Urodynamics For Urogynecologists Vignoli2018

Giancarlo Vignoli
Urodynamics for
Urogynecologists
A Pocket Guide
for Clinical Practice
123
Urodynamics for
Urogynecologists
Giancarlo Vignoli
Urodynamics for
Urogynecologists
A Pocket Guide for Clinical Practice
Giancarlo Vignoli
Functional Urology Unit
Casa Madre Fortunata Toniolo
Bologna
Italy
ISBN 978-3-319-74004-1 ISBN 978-3-319-74005-8 (eBook)

https://doi.org/10.1007/978-3-319-74005-8
Library of Congress Control Number: 2018940775
© Springer International Publishing AG, part of Springer Nature 2018

This work is subject to copyright. All rights are reserved by the Publisher, whether
the whole or part of the material is concerned, specifically the rights of transla-
tion, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on
microfilms or in any other physical way, and transmission or information storage
and retrieval, electronic adaptation, computer software, or by similar or dissimi-
lar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service
marks, etc. in this publication does not imply, even in the absence of a specific
statement, that such names are exempt from the relevant protective laws and
regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and
information in this book are believed to be true and accurate at the date of pub-
lication. Neither the publisher nor the authors or the editors give a warranty,
express or implied, with respect to the material contained herein or for any errors
or omissions that may have been made. The publisher remains neutral with
regard to jurisdictional claims in published maps and institutional affiliations.
Printed on acid-free paper
This Springer imprint is published by the registered company Springer

International Publishing AG part of Springer Nature
The registered company address is: Gewerbestrasse 11, 6330 Cham,
Switzerland
Preface
In recent years gynecologists have shown an increasing inter-

est in lower urinary tract dysfunctions related to gynecologic
disease, but many of them are unfamiliar with urodynamics. It
is a common belief that urodynamics can reveal the underly-
ing mechanisms of lower urinary tract symptoms and that this
may help to select more rational treatments. Particularly
when the clinical evaluation is uncertain, urodynamics can
provide additional information that may help to define the
diagnosis. For decades urodynamic studies have been consid-
ered the gold standard to objectively diagnose a dysfunction
of the lower urinary tract. Unfortunately, the role of urody-
namic studies in patients with lower urinary tract dysfunction
is largely based on expert opinion and the conventional use
of urodynamic testing in clinical practice failed to support
this original assumption. The differentiation between several
types of lower urinary tract dysfunctions and the choice of
treatment according to urodynamics data doesn’t seem to
have significant predictive value in most of the patients.
Possible explanations for such unexpected conclusion
have been summarized by Griffiths et al.*: first, symptoms of
lower urinary tract have similar underlying pathophysiology
requiring similar treatment regardless of urodynamic data;
second, current urodynamic tests are too rough (or to poorly
done) to address the important pathophysiological differ-
ences that affect treatment outcome; third (more distressing)
current treatments are so nonspecific that the underlying
dysfunction is unimportant: treatment work equally well or
poorly in any case.
vi Preface
To make matters worse, urodynamic testing is time con-

suming, invasive, and costly and not without associated mor-
bidity. Furthermore, since the quality of the studies is crucial,
they also require special training.
Today, the pros and cons of performing routine urody-
namic testing have become a topic embroiled in controversy.
Particularly among gynecologists, since with the introduc-
tion of easy to administer mid-urethral slings, a simplified
reasoning has taken place that states that every type of SUI
may be treated in the same way, and therefore, no urody-
namic investigation would be needed.
Since 2006 the National Institute for Clinical Excellence
(NICE) recommends that the use of multichannel urodynam-
ics is not routinely needed before surgery in women with a
clearly defined clinical diagnosis of pure SUI.
LUTS in women, however, are not only urinary inconti-
nence, but include the overactive bladder syndrome, the emp-
tying disorders, and painful bladder syndrome, all of which
should require urodynamic investigation for a proper
assessment.
Despite the debate, there is no doubt that urodynamic
evaluation of lower urinary tract function is still the best
available tool for lower urinary tract function assessment.
The evidence for urodynamic testing of patients with lower
urinary tract dysfunction is extensive and solid. Urodynamics
is necessary because it contributes to knowledge of lower
urinary tract dysfunction, whether or not there is a narrow
evidence that it improves outcome. Although pragmatic
treatment of symptoms is possible as a first approach, only
urodynamic testing can disclose the function of the lower
urinary tract and provide the rationale for the most appropri-
ate therapy.
The objective of this book is to verify the role of urody-
namics in current urogynecological practice and the opinion
about the need to perform urodynamic investigation in the
various clinical situations that are part of female urology.
Each chapter is structured according to a specific scheme
including the background of the problem, the theoretical role
Preface vii
of urodynamics in clarifying the nature of the problem, and,

finally, the pros and cons of the investigation according to
literature review. The first part of the book is devoted to con-
ducting a urodynamic investigation properly, the so-called
“good urodynamic practice.” Some recent surveys indicate
that most of the personnel performing urodynamics believe
that their training had been inadequate. Training and educa-
tion raises the level of confidence and the ability to perform
and interpret urodynamic investigations, with obvious impli-
cations for the accuracy, reliability, and consistency of the
final report.
Finally, a chapter is devoted to neurogenic bladder in
women, which requires special considerations that are not
seen with many male neurogenic bladder patients.
Our purpose is to provide urogynecological practitioners
with a practical, easy-to-read, approach to indications, perfor-
mance, and analysis of urodynamic testing in the field of
female urology.
Bologna, Italy Giancarlo Vignoli
*Griffiths DJ, Kondo A, Bauer S, Diamant N, Liao L, Lose G, et al.

Chapter 11: Dynamic testing. In: Abrams P, Cardozo L, Khoury S, Wein
A, editors. Incontinence, Volume 1: Basics and evaluation, 3rd ICI,
Edition 21. Paris, France: Health Publication Ltd; 2005. pp 585–673.
Contents
1 Physiology of Micturition in Female . . . . . . . . . . . . . . 1

1.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.1.1 Central Neural Mechanisms
Controlling Storage and Voiding. . . . . . 1
1.1.2 Peripheral Neural Mechanisms
Controlling Storage and Voiding. . . . . . 8
1.1.3 Pressure Variations During
Micturition Cycle. . . . . . . . . . . . . . . . . . . 10
Suggested Reading. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
2 Pretest Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

2.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
2.2 Pretest Assessment. . . . . . . . . . . . . . . . . . . . . . . . 18
2.2.1 Clinical History. . . . . . . . . . . . . . . . . . . . . 19
2.2.2 Relevant Physical Examination. . . . . . . 19
2.2.3 Urinalysis. . . . . . . . . . . . . . . . . . . . . . . . . . 23
2.2.4 Voiding Diary. . . . . . . . . . . . . . . . . . . . . . 24
2.2.5 Pad Test. . . . . . . . . . . . . . . . . . . . . . . . . . . 26
3 Noninvasive Urodynamics. . . . . . . . . . . . . . . . . . . . . . . 31

3.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
3.1.1 Uroflowmetry. . . . . . . . . . . . . . . . . . . . . . 31
3.1.2 Postvoid Residual (PVR)
Assessment. . . . . . . . . . . . . . . . . . . . . . . . 37
3.1.3 Voided Percentage (Void%). . . . . . . . . . 37
x Contents
4 How to Perform Conventional Urodynamic

Investigation: The “Good Urodynamic Practice” . . . 41
4.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
4.2 Setup of the Equipment. . . . . . . . . . . . . . . . . . . . 42
4.3 Transducers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44
4.3.1 Water-Filled (External) Transducers. . . 44
4.3.2 Microtip Transducers. . . . . . . . . . . . . . . . 45
4.3.3 Air-Charged Catheters
(T-DOC System) . . . . . . . . . . . . . . . . . . . 46
4.3.4 Zeroing the External Water-Filled
Transducers. . . . . . . . . . . . . . . . . . . . . . . . 47
4.3.5 Reference Height of the External
Water-Filled Transducers. . . . . . . . . . . . . 48
4.3.6 Microtip and Air-Filled Systems. . . . . . . 49
4.4 Setup of the Patient . . . . . . . . . . . . . . . . . . . . . . . 50
4.5 Post-test Patient Care. . . . . . . . . . . . . . . . . . . . . . 58
5 Interpretation of Tracings and Identification

of Artifacts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
5.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
5.2 Conventional (Invasive) UDS: Relevant
Parameters. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
5.2.1 Cystometry. . . . . . . . . . . . . . . . . . . . . . . . 62
5.2.2 Leak Point Pressures. . . . . . . . . . . . . . . . 66
5.2.3 Pressure/Flow Study . . . . . . . . . . . . . . . . 68
5.3 Artifacts Identifications and Remedial
Actions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
5.3.1 Uroflowmetry: Knock to the
Equipment. . . . . . . . . . . . . . . . . . . . . . . . . 71
5.3.2 Pressure Traces. . . . . . . . . . . . . . . . . . . . . 72
5.3.3 EMG: 60 Hz artifact. . . . . . . . . . . . . . . . 76
Suggested Readings . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
6 Supplementary Urodynamic Tests. . . . . . . . . . . . . . . . 79

6.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
6.2 Urethral Profilometry. . . . . . . . . . . . . . . . . . . . . . 79
6.2.1 Technical Notes . . . . . . . . . . . . . . . . . . . . 80
6.2.2 UPP at Rest . . . . . . . . . . . . . . . . . . . . . . . 81
6.2.3 Stress UPP. . . . . . . . . . . . . . . . . . . . . . . . . 84
Contents xi
6.3 Electromyography. . . . . . . . . . . . . . . . . . . . . . . . . 85

6.4 Videourodynamic. . . . . . . . . . . . . . . . . . . . . . . . . 87
6.5 Ambulatory Urodynamics
Monitoring (AUM). . . . . . . . . . . . . . . . . . . . . . . . 89
7 UDS in Stress Urinary Incontinence

Syndrome (SUI-S) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
7.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
7.2 Types of Urinary Incontinence in Female. . . . . 93
7.3 Evaluation of Patients with SUI. . . . . . . . . . . . . 97
7.4 Office Evaluation of Female Incontinence. . . . 98
7.4.1 History. . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
7.4.2 Urinalysis. . . . . . . . . . . . . . . . . . . . . . . . . . 99
7.4.3 Physical Examination . . . . . . . . . . . . . . . 100
7.4.4 Demonstration of Stress
Incontinence. . . . . . . . . . . . . . . . . . . . . . . 100
7.4.5 Assessment of Urethral Mobility. . . . . . 100
7.4.6 Post-void Residual Urine (PVR). . . . . . 101
7.5 Invasive Urodynamic Testing . . . . . . . . . . . . . . . 102
7.5.1 Confirm SUI. . . . . . . . . . . . . . . . . . . . . . . 102
7.5.2 Assess Detrusor Activity
During Filling. . . . . . . . . . . . . . . . . . . . . . 102
7.5.3 Assess Detrusor Contractility
During Voiding. . . . . . . . . . . . . . . . . . . . . 103
7.5.4 Assess Intrinsic Urethral Function . . . . 103
7.6 The Debate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104
7.6.1 The Case Against. . . . . . . . . . . . . . . . . . . 104
7.6.2 The Case Pros. . . . . . . . . . . . . . . . . . . . . . 106
7.6.3 The Future. . . . . . . . . . . . . . . . . . . . . . . . . 107
8 UDS in Pelvic Organ Prolapse

Syndrome (POP-S). . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
8.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
8.2 Classification of Pelvic Organ Prolapse. . . . . . . 114
8.2.1 S-POP-Q: Practical Tips. . . . . . . . . . . . . 115
8.3 The Role of Urodynamics Before Prolapse
Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
8.4 POP and SUI Syndrome . . . . . . . . . . . . . . . . . . . 117
xii Contents
8.4.1 Incontinence Surgery

in all Patients. . . . . . . . . . . . . . . . . . . . . 119
8.4.2 Incontinence Surgery
in No Patients. . . . . . . . . . . . . . . . . . . . 119
8.4.3 Incontinence Surgery in Some
Patients (namely, Patients with
Coexisting and Occult SUI-S). . . . . . . 120
8.5 Testing for Occult SUI and Assessment
of Urethral Function. . . . . . . . . . . . . . . . . . . . . . 120
8.5.1 Provocative Tests . . . . . . . . . . . . . . . . . 121
8.5.2 Urodynamic Testing. . . . . . . . . . . . . . . 121
8.6 POP and OAB Syndrome . . . . . . . . . . . . . . . . . . 122
8.6.1 Key Facts About POP
and OAB Syndrome. . . . . . . . . . . . . . . 123
8.7 POP and Voiding Dysfunction Syndrome. . . . . 124
9 UDS in Overactive Bladder Syndrome (OAB-S). . . . 131

9.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
9.2 Current Concepts on Pathophysiology
of OAB Syndrome (OAB-S). . . . . . . . . . . . . . . . 133
9.2.1 Myogenic Hypothesis. . . . . . . . . . . . . . 133
9.2.2 Increased Afferent Activity. . . . . . . . . 135
9.2.3 Abnormal Handling
of Afferent Signals. . . . . . . . . . . . . . . . 137
9.3 Urodynamics in OAB-S. . . . . . . . . . . . . . . . . . . . 137
9.4 OAB-S in Female: Key Notes for Clinical
Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142
9.5 OAB-S in Female: Key Notes
for Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142
10 UDS in Voiding Dysfunction Syndrome (VD-S). . . . 149

10.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
10.2 Prevalence of Emptying Problems
in Women. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
10.3 Causes of Voiding Dysfunction in Females. . . . 150
10.4 Detrusor Underactivity . . . . . . . . . . . . . . . . . . . . 152
10.4.1 Detrusor Underactivity
and Aging . . . . . . . . . . . . . . . . . . . . . . . 152
Contents xiii
10.5 Obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

10.5.1 Obstruction and Previous
MUS Surgery. . . . . . . . . . . . . . . . . . . . . 154
10.5.2 Obstruction and POP. . . . . . . . . . . . . . 154
10.5.3 Dysfunctional Voiding (DV). . . . . . . . 155
10.5.4 Fowler’s Syndrome. . . . . . . . . . . . . . . . 156
10.6 Assessment of Voiding Dysfunction
in Female. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157
10.7 Urodynamic Challenges in the
Diagnosis of Female DU/BOO. . . . . . . . . . . . . . 157
10.7.1 Obstruction. . . . . . . . . . . . . . . . . . . . . . 157
10.7.2 Detrusor Underactivity. . . . . . . . . . . . 158
10.8 Keynotes on Clinical Diagnosis of VD
in Women. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
10.9 Keynotes on Clinical Management
of VD in Women. . . . . . . . . . . . . . . . . . . . . . . . . 162
11 UDS in Pain Bladder Syndrome (PBS)

and Overactive Pelvic Floor Dysfunction. . . . . . . . . . 169
11.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169
11.2 Diagnosis of PBS/IC. . . . . . . . . . . . . . . . . . . . . . . 173
11.2.1 Symptoms and Signs. . . . . . . . . . . . . . . 173
11.2.2 Confusable and Associated Diseases. 175
11.2.3 Specific Tests. . . . . . . . . . . . . . . . . . . . . 176
11.3 Outline of Available Treatments. . . . . . . . . . . . . 179
12 Neurogenic Lower Urinary Tract Dysfunction

Syndrome (NLUTD-S) in Female . . . . . . . . . . . . . . . . 183
12.1 Background. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183
12.2 Classification. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183
12.3 Clinical Assessment of Female with
NLUTD-S . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 186
12.4 Initial Assessment. . . . . . . . . . . . . . . . . . . . . . . . . 186
12.4.1 History and Physical Examination. . . 186
12.4.2 Routine Laboratory Investigations . . 187
12.4.3 Ultrasound. . . . . . . . . . . . . . . . . . . . . . . 187
12.5 Specialized Assessment . . . . . . . . . . . . . . . . . . . . 188
xiv Contents
12.5.1 Urodynamics with Imaging

Techniques. . . . . . . . . . . . . . . . . . . . . . . 188
12.5.2 Difficult Situation During Urodynamic
Testing in NLUTD-S: Autonomic
Dysreflexia (AD). . . . . . . . . . . . . . . . . 190
12.5.3 Reappraisal of Urodynamic
Testing and Videourodynamics
in NLUTD-S. . . . . . . . . . . . . . . . . . . . . 191
12.6 Complications and Follow-Up of Neurogenic
Bladder Dysfunction. . . . . . . . . . . . . . . . . . . . . .. 192
12.7 Principles of Treatment of NLUTD-S. . . . . . . . 193
12.8 Management of Bladder Emptying . . . . . . . . . . 194
12.8.1 Spontaneous Voiding. . . . . . . . . . . . . . 194
12.8.2 Intermittent Catheterization. . . . . . . . 194
12.8.3 Indwelling Urethral Catheters . . . . . . 197
12.9 Management of Storage Symptoms. . . . . . . . . . 198
12.9.1 Antimuscarinic Drugs . . . . . . . . . . . . . 198
12.9.2 Botulin Toxin. . . . . . . . . . . . . . . . . . . . . 199
12.9.3 Neuromodulation. . . . . . . . . . . . . . . . . 200
12.10 Surgery for Sphincteric Incompetence. . . . . . . . 202
12.10.1 Bulking Agents. . . . . . . . . . . . . . . . . . . 202
12.10.2 Autologous Sling. . . . . . . . . . . . . . . . . . 203
12.10.3 Artificial Sphincter. . . . . . . . . . . . . . . . 203
12.11 Diapers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
12.12 Types of Neurogenic Bladder
and Relative Care. . . . . . . . . . . . . . . . . . . . . . . . . 205
12.12.1 Dementia. . . . . . . . . . . . . . . . . . . . . . . . 205
12.12.2 Stroke. . . . . . . . . . . . . . . . . . . . . . . . . . . 206
12.12.3 Multiple Sclerosis. . . . . . . . . . . . . . . . . 206
12.12.4 Parkinson’s Disease . . . . . . . . . . . . . . . 207
12.12.5 Diabetes Mellitus. . . . . . . . . . . . . . . . . 208
12.12.6 Radical Pelvic Surgery. . . . . . . . . . . . . 209
12.12.7 Spinal Cord Injury . . . . . . . . . . . . . . . . 209
12.12.8 Spina Bifida. . . . . . . . . . . . . . . . . . . . . . 210
Contents xv
13 Making Sense of Urodynamic Testing for Women

with LUTS: Practical Conclusive Notes. . . . . . . . . . . . 217
ppendix A: What Do the Experts Say?—

A
Scientific Societies Recommendations
for UDS Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221
ppendix B: Informed Consent for

A
Invasive UDS Testing (Sample) . . . . . . . . . . . . . . . . . . . . . 225
Index. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
Abbreviations
ACC Anterior cyngulate cortex

ALPP Abdominal leak point pressure
AUA/SUFU
American Urological Association/Society of
Urodynamics and Female Urology
AUM Ambulatory urodynamic monitoring
BOO Bladder outlet obstruction
BOOI Bladder outlet obstruction index
BPS Bladder painful syndrome
CLPP Cough leak point pressure
CIC Clean intermittent catheterization
DHIC Detrusor hyperactivity with impaired
contractility
DLPP Detrusor leak point pressure
DO Detrusor overactivity
DU Detrusor underactivity
EMG Electromyography
FDV First desire to void
FSF First sensation of filling
FVC Frequency volume chart
GUP Good urodynamic practice
HSB Hypersensitive bladder
ICI International Consultation on Incontinence
ICS International Continence Society
ICI-RS International Consultation on Incontinence
Research Society
IDC Involuntary detrusor contraction(s)
IDO Idiopathic detrusor overactivity
ISD Intrinsic sphincteric deficiency
xviii Abbreviations
LPP Leak point pressure

LUT Lower urinary tract
LUTD Lower urinary tract dysfunction(s)
LUTS Lower urinary tract symptoms
MCC Maximum cystometric capacity
MS Multiple sclerosis
MUCP Maximum urethral closure pressure
MUP Maximum urethral pressure
MUS Mid-urethral sling
NDO Neurogenic detrusor overactivity
NDV Normal desire to void
NICE National Institute for Health and Clinical
Excellence
NLUTD-S Neurogenic lower urinary tract dysfunction
syndrome
NPV Negative predictive value
OAB-S Overactive bladder syndrome
PAG Periaqueductal grey
PCR Polymerase chain reaction
PBS/IC Pain bladder syndrome/interstitial cystitis
PFC Pre-frontal cortex
PFM Pelvic floor muscles
PFMF Pelvic floor muscles function
PFS Pressure-flow study
PHC Parahippocampal complex
PMC Pontine micturition center
POP Pelvic organ prolapse
POP-S Pelvic organ prolapse syndrome
PPV Positive predictive value
PVR Post-void residual
QoL Quality of life
SCI Spinal cord injury
SNM Sacral neuromodulation
SD Standard deviation
SDV Strong desire to void
SMA Supplementary motor area
SUI-S Stress urinary incontinence syndrome
UAB Underactive bladder
Abbreviations xix
UDS Urodynamic studies

UPP Urethral pressure profile/profilometry
USI Urodynamic stress incontinence
UTI Urinary tract infection
UUI Urgency urinary incontinence
VLPP Valsalva leak point pressure
VUD Videourodynamic
VUR Vesico-ureteric reflux
VD-S Voiding dysfunction syndrome
V V Voided volume
WMH White matter hyperintensities
Chapter 1
Physiology of Micturition
in Female
1.1 Background
The two major functions of lower urinary tract are the stor-
age and emptying of urine. Since voiding takes between 1 and
2 min and is performed four or five times a day, the bladder
is in the storage mode for most of the time of daily life
(Fig. 1.1). Going to the toilet is an essential everyday event
normally done without paying excessive attention to the con-
text. However, in order to accomplish this apparently simple
sequence of events, a whole range of complex interacting
systems are involved including the generation of information
from the lower urinary tract and its following processing in
the spinal cord, brain stem, and forebrain.
Furthermore, whereas many other visceral functions (i.e.,
cardiovascular system, GI tract) are regulated involuntarily, mic-
turition requires the integration of autonomic and somatic effer-
ent mechanisms to coordinate the activity of visceral organs (the
bladder and urethra) with that of urethral striated muscles.
1.1.1 C
entral Neural Mechanisms Controlling
Storage and Voiding
An early attempt to provide a simple picture of neural con-
trol of micturition was made by Bradley who suggested that
control was exerted by four neural circuits (“loops”). Loop I,
© Springer International Publishing AG, part of Springer 1

Nature 2018
G. Vignoli, Urodynamics for Urogynecologists,
https://doi.org/10.1007/978-3-319-74005-8_1
2 Chapter 1. Physiology of Micturition in Female
permission to void
bladder volume
>90% SD
Filling Voiding
60% FD
40% FS
time
Figure 1.1 Micturition cycle: FS first sensation at 40% of bladder

capacity, FD first desire at 60% of bladder capacity, SD strong desire
at 90% of bladder capacity. Bladder sensation has a pivotal role in
micturition cycle since the overall motivation of micturition is to
attain relief from the increasingly intense sensation of bladder filling
by emptying the bladder
consisting of connections between the brain stem and the

frontal cortex, initiates and inhibits switching between filling
and voiding states. Loop II, running spinally between the
brain stem and sacral cord, is the main pathway of micturition
reflex coordinating detrusor contraction and sphincter relax-
ation. Loops III and IV, connecting the sacral cord and blad-
der, are important in spinal reflexes that guarantee urethral
tone at rest and proper coordination between the detrusor
and sphincter during voiding. Loop V, from the motor cortex
and Onuf’s nucleus, is concerned with the voluntary control
of the sphincters and pelvic floor muscles (Fig. 1.2).
Over the past 15 years, functional brain imaging has
emerged as the most powerful technique for studying
human brain function, in particular for understanding the
relationship between activity in certain brain areas and
1.1 Background 3
Figure 1.2 Neural control of micturition—Bradley loops: Loop I is

a bidirectional pathway between the brain stem and cerebral cortex
that includes also connections to subcortical nuclei (e.g., thalamus,
basal ganglia, and amygdaloid nucleus). Loop II provides the brain
stem control of the detrusor muscle. It is also a bidirectional path-
way through the reticulospinal tract, including ascending impulses
from the detrusor muscle to the brain stem micturition centers and
descending impulses from the brain stem micturition centers to the
sacral spinal cord. Loops III and IV provide for segmental control of
pudendal pathways. Loop V provides for supraspinal control of stri-
ated muscles of periurethral area
specific functions. The micturition cycle is under control of

specific neural networks which behave as a switch between
storage of urine and voiding with the brain functioning as
the master control of the entire process. Basically, voiding
reflex can be broken into two parts: the long-loop, spinobul-
bospinal voiding and the forebrain circuits that modulate
this reflex. The PAG (periaqueductal gray) acts as a pivotal
region that distributes incoming signals from the bladder to
many regions of the forebrain where they generate sensations
such as the desire to void and receive back signals from

forebrain structures to decide whether or not the voiding
reflex should be triggered. A provisional model of brain-
bladder control has been developed in the last decade
including three neural “circuits” which by handling bladder
sensations can promote or delay the voiding reflex acting on
the midbrain (Fig. 1.3).
• Circuit 1 involves the PFC (prefrontal cortex), the PAG

(periaqueductal gray), and PMC (pontine micturition cen-
ter) and is responsible for voluntary initiation of
micturition.
• Circuit 2 involves the insula, the ACC (anterior cingulate
cortex), and the adjacent SMA (supplementary motor
area) and is mostly involved in handling of bladder
sensation.
• Circuit 3 involves subcortical regions such as the parahip-
pocampal complex which might send safety or unsafety
signals of voiding to pontine micturition center.
Storage phase occurs largely unconsciously and presum-

ably relies on a subcortical network which maintains inhibi-
tion of the voiding reflex during bladder filling and monitors
unusual or unexpected bladder events.
As the bladder fills, afferent signals increase in strength
until they exceed a threshold set in the brain stem, specifically
the midbrain periaqueductal gray (PAG).
PAG notifies the forebrain about bladder fullness through
the activation of insula and ACC, and people perceive this
signal as a strong desire to void or urgency (circuit 2).
Activation of ACC is strictly related to activation of SMA
that is known to tighten the pelvic floor muscles and the ure-
thral sphincter, and this appears to be the mechanism to
withholding urine. These informations are also passed to the
prefrontal cortex (PFC) where the decision to void or not is
made. If the decision is not to void, the PFC sends an inhibi-
tory signal to the periaqueductal gray (PAG) and pontine
micturition center (PMC) to inhibit the bladder to contract-
ing until a bathroom is found. The ability of the brain to con-
trol the PMC is part of the social training that children
1.1 Background 5
Figure 1.3 Neural control of micturition—Simple working model:

three neural circuitry control lower urinary tract acting as a switch
between storage of urine and voiding. As we know, a normal adult can
postpone or advance the moment of micturition ensuring that urination
occurs only if it is consciously desired and socially appropriate. During
storage phase, afferent signals from the bladder are conveyed with
increasing strength to the brain stem, specifically to the midbrain peri-
aqueductal gray (PAG) where they remain silent until they exceed a
threshold set. PAG afferents are mapped in the insula, forming the basis
of sensation and are conveyed to the anterior cingulate cortex (ACC)
which provides to inform the prefrontal cortex about the need of void-
ing (circuit 2). In addition, ACC is closely related to SMA. Activation of
SMA is known to tighten the pelvic floor and urethral sphincter, and this
appears to be a backup continence mechanism, used in critical situations
to prevent incontinence. Circuit 3, including the parahippocampal
region, tend to suppress voiding at PAG and might be part of a subcorti-
cal circuit which may send “safe” or “unsafe” signal to the pontine mic-
turition center. Voluntary voiding is initiated by the medial prefrontal
cortex which activates PAG and in turn PMC (circuit 1) .When activated
the PMC passes on a signal to the sacral spinal cord where inhibitory
interneurons in Onuf’s nucleus relax the urethral sphincter at the same
time as the bladder contracts ensuring a coordinated synergic voiding.
Abbreviations: PMC pontine micturition center, PAG periaqueductal
gray, ACC anterior cingulate cortex, SMA supplementary motor area,
PFC prefrontal cortex, PHC parahippocampal complex
experience during growth and development. In infants, the

brain is not mature enough to command the bladder, so the
control of micturition comes from the signals sent from the
spinal cord. When urine fills the infant bladder, an excitatory
signal is sent to the sacral cord. When this signal is received
by the sacral cord, the spinal reflex center automatically trig-
gers the detrusor to contract. The result is an involuntary
detrusor contraction with coordinated voiding.
In adults, when the decision to void is made, the PFC
relaxes its inhibition of the PAG which, in turn, relaxes the
PMC (circuit 1). The PMC sends descending motor output to
the sacral spinal cord that ultimately relaxes the urethral
sphincter and contracts the detrusor, so that voiding occurs.
Voiding is continued to completion by continuing afferent
input, probably to the PAG.
Relative to the other circuits, the role of circuit 3 is less
known and still speculative. The parahippocampal complex is
known to be involved in the retrieval of episodic memories
and recognition of scenes and social context. Since it behaves
like PFC, one might argue that it could send signals of
“safety” or “unsafety” of micturition event to the PMC.
OAB, urgency incontinence, as well as chronic retention of
urine may occur as a consequence of known cerebral lesions
but often are idiopathic implying that there is a subtle lesion
that may involve damage to cerebral connecting pathways or
simply dysfunction of cortical and/or subcortical circuits
capable of compromising the stability of voiding reflex.
The presence in some brain regions of white matter hyper-
intensities (WMH), which are structural abnormalities that
appear with aging and may be linked to small vessel disease,
is associated with LUT disorders (Fig. 1.4). The extent of
white matter changes relates to functional brain activity dur-
ing urgency. Activations in the posterior cortex and cerebel-
lum are increased in those subjects with more intense white
matter changes, while activity in the ACC and SMA is
decreased. Deactivation in PFC is less pronounced, and the
activity in this region increases with the increase of
WMH. Such findings suggest that structural changes in white
1.1 Background 7
Figure 1.4 White matter hyperintensities in elderly women.

Hyperintensities appear as “bright signals” (bright areas) on an
MRI image
matter affect the regional brain activity involved in conti-

nence control, possibly making efforts to regulate less effec-
tively. Structural damage of individual white matter pathways
connecting these functionally important regions is most likely
a mechanism of white matter effects on continence control.
Even emotions experienced in higher brain centers may
exert downstream effects on the PMC, which is why some
people can experience incontinence with excitement or fear.
In summary, regional brain activity differs in subjects with
different functional and phenotypic characteristics. Such
regions of difference may serve as potential markers for func-
tional characterization of continence impairment. Imaging
methods, when coupled with urodynamic studies, may give an

insight on neural correlates in clinical syndromes of impaired
continence control (the Griffiths “new urodynamics”).
1.1.2 P
eripheral Neural Mechanisms Controlling
Storage and Voiding
The control of the bladder provides a good example of the
interplay between the voluntary somatic nervous system and
the sympathetic and parasympathetic divisions of the auto-
nomic nervous system, which operate involuntarily.
As shown in Fig. 1.5, the sympathetic innervation arises in
the thoracolumbar outflow of the spinal cord (T11–L2),
whereas the parasympathetic and somatic innervation origi-
nates in the sacral segments of the spinal cord (S2–S4).
Afferent axons from the lower urinary tract also travel in
these nerves.
Parasympathetic nervous fibers—via the pelvic nerve—
release both cholinergic (ACh) and non-adrenergic, non-
cholinergic transmitters. Cholinergic transmission is the major
excitatory mechanism in the human bladder, resulting in
detrusor contraction and consequent urinary flow. The effect
is mediated principally by the M3 muscarinic receptor,
although bladder smooth muscle also expresses M2
receptors.
Non-cholinergic excitatory transmission is mediated by
ATP on P2X purinergic receptors in the detrusor muscle,
whereas inhibitory input to the urethral smooth muscle is
mediated by nitric oxide (NO).
Sympathetic nervous fibers—via the hypogastric nerve—
release noradrenaline, which activates β3-adrenergic
inhibitory receptors in the detrusor muscle to relax the blad-
der and α-adrenergic excitatory receptors in the urethra and
the bladder neck.
Somatic cholinergic motor nerves supply the striated mus-
cles of the external urethral sphincter. They arise in S2–S4
motor neurons in Onuf’s nucleus and reach the periphery
through the pudendal nerves. A medially placed motor
1.1 Background 9
bladder afferent neurons to CNS

A-delta & C fibers
detrusor muscle
M3(+) Ach
beta3 receptors(-) PARASYMPATHETIC INPUT
P2X(+) ATP (S2-S4)
Pelvic nerves
. .
NO2(-)
bladder neck
alpha receptors(+) NA SYMPATHETIC INPUT (T11-L2)
Hypogastric nerve
ACH SOMATIC INPUT (S2-S4)

Pudendal nerve
nicotinic receptors(+)
external urethral sphincter
Figure 1.5 Peripheral bladder innervation: Parasympathetic pelvic

nerve innervates the detrusor muscle. The parasympathetic neu-
rotransmitter acetylcholine induces micturition by activating M3
receptors. In addition parasympathetic fibers release NO that
relaxes actively the urethra. Sympathetic hypogastric nerve ensures
continence. The sympathetic neurotransmitter norepinephrine
inhibits the detrusor muscle by beta-receptors and increases the
urethral tonus by alpha-receptors. Somatic pudendal nerve inner-
vates the external urethral sphincter and pelvic floor muscles by
releasing ACh at the motor plate. Sensations of the bladder are
conveyed to CNS through A-delta fibers and C-fibers whose cell
bodies are located in the dorsal root ganglia (DRG) at the level of
S2–S4 and T11–L2 spinal segments
nucleus at the same spinal level supplies axons that innervate

the pelvic floor musculature (Fig. 1.6).
Activation of the pudendal nerve causes contraction of the
external sphincter, which occurs with activities such as Kegel
exercises which also target the pelvic floor muscles. Some
reflex activity may also occur through the pudendal nerve,
such as the sphincter contractions that occur during sneezing,
coughing, and laughing—the so-called guarding reflex.
Sensations of bladder fullness are conveyed to the spinal
cord by the pelvic and hypogastric nerves, whereas sensory
Afferent fibers
Substantia gelatinosa
Autonomic
intermediolateral
nuclei:
- Sympathetic (T11-L2)
- Parasympathetic (S2-S4)
Somatic motoneurons (S2-S4):
- Onuf’s mucleus, right
- Pelvic floor muscles, left
Figure 1.6 Organization of bladder motor nuclei (autonomic and

somatic) in lateral and ventral horns of the spinal gray matter
input from the bladder neck and the urethra is carried in the
pudendal and hypogastric nerves. The afferent components of
these nerves consist of myelinated (Aδ) and unmyelinated
(C) axons. The Aδ-fibers respond to passive distension and
active contraction and thus convey information about blad-
der filling. The C-fibers are insensitive to bladder filling
under physiological conditions (they are therefore termed
“silent” C-fibers) and respond primarily to noxious stimuli
such as chemical irritation or cooling.
1.1.3 P
ressure Variations During Micturition
Cycle
Bladder is a low-pressure reservoir. During filling phase,
sensory afferent signals are carried via the pelvic and hypo-
gastric nerves to the spinal cord, where they are relayed to
the pontine micturition center and, in turn, to the periaque-
ductal gray via the lateral spinothalamic tracts and dorsal
columns. Sympathetic tonus via the hypogastric nerve main-
tains smooth muscle-based activity of the urethral sphincter
and aids in detrusor relaxation, which thus promotes urine
storage keeping bladder pressure low with no phasic con-
tractions and high compliance.
1.1 Background 11
As afferent signaling increases in intensity with bladder

filling, a threshold of consciousness is reached, at which point
a socially appropriate opportunity to void is sought. During
urine storage, there are a number of physiologic mechanisms
to maintain continence. The external sphincter progressively
contracts with bladder filling and will also contract during
any sudden increase of abdominal pressure (i.e., during
cough)—the so-called guarding reflex. During straining or
Valsalva maneuver, there is equal transmission of pressure
from the abdomen to the urethra (Fig. 1.7).
With permission to void, external sphincter relaxation is
the first step in micturition event and precedes the detrusor
contraction. Pontine signaling to the sacral cord results in
relaxation of the striated muscle of the pelvic floor and
parasympathetic cholinergic activation of the detrusor and
which allows the voiding phase which can be defined a pres-
surized flow.
However, men and women have unique micturitional
characteristics. What is normal voiding pressure and flow
rate for men is not necessarily normal for women, since the
voiding dynamics of women are different from those of men.
COUGH VALSALVA (Straining)
Pura Pura
Pves Pves
Pabd Pabd
Pdet Pdet
EMG EMG
Figure 1.7 Pressure events during cough and straining (Valsalva

maneuver). Immediately prior to cough there is a reflex contraction
of the sphincter causing a rise in urethral pressure (Pura), while dur-
ing straining or Valsalva maneuver, there is equal transmission of
pressure from the abdomen to the urethra
MALE FEMALE
Pves Pves
Pabd Pabd
Pdet Pdet
Flow Flow
Figure 1.8 Voiding dynamic in men and women: unlike men, women
may be able to void by prevalent relaxation of the pelvic floor muscles
with lower contraction pressure or acontraction
In men a significant rise of detrusor pressure is recorded

during voiding because the detrusor has to exert a force
strong enough to move the urine through a relatively high-
resistance conduit due to the presence of prostatic
urethra.
Conversely, in normal women there is a very little increase
in detrusor pressure during voiding, even when bladder con-
tractility is normal, because the flow of urine encounters
minimal resistance against female urethra (Fig. 1.8).
In addition many women void by pelvic floor relaxation
rather than by detrusor contraction.
Valsalva-induced voiding across a relaxed pelvic floor is
the third common voiding pattern seen in women (see Box
1.1) (Fig. 1.9):
During voluntary interruption of voiding or attempting to
prevent voiding during an involuntary detrusor contraction,
the external sphincter is contracted, stopping the stream, and
Box 1.1: Micturition Patterns in Women

• Pelvic floor relaxation (60%)
• Detrusor contraction (20%)
• Abdominal straining (20%)
1.1 Background 13
MICTURITION PATTERNS IN WOMEN
Pves Pves Pves
Pabd Pabd Pabd
Pdet Pdet Pdet
EMG EMG EMG
Flow Flow Flow
Pelvic relaxation Detrusor contraction Abdominal straining
Figure 1.9 Micturition patterns in women
Flow
Pura
Pves
Pabd
Pdet
EMG
voluntary contraction
Figure 1.10 Voluntary interruption of voiding
then, through a reflex mechanism, the detrusor contraction, if

present, decreases (Fig. 1.10).
Due to anatomical and behavior differences in micturition
among men and women, one may expect regional brain activ-
ity to differ during bladder filling and voiding according to
gender. To date, however, no significant differences in brain
activation patterns between females and males have been
reported.
In addition, the different voiding mechanisms do not lead
to significant differences in parameters of the PFS and free
uroflowmetry except detrusor contractility.
However, these voiding peculiarities are very important,

since female patients unable to generate adequate detrusor
pressure may be at higher risk for prolonged postoperative
retention after anti-incontinence surgery and are less likely to
be cured by intervention.
Suggested Reading
Neural Control of Micturition

Arya N, Weissbart S, Xu S, Rao H. Brain activation in response to
bladder filling in healthy adults: an activation likelihood estima-
tion meta-analysis of neuroimaging studies. Neurourol Urodyn.
2017;36:960–5.
Arya N, Weissbarth S. Central control of micturition in women:
brain-bladder pathways in continence and urgency urinary incon-
tinence. Clin Anat. 2017;30:373–84.
Smith PP, Kuchel GA, Griffiths D. Functional brain imaging and the
neural basis of voiding dysfunction in older adults. Clin Geriatr
Med. 2015;31:549–65.
deGroat WC, Griffiths D, Yoshimura N. Neural control of the lower
urinary tract. Compr Physiol. 2015;5:327–96.
DeGroat WC, Yoshimura N. Anatomy and physiology of lower uri-
nary tract. Handb Clin Neurol. 2015;130:61–108.
Bortolini MA, Bilhar AP, Castro RA. Neural control of lower urinary
tract and targets for pharmacological therapy. Int Urogynecol J.
2014;25:1453–62.
DeGroat WC, Wickens C. Organization of the neural switching
circuitry. Underlying reflex micturition. Acta Physiol (Oxford).
2013;207:66–84.
Tadic SD, Tannenbaum C, Resnick NM, Griffiths D. Brain responses
to bladder filling in older women without urgency incontinence.
Neurourol Urodyn. 2013;32:435–40.
Fowler CJ, Griffiths D, deGroat WC. The neural control of micturi-
tion. Nat Rev Neurosci. 2008;9:453–66.
Fowler CJ. Integrated control of lower urinary tract—clinical per-
spective. Br J Pharmacol. 2006;147:S14–24.
DeGroat WC. Integrative control of the lower urinary tract: preclini-
cal perspective. Br J Pharmacol. 2006;147(52):S25–40.
Suggested Reading 15
Griffiths D. Cerebral control of bladder function. Curr Urol Rep.

