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Female Pelvic

Medicine and
Reconstructive
Surgery
NOTICE
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Female Pelvic
Medicine and
Reconstructive
Surgery
Clinical Practice and Surgical Atlas
Editor
Rebecca G. Rogers, MD, FACOG
Regent’s Professor
Vice Chair for Research, Department of Obstetrics and Gynecology
Chief, Division of Urogynecology
Fellowship Director, Female Pelvic Medicine and Reconstructive Surgery
University of New Mexico Health Sciences Center
Albuquerque, New Mexico

Associate Editors
Vivian W. Sung, MD, MPH
Associate Professor
Director of Research
Division of Urogynecology and Reconstructive Pelvic Surgery
Department of Obstetrics and Gynecology
Warren Alpert Medical School of Brown University
Providence, Rhode Island

Cheryl B. Iglesia, MD, FACOG


Director
Section of Female Pelvic Medicine and Reconstructive Surgery
National Center for Advanced Pelvic Surgery (NCAPS)
MedStar Washington Hospital Center
Associate Professor
Departments of Obstetrics and Gynecology and Urology
Georgetown University School of Medicine
Washington, District of Columbia

Ranee Thakar, MD, MRCOG


Consultant Urogynaecologist and Obstetrician
Honorary Senior Lecturer at St. George’s University of London
Croydon University Hospital
Croydon, CR7 7YE
United Kingdom

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Dedication

RG Rogers: This book is dedicated to my family, John, Zachariah, and Hannah.


Without them, I would be lost. In addition, I would like to express my appreciation
and gratitude to the many patients I have had the privilege of caring for and the
amazing team I work with. Special thanks to Yuko, Gena, Peggy, Gwendy, and
Judy.
V Sung: To Helen, Sam, Doug, Kelsey, and Isla
C Iglesia: Dedicated to the ones I love, most especially Jon, Julie, and Brittany
R Thakar: Dedicated to all I have learnt from……………..my mentors, my fellows,
my patients
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Contents

Contributors ix Part B: Functional Anorectal Disorders 153


Preface xv
9. Anal Incontinence 153
Dipal Patel and Anton Emmanuel

10. Defecatory Dysfunction 173


I I FUNDAMENTAL TOPICS Gena Dunivan and William Whitehead

11. Anorectal Investigations 191


W. Thomas Gregory and Milena M. Weinstein
1. Epidemiology 3
Pamela J. Levin and Jennifer M. Wu Part C: Pelvic Organ Prolapse 209
2. Normal Anatomy of the 12. Pelvic Organ Prolapse:
Pelvis and Pelvic Floor 19 Anterior Prolapse 209
Marlene M. Corton Richard P. Foon and Robert Freeman
3. Mechanisms of Disease 51 13. Posterior Vaginal Wall Prolapse 225
Victoria L. Handa Tristi W. Muir
4. Clinical and Quality of Life Evaluation 61 14. Apical Pelvic Organ Prolapse 245
Mamta M. Mamik and Rebecca G. Rogers Tyler M. Muffly, J. Eric Jelovsek,
and Mark D. Walters

15. Pelvic Imaging 265


Olga Ramm and Kimberly Kenton
II I DISEASE STATES
Part D: Other Pelvic Floor Disorders 279
16. Pain of Urogenital Origin 279
Part A: Lower Urinary Tract Dysfunction 83
Cassandra L. Carberry and Deborah L. Myers
5. Stress Urinary Incontinence 83
17. Urinary Tract Infections 301
Charles R. Rardin and Nicole B. Korbly
Charlotte Chaliha
6. Urgency and Mixed
Urinary Incontinence 99 18. Female Sexual Dysfunction 315
Husam Abed and Yuko Komesu Christine M. Vaccaro and Rachel N. Pauls

7. Evaluation of Bladder Function 119


Cynthia S. Fok and Elizabeth R. Mueller

8. Voiding Phase Dysfunction 135


Benjamin M. Brucker and Victor W. Nitti

vii
viii Contents

III I CLINICAL MANAGEMENT IV I SURGICAL ATLAS

19. Pessaries for Treatment 27. Instrumentation 449


of Pelvic Organ Prolapse Jeannine M. Miranne and Cheryl B. Iglesia
and Urinary Incontinence 339
28. Stress Urinary Incontinence 455
Ranee Thakar
Alicia C. Ballard, Robert L. Holley, and Holly E. Richter
20. Physical Therapy for
Pelvic Floor Dysfunction 353 29. Urgency Urinary Incontinence
and Overactive Bladder 475
Kari Bø
Karen L. Noblett and Stephanie Jacobs
21. Behavioral Treatment for
Pelvic Floor Dysfunction 371 30. Vaginal Hysterectomy
with Uterosacral Plication 487
Kathryn L. Burgio, Patricia S. Goode,
and Alayne D. Markland John B. Gebhart and Christine A. Heisler

22. Use of Graft Materials 31. Laparoscopic Hysterectomy 501


in Reconstructive Surgery 391 Deirdre Lum and Ted Lee
David D. Rahn and Vivian W. Sung 32. Anterior Compartment Surgery 513
23. Route of Pelvic Organ Surgery 407 Sandra R. Valaitis
Anthony Smith and Fiona Reid 33. Posterior Compartment Surgery 521
24. Perioperative Medical Evaluation 413 Amy Park
Danielle D. Marshall and Robert E. Gutman 34. Apical Procedures 529
25. Postoperative Care of Patients Sunil Balgobin and Marlene M. Corton
with Functional Disorders 35. Anal Incontinence 553
of the Pelvic Floor 425
Giulio Aniello Santoro and Abdul H. Sultan
Patrick A. Nosti and Andrew I. Sokol
36. Fistula Repair 571
26. Incorporation of New Treatments
Steven Arrowsmith
into Clinical Practice 441
Cynthia A. Brincat, Stergios K. Doumouchtsis, 37. Complications from
and Dee E. Fenner Pelvic Reconstructive Surgery 583
Matthew D. Barber and Howard Goldman

Index 603
Contributors

Husam Abed, MD Cynthia A. Brincat, MD, PhD


Clinical Assistant Professor Assistant Professor
Department of Obstetrics and Gynecology Department of OBGYN
Wayne State University Division of Gynecology
Director, Division of Female Pelvic Medicine The University of Wisconsin Hospitals and Clinics
and Reconstructive Surgery Madison, Wisconsin
Henry Ford Health System Chapter 26
Detroit, Michigan
Chapter 6 Benjamin M. Brucker, MD
Assistant Professor
Steven Arrowsmith, MD Female Pelvic Medicine and Reconstructive Surgery
Clinical Consultant Department of Urology
Engender Health Fistula Care Project New York, New York New York University Langone Medical Center
Clinical Consultant New York, New York
Fistula Foundation Chapter 8
San Jose, California
Clinical Consultant Kathryn L. Burgio, PhD
Worldwide Fistula Fund Professor of Medicine
Denver, Colorado University of Alabama at Birmingham
Clinical Consultant Associate Director for Research
Mercy Ships Geriatric Research, Education, and Clinical Center
Garden Valley, Texas Birmingham VA Medical Center
Chapter 36 Birmingham, Alabama
Chapter 21
Sunil Balgobin, MD
Assistant Professor Kari Bø, PhD
Department of Obstetrics and Gynecology Physiotherapist, Exercise Scientist
Division of Female Pelvic Medicine and Reconstructive Norwegian School of Sport Sciences
Pelvic Surgery Department of Sports Medicine
University of Texas Southwestern Medical Center Oslo, Norway
Dallas, Texas Chapter 20
Chapter 34
Cassandra L. Carberry, MD, MS
Alicia C. Ballard, MD Clinical Assistant Professor
Instructor/Fellow Division of Urogynecology and
Department of Obstetrics and Gynecology Reconstructive Pelvic Surgery
Division of Urogynecology and Pelvic The Alpert Medical School of Brown University
Reconstructive Surgery Women and Infants Hospital of Rhode Island
University of Alabama Providence, Rhode Island
Birmingham, Alabama Chapter 16
Chapter 28
Charlotte Chaliha, MBBChir, MA, MD, MRCOG
Matthew D. Barber, MD, MHS Consultant
Professor of Surgery and Vice Chairman of Clinical Obstetrician and Gynaecologist,
Research, Obstetrics Subspecialist in Urogynaecology
Gynecology and Women’s Health Institute Department of Obstetrics and Gynaecology
Cleveland Clinic Royal London Hospital
Cleveland, Ohio London, E11BB
Chapter 37 Chapter 17
ix
x Contributors

Marlene M. Corton, MD Richard P. Foon, MRCOG


Associate Professor Consultant Obstetrician and Gynaecologist
Department of Obstetrics and Gynecology Department of Obstetrics and Gynaecology
Division of Female Pelvic Medicine and Reconstructive Royal Shrewsbury Hospital
Pelvic Surgery Shropshire, United Kingdom
University of Texas Southwestern Medical Center Chapter 12
Dallas, Texas
Chapters 2, 34 Robert Freeman, FRCOG
Professor
Stergios K. Doumouchtsis, PhD, MRCOG Derriford Hospital
Consultant Obstetrician and Gynaecologist Derriford Road Crownhill
RCOG accredited Subspecialist in Urogynaecology Plymouth, Devon
Honorary Senior Lecturer Chapter 12
Lead Consultant for Childbirth Injury and
Pelvic Health after Childbirth John B. Gebhart, MD, MS
Urogynaecology – Female Pelvic Medicine Associate Professor
and Reconstructive Surgery Unit Department of Obstetrics and Gynecology
Department of Obstetrics and Gynaecology Division of Gynecologic Surgery
St. George’s Healthcare NHS Trust/St. George’s University Mayo Clinic
of London Rochester, Minnesota
London, United Kingdom Chapter 30
Chapter 26
Howard Goldman, MD
Gena Dunivan, MD Associate Professor of Surgery
Assistant Professor Glickman Urological and Kidney Institute
University of New Mexico Cleveland Clinic
Department of Obstetrics and Gynecology Cleveland, Ohio
Division of Urogynecology Chapter 37
University of New Mexico
Albuquerque, New Mexico Patricia S. Goode, MD
Chapter 10 Professor of Medicine
University of Alabama at Birmingham
Anton Emmanuel, MBBS, BSc (Hons), MD, FRCP Associate Director for Clinical Programs
Director Geriatric Research, Education, and Clinical Center
GI Physiology Unit Birmingham VA Medical Center
University College Birmingham, Alabama
London NW1 2BU Chapter 21
Chapter 9
W. Thomas Gregory, MD
Dee E. Fenner, MD Associate Professor and Fellowship Director
Furlong Professor of Women’s Health Department of Obstetrics and Gynecology
Director of Gynecology Division of Urogynecology and
Department of Obstetrics and Gynecology Reconstructive Pelvic Surgery
University of Michigan Hospital and Health Systems Oregon Health and Science University
Ann Arbor, Michigan Portland, Oregon
Chapter 26 Chapter 11

Cynthia S. Fok, MD Robert E. Gutman, MD


Fellow Associate Professor
Departments of Urology and Obstetrics/Gynecology Department of Obstetrics and Gynecology
Division of Female Pelvic Medicine Section of Female Pelvic Medicine
and Reconstructive Surgery and Reconstructive Surgery
Loyola University Chicago Stritch School of Medicine Washington Hospital Center
Maywood, Illinois Washington, District of Columbia
Chapter 7 Chapter 24
Contributors xi

Victoria L. Handa, MD, MHS Yuko Komesu, MD


Professor Assistant Professor
Department of Gynecology and Obstetrics Department of Obstetrics and Gynecology
Johns Hopkins University School of Medicine Division of Female Pelvic Floor Support Disorders
Baltimore, Maryland University of New Mexico Health Sciences Center
Chapter 3 Albuquerque, New Mexico
Chapter 6
Christine A. Heisler, MD, MS
Assistant Professor Nicole B. Korbly, MD
Department of Obstetrics and Gynecology Clinical Instructor
Division of Urogynecology Obstetrics and Gynecology
Spectrum Health Alpert Medical School of Brown University
Grand Rapids, Michigan Women and Infants Hospital
Chapter 30 Providence, Rhode Island
Chapter 5
Robert L. Holley, MSc, MD
Professor Ted Lee, MD
Department of Obstetrics and Gynecology Director, Minimally Invasive Gynecologic Surgery
Division of Urogynecology and Pelvic Department of Obstetrics and Gynecology and
Reconstructive Surgery Reproductive Health
University of Alabama at Birmingham Magee-Womens Hospital
Birmingham, Alabama University of Pittsburgh Medical Center
Chapter 28 Pittsburgh, Pennsylvania
Chapter 31
Cheryl B. Iglesia, MD, FACOG
Director Pamela J. Levin, MD
Section of Female Pelvic Medicine and Reconstructive Clinical Instructor
Surgery Department of Obstetrics and Gynecology
National Center for Advanced Pelvic Surgery (NCAPS) Division of Urogynecology and Pelvic
MedStar Washington Hospital Center Reconstructive Surgery
Associate Professor Duke University Medical Center
Departments of Obstetrics and Gynecology and Urology Durham, North Carolina
Georgetown University School of Medicine Chapter 1
Washington, District of Columbia
Chapter 27 Deirdre Lum, MD
Fellow
Stephanie Jacobs, MD Minimally Invasive Gynecologic Surgery
Clinical Instructor and Fellow Department of Obstetrics and Gynecology and
Division of Urogynecolgy Reproductive Health
University of California, Irvine Medical Center Magee-Womens Hospital
Orange, California University of Pittsburgh Medical Center
Chapter 29 Pittsburgh, Pennsylvania
Chapter 31
J. Eric Jelovsek, MD
Associate Professor of Surgery Mamta M. Mamik
Female Pelvic Medicine and Reconstructive Surgery Assistant Professor
Center of Urogynecology and Pelvic Floor Disorders Obstetrics and Gynecology
Obstetrics, Gynecology, and Women’s Health Institute Icahn School of Medicine
Cleveland Clinic New York, New York
Cleveland, Ohio Chapter 4
Chapter 14
Alayne D. Markland, DO, MSc
Kimberly Kenton, MD, MS
Associate Professor of Medicine
Professor University of Alabama at Birmingham
Departments of Obstetrics and Gynecology and Urology Director
Division of Female Pelvic Medicine Continence Clinic, Geriatric Research,
and Reconstructive Surgery Education, and Clinical Center
Loyola University Chicago Birmingham VA Medical Center
Stritch School of Medicine Birmingham, Alabama
Maywood, Illinois Chapter 21
Chapter 15
xii Contributors

Danielle D. Marshall, MD Victor W. Nitti, MD


Fellow Professor
Section of Female Pelvic Medicine and Departments of Urology and Obstetrics and Gynecology
Reconstructive Surgery Vice Chairman
Washington Hospital Center Department of Urology
Washington, District of Columbia Director of Female Pelvic Medicine and
Chapter 24 Reconstructive Surgery
New York University Langone Medical Center
Jeannine M. Miranne, MD New York, New York
Fellow Chapter 8
Section of Female Pelvic Medicine and
Reconstructive Surgery Karen L. Noblett, MD
MedStar Washington Hospital Center Professor
Georgetown University School of Medicine Department of Obstetrics and Gynecology
Washington, District of Columbia Director
Chapter 27 Division of Urogynecolgy
University of California, Irvine Medical Center
Elizabeth R. Mueller, MD, MSME, FACS Orange, California
Associate Professor Chapter 29
Departments of Urology and Obstetrics/Gynecology
Division of Female Pelvic Medicine Patrick A. Nosti, MD
and Reconstructive Surgery Fellow
Loyola University Chicago Stritch School of Medicine Female Pelvic Medicine and Reconstructive Surgery
Maywood, Illinois Washington Hospital Center
Chapter 7 Georgetown University
Washington, District of Columbia
Tyler M. Muffly, MD Chapter 25
Fellow
Female Pelvic Medicine and Reconstructive Surgery Amy Park, MD
Center of Urogynecology and Pelvic Floor Disorders Assistant Professor
Obstetrics, Gynecology, and Women’s Health Institute Departments of Obstetrics and Gynecology, and Urology
Cleveland Clinic Georgetown University School of Medicine
Cleveland, Ohio Washington Hospital Center
Chapter 14 Washington, District of Columbia
Chapter 33
Tristi W. Muir, MD
Associate Professor Dipal Patel, MBChB, BSc (Hons), MRCS
Department of Obstetrics and Gynecology Research Fellow
Associate Professor GI Physiology Unit
Department of Urology University College
Director London NW1 2BU
Pelvic Health and Continence Center Chapter 9
University of Texas Medical Branch, Galveston
Galveston, Texas Rachel N. Pauls
Chapter 13 Director of Research
Good Samaritan Hospital
Deborah L. Myers, MD Division of Urogynecology and
Professor Reconstructive Pelvic Surgery
Division of Urogynecology and Cincinnati, Ohio
Reconstructive Pelvic Surgery Chapter 18
The Alpert Medical School of Brown University
Women and Infants Hospital of Rhode Island David D. Rahn, MD, FACOG
Providence, Rhode Island Assistant Professor
Chapter 16 Department of Obstetrics and Gynecology
Division of Female Pelvic Medicine and
Reconstructive Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
Chapter 22
Contributors xiii

Olga Ramm, MD Giulio Aniello Santoro, MD, PhD


Fellow Head
Departments of Obstetrics and Gynecology and Urology Pelvic Floor Unit I
Division of Female Pelvic Medicine Department of Surgery
and Reconstructive Surgery Regional Hospital
Loyola University Chicago Stritch School of Medicine Treviso, Italy
Maywood, Illinois Honorary Professor
Chapter 15 Shandong University, China
Chapter 35
Charles R. Rardin, MD
Associate Professor Anthony Smith, MD, FRCOG
Obstetrics and Gynecology Consultant Urogynaecologist
Alpert Medical School of Brown University The Warrell Unit
Director St. Mary’s Hospital
Fellowship Program in Female Pelvic Medicine and Central Manchester Foundation Trust
Reconstructive Surgery Manchester, M13 9WL
Director Chapter 23
Robotic and Laparoscopic Surgery
Women and Infants Hospital Andrew I. Sokol, MD
Providence, Rhode Island Associate Director
Chapter 5 Minimally Invasive Surgery
Section of Female Pelvic Medicine and
Fiona Reid, MD, MRCOG Reconstructive Surgery
Consultant Urogynaecologist Washington Hospital Center
The Warrell Unit Associate Professor
St. Mary’s Hospital Georgetown University School of Medicine
Central Manchester Foundation Trust Departments of Obstetrics and Gynecology and Urology
Manchester, M13 9WL Washington, District of Columbia
Chapter 23 Chapter 25

Holly E. Richter, PhD, MD, FACOG, FACS Abdul H. Sultan, MB.ChB, MD, FRCOG
Professor Consultant Obstetrician and Gynaecologist
Departments of Obstetrics and Gynecology, Croydon University Hospital, Surrey
Urology and Geriatrics Honorary Reader
J Marion Sims Endowed Chair of Obstetrics St. Georges University of London
and Gynecology United Kingdom
Director Chapter 35
Division of Urogynecology and Pelvic
Reconstructive Surgery Vivian W. Sung, MD, MPH
University of Alabama Associate Professor
Birmingham, Alabama Director of Research
Chapter 28 Division of Urogynecology
and Reconstructive Pelvic Surgery
Rebecca G. Rogers, MD, FACOG Department of Obstetrics and Gynecology
Regent’s Professor Warren Alpert Medical School of Brown University
Vice Chair for Research, Department of Obstetrics Providence, Rhode Island
and Gynecology Chapter 22
Chief, Division of Urogynecology
Fellowship Director, Female Pelvic Medicine and Ranee Thakar, MD, MRCOG
Reconstructive Surgery Consultant Urogynaecologist and Obstetrician
University of New Mexico Health Sciences Center Honorary Senior Lecturer at St. George’s University of
Albuquerque, New Mexico London
Chapter 4 Croydon University Hospital
Croydon, CR7 7YE
United Kingdom
Chapter 19
xiv Contributors

Christine M. Vaccaro, DO William Whitehead, PhD


Fellow Professor
Good Samaritan Hospital University of North Carolina
Division of Urogynecology and Department of Medicine
Reconstructive Pelvic Surgery Division of Gastroenterology and Hepatology
Cincinnati, Ohio Department of Obstetrics and Gynecology
Chapter 18 Division of Urogynecology
University of North Carolina at Chapel Hill
Sandra R. Valaitis, MD Chapel Hill, North Carolina
Associate Professor Chapter 10
Department of Obstetrics and Gynecology
Chief Jennifer M. Wu, MD, MPH
Division of Gynecology and Reconstructive Pelvic Surgery Associate Professor
University of Chicago Duke University Medical Center
Chicago, Illinois Department of Obstetrics and Gynecology
Chapter 32 Division of Urogynecology and Pelvic
Reconstructive Surgery
Mark D. Walters, MD Durham, North Carolina
Professor of Surgery Chapter 1
Female Pelvic Medicine and Reconstructive Surgery
Center of Urogynecology and Pelvic Floor Disorders
Obstetrics, Gynecology, and Women’s Health Institute
Cleveland Clinic
Cleveland, Ohio
Chapter 14

Milena M. Weinstein, MD
Director of Research
Division of Female Pelvic Medicine
and Reconstructive Surgery
Department of Obstetrics, Gynecology
and Reproductive Biology
Massachusetts General Hospital
Instructor
Harvard Medical School
Boston, Massachusetts
Chapter 11
Preface

Pelvic floor disorders are common and severely affect treatment of pelvic floor dysfunction. The content is
the lives of women who suffer from them. Many of organized into four sections. Section I reviews fun-
these women are too embarrassed to seek care, and damental topics including epidemiology, anatomy,
the number of providers well versed in the treatment mechanisms of disease, and clinical and quality of life
of these disorders is limited. It is estimated that up to evaluation. Section II addresses disease states and is
half of women suffer from incontinence and/or pro- divided into four parts addressing lower urinary tract
lapse by age 80 years and a third of these women have dysfunction, functional anorectal disorders, pelvic
symptoms severe enough to seek surgical treatment. organ prolapse, as well as the diagnosis and treatment
Female Pelvic Medicine and Reconstructive of pain, urinary tract infections, and sexual dysfunc-
Surgery (FPMRS) has arrived as a new subspecialty tion. Section III addresses clinical management and
recently recognized by the American Board of Medical Section IV surgical management of pelvic floor dys-
Specialties. It is essential that practicing gynecologists function. With a clear, easy-to-follow layout and writ-
and urologists become familiar with the diagnosis of ing style the book comprehensively covers the breadth
these common problems and are prepared to offer of the field. Ample figures and tables accompany the
both medical and surgical treatments. Knowledge of text illustrating the concepts presented. Key Points in
pelvic floor anatomy as well as the physiology of con- each chapter highlight important conclusions made in
tinence and pelvic support is essential. Because the the text, and a Master Surgeons’ Corner outlines impor-
majority of pelvic floor disorders are functional prob- tant tips and tricks in surgical management.
lems that affect quality of life, the practitioner must We wish to acknowledge the many international
also be familiar with measures of symptom severity experts who contributed to this book. They represent
and quality of life impact. While many disorders are the leaders in our specialty and the foremost medi-
treated satisfactorily with medical management, surgi- cal institutions. The authors were eager to share their
cal therapies are an essential component of the treat- expertise with the gynecologists and urologists who
ment armamentarium. wish to be up to date in this emerging field and who
Within its 37 chapters, Female Pelvic Medicine and serve the many women seeking freedom from these
Reconstructive Surgery comprehensively presents the embarrassing problems.
anatomy, pathophysiology, and medical and surgical
The Editors

xv
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Section I Fundamental
Topics

1 Epidemiology 3

2 Normal Anatomy of the Pelvis and Pelvic Floor 19

3 Mechanisms of Disease 51

4 Clinical and Quality of Life Evaluation 61


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1 Epidemiology
Pamela J. Levin and Jennifer M. Wu

INTRODUCTION two epidemiologic concepts is that prevalence refers


to all cases of disease while incidence refers to new
Key Point cases of disease.

• Pelvic organ prolapse, urinary incontinence, and Defining Pelvic Floor Disorders
anal incontinence are the most common pelvic Although the concepts of prevalence and incidence
floor disorders encountered in women. may seem straightforward, rates vary widely based
on the disease definition and study population. A
major issue with determining the prevalence and
Pelvic floor disorders (PFDs) encompass a variety of incidence of PFDs is that each of these conditions
symptoms and anatomical changes related to the geni- is defined in a variety of ways—for example, POP
tourinary tract. Pelvic organ prolapse (POP), urinary can be diagnosed based on a physical examination
incontinence (UI), and anal incontinence (AI) are the or based on a questionnaire that addresses bother-
most common PFDs encountered in women. These some symptoms. Similarly, the prevalence of UI may
disorders have a tremendous impact on a woman’s be quite different when it is defined as the occur-
quality of life and function, and are associated with rence of involuntary leakage of urine in the last year
considerable healthcare costs. In this chapter, the versus the last month. The specific population stud-
epidemiology of PFDs will be discussed, focusing ied can also impact prevalence and incidence. For
on three main topics: (1) prevalence and incidence; example, the prevalence of AI will be different in a
(2) nonmodifiable demographic risk factors, including study of all adult community-dwelling women versus
age and race; and (3) economic impact. nursing home residents. In order to make meaning-
ful determinations of prevalence and incidence, it is
imperative to understand the disease definition and
PREVALENCE AND INCIDENCE the population studied. This chapter will exclusively
discuss the rates of PFDs in women in the United
Prevalence is defined as the total number of cases in a States.
given population at a specific time divided by the num- Methods for measuring UI and overactive bladder
ber of individuals at risk for disease in the same popu- (OAB) include the frequency of voids, frequency of
lation. Incidence, or incidence proportion, is defined incontinence episodes, volume of leakage, degree of
as the number of new cases of disease that develop bother, pad weight, urodynamic findings, clinically
in a given population over a period of time divided demonstrated leakage, or impact on quality of life.
by the total number of individuals followed for that Similarly, for AI, the frequency of incontinence, type
same time period. The key distinction between these of stool and/or flatus lost, degree of bother, and impact
3
4 Section I Fundamental Topics

on quality of life can also be used. Defining POP is is the loss of urine with urgency and effort, physical
equally varied, as it can be measured by symptoms, exertion, sneezing, or coughing.3 OAB syndrome is
including frequency, duration, severity or degree of defined as urinary urgency, usually accompanied by
bother, as well as physical examination. Currently, the frequency and nocturia, with or without UUI.3 Thus,
CHAPTER 1

majority of research studies on POP rely on the pelvic OAB is more inclusive and includes UUI. Although
organ prolapse quantification system (POP-Q);1 how- there are other forms of UI, we will focus on SUI,
ever, the Baden Walker system is another method of UUI, and MUI, as these are the most common forms
prolapse assessment.2 The use of validated question- of incontinence. In the following sections, the preva-
naires to assess symptoms, severity, degree of bother, lence and incidence of any type of UI will be discussed
and impact on quality of life has become a mainstay in followed by a review for each type of UI.
urogynecologic studies.
Prevalence of Urinary Incontinence
Urinary Incontinence Data from large epidemiologic studies, including the
Women’s Health Initiative (WHI), National Health
Types of Urinary Incontinence
and Nutrition Examination Survey (NHANES),
The type of UI impacts prevalence and incidence. UI, Group Health Cooperative (GHC), and Nurses’
in general, is the symptom of involuntary urine loss.3 Health Study (NHS), have reported prevalence rates
This symptom can be further characterized by the set- of 5% to 64% for UI within the adult female popula-
ting or activity during which urine loss occurs, such tion, using different definitions of disease based upon
as with stress or urgency. Stress urinary incontinence frequency of leakage (Table 1-1).4-9 The broad range
(SUI) is the involuntary loss of urine with effort, phys- of reported prevalence is likely related to the defini-
ical exertion, sneezing, or coughing.3 Urgency urinary tion of UI used in each study, as well as the age of
incontinence (UUI) is the involuntary loss of urine the population studied. In the WHI, the prevalence of
with urgency, and mixed urinary incontinence (MUI) UI was 64%, as UI was defined as having ever leaked

Table 1-1 Prevalence of Any Urinary Incontinence in Women

Study Population Definition of Urinary Incontinence Prevalence, %


Women’s Health Initiative Ever leaked even a very small amount of urine 64
Female, postmenopausal involuntarily and could not control it
50–79 y4
National Health and Nutrition Difficulty controlling bladder, including leaking
Examination Survey small amounts when you cough or sneeze
Female, 60 y and over5 • Any in last 12 mo 38
• Few times a y 5
• Few times a mo 9
• Few times a wk 10
• Every d 14
Female, 20 y and over6 At least weekly leakage or monthly leakage of 16
volumes more than just drops
Group Health Cooperative Leakage of any amount that occurred at least monthly 45
Female, 30–90 y7 • Monthly episodes among those reporting UI 44
• Weekly episodes among those reporting UI 30
• Daily episodes among those reporting UI 26
Nurses’ Health Study Leaked urine or lost control of urine in the last 12 mo
Female, 54–79 y8 • Never 31
• Less than one per mo 31
• Once per mo 6
• Two to three times per mo 12
• Once per wk 10
• Almost every d 10
Female, 30–55 y9 Leaked urine during the previous 12 mo
• At least once per mo 34
• One to three times per mo 16
• At least once per wk 18
Chapter 1 Epidemiology 5

Table 1-2 Prevalence of Stress Incontinence in Women

Study Population Definition of Urinary Incontinence Prevalence, %


Women’s Health Initiative Leaked urine related to coughing, sneezing, or laughing 51

CHAPTER 1
more than once in the last 3 mo
Female, postmenopausal Weekly leaked urine related to coughing, sneezing, 20
with intact uterus, or laughing
55–80 y15,16
National Health and Nutrition Leaked or lost control of even a small amount of urine 25
Examination Study with an activity like coughing over the last 12 mo
Female, 20 y and over13,14 • Mild—Few times per y 10
• Moderate—Few times per mo 5
• Severe—Daily or few times per wk 9
Kaiser Permanente Current symptoms of urine leakage related to activity, 15
Continence Associated Risks coughing, or sneezing
Epidemiologic Study
Female, 25–84 y12

even a small amount of urine for this cohort of post- women between 19 and 44 years and 21.5% in women
menopausal women.4 Comparatively, using data from between 45 and 64 years, whereas MUI is the most
NHANES that represents a similar age group, the prevalent type in women over 65 years and occurs in
prevalence of UI was 38% when UI was defined as dif- 16.8% of women.10 Prevalence rates of 2% to 21%
ficulty controlling your bladder in the last 12 months.5 have been reported for MUI across all ages, again
In this same population, when UI is stratified as every with notable differences in the definition of disease
day, a few times a week, a few times a month, or a (Table 1-3).7,13,14,16
few times a year, the prevalence rates changed to 14%,
10%, 9%, and 5%, respectively.5 Similar variability Prevalence and Incidence of
in both definition and prevalence is demonstrated Overactive Bladder Syndrome
for UI in the GHC7 and NHS8,9 as well (Table 1-1).
and Urgency Urinary Incontinence
When comparing the prevalence of UI in community-
dwelling women to those living in long-term care facil- For OAB, the prevalence has been reported to range
ities, UI is present in approximately 60% to 78% of from 8% to 29%, depending upon the age and defi-
nursing home residents.10 nition used (Table 1-4).12,15,17 The reported range
of prevalence is similarly broad for UUI from 2%
Incidence of Urinary Incontinence to 49% and depends upon the definition of UUI
(Table 1-4).7,13-16 The incidence of UUI has been
In a systematic review performed by the Agency found to range from 0.3% to 0.7% per year.18
for Healthcare Research and Quality (AHRQ), the
pooled annual incidence of UI was 6.25%, and there
was a trend of increasing incidence rates associated Remission of Urinary Incontinence
with older age.10 The NHS demonstrated an increase Reported remission for any UI is variable, and data
in incidence with age as well only through age 50, on the regression of specific UI types are sparse.
with a subsequent slight decline in older women.11 Assessment of remission rates is also further limited
The two-year incidence of UI in women age 54 to 79 by the lack of data regarding the institution of therapy
years in this study was 9.2%,8 whereas the two-year in studies evaluating remission or regression. Reported
incidence in women age 36 to 55 years was 13.7%.11 remission and improvement rates range from 2.0% for
complete remission in the 54- to 79-year-old women
Prevalence of Stress and to as high as 11.9% in 46- to 55-year-olds and 17.1%
Mixed Urinary Incontinence in 36- to 45-year-old women.8,11

The prevalence of UI varies by type of UI. Overall,


Surgery for Urinary Incontinence
the prevalence of SUI across several large studies
ranges from 5% to 51%, with considerable differences Surgery for urinary incontinence is an important
in the definition of disease (Table 1-2).12-16 SUI is the treatment option. The lifetime risk of surgery for UI
most prevalent type of UI and occurs in 12.8% of or POP in women, given the average life expectancy
6 Section I Fundamental Topics

Table 1-3 Prevalence of Mixed Urinary Incontinence in Women

Study Population Definition of Urinary Incontinence Prevalence, %


Women’s Health Initiative Weekly leaked urine related to coughing, sneezing, or 14
CHAPTER 1

Female, postmenopausal with laughing and associated with a feeling of urgency, which is a
intact uterus, 55–80 y16 strong sensation of needing to go to the bathroom
National Health and Nutrition Leaked or lost control of even a small amount of urine with 17
Examination Study an activity like coughing over the past 12 mo and leaked or
Female, 20 y and over13,14 lost control of even a small amount of urine with an urge or
pressure to urinate and you could not get to the toilet fast
enough in the last 12 mo
• Mild—Few times per y 2
• Moderate—Few times per mo 4
• Severe—Daily or few times per wk 8
Group Health Cooperative Leaking or losing urine during activities such as coughing, 21
Female, 30–90 y7 laughing, or walking at least monthly of any amount and
leaking or losing urine associated with an urge to urinate so
strong and sudden that the participant could not reach the
toilet fast enough at least monthly of any amount

Table 1-4 Prevalence of Overactive Bladder and Urge Incontinence in Women

Study Population Definition of Urinary Incontinence Prevalence, %


Overactive Bladder
Women’s Health Initiative Usually experience frequent urination in the last 3 mo 29
Female, postmenopausal Usually experience a strong feeling of urgency to empty 29
with intact uterus, 55–80 y15 your bladder in the last 3 mo
National Overactive Bladder OAB without urge incontinence: Feeling of urgency ≥4 in the 9
Evaluation last 4 wks and either >8 micturitions per day or the use
of at least one of the following: (1) restricting fluid intake,
(2) locating bathrooms in a new place, (3) limiting travel or
defensive voiding
Female, 18 y and over17 OAB with urge incontinence: Criteria for OAB without urge 8
incontinence plus ≥3 episodes of urinary leakage in the past
4 wks that was typical and was not exclusively due to stress
incontinence
Kaiser Permanente Continence Current symptoms of frequent urination, rushing to the 13
Associated Risks Epidemiologic bathroom to avoid leakage of urine, and/or urine leakage
Study related to a feeling of urgency
Female, 25–84 y12
Urgency Urinary Incontinence
Women’s Health Initiative Leaked urine associated with a feeling of urgency, that is 49
a strong sensation of needing to go to the bathroom, more
than once in the last 3 mo
Female, postmenopausal with Weekly leaked urine associated with a feeling of urgency, that 20
intact uterus, 55–80 y15,16 is a strong sensation of needing to go to the bathroom
National Health and Nutrition Leaked or lost control of even a small amount of urine 8
Examination Study with an urge or pressure to urinate and could not get
Female, 20 y and over13,14 to the toilet fast enough in the last 12 mo
• Mild—Few times per y 4
• Moderate—Few times per mo 2
• Severe—Daily or few times per wk 4
Group Health Cooperative Leaking or losing urine associated with an urge to urinate so 5
Female, 30–90 y7 strong and sudden that the toilet could not be reached fast
enough at least monthly of any amount
Chapter 1 Epidemiology 7

of 79 years, is 11.1%.19 In a study of a large health- splinting or digitation; low backache; and bleeding,
care maintenance organization, the annual incidence discharge, or infection related to dependent ulceration
of UI procedures increases with age from 0.4 per of the prolapse. POP can be further defined by the
10,000 women in those age 20 to 29 years to 31.9 per specific prolapsed compartment. Anterior vaginal wall
10,000 women in those age 70 to 79 years.19 National

CHAPTER 1
prolapse is typically caused by prolapse of the blad-
data showed that approximately 130,000 women (rate der, whereas posterior vaginal wall prolapse is typically
12 per 10,000) underwent inpatient SUI surgery in caused by rectal protrusion into the vagina.3 Vaginal
2003.20 Given the adoption of minimally invasive vault prolapse is the descent of the vaginal cuff scar,
slings, outpatient SUI surgery has become more com- versus the descent of the uterus or cervix.
mon, and in 2006, 105,656 women underwent out-
patient UI surgery, an age-adjusted rate of 9.6 per Prevalence of Prolapse
10,000 women.21
The prevalence of symptomatic POP has been
reported as low as 2.9% in a nationally representative
Pelvic Organ Prolapse survey of US women over the age of 20 years when the
POP is the descent of one or more of the anterior or diagnosis was based entirely on the reported symptom
posterior vaginal walls, uterus, cervix, or apex of the of bulging or something visibly or palpably falling out
vagina, associated with relevant symptoms.3 These (Table 1-5).6 In contrast, when prolapse was defined
symptoms include vaginal bulging; pelvic pressure; as any prolapse noted on examination, the prevalence

Table 1-5 Prevalence of Pelvic Organ Prolapse in Women

Study Population Definition of Prolapse Prevalence, %


National Health and Nutrition Experience bulging or something falling out that 3
Examination Study can be seen or felt in the vaginal area
Female, 20 y and over6
Women’s Health Initiative In the last 3 mo, experienced any of the
following more than once:
• Pressure in the lower abdomen 14
• Heaviness in your pelvic area 6
• A sensation of bulging from the vaginal area 4
• A bulge you can see or feel in the vaginal area 4
• Pelvic discomfort with standing 3
Female, postmenopausal POP-Q examination
with intact uterus, • Stage 0 2
55–80 y15,16 • Stage 1 35
• Stage 2 62
• Stage 3 2
• Stage 4 0
Female, postmenopausal Prolapse, grade 1–3
50–79 y22 • Intact uterus 41
– Cystocele 34
– Uterine prolapse 14
– Rectocele 19
• Prior hysterectomy 38
– Cystocele 33
– Rectocele 18
Kaiser Permanente On a typical day, the sensation of a bulge in the 7
Continence Associated vagina or that something is falling out of the vagina
Risks Epidemiologic Study
Female, 25–84 y12
Pelvic Organ Support Study POP-Q examination
Female, 18 y and over23 • Stage 0 24
• Stage 1 38
• Stage 2 35
• Stage 3 2
• Stage 4 0
8 Section I Fundamental Topics

was 41.2% in subjects with a uterus and 38% in sub- review in women of all ages. When FI was evaluated
jects who had had a hysterectomy in postmenopausal separately, a prevalence of 6% to 19% was identified,
women in WHI.22 The prevalence rates of prolapse and prevalence increased with age.10 The prevalence
vary considerably based on how prolapse is defined of defecatory symptoms in several large studies ranges
CHAPTER 1

(Table 1-5).6,12,15,16,22,23 One particular challenge in broadly from 0.4% to 35% (Table 1-6).6,12,15,26-28 For
defining prolapse is establishing the difference between AI, prevalence rates vary considerably based upon the
“disease” and “normal,” as there may be some degree type of stool and frequency of loss, as well as by the
of prolapse that could be considered normal changes typical bowel habits of the subjects. Limited data exist
on examination, especially as a woman ages. Thus, it regarding the incidence; however, one study demon-
is important to assess symptoms and degree of bother strated a nine-year cumulative incidence of 6.2% for
when evaluating prolapse. A general principle is that FI in women over the age of 50 years.28 Rates of AI
women tend to report more bothersome symptoms as in women living in long-term facilities are generally
the vaginal wall approaches the hymen.23 understood to be higher than that of community-
dwelling women. These rates vary considerably in the
Incidence and Remission of Prolapse literature and depend largely on the definition of AI
and the baseline status of the population.10 AI remis-
Limited data exist on the true incidence of pro- sion remains unstudied.
lapse, particularly given the disparity between rates
measured by bothersome symptoms versus physical
examination. In a study that defined prolapse as vag- Coexisting Urinary and Anal Incontinence
inal descent to the hymen or beyond, the one-year
AI is often found in association with urinary inconti-
and three-year incidence of prolapse was 26% and
nence. In women between the ages of 30 and 90 years
40%, respectively.24 In addition, the one-year pro-
with at least monthly FI, 70% also reported urinary
gression, measured as 2 cm or more of vaginal
incontinence at least monthly (Table 1-6).27 Similarly,
descent by POP-Q, was 5.8%.24
the rates of comorbid FI were found to increase with
Remission rates of POP are difficult to ascertain.
increased severity of urinary incontinence. Specifically,
The WHI observational study is one of few reports to
in subjects with increasing severity of UI, based upon
determine regression rates; the one-year regression
the Sandvik Severity Index of 1-2, 3-4, and 6-8, rates
rate was 1.2% when defined as regression by at least
of comorbid FI were found to be 8%, 15%, and 26%,
2 cm or more.24
respectively.27

Surgery for Pelvic Organ Prolapse


Surgery for Fecal Incontinence
For inpatient surgery, the number of women under-
going prolapse procedures has decreased between The number of women undergoing inpatient surgi-
1979 and 2006, from 231,000 to 186,900, respec- cal procedures for FI has remained stable between
tively, with the age-adjusted rate decreasing from 1998 and 2003, from 3,423 to 3,509, respectively.29
2.9 to 1.5 per 1,000 women.25 For outpatient sur- Limited data exist for outpatient FI surgery.21
gery, 44,394 women underwent outpatient prolapse
procedures in 2006, an age-adjusted rate of 0.41 per
1,000 women.21 These trends are likely influenced by DEMOGRAPHIC RISK
the emergence of minimally invasive surgeries with
abbreviated postoperative hospital stays.
FACTORS FOR PELVIC
FLOOR DISORDERS
Anal and Fecal Incontinence Key Point
AI is a more comprehensive term than fecal inconti-
nence (FI) as it is defined as the involuntary loss of • Age and race are nonmodifiable risk factors that
either feces or flatus.3 FI is defined as the involuntary can impact pelvic floor disorders.
loss of solid or liquid stool and flatal incontinence as
the involuntary loss of flatus.3
Several risk factors have been identified for the devel-
Prevalence and Incidence opment and progression of PFDs. Although some of
these factors are modifiable, both age and race impact
of Anal Incontinence
the rates of PFDs and are inherent to an individual.
The prevalence of AI when compared to FI was consis- Here we will discuss these demographic, nonmodifi-
tently two- to fourfold greater in an AHRQ systematic able risk factors as they relate to PFDs.
Chapter 1 Epidemiology 9

Table 1-6 Prevalence of Anal Incontinence in Women

Study Population Definition of Anal Incontinence Prevalence, %


Women’s Health Initiative In the last 3 mo, do you usually experience the following:

CHAPTER 1
Female, postmenopausal • Lose stool beyond your control if your stool is 2
55–80 y15 well formed
• Lose stool beyond your control if your stool is 11
loose or liquid
• Lose gas from the rectum beyond your control 33
National Health and Nutrition At least monthly involuntary loss of solid, liquid, 9
Examination Study or mucous stool, not including flatus
Female, noninstitutionalized Accidental bowel leakage at least once during the 8
20 y and over6,26 past month
• Liquid stool 6
• Solid stool 2
• Mucus 3
Frequency of fecal incontinence
• Leakage 1–3/mo 6
• Leakage 1/wk 0.4
• Leakage 2–6/wk 1
• Leakage ≥ 1/d 1
Accidental leakage of gas at least once in the last mo 51
Accidental leakage of gas daily 21
Kaiser Permanente • Lose gas from the rectum beyond control 10
Continence Associated Risks • Lose stool beyond control 17
Epidemiologic Study
Female, 25–84 y12
Group Health Cooperative Loss of liquid or solid stool occurring at least monthly 8
Female, 30–90 y27 • Comorbid urinary incontinence defined as leakage of any 70
amount occurring at least monthly in subjects with fecal
incontinence
• Comorbid fecal incontinence in subjects with urinary 12
incontinence
– Comorbid FI in subjects with mild UI 8
– Comorbid FI in subjects with moderate UI 15
– Comorbid FI in subjects with severe UI 26
Rochester Epidemiology Project Problems with leakage of stool (accidents or soiling 18
Female, 50 y or older28 because of the inability to control the passage of stool
until reaching a toilet)

Age of UI has also been found to be affected by age, as


the prevalence of severe UI was 28% in women 30 to
Pelvic Floor Disorders 39 years compared to 54% in women 80 to 90 years
The prevalence of women with at least one symp- (Figure 1-3).7
tomatic pelvic floor disorder increases from 9.7% in A relationship between the specific types of UI and
women age 20 to 39 years to 49.7% in women 80 years age has also been reported. SUI is the most common
or older (Figure 1-1).6 Variation also exists by age with type in women age 19 to 65 years, and MUI is the most
respect to the type of pelvic floor disorder (Figure 1-2 common type in women over 65.10 When stratified for
and Table 1-7 ).6 each decade of life from age 30 to 90, the prevalence of
UUI and MUI consistently increases with age, whereas
pure SUI gradually decreases with age (Table 1-8).7
Urinary Incontinence
The incidence of UI type is also impacted by
The prevalence of UI overall appears to increase with age. The two-year incidence of SUI has been found
age such that 6.9% of women age 20 to 39 years are to steadily increase with age from a rate of 1.2% in
affected by bothersome UI, compared to 31.7% of women age 36 to 40 years11 to 2.8% in women age
women 80 years or older (Table 1-7 ).6 The severity 53 to 59 years.8 The rate then decreases to 1.7% in
10 Section I Fundamental Topics

Prevalence rates of US women with ≥1 pelvic floor disorder


60

49.7
50
CHAPTER 1

40 36.8
Prevalence, %
30 26.5

20

9.7
10

0 20–39 40–59 60–79 ≥80


Age
FIGURE 1-1 Prevalence rates of nonpregnant US women with at least one symptomatic pelvic floor disorder based
on data from the National Health and Nutrition Examination Survey.6

Prevalence rates of pelvic floor disorders in US women


35
UI FI POP
30

25
Prevalence, %

20

15

10

0
20–39 40–59 60–79 ≥80
Age
FIGURE 1-2 Urinary incontinence, fecal incontinence, and pelvic organ prolapse prevalence rates of nonpregnant US
women based on data from the National Health and Nutrition Examination Survey.6 (Reproduced with permission from
the National Task Force on Technology and Disability, “Within Our Reach” Report © 2004 NTFTD. All rights reserved.)

Table 1-7 Age Stratified Prevalence of Urinary Incontinence, Pelvic Organ Prolapse,
and Fecal Incontinence6

Prevalence, % (95% Confidence Interval)


Age Urinary Incontinence Fecal Incontinence Pelvic Organ Prolapse
20–39 6.9 (4.9–9.0) 2.9 (1.9–3.9) 1.6 (0.6–2.6)
40–59 17.2 (13.9–20.5) 9.9 (7.4–12.5) 3.8 (2.0–5.7)
60–79 23.3 (17.0–29.7) 14.4 (10.4–18.3) 3.0 (0.9–5.1)
≥80 31.7 (22.3–41.2) 21.6 (12.8–30.4) 4.1 (1.1–7.1)
Chapter 1 Epidemiology 11

35

Slight Moderate Severe


30

CHAPTER 1
25

Prevalence, % 20

15

10

0
30–39 40–49 50–59 60–69 70–79 80–90
Age, y
FIGURE 1-3 The severity of urinary incontinence by decade of age. (Reproduced with permission from Ref.7 Copyright
© 2005 American Medical Association. All rights reserved.)

women age 70 to 79 years.8 The incidence of MUI symptomatic prolapse in women ages 20 to 39 years
has also been found to gradually increase from 0.3% is 1.6%, whereas in women over the age of 80 years,
to 0.9% across ages from 36 to 55.11 The incidence of the prevalence is 4.1% (Figure 1-2, Table 1-7).6
UUI has been found relatively stable from ages 36 to
60 years at 0.4%8,11 then steadily increases to 0.9% in Fecal Incontinence
women ages 70 to 79 years.8
FI has been found to increase with age in several
studies.6,26,27 The prevalence of FI has been found
Pelvic Organ Prolapse
as low as 2.9% in women ages 20 to 39 years with a
Rates of POP have also been found to increase con- steady increase to a rate of 21.6% in women over the
siderably with increasing age. The prevalence of age of 80 years (Figure 1-2, Table 1-7 ).6

Table 1-8 Prevalence and Symptom Types of Urinary Incontinence According to Decade of Life7

Symptom Types Among Women Reporting UI


Age, y Respondents/Reporting UI* Urgency Stress Mixed Unknown†
30–39 1,031/290 (28) 28 (10) 132 (45) 118 (41) 12 (4)
40–49 686/278 (41) 27 (10) 119 (43) 124 (44) 8 (3)
50–59 545/264 (48) 27 (10) 85 (33) 144 (54) 7 (3)
60–69 458/234 (51) 26 (11) 69 (29) 133 (57) 6 (3)
70–79 407/223 (55) 45 (20) 48 (22) 123 (55) 7 (3)
80–90 311/169 (54) 34 (20) 26 (16) 90 (53) 19 (11)
Total 3,438/1,458 (42) 187 (13) 480 (33) 732 (50) 59 (4)

Values are given as number (percentage).


*Of the 3,553 participants, 3,438 completely answered the questions necessary for a diagnosis of UI.

Unknown because 59 respondents did not answer the symptom questions.
12 Section I Fundamental Topics

The graying of the United States


35
85 and up 75–84 65–74 55–64
30
CHAPTER 1

25
Percentage

20

15

10

0
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000 2010 2020 2030 2040 2050
Year
FIGURE 1-4 The projected number of elderly individuals age 65 years or older in the United States from 2010 to
2050. (Reproduced with permission from the National Task Force on Technology and Disability, “Within Our Reach”
Report © 2004 NTFTD. All rights reserved.)

