Chapter 29 Urinary Tract
KEY POINTS
1 The lower urinary tract comprises of the bladder and urethra; it is under autonomic
and somatic nervous system control, and is anatomically supported by the pelvic
floor musculature.
2 Urinary incontinence, although underdiagnosed, is very common, has a significant
impact on quality of life, and is generally treated successfully with conservative or
surgical treatments.
3 Stress urinary incontinence is the most common subtype and occurs with increases in
abdominal pressure; it can be treated with pelvic floor exercises, pessaries,
behavioral modification, and surgery.
4 Urgency urinary incontinence occurs with a sudden desire to urinate that cannot be
postponed; it can be treated with bladder training, medications, behavioral
modification, bladder onabutulinumtoxinA injections, and neuromodulation.
5 Mixed urinary incontinence is the co-occurrence of stress and urgency incontinence;
it is the most bothersome and impactful subtype, and most common in late
adulthood.
6 Voiding dysfunction and bladder pain syndrome are less common than urinary
incontinence, but more challenging to treat successfully.
INTRODUCTION
[1] The urinary tract in women is comprised of the bladder that receives and
stores urine from the kidneys as it is propelled downstream via the right and
left ureters. The bladder expels the urine out of the body through the urethra
when it reaches capacity or when it is socially appropriate to do so. To help
accomplish this dual role of storage and voiding, the bladder and urethra are
enveloped with muscles whose fibers are innervated by an intricate network
of autonomous and somatic nerves, and they are anatomically supported by a
complex system of pelvic floor muscles, fascia, connective tissues, and nerves
within the pelvis.
Anatomy of the Lower Urinary Tract
In the supine position, the bladder is positioned between the pubic bone and
transversalis fascia anteriorly and the endopelvic fascia, vagina, and uterus
posteriorly. The lateral margins of the bladder abut the obturator fascia and the
condensation of muscle and connective tissue known as the arcus tendinous
muscle fascia (white line). The bladder is comprised of three layers including the
1659mucosa, detrusor (mostly smooth muscle), and serosa. The bladder mucosa
consists of the urothelium, basement membrane, and lamina propria. The latter is
composed of an extracellular matrix with different cell types, nerve endings,
lymphatic and blood vessels, all of which may play a role in maintaining bladder
compliance and act as a communication portal between the nervous system and
bladder muscle (1). The trigone, which is the base of the bladder, gets its name
from the triad of the two ureteral orifices and the proximal urethra that make up
the three corners of the triangle. The urethra is a 4-cm tubular structure
surrounded by skeletal muscles. It travels over the anterior wall of the vagina and
exits the urogenital diaphragm under the pubic symphysis as it opens into the top
of the introitus (Fig. 29-1).
Innervation of the Bladder and Urethra
The bladder is primarily innervated by the autonomic, the sympathetic and
parasympathetic, nervous systems. The sympathetic nervous system originates
from the thoracolumbar region of the spinal cord. Signal transmission occurs via
the paraspinal ganglia with norepinephrine being the primary postganglionic
neurotransmitter stimulating two different adrenergic receptor types: (a) the alpha
receptors are mostly located in the urethra and trigone; and (b) the beta receptors
are primarily located in the body of the detrusor muscle. The parasympathetic
nervous system originates from the sacral region of the spinal cord. Unlike the
sympathetic system, the parasympathetic system has long neurons that exit from
S2 to S4, synapse with their ganglia closer to the end organ (bladder), and
transmit their signals via short postganglionic neurons to the body of the detrusor
muscle. Here, transmission of messages occurs through acetylcholine
neurotransmitters stimulating muscarinic (or cholinergic) receptors. The somatic
nervous system plays a secondary role in the lower urinary tract system. It
originates from the sacral (S2–S4) region of the spinal cord via the pudendal
nerve; it provides motor innervation to the urethral sphincter and pelvic floor
muscles, and sensory innervation to the perineum (2).
1660FIGURE 29-1 Lateral view of the pelvic floor showing the anatomic location of the
bladder, urethra, vagina, and pelvic floor support structures transected at the level of the
vesical neck.
The central command of the sacral micturition center comes from impulses
generated at the level of the pontine micturition center located in the brain stem
which is regulated by signals that arise from higher levels of the cerebellum and
cortex of the brain. This complex interplay between the upper cortex, cerebellum,
and brainstem plays a key and dual role of: (a) inhibition that supports the storage
function during the filling phase; and (b) stimulation that facilitates the
micturition function of the bladder during the voiding phase (3).
The Physiology of Storage and Voiding
The primary role of the bladder is to store urine produced by the kidneys
and excreted through the ureters, and to subsequently eliminate the urine
outside the body through the urethra. The function of storage is made
possible by several factors including: (a) intrinsic factors to the bladder such
as the ability of its elastic smooth muscle fibers to stretch as the volume of
urine distends its capacity; (b) extrinsic factors to the bladder including
excitatory neurologic stimuli that constrict the proximal urethra and
urethral sphincter, and inhibitory neurologic stimuli that inhibit (or relax)
1661the detrusor muscle of the bladder. This reservoir function of the bladder,
which in effect translates into its continence mechanism, is dependent on the
proper functioning of the autonomic (sympathetic and parasympathetic)
nervous system, and the somatic nervous system (4).
Continence during storage is dependent on the integrity of the bladder
muscle, urethra, and the pelvic floor support structures surrounding the
lower urinary tract, including the levator ani muscles, endopelvic fascia, and
their attachments to the pelvic sidewall and the white line. The urethra has
several components within or around it that play an important role. These include
the striated muscles of the urethral sphincter, the smooth muscles of the urethra,
and the neurovasculature of the urethral wall, all of which help maintain elasticity
and the epithelial coaptation function of the urethra during times of bladder filling
(5,6). The extrinsic structures supporting the urethra and the intrinsic
urethral function are equally important, to the extent that a defect in the
former can lead to urinary incontinence resulting from hypermobility of the
urethrovesical junction, and a defect in the latter can lead to urinary
incontinence caused by intrinsic sphincter deficiency.
During the filling phase, the sympathetic nervous system through the lumbar
region of the spinal cord sends inhibitory signals to the beta receptors in the
bladder to relax, and excitatory signals to the smooth muscles of the trigone and
urethra to contract. As the bladder gets distended, afferent fibers from the bladder
send impulses to the central nervous system through the pelvic nerve to the sacral
spinal cord. This initiates two types of impulses: one that is transmitted
horizontally via the micturition reflex back to the bladder, and another that is
transmitted vertically up to the brain. The latter will make one of two conscious
decisions. If it is socially inappropriate to initiate micturition, it will send
excitatory impulses via the pudendal nerve to contract the pelvic floor muscles
and external urethral sphincter, and inhibitory impulses to supplement the
function of the sympathetic system (Fig. 29-2). Alternatively, the brain may
decide it is an opportune time to eliminate the urine. In this instance, it will send
voluntary impulses to the striated muscles to relax the pelvic floor and urethral
sphincter. It will also send facilitative impulses to the pontine micturition center
to release its bladder inhibition. This transmits impulses down the spinal cord to
activate the sacral micturition reflex via the parasympathetic system, resulting in
stimulation of the cholinergic receptors and bladder contraction while the urethra
is relaxed (7).
1662FIGURE 29-2 Detrusor–sphincter reflex during urine storage: The sympathetic system
promotes the bladder to relax (inhibition) and the outlet to contract (stimulation).
Concurrently, the pudendal nerve stimulates the urethral sphincter to contract. (DeGroat
WC. A neurologic basis for the overactive bladder. Urology 1997;50(Suppl 6A):36–52;
Figure 4, need permission.)
