium Pentosan Polysulfate
This is the only FDA-approved drug designated for the treatment of IC. Its mechanism of action
is thought to involve correction of defects in the glycosaminoglycan layer of the bladder urothe-
lium. It may possibly act by binding toxic agents in the urine (30). Various clinical studies indi-
cate that 30 –40% of patients report a 40– 50% improvement in their symptoms. The minimum
 Interstitial Cystitis 897

Table 1 Practical Approach for the Management

of Interstitial Cystitis

Visit 1
History and physical examination
Urine culture, urine cytology, M4 (ureaplasm, chlamydia)
Vaginal wet prep
Initiation of oral therapy (for a minimum of 3 months)
Elmiron
Elavil or Neurontin if dominant pain component
Atarax (particularly if allergy prone)
Visit 2
MRI: rule out urethral diverticulum
Possible urodynamic testing + KCl testing
If suspect OAB (sensory vs motor urgency)
Visit 3
Cystoscopy and hydrodistension
Possible bladder biopsy
Visit 4 (at least 3 months after first visit)
Continue oral therapy if no side effects
Intravesical therapy (DMSO, heparin)
Pelvic floor therapy
Discuss sacral neuromodulation
Visit 5 (at least 3 months after fourth visit)
Trial of sacral neuromodulation

effective dose is 100 mg TID, although there have been anecdotal reports indicating that higher
doses may be more efficacious. Phase IV trials evaluating the efficacy of higher doses (600 mg or
800 mg daily) have not shown a definite difference. Long-term therapy is recommended as it
may take 6 months to a year for some patients to experience optimal symptomatic relief.

2. Antihistamines
Reports of antihistamine use to control the symptoms of IC have been largely anecdotal, and to
date, there have been no controlled trials verifying their efficacy. Hydroxyzine (Atarax, Vistaril)
is a histamine-1 receptor antagonist that can inhibit neuronal activation of mast cells. It may be
effective in atopic IC patients or those with significant mast cells on biopsy. The variability
noted in the efficacy of antihistamines may be explained by the previously presented pathophy-
siologic model in which mast cell degranulation is only one step in the chain of events leading to
inflammation and its associated symptoms. Antihistamines may be helpful in preventing symp-
tomatic flares but would be of minimal benefit once the patient is symptomatic. Hydroxyzine is
given in doses from 10 to 75 mg at bedtime and it may take up to 3 months to see an improve-
ment in symptoms.

3. Antidepressants
Antidepressant therapy (TCA, SSRIs) has some efficacy in the treatment of IC largely due to their
mode of action as pain neuromodulators. They are prescribed in escalating doses, as the side
effects can be prohibitive. Treatment can be initiated early in the course of the disease, particularly
if pain is a dominant presenting symptom. Amitryptyline (Elavil) is commonly prescribed in doses
898 Tchetgen et al.

beginning at 10 or 25 mg 1 h before bedtime and may be increased up to 75 mg as tolerated. With

fluoxetine (Prozac), dosing is started at 20 mg/d and may be increased as needed to 40 mg. Sertra-
line (Zoloft) is another SSRI that can be used and is well tolerated. Treatment is initiated at 50 mg/d
and may be increased to 100 mg. The therapeutic effects of antidepressants are multifactorial: they
improve sleep and as a result decrease nocturia; they have a neuromodulating effect by increasing
pain thresholds; they elevate mood; and they have an anticholinergic effect on the bladder and thus
may improve frequency by controlling instability.

4. Gabapentin (Neurontin)
This is an antiseizure medication that is used increasingly in the management of chronic pain. It
is thought to have a neuromodulating effect by increasing pain thresholds and may be useful in
IC patients in whom pain is a dominant symptom (31).

5. Anticholinergics, Antispasmotics
Patients with mild symptoms or coexisting bladder instability may get relief with the use of these
agents, but in the face of moderated to severe symptoms, they appear to have little efficacy.

B. Intravesical Therapy
1. Dimethyl Sulfoxide
DMSO is an organic solvent with anti-inflammatory, analgesic, and muscle-relaxant effect.
It also has collagen dissolution effects, which raises the issue of possible fibrosis developing
with long-term use of DMSO, and could be the underlying factor leading to progressive resist-
ance characteristically seen after several cycles of therapy. A review of the published experience
with DMSO in over 300 treated patients indicates a favorable response in a significant number of
patients with minimal associated morbidity (32). It remains a mainstay of therapy and can be
used in combination with hydrocortisone, heparin, and sodium bicarbonate to enhance its effect.

2. Heparin
Chronic intravesical instillation of heparin has been reported to have clinical efficacy in IC
patients (33). It consists of daily instillations of 10,000 – 20,000 units in 10 cc saline. Time
lag to symptomatic relief varies between 2 and 6 months, with the best results seen after 1 – 2
years of treatment. The mechanism of action is likely similar to that of sodium pentosan poly-
sulfate, as heparin has also been shown to reverse epithelial “leaks.”

3. Bacillus Calmete-Guerin (BCG)

A randomized, prospective, double-blind, placebo-controlled trial evaluating the efficacy of
intravesical BCG in the treatment of IC noted a 60% BCG response rate compared to a 27%
placebo response rate at a mean follow-up of 8 months (34). Outcome measures using a vali-
dated IC survey indicated a 63% improvement in IC symptomatology. The mechanism of action
of BCG in this setting is poorly understood but is thought to be immune mediated. Phase III
studies confirming the clinical efficacy of BCG therapy in the management of IC are lacking.
 Interstitial Cystitis 899

C. Muscle Manipulation and Sacral Neurostimulation

Physical therapy aimed at the pelvic floor musculature can have a therapeutic effect in some IC
patients. This is based on the premise that a dysfunctional pelvic floor may be the initiating event
ultimately leading to bladder wall neurogenic inflammation and that increased pelvic floor ten-
sion may be both a source of pain as well as a trigger for neurogenic inflammation via antidromic
reflexes (35). Ten IC patients underwent myofascial manual therapy that consisted of transvagi-
nal one-finger compression and lateral traction of the periurethral tissues and pubourethralis
muscle against the symphysis pubis followed by posterior traction via the vagina, and isometric
contractions of the pubovaginalis muscle. Seven of the 10 patients reported moderate to marked
improvement (51 –99% improvement) in their symptoms at a mean follow-up of 19 months.
Patients with urgency-frequency syndrome (which many believe is a milder form of IC) with
or without pain also responded favorably to this form of therapy, with 83% reporting marked
to moderate improvement or complete resolution of symptoms (35). Transvaginal Theile
massage in IC patients has also yielded encouraging results, with 90% of patients showing
short-term improvement in their symptoms (36).
Sacral neurogenic stimulation with the use of the Interstim device has recently been applied
to IC patients with promising results. A recent multicenter clinical trial evaluated the clinical
benefit of sacral neuromodulation in 22 IC patients and reported a significant decrease in urinary
frequency and pain as well as a significant improvement in IC symptom and problem index score
in 60% of the patients (O’Leary-Sant IC symptom and problem index) (37). As other investigators
have reported similar findings (38,39), sacral neuromodulation is increasingly considered in
patients whose symptoms are refractory to oral or intravesical therapies, and in whom a cystectomy
with urinary diversion would otherwise be the next best treatment option. The mechanism of action
of this form of neuromodulation is unclear but likely fits within the paradigm of IC as a neurogeni-
cally mediated cystitis. Interestingly, normalization of two previously described urinary markers of
IC, heparin-binding epidermal growth factor (HB-EGF) and antiproliferative factor (APF), was
associated with symptomatic relief in IC patients treated with sacral neurostimulation (40).

D. Surgical Treatment
1. Cystoscopy and Hydrodistension
As alluded to earlier in the chapter, cystoscopy and hydrodistension may have a therapeutic
effect in some patients, inducing symptom resolution for a period of 4– 12 months in up to
60% of patients. The mechanism of symptomatic improvement is not clear, although there is evi-
dence that the stretch stimulus of hydrodistension increases HB-EGF and reduces APF activity
in urine up to 2 weeks after distension (41).

2. Cystectomy and Urinary Diversion

Bladder removal remains a treatment option of last resort for patients whose symptoms are
refractory to less invasive forms of treatment. Most patients are symptom free after simple
cystectomy or supratrigonal cystectomy with enterocystoplasty, although persistent pelvic
pain has been reported in a few patients (42).

E. Treatment Outcome
There is a lack of outcome studies in the literature when it comes to the various treatments
available for the management of IC, mostly due to the paucity of valid outcome measures.
900 Tchetgen et al.

The O’Leary-Sant IC symptom index was recently validated in a randomized double-blind clini-
cal study evaluating the therapeutic effect of higher dosing of sodium pentosan polysulfate, and
proved to be a reliable and responsive measure of clinical improvement. There is clearly a need
for randomized controlled studies that critically evaluate the outcome of each of the many IC
treatments, and the ICSI is a useful outcome instrument that, if used uniformly, would facilitate
comparisons between studies.

VI. THE FUTURE

The primary issue to be addressed in the near future remains elucidating the pathophysiology of
IC. Theories abound, but unifying concepts are sketchy at best. The role of neurogenic inflam-
mation is being actively investigated and has added a new dimension of neural-directed thera-
pies to the treatment armamentarium, though more long-term studies are needed to confirm early
promising results. Other potential therapies such as Montelukast (a cysteinyl leukotriene D4
receptor antagonist), capsaicin/resiniferatoxin (C-fiber neurotoxins), and quercetin (a bioflavo-
noid) also need to be further evaluated in larger randomized placebo-controlled trials.

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8. Novicki DE, Larson TR, Swanson SK. Interstitial cystitis in men. Urology 1998; 52:621 – 624.
9. Schuster GA. Interstitial cystitis in children: not a rare entity. Urology 2001; 57(suppl 6A):107.
10. Propert KJ, Schaeffer AJ, Bresinger CM. A prospective study of interstitial cystitis: results of longi-
tudinal follow-up of the interstitial cystitis database cohort. J Urol 2000; 163:1434 – 1439.
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Urology 2001; 57(6 suppl 1):95– 99.
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imidazole-acetic-acid) in a painful bladder disease. Br J Urol 1987; 60:39– 42.
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NY Acad Sci 1998; 840:619.
20. Pang X, Marchand J, Sant GR. Increased number of substance P positive nerve fibers in interstitial
cystitis. Br J Urol 1995; 75(6):744– 750.
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8:139– 145.
22. Suzuki H, Miura S, Liu YY. Substance P induces degranulation of mast cells and leukocyte adhesion
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J Urol 1999; 162:231.
24. Jasmin L, Janni G, Manz HJ. Activation of CNS circuits producing a neurogenic cystitis: evidence for
centrally induced peripheral inflammation. J Neurosci 1998; 18(23):10016 – 10029.
25. Jasmine L, Janni G, O’Hara PT. CNS induced neurogenic cystitis is associated with bladder mast cell
degranulation in the rat. J Urol 2000; 164(3):852– 855.
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stitial cystitis: results from the interstitial cystitis database study. Urology 2001; 57(suppl 6A):67–81.
30. Sadhukhan PC, Tchetgen BM, Rackley RR. Sodium pentosan polysulfate reduces urothelial
responses to inflammatory stimuli via an indirect mechanism. J Urol 2002; 168:289 – 292.
31. Sasaki K, Smith CP, Chuang YC. Oral gabapentin (neurontin) treatment of refractory genitourinary
tract pain. Tech Urol 2001; 7(1):47 – 49.
32. Parkin J, Shea C, Sant GR. Intravesical dimethyl sulfoxide (DMSO) for interstitial cystitis: a practical
approach. Urology 1997; 49(5A suppl):105 – 107.
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Urol 1994; 73:504 – 507.
34. Peters K, Diokno A, Steinert B. The efficacy of intravesical Tice strain bacillus Calmette-Guerin in
the treatment of interstitial cystitis: a double blind, prospective, placebo-controlled trial. J Urol 1997;
157(6):2090– 2094.
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frequency syndrome. J Urol 2001; 166(6):2226 – 2231.
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intervention for women with interstitial cystitis. Urology 2001; 57(6 suppl 1):120.
37. Whitmore KE, Lukban JC, Payne CK. Sacral neuromodulation in patients with interstitial cystitis:
a multicenter clinical trial. J Urol 2001; 165(5 suppl):69.
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able pelvic pain. Urology 2001; 57(6 suppl 1):124.
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cystitis. Urology 2001; 57(1):207.
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60
Chronic Pelvic Pain in Interstitial Cystitis

James Chivian Lukban

Urogynecology Associates of Colorado, Denver, Colorado, U.S.A.
Kristene E. Whitmore
Graduate Hospital, Philadelphia, Pennsylvania, U.S.A.

I. INTRODUCTION

Interstitial cystitis (IC) is a clinical condition of multifactorial etiology characterized by urinary

frequency, urgency, debilitating episodic bladder discomfort, and the potential for the develop-
ment of chronic pelvic pain (CPP). In a multicenter, observational study designed to evaluate
the treated history of IC, 379 of 424 patients (94%) reported the presence of pain, with 24%
of those suffering from severe discomfort (1). In a survey of 374 patients performed to charac-
terize the natural history of IC, 96% of respondents overall reported pain, with 54% of subjects
describing their discomfort as severe or excruciating (2). Of respondents with symptoms for
.15 years, 99% reported pain, with 62% reporting the presence of severe or excruciating
discomfort. Pelvic pain has been found to be a preponderant, durable, and potentially debilitating
component of IC symptomatology. This chapter will consider the etiology and treatment of CPP
in patients with IC.

II. ETIOLOGY OF CHRONIC PELVIC PAIN IN INTERSTITIAL CYSTITIS

Contributing mechanisms to IC etiopathogenesis include, but are not limited to, a deficient or
dysfunctional glycosaminoglycan layer, altered urothelial permeability, mastocytosis, “toxic
urine,” and autoimmunity (3 – 7). One common element contributing to IC symptomatology,
independent of etiology, is the presence of chronic inflammatory changes within the bladder
wall. Prolonged bladder epithelial inflammation leads to persistent peripheral afferent stimu-
lation, and the potential for the development of reduced nociceptive thresholds, neuronal hyper-
sensitivity and spontaneous neuronal activity within the central nervous system (CNS). This
phenomenon is termed central sensitization, and is an important mechanism in the evolution
of centrally derived CPP.
Patients with IC have also the potential to exhibit neurogenic pelvic floor muscle spasm
(high-tone pelvic floor dysfunction), which may add to the generation of CPP. Pelvic muscle
spasm in patients with IC occurs, in theory, as a result of centrally mediated sacral somatic effer-
ent activity following sacral afferent barrage. Nociceptive impulses created by a spastic pelvic
floor may also perpetuate IC pathology through the indirect trigger of antidromic (retrograde)
transmission along visceral afferent C fibers with resultant neurogenic bladder inflammation.

903
904 Lukban and Whitmore

III. CENTRALLY DERIVED CHRONIC PELVIC PAIN

The bladder wall contains parasympathetic afferents in the form of lightly myelinated Ad fibers
and unmyelinated C fibers, possessing predominantly mechanosensitive (tension) and chemo-
sensitive (nociception) properties, respectively (8). Upon bladder filling, Ad fibers respond to
physiologic, low-threshold intravesical pressure, while C fibers are typically silent. Unmyeli-
nated bladder afferents exhibit impulse transmission following chemical irritation and may dis-
play ongoing activity even after irritant removal (9). Significant inflammation of the bladder
epithelium may also provide chemosensitive afferents the ability to adopt a mechanosensitive
capacity, firing in response to low-threshold intravesical pressure (9,10). Such novel mechano-
sensitivity is thought to be mediated by nerve growth factor, as has been suggested in experimen-
tal rodent models (11). Myelinated mechanosensitive afferents may undergo a similar reactive
change and develop chemosensitive properties, responding to urinary toxins and inflammatory
mediators (12). Postinflammation C-fiber activation and peripheral afferent change play an
important role in the creation of visceral pain, as physiologic bladder filling and epithelial
exposure to mildly noxious stimuli may result in a significant afferent barrage.
Chronic nociceptive input from the periphery as mediated by the presynaptic release of
neuropeptides (e.g., substance P) and excitatory amino acids (e.g., glutamate) can establish
long-standing functional changes within the CNS essential to the development of central sensit-
ization (13). As substance P (SP)-laden C fibers bombard sacral dorsal horn cells, postsynaptic
upregulation of SP receptors (NK1 receptors) may occur (14). Upregulation following long-term
somatic stimulation has been observed, with evidence supporting similar changes in response to
chronic visceral inflammation having recently been reported (14,15). Ishigooka et al. studied
NK1 receptor immunoreactivity in the lumbosacral dorsal horn cells of 12 female rats following
cyclophosphamide-induced bladder inflammation. Significant increases in postsynaptic NK1
receptor staining intensity, consistent with enhanced neuronal receptor expression, was observed
in bladder-specific spinal segments L6 –S1. It has also been postulated that repetitive dorsal horn
cell depolarization, as triggered by SP, relieves a voltage dependent Mg2þ block of postsynaptic
glutamate receptors (NMDA receptors) (13,16). Both the upregulation of NK1 receptors and the
increased availability of NMDA receptors following chronic afferent nociceptive input increase
the total number of postsynaptic sites for neurotransmission. Such events may result in lower
nociceptive thresholds and postsynaptic hypersensitivity, consistent with a state of central
sensitization.
In an electrophysiologic study of postinflammation CNS changes in rats, McMahon
observed the behavior of dorsal horn cells in L6 and S1 following turpentine and mustard
oil –induced bladder inflammation (10). An evaluation of 14 postsynaptic neurons revealed pro-
gressive increases in response to subsequent electrical stimulation in eight dorsal horn cells
(57%) and spontaneous activity in 10 (71%). These findings provide further evidence for the
development of central sensitization in response to significant visceral insults. The durability
of these changes, however, is not known, with some advocating the essential need for continued
peripheral input in the maintenance of central sensitization (17,18).