Aging Population in the United States will have at least one bothersome PFD by 2050
(Figure 1-5).31 Furthermore, the number of women
The population in the United States is aging. The US
with each type of pelvic floor disorder will also increase
Census Bureau projects that the elderly population,
substantially (Table 1-9).
those 65 years and older, will double from 40.2 mil-
lion to 88.5 million from 2010 and 2050 (Figure 1-4).30
Given these population projections and the higher Race
prevalence of PFDs in the elderly, the rates of PFDs
Urinary Incontinence
are expected to increase substantially in the coming
decades. Using current prevalence rates of symptom- Although race as a risk factor for PFDs has been stud-
atic PFDs, it is projected that 58.2 million women ied, some data are conflicting. UI appears to be more

Projected number of women (in millions) with ≥1 pelvic floor disorder,


2010 to 2050
50

43.8
45
40.2
40
36.3
Number of women (millions)

35
31.9
28.1
30

25

20

15

10

5
FIGURE 1-5 The projected num-
ber of women (in millions) with 0
at least one pelvic floor disorder 2010 2020 2030 2040 2050
from 2010 to 2050.31 Year
Chapter 1 Epidemiology 13

Table 1-9 Projected Number of Women (in Millions) with Symptomatic Pelvic Floor
Disorders, 2010 to 205031

2010 2020 2030 2040 2050

CHAPTER 1
Urinary incontinence 18.3 20.7 23.5 26.1 28.4

Fecal incontinence 10.6 12.1 13.8 15.4 16.8

Pelvic organ prolapse 3.3 3.7 4.1 4.5 4.9

≥1 Pelvic floor disorder 28.1 31.9 36.3 40.2 43.8

common in white women compared to women of other women was found to be comparatively lower at a prev-
races. An AHRQ systematic review found that the alence of 4%.10 When evaluating the NHANES data,
majority of studies demonstrate a higher prevalence no significant relationship could be identified between
of all types of UI in white women, when compared race and the prevalence of FI.26
to black, Hispanic, and Asian women. Further, being
non-white was found to be associated with lower odds
of severe UI in all groups except Hispanic women.10 ECONOMIC IMPACT
The NHS also demonstrated similar findings. The
NHS found that both occasional and frequent leak- It is critical to understand the different types of eco-
age of urine was lower in black, Hispanic, and Asian nomic costs before discussing the “costs” of PFDs.
women, compared to white women, with the lowest In general, economic costs are divided into direct and
prevalence in black women.9 indirect costs. Direct costs refer to the cost of all the
The type of UI also seems to have an association goods, services, and other resources that are related
with race. SUI is more common in white compared to to managing a condition as well as the costs associ-
black or Asian women,10 and least common in black ated with future complications of that condition.
women compared to white and Mexican American Direct costs include costs to the affected individual or
women.13 Data on UUI and race have been incon- caregivers, supplies, and treatments. Indirect costs are
sistent,10 but at least one study demonstrated lower related to lost productivity of the affected individual or
odds of UUI in white women compared to black and caregivers (Table 1-10).
Mexican American women.13 No statistically signifi-
cant difference has been demonstrated in the preva-
lence of MUI between white, black, and Mexican Factors to Consider
American women.13 Regarding Cost of Illness
When evaluating studies on the cost of illness, it is
Pelvic Organ Prolapse important to remember that the total economic costs
Race appears to be a risk factor for POP. A lower also depend upon the prevalence of disease, and given
risk of uterine prolapse, cystocele, and rectocele in the underreporting of PFDs, the total cost of these con-
African American women compared to white women ditions may be underestimated. Determining the cost
has been demonstrated in at least one study.22 of a disease is challenging because no national dataset
Hispanic women have been found to have the greatest contains all relevant direct costs, which would include
risk of uterine prolapse in more than one study,22,23 evaluation, outpatient visits, outpatient surgery, inpa-
with an increased risk of cystocele specifically when tient surgery, and medication costs. Furthermore, it is
compared to white women.22 Asian women have particularly challenging to determine indirect costs.
been found to have the greatest rate of cystocele and Another important factor to consider is the year in
rectocele.22 which the costs were estimated. For example, the cost
of UI in 1995 dollars is different than the cost of UI in
2010 dollars given inflation. One method of adjusting
Fecal Incontinence
for cost in a previous year is to use the consumer price
The prevalence of FI was relatively similar in an index to adjust for inflation. Another issue is the per-
AHRQ systematic review between African American spective of the analysis. Costs may be measured from
and white women, with reported ranges of 9% to a societal perspective, therefore including all types of
19% for African American women and 7% to 21% for costs, or from the perspective of the healthcare system,
white women. The prevalence of FI in Asian-American specific businesses, the government, or participants
14 Section I Fundamental Topics

Table 1-10 Direct and Indirect Economic Costs

Direct Costs Indirect Costs


• Cost of evaluating the condition • Lost productivity of
CHAPTER 1

– Office visits with physician or other health care providers, affected individual
including nurse practitioner, physical therapists, and specialists • Lost productivity of
– Diagnostic costs, including laboratory tests, radiology costs caregiver
• Cost of managing the condition
– Home health care services
– Rehabilitation care
– Nursing home care
– Emergency room visits
– Hospitalizations
• Cost of treatment
– Medications
– Surgery (inpatient or outpatient)
– Medical supplies
• Cost of routine care
– Absorbent pads and products
– Laundry, dry cleaning
• Nonmedical direct costs
– Cost of transportation to healthcare providers
– Costs of changes to diet, house, or related items
• Cost of complications of the condition

and families.32 Thus, when reviewing a cost analysis for total annual costs of asthma was $16.1 billion, and the
PFDs, it is important to keep the above issues in mind. direct costs of breast cancer was $5.1 billion in 2004.34
In this next section, cost data for each of the PFDs will Another estimate for inpatient costs and physician
be presented; however, significantly more data exist on office visits for women with UI is $452 million (2000
cost for UI, and more specifically for OAB, compared dollars);35 however, this does not include outpatient
to prolapse or FI. surgical costs. Outpatient surgical costs are likely to be
substantial given the increase in the number of outpa-
tient UI surgeries from approximately 35,000 in 1996 to
Urinary Incontinence
106,000 in 2006.36 When focusing on women 65 years
Total Costs or older, data for Medicare beneficiaries showed a con-
tinued increase in total costs from $128.1 million in
The most comprehensive estimate for the total annual
1992 to $234.4 million in 1998 (Table 1-11).5,37
cost of UI in the United States was $19.5 billion, of
which $14.2 billion was from community residents
Overactive Bladder
and $5.3 billion was from institutional residents in
the year 2000 (Table 1-11). These values were based More extensive research has been conducted for the
upon the direct and indirect costs derived from the costs related to OAB than any other PFD. Using med-
National Overactive Bladder Evaluation program.33 ical and pharmaceutical claims data, several studies
The prevalence of UI was based on a rate of 12% in have evaluated the total medical costs for individuals
women and 5% in men for daily incontinence and the who filled prescriptions for medications to manage
number of US adults from the 2000 Census. Thus, OAB (Table 1-12).18,38-40 Annual per person total med-
these costs may underestimate the true current costs ical costs included health plan and member liability.
of UI because the costs for adults with less frequent When evaluating OAB, it is also important to consider
than daily incontinence were not included, cost should OAB-related health conditions such as falls and frac-
be adjusted for inflation, and the number of men and tures, depression, urinary tract infections, and skin
women have increased since 2000. Using a prevalence- conditions.41 Individuals with OAB have also been
based epidemiologic model to estimate direct costs shown to have higher work loss due to absenteeism
for UI, defined as any incontinence episode in the last and disability than those without OAB.42,43 When Hu
year, a total US cost of $16.3 billion ($12.4 billion for et al. evaluated the total costs of OAB, which included
women and $3.8 billion for men) was reported in 1995 direct, indirect, and OAB-related conditions, OAB
(Table 1-11). To put these costs into perspective, the was estimated to cost $9.1 billion and $3.5 billion
Chapter 1 Epidemiology 15

Table 1-11 National Costs of Urinary Incontinence

Author and Year Population Definition of Costs Cost Data


Hu et al. Community-dwelling Direct: Urinary incontinence

CHAPTER 1
200433 and institutionalized Diagnostic costs • Community dwelling: $14.2 billion
adult men and Treatment costs (in 2000 dollars)
women in the United Routine care costs • Institutionalized elderly: $5.3 billion
States Complication costs
Indirect: Overactive bladder
Lost productivity • Community dwelling: $9.1 billion
• Institutionalized elderly: $3.5 billion
Wilson et al. Community-dwelling Diagnostic costs Total cost: $16.3 billion (in 1995 dollars)
200151 and institutionalized Treatment costs • Women: $12.4 billion
adult men and Routine care • Men: $3.8 billion
women Complication costs
Nygaard et al. Women with urinary Inpatient costs Total cost: $452.8 million (in 2000 dollars)
200735 incontinence in Physician office costs • Inpatient: $329.2 million
the United States • Physician office visits: $123.6 million
Anger et al. Female Medicare Inpatient costs Total cost: $234.4 million (in 1998 dollars)
200637 beneficiaries Outpatient costs • Inpatient: $110.1 million
and Emergency room • Outpatient
Thom et al. – Physician office: $75.9 million
20055 – Hospital outpatient: $5.0 million
– Ambulatory surgery: $42.8 million
• Emergency room: $0.6 million

(in year 2000 dollars) by community-dwelling and other items for odor control, bed pads, and skin care.
institutionalized residents, respectively.33 These costs vary based on the type of incontinence
(stress vs urge vs mixed), the severity of leakage (amount
and frequency), as well as the population being evalu-
Routine Care Costs
ated, as data from community-dwelling women may
For the individual and the caregivers, routine care costs be quite different than women presenting for surgery
related to UI may be significant. Routine care includes (Table 1-13). In general, higher routine care costs have
cost of supplies such as incontinence pads and diapers, been associated with more severe incontinence as well
as well as costs related to laundry, dry cleaning, and as mixed or urge UI when compared to SUI.44-46

Table 1-12 Total Annual Medical Care Costs Among Individuals Filling Prescriptions
for Medication to Treat Overactive Bladder18

Average PPPY Total Cost Average PPPY Total Costs


Author and Year Type of Prescription Filled Before Treatment After Treatment Initiation
Nitz et al. 200538 Oxybutynin IR $4,956 ± 14,396 $7,083 ± 39,420
Oxybutynin ER $4,146 ± 8,695 $5,980 ± 13,263
Tolterodine ER $3,349 ± 6,715 $5,074 ± 11,007
Hall et al. 200140 Tolterodine $5,004 $7,020
Oxybutynin $5,688 $7,116
Flavoxate or other OAB drug $5,352 $7,380
No drug treatment for OAB $2,928 $5,040
Varadharajan et al. Oxybutynin ER — $8,862 ± 18,684
200539 Oxybutynin IR $10,521 ± 22,602
Tolterodine ER—group 1 $8,303 ± 18,802
Tolterodine ER—group 2 $9,975 ± 24,860

PPPY, per person per year.


16 Section I Fundamental Topics

Table 1-13 Routine Care Costs for Urinary Incontinence

Author
and Year Population Weekly Cost Yearly Cost*
CHAPTER 1

Subak et al. 293 community- Women with any UI cost ($2005) Women with any UI cost ($2005)
200644 dwelling women $10.59 ± 18 (mean ± SD) $494.12 (mean)
in Diagnostic $5.00 (2, 12) (median (IQR)) $190.45 (median)
Aspects of Median costs Median costs
Incontinence • Slight $0.37 (0, 4) • Slight $19.31
Study • Weekly $0.62 (0, 3) • Weekly $32.35
• Daily $5.00 (2, 12) • Daily $260.89
• Severe $10.98 (4, 21) • Severe $572.91
• Urge $6.57 (0, 19) • Urge $342.81
• Stress $2.31 (0, 18) • Stress $120.53
• Mixed $3.96 (1, 8) • Mixed $206.62
Subak et al. 528 community- Women with any UI cost ($2005) Women with any UI cost ($2005)
200745 dwelling women in $5.17 ± 11.46 (mean ± SD) $269.76 (mean)
Reproductive Risks $1.83 (0.5, 5.2) (median (IQR)) $195.48 (median)
for Incontinence Median costs Median costs
Study • Weekly $0.93 (0.4, 2.9) • Weekly $48.53
• Daily $3.16 (0.9, 7.2) • Daily $164.88
• Moderate $0.93 (0.4, 2.9) • Moderate $48.53
• Severe $3.61 (1.6, 7.2) • Severe $188.36
• Very severe $7.82 (5.0, 36.6) • Very severe $408.03
• Urge $1.86 (0.5, 5.6) • Urge $97.05
• Stress $1.15 (0.4, 3.6) • Stress $60.00
• Mixed $ 2.80 (1.1, 7.5) • Mixed $146.10
Subak et al. 655 women Stress incontinence only ($2006) Stress incontinence only ($2006)
200846 enrolled in Stress $8 ± 9 (mean ± SD) $417 (mean)
Incontinence $4 (2, 13) (median (IQR)) $209 (median)
Surgical Treatment Mixed incontinence Mixed incontinence
Efficacy Trial $16 ± 25 (mean ± SD) $834 (mean)
$9 (4, 19) (median (IQR)) $470 (median)
Median costs (IQR) for mean Median costs for mean
no. of incontinence episodes no. of incontinence episodes
per day per day
• 0–1.0 $3 (1, 9) • 0–1.0 $157
• 1.0–2.5 $6 (3, 9) • 1.0–2.5 $313
• 2.5–4.5 $11 (5, 20) • 2.5–4.5 $574
• >4.5 $18 (8, 27) • >4.5 $939
*Yearly costs calculated by multiplying weekly costs by number of weeks per year.

Pelvic Organ Prolapse performed for prolapse based on the National Survey
of Ambulatory Surgery.48 In addition to surgery, it is
Limited data exist regarding the costs of POP. important to consider outpatient costs, which were
Although estimates for direct and indirect costs exist estimated to be $96.9 million in 2005-2006.49 At this
for urinary incontinence, only direct costs are available point, data regarding indirect costs for prolapse are not
for prolapse. Subak et al. reported that the direct cost available but given the bothersome symptoms of this
of inpatient prolapse surgery based on the National condition, indirect costs for prolapse certainly exist.
Hospital Discharge Survey database was $1.0 bil-
lion (95% confidence interval $0.82, $1.2 billion) in
1997 dollars.47 Estimates of the cost for outpatient
Fecal Incontinence
surgery are not available despite knowing that a num-
ber of outpatient surgeries are performed annually. In Current estimates for the cost of FI in the United
2006, approximately 44,000 outpatient surgeries were States are also limited. In fact, the statement from
Chapter 1 Epidemiology 17

the NIH State of the Science conference on the REFERENCES


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for the cost of FI are available.50 Costs for FI need terminology of female pelvic organ prolapse and pelvic floor
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CHAPTER 1
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prevalence rates of 5% to 64% for UI within the col. 2006;107:1253–1260.
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of disease based upon frequency of leakage. The lence: results from the National Health and Nutrition Examina-
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through age 50, with a subsequent slight decline in women: variation in prevalence estimates and risk factors. Obstet
older women. The prevalence of symptomatic POP Gynecol. 2008;111:324–331.
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increases. The prevalence of defecatory symptoms a longitudinal study. Obstet Gynecol. 2008;111:1148–1153.
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18 Section I Fundamental Topics

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23. Swift S, Woodman P, O’Boyle A, et al. Pelvic Organ Support eficiaries. J Urol. 2006;176:247–251; discussion 51.
Study (POSST): the distribution, clinical definition, and epide- 38. Nitz NM, Jumadilova Z, Darkow T, Frytak JR, Bavendam T.
miologic condition of pelvic organ support defects. Am J Obstet Medical costs after initiation of drug treatment for overactive
Gynecol. 2005;192:795–806. bladder: effects of selection bias on cost estimates. Am J Manag
24. Bradley CS, Zimmerman MB, Qi Y, Nygaard IE. Natural his- Care. 2005;11:S130–S139.
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Gynecol. 2007;109:848–854. nomic impact of extended-release tolterodine versus immedi-
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Lowder JL. Trends in inpatient prolapse procedures in the insured persons with overactive bladder. Am J Manag Care.
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e1–501 e7. 40. Hall JA, Nelson MA, Meyer JW, Williamson T, Wagner S.
26. Whitehead WE, Borrud L, Goode PS, et al. Fecal inconti- Costs and resources associated with the treatment of overactive
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Census Bureau; 2010. 45. Subak L, Van Den Eeden S, Thom D, Creasman JM, Brown JS.
31. Wu JM, Hundley AF, Fulton RG, Myers ER. Forecasting the Urinary incontinence in women: direct costs of routine care.
prevalence of pelvic floor disorders in U.S. Women: 2010 to Am J Obstet Gynecol. 2007;197(6):596.e1–596.e9.
2050. Obstet Gynecol. 2009;114:1278–1283. 46. Subak LL, Brubaker L, Chai TC, et al. High costs of urinary
32. Luce BR, Manning WG, Siegel JE, Lipscomb J. Estimating incontinence among women electing surgery to treat stress
costs in cost-effectiveness analysis. In: Gold MR, Siegel JE, incontinence. Obstet Gynecol. 2008;111:899–907.
Russell LB, Weinstein MC, eds. Cost-effectiveness in Health and 47. Subak LL, Waetjen LE, van den Eeden S, Thom DH, Vitting-
Medicine. New York: Oxford University Press; 1996. hoff E, Brown JS. Cost of pelvic organ prolapse surgery in the
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Hunt T. Costs of urinary incontinence and overactive bladder 48. Erekson EA, Lopes VV, Raker CA, Sung VW. Ambulatory pro-
in the United States: a comparative study. Urology. 2004;63: cedures for female pelvic floor disorders in the United States.
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34. RTI International. Cost of Illness Studies: Cost-of-Illness Sum- 49. Sung VW, Washington B, Raker CA. Costs of ambulatory care
maries for Selected Conditions. Available at: http://www.rti. related to female pelvic floor disorders in the United States. Am
org/page.cfm?objectid=CA1E1F48-8B6C-4F07-849D6A4C J Obstet Gynecol. 2010;202:483.e1–483.e4.
12CBF3C3. Accessed January 20, 2011. 50. Landefeld CS, Bowers BJ, Feld AD, et al. National Institutes
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2 Normal Anatomy of the Pelvis
and Pelvic Floor
Marlene M. Corton

INTRODUCTION from the superficial perineal space to the thighs


or posterior perineal triangle. Anteriorly, the con-
Basic understanding of pelvic anatomy is key to tinuity of Colles with Scarpa fascia may allow the
understanding pathologic processes. Pelvic anatomy spread of blood and infection between these com-
must be understood as relationships among vis- partments. This continuity may also be apparent
ceral organs, connective tissues, muscles, and nerves. when subcutaneous gas is noted in the vulva during
Conceptualizing the three-dimensional (3D) aspects laparoscopic cases.
of these structures is useful when performing recon- • The inguinal canal allows communication between
structive pelvic surgery. the intra-abdominal cavity and the subcutaneous
tissue of the mons and labia majora. The round lig-
ament and obliterated processus vaginalis exit the
EXTERNAL GENITALIA (VULVA) inguinal canal through the external or superficial
inguinal ring and attach to the subcutaneous tis-
The female external genitalia, or vulva, include the sue or skin of the labia majora. An abnormally pat-
mons pubis, labia majora and minora, clitoris, vesti- ent processus vaginalis, also known as the canal of
bule, vestibular bulbs, greater (Bartholin) and lesser Nuck, can result in hydroceles or inguinal hernias.
vestibular glands, Skene glands, and the distal urethral Therefore, the differential diagnosis of a mass in the
and vaginal openings (Figure 2-1). labium majus should include a round ligament leio-
myoma and an inguinal hernia.
Mons Pubis and Labia Majora
The skin over the mons pubis and labia majora con- Labia Minora
tains hair, and the subcutaneous layer is similar to that
of the anterior abdominal wall. The subcutaneous layer In contrast to the skin that overlies the labia majora,
consists of a superficial fatty layer similar to Camper’s the skin of the labia minora does not contain hair and
fascia, and a deeper membranous layer, Colles’ fascia, the subcutaneous tissue consists primarily of loose
which is continuous with Scarpa’s fascia of the ante- connective tissue (Figure 2-3). The labia minora lie
rior abdominal wall (Figure 2-2). between the labia majora and contribute to the lat-
eral boundaries of the vestibule as described below.
Anteriorly, each labium minus separates to form
Clinical Correlations
two folds that surround the glans of the clitoris. The
• The firm attachments of Colles’ fascia to the ischio- prepuce is the anterior fold that overlies the glans, and
pubic rami laterally and the perineal membrane the frenulum is the fold that passes below the clitoris.
posteriorly prevent the spread of blood or infection Posteriorly, the labia minora end at the fourchette.
19
20 Section I Fundamental Topics

Prepuce Mons pubis


of clitoris
Glans
of clitoris
Labium
majus

Labium
Skene gland minus
openings
Vestibule
Hart’s line
CHAPTER 2

Bartholin’s gland Fossa


openings navicularis
Fourchette

FIGURE 2-1 External female


genitalia.

Clinical Correlations • Chronic dermatologic diseases such as lichen


sclerosus may lead to significant atrophy of the
• The loose connective tissue underlying the skin of
labia minora and vulvar pain conditions such as
the labia minora allows mobility of the skin dur-
vestibulitis can lead to significant vulvar irritation
ing sex and justifies the ease of dissection during
and pain.
vulvectomy.

Crus of clitoris

Vestibular bulb

A B

FIGURE 2-2 Dissection of labia majora with vestibular bulb (A) and Colles fascia (B) shown.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 21

Cut edge of
labium minus

Anterior urogenital Left crus of


triangle clitoris

Vestibular bulb
Bulbospongiosum Ischiocavernosus
muscle muscle, cut

Perineal Bartholin’s gland


membrane
Bulbospongiosum
muscle, cut
Superficial Ischial
transverse tuberosity
perineal muscle
Levator ani muscle
Sacrotuberous

CHAPTER 2
ligament
External anal Posterior
sphincter muscle perineal triangle

FIGURE 2-3 Anatomy anterior urogenital triangle and posterior anal triangle.

Clitoris • The incision for Bartholin gland drainage or marsu-


pialization should be kept medial or inside Hart line
This is the female erectile structure that is homolo- in attempts to restore normal gland duct anatomy1
gous to the penis. It consists of a glans, a body, and and avoid visible scars on the vulva.
two crura. The glans contains many nerve endings and
is covered by a mucous membrane. The body mea-
sures approximately 2 cm and is attached to the pubic Vestibular Bulbs
ramus by the crura.
These are homologues to the bulb of the penis and cor-
pus spongiosum of the male. They are two richly vascu-
lar erectile masses that surround the urethra and vaginal
Vaginal Vestibule opening, and are partially covered by the bulbocaver-
This area is bounded by Hart’s line (Figure 2-1) on nosus muscles (Figure 2-4). They are found superficial
the labia minora laterally, the hymeneal ring medi- to the perineal membrane and their posterior ends are
ally, the prepuce anteriorly, and the fourchette pos- in contact with Bartholin glands. Anteriorly, they are
teriorly (Figure 2-4). The Hart line represents the joined to one another and to the clitoris.
line of transition between the darker skin of the
labia minora and the lighter mucous membrane on Clinical Correlation
the inner surface of the labia minora. The vestibule
• The proximity of the Bartholin glands to the ves-
contains the openings of the urethra, vagina, greater
tibular bulbs accounts for the significant bleeding
(Bartholin) and lesser vestibular glands, and Skene
often encountered with Bartholin gland excision.
glands. A shallow posterior depression, known as the
navicular fossa, lies between the vaginal opening and
the fourchette. Greater Vestibular or Bartholin Glands
These are the homologues of the male bulbourethral
Clinical Correlations or Cowper glands. They are in contact with, and often
• Localized vestibulitis is characterized by pain with overlapped by, the posterior ends of the vestibular
vaginal penetration, localized point tenderness, and bulbs. Each gland duct opens at the vaginal vestibule
erythema of the vestibular mucosa. at approximately 5- and 7-o’clock positions.
22 Section I Fundamental Topics

Crus of clitoris
Body of clitoris Cut edge of
labium minus
Prepuce of clitoris
Vestibular bulb
Frenulum of clitoris Ischiocavernosus
muscle, cut

Bartholin’s gland
Labium minus, cut

Bulbospongiosum
muscle, cut
Superficial Ischial
transverse tuberosity
perineal muscle
Levator ani muscle
Sacrotuberous
ligament
CHAPTER 2

External anal
sphincter muscle

FIGURE 2-4 Dissection of labia minorum.

Clinical Correlations outlet. These include the pubic symphysis anteriorly,


ischiopubic rami and ischial tuberosities anterolater-
• Contraction of the bulbocavernosus muscle during
ally, coccyx posteriorly, and sacrotuberous ligaments
sexual arousal stimulates gland secretion of small
posterolaterally. An arbitrary line joining the ischial
amounts of mucous material, which may serve to
tuberosities divides the perineum into the anterior
lubricate the vaginal opening.
or urogenital triangle, and a posterior or anal triangle
• Obstruction of the Bartholin ducts from inflam-
(Figure 2-3).
mation or infection can lead to symptomatic cysts
or abscesses, which are surgically drained. As dis-
cussed above, the incision should be made inside Anterior (Urogenital) Triangle
the Hart’s line. Symptomatic or recurrent cysts may
require marsupialization or gland excision.
Key Point
• The perineal membrane further divides the anterior
perineal triangle into a superficial and a deep space.
PERINEUM The deep space is bounded superiorly by the infe-
rior fascia of the levator ani muscles.
Key Point
• An arbitrary line joining the ischial tuberosities The structures that comprise the external female
divides the perineum into the anterior or urogenital genitalia or vulva lie in the anterior perineal trian-
triangle, and a posterior or anal triangle. gle. The base of this triangle lies between the ischial
tuberosities and generally overlies the superficial trans-
verse perineal muscles. The perineal membrane further
The perineum is the diamond-shaped area between the divides the anterior perineal triangle into a superficial
thighs that extends from the skin in this area to the and a deep space (Figure 2-5). The superficial perineal
inferior fascia of the pelvic diaphragm superiorly. space lies below or inferior to the perineal mem-
The anterior, posterior, and lateral boundaries of the brane and the deep space lies above or superior to
perineum are the same as those of the bony pelvic the membrane.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 23

External urethral opening Compressor urethrae muscle


Urethrovaginal sphincter
muscle
Ischiocavernosus
muscle

Bulbospongiosum
muscle Perineal membrane cut

Dorsal nerve
of the clitoris
Perineal nerve
Perineal body

Superficial transverse Levator ani muscle


perineal muscle

CHAPTER 2
Inferior anal
nerve
External anal
sphincter muscle

FIGURE 2-5 Superficial and deep anterior and perineal triangles.

Superficial Space of the Anterior the superficial portion of the vestibular bulbs and
Perineal Triangle Bartholin glands. They attach to the body of the clito-
ris anteriorly and the perineal body posteriorly.
This space lies between Colles’ fascia inferiorly and
the perineal membrane superiorly. It contains the stri- Clinical Correlation
ated ischiocavernosus, bulbocavernosus, and superfi-
cial transverse perineal muscles, and branches of the • Contraction of the bulbocavernosus muscles may
pudendal vessels and nerve. In addition, the clitoris, contribute to the release of secretions from Bartholin
vestibular bulbs, and Bartholin glands lie within the glands. They may also contribute to clitoral erection
space and the urethra and vagina traverse it (Figure 2-5). by compressing the deep dorsal vein of the clitoris.

Ischiocavernosus Muscle Superficial Transverse Perineal Muscles


This muscle attaches to the medial aspect of the ischial These are narrow strips of muscles that attach to
tuberosities posteriorly and the ischiopubic rami later- the ischial tuberosity laterally and the perineal body
ally. Anteriorly, it attaches to the crus of the clitoris. medially.
The ischiocavernosus muscle is innervated by muscu-
lar branches of the perineal nerve, which is a branch Clinical Correlation
of the pudendal nerve. The dorsal nerve of the clitoris
courses deep into this muscle.1 • The superficial transverse perineal muscle may be
attenuated or even absent, but when present, con-
Clinical Correlation tribute to the perineal body as discussed later.

• Contraction of the ischiocavernosus muscle during Deep Space of the Anterior Perineal Triangle
sexual arousal may help maintain clitoral erection
by compressing the crus of the clitoris, thus delay- This “space” lies deep into the perineal membrane.
ing venous drainage. It is partially bounded superiorly by the inferior fas-
cia of the levator ani muscles. In women, the levator
Bulbocavernosus Muscles muscles lack direct attachments to the urethra and
These muscles, also termed bulbospongiosus muscles, thus, the “deep space” is continuous with the pel-
surround the vaginal opening and partially cover vic cavity as described below.2 Parts of urethra and
24 Section I Fundamental Topics

vagina, branches of the internal pudendal artery, and ATLA


portions of the dorsal nerve and vein of the clitoris ATFP PS OC
are found within this area. It also contains the com-
pressor urethrae, urethrovaginal sphincter, and exter-
nal urethral sphincter muscles as described later in LA
the chapter.

liac a.
O
Perineal Membrane (Urogenital Diaphragm) Bladder

External
Traditionally, the urogenital diaphragm is described
as consisting of the deep transverse perineal muscles
and sphincter urethrae muscles between the inferior
fascia of the urogenital diaphragm (perineal mem-
brane) and the superior fascia of the urogenital dia-
phragm. However, the term “diaphragm” generally
implies a closed compartment. As described above, FIGURE 2-6 Retropubic space of Retzius demonstrating
the white line (ATFP). PS, pubic symphysis; ATLA, arcus
the deep space is an open compartment. It is bounded
tendineus levator ani; ATFP, arcus tendineus fascia pelvis;
inferiorly by the perineal membrane and extends up
OC, obturator canal; LA, levator ani.
into the pelvis.2 As a result, when describing perineal
CHAPTER 2

anatomy, the terms urogenital diaphragm and inferior fas-


cia of the urogenital diaphragm are misnomers and have
been replaced by the anatomically correct term perineal • During cadaver dissections, attachments of the
membrane.3 perineal membrane to the lateral vaginal walls can
The perineal membrane has recently been shown generally be identified approximately at the level of
to consist of two histologically, and probably func- the hymeneal remnants.
tionally, distinct portions that span the opening of the
anterior pelvic outlet.4 The dorsal or posterior portion Perineal Body
consists of a sheet of dense fibrous tissue that attaches The perineal body is a mass of dense connective tissue
laterally to the ishiopubic rami and medially to the found between the distal third of the posterior vaginal
distal third of the vagina and to the perineal body. The wall and the anus below the pelvic floor (Figure 2-7).
ventral or anterior portion of the perineal membrane is It is largely formed by the midline connection between
intimately associated with the compressor urethrae and the two halves of the perineal membrane.6 Distal or
urethrovaginal sphincter muscles, previously called the superficial to the perineal membrane, the medial ends
deep transverse perineal muscles in the female.2 In addi- of the bulbocavernosus and superficial transverse
tion, the ventral portion of the perineal membrane is perineal muscles also contribute to the perineal body.
continuous with the distal insertion of the arcus ten- Deep into the perineal membrane, fibers of the pubo-
dineus fascia pelvis, which can best be appreciated visceral portion of the levator ani attach to the perineal
during dissection of the retropubic space (Figure 2-6). body. The perineal body has direct attachments to the
In the above-mentioned histology study, the deep or posterior vaginal wall anteriorly and the external anal
superior surface of the perineal membrane was shown sphincter posteriorly. In the sagittal plane, the perineal
to have direct connections to the levator ani muscles body is triangular in shape with a base that is much
and the superficial or inferior surface of the membrane wider than its apex. The apex of the perineal body
was fused with the vestibular bulb and clitoral crus. A extends 2 to 3 cm above the hymeneal ring. The rela-
follow-up magnetic resonance imaging (MRI) study tionships of the perineal body in reference to posterior
showed that many of the distinct anatomic features compartment anatomy were demonstrated in a recent
of the perineal membrane described above could be MRI study.7
seen with MRI.5
Clinical Correlations
Clinical Correlations
• Clinical assessment of perineal body length takes
• The perineal membrane provides support to the into account the anterior portion of the external
distal vagina and urethra by attaching these struc- anal sphincter as well as the posterior vaginal wall
tures to the bony pelvis. In addition, its attachments and anterior anal wall thickness.
to the levator ani muscles suggest that the perineal • The perineal body contributes to support the dis-
membrane may play a more active role in support tal vagina and rectum; therefore, during episiotomy
than what was previously thought. repairs and perineal reconstructive procedures
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 25

Obturator internus
muscle

Arcus tendineus
levator ani

Visceral connective Ischial spine


tissue

Levator ani Coccygeus


muscle

CHAPTER 2
muscle

Arcus tendineus Iliococcygeus


fascia pelvis muscle
Urethra
Levator
Perineal plate
membrane
Anus
Vagina
Levator ani Perineal
muscle body
FIGURE 2-7 Sagittal view of pelvic musculature. Attachments of the pelvic musculature to the sidewall is illustrated as
well as the location of the perineal body.

emphasis should placed on reapproximation of the Clinical Correlations


torn ends of the anatomic structures that form the
• The pudendal or Alcock canal (Figure 2-9) is a split-
perineal body.
ting of the obturator internus fascia on the lateral
walls of the posterior perineal triangle. It allows
Posterior (Anal) Triangle path of the internal pudendal vessels and puden-
dal nerve before these structures split into terminal
Key Point branches to supply the structures of the vulva and
perineum (Figure 2-9).
• The pudendal or Alcock canal is a splitting of the • The inferior rectal nerve often courses through
obturator internus fascia on the lateral walls of the ischioanal fossa without entering the pudendal
the posterior perineal triangle through which the canal.1
pudendal neurovascular bundle passes.
The ischioanal fossa, formerly known as the ischio-
rectal fossa, is primarily filled with adipose tissue
This triangle contains the anal canal, anal sphincter and contains branches of the pudendal vessels and
complex, ischioanal fossa, and branches of the internal pudendal nerve (Figure 2-10). The anal canal and
pudendal vessels and pudendal nerve (Figure 2-8). It anal sphincter complex lie in the center of this fossa.
is bounded deeply by the fascia overlying the inferior The boundaries of the fossa include (1) the inferior
surface of the levator ani muscles, and laterally by the fascia of the levator ani muscles superior and medi-
fascia overlying the medial surface of the obturator ally, (2) the fascia covering the medial surface of the
internus muscles. obturator internus muscles and ischial tuberosities
26 Section I Fundamental Topics

Compressor urethrae
muscle

Dorsal nerve
of the clitoris Perineal body

Perineal nerve

Superficial transverse Levator ani muscle


perineal muscle
CHAPTER 2

Inferior anal Posterior


nerve perineal triangle
External anal
sphincter muscle

FIGURE 2-8 Posterior anal triangle.

Internal iliac Cauda equina


artery
Superior gluteal
External iliac LST artery
artery

S1 Anterior sacral
S2 foramina
Inguinal ligament
S3
S4
Obturator canal Inferior gluteal
with entering artery
obturator nerve
and artery Coccyx
Obturator muscle
Arcus tendineus Internal pudendal
levator ani artery
Arcus tendineus Ischial spine
fascia pelvis Lesser sciatic
foramen
Levator ani muscle Obturator
internus muscle
Internal pudendal artery
and pudendal nerve in Alcock’s canal Ischial tuberosity

FIGURE 2-9 The pudendal (Alcock) canal and lumbosacral trunk (LST).
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 27

External iliac
artery and vein
Obturator internus
muscle

Obturator internus
fascia

Longitudinal smooth
Levator ani muscle
muscle layer
with superior and inferior
layers of parietal fascia
Circular smooth
muscle layer
Rectum

Plicae
Pudendal nerve
transversalis

CHAPTER 2
and internal pudendal
recti
vessels in pudendal
(Alcock) canal Ischioanal
fossa
External anal
sphincter muscle Pectinate line

Internal anal
sphincter muscle
FIGURE 2-10 Ischioanal fossa and anal canal.

laterally, and (3) the lower border of the gluteus maxi- The anal sphincter complex consists of the external
mus muscles and sacrotuberous ligaments posterior and internal anal sphincters and the puborectalis mus-
and laterally. The contents of the ischioanal fossa cle (Figure 2-10).
extend to the anterior perineal triangle deep into the
perineal membrane. Posterior to the anus, the con- External Anal Sphincter
tents of the fossa are continuous across the midline This sphincter consists of striated or skeletal muscle
except for the attachments of the external anal sphinc- and is responsible for the squeeze pressure of the anal
ter fibers to the coccyx. canal. It surrounds the distal anal canal and consists of
a superficial and a deep portion. The more superficial
Clinical Correlation fibers lie distal or below the internal sphincter and are
separated from the anal epithelium only by submu-
• The continuity of the ischioanal fossa across peri- cosa. The deep fibers blend with the lowest fibers of
neal compartments and across the midline pos- the puborectalis muscle. The external anal sphincter
teriorly allows fluid, infection, and malignancy to is primarily innervated by the inferior anal nerve, also
spread from one side of the anal canal to the other, known as the inferior rectal or inferior hemorrhoidal
and also into the anterior perineal triangle deep into nerve. This nerve can be a branch of the pudendal
the perineal membrane. nerve or may arise directly from the sacral plexus.1
The inferior anal nerve communicates with the peri-
Anal Sphincter Complex neal branch of the posterior femoral cutaneous nerve,
which also contributes to the innervation of the peri-
Key Point anal skin.

• The anal sphincter complex consists of the external Internal Anal Sphincter
and internal anal sphincters and the puborectalis This sphincter represents the distal thickening of the
muscle. circular smooth muscle layer of the anal wall. It is
under the control of the autonomic nervous system
28 Section I Fundamental Topics

and is responsible for approximately 80% of the rest- The ischial spines are clinically important bony
ing pressure of the anal canal.8 prominences that project posteromedially from the
medial surface of the ischium approximately at the
Puborectalis Muscle level of the fifth sacral vertebra (S5).
This muscle comprises the medial portion of the leva-
tor ani muscle that arises on either side from the inner
Pelvic Openings
surface of the pubic bones. It passes behind the rec-
tum, and forms a sling behind the anorectal junction, The posterior, lateral, and inferior walls of the pelvis
contributing to the anorectal angle and possibly to have several openings through which many important
fecal continence. structures pass. The large obturator foramen between
the ischium and pubis is filled almost completely by
the obturator membrane (Figure 2-12). In the supe-
BONY PELVIS rior portion of this membrane, a small opening known
as the obturator canal, allows passage of the obtura-
The bony pelvis comprises the two hipbones, also tor neurovascular bundle into the medial or adductor
known as the innominate or coxal bones; the sacrum; and compartment of the thigh.
the coccyx (Figure 2-11). The hipbones consist of the The posterolateral walls of the pelvis are not covered
ilium, ischium, and pubis, which fuse at the acetabulum, by bone. Two important ligaments, the sacrospinous
a cup-shaped structure that articulates with the head of and sacrotuberous, convert the greater and lesser sciatic
CHAPTER 2

the femur. The ilium articulates with the sacrum poste- notches of the ischium into the greater sciatic foramen
riorly at the sacroiliac joint, and the pubic bones articu- and lesser sciatic foramen. The piriformis muscle, supe-
late with each other anteriorly at the symphysis pubis. rior and inferior gluteal vessels (Figure 2-12A), internal
The sacroiliac joint is a synovial joint that connects the pudendal vessels and pudendal nerve, sciatic nerve,
articular surfaces of the sacrum and ilium. This joint and other branches of the sacral nerve plexus pass
and its ligaments contribute significantly to the stabil- through the greater sciatic foramen (Figure 2-12B).
ity of the bony pelvis. The symphysis pubis is a carti- The internal pudendal vessels, pudendal nerve, and
laginous joint, which connects the articular surfaces of obturator internus muscle tendon pass through the
the pubic bones through a fibrocartilaginous disc. lesser sciatic foramen.

Ala

Iliac crest

Posterior
superior Ilium Anterior
iliac spine superior
iliac spine

Greater sciatic
notch
Ischial spine
Acetabulum
Lesser sciatic
notch
Pubis

Inferior pubic
Ischium ramus
Ischial tuberosity
FIGURE 2-11 Bony pelvis. Obturator foramen
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 29

A Inguinal ligament

Obturator canal
Levator ani
muscle

Pudendal
nerve

Pudendal
canal
Obturator
muscle
Piriformis
muscle
Sacrotuberous
ligament
LSF

CHAPTER 2
Ischial spine
GSF

Sacrospinous
ligament
LST

Piriformis muscle

Superficial &
inferior gemelli

Quadratus
femoris
Obturator
internus muscle

FIGURE 2-12 Greater sciatic foramen (GSF) and


lesser sciatic foramen (LSF). A.  Ventral view of
greater sciatic foramen. B. Dorsal view of greater
sciatic foramen. LST, lumbosacral trunk.

Posteriorly, four pairs of pelvic sacral foramina Clinical Correlations


allow passage of the anterior divisions of the first
four sacral nerves and lateral sacral arteries and veins • Understanding the anatomy related to the greater
(Figure 2-13). sciatic foramen is critical to avoid neurovascular
The urogenital hiatus is the U-shaped opening in injury during sacrospinous ligament fixation pro-
the pelvic floor muscles through which the urethra, cedures and when administering pudendal nerve
vagina, and rectum pass. blockade.9
30 Section I Fundamental Topics

Common iliac
artery

Internal iliac
artery S1
S2
IGA
IPA S3

PN S4

S5
Ischial spine
Coccygeus
CHAPTER 2

muscle
Nerves to pelvic
floor
Iliococcygeus
muscle

FIGURE 2-13 Sacral foramina.


IGA, inferior gluteal artery; IPA, Pubococcygeus
internal pudendal artery. muscle

• Weakening and opening of the urogenital hiatus structures and contribute to the stability of the bony
from neuromuscular injury to the pelvic floor mus- pelvis. The round and broad “ligaments” of the uterus
cles is thought to contribute to urogenital prolapse consist of smooth muscle and loose areolar tissue,
as described later in the chapter. respectively, and do not contribute to the support of
the uterus and adnexae. In contrast, the cardinal and
uterosacral “ligaments” do contribute to the support of
Ligaments the uterus and upper third of the vagina. The cardinal
Key Point ligaments primarily consist of perivesical connective
tissue and nerves and are vertically oriented in the
• The round and broad ligaments of the uterus consist of anatomic or standing position. The uterosacral liga-
smooth muscle and loose areolar tissue, respectively, ments consist primarily of smooth muscle and contain
and do not contribute to the support of the uterus some of the pelvic autonomic nerves. In the anatomic
and adnexa. In contrast, the cardinal and uterosacral position, the uterosacral ligaments are directed posteri-
ligaments do contribute to pelvic organ support. orly and oriented almost horizontal to the floor.

Clinical Correlations
Although the term ligament is most often used to
describe dense connective tissue that connects • The sacrospinous and anterior longitudinal liga-
two bones, the “ligaments” of the pelvis are variable ment serve as suture fixation sites in suspensory
in composition, site of attachments, and function. procedures used to correct pelvic organ prolapse.
The pelvic ligaments range from connective tissue • The iliopectineal ligament, also termed Cooper’s
structures that support the bony pelvis and pelvic ligament, is a thickening in the periosteum of the
organs to smooth muscle and loose areolar tissue that pubic bone, which is often used to anchor sutures
add no significant support. The sacrospinous, sacrotu- in retropubic bladder neck suspension proce-
berous, and anterior longitudinal ligament of the sacrum dures such as the Burch urethropexy procedure
consist of dense connective tissue that join bony (Figure 2-14).
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 31

Iliopectineal (Cooper) ligament


and from the obturator membrane. It exits the pelvis
through the lesser sciatic foramen, attaches to the greater
PS
trochanter of the femur, and as the piriformis muscles,
it functions as an external hip rotator.
ATFP
U Fascia
The fascia that invests striated muscles is termed pari-
etal fascia. Histologically, this tissue consists of regular
Bladder arrangements of collagen. Pelvic parietal fascia pro-
vides muscle attachment to the bony pelvis and serves
as anchoring points for visceral fascia, also termed endo-
pelvic fascia, which will be described later in the chap-
ter. Condensations or thickening of the parietal fascia
covering the medial surface of the obturator internus
FIGURE 2-14 Cooper’s ligament. Sutures are placed and levator ani muscles serve special functions. The
from the periurethral fascia to Cooper’s ligament for a arcus tendineus levator ani is a condensation of fascia
Burch procedure. covering the medial surface of the obturator internus
muscle. This structure serves as the point of origin for

CHAPTER 2
parts of the very important levator ani muscles. The
PELVIC WALL MUSCLES arcus tendineus fascia pelvis is a condensation of fascia
AND FASCIA covering the medial aspect of the obturator internus
and levator ani muscles. It represents the lateral point
Muscles of attachment for the distal portion of the anterior
vaginal wall. The proximal portion of the arcus tendin-
The posterior, lateral, and inferior walls of the pel-
eus fascia pelvis also contributes to the lateral point of
vis are partially covered by striated muscles and their
attachment for the iliococcygeal muscles.
investing layers of parietal fasciae. The levator ani mus-
cles represent the main muscular component of the
pelvic floor and are discussed later in the chapter.
LOWER URINARY TRACT
Piriformis Muscle STRUCTURES AND SPHINCTERIC
This muscle arises from the anterior and lateral sur- MECHANISM
face of the sacrum and partially fills the posterolat-
eral pelvic walls. It exits the pelvis through the greater Bladder
sciatic foramen, attaches to the greater trochanter of The bladder is a hollow organ that allows storage
the femur, and functions as an external or lateral hip and evacuation of urine. Anteriorly, the bladder rests
rotator. The piriformis muscle also functions as a thigh against the anterior abdominal wall and posteriorly it
abductor when the thigh is flexed. rests against the vagina and cervix (Figures 2-15 and
2-16). Inferiorly and laterally, the bladder is in con-
Clinical Correlation tact with the inner surface of the pubic bones. In this
• The sacral nerves and sacral plexus branches are retropubic position, the bladder is devoid of perito-
intimately associated with the piriformis mus- neal covering and not in contact with other visceral
cle. Many variations in anatomy of the piriformis structures. The reflection of the bladder onto the
muscle and sacral nerve branches exist, including abdominal wall is triangular in shape. The apex of
sciatic nerve perforation of the muscle.10 Stretch this triangle is continuous with the median umbilical
injury to the piriformis muscle may cause “sciatic ligament or urachus, which represents the obliterated
nerve”–type pain or persistent hip pain that can be remnant of the fetal allantois.
confused with other pelvic pathology. Imaging and
physical therapy evaluation may be warranted in Clinical Correlations
women who present with these symptoms.
• Because the apex of the bladder is highest in the
midline, this is the area where bladder injury is most
Obturator Internus Muscle
likely to result during peritoneal entry. For this rea-
This muscle partially fills the sidewalls of the pelvis. It son, it is important to drain the bladder prior to
arises from the pelvic surfaces of the ilium and ischium, abdominal entry.
32 Section I Fundamental Topics

Dome
Peritoneum

Paravesical space Body of


(with perivesical bladder
venous plexus)
Left ureteral
Obturator orifice
internus
muscle Trigone

Levator ani Tendinous arch


muscle of pelvis fascia
Perineal membrane Compressor
urethrae
Urethrovaginal
Vagina
CHAPTER 2

sphincters
Urethra
FIGURE 2-15 Coronal view of bladder and urethra.

Aorta
Left
common
iliac vein
Ureter
Ovarian
artery
L5 Ovarian
vein
Psoas
muscle
Internal
iliac
artery
Rectum

Round
ligament

Uterine Uterus
artery

Ureter

Cut edge of
peritoneum

Cut section of
bladder dome

Right
ureteral
orifice
FIGURE 2-16 Lower urinary tract anatomy including course of the ureter.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 33

• Transection of a patent urachus can result in extrav- found at the vesical neck, the area where the urethra
asation of urine into the abdominal cavity. A pat- enters the bladder wall.
ent urachus may also lead to extravasation of urine
through the umbilicus or to urachal cysts and diver-
ticula. When symptomatic, a patent urachus can be Urethra and Striated Urogenital
excised or ligated. Sphincter Complex
• The preferred location for an intentional cystotomy
The female urethra is a complex organ that is 3 to
is the retropubic or extraperitoneal portion of the
4 cm in length. The lumen of the urethra begins at the
bladder close to the dome. In this location the blad-
internal urinary meatus, and then courses through the
der is not in contact with other visceral structures
bladder base for less than a centimeter. This region of
and the risk of fistula formation is minimal.
the bladder where the urethral lumen traverses the
The bladder wall consists of coarse bundles of smooth bladder base is called the vesical neck. The distal two-
muscle known as the detrusor muscle, which extends thirds of the urethra are fused with the anterior vagi-
into the upper part of the urethra. Although separate nal wall.
layers of the detrusor are described, they are not as The walls of the urethra begin outside the bladder
well defined as the layers of other viscous structures wall. They consist of two layers of smooth muscle, an
such as the bowel or the ureter. The innermost layer inner longitudinal and an outer circular, which is in
of the bladder wall is plexiform and can be seen from turn surrounded by a circular layer of skeletal muscle
referred to as the sphincter urethra or rhabdosphinc-

CHAPTER 2
the pattern of trabeculations often noted during cys-
toscopy. The mucosa of the bladder consists of transi- ter. Approximately at the junction of the middle and
tional epithelium. lower third of the urethra, and just above the perineal
The bladder can be divided into a dome and a base membrane, two strap skeletal muscles known as the
approximately at level of the ureteral orifices. The urethrovaginal sphincter and compressor urethrae are
dome is thin walled and distensible, whereas the base found. These muscles were previously known as the
has a thicker wall that undergoes less distention during deep transverse perineal muscles in females and together
filling. The bladder base consists of the vesical trigone with the sphincter urethrae constitute the striated uro-
and the detrusor loops, two U-shaped bands of fibers genital sphincter complex (Figure 2-17). Together, these

Bladder

Pubic
symphysis

Sphincte
urethrae
muscle

Vagina
Compressor
urethrae
Urethrovaginal muscle
FIGURE 2-17 Striated urogenital sphinc- sphincter
ter complex. muscle
34 Section I Fundamental Topics

three muscles function as a unit and have a complex similar to that of the sigmoid, but near its termination
and controversial innervation as described below. it becomes dilated to form the rectal ampulla, which
Their fibers combine to provide constant tone, with begins below the posterior cul-de-sac peritoneum
emergency reflex activity mainly in the distal half of and extends inferiorly to the level of the pelvic floor
the urethra where the urethrovaginal sphincter and com- muscles.
pressor urethrae are found. The rectum contains several, usually three trans-
Distal to the level of the perineal membrane, the verse folds, known as the plicae transversales recti, or
walls of the urethra consist of fibrous tissue, serving valves of Houston. The largest and most constant
as the nozzle that directs the urine stream. The ure- of these folds is located anteriorly and to the right,
thra has a prominent submucosal layer that is lined approximately 8 cm from the anal orifice.
by hormone-sensitive stratified squamous epithelium.
Within the submucosal layer on the dorsal or vaginal
surface of the urethra is a group of glands known as Clinical Correlations
the paraurethral glands, which open into the lumen • In the empty state, the transverse rectal folds may
of the dorsal surface of the urethra. Duct openings of overlap each other, making it difficult at times to
the two most prominent glands, termed Skene glands, manipulate an examining finger or endoscopy tube
are seen on the inner surface of the external urethral past this level.
orifice at the vestibule. • These folds may contribute to fecal continence by
supporting fecal matter above the anal canal.
CHAPTER 2

Clinical Correlation
• Obstruction of the paraurethral gland ducts can
result in cyst formation, and chronic infection BLOOD SUPPLY
of the paraurethral glands can lead to urethral
diverticula. Pelvis
The pelvic organs are supplied by the visceral
The urethra receives its blood supply from branches of branches of the internal iliac (hypogastric) artery
the vesical and internal pudendal arteries. The puden- and by direct branches from the abdominal aorta
dal nerve innervates the most distal part of the stri- (Figure 2-18). The internal iliac artery generally
ated urogenital sphincter complex. Somatic efferent divides into an anterior and posterior division in the
branches of the pelvic nerve, a component of the infe- area of the greater sciatic foramen. Each division has
rior hypogastric (pelvic plexus) variably innervate the three parietal branches that supply nonvisceral struc-
sphincter urethra. tures such as striated muscles. The iliolumbar, lateral
sacral, and superior gluteal arteries are the three pari-
Ureters etal branches of the posterior division (Figure 2-18).
The obturator, internal pudendal, and inferior gluteal
A detailed description of the pelvic ureter appears
under the pelvic sidewall retroperitoneal space section
on pages 27–28.
External iliac a. & v.