URINARY INCONTINENCE
1663[2] Disorders of urine storage are typically expressed by patients with a
limited number of bladder control symptoms that include urinary urgency,
frequency, nocturia, and urinary incontinence. Urgency is defined as a
sudden, compelling desire to pass urine which is difficult to defer (8).
Frequency (i.e., increased daytime voids) and nocturia (increased nighttime
voids) are surrogates of urgency, and they are more commonly used than
urgency in epidemiologic and clinical trials because they are easier to
measure (9). The present International Continence Society (ICS) guidelines
define nocturia as waking up one or more times to urinate; whereas
frequency occurs when the patient considers that she is going to the
bathroom more often than her normal (8).
[2] Urinary incontinence, defined as any involuntary leakage of urine, is easier
to measure or quantify than urgency. Of all the urinary storage symptoms, it tends
to be the most distressing, impactful, and costly. Although the signs and
symptoms of urinary incontinence appear to be a straightforward expression of
bladder disorder, its diagnosis and treatment is anything but simple. The
complexity of the bladder is in its simplicity. There are many underlying causes
that can potentially lead to urinary incontinence. In the following sections, we
will define urinary incontinence and its subtypes, describe its epidemiology and
impact, discuss the pathophysiology and associated risk factors, discuss
evaluation and examination of women with incontinence, explore the various
diagnostic tools, and propose available treatment modalities.
Definitions
Defining urinary incontinence has been challenging. Should urinary incontinence
be defined as any amount of urine loss, then the overwhelming majority of
women may fit the definition. Conversely, should urinary incontinence be defined
with stricter criteria, such as losing a certain volume of urine with a specific
number of episodes in a month, then only a minority of women would fit that
definition. A key consideration is to be able to distinguish normal from abnormal
lower urinary tract function. While much of the focus of clinical research is on
individuals with frank urinary incontinence, the ultimate challenge is to
understand when preclinical urinary incontinence starts, and more importantly the
trajectory it takes to progress into a clinically relevant and persistent condition.
Historically, urinary incontinence was defined as the involuntary loss of urine
represented as an objectively demonstrable event, and described to be a social or
hygienic problem (10). Although highly specific, this definition was clinically
impractical. Women who presented with subjective incontinence received little to
no attention if it was not observed by their clinicians during an examination, or if
it was not reported by patients to be a “hygienic” problem. Presently, urinary
1664incontinence is defined as the complaint of any involuntary leakage of urine
(8). Paradoxically, this new definition includes a substantial spectrum of women
who have experienced rare incidental urine loss events. Consequently, some
studies report urinary incontinence prevalence estimates of up to 60% (11).
Urinary incontinence has two main subtypes, stress and urgency urinary
incontinence, that either occur in isolation of each other, or they co-occur
and present as mixed urinary incontinence. [3] Stress urinary incontinence is
defined as loss of urine associated with activities such as coughing, sneezing,
lifting, or laughing. [4] Urgency urinary incontinence is defined as loss of
urine associated with a strong desire to urinate. Of note is that the term
“urgency” has replaced “urge” as a symptom of storage disorder; the latter is
considered to be a normal (nonpathologic) desire to void urine when the bladder
is full. [5] Mixed urinary incontinence is defined as urine loss associated with
activity and with a strong desire to urinate (8). Women with urinary
incontinence may express their symptoms continuously (continuous urinary
incontinence), with intercourse (coital incontinence), with change in position
(postural incontinence), with retention or incomplete bladder emptying
(overflow incontinence), during sleep (nocturnal enuresis), or without being
aware of it (insensible incontinence). Finally, the term functional incontinence
is used to define women who have an intact bladder function, but still report
incontinence caused by factors extrinsic to the bladder. Examples include
elderly women who have mental, psychological, or mobility ailments that prevent
them from making it to the bathroom on time. A summary of current definitions
of symptoms of lower urinary tract storage disorders is shown below (Table 29-
1).
Table 29-1 Classification and Definition of Lower Urinary Tract Symptoms in
Women
I. Abnormal
Storage
Symptoms and Signs
Incontinence
(symptom)
Any involuntary leakage of urine
Stress urinary
incontinence
(symptom)
Involuntary leakage on effort or exertion, or on sneezing or coughing
Stress urinary
incontinence
(sign)
Observation of involuntary leakage from the urethra, synchronous
with exertion/effort, or sneezing or coughing
1665Urgency
urinary
incontinence
(symptom)
Involuntary loss of urine associated with urgency
Mixed
incontinence
Involuntary loss of urine associated with urgency and also with effort
or physical exertion or on sneezing or coughing
Continuous
urinary
incontinence
Continuous involuntary loss of urine
Frequency Number of voids per day, from waking in the morning until falling
asleep at night
Increased
daytime
urinary
frequency
Micturition occurs more frequently during waking hours than
previously deemed normal by women (traditionally defined as more
than seven episodes)
Nocturia Interruption of sleep one or more times because of the need to
micturate (each void is preceded and followed by sleep)
Nocturnal
enuresis
Involuntary loss of urine that occurs during sleep
Urgency Sudden, compelling desire to pass urine, which is difficult to defer
Postural
urinary
incontinence
Involuntary loss of urine associated with change of body position, for
example, rising from a seated or lying position
Insensible
urinary
incontinence
Urinary incontinence where the women has been unaware of how it
occurred
Coital
incontinence
Involuntary loss of urine with coitus. This symptom might be further
divided into that occurring with penetration or intromission and that
occurring at organism.
Overactive
bladder
syndrome
(OAB)
Urinary urgency, usually accompanied by frequency and nocturia,
with or without urgency urinary incontinence, in the absence of
urinary tract infection or other obvious pathology
Although stress and urgency urinary incontinence are regarded as different
1666disease entities, it is important to note that women move among and between
stress and urgency urinary incontinence. In one large study of over 10,500
women, significant changes in incontinence status were reported over a 2-year
period: of those with baseline urgency urinary incontinence, 34% to 38%
remitted, 4% to 9% transitioned to stress urinary incontinence, and 16% to 20%
transitioned to mixed urinary incontinence; of those with baseline stress urinary
incontinence, 32% to 41% remitted, 4% transitioned to urgency urinary
incontinence, and 16% to 23% transitioned to mixed urinary incontinence; of
those with baseline mixed urinary incontinence, 22% to 27% remitted, 10% to
11% transitioned to urgency urinary incontinence, and 11% to 15% transitioned to
stress urinary incontinence (12).
Epidemiology of Urinary Incontinence
Prevalence
Prevalence estimates of urinary incontinence among community-dwelling
women range from 2% to 58% (11). This wide range in estimates results from
variation in definitions used, populations surveyed, age of study participants, and
other reasons. Over their lifetime, urinary incontinence affects more than one in
three women (13). Recent U.S. population data show that more than 20 million
women have urinary incontinence, and this is projected to increase by more than
50% in the coming decade (14). Although urinary incontinence prevalence overall
increases with age, prevalence patterns differ by incontinence subtype. [3] Stress
urinary incontinence peaks in the fifth decade of life and is the most common
subtype overall. Prevalence of urgency and mixed urinary incontinence is
relatively low up to the fourth decade of life, but gradually increases thereafter.
The average prevalence of stress, urgency, and mixed urinary incontinence is
13%, 5%, and 11%, respectively. [5] Mixed urinary incontinence becomes the
most dominant subtype in late adulthood (15) (Fig. 29-3).