2004;5:348–52.
Bannowsky A, Juenemann KP. Innervation and function of the
female urinary bladder and urethra. EAU Updat Ser. 2003;1:120–7.
Bradley WE. Physiology of the urinary bladder. In: Walsh PC, et al.,
editors. Campbell’s urology. Philadelphia: WB Saunders; 1986.
Voiding Dynamic in Women

Kira S, Mitsui T, Kobayashi H, Haneda Y, Sawada N, Takeda
M. Detrusor pressures in urodynamic studies during voiding in
women. Int Urogynecol J. 2017;28:783–7.
Onyishi SE, Twiss CO. Pressure flow studies in men and women.
Urol Clin North Am. 2014;41:453–67.
Bauer RM, Huebner W. Gender differences in bladder control: from
babies to elderly. World J Urol. 2013;31(5):1081.
Digesu GA, Hutchings A, Salvatore S, Selvaggi L, Khullar
V. Reproducibility and reliability of pressure flow parameters in
women. BJOG. 2003;110:774–6.
Lemack GE, Baseman AG, Zimmern PE. Voiding dynamics in
women: a comparison of pressure-flow studies between asymp-
tomatic and incontinent women. Urology. 2002;59:42–6.
Bathia NN. Dynamics of voiding in women. Curr Opin Obstet
Gynecol. 2000;12:383–6.
Chapter 2
Pretest Assessment
2.1 Background
Recently the ICS has updated the International Continence
Society Good Urodynamic Practice 2002 (GUP2002) with
the aim to include new evidence and information on urody-
namic practice and urodynamic quality control inclusive of
standard on urodynamic equipment.
It is well-known that urodynamics testing incorporates a
hierarchy of different evaluations, the most comprehensive of
these being the pressure flow study, to which the term “uro-
dynamics” is often applied.
In practice, there are two principal methods of urodynamic
investigation:
• Noninvasive urodynamics, done without the insertion of a
catheter (uroflowmetry, PVR)
• Invasive or conventional urodynamics that involves inser-
tion of one or more catheters into the bladder or other
body cavities, i.e., rectum or vagina, (cystometry, pressure-
flow study)
In addition, there are supplementary urodynamics test
(EMG, video, urethral pressure measurements, and ambula-
tory urodynamics) to be used in specific clinical situations.
Not all patients need invasive urodynamics. The diagnostic
process for patients with LUTD should be carefully

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_2
18 Chapter 2. Pretest Assessment
implemented and personalized to rationally select patients

for invasive UDS.
Standard urodynamic protocol should include:
• Pretest assessment
• Urodynamics testing
–– Noninvasive
–– Invasive
• Posttest patient care (invasive urodynamics only)
2.2 Pretest Assessment

According to ICS classical definition, each lower urinary tract
dysfunction includes four aspects:
• Clinical condition (i.e., stress urinary incontinence, voiding
dysfunction, etc.)
• Symptom (assessed by detailed history)
• Sign (verified by physical examination)
• Urodynamic observation
Note: Following the recent changing of paradigms of diag-
nosis and management of lower urinary tract dysfunctions,
the ICI-RS has suggested that symptoms and signs that
patients present with can be more precisely delineated as a
syndrome. A syndrome is a complex of medical signs and
symptoms that are correlated with each other. In some cases,
i.e., inherited disorders like Down syndrome, signs and symp-
toms are so specific for the disease that the word syndrome
ends up being used interchangeably for the name of the dis-
ease. In other instances, like in lower urinary tract dysfunc-
tions, a syndrome is not specific to only one disease. Female
incontinence or overactive bladder is not a disease but simply
a set of signs and symptoms, i.e., a syndrome.
Each patient undergoing UDS testing, both invasive and
noninvasive, should have preliminarily:
• A clinical history including a valid symptom and bother
score(s) and medication list
2.2 Pretest Assessment 19
• Relevant physical examination

• Urinalysis
This basic assessment should be implemented by a:
• Voiding diary and, optionally, a pad test
2.2.1 Clinical History
The purpose of history taking is to determine the type of

urinary symptom and how it is bothersome to the patient.
Several validated questionnaires can be used to evaluate
bother and severity of symptoms (see Box 2.1).
Obstetric history (number of pregnancies, length of labor,
size of the baby, episiotomies and tears, use of forceps during
delivery) and gynecological history (menstrual cycle, meno-
pausal status, previous surgery) should also be taken.
2.2.2 Relevant Physical Examination
An abdominal examination should always be performed

before moving onto vaginal examination. The lower abdomen
should be palpated or percussed to assess a distended bladder
Box 2.1: Examples of Validated Urinary Incontinence

Questionnaires
• Urogenital Distress Inventory (UDI)
• Incontinence Impact Questionnaire (IIQ)
• Questionnaire for Urinary Incontinence Diagnosis
(QUID)
• Incontinence Quality of Life Questionnaire (I-QoL)
• Incontinence Severity Index (ISI)
• International Consultation on Incontinence
Questionnaire (ICI-Q)
suggestive for a urinary retention. Then, bimanual vaginal

examination should be done to evaluate the presence of uter-
ine, adnexal, or other pelvic masses.
2.2.2.1 Structured Vaginal Examination
The structured vaginal examination should include evalua-

tion for prolapse, vaginal wall atrophy, pelvic muscle quality
and the ability to voluntarily contract them, and urinary leak-
age with strain or cough. The examination is usually done in
lithotomy position but may be repeated with the patient
standing when it is not representative of the reported symp-
toms. The vaginal mucosa is first inspected for signs of atro-
phic vaginitis, indicating estrogen deficiency. The anterior
vaginal compartment is examined next by applying a slight
pressure on the posterior vaginal wall with the blade of small
vaginal speculum. The positions of the urethra, bladder neck,
and bladder are observed at rest and with straining to evalu-
ate the support of these structures. With coughing and strain-
ing, the urethra should be observed for urine leakage
(positive stress test) and whether that leakage occurs with
urethral hypermobility. A Q-tip test may be performed to
assess the degree of urethral hypermobility. The central vagi-
nal compartment is examined next. This is best accomplished
by gently retracting both the anterior and posterior vaginal
walls. The uterus and cervix are evaluated at rest and during
straining to determine prolapse. If the patient had a hysterec-
tomy, the vaginal cuff should be assessed for an enterocele.
Finally the posterior vaginal compartment is examined by
retracting the anterior vaginal wall with the speculum blade.
Sometimes it may be difficult to distinguish between a high
rectocele and an enterocele. With simultaneous vaginal and
rectal examination, one may palpate the enterocele sliding
above the anterior rectal wall. For detailed description of
POPQ assessment, see Chap. 8.
Physical examination should also include routinely:
• Focused neuro-urological assessment
• Pelvic floor muscle assessment
Figure 2.1 Focused L1

neuro-urological
examination: perineal
dermatomes L1 L1
S2 S2
S3
S4
S5
L2 L2
2.2.2.2 Focused Neuro-urological Assessment
Observation of the patient’s gait, assessment of elementary

lower limb reflexes, and evaluation of sensation in different
perineal dermatomes (S2–S5) (Fig. 2.1) and volitional control
of the anal sphincter are important in the identification of
neuro-urological abnormalities. In particular, special atten-
tion should be paid to “saddle sensation,” tone, and volitional
control of the anal sphincter and some reflexes that are spe-
cific for the sacral function including:
• Anal reflex: pricking the perianal skin, the anal sphincter
contracts reflexly.
• Bulbocavernosus reflex: pricking the skin along the labia
leads to a contraction of the anal sphincter (Fig. 2.2).
In patients found to have a neuro-urological abnormality,
a complete neurological evaluation should be planned.
2.2.2.3 Pelvic Floor Muscle Assessment
Pelvic floor muscles play an important role in continence and

support of the pelvic organs. Assessment of pelvic floor mus-
cle strength can be useful in deciding nonsurgical treatment.
Figure 2.2 Focused

neuro-urological
examination:
bulbocavernosus reflex
prickling
contraction of the anal sphincter
PFM evaluation can easily be performed by instructing the

patient to contract their PFM and vaginally palpating the
effect. Several components of PFM contractility can be
assessed including power (strength); endurance, i.e., the length
of time that a maximal voluntary contraction can be sustained
(usually 10 s); the number of maximal voluntary contractions
necessary to overload the muscle (usually 10); and the number
of fast contractions that the subject is able to do after a short
rest and the presence of co-contractions.
Power is mostly measured using Oxford grading scale (see
Table 2.1).
Overall, it is difficult to evaluate and compare PFM func-
tioning, because there are many different methods and scales.
Over the past 20 years, three pelvic floor muscle assessments
have been used most commonly: the Laycock PERFECT
scale with a six-point scale to score muscle strength and
endurance, the number of repetitions, and fast contractions;
the Brink score to assess muscle strength, urethral lift, and
muscle endurance, all with four-point scales; and the Devreese
assessment scale, with more PFMF items, including co-
contraction of the transverse abdominal muscles. In 2005 the
ICS standardized the terminology relative to pelvic floor
muscle functioning. In particular they redefined the muscle
strength as absent, weak, normal, or strong.
Table 2.1 Oxford grading Grading Muscle response

scale of muscle 0 Nil
contraction
1 Weak
2 Flicker
3 Moderate
4 Good
5 Strong
In current clinical practice, the PFM are generally only

tested for strength and endurance, but it is not yet clear
whether these two functions cover total PFMF as proposed
by the ICS terminology.
Note: When possible the above PFMF should be docu-
mented for each side of pelvic floor in order to differentiate
unilateral defects and asymmetry.
2.2.3 Urinalysis
Before UDS testing it is considered standard to perform a
urinalysis by either using a dipstick test or examining the
sediment of urine. If a dipstick test is chosen, it is recom-
mended that the strip that includes fields for hematuria, glu-
cose, leukocyte esterase, and nitrite tests should be used.
Dipstick is not as accurate as urine culture, being specific for
infection but not sensitive.
Note 1: Historically urine was considered to be sterile, and
only recently, utilizing new molecular technique like PCR
and 16S ribosomal RNA sequencing, it has been appreciated
that the bladder contains its own microbiome (saprophytic
bacterial communities). Its role in different urological entities
is still under investigation.
Note 2: The clinical relevance of asymptomatic bacteriuria
(without pyuria) and pyuria (without bacteriuria) in the
elderly is controversial.
2.2.4 Voiding Diary
Voiding diary is a specific urodynamic investigation recording

fluid intake and urine output per 24-h period. Voiding diary
is an important and objective tool that can be used to assess
LUTD in patients seeking the diagnosis and treatment of
their bladder or voiding conditions.
The recording of micturition events can be done in three
main forms:
• Micturition time chart that records only the timing of voids,
day and night, for at least 24 h.
• Frequency volume chart (FVC) that records the time of
each micturition and the voided volume for at least 24 h.
• Bladder diary is the most complete form of recording and
includes fluid intake, incontinence episodes, pad usage, the
degree of incontinence as well as a record of episodes of
urgency and sensation, and activities performed during or
immediately preceding the involuntary loss of urine. (Fig. 2.3)
Bladder diary is the most suitable for a comprehensive
evaluation of urinary symptoms. However, documentation
24 Hour Bladder Diary Date 12/03/14

Drinks Urine
Time Amount Amount Bladder Pads
Type
(ml) (ml) Sensation
6am WOKE 400 2
7 am 100 Water
8 am 150 2
9 am
10 am Cup Tea LEAK 3
11 am
Midday
Figure 2.3 Sample of ICS paper voiding diary

Figure 2.4 Screenshot of
digital voiding diary, cour-
tesy of Synappz BV
of the frequency with each voided volume for at least 24 h

can already be extremely helpful in the initial assessment of
the patient. To facilitate patient compliance, several apps for
the iPhone and iPod are available on the market to create a
quick and reliable digital voiding diary (Fig. 2.4).
Note: Two to three days of recording generally provide
more useful clinical data.
The important parameters documented by a bladder diary
include:
• Urinary frequency during the day and night
• For practical purposes, normal voiding frequency varies
between five and eight times per 24 h in women and
increases with age (8.2 in the sixth decade), while voiding
once a night is normal for women over 75.
Note: The ICS definition of daytime frequency is when the

patient considers that she is voiding too often. Therefore, no
absolute number can be applied to define a cutoff value for
voiding frequency.
• Functional bladder capacity, i.e., the largest volume
recorded
• Typical voided volume, i.e., the most frequently observed
bladder volume which may reflect the usual voided vol-
ume or the most frequent bladder sensation with respect
to voiding desire
• Urgency or urgency incontinence episodes, i.e., discomfort
voiding sensation felt by the patient which usually cannot
be deferred
• The volume of water drunk
• Daily and nocturnal urine output (consisting of all voids
during sleep and the early morning void)
Polyuria is defined as a production of more than 2.8 L of
urine in 24 h. Polyuria can be due to an excessive fluid intake
(polydipsia) or owing to diabetes mellitus and diabetes
insipidus.
Nocturnal polyuria is defined by a nocturnal voided volume
greater than 20–30%, depending on age, of total daily urine out-
put. Nocturnal polyuria is a heterogeneous condition in which
water diuresis, solute diuresis, or a combination of both is the
underlying cause. Water diuresis is represented by low osmolar-
ity at night and is due to a low ADH excretion, while nocturnal
sodium diuresis is mostly due to cardiac decompensation.
Accordingly, treatment will be with vasopressin at night in the
first case and with diuretics during the day in the second case.
2.2.5 Pad Test
Pad test (Fig. 2.5) is complementary to voiding diary. The test

assesses the degree of incontinence in a semi-objective man-
ner. Pad weight gain in non-menstruating women can be
attributed mainly to urine and in small part to perspiration
and vaginal discharges. There are two types of pad test:
Figure 2.5 Pad test apparatus
• The short-term (1 h) pad test

• The long-term (24 h) pad test
Incontinence is diagnosed if pad weight is more than 1 g/h
on the short-term pad test and more than 8 g/24 h on the
long-term pad test. However, there are conflicting data con-
cerning the correlation between severity of incontinence and
increase in pad weight.
Suggested Reading
Overviews
Rosier PFWM, Schaefer W, Lose G, Goldman HB, Guralnick M,
Eustice S, et al. International continence society good urodynamic
practices and terms 2016: urodynamics, uroflowmetry, cystometry,
and pressure-flow study. Neurourol Urodyn. 2017;36:1243–60.
Medina C, Costantini E, Petri E, Mourad S, Singla A, Rodríguez-

Colorado S, et al. Evaluation and surgery for stress urinary
incontinence: a FIGO working group report. Neurourol Urodyn.
2017;36:518–28.
Rosier P, Giarenis I, Valentini F, Wein A, Cardozo L. Do patients
with symptoms and signs of lower urinary tract dysfunction need
a urodynamic diagnosis? Neurourol Urodyn. 2014;33:581–6.
Winters JC, Dmochowski RR, Goldman HB, Herndon CD, Kobashi
KC, Kraus SR, et al. Urodynamic studies in adults: AUA/SUFU
guideline. J Urol. 2012;188:2464–72.
Lenherr SM, Clemens JQ. Urodynamics with a focus on appropriate
indications. Urol Clin North Am. 2013;40:545–57.
Haylen BT, de Ridder D, Freeman RM, Swift SE, Berghmans B, Lee
J, et al. An International Urogynecological Association (IUGA)/
International Continence Society (ICS) joint report on the ter-
minology for female pelvic floor dysfunction. Neurourol Urodyn.
2010;29:4–20.
Questionnaires
Shumaker SA, Wyman JF, Uebersax JS, McClish D, Fantl JA. Health-
related quality of life measures for women with urinary incon-
tinence: the Incontinence Impact Questionnaire and the
Urogenital Distress Inventory. Continence Program in Women
(CPW) Research Group. Qual Life Res. 1994;3:291–306.
Uebersax JS, Wyman JF, Shumaker SA, McClish DK, Fantl JA. Short
forms to assess life quality and symptom distress for urinary
incontinence in women: the Incontinence Impact Questionnaire
and the Urogenital Distress Inventory. Continence Program for
Women Research Group. Neurourol Urodyn. 1995;14:131–9.
Abrams P, Avery K, Gardener N, Donovan J, ICIQ Advisory Board.
The international consultation on incontinence modular ques-
tionnaire: www.iciq.net. J Urol. 2006;175:1063–6.
Coyne KS, Thompson CL, Lai JS, Sexton CC. An overactive bladder
symptom and health-related quality of life short-form: validation
of the OAB-q SF. Neurourol Urodyn. 2015;34:255–63.
Bradley CS, Rahn DD, Nygaard IE, Barber MD, Nager CW, Kenton
KS, et al. The questionnaire for urinary incontinence diagnosis
(QUID): validity and responsiveness to change in women under-
going non-surgical therapies for treatment of stress predominant

urinary incontinence. Neurourol Urodyn. 2010;29:727–34.
Brown JS, Grady D, Ouslander JG, Herzog AR, Varner RE, Posner
SF. Prevalence of urinary incontinence and associated risk fac-
tors in postmenopausal women. Heart & Estrogen/Progestin
Replacement Study (HERS) Research Group. Obstet Gynecol.
1999;94:66–70.
Sandvik H, Seim A, Vanvik A, Hunskaar S. A severity index for
epidemiological surveys of female urinary incontinence: com-
parison with 48-hour pad-weighing tests. Neurourol Urodyn.
2000;19:137–45.
Avery K, Donovan J, Peters TJ, Shaw C, Gotoh M, Abrams P. ICIQ: a
brief and robust measure for evaluating the symptoms and impact
of urinary incontinence. Neurourol Urodyn. 2004;23:322–30.
Physical Examination
Panicker JN, Fowler CJ, Kessler TM. Lower urinary tract dysfunction
in the neurological patient: clinical assessment and management.
Lancet Neurol. 2015;14:720–32.
Al Afraa T, Mahfouz W, Campeau L, Corcos J. Normal lower urinary
tract assessment in women: I. Uroflowmetry and post-void resid-
ual, pad tests, and bladder diaries. Int Urogynecol J. 2012;23:681–5.
Newman D, Laycock J. Clinical evaluation of pelvic floor muscles. In:
Baessler K, Burgio K, Norton P, Schüssler B, Moore K, Stanton S,
editors. Pelvic floor re-education. Principles and practice. London:
Springer; 2008. p. 91–104.
Bø K, Sherburn M. Evaluation of female pelvic floor muscle func-
tion and strength. Phys Ther. 2005;85:269–82.
Messelink B, Benson T, Berghmans B, Bø K, Corcos J, Fowler
C. Standardization of terminology of pelvic floor muscle func-
tion and dysfunction: report from the pelvic floor clinical assess-
ment group of the International Continence Society. Neurourol
Urodyn. 2005;24:374–80.
Laycock J, Jerwood D. The pelvic floor muscles assessment. The
PERFECT scheme. Physiotherapy. 2001;87:631–42.
Brink CA, Sampselle CM, Wells TJ, Diokno AC, Gl G. A digital test
for pelvic muscle strength in older women with urinary inconti-
nence. Nurs Res. 1989;38:196–9.
Devreese A, Staes F, Weerdt W, Feys H, Van Assche A, Penninckx F,

et al. Clinical evaluation of pelvic floor muscle function in conti-
nent and incontinent women. Neurourol Urodyn. 2004;23:190–7.
Nitti V, Ficazzola M. Voiding dysfunction: diagnostic evaluation. In:
Appel R, editor. Voiding dysfunction: diagnosis and treatment.
Humana Press; 2000.
Voiding Diaries
Bright E, Drake MJ, Abrams P. Urinary diaries: evidence for the
development and validation of diary content, format, and dura-
tion. Neurourol Urodyn. 2011;30:348–52.
Van Kerrebroeck P, Andersson KE. Terminology, epidemiology,
etiology, and pathophysiology of nocturia. Neurourol Urodyn.
2014;33(Suppl 1):S2–5.
Goessaert AS, Krott L, Hoebeke P, Vande Walle J, Everaert
K. Diagnosing the pathophysiologic mechanisms of nocturnal
polyuria. Eur Urol. 2015;67:283–8.
UTI
Mody L, Juthani-Mehta M. Urinary tract infections in older women:
a clinical review. JAMA. 2014;26(311):844–54.
Buchsbaum GM, Albushies DT, Guzick DS. Utility of urine reagent
strip in screening women with incontinence for urinary tract
infection. Int Urogynecol J Pelvic Floor Dysfunct. 2004;15:391–3.
Yu Y, Sikorski P, Bowman-Gholston C, Cacciabeve N, Nelson KE,
Pieper R. Diagnosing inflammation and infection in the urinary
system via proteomics. J Transl Med. 2015;13:111.
Pad Test
Krhut J, Zachova RL, Smith P, Rosier PF, Valanský L, Martan A,
et al. Pad weight testing in the evaluation of urinary incontinence.
Costantini E, Lazzeri M, Bini V. Sensitivity and specificity of one-
hour pad test as a predictive value for female urinary inconti-
nence. Urol Int. 2008;81:153–9.
Chapter 3
Noninvasive Urodynamics
3.1 Background
Noninvasive urodynamics in female consists of two tests: uro-
flowmetry and postvoid residual urine (PVR) assessment.
From PVR and voided volume, a voided percentage (Void%)
can be calculated. While these tests are useful tools for
screening, they have evident limits since subsequent invasive
tests are necessary to confirm the diagnosis and refine the
findings. Owing to their limitations, such tests must always be
interpreted by an experienced urogynecologist with knowl-
edge of patient’s complaints and symptoms.
3.1.1 Uroflowmetry
Uroflowmetry is the analysis of urine flow rate over the time.

The technique is a simple way to measure bladder emptying
and is the first-line screening test for most patients with
LUTS. By itself, a uroflow is seldom able to determine the
cause of voiding dysfunction; however, in conjunction with a
careful history and physical examination, it can provide valu-
able information and select the patients for further invasive
urodynamic investigation.

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_3
32 Chapter 3. Noninvasive Urodynamics
Flow rate (ml/s)
Time (s)
Figure 3.1 Uroflowmetry curve
Uroflow is measured by a collecting electronic equipment

(uroflowmeter) which provides a graphic expression of the
flow rate as a function of time (Fig. 3.1).
Since uroflowmetry results are sensitive to patient coopera-
tion and emotion, all free uroflowmetry studies should be
performed in a completely private dedicated room. Females
usually void seated on the commode except patients with void-
ing dysfunction which could prefer the standing position.
When flow rate and voided volume are unexpectedly low and
conversely PVR is larger than expected basing on history, emo-
tional problems should be taken into account, and the test
should be repeated.
3.1.1.1 Interpretation of Uroflowmetry
Several parameters from the trace are automatically calcu-

lated and printed out together with the trace.
Note: In automated calculations, it is important that the
examiner verifies the presence of artifacts such as an acciden-
tal knock to the flowmeter and, in case, checks the parame-
ters of the curve manually (Fig. 3.2).
3.1 Background 33
Automated calculation : 45 ml/s

Manual calculation : 19 ml/s
Flow rate (ml/s)
50
40
20
Time (s)
Figure 3.2 Common uroflowmetry artifact: accidental knock to the

equipment
Uroflowmetry Parameters
Voided volume
Average flow rate =
Flow time
Flow rate
(ml/s)
Maximum
flow rate
Voided
volume
time to
maximum flow
Flow time
Time (s)
Figure 3.3 Parameters of uroflowmetry curve
Common parameters determined by uroflowmetry include

(Fig. 3.3):
• Maximum flow rate (Qmax), that is, the maximum mea-
sured value of the flow curve.
• Flow time, that is, the time over which a measurable flow
occurs. Flow time is easily measured if the flow is continuous.
Characteristic Flow Patterns

Continuous Flow Curves Interrupted Flow Curves
Prolonged flow Undulating
Constrictive Intermittent
Figure 3.4 Patterns of uroflowmetry curve
When urine flow is intermittent, the time intervals between

flow episodes are not considered. Similarly, when there is
a lengthy terminal dribbling, it may be noted but not
included in the flow time.
• Average flow rate, that is, the volume voided divided by the
flow time.
• Time to maximum flow, that is, the elapsed time from onset
of flow to maximum flow rate.
• Morphology of the curve. Flow curve shape is complemen-
tary to flow rate in the assessment of voiding. Despite
some disparities in the definition of the morphology of
flow curve, several patterns of flow curves can be recog-
nized (Fig. 3.4):
–– Normal flow curve is continuous and has a bell shape
with steep slope and short flow time.
–– Long flow, a long and constant flow rate during the
entire micturition.
–– Constrictive, flat plateau of low flow.
–– Undulating with multiple peaks: a long continuous curve
with multiple peaks, each representing 20% or more
than Qmax frequently seen in dysfunctional voiding.
3.1 Background 35
–– Interrupted curve. Discontinuous curve characterized

by repetitive flow peaks reaching zero in between,
which can be due to abdominal straining or detrusor
sphincter dyssynergia.
A long flow curve may be due either to urethral obstruc-
tion or to poor detrusor contraction. A pressure-flow study is
necessary to clarify the underlying mechanism. A constrictive
curve may be seen in urethral stricture (i.e., after placement
of obstructive mid-urethral sling).
In neurologically normal patients, undulating flow curve is
most often a result of anxiety or dysfunctional voiding.
Intermittent flow in neurologic patients may be a conse-
quence of detrusor sphincter dyssynergia in suprasacral
lesions or abdominal straining in sacral and sub-sacral lesions.
Again a pressure-flow study is mandatory to define the exact
mechanism.
Qmax in women ranges from 23 to 33 mL/s.
Unlike men, in women the relation between Qmax and
age is unclear. The same concept applies to pre-/postmeno-
pausal status. Some studies report a negative relation proba-
bly linked to the development of detrusor underactivity with
aging, while other studies do not indicate any significant
connection.
Voiding time in women is lower than in men due to the
shortness of the urethra and is about 20 s. Flow rate is closely
related to voided volume. Voided volumes lower than 150 mL
are considered unreliable, and the test should be repeated
asking the patient to drink water until she experiences a
strong but not uncomfortable desire to void. On the other
hand, a voided volume greater than 700 mL is usually associ-
ated with a decline of Qmax.
To overcome the problem of volume dependency, Haylen
constructed Liverpool nomograms based on maximum and
average flow rates of healthy asymptomatic volunteers over a
wide range of voided volumes (15–600 mL). Nomogram is in
centile form. Flow rates below the fifth centile may be
generally regarded as abnormal; abnormality can be suspected
in flow curves between fifth and tenth centiles (Fig. 3.5).
95th 90th
60
75th
50
Maximum urine flow rate (ml/s)
50th
40
25th
30
10th
5th
20
10
0
0 100 200 300 400 500 600
Voided volume (ml)
40
95th
Average urine flow rate (ml/s)
30 90th
75th
50th
20
25th
10th
5th
10
0
0 100 200 300 400 500 600
Voided volume (ml)
Figure 3.5 The Liverpool nomogram for maximum and average

flow for women
3.1 Background 37
3.1.2 Postvoid Residual (PVR) Assessment
The postvoid residual volume (PVR) is defined as the volume

of urine remaining in the bladder immediately following void-
ing. It provides information on the ability of the bladder to
empty as well as its functional capacity (voided volume plus
PVR). Normal lower urinary tract function is usually associated
with a negligible PVR (<50 mL); however, there is no agree-
ment as to what an “abnormal” or clinically significant value is.
Thus, elevated PVR is somewhat arbitrary. This being the case,
most would agree that a PVR of greater than 100 mL is ele-
vated, although perhaps not significant. Elevated PVR may be
an indication of detrusor hypocontractility or bladder outlet
obstruction and may require further evaluation depending on
the patient and the symptoms complained. PVR can be mea-
sured directly by urethral catheterization or, better, determined
noninvasively by ultrasonography. Portable bladder scanners
based on ultrasound technology are currently available to
determine bladder volume (Fig. 3.6).
3.1.3 Voided Percentage (Void%)

Void% is the numerical description of the voiding efficacy or
efficiency which is the proportion of bladder content emp-
tied. Void% can be calculated by the formula: [(volume
voided/volume voided + PVR) × 100].
Figure 3.6 The bladder scanner, courtesy of Echo-Son

Example: If a patient voids 300 mL leaving a postvoid

residual volume of 100 mL (total bladder capacity, 400 mL),
then she has a Void% of 75.
Voiding efficiency may be a relevant parameter in addition
to Qmax and PVR for the follow-up of treated patients.
Key Points
• Uroflowmetry helps to identify patients with voiding

problems. However, by itself, the procedure cannot
distinguish true obstruction from poor bladder con-
tractility. Thus, the test’s utility lies in its ability to
identify patients who need further urodynamic
studies.
• Measurement of postvoid residual urine volume
(PVR) is also useful in assessing voiding
dysfunction.
• PVR measurement can be performed by sterile cath-
eterization or by bladder ultrasound. Portable blad-
der scanners are convenient, noninvasive, accurate,
and cost-effective and carry no risk of urethral
trauma or urinary tract infection.
• However, there is no agreement as to what is an
“abnormal” PVR: a PVR lower than 50 mL is negli-
gible, while a PVR greater than 100 mL is probably
elevated, although perhaps not significant.
• Void% may be an additional parameter in the evalu-
ation of voiding process.
Suggested Reading
Uroflowmetry
Sorel M, Reitsma H, Rosier P. Uroflowmetry in healthy women: a
systematic review. Neurourol Urodyn. 2017;36:953–9.
Rane A, Iyer J. Posture and micturition: does it really matter how a
woman sits on the toilet? Int Urogynecol J. 2014;25:1015–21.
Al Afraa T, Mahfouz W, Campeau L, Corcos J. Normal lower uri-

nary tract assessment in women: I. Uroflowmetry and post-
void residual, pad tests, and bladder diaries. Int Urogynecol J.
2012;23:681–5.
2010;29:4.
Yang KN, Chen SC, Chen SY, Chang CH, Wu HC, Chou EC. Female
voiding postures and their effects on micturition. Int Urogynecol
J. 2010;21:1371.
Barapatre Y, Agarwal MM, Singh SK, Sharma SK, Mavuduru R,
Mete UK, et al. Uroflowmetry in healthy women: development
and validation of flow-volume and corrected flow-age nomo-
grams. Neurourol Urodyn. 2009;28:1003.
Kumar V, Dhabalia JV, Nelivigi GG, Punia MS, Suryavanshi M. Age,
gender, and voided volume dependency of peak urinary flow rate
and uroflowmetry nomogram in the Indian population. Indian J
Urol. 2009;25:46.
Haylen BT, Yang V, Logan V. Uroflowmetry its current clini-
cal utility for women. Int Urogynecol J Pelvic Floor Dysfunct.
2008;19:899–903.
Pauwels E, De Laet K, De Wachter S, Wyndaele JJ. Healthy, middle-
aged, history-free, continent women—do they strain to void? J
Urol. 2006;175:1403.
Haylen BT, Law MG, Frazer M, Schulz S. Urine flow rates and resid-
ual urine volumes in urogynecology patients. Int Urogynecol J
Pelvic Floor Dysfunct. 1999;10:378–83.
Wyndaele JJ. Normality in urodynamics studied in healthy adults. J
Urol. 1999;161:899.
Abrams P. Bladder outlet obstruction index, bladder contractil-
ity index and bladder voiding efficiency: three simple indices to
define bladder voiding function. BJU Int. 1999;84:14–5.
Haylen BT, Ashby D, Sutherst JR, Frazer MI, West CR. Maximum
and average urine flow rates in normal male and female
populations—the Liverpool nomograms. Br J Urol. 1989;
64:30–8.
Fantl JA, Smith PJ, Schneider V, Hurt WG, Dunn LJ. Fluid weight
uroflowmetry in women. Am J Obstet Gynecol. 1983;145:1017.
Post-Void Residual Urine

Asimakopoulos A, De Nunzio C, Kocjancic E, Tubaro A, Rosier
P, Finazzi-Agrò E. Measurement of post-void residual urine.
Goode PS, Locher JL, Bryant RL. Measurement of post-void resid-
ual urine with portable transabdominal bladder ultrasound scan-
ner and urethral catheterization. Int Urogynecol J Pelvic Floor
Dysfunct. 2000;11:296–300.
Chapter 4
How to Perform
Conventional Urodynamic
Investigation: The “Good
Urodynamic Practice”
4.1 Background
Invasive or conventional urodynamic testing includes:
• Transurethral cystometry for the assessment of bladder
filling
• Pressure/flow study for the assessment of voiding phase
The performance, the results, and the interpretation of
urodynamic testing are dependent on both the urodynamicist
involved and the equipment being used. Rapid development
of computer-based technology has led to sophisticated urody-
namic equipment (Fig. 4.1).
Therefore, it is of greatest importance that the clinician
performing the test is familiar with the urodynamic software
and all the equipment that is used during the study. Proper
calibration and standardization of equipment, together with
the expertise of the clinician, who should understand the
patients’ symptoms and decide on more appropriate test, are
of paramount importance for “a good urodynamic practice.”
Note: UDS may be inconvenient for some patients, result-
ing in poor cooperation, which may alter the accuracy of the

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_4
42 Chapter 4. The “Good Urodynamic Practice”
a b
Figure 4.1 Equipment for conventional urodynamic testing includ-

ing (a) pressure/flow workstation with superimposed X-ray image,
(b) urethral profilometer, and (c) uroflowmeter, courtesy HC Italia
results. Conflicting evidence exists about which precise infor-

mation is helpful to give to patients before urodynamic test-
ing to reduce distress. Often information leaflets about
urodynamic investigations are too difficult for patients to
understand. A good information with clear and unambiguous
wording may increase patient acceptance and confidence
reducing the stress of investigation.
4.2 Setup of the Equipment

Three types of pressures are recorded during standard urody-
namic test (Fig. 4.2):
• Vesical is the pressure recorded within the bladder and, as
such, is the only absolute pressure recorded.
• Abdominal is the pressure surrounding the bladder and
indicates both passive forces created when the abdominal
4.2 Setup of the Equipment 43
Figure 4.2 Pressures measured during conventional urodynamic

testing
structures lie on the bladder during patient’s position

changes (from supine to sitting or upright position) and
active forces created by physical exertion like coughing or
sneezing. Measuring Pabd helps the examiner differentiate
the effects of abdominal from detrusor forces. Pabd can be
measured in various locations, including the rectal vault
(most commonly), posterior vaginal vault, and abdominal
stoma in patient with urinary or fecal diversion. Regardless
of where it is measured, Pabd is a relative pressure; in
other words, it provides a reasonable estimate of abdomi-
nal forces, but it is not possible to directly measure Pabd in
the clinical setting. Furthermore it is vulnerable to physi-
ological artifacts like bowel contractions when measured
in the rectal vault or movements of fluid-filled balloon
when measured in the posterior vaginal vault of a woman
with significant pelvic organ prolapse.
• Detrusor is the pressure created by the tone of the smooth
muscle within the bladder wall and passive forces exerted
by the viscoelastic properties of the bladder wall. It is cal-
culated by subtracting Pabd from Pves (Pdet = Pves − Pabd).
Since Pdet is derived by subtracting a relative pressure
(Pabd) from an absolute pressure (Pves), it is also a relative
pressure and as such well subject to physiological artifacts.
4.3 Transducers
Pressure measurement can be obtained using different types
of transducers.
4.3.1 Water-Filled (External) Transducers

(Fig. 4.3)
These are the most common transducers and are located
between the patient and the urodynamic equipment.
Transmission lines extend from the catheters placed in the
patient (bladder, rectum, or posterior vaginal vault) and pres-
sure transducer (usually located on the stand), while an elec-
Figure 4.3 Schematic drawing of water-filled external transducers.

Water-filled system allows the transmission of intravesical and
abdominal pressures from the patient to the external pressure trans-
ducers, which are attached to the urodynamic equipment
4.3 Transducers 45
tronic cable connects the transducer to the urodynamic

equipment. Because this system depends on the transmission
of pressure through fluid (water), it is crucial that there are no
air bubbles in the transducer or tubing to avoid a signal
dampening.
The main limitation of the water-filled system is that
patient movement (i.e., provocative maneuvers to demon-
strate SUI or DO) causes high-frequency artifactual signals
that are transmitted to the transducer by the water column
and as a result make the urodynamic traces harder to inter-
pret. Furthermore a re-levelling of the transducers is required
every time the patient moves from supine to sitting and
standing positions.
4.3.2 Microtip Transducers (Fig. 4.4)
Strain gauges are miniaturized in order to fit the tip of a 6–8

French catheter. The external proximal end of the catheter is
connected directly to the electronic recording system, thus
making them simpler to set up than fluid-filled systems. In
addition, a reference height does not need to be set up since
unlike external fluid catheters, it is at the level of the internal
transducer. Nevertheless, they need to be calibrated regularly
before use.
Microtip transducers are advantageous in certain situa-
tions such as ambulatory urodynamics since they are not
affected by movement artifacts, but for conventional cystom-
etry, they are not recommended by the ICS. The main disad-
stiff catheter
microtip
transducers
Figure 4.4 Schematic drawing of dual-sensor microtip transducer

for simultaneous measurement of bladder and urethral pressure
vantage of this system is that the pressure readings are

directional and rely on what the transducer is facing or what
the transducer is lying against. In addition the catheters are
expensive and must be handled with care.
4.3.3 A
ir-Charged Catheters (T-DOC System)
(Fig. 4.5)
This is the newest type of transducer. The system consists of
permanent cables with incorporated transducers and dispos-
able catheters with a tiny balloon located on the distal end of
the catheter. After the catheter is inserted into the patient
and connected to the cable, the transducer is used to “charge”
the catheter by injecting a micro-volume of air into the cath-
eter balloon. This creates a closed sensitive system for accu-
rate recording of bladder, abdominal, and urethral pressures.
Air-charged catheter has gained popularity due to its simpler
and quicker setup than fluid-charged systems. In addition
pressure detection is not directional, and the catheters are
disposable unlike the microtip catheters. However, pressures
measured using air-charged catheters are not comparable
with water-filled catheters and are therefore not interchange-
open charge
T-DOC air-charged catheter

to the equipment to the patient
Circumferential
pressure sensing balloon
Figure 4.5 Schematic drawing of air-charged catheters (T-DOC

system). This catheter uses a miniature, air-filled balloon placed cir-
cumferentially around a polyethylene catheter. External forces on
the balloon are transmitted to the air-filled catheter lumen and com-
municated to an external transducer connected to the equipment
4.3 Transducers 47
able. The air-charged catheters consistently produce higher

mean pressures than the water-filled catheters. Caution,
thereby, must be used when comparing urodynamic parame-
ters using air-charged and water-filled catheters.
4.3.4 Zeroing the External Water-Filled

Transducers
The pressure measurements can be “zeroed” either to the
surrounding atmospheric pressure or to the internal pressure.
The ICS recommend that the surrounding atmospheric pres-
sure should be used as it facilitates standardization of the
technique and comparison of data from other centers.
Zero is established by exposing the pressure transducer to
the atmosphere and setting the pressure value at 0 cmH2O.
In practice, once the bladder and rectal catheters are in
place, they are connected through transmission lines to their
respective transducer domes via a three-way stopcock. At the
other end of the transducer dome, a 20-mL syringe filled with
saline is also connected using a three-way stopcock. The
syringe will be used to flush air out of the system. Zeroing the
system to the atmosphere is achieved by opening the dome of
the transducer to the air while the three-way stopcock con-
necting the patient and syringe are off and then pressing the
zero button on the software system. Once this is done, the
dome of the transducer is closed to the air while stopcock to
syringe and patient are opened to flush saline into the tubings
to eliminate air in the system. Once air bubbles are removed,
the syringe stopcock is turned off, and the system, opened
only to the patient, is ready for recording (Fig. 4.6).
At this point, the patient is asked to cough to check for
accuracy of recorded signals.
Because a cough reflects abdominal forces acting on the
bladder, Pves and Pabd tracings are expected to reflect a
twin image characterized by a rapid rise and rapid descent of
Transducer dome
Syringe ZEROING
three-way tap Syringe FLUSHING
Syringe RECORDING
Figure 4.6 Three-way tap positions during setting of water-filled

transducer. Various positions allow the transducer to be zeroed to
atmospheric pressure, tubing to be flushed, and pressure to be
recorded
pressure to baseline. In contrast, the Pdet tracing should

show no response (Fig. 4.7). In fact, a small biphasic pressure
spike is usually seen on the Pdet trace. The biphasic spike is
an accepted artifact caused by the maximum pressure in the
Pves and Pabd traces being recorded at different times.
4.3.5 Reference Height of the External Water-

Filled Transducers
The reference height is the level at which the transducers
must be placed so that all urodynamic pressures have the
same hydrostatic component. The transducer should be posi-
tioned at the level of the pressure to be measured during
zeroing and during measurement.
Since the urine into the bladder acts as a column of water,
the pressure at the dome of the bladder (at the top of the col-
umn) should be lower than the pressure at the base of the
bladder (at the bottom of the column of fluid). For that reason
the ICS has established the superior margin of the symphysis
pubis as the reference point for measuring all UDS pressures.
4.3 Transducers 49
Pves
Pabd
Pdet
Figure 4.7 Cough induces near-identical spikes in Pves and Pabd,

while in Pdet is seen a small biphasic spike due to the recording gap
between the two previous pressures
If the patient changes the position during the test (i.e., sitting
to standing), the height of the transducer should be adjusted
so that it remains at the level of the bladder. Moving the
patient bed during the examen (from supine to sitting and to
standing position) without modifying the position of the trans-
ducer will provide inaccurate readings.
4.3.6 Microtip and Air-Filled Systems
For microtip transducers the reference height is the transducer

itself; for air-filled transducers the reference height is at the
position of the internal balloon. Using these systems it is there-
fore difficult to be certain of the position of the reference
height or to ensure that the reference height of the intra-
abdominal and the intravesical lines is equal. In addition
changes of patient position can cause significant differences in
the positions of intravesical and intra-abdominal transducers/
balloons. In the supine position, the rectal line is likely to be
lower than the intravesical line; when standing the rectal line
may be higher than the intravesical line. In practice, however,

these differences in height are unlikely to result in a significant
effect on recorded pressures, and most of the UDS instruments
are equipped with an automatic zeroing system (Fig. 4.8).
Note: Pves-Pabd balance button in water-filled systems.
In water-filled systems, artificial adjust of the recorded
pressures goes against the principles of physiological mea-
surement, and this was described as a common mistake in
Good Urodynamic Practice.
4.4 Setup of the Patient

• Preparation
Although evidence indicates that urodynamics is generally
well tolerated, embarrassment, fear of pain, and apprehen-
sion are quite common in the majority of patients. An
explanatory leaflet with sufficient information about uro-
dynamic investigation, written with clear and unambigu-
ous words, may be particularly useful to defeat the anxiety.
Furthermore, the patient should be aware that the proce-
dure is interactive, and she should discuss her sensations
during the study and whether or not her symptoms are
reproduced during the study.
Note: In any patient undergoing UDS, a conventional uri-
nalysis or simply a urine dipstick to screen for infection
should be available. When infection is present, the examen
should be rescheduled after appropriate antibiotics treat-
ment. There are no emergencies in urodynamics!
• Informed consent
The patient should be aware of the risks of the procedure
and should be informed about the possibility of a urinary
tract infection, hematuria, and voiding dysfunction after
the procedure (see Appendix B).
• Position
The standard position during cystometry should be sitting
position because this is reported to have a higher sensitiv-
ity for the diagnosis of abnormalities during filling phase.
Also standing position can be used in patients able to do.
REFERENCE HEIGHT OF THE TRANSDUCERS
a EXTERNAL FLUID-FILLED b MICROTIP/T-Doc

transducer
higher pressure
zero symphisis pubis
lower pressure
lower pressure
higher pressure
Figure 4.8 (a) With the external water-filled transducers, the reference height is the superior margin of the symphysis
4.4 Setup of the Patient
pubis; (b) for microtip and air-filled transducers, the reference height is the position of the transducer or the balloon
itself
51
• Catheters
Bladder: a double-lumen catheter as thin as possible
(5–8 Fr) for filling and pressure recording is regarded as
the gold standard (Fig. 4.9). A double-lumen catheter
allows a smooth transition from storage to voiding and
permits the exam to be repeated without reinsertion of a
filling catheter. Ancillary dual catheter method seems dis-
advantageous because removal of the separate filling cath-
eter just before micturition may interfere with lower
urinary tract function and may also displace the intravesi-
cal pressure-sensing catheter.
Rectum/vagina: abdominal pressures are measured with a
balloon catheter (Fig. 4.10) inserted into the rectum for
5–10 cm. The balloon should be filled with a small
amount of fluid (10–20% of its capacity) to prevent
obstruction of the catheter by the rectal content.
Overfilling is a common mistake which can cause mis-
leading measurements. To prevent overfilling the balloon
can be punctured, but pressure can also be recorded
through an open fluid-filled tube without the balloon. As
alternative to the rectum, the catheter can be positioned
in the vaginal vault or stoma when the rectum is closed,
although the pressures recorded, in the latter case, seem
less reliable.
to fill
to record
Figure 4.9 Double-lumen catheter (5–8 Fr) for filling and recording

bladder pressure
4.4 Setup of the Patient 53
Figure 4.10 Rectal/vaginal balloon catheter
• EMG electrodes
Electromyography of pelvic floor muscles is a supplemen-
tary urodynamic test and is usually indicated in neurologi-
cal patients and in dysfunctional voiding. Two types of
electrodes are usually employed: surface and needle/wire
(see Chap. 6).
Note: Bladder and rectal catheters as well as EMG elec-
trodes are positioned with the patient in supine position
and should be securely fixed with adhesive tape
(Fig. 4.11).
• Filling medium
Saline solution at room temperature is the commonly used
fluid for bladder filling. When videourodynamics is per-
formed, a contrast solution is added.
The rate of filling is usually 50 mL/min in non-neurogenic
patient and 20 mL/min in neurogenic patient more prone
to develop detrusor overactivity with a high filling rate.
• Display of signals
All measured (Pabd and Pves) and derived (Pdet) signals
are displayed according to the ICS standards (Good uro-
dynamic practice, 2002) (Fig. 4.12):
–– Vesical pressure
–– Abdominal pressure
–– Detrusor pressure
–– Flow
Figure 4.11 Catheters and EMG electrodes should be securely

fixed with the patient in supine position
Inf.vol
Pves
Pabd
Pdet
Flow
EMG
Voided vol.
Figure 4.12 Display of tracings: in color, the ICS recommended

sequence of basic tracings (Pves, Pabd, Pdet, Flow) and in gray, the
sequence of optional tracings (infused volume, EMG, voided vol-
ume)
Filling volume, electromyography, and voided volume are

displayed in additional curves.
• Resting pressures
The initial resting pressures, if transducers are properly
zeroed and positioned, are 15–40 cmH2O (sitting) or
30–50 cmH2O (standing), both for the vesical and intrarectal
pressures. By consequence the subtracted detrusor pressures
are around zero. In the supine position, the vesical pressure
will be 5–20 cmH2O and the intrarectal pressure usually
somewhat higher as a consequence of the position. Then
small differences in detrusor pressures (< + or − 10 cmH2O)
can be considered to be a result from differences in catheter
tip position of bladder and rectal catheters and are therefore
acceptable (Fig. 4.13). If the pressure ranges are outside the
acceptable range, two possibilities have to be considered:
–– When vesical and abdominal pressures are similar but
outside the expected range, the height of the transducer
should be checked.
PLAUSIBLE INITIAL RESTING PRESSURES
Supine Seated Standing
Pves
30-50 cm H20
15-40 cm H20
Pabd
5-20 cm H20
Pdet
+/- 10 cm H20
movement movement
artefacts artefacts
Figure 4.13 Plausible ranges for initial values of Pves and Pabd.