RECTUM r ta
Ao
A
The rectum is continuous with the sigmoid colon RCI
approximately at the level of the third sacral verte-
bra (S3) and it functions as a temporary storage site
LCIV

for feces. It descends on the anterior surface of the


sacrum for about 12 cm and ends in the anal canal Iliolumbar
after passing through the levator hiatus. The anterior
and lateral portions of the proximal two-thirds of the Lateral sacral
rectum are covered by peritoneum. The peritoneum is Superior gluteal
then reflected onto the posterior vaginal wall forming
the posterior cul-de-sac of Douglas, also termed the rec- Posterior division of internal iliac a.
touterine pouch. In women, the posterior cul-de-sac is FIGURE 2-18 Hypogastric (internal iliac) artery. Posterior
located approximately 5 to 6 cm from the anal orifice division branches: iliolumbar, lateral sacral and superior
and can be palpated manually during rectal or vaginal gluteal arteries. LCIV, left common iliac vein; RCIA, right
examination. In its proximal portion, the rectal wall is common iliac artery.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 35

arteries are parietal branches that most commonly Clinical Correlations


arise from the anterior division (Figure 2-19). The
• Although great variation exists in the branching
remaining branches of the anterior division supply
pattern of the anterior division, the umbilical and
the pelvic viscera (bladder, uterus, vagina, and rec-
obturator arteries are commonly the first branches
tum) and accordingly are termed visceral branches.
of the anterior division and the internal pudendal
These include the uterine, vaginal, middle rectal, and
and inferior gluteal arteries are commonly the dis-
the superior vesical arteries. Several superior vesical
tal, or terminal branches, of the anterior division.
arteries generally arise from the patent part of the
• During internal iliac (hypogastric) artery ligation,
umbilical arteries. The distal and obliterated portions
efforts should be made to ligate the internal iliac
of the umbilical arteries course toward the ante-
distal to the posterior division branches to preserve
rior abdominal wall and form the medial umbilical
collateral blood supply.
ligaments. The inferior vesical artery, when present,
often arises from either the internal pudendal or the
The two most important branches of the aorta that
vaginal arteries (Figure 2-19).
contribute to the blood supply of the pelvic organs are

Aorta

CHAPTER 2
Iliolumbar
artery

Ureter
Superior
gluteal
artery Internal iliac
artery
Lateral
sacral External iliac
artery artery

Middle Inferior
rectal gluteal
artery artery

Rectum Deep
circumflex
iliac artery
Ovarian
ligament Internal
fallopian tube, pudendal
and round artery
ligament
(cut) Inferior
epigastric
artery
Uterus
Superior
vesical
Ascending artery
branch
of uterine Obliterated
artery umbilical
artery
Bladder Obturator
artery
Vaginal
artery
Uterine
FIGURE 2-19 Blood supply to the pelvis. artery
36 Section I Fundamental Topics

r us
Ute
Right ureter attached to
Uterine a. medial leaf of peritoneum
Umbilical a.
vix
Cer
External iliac a.

Ovarian vessels

Internal
iliac a.

m.
Psoas
L5

FIGURE 2-20 Right pelvic sidewall.


CHAPTER 2

the ovarian and superior rectal arteries (Figure 2-20). before it exits the pelvis; these vessels are called acces-
The ovarian arteries, which arise directly from the aorta sory pudendal or accessory perineal arteries.
just inferior to the renal vessels, anastomose with the
ascending branch of the uterine artery. These anasto- Key Point
moses contribute to the blood supply of the uterus and
adnexa. The superior rectal artery, which is the terminal • The blood supply to the pelvic viscera arises primar-
branch of the inferior mesenteric artery, courses pos- ily from the internal iliac arteries. Direct branches
terior to the rectum, and splits into two branches that of the aorta, such as the ovarian and superior rec-
anastomose with the middle rectal arteries on each tal, also contribute. Extensive collateral circulation
side of the rectum. The superior rectal artery thus con- between the aorta and iliac vessels exists.
tributes to the blood supply to the rectum and vagina.
Other important anastomoses between the aorta
and internal iliac arteries include those of the middle
sacral artery with the lateral sacral arteries and lum- Clinical Correlation
bar arteries with the iliolumbar arteries. These anas-
• Accessory pudendal and perineal arteries usually
tomosis contribute to the collateral blood supply to
reach the perineum by coursing through the retro-
the pelvis.
pubic space making them vulnerable to injury dur-
ing midurethral sling procedures. Injury to these
Perineum accessory vessels may account for the more severe
hemorrhage infrequently encountered during these
The external pudendal artery is a branch of the femoral procedures.
artery and supplies the skin and subcutaneous tissue
of the mons pubis. The internal pudendal artery is one
of the terminal branches of the internal iliac artery. It
has a long course from its origin and the association of
NEUROANATOMY
this vessel to other structures has clinical importance.
It exits the pelvis through the greater sciatic foramen
Visceral Innervation
below the piriformis muscle, passes behind the ischial Nerve supply to the visceral structures in the pelvis
spines, and reenters the perineum through the lesser sci- arises from the autonomic nervous system. The two
atic foramen. It has a variable course, usually 2 to 3 cm, most important components of this system in the pel-
through the pudendal or Alcock canal, and then divides vis include the superior and inferior hypogastric plexuses.
into terminal branches (Figure 2-9). These are the infe- The superior hypogastric plexus, also known as the pre-
rior rectal, perineal, and clitoral arteries. Branches to sacral nerve, is an extension of the aortic plexus found
the perineum sometimes arise from the pudendal artery below the aortic bifurcation. This plexus primarily
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 37

contains sympathetic fibers and sensory afferent fibers pudendal nerve is a branch of the sacral plexus and is
from the uterus. formed by the anterior rami of the second through the
fourth sacral nerves (S2–S4). It has a course and dis-
Clinical Correlation tribution similar to the internal pudendal artery.

• The sensory afferent fibers contained within the


Clinical Correlations
superior hypogastric plexus are targeted in presa-
cral neurectomy, a surgical procedure performed to • The clitoral and perineal branches of the pudendal
treat dysmenorrhea and central pelvic pain refrac- nerve should be at low risk for direct nerve injury
tory to medical management. during midurethral slings and similar procedures as
they course distal to the ventral portion of the peri-
The superior hypogastric plexus terminates by divid- neal membrane.
ing into the right and left hypogastric nerves. These • The inferior rectal nerve might be at risk for injury
nerves join parasympathetic efferents from the second during procedures that involve passage of needles
through the fourth sacral nerve roots (pelvic splachnic through the ischioanal fossa.
nerves or nervi erigentes) to form the inferior hypogas-
tric or pelvic plexus. The ilioinguinal and iliohypogastric nerves mainly
Fibers of the inferior hypogastric plexus accompany originate from the anterior rami of the first lumbar
the branches of the internal iliac artery to the pelvic vis- nerve (L1) with varying contributions from the 12th

CHAPTER 2
cera and are divided into three portions that are named thoracic (T12) nerve. Branches of these nerves also
according to the vessels they accompany. These are the contribute to the sensory innervation of the vulva. The
vesical, uterovaginal (Frankenhäuser ganglion), and iliohypogastric nerve provides sensation to the skin
middle rectal plexuses. The uterovaginal plexus com- over the suprapubic area, and the ilioinguinal nerve
municates with the ovarian plexus, an extension of supplies the skin of the lower abdominal wall and
the renal plexus, within the infundibulopelvic ligament. upper portion of the labia majora and medial portion
Clitoral erection requires parasympathetic visceral effer- of the thigh through its inguinal branch (Figure 2-21).
ents. Parasympathetic extensions of the inferior hypo- These two nerves pierce the internal oblique muscles
gastric plexus reach the perineum along the vagina and 2 to 3 cm medial and 2 to 3 cm inferior to the anterior
urethra to innervate the clitoris and vestibular bulbs. superior iliac spine.11,12
Sympathetic fibers reach the perineum with the puden-
dal nerve. Clinical Correlations
• The ilioinguinal and iliohypogastric nerves can
Key Point be entrapped during closure of low transverse inci-
sions, especially if incisions extend beyond the lat-
• The pelvic viscera are innervated by the autonomic eral borders of the rectus muscle. They may also be
nervous system via the superior (sympathetic) and injured by placement of lower abdominal accessory
the inferior hypogastric (parasympathetic) plexuses. trocars. Some women may present days to months
after surgery with sharp incisional pain or burning
sensation that radiates to the inguinal region.
• The risk of iliohypogastric and ilioinguinal nerve
Clinical Correlation
injury should be minimized when lateral trocars are
• Injury to the branches of the inferior hypogastric placed superior to the anterior superior iliac spines
plexus during cancer debulking or other exten- and low transverse fascial incisions are not extended
sive pelvic surgeries can lead to varying degrees of beyond the lateral borders of the rectus muscle.12
voiding, sexual, and defecatory dysfunction. These
organ dysfunctions have led to the development of
nerve-sparing radical cancer surgery. VAGINAL ANATOMY
AND SUPPORT
Somatic Innervation
Key Point
Perineum
The perineal nerve, dorsal nerve of the clitoris, and infe- • The interaction between the pelvic floor muscles
rior anal nerve are the terminal branches of the puden- and connective tissue is essential for normal pelvic
dal nerve that provide the majority of the sensory organ orientation and support.
and motor innervation to the perineal structures. The
38 Section I Fundamental Topics

Subcostal
nerve (T12)

Illiohypogastric
nerve (L1)

Illioinguinal
nerve (L1) Obturator
nerve (L2-L4)
Psoas
muscle

Lateral femoral Inguinal


cutaneous ligament
nerve (L2-3)

Femoral branch
of genitofemoral
nerve (L1-2) Femoral
nerve (L2-L4)
CHAPTER 2

Genital branch
of genitofemoral
nerve (L1-2)
Lumbosacral
Femoral nerve, plexus (L1-S4)
artery, and vein
in femoral
triangle

Sartorius
muscle

Adductor
longus
muscle

FIGURE 2-21 Nerves of the pelvic floor.

The etiology of pelvic floor prolapse is complex and mul- prevent constant or excessive strain on the pelvic “liga-
tifactorial. It likely includes a combination of acquired ments” and “fascia.” The normal resting contraction
dysfunction of pelvic floor muscles and/or connective of the levators is maintained by the action of type I
tissue as well as genetic predisposition. However, the (slow twitch) fibers, which predominate in this mus-
interaction between the pelvic floor muscles and con- cle.15 This baseline activity of the levators keeps the
nective tissue is essential for normal pelvic organ orien- urogenital hiatus closed and draws the distal parts
tation and support. The information presented in this of the urethra, vagina, and rectum toward the pubic
chapter is based on a current review of the literature.13 bones. Type II (fast twitch) muscle fibers allow for
reflex muscle contraction elicited by sudden increases
in abdominal pressure. The levators can also be volun-
LEVATOR ANI MUSCLE SUPPORT tarily contracted as with Kegel exercises. Relaxation of
the levators occurs only briefly and intermittently dur-
The levator ani muscles are the most important mus- ing the processes of evacuation (voiding, defecation)
cles in the pelvic floor and represent a critical compo- and parturition.
nent of pelvic organ support (Figure 2-22). The normal The levator ani muscle is a complex unit, which
levators maintain a constant state of contraction, thus consists of several muscle components with different
providing an active floor that supports the weight of origins and insertions and, therefore, different func-
the abdominopelvic contents against the forces of tions. Knowing the precise attachments, function, and
intra-abdominal pressure.14 This action is thought to innervation of each of the levator ani component allows
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 39

Pubcoccygeus
muscle
Cooper’s
ligament Urethra
or ileopectineal
ligament Arcus
tendineus
Obturator fascia pelvis
internus
muscle and Vagina
fascia

Arcus Rectum
tendineus
levator ani Levator
plate
Iliococcygeus
muscle Coccyx

Coccygeus
muscle

CHAPTER 2
Piriformis
muscle
FIGURE 2-22 View of levator ani muscles from above.

better understanding of the various clinical manifesta- The puborectalis muscle represents the most medial
tions that may result from specific injuries (ie, anterior fibers of the levator ani muscle and is considered part
vaginal wall prolapse and stress urinary incontinence of the anal sphincter complex as described above.
with injury to the pubovaginal muscle). The iliococcygeus, the most posterior and thinnest
The pubococcygeus, puborectalis, and iliococcy- part of the levators, has a primarily supportive role.
geus are the three components of the muscle recog- It arises laterally from the arcus tendenius levator ani
nized in Terminologia Anatomica. The pubococcygeus and the ischial spines, and muscle fibers from one side
is further divided into the pubovaginalis, puboanalis, join those from the opposite side at the iliococcygeal
and puboperineal muscles according to fiber attach- (anococcygeal) raphé and the coccyx.
ments. Due to the significant attachments of the pubo-
coccygeus to the walls of the pelvic viscera, the term
pubovisceral muscle is frequently used to describe this
Levator Plate
portion of the levator ani muscle.16,17 In an MRI study The levator plate is the clinical term used to describe
of 80 nulliparous women with normal pelvic support, the region between the anus and the coccyx formed
the subdivisions of the levator ani muscles were clearly primarily by the insertion of the iliococcygeus mus-
visible on magnetic resonance scans.18 cles (iliococcygeal raphé). This portion of the levator
The anterior ends of the pubococcygeus or pubovis- ani muscle complex forms a supportive shelf upon
ceral muscle arise on either side from the inner surface which the rectum, the upper vagina, and the uterus
of the pubic bone. The pubovaginalis refers to the medial rest away from the urogenital hiatus. A consequence of
fibers that attach to the lateral walls of the vagina. Berglas and Rubin 1953 landmark radiographic levator
Although there are no direct attachments of the levator myography study has been the prevailing theory that
ani muscles to the urethra in females, those fibers of in women with normal support, the levator plate lies
the muscle that attach to the vagina are responsible for almost parallel to the horizontal plane in the standing
elevating the urethra during a pelvic muscle contrac- position.20 A recent supine dynamic MRI study showed
tion and hence may contribute to urinary continence.19 that the levator plate in women with normal support
The puboperinealis refers to the fibers that attach to the has a mean angle of 44.3° relative to a horizontal refer-
perineal body and draw this structure toward the pubic ence line.21
symphysis. The puboanalis refers to the fibers that attach
to the anus at the intersphincteric groove between
the internal and external anal sphincter. These fibers Levator Ani Muscle Injury
elevate the anus and along with the rest of the pubo- Another existing theory suggests that neuromuscular
coccygeus, and puborectalis fibers keep the urogenital injury to the levators may lead to eventual sagging or
hiatus closed. vertical inclination of the levator plate and lengthening
40 Section I Fundamental Topics

Uterus
Uterosacral
ligament

Bladder Coccyx
CHAPTER 2

Levator
Pubovaginalis plate
muscle

Puboperinealis Rectum
muscle
Puboanalis
muscle

FIGURE 2-23 Sagital view of pelvis. The insertions of the pubovisceralis and levator plate are visualized.

of the urogenital hiatus (Figure 2-23).22 Consequently, portion as all muscle components are interrelated and
the vaginal axis becomes more vertical and the cervix is form part of the same complex unit. Further studies
oriented over the opened hiatus. The mechanical effect are needed that correlate anatomic location of the inju-
of this change is to increase strain on the connective tis- ries with clinical manifestations later in life.
sue “ligaments” and “fasciae” that supports the pelvic Recent data obtained from 2D and 3D computer
viscera. This concept does not preclude primary con- models of cystocele formation support clinical find-
nective tissue damage as a potential cause of prolapse, ings that levator ani muscle impairment and connec-
but explains how injury to the pelvic floor muscles tive tissue impairment play a critical role in cystocele
can eventually lead to disruption of the connective tis- formation.23,24
sue component of support. However, whether vertical
inclination of the levator plate or widening or lengthen-
ing of the urogenital hiatus occurs first is not known.
Levator Ani Muscle Innervation
A recent MRI study showed that 20% of primiparous Traditionally, a dual innervation of the levators has
women had defects in the levator ani muscles whereas been described where the pelvic or superior surface
no defects were identified in nulliparous women. of the muscles is supplied by direct efferents from the
Importantly, the majority of defects (18%) were iden- second through the fifth sacral nerves, and the peri-
tified in the pubovisceral portion of the levators; only neal or inferior surface is supplied by pudendal nerve
2% involved the iliococcygeal portion of the muscle, branches. Recent literature suggests the pudendal
which is the portion of the muscle that forms the leva- nerve does not contribute to levator muscle innerva-
tor plate. It is possible that birth-related neuromus- tion.25,26 The pudendal nerve does, however, innervate
cular injury to the pubovisceral portion of the muscle parts of the striated urethral sphincter and external
eventually leads to alterations of the iliococcygeal anal sphincter through separate branches. Different
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 41

innervation of the levators and the striated urethral anatomically and histologically from parietal fascia,
and anal sphincters may explain why some women the connective tissue that invests the striated mus-
develop pelvic organ prolapse and others develop uri- cles of the body as described earlier. Histologically,
nary or fecal incontinence. visceral fascia consists of loose arrangements of col-
lagen, elastin, and adipose tissue, whereas parietal
Other Pelvic Floor Structures fascia is characterized by organized arrangements of
collagen. Although parietal fascia provides attach-
The muscles that span the pelvic floor are collectively
ment of muscles to bones, visceral fascia allows for
known as the pelvic diaphragm. This diaphragm con-
expansion and contraction of the pelvic organs and
sists of the levator ani and coccygeus muscles along with
encases blood vessels, lymphatics, and nerves. This
their superior and inferior investing layers of fasciae.
tissue is intimately associated with the walls of the
Inferior to the pelvic diaphragm, the perineal membrane
viscera and cannot be dissected in the same fashion
and perineal body also contribute to the pelvic floor.
that parietal fascia (ie, rectus fascia) can be separated
from the corresponding skeletal muscle. Therefore,
PELVIC CONNECTIVE TISSUE designation of this tissue as fascia has led to signifi-
cant confusion and inconsistencies while describing
Visceral (Endopelvic) Fascia pelvic anatomy and procedural steps.
The questionable existence of a separate layer of vag-
inal fascia and the role of this tissue in supporting the
Anterior Vaginal Wall

CHAPTER 2
urethra and bladder anteriorly and the rectum poste- The terms pubocervical fascia and paravesical fascia
riorly has been another area where controversy has are commonly used to describe the layers that support
persisted for over a century. The subperitoneal peri- the bladder and urethra and the tissue that is used for
vascular connective tissue and loose areolar tissue that reconstructive pelvic surgeries. However, histologic
exist throughout the pelvis and connects the pelvic examination of the anterior vaginal wall has failed
viscera to the pelvic walls is known as endopelvic (vis- to demonstrate a separate layer of fascia between the
ceral) fascia. This visceral “fascia,” however, differs vagina and the bladder (Figure 2-24).27 The anterior

Rectum

Sacrum

Uterus

Bladder

Arcus
tendineus
levator ani
Uterosacral
Levator ani ligament
muscle
Ischial
Arcus spine
tendineus
fascia pelvis
Cardinal
ligament
Visceral
connective tissue
“endopelvic fascia”

Anterior vaginal Paracolpium


wall adventitia

Anus
FIGURE 2-24 Visceral connective tissue.
42 Section I Fundamental Topics

vaginal wall has been shown to consist of three layers: layer between the vagina and the bladder, it has been
a mucosal layer consisting of nonkeratinized squamous appropriately recommended that when describing the
epithelium overlying a lamina propia; a muscular layer anterior vaginal wall tissue and support, terms such as
consisting of smooth muscle, collagen, and elastin; and “pubocervical fascia” or “paravesical fascia” be aban-
an adventitial layer consisting of collagen and elastin. doned, and replaced by more accurate descriptive
The vagina is separated from the bladder anteriorly terms such as vaginal muscularis or fibromuscular wall.
by the vaginal adventitia (Figure 2-25). The tissue that
attaches the lateral walls of the vagina to the arcus
tendineus fascia pelvis (ATFP) is a condensation of
Posterior Vaginal Wall
connective tissue that contains blood vessels, lymphat- Another topic of ongoing controversy is the debat-
ics, and nerves. This paravaginal tissue attaches to the able presence of one or two separate fascial layer(s)
vaginal wall muscularis and adventitia on each side of between the vagina and the rectum.28,29 These layers
the vagina and is responsible for the appearance of the are often indiscriminately referred to as the rectovagi-
anterior vaginal sulci, especially in the distal half of nal septum (RVS) or rectovaginal fascia (RVF). The
the vagina. The vagina and bladder are not invested RVS is similar to the rectovesical septum originally
in their own separate layer of connective tissue cap- described by Denonvilliers and it is believed to be a
sule. Based on the histologic absence of a true “fascial” peritoneal remnant. It is described as extending for
CHAPTER 2

I
II
III

Uterosacral
ligament

Ischial spine and


sacrospinous
ligament Cardinal
ligament

Lev
el I

Lev
el I
Levator ani I

Arcus tendineus Lev


fascia pelvis el I
II

Arcus
tendineus
fascia pelvis
FIGURE 2-25 Pubocervical and rectovaginal fascia.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 43

Bladder

Cervix

Vesicocervical Obturator
ligament/bladder internus muscle
pillar

Uterine artery
Cardinal ligament

Sacrospinous ligament Ureter

Uterosacral Rectum
ligament/rectal pillar

CHAPTER 2
FIGURE 2-26 Cardinal and uterosacral ligaments.

2 to 3 cm proximal to the perineal body and being ligaments (Figure 2-26). These “ligaments” are con-
absent superior to the level of the rectovaginal pouch. densations of visceral connective tissue that have
However, many have failed to demonstrate a separate assumed special supportive roles. The cardinal (trans-
layer of fascia between the vagina and the rectum on verse cervical or Mackenrodt) ligaments consist primar-
histologic examination of this region.30 On histologic ily of perivascular connective tissue. They attach to
examination of the posterior vaginal wall, DeLancey the posterolateral pelvic walls near the origin of the
showed that the paravaginal connective tissue that internal iliac artery and surround the vessels supply-
attaches the posterior vaginal wall to the pelvic walls ing the uterus and vagina.33 The uterosacral ligaments
attaches primarily to the lateral wall of the posterior attach to a broad area of the sacrum posteriorly and
vagina on either side; only few connective tissue fibers form the lateral boundaries of the posterior cul-de-sac
were found to cross the midline between the posterior of Douglas. They consist primarily of smooth muscle
vaginal wall and rectum.6 Thus, similar to the ante- and contain some of the pelvic autonomic nerves.34
rior vaginal wall the tissue labeled as “fascia,” and the The parametria continues down the vagina as the
plane dissected surgically includes portions of the vag- paracolpium. This tissue attaches the upper part of
inal muscularis. the vagina to the pelvic wall, suspending it over the
The lateral attachments of the posterior vaginal pelvic floor. These attachments are also known as
walls are to the pelvic sidewalls at another condensa- level I support or the suspensory axis and provide the
tion of connective tissue called the ascus tendineus connective tissue support to the vaginal apex after a
fascia rectovaginalis (Figure 2-25).31 The apex of the hysterectomy.
posterior wall is attached to the uterosacral ligaments,
which extend down to the level of the cul-de-sac peri-
toneum, and the inferior wall has direct connections to Clinical Correlations
the perineal body and the levator ani muscles. • Clinical manifestations of parametrial and level I
Although the visceral connective tissue in the pel- support defects include cervical and posthysterec-
vis is continuous and interdependent, three levels of tomy apical prolapse, respectively.
vaginal connective tissue support have been described • Recent data describe the clinical correlation
that help understand various clinical manifestations of between anterior and apical compartment support
pelvic support dysfunction (Figure 2-25).32 and the important contribution of apical support to
development and size of cystoceles.35,36
Cervical and Upper Vaginal Support
The connective tissue that attaches lateral to the
Mid-Vaginal Support
uterus is called the parametria and consists of what The lateral walls of the mid-to-lower portions of the
is clinically known as the cardinal and uterosacral vagina are attached to the pelvic walls on each side by
44 Section I Fundamental Topics

A B C

FIGURE 2-27 Manifestations of Level I (apical) and Level II (anterior wall) support defects. A. Apical prolapse.
CHAPTER 2

B. Anterior prolapse with paravaginal defect. C. Combined anterior and apical prolapse.

visceral connective tissue. These lateral attachments attachments are referred to as level II support or the
of the anterior vaginal wall are to the arcus tendineus attachment axis.32
fascia pelvis and to the medial aspect of the levator
ani muscles (Figure 2-7). Attachment of the ante-
Clinical Correlation
rior vaginal wall to the levators is responsible for the
bladder neck elevation noted with cough or Valsalva. • Clinical manifestations of level II support defects
Therefore, these attachments may have significance include anterior vaginal wall prolapse and stress
for stress urinary continence.37 The midvaginal urinary incontinence (Figures 2-27 and 2-28).

A B

FIGURE 2-28 Manifestations of Level II support defects. A. Anterior prolapse. B. Anterior prolapse with urethral hyper-
mobility and objective stress urinary incontinence.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 45

CHAPTER 2
A B

FIGURE 2-29 Manifestations of Level III support defects. A. Distal defect of the rectovaginal septum to the perineal
body. B. Distal urethrocele.

Distal Vaginal Support the uterine or internal iliac arteries in the setting of
hemorrhage.
The distal third of the vagina is directly attached to
its surrounding structures. Anteriorly, the vagina
Pelvic Ureter
is fused with the urethra, laterally it attaches to the
pubovaginalis muscle and perineal membrane, and The ureter enters the pelvis by crossing over the bifur-
posteriorly to the perineal body (Figure 2-29). These cation of the common iliac artery just medial to the
vaginal attachments are referred to as level III support ovarian vessels (Figures 2-17 and 2-20). It descends
or fusion axis,32 and they are considered the strongest into the pelvis attached to the medial leaf of the pelvic
of the vaginal support components. sidewall peritoneum. Along this course, the ureter lays
medial to the internal iliac branches and anterolat-
eral to the uterosacral ligaments. The ureter then tra-
Clinical Correlations
verses the cardinal ligament approximately 1 to 2 cm
• Failure of this level of support can result in distal lateral to the cervix. Near the level of the uterine isth-
rectoceles or perineal descent. mus it courses below the uterine artery (“water under
• Anal incontinence may also result if the peri- the bridge”). It then travels anteromedially toward
neal body is absent from obstetrical trauma the base of the bladder, and in this path, it is in close
(Figure 2-29). proximity to the upper third of the anterior vaginal
wall. Finally, the ureter enters the bladder and travels
obliquely for approximately 1.5 cm before opening at
SURGICAL SPACES WITH the ureteral orifices. The pelvic ureter receives blood
CLINICAL CORRELATIONS supply from the vessels it passes: the common iliac,
internal iliac, uterine, and vesicles. Vascular anastomo-
Pelvic Sidewall ses on the connective tissue sheath enveloping the ure-
ter form a longitudinal network of vessels.
The retroperitoneal space of the pelvic sidewalls con-
tains the internal iliac vessels and pelvic lymphatics,
Clinical Correlation
pelvic ureter, and the obturator nerve (see retropu-
bic space below). Entering this space is especially • The majority of ureteral injuries occur during gyne-
useful for identifying the ureter and for ligation of cologic surgery for benign disease. Over 50% of
46 Section I Fundamental Topics

these injuries are not diagnosed intraoperatively. In A


a study that used universal cystoscopy, the rate of IVC
ureteral injury during benign gynecologic proce-
dures was reported to be 1.7%.38 In the same study,

IA
RC
a 7.3% ureteral injury rate was reported in patients

s m.

LC
undergoing concomitant procedures for urinary

IV
incontinence or pelvic organ prolapse.

Psoa
L5
• The most common sites of ureteral injury include Sacral
the pelvic brim area while clamping the infundib- sympathetic
ulopelvic ligament, the isthmic region while ligat- chain
S1
ing the uterine vessels, and the vaginal apex while

IIA
EI
clamping or suturing the vaginal cuff. In a recent
study that evaluated urinary tract injury during hys-
terectomy based on universal cystoscopy, the ure-
teral injury rate was 1.8%; the most common site of RS
ureteral injury in this study was at the level of the
uterine artery.39

Uterus
In pelvic reconstructive procedures, the ureter is
CHAPTER 2

especially vulnerable at the pelvic sidewall during


placement of the uterosacral ligament suspension
(USLS) sutures. Ureteral injury rates of up to 11%
FIGURE 2-30 Presacral space. A, aorta; EIA, external
have been reported during USLS.40 The ureter can iliac artery; IIA, internal iliac artery; IVC, inferior vena cava;
also be injured during plication of the anterior vaginal LCIV, left common iliac vein; L5, lumbar fifth vertebra;
wall or placement of the apical sutures in a paravagi- RCIA, right common iliac artery; RS, rectosigmoid colon;
nal defect repair. A 2% rate of ureteral injury during S1, first sacral vertebra.
anterior colporrhaphy has been reported.41 A ureteral
obstruction rate of 5.1% was recently reported during
vaginal surgery for anterior and/or apical pelvic organ from the basivertebral veins that pass through the pel-
prolapse.42 Because of the pelvic ureter’s proximity to vic sacral foramina. The median sacral artery, which
many structures encountered during gynecologic sur- courses in proximity to the median sacral vein, arises
gery, emphasis should be placed on its precise intra- from the posterior and distal part of the abdominal
operative identification. Several cadaver dissection aorta. In a study that looked at the vascular anatomy
studies have recently described the relationship of the of the presacral space in unembalmed female cadav-
ureter to the uterosacral ligaments and upper third of ers, the left common iliac vein was the closest major
the vagina.43-45 vessel identified both cephalad and lateral to the mid-
sacral promontory.46 The average distance of the left
Presacral Space common iliac vein to the midsacral promontory in this
study was 2.7 cm (range 0.9–5.2 cm).
The presacral space is a retroperitoneal space located
between the sacrum posteriorly and the rectosigmoid
and posterior abdominal wall peritoneum anteriorly Key Point
(Figure 2-30). It begins below the aortic bifurcation
and extends inferiorly to the pelvic floor. The internal • The pelvic surgical spaces are extraperitoneal
iliac vessels and branches and the ureters constitute spaces and include the pelvic sidewall, retropubic,
the lateral boundaries of this space. Contained within presacral, vesicovaginal, rectovaginal, and para-
the loose connective tissue in this space are the supe- rectal spaces. Knowledge of the boundaries and
rior hypogastric plexus, hypogastric nerves, and por- contents of these spaces is essential to avoid and
tions of the inferior hypogastric plexus (Figure 2-31A manage complications.
and B). The vascular anatomy of the presacral space
is complex and includes an extensive and intricate
venous plexus (sacral venous plexus) formed pri-
Clinical Correlation
marily by the anastomoses of the middle and lateral
sacral veins on the anterior surface of the sacrum. The • The presacral space is most commonly entered to
sacral venous plexus also receives contributions from perform abdominal sacral colpopexies and presacral
the lumbar veins of the posterior abdominal wall and neurectomies. The proximity of the left common
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 47

iliac vein to the sacral promontory makes this vessel


especially vulnerable to injury during entrance and

Aorta
dissection in this space. Additionally, bleeding from

IVC
the sacral venous plexus may be difficult to control
IMA as the veins often retract into the sacral foramina.
Therefore, careful dissection and knowledge of the
presacral space vascular anatomy is essential to pre-
IA vent or minimize potentially life-threatening vascu-
RC

lar complications.

LC
IV Retropubic Space
This space is also called the prevesical space or space
RHN of Retzius. It can be entered by perforating the trans-
versalis fascial layer of the anterior abdominal wall
(Figure 2-32). This space is bounded by the bony pel-
vis and muscles of the pelvic wall anteriorly and lat-
erally and by the anterior abdominal wall superiorly.
The bladder and proximal urethra lie posterior to this

CHAPTER 2
A space. Attachments of the paravaginal connective tis-
sue to the arcus tendineus fascia pelvis constitute the
posterolateral limit of the space and separate it from
the vesicovaginal and vesicocervical spaces. There
L5
are a number of vessels and nerves in this space. The
dorsal vein of the clitoris passes under the lower bor-
IV

der of the pubic symphysis and drains into the vesi-


RC

L5-S1 disc cal venous plexus, also termed the plexus of Santorini
(Figures 2-33 and 2-34). The obturator neurovascular
bundle courses along the lateral pelvic walls and enters
the obturator canal to reach the medial compartment
of the thigh. Additionally, in most women, accessory
SVP obturator vessels that arise from the inferior epigastric
or external iliac vessels are found crossing the superior
pubic rami and connecting with the obturator vessels
near the obturator canal.47

Clinical Correlations
• Injury to the obturator neurovascular bundle or
accessory obturator vessels is most often associ-
C ated with pelvic lymph node dissections and para-
vaginal defect repair procedures. Thus, knowledge
of the approximate location of these vessels and of
the obturator canal is critical when this space is dis-
sected. The obturator canal is found approximately
5 to 6 cm from the midline of the pubic symphysis
and 1 to 2 cm below the upper margin of the ilio-
B
pectineal (Cooper’s) ligament.47
FIGURE 2-31 Superior hypogastric plexus is shown • Bleeding from the vesical venous plexus is often
by the asterisk (*). IVC, inferior vena cava; IMA, infe- encountered while placing the sutures or passing
rior mesenteric artery; LCIV, left common iliac vein; the needles into this space during retropubic blad-
RCIA, right common iliac artery; RHN, right hypogastric der neck suspensions and midurethral retropubic
nerve; SVP, sacral venous plexus. procedures, respectively. This venous bleeding usu-
ally stops when pressure is applied or the sutures
are tied.
48 Section I Fundamental Topics

Prevesical/retropubic
space
Bladder
Vesicovaginal space

Paravesical space Cervix

Pararectal space
Rectovaginal space
CHAPTER 2

Presacral (retrorectal) space


FIGURE 2-32 Pelvic floor space including retropubic space, paravesical space, prevesical/retropubic space, vesico-
vaginal space, pararectal space, rectovaginal space.

With the advent of midurethral slings, anti-incon- iliac veins. The internal iliac vein was formed cepha-
tinence procedures once requiring entry and direct lad to the level of the ischial spine; the closest dis-
visualization of the retropubic space have declined. As tance between these structures was 3.8 (1.6–6.2) cm.
a result, pelvic surgeons are growing increasingly less The retropubic space is a richly vascular space with
familiar with the 3D anatomic relationships within considerable anatomic variation. A thorough under-
this space. In a recent cadaver study that evaluated standing of the relationship of bony landmarks to
the anatomic relationships of clinically relevant struc- neurovascular structures within this space becomes
tures in the retropubic space, the obturator vein was increasingly important as the popularity and wide-
the closest of the obturator neurovascular structures spread use of procedures that rely on blind placement
to the ischial spine, a median distance of 3.4 cm.48 of trocars increases.
The vesical venous plexus included two to five rows
of veins that coursed within the paravaginal tissue
parallel to the bladder and drained into the internal
Accessory obturator v.
Dorsal v. Obturator v.
of clitoris
PS
Ex

PS
ter
na
l ili

Obturator n.
ac
v.

Paravesical
venous plexus Bl
ad
(plexus of de
r
Santorini)
Obturator n.
Bladder
Internal
iliac v. Paravesical venous plexus

FIGURE 2-34 Retropubic space. Venous structure dyed


blue including the plexus of Santorini, accessory obturator
FIGURE 2-33 Retropubic space. Plexus of Santorini. vein, and dorsal vein of the clitoris.
Chapter 2 Normal Anatomy of the Pelvis and Pelvic Floor 49

A thorough understanding of pelvic anatomy and 19. DeLancey JOL, Starr RA. Histology of the connection between
anatomic relationships is essential for safe execution of the vagina and levator ani muscles: implications for the uri-
nary function. J Reprod Med. 1990;35:765–771.
gynecologic procedures and effective management of 20. Berglas B, Rubin IC. The study of the supportive structures of
complications. Efforts to clarify and standardize ter- the uterus by levator myography. Surg Gynecol Obstet. 1953;97:
minology as well as techniques to analyze the inter- 677–692.
active role of the supporting structures in their 3D 21. Hsu Y, Summers A, Hussain HK, Guire KE, DeLancey JOL.
environment should continue. Levator plate angle in women with pelvic organ prolapse com-
pared to women with normal support using dynamic MR imag-
ing. Am J Obstet Gynecol. 2006;194:1427–1433.
22. Smith ARB, Hosker GL, Warrel DW. The role of partial dener-
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Anatomic relationships of the pudendal nerve branches. Am J 23. Chen L, Ashton-Miller JA, Hsu Y, DeLancey JO. Interaction
Obstet Gynecol. 2011;205(5):504.e1–504.e5. among apical support, levator ani impairment, and anterior
2. Oelrich TM. The striated urogenital sphincter muscle in the vaginal wall prolapse. Obstet Gynecol. 2006;108:324–332.
female. Anat Rec. 1983;205:223–232. 24. Chen L, Ashton-Miller JA, Delancey JOL. A 3D finite element
3. Federative Committee on Anatomical Terminology. Terminolo- model of anterior vaginal wall support to evaluate mecha-
gia Anatomica. New York: Thieme Stuttgart; 1998. nisms underlying cystocele formation. J Biomech. 2009;42:
4. Stein TA, DeLancey JO. Structure of the perineal membrane 1371–1377.
in females: gross and microscopic anatomy. Obstet Gynecol. 25. Barber MD, Bremer RE,Thor KB, et al. Innervation of the female
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5. Brandon CJ, Lewicky-Gaupp C, Larson KA, et al. Anatomy 26. Pierce LM, Reyes M, Thor KB, et al. Innervation of the levator
of the perineal membrane as seen in magnetic resonance ani muscles in the female squirrel monkey. Am J Obstet Gynecol.
images of nulliparous women. Am J Obstet Gynecol. 2009;200: 2003;188:1141–1147.
583.e1–583.e6. 27. Weber AM, Walter MD. What is vaginal fascia? AUGS Quart
6. DeLancey JOL. Structural anatomy of the posterior pelvic Rep. 1995;13.
compartment as it relates to rectocele. Am J Obstet Gynecol. 28. Richardson AC. The rectovaginal septum revisited: its relation-
1999;180:815–823. ship to rectocele and its importance in rectocele repair. Clin
7. Hsu Y, Lewicky-Gaupp C, DeLancey JO. Posterior compart- Obstet Gynecol. 1993;36:976–983.
ment anatomy as seen in magnetic resonance imaging and 29. Kuhn RJP, Hollyock VE. Observations of the anatomy of the
3-dimensional reconstruction from asymptomatic nulliparas. rectovaginal pouch and rectovaginal septum. Obstet Gynecol.
Am J Obstet Gynecol. 2008;198:651.e1–651.e7. 1982;59:445.
8. Frenckner B, Euler CV. Influence of pudendal block on the 30. Kleeman SD, Westermann C, Karram MM. Rectoceles and
function of the anal sphincters. Gut. 1975;16:482–489. the anatomy of the posteriorvaginal wall: revisited. Am J Obstet
9. Roshanravan SM, Wieslander CK, Schaffer JI, Corton MM. Gynecol. 2005;193(6):2050–2055.
Neurovascular anatomy of the sacrospinous ligament region in 31. Leffler KS, Thompson JR, Cundiff GW, et al. Attachment of the
female cadavers: implications in sacrospinous ligament fixation. rectovaginal septum to the pelvic sidewall. Am J Obstet Gynecol.
Am J Obstet Gynecol. 2007;197(6):660.e1–660.e6. 2001;185:41–43.
10. Smoll NR. Variations of the piriformis and sciatic nerve with 32. DeLancey JOL. Anatomic aspects of vaginal eversion after
clinical consequence: a review. Clin Anat. 2010;23(1):8–17. hysterectomy. Am J Obstet Gynecol. 1992;166:1717.
11. Whiteside JL, Barber MD, Walters MD, Falcone T. Anatomy 33. Range RL, Woodburne RT. The gross and microscopic anat-
of ilioinguinal and iliohypogastric nerves in relation to trocar omy of the transverse cervical ligaments. Am J Obstet Gynecol.
placement and low transverse incisions. Am J Obstet Gynecol. 1964;90:460–467.
2003;189(6):1574–1578; discussion 1578. 34. Campbell RM. The anatomy and histology of the sacrouterine
12. Rahn DD, Phelan JN, Roshanravan SM, White AB, Corton ligaments. Am J Obstet Gynecol. 1950;59:1–12.
MM. Anterior abdominal wall nerve and vessel anatomy: clini- 35. Rooney K, Kenton K, Mueller ER, et al. Advanced anterior
cal implications for gynecologic surgery. Am J Obstet Gynecol. vaginal wall prolapse is highly correlated with apical prolapse.
2010;202(3):234.e1–234.e5. Am J Obstet Gynecol. 2006;195:1837–1840.
13. Corton MM. Anatomy of pelvic floor dysfunction [Review]. 36. Summers A, Winkel LA, Hussain HK, DeLancey JOL. The
Obstet Gynecol Clin North Am. 2009;36(3):401–419. relationship between anterior and apical compartment support.
14. Parks AG, Porter NH, Melzak J. Experimental study of the Am J Obstet Gynecol. 2006;194:1438–1443.
reflex mechanisms controlling muscles of the pelvic floor. 37. DeLancey JOL. Structural support of the urethra as it relates
Dis Colon Rectum. 1962;5:407–414. to stress urinary incontinence: the hammock hypothesis. Am J
15. Heit M, Benson T, Russell B, et al. Levator ani muscle in women Obstet Gynecol. 1994;170:1713–1720.
with genitourinary prolapse: indirect assessment by muscle his- 38. Vakili B, Chesson RR, Kyle BL, et al. The incidence of uri-
topathology. Neurourol Urodyn. 1996;15:17–29. nary tract injury during hysterectomy: a prospective analy-
16. Lawson JO. Pelvic anatomy. I. Pelvic floor muscles. Ann R Coll sis based on universal cystoscopy. Am J Obstet Gynecol. 2005;
Surg Engl. 1974;54:244–252. 192:1599–1604.
17. Kerney R, Sawhney R, DeLancey JOL. Levator ani muscle 39. Ibeanu OA, Chesson RR, Echols KT, et al. Urinary tract injury
anatomy evaluated by origin-insertion pairs. Obstet Gynecol. during hysterectomy based on universal cystoscopy. Obstet
2004;104:168–173. Gynecol. 2009;113:6–10.
18. Margulies RU, Hsu Y, Kearney R, Stein T, Umek WH, 40. Barber MD, Visco AG, Weidner AC, et al. Bilateral uterosacral
DeLancey JO. Appearance of the levator ani muscle subdivisions ligament vaginal vault suspension with site-specific endopelvic
in magnetic resonance images. Obstet Gynecol. 2006;107(5): fascia defect repair for treatment of pelvic organ prolapse. Am J
1064–1069. Obstet Gynecol. 2001;185:1009.
50 Section I Fundamental Topics

41. Kwon CH, Goldberg RP, Koduri S, Sand PK. The use of 45. Wieslander CK, Roshanravan SM, Wai CY, et al. Uterosac-
intraoperative cystoscopy in major vaginal and urogynecologic ral ligament suspension sutures: anatomic relationships in
surgeries. Obstet Gynecol. 2002;187:1466–1472. unembalmed female cadavers. Am J Obstet Gynecol. 2007;197:
42. Gustilo-Ashby AM, Jelovsek JE, Barber MD, et al. The inci- 672.e1–672.e6.
dence of ureteral obstruction and the value of intraoperative 46. Wieslander CK, Rahn DD, McIntire DD, et al. Vascular anat-
cystoscopy during vaginal surgery for pelvic organ prolapse. omy of the presacral space in unembalmed female cadavers.
Am J Obstet Gynecol. 2006;194:1478–1485. Am J Obstet Gynecol. 2006;195:1736–1741.
43. Buller JR. Thompson GW, Cundiff LK, et al. Uterosacral liga- 47. Drewes PG, Marinis SI, Schaffer JI, et al. Vascular anatomy over
ment: description of anatomic relationships to optimize surgical the superior pubic rami in female cadavers. Am J Obstet Gynecol.
safety. Obstet Gynecol. 2001;97:873–879. 2005;193:2165–2168.
44. Rahn DD, Bleich AT, Wai CY, et al. Anatomic relationships 48. Pathi SD, Castellanos ME, Corton MM. Variability of the ret-
of the distal third of the pelvic ureter, trigone, and urethra in ropubic space anatomy in female cadavers. Am J Obstet Gynecol.
unembalmed female cadavers. Am J Obstet Gynecol. 2007;197: 2009;201(5):524.e1–524.e5.
668.e1–668.e4.
CHAPTER 2
3
1 Mechanisms of Disease
Victoria L. Handa

INTRODUCTION identify women whose stress incontinence would be


more effectively treated by urethropexy or anterior
Key Point colporrhaphy. However, the bead chain cystoure-
throgram was ultimately found to be poorly repro-
• The mechanisms for most pelvic floor disorders are ducible and was eventually abandoned. An abnormal
unknown. Most pelvic floor disorders appear to be position of the posterior urethrovesical angle is no
multifactoral. longer thought to be a mechanism of SUI.
Several contemporary theories of SUI attribute
this condition to poor support of the urethrovesi-
Little is known about the underlying mechanisms cal junction during increased intra-abdominal pres-
that cause pelvic floor dysfunction. Historically, the- sure. Hypermobility of the bladder neck is thought to
ories regarding the pathophysiology of pelvic floor be one of several factors that result in poor pressure
disorders have been derived from observation of suc- transmission to the proximal urethra at the instant of
cess—or failure—of new surgical or medical therapies. increased intra-abdominal pressure (Figure 3-2). The
Therefore, our understanding of the possible mecha- concept of pressure transmission is important with
nisms behind pelvic floor disorders continues to evolve. respect to mechanisms of urinary incontinence. Spe-
In this chapter, mechanisms of pelvic floor dysfunction cifically, continence is maintained during increased
will be reviewed to address hypothesized theories of intra-abdominal pressure if the pressure in the urethra
the pathophysiology of urinary and anal incontinence, exceeds the pressure in the bladder. The absolute dif-
overactive bladder, and pelvic organ prolapse. ference between urethral pressure and bladder pres-
sure is described as the “closure pressure,” typically
measured during urodynamic testing. If the closure
STRESS URINARY INCONTINENCE pressure drops below zero (eg, if bladder pressure
exceeds urethral pressure), incontinence will occur. In
Historically, stress incontinence has been associ- women with stress incontinence, the closure pressure
ated with abnormal support or position of the blad- decreases to zero (or below zero) during increased
der neck and urethra. Early observations linked intra-abdominal pressure.
stress urinary incontinence (SUI) to the loss of the Pressure transmission is linked to urethral support.
“normal” angle between the bladder and urethra. Specifically, in a continent woman, the urethra is sup-
This angle was measured on bead chain cystoure- ported by a “hammock,”5 consisting of the vaginal wall
throgram (Figure 3-1).1- 4 An abnormal posterior ure- and its fibrous and muscular attachments (Figure 3-3).
throvesical angle was initially thought to be the cause If the bladder neck is hypermobile, the proximal urethra
of urinary stress incontinence and was later used to descends at the moment of increased intra-abdominal
51
52 Section I Fundamental Topics

Another potential mechanism for SUI is a loss


of intraluminal urethral pressure. Urethral pressure
measures were first made in the 1960s by Enhorn-
ing.17 Resting intraluminal urethral pressures are
lower in women with SUI than in continent con-
trols.18 Both the striated and smooth muscles of the
urethra contribute to urethral intraluminal pressure.19
However, equal in importance to each of those mus-
cular components is the mucosal coaptation provided
FIGURE 3-1 Bead chain cystogram. A metallic bead chain by the bulking effect of the submucosal vasculature.
has been inserted transurethrally and lateral radiography Coaptation maintains urethral closure via surface
demonstrates the angle formed by the posterior urethra
tension. Reduction in coaptation or in the striated
and bladder base. Before (left) and after (right) retropubic
or smooth muscle tone can leave the urethra open
urethropexy. (Reproduced with permission from Ref.2)
at rest, facilitating stress incontinence. Tradition-
ally, this type of SUI has been classified as “intrinsic
pressure and thus the urethra is not compressed. Fur- sphincter deficiency” (ISD), although precise defi-
thermore, if the urethra descends through the levator nitions of ISD vary. A reduction in urethral tone is
hiatus at the instant of increased intra-abdominal pres- associated with increasing age,20 providing one expla-
sure, the urethra will not be exposed to the increase in nation for the association between SUI and aging. A
intra-abdominal pressure. This may result in an unfa- transient reduction in urethral tone may be associ-
vorable pressure gradient between the bladder and ated with α-adrenergic antagonists.21 The reduction
urethra, resulting in incontinence. in intraluminal urethral pressure with a loss of muco-
For almost four decades, hypermobility of the ure- sal coaptation is the rationale for the use of urethral
thra has been defined by the “Q-tip test” or cotton bulking agents for treatment of SUI.22
swab test. A lubricated cotton swab is placed through In addition to biological mechanisms that cre-
the urethra until the tip is in the bladder and the patient ate conditions favorable to the development of SUI,
is asked to strain (Figure 3-4). A positive cotton swab a number of conditions and behaviors may promote
test is defined as rotation beyond 30% from the hori- SUI. For example, women who smoke may experi-
zontal during straining. Clinicians have observed that ence SUI because they cough more often and more
women with SUI are likely to demonstrate a hyper- forcefully than nonsmokers.23 For these women, a
mobile bladder neck. However, it has been recognized reduction in coughing may substantially reduce SUI
that many continent women also have evidence of ure- symptoms. Another example is obesity.24 The mecha-
thral hypermobility and, thus, a hypermobile bladder nisms linking obesity and SUI are uncertain but may
CHAPTER 3

neck is not synonymous with SUI. In contemporary be related to increased intra-abdominal pressure in
practice, the cotton swab test may be used to identify obese women.25,26 Both obesity and cigarette smoking
women most likely to benefit from surgical treatment are associated with incontinence severity.27
of SUI: a negative cotton swab test, indicating good
support of the urethrovaginal junction, is a strong pre-
dictor of the failure of Burch urethropexy and sling OVERACTIVE BLADDER
procedures for treatment of SUI.7-13
SUI may also be a manifestation of pelvic muscle The symptom complex of “overactive bladder” refers
weakness. Women with SUI have weaker levator ani to the symptom of urgency, usually in association
muscle strength than continent controls.14 Programs with frequency and nocturia, with or without urgency
to strengthen the pelvic muscles are effective treat- incontinence. Mostly, overactive bladder is thought to
ments for SUI.15 However, it is not known whether be a result of involuntary detrusor contractions.
loss of muscle strength is the catalyst that triggers The detrusor contracts involuntarily throughout
the development of SUI or whether pelvic muscle fetal life and infancy. However, in childhood, acqui-
strengthening simply compensates for other mecha- sition of bladder control is achieved through cortical
nisms contributing to SUI. The relationship between maturation, with the inhibition of involuntary detrusor
pelvic muscle weakness and SUI may be mediated via activity. This typically occurs between age of three and
poor pressure transmission. Weakness of the muscular five years. Children who fail to acquire this suppres-
component of the pelvic floor contributes to hyper- sion of detrusor activity may be prone to nocturnal
mobility. This theory is supported by the observation enuresis or other manifestations of overactive bladder.
that SUI may be treated effectively with the “Knack” Thus, the highest incidence of overactive bladder in
maneuver, a pelvic muscle contraction timed to coin- children occurs between five and seven years of age,28
cide with anticipated increased abdominal pressure.16 as these children present for evaluation of frequency,
Chapter 3 Mechanisms of Disease 53

UPP Pull 3 Start


UPP Pull 2 Stop

PTR = 115%

PTR = 224%
UPP Start 2

UPP Start 3
UPP Stop 2

UPP Stop 3
PTR = 87%
PTR = 29%
PTR = 85%

PTR = 78%
2:10

2:20

2:30

3:20
3:10
v v v v v v v vv v vv

110 110
110110
12

108 108

70 70

107
8

98 98
10

89
Vesical

8
pressure

40 40
68 68
73 73

64 64
8

63 63

62
6

51
6

7
Abdominal
pressure

30 30
42 42
36 36

44 44
5

35 35

46
1

34
5

1
Detrusor
pressure

113113
14848

249 249

121 121
1979
7

.93
7

79
9

6
Urethral
pressure

141 141
38 38
–5

9 9
3

.14
23 23
–1

.2
–2

–6
3
.2
Urethral

Title: Pull 3
closure
pressure

A B
177

185
173 173

6
7

10

178
154

202
170

206

12
7

CHAPTER 3
190

228

–2
199 199
3

218
143

233
4

102

243

6
3

–13

–44
–20 –20

8
4

–40
11

–33
6

–41

6
3

FIGURE 3-2 Urethral pressure profiles at


rest and with coughing. The urodynamic
catheter is drawn through the urethra, result-
174

193

–10
171 171
5

200
9

153

205

ing in a display of urethral pressure from


157

211

14
6

proximal to distal. In each panel, the trac-


ing, from top to bottom, represents blad-
der pressure, abdominal pressure, calculated
detrusor pressure, urethral pressure, and
calculated urethral closure pressure. Panel A
–3

–16
–1

–2 –2
–1

22
–2

was obtained at rest. Panel B was obtained


–0

–3

12

with serial coughing in a continent woman.