1667FIGURE 29-3 Prevalence of stress, urgency, and mixed urinary incontinence by age. Note
the peak prevalence of stress urinary incontinence at 50 years of age followed by a decline;
also note the continuous increase in mixed urinary incontinence into late adulthood where
it becomes the most prevalent subtype. SUI, stress urinary incontinence; UUI, urgency
urinary incontinence; MUI, mixed urinary incontinence. (Minassian VA, Stewart WF,
Hirsch A. Why do stress and urge incontinence co-occur much more often than expected?
Int Urogynecol J Pelvic Floor Dysfunct 2008;19:1429–1440; Figure 1, need permission.)
Incidence and Remission
Longitudinal studies report high variations in urinary incontinence incidence
rates that range between 5% and 20%. In one meta-analysis, age-specific
incidence varied between 2/1,000 person-years before age 40 and increased to
5/1,000 person-years at age 50 (16). Remission rates of urinary incontinence
are equally high and range between 3% and 12%. Data from longitudinal
studies suggest that urinary incontinence is highly dynamic where women
cycle in and out of active disease (17–20). It is noteworthy that most
longitudinal studies that describe incidence and remission of urinary incontinence
offer little insight on the natural history of the urinary incontinence subtypes and
transition rates between stress, urgency, and mixed urinary incontinence (12).
Impact of Urinary Incontinence
Urinary incontinence is an emotionally, socially, physically, and economically
burdensome condition (21,22). It has a significant impact on quality of life
(QOL), where urinary incontinence has been shown to be associated with
embarrassment, anxiety, and depression (22–24). These emotional burdens
may lead women to adopt coping strategies that further alienate them from their
1668social environment resulting in further deterioration of QOL. There is a
downward cycle of impairment resulting in worsening psychological function.
Studies examining the burden of disease have shown that mixed urinary
incontinence is more severe, bothersome, and impactful on QOL than stress or
urgency urinary incontinence (25,26).
Despite the wide-ranging impact of urinary incontinence, only a minority of
women seek or receive care for their condition, resulting in underdiagnosis and
undertreatment. Since most women with early stages of urinary incontinence (i.e.,
mild to moderate urinary incontinence) do not seek care, when they finally
present with advanced symptoms (severe urinary incontinence), there is lost
opportunity to prevent or reverse disease progression (11). Managing urinary
incontinence is a substantial burden and cost for caregivers and the community.
Presence of urinary incontinence increases risk of nursing home admissions, and
in community-dwelling women, total urinary incontinence costs (direct and
indirect) are about $11.2 billion/year (27,28).
Pathophysiology
Stress Urinary Incontinence
Historically, the key urethral support responsible for continence was
considered to be at the bladder neck and proximal urethra. The
pubourethral ligaments, extending from the undersurface of the pubic bone
down to the urethra, were thought to be structurally important to maintain
continence (29). DeLancey used cadaveric studies to formulate the Hammock
Theory where he proposed that the primary support of the bladder neck and
urethra to be an intact vaginal wall at the base of the bladder (30). Through
its fibrous and muscular attachments to the pelvic sidewall, namely to the
condensation of the levator ani muscles, the vagina was shown to act as a
hammock to support the bladder neck, compress the urethra, and therefore
maintain continence. Loss of integrity of the hammock resulted in stress
urinary incontinence (30).
Concurrently, Petros and Ulmsten proposed the Integral Theory of
continence (31). They built on the work by DeLancey and others, and
hypothesized that stress urinary incontinence occurs as a result of connective
tissue laxity in the vagina and its supporting ligaments, namely the
pubourethral, cardinal/uterosacral, and arcus tendineus fascia pelvis. The
integral theory highlighted the role of the suspensory ligaments supporting
the proximal vagina that supports the mid-urethra. It hypothesized that the
multidirectional movement of the pelvic floor muscles coordinated the
urethral continence mechanism: (a) the forward direction of the
pubococcygeus muscle stretches the mid-vagina forward against the
1669pubourethral ligament to close the urethra from behind; (b) the backward
direction of the levator plate stretches the upper vagina and bladder base
backward and downwards in a plane around the pubourethral ligament to
close off the proximal urethra (32). In subsequent years, using urodynamic,
radiologic, and clinical observations, DeLancey proposed that the integrity of the
urethra is as, if not more, important in maintaining continence than the underlying
support structures. These structures include the epithelial coaptation of the
urethral mucosa with its neurovasculature, smooth muscles, and the striated
sphincteric muscles (6). Therefore, the current most accepted theory of stress
urinary incontinence pathogenesis is loss of integrity of structures intrinsic to
the urethra, and, to a lesser extent, the pelvic support structures in close
proximity, but extrinsic, to the urethra.
Urgency Urinary Incontinence
The pathophysiology of urgency urinary incontinence is not well-developed,
as the etiology of this condition in most women remains idiopathic. The term
“urgency urinary incontinence” is often used interchangeably with the term
“overactive bladder (OAB).” OAB is a syndrome associated with urgency,
usually accompanied by frequency, nocturia with (OAB-wet) or without
(OAB-dry) urgency urinary incontinence, and in the absence of a urinary
tract infection or other obvious pathology (8). Certain neurologic conditions
are known to be associated with urgency urinary incontinence (33). Women with
multiple sclerosis, Parkinson, or spinal cord injuries have a disruption of the
neuronal circuits at different levels of the central nervous system resulting in loss
of inhibitory control on the bladder voiding mechanism (34). The micturition
center in the brain maintains continence while the bladder fills up by suppressing
the urgency to urinate (35). Any abnormality in the pathways between the
micturition center and the bladder can lead to urgency urinary incontinence
(36).
Several theories have been developed for nonneurogenic OAB or idiopathic
urgency urinary incontinence. The epithelial hypersensitivity theory proposes
presence of chemosensitizing agents leading to bladder instability. These are
believed to be inflammatory substances such as nerve growth factor,
prostaglandins, and acetylcholine that increase detrusor muscle sensitivity and
neuronal excitability. The influence of these agents may be compounded by the
presence of a defective uroepithelium that leads to increased sensitivity of the
detrusor muscle (33,37). The myogenic theory suggests that the pelvic floor
sustains a physical strain during the developmental years. Myogenic dysfunction
ensues secondary to altered structure or disordered function of a group of
myocytes within the detrusor smooth muscle independent of its nerve supply (38).
1670Prolonged bladder outlet obstruction or bladder ischemia (from atherosclerosis or
diabetic neuropathy) can lead to denervation of detrusor muscle, muscle damage,
and increased hyperexcitability to acetylcholine (38). These and other proposed
theories are likely influenced by psychosocial disturbances, genetic
predisposition, inflammatory, and drug-induced conditions (37).
Mixed Urinary Incontinence
Mixed urinary incontinence is the most common incontinence subtype in
later adulthood. Women with mixed urinary incontinence tend to have more
severe symptoms that are bothersome and with a higher impact on QOL.
Mixed urinary incontinence may represent a combination of bladder storage
conditions of different etiologies. These may include women with independently
co-occurring stress or urgency urinary incontinence where symptoms of both
conditions are expressed on the same day or at different time periods; or stress
urinary incontinence that has predated urgency urinary incontinence or resulted in
stress-induced urgency urinary incontinence; or stress urinary incontinence
associated with urgency (OAB-dry) without incontinence. It is likely that mixed
urinary incontinence comprises different pathophysiologic subtypes that are still
not well understood (39).
Other Causes of Urinary Incontinence
Other conditions that may be associated with urinary incontinence where urine
loss occurs through the urethra include urethral diverticuli, and ectopic urethra.