Resting pressure must be updated when the patient moves from
supine to standing position in relation to the position of the pressure
transducers
–– If only one pressure is outside the range, the correct

zeroing of the relevant transducer should be checked,
and then the catheter should be flushed and, in case,
repositioned.
• Control of quality of signals
Before and during the exam, it is necessary to verify that
both pressures are registering by asking the patient to
cough. Usually, this is done every 50 mL of filling. The
amplitude of Pves and Pabd should be similar. If the height
of one cough peak is less than 70% of the other, the line
with the lower value should be flushed with water and the
cough test repeated. Vital signs such as respiration, talking
of the patient, and movement should be visible in Pves and
Pabd throughout the entire examen as a sign of good qual-
ity of pressure signals (Fig. 4.14) (Box 4.1).
QUALITY OF SIGNALS
“ live signals” “ dead signals”
Pves
Pabd
Pdet
Figure 4.14 Pressure fluctuations within 10 cmH2O of initial resting

pressure are considered normal “live signals.” The absence of the
fine structure of a pressure trace can indicate an error in pressure
transmission
Box 4.1 Urodynamic Testings: Key Points for Clinical

Practice
1. Detailed clinical evaluation.
2. Informed consent.
3. Room intended for quiet and protected from unnec-
essary interruptions.
Noninvasive
4. Free uroflowmetry when the patient feels a normal
desire to void.
5. Assessment of PVR through ultrasounds or
catheter.
Conventional
6. Catheters positioned in supine position:
–– 5 Fr rectal balloon catheter inserted at the anus
–– 7 Fr double-lumen transurethral catheter inserted
into the urethra
–– EMG surface electrodes attached at both sides of
the anus
7. Good urodynamics is carried out by making pres-
sure measurements relative to atmospheric pres-
sure. This is achieved in a water-filled system by
placing the pressure transducers at the upper level
of the symphysis pubis and by zeroing the equip-
ment with the transducers closed off to the patient
and open to the atmosphere.
8. Catheters should be properly connected to the
external transducers avoiding any leakage of fluid
and flushed by the air.
9. Filling and voiding cystometry are usually con-
ducted with the patient in sitting position.
10. Check that resting values for abdominal, intravesi-
cal, and detrusor pressures are in a normal range.
11. Prior to bladder filling, signal control quality is done:
cough is used to ensure that abdominal and intra-
vesical pressure signals respond equally.
(continued)
Box 4.1 (continued)

2. The bladder is filled at a rate of 50 mL/min.
1
13. During filling quality control of the signal is checked
asking patient to cough. Any artifacts should be
immediately corrected.
14. Using annotation marks while running the test is
helpful.
4.5 Post-test Patient Care

Most people have urodynamic tests without experiencing any
problems. Drinking a large amount of fluid for 24 h is usually
enough to avoid mild voiding problems. Anti-inflammatory
drugs may be used to resolve burning during micturition. Routine
antibiotics are unnecessary and usually not recommended.
Risk factors accounting for a potential increase of UTI
following UDS for which a periprocedural antibiotics are
advisable include:
• Patients with relevant neurogenic lower urinary tract
dysfunction
• Patients with bladder outlet obstruction and/or elevated
post-void residual
• Advanced age (older than 70 years)
• Asymptomatic bacteriuria
• Patients with chronic catheters
• Immunosuppression, corticosteroids, and inherent immune
deficiency
• Orthopedic implant
Diabetes, menopausal status, history of recurrent UTI, and
cardiac vascular disease do NOT require routine antibiotic
prophylaxis.
The first choice for prophylaxis is a single oral dose of
trimethoprim-sulfamethoxazole before UDS, with alternative
antibiotics chosen in case of allergy or intolerance.
Suggested Reading
Overviews
Rosier PFWM, Schaefer W, Lose G, Goldman HB, Guralnick M,
Eustice S, et al. International continence society good urody-
namic practices and terms 2016 (ICS-GUP2016): urodynamics,
uroflowmetry, cystometry and pressure-flow study. Neurourol
Urodyn. 2017;36:1243–60.
Leitner L, Walter M, Sammer U, Knüpfer SC, Mehnert U, Kessler
TM. Urodynamic investigation: a valid tool to define normal
lower urinary tract function? PLoS One. 2016;11:e0163847.
Raz O, Tse V, Chan L. Urodynamic testing: physiological back-
ground, setting-up, calibration and artefacts. BJU Int. 2014;
114:22–8.
Gammie A, Clarkson B, Constantinou C, Damaser M, Drinnan M,
Geleijnse G, et al. International continence society guidelines
on urodynamic equipment performance. Neurourol Urodyn.
2014;33:370–9.
Rosier PF, Giarenis I, Valentini FA, Wein A, Cardozo L. Do patients
with symptoms and signs of lower urinary tract dysfunction
need a urodynamic diagnosis? ICI-RS 2013. Neurourol Urodyn.
2014;33:581–6.
Winters JC, Dmochowski RR, Goldman HB, Herndon CD, Kobashi
KC, Kraus SR, et al. Urodynamic studies in adults: AUA/SUFU
guideline. J Urol. 2012;188:2464–72.
2010;29:4–20.
Schäfer W, Abrams P, Liao L, Mattiasson A, Pesce F, Spangberg
A, et al. Good urodynamic practices: uroflowmetry, filling
cystometry, and pressure flow studies. Neurourol Urodyn.
2002;21:261–74.
Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U,
et al. The standardisation of terminology in lower urinary tract
function: report from the standardisation subcommittee of the
International Continence Society. Urology. 2003;61:37–49.
Pressure Measurement
Abrams P, Damaser M, Niblett P, Rosier PFWM, Toozs-Hobson
P, Hosker G, et al. Air filled, including “air-charged,” catheters
in urodynamic studies: does the evidence justify their use?
Gammie A, Abrams P, Bevan W, Ellis-Jones J, Gray J, Hassine A,
et al. Simultaneous in vivo comparison of water-filled and air-
filled pressure measurement catheters: Implications for good
urodynamic practice. Neurourol Urodyn. 2016;35:926–33.
Digesu GA, Derpapas A, Robshaw P, Vijaya G, Hendricken C,
Khullar V. Are the measurements of water-filled and air-
charged catheters the same in urodynamics? Int Urogynecol J.
2014;25:123–30.
Quality Control
MacLachlan LS, Rovner ES. Good urodynamic practice: keys to per-
forming a quality UDS study. Urol Clin North Am. 2014;41:363–73.
Hogan S, Jarvis P, Gammie A, Abrams P. Quality control in urody-
namics and the role of software support in the QC procedure.
Gammie A, Drake M, Swithinbank L, Abrams P. Absolute versus
relative pressure. Neurourol Urodyn. 2009;28:468.
Patient Care After Tests

Cameron AP, Campeau L, Brucker BM, Clemens JQ, Bales GT, Albo
ME, et al. Best practice policy statement on urodynamic antibi-
otic prophylaxis in the non-index patient. Neurourol Urodyn.
2017;36:915–26.
Okorocha I, Cumming G, Gould I. Female urodynamics and lower
urinary tract infection. BJU Int. 2002;89:863–7.
Chapter 5
Interpretation of Tracings
and Identification of Artifacts
5.1 Background
Correct interpretation of tracings and recognition of artifacts
in the pressure signals are critical for an accurate diagnosis. A
number of reports describe the interobserver variation and
short-term (i.e., within the session), intermediate-term, and
long-term reproducibility of urodynamic investigation. A
test–retest variation of 10–15% for various urodynamic
parameters has been reported. Basically, this variation can be
regarded as the physiological variation of lower urinary tract
function, but there is also some evidence that some parame-
ters may be observer-dependent. Therefore, application of
standard techniques and continuous quality control is of the
greatest significance. While the value of a well-done urody-
namics assessment is well established, comparatively few cli-
nicians have received formal training in the area. The
familiarity with the most relevant UDS parameters to ana-
lyze is of paramount importance to facilitate the correct
interpretation of tracings and improve the performance of
examinations in daily practice.

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_5
62 Chapter 5. Interpretation of Tracings and Identification
5.2 C
onventional (Invasive) UDS: Relevant
Parameters
5.2.1 Cystometry
The principal aim of cystometry is to reproduce patient stor-

age symptoms (frequency, urgency) and relate them to spe-
cific urodynamic events.
Several parameters are recorded during the filling phase
including (Fig. 5.1):
• Bladder sensation
• Bladder compliance
• Maximum cystometric capacity
• Detrusor function
5.2.1.1 Bladder Sensation
Bladder sensation during urodynamics is usually recorded by

the simple method of asking patients to inform the investiga-
tor when they experience different sensations. This is an ICS
standardized but subjective measurement with evident limits.
Cystometry
cm H2O
Detrusor function:
involuntary contractions
Compliance
ml
Sensation: FD ND SD Max Cyst. Capacity
Figure 5.1 Parameters monitored during cystometry

5.2 Conventional (Invasive) UDS: Relevant Parameters 63
Note: The need of strategies to record bladder filling sen-

sations in a more automated and objective way is widely
recognized. Toward this end, a keypad “urge score” device
was designed to measure sensations during bladder filling.
To date, however, the device has never found a wide use
into clinical practice.
In normal subjects, three types of sensations can be
observed:
(a) The first sensation of bladder filling (FS), which is felt
when the subject becomes aware of bladder filling (it is
perceived as a vague sensation in the lower pelvis, which
waxes and wanes, and could be easily ignored for few
minutes). Usually is felt at 40% of bladder capacity
(b) First desire to void (FD), a constant sensation felt in the
lower abdomen that gradually increases with bladder fill-
ing and would lead the patient to void in the next conve-
nient moment, but still voiding can be delayed. Usually is
felt at 60% of bladder capacity
(c) Strong desire to void (SD), a persistent desire to void felt
in the perineum or urethra, without fear of leakage.
Usually is felt at 90% of bladder capacity
Note: Volumes of filling sensations and cystometric capac-
ity have to be weighed against the information from the
patients’ voiding diary, since the laboratory situation may
cause a variation in the patient’s usual lower urinary tract
behavior.
5.2.1.2 Bladder Compliance
Bladder compliance is the relationship between changes in

volume and pressure. It is calculated by dividing change in
volume by change in Pdet and is expressed in milliliter/centi-
meter H2O. Normal bladder compliance values vary between
30 and 100 mL/cmH2O and are higher in women than in men
(usually >40 mL/cmH2O).
The ICS recommends two standard points for measuring
bladder compliance: detrusor pressure at empty bladder and
at maximum bladder capacity or immediately before the start

of any detrusor contraction that causes significant leakage.
Bladder compliance in women is considered abnormal if it
is below 40 mL/cmH2O. Values lower that 40 mL/cmH2O in
neurological patients have been associated with a high risk of
upper urinary tract complications.
Note: A rule of thumb is that a detrusor pressure of
10 cmH2O or less at expected bladder capacity for age is
acceptable.
5.2.1.3 Maximum Cystometric Capacity
Maximum cystometric capacity is the bladder volume at the

end of bladder filling when patients have a strong desire to
void and can no longer delay micturition. Normal cystometric
capacity varies widely, but is normally between 300 and
500 mL, with lower values in women than in men.
Note: Usually there is a discrepancy in bladder capacity
between voiding diary and urodynamics study since in daily
life the bladder is usually emptied before a strong or even a
“normal” desire to void is felt on cystometry.
5.2.1.4 Detrusor Function
Detrusor function during filling cystometry can be classified in:

(a) Normal, which allows filling with little or no change in
pressure and no involuntary contractions despite provo-
cation (usually cough)
(b) Detrusor overactivity (DO), which is the urodynamic
observation of involuntary detrusor contraction during
bladder filling that may be spontaneous or provoked by
cough, postural changes, or rapid filling
Typically, there are two patterns of DO (Fig. 5.2):
(a) Phasic DO, defined by the presence of fluctuating
waveform, which may or may not lead to urinary
incontinence
DETRUSOR ACTIVITY DURING FILLING CYSTOMETRY

Pressure
cm H20
terminal DO
phasic DO, not necessarely > 5 cmH20
compliance
( slope of the curve @ MCC)
FS FD SD MCC time
Figure 5.2 Patterns of DO
Originally, ICS stated that, in order to diagnose “detru-

sor overactivity,” the contraction should be at least
15 cmH2O. However, it was subsequently realized that
involuntary detrusor contractions of <15 cmH2O could
cause significant symptoms. In practice, there is no stan-
dardized minimum value for detrusor contractions
though it may be difficult to be certain whether an invol-
untary contraction has occurred if the phasic wave is
<5 cmH2O.
( b) Terminal DO, classified as a single involuntary detrusor
contraction occurring at cystometric capacity, which can-
not be suppressed and often results in complete bladder
emptying
Note: The incidence of detrusor overactivity is higher
when the patient is in the sitting position during cystometry,
rather than the supine position.
In summary, during filling phase the bladder should have
constantly low pressure that usually does not reach more than
6–10 cmH2O above baseline at the end of filling (end-filling
pressure), and there should be no involuntary contractions,
with normal first sensation ranging between 100 and 250 mL,
bladder compliance between 30 and 100 mL/cmH2O, and
maximum bladder capacity between 450 and 550 mL (see
Box 5.1).
Box 5.1: Urodynamic Parameters During Filling Phase

in Women
Pdet 6–10 cmH2O
FS 100–250 mL
MCP 450–550 mL
Compliance >40 mL/cmH2O
No involuntary contractions
5.2.2 Leak Point Pressures
During the filling phase are also evaluated the leak point
pressures.
There are currently two types of leak point pressures that
measure different functional areas of the lower urinary tract:
• Detrusor leak point pressure—bladder
• Abdominal leak point pressure—urethra
Detrusor leak point pressure (DLPP) is defined by the ICS
as the lowest Pdet at which urine leakage occurs in the
absence of either detrusor contraction or increased abdomi-
nal pressure. The rise in bladder pressure is secondary to low
bladder compliance. This value reflects resistance that the
urethra offers to the bladder, mainly by the action of the
external sphincter (Fig. 5.3).
In patients with neurogenic bladder, a high DLPP can
threaten upper urinary tract function: a DLPP ≥40 cmH2O is
usually associated with upper tract damage if not treated. The
bladder volume at which detrusor pressure equals 40 cmH2O
is considered the patient’s “safe” bladder capacity.
Abdominal leak point pressure (ALPP) or Valsalva leak
point pressure (VLPP) is intravesical pressure at which urine
leakage occurs because of increased abdominal pressure in
the absence of detrusor contraction. It measures the ability of
the urethra to resist an increase in abdominal pressure. ALPP
is usually tested during cystometry after the bladder has been
DETRUSOR LEAK POINT PRESSURE

100
Leakage
Detrusor pressure
( cm H20)
40
Safe bladder capacity
0 50 100 150 200 Infused bladder volume (ml)
Figure 5.3 Detrusor leak point pressure: the lowest intravesical

pressure at which leakage is noted around the catheter. The bladder
volume at which detrusor pressure equals 40 cmH2O is considered
the maximal “safe” bladder capacity
VALSALVA LEAK POINT PRESSURE
Pressure Valsalva maneuvers

(cm H20)
50
Stop of filling
Q
Leakage @ 48 cm H20
0 200
Infused volume (ml)
Figure 5.4 Leakage occurring during Valsalva maneuver at 200 mL

of filling
filled to at least 150–200 mL. The patient is then asked to do

cough or a Valsalva maneuver until she leaks. VLPP is the
lowest pressure at which incontinence occurs. The procedure
is facilitated by having one person observing for leakage ad
one person observe for pressure since only consistent leak-
ages can be recorded by the flowmeter (Fig. 5.4).
Box 5.2: Leak Point Pressures

• DLPP not suitable in normal females.
• With reduced bladder compliance (lower than
40 mL/cmH2O), a DLPP>40 cmH2O is considered
dangerous for upper urinary tract. Bladder volume
with pressure below 40 cmH2O is considered as “safe
bladder capacity.”
• ALPP not suitable in normal females.
• In incontinent women:
–– ALPP lower than 60 cmH2O indicates an ISD.
–– ALPP greater than 100 cmH2O indicates urethral
hypermobility.
–– Values between 60 and 100 cmH2O are suggestive
of both ISD and hypermobility.
In normal women, no incontinence should be recorded,

whatever the increase in abdominal pressure.
In incontinent women the test correlates with severity of
incontinence and may indicate the presence an intrinsic
sphincteric deficiency (ISD). A value of ALPP greater than
100 cmH2O is usually associated with urethral hypermobility.
A value lower than 60 cmH2O is usually associated with
ISD. Values between 60 and 100 cmH2O are suggestive of
both ISD and hypermobility (see Box 5.2).
5.2.3 Pressure/Flow Study
Voiding phase starts when “permission to void “is given or

when uncontrollable voiding begins and ends when the
patient considers voiding has finished. Voiding is usually
assessed by measuring urine flow rate and voiding pres-
sures. Pressure/flow study or voiding cystometry is the
method by which the relationship between pressure in the
bladder and urine flow rate is measured during bladder
emptying. Pressure/flow study is considered to be the gold

standard for quantifying and grading bladder outlet
obstruction (BOO), and differentiating between BOO and
detrusor underactivity (DU) Pdet at maximum flow and
maximum flow (Qmax) are the most significant parame-
ters. Their values can be plotted on pressure flow nomo-
grams to classify patients as being either obstructed or not
obstructed and, at the same time, grade the severity of
obstruction.
Different types of nomograms have been developed for
male, including ICS nomogram, Abrams–Griffiths nomo-
gram, and Schafer nomogram.
However, since male and female have unique voiding
characteristics, these nomograms do not apply to female.
The only nomogram currently used for the analysis of P/Q
in women is that described by Groutz and Blaivas (Fig. 5.5).
The nomogram consists of four zones, which classify patients
into four categories: zone 0 (normal or no obstruction), zone
1 (mild obstruction), zone 2 (moderate obstruction), and zone
3 (severe obstruction). Two parameters are needed to con-
struct this nomogram: Free Qmax and Pdet.max. Free Qmax
is preferred to Qmax during P/Q because Pdet at Qmax and
Qmax cannot be evaluated if the patient does not void during
the test. The nomogram does not include the assessment of
bladder contractility.
160
140 SEVERE OBSTRUCTION (3)
pdet.max (cmH2O)
120
100
80 MODERATE OBSTRUCTION (2)
60
40 MILD OBSTRUCTION (1)
20 NO OBSTRUCTION (0)
0
0 10 20 30 40 50
Free Qmax (ml/sec)
Figure 5.5 The Groutz and Blaivas nomogram

Box 5.3: Urodynamic Parameters During Voiding Phase in

Women
Voiding by urethral 60%
relaxation
Voiding by abdominal 20%
straining
Voiding by detrusor 20%
contraction
Qmax 13–25 mL/s
Pdet at Qmax 18–30 cmH2O
Pdet max 22–46 cmH2O
VV 250–650 mL
Mild obstruction Pdet max: 10–60 cmH2O/
Qmax<12 mL/s
Moderate obstruction Pdet max: 60–110 cmH2O/
Qmax<12 mL/s
Severe obstruction Pdet max: 110–160 cmH2O/
Qmax<12 mL/s
As mentioned before (Chap. 1), 60% of females void by

pelvic floor relaxation only without any increase in detrusor
pressure, 20% utilizes abdominal straining, and the other
20% void by detrusor contraction like male.
Qmax ranges from 13 to 25 mL/s, Pdet at Qmax ranges
from 18 to 30 cmH2O, Pdet.max ranges from 22 to 46 cmH2O,
and voided volume (VV) ranges between 250 and 650 mL
(see Box 5.3).
Note: The majority of female patients are able to void rela-
tively well provided the catheters are properly fixed.
Nevertheless, investigators should interpret pressure–flow
voiding parameters and the subsequent post-void residual
urine together with the catheter-free voiding parameters,
5.3 Artifacts Identifications and Remedial Actions 71
preferably of multiple flows to avoid misinterpretations due

to the obstructive effects of catheter.
5.3 A
rtifacts Identifications and Remedial
Actions
Minimizing all equipment artifacts and ensuring the quality
of pressure recording makes the trace easier to interpret and
enables clear identification of pathophysiological features.
5.3.1 U
roflowmetry: Knock to the Equipment
(Fig. 5.6)
The knock to the equipment is recognized by a spike of less
than 2 s over the flow curve.
The artifact is less common in female than in male since
female void seated in the commode except in cases of voiding
dysfunction when she may decide to void in semi-seated
position.
Flow
(ml/s)
Time (s)
Figure 5.6 Spike of less than 2 ms over the flow curve due to an
accidental knock to the equipment
5.3.2 Pressure Traces
The most common pressure trace artifacts include:

(a) Poor pressure transmission—(damping of the signal due
to air bubbles in the system) (Fig. 5.7)
Accurate and high-quality pressure transmission is essen-
tial during urodynamic examination. The definition of good
pressure transmission is that changes in intraabdominal pres-
sure should be recorded equally on both Pves and Pabd, with
the result that Pdet is unchanged. In most of the cases, poor
pressure transmission is a consequence of air bubbles in the
system with a damping of the signal.
If pressure spikes are of unequal height, the catheter with
the smaller spike is to be flushed, and the patient is asked to
provide a cough signal again. If the problem persists, the
affected catheter should be checked for problems.
Note: Once the test is underway, cough signal spikes are
used every minute to assess the quality of pressure recording
and to take any necessary corrective steps as problems occur.
Damping due to air bubbles in the line
cough cough
Pves
damping signal restored

Pabd
flushing
Pdet
Figure 5.7 Poor quality signal in Pabd with Pdet negative. Following
flushing of the line, pressure transmission is restored
A lack of regular cough signals and failure to correct a prob-

lem once it has occurred can lead to traces being rejected on
quality base.
(b) Pressure line descent—leakage (Fig. 5.8)
A pressure line descent is usually caused by a leak some-
where between the pressure transducer and patient. It may
occur also when the taps are left open to both the syringe and
the patient. Initially a leak will affect pressure transmission and
may be mistaken for a displaced catheter or air bubble due to
the lack of agreement in the height of cough signal peaks
between Pves and Pabd. The affected tube should be checked
for taps position and leakage, and then it should be flushed to
remove any trapped air and restore transmission of pressure.
(c)
Negative fluctuations of Pdet—rectal contractions
(Fig. 5.9)
Rectal contractions may cause temporary increases in the
Pabd reflecting negatively in Pdet, without any change in
Descending pressure due to leakage in the line
Pves
pressure restored
Pabd
leakage
flushing
Pdet
Figure 5.8 Leakage in Pabd line. Remedial action consists in check-

ing the site of leakage. Then the line should be flushed to remove air
bubbles and restore good quality transmission of pressure
Rectal contractions
Pves
Pabd
Pdet
Figure 5.9 The peaks in Pabd due to rectal contractions cause nega-
tive waves in Pdet
Catheter displacement during voiding
micturition cough cough

loss of pressure
transmission
Pves
Pabd
pressure
transmission
Pdet restored
respositioning &
flushing
Flow
Figure 5.10 Displaced catheter result in poor quality cough signal

in Pves after voiding. After repositioning of the catheter and flush-
ing, good quality pressure transmission is restored
Pves. Sometimes rectal contractions can be mistaken for DO,

as wavelike pressure changes will occur on the Pdet line,
although there is no change in Pves which would occur in DO.
There are no remedial actions, but care should be taken
not to identify such Pdet decreases as DO.
(d) Displaced catheter during voiding (Fig. 5.10)
If a catheter moves down into either the urethral or anal
sphincter region, the resting pressure may increase, usually
Expelled catheter during voiding
Pves
Pabd
Pdet
Flow
Figure 5.11 Sharp drop in Pves and Pdet pressures indicate that

vesical catheter has been expelled during micturition
with reduction in pressure transmission. Catheter movement

is recognized by assessing pressure transmission after voiding.
If there is poor pressure transmission post void, care must be
taken when using the pressure readings recorded during the
void, as their validity may be unreliable.
(e) Expelled catheter (vesical or rectal/vaginal) at void

(Fig. 5.11)
When a catheter is expelled, live signal is lost, and pressure
drops abruptly, usually to an implausible pressure value. The
significance of an expelled catheter depends on whether the
urodynamic question has been answered before the catheter
is expelled.
If the urodynamic question cannot be answered because of
the expelled catheter, a new one should be inserted, the
patient refilled, and the voiding phase repeated.
Note: The reported descriptions are all with reference to
water-filled pressure measurement systems, although some of
these artifacts may occur in other types of recording system
as well.
Figure 5.12 Alternating current (60 Hz) artifact. The noise presents

at exact frequency of 60 Hz, as its name indicates
5.3.3 EMG: 60 Hz artifact (Fig. 5.12)
A 60 Hz or alternating current artifact is the most common

ambient noise during EMG recording. The problem arises
when the impedance of the active electrode becomes inade-
quate. In this situation, the ground becomes an active elec-
trode that, depending on its location, produces the 60 Hz
artifact. Essentially any device (computer, radio, lamp, etc.)
that is plugged into the wall AC (alternating current) outlet
may emit ambient noise.
A 60 Hz frequency from power line may overlay or cancel
the signal being recorded from the muscle.
Remedial action include switching-off any possible source
of interference (power line, phone line, radio waves) and
checking the electrode-to-skin contact including the ground
(poor skin prep, too little conducting gel).
Suggested Readings
Interpretation of Tracings
D’Ancona CA, Gomes MJ, Rosier PF. ICS teaching module: cystom-
etry (basic module). Neurourol Urodyn. 2017;36:1673–6.
Tarcan T, Demirkesen O, Plata M, Castro-Diaz D. ICS teaching mod-
ule: detrusor leak point pressures in patients with relevant neuro-
logical abnormalities. Neurourol Urodyn. 2017;36:259–62.
Rosier PF, Kirschner-Hermanns R, Svihra J, Homma Y, Wein AJ. ICS
teaching module: analysis of voiding, pressure flow analysis (basic
module). Neurourol Urodyn. 2016;35:36–8.
Suggested Readings 77
Mahfouz W, Al Afraa T, Campeau L, Corcos J. Normal urody-

namic parameters in women: part II—invasive urodynamics. Int
Urogynecol J. 2012;23:269–77.
Nager CW, Albo ME, Fitzgerald MP, McDermott S, Wruck L, Kraus
S, et al. Reference urodynamic values for stress incontinent
women. Neurourol Urodyn. 2007;26:333–40.
Craggs MD. Objective measurement of bladder sensation: use of a
new patient-activated device and response to neuromodulation.
BJU Int. 2005;96(Suppl 1):29–36.
Artifacts Recognition
Gammie A, D’Ancona C, Kuo H-C, Rosier P. ICS teaching mod-
ule: Artefacts in urodynamic pressure traces (basic module).
Hogan S, Gammie A, Abrams P. Urodynamic features and artefacts.
Chapter 6
Supplementary Urodynamic
Tests
6.1 Background
In 2016 the ICS Standardisation Steering Committee has
published a report to update the International Continence
Society’s Good Urodynamic Practice 2002 (GUP2002) with
the aim of including new evidence and information on urody-
namic practice and urodynamic quality control and the
revised ICS standard on urodynamic equipment. The ICS-
GUP2016 makes a distinction between the ICS standard
urodynamic test including uroflowmetry and PVR plus trans-
urethral cystometry and pressure-flow study and ICS supple-
mentary urodynamic test including urethral profilometry,
EMG and video. Ambulatory urodynamics monitoring has
not been further discussed in the new report and still refers
to ICS 2000 standards.
6.2 Urethral Profilometry

The urethral pressure profilometry (UPP) is a graph indicat-
ing changes in intraluminal pressure along the length of the
urethra.
UPP quantifies the occlusive pressure generated by active
(smooth and striated muscles) and passive structures (spongy
mucosal layer and fibroelastic connective tissue) and of the

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_6
80 Chapter 6. Supplementary Urodynamic Tests
Structure of middle third of female urethra and urethral pressure profile
fibroelastic coat
smooth muscolar coat
spongy lamina propria coat
epithelial layer
Figure 6.1 Structure of female urethra with superimposed urethral

pressure profile
urethra allowing the evaluation of urethral competence

(Fig. 6.1). Two variations of this measurement are commonly
reported:
• UPP at rest
• UPP under cough with the assessment of pressure trans-
mission ratio
6.2.1 Technical Notes
The three main methods for UPP measurement are:

–– Perfused catheters
–– Microtip catheters
–– Air-filled balloon catheters
The technique of perfused catheters is the most popular
and is mainly based on the description by Brown and
Wickham. The perfusion rate should be 2 mL/min and with-
drawal rate of 1 mm/s for an accurate measurement of closure
pressure. Perfusion rates lower than 2 mL/min usually fail to
record the true urethral pressure unless the withdrawal rate is
extremely slow. Withdrawal rate is irrelevant with the stress
profile since the % PTR is assessed in specific points (usually
6.2 Urethral Profilometry 81
each half centimetre) from the bladder neck to the external

meatus.
Because of the rapid frequency response, microtip cathe-
ters are particularly suitable for recording very rapid changes
in intra-urethral pressure, such as those occurring during
cough.
However, their stiffness may lead to an interaction between
the transducer and the urethral wall resulting in a directional
artefact. The results obtained with the transducer in the lat-
eral orientation (3 or 9 o’clock) compared with the anterior
position seems to be more reliable.
Air-filled catheters (AFCs) have been actively marketed
for the past few years since they seem faster and simpler to set
up than any other technology.
Studies comparing measurement of urethral pressure by
air-filled catheters with measurement by microtip catheters
have indicated that the values obtained are statistically sig-
nificantly different but are more reproducible with the air-
filled systems.
Compared with water-filled catheters, air-filled catheters
act as an overdamped system less sensitive to artefacts but
lower in response. In addition, the air-filled catheters consis-
tently produce higher mean pressure values than the water-
filled catheters. Therefore, the techniques are not
interchangeable, and caution must be used when comparing
urodynamic parameters using air-charged and water-filled
catheters.
6.2.2 UPP at Rest
Parameters recorded in the resting UPP include (Fig. 6.2):

–– Maximum urethral pressure
–– Maximum closure pressure
–– Functional length
Reference values are reported in the Box 6.1.
FEMALE RESTING URETHRAL PRESSURE PROFILE
Pressure
(cm H20) maximum urethral pressure a
maximum
urethral
closing
pressure b
bladder pressure c functional urethral length d
0 1 2 3 4 Distance (cm)
Figure 6.2 Diagram of female resting pressure profile indicating (a)

maximum urethral pressure, (b) maximum urethral closure pressure,
(c) intravesical pressure, (d) functional profile length
Box 6.1: Magnitude of Reference Values of Static UPP

Parameter Value
Maximum urethral pressure (MUP) 50–80 cm H2O
Maximum urethral closing pressure 40–70 cm H2O
(MUCP)
Functional length 3–4 cm
It is well established that in women the UPP changes with

age. MUP, MUCP and the urethral length increase from
infancy to the age of 20–25 years. Thereafter, a gradual
decline in the MUCP of approximately 15% per decade can
be observed (Fig. 6.3).
Both MUP and MUCP are reduced in stress-incontinent
women. However, since the overlap between the values from
continent and incontinent women is substantial, it is impos-
sible to define a cut-off level that allows differentiation
between women with and without stress incontinence.
6.2 Urethral Profilometry 83
MUCP
( cm H20 ) 120
100
80
60
40
20
20 30 40 50 60 70
Age (yrs)
Figure 6.3 MUCP against age group
An MUCP value less than 20 cm H2O is the most popular

single predictor of ISD and has been considered suggestive of
poor outcome of conventional antiincontinence surgery.
An MUCP value greater than 75 cm H2O may be indica-
tive of sphincter overactivity and in presence of an inter-
rupted flow may be suggestive of a dysfunctional voiding.
Several studies have shown considerable test-retest varia-
tion of all urethral pressure. Measurements or parameters
and those normal and pathological values of urethral pres-
sure parameters are largely overlapping.
Due to poor sensitivity and specificity and significant test-
retest variation, urethral profilometry is not recommended as
the only measurement in females with urinary incontinence,
but it should be judged in relation to other urodynamic tests
(i.e. urodynamic stress incontinence, Valsalva leak point pres-
sure) and physical examination.
6.2.3 Stress UPP
Stress UPP measures the rise in intra-abdominal pressure

transmitted to the proximal urethra. In normal women
without urethral hypermobility, increases in intravesical
pressure and proximal urethral pressure should be similar
(Fig. 6.4).
The pressure transmission ratio is a different parame-
ter, recording the increment of urethral pressure under
cough as a percentage of intravesical pressure elevation.
Pressure transmission ratio (% PTR) decreases progres-
sively from the bladder neck to the external meatus. In
normal women, its value should exceed 90% in the proxi-
mal urethra.
Values lower than 90% indicates urethral hypermobility,
but do not necessarily indicate incontinence (Box 6.2).
STRESS URETHRAL PROFILOMETRY

cough
Pves
a 100%
Pura
PTR b
0
Pura-Pves distance (cm)
catheter withdrawn
1 1.5 2 2.5 3 3.5 4 distance (cm)
Figure 6.4 Diagram of female stress urethral pressure profile indi-

cating Pves, Pura and Pura minus Pves under cough (a). Pressure
transmission ratio is calculated as Pura/Pves × 100 along the
functional urethral length divided in quartiles and decreases from
bladder neck to the external meatus (b)
6.3 Electromyography 85
Box 6.2: Urethral Profilometry

–– MUCP unsuitable for diagnosis of SUI
–– MUCP below 20 cm H2O raises the possibility of
ISD
–– MUCP values above 75 cm H2O for women are
considered hypertonic and suggestive of dysfunc-
tional voiding
–– %PTR <90% indicates hypermobility, but not
incontinence
Note: Current urethral function tests are only very mod-

estly suited to further “subcategorize” patients with stress
predominant urinary incontinence for treatment or to judge
the severity of incontinence. There is conflicting evidence
that low urethral closure pressures are associated with poorer
success rates of retropubic and transobturator midurethral
slings. On the other hand, the surgical procedures that are
more “obstructive” (retropubic vs. transobturator slings)
increase the risk of de novo overactive bladder syndrome.
6.3 Electromyography
Sphincter EMG records bioelectric potentials generated dur-
ing muscle depolarization allowing clinicians to completely
evaluate the striated sphincter complex and pelvic floor activ-
ity during bladder filling and voiding.
Clinically, the most important information obtained from
sphincter EMG is coordination or discoordination between the
external urethral sphincter (EUS) and the bladder. Investigation
may be performed with a variety of electrodes including sur-
faces, needle and wire electrodes. Surface electrodes (the most
commonly employed) are placed in the buttock close to the

anus. Needle and wire electrodes are placed lateral to the ure-
thral meatus and advanced parallel to the urethra to a distance
of about 1–2 cm. Unlike surface electrodes, they are positioned
in the muscle of interest, allowing the detection of activity in
individual motor units. In addition, since wire electrodes are
self-retaining, they are preferable when one expect changes in
patient position during the examination.
Normally, EMG activity from the EUS is low at rest. It
intensifies as fluid volume in the bladder grows, during bladder
filling, due to EUS contraction. It is known as the “guarding
reflex”. During voiding, EMG activity disappears completely
for a few seconds before detrusor contraction starts. Once the
bladder is empty, EMG activity resumes. With any increase of
abdominal pressure (cough, straining), there is an increase of
EMG activity proportional to the level of stress (Fig. 6.5).
Clinically, the most important information obtained from
sphincter EMG is coordination or discoordination between
EMG during MICTURITION CYCLE
cough voiding
Pves
EMG
Flow
Figure 6.5 EMG activity during micturition cycle. During bladder

filling, there is a gradual increase in sphincter EMG activity. During
cough there is a reflex contraction of the sphincter to prevent
incontinence. This process is organized by urethral reflexes known
collectively as the “guarding reflex”. During voiding the sphincter
EMG tracing becomes silent
6.4 Videourodynamic 87
Box 6.3: Electromyography

–– EMG activity increases progressively during blad-
der filling.
–– EMG activity increases with any increase of
abdominal pressure (cough, straining).
–– EMG activity is silent during voiding.
–– Persistent EMG activity during voiding is termed
detrusor sphincter dyssynergia in neurologic
patient.
–– Persistent EMG activity during voiding in neuro-
logically normal subjects is termed dysfunctional
voiding.
the external urethral sphincter (EUS) and the bladder.

Failure of the sphincter to relax or stay completely relaxed
during micturition is abnormal. When it occurs in patients
with neurologic disease, it is termed detrusor sphincter dys-
synergia. The term detrusor sphincter dyssynergia cannot be
used in the absence of neurologic disease. In these conditions,
the preferred term is dysfunctional voiding (Box 6.3).
6.4 Videourodynamic
Videourodynamic combines simultaneously anatomical and
functional information (Fig. 6.6). For many years, videouro-
dynamic (VUD) has been considered the gold standard for
the functional evaluation of lower urinary tract.
The importance of VUD is based upon the concept that
synchronous visualization of anatomy of lower urinary tract
and assessment of function may give more accurate diagnoses.
Anatomical observations, during filling phase, include blad-
der neck closure at rest and during stress, its position in rela-
tion to the pubis symphysis, bladder wall morphology and any
diverticula and vesico-ureteral reflux (VUR). During voiding
phase, VUD allows the distinction of bladder neck versus
external sphincter dyssynergia in neurologic patients and
accurate localization of obstruction after mid-urethral sling
Figure 6.6 Videourodynamics. The bladder is filled with a radio-

opaque contrast medium, with the simultaneous measurement of
intravesical pressure and intra-abdominal pressure. The subtracted
detrusor pressure is calculated automatically and flow is recorded
with the flowmeter. Pressure measurements and accompanying
radiographic pictures are mixed together allowing subsequent
review and analysis
insertion. In a broader context, VUD has been advocated in

situations in which UD alone fails to provide sufficient diag-
nostic information to guide therapy, especially in patients
with relevant neurological diseases.
In the recent years, it has become controversial whether
VUD is always necessary for every patient. Most of critical
questions can often be answered by conventional urody-
namics sometime supplemented by a separate voiding cysto-
urethrography (VCUG). The necessity of special equipment
and radiation exposure mean that the benefits should be
weighed against the potential disadvantages. The basic ques-
tion is under what circumstances does the anatomic infor-
mation obtained by video provide either useful or critical
information.
Low-grade evidence supports the use of VUD in the fol-
low-up of the patient with NLUTD and potential hazard to
the upper urinary tract.
Note: “Unsafe bladder “is defined by a filling pressure
greater than 40 cm H2O, compliance lower than 10 mL/cm H2O
and detrusor leak point pressure greater than 40 cm H2O.
According to EAU guidelines, in high-risk patients, the
upper urinary tract should be checked by creatinine and renal
6.5 Ambulatory Urodynamics Monitoring (AUM) 89
ultrasound once every 6 months, and VUD should be recom-

mended if either is abnormal.
There is only low-grade evidence for the added value of
VUD in non-neurogenic LUTS/LUTD.
In women, the use of VUD has been advocated to distin-
guish bladder neck dyssynergia (a quite rare condition) from
dysfunctional voiding since conventional UD with EMG do
not correlate well with visual assessment of urethral opening
characteristics.
In the past VUD was recommended for the assessment of
female SUI (Blaivas SUI classification), but recent data indi-
cate that it has no impact on surgery outcome.
Recurrent SUI in female is probably the only real indica-
tion for VUD.
In recurrent SUI, the assessment of bladder neck and ure-
thral hypermobility is crucial, since secondary procedures have
been associated with reduced cure rates in the presence of lim-
ited urethral mobility and intrinsic sphincter deficiency. VUD
may improve the evaluation of bladder neck and urethral
hypermobility facilitating optimal preoperative counselling.
Finally, radiation exposure during VUD (currently 488
(± 336) cGy × cm2 with an exposure time of 97.5 (± 34) s)
should further be evaluated in order to keep radiation doses
as low as reasonably achievable (ALARA). This might be
achieved by using the newest techniques such as pulsed fluo-
roscopy and image area reduction.
6.5 A
mbulatory Urodynamics Monitoring
(AUM)
Urodynamic investigations may be considered as nonphysio-
logical tests because of several artificial factors, such as pri-
vacy issues and patient embarrassment, catheterization,
supraphysiological filling rates and patients’ immobile posi-
tion during evaluation.
Ambulatory urodynamics monitoring (AUM) is performed
in a similar way to conventional urodynamics but differs in
some specific elements: It uses natural filling of the bladder
(the patients are usually asked to drink extra), and testing lasts
Pabd
Pves
Pdet
detrusor overactivity
Figure 6.7 Downloaded tracing of AUM indicating the presence of

for approximately 2–4 h. Patients are fully dressed after the
initiation of the test and are able to leave the urodynamic
room, which may reduce anxiety and embarrassment.
The investigation is considered as a supplementary urody-
namic test and may be a useful tool to investigate lower urinary
tract dysfunction in patients with inconclusive results on labo-
ratory urodynamic testing. The specific technical demands and
technical reliability of the investigation are well known, but its
clinical sensitivity and specificity are not well established.
In particular, AUM has been showed to be more sensitive
than laboratory urodynamics in diagnosing detrusor overac-
tivity (Fig. 6.7), but the level of evidence for this measure-
ment is low. Furthermore, the fact that AUM shows
abnormalities of bladder function, especially detrusor overac-
tivity, in healthy volunteers may also be considered a sign of
lesser specificity.
Suggested Readings
Urethral Profilometry
Gajewsy J, Rosier P, Rahnama’i S, Abrams P. Do we assess ure-
thral function adequately in LUTD and NLUTD? ICI-RS 2015.
Moe K, Schiøtz HA, Kulseng-Hanssen S. Outcome of TVT opera-

tions in women with low maximum urethral closure pressure.
Klünder M, Sawodny O, Amend B, Ederer M, Kelp A, Sievert KD,
et al. Signal processing in urodynamics: towards high definition
urethral pressure profilometry. Biomed Eng Online. 2016a;15:31.
Klünder M, Amend B, Vaegler M, Kelp A, Feuer R, Sievert KD.
High definition urethral pressure profilometry: evaluating a
novel microtip catheter. Neurourol Urodyn. 2016b;35:888–94.
Burden H, Warren K, Abrams P. Leak point pressures: how useful
are they? Curr Opin Urol. 2015;25:317–22.
Kapoor D, Housami F, White P, Swithinbank L, Drake M. Maximum
urethral closure pressure in women: normative data and evaluation
as a diagnostic test. Int Urogynecol J. 2012;23:1613–8.
Mikhail MS, Rosa H, Palan P, Anderson P. Comparison of preoperative
and postoperative pressure transmission ratio and urethral pressure
profilometry in patients with successful outcome following the vagi-
nal wall patch sling technique. Neurourol Urodyn. 2005;24:31–4.
Trowbridge ER, Wei JT, Fenner DE, Ashton-Miller JA, Delancey JO.
Effects of aging on lower urinary tract and pelvic floor function in
nulliparous women. Obstet Gynecol. 2007;109:715–20.
Lemack GE. Urodynamic assessment of patients with stress incon-
tinence: how effective are urethral pressure profilometry and
abdominal leak point pressures at case selection and predicting
outcome? Curr Opin Urol. 2004;14:307–11.
Khullar V, Cardozo L. The urethra (UPP, MUPP, instability, LPP).
Eur Urol. 1998;34(Suppl 1):20–2.
Electromyography
Krhut J, Zachoval R, Rosier P, Shelly B, Zvara P. ICS Educational
Module Electromyography in the assessment and therapy of
lower urinary tract dysfunction in adults. Neurourol Urodyn.
2017;37(1):27–32.
Kirby AC, Nager CW, Litman HJ, Fitzgerald MP, Kraus S, Norton P,
Sirls L, Rickey L, Wilson T, Dandreo KJ, Shepherd J, Zimmern P;
Urinary Incontinence Treatment Network. Perineal surface elec-
tromyography does not typically demonstrate expected relax-
ation during normal voiding. Neurol Urodyn. 2011;30:1591–6.
Mahajan ST, Fitzgerald MP, Kenton K, Shott S, Brubaker
L. Concentric needle electrodes are superior to perineal
surface-patch electrodes for electromyographic documenta-

tion of urethral sphincter relaxation during voiding. BJU Int.
2006;97:117–20.
Mayo ME. The value of sphincter electromyography in urodynamics.
J Urol. 1979;122:357–60.
Vereecken RL, Derluyn J, Verduyn H. Electromyography of the per-
ineal striated muscles during cystometry. Urol Int. 1975;30:92–8.
Videourodynamic
Peng CH, Chen SF, Kuo HC. Videourodynamic analysis of the ure-
thral sphincter overactivity and the poor relaxing pelvic floor
muscles in women with voiding dysfunction. Neurourol Urodyn.
2017;36(8):2169–75.
Anding R, Rosier P, Smith P, Gammie A, Giarenis I, Rantell A, et al.
When should video be added to conventional urodynamics in
adults and is it justified by the evidence? ICI-RS 2014. Neurourol
Urodyn. 2016;35:324–9.
Giarenis I, Phillips J, Mastoroudes H, Srikrishna S, Robinson D,
Lewis C, Cardozo L. Radiation exposure during videourodynam-
ics in women. Int Urogynecol J. 2013;24:1547–51.
Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in
women. J Urol. 1999;161:1535–40.
AUM
Digesù A, Gargasole C, Hendricken C, Gore M, Kociancic E,
Khulla V, Rosier PF. ICS teaching module: ambulatory urody-
namic monitoring. Neurourol Urodyn. 2017;36:364–7.
Salvatore S, Khullar V, Cardozo L, Anders K, Zocchi G, Soligo M.
Evaluating ambulatory urodynamics: a prospective study in
asymptomatic women. BJOG. 2001;108:107–11.
Radley SC, Rosario DJ, Chapple CR, Farkas AG. Conventional and
ambulatory urodynamic findings in women with symptoms sug-
gestive of bladder overactivity. J Urol. 2001;166:2253–8.
van Waalwijk van Doorn E, Anders K, Khullar V, Kulseng-Hanssen
S, Pesce F, Robertson A, Rosario D, Schafer W. Standardisation of
ambulatory urodynamic monitoring: report of the standardisation
sub-committee of the international continence society for ambula-
tory urodynamic studies. Neurourol Urodyn. 2000;19:113–25.
Chapter 7
UDS in Stress Urinary
Incontinence Syndrome
(SUI-S)
7.1 Background
There remains no clear consensus as to whether urodynamic
testing enhances surgical outcome of stress urinary inconti-
nence treatments by improving case selection or altering the
surgical approach based on study findings. As treatment strat-
egies for stress urinary incontinence have developed over the
last several years to a more uniform approach, it is less clear
that urodynamic testing will influence the choice of surgical
technique.
7.2 Types of Urinary Incontinence in Female

The main types of urinary incontinence (UI) in female are
stress (SUI), urgency (UUI), and mixed urinary incontinence
(MUI). The overall prevalence of UI in female is 19–26%,
increasing with age; this is most apparent for urgency urinary
incontinence (UUI) and mixed urinary incontinence (MUI),
since, interestingly, the prevalence of stress urinary inconti-
nence (SUI) do not seem to increase with age. UI is associ-
ated with a negative impact on a woman’s social, physical, and
psychological well-being, leading to embarrassment, low self-
esteem, and negative effects on the productivity of working
women.