Panel C was obtained with serial coughing
in a woman with stress urinary incontinence,
illustrating that urethral closure pressure
C drops to zero with coughing.
54 Section I Fundamental Topics

are more likely to experience detrusor overactivity.32


It is hypothesized that detrusor hypertrophy, caused
by increased voiding pressures against an obstruction,
leads to involuntary detrusor activity.
There are many potential neurogenic mechanisms
for detrusor dysfunction. The bladder and lower
urinary tract are regulated by both the autonomic
nervous system and the central nervous system and
therefore a variety of neurological conditions can
affect bladder function. If detrusor overactivity is
identified in an adult with a known neurological con-
dition, this is classified as “neurogenic detrusor over-
activity”. Examples of neurologic conditions that
precipitate detrusor hyperreflexia include multiple
sclerosis, Parkinson disease, stroke, and traumatic
brain injury. These conditions cause bladder over-
FIGURE 3-3 Lateral view of pelvic floor with urethra, activity due to a reduced tonic inhibition of bladder
vagina, and fascial tissues transected at level of vesi- contractions.33
cal neck drawn from three-dimensional reconstruction The degree of volitional control exerted over blad-
indicating compression of urethra by downward force der function contrasts sharply with the much more
(arrow) against supportive tissues indicating influence limited control exerted over other visceral organs,
of abdominal pressure on urethra (arrow). (Reproduced such as the rectum. Subtle derangements of the auto-
with permission from Ref.5 Copyright Elsevier 1994.)
nomic nervous system and the central nervous sys-
tem can result in bladder dysfunction. In the central
nervous system, the pontine micturition center is the
nocturia, and incontinence. Evidence suggests that
source of parasympathetic efferents to the detrusor,
pediatric overactive bladder is familial and strongly
which travel via the pelvic nerves. The pontine center
associated with overactive bladder later in life.29,30
is thought to mediate the voluntary control of detrusor
The specific factors that cause involuntary detrusor
function. Specifically, stimulation of the parasympa-
activity are not known. Theories are divided between
thetic efferent pathways results in bladder contrac-
“myogenic” and “neurogenic.” One example of a “myo-
tion. Bladder sensory afferents travel in the pelvic
genic” mechanism is bladder neck obstruction. It has
nerve and hypogastric nerve. Rapid distention of the
long been recognized that men with prostate enlarge-
bladder, especially with chilled fluid, can trigger a
ment have a higher prevalence of detrusor overactiv-
CHAPTER 3

detrusor contraction, demonstrating the potential role


ity.31 Similarly, women with obstructed voiding from
for afferent signaling in the genesis of detrusor over-
either severe prolapse or prior bladder neck surgery
activity. Other examples of a possible role for affer-
ent stimulation in the genesis of involuntary detrusor
Q-tip test
contractions include a variety of irritative conditions,
including cystitis, and their association with overac-
Symphysis pubis tive bladder symptoms.
A sustained and coordinated contraction of the
detrusor muscle is typical for normal voluntary void-
ing. Less coordinated or localized detrusor contrac-
tions are associated with sensory urgency34 and may
30º play a role in overactive bladder.
Uterus In some cases, superimposed conditions increase
symptoms related to overactive bladder. Examples
Bladder
include polyuria and medications that impact the
autonomic nervous system. Overactive bladder is
Rectum
also strongly associated with aging. However, it is not
known whether the increase in bladder overactivity
Spinal column associated with age is due to age-related changes in
FIGURE 3-4 The “Q-tip” test may be used to identify bladder function or to the acquisition with age of co-
women with urethral hypermobility, defined as a strain- morbid conditions. Additional age-related changes in
ing angle greater than 30% above the horizontal line. detrusor function include decreased contractility and
(Modified with permission from Ref.6 Urol Nurs © 2008. decreased compliance, both of which can mimic the
Society of Urologic Nurses and Associates.) effects of detrusor overactivity.
Chapter 3 Mechanisms of Disease 55

ANAL INCONTINENCE 2.0


1.9

Mean fiber density


The anal sphincter consists of an internal and external 1.8
component. Most of the resting tone is provided by 1.7
the internal sphincter.35 The external anal sphincter, 1.6
a striated muscle, provides voluntary tone. Injury to 1.5
1.4
either component can disrupt continence. Other fac-
1.3
tors that contribute to continence include rectal sen-
1.2
sation, the anal mucosal folds and vascular cushions,
1.1
the posterior anorectal angle, stool volume and consis- Antenatal 2 mo 5y Controls
tency, as well as the compliance of the rectum. Among A (6 mo)
adult women, the most common anal incontinence
symptoms include incontinence of flatus and fecal

Mean pudendal nerve terminal


2.4
urgency.36,37 In contrast, frank incontinence of solid
2.3

motor latency, ms
stool is less common. Pelvic floor mechanisms con-
tributing to symptoms of anal incontinence include 2.2
anal sphincter injury, pelvic organ prolapse, and rectal 2.1
prolapse. Other mechanisms include gastrointestinal
disorders and peripheral neuromuscular disorders. 2.0
Obstetrical injuries to the anal sphincter complex 1.9
are possibly the most well-recognized pelvic floor cause
of anal incontinence in young women. The incidence 1.8
B 48 h 2 mo 5y Controls
of anal sphincter injury at the time of vaginal birth
is not known but thought to be approximately 5%.38 120
Maximum anal canal pressure,

Injury to the external anal sphincter is more common 110


than injury to the internal sphincter. Six months after 100
recognized obstetrical anal sphincter laceration and 90
cm H2O

immediate repair, anal incontinence is reported by 80


17% of primigravid women,37 indicating a substantial 70
prevalence in this setting. Incontinence after sphincter 60
repair can occur due to chronic dehiscence of at least 50
one component of the repair.39,40 40
In 1993, Sultan and colleagues reported that 35% 30

CHAPTER 3
to 45% of women had evidence of occult sphincter lac- C Antenatal 48 h 2 mo 5y Controls
erations after vaginal childbirth.41 These occult lacera- FIGURE 3-5 A. Single fiber electromyography. Mean fiber
tions, detected postpartum on endoanal ultrasound, density (bars represent ±1 s.e.). There was an increase in
were associated with incontinence symptoms. How- mean fiber density in the 14 multiparous subjects during the
ever, this high incidence of occult laceration has since five years following entry. B. Pudendal nerve terminal motor
been attributed to inadequate training of obstetrical latency (standard errors omitted for clarity). Mean pudendal
providers in the recognition of such injuries at the time nerve terminal motor latency was increased at the five-year
of delivery.42 With improved detection, the incidence of follow-up. The control (•) represents the combined mean of
occult sphincter injuries has been estimated at less than the right (□) and left (■) data, which were identical in value.
10%.43,44 Recent evidence from magnetic resonance C. Anal canal pressure during a maximal squeeze contrac-
tion (bars represent ±1 s.e.). These multiparous women
imaging suggests that incontinent women may be
generally showed lower maximal anal canal pressures than
more likely to have evidence of levator ani injuries.45,46 the age-matched control group, and the anal canal pressure
Neuromuscular injuries have also been suggested as did not return to the level recorded at the first examination.
a possible mechanism for anal sphincter dysfunction (Reproduced with permission from Ref.52)
after childbirth. The pudendal nerve can be compressed
or stretched during vaginal childbirth.47 Evidence of
peripheral denervation of the levator ani is associated atrophy or dysfunction,53,54 raising questions about the
with obstetrical anal sphincter injury48-50 and also with mechanism for this observed association.
idiopathic anal incontinence.51 In a study of parous Although women with pelvic organ prolapse are
women followed five years from delivery,52 evidence of more likely to report anal incontinence than women
pudendal neuropathy was persistent postpartum and with normal pelvic organ support,55,56 it does not
associated with reduced anal canal pressures (Figure 3-5). seem likely that pelvic organ prolapse is a direct
However, animal models in which the pudendal nerve cause of anal incontinence. For example, there is no
is stretched or compressed do not produce sphincter correlation between uterovaginal prolapse and anal
56 Section I Fundamental Topics

incontinence.57,58 However, there is some evidence


that symptoms of anal incontinence may improve after
surgical treatment of prolapse.59,60 The specific role
played by pelvic organ prolapse in the development of
anal incontinence remains to be clarified.
Perineal descent is thought to be a possible cause
of anal incontinence. Normally, the perineal body
descends between 1 and 3.5 cm during defecation.61
Abnormal perineal descent is defined as descent of the
perineal body beyond the plane of the ischial tuber-
osities on defacography. In women with abnormal
Levator ani
perineal descent, chronic straining, such as may be
associated with chronic constipation, leads to stretch-
ing of the pudendal nerve, which in turn may lead to
pudendal neuropathy.62 It is thought that the resultant
neuropathy may contribute to weakness and dysfunc- FIGURE 3-6 Drawing of the normal vaginal axis, show-
tion of the anal sphincter complex. However, this ing an almost horizontal upper vaginal and rectum lying
on and parallel to the levator plate. The latter is formed
observation is based largely on cross-sectional stud-
by fusion of pubococcygeus muscles posterior to rectum.
ies and a causal role cannot be assumed. Longitudinal Anterior limit of point of fusion is shown, which is the margin
studies of adults with chronic constipation have not of genital hiatus. (Reproduced with permission from Ref.67)
been conducted and therefore this mechanism for anal
incontinence remains hypothetical.
Among women with rectal prolapse, a majority have recognized that the vaginal axis is an important com-
anal incontinence. Rectal prolapse causes anal inconti- ponent of normal support. The proximal vagina is
nence via reflex relaxation of the internal anal sphinc- horizontal when a woman is in the standing position,
ter.63 Although complete rectal prolapse is typically with the apex toward the third and fourth sacral verte-
diagnosed on physical examination, internal or occult brae.66,67 The upper vagina is thereby supported by the
rectal prolapse may be more difficult to detect and levator plate (Figure 3-6).68
should be suspected as a cause of anal incontinence, The connective tissue supports of the cervix and vag-
especially in the setting of difficult defecation. inal apex maintain the position of these structures over
At any age, gastrointestinal disorders contrib- the levator plate. As a result of this position, increases in
ute to anal incontinence via impact on stool volume intra-abdominal pressure compress the vagina against
and consistency, the development of stool impaction, the levator plate,68 rather than through the levator hia-
CHAPTER 3

or altered intestinal motility.64 Colonic function and tus (Figure 3-7).69 Prolapse might result if this anatomy
transport are important determinants. Dietary factors is altered. For example, if the levator ani muscles are
and habits also play a role. Recognized gastrointesti- elongated or detached, the levator hiatus will widen. A
nal conditions that contribute to anal incontinence wider hiatus would favor descent of the vagina through
include conditions that promote diarrhea (inflamma- the hiatus (Figure 3-8).68 Alternatively, if the connective
tory bowel disease, laxative use and abuse, and hyper- tissue supports are disrupted, the upper vagina might
motility disorders). Anal incontinence may also be be positioned over the levator hiatus. This could also
more common after cholecystectomy.64,65 result from surgical procedures that change the vaginal
Anal incontinence is more common in elderly axis, displacing the proximal vagina anteriorly. In either
women. Possible causes of anal incontinence in older circumstance, positioning of the vaginal apex over the
adults include age-related changes in striated mus- levator hiatus would favor descent of the vagina through
cle strength, decreased anorectal sensation, and the the levator hiatus at the instant of increased intra-
impact of co-morbid conditions. Conditions that favor abdominal pressure. This downward displacement of
the development of anal incontinence in older adults the vagina could predispose to additional disruption
include diabetes, vascular insufficiency, congestive of connective tissue supports, thus perpetuating a fur-
heart failure, neurologic diseases (such as Parkinsons, ther deterioration in support. Berglas and Rubin, using
stroke, dementia), decreased mobility, and frailty. contrast radiography in the early 1950’s to image the
levator ani muscle in living women, confirmed these
principles and demonstrated the dynamic support of
PELVIC ORGAN PROLAPSE the uterus and cervix by the levator plate during Val-
salva maneuvers. They also demonstrated levator laxity
Pelvic organ prolapse is thought to result from weak- in some women and found that the angle of the levator
ening of the muscular and connective tissue supports plate was directly correlated with the size of the levator
of the uterus and vagina. As early as the 1950s, it was hiatus and also with uterine support.68
Chapter 3 Mechanisms of Disease 57

Coccyx

Symphysis

Levator plate
A B
Hiatus

C D E

FIGURE 3-7 Diagrammatic display of vaginal support.


A. Invaginated area in a surrounding compartment; B. the
prolapse opens when the pressure (arrow) is increased;
C. closing the bottom of the vagina prevents prolapsed
by constriction; D. ligament suspension; E. flap valve clo-
sure where suspending fibers hold the vagina in a position
against the wall allowing increases in pressure to pin it in
place. (Reproduced with permission from Ref.69)

This description illustrates the importance of the


uterosacral and cardinal ligaments, which are the pri- FIGURE 3-8 With the same length of the levator plate,
mary supports of the vaginal apex and maintain the nor- its varying inclination determines extent of levator hia-
mal vaginal axis.70 The cardinal ligament originates at tus. If the levator ani muscles are detached from the pelvic
the greater sciatic foramen and the uterosacral ligament bones or if they become lax, the levator hiatus will widen.
originates over a broad surface of the sacral vertebrae.71 (Reproduced with permission from Ref.68)
Together, these structures provide support to the prox-
imal vagina and cervix. It has been hypothesized that

CHAPTER 3
stretching or tearing of these ligaments is a fundamental in connective tissue properties have been suggested as
step in the development of prolapse. However, it remains possible mechanisms for a genetic predisposition to
unclear whether such injuries to the ligaments occur and prolapse. Women with joint hypermobility may be at
what processes could lead to such injuries. Indeed, there increased risk for prolapse.75,76 There has been some
is very little evidence that such injuries occur. evidence to suggest that Marfan syndrome might
Connective tissue factors may contribute to the increase a woman’s propensity to develop prolapse,77
development of prolapse. For example, the vaginal presumably resulting from abnormalities of elastic
walls of women with severe prolapse are more extensi- fibers. A possible association with Ehlers-Danlos, a dis-
ble and less stiff than those without prolapse.72 Connec- order of collagen synthesis, has also been observed.78
tive tissues could be impacted by metabolic processes, There are a number of candidates with respect
such as hypoestrogenism. Although menopause is tem- to biochemical alterations in connective tissue.79,80
porally associated with the incidence of prolapse, this Hypothesized connective tissue mechanisms include
seems to be due to the confounding effects of aging. alterations in elastin turnover,81-86 collagen turnover,87-91
There is no question that prolapse is more common collagen content,90-94 and laminin proteins.95 Recent
with advancing age, but no link between hypoestrogen- observations have suggested the importance of connec-
ism and prolapse has been established. For example, in tive tissue remodeling following vaginal delivery, with
the Women’s Health Initiative, pelvic organ prolapse changes in collagen types96 and replacement of elas-
was not impacted by estrogen therapy.73 The precise tin. In animal models, genetic deficiencies in elastin
role of ovarian steroids in the biology of pelvic organ replacement are associated with prolapse that develops
prolapse remains to be explained. with aging or in response to vaginal delivery.83,85,97,98
Because familial associations for prolapse have been From an epidemiologic perspective, vaginal deliv-
observed,74 investigators have speculated regarding pos- ery seems to be an important risk factor for pelvic
sible genetic causes of prolapse. Phenotypic alterations organ prolapse.99-103 Studies comparing vaginal and
58 Section I Fundamental Topics

cesarean birth seem to suggest that vaginal birth con- 8. Walters MD, Diaz K. Q-tip test: a study of continent and
fers a greater risk of prolapse than does cesarean birth. incontinent women. Obstet Gynecol. 1987;70:208–211.
9. Bergman A, Koonings PP, Ballard CA. Negative Q-tip test as a
Possible mechanisms for this association include the risk factor for failed incontinence surgery in women. J Reprod
role of levator ani injuries, denervation of the levator Med. 1989;34:193–197.
ani muscles, and the potential impact on connective 10. Summitt RL Jr, Bent AE, Ostergard DR, Harris TA. Stress
tissue supports of the vaginal apex. incontinence and low urethral closure pressure. Correlation
Research on childbirth trauma to the pelvic floor of preoperative urethral hypermobility with successful subure-
thral sling procedures. J Reprod Med. 1990;35:877–880.
has been facilitated through the development of mag- 11. Klutke JJ, Carlin BI, Klutke CG. The tension-free vagi-
netic resonance104 and three-dimensional ultrasound nal tape procedure: correction of stress incontinence with
imaging.105,106 Studies suggest that avulsion of the minimal alteration in proximal urethral mobility. Urology.
levator ani muscle from its attachments at the pubic 2000;55:512–514.
ramus may be identified in up to one-third of vaginally 12. Bakas P, Liapis A, Creatsas G. Q-tip test and tension-free vagi-
nal tape in the management of female patients with genuine
parous women, presumably due to trauma during stress incontinence. Gynecol Obstet Invest. 2002;53(3):170–173.
delivery.105,107 Women with avulsion injuries identified 13. Liapis A, Bakas P, Christopoulos P, Giner M, Creatsas G.
on magnetic resonance or ultrasound imaging are at Tension-free vaginal tape for elderly women with stress urinary
substantially higher risk for prolapse.108,109 incontinence. Int J Gynaecol Obstet. 2006;92(1):48–51.
14. Amaro JL, Moreira EC, De Oliveira Orsi Gameiro M, Pado-
vani CR. Pelvic floor muscle evaluation in incontinent patients.
Int Urogynecol J Pelvic Floor Dysfunct. 2005;16:352–354.
Key Points 15. Dumoulin C, Hay-Smith J. Pelvic floor muscle training ver-
sus no treatment, or inactive control treatments, for urinary
• Some common underlying mechanisms associated incontinence in women. Cochrane Database Syst Rev. 2010;(1):
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JO. Clarification and confirmation of the Knack maneuver: the
• Further research is needed to identify the pre- effect of volitional pelvic floor muscle contraction to preempt
cise mechanism for development of pelvic floor expected stress incontinence. Int Urogynecol J Pelvic Floor Dys-
disorders. funct. 2008;19:773–782.
17. Enhorning G. Simultaneous recording of the intravesical
and intraurethral pressure. Acta Obstet Gynecol Scand. 1961;
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simulation. Am J Obstet Gynecol. 2005;192(5):1669–1676. 677–692.
48. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to inner- 69. Delancey JOL, Shobeiri SA. State of the art pelvic floor anat-
vation of pelvic floor sphincter musculature in childbirth. omy. In: Santoro GA, Wieczorek AP, Bartram CI, eds. Pelvic
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72. Epstein LB, Graham CA, Heit MH. Systemic and vagi- N, Creatsas G. Changes of collagen type III in female patients
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2007;197(2):165.e1–165.e6. 93. Lin SY, Tee YT, Ng SC, Chang H, Lin P, Chen GD. Changes
73. Bradley CS, Zimmerman MB, Qi Y, Nygaard IE. Natural in the extracellular matrix in the anterior vagina of women
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4
1 Clinical and Quality
of Life Evaluation
Mamta M. Mamik and Rebecca G. Rogers

INTRODUCTION CLINICAL EVALUATION


OF A PATIENT WITH PELVIC
Pelvic floor disorders, including urinary and anal FLOOR DYSFUNCTION
incontinence, pelvic organ prolapse (POP), sexual
dysfunction, and pelvic pain consist of an array of Pelvic floor disorders comprise a group of diseases that
functional and anatomical diseases that significantly patients may find difficult to bring up during a medical
impact the quality of life (QOL) of women. Central to interview. Although common, many patients are reluc-
the diagnosis and treatment of these disorders is the tant to discuss these problems with providers because
amount of bother and impact on QOL women experi- of embarrassment or because women are unaware of
ence from their pelvic floor problems. For the major- treatment options. In addition, many providers are
ity of pelvic floor disorders, no universally accepted not familiar with the diagnosis and treatment of pelvic
definition of the disease state on physical examination floor dysfunction or feel that these disease states can
or on ancillary testing exists. For this reason, diagno- only be treated by a specialist. Family members may
sis of disorders must not only take into account ana- believe that the lack of urinary or bowel control is voli-
tomic and functional measures, but also must include tional. Challenges faced by families are underlined by
evaluation of symptom severity and impact on QOL. the fact that incontinence is a major reason for nursing
This is not meant to trivialize the importance of the home admissions in the elderly.1
diagnosis and treatment of these problems, but rather The National Center for Quality Assurance empha-
to emphasize the need for pelvic floor disorders to be sized the importance of screening for pelvic floor
evaluated within the context of the patients’ personal problems by determining that a quality indicator for
experience. In this chapter, we review the clinical and primary care provider is to identify individuals with uri-
QOL evaluation of the women with pelvic floor dys- nary incontinence.2 In a busy primary care or obstet-
function; detailed descriptions of specific tests will not rics and gynecology practice, finding time to ask about
be presented here, but will be covered in more detail in incontinence or prolapse may be challenging. Many
chapters addressing specific pelvic floor dysfunctions. providers ask women general questions about whether
or not they have bowel, bladder, or sexual complaints
Key Point on their intake history. This simple intervention opens
the door for women to feel more comfortable to seek
• Central to the diagnosis and treatment pelvic floor treatment. Often patients have more than a single
disorders is the amount of bother and impact on disorder; it is critical that women who present with a
quality of life women experience from their pelvic single disorder be screened for others as well. Because
floor problems. of their central importance in detection and evalua-
tion of functional problems, following is a discussion
61
62 Section I Fundamental Topics

of the psychometric properties of questionnaires in measures that have not undergone rigorous analysis,
general and a brief discussion of questionnaires used referred to as an ad hoc questionnaire, to measures that
to screen pelvic floor disorders, as well as question- have been extensively evaluated or validated question-
naires that evaluate a spectrum of pelvic floor dysfunc- naires. Validated measures can be further divided into
tion. Clinical and physical examination assessment of those that are condition-specific, or were designed to
urinary and bowel complaints and POP will then be measure clinical problems in a specific group of indi-
presented, with questionnaires specific to the particu- viduals, or generic, meaning the questionnaire is best
lar dysfunction included in its respective section. used to evaluate differences between a variety of disease
states. Questionnaires used to evaluate pelvic floor dys-
Key Point function range in size from a single question to much
longer questionnaires. Often, both long- and short-form
• Evaluation of pelvic floor dysfunction involves versions of a questionnaire will be developed. Although
eliciting history, physical examination, and clinic- the long-form version of a questionnaire will provide
based tests and advanced studies. more detail than a shorter version, shorter forms reduce
patient burden and are often the most appropriate for
use in clinical practice. Some questionnaires have sub-
sections, which focus on a particular aspect of QOL or
QUESTIONNAIRES symptoms; these are referred to as domains. Choosing
which questionnaires to use depends on the goals
Although a complete discussion of the science behind of their use; although the International Continence
questionnaire development is beyond the scope of Society (ICS) rates questionnaires based on their
this chapter, a general understanding of the central quality, no standard measures have been determined.
concepts of questionnaire development is important Questionnaires are evaluated by their psychometric
because pelvic floor disorders are largely functional properties, including validity, reliability, and respon-
problems that cannot be diagnosed by objective test- siveness, or ability to measure changes in clinical con-
ing. Questionnaires transform “subjective” informa- dition (Table 4-1). Questionnaires are rated by the ICS
tion into “objective” measures of the presence and based on their validity, reliability, and responsiveness,
severity of symptoms as well as their effect on QOL. and given a “Grade” of A, B, or C. Initial questionnaire
Information should be collected in a nonbiased and validation is a process and not necessarily the endpoint
reproducible fashion. Questionnaires range from of questionnaire assessment.

Table 4-1 Properties of Questionnaires

Validity Determines whether the questionnaire measures what is intended to measure.


There are three aspects to validity, listed below.
i Criterion Validity This describes correlation of a questionnaire with a gold standard measure such
as a clinical or other self-report validated measure.
ii Construct Validity This examines the relationship between a questionnaire and underlying theories.
“Convergent” and “discriminant” validity are assessed, which show how closely a
new questionnaire is related to other measures of the same construct or the absence
of relationships between constructs that are postulated to be independent.
iii Content/Face Validity This is an assessment whether the questionnaires makes sense to those being
measured and to experts in the clinical area.
Reliability This is an assessment of a questionnaire’s ability to measure in a reproducible fashion.
Internal consistency, reproducibility, and stability are assessed.
i Internal Consistency This measures the correlations between different items and is measured by item-total
correlation or Cronbach α coefficient.
CHAPTER 4

ii Reproducibility Assesses the variability between and within observers and includes both inter-
and intrarater reliability.
iii Stability Assesses whether the questionnaire measures consistently in the same person
over a period of time in the absence of clinical change and is usually assessed by
test-retest analysis.
Responsiveness This is a questionnaire’s ability to measure clinical changes that are reflected in
changes in item, domain, or total scores.
Chapter 4 Clinical and Quality of Life Evaluation 63

Key Points Questionnaires that Evaluate a


Range of Pelvic Floor Dysfunction
• Questionnaires help in detection and evaluation
Although many measures focus on a specific aspect of
of functional problems and transform “subjec-
pelvic floor function, such as urinary incontinence or
tive” information into “objective” measures of the
POP, a number of questionnaires have been developed
presence and severity of symptoms as well as their
to assess an array of disorders. Two commonly used
effect on quality of life.
measures include the Pelvic Floor Distress Inventory
• Questionnaires can be generic or condition-specific
(PFDI)7 and the Pelvic Floor Impact Questionnaire
and are rated by the International Continence Soci-
(PFIQ).7
ety based on their validity, reliability, and respon-
siveness and given a “Grade” of A, B, or C.
Pelvic Floor Distress Inventory (PFDI)
(Grade A)7
This 46-item (long-form) questionnaire was devel-
Screening Questionnaires oped for use in women with all major pelvic floor dis-
for Pelvic Floor Dysfunction orders. Both long (46 questions) and short forms (20
To overcome screening barriers, several screening ques- questions) consist of three scales, individually focused
tionnaires for pelvic floor dysfunction have been devel- on urinary symptoms, bowel symptoms, and prolapse
oped. The most extensive of these is the Epidemiology symptoms. Patients are asked if they have a particu-
of Prolapse and Incontinence Questionnaire (EPIQ), lar symptom and asked to rate the level of bother of
which consists of 49 questions that evaluate uri- that symptom, if present, on a four-point scale. The
nary and anal incontinence, POP, and sexual health. measure has undergone extensive psychometric test-
On this measure, for items with a positive response, ing, which has established its reliability, validity, and
bother/satisfaction measures are reported on a 0 to responsiveness.
100 visual analog scale. Question no. 35, which asks
the patient “Do you have a sensation that there is a Pelvic Floor Impact Questionnaire (PFIQ)
bulge in your vagina or that something is falling out (Grade A)7
from your vagina?” has been used as a screening ques-
tion for POP in epidemiologic studies.3,4 Because of its This measure assesses QOL impact of urinary and/
length, the EPIQ questionnaire is not well suited for or anal incontinence and/or prolapse. The long-form
most clinical settings. version of the PFIQ has three scales and a total of
To identify women with incontinence, the 3IQ con- 92 items, whereas the short-form version consists
sists of three questions that screen for incontinence of 21 questions, also divided in three scales. These
symptoms and determines the type of incontinence.5 include the Incontinence Impact Questionnaire (IIQ),
Using an extended evaluation as a gold standard, the Colorectal-anal Impact Questionnaire, and Pelvic
sensitivity of the 3IQ for urgency incontinence was Organ Prolapse Impact Questionnaire. Each scale
0.75 (95% CI, 0.68–0.81) and a specificity of 0.77 consists of four domains that include physical activity,
(95% CI, 0.69–0.84); for stress incontinence, the sen- social, emotional, and travel. Again, the PFIQ has been
sitivity was higher at 0.86 (95% CI, 0.79–0.90) and extensively validated and has proved responsiveness.
the specificity lower at 0.60 (95% CI, 0.51–0.68). The
3IQ can easily be incorporated into intake question-
naires in a clinical setting. CLINICAL ASSESSMENT OF
Other screening questionnaires include the Simple URINARY INCONTINENCE
Questionnaire for sexual function.6 This question-
naire consists of three questions that ask whether or
not a patient is sexually active, if active, whether they
History
have any sexual problems and whether or not they A history of urinary incontinence should document
CHAPTER 4

have pain with sexual activity. This simple question- both the presence of incontinence as well as delin-
naire was able to identify women with sexual dysfunc- eate the major types of incontinence, including stress,
tion as well as those who underwent detailed analysis urgency, and mixed urinary incontinence. The precise
with a psychologist. Although these validated ques- nature of leakage should be queried. Patients may
tionnaires are available for use in the clinical setting, complain of leakage of urine with stress such as cough-
many providers have incorporated ad hoc screening ing, laughing or sneezing or exertion, Valsalva maneu-
questions that they develop themselves into their vers during exercise, or sexual intercourse, all of which
intake history. are associated with an increase in abdominal pressure
64 Section I Fundamental Topics

and the diagnosis of stress incontinence. Patients with may lead to simple interventions, such as modifying
urgency incontinence have loss of urine after a sensa- excessive fluid intake or if voiding very infrequently,
tion of urgency and often report failing to make it to planned voids to avoid overflow incontinence.
the bathroom in time. These patients typically practice
“toilet-mapping” and are aware of restrooms in the
vicinity of all the places they usually visit. Women with Physical Examination
urgency incontinence also report urgency “triggers” After taking a history, a physical examination, includ-
or association of having urgency when they hear the ing pelvic examination, is performed. A neurological
sound of running water. Patients may have a combina- examination should be performed to assess perineal
tion of these symptoms and are diagnosed with mixed sensation and cutaneous nerve reflexes (Figure 4-2).
urinary incontinence. An abdominal examination should be performed
The severity of the incontinence must be ascer- with attention to masses and previous surgical scars.
tained, as well as the bother that the patient experi- Perineal and genital inspection should include atten-
ences. Surrogate markers for bother include frequency tion to markers of incontinence such as erythema and
of leakage, pad use, type of pads, degree of pad satura- excoriation due to incontinence and the wearing of
tion and number of voids during the day and night. pads. An assessment of prolapse, described in more
Documentation of symptom onset and past medical detail below, is included.
history is important as well as any precipitating events Direct observation of incontinence on physi-
including recent medication changes (Table 4-2). cal examination can often confirm the diagnosis.
Patients with rare leakage may not be bothered by One such test is the empty supine cough test. This
their symptoms. is performed while the patient lies in a supine posi-
Not all lower urinary tract problems are associ- tion, immediately after voiding. The patient is asked
ated with incontinence; patients may have difficulty to cough with subsequent observation of involuntary
voiding or more commonly, complain of overactive loss of urine on examination. Stress incontinence
bladder (OAB). OAB, an umbrella term that encom- can sometimes be only observed after the reduction
passes urgency urinary incontinence, is defined as of coexistent prolapse. Urgency urinary incontinence
urinary urgency, usually accompanied by frequency may also be observed; the patient has loss of urine
and nocturia, with or without urgency urinary incon- synchronous with the sensation of a sudden, compel-
tinence, which occurs in the absence of urinary tract ling desire to void that is difficult to defer. Typically,
infection or other obvious pathology. Although not urgency losses are larger than urine loss associated
all women with OAB are incontinent, the condition with stress incontinence.
is associated with significant bother and decreased
QOL. Risk factors for urinary incontinence and rel-
evant past medical history should be ascertained as CLINIC-BASED TESTS
outlined in Table 4-2.
Voiding dysfunction, although relatively uncom- Other clinically based tests performed on physical
mon in women, may occur in patients with severe POP examination include assessment of the ability of the
or after pelvic surgery or complicated vaginal birth. patient to completely empty her bladder, and whether
Although some patients may develop overflow incon- or not she has a urinary tract infection.
tinence as a result of voiding dysfunction, others will Particularly in women with complaints of incomplete
report a slow stream or having to perform maneuvers emptying, a postvoid measure of urine volume should
in order to empty their bladders. be obtained, either by catheterization or by bladder
scan. Although the exact definition of an elevated post-
void residual has not been ascertained, less than one-
Bladder Diaries
third of the voided volume or less than 100 to 150 mLs
Bladder diaries are central to the evaluation of women is often considered “normal.” If it is unclear as to how
with urinary incontinence and OAB. On a bladder much is left in the bladder on bladder scan, straight
diary, patients prospectively record the number of vol- catheterization is performed to determine the exact
CHAPTER 4

untary voids and volumes, incontinent episodes, and volume. A urine sample should be obtained to assess
fluid intake. The National Institutes of Health recom- for hematuria, as well as markers for urinary infec-
mends a three-day bladder diary that records at least tion. Although rare, hematuria may be an indication of
urinary incontinence episodes, voiding frequency, and underlying bladder pathology such as transitional cell
pad usage8 (Figure 4-1). Bladder diaries are both diag- carcinoma, or stone disease, and urinary tract infec-
nostic and therapeutic, as women who complete them tion can be associated with stress incontinence or OAB
can identify patterns of fluid intake and voiding that symptoms that resolve with treatment of the infection.
Chapter 4 Clinical and Quality of Life Evaluation 65

Table 4-2 History Related to Urinary Incontinence, Anal Incontinence, and/or Pelvic
Organ Prolapse*

Urinary Incontinence
Symptom Documentation Past Medical History
Leakage with cough/laugh/sneeze History Associated with Stress Incontinence
Leakage with activity/sexual intercourse Prolonged labor
Leakage with urgency Operative vaginal delivery
Unconscious leakage Increased parity
Duration of symptoms Prior radiation therapy
Number of voids during the day and at night Prior incontinence surgery
Leaks per day Medications (eg, alpha-adrenergic blockers such
as prazosin, terazosin, and doxazosin, angiotensin-
converting enzyme inhibitors)
Amount of urine with leaks (large/small) History Associated with Overactive Bladder
Number of pads per day History of urinary tract infection
Digitalization prior to voiding Obstruction from prolapse
Change of position prior to voiding Prior incontinence surgery
Fluid intake Impaired bladder contractility
Associated anal and/or prolapse symptoms Bladder abnormalities or inflammation (eg, tumors,
calculi, interstitial cystitis)
Neurologic causes: (eg, Stroke, Alzheimer disease,
Multi-infarct dementia, multiple sclerosis, disk herniation,
Other dementias)
Estrogen deficiency
Systematic conditions (eg, heart failure, diabetes, sleep
disorders)
Functional and behavioral conditions (eg, excessive fluid
intake, poor bowel habits and constipation, impaired
mobility, psychological conditions, environmental
barriers to voiding)
Medications (eg, alpha adrenergics, anticholinergics,
antihistamines, antipsychotics, skeletal muscle relaxants,
tricyclic antidepressants, calcium channel blockers,
diuretics)
Anal Incontinence
Symptom Documentation Past Medical History
Number of incontinence episodes Anal injury (eg, obstetrical, fistulotomy,
hemorrhoidectomy, sphincterotomy, stretch)
Type of bowel content loss (eg, liquid stool, solid stool, Intestinal disorders (eg, colitis, or proctitis, irritable
mucus, or gas) bowel syndrome, bowel resection, tumors, fecal
impaction, constipation, rectal prolapse)
Volume of stool lost Neurological disorders (eg, dementia, neoplasia, stroke,
trauma, multiple sclerosis, spinal cord injury, psychosis)
CHAPTER 4

Pad use Infectious etiologies


Urgency Medications (eg, laxatives, enemas)
Number of bowel movements per week
Associated urinary and/or prolapse symptoms
(continued )
66 Section I Fundamental Topics

Table 4-2 History Related to Urinary Incontinence, Anal Incontinence, and/or Pelvic
Organ Prolapse* (Continued)

Pelvic Organ Prolapse


Symptom Documentation Past Medical History
Vaginal bulge Vaginal childbirth
Pressure Activities with increased abdominal pressure (eg, chronic
constipation, chronic obstructive pulmonary disease,
obesity, heavy lifting)
Vaginal bleeding/discharge Hysterectomy
Backache Prior incontinence or prolapse repair
Splinting/digitalization during urination or defecation Connective tissue disorders
Voiding dysfunction/difficulty in emptying bladder Congenital abnormalities (eg, spina bifida)
Associated urinary or anal symptoms

*Examples given in each section; lists not meant to be exhaustive.

Assessment of urethral mobility is of limited clini- greater than 10 degrees of movement on ultrasound.
cal value for patients not undergoing surgical interven- Women with immobile urethras who continue to leak
tion. To assess mobility, a cotton-tipped swab is placed urine are less likely to respond to surgical therapy than
in the urethra and withdrawn until it is at the urethro- women with mobile urethras.9
vesical junction (Figure 4-3). The patient is then asked Pelvic muscle strength is then assessed. It is impor-
to cough or Valsalva and the mobility of the urethra is tant to assess whether or not the patient is able to voli-
noted. A mobile urethra is defined as one that moves tionally contract their pelvic floor muscles, as many
greater than 30 degrees on cotton swab testing, or initial therapies for pelvic floor dysfunction hinge

To be maintained for 3 consecutive days

Name_________________________ Date_____________________________

Time of Amount Leakage If leakage Activity at Urgency prior Pads used/ Amount and
void (mls/oz) (Yes/No) present, how the time of to voiding changed type of fluid
much (small, leakage eg, (Yes/No) consumption
moderate, large coughing, eg, 4 oz tea
amounts) lifting, running
CHAPTER 4

FIGURE 4-1 Bladder diary.


Chapter 4 Clinical and Quality of Life Evaluation 67

ranging from 3 to 12.11 The Oxford grading scale12 is


L1
a scale that quantifies pelvic floor muscle strength as
no contraction (0), flicker (1), weak (2), moderate (3),
good (4), and strong (5).

Pad Testing
S2 S2 Pad testing quantifies the amount of urine lost over
the duration of testing, by measuring the increase in
S5 S4 S3 the weight of the perineal pads (weighed pre- and
posttesting) used. This may give a guide to the sever-
ity of incontinence. Testing duration varies and ranges
from a short (one hour) test in a clinical setting to a
24- and 48-hour test. Provocation during the test like-
S1 S1 wise varies from normal everyday activities to defined
regimens. The regimen recommended for a one-hour
FIGURE 4-2 Dermatomes of perineal body.
test includes the patient drinking 500-mL fluid within
a short period. After 15 minutes, the patient then
walks or climbs stairs for half an hour and during the
on the performance of pelvic floor exercises. Women remainder of the time patient stands up from sitting
unable to volitionally contract their pelvic floor muscu- position, coughs vigorously, runs in place, bends to
lature are unlikely to benefit from these interventions pick up small object, and washes their hands in run-
without the aid of a physiotherapist. The ICS recom- ning water. At the end of one hour, the pad is removed
mends assessment of pelvic floor strength to include and weighed.13,14 According to the ICS, women leaking
notation of the ability to both volitionally contract and less than 1 g during the one-hour pad test can be con-
relax the pelvic floor muscles, and the use of “absent,” sidered dry. Pad weight gains above these levels should
“weak,” “normal,” and “strong” to assess the strength indicate that incontinence occurred. Long-term tests
of pelvic floor contraction.10 Two other measures are are done for 24 or 48 hours of normal activities while
commonly used to assess pelvic floor muscle strength; wearing pads and then brought in by the patient for
the Brink scale, and the Oxford grading scale. For weighing. The upper limit of the 95% confidence
the Brink scale, pelvic floor strength is assessed after interval is between 5.5- and 8-g gain in pad weight for
inserting two lubricated fingers into the vagina. The the 24-hour home pad test.15,16
examiner then asks subjects to “squeeze and hold their In addition to screening for the severity of inconti-
pelvic muscles.” The Brink scale assesses three aspects nence, in patients where the diagnosis of incontinence
of pelvic floor muscle contraction, including vaginal is not clear, a test using an agent, such as phenazopyri-
pressure, displacement of the examiner’s fingers, and dine, that dyes the urine can be used. The patient is
duration of contraction. Each subscale is a four-point asked to take the phenazopyridine and engage in activi-
scale with a minimum score of one and maximum of ties that are thought to cause incontinence. During
four. The scores are added to provide a total score the activity, the patient observes whether their pad is
stained yellow. This test can aid in sorting out whether
or not the patients’ “wetness” is from urine or is from
another source, such as sweat or vaginal discharge.

Advanced Studies
Simple Cystometry
Also referred to as “bedside” urodynamics, simple
CHAPTER 4

cystometry utilizes a catheter inserted into the ure-


thra to check the postvoid residual volume of urine
after voiding. The bladder is then retrograde-filled,
with confirmation of when the patient experiences
sensation of first fill, initial desire to void, strong
desire to void, and maximum capacity. The bladder
is filled via an open syringe attached to the catheter.
FIGURE 4-3 ‘Q-tip’ or cotton-swab test. Before maximum capacity, the catheter is removed
68 Section I Fundamental Topics

and the patient asked to perform provocative maneu- asking the patient to void, in order to evaluate the
vers including coughing and Valsalva. Loss of urine anatomy of the urethra, bladder and distal ureters.
with stress maneuvers indicates the diagnosis of stress
incontinence, whereas a sudden loss of a large volume
of urine with a rise in the meniscus in the syringe indi- Magnetic Resonance Imaging
cates urgency incontinence. Magnetic resonance imaging (MRI) in urogynecol-
ogy provides the opportunity to examine the soft tis-
Urodynamics sue structures of the pelvic support. It is noninvasive,
has excellent soft tissue contrast resolution without
Urodynamics is the functional study of the lower uri- exposure to ionizing radiation, and allows the study
nary tract, and will be further addressed in Chapter 7. of function of pelvic floor structures under differ-
The sequence of testing involves testing with a com- ent dynamic conditions such as increased abdominal
fortably full bladder for free (no catheter) uroflow- pressure during Valsalva. Several anatomical land-
metry and postvoid residual urine volume (PVR) marks used for pelvic measurements are also easily
measurement prior to filling and voiding (with cath- identified in MRI, and most measurements are thus
eter) cystometry. Uninstrumented uroflowmetry highly reproducible. Currently, the clinical value of
measures the rate, time, and volume of urine voiding. these examinations is still under investigation with its
Filling cystometry is the pressure/volume relationship impact on therapeutic decisions not yet fully evalu-
of the bladder during bladder filling. It begins with ated; MRI is not commonly used for the diagnosis of
the commencement of filling and ends when a “per- urinary incontinence.
mission to void” is given by the urodynamicist. Aims
of filling cystometry are to assess bladder sensation,
bladder capacity, detrusor activity, and bladder com- Ultrasound
pliance. Stress incontinence is evaluated by asking
Ultrasound is commonly used to assess postvoid resid-
patient to cough when supine, Valsalva when supine,
ual volumes. “Bladder scanners” give a volumetric
and then cough when standing up. Urethral pressure
assessment of residual urine volumes and are less inva-
profiles can also be performed, which indicate intra-
sive but more inaccurate than postvoid residual testing
luminal pressure along the length of the urethra. At
with a catheter. In addition to postvoid residual test-
the conclusion of the testing, women typically perform
ing, ultrasound is most commonly used for assessment
a second instrumented uroflowmetry, which not only
of the urethra for diagnosis of anatomic abnormalities,
measures the rate, time, and volume of the void, but
such as urethral diverticula.
also the pressures in the urethra, bladder, and rectum,
as a proxy for abdominal pressures.

URINARY INCONTINENCE/
Intravenous Urography OVERACTIVE BLADDER
Intravenous urography provides an anatomical outline QUESTIONNAIRES
of the urinary tract including the calyces, renal pel-
vis, ureter, and bladder. An injection of x-ray contrast In addition to the questionnaire that assesses a vari-
media is given to the patient intravenously. The con- ety of pelvic floor disorders in a single questionnaire,
trast media becomes visible on x-rays after injection such as the PFDI and the PFIQ, a variety of validated
because it is excreted by the kidneys. x-Rays are taken questionnaires specifically focus on the evaluation of
at specific time intervals to capture the contrast as it urinary incontinence and OAB. A sample of both
travels through the different parts of the urinary sys- symptom severity and QOL measures for urinary
tem. This gives a comprehensive view of the patient’s incontinence with their rating by the ICS is outlined
anatomy and some information on the functioning of in Table 4-3. Questionnaires are rated by the ICS
the renal system. based on their validity, reliability and responsiveness
and given a “Grade” (Table 4-4).
CHAPTER 4

Micturating Cystourethrogram
Incontinence Severity
Micturating cystourethrogram is used in the detection
of vesicoureteric reflux, stress incontinence, urethral
Index (ISI) (Grade A) 18-20
stricture, some fistulae, and diverticula. A micturat- This questionnaire provides a severity index of female
ing cystourethrogram is a specific radiological proce- incontinence. Two questions ask how often urine leak-
dure that is performed under fluoroscopic screening to age is experienced and how much urine is lost. The
visualize the bladder by filling it with contrast material two responses are multiplied together and categorized
Chapter 4 Clinical and Quality of Life Evaluation 69

Table 4-3 Psychometric Characteristics of Urinary Incontinence Questionnaires

Reliability Validity International


Continence
Construct
Number of Test- Face/ Society
Questionnaire Questions IC* retest content Criterion Concurrent Divergent Rating
Incontinence Severity 2 ¸ ¸ ¸ A**
Index (ISI)18-20
Urogenital distress 19 ¸ ¸ ¸ ¸ ¸ A
inventory long form
(UDI)21
Urogenital distress 6 ¸ ¸ ¸ ¸ ¸ A
inventory short form
(UDI-6)22
Incontinence Impact 30 ¸ ¸ ¸ ¸ A
Questionnaire long form
(IIQ)21
Incontinence Impact 7 ¸ ¸ ¸ A
Questionnaire short form
(IIQ-7)22
King’s Health 32 ¸ ¸ ¸ ¸ ¸ ¸ A
questionnaire (KHQ)23
Overactive Bladder 33 ¸ ¸ ¸ ¸ ¸ ¸ A
Questionnaire (OABq)24
Bristol Female Lower 12 ¸ ¸ ¸ ¸ A
Urinary Tract Symptoms
Questionnaire-short
form Incontinence
Symptoms (BFLUTS-SF)25
Patient perception 1 ¸ ¸ ¸ ¸ ¸ ¸ A
of bladder condition
(PPBC)27

¸ indicates that testing has been done on this property. Modified with permission from Ref.17
*Internal consistency.
**Graded in 2005 International consultation on Incontinence.

into slight (1–2), moderate (3–4), and severe (6–8).