A urethral diverticulum is a localized herniation of urethral mucosa into the
surrounding tissues. Diverticuli occur mostly in the distal urethra of women
between the ages of 30 and 60 years. The etiology of acquired diverticula is
unknown, but one accepted hypothesis is injury and blockage of periurethral
glands from repeated urinary tract infections with subsequent rupture into the
urethral lumen resulting in formation of a diverticulum. Diverticuli could be
congenital in nature likely representing a remnant of Gartner duct (40). Although
urine loss (dribbling) is reported with urethral diverticuli, women commonly
present with symptoms similar to urinary tract infections such as dysuria, urethral
pain, dyspareunia, and hematuria. On examination, a tender urethral mass is often
palpable (Fig. 29-4). An ectopic ureter is a congenital anomaly where the ureter
opens distally into the urethra or more commonly into the vagina. Here, the
mother of a baby girl usually presents to her pediatrician complaining of constant
wetness in the perineum of her child resulting from absence of any sphincteric
control.
1671FIGURE 29-4 Urethral diverticulum. (Iyer S, Minassian VA. Resection of urethral
diverticulum in pregnancy. Obstet Gynecol 2013;122:467–469; Figure 2, need permission.)
Extraurethral incontinence occurs when a part of the urinary system drains
through an abnormal opening bypassing the urethra. These are conditions that
could be either congenital such as bladder extrophy, or traumatic such as a fistula.
A bladder extrophy is a rare condition that involves a congenital absence of the
anterior vaginal wall and base of the bladder/urethra. This is usually identified at
birth and may require several and complicated surgical procedures to reconstruct.
A fistula is an acquired condition where there are one or more direct
communications between the vagina and ureter (ureterovaginal fistula), bladder
(vesicovaginal fistula), or the urethra (urethrovaginal fistula). The vesicovaginal
fistula is the most common, and usually arises from a prolonged obstructed labor,
1672in younger and poorly developed women in rural, underdeveloped regions of the
world. With prolonged labor, caused by malpresentation or inadequately sized
pelvis, the lower urinary tract and vagina are compressed between the head of the
unborn child and the maternal pelvic bones, sometimes for days. This leads to
ischemic injuries resulting in tissue breakdown, necrosis, and development of a
fistula (Fig. 29-5). Another obstetrics-related condition, known as Youssef
syndrome, may arise from a fistulous tract developing between the uterus and
vagina, commonly after repeated cesarean sections. Here, patients present with
cyclic hematuria, urinary incontinence, and amenorrhea.
Unlike obstetric causes of fistula formation, in the developed countries, a
genitourinary fistula usually arises from gynecologic causes. These include
pelvic malignancies, gynecologic surgeries such as hysterectomy, and pelvic
irradiation. Undiagnosed bladder or ureteral trauma, or an inadequately treated
injury during a hysterectomy (vaginal, laparoscopic, or abdominal) can result in
fistula formation, usually within the first 2 weeks after surgery. An alternate
process of fistula formation occurs from an occult injury to the bladder or ureter,
typically during a laparoscopic hysterectomy where an energy source is used to
transect the uterine pedicles. Here, the fistula may develop as a result of a latent
injury from spread of energy to the genitourinary system.
FIGURE 29-5 Vesico-vaginal fistula.
Risk Factors of Urinary Incontinence
To better understand the pathophysiology of urinary incontinence and its
1673subtypes, it is important to identify risk factors associated with, or that mediate
onset and progression of disease. Known risk factors for urinary incontinence
include: race, age, parity, obesity, diabetes, chronic cough, COPD and
smoking, previous pelvic surgery, medications, and functional and motor
impairment (Table 29-2). Evidence for an association between risk factors and
urinary incontinence is strong for some, and inconclusive for others. Race has
been shown to have a variable effect on urinary incontinence by subtype. In
general, white women have a higher prevalence and incidence of urinary
incontinence than Hispanic, Asian and black women. More specifically, across
urinary incontinence subtypes, white women are at a higher risk of developing
stress urinary incontinence, whereas black women are at a higher risk of
developing urgency urinary incontinence (41,42).
Age has a variable effect on urinary incontinence subtypes. Prevalence of
stress urinary incontinence peaks in the fifth decade and then declines
thereafter. Advancing age past the 50s is not a risk factor for stress urinary
incontinence alone (15). This is because vaginal birth is strongly associated
with stress urinary incontinence in the first two decades after childbirth, but
has little to no effect beyond that. Hence, as the time interval increases between
a woman’s age and the birth of her children, there is decreasing effect of
childbirth and onset of stress urinary incontinence (43,44). In contrast, advancing
age is a strong predictor of both urgency and mixed urinary incontinence.
Pregnancy increases the risk of stress urinary incontinence with about
50% of pregnant women reporting symptoms. Although most women report
resolution of their stress incontinence symptoms after birth, recurrence
within 5 years is high. Parity, is another strong risk factor of urinary
incontinence, and primarily for stress urinary incontinence. A recent 2016
meta-analysis showed that vaginal birth had a twofold increased risk of stress
urinary incontinence when compared with cesarean delivery (43). Parity is a risk
factor for mixed urinary incontinence; however, controlling for its association
with stress urinary incontinence in women with mixed urinary incontinence,
parity is not a risk factor for urgency urinary incontinence (45). Most
epidemiologic data suggest that having a cesarean section reduces the risk of
subsequent urinary incontinence (43,46).
Table 29-2 Common Risk Factors by Urinary Incontinence Subtype
1674Obesity is another major risk factor for urinary incontinence and its
subtypes (47,48). Similar to vaginal birth, the effect of increasing weight on the
pelvic floor may lead to pudendal nerve injury with subsequent levator ani muscle
atrophy leading to weakening of the pelvic floor urethral support structures (49).
The effect of increased weight is a risk for new-onset stress urinary
incontinence, and for urgency urinary incontinence secondary to detrusor
overactivity (50). Diabetes and obesity are strongly correlated, but controlling for
obesity, diabetes still stands out as an independent risk factor for urgency
urinary incontinence, and to a lesser extent, for stress and mixed urinary
incontinence (51). The mechanism of action of diabetes is believed to be
multifactorial including: (a) its diuretic effect leading to frequency and urgency
urinary incontinence; (b) microvascular injury to the nerves supplying the
detrusor muscle leading to detrusor overactivity; and (c) microvascular injury to
the pudendal somatic nerve supplying the urethral sphincter (37).
Risk factors such as previous pelvic surgery, chronic cough or pulmonary
disease, and smoking have potentially similar detrimental effects on the
pelvic floor resulting in urinary incontinence. For instance, previous
hysterectomy has been shown to be associated with stress and urgency
urinary incontinence (15), surgery for prolapse increases risk of new-onset
stress urinary incontinence (52), and surgery for stress urinary incontinence
1675may lead to de novo or worsening urgency urinary incontinence. History of
smoking is associated with all urinary incontinence subtypes (48). Other risk
factors, also referred to urinary incontinence caused by functional or transient
causes, are described within the DIAPPERS mnemonic (Table 29-3). These
include certain medications (e.g., psychotropic medications), urinary tract
infections, stool impaction, and psychologic and motor impairment. Unlike age,
race, and parity, these risk factors are modifiable by directly treating or altering
their effect on the individual, and more specifically on the bladder.
Table 29-3 Reversible Causes of Urinary Incontinence
D Delirium
I Infection
A Atrophic urethritis and vaginitis
P Pharmacologic causes
P Psychological causes
E Excessive urine production
R Restricted mobility
S Stool impaction
From Resnick NM, Yalla SV. Management of urinary incontinence in the elderly. N Engl
J Med 1985;313: 800–805, with permission.