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_7
94 Chapter 7. UDS in Stress Urinary Incontinence
CROSS-SECTION OF FEMALE URETHRA

mucosal lining
lamina propria
smooth muscolar coat
striated muscolar coat
Figure 7.1 Structure of female urethra. The female urethra is com-

posed of four separate tissue layers that keep it closed. The inner
mucosal lining keeps the urothelium moist and the urethra supple.
The vascular spongy coat of lamina propria has an important role in
the mucosal seal mechanism. Compression from the middle smooth
muscular coat, inner longitudinal and outer circular, helps to main-
tain the resting urethral closure mechanism. The outer striated sero-
muscular layer augments, during sudden increase of abdominal
pressure, the closure pressure provided by the smooth muscular
layer
Stress incontinence is defined by ICS as an involuntary

leakage of urine that occurs with increases in intra-abdominal
pressure (e.g., with exertion, sneezing, coughing, laughing) in
the absence of a bladder contraction. Stress incontinence is
the most common type of incontinence in younger women,
with the highest incidence between 45 and 49 years.
Anatomically the female urethra (Fig. 7.1) is a multilay-
ered tube, containing mucosa, smooth and striated muscle,
and vascular and nerve tissue and is integrated with its sur-
roundings, i.e., striated pelvic floor muscles and connective
tissue including the endopelvic fascia. Anatomical abnormali-
ties are relevant in relation to its function.
Mechanisms of stress incontinence include urethral hyper-
mobility and intrinsic sphincteric deficiency (ISD). In most of
the patients, the two mechanisms coexist (Fig. 7.2).
7.2 Types of Urinary Incontinence in Female 95
Figure 7.2 Mechanisms of stress urinary incontinence
Urethral hypermobility originates from an insufficient

support of the urethra and bladder neck by weak pelvic floor
musculature and/or poor vaginal connective tissue.
This causes the urethra and bladder neck to lose the ability to
completely close against the anterior vaginal wall with the
increases in intra-abdominal pressure (e.g., from coughing or
sneezing) leading to incontinence. Insufficient urethral support
may be related to loss of connective tissue and/or muscular
strength due to chronic pressure (i.e., high-impact activity, chronic
cough, or obesity) or trauma due to childbirth, particularly vagi-
nal deliveries. Mid-urethral slings and traditional urethropexies
are aimed at providing a backboard of support for the urethra.
Intrinsic sphincteric deficiency (ISD) is another form of
stress urinary incontinence (SUI) that results from a loss of
urethral tone that normally keeps the urethra closed. This can
occur in the presence or absence of urethral hypermobility
and typically results in severe urinary leakage even with mini-
mal increases in abdominal pressure. In general, ISD results
from neuromuscular damage and can be seen in women who
have had multiple pelvic or incontinence surgeries. In general
it is a challenge to treat women with ISD, since they have
worse surgical outcomes.
A third mechanism, still poorly understood, is that of “ure-

thral instability.” Urethral instability is the urodynamic obser-
vation of urethral pressure variations in patients with
symptoms of LUTD, apart from detrusor overactivity.
Interstitial cells (ICs) in the urethra have, in analogy with
these in the intestine, i.e., the interstitial cells of Cajal (ICC),
been proposed as specialized pacemakers that are involved in
the generation of urethral tone. Failure to maintain sufficient
and continuous urethral muscle contraction may be a specific
pathophysiological entity.
Urgency incontinence is defined by ICS the complaint of
involuntary loss of urine associated with urgency, where
urgency is defined as a sudden, compelling desire to void
which is difficult to defer.
The amount of leakage ranges from a few drops to com-
pletely soaked undergarments. Urgency incontinence is more
common in older women and may be associated with comor-
bid conditions that occur with age. It is believed to result from
detrusor overactivity, leading to uninhibited (involuntary)
detrusor muscle contractions during bladder filling. First line
of treatment includes lifestyle modifications, timed micturi-
tions, pelvic floor muscles exercises, and topical estrogens for
postmenopausal women. Second line of treatment includes
pharmacotherapy with antimuscarinics and mirabegron and
percutaneous tibial nerve stimulation. For refractory cases,
third line of treatment includes botulinum toxin and sacral
neuromodulation.
Mixed urinary incontinence is a condition of both stress
and urgency urinary incontinence, is prevalent in 20–36% of
women, and is challenging to diagnose and treat because uri-
nary symptoms are variable and guidelines for treatment are
not clear. The role of surgery in the treatment of mixed incon-
tinence is controversial because there is thought to be a high
failure rate, related in part to preexisting symptomatic or
asymptomatic DO. However, there is some evidence that
surgery may relieve symptoms of DO, especially if stress
symptoms prevail over urge symptoms. Because high-quality
evidence is lacking regarding the treatment of mixed urinary
7.3 Evaluation of Patients with SUI 97
incontinence, treatment generally begins with conservative

management emphasizing the most bothersome component.
In addition, it has been also hypothesized that transobturator
tapes could be preferred in women with MUI compared to
retropubic tension-free vaginal tapes due to the more hori-
zontal position of the tape and, consequently, less obstructive
mechanism.
7.3 Evaluation of Patients with SUI

Identifying predictors for treatment failure would facilitate
improved counseling for women considering surgery to
manage their SUI and potentially allow surgeons to modify
their approach to improve the outcome for individual
patients.
Unfortunately, a standardized process to evaluate patients
complaining of SUI is currently lacking; however, specialized
societies and health organizations (ICI, AUA/SUFU, EAU,
NICE) have published specific recommendations.
The initial goal of the evaluation is to determine whether
the patient has uncomplicated SUI (index patient) or compli-
cated SUI (non-index patient).
Note: The index patient is that of an otherwise healthy
female with stress urinary incontinence with or without pelvic
organ prolapse.
Uncomplicated SUI (index patient) should include the fol-
lowing features:
• Predominant SUI symptom
• A history without having extensive pelvic or anti-
incontinence surgery
• Absence of POP beyond the hymen
• Confirmation of incontinence under stress (usually cough)
• Urethral hypermobility
• Absence of a UTI
• PVR (≤150 mL)
Conversely complicated SUI (non-index patient) is desig-

nated by:
• Additional storage and voiding symptoms
• Recurrent UTI
• Poorly controlled diabetes mellitus
• Neurological disease affecting the lower urinary tract
• Prolapse beyond the hymen
• Absence of urethral hypermobility (<30° deflection)
• PVR ≥ 150 mL
The two opposing components of the evaluation process
include, on the one hand, a simple office assessment and, on
the other, the invasive urodynamic testing.
7.4 O
ffice Evaluation of Female
Incontinence
Office evaluation should be urodynamically oriented. If the
symptoms and signs are interpreted in the context of func-
tional urodynamic information, then it may be possible to
produce a provisional urodynamic diagnosis, and the follow-
ing invasive investigations may be omitted or used to test the
clinical hypothesis.
According to ACOG and AUGS, basic office evaluation
should include six steps:
• History
• Urinalysis
• Physical examination
• Demonstration of stress incontinence
• Assessment of urethral mobility
• Measurement of post-void residual urine
7.4.1 History
The statement “bladder is an unreliable witness” was made

by Bates in 1970 in one of the early papers on urodynamics.
Despite the shortcomings of the patient’s symptoms on
7.4 Office Evaluation of Female Incontinence 99
Box 7.1: Examples of Validated Urinary Incontinence

Questionnaires
Urogenital Distress Inventory (UDI)
Incontinence Impact Questionnaire (IIQ)
Questionnaire for Urinary Incontinence Diagnosis
(QUID)
Incontinence-Quality of Life Questionnaire (I-QoL)
Incontinence Severity Index (ISI)
International Consultation on Incontinence
Questionnaire (ICIQ)
diagnosis, they are important and should be assessed in a

systematic way, analyzing both filling and voiding phases.
Storage symptoms include frequency, nocturia, and urgency.
Emptying symptoms include hesitancy, slow stream, inter-
mittency, straining to void, position-dependent micturition,
feeling of incomplete emptying, and dysuria.
Views on both symptoms severity and QoL might differ
between patients and clinicians. Thus, it is important to
include reports of QoL and symptom severity directly from
the patient. These reports can be collected in a standardized
manner with validated self-assessment questionnaires (see
Box 7.1).
Patients with uncomplicated SUI will have classic symp-
toms of leakage on effort or physical exertion. In contrast,
inability to reach the toilet that is associated with urgency
indicates the presence of urge UI.
7.4.2 Urinalysis
Urinary tract infections should be identified and treated

before initiating further investigation or therapeutic inter-
vention for UI. A urine dipstick assessment should be per-
formed to exclude a UTI and a specimen sent for microscopy
and culture if abnormal. If the urinalysis result is negative, the
patient’s condition is still consistent with uncomplicated SUI.
7.4.3 Physical Examination
Physical examination should include abdominal, vaginal, and

neuro-urologic assessment (see Chap. 2) and, specifically, in
incontinent female should include the demonstration of
stress incontinence and the assessment of urethral
hypermobility.
7.4.4 Demonstration of Stress Incontinence
Visualization of fluid loss from the urethra simultaneous with

a cough is diagnostic of SUI. Conversely, delayed fluid loss
suggests a cough-induced detrusor overactivity.
The cough stress test can be performed with the patient in
the supine position during the physical examination. However,
if urine leakage is not observed, the cough stress test needs to
be repeated with the patient standing and with a full bladder
to maximize test sensitivity.
Note: To perform the cough stress test in the standing posi-
tion, the patient stands near the examination table with 1 ft
on the table step, whereas the examiner keeps the labia sepa-
rated to observe the urethral meatus. If the stress test results
negative despite the patient symptoms of SUI, then multi-
channel UDS is recommended.
7.4.5 Assessment of Urethral Mobility
Anti-incontinence surgery is more successful in women with

urethral hypermobility, defined as a 30° or greater displace-
ment from the horizontal plane when the patient is straining
in a supine lithotomy position. Lack of urethral hypermobil-
ity is associated with an increase in the failure rate of mid-
urethral sling. Patients who lack urethral hypermobility may
be better candidates for urethral bulking agents or retropubic
7.4 Office Evaluation of Female Incontinence 101
Q- TIP test
cough or straining
pubis
bladder
> 30º cotton swab

horizontal line
URETHRAL HYPERMOBILITY
Figure 7.3 Q-tip test determines the descent of the normal urethro-
vesical junction contributing to stress incontinence in women. More
than 30-degree increase during exertional activities (cough, Valsalva)
indicates a hypermobile urethrovesical junction
tape (more obstructive) rather than a transobturator tape

(less obstructive).
Q-tip test with cotton swab has been the traditional assess-
ment of urethral mobility (Fig. 7.3).
Bladder neck descent can be also determined by measur-
ing the vertical distance between infero-posterior margin of
the symphysis pubis and the bladder neck, at rest, and maxi-
mal Valsalva maneuver via perineal ultrasound.
7.4.6 Post-void Residual Urine (PVR)
The presence of a post-void residual urine greater than

150 mL can indicate a bladder-emptying abnormality or
incontinence associated with chronic urinary retention (pre-
viously referred to as overflow incontinence). An elevated
post-void residual urine volume in the absence of POP is
uncommon and should lead an evaluation of the bladder-
emptying mechanism, usually with a pressure-flow study.
Note: Basic office evaluation may be implemented by

some supplementary test for a better assessment of the
patient. These include voiding diary, pad test, and, when avail-
able, uroflowmetry.
7.5 Invasive Urodynamic Testing

The aim of invasive urodynamic testing, apart from confirm-
ing SUI, is to differentiate between types of incontinence so
that the most effective method of treatment can be selected.
To do that, detrusor function is assessed during filling and
voiding phases, and intrinsic urethral function is evaluated
during filling phase (see Box 7.2).
7.5.1 Confirm SUI
Traditionally, cystometry with cough tests at representative

volumes (150 mL) has been the core test for the urodynamic
diagnosis of SUI. Urodynamic stress incontinence is the
involuntary leakage of urine during increased abdominal
pressure in the absence of a detrusor contraction (Fig. 7.4).
7.5.2 Assess Detrusor Activity During Filling
Given that patients undergoing stress incontinence surgery

expect not only the resolution of urine leakage but also
urgency and frequency symptoms and given that these symp-
toms are among those that baseline predict postsurgery
Box 7.2: Goals of UDS in SUI

• Confirm SUI
• Assess detrusor activity during filling
• Assess detrusor contractility during voiding
• Assess intrinsic urethral function
7.5 Invasive Urodynamic Testing 103
URODYNAMIC STRESS INCONTINENCE
Pves
Pabd
Pdet
leakage
Flow
Figure 7.4 Urodynamic stress incontinence. Involuntary leakage of

urine during increased abdominal pressure in the absence of a
detrusor contraction. The patient is usually asked to give sets of
strong coughs, and leakage can be assessed by inspection of urethral
meatus or recorded through the flowmeter
issatisfaction, the assessment of detrusor activity may be

d
extremely useful.
7.5.3 A
ssess Detrusor Contractility During
Voiding
Unlike OAB, underactive bladder in women is a novel con-
cept, and detrusor underactivity is a difficult to define urody-
namic finding (see Chap. 9).
7.5.4 Assess Intrinsic Urethral Function

Since combined hypermobility and ISD occurs in the vast
majority of incontinent patients, the challenge is to determine
the position of a given patient within the spectrum since it may
influence the treatment outcome. ISD is commonly associated
with more severe symptoms and often is associated with failed
previous surgery. In addition to clinical features, most studies
base the diagnosis of ISD upon urodynamic appearances using
recognized criteria like Valsalva leak point pressure <60 cm

H2O or a maximum urethral closure p ressure <20 cm H2O).
However, the uncertainty over this categorization is recog-
nized by the ICS, which has called for further research in this
area. Ranges of surgical treatments, from bulking agents to
artificial sphincter, can be used in ISD. A general agreement
exists that retropubic slings are more efficacious than transob-
turator slings. It is acknowledge, however, a need for larger
randomized trials, investigating the role of urethral function
parameters with relation to effective surgical management of
incontinence before reaching definitive conclusions.
7.6 The Debate

The role of urodynamic testing prior to surgery of stress uri-
nary incontinence is under constant debate.
There is lack of universal consensus regarding its value.
Whereas some studies support using it, others have failed to
demonstrate its routine utility. Detrusor overactivity is the
mostly emphasized aspect, but also ISD and detrusor under-
activity may play a significant role.
7.6.1 The Case Against
• NICE guidelines (2006)

UDS in women with “pure SUI” is no longer recom-
mended. UDS is indicated only in women with urinary
incontinence when there is a clinical suspicion of DO or in
patients who have undergone surgery for SUI or anterior
compartment prolapse or in women with symptoms sug-
gestive of voiding dysfunction.
• ValUE (Value of Urodynamic Evaluation) trial (2009)
A multicentric US study purely focused on UDS. Women
meeting criteria for an anti-incontinence procedure were ran-
domized to preoperative UDS or a simple office-based evalu-
ation. One of the outcomes was to determine if preoperative
UDS findings in women with stress predominant incontinence
7.6 The Debate 105
would affect surgical outcome, with secondary outcomes

being cost and utility of performing UDS. At 12 months, no
significant difference was seen between the urodynamic test-
ing group and the evaluation-only group with respect to treat-
ment success (76.9% and 77.2%, respectively). The report
concluded that UDS did not improve the rate of treatment
success and was not necessary in place of a well-performed
office-based evaluation (including demonstration of SUI) in
women with uncomplicated SUI.
Note: The ValUE trial found that urodynamic studies
rarely changed the primary diagnosis of SUI (<1%) but fre-
quently changed the listing of secondary diagnoses of OAB-
wet, OAB-dry, voiding dysfunction, or suspected intrinsic
sphincter deficiency in over half of women undergoing
UDS. Surprisingly, however, these changes of secondary diag-
noses rarely changed treatment plans, and therefore, no treat-
ment benefit was realized by the additional UDS.
• TOMUS (Trial Of Mid-Urethral Slings) trial, 2010 (ISD
do not influence the outcome of sling surgery)
Preoperative UDS was performed before randomization
into a retropubic mid-urethral sling (RMUS) or a transobtu-
rator mid-urethral sling (TMUS) and repeated at 12 months
post-surgery. Patients and surgeons were blinded to the find-
ings of the preoperative UDS so that they would not be influ-
enced in their treatment decision. The study supported the
fact that VLPP did not impact surgical outcome.
• VUSIS (Value of Urodynamics prior to Stress Incontinence
Surgery) I and II (different recruitment process) trials (2013)
This multicentric Dutch RCT was examining the role of UDS
in women with symptoms of SUI who had UDS findings discor-
dant from history and physical findings and where then random-
ized to receive either mid-urethral sling or “individual treatment.”
Individual treatment can include pessary, medical treatment,
physiotherapy, or surgery at the discretion of the provider.
Despite the relatively small number of patients (the trial
was stopped prematurely because of slow recruitment.), the
omission of urodynamics was not inferior to the use of urody-
namics in the preoperative workup of women with SUI. Women
with SUI undergoing urodynamics had the risk of a choice for

more prudent treatment (other than surgery), which seemed to
result in a delay until effective treatment (surgery).
Note: Both ValUE and VUSIS I and II trials are non-
inferiority designed trials. A non-inferiority trial is a clinical
trial whose objective is to establish a new approach/treatment
that is not clinically worse than the active comparison approach/
treatment by more than a small predetermined margin.
Example: if office evaluation of SUI cost 200 Euro and UDS
testing 600 Euro and the difference between them is clinically
negligible, then my patient can use the less expensive alternative.
7.6.2 The Case Pros
• Hermieu from the Association Francaise d’Urologie (2007)

In the presence of pure stress urinary incontinence with no
other associated clinical symptoms, a complete urodynamic
assessment is not mandatory but can be helpful to define the
prognosis and inform the patient about her vesicosphincteric
function. On the other hand, a complete urodynamic assess-
ment is recommended to investigate complex or complicated
urinary incontinence.
• Agur et al. (2009)
Only a very small proportion of patients (5.2%) referred with
urinary incontinence could be diagnosed as “uncomplicated
stress-predominant urinary incontinence” on the basis of symp-
toms and the sign of urinary loss during stress testing. Furthermore
26.1% of women with a “clearly defined clinical diagnosis” of
pure SUI may have important alternative/associated diagnoses
that could affect the outcome of surgery for UI. Clinical criteria
do not ensure that all women with potentially important urody-
namic findings are evaluated appropriately.
• Digesù et al. (2009)

Even patients with a history of “uncomplicated” SUI may
take advantage from urodynamics since as many as 20% of
7.6 The Debate 107
them might not need surgery as the first line of treatment due
to presence of DO and voiding dysfunction.
• Guerrette and Davila (2008)
Mid-urethral sling (Monarch) should be used with caution
in women with impaired urethral function.
The maximum urethral closure pressure (MUCP) had a
median of 20 cm H2O in the failures and 45 cm H2O in the
successful patients (p > 0.001).
The median VLPP at cystometric capacity (VLPPcap) in
the failures was 32 cm H2O compared to 71 cm H2O in the
successes (p > 0.001).
• Serati et al. (2013)
UDS is able to show that several patients (approx. 20%)
with symptoms of pure SUI present an underlying DO and
do not require surgery, even 1 year after UDS. In these
patients, antimuscarinic treatment appears to ensure a good
rate of cure; thus, UDS could lead to the avoidance of several
surgical procedures.
• Finazzi-Agrò et al. from the Società Italiana di Urodinamica
(2013)
“Uncomplicated” patients represent a minority of patients
evaluated before surgery for female SUI. According to the
data of six referral centers in Italy, the role of urodynamics in
female incontinence has not been challenged yet, and the
investigation seems still mandatory.
7.6.3 The Future
• INVESTIGATE-I (INVasive Evaluation before Surgical

Treatment of Incontinence Gives Added Therapeutic
Effect?)
A mixed-methods study comprising a pragmatic multi-
center randomized pilot trial, economic evaluation, survey of
clinicians’ views about invasive urodynamic testing, and
qualitative interviews with clinicians and trial participants.
The study should be a definitive randomized controlled

trial of invasive urodynamic testing compared with basic clini-
cal assessment and noninvasive testing in women potentially
suitable for surgical treatment for urinary incontinence.
Key Notes for Clinical Practice

• Patients with stress urinary incontinence desiring to
undergo surgical treatment should be divided in:
Index patient Non-index patient
(uncomplicated SUI) (complicated SUI)
History of SUI or MUI Urgency-predominant SUI
with prevalent SUI
Objective demonstration of Inability to demonstrate SUI
SUI with full bladder
Absent post-void residual Elevated post-void residual
urine urine
Negative urinalysis Positive urinalysis or
hematuria
POP-Q stage 3 or higher
Failure of prior surgery
Known or suspected NLUTD
• Physicians may omit urodynamics testing for the

index patient.
• Physicians should perform urodynamic testing for
the non-index patient.
• Despite urodynamic findings, physicians should
counsel the patients on potential complications of
surgery.
(Modified from Kobashi K, Albo M, Dmochowsky R,
Ginsberg DA, Goldman HB, Gomelsky A, et al. Surgical
treatment of female stress urinary incontinence. AUA/
SUFU Guidelines, 2017)
Note: Despite the clear indications of the guidelines, a

recent survey reported the 51% of urogynecologsts would
perform UDS before surgical correction of uncomplicated
SUI, while 79% would perform UDS only if no urine leakage
can be demonstrated on physical examination. Furthermore,
87% of clinicians would perform UDS before surgical correc-
tion of SUI in patients with mixed urinary incontinence.
Prior to surgical repair of POP, 27% of urogynecologists
would only perform a physical examination to rule out SUI,
while 34% would perform UDS as well.
Suggested Readings
Overviews
Serati M, Ghezzi F. The epidemiology of urinary incontinence: a case
still open. Ann Transl Med. 2016;4:123.
Hannestad YS, Rortveit G, Sandvik H, Hunskaar S. A community-
based epidemiological survey of female urinary incontinence: the
Norwegian EPINCONT study. Epidemiology of incontinence in
the County of Nord-Trøndelag. J Clin Epidemiol. 2000;53:1150–7.
Ebbesen MH, Hunskaar S, Rortveit G, Hannestad YS. Prevalence,
incidence and remission of urinary incontinence in women: lon-
gitudinal data from the Norwegian HUNT study (EPINCONT).
BMC Urol. 2013;13:27.
McGuire EJ. Urodynamic findings in patients after failure of stress
incontinence operations. Prog Clin Biol Res. 1981;78:351–60.
Chaikin DC, Rosenthal J, Blaivas JG. Pubovaginal fascial sling for
all types of stress urinary incontinence: long-term analysis. J Urol.
1998;160:1312–6.
Ghoniem G, Hammett J. Female pelvic medicine and reconstructive
surgery practice patterns: IUGA member survey. Int Urogyn J.
2015;26(10):1489–94.
Park K, Kim S, Huh J-S, Kim Y-J. A study of clinical predictors asso-
ciated with intrinsic sphincter deficiency in women with stress
urinary incontinence. Int Neurourol J. 2017;21:139–42.
Kirschner-Hermanns R, Anding R, Rosier P, Birder L, Andersson

KE, Djurhuus JC. Fundamentals and clinical perspective of ure-
thral sphincter instability as a contributing factor in patients
with lower urinary tract dysfunction—ICI-RS 2014. Neurourol
Urodyn. 2016;35:318–23.
Komesu YM, Schrader RM, Ketai LH, Rogers RG, Dunivan GC.
Epidemiology of mixed, stress, and urgency urinary incontinence
in middle-aged/older women: the importance of incontinence his-
tory. Int Urogynecol J. 2016;27:763–72.
Malek JM, Ellington DR, Jauk V, Szychowski JM, Parden AM,
Richter HE. The effect of age on stress and urgency urinary
incontinence outcomes in women undergoing primary midure-
thral sling. Int Urogynecol J. 2015;26:831–5.
Myers DL. Female mixed urinary incontinence: a clinical review.
JAMA. 2014;311:2007–14.
The Debate: Cons

NICE. National Institute for Health and Care Excellence Urinary
incontinence: the management of urinary incontinence in women.
NICE clinical guideline, vol 40. London: National Institute for
Health and Care Excellence; 2006. p. 1–36.
Nager CW, Brubaker L, Daneshgari F, Litman HG, Dandreo KJ,
Sirls L, et al. Design of the value of urodynamic evaluation
(ValUE) trial: a non-inferiority randomized trial of preoperative
urodynamic investigations. Contemp Clin Trials. 2009;30:531–9.
Nager CW, Brubaker L, Litman HJ, Zyczynski HM, Varner RE,
Amundsen C, et al. A randomized trial of urodynamic testing
before stres sincontinence surgery. N Engl J Med. 2012;366:1987–97.
Richter H, Albo M, Zyczynsky H, Kenton K, Norton PA, Sirls LT,
et al. Retropubic versus transobturator midurethral slings for
stress incontinence. New Engl J Med. 2010;362:2066–76.
Rachaneni S, Latthe P. Does preoperative urodynamics improve
outcomes for women undergoing surgery for stress urinary
incontinence? A systematic review and meta-analysis. BJOG.
2015a;122:8–16.
Clement KD, Lapitan MC, Omar MI, Glazener CM. Urodynamic
studies for management of urinary incontinence in children and
adults. Cochrane Database Syst Rev. 2013;29:CD003195.
Glazener CM, Lapitan MC. Urodynamic investigations for manage-
ment of urinary incontinence in adults. Cochrane Database Syst
Rev. 2002;3:CD003195.
van Leijsen SA, Kluivers KB, Mol BW, Broekhuis SR, Milani AL,
Bongers MY, et al. Can preoperative urodynamic investiga-
tion be omitted in women with stress urinary incontinence? A
non-inferiority randomized controlled trial. Neurourol Urodyn.
2012;31:1118–23.
van Leijsen SA, Kluivers KB, Mol BW, Hout Ji, Milani AL, Roovers
JP, et al. Value of urodynamics before stress urinary inconti-
nence surgery: a randomized controlled trial. Obstet Gynecol.
2013;121:999–1008.
van Leijsen SA, Mengerink BB, Kluivers KB. Urodynamics before
stress urinary incontinence surgery. Curr Opin Obstet Gynecol.
2014;26:398–403.
Zimmern P, Litman H, Nager C, Sirls L, Kraus SR, Kenton K, et al.
Pre-operative urodynamics in women with stress urinary inconti-
nence increases physician confidence, but does not improve out-
comes. Neurourol Urodyn. 2014;33:302–6.
Rachaneni S, Latthe P. Does preoperative urodynamics improve
outcomes for women undergoing surgery for stress urinary
incontinence? A systematic review and meta-analysis. BJOG.
2015b;122:8–16.
Norton P, Nager C, Brubaker L, Lemack GE, Sirls LT, Holley R, et al.
The cost of preoperative urodynamics: a secondary analysis of the
ValUE trial. Neurourol Urodyn. 2016;35:81–4.
Suneetha R, Pallavi L. Urodynamics before surgery for stress uri-
nary incontinence. Eur Urol Focus. 2016;2:275–6.
Medina C, Costantini E, Petri E, Mourad S, Singla A, Rodriguez-
Colorado S, et al. Evaluation and surgery for stress urinary
incontinence: a FIGO working group report. Neurourol Urodyn.
2017;36:518–28.
The Debate: Pro

Hermieu JF, Comitéd’Urologie et de Pelvi-périnéologie de la
Femme Association Francaise d’Urologie. Recommendations
for the urodynamic examination in the investigation of non-
neurological female urinary incontinence. Prog Urol. 2007;17(6
Suppl 2):1264–84.
Agur W, Housami F, Drake M, Abrams P. Could the National Institute
for Health and Clinical Excellence guidelines on urodynamics in
urinary incontinence put some women at risk of a bad outcome
from stress incontinence surgery? BJU Int. 2009;103:635–9.
Digesu GA, Hendricken C, Fernando R, Khullar V. Do women with

pure stress urinary incontinence need urodynamics? Urology.
2009;74:278–81.
Guerrette N, Davila B. Transobturator slings for stress inconti-
nence: using urodynamic parameters to predict outcomes. Int
Urogynecol J. 2008;19:97–102.
Serati M, Cattoni E, Siesto G, Braga A, Sorice P, Cantaluppi S, et al.
Urodynamic evaluation: can it prevent the need for surgical
intervention in women with apparent pure stress urinary inconti-
nence? BJU Int. 2013;112:E344–50.
Dillon BE, Zimmern PE. When are urodynamics indicated in patients
with stress urinary incontinence? Curr Urol Rep. 2012;13:379–84.
Giarenis I, Cardozo L. What is the value of urodynamic studies
before stress incontinence surgery? BJOG. 2013;120:130–2.
Finazzi-Agrò E, Serati M, Salvatore S, Del Popolo G. Comments
on “A randomized trial of urodynamic testing before stress-
incontinence surgery” (N Engl J Med. 2012 May 24;366(21):1987-
1997) From the Italian Society of Urodynamics. Neurourol
Urodyn. 2013;32:301–2.
Topazio L, Frey J, Iacovelli V, Perugia C, Vespasiani G, Finazzi-Agrò
E. Prevalence of “complicated” stress urinary incontinence in
female patients: can urodynamics provide more information in
such patients? Int Urogynecol J. 2015;26:1333–9.
Serati M, Finazzi-Agrò M. Urodynamics before surgery for stress
urinary incontinence: the urodynamic examination is still one of
the best friends of the surgeon and of patients with stress urinary
incontinence. Eur Urol Focus. 2016;2:271–3.
Serati M, Topazio L, Bogani G, Costantini E, Pietropaolo A,
Palleschi G, et al. Urodynamics useless before surgery for female
stress urinary incontinence: are you sure? Results from a multi-
center single nation database. Neurourol Urodyn. 2016;35:809–12.
Future Research
Hilton P, Armstrong N, Brennand C, Howel D, Shen J, Bryant A, et al.
A mixed methods study to assess the feasibility of a randomised
controlled trial of invasive urodynamic testing versus clinical
assessment and non-invasive tests prior to surgery for stress uri-
nary incontinence in women: the INVESTIGATE-I study. Trials.
2015;16:400.
Chapter 8
UDS in Pelvic Organ
Prolapse Syndrome (POP-S)
8.1 Background
Pelvic organ prolapse (POP) is the herniation of the pelvic
organs to or beyond the vaginal walls. It is an age-dependent
problem which has been reported to affect 50% of the parous
women causing a variety of pelvic, urinary, bowel, and sexual
symptoms. Up to 20% of women will require at least one
surgery for correction of POP in their lifetime, with an esti-
mated 30% reoperation rate.
POP is categorized according to the affected
compartment:
• Anterior (cystocele)
• Posterior (rectocele)
• Apical (descent of the uterus or bowel—enterocele—
following hysterectomy)
The presence of associated symptoms is very important
since treatment of urinary or fecal symptoms is typically
coordinated with treatment for POP. Asymptomatic POP
may not require treatment.
Note: Women may not be aware of a vaginal prolapse
until it reaches the hymen. It follows that many women can
be categorized as having prolapse on physical examination,
although they do not manifest any symptoms consistent with

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_8
114 Chapter 8. UDS in Pelvic Organ Prolapse Syndrome
prolapse. Terms such as “subclinical” or “preclinical” pro-

lapse have been suggested, in order to distinguish asymp-
tomatic women from those with symptoms of prolapse. It is
not known whether women with subclinical prolapse are at
higher risk for the development of clinically evident pro-
lapse. However, there are no data that supports intervention
to promote prevention of possible future pelvic floor
disorders.
8.2 Classification of Pelvic Organ Prolapse

The large number of different grading systems that have
been used is reflective of the difficulty in designing an
objective, reproducible system of grading prolapse. Intra-
and interobserver variability is often important and may
lead to confusion. This makes it difficult to compare succes-
sive examinations over time in the same woman or between
different women.
Evaluation for POP can be done using one of several
clinical quantification systems. The Baden Walker classifica-
tion (1971) was one of the first classification systems used.
The POP-Q system introduced in 1996 has become the
internationally accepted standard for reporting POP in
research today. POP-Q system includes nine measurements
taken in centimeters from fixed points. The six points are
measured to evaluate anterior, posterior, and apical descent
of pelvic organs in relation to a fixed point of reference—
the hymen—at maximum Valsalva. Additionally, measure-
ments were taken of the genital hiatus, perineal body, and
total vaginal length. The POP-Q system has not been widely
adopted in clinical practice particularly by non-urogynecol-
ogist, owing somewhat to difficulty in learning the assess-
ment. Because of the complexity of the POP-Q, a more
simplified version (S-POP-Q) has been developed by Swift
in 2002 and subsequently adopted by the IUGA. Because of
its simplicity, the S-POP-Q system is now recommended for
routine clinical practice over the more complex standard
POP-Q system.
8.2 Classification of Pelvic Organ Prolapse 115
8.2.1 S-POP-Q: Practical Tips
For the S-POP-Q, the four areas examined include the ante-
rior and posterior vaginal walls, the apex, and the cervix
(Fig. 8.1). If the patient underwent hysterectomy, then only
three measurements are taken: the anterior and posterior
vaginal walls and the cuff. No measuring devices are required
for the S-POP-Q, and the investigators have to use rough
estimation for identifying those points on the anterior and
posterior vaginal segments that are used to represent the
respective walls. For examination of the anterior vaginal seg-
ment, the speculum is placed into the vagina, and the poste-
rior vaginal wall is retracted to allow for full visualization of
the anterior vaginal wall. A point approximately halfway up
the anterior vaginal wall or approximately 3 cm proximal to
the urethral meatus or hymenal plane is identified. The
Figure 8.1 S-POP-Q landmarks and relationship between measure-

ments and POP stage
subject is then instructed to Valsalva or cough in a forceful

fashion and where that point descend in relation to the
hymenal plane is recorded as the suitable stage of the anterior
vaginal wall. The posterior segment is examined in a similar
fashion. The cervix is evaluated by placing a Sims speculum in
the vagina and directly observing its descent during a Valsalva
or cough to determine its stage in relation to the hymenal plane.
The staging system for each segment is:
• Stage 1: Prolapse where the given point remains at least
1 cm above of the hymenal remnants.
• Stage 2: Prolapse where the given point descends to the
introitus, defined as an area extending from 1 cm above to
1 cm below the hymenal remnants.
• Stage 3: Prolapse where the given point descends greater
than 1 cm past the hymenal remnants, but does not repre-
sent complete vaginal vault eversion or complete proci-
dentia uteri. This implies that at least some portion of the
vaginal mucosa is not everted.
• Stage 4: Complete vaginal vault eversion or complete
procidentia uteri. This implies that the vagina and/or
uterus is maximally prolapsed with essentially the entire
extent of the vaginal mucosa everted.
Note: With the introduction of MRI, prolapse description
uses a nomenclature based on a different axis to clinical exami-
nation (i.e., sagittal section). The discrepancy between MRI and
POP-Q is significant. However, the concept of the H and M
lines, while measureable and reproducible, has not demon-
strated any advantage over clinical examination. Until we have
a clinically relevant staging system, attempting to correlate
radiologic findings with clinical findings will prove problematic.
8.3 T
he Role of Urodynamics Before
Prolapse Surgery
The role of urodynamic testing before prolapse surgery is
contentious and a hotly debated topic in urogynecology.
8.4 POP and SUI Syndrome 117
Prolapse surgery has to deal with three main functional

problems:
• SUI syndrome
• OAB syndrome
• Voiding dysfunction syndrome
• POP and SUI Syndrome
8.4 POP and SUI Syndrome

Urogynecologists are often challenged by the persistence or
the de novo development of stress urinary incontinence fol-
lowing POP repair.
About 40% of all patients with genital prolapse report
stress incontinence. In about half of the 60% patients that do
not report stress incontinence, occult urinary stress inconti-
nence can be detected. In these patients, stress incontinence
is masked due to kinking or compression of the urethra by
the prolapse (see Box 8.1).
Box 8.1: Incidence of POP and SUI

60% of pts with POP are continent.
40% of pts with POP complain SUI.
20% of continent pts with POP have “occult SUI.”
Note: “Occult SUI” is an incontinence observed
only after the reduction of a coexistent prolapse.
The combination of prolapse surgery with an anti-

incontinence procedure is frequently considered as a suitable
option to overcome the problem. In particular, three groups
of patients can be considered:
• Women with coexisting SUI
• Women asymptomatic for SUI
• Women asymptomatic for SUI with occult SUI
The advantage of combining prolapse and stress incon-

tinence surgery is that only few patients report stress
incontinence following such combination. However, this
combination has been associated with an increased risk on
complications, of which the development of obstructive
micturition symptoms, overactive bladder symptoms, and
bladder retention are the most important ones. Furthermore,
combining two procedures may be unnecessary as per-
forming only prolapse surgery may cure stress inconti-
nence. Thus, the relative benefit of adding an
anti-incontinence procedure as a primary option requires
evaluation.
To date, there are three main approaches to this issue:
• Perform an incontinence procedure in all patients under-
going POP surgery.
• Perform an incontinence procedure in no patients under-
going POP surgery.
• Perform an incontinence procedure in some patients
undergoing POP surgery (namely, those with symptoms of
SUI or those with demonstrable SUI on stress testing or
those with occult SUI on stress testing after prolapse
reduction).
Note: Currently, there are two main methods to repair
POP:
• Vaginally through fascial repair or MESH reinforcement
• Abdominally with sacrocolpopexy (open, laparoscopic,
and robotic)
Likewise, in the treatment of SUI, there are two proce-
dures considered to be gold standard because of similar cure
rates:
• Vaginally with the introduction of a midurethral sling
(MUS)
• Abdominally with a Burch colposuspension
When combination surgery is performed vaginally, repair
is often combined with a MUS, whereas sacrocolpopexy is
more likely to be combined with a Burch colposuspension.
8.4 POP and SUI Syndrome 119
8.4.1 Incontinence Surgery in all Patients
Evidence to support this approach come from:

• CARE trial. Women undergoing abdominal sacrocolpo-
pexy who did not have any significant symptoms of SUI
(answers of never or rarely to the SUI questions on the
MESA questionnaire) were randomized to either a Burch
suspension or no Burch suspension (the control).
Postoperatively significantly more women in the no Burch
group developed bothersome SUI than in the Burch group
(24.5% vs. 6.1%). No significant postoperative difference
in the frequency of urge incontinence was observed.
• OPUS trial. Women without stress urinary incontinence
undergoing vaginal surgery for pelvic organ prolapse (stage
2 or higher) were randomly assigned to receive either a
midurethral sling or sham incisions during surgery. At
12 months, urinary incontinence (allowing for subsequent
treatment of incontinence) was present in 27.3% and 43.0%
of patients in the sling and sham groups. Adverse events
including urinary tract infection (31% vs. 18.3%) and incom-
plete bladder emptying 6 weeks after surgery (3.7% vs. 0%)
were higher in the sling group than in the sham group.
• CUPIDO 1 (women with incontinence) and 2 (women with
occult SUI) trials. Women were randomly assigned to
undergo vaginal prolapse repair with or without
MUS. Women with POP and coexisting SUI are less likely
to have UI after vaginal prolapse repair with MUS com-
pared with prolapse repair only and are less likely to
undergo additional treatment for SUI.
8.4.2 Incontinence Surgery in No Patients
At the opposite end of the spectrum, there is the strategy to not

perform an incontinence surgery in patients undergoing POP
repair whether or not they have symptoms or signs of SUI pre-
operatively. Patients with bothersome SUI postoperatively will
be candidate for an antincontinence procedure. The clear advan-

tage of this approach is that no patient who does not have SUI
postoperatively will have had an unnecessary antincontinence
procedure. The disadvantage of course is that many patients will
have SUI postoperatively and require secondary surgery.
Evidence to support this approach comes from the obser-
vation that 45% of the patients, even with clinical SUI, have
resolution of SUI after POP surgery alone. The disadvantages
with this approach include the fact that many women—
apparently greater than 50%—will require a second supple-
mentary surgery. The situation could be particularly stressful
in patients who have an occult SUI for which the manage-
ment of an “unknown” incontinence, while waiting the second
intervention, may be significantly disappointing.
8.4.3 I ncontinence Surgery in Some Patients