Table 4-4 Criteria for Recommendation
This questionnaire has good levels of validity, reliabil-
of Questionnaires for UI and UI/LUTS
ity, and responsiveness.
at the International Consultation on
Incontinence 200826
Urogenital Distress Inventory
Long and Short Forms (UDI/UDI-6) Grade Definition
(Grade B/A)21,22 A Validity, reliability, and responsiveness
established with rigor in several data
This questionnaire was developed to assess the
sets
CHAPTER 4

degree to which symptoms are bothersome to indi-


viduals. The long form contains 19 lower urinary tract A new Validity, reliability, and responsiveness
indicated with rigor in one data set
symptoms grouped into three subscales of irritative
symptoms (nine questions), obstructive/discomfort B Validity, reliability, and responsiveness
(11 questions), and stress symptoms (two questions). indicated but not with rigor. To be used
Transformation of scores is done by subtracting one if suitable questionnaires not available in
ICIQ modular format or Grade A or
and multiplying times 100/3, which gives each sub-
Grade A new
scale a total possible score of 0 to 100 and a total
70 Section I Fundamental Topics

score ranging from 0 to 300. Reliability assessment The IIQ has been assessed in multiple clinical
included calculation of Cronbach α and for irritative trials.
symptoms (α values of 0.7), obstructive/discomfort The IIQ has also been shortened to seven items and
(α values of 0.77), and stress symptoms (α values of has been proven to have good validity and reliability.
0.48). Construct validity (convergent and divergent) Correlation with the long-form responses of the IIQ
was assessed using scores on measures including was 0.97. The correlations of the short form informal
the 36 item Short Form Health Survey, the Centers subscales with the long-form subscales ranged from
for Epidemiologic Studies-Depression Scale, the r values of 0.88 to 0.94, which verifies that the IIQ-7
Medical Outcomes Study measure of Social Support retains excellent representation of each separate life
1992, and the Profile of Mood States. Pad tests and impact domain. The IIQ-7 is part of the PFIQ dis-
urinary incontinence diaries were also used for con- cussed above.
vergent validity. Divergent construct validity was
assessed using age. Criterion validity was investigated
using physicians who were blind to the questionnaire King’s Health Questionnaire (KHQ)
responses to make the diagnosis of stress inconti- (Grade A)23
nence or detrusor instability with or without stress
This measure was developed at King’s College Hospi-
incontinence. Responsiveness to change was also ana-
tal in London as part of a large longitudinal study of
lyzed by assessing scores at baseline and 12 weeks’
QOL. The questionnaire has three sections. The first
follow-up visit. Data on the reliability, validity, and
section consists of two questions that measure over-
sensitivity to change of these measures demonstrate
all health as it relates to urinary symptoms. The sec-
that they are psychometrically strong. A short-form
ond section has 19 questions divided into domains of
version of the urogenital distress inventory (UDI-6)
QOL, which are incontinence impact, role limitations,
has been shown to be valid and reliable. The UDI is
physical limitations, social limitations, personal rela-
part of the PFDI discussed above.
tionships, emotions, sleep and energy, severity-coping
measures, general health perception, and symptom
Incontinence Impact Questionnaire severity. The third section measures level of bother or
Long and Short Forms (IIQ/IIQ-7) impact of urinary symptoms. The questionnaire has
(Grade A/A)21,22 been shown to have excellent reliability and validity
for women. Sensitivity to change has been shown suc-
The IIQ has a total of 30 items. Twenty-four of these cessfully in observational studies and in increasing
assess the degree to which urinary incontinence affect numbers of clinical trials.
daily activities such as shopping, recreation, and enter-
tainment and six assess the effects of urinary inconti-
nence on feelings such as fear, frustration, and anger. Overactive Bladder
Responses for these items range from 1 = not at all to Questionnaire (OABq) (Grade A)24
4 = greatly. IIQ is divided into four subscales; Physical
Activity (A; six items), Travel (T; six items), Social This questionnaire was developed to assess OAB symp-
Relationships (So; 10 items), and Emotional Health toms in both continent and incontinent patients. It
(E; eight items). Reliabilities for the subscales of IIQ consists of 33 items that assess symptoms (eight items)
were Physical Activity (α values of 0.87), Travel (α val- and health-related QOL impact of OAB (25 items).
ues of 0.87), Social (α values of 0.90), and Emotional High internal consistency has been shown with
(α values of 0.90). Construct validity using measures Cronbach α ranging from 0.86 to 0.94. This question-
including the 36 item Short Form Health Survey, naire has also demonstrated good responsiveness. The
the Centers for Epidemiologic Studies-Depression OABq showed moderate correlation (r = 0.16–0.52)
Scale, the Medical Outcomes Study measure of Social with subscales of the SF-36.
Support 1992, and the Profile of Mood States was
performed. There was moderate correlation (mean
Bristol Female Lower Urinary Tract
r value = 0.37) indicating that the IIQ measures more
Symptoms (BFLUTS-SF) (Grade A)25
CHAPTER 4

than the general health state and therefore supports


the construct validity. The number of incontinent epi- The short-form questionnaire was derived from a lon-
sodes and pad test results correlated significantly with ger questionnaire that assessed the occurrence and
the IIQ during assessment of convergent construct symptom bother relating to incontinence and other
validity. The only significant difference was lower lower urinary tract symptoms for women. Factor
scores on the Travel subscale for detrusor instability analysis and clinical judgment were used to develop
with or without genuine stress incontinence. The IIQ a shortened scored version of the BFLUTS ques-
is also responsive to change. tionnaire that comprises three subscales consisting of
Chapter 4 Clinical and Quality of Life Evaluation 71

BFLUTS-IS (incontinence symptoms), BFLUTS-VS cause, colonoscopy is indicated to evaluate for neo-
(voiding symptoms), and BFLUTS-FS (filling symp- plasm, or inflammatory bowel disease. Sudden-onset
toms) with the addition of subscales for sexual function anal incontinence associated with diarrhea should
(BFLUTS-sex) and QOL impact (BFLUTS-QoL). trigger evaluation for infections such as those respon-
Validity assessment included content/face valid- sible for acute gastroenteritis, such as Campylobacter,
ity by interviewing clinicians and construct valid- Shigella, or Clostridium difficile.
ity by comparing answers from a community group
and a clinical group. Women in community group Physical Examination
reported lower prevalence of symptoms than those
in clinical setting. Criterion validity was assessed by Careful inspection of the anus and perineum should
correlation with pad testing and frequency/volume be performed. There may be evidence of fecal incon-
charts. Reliability and responsiveness were assessed. tinence in the form of stool soiling. Assessment is also
Reliability testing of all symptom questions gave a performed to look for scars, perineal body length,
high Cronbach α of 0.78. Subgrouping of catego- hemorrhoids, rectal prolapse, “dovetail” sign and peri-
ries into storage, voiding, and incontinence showed rectal dimpling, and other anatomic abnormalities. A
Cronbach α of 0.48, 0.72, and 0.82 for incontinence, dovetail sign is associated with radial folds posteriorly
voiding, and filling symptoms, respectively. Test-retest to the anus, with loss of those folds anteriorly, pre-
reliability was assessed at two weeks’ interval and was sumably secondary to sphincter injury (Figure 4-4).
similarly found to be high. Dimpling can be observed on the perineum where
the ends of the sphincter lie when the sphincter con-
tracts. Perianal reflexes specific to the anus include a
Patient Perception of Bladder perianal wink, which assesses pudendal innervation of
Condition (PPBC) (Grade A) 27 the external anal sphincter. The perianal skin is gen-
This is a questionnaire consisting of a single question tly stroked with a cotton-tipped swab and cutaneous
that assesses patients’ perception of their bladder con- anal wink is elicited. Rectal examination is performed.
dition. The questionnaire has a choice of one of six
statements that best describe present bladder condi-
tion. This questionnaire has been validated in two clin-
ical studies evaluating the tolerability and efficacy of
tolterodine in patients with OAB and correlated with
responses to OABq and KHQ.

CLINICAL ASSESSMENT
OF BOWEL DISORDERS
Anal Incontinence
History
The history of patients with anal incontinence should
also include past medical, obstetrical and surgical
history; current medication use, including the use of
laxatives and enemas and bowel habits (Table 4-2).
In addition, a history of food sensitivities should be
included. Risk factors that predispose to fecal incon-
tinence include obstetric injury to the anal sphincter
at the time of delivery, increasing parity and medical
conditions such as stroke, diabetes, and constipation.
CHAPTER 4

An anal incontinence history should include number


of incontinence episodes, type of loss (gas, mucus,
stool), consistency of stool at the time of incontinence,
amount of stool lost, use of pads, type and number of
pads used. The patient’s history of colonoscopy, irrita-
ble bowel syndrome, as well as history of inflammatory
bowel disease should be noted. For patients with new- FIGURE 4-4 Dovetail sign. Radial folds are seen posteri-
onset incontinence without an underlying infectious orly with loss of radial folds anterior to the anal opening.
72 Section I Fundamental Topics

The integrity of the external anal sphincter, resting Advanced Studies


and squeeze tone, is then assessed. Although vali-
Magnetic Resonance Imaging/
dated measures of anal tone do not exist, a compar-
Endoanal Magnetic Resonance Imaging
ison of anal sphincter tone to manometry measures
Endoanal MRI has a complementary role with endo-
indicated that digital examination was effective in
sonography. It has the advantages of multiplanar imag-
identifying weak sphincters.28 The patient should be
ing and of defining the striated components of the
asked to perform a Valsalva maneuver at the end of the
sphincter with great clarity, although its clinical util-
examination to see whether dyssynergia or rectal pro-
ity is limited not only because of limited availability,
lapse is present. Dyssynergia occurs when the patient
but also because of discomfort of patients with the
contracts the pelvic floor rather than relaxing when
examination.
attempting to defecate.

Clinic-based Tests Constipation


Anorectal Manometry Functional constipation comprises a group of disor-
Rectal pressure is measured using this technique. ders that present as persistent, difficult, infrequent,
The test consists of inserting a small, flexible tube or incomplete defecation, and is a common com-
that has an inflatable balloon tip and a pressure plaint among women with pelvic floor dysfunction.
transducer. Resting and squeeze pressures are mea- Constipation occurs in up to 20% of women, depend-
sured, as well as various anorectal reflexes and rectal ing on demographic factors, sampling, and the defini-
and anal sensation. Anal manometry can be used to tion used. Rome criteria were developed for defining
identify women with Hirschsprung’s disease by the bowel dysfunction (Table 4-5). The Rome II commit-
absence of the rectoanal inhibitory reflex. The reflex tees30 and, more recently, the Rome III Board29 took on
is elicited with the transient distension of the rectum, the responsibility to enhance these criteria. According
inducing a temporary relaxation of the anal internal to these criteria, patients have at least 12 weeks, which
sphincter, and plays a major role in the continence need not be consecutive, in the preceding 12 months
and defecation. Anal manometry is discussed further of two or more of the symptoms listed in Table 4-5.
in Chapter 11. Women with constipation should be assessed for
general health, psychological status, use of constipat-
ing medications, dietary fiber intake, and medical ill-
Imaging
nesses (eg, hypothyroidism). In patients who do not
Anal endosonography is used to assess disruption
respond to increased fluid intake and fiber supplemen-
of internal and external anal sphincters and helps
tation, measurements of whole gut transit time and
guide surgical management. The technique involves
anorectal function may be indicated.
placing a transducer in the rectum, which provides
a 360-degree evaluation of the anal canal. Images
can be obtained which are both two-dimensional Physical Examination
(2D) and 3D. In addition to endoanal imaging, Findings on digital rectal examination may include
transperineal, also termed translabial, imaging of anal stricture or mass, paradoxical contraction of the
the sphincter complex is also performed. This tech- puborectalis, nondescent of perineum and rectocele/
nique utilizes a vaginal probe, which is placed at the enterocele.
vaginal introitus and angled posteriorly. The trans-
perineal technique has the added advantage of not
distorting the anal sphincter complex and is less Table 4-5 Rome Criteria II29
uncomfortable for the patient. Transperineal images
can be obtained in both 2D and 3D. Both techniques 1. Straining in more than one-fourth defecations
also allow for imaging of the muscles of the levator 2. Lumpy or hard stools in more than one-fourth
ani. Defecography demonstrates normal anatomy of defecations
the anorectum as well as disorders of rectal evacu- 3. Sensation of incomplete evacuation in more than
CHAPTER 4

ation. Barium paste is inserted rectally prior to def- one-fourth defecations


ecation over a translucent commode. The anorectal 4. Sensation of anorectal obstruction/ blockade in
angle is the angle made by the puborectalis muscle more than one-fourth defecations
and is measured in degrees using this modality. In
5. Manual maneuvers to facilitate more than one-
addition, the presence, size, or emptying of any rec- fourth defecations (eg, digital evacuation, support
tocele is noted. Enteroceles, rectal intusssusception, of the pelvic floor)
and mucosal prolapse as well as anismus, or a spastic
6. <3 Defecations/wk
pelvic floor, may be diagnosed.
Chapter 4 Clinical and Quality of Life Evaluation 73

Further Studies
A colonoscopy should be performed to seek intralumi-
nal pathology as the cause of constipation. In addition
to colonoscopy, a barium enema can help identify a
variety of colonic abnormalities such as a redundant
colon or extrinsic compression.
The next step should be physiologic testing
explained in more detail in Chapter 10. The radi-
opaque marker method, first described by Hinton,31
involves ingesting 24 markers and taking an abdomi-
nal radiograph on day three and five. Colonic transit
is assessed by the distribution of the markers with
at least 80% of the markers eliminated by day five.
Similarly a scintigraphic technique involves ingest- FIGURE 4-5 Rectal prolapse.
ing pellets labeled with either technetium-99m or
indium-111 and identifying the distribution of signal
when performing a scan. This technique can iden- rectal prolapse including chronic constipation and
tify delayed segmental colonic transit, and delayed straining should be gathered. A screening evaluation
small bowel transit. Paradoxical contraction of the of the colon with endoscopy or barium enema is rec-
puborectalis causing constipation may be assessed by ommended in adults to exclude coexisting conditions
anal sphincter electromyography. such as diverticular disease, which may influence the
choice of procedure to correct the prolapse. Common
testing options include cinedefecography to check
Fecal Urgency movement of the pelvic floor, anorectal manometry
Fecal (rectal) urgency is defined as a sudden, compel- to measure the pressure generated by the sphincter
ling desire to defecate that is difficult to defer. Fecal muscles, and electromyography to check for denerva-
(flatal) urgency incontinence is the involuntary loss of tion and colon transit studies. It is postulated that an
feces (flatus) associated with urgency. Fecal urgency is increased sigmoid transit time is a significant factor in
a symptom rather than a condition. The Rome diag- the cause of incontinence that is associated with rectal
nostic30 criteria for functional bowel disorders con- prolapse.31
sider fecal urgency to be a supportive symptom for
the diagnosis of irritable bowel syndrome, defined as
“having to rush to have a bowel movement.” This may BOWEL DISORDER
predispose individuals to fecal incontinence.
QUESTIONNAIRES
Rectal Prolapse Questionnaires for functional bowel disorders are not
in general as developed as those for urinary symptoms
Rectal prolapse is the complaint of external protru- and the grading of these scales by the International
sion of the rectum. The classic description of rectal Continence Society is less rigorous. (Table 4-6). There
prolapse, or procidentia, is a protrusion of the rec- are no Grade A scales recommended.
tum beyond the anus. The symptoms of rectal pro-
lapse closely mimic the warning signs that the public
is taught for rectal cancer: presence of a mass, bleed- Table 4-6 Criteria for Recommendation
ing, protrusion and a change in bowel habits. Earliest of Questionnaires for POP and FI at the
symptoms include a reducible protrusion that may International Consultation on Incontinence34
be associated with a mucous discharge (Figure 4-5).
Early in the course, rectal prolapse may only occur Grade Definition
CHAPTER 4

in association with bowel movements. The patient


A Validity, reliability, and responsiveness
may complain of a feeling of incomplete evacuation established with rigor
or tenesmus. Later, after the prolapse has been pres-
B Validity and reliability established with rigor,
ent for some time, the patient may experience loss of
or validity, reliability, and responsiveness
control of stool because of stretching of the sphincter
indicated.
muscles and damage to the pudendal nerves.
A complete history and a physical examination are C Early development –further work required
and encouraged
required. An assessment of specific risk factors for
74 Section I Fundamental Topics

Table 4-7 Psychometric Characteristics of Fecal Incontinence Questionnaires

Reliability Validity International


Continence
Construct
Number of Test- Society
Questionnaire Questions IC* retest Face Criterion Concurrent Divergent rating
Fecal Incontinence 29 ¸ ¸ ¸ ¸ B
Quality of Life Scale
(FIQL)35
Manchester Health 31 ¸ ¸ ¸ ¸ ¸ B
Questionnaire (MHQ)38
Birmingham Bowel 22 ¸ ¸ ¸ ¸ ¸ B
and Urinary Symptoms
Questionnaire
(BBUSQ)32, 33
*Internal consistency.

Birmingham Bowel and Urinary divergent validity, patients with fecal incontinence had
Symptoms Questionnaire (BBUSQ) a significantly lower QOL score than the controls for
(Grade B)32,33 each of the four scales (P < 0.01). There is no report
yet on unscreened populations and responsiveness.
This is a 22-item questionnaire covering various bowel
and urinary symptoms (Table 4-7). The question-
naire evaluates passive and urge incontinence (four Manchester Health
items), evacuatory function (seven items), stool con- Questionnaire (MHQ) (Grade B)38
sistency (one item), frequency of laxative use or medi- This questionnaire is adapted from the King’s
cal consultation (two items), and urinary symptoms Health Questionnaire. A five-point scoring assesses
(eight items). Feedback was obtained from patients the domains of general perception of health, general
after the questionnaire was constructed for readabil- impact of incontinence, role, physical function, social
ity and clarity. The questionnaire was tested in various function, personal relationships, emotion, sleep/energy,
clinics including an urogynecology clinic, gynecology and severity/coping measures. There is a separate scale
departments of three hospitals, a functional bowel for the assessment of the severity of symptoms.
clinic, and a general practice. Content and construct Content validity was performed by two experts by
validity was performed by expert clinicians and scien- sending out the questionnaires to 15 patients with
tists and by factor analysis respectively. known fecal incontinence for three cycles. Criterion
and convergent validity was assessed against SF-36
questionnaire. Pearson correlations ranged from 0.30
Fecal Incontinence Quality to 0.65 for all domains and were all statistically sig-
of Life Scale (FIQL) (Grade B)37 nificant. Internal consistency (Cronbach α) ranged
This questionnaire measures the impact of fecal incon- from 0.73 to 0.91 for all domains. Test-retest reliability
tinence of health-related QOL (HRQL). Twenty- conducted between one and two weeks after the initial
nine items were developed and tested consisting of four questionnaire was answered, showed a range of 0.81 to
scales of HRQL including Lifestyle (ten items), Coping/ 0.93 using Pearson correlation. Responsiveness has not
behavior (nine items), Depression/self-perception yet been assessed.
(seven items), and Embarrassment (three items).
Internal reliability on all four scales showed Fecal Incontinence
CHAPTER 4

Cronbach α values of 0.70. The test re-test reliabil-


ity showed no significant differences between tests.
Severity Index (FISI) (Ungraded)35
Convergent and discriminant validity was assessed. This instrument was developed for assessment of
For convergent validity, FIQL scales were correlated severity of fecal incontinence including gas, mucus,
with comparable scales found in SF-36. These ranged liquid, and solid stool incontinence. A type and fre-
from r values of 0.65 (FIQL depression, SF-36 Mental quency of 20-cell matrix was filled out by surgeons
Health) to 0.28 (FIQL embarrassment, SF-36 Role and patients to rank the severity of symptoms relative
Physical) and were all statistically significant. For to each other assigning a “1” to most severe and “20”
Chapter 4 Clinical and Quality of Life Evaluation 75

to least severe symptom. Severity rankings showed vaginal bleeding should be evaluated for other causes
that rankings for surgeons and patients correlated very of the bleeding, particularly in postmenopausal
highly. Correlations were high between each of the women with a uterus, who should undergo endome-
four FIQL scale scores filled out by patients and sur- trial evaluation.
geons and severity weights. Patients with prolapse often need to splint or digi-
tate in order to defecate or urinate. Splinting is the
complaint of the need to digitally replace the prolapse
Patient Assessment of Constipation or to otherwise apply manual pressure to the vagina or
(PAC-SYM/PAC-QOL) (Ungraded)36 perineum (splinting), or to the vagina or rectum (digi-
This is a self-report instrument consisting of two com- tation) to assist voiding or defecation. Patients may
plementary components: the Symptom Questionnaire complain of low, sacral (or “period like”) backache
(PAC-SYM) and the QOL Questionnaire (PAC- associated temporally with POP (Table 4-2).
QOL). Items for symptom development (PAC-SYM)
were developed through literature review and focus-
Physical Examination
group patient interviews. The questionnaire consists of
12 items and three domains: rectal, abdominal, and The choice of the woman’s position during examina-
stool symptoms. Intraclass correlations for the sub- tion, for example, left lateral (Sims), supine, standing,
scales on test-retest were 0.70 or more. The Cronbach or lithotomy, is that which can best demonstrate POP
α for the entire questionnaire was 0.89. Concurrent in that patient and which the woman can confirm, by
and discriminant validity and responsiveness have use of a mirror or digital palpation, the severity of the
also been assessed, and this instrument was noted to prolapse that she has experienced. The hymen remains
be valid and responsive. PAC-QOL is a 28-item self- the fixed point of reference for prolapse description.
administered condition-specific QOL instrument for All examinations for POP should be performed with
constipation with four subscales: physical discomfort, the woman’s bladder empty and, if possible, an empty
psychosocial discomfort, worries and concerns, and rectum. Increasing bladder volume has been shown to
satisfaction. Total score and scores for subscales range restrict the degree of descent of the prolapse.39
from 0 to 4 with lower scores indicating better QOL.
This instrument has also been shown to be reliable Pelvic Organ Prolapse Measurement
and valid.
POP has been graded using multiple systems over
time. These include the Pelvic Organ Prolapse Quan-
tification (POP-Q) examination, Baden-Walker sys-
PELVIC ORGAN PROLAPSE tem,40 Beecham system,41 or nonstandardized systems,
which only addresses the type of defect but not sever-
History ity.42 The attempt to standardize POP description has
Prolapse symptoms include abnormal sensation, evolved, and currently the ICS recommends using the
structure or function, experienced by the woman in POP-Q for measuring degree of prolapse.43
reference to the position of her pelvic organs. In gen- The POP-Q is a site-specific system that consists of
eral, symptoms are worse at times when gravity makes six points, two on the anterior vaginal wall, two in the
prolapse worse, such as after long periods of stand- superior vagina, and two on the posterior vaginal wall
ing or exercise, and better when gravity is not a fac- whose position is described in relationship to the plane
tor, for example, when the patient is lying supine. of the hymen.
Prolapse may be more prominent at times of abdomi- The measurements are then recorded in a “3 by 3”
nal straining, which occurs with lifting and defecation. grid as noted in Figure 4-6 followed by staging.
Symptoms associated with prolapse include vaginal
bulging, pelvic pressure, bleeding, and low backache.
Vaginal bulging consists of a complaint of a “bulge” Aa Ba C
or “something coming down” toward or through the
CHAPTER 4

vaginal introitus. The woman may state she can either


feel the bulge by direct palpation or see it aided with GH PB TVL
a mirror. With pelvic pressure, patients complain of
increased heaviness or dragging in the suprapubic area
and/or pelvis. Complaints of vaginal bleeding, dis- Ap Bp D
charge, or infection can be related to dependent ulcer-
ation of the prolapse and may accompany symptoms
of pressure. Nonetheless, patients with unexplained FIGURE 4-6 POP-Q measurements in a “3 by 3” grid.
76 Section I Fundamental Topics

Table 4-8 Staging of Pelvic Organ Prolapse43 To assess the anterior vaginal wall, a half speculum
is inserted to reduce the posterior vaginal wall and the
Stage Definition patient is asked to Valsalva. Patients who are unable
Stage 0 No prolapse is demonstrated. Points to volitionally Valsalva may be asked to cough to dem-
Aa, Ap, Ba, and Bp are all at −3 cm and onstrate pelvic organ descent, although reflexive con-
points C and D are <2cm of descent traction of the pelvic floor may diminish the amount
Stage I The criteria for stage 0 are not met,
of prolapse observed. The posterior vaginal prolapse
but the most distal portion of the is assessed similarly, with reduction of the anterior
prolapse is >1 cm above the level of vaginal wall with a split speculum. The apex can be
the hymen assessed by placing the calibrated scopette on the
Stage II The most distal portion of the prolapse cervix or cuff and asking the patient to strain; assess-
is within 1 cm above or below the plane ment of point D of the POP-Q is assessed in a similar
of the hymen, descends no further than fashion (Figure 4-8). It is important to confirm that
2 cm less than TVL the degree of prolapse observed during examination
Stage III The most distal portion of the prolapse recapitulates the degree of prolapse that the patient
is >1 cm below the plane of the hymen has experienced outside of clinic. Use of a handheld
but protrudes no further than 2 cm mirror can help confirm that the POP-Q findings are
less than the total vaginal length accurate. Further description of each of the stages is
Stage IV Complete eversion of the total length noted in Table 4-8.
of the vagina is demonstrated. The distal
portion of the prolapse descends to at
least (TVL-2) cm. Mostly instances, the
Clinic-based Tests
leading edge of stage IV prolapse is the In patients with significant prolapse, postvoid residual
cervix or vaginal cuff testing is indicated, particularly if women have urinary
TVL, total vaginal length. as well as prolapse symptoms.

Imaging
Staging Although clinical assessment of prolapse does not
typically require imaging, several modalities, including
Based on the degree of prolapse, staging further ultrasound and MRI, have been used to further assess
describes the severity of prolapse (Table 4-8). Stages pelvic anatomy in women with prolapse. Most of these
range from 0 to 4, with Stage 0 indicating perfect vagi- modalities are utilized in the research setting.
nal support and Stage 4 indicating complete vaginal
eversion. In order to assess prolapse, an instrument
to measure descent, such as a calibrated scopette Magnetic Resonance Imaging
(Figure 4-7) as well as speculum, is required. To determine the presence and extent of POP, a point
of reference for rest and Valsalva measurements is
required. Several reference points and lines for mea-
suring and staging POP on MRI have been proposed.
The two most commonly used lines are a line con-
necting the inferior aspect of the pubic symphysis
to the anterior margin of the sacrococcygeal junc-
tion, the pubococcygeal line (PCL) which approxi-
mates the levator plate and a line extending caudally
along the long axis of the pubic bone, the midpubic
line (MPL). After choosing the reference line, staging
of POP in the anterior, apical and posterior compart-
CHAPTER 4

ments may be performed. This is done by perpen-


dicularly measuring the distance from the anatomic
reference point in each compartment to the reference
line. The reference point in the anterior compartment
is the most posteroinferior part of the bladder base, in
the apical compartment is the anterior cervical lip or
the vaginal apex in a post-hysterectomy patient and
FIGURE 4-7 Calibrated scopette. in the posterior compartment is the anterior aspect
Chapter 4 Clinical and Quality of Life Evaluation 77

A B

FIGURE 4-8 Pelvic organ prolapse. A. Anterior defect (cystocele). B. Posterior defect (rectocele).

of the anorectal junction. The largest measurement PELVIC ORGAN PROLAPSE


below or closest to the reference line during Valsalva QUESTIONNAIRES
or evacuation is used to stage POP.
Prolapse questionnaires are limited. The most com-
Ultrasound monly used are the PFDI and PFIQ, which evaluate
Ultrasound imaging can identify a number of entities all three pelvic floor disorders including prolapse.
that may be difficult to distinguish clinically and can
enhance clinical examinations and help tailor treat-
ment appropriately. Occasionally, anterior prolapse Pelvic Floor Distress Inventory
will turn out to be due to a urethral diverticulum, a (Grade A Described Above) and
Gartner duct cyst, or an anterior enterocele, which Pelvic Floor Impact Questionnaire
may be missed on clinical examination. Synthetic (Grade A Described Above)7
mesh implants used in incontinence and prolapse sur- The PFDI and PFIQ have been discussed earlier under
gery are visible on ultrasound imaging; their identifi- the section “Questionnaires that Evaluate a Range of
cation may aid in planning for another repair or for Pelvic Floor Dysfunction.” The PFIQ accompanies the
removal if the previous repair has failed. PFDI and assesses the impact of POP, lower urinary
In the posterior compartment, prolapse could be tract and gastrointestinal tract on QOL (Table 4-9).
due to a true “rectocele,” that is, a defect of the recto-
vaginal septum, or due to an abnormally distensible,
intact rectovaginal septum, a combined rectoentero-
cele, an isolated enterocele, a deficient perineum
OTHER QUESTIONNAIRES AND
(perineocele) giving the impression of a “bulge,” or MEASURES USED TO EVALUATE
PELVIC FLOOR DYSFUNCTION
CHAPTER 4

even a rectal intussusception, a condition that is not


uncommon among urogynecological patients, and
almost always overlooked. Translabial ultrasound is Sexual Health Questionnaires
a suitable screening tool for these conditions, with
Sexual Function Questionnaires
results largely comparable to defecation proctogra-
phy. Ultrasound is increasingly being used not just Sexual function is an important component of
by gynecologists but also by colorectal surgeons and HRQL (Table 4-10). The Pelvic Organ Prolapse/
gastroenterologists.44 Urinary Incontinence Questionnaire (PISQ) long
78 Section I Fundamental Topics

Table 4-9 Psychometric Characteristics of Pelvic Organ Prolapse Questionnaires

Reliability Validity International


Continence
Construct
Number of Test- Society
Questionnaire Questions IC* retest Face Criterion Concurrent Divergent Rating
Pelvic Floor Distress 46 ¸ ¸ ¸ ¸ ¸ ¸ A
Inventory (PFDI)7
Pelvic Floor Impact 93 ¸ ¸ ¸ ¸ ¸ ¸ A
Questionnaire (PFIQ)7

*Internal consistency

and short forms are the only condition-specific the questionnaire PISQ-31 (r = 0.75–0.95) and the
questionnaires for assessment of sexual function in Sexual History Form-12 and the IIQ-7. Test-retest
patients with pelvic organ prolapse and/or urinary reliability was moderate to high. Good agreement was
incontinence. noted in 30 out of 31 items (Table 4-10).

Pelvic Organ Prolapse/Urinary Incontinence Sexual Golombok-Rust Inventory of


Questionnaire (PISQ/PISQ-12) (Grade A)45,48 Sexual Satisfaction (GRISS) (Grade A)46
The 31 items in the questionnaire are divided into This is a questionnaire that is designed to assess
three domains: Behavior-Emotive, Physical, and the quality of a sexual relationship in a heterosexual
Partner-related. Questions specifically address the couple. It consists of 56 questions 28 of which are
impact of urinary incontinence and/or POP on sex- for females and the remainder for males. There are
ual function. The measure has been found to have 12 domain scores, five of which are female-specific
convergent and divergent validity. A short-form ver- (Dissatisfaction, Nonsexuality, Avoidance, Vaginismus,
sion of the questionnaire has also been developed and Anorgasmia), five are male-specific, and two
(PISQ-12). Construct validity of the PISQ-12 was (Noncommunication and Frequency of Sexual
examined through correlations with the long form of Contact) are not related to gender (Table 4-10).

Table 4-10 Psychometric Characteristics of Sexual Function Questionnaires

Reliability Validity International


Continence
Construct
Number of Test- Society
Questionnaire Questions IC* retest Face Criterion Concurrent Divergent Rating
Pelvic Organ 31 ¸ ¸ ¸ ¸ ¸ ¸ A
Prolapse/Urinary
Incontinence Sexual
Questionnaire- long
form (PISQ)45
Pelvic Organ 12 ¸ ¸ ¸ ¸ ¸ ¸ A
Prolapse/Urinary
Incontinence Sexual
Questionnaire- short
CHAPTER 4

form (PISQ-12)48
Golombok Rust 56 (28 for ¸ ¸ ¸ ¸ ¸ ¸ A
Inventory of Sexual females)
Satisfaction (GRISS)46
Female Sexual 19 ¸ ¸ ¸ ¸ B
Function Index (FSFI)47

*Internal consistency
Chapter 4 Clinical and Quality of Life Evaluation 79

Female Sexual Function Index (FSFI) (Grade B)47 7. Barber MD, Kuchibhatla MN, Pieper CF, Bump RC. Psycho-
The 19-items in this questionnaire are divided into metric evaluation of 2 comprehensive condition-specific quality
of life instruments for women with pelvic floor disorders. Am J
six sexual function domains consisting of Desire, Obstet Gynecol. 2001;185(6):1388–1395.
Lubrication, Orgasm, Arousal, Pain, and Satisfaction. 8. National Institute for Health and Clinical Excellence. Uri-
Psychometric properties including internal consistency, nary incontinence: the management of urinary incontinence in
test-retest reliability, and discriminant validity has been women. (Clinical guideline 40.) 2006. Available at: www.nice.
assessed. A short form, the Female Sexual Funtion org.uk/nicemedia/pdf/CG40fullguideline.pdf.
9. Bergman A, Koonings PP, Ballard CA. Negative Q-tip test as a
Index-6, has also been developed and its psychometric risk factor for failed incontinence surgery in women. J Reprod
properties assessed. Reliability, internal consistency, and Med. 1989;34(3):193–197.
stability on retest were good.49 10. Haylen BT, de Ridder D, Freeman RM, et al. An Interna-
tional Urogynecological Association (IUGA)/International
Continence Society (ICS) joint report on the terminology for
General Health female pelvic floor dysfunction. Neurourol Urodyn. 2010;29(1):
4–20.
HRQL measures refer to a person’s complete well- 11. Brink CA, Sampselle CM, Wells TJ, Diokno AC, Gillis GL. A
being and take into consideration several dimensions digital test for pelvic muscle strength in older women with uri-
including social, physical, and emotional health. These nary incontinence. Nurs Res. 1989;38:196–199.
measures may be condition-specific or generic. One 12. Laycock J. Clinical evaluation of pelvic floor. In: Schussler B,
of the most commonly used generic questionnaires in Laycock J, Norton P, Stanton S, eds. Pelvic Floor Re-education.
London: Springer-Verlag; 1994:42–48.
women with pelvic floor disorders is the SF-36. 13. Sutherst J, Brown M, Shawer M. Assessing the severity of uri-
nary incontinence in women by weighing perineal pads. Lancet.
Medical Outcomes Study Short 1981;1:1128–1130.
form SF-36/SF-20 and SF-1250–52 14. Versi E, Cardozo LD. Perineal pad weighing versus video-
The SF-36 is a 36-item questionnaire developed as part graphic analysis in genuine stress incontinence. Br J Obstet Gyn-
aecol. 1986;93:364–366.
of the Medical Outcomes Study in the United States. 15. Lose G, Jorgensen L, Thunedborg P. 24-hour home pad weigh-
It has eight domains which are physical functioning, ing test versus 1-hour ward test in the assessment of mild stress
bodily pain, role limitations due to physical health incontinence. Acta Obstet Gynecol Scand. 1989;68:211–215.
problems, role limitations due to personal or emotional 16. Mouritsen L, Berild G, Hertz J. Comparison of different meth-
problems, general mental health, social functioning, ods for quantification of urinary leakage in incontinent women.
Neurourol Urodyn. 1989;8:579–587.
energy/fatigue, and general health perceptions. This 17. Abrams P, Cardozo L, Khoury S, Wein A. Incontinence. In:
instrument has good construct, discriminant validity, Committee 5B–A. Patient-reported Outcome Assessment. 4th Inter-
and internal consistency. national Consultation on Incontinence. 4th ed. 2009:363–413.
For the most part, general health questionnaires 18. Sandvik H, Hunskaar S, Seim A, Hermstad R, Vanvik A, Bratt
have limited responses to changes in pelvic floor func- H. Validation of a severity index in female urinary incontinence
and its implementation in an epidemiological survey. J Epide-
tion, and for assessment of changes in quality of life, miol Community Health. 1993;47:497–499.
condition-specific measures are recommended in addi- 19. Hanley J, Capewell A, Hagen S. Validity study of the severity
tion to a thorough history and physical examination. index, a simple measure of urinary incontinence in women.
BMJ. 2001;322(7294):1096–1097.
20. Hagen S, Hanley J, Capewell A. Test-retest reliability, validity,
and sensitivity to change of the urogenital distress inventory
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Gynecol. 2004;191(1):73–82. conventional concepts of pelvic floor weaknesses. Neurourol
26. Abrams P, Cardozo L, Khoury S, Wein A, ed. Incontinence. Ini- Urodyn. 1993;12:310–311.
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in women. BJOG. 2002;109(4):424–430. Qualls C. A short form of the Pelvic Organ Prolapse/Urinary
34. Abrams P, Cardozo L, Khoury S, Wein A, ed. Incontinence. Ini- Incontinence Sexual Questionnaire (PISQ-12). Int Urogynecol J
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and female patients. In: 4th International Consultation on Inconti- 49. Isidori AM, Pozza C, Esposito K, Giugliano D, Morano S,
nence, Paris, July 5–8, 2008. 4th ed. Editions 21, France: Health Vignozzi L, Corona G, Lenzi A, Jannini EA. Development and
Publication Ltd; 2009:369. validation of a 6-item version of female sexual function index
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Dis Colon Rectum. 1999;42(12):1525–1532. health survey (SF-36). I. Conceptual framework and item selec-
36. Frank L, Kleinman L, Farup C, Taylor L, Miner P Jr. Psycho- tion. Med Care. 1992;30(6):473–483.
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37. Rockwood TH, Church JM, Fleshman JW, et al. Patient and cal tests of validity in measuring physical and mental health
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38. Bug GJ, Hosker GL, Kiff ES. Routine symptom screen- quality, scaling assumptions, and reliability across diverse
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CHAPTER 4
Section II Disease States

Part A: Lower Urinary Tract Dysfunction


5 Stress Urinary Incontinence 83

6 Urgency and Mixed Urinary Incontinence 99

7 Evaluation of Bladder Function 119

8 Voiding Phase Dysfunction 135

Part B: Functional Anorectal Disorders


9 Anal Incontinence 153

10 Defecatory Dysfunction 173

11 Anorectal Investigations 191

Part C: Pelvic Organ Prolapse


12 Pelvic Organ Prolapse: Anterior Prolapse 209

13 Posterior Vaginal Wall Prolapse 225

14 Apical Pelvic Organ Prolapse 245

15 Pelvic Imaging 265

Part D: Other Pelvic Floor Disorders


16 Pain of Urogenital Origin 279

17 Urinary Tract Infections 301

18 Female Sexual Dysfunction 315


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Part A: Lower Urinary Tract Dysfunction

5
1 Stress Urinary Incontinence
Charles R. Rardin and Nicole B. Korbly

DEFINITION Closure of the urethra is essential during filling and


storage of urine in order to prevent leakage. If the ure-
Urinary incontinence is defined by the International thral closure mechanism is incompetent, it allows leak-
Continence Society (ICS) as “the complaint of invol- age of urine in the absence of a detrusor contraction.
untary leakage of urine.” The most common forms of Both intrinsic and extrinsic factors contribute to the
urinary incontinence are classified as stress, urgency, symptoms of SUI. Intrinsic factors are those related to
and mixed urinary incontinence. The current ICS the function of the urethra, whereas extrinsic factors
definition of stress urinary incontinence (SUI) is sub- are secondary to influences apart from the urethra,
jective based on symptoms perceived by the patient: such as patient level of activity or weight and urethral
“stress urinary incontinence is the complaint of invol- support. Increasingly rigorous investigation into the
untary leakage on effort or exertion, or on sneezing or epidemiology, anatomy, physiology, and neurology of
coughing.”1 In contrast, urgency urinary incontinence SUI has promoted the understanding of normal and
is “the complaint of involuntary leakage accompanied incontinent states; this chapter provides an overview
by or immediately preceded by urgency,” and mixed of current understanding of these mechanisms, as well
urinary incontinence is “a combination of symptoms as their limitations.
of both stress and urgency urinary incontinence.”
The definition of SUI has evolved over time into
its current subjective definition. It was previously EPIDEMIOLOGY
referred to as “genuine stress incontinence (GSI)”
by the 1990 ICS Standardization of Terminology of Prevalence rates for SUI are wide, with reported
Lower Urinary Tract Function. GSI was defined as ranges from as low as 4% to as high as 70%,2 and
“the involuntary loss of urine occurring when, in the vary by age. SUI is common in younger women with
absence of a detrusor contraction, the intravesical estimated rates of 4% to 23% in women age 20 to
pressure exceeds the maximum urethral pressure.” 39 years. Prevalence rates peak by age 50 to 60 years,
With the revision of the ICS terminology in 2002, with estimated rates of 16% to 36% in women age
GSI was replaced by the term “urodynamic stress 40 to 59 years.2 Older women are more likely to be
incontinence.” Urodynamic stress incontinence is the affected by urgency urinary incontinence and mixed
observation during filling cystometry of involuntary urinary incontinence than SUI.
leaking of urine during increased abdominal pressure, Multiple studies report different prevalence rates
in the absence of a detrusor contraction. The evolu- of urinary incontinence between different racial
tion of the definition of SUI underlines the impor- groups. African-American women are less affected
tance of eliciting the patients’ subjective experience of by SUI compared to Caucasian women, with one
the condition. population-based study showing prevalence rates
83
84 Section II Disease States

of SUI in Caucasian women of 39.2% compared to • Type I: Well-supported bladder neck, with mild
25.0% in African-American women3; other population (2 cm) descent and urethral opening during Valsalva
studies have supported this finding.4 The explanation • Type II: Greater than 2 cm descent of the bladder
for the racial differences is unclear, but it is plausible neck
CHAPTER 5

that genetic, anatomic, social, and cultural factors • Type III: Open bladder neck and proximal urethra
contribute. at rest11
Pregnancy and childbirth appear to be risk fac-
tors for the development of SUI. Pregnancy, in and Key Point
of itself, is a risk factor for urinary incontinence; how-
ever, there also appear to be differences in risk based • A key to understanding the pathophysiology of
on delivery type. Women who undergo vaginal delivery stress incontinence is an understanding of the anat-
may have up to twice the risk of developing SUI symp- omy of the sphincteric mechanism and surround-
toms compared to women who deliver by cesarean ing structures.
section.5 In a large epidemiologic study conducted in
Norway, women who delivered vaginally appear to be
at significantly higher risk for SUI than women deliv- The anatomy of the lower urinary tract is discussed
ered by cesarean section. This difference diminished below. In addition, we present data that illustrate the
over time.6 Most studies agree in the conclusion that various mechanisms that contribute to continence.
cesarean delivery is not entirely protective of the devel- The detrusor, the main structural element of the
opment of SUI. urinary bladder, is composed primarily of smooth
Both obesity and smoking are modifiable risk fac- muscle under autonomic control and connective tis-
tors associated with SUI. Increases in body mass index sue. It is lined internally by transitional urothelium,
(BMI) have been associated with increased symptoms with a loose connective tissue layer referred to as the
of SUI.7 It is hypothesized that the increased weight lamina propria. In the base of the bladder, the trigone
causes chronic strain, stretching, and weakening of is found. Its deep layer is continuous with Waldeyer
the pelvic floor. Weight loss can be associated with sheath in the distal ureter, and is similar in its para-
improvement in SUI symptoms and a decrease in sympathic innervation to the detrusor muscle, whereas
symptom bother.8 Smoking is another modifiable risk the superficial layer of the trigone is continuous with
factor; the mechanism behind the increased risk for the smooth muscle of the urethra, and has similar
stress incontinence in women who smoke is likely mul- sympathetic predominance of innervation. During the
tifactorial and includes direct toxic effects on urinary filling phase, the detrusor exhibits remarkable compli-
tract tissue in combination with the increased abdomi- ance, with minimal increases in pressure as the bladder
nal pressures associated with chronic pulmonary con- fills, until it approaches its capacity. SUI is a disorder
ditions and coughing. of the filling phase, and is not attributed to detrusor
dysfunction.
The epithelium of the proximal urethra is the same
PATHOPHYSIOLOGY transitional urothelium as that found in the bladder;
more distally, the epithelium becomes squamous, like
The mechanisms that allow continence, and the that of the vulva. During the filling phase, the epi-
nature of the failures of those mechanisms, have thelium of the urethra is compressed into longitudi-
been a source of debate for as long as the condi- nal rugations. These rugations, in addition to the rich
tion has been addressed scientifically. In the early venous vasculature of the underlying lamina propria,
twentieth century, Bonney promoted the idea of a contribute to urethral coaptation and resultant ure-
loss of suburethral support as the underlying mecha- thral resistance to urine flow. Surrounding the lamina
nism of incontinence,9 while Kelly described a more propria are two layers of smooth muscle of the ure-
intrinsic urethral dysfunction as the cause, such thra known as the intrinsic sphincter mechanism: an
as an open bladder neck and urethra.10 Although internal, longitudinally oriented layer, and an exter-
no longer used, the multifactorial nature of stress nal, circumferentially oriented layer. These fibers are
incontinence came into greater focus with the clas- under autonomic control, and show predominance
sification of various subtypes of stress incontinence, of α-adrenergic receptors of the sympathetic system
as follows: (Figure 5-1).12
Surrounding these layers, the rhabdosphincter, or
• Type 0: Reports of SUI, but well-supported blad- external urethral sphincter, is found in the proximal
der neck, no abnormality on videourodynamics. and midurethra. The appearance of the striated ure-
Thought to represent voluntary contraction during thral sphincter of the urethra in normal, continent
testing women on magnetic resonance imaging shows that
Chapter 5 Stress Urinary Incontinence 85

Sympathetic
IMG Urethra

Somatic

CHAPTER 5
Lumbar
spinal cord

Hypogastric Sacral
nerve spinal cord
Parasympathetic
Lumen Onuf’s
Pudendal nucleus
nerve

Sacral Pelvic Rhabdosphincter


spinal cord nerve Pelvic
ganglia Circular smooth muscle

Longitudinal smooth muscle


FIGURE 5-1 Sympathetic and parasympathetic innervation of the intrinsic urethral sphincter (smooth muscle), and
the somatic innervation from Onufruwicz (or, Onuf) nucleus in the sacral spinal cord. IMG, inferior mesenteric gan-
glion. (Reproduced with permission from Ref.12)

the appearance of striated sphincter muscle decreased


along the longitudinal axis, until the level of the peri-
neal membrane, where there is no muscular content
of the urethra.13 The axial structure of the rhabdo- B
sphincter may vary. In nulliparous women, it has been
described as a continuous ring structure. Other stud-
ies, examining women as they age, and/or those with
stress incontinence, demonstrate a diminution of the
posterior or dorsal fibers.14,15 Some have postulated
that this finding may be a result of compressive forces
of vaginal delivery on the muscle fibers of the posterior US VW
urethra. Distally, the extrinsic continence structures
include two discrete bands of muscle (the compressor VW CU
urethrae and the urethrovaginal sphincter muscles),
contained within the anterior segment of the perineal
membrane, which exert compressive forces from above U
the urethra (Figure 5-2).16
IR
The bladder base and urethra are adjacent to the
anterior vagina, and are supported by it. Although V
the connective tissue between the vaginal epithelium
UVS
and the bladder base and urethra can often appear
surgically as a distinct fascial layer referred to as
the pubocervical fascia, histologic studies have con-
firmed that this tissue contains no true fascial fibers,
FIGURE 5-2 Oblique view of the urogenital sphincter
and are more correctly referred to as the fibromus-
musculature. The urethral sphincter (US) provides radial
cularis of the vagina and its surrounding adventitia. compression, whereas the compressor urethrae (CU)
Nonetheless, the connective support of the ante- and urethrovaginal sphincter (UVS) provide downward
rior sulci of the vagina to the surrounding pelvic compression against the vaginal wall (VW). U, Urethra;
structures plays an important role in maintaining V, vagina; IR, inferior ramus. (Reproduced with permission
continence. from Ref.16)
86 Section II Disease States

Vaginal supports have been described in three dif-


ferent levels, with Level I representing posterolateral
support to the vaginal apex, Level II representing
lateral support of the anterior vaginal fornices, and A B
C
CHAPTER 5