Diagnosis
Historically, diagnosis of urinary incontinence required a big workup. First, a
detailed history and extensive physical and pelvic examination including Q-tip
testing were performed. Exhaustive 7-day long bladder diaries were required of
patients, and multiple urogynecologic surveys were administered. Laboratory and
bladder testing including urine analysis and urine culture, 24-hour pad test,
cystoscopy, urodynamics, and other tests were frequently performed. Mounting
evidence indicates that most of these diagnostic modalities are not cost-effective,
and unnecessary during the initial workup of a woman with urinary incontinence.
Based on the new AUA and ACOG guidelines, the workup of urinary
incontinence has become more streamlined (53,54). The urethral Q-tip test
has mostly been eliminated, and the 7-day bladder diary has been replaced
with a 2- to 3-day diary (55–57). Similarly, simpler and shorter forms of
1676QOL, bother, and sexual dysfunction questionnaires, specific to urinary
incontinence, have been developed. Cystoscopy is rarely an indication for
uncomplicated urinary incontinence, and urodynamics is no longer necessary
prior to treatment for simple urgency urinary incontinence, or prior to
surgery for uncomplicated stress urinary incontinence (58,59).
History Taking
Medical history taking from a woman with urinary incontinence should
explore the duration of time with urine loss, associated symptoms, and their
severity. Questions are asked to identify incontinence subtype based on the
circumstances surrounding the urinary incontinence episodes. Urine loss
associated mostly with activities such as coughing, sneezing, or laughing is
suggestive of stress urinary incontinence; women with stress urinary
incontinence report urine loss that occurs while they are on the trampoline
with their children, during activities such as running and jumping, and at
times, with intercourse. Symptoms associated with or immediately preceded
by an urgency episode are indicative of urgency urinary incontinence. The
latter may present with reports of increased urinary frequency, or nocturia.
Women describe symptoms of urgency with or without incontinence
provoked by the sound of running water (e.g., washing dishes), change in
temperature, getting out from the car, or as they open the door to get into
their homes. Many women, especially the older age group, report mixed
symptoms of stress and urgency urinary incontinence, and information on
bother and impact on QOL by subtype should be solicited.
Other relevant clinical information is history of previous medical or surgical
treatment for incontinence, coexisting urinary tract infection with symptoms such
as dysuria, hematuria, or suprapubic pain, fluid intake, and other health conditions
(e.g., neurologic), or medications that may be associated with incontinence. For
example, a woman with past history of stress urinary incontinence who underwent
a mid-urethral sling may now be presenting with urgency symptoms; another
woman presenting with occasional urgency urinary incontinence, a frequency of
15 episodes during the day and only once at night may admit to drinking a gallon
(about 4 L) of liquids, including coffee and soda; alternatively, a poorly
controlled diabetic woman who is a smoker may present with urgency (diuretic
effect of sugar) and stress (chronic cough effect from smoking) urinary
incontinence symptoms. Many medications taken for other medical conditions
can impact the lower urinary tract and should be discussed with patients as
potential contributors to their symptoms (Table 29-4).
Table 29-4 Medications that May Affect the Function of the Urinary Tract
16771. Sedatives such as the benzodiazepines may cause confusion and secondary
incontinence, particularly for elderly patients
2. Alcohol may have similar effects to benzodiazepines and also impairs mobility and
causes diuresis
3. Anticholinergic drugs may impair detrusor contractility and may lead to voiding
difficulty and overflow incontinence. Drugs with anticholinergic properties are
widespread and include antihistamines, antidepressants, antipsychotics, opiates,
antispasmodics, and drugs used to treat Parkinson disease
4. Alpha agonists, which are often found in over-the-counter cold remedies, increase
outlet resistance and may lead to voiding difficulty
5. Alpha blockers, sometimes used to treat hypertension (e.g., prazosin, terazosin), may
decrease urethral closure pressure and lead to stress incontinence
6. Calcium channel blockers may reduce bladder smooth muscle contractility and lead to
voiding problems or incontinence; they may also cause peripheral edema, which may
lead to nocturia or nighttime urine loss
7. Angiotensin-converting enzyme inhibitors may result in a chronic and bothersome
cough that can result in increasing stress urinary incontinence in an otherwise
asymptomatic patient
Physical Examination
All women presenting for evaluation of urinary incontinence should undergo a
routine general physical examination with particular attention given to conditions
that may impact their incontinence. These include: mental and cognitive function
(e.g., dementia and its association with urgency, frequency, and enuresis),
neurologic function (e.g., Parkinson disease and multiple sclerosis and their effect
on urgency urinary incontinence), cardiovascular status (e.g., vascular
insufficiency and lower extremity edema and their association with nocturia
secondary to night time fluid mobilization in the recumbent position), pulmonary
function (e.g., chronic obstructive pulmonary disease and its effect on stress
urinary incontinence), nutritional status (effect of obesity on stress and urgency
urinary incontinence), mobility, gait, and dexterity (urgency urinary
incontinence).
The pelvic examination includes palpation of the pelvis and lower abdomen for
presence of masses. Lower extremity (deep tendon reflexes) and perineal
sensation and sacral nerve reflexes, including the anal wink and bulbocavernosus
reflexes, are evaluated. The latter reflexes are elicited by gently stroking or
tapping the clitoral and perianal skin to elicit a contraction of the external anal
1678sphincter. The goal of the pelvic examination is to investigate the underlying
cause of urinary incontinence and to identify associated pelvic support
defects. Examination is performed in the lithotomy position, but may require
a semi-upright or standing position. Evaluation of the vulva and vagina may
reveal atrophy, vaginitis, dermatoses, or pain associated with symptoms of
incontinence, urgency, and frequency. Inspection or palpation of the urethra may
reveal tenderness or mass, suggestive of an infection or diverticulum. Prolapse
staging of the different pelvic floor compartments is performed (see Chapter
30). Integrity of the pelvic floor and levator ani muscles can be assessed.
With two fingers in the vagina, the patient is asked to contract the muscles
used to “hold urine” or to “avoid passing gas.” The ability to contract and
strength and duration of the contraction are all measured. Finally, bimanual
and rectovaginal examinations are performed to assess for pelvic or adnexal
masses, integrity of the anal sphincter, and pelvic tenderness.
Q-tip Test
The Q-tip test, which is no longer recommended, involves introducing a
cotton-tipped swab into the urethra and asking the patient to Valsalva to
measure the angle deviation of the urethra from baseline. More than a 30-
degree deviation is consistent with hypermobility of the urethra, and/or
urethrovesical angle. Minimal to no angle deviation in a woman with stress
urinary incontinence may indicate intrinsic sphincter deficiency, also known
as stove-pipe urethra. The Q-tip test is no longer recommended because of the
discomfort associated with inserting the cotton swab into the urethra. Equivalent
information can be obtained from a vaginally placed swab to measure urethral
mobility while the patient is asked to Valsalva (55).
Cough Stress Test
During the pelvic examination, a cough stress test is performed. This can be
done either with a full or an empty bladder. The advantage of doing it with a
full bladder is that it is easier to demonstrate urine loss from the urethra in a
woman with stress urinary incontinence. If history is suggestive, but urine
loss is not observed in the lithotomy position, the patient may be asked to
stand up and possibly jump and/or cough vigorously while the examiner
observes for urine loss. Note that a positive cough test with a full bladder cannot
rule out overflow incontinence; here, a patient may demonstrate objective
evidence of urine loss with a stress activity, but may concurrently have
incomplete bladder emptying. Clearly, offering a surgical intervention, like a midurethral sling, to such a patient is not ideal because it can result in urinary
retention. Alternatively, a cough test can be done after asking the patient to empty
1679her bladder. A positive empty bladder cough test is strongly indicative of stress
urinary incontinence and at times may be suggestive of intrinsic sphincter
deficiency.