IV. NEUROGENIC PELVIC FLOOR MUSCLE SPASM

A. Anatomy of the Pelvic Floor
The pelvic floor contains layers of connective tissue and muscle that provide support to the
pelvic viscera. The urethra, vagina, and rectum are attached to the pelvic sidewalls by the endo-
pelvic fascia (vesico vaginal adventitia), penetrating the pelvic floor at the urogenital hiatus.
 Chronic Pelvic Pain in IC 905

Immediately beneath the endopelvic fascia is the pelvic floor musculature (PFM). It is composed
of the puborectalis, levator ani (pubococcygeus and iliococcygeus), and coccygeus muscles. The
puborectalis originates from the pubis and runs posteriorly to join its contralateral muscle behind
the anorectal junction, forming a U-shaped sling. The pubococcygeus muscle emanates from the
pubis, traveling posteromedially to insert on the superior surface of the coccyx and the anococ-
cygeal raphe. The iliococcygeus arises from the arcus tendineus levator ani, running posterome-
dially to insert on the coccyx and anococcygeal raphe. The coccygeus muscle originates from the
ischial spine and sacrospinous ligament, inserting onto the lateral coccyx and lower sacrum.
Beneath the PFM is the perineal membrane, which together with the PFM defines the pelvic
floor. The perineal membrane is a triangular sheet of dense fibromuscular tissue spanning the
anterior half of the pelvic outlet. Its attachments include the urethra, vagina, and perineal
body medially, and the inferior ischiopubic rami laterally (19).

B. Innervation of the Pelvic Floor and Bladder

The nerve supply to the pelvic floor and bladder is of somatic and autonomic origin respectively.
Somatic fibers from S2 – S4 form the pudendal nerve, which supplies the perineal surface of the
PFM. Sacral nerve root branches also innervate the pelvic floor directly through fibers traveling
to the visceral surface of the PFM. Parasympathetic innervation of the bladder begins with pre-
ganglionic fibers emanating from S2 – S4 and ends in the postganglionic muscarinic receptors of
the bladder wall. Sympathetic innervation arises from T10 – L2, with postganglionic fibers travel-
ing to beta-adrenergic receptors in the smooth muscle of the bladder wall, and alpha-adrenergic
receptors in the smooth muscle of the bladder neck and proximal urethra (20).

C. Normal Pelvic Floor Function

The PFM performs an important role in tonic support of the pelvic viscera. Such support is pro-
vided by a preponderance of type I (slow-twitch) fibers within the PFM. In the maintenance of
urinary continence, tonic muscular forces are provided by the external striated urethral sphincter
(composed of the intramural striated sphincter and the periurethral levator ani musculature) and
are important in effecting adequate urethral support. In addition, a minority population of type II
(fast-twitch) fibers within the levator ani musculature provides a mechanism for active periure-
thral muscular contraction at the time of provocative increases in intra-abdominal pressure (21).
Less perceptible tonic increases in the PFM occur during bladder filling as part of a sacral spinal
mechanism known as the guarding reflex whereby parasympathetic impulses triggered by vesi-
cal distension lead to somatic efferent stimulation of the PFM and the external striated urethral
sphincter (20).

D. High-Tone Pelvic Floor Dysfunction

High-tone PFD refers to the clinical condition of hypertonic, spastic PFM with resultant impair-
ment of muscle isolation, contraction, and relaxation. Manifestations include voiding dysfunc-
tion, urinary frequency, urinary urgency, pelvic pain, painful bowel movements, and impaired
rectal evacuation. High-tone PFD, as a chronic, painful clinical condition, was introduced in
the colorectal literature, having been reported as any one of the following clinical entities:
coccygodynia; tension myalgia of the pelvic floor; coccygeus-levator spasm syndrome; levator
syndrome; and levator ani spasm syndrome.
906 Lukban and Whitmore

Thiele described coccygodynia in 1937 as an entity not only characterized by pain loca-
lized to the coccyx, but as a syndrome also noteworthy for the presence of levator ani and
coccygeus muscle spasm (22). In his original communication, 64 of 69 patients with coccygeal
pain were found to have spastic PFM on rectal examination. Work published by the same author
in 1963 further characterized coccygodynia based on a review of 324 case records (23).
Patient symptoms included pain localized to the lower sacrum and coccyx, often exacerbated
by prolonged sitting. Few of his patients, however, exhibited tenderness of the coccyx
upon direct palpation or manipulation, a finding consistent with pain born of PFM spasm,
and not of primary sacrococcygeal pathology. Common etiologic factors included anal
infection and chronic trauma as identified in 178 (55%) and 106 (33%) patients, respectively.
Anal infection was thought to cause reflex PFM spasm through lymphatic drainage of
organism-laden lymph. Chronic trauma included poor sitting posture and extended vehicle
rides.
Sinaki et al. employed the term tension myalgia of the pelvic floor to describe a sample of
94 patients with spastic, tender PFM (24). Common symptoms included low back pain in 82%
and a “heavy feeling in the pelvis” in 64%, with the appearance of symptom aggravation in 88%
of patients following prolonged sitting. Pelvic floor muscle spasm was attributed to habit con-
traction of the pelvic floor in addition to a component of hypochondriasis.
Paradis and Marganoff used the term coccygeus-levator spasm syndrome to characterize
92 patients with pelvic floor spasm and “rectal” pain (25). Patients were found to be particularly
tender at muscular sites adjacent to the ischial spines and coccyx, with a suggestion by the
authors of a more significant involvement of musculofascial, ligamentous, and tendinous struc-
tures than of the muscles themselves. Neither infection nor trauma was identified in his patients
as an etiologic factor, with the attribution of disease presence to psychoneurosis.
Grant et al. employed the term levator syndrome to describe a sample of 316 patients exhi-
biting PFM spasm and tenderness (26). The predominant symptom was that of rectal discomfort.
The etiology of levator syndrome was reported as unknown.
All of the syndromes as presented above represent a similar clinical condition character-
ized by tender, spastic PFM manifesting as pain localized to the coccyx and lower sacrum, rectal
pain, or generalized pelvic discomfort. Etiologic factors as reported are varied and include infec-
tion, chronic sacrococcygeal trauma from poor posture or prolonged sitting, and hypochondria-
sis or hysteria. A definitive cause of high-tone PFD as encountered in patients with IC has not
been established and is most likely the result of several coexisting factors.

E. High-Tone Pelvic Floor Dysfunction in Patients with Interstitial Cystitis

In 1973, Lilius et al. published a thoughtful study on the prevalence of levator spasm in patients
with IC (27). As many of their patients complained of pain not only in the area of the bladder but
also in the regions of the sacrum, coccyx, and anus, they investigated the presence of concomi-
tant PFM spasm. Twenty-five of 31 patients (81%) with IC were found to have spasm and
tenderness of the levator ani musculature, which they termed levator ani spasm syndrome. Lilius
and coworkers postulated that frequent restraint of urine led to sustained PFM spasm, and in
cases of more severe bladder disease, high-tone pelvic floor musculature was thought to appear
in response to afferent autonomic pain impulses from the bladder wall. The researchers also
assigned importance to poor sitting or working posture as contributing factors to the develop-
ment of levator ani spasm syndrome. Their excellent clinical observations, which have since
been supported by Schmidt and Vapnek (28) and Moldwin and Mendelowitz (29), suggest
both a neurologic and musculoskeletal etiology to the development of high-tone pelvic floor dys-
function in patients with IC.
 Chronic Pelvic Pain in IC 907

One speculative possibility in the neurogenic development of high-tone PFD is that the affer-
ent “bombardment” seen in patients with IC may enhance and sustain the guarding reflex which
manifests as pelvic floor hypertonus. This concept has been alluded to previously by Chancellor
(30). A significant musculoskeletal component to high-tone PFD has been suggested by several
authors. Thiele (23), Sinaki et al. (24), and Lilius et al. (27) have associated PFM spasm with
poor posture and prolonged sitting. The “typical pelvic pain posture” as described by Baker,
characterized by exaggerated lumber lordosis, anterior pelvic tilt, and thoracic kyphosis, has
been implicated in the subsequent development of sacroiliac pathology (31). As the sacroiliac
joint moves, however slightly, through upslip, downslip, or torsion, the PFM to which it is attached
is also subject to dynamic change (32). Muscles that are stretched or compressed are prevented
from maintaining a normal resting tone and are prone to trigger point formation and hypertonicity
(31). Pelvic floor dysfunction is also thought to appear in reaction to overflexion of the coccyx
while sitting with incorrect posture (23). Spasm in these cases may be the result of a change in
tension of the PFM to which the coccyx is attached (23). The presence of sacroiliac dysfunction
with or without a contribution of poor posture may reasonably serve as a trigger for the develop-
ment of high-tone PFD. It is likely that the degree of high-tone PFD encountered in IC represents
the sum of both neurologic and musculoskeletal components (33). Of interest is the report of lateral
sacral shift in an unknown number of patients with coccygeus spasm (34).

V. ANTIDROMIC NEUROINFLAMMATION

Painful pelvic floor musculature may perpetuate bladder pathology through the induction of
CNS-mediated antidromic impulse transmission along visceral bladder afferents with resultant
neurogenic inflammation. Experimental evidence for centrally mediated neurogenic bladder
inflammation was reported by Pinter and Szolcsanyi, who created an animal model to prove anti-
dromic transmission through capsaicin-sensitive afferents (C fibers) to the bladder following
CNS stimulation (35). Electrical stimulation of the lumbosacral dorsal nerve roots in anesthe-
tized rats resulted in significant plasma extravasation as quantified by the accumulation of
Evans Blue tracer in bladder tissue. Extravasation indicative of neurogenic bladder inflammation
was significantly reduced following the functional inactivation of visceral bladder afferents
through pretreatment with capsaicin.
Jasmin et al. employed the neurotropic pseudorabies virus (PRV) to illustrate the appearance
of immune-mediated hemorrhagic cystitis following sacral somatic inoculation (36,37). Following
injection of PRV into the abductor caudae dorsalis (ACD) tail muscle of the rat, behavioral and
histologic evidence of cystitis appeared 84 h postinjection. A specific sacral somatic fiber—dorsal
horn cell—bladder afferent (C-fiber) circuit was suggested, as systemic examination of other abdo-
minopelvic viscera revealed the absence of postinoculation inflammation. Additionally, selective
peripheral and central denervation prevented the appearance of cystitis. These researchers theo-
rized that sacral somatic neurons within the dorsal horn have the capacity to trigger neighboring
visceral afferent neurons, resulting in antidromic C-fiber impulse transmission with subsequent
neurogenic bladder inflammation. In additional work by the same investigators, local neuroinflam-
mation as a mast cell–mediated event was proved as a significant reduction in the number of
microscopically visible mast cells (consistent with degranulation) was detected in the bladder
wall post-PRV inoculation (37). Additionally, pre-emptive mast cell degranulation with the
mast cell degranulator, compound 48/80, resulted in the absence of cystitis.
Clinical evidence of antidromic bladder neuroinflammation following pelvic floor muscle
spasm was offered by Weiss, who noted moderate to marked symptom improvement in 35 of
42 patients (83%) with urgency-frequency syndrome and similar improvement in seven of
908 Lukban and Whitmore

Figure 1 Proposed mechanism for concomitant IC and PFD.

10 patients with IC following internal pelvic floor myofascial trigger point massage (38).
A proposed mechanism for concomitant IC and PFD is presented in Figure 1.

VI. TREATMENT OF CENTRALLY DERIVED CHRONIC PELVIC PAIN

A. Opioids
Pain relief from the administration of opioids occurs in part through the activation of opioid recep-
tors in the periaqueductal gray (PAG) of the midbrain, with descending inhibitory impulses pro-
viding pain relief by raising nociceptive thresholds within dorsal horn cells. Inhibitory control
from the PAG is transmitted through the rostral ventromedial medulla and the dorsal lateral funi-
culi with spinal nociceptive inhibition mediated by serotonin, norepinephrine, and acetylcholine
(39).
In patients with severe pelvic pain from interstitial cystitis, narcotics are added to the treat-
ment regimen. We typically employ short-acting oxycodone or hydrocodone for significant episo-
dic discomfort. Long-acting formulations of oxycodone or morphine serve a role in the treatment
of severe persistent pelvic pain, and are administered in conjunction with immediate-release
opioids for breakthrough discomfort. The quantification of immediate-release drug consumption
daily is used to titrate an appropriate dose of long-acting narcotic (40). We begin with an
initial regimen of long-acting, controlled-release oxycodone at a dose of 10 mg BID, and titrate
as appropriate. Opioids may be used in conjunction with other oral IC agents, with both hydroxy-
zine and amitriptyline exhibiting the ability to potentiate narcotic pain relief (40).
 Chronic Pelvic Pain in IC 909

B. Amitriptyline
Tricyclic antidepressants have been employed as analgesic agents in nonurologic popula-
tions, with clinical benefit proved in patients with postherpetic neuralgia, diabetic peripheral
neuropathy, and chronic low back pain (41 – 43). Its use in those with IC has more recently
been reported (44,45). The mechanism of tricyclics in alleviating pain is thought to result
from the inhibition of serotonin and noradrenaline reuptake (46). Its analgesic benefit is thought
to be independent of its effect on mood (42).
Hanno et al. evaluated 20 IC patients treated with amitriptyline employing an initial dose
of 25 mg at bedtime, with increases to 50 mg and 75 mg in weeks 2 and 3, respectively (44).
Treatment resulted in a significant decrease in daytime frequency (average minutes between
voids: pretreatment, 62.8; posttreatment, 117) and in pain as rated on a 1 to 10 scale (mean
value: pretreatment, 6.1; posttreatment, 3.3). Eleven of 19 patients reported an improvement
in urinary urgency. Kirkemo et al. evaluated 30 IC patients administered 25– 75 mg of amitripty-
line nightly (45). Patients were issued questionnaires and voiding diaries to assess symptom
improvement. Ninety percent reported subjective improvement at 2 months. A 50% reduction
in frequency and nocturia was reported in those with a maximum cystometric capacity under
anesthesia .450 cc. In patients with a bladder capacity ,450 cc, despite persistent frequency,
an improvement in suprapubic pain was reported.
Initial doses of amitriptyline should begin with 10 mg at bedtime. Increases to 25 mg,
50 mg, and 75 mg at 2- and 3-week intervals may follow with a maximum dose of 150 mg
recommended. Dry mouth and sedation are typically the two most common side effects (41,42).

C. Gabapentin
Gabapentin is an anticonvulsant medication with proven effectiveness in neuropathic pain syn-
dromes (47,48). It has been employed more recently as an agent in the treatment of pain in those
with IC. Its mechanism of action has not been completely elucidated. Gabapentin is a structural
analog to gamma-aminobutyric acid (GABA); however, it does not stimulate GABA receptors,
nor does it alter GABA reuptake (49). In two case studies reported by Hansen, IC patients taking
1600 mg gabapentin daily (one for 6 weeks and one for an undefined period of time) exhibited a
substantial improvement in pain, with a concomitant decrease in narcotic use (50). Sasaki et al.
recently reported data on 21 patients with refractory genitourinary pain treated with gabapentin
(51). A mean dose of 1200 mg daily (range 300 –2100 mg) was administered over a 6-month
period. Pain severity was evaluated by a 1 to 5 subjective severity index and a 10-cm visual
analog scale. Ten of 21 patients reported subjective improvement in pain, with five out of
eight patients diagnosed with IC reporting benefit.
Dosing may begin with 100 mg at bedtime, with increases in increments of 100 mg every
3 –7 days as tolerated. In our practice, we begin with dosing at bedtime followed by the addition
of medication in the morning, and then at midday as warranted. Doses up to 3600 mg daily have
been administered, with dizziness and somnolence noted to be the most common side effects
(47,48).