Level III representing distal or perineal support.17


The Level II paravaginal attachments of the vagina to
the arcus tendineus of the fasciae pelvis support the
anterior vagina bilaterally, and the vagina thus forms
a sling against which the bladder base and urethra FIGURE 5-3 Schematic diagram of sources of urethral
are supported. Abdominal pressure during exertion is pressure. The musculature (smooth and striated) of the
transmitted to the bladder, increasing bladder pres- urethra A. produces radial pressures; compressive pres-
sures are derived from the compressor urethrae and ure-
sure, but simultaneously, that pressure is passively
throvaginal sphincter muscles B. and the urethral and
transmitted to the urethra, pushing it against the vaginal supports C. provide a hammock effect from below.
anterior vagina, resulting in coaptive pressure. As the (Reproduced with permission from Ref.21)
fibers of the arcus tendineus fasciae pelvic travel dis-
tally, they merge with the inner aspects of the perineal
membrane. These connective condensations have
been termed pubourethral ligaments.18 More recent supporting structures is not sufficient explanation
studies demonstrate that these structures represent of continence.22 Conversely, patients with clinically
the continuity of lateral support between Level II and adequate urethral support who still experience SUI
Level III. also demonstrate that support is not the whole story.
The perineal membrane is a complex collection Similarly, urethral pressure measurements on their
of structures, formerly known as the urogenital dia- own are poor predictors of continence status.23
phragm, and erroneously thought to consist of a sheet Multiple intrinsic and extrinsic forces may explain
of striated muscle between two fascial layers, span- some of the variability observed in urethral pressure
ning the area between pubic rami and penetrated by measurements on urodynamic testing depending on
the vagina and urethra. More recent study shows it to the orientation of the catheter.24 One study demon-
be comprised of a dorsal portion that covers the area strated, in a small number of women undergoing pel-
between the pubic rami to the vagina/perineal body and vic surgery, that by blocking the striated muscle of the
a ventral portion, which is continuous with the para- sphincter, urethral pressure was reduced by roughly
vaginal connective tissue and contains the compressor one-third. Vascular clamps were then (temporarily)
urethrae and urethrovaginal sphincter muscles.19 applied to the iliac vessels, reducing urethral pressure
It is likely that the muscles of the pelvic floor play by an additional one-third.25 This model suggested
an important role in the stabilization and support of that the striated (external) sphincter, smooth muscle
the lower urinary tract and in maintenance of con- (internal) sphincter, and vascular plexi of the lamina
tinence. Women with SUI were observed to have propria of the urethra contribute equally to urethral
greater acceleration and posterior displacement of the pressure in the continent woman.
urethra, associated with a lengthening of the muscles, Innervation of the urethra comprises somatic, sym-
compared to continent controls, where shortening pathetic, and parasympathetic innervation via the
and stiffening of the pelvic floor muscles resulted pudendal, hypogastric, and pelvic nerves, respectively,
in improved and more balanced stabilization of the illustrated in Figure 5-1. The pelvic nerves contain the
urethra.20 afferent fibers that bring signals from the stretch and
In addition to the passive support of the anterior pressure receptors in the detrusor, as well as some
vaginal wall to the urethra, other intrinsic and extrin- nociceptive C-fibers that may contribute to inflamma-
sic factors that contribute to continence have been tory pain conditions.12
described. The circular striated muscle fibers of the Two reflex pathways contribute to the storage
sphincter urethrae are intrinsic to the urethra and mechanisms of the lower urinary tract. The sympa-
extrinsic forces including structures surrounding the thetic storage reflex, mediated through the hypo-
urethra contribute to the maintenance of continence. gastric nerve, responds to activation of the stretch
Together, these intrinsic and extrinsic systems as well receptors in the detrusor with a postganglionic
as vagina support structures provide three different release of norepinephrine, which in turn activates β
types of support and/or compression to the urethra, receptors in the bladder, which inhibit detrusor tone,
as seen in Figure 5-3.21 The observation that urethral and α receptors in the urethral smooth muscle, which
pressures both precede (by 240 ms) and exceed vesi- increase tone. This reflex is suppressed by higher
cal pressures (by up to 170%) during a cough is an central nervous system (CNS) mechanisms during
indication that passive pressure transmission to the micturition. The somatic storage reflex also responds
Chapter 5 Stress Urinary Incontinence 87

to sudden increases in bladder pressure. Efferent induced by the vaginal distension method. Leak point
pathways signal a spinal reflex through Onufruwicz pressures in the incontinent rats were increased from
nucleus. Motor neurons, traveling through the 39 to 92 cm H2O after the administration of duloxetine.
pudendal nerve, then stimulate activity of the stri- Sympathomimetic agents such as ephedrine and

CHAPTER 5
ated urethral sphincter and the perineal membrane phenylpropanolamine have been studied for use
muscles including the compressor urethrae and the in humans in the hopes of increasing urethral pres-
urethrovaginal sphincter muscle. Similar to the sym- sures.34 However, their lack of specificity to the
pathetic storage reflex, the somatic storage reflex is lower urinary tract has limited safety and tolerability.
suppressed by spinal and supraspinal activity when Phenylpropanolomine was withdrawn from the US
micturition is appropriate. market after being linked to increased rates of hemor-
rhagic stroke. In humans, duloxetine has been shown
to increase the resting tone of the urethra.35 In addi-
PHARMACOLOGIC INSIGHT INTO tion, it appears to lower the excitability threshold of
CONTINENCE MECHANISMS the external urethral sphincter contractions,36 and to
potentiate the benefits of pelvic floor muscle rehabili-
Estrogens exert trophic effects on the urethral epithe- tation therapy in women with SUI.37 The motor neu-
lium, vascular beds, and connective tissue, and have rons in Onufruwicz nucleus appear to be particularly
been demonstrated to increase both urethral pres- sensitive to the effects of some medications, including
sure and pressure transmission ratios in experimen- duloxetine, which led to interest in its use as a therapy
tal models.26 However, clinical results from estrogen for SUI. Although it is currently indicated for treat-
supplementation and its effects on SUI have not been ment of SUI in Europe, it is not currently approved
supportive of its clinical efficacy, where women who by the Food and Drug Administration for treatment of
were taking hormone replacement therapy reported urinary symptoms in the United States.
more incontinence than those not taking hormone
replacement therapy.27 As previously discussed, the
intrinsic sphincter mechanisms contain both stri- INSIGHTS FROM ANIMAL
ated (external urethral sphincter) and smooth muscle MODELS OF STRESS URINARY
(internal urethral sphincter) components, both of INCONTINENCE
which contribute to closure pressures. Pharmacologic
studies can be used to observe the relative contribu- Rat models of SUI have included the vaginal bal-
tions of each component, as manipulation of either loon catheter distension technique, which seeks to
component will affect overall urethral closure pres- mimic tissue damage observed during vaginal deliv-
sure. Voluntary pelvic floor contraction (striated com- ery; this model has been shown to result in levator
ponent) and pharmacologic stimulation of smooth and bladder/urethral muscle injury, neurologic injury,
muscle both result in increases in urethral closure as well as generalized hypoxia/reperfusion injuries
pressure, whereas pharmacologic blockade of both similar to those experienced during human vaginal
striated and smooth muscle components result in birth.38,39 Other models include the extensive dam-
decreases in closure pressures.28-31 age to the urethral support structures (urethrolysis),40
Urethral closure pressures, however, measure the focused transection of the puburethral supports,41 or
tonic, or resting activity of the sphincter mechanisms. direct nerve injury to the pudendal nerves.42 This lat-
Other techniques are used to assess the contributions ter technique demonstrates a one-third decrease in
of the neurologic and muscle activity of the reflex leak point pressures, with a nadir at 4 days; thereafter,
mechanisms involved in continence. In a rat model, the some neuroregeneration, which is enhanced by estro-
intravenous adrenergic agonist nisoxetine enhanced the gen, is observed. This model serves to illustrate some
sneeze-induced reflex of increased midurethral pres- of the injury/recovery/compensation of the continence
sure, without affecting baseline urethral tone. The intra- mechanism in response the neurologic injury.43
thecal administration of the α-adrenergic antagonists In intact anesthetized cats, sneeze-induced conti-
prazosin and phentolamine eliminated this effect.32 The nence reflex is most pronounced in the distal urethra,
authors postulated that at least two adrenergic reflex and lasted longer than the contractions induced in the
systems are in place: one central system in the spinal bladder, proximal and midurethra. Unilateral pudendal
cord, and another in the peripheral system. Conversely, nerve lesions most notably decreased this distal urethral
the administration of duloxetine, a serotonin- and reflex, and bilateral pudendal nerve lesions reduced this
norepinephrine-reuptake inhibitor, enhanced both the reflex contraction throughout the length of the urethra.44
baseline urethral pressure and the amplitude of the All of these types of intervention have been shown
sneeze-induced reflex contraction.33 This effect was to produce durable models of SUI, as measured by
observed both in normal rats, and in rats with SUI suprapubic tube placement and measurement of
88 Section II Disease States

induced leak point pressures. The variety of methods SUI relate to the adequacy of suburethral/anterior
to model the condition of stress incontinence provides vaginal support, thickness and vascular support of the
some insight into the likely overlapping structures urethral epithelium, the tone and quality of the inter-
and functions of the lower urinary tract continence nal (smooth muscle) sphincter mechanisms, the integ-
CHAPTER 5

mechanisms. rity and rapidity of response of the external urethral


apparatus and that of the pelvic floor musculature as
a whole, as well as the myriad peripheral and central
INSIGHTS INTO CONTINENCE neurologic pathways and reflex arcs.
MECHANISMS FROM
HUMAN DATA
EVALUATION OF PATIENTS WITH
Much of our understanding of the risk factors and STRESS URINARY INCONTINENCE
associations with the development of SUI comes from
the comparison of women with incontinence to con- The evaluation of patients with complaints of SUI
tinent controls. The relative contributions of support starts with careful but directed questioning about any
and urethral function toward continence have been leakage of urine. The prevalence of incontinence in the
assessed using a variety of measurement techniques. population may lead some women to assume that some
DeLancey et al. demonstrated that reductions in ure- degree of leakage is normal, and not worth discussing
thral closure pressures were a better predictor of de or evaluating. Questions that may help to differenti-
novo SUI in women following vaginal delivery than ate SUI from other forms of incontinence, including
loss of vesical support as measured by ultrasonography detrusor overactivity or overflow incontinence, include
during a cough.45 The coexistence of both variables “do you leak with coughing, sneezing, or laughing,”
in women, however, was able to predict only 37% of “do you leak with physical activity,” and “is the leakage
incontinence in these women, once again indicating brief or sustained?” These and other questions may
that multiple mechanisms are involved. help guide the clinician to an understanding about the
The contribution of the pelvic floor to urethral sup- causes of leakage, and they may aid the patient with
port has generally been understood to represent reflex- mixed urinary incontinence to differentiate between
ive contraction of the levator musculature secondary leakage types. This can be important in managing the
to stretching experienced during stress. In normal patient’s expectations for treatments, as the thera-
women, pelvic muscle reflexive contractions have been pies for stress and urgency incontinence are different.
shown to increase with increasing intensity of cough Other aspects of the patient history, including medical,
and other increased abdominal pressures.46 Some have surgical, and gynecologic issues, should be obtained. A
postulated that this graduated response, rather than a wide variety of cardiovascular, neurologic, pulmonary,
simple on-or-off reflexes, indicates the central nervous endocrine, and other health conditions may manifest
system’s involvement in modulating the reflex arc, and as urinary incontinence. Medications may also play a
the central nervous system must be “programmed” role. α-adrenergic antagonists, sometimes used in the
to allow for this nuanced reaction.47 One study evalu- treatment of hypertension, can reduce urethral pres-
ated women undergoing a Manchester procedure for sures and result in SUI.
the treatment of uterovaginal prolapse, where 22% The physical examination should be thorough and
of women demonstrated stress incontinence after the evaluate the developmental, structural, and neurologic
procedure.48 Analysis of preoperative and postopera- components of pelvic and lower extremity anatomy.
tive data in this cohort showed that low preoperative Strength and symmetry of the levator musculature
urethral pressures were associated with high risk for and anal sphincter should be assessed, both at rest and
the development of stress incontinence. with voluntary contraction. Defects in levator muscle
Despite multiple theories and explanations of the may represent loss of motor units from neurologic
mechanisms of continence and failures of current injury. Assessment of the anal and clitoral reflexes can
therapies, our understanding is incomplete. In isola- help identify potential underlying neurologic issues,
tion, urodynamic parameters perform poorly in distin- although these have poor specificity and may be absent
guishing incontinent women from asymptomatic ones. in neurologically intact women.
Additionally, interventions known to improve symp- The presence and degree of prolapse in all vaginal
toms of SUI demonstrate little or no change in our compartments should be recorded according to the
testing parameters. A more complete understanding Pelvic Organ Prolapse Quantification (POP-Q) exami-
of the pathophysiology almost certainly invites con- nation. Anterior vaginal prolapse can be very closely
sideration not of a single underlying mechanism but related to the pathophysiology of SUI, as described
rather multiple mechanisms acting in concert. Within later in this chapter, but apical and posterior compart-
any individual, the underlying problems resulting in ment prolapse can also affect the suburethral support
Chapter 5 Stress Urinary Incontinence 89

in positive or negative ways. Bimanual examination of be present, whereas transurethral leakage of urine will
gynecologic anatomy and rectovaginal examination result in staining of the distal end of the tampon.
both provide critical information about relevant ana- Some form of confirmation of transurethral urine
tomic and neurologic considerations. Careful evalua- leakage with increased abdominal pressure is con-

CHAPTER 5
tion of the bladder and urethra can help identify other sidered obligatory prior to anti-incontinence surgery.
causes of urinary leakage, including urethral diver- Positive CST or perineal pad test (with or without
ticula or urogenital fistula. Provocative maneuvers phenazopyridine) may be considered confirmatory
such as the cough stress test (CST) are important. of SUI. Single-channel cystometry, in which bladder
During filling, a leak with cough represents a positive filling is carried out through a simple catheter, can
CST and confirms the finding of SUI. A positive CST further distinguish between detrusor overactivity iden-
after voiding is considered by many to be suggestive of tified by a rise in the meniscus of the fluid in the open
intrinsic sphincter deficiency (ISD). Sustained leakage filling syringe. SUI is identified after filling, with the
after a provocative maneuver may be indicative not of catheter removed upon provocative maneuvers such
SUI, but rather of provoked detrusor overactivity. as cough or Valsalva with observation of transurethral
Bladder neck mobility can be assessed with the cot- urine loss. This simple office-based test fulfills the cri-
ton swab test, in which a lubricated cotton swab is teria for the diagnosis of urodynamic SUI. In addition,
introduced through the urethra into the bladder, then this form of basic office evaluation permits accurate
withdrawn until gentle resistance is met, signifying the testing of postvoid residual through urethral catheter-
location of the internal urethral meatus. The angle of the ization. Identification of elevated postvoid residual
swab relative to the ground is measured at rest, and again should prompt more extensive testing.
with maximum Valsalva. A straining angle of greater
than 30°, or a change from resting to straining angle
of more than 30°, is considered urethral hypermobil- Key Point
ity. Other forms of assessment of urethral hypermobility
included fluoroscopy and ultrasound. The importance • The role of multichannel urodynamics for simple
of the assessment of urethral mobility is unclear, how- stress urinary incontinence is controversial.
ever, especially in primary SUI.The presence of urethral
hypermobility cannot distinguish between continent
and incontinent women, and midurethral slings have The role of complex, multichannel electronic uro-
been shown not to change urethral mobility. SUI in the dynamic testing in the setting of primary, uncompli-
absence of hypermobility, however, may represent a dif- cated SUI remains controversial. Its popularity in this
ferent entity (Type III incontinence), which, in many setting stems from its ability to distinguish detrusor
reports, is a more challenging condition to correct, and contractions from increased abdominal pressure, and
results of urethral mobility testing may therefore be use- thereby to distinguish SUI from detrusor overactivity.
ful in counseling these patients. The cotton swab test Its usefulness in the treatment of SUI depends on the
may play a more important role in the assessment of prevalence of detrusor overactivity in the population.
recurrent SUI, or in voiding dysfunction following anti- Complex multichannel urodynamic testing was found
incontinence procedures. to be more cost-effective than single-channel evalua-
Objective information, including a bladder diary, tion when the prevalence of DO in the community was
provides information about frequency and amount of over 8%.49
leakage. A three-day diary, in which a patient records Some clinicians advocate the use of multichan-
all fluid intake, voiding episodes, volumes, and degree nel urodynamics in women with stress incontinence
of urgency, as well as leakage episodes and the circum- symptoms to assess for the presence of ISD, or a low-
stances leading to them, is clinically useful. A peri- pressure urethra. Unfortunately, there is no consen-
neal pad test, in which a collecting absorbent pad is sus agreement on definition of ISD. Table 5-1 is an
weighed, and then worn by the patient during 1 hour
of activity and then reweighed, can also be useful when
assessing incontinence. Oral phenazopyridine stains Table 5-1 Criteria Used to Define Intrinsic
urine orange-red; in conjunction with a perineal pad Sphincter Deficiency
test, orange staining of the pad can help to distinguish
leakage of urine from other forms of perineal wetness, • Open bladder neck at rest (by cystoscopy or
including sweat or vaginal discharge. In circumstances videourodynamics)
where anatomic abnormalities such as urogenital fis- • Maximal urethral closure pressure of less than
tula or ectopic ureter are suspected, phenazopyridine 20 cm H2O
tampon testing can be used. If staining of the proxi- • Valsalva leak point pressure of less than 60 cm H2O
• SUI in the absence of bladder neck hypermobility
mal end of the tampon is found, these conditions may
90 Section II Disease States

Table 5-2 When to Perform Urodynamic Flange Fluid-filled Bulbous tip


Testing sheath

• When the diagnosis remains uncertain after an initial


CHAPTER 5

history and physical examination


• When patient symptoms do not correlate with
objective physical findings
• If the patient fails to improve with treatment
• In a clinical trial setting
cm
0 1 2 3 4 5

FIGURE 5-4 The FemSoft urethral insert device (Roch-


ester Medical Corp, Stewartville, MN). A disposable
incomplete listing of criteria some have used to apply silicone reservoir filled with mineral oil is inserted, using
the definition of ISD. Given the variation in param- a small plastic obturator (not shown); the bulbous tip is
eters and lack of consensus on definition, the ICS cur- held against the internal urethral meatus, and the external
rently discourages the use of the category “intrinsic flange rests against the external meatus. Traction on the
sphincter deficiency.” However, certain components flange is used to remove the device prior to voiding. (With
of these criteria including urethral closure pressures kind permission from Ref.54)
and Valsalva leak point pressures have been shown to
confer different outcomes of certain anti-incontinence
procedures, as described below, and so still may play a
support in the form of vaginal inserts or pessaries
clinical role in some circumstances.
can provide some relief. Details of continence pes-
Table 5-2 provides recommendations on urody-
saries are provided in Chapter 20. Women describe
namic testing per The Agency for Healthcare Quality
reduced leakage while wearing a tampon, and a vari-
and Research (AHQR).
ety of pessaries have been developed specifically with
the goal of reducing SUI. When pessaries are used
THERAPIES FOR STRESS to treat vaginal prolapse, a variety of factors influ-
ence the benefit and acceptability to women. These
URINARY INCONTINENCE include patient age, vaginal length, previous surgery,
and the patient’s expectations. Long-term continued
Nonsurgical Options usage of pessaries specifically for the treatment of
incontinence varies widely, with reported one-year
Key Point continued use rates between 16% and 75%, in the
few small studies designed to look at this ques-
• The least invasive treatments including behavioral tion.52,53 Similarly, a variety of urethral inserts have
modification and pelvic floor muscle exercises been developed. The most researched of these is the
should be considered as first-line therapies. FemSoft Device (Rochester Medical Corp), a dis-
posable single-use silicone device with a reservoir
of mineral oil that is introduced transurethrally and
The Agency for Health Care Policy and Research rec- left in place after removal of the plastic obturator
ommends the ‘least invasive and least dangerous’ treat- (Figure 5-4).54 This device, in appropriately selected
ments should be considered as first-line therapies for individuals with stress incontinence, significantly
SUI.50 Behavioral modification and pelvic floor mus- reduces daily incontinence episodes and pad weight
cle exercises and rehabilitation play an important role tests, with a mean follow-up of 15 months. Although
in the treatment of women with SUI, and should be there is an increased urinary tract infection rate of
reviewed with every patient seeking treatment options up to 11% in the first month of use, the infection
for this condition. These therapies are covered in detail rate stabilized to 2% to 3% per month thereafter.54
in a subsequent chapter of this textbook. Variations on Ease of use and satisfaction rates were high with this
pelvic muscle contracture, known as “prekegels” or device in studied women.
“the Knack,” where women learn to contract the pel-
vic floor in anticipation of an increase in abdominal
Surgical Treatment Options
pressure, can be taught, and provides improvement in
stress incontinence, or at least in the volume of leakage
for Stress Urinary Incontinence
with each episode.51 Over the past century, an extraordinarily wide variety
Especially in situations in which urinary inconti- of surgical procedures for the treatment of SUI have
nence is associated with loss of support, mechanical been described. This is an indicator of the complex
Chapter 5 Stress Urinary Incontinence 91

nature of the continence mechanisms and methods of Retropubic Colposuspension Procedures


correcting their dysfunction. Although variations are (Marshall-Marchetti-Krantz, Burch, and
innumerable, described procedures generally fall into Paravaginal Defect Repair Procedures)
the following categories.
In 1949, the Marshall-Marchetti-Krantz (MMK)

CHAPTER 5
Anterior Colporrhaphy retropubic vesicourethral suspension procedure was
described, wherein the space of Retzius was opened
Based on the observation that urinary incontinence and permanent sutures were used to secure the para-
was associated with an open or gaping bladder neck vaginal tissue on either side and support it to the peri-
on cystoscopy, anterior colporrhaphy was designed to osteum of the pubic symphysis.58 Concern about the
plicate the vaginal connective tissue, effectively tight- possibility of osteitis pubis, which occurred in up to
ening the hammock upon which the bladder neck 2.5% of patients,59 as well as the technical difficulty
rests. This procedure gained popularity and fairly in securing the periosteum led to modifications. In
wide usage, under a variety of monikers including 1961 Burch described a similar procedure in which
Kelly Plication, Kelly-Kennedy Plication, Bologna Cooper’s ligament provided the anchoring points.60
Procedure, and others,67 in part due to the rela- The Tanagho modification, characterized by place-
tive ease of the procedure, the lack of entry into the ment of absorbable sutures at the level of the midure-
abdominal or retropubic spaces, and low patient mor- thra and the urethrovesical junction as laterally as
bidity. More recent scientific scrutiny, however, has possible, is essentially the procedure known as the
shown the anterior colporrhaphy is less efficacious in Burch procedure today, although many surgeons pre-
restoring continence than other procedures. A panel fer the use of permanent suture material.61
summary report published for the American Urologic In addition to the MMK and Burch procedures,
Association (AUA) determined that its success rates some have advocated the paravaginal defect repair as
in curing SUI was inferior to other methods, and they described by White in 1912 and Richardson in 1976,
recommended that the procedure be considered only as another form of retropubic colposuspension for
if the risks of slings, colposuspensions, and needle the treatment of urinary incontinence.62 Although the
suspensions were considered too high in particular paravaginal repair continues to enjoy popularity as a
patients.55 A Cochrane Database systematic review means to correct anterior compartment prolapse, its
concluded that the failure rates and reoperation rates disappointing cure rates of 61% at three years have
were inferior compared to the retropubic colposus- removed it from the list of preferred anti-inconti-
pension, and dyspareunia was sometimes observed nence procedures along with anterior colporraphy
when anterior and posterior colporrhaphies were per- and needle procedures.63 Studies comparing MMK
formed concurrently.56 to Burch have demonstrated improved efficacy of the
Burch procedure. These findings caused the authors
Bladder Neck Needle Suspension of a Cochrane Database systematic review to state, “it
Bladder neck needle suspension procedures were is reasonable to conclude that the Burch technique
developed as an alternative to retropubic colposuspen- should be regarded as the standard open retropubic
sion procedures, and are characterized by the passage colposuspension procedure.”64
of slender needles or suture carriers through the ret- The Burch colposuspension is the most widely
ropubic space to allow suspension of the paraurethral studied of the retropubic colposuspension procedures.
vaginal fibromuscularis from the rectus fascia above. A systematic review of available literature in 1996
Many variations have been described, including the demonstrated a success rate of approximately 85% at
Raz, Stamey, Pereyra, and Gittes procedures, and sub- one year from surgery, and that technical differences
sequent modifications; these differed in the route of in the procedure were not associated with different
needle passage, number of paraurethral suture bites, success rates.65 The Burch procedure appears to have
and the use of synthetic bolsters or other materials better durability compared to anterior colporrhaphy
placed in an effort to improve the durability of the and needle suspensions. At 10 to 20 years, roughly
procedure. Collectively, however, the success rates 70% of women remained continent.66 Although open
have been disappointing; the AUA Consensus Panel colposuspension procedures have lost popularity
observed a higher failure rate among needle sus- among surgeons following the advent of the minimally
pensions than colposuspension or sling procedures invasive suburethral slings, renewed interest has been
and a Cochrane Database systematic review con- invigorated with the observation that Burch procedure
cluded, among the limited comparative data avail- at the time of open sacrocolpopexy for apical vaginal
able, that cure rates seemed roughly similar to those prolapse in women without incontinence prior to sur-
of anterior colporrhaphy, and inferior to slings and gery reduces by half the likelihood that the patient will
colposuspensions.57 report SUI following surgery.67 In addition, recent
92 Section II Disease States

concerns by women regarding the use of synthetic


mesh materials and their complications have increased
the performance of retropubic anti-incontinence
procedures.
CHAPTER 5

Laparoscopic Burch Colposuspension


In 1991, a laparoscopic technique for retropubic col-
posuspension of the MMK variety was described.68
Since that time, a wide variety of modifications have
been described. Laparoscopic suturing was a develop-
ing skill, and several techniques were described that
involved the use of tackers, staples, and/or mesh as
an alternative to intracorporeal suturing. Many sur-
geons, however, feel laparoscopy is a mode of access
rather than a type of intervention, and laparoscopic
techniques should duplicate the methods and goals
of open surgery. For example, when the laparoscopic
procedures as described commonly involved using one
suture on each side, rather than the traditional two
sutures per side, objective and subjective success rates
of the Burch colposuspension were reduced.69 In addi-
tion, a new group of complications related to these
techniques, including intravesical metal tacks and
staples,70 as well as retropubic pain syndromes, were
encountered. As a result, most recent studies describ-
ing laparoscopic Burch colposuspension involve mini-
mally invasive access for a traditional technique with
the placement of two sutures on each side and fixation
to Cooper’s ligament (Figure 5-5).71
As the technology and techniques of procedures
have proliferated and evolved rapidly, it is difficult to
interpret findings of the numerous articles published FIGURE 5-5 Laparoscopic Burch procedure, in which
double sutures are placed in the vaginal fibromuscularis
on laparoscopic compared with open colposuspen-
at the level of the midurethra and the urethrovesical junc-
sion. A meta-analysis published in 2003 demonstrated tion bilaterally, and supported from Cooper ligament.
similar subjective success rates and a trend toward See the Atlas section for further details. (Reproduced with
lower objective success, whereas patients undergo- permission from Ref.71)
ing laparoscopic procedures had shorter hospital-
ization, lower blood loss, and lower rates of urinary
retention.72 In a more recent systematic review of 22
success rates.74 Others state bladder neck mobility
randomized trials from the Cochrane Collaboration,
measured by the cotton swab test is an imperfect mea-
10 trials compared laparoscopic to open techniques
sure of the support provided to the posterior urethra.
and found no significant differences in subjective or
This is because passing a rigid swab through the ure-
objective cure rates beyond 18 months.73 Laparoscopic
thra over the course of its anatomic path causes it to
Burch was associated with greater improvements in
become temporarily rigid. Thus, the urethra does not
quality-adjusted life years (QALYs) at a somewhat
behave as it would without a cotton swab.
higher cost, despite shorter hospitalization, compared
Pressure transmission ratios appear to demon-
to open Burch.
strate better correlation between urodynamic change
and clinical improvement following Burch colposus-
Colposuspension: Mechanisms of Action
pension.75-77 In women following Burch procedures,
and Insights into the Nature of Continence
urethral pressure profiles demonstrated that the ana-
The Burch retropubic colposuspension is designed to tomic location of the area of maximal pressure trans-
restore bladder neck support of the underlying vagi- mission was more proximal at the bladder neck, the
nal tissues. Although conflicting data do exist, most area targeted by the procedure, than what was seen in
reports suggest that the absence of preoperative blad- normal controls. This suggests the mechanism of the
der neck hypermobility is associated with reduced Burch procedure is, at least in part, compensatory
Chapter 5 Stress Urinary Incontinence 93

rather than restorative. In women who had under- was associated with laxity of the bladder neck and
gone laparoscopic Burch procedures, ultrasound proximal urethra. Many consider the rectus fascia
measurements demonstrated a significant stabiliza- sling to represent the gold standard of traditional
tion and reduction of descent and rotation during pubovaginal slings. Two cohort studies, representing
Valsalva.78

CHAPTER 5
nearly 500 women, showed success rates of 84% to
Studies are consistent in finding women with res- 92% at one year or greater from surgery, with high
toration of their continence after a Burch colposus- rates of patient satisfaction.80 Few comparative stud-
pension demonstrate no change in the resting tone ies compare one type of pubovaginal sling to another.
of the urethra. This is in keeping with the concept A systematic review from the Cochrane Collaborative
that resting tone is related to the intrinsic sphincter concluded that autologous rectus fascial sling was
mechanism, rather than the extrinsic mechanisms or superior to Pelvicol and FortaPerm, both of which are
suburethral support altered with the attachment of xenograft materials.81
the periurethral tissues to Cooper ligament. Despite
this, other mechanisms of continence play a role in the
clinical outcomes of patients undergoing procedures Midurethral Slings
for SUI. Preoperative rhabdosphincter activity, as Introduced in 1995 by Ulmsten, the Tension-Free
measured by urethral electromyography of motor unit Vaginal Tape (TVT) was the first of an extensive
activation, was predictive of outcomes after Burch col- array of minimally invasive slings introduced for the
posuspension with women with higher electromyogra- surgical treatment of SUI.82 TVT differed in princi-
phy (EMG) activity are more likely to experience cure ple and technique from previous sling procedures in
with the Burch procedure than those with low EMG three important ways. Firstly, the procedure involved
activity.79 The EMG parameters were more predictive passing trocars blindly through the retropubic space.
of clinical success than the urodynamic parameters of Secondly, the synthetic mesh was delivered in such a
Valsalva leak-point pressure or urethral closure pres- way that the mesh was self-retaining throughout its
sures. These findings support the idea that there are length, and required no anchoring suture or mecha-
several overlapping potential causes for SUI, and that nism. Thirdly, the sling was intended to be placed
determination of the underlying dysfunction may be at the level of midurethra, rather than the bladder
important in its clinical correction. neck. Contrary to the prevailing theories of conti-
nence, Ulmsten and Petros developed their Integral
Theory of Continence.83 Although quite complex,
Pubovaginal Sling
and based on the authors’ intuitive understand-
Among the oldest of published descriptions of sur- ing of physiology and some degree of speculative
gery for the treatment of SUI is von Giordano’s 1907 anatomy, the Integral Theory did provide a basis for
description of a gracilis muscle sling. Since then, a understanding the role of the midurethral support.
wide variety of procedures have been described. The The relative ease of performing the procedure, rapid
evolution of the pubovaginal sling has seen a change postoperative recovery and success rates comparable
both in surgical approach and in materials. Early to those of more invasive procedures brought mini-
surgeries involved pedicled flaps secured below the mally invasive midurethral slings to the forefront of
urethra with an abdominal approach. Subsequently, surgical management of SUI. By some estimates,
a combined abdominal-and-vaginal approach was TVT is among the most studied of all gynecologic
described, and in recent years, the vaginal-only surgical procedures.
approach has gained favor. In terms of materials, the In response to rare but significant injuries reported
quest to reduce harvest site morbidity commonly with the retropubic TVT and similar variations, a
seen with earlier slings has prompted a change from midurethral sling variation involving similar materi-
autologous materials (fascia lata, pyramidalis mus- als and suburethral dissection, known as the tran-
cle, rectus fascia, or vaginal epithelium) to cadaveric sobturator tape (TOT), was introduced by DeLorme
materials and synthetic meshes. To date, no data have in 2001.84 The transobturator placement of the sling
been offered demonstrating conclusive superiority of avoided blind passage through the retropubic space,
one material over another. and thus proximity to the peritoneal cavity as well
The traditional pubovaginal sling, along with its as the iliac vasculature. Complications involving
various modifications of patch-type slings, in which perforation of major vessels, the bowel, or bladder
the sling material is suspended indirectly by way of from transobturator placement of the sling seem to
sutures, and in situ vaginal wall slings, as well as most be reduced when compared to slings placed through
bone-anchored sling procedures, is characterized by its the retropubic space. According to meta-analyses
fixed location under the bladder neck. This choice of of randomized trials comparing retropubic to tran-
fixation was based on observations that incontinence sobturator midurethral slings, bladder injury and
94 Section II Disease States

pelvic hematoma formation do appear to occur less variation in the postsurgical location of the sling. A
frequently following transobturator placement.85,86 cadaveric study evaluating the path of the sling dem-
Some studies have shown decreased rates of void- onstrated that the device passed cephalad, or deep, to
ing dysfunction and/or de novo urgency or urgency the perineal membrane. The urethrovaginal sphincter
CHAPTER 5

incontinence with transobturator placement, whereas muscle, pubococcygeus muscle, and periurethral con-
others demonstrate no differences in these outcomes. nective tissue were variably penetrated.91 In a study of
A summary of available comparative data of the effi- women undergoing three-dimensional ultrasonogra-
cacies of these two types of midurethral slings is pre- phy following TVT placement, only two-thirds were
sented in the following section. noted to have the sling located at the midurethra. Ten
More recently, new variations of the midurethral percent were in the proximal third, and 23% in the dis-
sling have been introduced, collectively known as tal third. This variability in placement does not appear
single-incision, or mini-slings. These are character- to influence success rates.
ized by a shorter length of mesh material, and inser-
tion techniques where the mesh is pushed into place
through a single incision. A variety of anchoring Periurethral Bulking
or stabilizing systems are used. These devices offer Periurethral bulking injections can be performed
the theoretical advantage of reduced total mesh via the periurethral and transurethral routes, and
burden, and possibly reduced adverse outcomes demonstrate highly variable success rates ranging
related to the mesh close to the exit points of the between 26% and 75%. A wide variety of materials
full-length midurethral slings, such as groin pain in have been used, although gluteraldehyde cross-linked
the TOT devices. However, scant comparative data (GAX) collagen (Contigen) is most widely studied.
are available to assess either safety or efficacy of these Other available injectable materials have included
new devices. silicone particles (Macroplastique), carbon beads
(Durasphere), calcium hyroxylapatite (Coaptite), and
ethinyl vinyl alcohol copolymer (Uryx and Tegress).
Slings: Mechanisms of Action and Insights
Although success rates are modest, associated risk is
Into the Nature of Continence
low, and the Cochrane systematic review concludes
Postsurgical evaluation of traditional pubovaginal that injection therapy may represent a useful option
sling procedures indicate, as is the case with Burch for short-term symptomatic relief among selected
colposuspension, that successful treatment of stress women.92 Contigen can be highly antigenic, and
incontinence is dependent upon correction of hyper- requires skin injection testing prior to urethral implan-
mobility of the bladder neck. Forty women undergoing tation. Its popularity has diminished over time, and
suburethral sling surgery demonstrated that restora- recently production was ceased by the manufacturer.
tion of continence occurred when hypermobility was Tegress and Uryx (ethinyl vinyl alcohol copolymer)
corrected, even though increases in urethral pressures were associated with urethral erosions, and are no
were modest. Another study of polypropylene pubo- longer available. Among available comparative stud-
vaginal slings demonstrated that success was associ- ies included in the Cochrane analysis, no significant
ated with an elevation of the bladder neck by over 2 cm differences between the different injectable materials
at rest and 3 cm during Valsalva.87 were seen.
Midurethral slings also improve continence without One recent study evaluated the post-injection uro-
significant effects on urethral pressures. After TVT, in dynamic effects of transurethral collagen injection
women with both low and normal pressure urethrae, and found that urethral pressures were significantly
cure rates of 83% to 91% were not associated with increased, and improved continence scores. This study
increases in urethral pressures, or with correction of further evaluated the effect of the location of the point
hypermobility, but with increased pressure trans- of injection. Although not achieving statistical signifi-
mission ratios.88 Another investigation of TOT con- cance, collagen injection at the midurethra, compared
cluded restoration of continence was associated with to the more traditional location of the bladder neck,
decreased mobility of the mid-portion of the urethra appeared to result in a greater increase in urethral
as measured by ultrasound, but mobility of the proxi- pressure, as well as a higher urinary retention rate. The
mal and distal urethra was not significantly altered.89 A authors postulate that this may represent the effect of
small series of patients with failed pubovaginal slings the striated urethral sphincter. The paucity of these
revealed that sling placement too proximal was associ- fibers at the bladder neck may minimize the centrip-
ated with failure, and was corrected with revision and etal compression effects, compared to the midurethra,
replacement of the sling.90 where the striated urethral fibers may help to contain
Midurethral slings are intended to be placed at the injected material and increase the effects seen in
the level of the midurethra; however, there is broad the urethral lumen.
Chapter 5 Stress Urinary Incontinence 95

Efficacy Differences Between although variability of inclusion criteria and meth-


Surgical Options for SUI odology of the trials was significant. A randomized
trial of 180 women compared TVT to TOT success
Burch Versus Pubovaginal Sling rates, using a composite definition including “any

CHAPTER 5
In 2007, the Urinary Incontinence Treatment Network incontinence,” objective SUI, retreatment, or urinary
published the results of their randomized trial investi- retention, showed the transobturator approach to be
gating 655 women who were randomized to undergo noninferior to the retropubic sling. Bladder injury
either rectus fascia pubovaginal sling or open Burch rates were lower among patients in the TOT group.98
colposuspension. Two years postoperatively, women More recently, the Urinary Treatment Incontinence
undergoing the sling procedure were more likely to Network published a large, multicenter trial in which
demonstrate SUI cure than their counterparts under- 565 women were followed for one year following ran-
going Burch colposuspension (66% vs 49%); however, domization to either TVT or TOT.99 Objective com-
this was at the cost of increased rates of voiding dys- posite measures of success, including negative CST
function and urgency incontinence.93 and pad weight test, and no retreatment for SUI,
were equivalent between the groups (81% vs 78% in
the TVT and TOT groups, respectively); subjective
Burch Versus Tension-free Vaginal Tape outcomes were similar, although they did not achieve
predetermined criteria for equivalence. Women in the
In 2002, Ward and Hilton published a randomized
TVT group were more likely to be treated for void-
trial comparing TVT to open Burch colposuspension.
ing dysfunction (2.7% vs none), whereas they were
Neither procedure demonstrated an efficacy advan-
less likely to experience “neurologic” issues, primar-
tage over the other, with objective cure of SUI in 66%
ily in the form of upper leg weakness or discomfort
and 57% of women in the TVT and Burch groups,
(4% vs 9.4%) compared to those in the TOT group.
respectively.94 Five years after surgery, 81% of women
Procedure satisfaction was similar between groups.
in the TVT group and 90% of women in the Burch
Of note, neither of the above studies evaluated
group demonstrated negative one-hour pad tests.95 In
patients with intrinsic sphincter deficiency (ISD)
this study, higher rates of bladder injury were associ-
or low-pressure urethrae separately. Some surgeons
ated with TVT, while hospitalization, delayed return
hypothesized that the gentler angle of suspension from
to normal functioning, and the development of apical
the sling might lead to less relative obstruction from
and posterior prolapse were associated with the Burch
TOT than from the retropubic approach. One pub-
procedure.
lication found, retrospectively, among women with
maximal urethral closure pressures less than 42 cm
Laparoscopic Burch Versus H2O, TOT was associated with significantly higher
Tension-free Vaginal Tape failure rates.100 Subsequently, a randomized trial pro-
vided more robust support for this finding. Among
Laparoscopic Burch was compared to TVT in women women with ISD (defined as urethral closure pressure
with SUI, with normal-pressure urethrae in a ran- less than 20 cm H2O or a Valsalva leak point pressure
domized trial.96 In this trial, laparoscopic Burch was less than 60 cm H2O), failure rates were twice as high
associated with longer operative times (132 vs 79 min- (45%) in the TOT group as seen in the TVT group
utes), higher objective failure rates (19% vs 3%), and (21%, P = 0.004).101
higher subjective complaints of incontinence one year
after surgery. Enrollment for this study was stopped
due to funding and recruitment issues, and objective RECURRENCE
failures in the Burch group were significantly higher
than expected. The women in this trial were followed Although generally high success rates are reported
for an additional three to seven years. At that point, with modern anti-incontinence surgery, patients and
there were no statistically significant differences in surgeons can expect a failure rate of up to 10% to 20%
the rates of any incontinence and SUI between the in the long term, although heterogeneity of reporting
two treatment groups.97 and diagnostic methods make generalizing statements
about relative failure rates difficult to determine. The
evaluation of patients who fail a primary surgery
Midurethral Slings: Retropubic
needs to be more exhaustive, and should include both
Versus Transobturator
multichannel urodynamic testing as well as cystoure-
Meta-analyses of trials comparing retropubic midure- throscopy, as previous surgery introduces a greater
thral and transobturator slings did not detect differ- likelihood of foreign body erosion, fistula formation,
ences in success rates between the two techniques, or other anatomic abnormality. Other components
96 Section II Disease States

of evaluation, including cotton swab-tip testing, 4. Dooley Y, Kenton K, Cao G, et al. Urinary incontinence prev-
pressure-flow evaluation of voiding mechanisms, or alence: results from the National Health and Nutrition Exami-
nation Survey. J Urol. 2008;179(2):656–661.
videourodynamic testing, may also reveal underlying 5. Goldberg RP, Abramov Y, Botros S, et al. Delivery mode is
complexities of the nature of the incontinence in this a major environmental determinant of stress urinary incon-
CHAPTER 5

population. tinence: results of the Evanston-Northwestern Twin Sisters


Recurrent SUI after surgical management can Study. Am J Obstet Gynecol. 2005;193(6):2149–2153.
be a particular challenge, and nearly all of the pro- 6. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S. Norwe-
gian EPINCONT Study. Urinary incontinence after vaginal
cedures outlined above have been described in the delivery or cesarean section. N Engl J Med. 2003;348(10):
treatment of SUI recurrence with lower success than 900–907.
that reported for primary procedures. Few com- 7. Richter HE, Kenton K, Huang L, et al. The impact of obe-
parative data exist comparing surgical management sity on urinary incontinence symptoms, severity, urody-
techniques for recurrent SUI. One long-term cohort namic characteristics and quality of life. J Urol. 2010;183(2):
622–628.
trial evaluated Burch and pubovaginal slings for the 8. Vella VL, Jaffe W, Lidicker J, Meilahn J, Dandolu V. Prevalence
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all failure rate using both objective and subjective after bariatric surgery. J Reprod Med. 2009;54(10):597–602.
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serotonin and norepinephrine reuptake inhibitor, on central funct. 2008;19(6):773–782.
neural control lower urinary tract function in the chloralose- 52. Farrell SA, Baydock S, Amir B, Fanning C. Effectiveness of a
anesthetized female cat. J Pharmacol Exp Ther. 1995;274(2): new self-positioning pessary for the management of urinary
1014–1024. incontinence in women. Am J Obstet Gynecol. 2007;196(5):
36. Mehnert U, Boy S, Widmer-Simitovic S, Reitz A, Schurch 474.e1–474.e8.
C. The facilitory effect of duloxetine combined with pelvic 53. Robert M, Mainprize TC. Long-term assessment of the incon-
floor muscle training on the excitability of urethral sphincter tinence ring pessary for the treatment of stress incontinence.
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20(6):659–666. 54. Sirls LT, Foote JE, Kaufman JM, et al. Long-term results of
37. Ghoniem GM, Van Leeuwen JS, Elser DM, et al. A random- the FemSoft1 urethral insert for the management of female
ized controlled trial of duloxetine alone, pelvic floor muscle stress urinary incontinence. Int Urogynecol J Pelvic Floor Dys-
training alone, combined therapy, and no active treatment in funct. 2002;13(2):88–95.
women with stress urinary incontinence. J Urol. 2005;173(5): 55. Leach GE, Dmochowski RR, Appell RA, et al. Female Stress
1647–1653. Urinary Incontinence Clinical Guidelines Panel summary
38. Lin AS, Carrier S, Morgan DM, Lue TF. Effect of simulated report on surgical management of female stress urinary incon-
birth trauma on the urinary continence mechanism in the rat. tinence. The American Urological Association. J Urol. 1997;
Urology. 1998;52(1):143–151. 158(3 pt 1):875–880.
39. Cannon TW, Wojcik EM, Ferguson CL, et al. Effects of vagi- 56. Glazener CMA, Cooper K. Anterior vaginal repair for uri-
nal distension on urethral anatomy and function. BJU Int. nary incontinence in women. Cochrane Database Syst Rev.
2002;90(4):403–407. 2001;(1):CD001755. doi: 10.1002/14651858.CD001755.
40. Rodríguez LV, Chen S, Jack GS, et al. New objective measures 57. Glazener CMA, Cooper K. Bladder neck needle suspen-
to quantify stress urinary incontinence in a novel durable ani- sion for urinary incontinence in women. Cochrane Database
mal model of intrinsic sphincter deficiency. Am J Physiol Regul Syst Rev. 2004;(2):CD003636. doi: 10.1002/14651858.
Integr Comp Physiol. 2005;288(5):R1332–R1338. CD003636.pub2.
41. Kefer JC, Liu G, Daneshgari F. Pubo-urethral ligament injury 58. Marshall VF, Marchetti AA, Krantz KE. The correction of
causes long-term stress urinary incontinence in female rats: stress incontinence by simple vesicourethral suspension. Surg
an animal model of the integral theory. J Urol. 2009:181(1): Gynecol Obstet. 1949;88(4):509–518.
397–400. 59. Mainprize TC, Drutz HP. The Marshall-Marchetti-Krantz
42. Damaser MS, Broxton-King C, Ferguson C, Kim FJ, Kerns procedure: a critical review. Obstet Gynecol Surv. 1988;43(12):
JM. Functional and neuroanatomical effects of vaginal disten- 724–729.
sion and pudendal nerve crush in the female rat. J Urol. 2003; 60. Burch JC. Urethrovaginal fixation to Cooper’s ligament for
170(3):1027–1031. correction of stress incontinence, cystocele and prolapse. Am J
43. Kane DD, Kerns JM, Lin DL, Damaser MS. Early structural Obstet Gynecol. 1961;81:281–290.
effects of oestrogen on pudendal nerve regeneration in the rat. 61. Tanagho EA. Colpocystourethropexy: the way we do it. J Urol.
BJU Int. 2004;93(6):870–878. 1976;116(6):751–753.
44. Bernabé J, Julia-Guilloteau V, Denys P, et al. Peripheral neu- 62. Bruce RG, El-Galley RE, Galloway NT. Paravaginal defect
ral lesion-induced stress urinary incontinence in anesthetized repair in the treatment of female stress urinary incontinence
female cats. BJU Int. 2008;102(9):1162–1167. and cystocele. Urology. 1999;54(4):647–651.
98 Section II Disease States

63. Columbo M, Milani R, Vitobello D, Maggioni A. A random- 85. Sung VW, Schleinitz MD, Rardin CR, Ward RM, Myers DL.
ized comparison of Burch colposuspension and abdominal Comparison of retropubic vs transobturator approach to
paravaginal defect repair for female stress urinary inconti- midurethral slings: a systematic review and meta-analysis. Am
nence. Am J Obstet Gynecol. 1996;175(1):78–84. J Obstet Gynecol. 2007;197(1):3–11.
64. Lapitan MCM, Cody JD, Grant A. Open retropubic colposus- 86. Latthe PM, Foon R, Toozs-Hobson P. Transobturator and
CHAPTER 5

pension for urinary incontinence in women. Cochrane Data- retropubic tape procedures in stress urinary incontinence: a
base Syst Rev. 2009;(4):CD002912. doi: 10.1002/14651858. systematic review and meta-analysis of effectiveness and com-
CD002912.pub4. plications. BJOG. 2007;114(5):522–531.
65. Black NA, Downs SH. The effectiveness of surgery for stress 87. Kuo HC. Anatomical and functional results of pubovaginal
urinary incontinence in women: a systematic review. Br J Urol. sling procedure using polypropylene mesh for treatment of
1996;78(4):497–510. stress urinary incontinence. J Urol. 2001;166(1):152–157.
66. Alcalay M, Monga A, Stanton SL. Burch colposuspension: 88. Mutone N, Mastropietro M, Brizendine E, Hale D. Effect of
a 10-20 year follow up. Br J Obstet Gynaecol. 1995;102(9): tension-free vaginal tape procedure on urodynamic continence
740–745. indices. Obstet Gynecol. 2001;98(4):638–645.
67. Brubaker L, Cundiff G, Fine P, et al. Abdominal sacrocol- 89. Shek KL, Chantarasorn V, Dietz HP. The urethral motion
popexy with Burch colposuspension to reduce urinary stress profile before and after suburethral sling placement. J Urol.
incontinence. N Engl J Med. 2006;354(15):1557–1566. 2010;183(4):1450–1454.
68. Vancaillie TG, Schuessler W. Laparoscopic bladderneck sus- 90. Poon C, Zimmern P. When the sling is too proximal: a specific
pension. J Laparoendosc Surg. 1991;1(3):169–173. mechanism of persistent stress incontinence after pubovaginal
69. Persson J, Wølner-Hanssen P. Laparoscopic Burch colposusu- sling placement. Urology. 2004;64(2):287–91.
pension for stress urinary incontinence: randomized compari- 91. Rahn DD, Marinis SI, Schaffer JI, Corton MM. Anatomical
son of one or two sutures on each side of the urethra. Obstet path of the tension-free vaginal tape: reassessing current teach-
Gynecol. 2000;95(1):151–155. ings. Am J Obstet Gynecol. 2006;195(6):1809–1813.
70. Kenton K, FitzGerald MP, Brubaker L. Multiple foreign body 92. Keegan PE, Atiemo K, Cody JD, McClinton S, Pickard R.
erosions after laparoscopic colposuspension with mesh. Am J Periurethral injection therapy for urinary incontinence in
Obstet Gynecol. 2002;187(1):252–253. women. Cochrane Database Syst Rev. 2007;(3):CD003881.
71. Rardin CR. Laparoscopic reconstructive surgery, female doi: 10.1002/14651858.CD003881.pub2.
patient. 2004;29:11–24. 93. Albo ME, Richter HE, Brubaker L, et al. Burch colposuspen-
72. Moehrer B, Carey M, Wilson D. Laparoscopic colposuspen- sion versus fascial sling to reduce urinary stress incontinence.
sion: a systematic review. BJOG. 2003;110(3):230–235. N Engl J Med. 2007;356(21):2143–2155.
73. Dean N, Ellis G, Herbison GP, Wilson D. Laparoscopic colpo- 94. Ward K, Hilton P. Prospective multicentre randomised trial
suspension for urinary incontinence in women. Cochrane Data- of tension-free vaginal tape and colposuspension as primary
base Syst Rev. 2006;(3):CD002239. doi: 10.1002/14651858. treatment for stress incontinence. BMJ. 2002;325(7355):67.
CD002239.pub2. 95. Ward KL, Hilton P. Tension-free vaginal tape versus colposus-
74. Bergman A, Koonings PP, Ballard CA. Negative Q-tip test as a pension for primary urodynamic stress incontinence: 5-year
risk factor for failed incontinence surgery in women. J Reprod follow up. BJOG. 2008;115(2):226–233.
Med. 1989;34(3):193–197. 96. Paraiso MF, Walters MD, Karram MM, Barber MD. Lapa-
75. Karram MM, Bhatia NN. Management of coexistent stress and roscopic Burch colposuspension versus tension-free vagi-
urge urinary incontinence. Obstet Gynecol. 1989;73(1):4–7. nal tape: a randomized trial. Obstet Gynecol. 2004;104(6):
76. Dainer M, Hall CD, Choe J, Bhatia NN.The Burch procedure: a 1249–1258.
comprehensive review. Obstet Gynecol Surv. 1998;54(1):49–60. 97. Jelovsek JE, Barber MD, Karram MM, Walters MD, Paraiso
77. Ross JW. Multichannel urodynamic evaluation of laparoscopic MF. Randomised trial of laparoscopic Burch colposuspension
Burch colposuspension for genuine stress incontinence. Obstet versus tension-free vaginal tape: long-term follow up. BJOG.
Gynecol. 1998;91(1):55–59. 2008;115(2):219–225.
78. Yang JM, Yang SH, Huang WC. Dynamic morphological 98. Barber MD, Kleeman S, Karram MM, et al. Transobturator
changes in the anterior vaginal wall before and after laparo- tape compared with tension-free vaginal tape for the treatment
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incontinence. Ultrasound Obstet Gynecol. 2005;25(3):289–295. Obstet Gynecol. 2008;111(3):611–621.
79. Kenton K, FitzGerald MP, Shott S, Brubaker L. Role of ure- 99. Richter HE, Albo ME, Zyczynski HM, et al. Retropubic ver-
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pubic urethropexy. Am J Obstet Gynecol. 2001;185(1):51–55. N Engl J Med. 2010;362(22):2066–2076.
80. Morgan TO, Westney OL, McGuire EJ. Pubovaginal sling – 100. Miller JJ, Botros SM, Akl MN, et al. Is transobturator tape as
4-year outcome analysis and quality of life assessment. J Urol. effective as tension-free vaginal tape in patients with border-
2000;163(6):1845–1848. line maximum urethral closure pressure? Am J Obstet Gynecol.
81. Rehman H, Bezerra CCB, Bruschini H, Cody JD. Tradi- 2006;195(6):1799–1804.
tional suburethral sling operations for urinary incontinence 101. Schierlitz L, Dwyer PL, Rosamilia A, et al. Effectiveness of
in women. Cochrane Database Syst Rev. 2011;(1):CD001754. tension-free vaginal tape compared with transobturator tape in
doi: 10.1002/14651858.CD001754.pub3. women with stress urinary incontinence and intrinsic sphinc-
82. Ulmsten U, Henriksson L, Johnson P, Varhos G. An ambula- ter deficiency: a randomized controlled trial. Obstet Gynecol.
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of female urinary incontinence. Int Urogynecol J Pelvic Floor 102. Amaye-Obu FA, Drutz HP. Surgical management of recurrent
Dysfunct. 1996;7(2):81–85. stress urinary incontinence: A 12-year experience. Am J Obstet
83. Petros PE, Ulmsten UI. An integral theory and its method Gynecol. 1999;181(6):1296–1307.
for the diagnosis and management of female urinary inconti- 103. Ashok K, Wang A. Recurrent urinary stress incontinence: an
nence. Scand J Urol Nephrol. 1993;153(suppl):1–93. overview. J Obstet Gynaecol Res. 2010;36(3):467–473.
84. Delorme E. Transobturator urethral suspension: mini-invasive 104. Isom-Batz G, Zimmern PE. Collagen injection for female uri-
procedure in the treatment of stress urinary incontinence in nary incontinence after urethral or periurethral surgery. J Urol.
women. Prog Urol. 2001;11(6):1306–1313. 2009;181(2):701–704.
6
1 Urgency and Mixed
Urinary Incontinence
Husam Abed and Yuko Komesu