Postvoid Residual
The postvoid residual (PVR) volume of urine is the amount of urine
remaining in the bladder within 10 minutes from voiding. This can be
measured either using a small-caliber catheter during the pelvic examination or
via ultrasound. The latter is less invasive and has a standard error of less than
20%, with more accuracy for smaller PVRs (i.e., less than 200 mL) (60).
Alternatively, using the catheter to measure a PVR may result in a more exact
volume of urine, especially for large bladder volumes, and has the added benefit
of testing a more sterile urine specimen for a urine analysis or urine culture, if
indicated. Normal values for PVRs are not well established; however, most
would consider a PVR <50 mL to be within normal and a PVR >150 mL to
be abnormally elevated (61,62).
Simple Bladder Testing
Other simple tests are available that can be administered before (bladder diary),
during (urinalysis), or after (pad test) a clinical encounter to assist the clinician in
making a firm diagnosis.
Bladder Diary
The bladder diary, also referred to as the voiding diary, is meant to
represent the total amount of fluid intake, by type, in a 24-hour period.
Historically, voiding diaries were administered over a 7-day period. But these
were too inconvenient for patients to complete, and evidence shows that a 2- to 3-
day diary is equally reliable (56). The information gained from fluid intake is
important because it helps put into context symptoms of urgency, frequency,
and nocturia. In addition to fluid intake, the bladder diary offers information on
various measures of urine output, urinary incontinence, and circumstances
surrounding the urinary incontinence episode(s). The patient is asked to measure
the amount of voided urine by time of day and night; here, one can assess the 24-
hour total urine output, number of voids per day, average voided volume, and
bladder capacity (largest voided volume). The patient also documents the time a
urine loss occurs, and whether the event is associated with a stress activity (e.g.,
with a cough, sneeze, or laugh) or with urgency (Fig. 29-6).
1680FIGURE 29-6 An example of a voiding diary including time and amount of urination
during the day and at night, urinary incontinence episodes and associated activity, volume,
type, and time of fluid intake.
The bladder diary helps clarify the diagnosis when information gathered
during the history and pelvic examination is inconclusive. For example, intake
of large fluid volumes or consumption of large amounts of caffeine and alcohol
can easily explain why a woman may report a physiologic increase in urinary
frequency and urgency. Alternatively, a voiding diary that shows a 24-hour fluid
intake of 50 ounces (1.5 L), and nothing to drink 3 hours before bedtime in a
patient who reports a daytime frequency of every 2 hours, nocturia of 3 to 4
times, and with small voided volumes may represent a pathologic condition like
OAB or urgency urinary incontinence.
Urinalysis
The urinalysis by simple dipstick is helpful to rule out a urinary tract
infection, especially in the presence of irritative lower urinary tract
symptoms such as urgency, frequency, nocturia, and dysuria. Presence of
nitrites, leukocytes and/or hematuria on dipstick may indicate the presence of a
1681urinary tract infection. It is important to note that hematuria on a dipstick is not
conclusive for presence of blood in the urine and should be confirmed by a formal
microscopic evaluation. A urine culture can be sent to confirm the presence of a
urinary tract infection. Treatment of a urinary tract infection may help improve
these symptoms. It is generally not recommended to treat bacteriuria in a woman
who is otherwise asymptomatic.
Pad Tests
These are not routinely performed in the clinical setting. They are helpful
objective tools used in research since they quantify the volume and frequency of
urine loss by counting and weighing the pads used in a 24- to 48-hour period. One
research application of pad tests may include a new drug trial to treat urgency
urinary incontinence. In this instance, patients may be asked to wear incontinence
pads before and after taking the medication, to determine if the drug (compared to
placebo) results in a decrease in the volume and frequency of urinary
incontinence episodes. Pad tests can be employed to help objectify the presence
of urinary incontinence that is not demonstrable in the clinical setting, even with a
full bladder (i.e., negative cough stress test). An example may be a competitive
female athlete who reports loss of urine that occurs only during strenuous exercise
and which significantly impedes her performance. The patient is given 100 mg of
phenazopyridine (changes the color of urine into orange) to take before her
exercise routine while wearing a pad. The presence of orange staining on the pad
may help in the diagnosis of stress urinary incontinence.
Table 29-5 Symptom Questionnaires for Women with Pelvic Floor Disorders
Urinary Incontinence:
• Incontinence Severity Index
• International Consultation on Incontinence Questionnaire Short Form (ICIQ-SF)
• Urogenital Distress Inventory (UDI)
• Urogenital Distress Inventory Short Form (UDI-6)
• Kings Health Questionnaire
• Bristol Female Lower Urinary Tract Symptom Questionnaire (BFLUTS)
All pelvic floor disorders (urinary incontinence, fecal incontinence, prolapse):
• Pelvic Floor Distress Inventory (PFDI)
• Pelvic Floor Distress Inventory Short Form (PFDI-20)
Adapted from Barber MD. Questionnaires for women with pelvic floor disorders. Int
Urogynecol J Pelvic Floor Dysfunct 2007;18:461–465; permission needed?
1682Quality of Life Measures
Although urinary incontinence is a health condition with limited immediate
physical sequelae to the individual woman, it can have tremendous
psychological, social, and general health effects. Some women stop exercising
as a result of constant urine loss with activity; others limit the amount of fluids to
reduce their urgency and urinary incontinence episodes; women may stop going
out because of fear of not finding a bathroom when one is needed; yet others may
not wish to have intercourse with their partner due to embarrassment from having
an accident. Clinical evaluation is not complete without an assessment of these
behavioral changes in response to bother from urinary incontinence that can lead
to profound consequences on an individual’s psychological, sexual, social, and
ultimately her physical well-being. There are several validated questionnaires
specifically developed to better assess severity of urinary incontinence, its
bother, impact on QOL, and sexual health (63). Many of those have short
versions that can be easily administered to patients during the initial visit,
and repeated in the future after an intervention, to measure change
(improvement) over time. The following two tables list a summary of
common symptom questionnaires (Table 29-5) and QOL and sexual function
scales for women with urinary incontinence pelvic floor disorders (Table 29-
6).
Table 29-6 Quality of Life and Sexual Function Scales for Women with Pelvic Floor
Disorders
Advanced Bladder Testing
Urodynamics
The hallmark of advanced bladder testing is the urodynamics test. This test
is an adjunct to history taking, clinical examination, and simple bladder
testing. The scope of its indications and use in clinical practice has narrowed over
time as clinicians have improved their diagnostic acumen in identifying different
1683bladder control conditions. Examples where urodynamics are not necessary
include: the diagnosis of incontinence is straightforward and consistent with
history, physical examination, and simple bladder testing; a woman with
predominantly subjective stress urinary incontinence symptoms with positive
cough test and minimal PVR, irrespective of whether an anti-incontinence surgery
is planned or not; a woman with urgency urinary incontinence symptoms, even
prior to initiation of medical treatment.
When performed, urodynamics provides objective data on lower urinary
tract function and serves two purposes: the first is to help characterize
bladder storage conditions by distinguishing stress, urgency, and mixed
urinary incontinence from each other; the second is to assist in establishing a
diagnosis for bladder voiding dysfunction. Urodynamics has many useful
applications in situations where: the diagnosis is not clear because of
inconsistencies between the history, physical examination, symptom scales,
and voiding diary; women have mixed or complex symptoms where
conservative treatment options have failed; surgery for prolapse is being
planned in a woman without any symptoms of urinary incontinence, or with
a negative cough stress test, to elicit the presence or absence of occult stress
urinary incontinence; previous surgery for incontinence has failed or
symptoms of urinary incontinence have recurred; incomplete bladder
emptying is reported (high PVR); symptoms of incontinence are
compounded by the presence of neurologic conditions like multiple sclerosis
(64).