D. Additional Therapeutic Considerations

1. Resiniferatoxin
Resiniferatoxin is an ultrapotent vanilloid receptor agonist which functions through C-fiber
desensitization following intravesical instillation. Sensory stimulation by this agent has been
found to occur without the intense noxious excitation as encountered with the instillation of
910 Lukban and Whitmore

capsaicin (52). A randomized, placebo-controlled study of resiniferatoxin in the treatment of

hypersensitive disorders of the bladder was performed by Lazzeri et al. (53). Eighteen IC
patients with a mean disease duration of 16.9 months were evaluated through a voiding pattern
assessment and pain scale. After a single treatment, patients receiving resiniferatoxin were noted
to exhibit a significant reduction in frequency and pain at a 30-day follow-up with loss of sig-
nificant pain relief at 90 days. A dose of 10 nM of resiniferatoxin was employed with no reported
neurotoxic effects. Four of the patients receiving drug complained of a transient light warm or
burning sensation at the suprapubic or urethral level. The efficacy of intravesical C-fiber desen-
sitization in the treatment of centrally derived pain is unknown, and completion recently of a
pilot RCT showed no clinical benefit.

2. Sacral Neuromodulation
Sacral nerve root stimulation has shown promise as a therapeutic modality in patients with IC. Its
mechanism of pain relief is thought to involve stimulation of sacral somatic afferents with com-
petitive inhibition of slow C-fiber transmission to the CNS (54,55). This theory is based on the
cutaneous “gate control” theory of pain in which large diameter fibers inhibit transmission of
small diameter fibers to higher centers (56).
Several recent studies have evaluated sacral nerve root stimulation in patients with pelvic
pain and the apparent absence of pelvic floor muscle spasm. Maher et al. prospectively evaluated
15 consecutive IC patients with a mean disease duration of 5.2 years who underwent a 7-to-10-
day trial of percutaneous third nerve root stimulation (57). Evaluation was in the form of voiding
diary, pain score (0 to 10), and quality-of-life questionnaire. Test stimulation resulted in statisti-
cally significant improvements in mean daytime frequency (decrease from 20 to 10 voids per
day), nocturia (decrease from six to two voids per night), mean voided volume (increase from
90 to 143 cc), and mean bladder pain (decrease from 8.9 to 2.4). The quality-of-life variables
of general health, social health, and bodily pain also exhibited significant improvement.
The efficacy of sacral nerve stimulation following permanent implantation in patients with
chronic intractable pelvic pain of a median duration of three years was considered by Siegel et al.
(58). Ten patients following successful percutaneous sacral nerve root stimulation were
implanted with a neuroprosthetic device, with lead placement in sacral foramen 3 or 4 in
eight and two cases, respectively. The permanent implant was found to decrease the severity,
number of hours (total duration of pain per week), and “rate of pain,” with six of 10 patients
reporting a significant improvement in overall pelvic pain symptomatology (median follow-
up of 19 months). No serious device complications were reported. A total of 27 adverse events
were listed, with the three most common found to be local wound complications (6 cases),
change in pain location (4), and implant site pain (4). The long-term benefit of sacral neuro-
modulation in the treatment of centrally derived pain is unknown. As patients in the aforemen-
tioned studies had symptoms of pelvic pain measured in years, it is likely that some possessed
centrally derived pain. Such patients in theory may receive therapeutic benefit from the elimin-
ation of peripheral contributions to dorsal horn cells which possess hypersensitivity and low
nociceptive thresholds. A summary of therapeutic measures for the treatment of IC patients
with central sensitization is offered in Table 1.

3. Surgical Therapy
Major surgical therapy is the final therapeutic option for patients with IC, of whom only 10%
may have disease severity appropriate for such intervention (59). Procedures including subtrigo-
nal or supratrigonal cystectomy with substitution cystolplasty are typically employed, with suc-
cess rates ranging from 25% to 100% (60). Urinary diversion with or without cystectomy may be
 Chronic Pelvic Pain in IC 911

Table 1 Therapy for Centrally Derived Chronic Pelvic Pain

Agent Proposed mechanism of action Initial dosage

Opioids (oxycodone) Stimulation of opioid receptors in 5 hrs 4–6 PRN

midbrain periaqueductal gray (immediate release)
10 mg BID (long acting)
Amitriptyline Inhibition of serotonin and 10 mg at bedtime
norepinephrine reuptake
Gabapentin Unknown 100 mg at bedtime
Resiniferatoxin Desensitization of C fibers Single treatment
Sacral neuromodulation Inhibition of C-fiber transmission to CNS Test stimulation

indicated following failure of substitution cystoplasty, or in patients who are inappropriate can-
didates for orthotopic substitution (e.g., severe stress incontinence or inability to catheterize via
urethra due to exacerbation of symptoms) (60). Despite technically appropriate surgical inter-
vention, patients may still suffer from persistent discomfort. In a report of four patients (three
with IC and one with voiding dysfunction) with severe intractable pelvic pain despite cystectomy,
hysterectomy, and bilateral salpingo-oophorectomy, Baskin et al. suggested the presence
of central sensitization or untreated pelvic floor dysfunction as potential contributors to
persistent symptomatology (61). Appropriate preoperative workup in IC patients prior to
embarking upon surgical therapy should thus include not only an appropriate genitourinary
and gynecologic assessment, but an evaluation of the pelvic floor, a visit to a pain specialist
(to rule out psychogenic pain and/or central sensitization), and a thorough psychological
assessment.

VII. TREATMENT OF HIGH-TONE PELVIC FLOOR DYSFUNCTION

A. Physical Therapy
Patients identified with high-tone PFD are subsequently sent to a physical therapist for assess-
ment to identify sacroiliac malalignment, also known as sacroiliac dysfunction. Evaluation in
brief includes a specific assessment of the following: pelvic alignment; lumbar and hip active
and passive range of motion; strength and flexibility of the spinal and pelvic stabilizers; and ten-
derness and spasm of the pelvic supportive musculature. Typical manual therapy techniques
employed in the correction of sacroiliac dysfunction, if identified, include myofascial release,
joint mobilization, muscle energy, strengthening, stretching, neuromuscular reeducation, and
instruction in an extensive home exercise program. The speculative logic in correcting sacroiliac
dysfunction in patients with high-tone PFD is such that if sacroiliac alignment is restored,
normal tension to the PFM returns, allowing for the resolution of a high-tone state.
In a pilot study of 16 patients with high-tone PFD, sacroiliac dysfunction, and IC, manual
physical therapy was performed to assess the benefit of such treatment in reducing IC symptoms
(frequency, urgency, nocturia, pain) as measured by the O’Leary-Sant Symptom Index (62).
Dyspareunia was also evaluated in these patients employing the “sex life” question as taken
from the Modified Oswestry Disability Scale. A comparison of pre- and posttreatment Modified
Oswestry scores revealed an improvement in dyspareunia in 15 (94%) patients. A comparison
of pre- and posttreatment O’Leary-Sant scores also showed improvement in 15 (94%) subjects.
Schroeder reported the use of an undefined regimen of physical therapy in a pediatric and
912 Lukban and Whitmore

adolescent population in which 20 of 21 patients with musculoskeletal pelvic pain were success-
fully treated (63).

B. Thiele Massage
Following sacroiliac realignment, patients are reassessed by digital exam and perineometry. If
PFM spasm persists as either diffuse or localized hypertonicity, subjects undergo a regimen
of Thiele massage. In his original description of this technique, Thiele reported a personal series
of 31 cases of coccygodynia and PFM spasm in which 19 (61.3%) were cured and 17 (35.5%)
were improved (undefined criteria) following transrectal massage (22). The author combined his
data with those taken from eight other proctologists employing the same technique, and reported
a 93.7% cured and improved rate in a total of 80 patients. Treatment consisted of an average of
11 treatments over an average of 11 weeks.
Weiss recently reported the use of PFM trigger point massage in 45 women and seven men
with “urgency-frequency syndrome” of whom 10 fulfilled undefined cystoscopic IC criteria (38).
Following one to two visits per week for 8– 12 weeks, seven of 10 IC patients exhibited .50%
improvement in overall symptoms.
In our practice, we perform Thiele massage transvaginally as this is more comfortable for
our patients. In performing this technique, pressure is applied to the PFM fibers longitudinally
from origin to insertion. Ten to 15 sweeps of maximally tolerated pressure are performed on
each side followed by myofascial massage (10 –15 sec of sustained pressure) to tender points.
Patients are treated once or twice a week for a duration of 6– 8 weeks, less frequently than prac-
ticed by Thiele, who applied therapy every day for 5– 6 days then every other day for 7 – 10 days
as an initial course.

C. Pelvic Floor Muscle Exercises and Biofeedback

Patients with persistent high-tone PFD despite manual physical therapy and Thiele massage may
benefit from PFME and BF. In a study of 60 patients with intractable rectal pain, 70% of whom
were diagnosed with either levator spasm or coccygodynia, Ger performed BF on 14 subjects
employing rectal EMG (64). Following a minimum of six weekly 30- to 60-min sessions,
pain relief was rated as excellent or good (undefined) in six (43%) patients at a mean follow-
up of 15 months. Heah prospectively treated 16 patients with levator ani syndrome with biofeed-
back employing a rectal manometric balloon (65). A significant improvement in pain was
achieved with scores recorded on a 0-to-10 linear analog scale (median pain score before BF,
8; median pain score after BF, 2). All patients exhibited nontender musculature posttherapy.
The theory behind BF in the treatment of high-tone PFD is that of achieving conscious control
over PFM contraction and relaxation, thus breaking the cycle of spasm.

D. Electrical Stimulation
The use of electrogalvanic stimulation (EGS) in patients with levator syndrome was first
described by Sohn (66). Seventy-two patients were treated with EGS at 80 Hz to a point of
mild discomfort for a duration of 1 h/d for three sessions over a 3-to-10 day period. Fifty
(69%) patients rated treatment as excellent (complete pain relief), and 15 (21%) rated therapy
as good (pain resolution with ,3 recurrences in the 6 –30 month follow-up). The mechanism
of pain relief in these patients was reported as muscle fatigue following sustained contractions
in addition to motoneuron suppression. Other investigators have reported the use of EGS in
 Chronic Pelvic Pain in IC 913

patients with levator syndrome reporting variable results with excellent or good improvement
ranging from 43% to 91% (67 –70). Electrical stimulation in patients with high-tone PFD is
delivered with the same intention as EGS in creating muscle fatigue with resultant relaxation;
however, ES employs low-voltage alternating current whereas EGS employs high-voltage direct
current (71). Electrical stimulation may be provided for patients with high-tone PFD at the time
of BF therapy.
Administration of anogenital electrical stimulation involves the use of an intravaginal
or intrarectal probe with delivery of current to the pudendal nerve or its branches. Electrical
stimulation in the treatment of PFD employs a frequency of 50 Hz (or higher) to ensure PFM
contraction and resultant fatigue. Therapy may be performed in combination with PFM exercises
and biofeedback in the form of weekly 23-min sessions over 6 weeks. Each session begins with
4 min of biofeedback during which time the patient is asked to offer PFM contractions for 5 sec
followed by 10-sec intervals of relaxation. Anogenital stimulation is then applied for 15 min fol-
lowed by four additional minutes of PFM exercises with biofeedback. Patients with high-tone
PFD may maintain PFM fitness with a home device.

E. Pharmacologic Therapy
Several authors have reported success in the treatment of high-tone PFD with diazepam. Grant
reported the use of this medication in conjunction with heat and transrectal massage, with 68%
of patients reporting good (symptom relief by three or fewer massage treatments) results (26). In
a smaller series of six females with external sphincter spasm, sustained relief from urgency,
suprapubic discomfort, and voiding dysfunction was achieved following a 2-to-6-month course
of diazepam taken in doses of 2– 6 mg/d (72).
We have had anecdotal success with tizanidine hydrochloride in relieving high-tone PFD.
As it is a centrally acting a-adrenergic agonist, it should be used with caution in patients taking
other centrally acting agents. We usually begin with a low dose of 2 mg/d and titrate as
appropriate.

Figure 2 Treatment of high-tone pelvic floor dysfunction.

914 Lukban and Whitmore

F. Sacral Neuromodulation
Subacute sacral nerve stimulation in 26 subjects with pelvic pain (with or without PFD) was
reported by Everaert et al. (73). Following unilateral percutaneous nerve evaluation of S3 for
a maximum of 4 weeks, 16 patients exhibited significant pain relief as defined by
50%
improvement on visual analog scale. All responders exhibited pain related to urodynamically
defined pelvic floor dysfunction. The mechanism of action of sacral neuromodulation in the
relief of painful pelvic floor muscle spasm may involve the aforementioned gate theory, with
inhibition of impulse transmission to the sacral spinal cord interneurons from which somatic
efferents to the pelvic floor emanate (54,74).

G. Treatment Algorithm for High-Tone Pelvic Floor Dysfunction

High-tone pelvic floor dysfunction is treated initially with manual physical therapy performed in
an effort to restore sacroiliac and sacrococcygeal alignment, with resultant relief from abnormal
muscular tension. Thiele massage is initiated if the PFM exhibits persistent hypertonus despite
appropriate bony alignment. Pelvic floor muscle exercise, biofeedback, and electrical stimu-
lation then provide a mechanism to achieve maximal PFM contraction and relaxation in the
restoration of normal muscular function. Pharmacologic therapy may be used as adjunctive
therapy in patients with high-tone PFD. Sacral neuromodulation testing may be considered in
patients with pain born of PFD refractory to other therapy. The treatment algorithm for PFD
is represented in Figure 2.

VIII. CONCLUSION

Pain can become the most debilitating symptom in a patient with long-standing IC. A better
understanding of the etiology of CPP in this population is essential to improve treatment and
restore quality of life. We propose the derivation of CPP in IC to be the product of centrally
induced changes (with or without the need for a measure of peripheral nociceptive input) in
addition to neurogenic pelvic floor muscle spasm. Evidence for central sensitization has been
well established in the pain literature. Experimental proof supporting generation of PFD from
nociceptive afferent barrage and dynamic changes in the bony pelvis is less well established.
Additionally, antidromic neuroinflammation in the perpetuation of bladder pathology is an
investigational consideration.
Clinically, we employ therapy to control centrally derived pain and maintain a high index
of suspicion for the presence of concomitant PFD in patients with IC. We eagerly treat the pelvic
floor in appropriate candidates, as any degree of therapeutic benefit achieved in a patient with
chronic debilitating discomfort outweighs the attendant risks of such therapy.

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61
Fecal Incontinence

Tracy Hull
Cleveland Clinic Foundation, Cleveland, Ohio, U.S.A.

I. INTRODUCTION

Fecal incontinence, although not a life-threatening condition, can be a life-altering problem. The
symptoms range from minor soiling to gross loss of stool. For some with this problem, the fear
of soilage prevents them from functioning outside their homes and away from a toilet. The inclusion
of a chapter on this subject in a book devoted to anterior pelvic organ problems is appropriate as the
pelvic floor is viewed more as a single entity due to shared innervation and muscular support. The
common etiology leading to most urogenital dysfunction is the same for fecal incontinence: namely,
childbirth. At our institution, we found that a third of women presenting to the urogynecologist for
urinary incontinence also had fecal incontinence (1). Similarly, Tetzcher et al. found that 18% of
women who had a previous obstetric anal sphincter disruption had both urinary and fecal inconti-
nence (2). Therefore, women presenting to the urogynecologist frequently have combined problems.