DEFINITION, EPIDEMIOLOGY, Attempts to ascertain OAB and UUI prevalence


AND IMPACT and incidence have been hampered by lack of stan-
dardization of definitions including the frequency
or severity of symptoms in epidemiologic studies.
Key Points
Nonetheless, based on a recent summary, estimates
of OAB and UUI prevalence in Europe, Asia, and the
• Urgency urinary incontinence is a subset of overac-
United States are relatively consistent.2 The preva-
tive bladder characterized by urinary urgency with
lence of OAB in the United States is approximately
incontinence.
15% and UUI is as high as 11%.2 Occurrence of
• Mixed urinary incontinence includes women with
both UUI and OAB is associated with increasing age
both urgency and stress urinary incontinence.
(Figure 6-2). UUI incidence in the United States is
four to five women per thousand in the 35- to 55-year
age group,3 and increases to 7 to 17 women per
The International Continence Society (ICS) has thousand4,5 in women older than 60 years. The few
defined bladder storage abnormalities that include uri- studies that address remission of UUI report annu-
nary incontinence, its subtypes, and overactive blad- alized remission rates ranging from 11% to 22.7%
der (OAB) syndrome.1 Although urinary incontinence in older women.4,5 These reports and other recent
is simply “involuntary loss of urine,” its three major work indicate that UUI is a dynamic state over the
subcategories are stress urinary incontinence (SUI), short term.4-6 Although no studies have evaluated the
urgency urinary incontinence (UUI), and mixed uri- lifetime natural history of OAB and UUI, data from
nary incontinence (MUI). SUI is the “involuntary loss the Agency for Healthcare Research and Quality
of urine on effort or physical exertion or on sneezing (AHRQ) suggest that over the long term women ulti-
or coughing.”1 UUI, the focus of this chapter, is incon- mately develop persistent symptoms.2
tinence associated “with the sensation of a sudden, Approximately one-third of women with incon-
compelling desire to void that is difficult to defer.”1 tinence are estimated to have MUI7 with prevalence
UUI is a subset of OAB syndrome, defined by the ICS varying from 27% to 36%.8,9 Similar to UUI, MUI
as urinary urgency, usually accompanied by frequency prevalence also increase with age (Figure 6-2).10 The
and nocturia, with or without UUI in the absence of prevailing opinion is that MUI represents a more
urinary tract infection or other obvious pathology.1 severe form of incontinence than pure UUI, and
Lastly, MUI is a combination of SUI and UUI and is although women with MUI are more likely to seek
defined as “involuntary loss of urine associated with care for their symptoms, their incontinence is more
urgency and also with effort or physical exertion or on refractory to treatment.7,9-12
sneezing or coughing.”1 The interrelationships between The spectrum of OAB, including UUI and MUI,
OAB, SUI, UUI, and MUI are illustrated in Figure 6-1. is an increasingly pressing problem due to the aging
99
100 Section II Disease States

muscle, or detrusor, relaxes while the urethra (smooth


muscle), the external urethral sphincter (EUS) (skel-
etal muscle), and the bladder neck contract. During
voiding, the bladder contracts and the outlet relaxes.
Stress Mixed Urgency Over
urinary urinary urinary active
These seemingly simple events require complex neu-
incontinence incontinence incontinence bladder rologic coordination.
UUI symptoms can be caused by several mecha-
nisms. Urinary urgency and urgency incontinence
can be a manifestation of a neurogenic bladder
caused by conditions such as stroke, spinal cord
FIGURE 6-1 Interrelationship of overactive bladder, injury, multiple sclerosis, or Parkinson disease. In
urgency urinary incontinence, mixed urinary inconti- men, UUI symptoms are most commonly related to
nence, and stress urinary incontinence. obstructive pathology of the prostrate. Traditionally,
UUI in women is thought to be due to idiopathic
detrusor overactivity and its mechanism is incom-
population. It extracts a personal toll on individu- pletely understood.15 Abnormalities of bladder mus-
als and poses an economic burden upon society. It cle and/or epithelium and their chemical products as
causes modification in work and social habits, which well as neurologic dysfunction may contribute to its
range in significance from bathroom mapping and occurrence.16,17
CHAPTER 6

sleep disturbance to social isolation.2 UUI, MUI,


and OAB are associated with depression, diminished
self-esteem, sexual dysfunction, and decreased work
Normal Voiding and Storage
productivity.2,13 The OAB population, which num- Physiology and Anatomy
bered 34 million in 2007, is projected to increase to A review of normal voiding and storage physiology of
41.9 million in 2020.14 OAB is also projected to con- the bladder assists in understanding its dysfunction.
sume 76.2 billion dollars in 2015 and 86.2 billion dol- Motor, or efferent, control of the bladder depends on
lars by 2020.14 OAB’s personal, social, and medical autonomic and somatic nerves. Autonomic nerves,
costs make it the principal contributor to the financial both the parasympathetic and sympathetic, control
burden of bladder storage disorders. lower urinary tract smooth muscle. Somatic nerves
control lower urinary tract skeletal muscle.
PATHOPHYSIOLOGY The autonomic nervous system’s sympathetic and
parasympathetic components function reciprocally.
Sympathetic stimulation results in urine storage,
Introduction and parasympathetic stimulation results in voiding.
The lower urinary tract, the bladder and its outlet, has Sympathetic efferents originate in the thoraco-lumbar
two functions: the coordinated storage and expulsion spinal cord. Most sympathetic preganglionic nerves
of urine. During storage, the pliable bladder smooth synapse with postganglionic nerves in the hypogastric18

70

60

50
Other UI

40
UUI

30
MUI
20

10 SUI
FIGURE 6-2 Prevalence of type
of incontinence (% on y axis) com- 0
pared to age (in years on x axis).
4

34

44

69

+
–2

–2

–3

–4

–5

–5

–6

–7

–7

–8

–8

90

(Reprinted with permission from


18

25

30

35

40

45

50

55

60

65

70

75

80

85

Ref.10) Age groups (years)


Chapter 6 Urgency and Mixed Urinary Incontinence 101

or inferior mesenteric plexus19 and travel via the hypo- afferents synapse with efferents to the lower urinary
gastric nerve to the bladder.18,20 Parasympathetic effer- tract and can initiate urinary reflex arcs. Lower urinary
ents originate in the parasympathetic nucleus at spinal tract afferents also synapse with secondary afferents
cord levels S2–S4. The preganglionic efferents travel that travel to the brainstem and upper CNS, which
via the pelvic nerve and synapse in the pelvic plexus modulate voiding responses.20
or synapse with postganglionic nerves located in the The supraspinal CNS modulates the previously
bladder wall (Figures 6-3 and 6-4).21 described reflexes and determines whether it is an
Neurotransmitters are responsible for pregangli- appropriate time to void. Recent reviews of brain
onic (nerve-to-nerve), and postganglionic (nerve- imaging correlated with laboratory investigation
to-muscle) communication. The major sympathetic have proposed a simplified model of CNS modula-
postganglionic neurotransmitter is norepinephrine tion of bladder storage and micturition (Figures 6-6
(NE), whereas the major parasympathetic postgan- and 6-7).25,26 Bladder afferents transmit information
glionic neurotransmitter is acetylcholine (ACh). NE from the spinal cord to the periaqueductal gray matter
stimulates bladder β-sympathetic receptors result- (PAG) in the midbrain (Figure 6-6). The PAG, com-
ing in bladder relaxation and urethral α-sympathetic posed of gray matter around the cerebral aqueduct,
receptors resulting in urethral contraction; the in turn relays neural signal to regions in the cerebral
net effect is urine storage. ACh release stimulates cortex, including the insula, anterior cingulate gyrus
the bladder’s muscarinic parasympathetic recep- (ACG), and prefrontal cortex (Figure 6-7). The PAG
tors (primarily M-2 and M-3) resulting in detru- also regulates output from these regions to the pontine

CHAPTER 6
sor contraction. The importance of ACh release in micturition center (PMC) (Figures 6-6 and 6-7). This
urethral relaxation is less certain; local release of output can inhibit voiding until voiding is appropriate,
nitric oxide (NO) also probably plays a significant at which time the PMC is disinhibited and voiding
role. In either case, the net effect of urethra dilation occurs25-28 (Figure 6-7). Urinary storage disorders may
and ACH-mediated detrusor contraction is voiding be caused by dysfunction at numerous points in this
(Figures 6-3, 6-4, and 6-5).21 complex pathway.
Somatic nerves control lower urinary tract skeletal
muscle, including the EUS. Somatic efferents originate
in Onuf nucleus in the ventral portion of S2–S4 and Pathophysiology of Storage Disorders
travel in the pudendal nerve to the EUS (Figure 6-3).19
Idiopathic Urgency Urinary Incontinence
More recent work reports an additional pathway of
innervation via the levator ani nerve.22 A number of abnormalities probably contribute to
The sensory, or afferent, nerves in the bladder what we currently classify as idiopathic UUI. These
include unmyelinated C-fibers and myelinated A-δ include alterations in neurotransmitters, sensory nerve
afferents. At birth, C-fiber afferents predominate18 fibers, and patterns of brain activation. For example,
but as the nervous system matures, A-δ fibers gain UUI is associated with increased release of nonad-
importance.18,23 A-δ fibers transmit bladder filling renergic noncholinergic (NANC) neurotransmitters
signals to the central nervous system (CNS) when in the bladder, such as ATP.17,29 ATP is an alternative
stretch receptors are activated. C-fibers transmit neurotransmitter that is increased in idiopathic detru-
unpleasant sensations such as pain or discomfort sor instability, and its release may explain why musca-
to the CNS.18 Neural insult, such as what occurs rinic blockade fails in some UUI patients.30 Injury or
following infection, inflammation, or trauma, may insult to sensory fibers in the bladder also potentially
cause A-δ fibers to revert to C-fibers and contributes contributes to UUI. Following infection, inflamma-
to the development of OAB, UUI, and painful blad- tion, or trauma, A-δ fibers may revert to C-fibers caus-
der syndrome.19 ing hyperexcitability of lower urinary tract afferents
Anatomically, the afferent system of the lower uri- and subsequent detrusor overactivity.19 Additionally, a
nary tract varies from the motor or efferent system. variety of potential mediators that affect neural activ-
Although afferents travel with the autonomic and ity can be synthesized within the bladder wall itself,
somatic efferent nerves, they are not segregated into and likely play a role in increased detrusor contrac-
sympathetic and parasympathetic autonomic and tility.16 Lastly, the advent of improved brain imaging
somatic pathways until they reach the dorsal root gan- has allowed research to focus on the role of the CNS
glia, located just outside the spinal cord.24 Nerves that in mediating UUI symptoms. The brain’s handling
originate in the bladder and urethra travel with the pel- of lower urinary tract afferent signals, with increased
vic, hypogastric, and pudendal nerves to cell bodies in limbic and decreased prefrontal cortical activation and
the dorsal root ganglia. It is here that afferents differ- alterations in brain connectivity in women with UUI,
entiate into sympathetic, parasympathetic, or somatic may be associated with decreased inhibition of voiding
tracts.19 In the spinal cord, autonomic and somatic and UUI.25-28
102 Section II Disease States

Bladder relaxation
(Sympathetic input)
and
Bladder contraction
(Parasympathetic input)
CHAPTER 6

Sympathetic
S
autonomic pathway
auton
(Hypogastric nerve)
(Hyp
α

Hypogastric
Hyp nerve β
and plexus

T10

T11
T12

L1

L2

Parasympathetic
Parasympat
Onufs
ufs autonomic papathway
nucleus
eus (Pelvic ne
nerve)

Pelvic nerve
Pe
S2
and plexus
a
S3
S4
Somatic pathway External urethral
(Pudendal nerve) sphincter
(Striated muscle)
Pudendal nerve
FIGURE 6-3 Bladder storage and elimination. A. Sympathetic nerves exit the spinal cord between levels T10-L2 (or
between T11-L2 according to some authorities) and either synapse in the paravertebral ganglion or proceed through the
paravertebral ganglion and synapse in the pelvic plexus. Postganglionic fibers travel to the bladder via the hypogastric
nerve. The sympathetic neurotransmitter, NE, stimulates α and β receptors resulting in detrusor relaxation and urethral
contraction. B. Parasympathetic nerves exit the spinal cord between levels S2–S4. Preganglionic fibers travel to the blad-
der via the pelvic nerve and synapse in ganglia within or near the bladder. The neurotransmitter, ACh, stimulates M2 and
M3 receptors, which result in detrusor contraction. C. The external urethral sphincter is innervated by motor neurons that
originate in Onuf nucleus and travel via the pudendal nerve to the EUS. (Reprinted with permission from Ref.21)
Chapter 6 Urgency and Mixed Urinary Incontinence 103

Urinary storage efferents

Cervical
vertebrae

Interomediolateral
nucleus
Thoracic
Paravertebral vertebrae
ganglia
T10-L2
Hypogastric
plexus Lumbar
vertebrae

S2–S4 Sacrum

Hypogastric nerve

CHAPTER 6
Onuf nucleus

Pudendal nerve
A External urethral sphincter
FIGURE 6-4 Storage and voiding efferent signals. A. During bladder storage and distension, afferent signals travel to
the spinal cord, which sends efferent signals to the bladder and the EUS resulting in urinary storage. Sympathetics travel
from the Intermediolateral Nucleus located from T10-L2 (or T11-L2), synapse in or pass through the paravertebral ganglia
and travel to the hypogastric plexus (or the inferior mesenteric plexus according to some experts) and travel to the blad-
der and urethra via the hypogastric nerve. Beta stimulation of the bladder results in detrusor relaxation and α stimulation
results in contraction of the internal urethral sphincter. Somatics travel from Onuf nucleus via the pudendal nerve to the
urethral sphincter, resulting in EUS contraction.

Neurogenic Bladder Neurologic illness, including multiple sclerosis


(MS) and Parkinson disease, is also commonly asso-
Spinal cord injury can result in lower urinary tract dys-
ciated with neurogenic detrusor overactivity. MS can
function. Spinal trauma superior to the lumbosacral
wax and wane but is often progressive as increasing
region eliminates voluntary and supraspinal control of
bladder dysfunction accompanies increased spinal
the bladder and results in “spinal shock” with bladder
cord involvement. MS disrupts supraspinal control of
areflexia and urinary retention. After a variable period,
the urinary tract and activates C-fibers32 with resul-
commonly six to eight weeks, detrusor hyperreflexia
tant detrusor overactivity and detrusor-sphincter-
and neurogenic detrusor overactivity ensue.16,20,31
dyssynergia. Detrusor overactivity in Parkinson disease
Despite the bladder’s overactivity, voiding may be inef-
may be due to a central defect in dopaminergic control
fective due to development of detrusor-sphincter-dys-
of micturition. Dopamine one, which inhibits micturi-
synergia caused by concomitant urethral and detrusor
tion, is depleted in the midbrain in Parkinson disease
contractions. The belief is that the normally quiescent
and results in detrusor overactivity.33
C-fiber afferents trigger reflex pathways, which result
Cerebrovascular accidents (CVA) frequently
in detrusor hyperreflexia due to morphologic, chemi-
result in urinary incontinence. Approximately 40%
cal, and electrical changes in bladder afferents follow-
of stroke victims are incontinent one week following
ing trauma.31
a CVA and 15% to 20% have persistent incontinence
104 Section II Disease States

Voiding efferents

Cervical
vertebrae

Thoracic
vertebrae

Lumbar
Parasympathetic vertebrae
nucleus

S2–S4
Sacrum
CHAPTER 6

Pelvic plexus

M2 & M3
receptors Pelvic nerve

M2 & M3
receptors

FIGURE 6-4 (Continued) B. When voiding is to occur the PAG sends signal to the Pontine Micturition Center (Figure 6-7),
which stimulates the efferent parasympathetics and inhibits the sympathetics and EUS. Parasympathetics from the
Parasympathetic nucleus travel to the pelvic plexus. Via the pelvic nerve, the neurotransmitter ACh results in stimulation
of muscarinic two and three receptors, which results in detrusor contractions. (Reprinted with permission from Ref.21)

at hospital discharge.34 The size, location, and sever- outlet obstruction may cause stretch-induced blad-
ity of a CVA affect the degree and type of lower der damage that upregulates C-fiber activity, facili-
urinary tract dysfunction.35 In animal experiments, tating the voiding reflex.16 Surgical relief of the outlet
occlusion of the middle cerebral artery resulted in obstruction can improve UUI. Among the women
damage to the cortex and putamen with decreased treated with colpocleisis above, the prevalence
bladder capacity.36 In clinical practice strokes often of UUI decreased to 15% at one-year follow-up.
damage centers that inhibit micturition resulted in Surgical series report resolution of UUI in 75%
detrusor instability.37 to 82%38,39 of women treated with anterior vaginal
prolapse repair. These clinical findings indicate that
Obstruction anterior prolapse–related UUI may be reversible in
many women.
Bladder outlet obstruction, though common in men
due to prostatic hypertrophy, is less common in
Mixed Urinary Incontinence
women and usually occurs due to advanced pelvic
organ prolapse or anti-incontinence procedures. In a Mixed UI is the combination of both UUI and SUI
multicenter study of women who underwent colpo- and constitutes one-third of incontinence cases, most
cleisis to treat prolapse, 41% of women had bother- prevalent in the elderly. It is more refractory to treat-
some OAB and UUI preoperatively. In such patients ment than other incontinence types, in part because
Chapter 6 Urgency and Mixed Urinary Incontinence 105

Parasympathetic Sympathetic
nerve nerve

M2 receptor

Norepinephrine
Acetycholine

M3 receptor β3 adrenergic
receptor

CHAPTER 6
G protein − +

+ Adenylate
cyclase
Phosholipase C

Inositol Cyclic AMP


triphosphate

Contraction of bladder Relaxation of bladder


smooth muscle smooth muscle

FIGURE 6-5 Representation of parasympathetic and sympathetic postjunctional receptors. (Reprinted with permis-
sion from Ref.21)

Anterior cingulate
gyrus/cortex

Periqueductal gray

Insula Pontine micturition


center

Prefrontal cortex

FIGURE 6-6 Diagram of some of the areas of brain activation during urinary storage. (Reprinted with permission from
Ref.26)
106 Section II Disease States

EVALUATION
ACG Key Point
• Initial evaluation of UUI includes history, examina-
PFC
tion, voiding diary, urinalysis, and postvoid residual
RI testing.
PAG
PMC
The International Consultation on Incontinence
(ICI) constructed algorithms for urinary inconti-
nence treatment and evaluation based on literature
review and expert opinion.43 The ICI is composed
of a panel of world experts organized by the
International Consultation on Urological Diseases
and the World Health Organization. Their algo-
Afferents rithms include initial management of uncomplicated
incontinence for use by all clinicians (Figure 6-9)43
and specialized management of complex incontinence
CHAPTER 6

intended for use by specialists (Figures 6-10 and


6-11).43 The following is largely taken from their
Motor
output recommendations.
Evaluation of urinary incontinence begins with a
careful history to distinguish between UUI, MUI,
FIGURE 6-7 Simplified model of supraspinal control and SUI (Figure 6-9). The history helps differenti-
system. Secondary bladder afferents synapse in the PAG ate more straightforward incontinence (Figure 6-9)
and are relayed to the insula (RI), forming the substrate from complex incontinence (Figure 6-10). Complex
for sensation. Insula representation may have slight incontinence may be associated with prior radia-
right-sided predominance. The ACG is responsible for tion or surgery, recurrent urinary tract infections,
monitoring, arousal, and efferent output to the PAG and or neurologic abnormalities (Figure 6-11). The his-
PMC. The prefrontal cortex (PFC) is involved in voluntary
tory also includes a complete review of medications.
decision about voiding and generates efferent signals to
control ACG and ultimately PMC. PMC provides motor
For instance, diuretics contribute to urgency and
output to cause voiding. (Reprinted with permission from frequency and change in dose or dosing intervals
Ref.27) may improve symptoms.44 In addition to the history,
screening questionnaires assist in urinary inconti-
nence diagnosis as most women will not admit to
bothersome incontinence.45 Questionnaires also
its etiology remains incompletely understood.7 One help determine the level of bother experienced by
hypothesis is that detrusor overactivity is initiated by patients due to their incontinence. Examples of such
increased afferent activity in response to the pres- questionnaires are discussed in Chapter 4.
ence of urine within the bladder neck, or funneling, Physical examination follows the history and
that occurs commonly in SUI.40 The hypothesis is includes a pelvic and screening neurologic examina-
supported by laboratory work showing that urethral tion (Figure 6-9). On pelvic examination, evidence of
fluid infusion cause reflexive detrusor contractions.41 vaginal prolapse, vaginal estrogen status, pelvic floor
This concept, “stress hyperreflexia” (Figure 6-8),42 is muscle strength, and urine leakage with Valsalva and
supported by both clinical and laboratory observa- cough, a sign consistent with SUI, should be noted.
tions. Alleviation of stress hyperreflexia may account Assessment of gait and sensation in the S2–S4 der-
for the observation that surgical repair of SUI pre- matomes comprise the basic neurologic examination.
dominant MUI can also cure UUI; UUI resolves in as Presence of the bulbocavernosus and perianal wink
many as 40% to 50% women with MUI treated with confirms the integrity of sacral reflexes.
stress incontinence surgery.7 Although surgical treat- Additional simple tests to evaluate incontinence
ment of MUI may resolve UUI in selected patients, include a urine dipstick or urinalysis, a voiding diary,
surgery also has the potential to irreversibly worsen and postvoid residual testing. As urinary tract infec-
UUI. Accordingly, the current recommendations are tions are a readily detected and treatable cause of
to initiate treatment of MUI with conservative mea- UUI and OAB, urine tests should be performed in
sures prior to surgical repair.7,43 the initial evaluation (Figure 6-9). Voiding diaries
Chapter 6 Urgency and Mixed Urinary Incontinence 107

Sacral spinal cord 3

Triggering of bladder
efferents in the sacral
parasympathetic nucleus

Parasympathetic bladder
efferents enhance the
detrusor contraction

CHAPTER 6
Bladder
1

Urine entering the


urethra
FIGURE 6-8 Stress hyper-
reflexia. In this diagram, the
2 presence of urine in the ure-
thra (voluntary or involuntary)
Stimulation of triggers afferents, which rein-
urethral afferents force the micturition reflex.
(Reprinted with permission
Urethra from Ref.42)

evaluate voiding frequency and volumes, episodes NONSURGICAL TREATMENT


and triggers of incontinence, and volume and types
of fluids consumed. An example of a voiding diary is Introduction
also included in Chapter 4. Evaluation also includes a
postvoid residual test, although no consensus regard- The mainstays of UUI and OAB treatment are non-
ing what constitutes an abnormal residual volume surgical and include lifestyle modification, behavioral
exists. A 1992 expert panel considered repeated resid- therapy, and medications (Figure 6-9). For women with
ual volumes >200 cc to be abnormal, whereas inter- MUI, treatment should first focus on the predomi-
mediate values of 50 to 199 cc warranted exercise of nant symptom, either SUI or UUI (Figure 6-9).15,43
clinical judgment.46 Studies performed subsequent Symptoms and patient perception of symptom bother
to that recommendation have found that only 5% to will help women and their providers establish treat-
11% of women have residual volumes >100cc.47-49 ment goals.50 Patient and provider judgment regarding
Determination of clinically significant postvoid vol- risks, benefits, and likelihood of treatment adherence
umes continues to be debated. Despite lack of con- also dictate treatment choice.
sensus regarding the lower limit of abnormal postvoid
residuals, possible elevations in residuals represent Lifestyle Modification
complex incontinence problems and justify specialty
and Behavioral Therapy
consultation (Figures 6-10 and 6-11). Complicated
urinary incontinence often requires specialized assess- Lifestyle modification includes alteration of fluid
ment with urodynamic tests and urethrocystoscopy intake, weight loss, and avoidance of bladder stimu-
(Figure 6-10). lants. At times, lifestyle modifications may run counter
108 Section II Disease States

Initial management of urinary incontinence in women

Incontinence Incontinence Incontinence/ Complicated incontinence


History on physical with mixed frequency with
activity symptoms urgency • Recurrent incontinence
• Incontinence associated
with:
• General assessment (see Chapter 4) - Pain
• Urinary symptom assessment (including frequency-volume - Hematuria
chart and questionnaire) - Recurrent infection
• Assess quality of life and desire for treatment - Significant voiding
• Physical examination: abdominal, pelvic, and perineal symptoms
Clinical
• Cough test to demonstrate stress incontinence if appropriate - Pelvic irradiation
assessment
• Urinalysis ± urine culture if infected, treat, and reassess - Radical pelvic surgery
if appropriate - Suspected fistula
• Assess oestrogen status and treat as appropriate
• Assess voluntary pelvic floor muscle contraction
• Assess postvoid residual urine

Stress incontinence Mixed incontinence OAB -with or without • If other abnormality


Presumed
presumed due to (treat most urgency incontinence found eg,
diagnosis
sphincteric bothersome presumed due to • Significant post
CHAPTER 6

incompetence symptom first) detrusor overactivity void residual


• Significant pelvic
organ prolapse
• Life style interventions • Pelvic mass
• Pelvic floor muscle training for SUI or OAB
Management
• Bladder retraining for OAB
• Duloxetine* (SUI) or antimuscarinic (OAB ± urgency incontinence)

• Other adjuncts, such as electrical stimulation


• Vaginal devices, urethral inserts
* Subject to local Failure
regulatory approval
(see black box warning). Specialized management

FIGURE 6-9 Initial evaluation and management of urinary incontinence in women, recommendations from the 4th
International Consultation on Incontinence. (Reprinted with permission from Ref.43)

to popular culture. Websites advocate the many ben- who lost 5% to 10% of their body weight had sig-
efits of increased water consumption, some recom- nificant improvement in UUI episodes when com-
mending eight-ounce glasses of water per day to pared to women who gained weight.54 Women in the
remove dangerous “poisons.”51 Overly liberal interpre- weight loss group were two to four times more likely
tation of these popular recommendations can result to achieve a 70% reduction in UUI episodes, which
in excessive fluid intake and increased incontinence.52 was maintained at 6-, 12-, and 18-month follow-up.55
As appropriate fluid intake depends on activity levels Caffeine has been associated with detrusor overac-
and metabolic needs, a practical approach assesses tivity in urodynamic studies56,57 but clinical studies of
voided volumes on patient diaries. Reasonable voided caffeine restriction are not conclusive. A prospective
volumes are 40 to 50 ounces/d (or 1500 cc/d)52 and study of 69 incontinent women reported no change in
patients who void in excessive amounts, defined by urgency, frequency, and UUI episodes following caf-
some as >3000 cc/d,15 may benefit from fluid restric- feine restriction, although baseline caffeine intake was
tion. In a small trial of 25 patients, the effect of alter- not reported.58 In contrast, an RCT (n = 74) found
ing fluid intake was examined.53 Patients who reduced that caffeine reduction with bladder training decreased
their fluid intake by 25% also reduced voids (mean = frequency and urgency symptoms greater than blad-
2.2/d), reduced UUI episodes (mean = 1.3/d), and had der training alone. UUI episodes also trended toward
decreased urgency symptoms. a decrease in the caffeine-restricted group (56% vs
The effect of weight loss on UUI has also been 26%) but did not reach significance, in part due to
studied in a randomized controlled trial (RCT), the subject dropout that left the study underpowered.59
Program to Reduce Incontinence by Diet and Exercise Behavioral therapy consists of bladder training
(PRIDE). In that study, overweight and obese women and pelvic floor muscle training. A comprehensive
Chapter 6 Urgency and Mixed Urinary Incontinence 109

Specialized management of urinary incontinence in women

Incontinence Incontinence Incontinence “Complicated” incontinence:


History/symptom
on physical with mixed with urgency/
assessment • Recurrent incontinence
activity symptoms frequency
• Incontinence associated
with:
• Assess for pelvic organ mobility/prolapse - Pain
Clinical
• Consider imaging of the uterus/pelvic floor - Hematuria
assessment
• Urodynamics - Recurrent infection
- Voiding symptoms
- Pelvic irradiation
- Radical pelvic surgery
Urodynamic Mixed Detrusor Incontinence - Suspected fistula
stress incontinence overactivity associated with
incontinence (treat most incontinence poor bladder
Consider:
bothersome emptying
• Urethrocystoscopy
symptom first)
Diagnosis • Further imaging
• Urodynamics
Bladder Underactive
outlet detrusor
obstruction

CHAPTER 6
Lower urinary
tract anomaly/
If initial therapy fails: If initial therapy fails: • Correct anatomic pathology
• Stress incontinence • Botulinum toxin bladder outlet
surgery • Neuromodulation obstruction (eg,
Treatment - Bulking agents • Bladder genitourinary
- Tapes and slings augmentation prolapse)
- Colposuspension • Intermittent • Correct anomaly
catheterization • Treat pathology

FIGURE 6-10 Specialized evaluation and management of urinary incontinence in women, recommendations from the
4th International Consultation on Incontinence. (Reprinted with permission from Ref.43)

meta-analysis prepared for the AHRQ supported reflex; the EUS contraction sends afferent signals to the
behavioral therapy to treat OAB/UUI.2 Behavioral sacral cord that inhibit parasympathetic stimulation of
therapy included both bladder training and pelvic the detrusor.63,64 Detrusor inhibition allows the patient
floor muscle training. The report suggested that multi- time to reach the toilet to void.64 Importantly, when
component behavioral therapy was most effective.2 patients are asked to perform pelvic floor contractions
Bladder training increases time between voids and approximately 25% may perform Valsalva maneuvers
is widely used to treat incontinence. It includes patient instead.65 This only serves to exacerbate problems with
education and positive reinforcement as well as timed urine leakage and emphasizes the need for patient educa-
voiding.60 The goal of therapy is to achieve continence tion and coaching on physical examination. A Cochrane
by increasing bladder capacity.61 Patients record their review supports pelvic floor training to treat SUI, UUI,
voids, learn methods of distraction and relaxation, and and mixed incontinence. In this review, patients per-
gradually increase voiding intervals to two to three formed anywhere from 30 to 200 pelvic floor contrac-
hours during waking hours over six to eight weeks.15 A tions per day.64 A pragmatic recommendation by some
recent Cochrane review concluded that bladder train- physical therapists would be for patients to perform fif-
ing may be a useful treatment for UUI.60 teen ten-second contractions three times a day.15,50
Bladder training is frequently augmented by teach-
ing patients self-monitoring (eg, via voiding diaries) and Pharmacologic Therapy
urge-suppression techniques. The latter includes iso-
lated contraction of the pelvic muscles as part of pelvic Key Point
floor muscle training.60 Pelvic floor muscle training, fre-
quently called “Kegel” exercises, was first described to • First-line treatment includes behavioral therapy
treat SUI.62 It is now recommended for UUI treatment and pelvic floor therapy with or without pharma-
as well. The hypothesis is that pelvic floor muscle con- ceutical treatment.
traction inhibits detrusor contractions via the guarding
110 Section II Disease States

Initial management of neurogenic urinary incontinence

Suprapontine cerebral Suprasacral infrapontine Peripheral nerve lesion


History lesion (eg, Parkinson spinal cord lesion (eg, radical pelvic surgery)
level of lesion disease, stroke, (eg, trauma, multiple Conus/cauda equina lesion
multiple sclerosis) sclerosis) (eg, lumbar disc prolapse)

• Further history
• General assessment including home assessment
• Urinary diary and symptom score
• Assessment of functional level, quality of life, and desire for treatment
Clinical
• Physical examination: assessment of sensation in lumbosacral dermatomes, anal tone and
assessment
voluntary contraction of anal sphincter, bulbocavernosus and anal reflexes, gait
• Urine analysis + culture (if infected: treat as necessary)
• Urinary tract imaging, serum creatinine: if abnormal: specialized management
• Post void residual (PVR) by abdominal examination or optional by ultrasound

This assessment will give basic information, but does not permit a precise neurourological diagnosis

Stress urinary incontinence Urinary incontinence due to detrusor overactivity


Presumed
due to sphincter
diagnosis
CHAPTER 6

incompetence
With poor bladder With negligible PVR
emptying
(significant PVR)
• Depending on cooperation
and mobility:
• Behavioural modification
Management
• Intermittent catheterisation • Antimuscarinics
• Behavioural modification with or without • External appliances
• External appliances • Antimuscarinics • Indwelling catheter
Failure Failure Failure
specialized management preferable for more “tailored” treatment

FIGURE 6-11 Initial evaluation and management of neurogenic urinary incontinence in women, recommendations
from the 4th International Consultation on Incontinence. (Reprinted with permission from Ref.43)

Anticholinergic medications are also a first-line ther- superior to others including those recent medications
apy for OAB, UUI, and MUI. As ACh stimulates designed to target M-2 and M-3 receptors.2 The same
bladder muscarinic receptors and results in detru- report concluded that extended-release formulations
sor contraction, anti-muscarinics, which block this had modestly better effects than immediate-release
effect, may be used to treat OAB. Unfortunately, sys- preparations.2 A Cochrane review also reached a simi-
temic side effects of nontargeted muscarinic blockade lar conclusion.67
include dry mouth, dry eyes, and constipation,66 as Pharmacotherapy side effects are usually mild. The
well as altered cognition.2 Some muscarinic receptors, same AHRQ meta-analysis reported that the most
the M-2 and M-3 receptors, are more bladder-specific. common side effects were dry mouth (2%–99%), con-
In an attempt to decrease anticholinergic medications’ stipation (0%–32%), impaired urination (0%–29%),
systemic effects, these receptors are the most recent and urinary tract infection (<1%–18%).2 Notably,
targets in OAB treatment. many of these symptoms were not severe enough to
Six anticholinergic medications are approved for result in subject withdrawal and resulted in a study
use in the United States and include oxybutynin, dropout of only 17% (some of whom were controls).2
tolterodine, fesoterodine, solifenacin, trospium, and Cardiac events, more serious adverse events, were rare
darifenacin. These medications, their dosages, and and occurred in <1% of patients at rates similar to the
methods of delivery are listed in Table 6-1.15 The frequency seen in the placebo groups.2 Despite phar-
AHRQ reviewed these medications and concluded macotherapy’s mild side effects, these side effects limit
that all were more effective than placebo in decreas- long-term adherence to treatment outside of a drug
ing both urinary frequency (range of decrease from trial setting. A new class of OAB medication, mirabe-
0.7–4.2 voids/d) and UUI (range of decrease from gron targets β-receptors in the detrusor to facilitate
0.9–4.6 episodes/d). No single drug was definitely urine storage (Table 6-1).2,68
Chapter 6 Urgency and Mixed Urinary Incontinence 111

Table 6-1 Pharmacologic Therapies Indicated for Overactive Bladder with or Without
Urgency Incontinence

Compound Usual Dose


Oxybutynin chloride (Ditropan, Ortho-McNeil-Janssen 5 mg by mouth 3–4 times daily
Pharmaceuticals and available as generic formulation)
Oxybutynin chloride extended release (Ditropan XL, Ortho-McNeil- 5, 10, or 15 mg by mouth once daily
Janssen Pharmaceuticals and available as generic formulation)
Oxybutynin transdermal patch (Oxytrol, Watson Pharmaceuticals) One patch applied twice weekly
Oxybutynin gel 10% (Gelnique, Watson Pharmaceuticals) One sachet applied daily
Tolterodine tartrate (Detrol, Pfizer and available as generic 2 mg by mouth twice daily
formulation)
Tolterodine tartrate long-acting (Detrol LA, Pfizer and available 4 mg by mouth once daily
as generic formulation)
Fesoterodine fumarate (Toviaz, Pfizer) 4 or 8 mg by mouth once daily
Solifenacin succinate (Vesicare, Astellas Pharmaceuticals) 5 or 10 mg by mouth once daily
Trospium chloride (Sanctura, Allergan) 20 mg by mouth twice daily

CHAPTER 6
Trospium chloride extended release (Sanctura XR, Allergan) 60 mg by mouth once daily
Darifenacin (Enablex, Novartis Pharmaceuticals) 7.5 or 15 mg by mouth once daily
Mirabegron (Myrbetrig, Astellas) 25 or 50 mg by mouth once daily

Printed with permission from Ref.15

A Cochrane review that compared medications to completed 12 treatment sessions, 58% were “with-
bladder training concluded that improvement was more out symptoms,” 28% were “improved,” and 14%
common with anticholinergic medications compared were unchanged.70 An RCT randomized women to
to bladder training alone (relative risk [RR] 0.73; reflexology, which employs a variation of acupres-
95% confidence interval [CI] 0.59–0.9).66 The review sure on specific points on the foot, or sham reflexol-
also concluded that improvement was more common ogy to treat UUI. Investigators reported decreased
with anticholinergics combined with bladder training daytime voids in the reflexology group (1.99 vs 0.55
as compared to each modality alone.66 Combination per day, P = 0.03) without group differences in UUI,
behavioral and pharmacotherapy may also improve urgency, or night-time voids.71 A third study, also an
patient satisfaction and quality-of-life measures.2 The RCT, randomized 85 women with UUI to acupunc-
addition of anticholinergics to behavioral therapy in ture therapy or sham acupuncture.72 They found that
clinical practice is commonly influenced by potential although the decrease in UUI episodes did not differ
impact of these drugs on patient comorbidities, such between groups, frequency, urgency, and quality-of-
as the increased risk of CNS symptoms in elderly life measures were significantly better in the acupunc-
women with underlying cognitive impairment. ture group.72 In summary, despite the general public’s
interest and use of CAM, evidence is sparse regarding
its efficacy in treatment of UUI and OAB.
Complementary and Alternative
Medicine Therapies
Despite widespread use of complementary and alter- RECURRENT/REFRACTORY
native medicine (CAM) therapy, literature is sparse URGENCY URINARY
regarding its use in UUI and OAB. A survey of gyne- INCONTINENCE
cologic and urogynecologic patients found that 45%
of patients were present or past CAM users (32% in SURGICAL TREATMENT
gynecology, 51% in urogynecology), and that both
groups expressed willingness to use CAM as a adjunc-
tive therapy (60% in gynecology, 76% in urogynecol-
Introduction
ogy).69 Three studies have reported results of CAM The mainstays of UUI treatment are medical and
therapies in UUI/OAB treatment. In a prospective behavioral. However, for patients refractory to these
hypnotherapy case series of 50 UUI patients who treatments, other Federal Drug Administration (FDA)
112 Section II Disease States

approved interventions include sacral neuromodula-


tion and peripheral neuromodulation, which are dis-
cussed subsequently (Figure 6-10). Botulinum toxin
injection is increasingly used to treat UUI but is FDA 60°
90°
approved only for individuals with a neurogenic blad-
der (Figure 6-10).

Sacral Neuromodulation
Sacral neuromodulation is a procedure that treats UUI
and OAB via stimulation of the S-3 (and occasionally
S-2 or S-4) nerve root. The first human sacral nerve
stimulator was successfully implanted in 1986.73 The
procedure ultimately received FDA approval in 1997
for UUI, followed by approval for treatment of urinary A
frequency and retention in 1998. It is used in patients
who have failed established treatments, including
pharmacotherapy and behavioral therapy.
Sacral neuromodulation’s specific mechanism of
CHAPTER 6

action is unknown. Because it results in both detrusor


relaxation and stimulation and treats the contradictory
problems of urinary retention and incontinence, it is
unlikely that it targets neural efferents. The current
belief is that sacral neuromodulation acts upon neural
afferents and alters C-fiber activity, regulates sensory
input at the spinal cord, or affects reflex pathways at
the spinal or supraspinal level. All these or their com-
binations are possible mechanisms of action.74
Sacral neuromodulation is a two-step procedure.
Step 1 (Figure 6-12A–C) is a test phase that determines B
whether a patient’s therapeutic response justifies per-
manent implantation of a neuromodulator. Step 2, per-
manent implantation, follows if the patient responds
favorably. Clinicians use two methods for the test phase:
either in-office temporary lead placement or outpatient
surgery placement of tined or small pronged leads,
which are less likely to migrate during the test phase
(Figure 6-13A–C). In-office percutaneous lead place-
ment is followed by a one- to two-day trial period. Tined
lead placement in outpatient surgery, performed under
fluoroscopic guidance, is followed by a one- to two-week
trial period. In the latter method, the tined leads are also
C
used as permanent leads if the trial period is success-
ful.75 For both methods, the leads are usually placed in FIGURE 6-12 A-C. Test phase using percutaneous leads.
the third sacral nerve root foramen and attached to a A and B. S3 foramen identified. C. Tined leads places for
temporary nerve stimulator. No studies have compared test phase. (Figures courtesy of Medtronics® Corp.)
the two test phase methods to determine which is most
efficacious and cost-efficient. A 50% improvement in
targeted symptoms defined as improved incontinence
episodes, urinary frequency or retention, during the test Contraindications to sacral neuromodulation
phase is considered a favorable response.75 Following a include limited cognitive function or need for future
positive response, permanent implantation is performed magnetic resonance imaging (MRI). Abnormal cogni-
in the operating room. The tined leads are attached tive function could interfere with patients’ ability to
to a permanent battery or internal pulse generator operate the device. An MRI is contraindicated with
(Figure 6-14). If the response is negative, the leads are sacral neuromodulation as implanted metallic devices
removed and implantation is not performed. could heat and damage surrounding tissue.76 Relative
Chapter 6 Urgency and Mixed Urinary Incontinence 113

CHAPTER 6
B

FIGURE 6-13 A-C. Test phase tined leads. A. Tined lead.


B and C. x-Rays of tined leads placed in S3 foramen.
Leads are tunneled subcutaneously and are used per-
manently if test phase is successful. (Figures courtesy of
C
Medtronics® Corp.)

contraindications include psychologic instability,


unacceptable risk for infection, and rapidly progres-
sive neurologic disease, particularly in individuals who
would require MRI evaluations.76
Evidence of the efficacy of neuromodulation in
the treatment of refractory UUI was summarized in
an AHRQ review2 that included a single RCT.77 The
RCT compared patients randomized to sacral neuro-
modulation or standard medical therapy. At 6-month
follow-up, the sacral neuromodulation group (N = 34)
had a decrease in UUI episodes (9.7 to 2.6 per day)
whereas the standard therapy group (N = 42) had
an increase in UUI episodes (9.3 to 11.3 per day)
(P < 0.001).77 The lack of improvement in the medi-
cal therapy group may have been due to the fact that
this group had previously failed standard treatment.2
Longer follow-up comparing group differences in this
FIGURES 6-14 Tined lead is placed in S3 foramen and trial is unavailable because many patients randomized
attached to a permanent battery, which is placed in a to standard therapy underwent sacral neuromodula-
skin pocket made for battery placement. tion after six months.
114 Section II Disease States

The AHRQ review also included six case series


evaluating the success of neuromodulation.2 These
studies reported that incontinence episodes decreased
from 50% to 80% per day. Follow-up ranged between
six months to five years.2 Findings from one of the
studies suggested that the long-term success of the
procedure was predicted by success at one years.
There was a high correlation between one- and five-
year success rates; 84% of the UUI patients with good
one-year outcomes had continued success at five years
after implantation.78
Neuromodulation adverse events include pain or
discomfort usually due to stimulation or pain at the
implant site (15%–27%),77-79 lead migration or dis-
ruption (3%–11%),77-81 and infection (2%–6%).77,79-81
Reported surgical revision rates are high and range
from 33% to 48%.77,79,80 Some investigators report FIGURE 6-15 Percutaneous tibial nerve needle and
decreased revision rates with the use of tined leads and stimulator. (Reprinted from Ref.86 with permission from
increased surgeon experience.80 Elsevier.)
CHAPTER 6

The greatest concern regarding sacral neuromod-


ulation is its expense. The estimated 2008 cost for
sacral neuromodulator placement was approximately significant improvement in UUI. At 13-week fol-
$17,000 (Stage 1 = $5,720 and stage 2 = $11,280).82 low-up, median UUI episodes in the PTNS group
The ICI recommends that sacral neuromodula- decreased from 3.0 to 0.3 per day, compared to the
tion be used as a second-line treatment for UUI,43 sham group that decreased from 1.8 to 1.0 UUI/d
and these recommendations are reasonable given its (P = 0.002).84 The OrBIT trial found that there
potential complications, significant revision rates, and was no significant difference in urinary frequency
cost. In light of these issues, it will be important to and UUI symptoms between PTNS subjects (N =
continue to identify predictors of sacral neuromodula- 41) compared to extended-release tolterodine sub-
tion’s success or failure. To date, age greater than 55 jects (N = 43).85 At 12-week follow-up, both groups
and presence of >3 medical comorbidities have been noted decreased mean voids per day and decreased
reported to predict poor therapeutic response.83 The UUI episodes with no difference between groups.
greatest predictor of success, however, is a successful PTNS subjects did have greater subjective impres-
stage 1 trial.76 sion of improvement compared to tolterodine sub-
jects (79.5% vs 54.8%, P = 0.01). At 6- to 12-month
follow-up, subjects who continued PTNS treatment
sustained their initial UUI improvement.86 Serious
Posterior Tibial Nerve Stimulation adverse effects of PTNS were minimal in these and
Posterior tibial nerve stimulation (PTNS), or percuta- other reports.84,85
neous nerve stimulation, is a method of peripheral neu- In summary, PTNS is a low-risk treatment for
romodulation. The FDA approved PTNS for treatment UUI subjects. It is used in patients who are refrac-
of UUI in 2000 and OAB in 2010. The mechanism of tory to first-line treatments, who do not tolerate
action of PTNS, similar to that of sacral neuromodula- antimuscarinics, or for those patients who cannot or
tion, is unknown. Like sacral neuromodulation, PTNS choose not to have an implantable device placed.85
probably affects S2–S4 afferents via the tibial nerve.84,85 Further study will determine whether the general
PTNS is performed in the office. The posterior public will find PTNS in-office visits acceptable over
tibial nerve is stimulated percutaneously via a small the long term.
needle electrode inserted cephalad to the medial mal-
leolus and attached to an external pulse generator
(Figure 6-15). Sessions last for 30 minutes and are per-
Botulinum Toxin
formed weekly for 12 weeks.86 In the last ten years, Botulinum toxin has been
Two RCTs, the SUmit and OrBIT studies, have increasingly used to treat OAB and UUI. The ICI43
been performed to evaluate PTNS.85,86 The SUmiT recommended its use as an alternative, specialized
trial was a double-blind placebo-controlled study treatment for refractory detrusor overactivity and
that found that subjects treated with PTNS (N = mixed incontinence. A European Consensus Panel
103) versus a sham needle procedure (N = 105) had also determined that Grade A evidence recommended
Chapter 6 Urgency and Mixed Urinary Incontinence 115

Table 6-2 FDA Recommended Drug Name Changes for Botulinum Toxin

Trade Name New Drug Name Old Drug Name


Botox Onabotulinumtoxin A Botulinum toxin type A
Dysport Abobotulinumtoxin A Botulinum toxin type A
Myobloc Rimabotulinumtoxin B Botulinum toxin type B

http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/
ucm174949.htm

its use in neurogenic and idiopathic detrusor overac- Botulinum toxin injection, approximately 69% (range:
tivity.87 OnabotulinumtoxinA was FDA approved in 36.4%–89%) of subjects improve, there is a 65%
2011 for intravesical injection for treatment of neu- decrease in UUI episodes, and complete continence
rogenic UUI. is achieved in 58% (range: 32%–86%) of subjects.87
Botulinum toxin is a protein produced by the Benefits of a single injection are reported to last an
Clostridium family of bacteria, which temporarily average of 6 months87 with a wide range in therapeu-
denervates or decreases neural activity.88 Directly tic duration (4–14 mo),87,88 which depends on dosage,
injected into the bladder, it paralyses the detrusor. It site, and depth of injection.