(namely, Patients with Coexisting
and Occult SUI-S)
This selective approach is used by the majority of clinicians.
According to AUA SUI-S Guidelines, “few would disagree
that operations for SUI should be confined to those patients
who actually have demonstrable SUI including occult SUI
demonstrable only after reduction of pelvic organ prolapse.”
The advantage of this approach is that very few patients
with SUI will be missed, and unnecessary treatment with the
related risks will be avoided in most patients who do not need
an antincontinence surgery.
In this group of patients, preoperative screening for coex-
isting and occult SUI seems pivotal.
8.5 T
esting for Occult SUI and Assessment
of Urethral Function
Occult SUI is defined as an incontinence that is not symp-
tomatic but becomes apparent only during clinical or urody-
namic testing when the prolapse is reduced. Occult stress
8.5 Testing for Occult SUI and Assessment of Urethra 121
incontinence is also referred to as latent, hidden, iatrogenic,

or potential incontinence.
Signs in medical history that may suggest occult SUI
include:
• Incontinence that improved or resolved as prolapse
worsened
• The need to manually replace the prolapsed structures
into the vagina to void
• Worsening or development of SUI with use of a pessary
8.5.1 Provocative Tests
Prolapse reduction testing may be performed as part of office

testing of SUI or during urodynamic evaluation. Both
approaches appear to have a similar predictive value for the
development of postoperative SUI.
Prolapse reduction may be performed in semilithotomic
position using fingers, large cotton swab, single speculum
blade, or pessary. The bladder should be filled at a volume
between 100 and 300 mL, the latter being more reliable in
predicting postoperative SUI.
Pessaries may be less effective at detecting SUI than other
methods because they increase the maximum urethral clo-
sure pressure and functional urethral length. However, once
positioned, the pessary should be left in situ for at least
1 week to see whether continuous use would elicit UI, regard-
less of any leakage on the objective tests. Care should be
taken in positioning the pessary. While elevating the pro-
lapsed structures, it is important to avoid obstructing the
urethra and placing the anterior vaginal wall under excessive
tension, which could mask incontinence by distorting the
pelvic anatomy.
8.5.2 Urodynamic Testing
Invasive UDS provides more information on urethral func-

tion than office provocative stress test.
Urodynamic parameters of urethral function include:

• Urodynamic observation of SUI (leakage under cough or
Valsalva without any concomitant detrusor contraction)
• VLPP with a cutoff (normal vs. ISD) greater than 60 cm
H2O
• MUCP with a cutoff (normal vs. ISD) greater than 20 cm
H2O
• (Less commonly) % pressure transmission with a cutoff
(normal vs. defect in support) greater than 90%
Despite lack of solid evidence, these parameters may be
useful in choosing the type of incontinence surgery to be used
concurrently with POP repair, according to comparative data
on the effectiveness of different types of mid-urethral slings.
Note: The retropubic tape in that is closer to perpendicular
to the urethral axis creates greater circumferential compres-
sion of the urethra providing a better support.
Figure 8.1 summarizes the risk of SUI after POP repair
according to different approaches.
8.6 POP and OAB Syndrome

Since both POP-S and OAB-S are frequently seen in the
elderly female population, it would be expected that the two
conditions are frequently encountered in the same patient.
Up to 96% of women with POP report LUTS with mixed
urinary incontinence predominating. If there is a causal rela-
tionship, it could be anticipated that OAB symptoms would
improve after successful treatment of POP. Unfortunately,
this is not the rule, and it is still unclear whether there is a
causal relationship between the two conditions. Nevertheless,
many women with either urgency or urge incontinence are
sent to POP surgery for solving their problems. Persistent
OAB symptoms are associated with poor patient satisfaction
as the majority of the patients expect complete postoperative
resolution of all their LUTS.
8.6 POP and OAB Syndrome 123
8.6.1 Key Facts About POP and OAB Syndrome
• The prevalence of OAB symptoms is greater in the POP

patients than in patients of the same age group without
POP, accounting for some role of POP in development of
OAB symptoms.
• POP can cause bladder outlet obstruction, and this is
often regarded as an important mechanism for develop-
ing OAB in these patients in a way not dissimilar to that
of men with prostatic bladder outlet obstruction. Patients
with prolapse have a lower maximum flow rate (Qmax)
during voiding and higher PVR than patients without a
prolapse. These findings suggest that some degree of
obstruction during voiding may play a role in DO con-
comitant with POP.
• Unfortunately, diagnosis of obstruction is a difficult issue
in female (see Chap. 10). Recently, it has been reported
that the criterion (pdetmax > 2Qmax) is the best determi-
nant of BOO in women (ICI-RS 2014).
• Treatment of POP (by surgery or simple pessary) gives an
improvement in OAB complaints as well as DO symptoms
in approximately 60% of the patients.
• In the remaining 40% of patients with persistent symp-
toms after POP repair, pathophysiological mechanisms
other than obstruction should be considered, including
increased afferent activity from the urothelium and abnor-
mal handling of afferent signals by brain areas, particularly
in elderly patients (see Chap. 9).
In support of this view, there are studies indicating a
lack of correlation between the prolapsed compartment
and the presence of OAB symptoms, when intuitively one
would consider an anterior prolapse more at risk of devel-
oping OAB symptoms than a central or posterior one. In
addition, urgency and urgency incontinence seem to occur
more often in women with a less advanced prolapse
overall.
• Mechanisms alternative to bladder outlet obstruction should

also be applied to 20% of patients who develop de novo
urgency urinary incontinence (UUI) after prolapse repair.
Note: The term de novo urgency urinary incontinence is
used to describe urgency incontinence that develops following
surgical correction of the prolapse and persists after 6 months
among women who did not have any urgency preoperative.
In summary, with the current state of our knowledge, there
are no means to discern which factors will determine the per-
sistence or disappearance of OAB symptoms after POP
repair, and patients should be adequately counseled on that
possibility. In any case, prolapse repair should not be offered
to women as a primary treatment for detrusor overactivity.
8.7 POP and Voiding Dysfunction Syndrome

A third of women with stage 2 or more POP experience dif-
ficulties in emptying the bladder. Voiding difficulties usually
disappear postoperatively because the obstruction caused by
the prolapse has been corrected. In contrast, voiding dys-
function might develop after surgery because of kinking of
the urethra due to the surgical technique. Postoperative
voiding dysfunction (including postoperative urinary reten-
tion) is a frequent consequence of gynecologic surgery. Its
prevalence ranges from 2.5 to 24% after only prolapse sur-
gery reaching the 43% when a concomitant sling placement
is undertaken. In most of the patients is a consequence of a
failure to relax appropriately the pelvic floor muscles during
voiding and is usually temporary. Prolonged retention, last-
ing 4 weeks or longer after surgery, has a prevalence of
2–4%. In these patients, surgical obstruction should be ruled
out through a pressure-flow study in order to decide a sling
cut within few weeks. In female complaining voiding difficul-
ties preoperatively, no valid conclusions regarding voiding
dysfunction following POP surgery can be drawn from pre-
operative urodynamic testing due to difficulties in defining
and assessing detrusor underactivity in female patents (see
Chap. 10).
8.7 POP and Voiding Dysfunction Syndrome 125
Key Notes for Clinical Practice
To date, it has not been possible to reach a universal

consensus on the role of UDS before prolapse surgery.
It is clear that UDS could add some information in
women undergoing pelvic organ prolapse surgery and
could facilitate counseling of patients. However, there is
no evidence that the outcome of surgery is altered by
prior UDS.
• Prolapse + SUI
In women with prolapse and SUI symptoms, pro-
lapse procedures alone are associated with low success
rates for SUI. Concomitant continence procedures
(MUS, Burch colposuspension) reduce the risk of post-
operative SUI.
• Prolapse + occult SUI
In continent women undergoing POP surgery with
occult SUI, the addition of continence surgery reduces
the rate of postoperative SUI.
• Prolapse without SUI
No clear conclusion can be made regarding the man-
agement of continent women undergoing prolapse sur-
gery without occult SUI. The risk of incontinence after
simple POP repair is relatively low (7%), and the NNT
(number need to treat) is probably considerable. To
prevent incontinence in one woman, 20 patients should
undergo combined surgery, and the benefits of reduced
surgery might outweigh the risks of combined surgery.
• Antincontinence procedure
A retropubic tape appears to be more suitable than a
transobturator tape in women with intrinsic sphincter
deficiency, diagnosed using urethral pressure profilom-
etry and/or Valsalva leak point pressures.
• OAB symptoms
Preoperative bladder overactivity may resolve in
40% of patients undergoing POP surgery, and de novo
bladder overactivity may occur in 20%. No clear con-
clusions can be drawn from preoperative urodynamic
testing, and patients should be counseled about persis-
tent postoperative OAB symptoms.
• Voiding dysfunction
Except the evident cases of obstruction, urodynamic
testing are not particularly useful in predicting the reso-
lution of voiding symptoms after POP surgery due to
the difficulties in assessing detrusor underactivity in
female patients.
Overall, when preoperative UDS are suggestive of
detrusor overactivity (DO) or detrusor underactivity
(DU) and even in patients who habitually void by
abdominal straining, an interval rather than a concomi-
tant continence procedure is advisable even in women
with occult SUI.
Suggested Readings
POP Classification Systems

Baden WF, Walker TA. Physical diagnosis in the evaluation of vagi-
nal relaxation. Clin Obstet Gynecol. 1972;15:1055–69.
Bump R, Mattiasson A, Bo K, Brubaker L, Delancey JO, Klarskov P,
et al. The standardization of terminology of female pelvic organ
prolapse and pelvic floor dysfunction. Am J Obstet Gynecol.
1996;175:10–7.
Swift S. Current opinion on the classification and definition of geni-
tal tract prolapse. Curr Opin Obstet Gynecol. 2002;14:503–7.
Ghoniem G, Stanford E, Kenton K, Achtari C, Goldberg R,
Mascarenhas T, et al. Evaluation and outcome measures in the
treatment of female urinary stress incontinence: International
Urogynecological Association (IUGA) guidelines for research
and clinical practice. Int Urogynecol J. 2008;19:5–33.
Haylen BT, De Ridder D, Freeman RM, Swift SE, Berghmans B, Lee

minology for female pelvic floor dysfunction. Int Urogynecol J.
2010;21:5–26.
Haylen BT, Mahen CHF, Barber MD, Camargo S, Dandolu V, Digesu
A, et al. An International Urogynecological Association (IUGA)
/International Continence Society (ICS) joint report on the ter-
minology for female pelvic organ prolapse (POP). Int Urogynecol
J. 2016;27:165–94.
Overviews
Serati M, Giarenis I, Meschia M, Cardozo L. Role of urodynamics
before prolapse surgery. Int Urogynecol J. 2015;26:165–8.
Adelowo A, Dessie S, Rosenblatt PL. The role of preoperative
urodynamics in urogynecologic procedures. J Minim Invasive
Gynecol. 2014;21:217–22.
Ballert KN. Urodynamics in pelvic organ prolapse when are
they helpful and how do we use them? Urol Clin North Am.
2014;41:409–17.
Baessler K, Maher C. Pelvic organ prolapse surgery and bladder
function. Int Urogynecol J. 2013;24:1843–52.
Dillon B, Lee D, Lemack G. Urodynamics role in incontinence
and prolapse: a urology perspective. Urol Clin North Am.
2012;39:265–72.
Whiteside JL. Making sense of urodynamic studies for women with
urinary incontinence and pelvic organ prolapse a urogynecology
perspective. Urol Clin North Am. 2012;39:257–63.
Serati M, Salvatore S, Siesto G. Urinary symptoms and urody-
namic findings in women with pelvic organ prolapse: is there a
correlation? Results of an artificial neural network analysis. Eur
Urol. 2011;60:253–60.
Costantini E, Lazzeri M. Urodynamics for pelvic organ prolapse sur-
gery: “par for the course”. Eur Urol. 2011;60(2):261.
Roovers JP, van Laar JO, Loffeld C, Bremer GL, Mol BW, Bongers
MY. Does urodynamic investigation improve outcome in patients
undergoing prolapse surgery? Neurourol Urodyn. 2007;26:170–5.
Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse
on voiding. J Urol. 1999;161:581–6.
POP and SUI-S

Khullar V, Anding R, Robinson D, Castro-Diaz D, Dmochowski R,
Cardozo L. Under what circumstances should stress incontinence
surgery be performed at the same time as prolapse surgery?
ICI-RS 2015. Neurourol Urodyn. 2017;36:909–14.
Visco AG, Brubaker L, Nygaard I, Richter HE, Cundiff G, Fine P,
et al. The role of preoperative urodynamic testing in stress-con-
tinent women undergoing sacrocolpopexy: the Colpopexy and
Urinary Reduction Efforts (CARE) randomized surgical trial.
Int Urogynecol J Pelvic Floor Dysfunct. 2008;19:607–14.
Brubaker L, Nygaard I, Richter HE, Visco A, Weber AM, Cundiff
GW, et al. Two-year outcomes after sacrocolpopexy with and
without Burch to prevent stress urinary incontinence. Obstet
Gynecol. 2008;112:49–55.
Maher C, Feiner B, Baessler K, Adams EJ, Hagen S, Glazener
CM. Surgical management of pelvic organ prolapse in women.
Cochrane Database Syst Rev. 2010;4:CD004014.
van der Steen A, van der Ploeg M, Dijkgraaf MG, van der Waart
H, Roovers JP. Protocol for the CUPIDO trials; multicenter ran-
domized controlled trials to assess the value of combining pro-
lapse surgery and incontinence surgery in patients with genital
prolapse and evident stress incontinence (CUPIDO I) and in
patients with genital prolapse and occult stress incontinence
(CUPIDO II). BMC Womens Health. 2010;10:16.
Wei J. A mid urethral sling prevents incontinence among women
undergoing vaginal prolapse repair—the OPUS trial. Neurourol
Urodyn. 2011;30:809–10.
van der Ploeg JM, van der Steen A, Oude Rengerink K, van der
Vaart CH, Roovers JP. Prolapse surgery with or without stress
incontinence surgery for pelvic organ prolapse: a system-

atic review and meta-analysis of randomised trials. BJOG.
2014;121:537–47.
van der Ploeg JM, Oude Rengerink K, van der Steen A, van Leeuwen
JH, Stekelenburg J, Bongers MY, et al. Transvaginal prolapse
repair with or without the addition of a midurethral sling in
women with genital prolapse and stress urinary incontinence: a
randomised trial. BJOG. 2015;122(7):1022–30.
POP and OAB-S

Tran H, Chung DE. Incidence and management of de novo lower
urinary tract symptoms after pelvic organ prolapse repair. Curr
Urol Rep. 2017;18:87.
Kim MS, Lee GH, Na ED, Jang JH, Kim HC. The association of
pelvic organ prolapse severity and improvement in overactive
bladder symptoms after surgery for pelvic organ prolapse. Obstet
Gynecol Sci. 2016;59:214–9.
Tomoe H. Improvement of overactive bladder symptoms after
tension-free vaginal mesh operation in women with pelvic organ
prolapse: correlation with preoperative urodynamic findings. Int
J Urol. 2015;22:577–80.
Dieter AA, Edenfield AL, Weidner AC, Siddiqui NY. How does site
of pelvic organ prolapse repair affect overactive bladder symp-
toms? Female Pelvic Med Reconstr Surg. 2014;20:203–7.
Basu M, Wise B, Duckett J. Urgency resolution following prolapse
surgery: is voiding important? Int Urogynecol J. 2013;24:1309–13.
Maher CM, Feiner B, Baessler K, Glazener CM. Surgical manage-
ment of pelvic organ prolapse in women: the updated summary
version Cochrane review. Int Urogynecol J. 2011;22:1445–57.
Long CY, Hsu CS, Wu MP, Liu CM, Chiang PH, Juan YS, Tsai
EM. Predictors of improved overactive bladder symptoms
after transvaginal mesh repair for the treatment of pelvic organ
prolapse: predictors of improved OAB after POP repair. Int
Urogynecol J. 2011;22:535–42.
Foster RT Sr, Barber MD, Parasio MF, Walters MD, Weidner AC,
Amundsen CL. A prospective assessment of overactive bladder
symptoms in a cohort of elderly women who underwent trans-
vaginal surgery for advanced pelvic organ prolapse. Am J Obstet
Gynecol. 2007;197:82e1–4.
POP and VD-S

Zhang L, Zhu L, Liang S, Xu T, Lang J. Short-term effects on void-
ing function after mesh-related surgical repair of advanced pelvic
organ prolapse. Menopause. 2015;22(9):993.
Geller E. Prevention and management of postoperative urinary

retention after urogynecologic surgery. Int J Women Health.
2014;6:829–38.
Maher C, Schmid C, Baessler K, Feiner B. Surgical management of
pelvic organ prolapse in women. Cochrane Database Syst Rev.
2013;(4):CD004014.
Hakvoort RA, Dijkgraaf MG, Burger MP, Emanuel MH, Roovers
JP. Predicting short-term urinary retention after vaginal prolapse
surgery. Neurourol Urodyn. 2009;28:225–8.
Fitzgerald MP, Kulkarni N, Fenner D. Postoperative resolution of
urinary retention in patients with advanced pelvic organ prolapse.
Am J Obstet Gynecol. 2000;183:1361–3.
Chapter 9
UDS in Overactive Bladder
Syndrome (OAB-S)
9.1 Background
Overactive bladder syndrome (OAB-S) is a symptom com-
plex whose hallmark is the urinary urgency (the sudden com-
pelling desire to void that is difficult to defer), usually
accompanied by frequency and nocturia, and sometimes
urgency incontinence in the absence of any urinary tract
infection or another obvious pathology.
OAB is further subclassified as “OAB wet” if associated
with urinary incontinence or “OAB dry” without inconti-
nence. OAB may be idiopathic (non-neurological) or second-
ary to a neurological cause (e.g., multiple sclerosis, spinal cord
injury). The overall prevalence is approximately 16% in gen-
eral population. Both men and women demonstrate an age-
related increase in the prevalence of OAB; however, this is
more pronounced in women, particularly after the age of 40
(Fig. 9.1).
In addition, men are more likely to have OAB dry and
females to suffer from OAB wet. OAB has a significant effect
on quality of life (QoL), particularly if associated with
incontinence.
The definition of OAB is based on symptoms only.
Although the symptoms are suggestive of detrusor overactiv-
ity, this is not a rule of thumb, since only a proportion of
patients have detrusor overactivity on urodynamic testing.

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_9
132 Chapter 9. UDS in Overactive Bladder Syndrome (OAB-S)
PREVALENCE OF OAB IN WOMEN by AGE
35
30
25
Prevalence %
20
15
10
0
<25 25-34 35-44 45-54 55-64 65+
Age (years)
Figure 9.1 Prevalence of OAB in women by age
Thus, the terms overactive bladder and detrusor overactivity

are distinct, with the latter being a finding in an urodynamic
examination.
Historically, urodynamics evaluation has not been recom-
mended in the initial evaluation of OAB, since it is defined
primarily by clinical symptoms. Urinalysis and voiding diary
are the two most important tools for the initial assessment of
the condition. In particular, voiding diary provides quantifi-
able, objective data that are also useful to analyze the evolu-
tion after the prescription of treatment. In postmenopausal
women, atrophic vaginitis should be excluded. Assessment of
post-void residual (>150 mL) should exclude a chronic uri-
nary retention.
Note: Among noninvasive investigations, urinary NGF has
been proposed for the diagnosis of OAB. The neuronal
growth factor (NGF) is produced in the urothelium and vesi-
cal smooth musculature and modulates the release of neu-
rotransmitters reducing the sensitivity threshold of nociceptive
9.2 Current Concepts on Pathophysiology of OAB 133
fibers. Patients with overactive bladder symptoms show

higher urinary NGF levels than healthy individuals and
achieve lower NGF levels after having been effectively
treated. However, an issue in the use of NGF as an overactive
bladder biomarker is the fact that it can be elevated in other
clinical conditions as well, such as painful bladder syndrome,
urinary infections, urinary lithiasis, and bladder tumors.
As the pathophysiology of the OAB syndrome has become
more clearly elucidated from recent studies, the role of UDS
has again become a topic of discussion as a tool that can pro-
vide objective data to reflect these new findings. The utility of
UDS in the diagnosis and treatment of OAB is still evolving,
but in certain clinical scenarios, especially when empiric
treatment has failed, it can provide definitive information
that can identify associated pathologies and/or alter the treat-
ment course.
9.2 C
urrent Concepts on Pathophysiology
of OAB Syndrome (OAB-S)
OAB-S is a well-defined symptom complex but not very spe-
cific for the pathophysiology. The mechanisms behind OAB
symptoms remain the subject of debate and ongoing scientific
research.
Until the last decade, studies had focused more on the
detrusor muscle.
9.2.1 Myogenic Hypothesis
In the myogenic hypothesis, involuntary contractions are

caused by changes in myocyte excitability and coupling of
myocytes with other myocytes or myofibroblasts. The
involuntary contractions that result will provide increased
afferent activity and generation of OAB symptoms. Among
myogenic mechanisms, great interest has focused in recent
years on bladder micromotions. The isolated bladder
BLADDER MICROMOTIONS
isolated bladder
inhibition by CNS inhibition by CNS

during storage during voiding
Figure 9.2 Bladder micromotions. In vitro, the bladder shows

autonomous micromotions, which increase with bladder distension
and generate sensory nerve activity. In vivo, micromotions are sub-
ordinate to the efferent control of the central nervous system. The
loss of efferent inhibition may allow unregulated micromotility with
consequent afferent stimulation, which may be responsible for uri-
nary urgency
shows autonomous micromotions, which increase with

bladder distension and generate sensory nerve activity
(Fig. 9.2).
In vivo, these micromotions are subordinate to the effer-
ent control of the central nervous system, which, in the stor-
age phase, keep the autonomic activity at low level allowing
just a signal of a “state of fullness” while maintaining a nor-
mal compliance. In OAB, efferent control of the bladder can
be impaired, for example, due to peripheral “patchy” dener-
vation. In this case, loss of efferent inhibition may allow an
unregulated micromotility, with subsequent afferent stimula-
tion that will predispose to urinary urgency.
9.2 Current Concepts on Pathophysiology of OAB 135
Next to myogenic hypothesis, two more underlying mecha-

nisms for OAB symptoms have been suggested by ICS
including:
• An increased afferent activity
• An abnormal handling of afferent signals by the brain
9.2.2 Increased Afferent Activity
In the last years, new evidence has highlighted the role of the
afferent system and, in particular, emphasized the important
afferent role played by the urothelium/suburothelium. The
urothelium is an epithelial tissue that lines the urinary tract.
It is composed of approximately three to five urothelial cell
layers and forms an effective barrier to harmful components
in urine. In addition to this barrier function, the urothelium
also has sensory and signaling functions, which are currently
hot topics in urology research. Urothelial cells are primary
transducers of physical and chemical stimuli. The urothelium
has been shown to release various transmitters, such as ATP
and ACh, in response to mechanical and chemical stimuli.
These transmitters may regulate the activity of primary blad-
der afferent nerves, which are anatomically located in close
proximity to the urothelium. In addition, lamina propria
contains a dense layer of spindle-shaped cells categorized as
myofibroblast or interstitial cells (ICs) and characterized by
comparison with ICs of Cajal in the gastrointestinal tract.
The role of bladder ICs has not yet been established, but
they may constitute a structural and functional link between
urothelial cells and sensory nerves and/or between urothelial
cells and detrusor smooth muscle cells (Fig. 9.3).
In the urothelium-based hypothesis, changes in urothelial
receptor function and neurotransmitter release, as well as
changes in the sensitivity and coupling of the suburothelial
myofibroblasts/interstitial cells, are suggested to contribute to
increased afferent activity. This increased afferent activity
amplifies the sensations of bladder fullness, thereby leading to
urgency and predisposing to activation of the micturition reflex.
136
BLADDER DISTENTION
interstitial cells urothelial cells
ATP NO Ach
UROTHELIUM
SUBUROTHELIAL
LAYER
INCREASED
NERVE ACTIVITY
DETRUSOR SMOOTH
MUSCLE LAYER
detrusor smooth muscle
Figure 9.3 Urothelial signaling. A schematic view of the cellular structures in the different bladder layers. At present,
there is still a debate on what precisely defines an interstitial cell in the human bladder. However, the stretch of the
bladder during filling may evoke activity in afferent nerves directly or via interstitial cells
Chapter 9. UDS in Overactive Bladder Syndrome (OAB-S)
9.3 Urodynamics in OAB-S 137
9.2.3 Abnormal Handling of Afferent Signals
As fully described in Chap. 1, in the past few decades, various

methods of functional brain imaging have been used to study
cerebral control of the bladder and urethra. Bladder control
depends on an extensive network of brain regions. Dysfunction
in various parts may contribute to Urgency incontinence
suggesting that there are different phenotypes requiring

different treatments.
Studies of older females with urgency incontinence, with-
out DO, have linked bladder filling sensations such as desire
to void and urgency to an exaggerated activation of the
insula, the dorsal anterior cingulate cortex (ACC) and sup-
plementary motor area (SMA). Similar activation is seen in
healthy individuals, but with little awareness of bladder filling
until a substantial volume of urine has accumulated, a desire
to void is felt, and an opportunity to empty the bladder is
sought. Conversely, the neural signature of DO itself seems to
be a prefrontal cortex deactivation.
Clearly, different causes or combinations of causes may be
responsible for Urgency incontinence in different individuals,
implying that there are different phenotypes that may require
different treatments. Understanding these differences and
their causes will be the next great advance in diagnosis and
therapy of this difficult problem.
9.3 Urodynamics in OAB-S

Urodynamic evaluation is potentially part of specialist
assessment of OAB-S. It applies when conservative and
medical management is suboptimal and when overactive
bladder syndrome has a significant impact on a patient’s
quality of life. A major challenge in profiling patients with
subtypes of idiopathic OAB is the lack of validated pheno-
typic markers to identify patients with different underlying
pathophysiologies.
Note: Less than 20% of treatment trials profile patients

according to suspected underlying pathophysiology of
OAB. Detrusor overactivity on urodynamic testing is by far
the most common categorization. The cost of subclassifying
OAB by pathophysiologic condition would be far more
expensive than a more “empiric” approach, and probably the
treatment effects of current OAB therapies target a common
symptomatic mechanism of urgency (i.e., DO) for different
pathophysiologic conditions.
Urodynamically, patients with OAB-S can be stratified into
clinical groups based on the presence or absence of involun-
tary detrusor contractions, the ability to abort contractions,
and the ability to contract the urinary sphincter in response to
contractions. Then, the urodynamic diagnoses associated with
OAB symptoms should include at least three findings:
• Detrusor overactivity
• Increased filling sensation
• The ability or not to contract the external sphincter in
response to detrusor behavior
Detrusor overactivity can be:
• Phasic, characterized by increasing amplitude in contrac-
tions when the bladder volume increases (Fig. 9.4).
Detrusor overactivity is observed only in half of the
patients with OAB symptoms. The association between
OAB and DO appears to be more common in patients
with urgency incontinence than in those without
incontinence.
Note: If detrusor overactivity isn’t observed during blad-
der filling, then a provocation test can be initiated, such as
asking patient to cough, changing the position from sitting to
standing, and/or generating the sound of running water.
• Terminal, a single involuntary detrusor contraction at cys-
tometric capacity, causing incontinence often leading to
bladder emptying (Fig. 9.5).
Pves
Pabd
Pdet
Flow
Figure 9.4 Phasic detrusor overactivity. Phasic DO is an involun-

tary detrusor contraction recognizable as a temporary increase in
Pvess and Pdet. The ancient concept of minimum size of 5 cm H2O
has been updated. There is no minimum size for DO, but it should
be just an observable increase of pressure
Pves
strong desire
Pabd
Pdet
Flow
Figure 9.5 Terminal detrusor overactivity. Terminal DO is defined

as a single involuntary contraction occurring at cystometric capacity
which cannot be suppressed and usually results in a complete blad-
der emptying
The reduction of “warning time,” i.e., the time between the

compelling desire to void and the effective voiding, has been
interpreted as the result of poor brain handling of afferent
signals from the bladder. Timed voiding is probably the best
therapeutic option for this group of patients.
In the absence of detrusor overactivity, the patient may
report an increased bladder sensation during filling, that is, an
early and persistent desire to void usually at a volume lower
than 100 mL (Fig. 9.6). By some authors this finding is con-
sidered as the first step of a pain bladder syndrome (PBS).
While urgency is the defining symptom of OAB and pain on
bladder filling is the hallmark symptom of PBS, the relation-
ship between urgency and pain, as well as the different affer-
ent mechanisms associated with the genesis of these sensory
symptoms, remains unknown. From a practical point of view,
the efficacy of antimuscarinics is significantly lower in this
group of patients.
Pves
Pabd
Pdet
fd sd
0 50 100 150
volume (ml)
Figure 9.6 Increased bladder sensation. Bladder hypersensitivity is

defined as an early first sensation of bladder filling which occurs at
low bladder volume (usually lower than 100 mL) without any invol-
untary contraction
Filling cystometry
Pves
Pabd
Pdet
phasic Do phasic Do
EMG
sphincter contracts sphincter relaxes

FLOW
(a) OAB-dry (b) OAB-wet
Figure 9.7 Sphincter behavior in OAB dry (a) and OAB wet (b). In
OAB dry patient is aware of detrusor contraction and can volun-
tarily contract the sphincter aborting detrusor contraction and pre-
venting incontinence. In OAB wet the patient is neither able to
voluntarily contract the sphincter nor abort the detrusor contraction
and voids involuntarily
Sphincter behavior during filling may account for an

“OAB dry” (when patient is able to compensate detrusor
contraction) or an “OAB wet” (when patient is unable to
contract the sphincter) (Fig. 9.7).The inability to contract the
sphincter may justify the practice of Kegel exercises.
In summary, it is likely that the OAB syndrome represents
a spectrum of underlying pathophysiologic conditions.
Unfortunately, few randomized clinical trials currently make
an attempt to profile idiopathic OAB patients according to
specific findings. In order to better target therapy based on
pathophysiology, future studies should explore and validate
standardized criteria for classification of idiopathic OAB
subtypes.
9.4 O
AB-S in Female: Key Notes for Clinical
Assessment
• OAB is a syndrome (i.e., a symptom complex common to
several clinical conditions).
• Comorbid conditions should be completely excluded.
• A urinalysis to rule out UTI and hematuria should be per-
formed in any patient.
• In postmenopausal women, pelvic examination should
exclude atrophic vaginitis and pelvic organ prolapse.
• Bladder diary may be useful in patients who cannot
describe their voiding behavior.
• Post-void residual may be useful to exclude a voiding dys-
function and before antimuscarinics.
• Urodynamic testing is not indicated in the initial diagnos-
tic workup.
• Urodynamic testing should be recommended in refractory
patient who have failed multiple OAB treatments in order
to identify the exact mechanisms of urgency. In particular,
urodynamic testing should be recommended when inva-
sive, potentially morbid and irreversible treatments are
considered.
9.5 O
AB-S in Female: Key Notes
for Treatment (Fig. 9.8)
A detailed discussion of OAB treatments is beyond the scope
of the chapter. Below are the most significant points:
• Initial management is conservative and includes educa-
tion, bladder training, and advice on fluid intake. Drug
therapy options include antimuscarinic medications (with
ER formulations more efficacious than the correspondent
IR formulations) and beta-3 adrenergic receptor
agonists.
• Persistent symptoms may require adjustment of medica-
tion including association of different drugs.
OAB Diagnosis
Lifestyle interventions
Behavioural therapy/PFMT
if inadequate efficacy
AM or MIR ( depending on co-morbidities and

contraindications)
if inadequate efficacy if side effects
Titrate to max.dose if using AM or Switch to another AM or

switch to MIR or switch to AM if TDS or MIR
using MIR
Legend:
if inadequate efficacy PFMT pelvic floor muscle training
Combination AM+MIR PNTS or BOTOX* or SNM AM antimuscarinics
( patient / physician preference) MIR mirabregon
TDS transdermal delivery system
* Patient willing and able to do CIC
PNTS posterior tibial nerve
stimulation
9.5 OAB-S in Female: Key Notes for Treatment
Augmentation cystoplasty SNM sacral neuromodulation

( selected cases)
143
Figure 9.8 OAB treatment algorithm

• There is considerable variation in the current guidelines

regarding the use of oral pharmacotherapy, with antimus-
carinics. The discrepancies reflect the lack of adequate
comparative head-to-head studies between AMs as well as
of well-designed pharmacoeconomic studies. The EAU
Guidelines 2015 propose the use of either immediate-
release (IR) or extended-release (ER) formulations as
first-line drugs, while AUA/SUFU Guidelines favor the
ER formulations over the IR ones and NICE Guidelines
(largely cost-driven) favor mostly IR formulations.
Likewise, there is no unanimity concerning the use of the
new beta-3 agonist mirabegron, and no recommendations
currently stand on combination pharmacotherapy.
For refractory cases (ineffective treatment with AMs for
3 months or intolerance due to side effects), BoNT/A bladder
injections can be used, provided the patient is able and will-
ing to do intermittent self-catheterization, which is necessary
in about 5% of treated patients.
• Bladder instillation of liposome-encapsulated BoNT/A is
a new approach, deserving further research.
• Posterior tibial nerve stimulation and sacral nerve stimula-
tion are other approaches. (See Chap. 12 for further
details.)
• Major reconstructive surgery, such as auto-augmentation
via detrusor myectomy or augmentation cystoplasty with
the use of bowel, is rarely undertaken in modern practice
but remains a possibility in extreme cases.
Suggested Readings
Overviews
Truzzi JC, Gomes CM, Bezerra CA, Plata IM, Campos J, Garrido GL,
et al. Overactive bladder—18 years—Part I. Int Braz J Urol.
2016a;42:188–98.
Truzzi JC, Gomes CM, Bezerra CA, Plata IM, Campos J, Garrido GL,
et al. Overactive bladder—18 years—Part II. Int Braz J Urol.
2016b;42:199–214.
Wallace KM, Drake MJ. Overactive bladder. F1000Res. 2015;4. pii:

F1000 Faculty Rev-1406.
Gormley EA, Lightner DJ, Faraday M, Vasavada SP, American
Urological Association.; Society of Urodynamics, Female Pelvic
Medicine. Diagnosis and treatment of overactive bladder (non-
neurogenic) in adults: AUA/SUFU guideline amendment. J Urol.
2015;193:1572–80.
Nambiar A, Lucas M. Chapter 4: guidelines for the diagnosis and
treatment of overactive bladder (OAB) and neurogenic detrusor
overactivity (NDO). Neurourol Urodyn. 2014;33(Suppl 3):S21–5.
Haab F. Chapter 1: the conditions of neurogenic detrusor overac-
tivity and overactive bladder. Neurourol Urodyn. 2014;33(Suppl
3):S2–5.
Robinson D, Cardozo L. Overactive bladder: diagnosis and manage-
ment. Maturitas. 2012;71:188–93.
Pathophysiology
Chapple C. Chapter 2: pathophysiology of neurogenic detrusor
overactivity and the symptom complex of “overactive bladder”.
Neurourol Urodyn. 2014;33(Suppl 3):S6–13.
Gajewski JB, Kanai AJ, Cardozo L, Ykeda Y, Zabbarova IV. Does
our limited knowledge of the mechanisms of neural stimulation
limit its benefits for patients with overactive bladder? ICI-RS
2013. Neurourol Urodyn. 2014;33:618–21.
Hanna-Mitchell AT, Kashyap M, Chan WV, Andersson KE,
Tannenbaum C. Pathophysiology of idiopathic overactive blad-
der and the success of treatment: a systematic review from ICI-RS
Chacko S, Cortes E, Drake MJ, Fry CH. Does altered myogenic
activity contribute to OAB symptoms from detrusor overactiv-
ity? ICI-RS 2013. Neurourol Urodyn. 2014;33:577–80.
Kitta T, Mitsui T, Kanno Y, Chiba H, Moriya K, Shinohara N. Brain-
bladder control network: the unsolved 21st century urological
mystery. Int J Urol. 2015;22:342–8.
Morris CL. Urge urinary incontinence and the brain factor.
Tadic SD, Griffiths D, Schaefer W, Murrin A, Clarkson B, Resnick
NM. Brain activity underlying impaired continence control
in older women with overactive bladder. Neurourol Urodyn.
2012;31:652–8.
Chai TC, Russo A, Yu S, Lu M. Mucosal signaling in the bladder.

Auton Neurosci. 2015;200:1566–10702.
Andersson KE, McCloskey KD. Lamina propria: the functional cen-
ter of the bladder? Neurourol Urodyn. 2014;33:9–16.
Kanai A, Fry C, Hanna-Mitchell A, Birder L, Zabbarova I, Bijos D,
Ikeda Y. Do we understand any more about bladder interstitial
cells? -ICI-RS 2013. Neurourol Urodyn. 2014;33:573–6.
Birder LA, Andersson KE, Kanai AJ, Hanna-Mitchell AT, Fry CH.
Urothelial mucosal signaling and the overactive bladder-ICI-RS
Castro-Diaz D, Cardozo L, Chapple C. Urgency and pain in patients
with overactive bladder and bladder pain syndrome. What are the
differences? Int J Clin Practice. 2014;68:356–62.
De Wachter SG, Heeringa R, van Koeveringe GA, et al. On the
nature of bladder sensation: the concept of sensory modulation.
Banakhar MA, Al-Shaiji TF, Hassouna MM. Pathophysiology of
overactive bladder. Int Urogynecol J. 2012;23:975–82.
Roosen A, Chapple CR, Dmochowski RR, et al. A refocus on the
bladder as the originator of storage lower urinary tract symptoms:
a systematic review of the latest literature. Eur Urol. 2009;56:810–9.
Diagnosis
Bhide AA, Cartwright R, Khullar V, Digesu GA. Biomarkers in
overactive bladder. Int Urogynecol J. 2013;24:1065–72.
Scarpero H. Urodynamics in the evaluation of female LUTS when
are they helpful and how do we use them? Urol Clin North Am.
2014;41:429–38.
Rovner ES, Goudelocke CM. Urodynamics in the evaluation of
overactive bladder. Curr Urol Rep. 2010;11:343–7.
Rutman MP, Cha DY, Blaivas JG. How do urodynamics findings
influence the treatment of the typical patient with overactive
bladder? Curr Urol Rep. 2012;13(5):370–8.
Rosier PF, Giarenis I, Valentini FA, Wein A, Cardozo L. Do patients
with symptoms and signs of lower urinary tract dysfunction
need a urodynamic diagnosis? ICI-RS 2013. Neurourol Urodyn.
2014;33:581–6.
Flisser AJ, Blaivas JG. Role of cystometry in evaluating patients with
overactive bladder. Urology. 2002;60(Suppl 1):33–42.
Al-Zahrani AA, Gajewski J. Urodynamic findings in women with
refractory overactive bladder symptoms. Int J Urol. 2016;23:75–9.
Treatment
Apostolidis A, Averbeck MA, Sahai A, Rahnamai’s MS, Anding R,
Robinson D, et al. Can we create a valid treatment algorithm for
patients with drug resistant overactive bladder (OAB) syndrome
or detrusor overactivity (DO)? Results from a think tank (ICI-RS
2015). Neurourol Urodyn. 2017;36:882–93.
Vouri SM, Kebodeaux CD, Stranges PM, Teshome BF. Adverse
events and treatment discontinuations of antimuscarinics for
the treatment of overactive bladder in older adults: a systematic
review and meta-analysis. Arch Gerontol Geriatr. 2017;69:77–96.
Olivera CK, Meriwether K, El-Nashar S, Grimes CL, Chenn CC,
Orejuela F, et al. Nonantimuscarinic treatment for overactive blad-
der: a systematic review. Am J Obstet Gynecol. 2016;215:34–57.
Visco AG, Fraser MO, Newgreen D, Oelke M, Cardozo L. What is the
role of combination drug therapy in the treatment of overactive
bladder? ICI-RS 2014. Neurourol Urodyn. 2016;35:288–92.
Madhuvrata P, Singh M, Hasafa Z, Abdel-Fattah M. Anticholinergic
drugs for adult neurogenic detrusor overactivity: a systematic
review and meta-analysis. Eur Urol. 2012;62:816–30.
Linsenmeyer TA. Use of botulinum toxin in individuals with neuro-
genic detrusor overactivity: state of the art review. J Spinal Cord
Med. 2013;36:402–19.
Andersson KE. New pharmacologic targets for the treatment of the
overactive bladder: an update. Urology. 2004;63:32–41.
Chapter 10
UDS in Voiding Dysfunction
Syndrome (VD-S)
10.1 Background
Although emptying problems are more commonly reported
in men, a significant number of women also complain of void-
ing dysfunction (VD). Despite the recent advances in the
standardization of terminology of lower urinary tract dys-
function at present, there is a lack of consensus regarding a
precise diagnosis and definition of voiding abnormalities in
women.
According to the latest terminology report from ICS, void-
ing dysfunction (VD) is defined as an “abnormally slow and/
or incomplete micturition, based on symptoms and urody-
namic investigations.”
Note: As mentioned before (Chap. 1), the voiding mecha-
nism in female is increasingly recognized as more complex
than in men. The conventional idea of a detrusor contraction
has been overtaken by various studies showing women void
via a variety of mechanisms, including abdominal straining
plus pelvic floor relaxation, with or without a detrusor
contraction.
Emptying problems in women encompass a complex of
complaints characterized by poor and/or intermittent stream,
sensations of incomplete emptying, double voiding, and pos-
sibly hesitancy and terminal dribbling. These symptoms rarely

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_10
150 Chapter 10. UDS in Voiding Dysfunction Syndrome (VD-S)
exist in isolation and often are found in association with other

storage-related symptoms such as frequency, urgency, and
nocturia. In addition recurrent UTIs and urinary inconti-
nence may be present.
10.2 P
revalence of Emptying Problems
in Women
The evidence from two epidemiological studies (EPIC,
EpiLUTS) suggest that, overall, voiding problems are less
common in women than in men.
The prevalence varies from 5 to 10% depending on the
definition of post-void residual used. It would seem reason-
able to consider a post-void residual of >100 ml to be signifi-
cant although many women may still remain asymptomatic
with a PVR of >200 ml, and hence it is imperative to consider
the clinical context.
10.3 C
auses of Voiding Dysfunction
in Females
The causes of female VD can be broadly divided into detru-
sor underactivity (DU) and bladder outflow obstruction
(BOO) which may either be anatomical and functional (Box
10.1).
Classically, diminished bladder emptying has been reported
to occur because of decreased quality of detrusor contractil-
ity or impairment of the outflow tract. In some cases a com-
bination of both may coexist.
Recent studies, however, have demonstrated that impaired
voiding is more than a simply issue of contractile properties
of detrusor smooth muscle or outflow obstruction but is a
complex interplay of sensory function and central processing
of afferent signals by the brain, which implement the detrusor
muscular function and the resistance offered by the lower
urinary tract (Fig. 10.1).
10.3 Causes of Voiding Dysfunction in Females 151
Box 10.1: Causes of Female Voiding Dysfunction

• Detrusor underactivity
–– Myogenic (age)
–– Neurogenic (diabetes)
–– Iatrogenic (radical pelvic surgery)
–– Idiopathic
• Bladder outlet obstruction
Anatomical
–– Anti-incontinence surgery
–– POP
Functional
–– Dysfunctional voiding (including Fowler’s
syndrome)
• Mixed forms
Brain - FAILURE OF PROCESSING SIGNALS

- aging
- neurological disease
- neurological disease
- neurological disease - aging
- aging
Detrusor muscle - LOSS OF INTRINSIC CONTRACTILITY