II. PREVALENCE

The true incidence of fecal incontinence is unknown. Factors that lead to an inaccurate esti-
mation of how many people are afflicted with this problem include the lack of a standard and
accepted definition for severity and frequency; reluctance of patients to discuss it with health
care providers; lack of awareness of the problem and treatment options by health care providers;
and the wide variety of populations sampled when calculating the incidence (3). The prevalence
has been estimated in the general population by an English postal survey to be 1.7/1000 women
aged 15 – 64 and 13.3/1000 women over 65 years of age (4). A study of patients visiting primary
care doctors or gastroenterologists in Illinois found the prevalence of fecal incontinence to be
18.4% (5). One-third of symptomatic patients had not discussed their problem with their doctor.
Similarly in a Swiss study 5.6% of women in a general outpatient clinic had incontinence, but
only 20% reported symptoms to their medical practitioner (6). In a random telephone survey in
Wisconsin, 2.2% had fecal incontinence (7). In this study one-third were .65 years old and 63%
were women. A recent British study reported that 2% of the population has fecal incontinence
and it afflicts 7% of those over 65 years (8). Therefore an accurate assessment of the number of
people afflicted with this problem is not clear. It is safe to say that it is probably underestimated
and a significant issue.
919
920 Hull

III. ETIOLOGY

As stated in the introduction, the most common etiology is childbirth during a vaginal delivery. After
review of 11 studies, Sultan found fecal incontinence after an obstetric injury to be 20–50% with a
median follow-up of 6–12 months (9). In his landmark study, Sultan found that 35% of primiparous
women had a sphincter defect after a vaginal delivery, and 44% of multiparous (10). Others have
found the incidence of anal sphincter defects to be 7–34% for primiparous women and 12–37%
for multiparous (11–13). Therefore, a significant group of women will have a sphincter defect
after a vaginal delivery. Not all these women have incontinence initially. Normal aging may influ-
ence problems in older women. Until long-term prospective data are collected, the actual influence
of a remote childbirth disruption of the sphincter complex versus natural aging will not be known.
Additional causes of fecal incontinence include surgical sphincter damage (i.e., hemor-
rhoidectomy or sphincterotomy), irradiation, trauma, congenital abnormalities, rectal prolapse,
bowel tumors, inflammation, neurologic conditions (i.e., diabetes, dementia, multiple sclerosis),
and others (i.e., diarrhea, scleroderma).

IV. EVALUATION

A comprehensive history is the first step in evaluating these patients. This includes questions
about the duration and frequency of incontinence. Additionally, the quality of the stool that is
lost and the ability to control flatus are elucidated. The use of pads in fecal urgency is questioned.
Effect on the patient’s quality of life is important to determine for optimal treatment options.
Owing to its frequent coexistence, questions about urinary incontinence should be asked.
A past obstetric and surgical history along with other medical problems is obtained to give
clues regarding etiology. Some medications can contribute to fecal incontinence by producing
loose stools, and therefore all medicines and their side effects are reviewed.
On physical exam, looking at the undergarments for soiling and the perineum for scarring
or anal gapping is the initial step. The anus should be visualized while the patient is asked to
strain and squeeze to view muscle movement. This should be repeated with a finger in the
anus to assess sphincter movement. It is important to distinguish puborectalis contraction
from external sphincter contraction. Stool retained in the rectum or fecal impaction is noted.
Visualization of the distal large bowel with proctoscopy or a flexible sigmoidoscopy will
rule out any rectal abnormalities predisposing to incontinence. If the diagnosis is still in ques-
tion, a 100-cc tap water enema can be administered. If the patient can hold this, her fecal incon-
tinence is probably not significant.

V. DIAGNOSTIC TESTING

Objective testing may be beneficial to determine the degree of impairment. It is not mandatory
for an uncomplicated sphincter disruption, but may be needed for redo procedures or those that
do not appear straightforward.
Anorectal manometry reflects pressures that are generated by the anal sphincters. The
internal anal sphincter is the primary determinant of the resting pressures. The external anal
sphincter primarily determines the squeeze pressures. There are many types of catheters avail-
able to do these measurements, but most are water perfused with four or eight radial port chan-
nels. The length of the anal canal can also be determined as the distance of increased pressure
from the rectum to the outer skin. Additionally, rectal compliance (which is responsible for the
degree of urgency to evacuate) can be calculated. The amount of air inserted in a balloon until
 Fecal Incontinence 921

the patient first senses it and the maximal tolerated volume are measured. The rectal compliance
can be calculated from this. It is the rectal capacity (maximum tolerated volume minus the first
sensation) divided by gradient pressure. The sensation of urgency has been correlated with rectal
compliance (14). Thus, patients with a low compliance may have difficulty waiting to defecate
and thus have severe urgency, which may be misinterpreted or contribute to fecal incontinence.
Traditionally, needle electromyography (EMG) was used to evaluate the striated muscle of
the anorectum. Cutaneous surface electrodes placed in pairs at the anal orifice were developed
because of the pain from EMG. They may be inaccurate owing to electrical activity of adjacent
large muscles such as the gluteus (15). However, this has not been a uniform finding, and surface
EMG has been found to be accurate and comparable to needle EMG (16). Currently, EMG has been
replaced by anal ultrasound (17), which is much more accurate at delineating defects and differen-
tiating scar from muscle. However, EMG still has a place in evaluating neuromuscular integrity.
Pudendal nerve terminal motor latency is the length of time needed after the pudendal nerve
is stimulated at the ischial spine, until the sphincter muscle contracts. A prolonged pudendal nerve
motor latency has been shown by some to decrease success after sphincter repair (18,19).
Endoanal ultrasonography has emerged as a preferred tool to map the sphincters. The
internal anal sphincter appears as a hypoechoic circular band that is best visualized in the mid-
anal canal. The external sphincter is thicker and of mixed echogenicity (Fig. 1). Correlation of

Figure 1 This is an anal sphincter ultrasound (done transanally) of the mid anal canal. This is a woman
who has fecal incontinence 10 years after the birth of her last baby. The probe of the transducer is faintly
seen in the center. The internal anal sphincter is the black hypoechoic circle, which has an anterior defect.
The ends are shown with the small arrows. The external anal sphincter (with mixed echogenicity) also has
an anterior defect. The ends of the muscle are shown with the fat arrows. ANT, anterior; POST, posterior;
R, right; L, left; T, transducer in lumen of anal canal.
922 Hull

preoperative detected lesions with intraoperative findings is high, close to 100% in two studies
(20,21). However, Sentovich et al. found that even though the accuracy correlated 100% with
intraoperative findings, transanal ultrasound falsely showed a sphincter injury in 5– 25% of
nulliparous women (22). Recent innovations to improve preoperative sphincter visualization
include three-dimensional anal ultrasound and magnetic resonance imaging (MRI) with endo-
anal receiver coil (23). One study suggests that endoanal ultrasound and endoanal MRI are
equivalent in diagnosing external anal sphincter injury, but MRI is inferior at diagnosing internal
anal sphincter defects (24).
Defecography is not routinely used to evaluate fecal incontinence unless defecation
dysfunction exists. The study is done looking for rectal prolapse or internal intussusception.

VI. NONSURGICAL TREATMENT

All treatment of fecal incontinence starts with optimization of any medical condition (such as
proctitis). Diarrhea should be evaluated and aggressively treated (25). Sometimes treating diar-
rhea will eliminate fecal incontinence. Some commercial bulking agents such as Metamucil,
Citrucel, or Konsyl improve the consistency of stool and improve incontinence. In one prospec-
tive randomized study, patients using psyllium had 50% fewer episodes of incontinent stools
over controls due to improvement in stool consistency (26). Agents such as loperamide (Imo-
dium) and diphenoxylate hydrochloride with atropine (Lomotil) are used for patients with diar-
rhea of no obvious etiology. Similarly, patients with constipation and overflow incontinence
require aggressive enemas or laxatives to keep the rectum empty.
More recently, amitriptyline (20 mg at bedtime) may improve fecal incontinence (27). It is
felt that this agent works by decreasing the amplitude and frequency of rectal motor complexes.
This leads to firmer stools.
There are multiple barrier creams on the market today. Aggressive protection of the anal
skin with these agents is needed to protect skin from excoriation. Some patients benefit from an
enema program, which washes out the rectum to prevent stool loss. Special cone-tipped catheters
can be used for patients with poor tone and difficulty administering an enema.
Biofeedback involves providing patients visual (and occasionally auditory) feedback
about contraction of the external sphincter. Many methods and forms exist. A popular method
involves placing a balloon in the rectum to simulate stool and measuring anal sphincter contrac-
tion with a separate balloon in the anal canal, or by an anal plug, or by perianal surface electro-
des. Patients are encouraged when the proper sphincter response is made. The goal is to increase
sphincter strength and to teach patients to respond to smaller volumes of material in the rectum.
A recently published study looked at 46 studies from the English literature where biofeedback
was used to treat fecal incontinence in adults (28). After biofeedback 49% were said to be cured
of their fecal incontinence, and 72% were cured or improved. The limitations of this study were
that methods of biofeedback varied and few studies used controls. Also, no standard tool was
used to assess outcome. However, the authors felt that their results suggest that biofeedback
helps the majority of patients. In another review of articles published on biofeedback, comparing
coordination training (coordination of pelvic floor muscle contraction with the sensation of
rectal filling) with strength training (like kegels), the success rate was 70% for both (29). Bio-
feedback requires a dedicated, caring therapist to teach and encourage the biofeedback. Patients
must be alert and extremely motivated. Multiple sessions are usually required. Long-term results
do not seem to diminish with time (30,31). One interesting application was the use of biofeed-
back in patients who did not have functional improvement after “successful” sphincteroplasty.
These patients were found to improve after biofeedback (32).
 Fecal Incontinence 923

VII. SURGICAL TREATMENT

A. Sphincteroplasty
The most common surgical procedure is directed at repair of the muscle. The most common type
of repair is after an obstetric injury, and thus an anterior repair is performed. A few are per-
formed to repair defects from anorectal surgery. Attempts are usually made to repair obstetric
injury at the time of occurrence; thus, this repair is done in a delayed fashion when the original
repair at childbirth has failed. Originally the ends were reapproximated end to end. Currently,
the scar is divided but retained, and an overlapping repair as described by Parks and McPartlin
is performed (33). Patients can be positioned in the lithotomy or prone position. The surgery can
be done under regional or general anesthesia. I prefer a full bowel preparation; however, some
only administer enemas in the preoperative area. I also prefer perioperative antibiotics continu-
ing for several days after the procedure. A curvilinear incision is made over the perineal body.
To avoid injury to the pudendal nerve, the arc of the incision should not extend to the extreme
posterior lateral position. The dissection is deepened and carried laterally into the ischiorectal
fat. Since the medial border of the ischiorectal fossa is the external sphincter muscle, it is ident-
ified in this area. The same procedure is carried out on the other side (Fig. 2). Then the midline
scar is divided and further elucidation of the ends is done (Fig. 3). If both the internal and exter-
nal sphincters are injured, sometimes leaving them intact as a unit facilitates repair. If only the
external sphincter is injured, then the internal is not mobilized.
The levator ani muscle may be plicated at this point using No. 0 or 2-0 delayed absorbable
sutures. The vagina should be checked after the plication to ensure that no ridge or narrowing
was created. The sphincter complex is next overlapped and approximated using 2-0 polyglactin

Figure 2 This is a schematic in the prone position. A semicircular incision is made over the perineal
body. The muscle is identified with a scar in the anterior midline. (Reprinted with permission of the
Cleveland Clinic Foundation, Cleveland, OH.)
924 Hull

Figure 3 The scar is divided in the middle, leaving scar on the ends of the muscle. The ends are further
dissected. (Reprinted with permission of the Cleveland Clinic Foundation, Cleveland, OH.)

mattress sutures. Approximately three or four sutures are placed on each side (Fig. 4). During the
procedure irrigation of the wound is carried out with antibiotic solution. The skin edges are
reapproximated (Fig. 5). Sometimes it must be closed in a V-Y fashion owing to tension
from lengthening the perineal body. I usually leave the middle open to facilitate drainage of
any fluid collection.
Postoperatively I prefer 2 days of IV antibiotics and withhold oral intake. I do not use sitz
baths due to the tendency to macerate tissue. However, showers are permitted. I also do not use
constipating agents. At discharge one of the most important points is to ensure that patients do
not get constipated. I prefer to use a bulking fiber agent along with an ounce of mineral oil each
morning for the first 2 weeks. Also, if the patient has not had a bowel movement by postoperative
day 4, milk of magnesia 1 ounce twice daily is advised until there is a bowel movement.
The use of a diverting stoma is reserved for redo procedures, complicated repairs (such as
a cloaca), and patients with concomitant inflammatory bowel disease or diarrhea. Not all of these
patients require a stoma, and its use does not guarantee success; the question is therefore left up
to the surgeon’s discretion.
Table 1 shows the success rates for this repair in a number of recent studies. Unfortunately,
it appears that long-term results are not as optimistic as once thought. Other treatment options
are therefore considered for those who fail.

B. Gluteal Muscle Transposition

This was popular 8 –10 years ago, but has now been replaced by other techniques. Similarly, the
posterior anal imbrication (Park’s postanal repair) has also been nearly abandoned as has the
Thiersch encirclement procedure.
 Fecal Incontinence 925

Figure 4 An overlapping repair is done taking advantage of the strength of the scar versus the muscle
belly. The sutures go through the scar and anchor it to the opposite muscle with mattress sutures.
(Reprinted with permission of the Cleveland Clinic Foundation, Cleveland, OH.)

The stimulated gracillis transposition and encirclement around the anus emerged as a
promising treatment option over the past 15 years. Even though this remains in the armamentar-
ium of incontinence surgeons in Canada and Europe, the stimulator is no longer available in the
United States. This procedure has a steep learning curve with a high morbidity rate. The gracilis
muscle is mobilized from the inner thigh, preserving the neurovascular bundle proximally. The
tendon of insertion is divided at the knee. The muscle is wrapped around the anus and the tendon
is sewn to the opposite ischial tuberosity. An electrical stimulator is placed at an optimal site on
the abdomen, and leads are tunneled from the stimulator to the muscle. The leads are positioned
in the proximal aspect of the nerve.
The results of a multicenter study showed that 74% had adverse events (infection, muscle
wrap problems, pain, device problems, and other problems) with 40% requiring one or more
operations to treat complications (39). Successful results (50% reduction in incontinence
episodes) were obtained in 57% of patients at 18 months.

C. Artificial Anal Sphincter

This has emerged as the newest accepted option for patients with intractable fecal incontinence.
American Medical Systems, Minnetonka, MN, has modified the device used in urinary inconti-
nence for fecal incontinence. It consists of three parts: an inflatable cuff which surrounds the
anus; a central pump positioned in the labia for women and the scrotum for men; and a regulating
balloon in the space of Retzius (Fig. 6). When a patient needs to defecate, the central pump is
pumped, which forces the fluid into the regulating balloon. Then over the next 8 min, the fluid
gradually returns to the cuff which surrounds the anus to occlude the opening. Problems with the
926 Hull

Figure 5 The skin is reapproximated. (Reprinted with permission of the Cleveland Clinic Foundation,
Cleveland, OH.)

procedure include infection, erosion, mechanical failure, and difficult evacuation. Complications
range from 23% to 67% (40 –43). The results of 33 patients being implanted at an experienced
European center revealed that 83% of patients had an activated device at a minimum of 6
months’ follow-up (44). Good to excellent results were obtained in 75% of these patients.

VIII. NEW INVESTIGATIONAL TREATMENTS

The internal anal sphincter contracts in response to adrenergic stimulation. Phenylephrine is

an alpha1 adrenergic agonist. It has been shown to increase resting pressure when applied
topically (45). Carapeti et al. applied 10% cream to patients with an intact sphincter and fecal

Table 1 Success Rates of Sphincteroplastya

Mean
N Excellent Good Fair Poor follow-up

Yugoslavia (34) 53 47% 23% 21% 9% ?

Miami (35) 22 74% 6% 14% 6% 20 mos
France (36) 74 28% 23% —49 %—b 40 mos
St. Marks, U.K. (37) 38 0 11% —89 %—b 77 mos
CCF, Ohio (38) 48 14% 30% —56 %—b 63 mos
a
Excellent ¼ no incontinence; good ¼ incontinence to gas only; fair ¼ incontinence to gas and liquid stool; poor ¼
incontinence to solid stool.
b
Combined fair and poor into one group.
 Fecal Incontinence 927

Figure 6 This is the artificial bowel sphincter implanted in a woman. The cuff is seen encircling the
anus. The pump would be in the labia. A reservoir balloon sits in the space of Retzius anterior to the
bladder. (Reprinted with permission of American Medical Systems, Inc., Minnetonka, MN.)

incontinence in a double-blind crossover study (46). Six of 18 in the treatment arm and two of 18
in the placebo crossover arm had more than 75% subjective improvement. They concluded that
further studies are needed to determine the exact subgroup of patients, which would respond.
Radiofrequency energy delivered to a target temperature of 858C for 1 min 23 –32 times in
the anal canal has been shown to be safe and effective. In a poster presentation at the American
Society of Colorectal Surgeons meeting, there was significant improvement at 12 months in all
parameters tested (47). The exact mechanism for this improvement is unknown.
Another new treatment is sacral spinal nerve stimulation. Originally, attempts were made
to stimulate the muscle directly in patients with intact but functionally suboptimal sphincters.
However, infection, migration, and fibrotic reactions led to failure. Based on a urology
model, the site for electrostimulation was shifted to the peripheral nerve supply at the level of
the sacral spinal nerves. The level of the sacral nerve is chosen (S2, S3, or S4) by passing a per-
cutaneous electrode through the sacral foramen and stimulating each sacral nerve (at the S2, S3,
or S4 level). The sacral nerve is chosen based on maximal contraction of the pelvic floor and
minimal affect on the lower extremities (48). It is usually S3. The patient then undergoes stimu-
lation with temporary electrodes and an external generator. If their fecal incontinence improves,
a permanent generator and leads are implanted. Thus far, results from Europe in small groups of
patients show incontinence improves in most patients through increased striated anal sphincter
function (48 –50).
928 Hull

Finally, for patients who have failed or who are not candidates for other surgical repairs, a
stoma may improve their quality of life. It may allow patients the opportunity to leave home,
attend work, and enjoy social functions. However, patients deserve evaluation at a center that
specializes in all options of evaluating and treating fecal incontinence before a stoma is felt
to be the final treatment option.