CHAPTER 6
is also believed to block presynaptic release of ACh In general, the safety profile of this medication is
as well as other transmitters, including ATP and sub- good, although there have been infrequent reports
stance P, and down-regulate purinergic and capsa- of weakness or paralysis of distant muscle groups.87
icin receptors in the urothelium.89 Decreased release A Danish registry reports that this may occur in
of these neurotransmitters in turn decreases afferent <10/10,000 patients, with several deaths possibly
stimulation of the CNS, further decreasing sensation due to respiratory complications.98 Additionally,
of urgency.89 in clinical trials specific concern arose94 about the
Various bladder injection techniques have been association between Botulinum toxin and ele-
described for botulinum treatment of OAB. The num- vated postvoid residuals (19%–43%); this resulted
ber of injection sites, decisions whether or not trigonal in self-catheterization in a number of subjects
injection should be avoided or targeted, and the opti- (4%–43% depending on the criteria used) and uri-
mal location for injection have yet to be determined.87 nary tract infections (10%–43%).88 A recent trial
Prior work used 10 to 30 injection sites in the blad- of 313 patients randomized to placebo or varying
der,88 advocated intramuscular rather than suburothe- doses of OnabotulinumtoxinA (50,100,150,200, and
lial injections,87,90 and avoided the trigone because of 300 Units) reported that doses ≥100 Units demon-
concerns of vesicoureteral reflux.87,90 Some investiga- strated durable efficacy.95 Furthermore, increased
tors90 have called the latter concern into question.87,88 residuals and need for self-catheterization were
In 2009 the FDA recommended changes to the dose-dependent events.95 The researchers suggested
previously established Botulinum toxin drug names.91 that 100 Units may be the appropriate dose, which
The FDA made this recommendation to reinforce balances benefits versus side effects.95 Continued
differences in Botulinum medications. These medica- evaluation of this drug will help determine appropri-
tions are not interchangeable. Different Botulinum ate patient selection, medication dosage, as well as
preparations have different potencies and doses. its limitations.
The former names, new names, and trade names
are listed in Table 6-2. Most UUI/OAB clinical trials
have used OnabotulinumtoxinA (Botox),92-95 although
Other Surgical Procedures
RimabotulinumtoxinB (Myobloc) has also been Bladder augmentation, or augmentation cystoplasty,
used.96 Botulinum toxin dosing recommendations, is a surgical procedure used for patients with either
efficacy, and safety data should be considered to be severe neurogenic or idiopathic detrusor instability
product specific.97 refractory to all other treatments.99 The ICI included
All four RCTs that compared intravesical Onabotu- bladder augmentation in the list of specialized treat-
linumtoxinA injection to placebo found the former to ment of women with UUI (Grade C).43 In this pro-
be more effective than placebo.91,92,94,95 cedure, the bladder is bisected and augmented with a
It is not possible to pool the RCT results due to portion of bowel to increase bladder volume.99 Case
heterogeneity in procedures, medication dosages, and series report UUI cure rates of 69% to 100% (sample
reported outcomes. With respect to UUI, review of sizes range 12–32 patients).99 A larger study of 76 sub-
observational studies and trials indicate that following jects followed for an average of 106.8 months reported
116 Section II Disease States

≥50% improvement in the vast majority (97%) of 13. Kannan H, Radican L, Turpin RS, Bolge SC. Burden of illness
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7
1 Evaluation of Bladder Function
Cynthia S. Fok and Elizabeth R. Mueller

INTRODUCTION The ureters are also located in the retroperitoneum.


They vary in length from 22 to 26 cm and travel from
Many patients are initially reluctant to seek treatment the renal pelvis located at the level of the 1st to 2nd
for pelvic organ prolapse and will later cite that it was lumbar vertebral body to the posterior bladder base.1
a change in their bladder function, including difficulty There are three distinct regions where the ureteral
emptying, suprapubic pressure, nocturia, new-onset lumen narrows: the ureteropelvic junction, where
urgency, or urinary incontinence, that prompted them the ureter crosses over the iliac vessels and also upon
to consult a specialist. Although pelvic floor disorders entering the bladder, or ureterovesical junction. The
can cause these symptoms, there are other pathologies, distal ureter traverses obliquely through the muscular
such as pelvic or bladder wall carcinoma, that may layers of the bladder base and terminates at the ure-
present with similar symptoms. In this chapter, we will teral orifice on the trigone. This results in distal ureter
briefly review the pertinent anatomy, physiology, and constriction when the bladder contracts. For this rea-
diagnostic tools that are utilized when evaluating blad- son, ectopic ureteral orifices that are positioned lateral
der function. Our discussion will focus primarily on to the trigone are at risk for urinary reflux. Ureteral
the lower urinary tract. orifices that are medial to the normal placement on
the trigone traverse thicker muscular layers that sur-
round the bladder neck and proximal urethra and are
LOWER URINARY TRACT more susceptable to ureteral obstruction.2
STRUCTURE AND FUNCTION The bladder is located in the lower pelvis and the
superior surface of the bladder (located at the level of
the pubic bone) has an apex where a fibrous remnant
Anatomy of the allantois, the urachus, once drained the fetal
The genitourinary system is divided into upper and bladder. The posterior-inferior surface of the bladder
lower tracts. The upper urinary tract (UUT) consists including the trigone is called the base. The remaining
of the renal parenchyma and the collecting system two bladder surfaces on the left and right are described
components (renal pelvis and ureters). The bladder as being positioned inferior-lateral.
and urethra compose the lower urinary tract (LUT). The internal surface of the bladder, ureters, and
The kidneys lie in the retroperitoneum and weigh renal pelvis are lined with transitional epithelium
approximately 135 g in women. The superior margin called the “urothelium.” This layer is usually six to
of the left kidney is located at the level of the 12th tho- seven cells thick and rests on the lamina propria, a
racic vertebral body and the right kidney is 1 to 2 cm supporting structure (Figure 7-1).1 The urothelium
lower due to displacement by the liver.1 is smooth when the bladder is full and contracts into

119
120 Section II Disease States

fibers are lost per year as a woman ages. The overall


Urothelium
decrease in urethral sphincter muscle density with age
is also correlated with a shorter urogenital sphincter
Lamina propria and longer vesical neck, all of which more commonly
associated with stress urinary incontinence and poorer
pelvic floor muscle function.3
Smooth muscle
Function
Innervation
FIGURE 7-1 The six to seven cell layered urothelium, the
Sensory impulses from the bladder relay information
intervening lamina propria and the smooth muscle (muscu-
laris mucosae) layer. (Figure from Urodynamics Curriculum
about distension, inflammation, and other stimuli
for Urology Residents, http://sufuorg.com/elearning/.) along afferent nerves that accompany primarily the
(efferent) parasympathetic (pelvic, S2–S4) and the
sympathetic (hypogastric, T10-L2) nerves. The affer-
folds when the bladder empties. The lamina propria is ents terminate on interneurons mainly in the posterior
composed of fibroelastic connective tissue that allows horn of the spinal cord. Targets of the interneurons
distension and contains numerous blood vessels and include the periaqueductal gray matter of the mid-
smooth muscle fibers called the muscularis mucosae. brain and eventually the pontine micturition center.6
The lamina propria is an anatomic landmark that is Bladder afferents include A-δ fibers and C fibers.
critical for the staging and prognosis of bladder can- A-δ fibers are myelinated mechanoreceptors that
cers. Bladder tumors confined to the urothelium are increase their firing with increases in bladder wall ten-
considered superficial. Once a tumor has invaded the sion, whereas C fibers are unmyelinated nocioceptors
lamina propria it is called an “invasive” bladder cancer thought to be primarily involved in sensations of uri-
and carries the risk of hematogenous spread. nary urgency and bladder pain. They fire when in con-
Lateral to the lamina propria lays the branching and tact with noxious chemical irritants, increased urinary
interlacing smooth muscles of the bladder wall. The potassium, and decreased pH or cold temperatures.
3 muscle types are inner longitudinal, middle circu- During normal bladder filling, A-δ fibers are active
lar, and outer longitudinal. In the upper part of the and C fibers are silent.6 During noxious filling, for
bladder near the urachus these layers are not very pro- example, during acute urinary tract infection (UTI),
nounced or distinct. Near the bladder base and blad- C fibers become more active and generate the sensa-
der neck the detrusor muscle is clearly layered2 and tion of discomfort.
funnels to the internal urethral meatus. Motor innervation of the LUT occurs through the
CHAPTER 7

On magnetic resonance imaging (MRI), the female autonomic and somatic nervous systems. The hypo-
urethra measures approximately 2.65 cm in length, gastric nerve carries preganglionic sympathetic nerve
extending from the bladder neck to the urethral fibers that originated in the T11 to L2 segments in the
meatus.3 The sphincter muscle is composed of both spinal cord, to the bladder and urethra.7 Stimulation
striated and smooth muscle layers. The striated uro- of these fibers results in activation of the β-adrenergic
genital sphincter muscle is intimately associated with inhibitory receptors in the bladder wall resulting in
the distal two-thirds of the urethra.3 Urethral function detrusor relaxation and the α-adrenergic excitatory
is less well studied than bladder function; however, receptors in the urethral smooth muscle resulting in
Rud et al. attempted to determine the factors respon- urethral contraction (Figure 7-2). This promotes uri-
sible for continence by measuring urethral pressure nary storage easily remembered with the mneumonic
awake and under general anesthesia. By comparing “sympathetic = storage.” The pelvic nerve carries
pressures between awake and anesthetized patients, preganglionic parasympathetic nerve fibers that orig-
they determined that one-third of the resting pres- inated from spinal segments S2 to S4. Their stimula-
sure of the urethra is derived from the striated urethral tion results in excitation of muscarinic receptors in the
sphincter, one-third from the smooth urethral sphinc- bladder wall with an end result of bladder contraction
ter, and final third from mucosal coaptation from ure- and release of nitrous oxide at the proximal urethra
thral intravascular blood pressure.4 causing relaxation of the urethral smooth muscle
Radiographic and histologic studies have shown that (Figure 7-3). These actions promote bladder empty-
over time there is loss of the striated urethral sphincter ing “parasympathetic = pee.” The pudendal nerve is
muscle that corresponds to the increasing incidence of a somatic motor nerve that activates the striated ure-
urinary incontinence with aging.5 Perucchi et al. used thral sphincter. It arises in S2–S4 motor neurons in
histologic sectioning of female cadaveric urethras to Onuf nucleus and when stimulated results in striated
estimate that approximately 2% of sphincter muscle sphincter contraction.
Chapter 7 Evaluation of Bladder Function 121

Pontine
continence
center

β Hypogastric nerve

L1–L2

Bladder afferents

α +
Onuf
Pudendal nerve
+ nucleus
Nicotinic
+ S2–S4

FIGURE 7-2 Bladder filling: during filling, distension of the bladder wall results in low-afferent firing from the
mechanoreceptors. Interneurons in the spinal cord and the contralateral pontine continence center are activated and in
turn activate the hypogastric and pudendal nerves. (Figure from Urodynamics Curriculum for Urology Residents, http://
sufuorg.com/elearning/.)

CHAPTER 7
Pontine
micturition
center

M3/M2 L1–L2
+
Pelvic nerve

Onuf
− nucleus
Nitrous oxide S2–S4

FIGURE 7-3 Bladder emptying: once voiding is appropriate, the storage phase is switched to the voiding phase.
The end result is activation of the pelvic nerve and deactivation of the pudendal and hypogastric nerve. (Figure from
Urodynamics Curriculum for Urology Residents, http://sufuorg.com/elearning/.)
122 Section II Disease States

Normal Storage and Emptying Terminology


Normal bladder filling and storage require the blad- Confusion surrounding the description of patient
der to accommodate increasing volumes of urine, with symptoms, prolapse quantification, LUT syndromes,
appropriate sensation and minimal increases in intra- and urodynamic diagnoses has been significantly
vesical pressure. To maintain continence, the urethral reduced due to the collaborative work of the Inter-
sphincter has to remain closed at rest and remain closed national Urogynecologic Association (IUGA) and
with increases in intravesical pressure. As bladder fill- International Continence Society (ICS). Both of these
ing increases, the forces at the bladder neck increase organizations have standardized the terminology used
and the intraluminal pressure of the urethra increases. to describe female pelvic floor function and dysfunc-
This is known as the “guarding reflex.” As the blad- tion.8 Table 7-2 lists terminology used to describe
der continues to fill, the afferent activity increases and patient storage and voiding symptoms. According to
alerts higher brain centers. Once voiding is appropri- IUGA/ICS Terminology, symptoms are any departure
ate, the storage phase is then switched to the voiding from normal structure, function, or sensation, experi-
phase by the activation of the pontine micturition cen- enced by a woman and indicative of disease or a health
ter and inhibition of the pontine continence center. problem. Symptoms can be described by the patient
For the bladder to empty effectively, the smooth and or the caregiver.8 Signs are any abnormality indica-
striated urethral sphincters and the pelvic floor need to tive of disease or a health problem that can be seen by
relax to allow the outflow of urine. This is followed by a the examiner. Examples of signs are stress or urgency
coordinated contraction of the bladder smooth muscle. urinary incontinence, extraurethral incontinence (fis-
tula), or stress incontinence with prolapse reduction
(occult or latent incontinence). Lastly, diagnoses are
DESCRIBING LOWER URINARY made based on the correlation between symptoms,
TRACT DYSFUNCTION signs, and any relevant diagnostic investigations.
Diagnosis of bladder dysfunction is highly reli-
Functional Classification ant on patient history. A detailed history of the
patient’s urinary storage and voiding habits should
Key Point be obtained. The best way to elicit patient symptoms
is to simply ask. Each symptom can be explored by
• Lower urinary tract symptoms related to storage or inquiring when the symptom started, what it is asso-
emptying failure and can usually be attributed to ciated with, how long it lasts, and what makes it bet-
the bladder or urethra. ter or worse. It is also important to ask specifically
about how much the symptom bothers the patient.
Some symptoms may occur infrequently but because
CHAPTER 7

The function of the LUT is to store urine between of their unpredictability be the most bothersome (ie,
voids and to empty the bladder when appropriate. urgency incontinence).
When patients present with LUT symptoms related to Many diseases of the central nervous system may
urine storage or voiding, the dysfunction can usually result in lower urinary tract dysfunction (LUTD).
be categorized as being a failure to store or a failure Lesions may be located at or above the brainstem, within
to empty and can be attributed to either the bladder the spinal cord, or locally within the bladder itself. To
or the urethra. For example, a woman who presents elicit these symptoms, women should be asked about
with urinary incontinence may have a bladder etiol- any changes in their overall health before or at the time
ogy such as overactive bladder or a urethral etiology their LUT symptoms started. Additional questions to
such as stress urinary incontinence. This “Functional explore LUT changes should include questions about
Classification System” was introduced by Alan Wein changes in gait, balance, sensory, or motor function of
(Table 7-1). It provides a logical framework for under- the lower extremities, and bowel function.
standing the possible etiologies of patient symptoms. Women who have recently undergone surgery and
present with new LUT symptoms may have a surgi-
cal complication. Complaints of continuous urinary
Table 7-1 Functional Classification System leakage at rest and activity herald the development of
a genitourinary fistula. Women who have undergone
Failure to Store Failure to Empty radical resections of the colon or uterus for cancer
can present with injuries of the pelvic plexus that
Bladder Detrusor Acontractile
overactivity detrusor
manifest as urinary incontinence due to incomplete
emptying of the bladder. The increasing use of surgi-
Outlet/ Stress Bladder outlet
cal mesh in surgeries for pelvic floor reconstruction
urethra incontinence obstruction
requires a low threshold for suspecting that the LUT
Chapter 7 Evaluation of Bladder Function 123

Table 7-2 Summary of International Urogynecological Association/International Continence


Society Joint Report Terminology

Symptoms
Urinary incontinence symptoms Stress
Urge
Postural
Nocturnal
Mixed
Continuous
Insensible
Coital
Bladder storage symptoms Increased daytime frequency urgency
Nocturia
Overactive bladder syndrome
Sensory symptoms Increased bladder sensation
Reduced bladder sensation
Absent bladder sensation
Voiding and postmicturation symptoms Hesitancy
Slow stream
Intermittency
Straining to void
Spraying stream
Feeling of incomplete bladder emptying
Need to immediately re-void
Postmicturition leakage
Position dependent micturition
Dysuria
Urinary retention
Signs
Incontinence signs Involuntary urine loss on examination
Other signs Neurologic signs
Abdominal signs (scars, masses, bladder distension)
Pad testing

CHAPTER 7
Bladder diary
Diagnosis
Urodynamic stress incontinence Symptoms, signs, and urodynamic findings of involuntary
leakage are associated with increased intra-abdominal pressure,
in the absence of detrusor contraction
Detrusor overactivity Symptoms and urodynamic findings of women with lower urinary tract
symptoms with involuntary detrusor contraction during filling cystometry
Bladder oversensitivity Symptoms and urodynamic findings of women with frequency, nocturia,
reduced average voided volume with increase perceived bladder
sensation during early filling
Voiding dysfunction Symptoms and urodynamic findings of abnormally slow and/or
incomplete micturition. Can include acute or chronic retention of urine

symptoms may be due to “foreign-body” in either the during a supine stress test (stress incontinence), leak-
bladder or urethra. age of urine with a sudden, compelling desire to void
Physical examination of the abdomen, back, (urgency incontinence), urine leaking from channels
and lower extremities should be performed in addi- other than the urethral meatus (extraurethral incon-
tion to a routine genitourinary examination. Signs tinence), or the observation of transurethral urine
of urinary incontinence that can be observed during loss during stress maneuvers with prolapse reduction
physical examination are involuntary leakage of urine (occult incontinence).
124 Section II Disease States

TESTS TO EVALUATE LOWER Patients are typically given pre-printed 24-hour forms
URINARY TRACT FUNCTION that instruct the patient to record the time, volume,
and type of fluid consumed. The time and volume
of urine excreted is also noted and can be facilitated
Key Point
by providing the patient with a measuring device of
“hat” the fits on the toilet. Instruct the patient that
• There are a variety of tests to evaluate the lower
the diary represents a “typical day and night” and that
urinary tract and each test has its own strengths
fluid intake should not be modified. In addition, some
and limitations.
forms track incontinence episodes and associated
activity or sensation. Once the diary is returned, total
fluid intake, number of voids, and urine output are
The purpose of most investigational studies of the LUT
calculated along with mean and maximal functional
is to aid in the evaluation of patient’s symptoms or to
bladder capacities.
understand the LUT function. It is critical, therefore,
Normal values for bladder diaries can be easily
that the patient’s symptom history is well understood
found but are not helpful for analysis as much as
and that diagnostic testing answers a specific question.
reviewing the “story” from the diary. For example,
For example, a woman who describes urgency incon-
two women may have 20 voids in a 24-hour period,
tinence requiring daily pad usage that has worsened
which is much higher than the expected median of
over the last five years may not have the same etiology
8. For a woman drinking over 4 L/d the diagnosis is
as a woman who presents with a sudden three-month
that the bladder is normal but the intake is excessive
onset of urinary urgency incontinence. In the example
resulting in polyuria (>40 mL/kg body weight/24 h).
provided, the patient with slowly worsening symptoms
Another woman may have the same number of voids
fits the typical course of urgency incontinence, and
with 1,200 mL intake due to frequent small voids
there maybe little justification to perform additional
characteristic of the voiding pattern with urinary
testing prior to treating her symptoms. In contrast, the
retention or with overactive bladder symptoms. Often
acute onset of the bladder symptoms warrants further
bladder diaries can provide objective measure of the
investigation.
patient’s symptoms. Diaries are helpful in evaluating
patients with complaints of nocturia because sleep
Postvoid Residual Urine Measurement apnea and other chronic medical conditions may
have coexisting nocturnal polyuria, defined as noc-
The postvoid residual (PVR) urine measurement turnal voided volume of at least 30% of the 24-hour
refers to the volume of urine in the bladder after a total.9 Patients with this finding should be referred to
voluntary void. This is done by straight catheterization their primary care provider or nephrologists for fur-
or bladder ultrasound (US) within 10 minutes of void-
CHAPTER 7

ther work-up.
ing. Any urine specimen obtained on the initial visit
can be tested by dipstick analysis for the presence of
red cells, white cells, and nitrates. Urine specimens Urodynamics
suspicious for UTIs are sent for culture and sen-
sitivities. It may be helpful to reevaluate the patient Key Point
while she in on antibiotics to see if her symptoms
have improved and are attributable to the UTI. Most • Urodynamics are indicated when they will benefit
women have PVR >10 mL in their bladders follow- the patient or change the treatment plan.
ing voiding because urine production is continuous.
In order to determine if PVR is elevated it needs to
be put in context with the amount of urine voided. Urodynamics refers to a group of studies that assess
Residual volumes greater than 100 mL and/or greater LUT function during urine storage and emptying.
than one-third of the total volume (voided + PVR) Urodynamics can play a critical role in the function,
are generally considered abnormal. That said, asymp- evaluation, and treatment of LUT symptoms. Not all
tomatic women with higher than these PVR measure- urinary tract conditions require urodynamics. In fact,
ments can be conservatively managed once their renal many patients can be diagnosed and offered treat-
function is verified as normal. ment options based on their LUT symptoms alone.
Urodynamics are indicated when they will benefit the
patient or change the treatment plan. They can provide
Bladder Diaries
information in situations when the clinical diagnosis is
Bladder diaries are a record of the patient’s fluid uncertain. Lastly, they are used when a patient does
intake and urinary output over a specified time. not respond to empiric first-line medical or surgical
Chapter 7 Evaluation of Bladder Function 125

FIGURE 7-4 An example of a complex uroflow study.

CHAPTER 7
therapy. Urodynamics consist of one or more of the visually inspecting the tracing. The time to maximum
following tests: uroflowmetry, cystometrogram, pres- flow usually occurs in the first third of the total void-
sure-flow studies, urethral-pressure profiles (UPPs), ing time. A typical normal uroflowmetry curve from
leak point pressures, electromyography (EMG), and an electronic device is shown in Figure 7-4. The urine
fluoroscopy. flow rate is plotted versus time. Notice that the plot
is continuous and smoothly shaped. The flow curve is
printed along with the values for the following vari-
Uroflowmetry
ables: maximum and average flow rates, voiding time,
Uroflowmetry, or urine flow studies, measure urinary time to peak flow, and voided volume. The postvoid
flow rates and voided volume. They are often used for residual is typically a manual entry and is obtained by
screening or diagnosing patients with a clinical history performing a bladder scan or catheterization.
or symptoms of voiding dysfunction. Uroflowmetry is Average and maximum flow rates for an individual
obtained by having a patient arrive with a comfortably vary and are dependent on the voided volume, age,
full bladder. She is then taken into a private room and and position. Many experts believe that urine flow
allowed to void while seated into a measuring device. rates are not valid unless voided volumes are greater
Prior to the use of electronic devices, the flow time than 125 to 150 mL. The advantages of uroflowme-
and voided volume were measured, and an average try are that it is noninvasive, easy to perform, and the
flow rate was calculated. Now, electronic flow devices equipment is relatively inexpensive. The major limita-
are used. tion of uroflowmetry is that the etiology of a low urine
The maximum and the average urine flow rates are flow rate is not identified and may be due to inad-
electronically calculated, but should be confirmed by equate voided volumes, poor detrusor contractility, or
126 Section II Disease States

obstruction. Women can have normal values for urine Changes in the fluid level represent changes in bladder
flow rates in the presence of obstructed voiding by pressure that may be due to the intrinsic pressure of
increasing their abdominal pressure. As a result, nor- the bladder or abdominal pressure on the bladder. An
mal uroflowmetry flow rates cannot be used to rule abrupt rise in the fluid column usually signifies a blad-
out obstruction. der contraction during filling.
In single channel cystometry, a catheter is placed
into the bladder to measure pressure and deliver fluid
Filling and Storage Cystometry
at a constant rate. This measured pressure is called
Cystometry is the measurement of the pressure and “vesical” pressure, which is composed of the bladder
volume relationship of the bladder. When the test is wall pressure (also known as the detrusor pressure)
performed at the same time fluid is being infused into and the pressure exerted on the bladder by the abdo-
the bladder, which replicates bladder filling, it is called men (or the abdominal pressure). The major limita-
“filling cystometry.” During attempts to expel urine, tion of simple and single channel cystometry is that
it is called “voiding cystometry” and is part of the there is no way to determine if a rise in pressure is due
pressure-flow study. A cystometrogram is the graphi- to intrinsic detrusor pressure or abdominal pressures
cal recording of the bladder pressure and volume external to the bladder.
over time. The final and most common cystometry performed
Filling cystometry is typically performed with the is dual-channel. During this procedure, both abdomi-
patient in a comfortable position, usually seated, with nal pressure and vesical pressures are obtained. A
an empty bladder. A transurethral catheter is placed catheter is placed transurethrally into the bladder to
to measure bladder pressure. During simple cystom- measure vesical pressure and infuse fluid, and a sec-
etry, also called “eyeball” cystometry, a Foley catheter ond catheter is placed at the vaginal apex or rectum
is fitted with a Toomey syringe and is gravity-filled to measure abdominal pressure. The detrusor pressure
with fluid until the bladder is at capacity or the patient is electronically calculated and recorded in a process
reports discomfort (Figure 7-5). The bottom of the called subtraction cystometry. The detrusor pressure is
syringe is held at the level of the pubic symphysis. The obtained by subtracting the abdominal pressure from
distance of the meniscus above the pubic symphysis the vesical pressure (Figure 7-6).
estimates bladder pressure in centimeters of water. Urethral pressures can also be measured during fill-
The fluid meniscus is watched for a change in height. ing cystometry. This can be done by withdrawing the
CHAPTER 7

FIGURE 7-5 Graphic representation


of “eyeball cystometry.”
Chapter 7 Evaluation of Bladder Function 127

FIGURE 7-6 Dual-channel cystometrogram: the horizontal or “x-axis” is time, and the vertical or “y-axis” is pressure
in centimeters of water. The bladder is being filled at a rate of 50 mL/min. The top tracing is the vesical pressure and
there are fluctuations in the tracing that represent increases in bladder pressure. At the time marked the vesical pressure is
41 cm H2O. The abdominal catheter has been placed transvaginally and demonstrates a constant pressure of 28 cm H2O.
Thus, the detrusor pressure is actually fluctuating during filling.

catheter measuring vesical pressure into the urethra or during the filling cystometry. A profilometer is used to
by a catheter that can simultaneously measure vesical hold the catheter in place and to allow for the catheter
and urethral pressure. Because continence is depen- to be withdrawn at a set rate of 1 mm/s. The result-
dent on urethral pressures exceeding vesical pressure, ing pressure tracing is then analyzed (Figure 7-8).The
urethral closing pressures are often reported and are most common measurements obtained from an UPP
calculated by subtracting the vesical pressure from the are the maximal urethral pressure, the maximum ure-
urethral pressure (Figure 7-7). thral closure pressure, the total urethral length, and
As urethral pressure varies along the length of the the functional urethral length. The maximal urethral
urethra, many clinicians perform an UPP. UPPs are closure pressure is obtained by subtracting the vesical
typically performed at rest and at a set bladder volume pressure from the maximal urethral pressure.

CHAPTER 7

FIGURE 7-7 Cystometrogram with urethral pressure: in this tracing of a filling cystometrogram we see a normally
compliant bladder with no rise in vesical, abdominal, or detrusor pressure as the bladder fills from 0 to 300 mL. We
do see a rise in the urethral and urethral closure pressure (urethral pressure – vesical pressure) as the bladder fills repre-
senting the “guarding reflex.”
128 Section II Disease States

FIGURE 7-8 Urethral-pressure profile. A. Urethral port advanced into the bladder (urethral closure pressure [Pclo] = 0).
B. Urethral port withdrawn into the urethral lumen and the pressure reaches a maximum at (C) and starts to decline as
shown by (E). The functional urethral length is the length that Pclo is greater than zero (D).

Urethral length measurements are possible because should be present during a study to ensure proper
the profilometer withdraws the transurethral catheter measurements and interpretation. Cystometry stud-
measuring pressure through the urethra at a set rate of ies are valuable because they allow for a continuous
1 mm/s. Two urethral lengths are calculated. The first assessment of bladder pressure during filling and can
is total urethral length, which is the length of the ure- provide information that can be correlated with LUT
thra that has any pressure from the bladder neck to symptoms. Although cystometry is invasive, it is easy
the urethral meatus. The second is functional urethral to perform and generally well tolerated in patients who
CHAPTER 7

length. Functional urethral length is the length of the have been told what to expect.
urethra where the urethral pressure exceeds the intra- The major limitation of cystometry is that the pro-
vesical pressure. cess is done in a laboratory and does not represent
A cystometrogram report should include mea- normal bladder filling. The fill rates on average are
sures of compliance, sensation, pressure, and volume. 50 mL/min, the fluid is nonphysiologic, and the pres-
Bladder compliance is calculated by dividing the ence of the catheter can be a bladder wall irritant. To
change in bladder volume by the change in detrusor mitigate these limitations, it is important that the per-
pressure. Normal compliance is defined as >20 mL/ son performing urodynamics be technically qualified
cm H2O. Filling rates, intrinsic properties of the detru- to perform urodynamics and troubleshoot common
sor, such as previous radiation exposure, and the start- problems.
ing and ending volumes chosen for the calculation
can affect compliance. In general, bladder sensation
Voiding Cystometry (Pressure-flow Studies)
is measured during filling and is typically reported as
the infused volume at which the patient experiences When voiding cystometry is performed simultane-
the following sensations: the first sensation of blad- ously with uroflow measurements, the test is called
der filling (awareness), the first desire to void, a strong a pressure-flow study. Pressure-flow studies assess
desire to void, and the maximum cystometric capacity bladder characteristics and urine flow during bladder
defined as the bladder volume when micturition can emptying. They are commonly performed following
no longer be delayed. filling cystometry. Once the patient has been filled to
During filling the bladder and abdominal pressure maximum capacity and all bladder storage questions
tracings are monitored for any sudden rises in detrusor have been answered, the patient is assisted into a com-
pressure that can be associated with urgency or trans- fortable position and allowed to urinate with catheters
urethral urine loss. This is one reason why a clinician in place. Each catheter position should be confirmed
Chapter 7 Evaluation of Bladder Function 129

function. Women who cannot void during a pressure-


flow study may have normal voiding once they are out
of an artificial environment. Flow rate parameters are
maximum and average flow rates, total voided volume,
and time to maximum flow rate.
Pressure-flow studies allow assessment of bladder
function during voiding. The results of pressure-flow
studies are used to provide insight into LUT symp-
toms. Like other urodynamic tests, pressure-flow stud-
ies are easy to perform and well-tolerated in patients
who are appropriately counseled for the procedure. It
is important to remember that the pressure-flow study
is an artificial test and some patients may not be able
to urinate in this setting.

Measures of Urethral Function


In addition to urethral pressure, urethral function can
be assessed by bladder leak point pressures and EMG
of the striated urethral sphincter. The ICS defines
two leak point pressures: the detrusor leak point pres-
FIGURE 7-9 Pressure-flow study. The rise in vesical pres-
sure (Pves) along with some decrease in the abdominal
sure and the abdominal leak point pressure. It is not
pressure (Pabd) with resulting rise in detrusor pressure normal to leak during filling cystometry; both tests are
(Pdet). The rise in Pdet is results in a steady flow of urine considered as abnormal if positive. The detrusor leak
with the voided amount 280 mL in this example. point pressure is considered to be a static test and is
the lowest value of the detrusor pressure at which leak-
age is observed, in the absence of increased abdominal
pressure or a detrusor contraction. Detrusor leak point
by reviewing the tracing and making necessary adjust- pressures are often observed in patient with neurologic
ments. Monitoring of the urethral pressure will allow disorders. High detrusor leak point pressures (>40 cm
the clinician to determine if the urethra opens and H2O) may put patients with neurologic disorders at
stays relaxed to allow voiding at normal pressures. increased risk for UUT deterioration.
Usually, pressure-flow studies are performed using The abdominal leak point pressure is defined as the
dual-channel cystometry because it allows the exam- intravesical pressure at which urine leakage occurs with

CHAPTER 7
iner to determine if abdominal force is being used dur- provocative measures—such as coughing or perform-
ing voiding (Figure 7-9). ing a Valsalva maneuver—in the absence of a detrusor
In addition to measuring vesical and abdominal contraction. Low abdominal leak point pressures are
pressures, flow rate is measured. One significant differ- suggestive of poor urethral function and may predict
ence between the flow rates obtained during uroflow lower surgical success in women with the diagnosis of
and pressure-flow studies is the presence of a catheter urodynamic stress incontinence. Values for leak point
in the urethra. Studies have consistently demonstrated pressure are difficult to reproduce and are influenced
lower urinary flow rates in the presence of a urethral by the size of the transurethral catheter, patient posi-
catheter for women with normal anatomy. Typically, tion, and the bladder volume.
flow rates obtained during pressure-flow studies are Another test often performed to measure urethral
called “instrumented” flow because of the presence of sphincter function is EMG, which is the recording
the catheter. Again, the primary aim of pressure-flow and study of electrical activity from striated muscles.
studies is to reproduce the patient’s symptoms dur- It can be used to distinguish between normal, dener-
ing urination to see if the symptoms relate to pressure- vated, and myopathic muscles. EMG is most often
flow observations. performed using patch electrodes. Surface patch elec-
Commonly recorded bladder pressures are the pre- trodes are placed on the perineal skin of either side
micturition pressures, maximum pressures observed of the urethra. They record the neuromuscular activity
during voiding and the pressures at the maximum flow from all nearby muscles, including the levator ani. As
rate. Often voiding pressures are interpreted as nor- a result, they cannot be used to diagnose or quantify
mal, underactive, or acontractile. Urethral function is neuropathy or myopathy. They are simply a qualitative
assessed as normal, dysfunctional, or dysynergic, and measure of pelvic floor muscle activity, not the urethral
requires a simultaneous assessment of the bladder sphincter. The limitations of surface patch electrodes
130 Section II Disease States

are that the recordings are difficult to interpret, they pressures, profuse sweating, and pounding headache.
are not reproducible and the urethral sphincter cannot As a result, these patients should have blood pressure
be isolated. monitoring during any study involving the bladder or
Another method of measuring urethral sphincter bowel and if they develop the symptoms of autom-
function uses needle electrodes that are placed directly nomic dysreflexia, the bladder should be immediately
in the urethral sphincter and record the neuromuscu- emptied and all catheters removed.
lar activity directly from the striated urethral sphincter. Whether or not medications for LUT symptoms
These EMG studies are considered the “gold stan- should be withdrawn prior to urodynamic studies is
dard” for identifying neuromuscular disease in striated dependent on the urodynamic question. For example,
muscle and allow for both qualitative and quantitative if the urodynamic question is, “does this patient have
analyses or the urethral sphincter. A variety of needle stress incontinence?” then leaving her on an anti-
electrodes are available and each has unique recording cholinergic for the urodynamic study may allow the
properties. The limitations of needle electrodes are that filling cystometry and leak point pressures to be per-
they require increased skill and training to accurately formed completely if her overactive bladder symptoms
place, and the test is uncomfortable for the patient. are more controlled.
Some basic principles that help improve the reliabil-
Video-Urodynamics ity of urodynamic testing is to make sure the specific
question you are trying to answer is stated when order-
Video-urodynamics is the term given for the use of
ing the studies. Also, as a clinician, you are respon-
fluoroscopic imaging during filling and voiding cys-
sible for insuring that the studies are being performed
tometry. This test is typically reserved for more com-
in a technically correct fashion. You must be properly
plicated cases of LUTD where there is a high chance
trained to perform and interpret the results of urody-
of having an anatomic abnormality that would explain
namics. Lastly, at the end of every urodynamic study
LUT symptoms. The imaging for video-urodynamics
you should ask whether or not the urodynamic testing
is typically done with a fluoroscopic unit, which can
reproduced the patient’s symptoms.
be fixed or mobile. Some practices use US, although
this modality has significant limitations in imaging the
UUT. With fluoroscopy, a shielded room in the uro- Cystoscopy
dynamics laboratory or radiology suite is required due Cystourethroscopy plays a critical role in evaluating
to the use of x-ray. In order to mimic normal voiding, women who present with lower urinary tract symp-
accommodations need to be made for men to stand toms (LUTS). It is used for the visual detection of
and women to sit. Images of the urinary tract during bladder and urethral lesions such as carcinoma
bladder filling and storage can delineate the bladder (Figure 7-10), intravesical leiomyoma, endometriosis,
outline and shape, allowing for the detection of blad- bladder or kidney stones, and the presence of a for-
CHAPTER 7

der diverticulum or herniation. Cough and Valsalva eign body, particularly in patients who have had prior
maneuvers are performed looking for bladder neck
descent and competence. During voiding, the out-
line of the urethra is examined for abnormalities,
strictures or failure of the urethral sphincter to relax.
Ureteral reflux can be seen with bladder filling, rises
in abdominal pressure or during attempts to void.
Lastly, postvoid images are reviewed for the volume
of residual urine.

Preparing a Patient for Urodynamic Testing


Patients should be counseled about urodynamic test-
ing. Studies have shown that patients who are given
simple explanations about why the test is indicated and
what to expect, tolerate the testing well. Antibiotics
should be given based on recent American Urological
Association guidelines and patient specifics. Spinal
cord injury patients with lesions above spinal cord
level T-6 may develop autonomic dysreflexia with the
bladder stimulation from urodynamics. Autonomic
dysreflexia is a syndrome of massive reflex sympa- FIGURE 7-10 Papillary urothelial tumor viewed through
thetic discharge resulting in dangerously high blood a cystoscope.
Chapter 7 Evaluation of Bladder Function 131

FIGURE 7-11 The 3 components of the


cystoscope.

pelvic surgery. Upper tract lesions can also be identi- of the study is when a catheter is placed and the blad-
fied by cystoscopy. In women with gross hematuria, der is filled with contrast. Filling defects on x-ray in
cystoscopy may identify blood coming from a unilat- the bladder can be related to foreign body, uretero-
eral ureteral orifice implicating the UUT as the source cele, or tumor. Retrograde filling of the bladder with
of the bleeding. In addition, washings taken from the a radiopaque solution can also assess the integrity of
bladder may indicate malignant cells that are com- the bladder to assess for rupture after trauma or pres-
ing from the transitional cell lining for the ureter and ence of a genitourinary fistula following pelvic sur-
renal pelvis. gery. After the bladder is filled, the patient is asked
Cystoscopes have three components: lens, bridge, to void. The position of the patient is important dur-
and sheath (Figure 7-11) and require a distension ing the voiding phase. Most women do not void in
medium and light source. Most teaching institutions the supine position, yet this is often the position that
utilize a camera so that the findings may be reviewed women are asked to void for VCUG. It may be neces-
on a monitor. There are three lenses commonly used sary to discuss with the radiologist that you would like
in office cystoscopy. The 70° lens is the best lens for images from the voiding phase with the patient seated.
diagnostic studies because it provides a wide-angle During the voiding phase, fluoroscopy can assess for
view of the bladder topography. A 30° or 0° lens is best ureteral reflux (Figure 7-12). Finally, the bladder is
for examination of the urethra or if instrumentation is
going to be passed through the scope such as a flexible
grasper to remove an ureteral stent. When cystoscopy

CHAPTER 7
is being performed to rule out a urethral or bladder
carcinoma, the filling medium should be normal saline
so that the bladder cells being sent for cytology remain
normally shaped from an isotonic solution.

Radiology
It is important to understand the question you are ask-
ing before ordering imaging tests. This is also impor-
tant as many patients are concerned about unnecessary
exposure to the radiation that is involved in some of
these imaging modalities.

Voiding Cystourethrogram
Voiding cystourethrogram (VCUG) is a test very
commonly used by pediatric urologists, but is also an
important test for the urogynecologist. A VCUG is a
set of plain x-rays. The first image is a plain film of the
pelvis. This allows for evaluation of the bony struc-
tures and will help detect spina bifida occulta or other
neurologic diseases with bony landmark findings that FIGURE 7-12 Voiding cystourethrogram demonstrating
may be affecting urinary tract function. The next part bilateral ureteral reflux during voiding.
132 Section II Disease States

imaged after voiding to assess for any residual con- dependent on the skills of the ultrasonographer and
trast that may signify loss of bladder integrity or pres- the patient’s body habitus.
ence of a fistula.
Intravenous Pyelogram
Renal and Bladder Ultrasound
Intravenous pyelogram (IVP) is an x-ray test that is
Renal and bladder US can be a useful modality that not commonly performed as it has been surpassed by
does not use ionizing radiation. Renal US can assess the computed tomography (CT) urogram. An IVP
hydronephrosis, renal lesions, and some nephrolithia- consists of several x-rays. The initial x-ray is without
sis. Bladder US can delineate intraluminal lesions if the contrast and serves as a general survey of the abdo-
bladder is well-filled, bladder wall thickness, uretero- men and pelvis. After IV contrast is administered, sev-
celes, the presence of ureteral jets, and bladder stones. eral images are taken at different time points. These
US equipment is often available in the outpatient postcontrast images are used to assess contrast in the
clinic settings of urogynecologists/urologists, and, as a kidney, into the collecting system, and finally into the
result, offers the opportunity to quickly answer a clini- bladder. This test is much more cumbersome and does
cal question. Limitations of US are that the images are not provide as much information as a CT urogram.

Table 7-3 Summary of How to Answer Common Urogynecologic Questions

Clinical Question
Does the Patient have… Additional Tests to Perform
Stress urinary incontinence? 1. Empty supine stress test
2. Urinalysis and urine culture to rule out UTI
3. Consider CMG/UDS if planning surgical intervention
Urgency urinary incontinence? 1. Postvoid residual
2. Urinalysis and urine culture to rule out UTI
3. Consider CMG/UDS if planning surgical intervention
4. Consider cystoscopy and urine barbotage to evaluate for bladder cancer
if risk factors (ie, sudden onset, heavy smoker, history of pelvic radiation,
nonresponsive to therapy, hematuria, recurrent UTI despite adequate treatment)
5. Consider MRI any concern for neurologic etiology
Genitourinary fistula? 1. Cystoscopy to look for fistula ± tampon test (Is it bladder or ureter?)
CHAPTER 7

Secretions that are not urine? 1. Pyridium pad test (is it urine?) if not detected on physical examination
Obstructive voiding? 1. Pressure flow, with urethral needle EMG to see if urethral quieting occurs
2. If post-op synthetic sling procedure, consider possibility of urethral erosion
(urethroscopy)
3. CT or MRI to evaluate for pelvic mass (even pregnancy) or neurologic etiology if
symptoms suddenly appear
4. Physical examination to see if “dysfunctional voider”
Urothelial tumor? 1. Cystoscopy
2. Cytology obtained at the time of cystoscopy
3. Upper tract imaging (CT urogram or renal US to look for stones,
filling defects, masses, etc)
Recurrent UTI? 1. Post void residual to rule out obstruction
2. Voided cytology (tumors can be nidus for infection) or cystoscopy with bladder
barbotage
3. Upper urinary tract imaging (CT scan or renal US to look for kidney stones,
renal tumors, embryologic)
4. Consider VCUG if concern for ureteral reflux
5. Consider Lasix renal scan if concerned for ureteral obstruction
Nocturnal polyuria? 1. Bladder diary (Is it nocturnal polyuria? If yes, needs sleep study)
Urethral diverticulum? 1. Urethroscopy with 0° of 30° scope
2. Consider MRI or transvaginal ultrasound for surgical planning

CMG, cystometrogram; CT, computed tomography; EMG, electromyography; MRI, magnetic resonance imaging; UDS, urodynamics; US, ultrasound;
UTI, urinary tract infection; VCUG, voiding cystourethrogram.
Chapter 7 Evaluation of Bladder Function 133

Currently, IVP is most commonly used in trauma situ- an anxietolytic so that they can complete it. Patients
ations to assess if there are indeed two kidneys present. with an implanted sacral neuromodulator cannot
This “one-shot IVP” is done by taking a scout film undergo an MRI study due to safety concerns with
followed by administering IV contrast, and then taking implanted magnetic medical devices.
another image from two to ten minutes after adminis- There are a multitude of ways to evaluate the LUT.
tering contrast. It is important to remember that these testing modali-
ties each have their own strengths and limitations. The
value of these testing modalities is related to their abil-
Computed Tomography Urogram ity to answer a specific clinical question. A summary of
CT urogram is a specific triple phase CT scan. There this is provided in Table 7-3. A clinician should have a
is a noncontrast phase that assesses overall anatomy, clear understanding of what clinical question is being
as well as for the presence of nephrolithiasis as most asked before deciding which test should be performed
kidney stones are calcium-based. The contrast phase for a particular patient.
of the study is done to assess the vasculature and renal
function. The final phase of the study is a delayed
phase, which is a 2D reconstruction of a delayed scan REFERENCES
and allows the viewer to see the collecting system
opacified with contrast that has been excreted. In this 1. Hinman F. Atlas of Urosurgical Anatomy. Philadelphia, PA: W.B.
Saunders; 1993.
way, it mimics the images obtained with IVP and can
2. Stephens FD. Congenital Anomalies of the Kidney, Urinary and
detect filling defects that may represent upper tract Genital Tracts. 2nd ed. London: Martin Dunitz; 2002.
cancers of the urothelium. 3. Morgan DM, Umek W, Guire K, Morgan HK, Garabrant A,
CT urograms are used in the work-up for gross and DeLancey JO. Urethral sphincter morphology and function with
concerning microscopic hematuria because they can and without stress incontinence. J Urol. 2009;182(1):203–209.
4. Rud T, Andersson KE, Asmussen M, Hunting A, Ulmsten U.
detect renal parenchymal masses, renal and ureteral
Factors maintaining the intraurethral pressure in women. Invest
stones, congenital anatomic abnormalities, and can- Urol. 1980;17(4):343–347.
cers of the urothelium.10 They are also used to evaluate 5. Perucchini D, DeLancey JO, Ashton-Miller JA, Peschers U,
masses extrinsic to the genitourinary system. Kataria T. Age effects on urethral striated muscle. I. Changes
in number and diameter of striated muscle fibers in the ventral
urethra. Am J Obstet Gynecol. 2002;186(3):351–355.
Magnetic Resonance Imaging 6. de Groat WC, Yoshimura N. Changes in afferent activity after
spinal cord injury. Neurourol Urodyn. 2010;29(1):63–76.
Pelvic MRI is considered to be the gold standard for 7. Fowler CJ, Griffiths D, de Groat WC. The neural control of
assessing lesions of the lower bladder, vagina, and micturition. Nat Rev Neurosci. 2008;9(6):453–466.
8. Haylen BT, de Ridder D, Freeman RM, et al. An International
urethra because of its ability to distinguish soft tis-
Urogynecological Association (IUGA)/International Conti-

CHAPTER 7
sue masses. MRI of the brain and spinal cord are nence Society (ICS) joint report on the terminology for female
also used to assess for neurologic disorders that pelvic floor dysfunction. Neurourol Urodyn. 2010;29(1):4–20.
may be causing LUTS. It is important to remem- 9. Van Kerrebroeck PE, Dmochowski R, FitzGerald MP, et al.
ber that women with multiple sclerosis may initially Nocturia research: current status and future perspectives.
Neurourol Urodyn. 2010;29(4):623–628.
present with urinary complaints. Patients may find
10. Grossfeld GD, Litwin MS, Wolf JS, et al. Evaluation of asymp-
MRIs disconcerting based on the length of the study tomatic microscopic hematuria in adults: The American Uro-
and the noise level, and should be counseled in logical Association Best Practice Policy-Part I: Definition,
advance about the necessity of the test and offered Detection, Prevalence, and Etiology. Urology. 2001;57:599–603.
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8
1 Voiding Phase Dysfunction
Benjamin M. Brucker and Victor W. Nitti

The purpose of the lower urinary tract is to allow for diagnosis of “acontractile” or “hypocontractile” blad-
low-pressure bladder filling and storage of urine with- der, as behavior during urodynamics may not mimic
out incontinence and voluntary complete expulsion that of daily living. For example, if a patient normally
of urine. This is made possible by an intricate balance voids yet cannot do so during a urodynamics study,
of neural control, numerous neurotransmitters, subtle she may not truly have an acontractile bladder.
anatomic relations, and a variety of pharmacologi-
cal and mechanical properties. This complex system
can be simplified into the two phases of the micturi- Key Points
tion cycle: bladder filling with urine storage and blad-
der emptying or voiding.1 The focus of this chapter • The micturition/voiding phase requires a detru-
will be on problems that women face in regard to their sor contraction that is of sufficient strength and
ability to successfully empty their bladder, termed duration to overcome the resistance of the bladder
voiding phase dysfunction. outlet.
• Ineffective or incomplete emptying can be caused
by a problem with the bladder (impaired contrac-
DEFINITION tility) or a problem with the outlet (obstruction).

Ineffective Emptying
This chapter will review the pathophysiology under-
In the simplest terms, the micturition/voiding phase lying the different etiologies for common conditions
requires a detrusor contraction that is of sufficient causing ineffective emptying, general evaluation of
strength and of sufficient duration to overcome the voiding dysfunction, followed by treatment options for
resistance of the bladder outlet. Any alterations, or each condition.
combinations of alterations, that affect the strength/
duration of the detrusor contraction, that increase
the resistance of the outlet, or that affect the coor-
dination of these actions, are potential causes of
PATHOPHYSIOLOGY
impaired emptying. Ineffective or incomplete emp-
tying can be caused by a problem with the bladder
Detrusor Underactivity
(impaired or absent contractility) or a problem with Detrusor underactivity is defined by the International
the outlet (obstr