- aging
Bladder outlet - ANATOMICAL or FUNCTIONAL OBSTRUCTION

- POP
- sling surgery
- dysfunctional voiding
MECHANISMS
ETIOLOGIES redrawn from Osman N, Chapple C. Contemproary concepts on the aetiopathogenesis of detrusor underactivity
Nature Reviews Urology 2014;11:639-648
Figure 10.1 Major etiologies sites of dysfunction and pathogenic

mechanisms that result in DU
Understanding the pathophysiology of voiding dysfunc-

tion is a necessary step to interpret the diagnostic procedures
and provide appropriate treatment.
10.4 Detrusor Underactivity

The International Continence Society defines detrusor under-
activity (DU) as a “contraction of reduced strength and/or
duration, resulting in prolonged bladder emptying and/or a
failure to achieve complete bladder emptying within a nor-
mal time span” and underactive bladder (UAB) as a symptom
complex suggestive of detrusor underactivity, usually charac-
terized by prolonged micturition time with or without a sen-
sation of incomplete bladder emptying, usually with hesitancy,
reduced sensation on filling, and a slow stream.
DU is observed in patients with pathological conditions
such as diabetic neuropathy or bladder dysfunction after sur-
geries of intra-pelvic organs. However, DU frequently occurs
without obvious etiology, suggesting that, in some cases, it
may be a distinct disease entity. Detrusor overactivity some-
times coexists with DU in the elderly population. The condi-
tion is called detrusor hyperactivity with impaired contractility
(DHIC).
10.4.1 Detrusor Underactivity and Aging
Bladder contractility is reduced by 35% in women between

50 and 80 years of age. Uroflow studies have demonstrated an
age-dependent decrease in Qmax which is similar in both
sexes. Increasing age is associated with an increase of the col-
lagen: muscle ratio in bladder wall that is reflected in a
decline of contractility. Specific ultrastructural features
described as “degeneration patterns” have been described in
the bladder of elderly people including shrinked appearance
of the cells, disrupted sarcolemma, and deposition of collagen
in the interstitium.
10.5 Obstruction 153
Note: As well as in elderly, “degeneration patterns” have

been described in diabetic patients and in patients who
undergone extended pelvic surgery like radical hysterectomy,
or anterior/abdominoperineal resection, and thus may be
considered neurogenic in origin.
Recently, attention has been focused on bladder isch-
emia as a common pathophysiologic mechanism for age-
related bladder dysfunction, including DO and
DU. Atherosclerosis is one of the important causes of
reduction of blood flow of the bladder, leading to chronic
bladder ischemia. Studies in animal models suggest that
the extent of bladder dysfunction in chronic bladder isch-
emia depends on the degree and duration of ischemia.
Moderate ischemia may cause DO and OAB symptoms via
sensitization of afferent pathways. When bladder ischemia
becomes severe, progression of damage to nerves (both
afferent and efferent) and detrusor muscle may cause DO
and inability to empty the bladder.
Finally, an abnormal handling of afferent bladder signals
by the brain, frequently reported in association with increas-
ing age, may contribute to DU. To void efficiently, a feed-
forward mechanism by which urinary flow in the urethra
helps to enhance and maintain adequate contractile func-
tion of the bladder, until the bladder is empty is required.
FMRI in older people with voiding dysfunction found
diminished response to bladder filling in the insula, the
area of the brain responsible for mapping visceral
sensations.
10.5 Obstruction
Bladder outlet obstruction (BOO) is defined by the ICS as a
“generic term for obstruction during voiding.” Although
BOO is one of the most common clinical complaints in adult
men, it is a condition less common in women. BOO in women
is subdivided by cause into anatomic and functional
subgroups.
Anatomic causes are generally more obvious than func-

tional causes and include:
• Previous anti-incontinence surgery (MUS)
• Pelvic organ prolapse
10.5.1 Obstruction and Previous MUS Surgery
One potential complication of mid-urethral sling surgery is

postoperative voiding dysfunction, with reported rates vary-
ing between 5 and 20% and need of surgical re-intervention
in 0–4% of patients. Because symptoms are misleading and
not indicative of urinary obstruction, diagnosis and subse-
quent treatment are often late. Peculiar symptoms of obstruc-
tion are the need to immediately re-void and
position-dependent micturition. However they are often
masked by OAB symptoms or recurrent UTI. Pressure-flow
study is the only way to diagnose an obstruction (see below).
Surgery, generally performed through vaginal route,
includes simple transection or partial removal of the sling at
the surgeon’s discretion at the time of surgery. However,
there is still an active discussion on how to optimally treat
this condition. Satisfaction rate is around 75%. Dissatisfied
patient complains both recurrent SUI and OAB symptoms.
Performing surgical release more than 180 days after obstruc-
tive anti-incontinence surgery seems associated with less
recurrent SUI, while a surgical release before 70 days seems
to have a decrease of postoperative OAB symptoms.
10.5.2 Obstruction and POP
Prolapse greater than Stage 2 is sufficient to cause a lack of

proximal urethral funnelling with urethral kinking that can
result in bladder outlet obstruction. Again the diagnosis of
obstruction is done during a pressure-flow study (see below).
Note: In some cases of POP, urethral kinking may be dif-
ficult to measure or observe even under fluoroscopy because
10.5 Obstruction 155
the catheter tends to straighten the urethra during the pres-

sure/flow investigation.
There is an overall agreement that prolapse-induced blad-
der outlet obstruction may trigger bladder OAB symptoms.
Surgical management of prolapse leads to improvements of
OAB symptoms in most of the patients. The topic is widely
discussed in Chap. 8.
Functional—Functional obstruction is caused by abnormal
contraction of the periurethral muscles or failure to relax
them during voiding. Functional obstruction includes:
• Dysfunctional voiding
• Fowler’s syndrome
10.5.3 Dysfunctional Voiding (DV)
DV is defined as “an intermittent and/or fluctuating flow

rate due to involuntary intermittent contractions of the peri-
urethral striated muscle during voiding in neurologically
normal individuals”. In contrast to detrusor sphincter dyssyn-
ergia, there is no neurologic cause for the findings. DV
appears to be a learned behavior since in physiologic void-
ing, the pelvic floor muscles and external striated sphincter
should relax just prior to detrusor contraction. A precise
urodynamically quantifiable definition does not exist for DV,
and urethral voiding dysfunction is usually diagnosed on the
basis of abnormalities of flow and pelvic floor EMG, with
either Qmax reduced or a flow curve interrupted or fluctuat-
ing due to the persistence of EMG activity during voiding
(Fig. 10.2).
Note: Difficulty in initiating the voiding reflex may occur
as a consequence of embarrassment or mental stress in the
urodynamic room, the so-called “bashful” or “shy bladder”
syndrome. In these conditions flow rate may not be represen-
tative for the actual physiology of the lower urinary tract of
the women. Not much is known about the prevalence of psy-
chogenic voiding dysfunction and its influence on the final
diagnosis among patients referred to urodynamic clinic.
Pves
Pabd
Pdet
EMG
Flow
Figure 10.2 Urodynamic findings in DV. During voiding there is a

patchy increase of EMG activity that induces a fluctuating stream
Dysfunctional voiding is essentially a problem of striated

musculature. The relative importance of urethral smooth
muscle in women with voiding dysfunction is unclear. There
is no histological evidence of sympathetic alpha-adrenergic
receptors in the female urethra nor for its significance at the
bladder neck level. Alpha-blockers have never consistently
demonstrated objective effect on female voiding dysfunction
despite some reports on subjective improvement of
micturition
10.5.4 Fowler’s Syndrome
Another type of urethral abnormality that can result in func-

tional BOO is Fowler’s syndrome. Fowler’s syndrome typi-
cally presents in young women as painless urinary retention
(often in excess of 1 L) with no neurologic or anatomic etiol-
ogy. It is not known if Fowler’s syndrome represents a sub-
group of patients with VD or a distinct clinical entity in young
women with chronic urinary retention. The diagnosis is made
by a characteristic electromyography pattern that demon-
strates failure of urethral sphincter relaxation and decrease in
bladder sensation.
10.7 Urodynamic Challenges in the Diagnosis 157
10.6 A
ssessment of Voiding Dysfunction
in Female
“The female bladder is an even less reliable witness.”
Most of the patients complain both storage and voiding

symptoms. The predictive value of voiding symptoms has
been shown to be poor when predicting female VD. Women
are most concerned with leakage than with retention and
generally fail to describe their stream and compare it with the
past. Recurrent UTI may be a red flag symptom.
The diagnosis of emptying problems in women relies
mostly on urodynamics although the extent of investigation is
dependent upon the clinical setting. All women complaining
of difficulty in micturition should be investigated first with a
free flowmetry and post-void residual. If abnormal, filling
cystometry with a pressure-flow study will help to determine
whether the cause is detrusor underactivity or outlet
obstruction.
10.7 Urodynamic Challenges

in the Diagnosis of Female DU/BOO
To date, there are no universally accepted criteria to diagnose
and quantify obstruction and detrusor underactivity in
women.
10.7.1 Obstruction
Several definitions for female BOO have been proposed

using various combinations of clinical parameters,
pressure-flow criteria, and radiographic evidence of BOO
(see Box 10.2).
There is a general agreement that absolute pressure and
flow values are imprecise, and urodynamic tracings alone are
insufficient to diagnose BOO in women. Probably only
Box 10.2: Urodynamics Criteria for Diagnosing BOO in

Women
Author Qmax Pdet@Qmax
Axelrod and Blaivas <12 mL/s > 20 cmH2O
Massey and Abrams <15 mL/s > 20 cmH2O
Chassagne <15 mL/s > 20 cmH2O
Lemack and Zimmern (2000) < 11 mL/s > 21 cmH2O
Lemack and Zimmern (2004) <12 mL/s > 25 cmH2O
Nitti fluoroscopic evidence of
obstruction with any low flow
and high Pdetmax
fluoroscopic evidence of obstruction between the bladder

neck and distal urethra in the presence of a sustained detru-
sor contraction of any magnitude, usually associated with a
reduced or delayed flow, has the highest concordance with a
clinical suspicion of obstruction.
Only recently has been reported (ICI-RS 2014) that the
criterion Pdetmax > 2Qmax is the best determinant of BOO
in women.
Note: Technically, a proportion of women may be unable
to void during urodynamic testing, and concerns have been
expressed that the use of certain urethral catheter sizes dur-
ing pressure-flow study may lead to over diagnosis by
increasing outlet resistance.
10.7.2 Detrusor Underactivity
Bladder contractility in women has received less attention

than in male.
The isovolumetric pressure attained when flow is inter-
rupted (the stop test) provides in theory a good estimate of
10.7 Urodynamic Challenges in the Diagnosis 159
contraction strength (Coolsaet). However, mechanical inter-

ruption of flow by occlusion with a balloon catheter may be
difficult to perform and may induce discomfort in the patient.
Therefore others methods of estimating bladder contractility
have been proposed.
Several algorithms have been proposed to quantify detru-
sor power during voiding, like the Griffiths’ Watt factor,
Schafer’s nomogram, and bladder contractility index.
All are based on the bladder output relation (BOR), an
inverse relation between pressure and flow that is analogous
to Hill’s equation for contracting muscle. If the slope and
curvature of the BOR are known, the isovolumetric detrusor
pressure can be estimated by extrapolating (projecting) the
actual pressure back to the pressure axis. PIP (projected iso-
volumetric pressure) can be calculated by the formula
PIP = Pdet + KQ where Q is the maximum flow rate and Pdet
is the corresponding pressure (Fig. 10.3).
PIP- Projected Isovolumetric detrusor Pressure

200
pressure
cmH2O ST
PIP
N
100
W
Actual Qmax and
Pdet@Qmax
0 VW
0 10 20 flow rate (ml/s)
Figure 10.3 Projected isovolumetric pressure. The isovolumetric

detrusor pressure can be estimated by extrapolating (projecting) the
actual pressure back to the pressure axis
Schafer took K to be 5 cmH2O/mL/s and suggested that

values of PIP greater than150 cmH2O represented strong
contractions (ST); values from 100 to 150 cmH2O, normal
contractions (N); values from 50 to 100 cmH2O, weak con-
tractions (W); and values below 50 cmH2O, very weak con-
tractions (VW). He constructed his well-known contractility
nomogram that together with possible information on blad-
der outlet obstruction allows contraction strength to be clas-
sified in one of these classes (Fig. 10.4).
The problems with these methods are that they are calcu-
lated for male pressure-flow study and when applied in
female tend to overestimate the value of bladder contractility.
The female void with lower detrusor pressure and higher flow
rate. Adjustments of PIP have been proposed, modifying the
value of constant K in calculation of female bladder contrac-
tility from K = 5 to K = 1 cmH2O/mL/s, thus obtaining more
reliable estimates of bladder contractility in females still
maintaining the categories proposed for men.
To date, there is only one validated nomogram for women,
the Blavais-Groutz nomogram, which, however, does not
Schafer Nomogram
25
N- N+ ST
20
W+
Qmax (ml/s)
15
W-
10
5 O I II III IV V VI
VW
0
0 20 40 60 80 100 120 140
Pdet (cmH2O)
Figure 10.4 The Schafer’s nomogram

10.8 Keynotes on Clinical Diagnosis of VD in Women 161
consider detrusor contractility. The nomogram identifies

three degrees of obstruction but has received criticism con-
cerning its sensitivity, particularly in the mild obstruction
zone (Fig. 5.4). Blaivas and Groutz described as important the
obstructive effect of 7Fr urethral catheters accounting for
misleading results of pressure/flow curves in women. They
proposed using the value of maximum flow from the non-
intubated free flowmetry just previous to cystometry plotted
against the maximum detrusor pressure (Pdetmax) instead of
detrusor pressure at the maximum flow (Pdet@Qmax) since
they found no statistical differences between Pdetmax and
Pdet@Qmax. In addition Pdetmax can be used even in
absence of flow, fairly common in women (see note).
Note: As additional problem, the vast majority of computer-
urodynamic investigations are performed as in-office proce-
dures; however, there is ongoing debate about their universal
validity because relevant urethral sphincter activity may
interfere with voiding. Recently it has been reported that
84% of patients with acontractile detrusor during office uro-
dynamics have detrusor contractions during ambulatory uro-
dynamics. Therefore, in patients with VD-S, results of
conventional in-office urodynamics should be compared,
when possible, with ambulatory urodynamics to avoid
misinterpretations.
10.8 K
eynotes on Clinical Diagnosis of VD
in Women
1. Mixed symptoms (storage and voiding)
2. Recurrent UTI
3. Interrupted flow
4. PVR > 100 ml
5. Qmax <12–15 mL/s
6. Pdet@Qmax >20–25 cmH2O
7. Pdetmax>2Qmax
8. Videourodynamics: mid-urethral narrowing during voiding
9. Dysfunctional voiding: increase in EMG activity during
voiding
10.9 K
eynotes on Clinical Management
of VD in Women
The management of women with voiding dysfunction should
be individualized to each patient.
The following clinical scenarios can be outlined:
1. Patient asymptomatic with low PVR: double voiding and
periodic PVR measurements is all that is required.
2. Patient with mixed symptoms and low PVR: antimusca-
rinic therapy with frequent residual assessments to ensure
voiding function is not deteriorating.
3.
Patient with voiding dysfunction following anti-
incontinence surgery:
• Short-term urethral catheter since evidence suggest
that <5% of patients require catheterization for more
than 1 week.
• Women with persistent symptoms: short-term CIC since
the majority of postoperative voiding difficulties will
resolve, and by delaying intervention the risk of recur-
rent stress incontinence (SUI) would appear to be
reduced.
• Women with persistent symptoms, who are unwilling to
self-catheterize: urethral dilatation or urethrolysis. Both
procedures improve symptoms (at least in the short
period), but SUI may recur.
4. Patient with voiding dysfunction and POP: surgical

correction.
Evidence suggest that surgical correction of urogenital
prolapse is effective both in improving symptoms of VD
and those concomitant with storage phase.
5. Dysfunctional voiding: pelvic floor rehabilitation.
In a small Italian study, treatment with tamsulosin
resulted in a significant improvement in symptoms (62.5%
of pts) implying that pharmacological therapy may have a
role in management of dysfunctional voiding.
Suggested Readings
Overviews
Hoffman DS, Nitti VW. Female Bladder Outlet Obstruction. Curr
Urol Rep. 2016;17:31.
King AB, Goldman HB. Bladder outlet obstruction in women: func-
tional causes. Curr Urol Rep. 2014;15:436.
Robinson D, Staskin D, Laterza RM, Koelbl H. Defining female void-
ing dysfunction: ICI-RS 2011. Neurourol Urodyn. 2012;31:313–6.
Tunuguntla HS, Tunuguntla R, Barone J, Kanagarajah P, Gousse
AE. Voiding dysfunction in the female patient: is the “syndrome”
paradigm valid? Curr Urol Rep. 2011;12:377–80.
Abdel Raheem A, Madersbacher H. Voiding dysfunction in women:
how to manage it correctly. Arab J Urol. 2013;11:319–30.
Cohn JA, Brown ET, Kaufman MR, Dmochowski RR, Reynolds
WS. Underactive bladder in women: is there any evidence? Curr
Opin Urol. 2016;26:309–14.
Robinson D, Staskin D, Laterza RM, Koelbl H. Defining female void-
ing dysfunction: ICI-RS 2011. Neurourol Urodyn. 2012;31:313–6.
Epidemiology
Irwin DE, Milson I, Hunskaar S, Reilly K, Kopp Z, Herschorn S,
et al. Population based survey of urinary incontinence, overactive
bladder, and other lower urinary tract symptoms in five countries:
results of the EPIC study. Eur Urol. 2006;50:1306–14.
Coyne KS, Sexton CC, Thompson CL, Milsom I, Irwin D, Kopp ZS,
et al. The prevalence of lower urinary tract symptoms (LUTS)
in the USA, UK and Sweden: results from the epidemiology of
LUTS (EpiLUTS) study. BJU Int. 2009;104:352–60.
Clinical Assessment
Gammie A, Kirschner-Hermanns R, Rademakers K. Evaluation of
obstructed voiding in the female: how close are we to a defini-
tion? Curr Opin Urol. 2015;25:292–5.
Espuña-Pons M, Cardozo L, Chapple C, Sievert KD, van

Kerrebroeck P, Kirby MG. Overactive bladder symptoms and
voiding dysfunction in neurologically normal women. Neurourol
Urodyn. 2012;31:422–8.
Lowenstein L, Anderson C, Kenton K, Dooley Y, Brubaker
L. Obstructive voiding symptoms are not predictive of elevated
post void residual urine volumes. Int Urogynaecol J Pelvic Floor
Dysfunct. 2008;19:801–4.
Al-Sharani M, Lovatis D. Do subjective symptoms of obstructive
voiding correlate with the post void residual urine in women? Int
Urogynaecol J. 2008;16:12–4.
Gehrich A, Stany MP, Fischer JR, Buller J, Zahn CM. Establishing
a mean postvoid residual volume in asymptomatic peri-
menopausal and postmenopausal women. Obstet Gynaecol.
2007;110:827–32.
Luckacz ES, DuHamel E, Menefee SA, Luber KM. Elevated post-
void residual in women with pelvic floor disorder: prevalence and
associated risk factors. Int Urgynaecol J. 2007;18:397–400.
Urodynamics
Rosier P, GaJewski J, Sand P, Szabó L, Capewell A, Hosker
G. Executive Summary: The International Consultation on
Incontinence 2008—Committee on: “Dynamic Testing”; for uri-
nary incontinence and for fecal incontinence. Part 1: innovations
in urodynamic techniques and urodynamic testing for signs and
symptoms of urinary incontinence in female patients. Neurourol
Urodyn. 2010;29:140–5.
Axelrod S, Blaivas J. Bladder neck obstruction in women. J Urol.
1987;137:497–9.
Massey JA, Abrams PH. Obstructed voiding in the female. Br J Urol.
1988;61:36–9.
Chassagne S, Bernier PA, Haab F, Roehrborn CG, Reisch JS,
Zimmern PE. Proposed cutoff values to define bladder outlet
obstruction in women. Urology. 1998;51(3):408–11.
Lemack GE, Zimmern PE. Pressure flow analysis may aid in identify-
ing women with outflow obstruction. J Urol. 2000;163(6):1823–8.
Defreitas GA, Zimmern PE, Lemack GE, Shariat SF. Refining diag-
nosis of anatomic female bladder outlet obstruction: comparison
of pressure-flow study parameters in clinically obstructed women
with those of normal controls. Urology. 2004;64(4):675–9.
Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in

women. J Urol. 1999;161:1535–40.
Rademakers K, Apostolidis A, Constantinou C, Fry C, Kirschner-
Hermanns R, Oelke M, et al. Recommendations for future devel-
opment of contractility and obstruction nomograms for women.
ICI-RS 2014. Neurourol Urodyn. 2016;35:307–11.
Groutz A, Blaivis JG, Chaikin DC. Bladder outlet obstruction
in women: definition and characteristics. Neurourol Urodyn.
2000;19:213–20.
Groutz A, Blaivas JG, Sassone AM. Detrusor pressure uroflowmetry
studies in women: effect of a 7Fr transurethral catheter. J Urol.
2000;164:109–14.
Massolt ET, Groen J, Vierhout M. Application of the Blaivas–Groutz
bladder outlet obstruction nomogram in women with urinary
incontinence. Neurourol Urodyn. 2005;24:237–42.
Kuo HC. Videourodynamic characteristics and lower urinary
tract symptoms of female bladder outlet obstruction. Urology.
2005;66:1005–9.
Detrusor Underactivity
Osman N, Mangera A, Hillary C. The underactive bladder: detec-
tion and diagnosis. F1000Res. 2016;25:5; pii: F1000 Faculty
Rev-102.
Cohn JA, Brown ET, Kaufman MR, Dmochowski RR, Stuart
Reynolds W. Underactive bladder in women: is there any evi-
dence? Curr Opin Urol. 2016;26:309–14.
Smith P, Birde L, Abrams P, Wein A, Chapple C. Detrusor underac-
tivity and the underactive bladder: symptoms, function, cause—
what do we mean? ICI-RS think tank 2014. Neurourol Urodyn.
2016;35:312–7.
Park J, Lavelle JP, Palmer MH. Voiding dysfunction in older women
with overactive bladder symptoms: a comparison of urodynamic
parameters between women with normal and elevated post-void
residual urine. Neurourol Urodyn. 2016;35:95–9.
Osman NI, Chapple CR, Abrams P, Dmochowski R, Haab F, Nitti
V, et al. Detrusor underactivity and the underactive blad-
der: a new clinical entity? A review of current terminology,
definitions, epidemiology, aetiology, and diagnosis. Eur Urol.
2014;65:389–98.
Yoshida M, Yamaguchi O. Detrusor underactivity: the current

concept of the pathophysiology. Low Urin Tract Symptoms.
2014;6:131–7.
Osman NI, Chapple CR, Abrams P, Dmochowski R, Haab F, Nitti
V, et al. Detrusor underactivity and the underactive blad-
der: a new clinical entity? A review of current terminology,
definitions, epidemiology, aetiology, and diagnosis. Eur Urol.
2014;65:389–98.
Osman NI, Chapple CR. Contemporary concepts in the aetio-
pathogenesis of detrusor underactivity. Nat Rev. Urol.
2014;11:639–48.
Koeveringe G, Rademakers K, Birder L, Korstanje C, Daneshgari
F, Ruggieri MR, et al. Detrusor underactivity: pathophysiological
considerations, models and proposals for future research. ICI-RS
van Koeveringe GA, Vahabi B, Andersson KE, Kirschner-Herrmans
R, Oelke M. Detrusor underactivity: a plea for new approaches
to a common bladder dysfunction. Neurourol Urodyn.
2011;30:723–8.
van Koeveringe GA, Rahnama’i MS, Berghmans BC. The addi-
tional value of ambulatory urodynamic measurements com-
pared with conventional urodynamic measurements. BJU Int.
2010;105:508–13.
Griffiths D, Tadic SD, Schaefer W, Resnick NM. Cerebral control of
the bladder in normal and urge-incontinent women. NeuroImage.
2007;37:1–7.
Bladder Aging
Vahabi B, Wagg AS, Rosier P, Rademakers KLJ, Denys MA, Pontari
M, et al. Can we define and characterize the aging lower urinary
tract? -ICI-RS 2015. Neurourol Urodyn. 2017;36:854–8.
Camões J, Coelho A, Castro-Diaz D, Cruz F. Lower urinary tract
symptoms and aging: the impact of chronic bladder ischemia on
overactive bladder syndrome. Urol Int. 2015;95:373–9.
Daly DM, Nocchi L, Liaskos M, McKay NG, Chapple C, Grundy
D. Age-related changes in afferent pathways and urothelial func-
tion in the male mouse bladder. J Physiol. 2014;592:537–49.
Elbadawi A, Yalla SV, Resnick NM. Structural basis of geriatric void-
ing dysfunction. II. Aging detrusor: normal versus impaired con-
tractility. J Urol. 1993;150:1657–67.
Dysfunctional Voiding
Peng CH, Chen SF, Kuo HC. Videourodynamic analysis of the ure-
thral sphincter overactivity and the poor relaxing pelvic floor
muscles in women with voiding dysfunction. Neurourol Urodyn.
2017;36(8):2169–75.
Artibani W, Cerruto MA. Dysfunctional voiding. Curr Opin Urol.
2014;24:330–5.
King AB, Goldman HB. Bladder outlet obstruction in women: func-
tional causes. Curr Urol Rep. 2014;15(9):436.
Osman NI, Chapple CR. Fowler’s syndrome—a cause of unex-
plained urinary retention in young women? Nat Rev Urol.
2014;11(2):87–98.
Brucker BM, Fong E, Shah S, Kelly C, Rosenblum N, Nitti
VW. Urodynamic differences between dysfunctional void-
ing and primary bladder neck obstruction in women. Urology.
2012;80:55–60.
Groutz A, Blaivas JG, Pies C, Sassone AM. Learned voiding dys-
function (non-neurogenic, neurogenic bladder) among adults.
Various
Cohn JA, Brown ET, Reynolds WS, Kaufman MR, Dmochowski
RR. Pharmacologic management of non-neurogenic func-
tional obstruction in women. Expert Opin Drug Metab Toxicol.
2016;12:657–67.
Costantini E, Lazzeri M, Bini V, Zucchi A, Fioretti F, Frumenzio E,
et al. Open-label, longitudinal study of tamsulosin for functional
bladder outlet obstruction in women. Urol Int. 2009;83:311–5.
Chapter 11
UDS in Pain Bladder
Syndrome (PBS)
and Overactive Pelvic Floor
Dysfunction
11.1 Background
Bladder pain syndrome (BPS) is an enigmatic condition diffi-
cult to be diagnosed and treated. Its etiology and pathogenesis
remain unknown, and a number of theories based on clinical
and experimental observations have been developed without
convincing evidence. Treatment strategies are empirical, with
limited efficacy, and affected patients have a poor quality of life.
Much confusion regarding the diagnosis of pain bladder
syndrome is due to many changes in definition and nomen-
clature since its first description in 1887 by Skene. The condi-
tion classically known as interstitial cystitis (IC) was reserved
for patients with typical cystoscopic findings, such as glo-
merulations or the Hunner’s ulcer (Fig. 11.1). Up until 2002,
the National Institute for Diabetes and Digestive and Kidney
Diseases (NIDDK) criteria, mostly based on glomerulations
at cystoscopy under hydrodistention, were used to define IC.
Since NIDDK criteria were considered overly restrictive,
in 2002 the ICS defined painful bladder syndrome (PBS) as
“the complaint of suprapubic pain, related to bladder filling
accompanied by other symptoms, such as increased daytime

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_11
170 Chapter 11. UDS in Pain Bladder Syndrome (PBS)
a b
Figure 11.1 (a) Glomerulations are tiny areas of bleeding in the

mucosa after bladder hydrodistention. (b) Hunner’s ulcer is a muco-
sal lesion intermixed to normal capillary structure. Often it is cov-
ered by fibrin clots and associated with scars in the vicinity
and nighttime frequency, in the absence of proven urinary

infection or other obvious pathology” of the lower urinary
tract. Subsequent to this definition, some used IC to reflect
patients who meet the classic NIDDK criteria and PBS to
reflect those with identical symptoms but who did not
undergo formal hydrodistention or did not meet all of the
NIDDK criteria.
In the subsequent years, two more definitions have been
proposed.
The ESSIC defined PBS as “chronic pelvic pain, pressure,
or discomfort, perceived to be related to the urinary bladder
accompanied by at least one other urinary symptom: persis-
tent urgency or urinary frequency.” This revised definition has
been accepted by ICI.
The SUFU defined PBS as “an unpleasant sensation
(pain, pressure, discomfort) perceived to be related to the
urinary bladder, associated with lower urinary tract symp-
toms for more than six weeks duration, in the absence of
infection or other identifiable causes.” This definition is
used by AUA.
11.1 Background 171
There is a further Japanese and Asian view, in which uri-

nary frequency/urgency is the primary symptom, with overac-
tive bladder (OAB) and hypersensitive bladder (HSB) listed
as subgroups and with painful bladder syndrome (PBS) as its
extreme form (Fig. 11.2).
Beside terminology issues, 50–87% of patients suspected
of having PBS manifest a voiding dysfunction due to an over-
active pelvic floor.
Voiding dysfunction is defined by ICS as an intermittent
and/or fluctuating flow rate due to an involuntary intermit-
tent contraction of the peripheral striated muscle during
voiding in neurologically normal individuals.
The overactive pelvic floor is “A condition in which the
pelvic floor muscles do not relax, or may even contract when
relaxation is functionally needed, for example during micturi-
tion or defecation” (2005 report from the Pelvic Floor
Clinical Assessment Group of the ICS).
While in children this dysfunctional behavior may be the
result of an improper learning of pelvic floor muscle control,
in adults it is usually related to a voluntary prolonged holding
FREQUENCY-URGENCY SYNDROME
OAB HSB
IC: PBS
OAB wet Hunner lesion
Figure 11.2 East Asian view of IC/PBS taxonomy. Symptoms of

OAB and HSB substantially overlap. HSB is a condition of
increased bladder sensation usually associated with urinary fre-
quency and urgency with or without pain. The use of term “PBS/IC”
is limited to patients with HSB symptoms and bladder pathology
such as a Hunner’s lesion or glomerulations after bladder overdis-
tention. Controversial is the role of the finding of glomerulations
following bladder hydrodistention since it has not proven to be of
any significance
(habit, lifestyle, occupation, psychological distress) or may be

a consequence of direct trauma of pelvic musculature (vagi-
nal delivery, pelvic surgery).
Symptoms of overactive pelvic floor fall into three
categories:
• Pain
• Bladder function
• Bowel function
In addition to voiding and defecation, other conditions
such as sexual dysfunction and genital/pain syndromes (i.e.,
vulvodynia) are also commonly associated with pelvic floor
muscle overactivity.
There is a very close relationship between overactive pel-
vic floor and chronic pelvic pain although the mechanisms of
association are not completely understood. An overactive
pelvic floor shares several mechanisms with myofascial pain
syndrome. Myofascial pain syndrome typically occurs after a
muscle has been contracted repetitively. The subsequent
muscle spasm may induce the development of palpable taut
bands and trigger points which are hypersensitive painful
spots located within a definite set of tense muscle fibers
(Fig. 11.3). In addition abnormal tension can cause the accu-
mulation of inflammatory substances within the muscle
Trigger point complex
Normal fibers
Taut band
Nodule
Contraction knot
Figure 11.3 Trigger point complex. A hyperirritable spot in skeletal

muscle that is associated with a hypersensitive palpable nodule in a
taut band (group of tense muscle fibers extending around a trigger
point)
11.2 Diagnosis of PBS/IC 173
which cause pain. Pain in turn increases muscle spam becom-

ing a self-maintaining vicious cycle.
The role of pelvic floor overactivity is often neglected in
the assessment of patients with pelvic problems despite the
fact that a normalization of pelvic floor muscle function
through physical therapy may be crucial for the successful
management of symptoms.
11.2 Diagnosis of PBS/IC

Much work has been put into the attempt to define objective
diagnostic criteria for PBS/IC based on cystoscopy during
bladder hydrodistention, bladder wall biopsies, and urody-
namics. Results have, however, been frustrating. A more
advantageous approach is probably to establish a broad clini-
cal diagnosis, mainly on the basis of symptoms and exclusion
of other diseases, and then stratify patients by urodynamics,
cystoscopy, histology, and other tests according to the
significance of these findings regarding the treatment and
prognosis of the disease.
Note: In PBS delay of diagnosis is common, with an average

time of 3–7 years from the time of presentation to the general
practitioner to diagnosis by a specialist.
11.2.1 Symptoms and Signs
The characteristic presentation of PBS/IC includes a combi-

nation of pain, frequency, nocturia, and urgency, with pain
being the most common complaint. Typically pain, often
described as “pressure,” is felt in the suprapubic area, but it
can be referred to other areas in the pelvis such as the ure-
thra, vagina, labia, and perineum.
Worsening of symptoms (“flares”), triggered by stress,
intercourse, menses, or diet are commonly reported. Frequency
urgency is also prevalent and cannot distinguish PBS/IC from
OAB. A poor response to antimuscarinics may suggest a
PBS. In addition, pain is usually relieved by micturition,

which is not the case with OAB. Despite the absence of uri-
nary infection (UTI) being a prerequisite at the time of diag-
nosis, up to 50% of patients will have a previous history of
UTI.
A self-administered symptom score (also known as the
O’Leary-Sant Symptom Score) may be useful to establish
baseline symptoms severity.
The physical exam should include an abdominal and pelvic
exam. A suprapubic tenderness particularly at the bladder
neck level is often observed. In addition, palpating the ante-
rior vaginal wall along the course of the urethra up to the
bladder neck may elicit pain. Furthermore, in 50%–80% of
the patients, a pelvic floor overactivity may be present. A
systematic palpation of the pelvic floor muscles, looking for
tenderness, spasm/taut bands, and/or trigger points, is impor-
tant (Fig. 11.4).
Figure 11.4 Pelvic floor muscles systemic palpation: relevant land-

marks include anal sphincter, pubo-rectalis m. and pyriformis muscle
Also voiding diary helps to determine the severity of stor-

age symptoms. Usually the average voided volume is less
than 100 mL, and the average number of daytime voids
ranges from 17 to 25 compared to 6 in an asymptomatic
women. Pain should be recorded using a visual analogue scale
(VAS) for pain during the 24 h of voiding diary.
A urine dipstick represents the minimum required labora-
tory test. If signs of UTI are identified, a culture and sensitiv-
ity are required.
11.2.2 Confusable and Associated Diseases
According to ESSIC, confusable disease is a disease which

may show similar symptoms and/or signs to those of BPS/
IC. In general, such a confusable disease needs to be excluded
as the main cause of the symptoms and/or signs before a diag-
nosis of BPS can be made. Confusable diseases include malig-
nancies, UTI, gynecological conditions, and other bladder
conditions (see Box 11.1).
Box 11.1: PBS/IC—Relevant Confusable Diseases
Malignancies Other bladder conditions

Bladder ca in situ OAB-S
Cervical, uterine, ovarian cancer VD-S
Urinary tract infections Gynecological conditions
Intestinal bacteria Endometriosis
Chlamydia, ureaplasma, Candidiasis
mycoplasma
Herpes simplex POP
HPV
Various
Pudendal nerve entrapment
Box 11.2: PBS/IC—Relevant Associated Diseases

• Allergic disorders
• Crohn’s disease
• Fibromyalgia
• Irritable bowel syndrome
• Rheumatoid arthritis
• Sjogren’s syndrome
• Lupus erythematosus
• Thyroid disorders
• Vulvodynia
Confusable diseases should be distinguished from associ-

ated diseases. Associated diseases are diseases with a higher
prevalence among patients with BPS than in the general
population. The practical consequence of associated dis-
eases is that medical professionals should know these asso-
ciations and should have a higher index of suspicion for
PBS/IC.
Relevant associated diseases are reported in the Box
11.2.
11.2.3 Specific Tests
11.2.3.1 Cystoscopy
Cystoscopy performed alone, without hydrodistention, is

expected to be normal (except for discomfort and reduced
“functional” bladder capacity) in the majority of patients. The
classic findings of glomerulations are reliably identified only
after a formal hydrodistention under anesthesia. Therefore,
the purpose of cystoscopy alone should only be viewed as a
tool to rule out bladder cancer/carcinoma in situ.
11.2.3.2 Potassium Sensitivity Test
The potassium sensitivity test is no longer recommended as a

standard evaluation for IC/BPS. The test is unreliable and
mostly distressing, with patients experiencing severe pain
both during and after the procedure.
11.2.3.3 Urodynamics
Overall, UDS studies are not recommended in the standard

diagnostic evaluation of a patient suspected of having IC/
BPS. Common findings on filling cystometry are a stable blad-
der with reduced first sensation of void (<100 mL) and reduced
cystometric capacity (Fig. 9.5). Detection of detrusor overactiv-
ity, present in 15% of patients suspected of having IC/PBS,
should exclude automatically the diagnosis, but may lead the
clinician to initiate therapy with antimuscarinics. Whether these
patients respond better to antimuscarinics than BPS patients
with stable bladders has never been systematically investigated.
Micturition assessment through pressure flow studies, with or
without electromyography, may be useful in patients which
complain coexistent voiding symptoms. In these cases a dys-
functional voiding due to an overactive pelvic floor is frequently
seen (Fig. 10.1). Resting urethral profilometry usually indicate
an high MUCP. Voiding dysfunction may be presumed less
invasively by an intermittent “free” flowmetry pattern and by
an ultrasound evaluation of post-void residual urine.
11.2.3.4 Hydrodistention
Hydrodistention under general anesthesia allows for stratifica-

tion of patients into those with more classic disease associated
with Hunner’s lesion and glomerulations from those with no
obvious mucosal abnormalities. The technique involves gravity
filling of the bladder at 70–100 cmH2O for a minimum of
2 min. Bladder capacity is fixed when the inflow backs up in
the drip chamber or leakage occurs per urethra. A reduced
bladder capacity (< 400 mL) does correlate with pain, but
more than 50% of patients with IC/BPS show capacities more
than 800 mL under anesthesia. The presence of terminal hema-
turia upon draining the infusion fluid and the appearance of
petechial submucosal hemorrhages (glomerulations) has been
suggested to be characteristic of IC/BPS. A recent review of
the literature, however, found no convincing evidence that
glomerulations should be included in the diagnosis or pheno-
typing of bladder pain syndrome/interstitial cystitis.
Glomerulations do not correlate with symptoms and are found
in patients without bladder pain syndrome/interstitial cystitis.
In addition, approximately 8% of patients with a diagnosis of
IC/BPS do not show glomerulations. Hunner’s ulcer seems
more specific for IC. However, over the years, controversy has
developed as to the prevalence and even the actual existence
of the Hunner’s lesion, and some urogynecologists believe that
they are rare, or do not exist. Despite these limitations, hydro-
distention is still the most accepted diagnostic criteria.
11.2.3.5 Bladder Biopsies

There are no specific features found on bladder biopsy to
confirm a diagnosis of IC/BPS. Findings related to chronic
inflammation are not specific, overlapping with other etiolo-
gies, and they correlate poorly to cystoscopic findings. In
addition, between 30 and 43% of patients with a clinical diag-
nosis of IC/BPS may have normal histology.
Keynotes for Clinical Practice

• IC/PBS is a clinical and cystoscopic diagnosis.
• Urodynamic testing is not recommended for routine
clinical use in IC/PBS diagnosis but only in patients
refractory to first-line therapy.
• Pain during filling cystometry with a stable bladder
(hypersensitivity) is consistent with IC/PBS.
11.3 Outline of Available Treatments 179
• Detrusor overactivity is seen in approximately

15–20% of IC/BPS patients. In these cases, it can be
difficult to determine whether the diagnosis is DO
alone or IC/BPS in combination with DO. Usually,
patients with IC/PBS are less responsive to antimus-
carinic drugs.
• Most patients will have normal compliance.
• Urodynamic evaluation may provide information
regarding concomitant voiding dysfunction.
• Pelvic floor muscle dysfunction may manifest as
intermittent flow and high resting urethral pressure.
• On pressure/flow study preferably with pelvic floor
EMG, functional bladder obstruction can be diag-
nosed by a poor relaxing sphincter sometimes asso-
ciated with poor detrusor contractility due to
bladder inhibition from non-relaxing pelvic floor
muscles.
11.3 Outline of Available Treatments

A complete discussion of the subject is beyond the goal of the
chapter.
PBS/IC is a heterogeneous condition challenging to man-
age, with no treatment that is successful for all patients.
Multiple options exist, ranging from conservative therapies
with few side effects to major abdominal surgery. Patients can
be identified with characteristic phenotypic patterns based on
proposed mechanisms and symptom complexes. The UPOINT
phenotypic classification system, recently described by Nickel
and adopted by the EAU, may be a useful tool to characterize
patients with PBS/IC and guide potential therapies (see
Box 11.3).
180
Box 11.3: Phenotypic Management Paradigm for the Treatment of BPS/IC

UPOINT*
SYMPTOMS PHENOTYPES adapted from Nickel et al., 2014
Organ-specific
Urinary Infectious Neurologic/systemic Tenderness
Psychosocial Non-Hunner’s Hunner’s
Bladder training Antimicrobials Gabapentanoids Pelvic floor
Anticholinergics Stress management Amitriptyline Hydroxyzine physiotherapy,
and Cimetidine Endoscopic Cimetidine massage,
psychological support Hydroxyzine (Fulguration, Sacral neuromodulation acupuncture,
PPS laser, resection, trigger point
Quercelin steroid injection) injections
Hydrodistention Intravesical agents
Botulinum toxin A (DMSO, Hep, HA,
Sacral neuromodulation CS, alkalinized
Radical surgery lidocaine, PPS)
Hydrodistension
Botulinum Toxin A
Radical surgery
*UPOINT (Urinary, Psychosocial, Organ-specific, Infective, Neurologic, Tenderness)

Chapter 11. UDS in Pain Bladder Syndrome (PBS)
Suggested Readings
Overviews and Guidelines