IX. CONCLUSION

Fecal incontinence is a complicated problem. The choice of treatment depends of the etiology of
incontinence, the sphincter anatomy, and the impact of incontinence on the patient’s quality of
life. Usually nonsurgical treatment is the first choice. It is important to treat diarrhea first and be
alert to anal skin problems. The best surgical option is a sphincter repair in a patient with an iso-
lated anterior defect and otherwise good muscle function. In the past 10 years, many new treat-
ments have been developed for patients with fecal incontinence that has not responded to
traditional therapies. Considerable enthusiasm has been directed toward these new treatments,
many of which are still in the preliminary stages.

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Index
Abdominal hysterectomy, 530, 536, 548– 549 Urinary Incontinence Guideline Panel, 217,
complications, 549– 550 220
operative mortality, 546 Agency for Healthcare Research and Quality
risk factors, 549– 560 (AHRQ), 233
Abdominal leak point pressure (ALPP), 157– 160, Alcohol and urinary tract infections (UTIs), 236
163, 169, 171– 172, 179, 679 a-Adrenergic agonists, 225
measurement, 157– 160 a-Adrenergic antagonists, 223
Abdominal paravaginal repair, 568– 569 American College of Obstetricians and
outcomes, 627– 628 Gynecologists (ACOG), 98
Abdominal pressure, 172 American Foundation of Urologic Disease
Abdominal retrupubic paravaginal repair, 585 (AFUD) Consensus Panel, 65
Abdominal sacral colpoperineopexy, technique, American Urogynecologic Society, 131, 273, 561
684 American Urologic Association (AUA), 296, 399,
Abdominal sacral colpopexy, 677– 689 423
comparative studies, 686 Clinical Guidelines Panel, 280– 281, 393, 395,
complications, 684, 686 418
failure rates, 683– 684, 686 Amitriptyline
graft material, 685 in fecal incontinence, 922
modifications, 686– 687 in interstitial cystitis (IC), 909
present role, 685–686 AMPA, 32 – 33
results, 683 Anal sensors, 246
surgical technique, 679–685 Anal sphincter, 19, 921
treatment success, 686 artificial, 925– 926
Abdominal symptoms of urogynecologic disease, in pregnancy, 96 – 97
123 injuries, 111
Abductor caudae dorsalis (ACD) tail muscle of lacerations, 109
the rat, 891, 907 reflex, 152
Acetylcholine (ACh), 191, 216– 217 Anesthesia, 545
N-acetylcysteine, 207 Anorectal angle, 597
Adenosine, 31 Anorectal physiologic testing, 509
Adenosine triphosphate (ATP), 24, 31, 34, Anorectal studies, 742– 743
222 Anterior colporrhaphy, 565– 568, 584, 606, 610,
Adnexal removal, 555 675
Adnexectomy, 552 comparison with Burch urethropexy, 299–300
b-Adrenergic agonists, 223 Anterior flap extraperitoneal cystoplasty (AFEC),
b-Adrenergic receptors, 223 465– 472
Adrenergic mechanisms, 29 –30 bowel preparation, 466
Adrenergic responses, a-1 and a-2, 67 postoperative procedure, 468
Agency for Health Care Policy and Research preoperative evaluation, 466
(AHCPR) results, 471– 472
Clinical Practice Guideline, 45, 226, 233, technique, 466– 471
280– 281 Anterior pelvic exenteration, 824, 860

931
932 Index

Anterior pelvic organ prolapse, conservative outcomes, 325

therapies, 563– 565 patient selection, 321
Anterior pelvis, 508 potential advantages, 325– 326
Anterior rectal wall, 755– 757 techniques, 321– 325
Anterior vaginal wall prolapse, 615, 617, Asepsis, 546
625– 626, 638 Association of Women’s Health Obstetric and
adjunctive materials to enhance long-term Neonatal Nurses (AWHONN), 245
success, 570– 571 ATP-dependent pumps (ATPases), 24
anatomic supports and histology, 562–563 Atrial fibrillation, 177
combined central and lateral defect repairs, Atropine resistance, 30
588– 591 Atropine sulfate (DL-hyoscyamine), 217
effect of concomitant operations, 571 Augmentation cystoplasty, 444, 473
laparoscopic repair, 587– 588 Autologous fat injection, 337– 338
mild/moderate cystoceles, 575– 594 complications, 338
outcomes, 628 results, 337– 338
pathophysiology, 562– 563 Autonomic nervous system, 26
predisposing factors, 563 Autonomous bladder, 223
repair of central defects, 584– 585 AVWS, 283– 290, 379– 385
repair of lateral defects, 585– 587 anchoring point, 290
stages III and IV, 561– 573 complications, 384
surgical outcomes, 582 efficacy reports, 383
surgical repair techniques, 565– 571 evolution, 283–284
Anterior vaginal wall relaxation, 596 indications/contraindications, 284
Anterior vaginal wall sling (see AVWS) initial setup, 285
Anterior vaginal wall support, 13, 508, operative technique, 284– 286
632– 633 outcomes, 286– 290
anatomy, 616– 618 patient selection, 379– 380
Anterior vaginal wall suspension (see AVWS) reported success rates, 382
Anticholinergic agents results, 382
in interstitial cystitis (IC), 898 sexual function following, 288
relatively pure, 216– 219 surgical technique, 380–381
with mixed actions, 219
Antidepressants in interstitial cystitis (IC), 897 Bacillus Calmete-Guerin (BCG) in interstitial
Antidiuretic hormone (ADH), 236 cystitis (IC), 898
Antihistamines in interstitial cystitis (IC), 897 Behavior modification, 234– 238
Antimuscarinic agents, 191 Behavioral management for continence (BMC)
side effects, 217 program, 249
Antiproliferative factor (APF), 894– 895 Behavioral treatments, 233– 265
Antisepsis, 546 and drug therapy, 252
Antispasmotics in interstitial cystitis (IC), 898 Benign prostatic hyperplasia, 168
Apical prolapse, 678 Bethanechol chloride, 29
Arcus tendineus fascia pelvis (ATFP), 292, 294, Bilateral hydroureteronephrosis, 161
296, 568–569, 597, 606, 615– 618, Biofeedback
620– 622 in fecal incontinence, 922
Arcus tendineus levator ani (ATLA), 597, 604 in high-tone PFD, 912
Artificial anal sphincter, 925– 926 Biofeedback therapy, 248– 252
Artificial urinary sphincter (AUS), 319 Bladder (see also Overactive bladder)
advantage of transvaginal approach, 328 antidromic neuroinflammation, 907– 908
continence rate, 326 inferior hypogastric innervation, 441
erosion, 327 innervation, 905
insertion, 319– 328 Bladder augmentation, 457– 465, 485
long-term reliability, 326 laparoscopic, 473
long-term social continence, 328 Bladder biopsy, 895– 896
 Index 933

Bladder cancer Bladder voiding (see Voiding)

muscle-invasive, 859 Bladder volume, 158– 159
see also Transitional cell carcinoma (TCC) of Bladder wall, properties of, 23 – 25
the bladder Body mass index (BMI), 234– 235
Bladder capacity, 168, 204 Bony pelvis in childbirth, 100– 101
therapy to increase, 216– 225 Botulinum toxin, 29
Bladder compliance, 25, 168– 171, 204, 206 Bowel anastomosis, 476
Bladder complications of retropubic urethropexy, Bowel complaints, 702
303– 304 Bowel mobilization, 863–864
Bladder contractions, 440 Bowel regularity
Bladder control strategies, 241 and lower urinary tract symptoms (LUTS),
Bladder denervation, 442– 444 237– 238
Bladder diary, 126– 127, 241, 254 patient guide, 262
Bladder dysfunction, 473 Bradley’s loop concept, 35– 38
Bladder emptying assessment, 581 Brainstem sacral loop (loop 2), 36
Bladder filling Brief Index of Sexual Function in Women
phases, 174 (BISF-W), 70
requirements, 215 Bristol Female Lower Urinary Tract Symptoms
Bladder flap techniques, 854– 855 (BFLUTS), 57, 60
general principles, 855 Bulbocavernosus muscle, 509, 596
Bladder function, 81 – 82 Bulbocavernosus reflex, 128, 152
Bladder hyperactivity, 220 Bulbocavernous flap, mobilization, 808
Bladder injuries, 591 Burch bladder neck suspension, 289
Bladder instability, 602 Burch colposuspension, 15, 61, 298 –299, 604
Bladder irritants and lower urinary tract Burch procedures, 293, 296–300
symptoms (LUTS), 236– 237 laparoscopic, 302– 303
Bladder mucosa autografting, 792 Burch urethropexy, 298, 634
Bladder neck, 510, 577 candidates for, 301
anatomic position, 10 – 11 comparison with anterior colporrhaphy,
descent, 511, 513, 520 299– 300
funneling, 511, 519 mini-incision outpatient modification, 299– 300
hypermobility, 510, 513
associated with stress incontinence, 11 – 12 Cadaveric dermis, 606
Bladder neck support, 268, 271 Cadaveric fascia lata, 606
Bladder neck suspension, 512 Cadaveric fascia lata allograft (CFLA), 357– 366
concomitant with excision of urethral Cadaveric transvaginal sling (CATS), 387– 397
diverticula, 828– 829 bone anchors, 389
Bladder outlet abnormalities, 223 choice of sling material, 387– 388
Bladder outlet obstruction (BOO), 173, 217, 268 complication rates, 395
diagnosis, 439– 440 indications, 387
Bladder outlet resistance, 9 operative procedure, 389– 392
therapy to increase, 225– 227 patient selection, 387
Bladder pathology and pelvic floor musculature postoperative care, 393
(PFM), 907 preoperative preparation, 389
Bladder perforations, 207 response score for assessment of surgical
Bladder pressure, 172 outcomes, 397
Bladder removal, 899 results, 393– 395
Bladder retraining, 233 surgical technique, 389– 393
patient guide, 262– 263 Caffeine, and lower urinary tract symptoms
Bladder smooth muscle, 30 (LUTS), 236– 237
Bladder storage disorders, 215 Caffeine chart, patient guide, 261
Bladder symptoms, 81 Calcium antagonists, 222
Bladder training (BT), 239– 241 Calcium channel blocker, 60
934 Index

Calcium hydroxylapatite, 339 outcomes, 709– 714

Capio CL device, 430 partial (see Partial colpocleisis)
Capsaicin, 224– 225 results, 706– 707
Carcinoembryonic antigen (CEA), 823 surgical techniques, 705– 709
Cardinal ligaments, 577, 597 traditional approach, 701
Cardinal-sacrouterine ligament complex, 597 Colpocystodefecography, 600– 601
Cardinal-uterosacral ligament complex, 533, 535 Colpocystourethrography, 512– 513
Cecocolocystoplasty, 479 Colpopexy, 558
Centers for Disease Control (CDC), 549 Combined incontinence, 369
Central defect, 607 Complex enteroceles, 15
Cerebral-brainstem circuit (loop I), 35 – 36 Complex fistulae, 773– 780
Cerebral-sacral loop (loop IV), 37 –38 tissue interposition, 773– 779
Cervical ligament pedicles, 556 Computed tomography (CT), 510, 514
Cervix, amputation, 553 Congenital enteroceles, 15
Cesarean delivery, 108– 109 Connective tissue, 25
Childbirth (see also Delivery; Labor; Pregnancy), Connective tissues, in childbirth, 100– 101
717– 718 Constipation, 702, 721
bowel and bladder habits after, 110 and lower urinary tract symptoms (LUTS), 237
levator muscles in, 98 –99 Continence, determinant of, 9
Cholinergic mechanisms, 28 – 29 Continence Guard, 270– 271
Chronic pelvic pain (CPP) (see Interstitial cystitis Continence ring, 271, 274
(IC)) Contraceptive diaphragm, 269
Cigarette smoking in urinary incontinence, 47, Contrast sonography, 513– 514
234 Cooper’s ligament (see Transvaginal Cooper’s
Citrobacter, 352 ligament sling)
Clean intermittent catheterization (CIC), 466, Cough test, 400
472, 705 Cough urethral pressure profile, 150–151
Clear cell adenocarcinoma, 823 Creutzfeldt-Jakob disease, 347
Clitoral reflexes, 128 C-SSL, 667– 669
CLPP, 157– 158 Culdoplasty, 555
vs. VLPP, 159 sutures, 537– 538
Coccygeus, 597 Cushing’s syndrome, 72
Coccygeus-sacrospinous ligament (C-SSL), 666 Cyclic AMP, 24
Cochrane Collaboration, 238 Cyclic gyanylate monophosphate (cGMP), 67
Cochrane database, 240 Cystectomy, 186, 899
Collaborative Review of Sterilization (CREST) nerve-sparing, 885
study, 549 Cystocele, 12 – 14, 172, 510, 517– 518, 615, 664
Collagen central defect, 13, 578
and hypermobility, 335– 336 classifications, 596
as urethral injectables, 330– 339 complications, 591– 592
comparison of parameters and results, 333– 334 cystoscopic transillumination, 603
injection results, 331– 335 defined, 12
treatment-related morbidity, 336 grade IV, 589
Collagen fibers, 598 grading systems, 578– 579
Collagen injections, 707 high-grade, 14
durability, 340 lateral defect, 578
safety, 340 mild/moderate, 575– 594
viable minimally invasive alternative, 340 natural history, 595
Collagen, estrogen effect on, 82 nonsurgical management, 582– 583
Colpocleisis, 530, 641, 703 preoperative evaluation, 579–582
complications, 709– 714 radiography, 581
for vaginal vault prolapse, 701–715 stage IV, 595– 614
indications, 702 abdominal approach, 604– 605
 Index 935

central defect repair, 611 Detrusor external sphincter dyssynergia (DESD),

clinical evaluation, 599 149, 163, 167, 174, 179
clinical presentation, 599– 603 Detrusor function, 82
fluoroscopy, 602 disorders of, 843
four-defect repair, 607– 612 Detrusor hyperactivity, 35
imaging studies, 600– 601 Detrusor hyperreflexia (DH), 167
laboratory evaluations, 603 Detrusor hypocontractility, 411
laparoscopic approach, 605– 606 Detrusor instability, 60, 178
magnetic resonance imaging (MRI), 601 conservative management, 440– 441
physical examination, 599– 600 de novo, 303–304
symptoms, 599 pharmacologic management, 191– 199
treatment, 604– 606 postoperative, 437– 445
upper urinary tract evaluation, 603 surgical management, 199– 207
urodynamic study (UDS), 602 treatment, 440– 444
vaginal approach, 606 Detrusor leak point pressure (DLPP), 157,
video urodynamic study, 602 162– 163, 169– 171
surgical management, 583– 584 clinical application, 162– 163
use of term, 579 technique, 162
Cystogram, 517 Detrusor muscle, properties of, 23 – 25
Cystography, 461, 510– 511, 793 Detrusor myectomy, 203– 204, 444
Cystolysis, 201 Detrusor myomectomy, 457– 464, 485
Cystometrogram (CMG), 168–174, 176, 179 application, 463
Cystoscopy, 314, 371, 392, 439, 449, 527, clinical results, 462– 463
556– 557, 582, 635, 673, 763, 842, extraperitoneal approach, 459
893, 899 history, 457– 458
Cystotomy, 479– 480, 557 intraperitoneal approach, 459
Cystourethrocele, 634– 635 operative technique, 459– 461
grade I and II, 12 – 13 postoperative care, 461– 462
grade III, 13 preoperative preparation, 459
Cystourethrography, 600 techniques, 459–462
Cystourethroscopy, 602– 603 Detrusor pressure, 168
Detrusosphincteric inhibitory reflex (DSIR), 39
Darifenacin, 219 Detrusourethral inhibitory reflex (DUIR), 38
Defacography, 512 Diabetes, 177
Defecating proctography, 739– 742 Diabetic cystopathy, 168
Defecatory dysfunction, 737, 739 Diazepam in high-tone PFD, 913
Defecography, 922 Dicyclomine hydrochloride, 221
Deficient extrinsic continence mechanism, 121 Dietary habits and lower urinary tract symptoms
Delivery (see also Childbirth; Labor; Pregnancy) (LUTS), 235– 237
implications for subsequent pelvic floor Dimethyl sulfoxide (DMSO) in interstitial cystitis
function, 104 (IC), 898
operative vaginal, 106– 107 Distal urethral polypropylene sling (DUPS),
pelvic floor in, 95 – 101 417– 427
pushing positions and techniques, 105 adjusting sling tension using two Allis clamps,
Denonvillier’s fascia, 736, 869 424
De novo detrusor instability, 303– 304, 592 failures, 424
De novo dyspareunia, 747 pathophysiology, 418– 419
De novo urge, 452 quality of life (QOL) assessment, 423
N-Desethyloxybutynin, 196 surgical outcomes, 422–424
Detrosodetrusor facilitative reflex (DDFR), 38 surgical technique, 420– 421
Detrusor areflexia (DA), 167 Distal urethral prolene sling (DUPS), 608
Detrusor contractility, therapy to decrease, Diuresis scintigraphy, 179
216– 225 Diverticulectomy, 824
936 Index