Urodynamics can be simple or complex. A summary of all the definitions and
terms used in urodynamics is shown (Table 29-7) (65). A simple urodynamics
consists of uroflowmetry, PVR, and simple filling cystometry. This may be the
procedure of choice when someone has predominant stress urinary incontinence
with a negative cough stress test.
Table 29-7 Urodynamic Definitions
I. Bladder sensation
A. First sensation First becomes aware of bladder filling
B. First desire to
void
Feeling that would lead the person to void at next
convenient moment, but voiding can be delayed if necessary
C. Strong desire to
void
Persistent desire to void without the fear of leakage
D. Sensation Classified as:
16841. Increased
2. Reduced
3. Absent
4. Nonspecific bladder sensations (other symptoms make
person aware of bladder filling, like abdominal fullness)
5. Bladder pain (is abnormal)
6. Urgency (sudden compelling desire to void)
II. Detrusor function
A. Normal Allows bladder filling with little or no change in pressure;
no involuntary phasic contractions
B. Detrusor
overactivity
Involuntary detrusor contractions during filling
1. Phasic Characteristic wave form; may or may not lead to
incontinence
2. Terminal Single involuntary detrusor contractions occurring at
cystometric capacity, which cannot be suppressed, and
results in incontinence usually resulting in bladder emptying
3. Detrusor
overactivity
incontinence
Incontinence that is due to an involuntary leakage episode
4. Neurogenic
detrusor
overactivity
There is a relevant neurologic condition (replaces term
detrusor hyperreflexia)
5. Idiopathic
detrusor
overactivity
No definite cause (replaces term detrusor instability)
C. Bladder
compliance
Fill volume/change in detrusor pressure (Pdet)
1. Calculate at start of bladder filling (usually 0)
16852. At cystometric capacity (excluding any detrusor
contraction)
D. Bladder capacity
1. Cystometric
capacity
Volume at end of cystometrogram; capacity is volume
voided together with any residual urine
2. Maximum
cystometric
capacity
Volume at which person feels she can no longer delay
voiding
III. Urethral function
A. Normal urethral
closure
mechanism
Maintains a positive urethral closure pressure during bladder
filling
B. Incompetent
urethral closure
mechanism
Allows leakage of urine in the absence of a detrusor
contraction
C. Urethral
relaxation
incontinence
Leakage that is due to urethral relaxation in the absence of
raised abdominal pressure or detrusor overactivity
D. Urodynamic stress
incontinence
Involuntary leakage of urine during increased abdominal
pressure, in the absence of detrusor contraction (replaces
term genuine stress incontinence)
E. Urethral pressure
(Pura)
Fluid pressure needed to open closed urethra
1. Pressure
profile
Pressure along length of urethra
2. Urethral
closure
pressure
P
ura – Pves
3. Maximum
urethral
closure
pressure
(MUCP)
Maximum difference between P
ura and Pves
16864. Pressure
transmission
ratio
Increment in urethral pressure on stress as percentage of
simultaneously recorded increment in intravesical pressure
F. Abdominal leak
point pressure
Intravesical pressure at which urine leakage occurs because
of increased abdominal pressure
IV. Pressure flow studies
A. Urine flow Defined as:
1. Continuous
2. Intermittent
a. Flow rate Volume voided/unit time
b. Voided volume Total volume voided
c. Maximum flow
rate
d. Voiding time Includes interruptions
e. Flow time Time over which measurable flow actually occurs
f. Average flow
rate
Voided volume/flow time
g. Closing
pressure
Pressure measured at end of measured flow
h. Detrusor
function during
voiding
Classified as:
1. Normal
2. Detrusor
underactivity
Contraction of reduced strength resulting in prolonged
bladder emptying and/or a failure to achieve complete
bladder emptying
3. Acontractile Cannot be demonstrated to contract
i. Urethral
function during
Classified as:
1687voiding
1. Normal Continuously relaxed
2. Dysfunctional
voiding
Intermittent and/or fluctuating flow rate that is due to
involuntary intermittent contractions of the periurethral
striated muscle during voiding in neurologically normal
people
3. Detrusor
sphincter
dyssynergia
Detrusor contraction concurrent with an involuntary
contraction of the urethral and/or periurethral striated muscle
4. Nonrelaxing
urethral
sphincter
obstruction
Usually occurs in people with a neurologic lesion
From Abrams P, Cardozo L, Fall M, et al. The standardization of terminology of lower
urinary tract function: Report from the Standardization Sub-committee of the International
Continence Society. Neurourol Urodyn 2002;21:167–178, with permission.
Uroflowmetry
This a study that assess voiding function. Here, the patient is asked to come
to the office with a comfortably full bladder and void while sitting on a
special commode attached to a funnel that directs the voided volume into a
spinning receptacle that measures the amount of voided volume of urine over
time. Several data points are obtained through this study that include the
total amount of voided urine, the average and peak flow of urine, the time to
peak flow, flow time, and total time to void. A normal uroflow has a
continuous bell-shaped configuration, a short time to peak flow, and a high
peak flow (Fig. 29-7); whereas an obstructed flow may have two or more
lower peaks with an interrupted flow pattern or a prolonged tail (Fig. 29-8).
1688FIGURE 29-7 Normal uroflow with a bell-shaped pattern, a short time to peak flow, and a
continuous flow with complete bladder emptying.
FIGURE 29-8 Abnormal uroflow showing a prolonged and interrupted voiding pattern
with an initial high peak followed by several smaller peaks.
1689Filling Cystometry
After completion of the uroflowmetry, the patient is placed in a lithotomy position
and a catheter is placed to measure the PVR volume, which, if normal, is
generally less than 50 mL. In a simple urodynamics, filling cystometry involves
backfilling the bladder manually through the catheter at 60 mL increments or via
a water pump at a rate of 50 to 100 mL per minute. There are several sensory
parameters that are measured during the filling phase including (with their typical
normal values): first filling sensation (50 mL); first desire to void (150 mL);
strong desire to void (250 mL), and maximum cystometric capacity (400 mL).
Reduced volumes in several of these parameters may be consistent with OAB or
urgency urinary incontinence. Once the bladder capacity is attained, the catheter
is removed, and the patient is asked to cough or Valsalva. Loss of urine associated
with an increased abdominal pressure is indicative of stress urinary incontinence.
Complex Urodynamics
Women with predominant urgency urinary incontinence, mixed or complex
symptoms, with previous failed incontinence surgery, or neurologic conditions
may be more suited for a complex urodynamics. In addition to the uroflowmetry,
this test includes complex filling cystometry, urethral pressure profilometry, and
pressure flow studies. In addition, electromyography (EMG) of the urethral
sphincter is commonly performed. Although complex urodynamics is a more
advanced form of bladder testing, it is not a perfect test. A false negative test can
occur in a woman with subjective stress urinary incontinence where no urine loss
is observed even with a full bladder in the lying or standing position; it can also
occur with urgency urinary incontinence where a patient may report sensory
urgency, but no detrusor activity is visible. A false positive is uncommon with
stress but may happen with urgency urinary incontinence where the presence of
the catheter or patient’s anxiety may provoke an iatrogenic bladder contraction.