Hanno P, Cervigni M, Dinis P, Nickel C, Nordling J, van Ophoven
A, et al. Bladder pain syndrome. In: Abrams P, Cardozo L,
Wagg A, Wein A, editors. Incontinence. Tokyo: ICS-ICUD; 2017.
p. 2203–301.
Doggweiler R, Whitmore KE, Meijlink JM, Drake MJ, Frawley H,
Nordling J, et al. A standard for terminology in chronic pelvic
pain syndromes: a report from the chronic pelvic pain working
group of the international continence society. Neurourol Urodyn.
2017;36:984–1008.
Cox A, Golda N, Nadeau G, Curtis Nickel J, Carr L, Corcos J,
Teichman J. CUA guideline: diagnosis and treatment of inter-
stitial cystitis/bladder pain syndrome. Can Urol Assoc J.
2016;10:E136–55.
Hanno PM, Erickson D, Moldwin R, Faraday MM, American
Urological Association. Diagnosis and treatment of interstitial
cystitis/bladder pain syndrome: AUA guideline amendment. J
Urol. 2015;193:1545–53.
Davis NF, Gnanappiragasam S, Thornhill JA. Interstitial cystitis/
painful bladder syndrome: the influence of modern diagnostic
criteria on epidemiology and on Internet search activity by the
public. Transl Androl Urol. 2015;4:506–11.
van de Merwe JP, Nordling J, Bouchelouche P, Bouchelouche K,
Cervigni M, Daha LK. Diagnostic criteria, classification, and
nomenclature for painful bladder syndrome/interstitial cystitis:
an ESSIC proposal. Eur Urol. 2008;53(1):60–7.
Offiah I, McMahon SB, O’Reilly BA. Interstitial cystitis/bladder
pain syndrome: diagnosis and management. Int Urogynecol J.
2013;24(8):1243–56.
Homma Y. Hypersensitive bladder: a solution to confused termi-
nology and ignorance concerning interstitial cystitis. Int J Urol.
2014;21(Supp 1):43–7.
Cervigni M, Natale F. Gynecological disorders in bladder pain syn-
drome/interstitial cystitis patients. Int J Urol. 2014;21(Supp 1):85–8.
Fall M, Logadottir Y, Peeker R. Interstitial cystitis is bladder pain syn-
drome with Hunner’s lesion. Int J Urol. 2014;21(Suppl 1):79–82.
Wennevik GE, Meijlink JM, Hanno P, Nordling J. The role of
glomerulations in bladder pain syndrome: a review. J Urol.
2016;195:19–25.
Urodynamics
Kuo YC, Kuo HC. The urodynamic characteristics and prognostic
factors of patients with interstitial cystitis/bladder pain syndrome.
Int J Clin Pract. 2013;67(9):863.
Kirkemo A, Peabody M, Diokno AC, Afanasyev A, Nyberg LM Jr,
Landis JR, et al. Associations among urodynamic findings and
symptoms in women enrolled in the Interstitial Cystitis Data
Base (ICDB) study. Urology. 1997;49:76.
Steinkohl WB, Leach GE. Urodynamic findings in interstitial cystitis.
Urology. 1989;34:399.
Kuo HC, Chang SC, Hsu T. Urodynamic findings in interstitial cysti-
tis. J Formos Med Assoc. 1992;91:694.
Various
Ogawa T, Ishizuka O, Ueda T, Tyagi P, Chancellor MB, Yoshimura
N. Current and emerging drugs for interstitial cystitis/bladder pain
syndrome (IC/BPS). Expert Opin Emerg Drugs. 2015;20:555–70.
Nickel JC, Irvine-Bird K, Jianbo L, Shoskes DA. Phenotype-directed
management of interstitial cystitis/bladder pain syndrome.
Urology. 2014;84:175–9.
Chapter 12
Neurogenic Lower Urinary
Tract Dysfunction Syndrome
(NLUTD-S) in Female
12.1 Background
Neurogenic bladder or neurogenic lower urinary tract
dysfunction syndrome (NLUTD-S) is a bladder symptom

complex caused by a lesion in the brain or spinal cord associ-
ated with a congenital condition (e.g., myelomeningocele), an
acquired stable condition (e.g., stroke, spinal cord injury), or
an acquired progressive condition (e.g., multiple sclerosis,
Parkinson’s disease, dementia).
The type of bladder dysfunction depends on the site,
extent, and evolution of the lesion. From the functional point
of view, the two most significant urodynamic findings are
neurogenic detrusor overactivity (NDO), responsible of uri-
nary incontinence, and detrusor sphincter dyssynergia (DSD),
responsible of poor bladder emptying. Both result in elevated
bladder pressure during the storage and voiding phases that
often lead to structural bladder damage, vesicoureteral reflux
(VUR), upper urinary tract dilation, and renal failure.
12.2 Classification
Several classification systems have been proposed. A simple
classification system for use in daily practice that focuses
mainly on therapeutic consequences has been proposed by

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_12
184 Chapter 12. NLUTD-S in Female
Madersbacher and adopted by the EAU. This classification

describes several NLUTD symptoms and findings on the
basis of the contraction state of the bladder and external ure-
thral sphincter during voiding and the filling phase (Fig. 12.1).
• Supraspinal lesion
Supraspinal lesions (above the pons) have predominantly
storage symptoms, DO on urodynamics and absent PVR on
ultrasounds.
• Spinal lesion
Spinal lesions (between the pons and sacral cord) have
both storage and voiding symptoms, DO with DSD on urody-
namics and PVR usually raised on ultrasounds.
• Sacral/infrasacral lesion
Sacral/infrasacral lesion (sacral cord and peripheral
nerves) have predominantly voiding symptoms, hypocontrac-
tile or acontractile detrusor on urodynamics.
Note: Since bladders at the same level of lesion may
behave differently over time depending on the etiology of
neurogenic lesion, recently Powell proposed a new classifica-
tion named SALE (Stratify by Anatomic Location and
Etiology) to better guide the management of the bladder as
well as inform about prognosis. The classification includes
seven categories, each having a neurologic defect in a distinct
anatomic location. In addition to bladder dysfunction, the
presence or absence of bowel dysfunction and autonomic
dysreflexia is reported. Furthermore, as more definite data
will be gathered from the assessment of biomarkers, urinary
nerve growth factor (NGF), and urinary brain-derived neuro-
trophic factor (BDNF), levels will be added to the classifica-
tion to give more prognostic information.
Suprapontine lesion
overactive
History predominanatly storage symptoms
Ultrasound insignificant PVR
Urodynamics detrusor overactivity
normoactive
Spinal (infrapontine-suprasacral) lesion
History both storage and voiding symptoms overactive
Ultrasound PVR usually raised
Urodynamics detrusor overactivity,detrusor-sphincter dyssinergia
overactive
Sacral/Infrasacral lesion
underactive underactive
History predominanatly voiding symptoms
Ultrasound PVR raised
Urodynamics hypocontractile or acontractile detrusor normoactive underactive
12.2 Classification
Figure 12.1 NLUTD classification

185
12.3 Clinical Assessment of Female

with NLUTD-S
Despite the complexity of neural control, symptoms of neu-
rogenic bladder dysfunctions can be simply classified in fail-
ure to store and failure to emptying with a large group of
patients showing a combination of incomplete emptying and
bladder overactivity.
Clinical assessment can be divided in:
• Initial assessment (noninvasive)
• Specialized assessment (mostly invasive)
12.4 Initial Assessment
12.4.1 History and Physical Examination
Neurologic history and neurological status including mobility,

hand function, mental status, comprehension, spasticity,
motor, and sensory status should be evaluated and prior sur-
gery (hysterectomy, anti-incontinence surgery) and medica-
tions recorded. In parallel to the bladder symptoms, clinicians
should ask about sexual and bowel dysfunction. Special
attention should be paid to potential symptoms and signs that
may indicate the presence of complications (i.e., pain, infec-
tion, hematuria, and fever). Quality of life should be assessed
as well. Information obtained from the history can be supple-
mented by a bladder diary that records the time and volume
of each voiding, urinary output and episodes of incontinence
and urgency.
Physical examination should include the assessment of
sensation in lumbosacral dermatomes, anal tone, and volun-
tary contraction of the anal sphincter, bulbocavernosus, and
anal reflexes.
12.4 Initial Assessment 187
12.4.2 Routine Laboratory Investigations
Blood tests are performed to assess renal functions including

serum creatinine. Urine dipsticks and, if necessary, urine cul-
ture are sent to exclude urinary tract infections, and this
should also be carried out before invasive procedures such as
urodynamics or cystoscopy.
Blood tests are performed to assess renal functions includ-
ing serum creatinine. Urine dipsticks and, if necessary, urine
culture are sent to exclude urinary tract infections, and this
should also be carried out before invasive procedures such as
urodynamics or cystoscopy.
12.4.3 Ultrasound
Ultrasound scanning can be used to assess morphological

changes in the upper or lower urinary tract, such as upper
urinary tract dilatation, stones, pyelonephritic scars, and, in
advanced kidney disease, renal atrophy. Bladder ultrasound
can detect stones, bladder wall thickness, and any large muco-
sal lesions. Bladder ultrasound is also performed in patients
who can void, to assess the post-void residual (PVR) volume.
In patients with impaired voiding, a PVR of more than
100 mL is thought likely to contribute to bladder dysfunction,
although there is no consensus about the figure of PVR at
which intermittent self-catheterization should be initiated.
Initial assessment will provide a presumed diagnosis of:
• Incontinence due to sphincteric weakness with negligible
PVR
• Incontinence due to detrusor overactivity with negligible
PVR
• Incontinence due to detrusor overactivity with associated
emptying disorder (high PVR)
allowing an empirical treatment with intermittent catheter-
ization and/or antimuscarinics alone or in combination.
12.5 Specialized Assessment
12.5.1 Urodynamics with Imaging Techniques
Often it is impossible to anticipate the nature of NLUTD-S

from initial assessment alone, particularly in incomplete
lesions. In addition, severity of NLUTD-S does not necessar-
ily correspond with severity of neurological lesion. Despite a
recent criticism, the use of multichannel cystometry and pres-
sure flow studies with synchronous imaging (videourodynam-
ics (VUD)) is considered the gold standard for the evaluation
of patients with NLUTD-S.
Urodynamic investigation evaluates multiple functional
parameters in NLUTD-S including:
• Bladder sensation during filling cystometry
• Detrusor function and compliance during filling
cystometry
• Detrusor leak point pressure in patients with impaired
detrusor compliance
• Cystometric bladder capacity
• Sphincter function during bladder filling
• Detrusor/sphincter function during voiding
• Post-void residual
Bladder pressure and sphincter EMG measurement, com-
bined with fluoroscopy, are the ideal methods to investigate
NLUTD-S. If videourodynamic facilities are not available, a
simple cystography with voiding phase can be carried out.
This will evaluate vesicoureteral reflux, indicate the level of
bladder outlet obstruction (bladder neck, external urethral
sphincter), and show the appearance of the bladder wall.
Compliance, detrusor leak point pressure, and “safe blad-
der capacity” are the most significant parameters recorded
during filling phase. Detrusor leak point pressure is the low-
est intravesical pressure at which leakage occurs around the
catheter. The bladder volume at which detrusor pressure
equals 40 cm H20 is considered patient’s maximal “safe blad-
der capacity.” Therefore, if the bladder volume remain below
the maximal “safe bladder capacity,” the detrusor pressure
should remain safe for the upper urinary tract.
12.5 Specialized Assessment 189
EMG of the urethral sphincter has been used for decades

in the diagnosis of NLUTD-S; however, its value in practice
remains uncertain. The use of needle or surface electrodes is
debated. Urethral concentric needle electrodes were found to
be superior to surface patch electrodes for evaluating relax-
ation of the muscle during voiding. Furthermore, with surface
electrodes bladder dysfunction is related more to the anal
sphincter than to the urethral sphincter. However, patch elec-
trodes are more convenient for routine clinical practice.
Rhythmic detrusor contractions on cystomanometry with
associated marked increase in EMG activity on attempted
voiding are the relevant characteristics of patients with
DSD. There are three types of DESD (Fig. 12.2). Type 1 has
a crescendo increase in EMG activity that reaches a maxi-
mum at the peak of the detrusor contraction and then relaxes
allowing unobstructed micturition, type 2 has clonic sphincter
contractions interspersed throughout the detrusor contrac-
tion with a typically interrupted flow, and type 3 is
characterized by a sustained sphincter contraction that
DESD TYPES
TYPE 1
TYPE 2
TYPE 3
Figure 12.2 Types of DESD. Type 1 shows a temporary failure of

the EMG to silence during detrusor contraction and is not obstruct-
ing. Type 2 is intermittent but not obstructing. Type 3 shows a cre-
scendo of the EMG throughout the detrusor contraction and is
obstructing
coincides with the detrusor contraction and does not permit

any kind of flow. In some patients this high bladder pressure
condition can give rise to autonomic dysreflexia (see below).
Note: A recent ICS report on terminology for adult neuro-
genic lower urinary tract dysfunction (ANLUTD) introduced
two new types of neurogenic detrusor overactivity in addition
to pre-existing phasic and terminal detrusor overactivity: sus-
tained detrusor overactivity, defined as a continuous detrusor
contraction whithout returning to the detrusor resting pres-
sure and compound detrusor contraction, defined as a phasic
detrusor contraction with subsequent increase in detrusor
base pressure.
12.5.2 D
ifficult Situation During Urodynamic
Testing in NLUTD-S: Autonomic
Dysreflexia (AD)
Spinal cord injuries above the sixth thoracic neurotome (tet-
raplegia or high paraplegia) may be complicated by a phe-
nomenon known as autonomic dysreflexia. AD is a potentially
life-threatening acute condition due to excessive sympathetic
responses to noxious stimuli below the level of lesion which
leads to diffuse vasoconstriction and hypertension. A compen-
satory parasympathetic response produces bradycardia and
vasodilation above the level of the lesion, but this is not suf-
ficient to reduce elevated blood pressure. Typical stimuli
include bladder distention and bowel impaction but also
medical procedures such as urodynamic testing and cysto-
urethroscopy. Common clinical manifestations of this
troublesome event are headache, flushing, blurred vision,
nausea, and increased blood pressure. Bradycardia is common.
Note: Patients with SCI above T6 have normal/baseline
systolic blood pressure in the 90–110 mmHg range. Systolic
blood pressure elevations more than 20 mm–40 mmHg above
baseline may be a sign of AD.
Autonomic dysreflexia is the only urodynamic emergency.
Management of acute attacks includes immediately sitting
12.5 Specialized Assessment 191
the patient upright to orthostatically lower blood pressure,

removal of any tight-fitting garments, correcting noxious elic-
iting stimuli (i.e., bladder distension), and prompt reduction
of blood pressure with a rapid-onset/short-duration agent
like nifedipine (10 mg SL) or captopril (25 mg SL).
Note: Unfortunately, it is not always possible to start the
management on time, since the AD episode may be “silent”,
i.e., without clear symptoms. In these conditions, a further
increase in blood pressure may end in a life-threatening
condition. High index of suspicion is needed. Monitoring
blood pressure during UDS testing is of utmost importance.
Avoidance of provoking stimuli is important in preventing
attacks. Nifedipine, prazosin, and terazosin should be also
used prophylactically to prevent an attack. Recently, a single
cycle of 200 units of intradetrusor injected of onabotulinum-
toxinA has been shown to decrease the severity and fre-
quency of bladder-related AD episodes improving bladder
function and quality of life.
12.5.3 Reappraisal of Urodynamic Testing

and Videourodynamics in NLUTD-S
As mentioned before, the role of urodynamics and videouro-
dynamics has been recently questioned since there are inad-
equate data to support its routine use in NLUTD-S. Overall,
routine urodynamics should be recommended in conditions
of “high-pressure bladder” as opposed to urodynamically
“safe” bladder.
More specifically, the EAU recommend that in high-risk
patients (defined by a high filling pressure (>40 cmH2O),
poor compliance (<10 mL/cm H2O), and high detrusor leak
point pressure (>40 cmH2O)), upper urinary tract should be
checked by urine laboratory, creatinine, and renal ultrasound
once every 6 months (LE 4, Grade A) reserving conventional
UDS or VUD when either are abnormal (expert opinion).
Likewise, the evidence regarding the added value of video
to conventional urodynamics is controversial. In a broader
context, VUD has been advocated in situations in which UDS
alone fails to provide sufficient diagnostic information to

guide therapy, especially in patients with relevant neurologi-
cal disease. Nevertheless, it is debated whether VUD is
always necessary for every patient with NLUTD-S. As
previously said, critical questions such as storage pressures
and mechanisms of emptying can often be answered with
simpler UDS testing eventually joined to a voiding cystoure-
thrography (VCUG) if VUD facilities are unavailable.
Current guidelines (ICS, ICI, AU, AUA/SUFU, NICE) do not
specify the added value of imaging to urodynamics neither
for management nor for outcome. In addition, none of these
guidelines discusses the potential drawbacks (necessity of
special equipment, time, and expense) and harm (radiation
exposure) of the investigation. Recommendations are based
on single center series and expert opinion.
12.6 Complications and Follow-Up

of Neurogenic Bladder Dysfunction
Complications of neuropathic bladder dysfunction have
been reported most often in patients with spinal cord injury.
Up to the 1950s, upper urinary tract damage was the primary
cause of mortality in this group of patients, but with newer
advances, urinary complications are now relatively low. The
commonest complications include upper and lower urinary
tract infections and stones. Less commonly, morphological
damage may occur in the lower urinary tract, such as diver-
ticula, trabeculae, wall thickening, and pelvic organ prolapse.
Upper tract complications include vesicoureteral reflux and
kidney failure. In addition, the risk of squamous-cell carci-
noma of the bladder is increased in patients with a long-term
history of an indwelling catheter and recurrent urinary tract
infections.
Patients with neurogenic bladder dysfunction, especially
those with MS and spinal cord injury, need a regular neuro-
urological follow-up. Optimum frequency and components of
follow-up evaluations remain controversial. In spinal cord
injury, most guidelines propose an assessment of the upper
urinary tract functions using serum creatinine and ultrasound
12.7 Principles of Treatment of NLUTD-S 193
every year reserving multichannel urodynamics to specific

clinical situations like periodic control of high-pressure
systems and uncontrollable UTI.
12.7 Principles of Treatment of NLUTD-S

The primary goals for treatment of NLUTD-S should be:
• Protection of the upper urinary tract
• Restoration of the LUT function (complete bladder emp-
tying and dryness) and improvement of the patient’s QoL
Note: The risk of developing upper urinary tract damage
and renal failure is much lower in patients with slowly pro-
gressive non-traumatic neurological disorders than in those
with spinal cord injury or spina bifida.
The principles of treatment of NLUTD-S are the same in
female and male. However, practical management may be
different between genders. Female patients usually have
more severe urinary incontinence due to anatomical reasons
but, unlike the male, cannot use external appliances to
collect urine and prevent urine soiling. In addition, CIC
may require more facilities and resources for women. It
follows that women may need a larger amount of diapers to
manage their incontinence and often recur to an indwelling
catheter.
Restoration of LUT function includes:
• Management of bladder emptying
• Management of storage symptoms
Management typically begins with anticholinergic medica-
tions and clean intermittent catheterization. Patients who fail
this treatment because of inefficacy or intolerability are can-
didates for a spectrum of more invasive procedures. Patients
with incompetent sphincters are candidates for sling surgery
or artificial sphincter implantation. Coordinated bladder
emptying is possible with neuromodulation in selected
patients. Bladder augmentation, usually with an intestinal
segment, and urinary diversion are the last resort.
12.8 Management of Bladder Emptying
12.8.1 Spontaneous Voiding
Patients can be instructed to void by abdominal stimulation

(triggered reflex voiding), the Crede maneuver, or abdominal
straining (Valsalva). However, spontaneous voiding with and
without triggered voiding and/or bladder expression has been
proven to be less safe than CIC.
12.8.2 Intermittent Catheterization
Impaired emptying is most often managed by clean intermit-

tent self-catheterization, and this should be initiated if the
post-void residual urine is greater than 100 mL or exceeds
one-third of bladder capacity or, rarely, if spontaneous void-
ing is dangerous due to high detrusor pressure.
Intermittent catheterization is designed to simulate nor-
mal voiding. Usually, the average adult empties the bladder
four to five times a day. Thus, catheterization should be done
four to five times a day; however, individual catheterization
schedules may vary, depending on the amount of fluid taken
in during the day.
CIC can be done by patient himself or by a caregiver.
The most common barriers on IC are insufficient hand
function, inability to sit properly, and spasticity. IC may be
easily applicable for patients with paired hand functions such
as paraplegics, but it can be difficult for the patients who do
not have enough hand functions. Unlike male, female patient
presents several potential difficulties with IC in that the ure-
thral meatus is more difficult to access particularly for
patients confined to a wheelchair. In fact, the need to cathe-
terize four to six times daily can be quite a challenge for
many women confined to a wheelchair, since they need to
recline or lie flat and remove clothing in order to access the
urethral meatus and, unfortunately, in most cases, the acces-
sible bathrooms are not large enough to recline or lie down.
12.8 Management of Bladder Emptying 195
In addition, for women who cannot successfully perform

regular IC, there are no reliable devices to collect urine leak-
age. Therefore, many female patients confined to a wheel-
chair are more likely to use a chronic indwelling catheter or
wear a diaper with all potential inherent dangers.
Fear of accidentally injuring self is another common con-
cern among patients not confined to a wheelchair.
Appropriate instruction to the patient can help overcome
natural reluctance (Fig. 12.3). Catheterization may be per-
formed in any clean washroom, possibly with a counter space
within reach. “Clean” technique, without disinfectant or
gloves, usually prevents infection without the need for abso-
lute sterility. Hands must be washed thoroughly with soap
and water and then rinsed and dried. Fingernails should be
short and clean. Position should be comfortable. At the begin-
ning, a mirror could be helpful in outlining the anatomy.
Vagina should be washed from front to back with soap and
water. Catheters are usually pre-lubricated. Using non-
dominant hand (i.e., left hand for right-handed women), labia
should be spread with index and ring fingers, whereas the tip
of middle finger feel the urethral meatus. Then, using
1 - enlarge labia
meatus
2 - insert catheter
vagina
Figure 12.3 Technique of self-intermittent catheterization in women

(see text)
ominant hand, catheter is slowly inserted into the urethra

d
for about 5 centimeters until the urine begins to flow. Urine
can be drained into a container or directly into the toilet if
there is no need to measure the amount drained. Gentle
straining may help bladder emptying. Catheter is then gently
withdrawn (Box 12.1).
Box 12.1: Self-catheterization technique

1. Assemble the necessary supplies and have them close
at hand.
2. Wash your hands with water and soap.
3. Get into a comfortable sitting position over the toilet
rim or lying on the bed; then spread your thighs wide
apart and separate vaginal labia with one hand.
4. Wash vaginal ostium from front to back with soap
and water; then rinse and dry.
5. Squeeze the envelope of the catheter in order to
lubricate it.
6. Using non-dominant hand spread labia to expose

urethral opening; using the middle finger, feel the
meatus.
7. Using dominant hand gently insert the catheter into the
urethra for about 5 cm until the urine begins to flow.
8. Drain urine into a container or directly into the toilet
if there is no need to know the amount of urine
drained.
9. When urine stops flowing, withdraw the catheter

slowly.
Another important concern about the IC is the infection.

Although infection is a common problem in patients on IC,
potential risk of infection is lower in patients on IC than in
patients on indwelling catheterization. Usually, the infections
that do occur are managed without complications. In general,
routine use of long-term suppressive therapy with antibiotics
in patients with chronic clean intermittent catheterization is
not recommended since the use of chronic suppressive
12.8 Management of Bladder Emptying 197
antibiotic therapy may result in the emergence of resistant

bacterial strains.
12.8.3 Indwelling Urethral Catheters
Many female patients prefer the simplicity of an indwelling

catheter, and this view is also shared by many urologists. With
an indwelling catheter, bladder pressures are not a problem,
and the bladder is always adequately drained. However, an
indwelling catheter is associated with significant potential mor-
bidity including risks of recurrent urinary tract infection, hema-
turia, bladder stones, vesicoureteral reflux, and bladder cancer.
Indwelling catheters must be changed at least once a month.
They may be changed at an office, a clinic, or at home by a visit-
ing nurse. The standard catheter size is 16F or 18F, with a bal-
loon filled with 10 mL of sterile water. Catheters that develop
encrustations and problems with urine drainage must be
changed more frequently. Routine irrigation of catheters is not
required. However, some authors favor the use of 0.25% acetic
acid irrigation (30 mL) because it is bacteriostatic, minimizes
catheter encrustation, and diminishes the odor.
All indwelling catheters that remain in the urinary bladder
for more than 2 weeks become colonized with bacteria.
Bacterial colonization does not mean the patient has clinical
bladder infection. When bladder infection occurs (foul odor,
purulent urine, hematuria), the catheter and drainage system
should be changed.
One of the major problems in females with an indwelling
catheter is the erosion of the urethra. The typical presentation
is that of a patient who has required a gradual increase in
catheter diameter to stay dry with a progressive increase in
the balloon fluid. Urethral erosion can be a very difficult
problem that, invariably, requires surgical intervention.
Reconstruction of damaged urethra with simultaneous autol-
ogous sling can be attempted with small urethral erosion and
in patients willing to accept the practice of CIC after surgery.
Otherwise, when urethral erosion is not amenable to sling
placement, transabdominal bladder neck closure done in con-
junction with a urinary diversion is a viable option.
12.9 Management of Storage Symptoms

Storage symptoms are most often managed using antimusca-
rinic medications. Other options include desmopressin to
reduce urine output or intradetrusor injection of botulinum
toxin type A to reduce detrusor overactivity.
12.9.1 Antimuscarinic Drugs
Anticholinergic treatment is the first-line therapy for neuro-

genic detrusor overactivity. This treatment works by blocking
cholinergic transmission at muscarinic receptors. Several
drugs are currently available including:
Anticholinergic agents have similar efficacy; however, they
have different side effect and tolerability profiles that depend
on their muscarinic receptor selectivity and the rate of drug
distribution. Anticholinergic drugs that bind M1 receptors
might produce impairments of memory and cognition. Agents
that bind M2 receptors can produce QT interval prolongation
that causes tachycardia and arrhythmias. Anticholinergic
drugs that bind M3 receptors might produce constipation
visual blurring and xerostomia.
The side effects of anticholinergic therapy have led to poor
compliance with long-term use. In attempts to improve the
efficacy and tolerability of anticholinergic therapy, several
newer drugs have been developed that are available in
sustained release formulations.
Sustained release formulations seem to have less side
effects of the correspondent immediate release formulations.
In addition, different routes of application have been pro-
posed. A transdermal oxybutynin system was found to be
efficacious in SCI patients with neurogenic detrusor overac-
tivity and was well tolerated at up to three times the standard
dose; however, skin irritation was a common side effect.
12.9 Management of Storage Symptoms 199
12.9.2 Botulin Toxin
Intradetrusor injections of onabotulinumtoxinA have trans-

formed the management of neurogenic detrusor overactivity.
Botulinum toxin A blocks neuromuscular transmission by
binding to acceptor sites on motor or autonomic nerve termi-
nals and inhibiting the release of acetylcholine. The inhibition
occurs as the neurotoxin cleaves a protein critical to the
successful docking and release of acetylcholine from presyn-
aptic vesicles located within the nerve endings.
When injected into the muscle at therapeutic doses, botu-
linum toxin A produces a temporary chemical denervation of
the muscle, resulting in a localized reduction in muscle activ-
ity. Evidence exists that reinnervation of the muscle may
occur, thus slowly (6 months) reversing the muscle denerva-
tion produced by botulinum toxin A. Another mechanism for
the effect of botulinum toxin A on detrusor overactivity may
be related to its effect on sensory receptor expression in
suburothelial fibers that may play a role in the pathophysiology
of detrusor overactivity.
Botulinum toxin A may be used as monotherapy or in
conjunction with anticholinergic therapy.
Intradetrusor injection of botulinum toxin A may be per-
formed via rigid or flexible cystoscopy, depending on the
urogynecologist’s preference (Fig. 12.4).
The recommended dose is 200U per treatment, but doses
of 150U and 100U achieve a similar rate of excellent results
with significantly fewer adverse events including the duration
of therapeutic effectiveness. The effects of treatments last at
least 9 months.
The most common adverse event of intradetrusor injection
of botulinum toxin A is an increased post-void residual,
which may necessitate clean intermittent catheterization.
Thus, patients should be counseled about the potential need
for clean intermittent self-catheterization. Other side effects
DETRUSOR INJECTIONS OF BOTULINUM TOXIN A
100 ml bladder volume
1 ml Botox©
Avoid the trigone
Figure 12.4 Schematic representation of intradetrusor injections of

Botox (Allergan, Irvine, CA). At equally spaced points, several dis-
tinct injections according to the chosen dosage, each containing
1 mL of reconstituted onabotulinumtoxinA, are made sparing the
trigone
include mild hematuria and urinary tract infection. Usually,

there are no systemic side effects, but one study reported a
mild case of asthenia after injection of botulinum toxin
A 300U, which persisted for 10 days.
12.9.3 Neuromodulation
When pharmacotherapy fails to relax an overactive detrusor,

neuromodulation may be considered a suitable option.
Neuromodulation can be performed at different sites includ-
ing sacral, pudendal, and tibial nerves. However, the most
commonly described site of neuromodulation for treatment
of OAB is the third sacral nerve root (S3).
Despite the substantial usage of the technique over the
past two decades, the exact mechanism remains poorly
12.9 Management of Storage Symptoms 201
e lucidated. The current leading hypothesis suggests that neu-

romodulation works by stimulating peripheral somatic affer-
ent nerves (C fibers). Stimulation of the peripheral afferent
nerve blocks competing abnormal visceral afferent signals
from the bladder and prevents reflex bladder hyperactivity or
retention However, the effects of neuromodulation are not
just limited to spinal cord reflexes since functional magnetic
resonance imaging (MRI) studies demonstrate changes of
brain activity with SNM (Fig. 12.5).
(–)
Bladder C-fiber afferents (+)

PTNS
(–) SNM
Posterior tibial (–)
afferent (+)
Bladder efferent (–)
Pudendal afferent (+)
PNM
Figure 12.5 Techniques of neuromodulation. Neuromodulation is

postulated to work in the setting of bladder overactivity by activat-
ing peripheral somatic afferent nerves (i.e., the pudendal or poste-
rior tibial nerve) which in turn inhibit signals from the bladder
afferents at the level of the spinal cord and thus disrupt an aberrant
micturition reflex. Conversely, neuromodulation is postulated to
work in the setting of urinary retention by restoring normal afferent
signaling from the bladder in the midbrain and reducing cortical
activity which stimulates the guarding reflex
Sacral and pudendal neuromodulation are performed as a

staged procedure in order to demonstrate efficacy in the first
phase prior to permanent implantation in the second phase.
With PTNS the technique consists of stimulating the nerve by
means of a 34 gauge needle electrode inserted 4–5 cm cepha-
lad to the medial malleolus. Once the current is applied, the
flexion of the big toe or the movement of the other toes con-
firms the correct positioning of the needle electrode. The
electric current is a continuous, square wave form with a
duration of 200 μs and a frequency of 20 Hz. The current
intensity is determined by the highest level tolerated by the
patient. The stimulation sessions last for 30 min and are
performed once a week for 10–12 weeks in the majority of
published papers.
Overall, neuromodulation techniques can only be used if
there is little or no damage to the CNS-bladder axis. Data in
the neurogenic population is limited to patients with stroke,
Parkinson’s disease, MS, and incomplete spinal cord injury.
The current literature is generally positive and indicates that
neuromodulation demonstrates a good efficacy among the
neurogenic patients in terms of successful outcomes. However,
the proportion of patients whose condition is improved is
much less than in non-neurological pathologies. In addition,
like in non-neurogenic patients, there is limited evidence for
long-term efficacy (beyond 12–36 months), and maintenance
of therapeutic effect requires reprogramming and surgical
revision rate in a substantial number of patients.
Note: SNM is better utilized for treatment of bladder over-
activity than for urinary retention. DESD is not an FDA-
approved indication for SNM.
12.10 Surgery for Sphincteric Incompetence
12.10.1 Bulking Agents
Bulking agents can be used to treat neurogenic stress incon-

tinence when there is a demand for a minimally invasive
12.10 Surgery for Sphincteric Incompetence 203
treatment. The patient should be aware that the technique

has a low success rate. Macroplastique (polymethylsiloxane)
and Zuidex (dextranomer hyaluronic acid copolymer) are the
most common synthetic products utilized. One of the main
advantages of periurethral injections of bulking agents is that
they are minimally invasive and can even be carried out as an
outpatient procedure. The product is usually injected in the
region of the bladder neck using a retrograde endoscopic
approach. The bulking agent is injected at up to three sites
with the aim of achieving urethral coaptation. The success
rate, intended as “dryness for some hours” between voiding
and catheterization, ranges between 0 and 36% with a mean
follow-up that rarely exceeds 2 years.
12.10.2 Autologous Sling
In women with neurogenic lower urinary tract dysfunction,

the use of an autologous fascial sling to support the urethra
(usually close to the bladder neck) has been widely used to
treat stress incontinence with a success rate of 83–89%. The
procedure has a low morbidity rate. In particular, the risk of
urethral erosion is very low when fascial slings are used.
After surgery, most of the patients will be dependent on
bladder emptying using IC, because the patient’s neurological
dysfunction may preclude voluntary voiding and because the
sling may have to be inserted under tension in order to pro-
vide sufficient outflow resistance in the face of neurogenic
intrinsic sphincter deficiency.
Synthetic midurethral tapes have not been adopted for the
treatment of neurogenic stress incontinence due to concerns
about the risk of urethral erosion.
12.10.3 Artificial Sphincter
The AUS is recognized as one of the most effective treat-

ments for urinary incontinence. It has the inherent advantage
that it provides an adequate urethral closure pressure during
the urine storage phase allowing voiding to take place with a

low bladder outlet resistance. In patients with SUI, it is able
to deliver either complete or “social” continence in 75–87%
with satisfaction rates ranging between 85 and 95%. Most of
the series are related to male patients with non-neurogenic
incontinence. Many teams are still reluctant to implant AUS
devices in women because of technical difficulties related to
the short length of female urethra, which can lead to
subsequent complications. However, the device has been

effectively used also in female patients with neurological dis-
ease provided that they had a low-pressure bladder. Data are
scarce regarding the long-term functional outcomes of AUS
among adult female neurological patients. In addition, the
outcomes in the female neurological population, when avail-
able, are not analyzed separately from non-neurological
patients. A thorough urodynamic assessment of the bladder is
mandatory in order to evaluate the potential impact of blad-
der compliance following AUS implantation. In the event of
any doubt about the quality of the bladder reservoir, bladder
augmentation should be performed. Device infection, cuff
erosion into the urethra, and loss of fluid from the implant are
the main causes of failure of an AUS.
12.11 Diapers
Diapers are necessarily used in patients with storage symp-
toms when the aforementioned treatment regimens are not
fully effective.
Diapers are pads designed to absorb urine to protect the
skin and clothing. Usually available in disposable forms, they
are a temporary means of keeping the patient dry until a
more permanent solution becomes available or when the
treatment gives less-than-optimal results.
By reducing wetness and odor, they help maintain the
patient’s comfort and allow them to function in normal activi-
ties. The improper use of pads may contribute to skin break-
down and urinary tract infections. Thus, appropriate use,
12.12 Types of Neurogenic Bladder and Relative Care 205
meticulous care, and frequent changes are needed when

absorbent products are used.
With diapers it is important to implement a skin care pro-
gram to avoid the development of moisture lesions. The aim
is to keep the skin clean and dry. This can be achieved
through the use of protective skin barrier products, gentle
cleanser, and simple moisturizers. Following an episode of
incontinence, the area should be cleaned using a foam
cleanser (or similar). The skin should then be carefully dried,
and either a moisturizer or skin barrier is applied depending
on the condition of the skin and amount or frequency of
incontinence. Skin care should routinely be done according to
the degree of incontinence with timely cleansing of soiled and
wet skin.
12.12 T
ypes of Neurogenic Bladder
and Relative Care
Some types of neurogenic bladder are common findings in
urogynecological practice, while others are usually managed
in high specialized centers. The first include dementia, stroke,
multiple sclerosis, Parkinson’s disease, diabetes mellitus, and
radical pelvic surgery. The latter include spinal cord injury
and spina bifida.
12.12.1 Dementia
Incontinence in dementia is complex because it is often mul-

tifactorial and does not lend itself to easy solutions. Detrusor
overactivity (DO) was traditionally thought to be the princi-
pal cause of incontinence in dementia. However, much of the
incontinence seen in dementia may be functional inconti-
nence where the cognitive impairment interferes with the
ability to toilet. Management is directed at ameliorating the
predisposing causes with the ultimate goals of maintaining
independence, self-esteem, and health of the person.
Anticholinergics have been used to reduce detrusor overac-

tivity. However, the side effects of these drugs are a concern,
as they can worsen cognition, raising the risk of delirium.
More than drugs effective communication is the key to alle-
viating caregiving problems in dementia.
12.12.2 Stroke
Urinary incontinence following stroke is a common problem

affecting more than one-third of acute stroke patients and
persisting in up to a quarter at 1 year. It is well established that
this condition is a strong marker of stroke severity and is asso-
ciated with poorer functional outcomes and increased institu-
tionalization and mortality rates compared with those who
remain continent. Urodynamic findings vary depending upon
timing of the study and associated comorbidities. Detrusor
overactivity is predominant, and detrusor underactivity is
somewhat less prevalent. Patients with detrusor underactivity
should be managed with clean intermittent catheterization or
indwelling Foley catheter, while timed voiding with or without
anticholinergic therapy may be an effective treatment for
patients with detrusor overactivity after stroke.
12.12.3 Multiple Sclerosis
Lower urinary tract dysfunction is a common problem in

patients with multiple sclerosis (MS), with a prevalence of
75%. Urinary symptoms can vary in patients with MS, but
usually the most common are urgency, frequency, nocturia,
and urgency incontinence. In addition, patients can also pres-
ent voiding symptoms, like hesitancy and intermittency, which
can be present alone or in combination with the previous
ones. This is well reflected by urodynamic findings, which
shows that detrusor overactivity is the most common sign,
present in up to 81% of patients. The second most common

finding is detrusor sphincter dyssynergia (DSD), which is
associated to detrusor overactivity in 93% of cases. Treatment
of detrusor overactivity in patients with MS is still based on
anticholinergic drugs, after having assessed the post-
micturition residual volume (PVR). However, anticholinergic
drugs often fail to adequately control urinary symptoms or
are abandoned due to side effects. Recently, the use of
intradetrusor botulinum toxin type A, alone or associated to
CIC, has proven to be effective in increasing continence, in
improving urodynamic parameters, and in ameliorating qual-
ity of life.
12.12.4 Parkinson’s Disease
Urinary disturbances are frequently observed in patients suf-

fering of Parkinson’s disease resulting in significant impact to
the individual’s quality of life. They may occur at any stage of
the illness and get worse with advancing and aggravating dis-
ease. Storage symptoms are present in 57–83% of patients,
whereas voiding symptoms are seen in 17–27% patients. Out
of all the urinary symptoms, nocturia is the most common
complaint in >60% patients with PD. Detrusor overactivity
(DO) is the commonest urodynamic abnormality in patients
with PD. The main differential to consider is multiple system
atrophy (MSA) in which all patients are ultimately afflicted
with urinary disturbance. It is well recognized that patients
initially diagnosed with PD may in fact have MSA, and it is
important to distinguish the two as their urological manage-
ment is different. The post-void residual (PVR) volume is
minimal in PD, which differs significantly from multiple sys-
tem atrophy (MSA) patients who have a more progressive
disease that leads to urinary retention. Anticholinergic drugs
and, in selected cases, local injections of botulinum toxin are
the mainstay of treatment.
12.12.5 Diabetes Mellitus
Over 50% women with diabetes of type 2 have bladder dys-

function. The incidence is correlated with the duration of
diabetes and glycemic control.
The classic symptoms of diabetic cystopathy are decreased
bladder sensation, increased bladder capacity, and impaired
bladder emptying with resultant increased post-void residual
volume. The syndrome, also known as diabetic cystopathy
most likely represents end-stage bladder failure and is rela-
tively uncommon. Recent clinical evidence indicates a preva-
lence of storage symptoms, such overactive bladder
symptoms, in 39–61% of diabetic patients. The pathophysiol-
ogy of diabetic cystopathy is multifactorial, including distur-
bances of the detrusor muscles, nerves, and urothelium.
Hyperglycemia, oxidative stress, and polyuria play also
important roles in inducing voiding dysfunction. A “tempo-
ral theory of diabetic bladder dysfunction” has been pro-
posed. Hyperglycemia- induced polyuria plays a major
pathophysiological role during the early stages of diabetes
polyuria, causing compensatory bladder hypertrophy and
associated myogenic and neurogenic alterations. This stage is
compatible with findings of a hyperactive bladder during
urodynamic evaluation when patients present with bladder
storage concerns (urgency or urge incontinence). With time
and accumulation of toxic metabolites, decompensation of
bladder tissue and function ensues, resulting in the classical
signs and symptoms of diabetic cystopathy (hypocontractile
detrusor or atonic bladder) in patients with urinary voiding
problems. The first line of treatment of urge incontinence is
an oral anticholinergic drug. In case of empty failure, fre-
quent clean intermittent catheterization is the best choice to
avoid long-term indwelling catheter because of the risk of
increased infection rate.
12.12.6 Radical Pelvic Surgery
Dysfunction of the lower urinary tract is the most common

long-term complication of radical surgery for cervical cancer.
Bladder disorders are related to the extent of radical surgery.
The sympathetic and parasympathetic systems innervating
the lower urinary tract may be disrupted due to resection of
uterosacral and rectovaginal ligaments, the dorsal and lateral
paracervix, the caudal part of the vesico-uterine ligaments,
and the vagina. Nerve-sparing techniques appear to improve
bladder function without compromising overall survival of
the patients.
Typically there are two phases of dysfunction after surgery.
In the immediate postoperative period, there is usually a
transient spastic bladder with a decreased capacity but also
with diminished sensation which may require urethral cathe-
terization for a few days or for a few weeks. After this period
the patient may recover an efficient voiding function, with
some changes in bladder sensation and in detrusor and ure-
thral function but without any symptoms. Permanent dys-
functions (beyond 6–12 months) are reported in 30–50% of
patients. Hypocontractile bladder is the cause of persistent
voiding dysfunction, and these patients need abdominal
straining to void.
12.12.7 Spinal Cord Injury
Spinal shock occurs following an acute SCI and can last up to

3 months. Interruption of the nervous pathways eliminates
the micturition reflex, the bladder becomes atonic, and there
is no conscious awareness of bladder filling. The resulting
urinary retention should be managed by clean intermittent
catheterization (CIC) or with an indwelling catheter. Initial
urodynamic studies should be performed after the patient is

beyond the spinal shock phase.
The subsequent evolution of bladder function will depend
on the level of lesion:
• In suprasacral lesion, reflex bladder function will occur.
Consciousness of bladder filling might not be totally
absent; however, voluntary inhibition of the micturition
reflex is lost. Typical urodynamic findings include detrusor
overactivity and detrusor striated sphincter dyssynergia
(DESD). Discoordinated micturition will result in urinary
incontinence with high voiding pressure and residual urine
volume, which, if not treated, will result in upper tract
deterioration and renal failure.
• Sacral lesions will result in denervation of the bladder
and sphincter. Micturition reflex is absent, and, in cases
of complete lesion, conscious awareness of bladder filling
is lost. Bladder is acontractile and usually highly compli-
ant (in some cases low bladder compliance can occur)
with competent but nonrelaxing smooth and striated
sphincters that retain some fixed tone out of voluntary
control.
12.12.8 Spina Bifida
Spina bifida, especially when it is associated with myelome-

ningocele, is the commonest congenital cause of neurogenic
voiding dysfunction. More than 90% of children with spina
bifida have bladder dysfunction. The most common finding is
a urinary sphincter incompetence associated with bladder
underactivity. However, detrusor overactivity can occur as
well. The major problem with spina bifida is the risk of upper
urinary tract damage which tends to increase with age. Adults
with spina bifida have eight times the age-standardized risk

of renal failure compared to the general adult population.
Key Notes for Clinical Practice: Initial Assessment and