Dopaminergic mechanisms, 31 – 32 Excitation-contraction coupling, 23 – 24

Drug delivery, metabolism and distribution, 216 External iliac artery, 865– 866
Drug therapy and behavioral treatments, 252 External urethral sphincter (EUS), 26
Duloxetine, 227 physiology, 34 – 35
Durasphere, 339 Extracellular matrix (ECM), 25
Dynamic fluoroscopy, 512, 600 Extraperitoneal levator myorraphy, 646
Dynamic proctography, 512
Dyspareunia, 123– 124, 288 Fecal incontinence, 19, 919– 930
amitriptyline in, 922
EEA sizer, 693– 694 biofeedback in, 922
Electrical stimulation (ES) for treatment of diagnostic testing, 920– 922
urinary incontinence, 201 due to childbirth, 920
Electrogalvanic stimulation (EGS) high-tone etiology, 920
PFD, 912– 913 evaluation, 920
Electromyography (EMG), 174, 179, 248– 249, new investigational treatments, 926– 928
509, 816, 912 nonsurgical treatment, 922
multichannel, 246 overview, 919
pelvic floor muscles, 246 prevalence, 919
Endoanal ultrasonography, 509 psyllium in, 922
Endopelvic fascia (EPF), 576– 578, 581, 597– 598 radiofrequency energy in, 927
Endopelvic fascia repair, 669– 670 sacral spinal nerve stimulation in, 927
Entercoccus, 352 stoma in, 928
Enterocele, 15 –16, 517, 608, 643– 645, 671, 682, surgical treatment, 923– 926
707 Female Stress Urinary Incontinence Clinical
after colposuspension, 304 Guidelines Panel, 437, 453
defined, 15 Fetal position, effects on pelvic floor, 108
formation, 512 Fiberoptic catheters, 143
repair, 671 Fibroids, 552
use of term, 579 Flavoxate hydrochloride, 221– 222
Enterocystoplasty, 204– 207 Fluid management and urinary tract infections
choice of bowel segments, 205– 206 (UTIs), 235– 237
early complications, 206 Fluoroscopic urodynamics, 186
efficacy of, 457 Fluoroscopy, 179, 510– 513
history, 457– 458 cystocele stage IV, 602
late complications, 206– 207 Fluoroscopy unit, 167
Ephedrine, 226 Food and Drug Administration (FDA), 348– 349
Epidural analgesia, effects on pelvic floor, 108 Forceps delivery, 106
Episiotomy, 97 – 98, 720 Free mucosal graft, 791– 792
Estradiol, 88 Full-thickness labial (Martius) flap, 777
dosages, 88
Estrogen, 72 – 73 Gabapentin in interstitial cystitis (IC), 898, 909
in sexual function, 68 Gamma-aminobutyric acid (GABA), 909
Estrogen deficiency, 83 inhibitory mechanisms, 33
Estrogen receptors, 79 – 82 Gastrointestinal anastomosis stapling device (GIA
Estrogen replacement therapy (ERT), 73, 81, 83, stapler), 477
558 Gastrointestinal injury, 557
Estrogens, 80 Gastrointestinal symptoms of urogynecologic
in recurrent urinary tract infection, 86 disease, 123
in urinary incontinence, 84 – 85, 89, 227–228 Genital hiatus (GH), 502
urogenital atrophy, 86 – 88 Genital prolapse, 545
Ether as general anesthetic agent, 545 pessaries for, 273– 274
Euphorbia resinifera, 33, 225 Gilliam suspension, 529, 548
Evacuation proctography, 512 Glutaminergic mechanisms, 32 – 33
 Index 937

Gluteal flap, 777– 779 Hypotonic bladder, 328

Gluteal muscle transposition, 924– 925 Hysterectomy, 305, 312, 530–531, 616
Glycoprotein-51 (GP-51), 894– 895 complications, 530
Gracilis myocutaneous flap, 779 contemporary practice and incidence, 548
Guanosine triphospahte (GTP), 24 death from, 546
sexual function following, 540– 541
Habit training, 238 vault prolapse repair after, 642– 646
Halban culdeplasty, 682 vesicovaginal fistula (VVF) after, 761
Halban procedure, 698 see also Abdominal hysterectomy;
HASTE sequence, 515, 519 Laporoscopic hysterectomy;
Health-related quality-of-life (see HRQOL) Posthysterectomy vault prolapse; Vaginal
Heart and Estrogen/Progestin Replacement Study hysterectomy
(HERS), 73 Hysteropexy, 529
Heparin, use in interstitial cystitis (IC), 898
Heparin-binding epidermal growth factor-like Iatrogenic enteroceles, 15
growth factor (HB-EGF), 895 Ileocytoplasty, 476
High-tone pelvic floor dysfunction, treatment Iliococcygeus, 597
algorithm, 914 Iliococcygeus fascia suspension, 670– 671
High-tone PFD, pharmacologic therapy, 913 Iliococcygeus trauma, 517
High uterosacral ligament suspension with fascial Imgelman – Sundberg bladder denervation
reconstruction, 671– 674 technique, 200
HIV, 347 Imipramine, 224, 227
Hormonal influences, 79 – 80 Incontinence (see also Fecal incontinence;
on lower urinary tract, 79 – 94 Urinary incontinence), reversible causes,
on sexual function and response, 67 – 68 124
on urinary tract infection, 81 Incontinence Impact Questionnaire (IIQ), 56 – 57,
Hormone replacement therapy (HRT), 68, 73, 60 – 61
80 – 81, 86 Infralevator obturator fascia, 611
Hormones and Urogenital Therapy (HUT) Ingelman– Sundberg partial bladder denervation,
committee, 84 – 86 444
HRQOL Inositol triphosphate (IP3), 24
construct validity, 55 Intermittent self-catheterisation (ISC), 174
content validity, 55 International Consultations on Incontinence (ICI),
criterion validity, 55 280
development and evaluation of new International Continence Society (ICS), 157, 561,
instruments, 54 – 55 578, 595
disease-specific, 60 – 61 Committee on Terminology, 500
disease-specific instruments, 56 – 58, 125 International Federation of Gynecologists and
general instruments, 55 – 56 Obstetricians (FIGO), 504
pilot testing, 55 International Incontinence Society, 131
reliability, 55 International Urogynecological Association
research, 54 (IUGA), 504
urinary incontinence in, 53 – 64 Interposition operation, 547
validity, 55 Interstitial cystitis (IC), 889– 901
Hydrodistension, 893, 899 amitriptyline in, 909
for irritative bladder symptoms, 199 and pelvic floor dysfunction (PFD), proposed
Hydronephrosis, 711 mechanism, 908
Hydroureteronephrosis, 518, 520, 603 anticholinergics in, 898
Hypermobility, 340 antidepressants in, 897
and collagen, 335– 336 antihistamines in, 897
management of, 329– 343 antispasmotics in, 898
Hypogastric artery, 868 Bacillus Calmete-Guerin (BCG) in, 898
Hypothyroidism, 72 characteristic symptoms, 891
938 Index

[Interstitial cystitis (IC)] Involuntary bladder contractions (IVC),

chronic pelvic pain, 903– 917 216– 217
centrally derived, 904, 908– 911 I-QOL, 58, 61
etiology, 903
clinical presentation, 893 Kaplan-Meier curve, 335
definition, 890 Kelly procedure, 299
diagnosis, 891, 893– 896 Kelly-type plication, 283
dimethyl sulfoxide (DMSO) in, 898 Kidney function, 169
epidemiology, 889– 890 King’s College Prolapse Quality of Life tool
etiology, 890–892 (P-QOL), 499
gabapentin in, 898, 909 King’s Health Questionnaire, 57, 61
heparin in, 898 “KNACK”, 264
high-tone pelvic floor dysfunction,
906– 907 Labia minora flap, 853
intravesical therapy, 898 Labor (see also Childbirth; Delivery; Pregnancy)
management approach, 897 implications for subsequent pelvic floor
muscle manipulation, 899 function, 104
opioids in, 908 pelvic floor in, 95 – 101
oral therapy, 896– 898 pushing positions and techniques, 105
outcome, 899– 900 second-stage strategies, 105– 106
proposed model of pathogenesis, 892 Laparoscopic abdominal sacral colpopexy,
resiniferatoxin in, 909– 910 691– 700
sacral nerve root stimulation, 910 clinical outcome, 699
sacral neuromodulation, 910 indications, 691– 692
sacral neurostimulation, 899 operative technique, 692– 698
sodium pentosan polysulfate in, 896– 897 Laparoscopic anterior vaginal wall prolapse
surgical treatment, 899– 890, 910– 911 repair, 587– 588
theories, 890 Laparoscopic approach to abdominal
treatment, 896– 900 vesicovaginal fistula (VVF) repair, 792
urodynamic evaluation, 893 Laparoscopic bladder augmentation, 473
Interstitial Cystitis Association, 889 Laparoscopic Burch procedures, 302– 303
Interstitial Cystitis Database (ICDB), 893 Laparoscopic Burch urethropexy, follow-up, 314
Intra-abdominal catheter, 143 Laparoscopic enterocystoplasty, 473– 483
Intravaginal devices, 267– 278 bladder mobilization and cystotomy, 479– 480
Intravaginal slingplasty (IVS), 400, 408 bowel selection and mobilization, 476
Intravenous pyelography, 843 case details, 482
Intravenous urogram (IVU), 509– 510 enterovesical anastomosis, 480– 481
Intravesical pressure, 80 exclusion and reanastomosis of the bowel, 476
Intrinsic sphincter function, 329 indications, 474
Intrinsic sphincteric deficiency (ISD), 11, options for selection of port sizes and location,
160– 161, 163, 284, 310– 311, 319, 329, 475
340, 368, 387, 399, 409, 417, 429, 702, patient preparation, 474
705, 709, 714 patient selection, 474
evaluation, 319– 321 postoperative management, 481– 482
in stress incontinence, 12 refashioning of isolated bowel segment,
physical examination, 320 477– 478
radiographic evaluation, 320 results, 482– 483
urodynamic studies, 320– 321 surgical technique, 474–475
Intrinsic urethral deficiency, challenge of, Laparoscopic hysterectomy, 530– 531, 549
327– 328 Laparoscopic hysteropexy, 530
Intrinsic urethral dysfunction, 12 Laparoscopic paravaginal repair, 588, 631–639
Introl bladder neck support prosthesis (BNSP), clinical results, 637– 638
269– 271 incision sites, 636
 Index 939

preoperative considerations, 632 sympathetic nervous system, 30

surgical technique, 632–635 symptoms, 82 –84
Laparoscopic prolapse surgery, advantages, 691 Lower urinary tract function/dysfunction, 217
Laparoscopic rectocele repair, 749– 750 drug therapy, 216
Laparoscopic retropubic bladder neck suspension, hormonal influences on, 81
605– 606 Lower urinary tract symptoms (LUTS), 57, 228,
Laparoscopic sacral colpoperineopexy, 692 233– 234
anatomic landmarks, 692
Laparoscopic sigmoidoplasty, selection of port McCall culdeplasty, 652, 669–670, 675
sizes and location, 477 Macrosomia, physical effects, 107
Laparoscopic urinary stress incontinence Magnetic resonance imaging (MRI), 510,
procedures, 309– 317 514– 520, 739, 817
clinical outcomes, 311 cystocele stage IV, 601
patient position, 312 dynamic defecography, 742
technique, 311 female anatomic structures, 516
Laparoscopically directed pelvic floor paravaginal defect repair, 619
reconstruction, 314– 315 pelvic organ prolapse, 516
Lateral urethrocystography, 402 pelvis, 19, 581– 582
Lateral vascular pedicle, ligation to bladder, 866 rectocele, 722
Leak point pressure (LPP), 157–165 urethral diverticula, 820, 822– 824
definitions, 157– 158 uterine prolapse, 527
introperative use, 162 Maladaptive neurogenic inflammation, 891
LeFort colpocleisis, 547– 548 Manchester-Fothergill operation, 547
LeFort partial colpocleisis, 712– 713 Manchester operation, 529
Levator ani muscular sling, 718 Manometric measurement of pelvic floor muscles,
Levator hiatus, 719– 720 246
Levator muscle fascia, 4 Manometry, 246– 247
Levator musclulature, 401 Marshall-Marchetti-Krantz (MMK) bladder neck
fascial covering, 508 elevation, 283, 292–295, 299–300, 304,
in childbirth, 98 – 99 309– 312, 625, 809
magnetic resonance imaging (MRI), 515 outpatient mini-incision, 295– 296
Levator musculature, 4, 17, 134, 597– 598, 644, Marshall-Marchetti-Krantz (MMK) retropubic
724, 923 urethropexy, 389
myography, 510 Marshall-Marchetti-Krantz (MMK)
Levator syndrome, 912 vesicourethropexy, 389
Lifestyle practices, 234 Martius flap, 773– 775, 851– 853
Ligaments in childbirth, 100– 101 Martius graft, 847
Lower urinary tract Mastocytosis, 891
adrenergic receptors, 29 – 30 Maximal urethral closing pressure (MUCP),
central nervous connections, 35 –39 clinical application, 160
clinical uropharmacology, 215 Maximal urethral closure pressure (MUCP), 145,
drugs affecting, 125 147, 160, 225, 227
functions, 23 Medical Outcomes Study, 56
hormonal influence on, 79 – 94 Membrane catheters, 142– 143
innervation, 25 – 27 Meningomyelocele, 148
neurotransmission and receptors, 27 –33 Menopause, 83 – 84, 86
parasympathetic nerve terminals, 27 Menstrual cycle, 80
parasympathetic supply, 25 – 26 Mesonephric carcinoma, 823
proliferation rates, 80 Messenger RNA, 33
reconstruction, 859, 874– 879 Microballoon, implantation system, 339
somatic supply, 26 – 27 Microtransducer catheters, 143
sympathetic innervation, 26 Micturition
sympathetic nerve terminals, 27 central neurological control, 81
940 Index