Empirical Treatment of NLUTD-S
• History including of home circumstance
• Urinary diary
• Physical examination:
–– Assessment of mobility and hand function
–– Assessment of sensation in lumbosacral derma-
tomes, anal tone and voluntary contraction of anal
sphincter, bulbocavernosus, and anal reflexes
• Urine analysis + culture
• Urinary tract imaging and serum creatinine
• PVR assessment
Presumed diagnosis according to level of lesion
Suprapontine Suprasacral Sacral cord/cauda equina

lesion (Stroke, lesion (Spinal lesion (Disc prolapse,
Parkinson’s) cord injury) radical surgery)
Empirical Treatment
Antimuscarinics a
Intermittent Physical therapya
self-
catheterizationa
Modified from Drake M, Apostolidis A, Cocci A, Emmanuel
A, Gajewski JB, Harrison SC et al. Neurogenic lower urinary
tract dysfunction: Clinical management recommendations of
the Neurologic Incontinence Committee of the Fifth
International Consultation on Incontinence 2013
a
External pads and/or indwelling catheter can be used in
support of the specific treatment
Key Notes for Clinical Practice: Specialized Assessment

and Treatment of NLUTD-S
Urodynamic (usually videourodynamic) diagnosis
Detrusor Poor bladder Poor bladder Sphincter

overactivity emptying due to emptying due incompetence
without DESD DESD to detrusor
underactivity
Conservative treatment
AM + timed AM + IC IC None

voiding
BonTA Straining (?)
detrusora + IC
Triggered voiding
(?) + alpha1-
antagonists
Surgical treatment
Neuro SDAF + IC
b
None Bulking agent
modulation
SDAFb + SARSc MUS
(retropubic)
+ IC
Enterocystoplasty Artificial
+ IC sphincter
Modified from Drake M, Apostolidis A, Cocci A, Emmanuel
A, Gajewski JB, Harrison SC et al.Neurogenic lower urinary
tract dysfunction: Clinical management recommendations of
the Neurologic Incontinence committee of the fifth
International Consultation on Incontinence 2013
a
BoNTA sphincteric injections are not currently licensed
b
SDAF sacral deafferentation
c
SARS sacral anterior-root stimulation
Note 1: Described by Brindley in 1970, SARS with poste-

rior root rhizotomy can be performed only in patients with
SCI with preserved sacral reflex and normal detrusor compli-
ance. Because all or a part of the posterior sacral nerves are
destroyed, the technique cannot be performed in patients with
conserved lower limb motility. Furthermore, the deafferenta-

tion induces sensory loss in the sacral dermatomes, and female
patients could lose vaginal lubrification. Despite the efficacy,
the technique is not commonly used because of the irrevers-
ibility and consequences of the posterior rhizotomy.
Note 2: Urinary diversion may be an option in selected
cases of female patients with neurogenic bladder.
Note 3: Recent research suggest there are discrepancies
between the goals of experts about how to best manage blad-
der problems in comparison to the goals of patients with
neurogenic bladder. Obviously, nonadherence to codified
programs can result in serious health problems (i.e., kidney
stones, skin sores, urinary tract infection). On the other hand,
proper adherence to bladder program may make it difficult to
participate in social activities, especially for women. Updated
clinical practice guidelines and standards for how to best
assess and treat these problems in women are needed.
Suggested Readings
Overviews
Gajewsky JB, Schurch B, Hamid R, Averbeck M, Sakakibara R,
Finazzi-Agrò E, et al. An International Continence Society (ICS)
report on terminology for adult neurogenic lower urinary tract
dysfunction (ANLUTD). Neurourol Urodyn. 2018;37:1152–61.
Drake M, Apostolidis A, Cocci A, Emmanue A, Gajewski JB,
Harrison S, et al. Neurogenic lower urinary tract dysfunction:
clinical management recommendations of the neurologic inconti-
nence committee of the fifth international consultation on incon-
tinence 2013. Neurourol Urodyn. 2016;35:657–65.
Panicker J, Fowler C, Kessler T. Lower urinary tract dysfunction in
the neurological patient: clinical assessment and management.
Lancet Neurol. 2015;14:720–32.
Goldmark E, Niver B, Ginsberg DA. Neurogenic bladder: from diag-
nosis to management. Curr Urol Rep. 2014;15:448.
Nambiar A, Lucas M. Chapter 4: guidelines for the diagnosis and
treatment of overactive bladder (OAB) and neurogenic detrusor
overactivity (NDO). Neurourol Urodyn. 2014;33(Suppl 3):S21–5.
Pannek J, Blok B, Castro-Diaz D, Del Popolo G, Kramer G,

Radziszewski P, et al. EAU Guidelines on neurogenic lower uri-
nary tract dysfunction. 2013.
Ginsberg D. The epidemiology and pathophysiology of neurogenic
bladder. Am J Manag Care. 2013;19(10 Suppl):s191–6. Online.
Classification
Madersbacher HG. Neurogenic bladder dysfunction. Curr Opin
Urol. 1999;9:303–7.
Powell C. Not all neurogenic bladders are the same: a proposal for
a new neurogenic bladder classification system. Transl Androl
Urol. 2016;5:12–21.
Assessment
Musco S, Padilla-Fernández B, Del Popolo G, Bonifazi M, Blok
BFM, Groen J. Value of urodynamic findings in predicting upper
urinary tract damage in neuro-urological patients: A systematic
review. Neurourol Urodyn 2018, Feb 2. [Epub ahead of print]
Allio BA, Peterson AC. Urodynamic and physiologic patterns asso-
ciated with the common causes of neurogenic bladder in adults.
Transl Androl Urol. 2016;5:31–8.
Collins CW, Winters JC. AUA/SUFU adult urodynamics guideline: a
clinical review. Urol Clin North Am. 2014;41:353–62.
Cruz F, Nitti V. Chapter 5: clinical data in neurogenic detrusor
overactivity (NDO) and overactive bladder (OAB). Neurourol
Urodyn. 2014;33(Suppl 3):S26–31.
Danforth TL, Ginsberg DA. Neurogenic lower urinary tract dysfunc-
tion: how, when, and with which patients do we use urodynamics?
Urol Clin North Am. 2014;41(3):445–52.
Nitti VW. Evaluation of the female with neurogenic voiding dysfunc-
tion. Int Urogynecol J Pelvic Floor Dysfunct. 1999;10:119–29.
Management
Nevedal A, Kratz AL, Tate DG. Women’s experiences of living with
neurogenic bladder and bowel after spinal cord injury: life con-
trolled by bladder and bowel. Disabil Rehabil. 2016;38:573–81.
Ginsberg DA. Management of the neurogenic bladder in the female

patient. Curr Urol Rep. 2006;7:423–8.
Chartier-Kastler E, Denys P. Intermittent catheterization with
hydrophilic catheters as a treatment of chronic neurogenic uri-
nary retention. Neurourol Urodyn. 2011;30:21–31.
Jamison J, Maguire S, McCann J. Catheter policies for management
of long term voiding problems in adults with neurogenic bladder
disorders. Cochrane Database Syst Rev. 2013;11:CD004375.
Smith CP, Chancellor MB. Botulinum toxin to treat neurogenic blad-
der. Semin Neurol. 2016;36:5–9.
Kurpad R, Kennelly MJ. The evaluation and management of refrac-
tory neurogenic overactive bladder. Curr Urol Rep. 2014;15:444.
Cruz F, Herschorn S, Aliotta P, Brin M, Thompson C, Lam W, et al.
Efficacy and safety of onabotu-linumtoxinA in patients with
urinary incontinence due to neurogenic detrusor overactivity:
a randomised, double-blind, placebo-controlled trial. Eur Urol.
2011;60:742–50.
Giannantoni A, Mearini E, Del Zingaro M, Porena M. Six-year fol-
low-up of botulinum toxin a intradetrusorial injections in patients
with refractory neurogenic detrusor overactivity: clinical and uro-
dynamic results. Eur Urol. 2009;55:705–11.
Del Popolo G, Filocamo MT, Li Marzi V, Macchiarella A, Cecconi F,
Lombardi G, et al. Neurogenic detrusor overactivity treated with
english botulinum toxin a: 8-year experience of one single centre.
Eur Urol. 2008;53:1013–9.
Karsenty G, Denys P, Amarenco G, De Seze M, Gamé X, Haab F, et al.
Botulinum toxin A (Botox) intradetrusor injections in adults with
neurogenic detrusor overactivity/neurogenic overactive bladder:
a systematic literature review. Eur Urol. 2008;53:275–87.
Church B, Denys P, Kozma CM, Reese PR, Slaton T, Barron
RL. Botulinum toxin A improves the quality of life of patients
with neurogenic urinary incontinence. Eur Urol. 2007;52:850–8.
Sanford MT, Suskind AM. Neuromodulation in neurogenic bladder.
Transl Androl Urol. 2016;5:117–26.
Joussain C, Denys P. Electrical management of neurogenic lower uri-
nary tract disorders. Annals Physical Rehab Med. 2015;58(4):245–50.
Lay AH, Das AK. The role of neuromodulation in patients with neu-
rogenic overactive bladder. Curr Urol Rep. 2012;13:343–7.
Cameron AP. Medical management of neurogenic bladder with oral
therapy. Transl Androl Urol. 2016;5:51–62.
Abdul-Rahman A, Attar KH, Hamid R, Shah PJ. Long-term out-
come of tension-free vaginal tape for treating stress incontinence
in women with neuropathic bladders. BJU Int. 2010;106:827–30.
Pannek J, Bartel P, Gocking K. Clinical usefulness of the transobtu-

rator sub-urethral tape in the treatment of stress urinary incon-
tinence in female patients with spinal cord lesion. J Spinal Cord
Med. 2012;35:102–6.
Phè V, Leon P, Granger B, Denys P, Bitker MO, Mozer P, et al. Stress
urinary incontinence in female neurological patients: long-term
functional outcomes after artificial urinary sphincter (AMS
800TM) implantation. Neurourol Urodyn. 2017;36:764–9.
Averbeck M, Madersbacher H. Follow-up of the neuro-urological
patient: a systematic review. BJUI. 2015;115:39–46.
Specific Types of NLUTD

Ransmayr GN, Holliger S, Schletterer K, Heidler H, Deibl M, Poewe
W, et al. Lower urinary tract symptoms in dementia with Lewy
bodies, Parkinson disease, and Alzheimer disease. Neurology.
2008;70:299–303.
Mehdi Z, Birns J, Bhalla A. Post-stroke urinary incontinence. Int J
Clin Pract. 2013;6:1128–37.
Winge K. Lower urinary tract dysfunction in patients with par-
kinsonism and other neurodegenerative disorders. Handb Clin
Neurol. 2015;130:335–56.
Phè V, Chartier-Kastler E, Panicker J. Management of neuro-
genic bladder in patients with multiple sclerosis. Nat Rev Urol.
2016;13:275–88.
Laterza RM, Sievert KD, de Ridder D, Vierhout ME, Haab F,
Cardozo L, et al. Bladder function after radical hysterectomy for
cervical cancer. Neurourol Urodyn. 2015;34:309–15.
Daneshgari F, Liu G, Birder L, Hanna-Mitchell AT, Chacko
S. Diabetic bladder dysfunction: current translational knowledge.
J Urol. 2009;182(6 Suppl):S18–26.
Kirschner-Hermanns R, Daneshgari F, Vahabi B, Birder L, Oelke
M, Chacko S. Does diabetes mellitus-induced bladder remodel-
ing affect lower urinary tract function? ICI-RS 2011. Neurourol
Urodyn. 2012;31:359–64.
Taweel WA, Seyam R. Neurogenic bladder in spinal cord injury
patients. Res Rep Urol. 2015;7:85–99.
Mourtzinos A, Stoffel JT. Management goals for the spina bifida
neurogenic bladder: a review from infancy to adulthood. Urol
Clin North Am. 2010;37(4):527–35.
Chapter 13
Making Sense of Urodynamic
Testing for Women
with LUTS: Practical
Conclusive Notes
The enthusiasm of routine urodynamic testing in the manage-
ment of women with lower urinary tract dysfunction, in par-
ticular urinary incontinence and pelvic organ prolapse, has
been tempered in the last few years. Controversy exists
whether routine urodynamic testing provides a real benefit
for the patient since there is a growing evidence that they
give little additional information over basic office assessment,
including focused history with quality of life (QoL) assess-
ment, bladder diaries, pelvic examination, cough test, uro-
flowmetry, measurement of post-void residual urine, and
urine analysis.
Clearly, the exclusion of preoperative urodynamics in
favor of comprehensive office evaluation in women with SUI
or stress-predominant MUI might lead to significant savings
for healthcare systems and could also save women from the
embarrassment of the examination and from potential uri-
nary tract infections. In addition, some reports demonstrated
that immediate sling placement for women with pure SUI or
MUI was less costly and more effective than a delayed treat-
ment based on UDS finding.
The problem turn around the distinction between pure
stress urinary incontinence and complicated urinary inconti-
nence with mixed urinary incontinence staying between
the two.

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8_13
218 Chapter 13. Making Sense of Urodynamic Testing
The National Institute for Health and Care Excellence

(NICE) guideline recommends that urodynamics not be per-
formed in the small group of women where pure SUI is diag-
nosed based on a detailed clinical history and physical
examination.
ICS defines complicated urinary incontinence as inconti-
nence with significant pelvic organ prolapse, recurrent infec-
tions, pain or hematuria, suspected or proven voiding
problems, failed previous incontinence surgery, or inconti-
nence following radical pelvic surgery. This group of women
with complicated UI will still need urodynamics.
Mixed urinary incontinence, highly prevalent among
elderly patient, is a challenge. Women with mixed symptoms
may present underlying pure detrusor overactivity or different
combinations of stress incontinence with detrusor overactiv-
ity, urethral hypermobility, and intrinsic sphincteric deficiency
with or without voiding dysfunction.
The relationship between SUI and the overactive bladder
(OAB) syndrome is still poorly understood. At least 50% of
patient could benefit from treatment directed at the urethra,
but the other 50% could complain a worsening of symptoms.
Given that patients undergoing stress incontinence surgery
expect not only the resolution of urine leakage but also
urgency and frequency symptoms and given that these symp-
toms are among those that predict postsurgery dissatisfac-
tion, UDS has a pivotal role in defining detrusor function not
only in terms of the presence or absence of detrusor overac-
tivity but also in terms of increased afferent activity and brain
handling of peripheral bladder informations.
The question remains whether the overall outcome of sur-
gery could have a better success rate when a more structured
UDS diagnosis had been used.
Beyond precluding indication to surgery, urodynamic
information can facilitate tailored counseling of patients
regarding the need for postoperative treatment for urgency/
urgency incontinence.
Currently, there is no adequate consensus on how to
categorize SUI in terms of the two principal postulated

Chapter 13 Making Sense of Urodynamic Testing 219
pathophysiological mechanisms: intrinsic sphincter deficiency

and urethral hypermobility. These represent extremes of a
spectrum and coexist in the vast majority of patients. The
uncertainty over this categorization is recognized by the ICS,
which has called for further research in this area.
Despite abdominal leak point pressure or maximum ure-
thral closure pressure does not seem to alter the surgical
outcome of a MUS, a retropubic tape appears to be more
suitable than a transobturator tape in women with intrinsic
sphincter deficiency, diagnosed using urethral pressure pro-
filometry and/or abdominal leak point pressures.
In the case of pelvic organ prolapse, UDS testing should
clarify which patients might have lower urinary tract dysfunc-
tion following repair, i.e., incontinence, OAB symptoms, and
voiding dysfunction. Clinical testing would seem easier for
most patients and physicians, but it is conceivable that UDS
testing may offer the most efficient way to identify the rele-
vant information necessary to make a clinical decision. Once
again, it should be acknowledged that particularly for OAB
symptoms and voiding dysfunction, the final decision will be
no better than without UDS testing and the results, in fact,
will be used only to counsel the patients about the possible
persistence of symptoms following surgery.
Voiding dysfunction in female is a relatively new field.
Mechanical obstruction, detrusor underactivity, and overactive
pelvic floor are the acknowledged underlying mechanisms.
Mechanical obstruction, although the intriguing difficulties are
associated with the unclear definition of obstruction in female,
is probably the easier urodynamic diagnosis.
Poor detrusor contractility is an aging-related problem
that may be associated with a postoperative voiding dysfunc-
tion that may create significant care problems in elderly
patients.
The mechanisms are still poorly understood. However,
identifying patients likely to develop postoperative VD may
be useful in better defining patient expectations and identify-
ing those most likely to benefit from preoperative teaching of
clean intermittent self-catheterization.
220 Chapter 13. Making Sense of Urodynamic Testing
Finally, the recognition of pelvic floor overactivity may be

a key element to address patient to physical therapy instead
of surgery.
In summary, the use of urodynamics depends on whether
the clinician feels that the extra information provided by the
investigation translates into better outcomes and so would be
worth the associated risks and costs of the examen. From
urodynamic perspective the pathophysiology of symptoms is
multifactorial in women with LUTS, and UDS testing is the
only objective way to determine the underlying mechanisms.
Irritative symptoms and emptying problems are probably
the clinical situations that take the best advantage from uro-
dynamic examination. Cystometry is the only method by
which bladder sensations and control can be evaluated, and
pressure-flow study is the only proven method to evidentiate
voiding problems other than obstruction, i.e., detrusor under-
activity and pelvic floor overactivity. UDS add a dimension of
precision to evaluation of female with LUTS and sometimes,
according to the current views, may significantly influence
technique and outcome measures in this group of patients.
Despite the passionate debate, many clinicians still perform
preoperative multichannel UDS. A recent survey of urolo-
gists and urogynecologists concluded that many of them
would arrange urodynamics for women with LUTS prior to
surgery while recognizing the need for further better designed
clinical trials to address this question.
Suggested Reading
Hilton P, Bryant A, Howel D, McColl E, Buckley BS, Lucas M, et al.
Assessing professional equipoise and views about a future clini-
cal trial of invasive urodynamics prior to surgery for stress uri-
nary incontinence in women: a survey within a mixed methods
feasibility study. Neurourol Urodyn. 2012;31:1223–30.
ppendix A: What Do
A
the Experts Say?—Scientific
Societies Recommendations
for UDS Testing
Acronyms
AHPCR Agency for Healthcare Policy and Research
SOGC The Society of Obstetricians and Gynecologists
of Canada
ACOG The American College of Obstetricians and
Gynecologists
ICS International Continence Society
RCOG Royal College of Obstetricians and Gynecologists
NICE National Institute of Clinical Excellence
EAU European Association of Urology
ICI The International Consultation on Incontinence
AUA American Urological Association
SUFU Society of Urodynamics, Female Pelvic Medicine
& Urogenital Reconstruction
Numerous scientific societies have provided opinions on
the indications for urodynamic testing. Below are summa-
rized the main clinical guidelines.
• AHPCR
Multichannel urodynamic testing should be reserved only
for women with “complicated diagnostic situations or
involved therapeutic plans.”
Fantl JA, Newman DK, Colling J, DeLancey JOL, Keeys C,
Loughery R, et al. Urinary incontinence in adults: acute and

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8
222 Appendix A: What Do the Experts Say?
chronic management. Rockville, MD. Department of Health

and Human Services (US), Public Health Service, Agency for
Health Care Policy and Research, 1996. Clinical practice
guideline N0. 2, AHPCR publication No. 96–0682 24.
• RCOG
Prior to performing irreversible bladder neck surgery, it
would appear to be beneficial to have assessed objectively
the type of incontinence and the presence of any complicat-
ing factors.
Adams EJ, Barrington JW, Brown K, Smith ARB. Surgical
Treatment of Urodynamic Stress Incontinence. Royal College of
Obstetricians and Gynaecologists Guideline No. 35, October 2003.
• SOGC and ACOG
Preoperative urodynamic testing are not necessary in
women with pure stress incontinence that can be objectively
demonstrated in whom all appropriate preoperative investi-
gations have been performed.
Farrell SA. SOGC Urogynaecology Committee. The evalu-
ation of stress incontinence prior to primary surgery. SOGC
Clinical Practice Guideline No. 127. J Obstet Gynaecol Can.
2003;25(4):313–24.
American College of Obstetricians and Gynecologists.
Urinary incontinence in women. ACOG Practice Bulletin No.
63. Obstet Gynecol. 2005;105:1533–45.
• ICS
Non-invasive urodynamics, such as voiding diary, post-void
residual, and uroflowmetry, are recommended for all inconti-
nent patients.
Invasive urodynamic studies are not necessary prior to
treatment when the type of incontinence is clear and there
are no complicating factors involved.
Abrams P, Cardozo L, Khoury S, Wein A. Incontinence,
Basics and Evaluation, 3rd International Consultation on
Incontinence, Co-sponsored by the International Continence
Society, Edition 2005.
Appendix A: What Do the Experts Say? 223
• ICI
UDS should be used if results will alter treatment recom-
mendation and management.
Abrams P, Andersson KE, Birder L, et al. Fourth
International Consultation Incontinence Recommendations
of the International Scientific Committee: evaluation and
treatment of urinary incontinence, pelvic organ prolapse,
and fecal incontinence. Neurourol Urodyn.
2010;29:213–40.
• AUA/SUFU
Urodynamics may be “optionally” performed in patients
with UI if considering invasive treatment.
Appell RA, Dmochowski RR, Blaivas JM, et al. Guideline
for the Surgical Management of Female Stress Urinary
Incontinence: 2009 Update. American Urological Association
Education & Research, Inc, 2012 revision.
• NICE
Urodynamics is unnecessary in case of pure SUI.
Urodynamic testing should be considered if diagnosis is
unclear, with a history of previous surgery for SUI or for
symptoms suspicious for detrusor overactivity or voiding
dysfunction.
National Institute for Health and Care Excellence. Urinary
Incontinence in Women: The Management of Urinary
Incontinence in Women, 2013.
• Cochrane
While urodynamic tests may change clinical decision mak-
ing, there is some evidence that this do not result in better
outcomes in terms of a difference in urinary incontinence
rates after treatment.
Clement KD, Lapitan MC, Omar MI, Glazener
CM. Urodynamic studies for management of urinary inconti-
nence in children and adults. Cochrane Database Syst Rev.
2013.
224 Appendix A: What Do the Experts Say?
• EAU
Urodynamics is unnecessary if pursuing a conservative
treatment.
UDS should be used if results may alter treatment recom-
mendation and management.
Counseling the patient that UDS does not predict the
treatment outcome is advisable.
Test of urethral function by urethral pressure profile or
leak-point pressure measurement should not be used.
Burchard F, Bosch J, Cruz F, et al. EAU Guidelines on
Urinary Incontinence. Updated March 2017.
Suggested Reading
Syan R, Brucker B. Guidelines of guidelines: urinary inconti-
nence. BJU Int. 2016;117:20–33.
ppendix B: Informed
A
Consent for Invasive UDS
Testing (Sample)
Definition
Urodynamic testing is a sophisticated office-based procedure
used to help diagnose problems with difficult urination and/
or involuntary loss of urine. Urodynamic testing helps
increase the accuracy of diagnosis, uncovering in some
instances a completely unexpected finding. The test is short
and minimally invasive. In certain circumstances, even more
information can be obtained with the use of fluoroscopy (spe-
cial real-time X-rays) during the test. This is referred to as a
“videourodynamic test.”
Preparation
There is no particular preparation for a UDT. If you are in
child-bearing age, it is important that you are not pregnant
especially in cases where the use of X-ray is planned. So
please inform the examiner if there is any suspicion that you
may be. You should arrive to the office with a full bladder in
order to perform an uroflowmetry. Uroflowmetry is the ini-
tial portion of the test in which you urinate into a special
equipment that calculate the pattern and the force of your
stream.
226 Appendix B: Informed Consent
Procedure
The examen will take less than 1 hour.
Once your bladder is empty, you will be asked to lie
down on the examination table. Under sterile conditions a
small catheter will be inserted in your bladder through the
urethra. With the insertion you may feel a minimal discom-
fort. Next, a similar catheter with a small balloon on the
end will be inserted into the rectum or the vagina, and the
balloon will be filled with a little amount of fluid. The cath-
eters will be secured in place with a tape, the bed will be
put in sitting position, and the test will begin. Throughout
the filling, you will be asked to describe the sensations you
are having as the bladder fills. When you are full, you will
be asked to urinate and empty your bladder into a special
container. In certain instances, X-rays can be taken during
the filling and voiding portions of the test. In these cases,
bladder will be filled with an X-ray dye instead of saline
solution. Don’t worry about possible allergies to dye
because the fluid is only in your bladder and not in your
bloodstream. At the end of voiding, catheters are removed
and the test is over.
Post-procedure
After the procedure you might have a little burning in the
urethra that usually disappear with the following urination.
You may even see a tiny blood discoloration of your urine.
Possible Complications of the Procedure

All invasive procedures, regardless of complexity or time, can
be associated with unforeseen problems. These include:
Appendix B: Informed Consent 227
Urinary Tract Infection

It may be a simple bladder infection that presents with symp-
toms of burning urination, urinary frequency, and a strong urge
to urinate and usually resolve with a few days of antibiotics.
Bloodstream Infection (Urosepsis)
This type of infection often presents with the urinary
symptoms and any combination of the following: fevers, shak-
ing chills, weakness or dizziness, nausea, and vomiting. You
may need a short hospitalization for intravenous antibiotics,
fluids, and observation. This scenario is more common in dia-
betics, patients on long-term steroids, or patients with any
disorder of the immune system.
If you have high temperatures or any symptoms of severe
illness (fevers, shaking chills, weakness or dizziness, nausea
and vomiting, confusion), let your doctor know immediately,
or proceed to the nearest emergency room.
Blood in the Urine
In some patients, placing the catheters within the bladder
may cause a very small amount of bleeding in the urine. In
almost all instances, the urine clears on its own over the next
day or so.
Consent for Treatment
I understand that during the course of the procedure, unfore-
seen conditions might arise that could require other opera-
tions, procedures, or treatments.
I acknowledge that the procedure has been explained to
me in detail and all my questions concerning the procedures
have been answered to my satisfaction.
228 Appendix B: Informed Consent
I hereby consent to the above procedure accepting all of

the inherent risks.
Patient signature Physician signature

Index
A B
Abdominal leak point pressure Baden Walker classification, 114
(ALPP), 66, 68, 219 Bladder control, 4, 137
Abrams–Griffiths nomogram, 69 Bladder diary, 24, 25
Afferent signals, abnormal Bladder ischemia, 153
handling, 137 Bladder motor nuclei, 10
Afferent system, 135 Bladder outlet obstruction
Aging, 6, 35, 152, 153, 219 (BOO), 153
Air-charged catheters (T-DOC and POP, 154
system), 46, 47 clinical parameters, 157
Air-filled catheters (AFCs), 81 functional obstruction, 155
Ambulatory urodynamics postoperative voiding
monitoring (AUM), dysfunction, 154
89, 90 pressure-flow criteria, 157
Artifacts identifications and radiographic evidence, 157
remedial action urodynamics criteria, 158
alternating current artifact, 76 Bladder output relation (BOR),
displaced catheter during 159
voiding, 74 Bladder pain syndrome/
expelled catheter, 75 interstitial cystitis
interference, 76 (BPS/IC)
leakage in Pabd line, 73 associated diseases, 176
pressure line descent, 73 bladder biopsy, 178
Pves and Pdet pressures, 75 characteristic presentation,
rectal contractions, 73, 74 173
uroflowmetry, 71 confusable diseases, 175, 176
As low as reasonably achievable conservative therapies, 179
(ALARA), 89 cystoscopy, 176
Autonomic dysreflexia (AD), definitions, 170
184, 190–191 diagnostic criteria, 173

Nature 2018
https://doi.org/10.1007/978-3-319-74005-8
230 Index
Bladder pain syndrome/ patient storage symptoms, 62

interstitial cystitis types of sensations, 63
(BPS/IC) (cont.) urodynamic events, 62
etiology, 169
glomerulations, 170
hydrodistention, 177, 178 D
levator ani systemic De novo urgency urinary
palpation, 174 incontinence (UUI),
O’Leary-Sant Symptom 124
Score, 174 Detrusor hyperactivity with
pathogenesis, 169 impaired contractility
phenotypic patterns, 179 (DHIC), 152
physical examination, 174 Detrusor leak point pressure
potassium sensitivity test, 177 (DLPP), 66, 67
pressure/flow study, 179 Detrusor overactivity (DO), 126,
self-administered symptom 138, 140
score, 174 Detrusor sphincter dyssynergia
signs and symptoms, 173 (DSD), 35, 87, 155, 183,
taxonomy, 171 184, 189, 207
trigger point complex, 172 Detrusor underactivity (DU), 69,
UDS studies, 177 126, 152, 153, 158
voiding diary, 175 Digital voiding diary, 25
voiding dysfunction, 171 Double-lumen catheter, 52
Bladder scanner, 37 Dual-sensor microtip transducer,
Blaivas nomogram, 69 45
Blavais-Groutz nomogram, 160 Dysfunctional voiding (DV), 155,
Brain-bladder control, 4 156
C E
CARE trial, 119 Electromyography (EMG),
Complicated urinary 85–87, 89, 155, 188, 189
incontinence, 106, 217, electrodes, 53, 54, 57
218 recording, 76
Cough stress test, 100 External water-filled transducers,
CUPIDO 1 (women with 51
incontinence) and 2 reference height, 48, 49
(women with occult zeroing, 47, 48
SUI) trials, 119
Cystometry
bladder compliance, 63 F
bladder sensation, 62 Female incontinence, 18, 96, 108
detrusor function, 64, 65 Female resting pressure profile,
filling phase, 62 82
maximum cystometric Female stress urethral pressure
capacity, 64 profile, 84
Index 231
Fowler’s syndrome, 151, 155, 156 M

Frequency volume chart (FVC), Microtip and air-filled systems,
24 49–51
Microtip transducers, 45, 46
Micturition cycle, EMG activity,
G 86
Groutz nomogram, 69 Micturition, female
and male, voiding dynamics,
12
H functional brain imaging, 2
Hill’s equation, 159 neural control, 1, 3, 5
Hydrodistention, 177, 178 patterns, 13
pressure variations, 10, 11, 13,
14
I storage phase, 4
International Continence Society Micturition time chart, 24
(ICS), 17, 18, 22–24, 26, Midbrain periaqueductal gray
45, 47, 48, 53, 54, 62, 63, (PAG), 4, 5
65, 66, 69, 79, 94, 104, Mixed urinary incontinence
149, 153, 169, 171, 218, (MUI), 93, 96–97,
219, 224 217, 218
International Continence Society Myogenic hypothesis, 133–135
Good Urodynamic
Practice 2002, 17
Intrinsic sphincteric deficiency N
(ISD), 68, 94, 95 National Institute for Diabetes
INVasive Evaluation before and Digestive and
Surgical Treatment of Kidney Diseases
Incontinence Gives (NIDDK) criteria, 169,
Added Therapeutic 170
Effect National Institute for Health and
(INVESTIGATE-I), Care Excellence
107 (NICE) guideline, 97,
Invasive/conventional 104, 144, 192, 218, 223
urodynamic testing, 17, Neurogenic bladder/neurogenic
41 lower urinary tract
dysfunction syndrome
(NLUTD-S)
L anticholinergic therapy, 198
Laycock PERFECT scale, 22 artificial sphincter, 203, 204
Leak point pressures, types, 66 autologous fascial sling, 203
Liverpool nomogram, 35, 36 autonomic dysreflexia, 190
Lower urinary tract bladder emptying
emptying of urine, 1 management
dysfunction, 18, 149 abdominal stimulation,
storage, 1 194
232 Index
Neurogenic bladder/neurogenic pressure flow studies, 188

lower urinary tract radical surgery, 209
dysfunction syndrome rhythmic detrusor
(NLUTD-S) (cont.) contractions on
intermittent self- cystomanometry, 189
catheterization, sacral and pudendal
194–196 neuromodulation, 202
spontaneous voiding, 194 sacral lesions, 184, 210
bladder pressure, 188 self-intermittent
blood tests, 187 catheterization, 195
botulinum toxin A, 199 sphincter EMG measurement,
brain/spinal cord lesion, 183 188
classification systems, 183–185 sphincteric incompetence,
clean intermittent surgery, bulking agents,
catheterization, 209 202, 203
clinical assessment, 186 spinal lesions, 184
complications, 192, 193 spinal shock, 209
diabetes, 208 storage symptoms, 198
diabetic cystopathy, 208 stroke, 206
diapers, 204, 205 supraspinal lesions, 184, 210
EMG of the urethral treatment, 193
sphincter, 189 ultrasound scanning, 187
hyperglycemia-induced urinary diversion, 213
polyuria, 208 urodynamic investigation,
incontinence in dementia, 205 188
indwelling catheter, 197 urodynamics, 191
infrasacral lesion, 184 videourodynamics, 191
intradetrusor injections of Neuronal growth factor (NGF),
Botox, 200 132, 133, 184
LUT function, 193 Nocturnal polyuria, 26
multichannel cystometry, 188 Non-invasive urodynamics, 17,
multiple sclerosis, 206, 207 31–38
multiple system atrophy, 207 PVR, 37
neurogenic detrusor uroflowmetry, 31–36
overactivity, 183 voided percentage, 37–38
neurologic history, 186
neurological status, 186
neuromodulation, 200–202 O
onabotulinumtoxinA, 199 Occult stress incontinence
Parkinson’s disease, 207 definition, 120
patient’s neurological medical history, 121
dysfunction, 203 POP repair, 122
physical examination, 186 provocative tests, 121
post-micturition residual urethral function, 121
volume, 207 urodynamic parameters, 122
Index 233
Office provocative stress test, 121 Pelvic organ prolapse syndrome

OPUS trial, 119 (POP-S)
Overactive bladder syndrome age-dependent, 113
(OAB-S), 122–124, 142, anterior (cystocele), 113
144, 218 anti-incontinence procedure,
bladder filling sensations, 137 117, 118, 125
bladder hypersensitivity, 140 in no patients, 120
bladder micromotions, 134 in some patients, 120
clinical groups, 138 apical, 113
definition, 131 clinical practice, 125
diagnosis, 133 clinical quantification systems,
in female 114
clinical assessment, 142 grading systems, 114
treatments, 142, 144 nomenclature, 116
idiopathic (non-neurological), posterior (rectocele), 113
131 staging system, 116
pathophysiology, 133, 141 stress incontinence surgery,
prefrontal cortex 118
deactivation, 137 stress urinary incontinence,
prevalence, 132 117
secondary, neurological cause, subclinical prolapse, 114
131 treatment, 113
sphincter behavior, 141 types, 113
treatment, 133 urodynamic testing, 116
treatment algorithm, 143 Peripheral bladder innervation, 9
urge incontinence, 137 Peripheral neural mechanisms,
urinary urgency, 131 8, 9
urodynamic evaluation, 137, Phasic detrusor overactivity, 139
138 Polyuria, 26, 208
Overactive pelvic floor, 171, 172 Pontine micturition center
Oxford grading system of muscle (PMC), 4–7, 10
contraction, 22, 23 Postoperative voiding dysfunction,
124, 154, 219
Postvoid residual volume (PVR)
P assessment, 37, 38
Pad test, 19, 26, 27, 102 Potassium sensitivity test, 176
Pad test apparatus, 27 Preoperative bladder
Parahippocampal complex overactivity, 126
(PHC), 4, 6 Pressure/flow study, 41
Parasympathetic nervous fibers, 8 Pressure trace artifacts, 72
Pelvic floor overactivity, 173, 220 Pre-test assessment
Pelvic floor relaxation, 12, 70, 149 abdominal examination, 19
Pelvic organ prolapse clinical history, 19
quantification system focused neuro-urological
(POP–Q), 114, 116 assessment, 21, 22
234 Index
Pre-test assessment (cont.) cystometry with cough tests,

obstetric history, 19 102
pelvic floor muscle detrusor activity, 103
assessment, 21 detrusor underactivity, 103
physical examination, 20 female urethra, structure, 94
structured vaginal invasive urodynamic testing,
examination, 20 102
voiding diary, 19 ISD, 103
Prolapse reduction testing, 121 mechanisms, 95
office evaluation, 98, 99, 102
patient evaluation, 97
Q physical examination, 100
Q-tip test, 20, 101 postoperative treatment, 218
post-void residual urine, 101
Q-tip test, 101
R surgical treatment, 108
Regional brain activity, 7, 13 uncomplicated SUI, 97
Retropubic mid-urethral sling urethral hypermobility, 100,
(RMUS), 105 101
urinary tract infections, 99
urodynamic testing, 93, 104
S Supplementary urodynamic
Schafer nomogram, 69 tests, 17
Somatic cholinergic motor dysfunctional voiding, 87
nerves, 8 EMG activity, 86
Spina bifida, 193, 205, 210 external urethral sphincter,
Spinal cord injuries (SCI), 131, 85, 87
183, 190, 192, 193, 202, sphincter EMG, 85
205, 209 Sympathetic nervous fibers, 8
Simplified version pelvic organ
prolapse quantification
system (S-POP-Q), T
114, 115 Terminal detrusor overactivity,
Stress incontinence, 94, 95, 139
100–102, 105, 117, 118, Transducers
202, 203, 218, 222 air-charged catheter, 46
Stress urethral pressure microtip, 45, 49
profilometry, 84, 85 reference height, 48
Stress urinary incontinence water-filled system, 45
(SUI), 93, 217 water-filled systems, 50
Stress urinary incontinence zero, external water-filled,
syndrome (SUI-S) 47, 48
bladder neck descent, 101 Transobturator mid-urethral
clinical testing, 219 sling (TMUS), 105
complicated SUI, 98 Transurethral cystometry, 41, 79
Index 235
Trial Of Mid-Urethral Slings saline solution, 53

(TOMUS) trial, 105 tracings and artifacts, pressure
signals, 61
transducers, 44, 46, 47, 49, 50
U urodynamic software, 41
UPOINT phenotypic classification vesical pressure, 42
system, 179 voiding phase, women, 70, 71
Urethral hypermobility, 94, 95 Uroflowmetry, 31–35, 38
Urethral pressure profilometry Urothelial signaling, 136
(UPP), 79–83 Urothelium-based hypothesis, 135
Urgency incontinence, 6, 26, 96,
123, 124, 131, 137, 138,
206, 218 V
Urgency urinary incontinence Validated Urinary Incontinence
(UUI), 93, 96, 124 Questionnaires, 19, 99
Urinalysis, 23, 99, 132 Valsalva leak point pressure
Urinary incontinence (UI), (VLPP), 66, 83, 104, 125
types, 93 Valsalva-induced voiding, 12
Urodynamic stress incontinence, Value of Urodynamic Evaluation
102, 103 (ValUE) trial, 104, 105
Urodynamics testing Value of Urodynamics prior to
abdominal pressure, 42 Stress Incontinence
anti-inflammatory drugs, 58 Surgery (VUSIS) I and
bladder, 52 II trials, 105, 106
clinical practice, 57 Videourodynamics (VUD),
detrusor pressure, 43 87–89
electromyography of pelvic Voided percentage, 37–38
floor muscles, 53 Voiding cystourethrography
EMG electrodes, 54 (VCUG), 88, 192
equipment, 42 Voiding diary, 24, 25, 132
informed consent, 50 Voiding dysfunction, 126, 157, 219
patient preparation, 50 Voiding dysfunction syndrome
posttest patient care, 58 (VD-S), 124
preoperative urodynamics, 217 bladder outflow obstruction,
pressure fluctuations, 56 150
pressure measurement, 43 causes, 150, 151
pressure types, 42 clinical diagnosis, 161
principal methods, 17 clinical management, 162
prophylaxis, 58 detrusor contraction, 149
quality of signals, 56 detrusor underactivity, 150,
rectal/vaginal balloon 152
catheter, 53 diagnostic procedures, 152
rectum/vagina, 52 diminished bladder emptying,
resting pressures, 55 150
risk factors, 58 epidemiological studies, 150
236 Index
Voiding dysfunction syndrome urodynamic findings, 156

(VD-S) (cont.) Voiding phase, 11, 41, 68, 70, 75,
isovolumetric detrusor 88, 99, 102, 183, 188
pressure, 159 Voluntary interruption of
pathophysiology, 152 voiding, 12, 13
prevalence, 150
projected isovolumetric
pressure, 159 W
Schafer’s nomogram, 160 Water-filled external transducers,
slow/incomplete micturition, 44, 45
149 White matter hyperintensities
urethral sphincter activity, 161 (WMH), 6, 7

Urodynamics For Urogynecologists Vignoli2018

Uploaded by

Copyright:

Available Formats

Urodynamics For Urogynecologists Vignoli2018

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Urodynamics For Urogynecologists Vignoli2018

Uploaded by

Copyright:

Available Formats

Giancarlo Vignoli

ISBN 978-3-319-74004-1 ISBN 978-3-319-74005-8 (eBook)

Library of Congress Control Number: 2018940775

© Springer International Publishing AG, part of Springer Nature 2018

Printed on acid-free paper

This Springer imprint is published by the registered company Springer

In recent years gynecologists have shown an increasing inter-

To make matters worse, urodynamic testing is time con-

of urodynamics in clarifying the nature of the problem, and,

Bologna, Italy Giancarlo Vignoli

*Griffiths DJ, Kondo A, Bauer S, Diamant N, Liao L, Lose G, et al.

1 Physiology of Micturition in Female . . . . . . . . . . . . . . 1

2 Pretest Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3 Noninvasive Urodynamics. . . . . . . . . . . . . . . . . . . . . . . 31

4 How to Perform Conventional Urodynamic

5 Interpretation of Tracings and Identification

6 Supplementary Urodynamic Tests. . . . . . . . . . . . . . . . 79

6.3 Electromyography. . . . . . . . . . . . . . . . . . . . . . . . . 85

7 UDS in Stress Urinary Incontinence

8 UDS in Pelvic Organ Prolapse

8.4.1 Incontinence Surgery

9 UDS in Overactive Bladder Syndrome (OAB-S). . . . 131

10 UDS in Voiding Dysfunction Syndrome (VD-S). . . . 149

10.5 Obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

11 UDS in Pain Bladder Syndrome (PBS)

12 Neurogenic Lower Urinary Tract Dysfunction

12.5.1 Urodynamics with Imaging

13 Making Sense of Urodynamic Testing for Women

 ppendix A: What Do the Experts Say?—

 ppendix B: Informed Consent for

ACC Anterior cyngulate cortex

LPP Leak point pressure

UDS Urodynamic studies

© Springer International Publishing AG, part of Springer 1

Figure 1.1 Micturition cycle: FS first sensation at 40% of bladder

consisting of connections between the brain stem and the

Figure 1.2 Neural control of micturition—Bradley loops: Loop I is

specific functions. The micturition cycle is under control of

such as the desire to void and receive back signals from

• Circuit 1 involves the PFC (prefrontal cortex), the PAG

Storage phase occurs largely unconsciously and presum-

Figure 1.3 Neural control of micturition—Simple working model:

experience during growth and development. In infants, the

Figure 1.4 White matter hyperintensities in elderly women.

matter affect the regional brain activity involved in conti-

methods, when coupled with urodynamic studies, may give an

bladder afferent neurons to CNS

ACH SOMATIC INPUT (S2-S4)

Figure 1.5 Peripheral bladder innervation: Parasympathetic pelvic

nucleus at the same spinal level supplies axons that innervate

Figure 1.6 Organization of bladder motor nuclei (autonomic and

As afferent signaling increases in intensity with bladder

COUGH VALSALVA (Straining)

Figure 1.7 Pressure events during cough and straining (Valsalva

In men a significant rise of detrusor pressure is recorded

Box 1.1: Micturition Patterns in Women

MICTURITION PATTERNS IN WOMEN

Pves Pves Pves

Pabd Pabd Pabd

Bologna, Italy Giancarlo Vignoli

1 Physiology of Micturition in Female . . . . . . . . . . . . . . 1

2 Pretest Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3 Noninvasive Urodynamics. . . . . . . . . . . . . . . . . . . . . . . 31

4 How to Perform Conventional Urodynamic

5 Interpretation of Tracings and Identification

6 Supplementary Urodynamic Tests. . . . . . . . . . . . . . . . 79

6.3 Electromyography. . . . . . . . . . . . . . . . . . . . . . . . . 85

7 UDS in Stress Urinary Incontinence

8 UDS in Pelvic Organ Prolapse

8.4.1 Incontinence Surgery

9 UDS in Overactive Bladder Syndrome (OAB-S). . . . 131

10 UDS in Voiding Dysfunction Syndrome (VD-S). . . . 149

10.5 Obstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

11 UDS in Pain Bladder Syndrome (PBS)

12 Neurogenic Lower Urinary Tract Dysfunction

12.5.1 Urodynamics with Imaging

13 Making Sense of Urodynamic Testing for Women

ppendix A: What Do the Experts Say?—

ppendix B: Informed Consent for

implemented and personalized to rationally select patients

2.2 Pretest Assessment

2.2.1 Clinical History

2.2.2 Relevant Physical Examination

2.2.2.1 Structured Vaginal Examination

2.2.2.2 Focused Neuro-urological Assessment

2.2.2.3 Pelvic Floor Muscle Assessment

2.2.4 Voiding Diary

2.2.5 Pad Test

Medina C, Costantini E, Petri E, Mourad S, Singla A, Rodríguez-

3.1.1.1 Interpretation of Uroflowmetry

3.1.2 Postvoid Residual (PVR) Assessment

3.1.3 Voided Percentage (Void%)