[Micturition] Obesity, and urinary incontinence, 234– 235

dopaminergic influence, 32 Obstetrical correlates of urinary incontinence,
initiation reflexes, 38 101– 102
intramicturition reflexes, 38 – 39 Obturator fascia, 612
neurophysiology, 23 – 43 Obturator fossa, 866, 868
sensory innervation, 33 Obturator lymph node, 866
storage-favoring reflexes, 38 Obturator vessels, 866
UCPP, 152 Occult stress incontinence, 268
Mid-to-distal suburethral slings, 419– 420 Occult stress urinary incontinence, 679
Midline-type defect, 756 O’Leary-Sant IC symptom index, 900
Minimally invasive vaginal sling procedures, 429 O’Leary-Sant Symptom Index, 911
Mixed urinary incontinence, 45, 122 Omental interposition, 776, 790
Modified Oswestry Disability Scale, 911 Omentum, 792
Moshcowitz procedure, 698 Opioids in interstitial cystitis (IC), 908
Multichannel urodynamics, 509 Organ selectivity, 216
Multiple pregnancy and childbirth effects on Orgasmic disorder, 65
pelvic floor, 107 Orthotopic neobladder substitution, 859– 887
Multiple sclerosis, 128, 176, 178 Orthotopic urinary diversion, 860
Muscarinic ACh receptors, 217 Osteomyelitis, 352
Muscarinic receptors, 191 Overactive bladder (OAB), 60, 191– 213, 219,
Muscle-invasive bladder cancer, 859 224, 227, 233, 241
Muscle manipulation in interstitial cystitis (IC), characterization, 191
899 telephone study, 59
Musculofascial support, 16 Overflow incontinence, 45
Myelodysplasia, 184 Oxybutynin, 218– 219
comparison with tolterodine, 221
National Center for Health Statistics, 525 extended-release, 195– 198
National Health and Social Life Survey (NHSLS), long-term tolerability and compliance, 198
65 safety and efficacy in the elderly, 197
Needle electrodes, 247 versus immediate-release oxybutynin, 197
Needle electromyography (EMG), 921 immediate-release, 191, 193
Needle suspension (see also Transvaginal needle Oxybutynin chloride, 219– 220
suspensions (TVNS)), 587– 588
Nephrogenic adenomas, 821 Pain in pelvic floor disorders, 122
Neurogenic cystitis, 891 Paracolpium, 597
Neurogenic pelvic floor muscle spasm, 904– 907 Parametrium, 597
Neurologic disease, 167 Parasympathetic nervous system, 191
Neurologic testing, abnormal findings, 129 Paraurethral dissection, 404
Neuropathic changes, in childbirth, 99 – 100 Paravaginal defect repair (PVDR), 292– 294, 302,
Neuropeptide Y (NPY), 67 310, 565, 568, 604, 606– 607, 618,
Neurotropic pseudorabies virus (PRV), 891, 907 634– 635
NIDDK, 889, 895– 896 abdominal (retropubic approach), 621
NIH-NIDDK, 889 anterior vaginal prolapse, 625– 626
Nimodipine, 60 complications, 626– 629
Nitric oxide (NO), 67 diagnosis, 618– 620
Nitric oxide synthetase (NOS), 67 – 68 genuine stress incontinence, 623– 625
NMDA, 32 laparoscopic approach (see Laparoscopic
Nonadrenergic, noncholinergic (NANC) paravaginal repair)
neurotransmitter system, 30 magnetic resonance imaging (MRI), 619
Nonadrenergic/noncholinergic mediated outpatient mini-incision technique, 294
responses, 67 physical examination, 618– 619
Nottingham Health Profile, 56 surgical correction, 615– 630
Nurses Health Study (NHS) I and II, 889 surgical outcomes, 623– 629
 Index 941

surgical techniques, 620–623 Pelvic floor injury

ultrasonography, 619–620 managing the next pregnancy, 110–111
vaginal approach, 621– 623 obstetrical, 103
Parkinson’s disease, 35 predicting, 104
Park’s postanal repair, 924 Pelvic floor musculature (PFM), 244, 248– 249,
Partial colpocleisis, 708– 709 899, 905
indications, 702 and bladder pathology, 907
results, 710–711 assessment, 251
Pedendal nerve injury, 110 dysfunction, definitions, 243
Pelvic anatomy, 507, 576, 701, 735– 736 electromyography (EMG), 246
bony and muscolofascial support, 507– 508 in men, 244
perineal support, 509 in women, 245
Pelvic denervation, 598 manometric measurement, 246
Pelvic diaphragm, 596 rating scale, 250
Pelvic diaphragm muscles, 597 reflex spasm, 906
Pelvic floor rehabilitation, 233, 241– 254
activity during increased intra-abdominal spasm and tenderness, 906
pressure, 10 spastic, 906
anatomy, 904– 905 strength measurement, 134
damage leading to urinary incontinence, training, 241– 242, 249
102 Pelvic floor relaxation, 507, 512, 517
in pregnancy, labor, and delivery, 95 –101 anatomy, 717– 720
innervation, 905 critical components, 718
laparoscopically directed reconstruction, pathophysiology, 717– 720
314– 315 Pelvic floor support, anatomy, 596– 597
normal function, 905 Pelvic fractures, 843
rehabilitation, 109 Pelvic lymphadenectomy, 864– 866
tension myalgia, 906 Pelvic muscle excercises (PMEs), 242, 244,
Pelvic floor disorders, 119– 139, 267– 278 251– 252, 254
ancillary studies for functional disorders, Pelvic organ classification systems, 130
740– 741 Pelvic organ function, evaluation, 679
evaluation, 679 Pelvic organ prolapse, 129– 131, 274, 701
general examination, 129 etiology, 597– 599, 664
gynecologic examination, 129– 131 imaging techniques, 509–520
high-tone, 905– 906, 911– 914 incidence, 664
in interstitial cystitis (IC), 906– 907 indications, 702
history, 119– 120 magnetic resonance imaging (MRI), 516
neurological examination, 126– 128 management, 663
pathophysiology, 8 – 11 normal support to pathologic prolapse,
physical examination, 126 497– 498
questionnaires, 125 pathology, 663– 664
symptoms, 120– 125 pathophysiology, 597– 599, 702
systemic manifestations, 121 physical examination, 722
Pelvic Floor Distress Inventory (PFDI), 57 physiologic evaluation, 509
Pelvic floor electrical stimulation (PFES), prevalence, 664, 735
252– 254 quality of life (QOL), 497
Pelvic floor exercises, 60, 109, 241– 245, 252, radiographic evaluation, 507– 523
583, 598 staging, 133, 596
in high-tone PFD, 912 surgical correction, 615
in pregnancy, 103–104 symptoms, 498–500
in sexual dysfunction, 66 Pelvic Organ Prolapse Quantification (POP-Q),
patient guide, 263– 265 131– 136, 497, 500–501, 503–505, 527,
Pelvic Floor Impact Questionnaire (PFIQ), 57 595, 739
942 Index

[Pelvic Organ Prolapse Quantification (POP-Q)] contraindications, 276– 277

examination, 132 cost issues, 276
ordinal staging system, 502, 504 fitting, 564
points of reference, 131– 132 for genital prolapse, 273–274
Pelvic organ support historical applications, 273
anatomy, 1 – 21, 692 ideal candidate for, 276
bone, 1 inability to fit, 276
defects, 507 incarceration, 565
deficiency of, 8 indications, 275
distribution of, 499 perceived drawbacks, 274– 276
levels of, 576– 577 removal and cleansing, 565
ligaments, 1 – 2 specially designed, 565
musculature, 2 test, 269
quantification, 580 types, 274– 275, 564
structures, 1 – 2 urodynamic effects, 272
Pelvic organ support defects, 497– 506 Peyrera needle suspension procedure, 283
codifying systems, 500 Phenoxybenzamine, 29
conditions for performing exam, 505 Phentolamine, 29
Pelvic reconstructive surgery, goals of, 692 Phenylpropanolamine (PPA), 226– 227
Pelvic trauma, 842 Phosphodiesterase type 5 (PDE5), 67
Pelvis Physical therapy in high-tone PFD, 911
magnetic resonance imaging (MRI), 19, 528, Polyglycolic acid (PGA) mesh, 584
581– 582 Polytetrafluoroetylene paste (PTFE, Teflon,
obstetric issues, 95 –118 urethrin), 336– 337
sagittal view, 17 complications, 336– 337
Percutaneous neuromodulation, 201 results for stress incontinence, 336– 337
Perfusion catheters, 142 Pontine micturition center (PMC), 32, 35
Periaqueductal gray (PAG) of midbrain, 908 Positive-contrast peritoneography, 513
Perineal body (PB), 2, 502 Positive-pressure urethrography (PPUG), urethral
Perineal laxity, 18 diverticula, 817
identification, 723 Posterior colporrhaphy, 288, 717– 732, 744– 745
Perineal massage in pregnancy, 103– 104 Posterior pedicle, ligation to bladder, 869– 872
Perineal musculature, 16 Posterior pelvis, 508
Perineal repair, indications, 724 Posterior vaginal wall, 754–755
Perineal support, 8 Posterior vaginal wall relaxation,
Perineal tears, grading, 721 symptomatology, 721
Perineobulbar detrusor facilitative reflex Posterior vaginal wall support, 508
(PBDFR), 38 restoration of, 717
Perineodetrusor inhibitory reflex (PDIR), 38 Posthysterectomy apical prolapse, 663
Perineum, 8, 16 – 19 Posthysterectomy vault prolapse, 651
in pregnancy, 96 –97 Postoperative urgency and urge incontinence, 437
Peripheral nerve evaluation (PNE), 489 Postpartum issues, 109– 110
Peripheral nerve stimulation, 202 Postprostatectomy incontinence, 160– 161
Peritoneal flap, 774 Potassium channel openers, 222
development of, 776 Potassium chloride test (KCl test), 893– 894
Peritoneum, 681 Pouch of Douglas, 869
Periurethral fascia, 831, 835– 836 Pregnancy
Perivesical fascia, 609– 610 pelvic floor in, 95 – 101
Pernicious anemia, 458 perineum in, 96– 97
Pessaries, 267– 278, 545, 563– 565, 641 urethral diverticula in, 824– 825
and stress incontinence, 268– 272 Prerectal fascia, 736
care recommendations, 274, 276 Pressure perineometer, 247
complications, 565, 583 Pressure transmission ratios, 152
 Index 943

Progesterone, 80 sling materials, 357

Progestogens, 80 – 81 sling placement, 361, 370–371
Prolapse sling tension, 372– 373
classification systems, 131 surgical technique, 358, 370– 374
grid for recording measurements, 133 suture techniques, 372
see also Anterior pelvic organ prolapse; Pelvic synthetic materials, 349– 351, 357
organ prolapse; Posthysterectomy apical vaginal dissection, 358– 361
prolapse; Posthysterectomy vault versus retropubic urethropexy (RPU),
prolapse; Urethral prolapse; Urogenital 291– 292
prolapse; Uterine prolapse; Uterovaginal xenografts, 357
prolapse; Vaginal apex prolapse; Vaginal Pubovesical muscle (PVM), 577
vault prolapse; Vaginal wall prolapse Pudendal nerve in childbirth, 99– 100
Prompted voiding (PV), 239 Pulsion enteroceles, 15
Propantheline bromide, 217– 218 Purinergic mechanisms, 31
Prostaglandin antagonists, 222 Purse-string suture, 538
Prostate-specific antigen (PSA), 823
Proximal urethra hypermobility, 520 Q-tip angle, 135
Proximal urethral support, 273 Q-tip test, 134– 136
Pseudoephedrine, 226 resting and straining angles, 136
Pseudomonas, 352 Quality-of-life (QOL)
Pseudorenal pain, 122– 123 pelvic organ prolapse, 497
Psyllium in fecal incontinence, 922 sexuality in, 65
Pubocervical fascia, 5 – 6, 577, 583– 584, 615 Questionnaires, 124– 136
Pubococcygeus muscle (PCM), 401, 597– 598 pelvic floor disorders, 125
Pubococcygeus trauma, 517
Pubourethral ligaments (PUL), 4, 401, 508 Radiation fistulae, 773
Pubovaginal sling (PVS), 61, 848– 851 Radical cystectomy, 859– 887
allograft fascia, 347– 349 abdominal exploration, 862
allograft preparation, 358 bowel mobilization, 863– 864
allografts, 357 complications, 884
anesthesia/position, 358 continence/voiding pattern, 880– 884
autologous fascia/tissue, 346– 347, 357 definition, 860
bone anchor technology, 353 incision, 861– 862
cadaveric fascia lata allograft (CFLA), overview, 860
357– 366 patient positioning, 861
choice of sling materials, 346– 353 post-operative care, 879
clinical results, 374 preoperative evaluation, 860 –861
complications, 374– 376 preoperative preparation, 861
contemporary results, 346 recurrence, 884
cystourethropexy, 369 results, 880– 884
autologous fascia lata, 367– 378 surgical technique, 861– 879
history, 367 survival, 884
erosion of synthetic slings, 350 urethral preparation, 873– 874
fascia lata graft harvest, 370 urinary diversion after, 859
history, 345– 346 Radical prostatectomy, incontinence following,
indications, 368– 370 175
infectious osseous complications, 352 Radiculitis, 122– 123
outcomes, 362– 364 Radiofrequency energy in fecal incontinence, 927
overview, 345 Radiography, cystoceles, 581
preoperative valuation, 357– 358 Radiologic imaging, 817
selection of graft material, 373– 374 RAND 36-item Health Survey (SF-36), 56, 59 – 60
selection of patients, 357 Receptor selectivity, 216
sling fixation techniques, 351– 353 Rectal pressure, 178
944 Index

Rectocele, 512, 664, 702, 707, 735– 759 Retropubic dissection, 372
adjunctive studies, 739 Retropubic urethropexy (RPU), 291– 307
after colposuspension, 304 candidates for, 292
bowel function, 721 concomitant gynecologic surgery, 305
classification, 720 history, 292– 293
defect-specific repair, 745– 747 long-term bladder complications, 303– 304
definition, 18, 735 techniques and efficacy of procedures,
diagnosis, 18, 722– 723, 739– 744 293– 300
etiology, 737–738 versus pubovaginal sling, 291–292
evaluation, 721– 723, 739– 744
formation, 718– 719 Sacral anatomy, 487
high-grade, 19 Sacral colpopexy, key anatomic landmarks, 692
history, 721 Sacral micturition center (SMC), 35
indications for repair, 723– 724 Sacral nerve root stimulation, 444, 485– 495
laparoscopic repair, 749– 750 acute nerve stimulation testing, 486– 488
magnetic resonance imaging (MRI), 722 complications, 493
nonsurgical approaches, 744 efficacy of, 491–493
operative criteria, 743 history, 485– 486
physical examination, 739 important responses, 488
prevalence, 720–721 interstitial cystitis (IC), 910
radiographic examination, 722– 723 multicenter randomized controlled trial
sexual function, 721 (MDT-103), 491– 493
surgical approaches, 744 patient selection, 486
surgical repair, 735 peripheral nerve evaluation (PNE), 489
symptoms, 18, 738– 739 permanent neurostimulator implantation,
transanal repair, 747– 749 489– 491
treatment, 744– 750 postimplantation activation and programming,
use of term, 579 491
with attenuated perineum, 753 subchronic phase, 489
Rectocele repair, 717–732 test procedure, 486– 489
complications, 750 two-stage sacral neurostimulator implantation,
criteria of patient selection, 743– 744 490– 491
defect-specific, 731– 732 urge incontinence, 492
outcomes, 732 urinary frequency, 492–493
summary of anatomic and functional outcomes, urinary retention, 493
751– 752 Sacral neuromodulation, 202– 203
surgical technique, 724– 732 in interstitial cystitis (IC), 910
use of mesh, 750 in pelvic pain, 914
Rectogenital septum, 736 Sacral neurostimulation, in interstitial cystitis
Rectovaginal fascia, 736, 748 (IC), 899
Rectovaginal septum, 8, 17, 508, 719, 747 Sacral spinal nerve stimulation in fecal
delineation, 694 incontinence, 927
tears in, 736 Sacrocolpopexy, 604
Rectus abdominis muscle, 790 Sacrospinous ligament suspension, 651– 661
Refractory detrusor instability, 485– 495 accompanying vaginal hysterectomy, 651– 652
management of, 465– 472 anatomic outcomes, 655– 657
Renal insufficiency, 520 anterior vaginal wall support, 656
Renal pain, 122 complications, 657– 658
Resiniferatoxin (RTX), 33, 225 exposing the ligament, 652–653
in interstitial cystitis (IC), 909– 910 pre- and perioperative considerations, 654– 655
Retrograde pyelography, 843 predictors of success, 657
Retropubic Burch cystourethropexy, 283 risk factors, 657– 658
Retropubic colposuspension, 309, 738 sexual function, 656– 657
 Index 945

support of vaginal apex, 655– 656 Sling procedures

surgical anatomy, 666 currently used materials, 419
surgical technique, 667–669 postoperative complications, 447– 455
suture placement, 653–654 variables between, 418
techniques, 652– 655 Smith-Hodge pessary, 268– 270, 274
unilateral versus bilateral, 654 Smoking, and urinary incontinence, 47, 234
uterine suspension, 652 Smooth muscle cell morphology, 24
vaginal anatomy, 656– 657 Society of Gynecologic Surgeons, 131, 561
Sacrouterine ligament complex, 607 Sodium morrhuate, 329
SEAPI incontinence score, 387, 397 Sodium pentosan polysulfate in interstitial cystitis
Self-catheterization, 438 (IC), 896– 897
Sensory dermatomes, 128 Sonography, 513– 514
Sensory disorders, 224 Spalding-Richardson procedure, 547
Serotonergic mechanisms, 32 SPARC procedure, 350
Serotonin (5HT), 32 Sphincteroplasty, 923–924
Sex hormone-binding globulin (SHBG), success rates, 926
67 – 68 Spinal cord injury (SCI), 163, 170
Sex hormones, 81 Splinting, 702
Sexual dysfunction, 65 – 78 Spongiform encephalopathy, 347
arousal disorder, 65 Staphylococcus aureus, 352
categories, 65 – 66 Stoma in fecal incontinence, 928
definition, 66 Stress incontinence (see also Urinary
diagnosis, 70 incontinence), 45, 121– 122, 168,
hormonal abnormalities, 68 – 69 267– 278
hormonal profile, 72 Stress incontinence (see also Urinary
hypoactive sexual desire, 65 incontinence)
investigational medications/devices, 73 – 75 clinical application, 160– 162
medical management, 72 –73 development of, 11
medical risk factors associated with, 68 –70 estrogens in, 89
medications in, 70 ISD in, 12
musculogenic factors, 70 secondary, 837
neurogenic factors, 69 – 70 techniques of repair, 704– 705
neurological exam, 72 videourodynamics, 179
pelvic floor exercises, 66 Stroller afferent nerve stimulator (SANS),
physical exam, 71 201– 202
prevalence, 65 Substance P, 33, 67, 891
psychogenic factors, 70 Subtotal hysterectomy, 530
treatment, 72 – 73 Subtrigonal dissection, 443
vascular factors, 68 Suprapubic catheter (SPT), 393
Sexual function and response, hormonal influence Surface skin electrodes, 246–247
on, 67– 68 Sympathetic-detrusor inhibition reflex (SDIR), 38
Sexual function questionnaire, 65 Sympathetic sphincter constrictor reflex (SSCR),
Sexual pain disorders, 65 38
Sexual response Symptom Impact Index (SII), 57
evaluation, 70 – 72 Symptom Severity Index (SSI), 57
neurogenic mediators, 66 – 67 Symptomatic anterior quadrant relaxation, 618
Sexual response cycle, 66
Sexuality, as quality-of-life issue, 65 T-shaped prolene mesh, 695– 697
Sickness Impact Profile (SIP), 56 Tanagho procedure, 856
Sigmoidocytoplasty, 476 Tension-free vaginal tape technique (see TVT
Silicone microimplant, 338– 339 procedure)
complications, 339 Testosterone, 67 – 68, 73
results, 338–339 Thiele massage in high-tone PFD, 912
946 Index

Thiersch encirclement procedure, 924 infection, 411

Tizanidine hydrochloride in high-tone PFD, 913 load-deformation curves for permanent
Toileting programs, 238– 241 materials, 402
Tolterodine, 191– 195, 241 mechanism of action, 405– 408
adverse effects, 193 obturator approach, 413
comparison with oxybutynin, 221 outcomes, 408– 409
dosage, 192 patient position, 402
extended-release, 198– 199 subpopulation studies, 409
safety, 195 surgical technique, 400–405
side effects, 195 vessel distance from needle, 411
tolerability, 193–195 Type 1 incontinence 180x
versus immediate-release oxybutynin, 194 Type 2 incontinence, 319
Tolterodine tartrate, 218 Type 2A incontinence, 181
Total vaginal length (TVL), 502 Type 2B incontinence, 182
Traction enteroceles, 15 Type 3 incontinence, 183, 319, 369
Transdermal oxybutynin patch, 60 Type I muscle fibers, 242
Transitional cell carcinoma (TCC) of the bladder, Type II muscle fibers, 242
859, 884
Translabial ultrasonography, 820 UDI-6, 61
Transurethral diverticulotomy, 825 Ultrasonography, 600– 601, 817
Transurethral electrocoagulation, 826 paravaginal defect repair, 619– 620
Transvaginal Cooper’s ligament sling, 429– 435 urethral diverticula, 818
choice of sling material, 431– 432 Ultrasound, 513– 514
complications, 434 Upper urinary tract evaluation, cystocele stage IV,
outcomes, 432– 433 603
procedure, 429– 431 Ureteral dissection, 864
Transvaginal diverticulectomy, 825 Ureteral injury, 557, 591
Transvaginal hysterectomy, 540 Ureteral obstruction, 518, 711
Transvaginal levator myorraphy, 641– 649 videourodynamics, 179– 183
preoperative evaluation, 641– 642 Ureteral pain, 123
technique, 641– 646 Ureterovaginal fistula, 540
Transvaginal needle suspensions (TVNS), Urethra, 82
279– 282 anatomy, 10 – 11, 141
complications, 281 hypermobility associated with stress
current status, 281 incontinence, 11 – 12
development and evolution, 279 low pressure, 147– 148
level of evidence, 280 multilayered reconstruction, 804
reported outcomes, 280– 281 pressure necrosis of musculofascial structure,
surgical techniques, 280 842
Transvaginal tape procedure (see TVT procedure) traumatic disruption, 800
Transverse cervical ligament pedicles, 555 Urethral catheter, 158
Transvesical phenol injections, 200– 201 Urethral closure, 9
Tricyclic antidepressants, 223– 224 Urethral closure pressure profile (UCPP), 145,
Trospium chloride, 218– 219 147
TURP, 160– 161 augmented, 148– 149
Tutoplast fascia, 388, 390 double-peaked, 148
TVT procedure, 61, 291, 301, 350– 351, dynamic, 149– 152
399– 416, 419, 423, 437, 453, 548 micturition, 152
bladder perforation, 411 Urethral continence, 9
comparative studies, 413 Urethral damage, causes of, 855
complications, 410– 413 Urethral diverticula, 811– 840
concomitant surgery, 412 benign pathology, 821– 822
historical background, 400 communication site, 834
 Index 947

complications, 830– 837 transurethral method, 330

diagnosis, 811, 815 Urethral injury
differential diagnosis of suburethral masses, common causes, 841
815 diagnosis, 797
endoscopic techniques, 825– 826 Urethral length, 9
etiology, 812–813 Urethral obstruction, 437
evaluation, 812– 814, 837 clinical presentation, 447– 448
excision, 826– 828, 833 cystoscopy, 449
and concomitant bladder neck suspension, diagnosis, 448– 449
828– 829 outcomes, 451
history, 811, 815 prevention, 451–452
identification, 812– 814 surgical management, 441– 444
in pregnancy, 824–825 treatment, 449– 451
incidence, 811–812 urodynamics, 448
initial incorrect diagnoses, 814 vaginal examination, 449
intraoperative complications, 830–831 Urethral pathology, 821– 824
intraoperative monitoring, 820 Urethral plication, 399
LNSC3 classification system, 813 Urethral preparation for radical cystectomy,
magnetic resonance imaging (MRI), 820, 873– 874
822– 824 Urethral pressure, 80, 82, 178
malignancies, 822– 824 Urethral pressure measurement, 141– 143
marsupialization, 825 clinical application, 160
most common initial complaints, 813 Urethral pressure profile, 147– 148
nonsurgical management, 824– 825 measurement, 402
physical examination, 815 Urethral pressure profilometry, 141– 155
positive pressure urethrography (PPUG), 817 technique, 143– 144
postoperative care, 829 Urethral prolapse, 11
postoperative complications, 831–837 Urethral reconstruction, 841–858
presentation, 813– 814 advancement flap, 845
recurrence, 831 ancillary procedures, 848– 853
surgical techniques, 825–829 basic techniques, 844– 847
ultrasonography, 818 diagnosis, 842– 843
urinary incontinence in, 816 indications for surgery, 843
voiding cystourethrography (VCUG), 817– 818 labia minora pedicle graft, 846– 847
Urethral diverticular disease, 511 pelvic examination, 842
Urethral erosion postoperative care, 847– 848
clinical presentation, 453 preoperative management, 843
diagnosis, 453 primary closure, 845
treatment, 454 results, 853– 855
Urethral floor studies, 854
linear loss, 808 surgical approaches, 844
slough of, 805– 809 surgical technique, 843– 844
Urethral hypermobility, 134– 136, 172, 429, 433, timing of surgery, 843
607, 704 tube graft, 845
Urethral hypermobility (type II incontinence), vaginal examination, 842
357, 368–369 videourodynamic testing, 842
Urethral injectables, 329– 343 Urethral sphincteric mechanism, 885
ideal agent, 330 Urethral support, 577
injection techniques, 330– 339 Urethrodetrusor facilitative reflexes (UDFR), 39
mechanism of action, 329–330 Urethrolysis, 441– 442
new injectables, 339 Urethropelvic ligament, 5, 11, 508, 597, 607
patient selection, 330 Urethroscopy, 817
periurethral method, 330 Urethrosphincteric guarding reflex (USGR), 38
948 Index

Urethrosphincteric inhibitory reflex (USIR), 39 pharmacologic management, 215– 231

Urethrovaginal fistula, 797– 810, 831 postpartum, 109– 110
causes of, 797 pregnancy as risk factor, 46 – 47
clinical presentation, 798 prevalence, 48 – 49, 82
etiology, 797 in older women, 49
incision and mobilization, 799 in younger women, 48
linear, 803– 805 quality-of-life issues, 53 – 64
multilayer closure, 799 race factor, 47 – 48
operative repair, 798– 800 risk factors, 45 – 48
Urethrovesical junction (UVJ), 267, 269, 297, surgical treatment, 61
360, 612, 623 type I and II, 417
use of term, 579 see also Laparoscopic urinary stress
Urge Impact Scale (URIS), 58 incontinence procedures; Mixed
Urge incontinence, 45, 122, 172, 200, 374 incontinence; Overflow incontinence;
and urgency, 438 Specific management techniques; Stress
sacral nerve root stimulation, 492 incontinence; Urge incontinence and
Urge-Incontinence Impact Questionnaire (U-IIQ), specific management techniques
57 Urinary retention, 128, 167, 207, 328, 374, 453,
Urge-Urinary Distress Inventory (U-UDI), 57 558
Urinary control inserts, 60 sacral nerve root stimulation, 493
Urinary diversion, 207, 885, 899 Urinary tract infection (UTI), 438, 453
after radical cystectomy, 859 hormonal influences on, 81
videourodynamics, 187– 188 recurrent, 86
Urinary division, 161–162 Urine leakage, 237
Urinary frequency, sacral nerve root stimulation, Urine markers, 894– 895
492– 493 Urine storage requirements, 215
Urinary incontinence, 81 – 83, 121, 167, 215, 233 Urodynamic assessment, 141– 155
age factor, 45 – 46, 82 Urodynamic evaluation, 439
assessment, 124 Urodynamic study, cystocele stage IV, 602
behaviorally based and other noninvasive Urodynamics, 167, 703, 816
interventions, 59 – 60 Urogenital atrophy, 83 – 84
cigarette smoking in, 47 estrogens, 86 – 88
defined, 45 prevalence, 83
epidemiology, 45 – 51 Urogenital diaphragm, 596–597, 723
estrogens for, 84 – 85, 227– 228 Urogenital Distress Inventory (UDI), 56 – 57
further evaluation, 119 Urogenital prolapse, prevalence, 83
heredity in, 46 Urogynecologic disease
history, 124, 310– 311 abdominal symptoms, 123
hysterectomy risk, 46 gastrointestinal symptoms, 123
impact of treatment on HRQOL, 59 – 61 Urologic disease, 167
impact on general health-related quality of life Uroselectivity, 216
58–59 Uterine anatomy, 525– 526
impact on psychological health, 59 Uterine pedicles, 537
in health-related quality of life (HRQOL), Uterine prolapse, 518, 545– 559
53 – 64 clinical evaluation, 526
incidence, 49, 82 complications, 536– 541
medical management, 60 –61 conservative treatment, 528
new-onset, 831 diagnostic tests, 527
obesity in, 46 grades I to IV, 14 – 15
objective measures, 53 history, 526, 545, 547
obstetrical correlates of, 101–102 magnetic resonance imaging (MRI), 527
parity as risk factor, 46 –47 pathophysiology, 526
pelvic floor damage leading to, 102 physical examination, 527
 Index 949

presentation, 526 levels, 617

surgical therapy, 525– 544 posterior, 8, 508
technique, 531– 535 Vaginal tampons, 269–270
therapeutic options, 528– 541 Vaginal ultrasound, 513
uterine sparing procedures, 529– 530 Vaginal vault prolapse, 14 – 16, 641– 649,
Uterine support, 6 – 7, 508 677– 689
Uterine suspension, sacrospinous ligament abdominal approach, 641
suspension, 652 complications, 647– 648
Utero-ovarian tie, 554 evaluation, 678– 679, 702– 705
Uterosacral-cardinal ligament complex, 558 grade 3, 707
Uterosacral ligament, 551, 555, 577, 597 grade 4, 707
Uterosacral vaginal vault suspension, 675 history, 702
Uterovaginal prolapse, 664– 665 overview, 677
Uterus, eversion of, 535 physical examination and studies, 703– 704
repair, 651–661
Vacuum-assisted deliveries 107d after hysterectomy, 642– 646
Vaginal apex prolapse sexual function, 647
general concepts of surgical repair 665p vaginal approach, 641
preoperative assessment, 665 Vaginal vault support, 6 – 7, 558
prevalence, 674 Vaginal wall flap, 836
transvaginal approaches, 663–676 Vaginal wall prolapse
Vaginal bleeding, 565 anterior, 11 – 14
Vaginal cuff, 555– 558 posterior, 16 – 19
cellulitis or abscess, 557 Vaginal wall support
Vaginal depth restoration, 539 anterior, 13, 508, 632– 633
Vaginal devices, 267– 278 posterior, 508, 717
Vaginal erosion Vaginal weights, 252
clinical presentation, 453 Vaginography, 600
diagnosis, 453 Valsalva leak-point pressure (VLPP), 158– 161,
treatment, 454 368, 380– 381, 383–384
Vaginal fascia, 736 interpretation of results, 159
Vaginal fascial condensation, 7 measurement, 158
Vaginal hysterectomy, 184, 531, 545– 559 Vanilloid receptor (VR1), 33
complications, 549– 550, 557 Vasoactive intestinal polypeptide (VIP), 67
conversion to abdominal approach, 550– 551 Vesical autoplasty, 791
historical perspective, 546 Vesical instability, 328
intraoperative complications, 557 Vesical pain, 123
operative mortality, 546 Vesical-sacral sphincter loop (loop III), 37
postoperative complications, 557 Vesicopelvic fascia, 13, 612
risk factors, 549– 560 Vesicopelvic ligament, 5– 7, 508, 577, 597
technique, 550– 557 Vesicoperitoneal fold, 534
Vaginal leiomyoma, 821 Vesicoureteral reflux, 168
Vaginal obturator, 692– 693 videourodynamics, 179
Vaginal paravaginal repair, 569– 570, 611, Vesicourethral reflux, 511
623– 626 Vesicovaginal fistula (VVF) repair, 511, 540, 558,
outcomes, 627 761– 773, 783– 795
Vaginal prolapse, 558, 598, 602 abdominal approach, 771, 787– 793
staging system, 527 abdominal versus vaginal approach, 765– 766
Vaginal sensors, 246 after hysterectomy, 761
Vaginal sling procedures, minimally invasive, 429 closure of fistula, 771
Vaginal sling surgery (PVS), 345– 356 complications, 772
Vaginal support conservative management, 764
anterior 3–6 creation of flaps, 771
950 Index

[Vesicovaginal fistula (VVF) repair] transvesical approach, 772

diagnosis, 761– 764, 784– 785 vaginal approach, 767– 771
etiology, 762, 783– 784 Videourodynamics, 61, 167– 190, 842
excision of fistulous tract, 766 applications, 174–188
history, 761– 762 cystocele stage IV, 602
indications for abdominal approach, 787–788 equipment and technique, 178– 179
interposition of tissue, 792– 793 Vitamin B12 deficiency, 458
isolation of fistula, 767 Voiding, 178
laparoscopic approach, 792 Voiding cystogram, 284
operative management, 764– 767 Voiding cystourethrography (VCUG), 287– 289,
overview, 783 510– 511, 581, 763, 817– 820
patient preparation, 767 urethral diverticula, 817– 818
pelvic examination, 785 Voiding dysfunction, 23, 174, 216, 224, 268, 281,
physical examination, 762– 763 399, 411, 433, 485
postoperative care, 771, 793 evaluation, 438– 440
postoperative drainage, 766 neurogenic and nonneurogenic, 462
post-radiation, 793 postoperative, 437– 445, 592
principles for success, 787 Voiding frequency, 192
radiation-induced, 773 Voiding habits, 192
results, 793 Voiding phases, 28, 174
sexual function following, 767 Voiding pressure, 172
standard O’Conor approach, 788– 791 Voiding reflexes, integral theory, 38 – 39
stress incontinence prior to fistula development, Vulvodynia, 123– 124
766
success rates, 772, 794
Watkins transposition operation, 547
surgical approaches, 767
Whitaker test, 179, 185
timing and success, 765
Window of Deaver, 876
timing of repair, 785– 786
timing of surgery, 764– 765
tissue interposition, 766 York Incontinence Perceptions Scale (YIPS), 58