Filling Cystometry (Complex)
Similar to the simple urodynamics, filling cystometry is performed to assess
bladder and urethral function during the filling phase. The catheter placed in the
bladder has two transducers, one is situated at the tip of the catheter measuring the
intravesical pressure, and another is positioned a few centimeters behind the tip
measuring the transurethral pressure. A pressure transducer is placed either inside
the vagina, or the rectum, to approximate the intra-abdominal pressure. Since the
intravesical pressure (Pves) is a measure of the detrusor pressure (Pdet) plus the
pressure of the abdomen and surrounding organs (Pabd), then the true detrusor
pressure is obtained by subtracting the value of the abdominal pressure from the
intravesical pressure:
1690Pdet = Pves - Pabd
The advantage of complex cystometry is a more accurate assessment of the
detrusor pressure (activity) during the filling phase. For instance, should the
patient inadvertently sneeze, Valsalva, or increase her intra-abdominal pressure
during the test, a stable Pdet in the presence of an increased Pves is expected in a
normal bladder because the rise in Pves and Pabd cancel each other.
Alternatively, if a woman develops an unprovoked bladder contraction, Pabd will
remain neutral while Pves and Pdet show a spike. In this situation detrusor
overactivity is observed (Fig. 29-9).
FIGURE 29-9 Detrusor overactivity on filling cystometrography. The patient begins to
sense urgency, accompanied by an unstable bladder contraction, when 88 mL of water are
instilled into the bladder. The detrusor pressure rises, and when 96 mL of water are
instilled, she leaks. Pabd, abdominal pressure; Pves, vesical pressure; Pdet, detrusor
pressure.
Urethral Pressure Profilometry
1691The urethral pressure profilometry is a measure of the function of the urethra.
When the bladder capacity is attained during cystometry, filling is stopped. The
pressure inside the bladder (Pves), and that of the urethra (Pure) are noted. In a
healthy normal bladder and urethra, the Pure is higher than Pves during filling,
the opposite is true during voiding. The difference between the urethral and
bladder pressures is denoted as Pclose where:
Pclose = Pure - Pves
Because the urethra is approximately 4-cm long and the urethral sphincter is
located in the proximal urethra, it is important to identify the maximum urethral
closure pressure (MUCP). The catheter inside the bladder is typically attached to
a pulley which, when engaged, will pull the catheter in and out of the bladder as
the urethral transducer measures the Pure. The MUCP is the highest value of
Pclose along the urethral pressure continuum. MUCP values of less than 20 cm of
H2O may represent intrinsic sphincter deficiency; whereas a normal urethra has
MUCP value >40 cm of H2O.
Another test of urethral integrity is known as the Valsalva leak point pressure
(VLPP) which represents the value of the intra-abdominal or intravesical pressure
at which point urine loss occurs. This is usually performed when the bladder is
comfortably filled to 200 cc and the patient is asked to Valsalva or cough with
gradually increasing force. The point at which leakage of urine is observed during
this exercise is marked and denoted as VLPP. Typically, a VLPP >60 cm of H2O
is used as a cut-off representing normal urethral function, and below which may
be consistent with diminished urethral sphincter tone (Fig. 29-10).
1692FIGURE 29-10 Valsalva leak point pressure. The abdominal Valsalva leak point pressure
(VLPP) is 114 cm H2O (the abdominal pressure at which the patient leaked urine).
Electromyography
EMG leads are usually placed around the external anus to indirectly assess the
activity in the urethral sphincter. Since the anal sphincter and urethra are
primarily innervated by the pudendal nerve, the EMG activity generally
represents a good estimation of the urethral striated muscle activity. In a normal
individual, and during the filling phase, there is increased EMG activity; during
the voiding phase, there is decreased EMG activity. In women with neurologic
conditions or spinal cord injuries with retention or dysfunctional voiding, there is
often dyssynergia between the detrusor function and the urethral muscle activity.
Pressure Flow Studies
1693The final component of a complex urodynamics study is the pressure flow study
or voiding cystometrogram. Here the Pves, Pabd, and Pure are measured
concurrently as the patient is asked to void. This study offers information on the
voiding mechanism of the bladder, presence of dysfunctional voiding, and the
potential risk for retention or incomplete bladder emptying after surgery for
incontinence. Normative values for all the components of a urodynamics study
are shown (Table 29-8).
Other Bladder Studies
Fluoroscopy
Fluoroscopy is sometimes used, but generally not recommended, in conjunction
with urodynamics (also referred to as video urodynamics) to assess for a cystocele
and hypermobility of the urethrovesical junction. This information could be
equally gathered during a pelvic examination; imaging studies do not have any
significant added value, and they expose patients to unnecessary radiation.
Moreover, the presence of funneling, or bladder neck opening with Valsalva does
not necessarily equate to stress urinary incontinence as many women with normal
functional urethras, and who are continent, show evidence of bladder neck
opening during fluoroscopy (66).
Cystoscopy
A typical office-rigid cystoscope consists of a 17-French caliber sheath, through
which the endoscope is introduced. This is attached to a fiber-optic light source,
camera, and distending medium (sterile water or normal saline). The lenses on the
endoscope are 0, 12, 30, 70, or 120 degrees. The lesser angle lenses are wellsuited to inspect the urethra (Fig. 29-11), and perform office procedures like
urethral bulking or bladder botox; whereas the 30- and 70-degree lenses are best
to identify the ureteral orifices, trigone and bladder walls, and stent the ureters.
The 120-degree scope, which is helpful to have a retroview of the bladder neck, is
not routinely used in women. Instead, a flexible cystoscope, that has a smaller
caliber and is more comfortable to patients, can be used in those instances. In fact,
many specialists preferentially use the flexible cystoscope. However, the
advantage of a rigid versus a flexible cystoscope is that the former has an
operative channel through which it is easier to take a biopsy, should an
abnormality be identified.
Table 29-8 Approximate Normal Values of Female Bladder Function
• Residual urine <50 mL
1694• First desire to void occurs between 150 and 250 mL infused
• Strong desire to void does not occur until after 250 mL
• Cystometric capacity between 400 and 600 mL
• Bladder compliance between 20 and 100 mL/cm H2O measured 60 sec after reaching
cystometric capacity
• No uninhibited detrusor contractions during filling, despite provocation
• No stress or urge incontinence demonstrated, despite provocation
• Voiding occurs as a result of a voluntarily initiated and sustained detrusor
contraction
• Flow rate during voiding is >15 mL/sec with a detrusor pressure of <50 cm H2O
From Wall LL, Norton P, DeLancey JO. Practical Urogynecology. Baltimore, MD:
Williams & Wilkins, 1993, with permission.
1695FIGURE 29-11 Cystoscopic view of a scarred urethra using a smaller angle lens.
Cystoscopy is a simple office procedure that is frequently performed in the
evaluation of various bladder conditions. But, it has a limited role in the initial
workup of basic urinary incontinence. Instances where cystoscopy is important
include stones, bladder tumors, foreign bodies, or chronic cystitis. Other
indications in women include: (a) microscopic hematuria (presence of red blood
cells in the urine) that is unrelated to a urinary tract infection; (b) OAB that is
refractory to conservative or medical treatment, especially in older women; (c)
urinary incontinence with suspected vesicovaginal fistula; (d) symptoms such as
frequency, urgency, dysuria, in the absence of a urinary tract infection; (e) women
presenting with recurrent urinary tract infections; (f) recurrent urinary
incontinence or OAB symptoms following previous anti-incontinence surgery; (g)
complications from previous vaginal mesh or sling procedures (54,67).
1696Experts agree that cystoscopy is essential intraoperatively during any prolapse,
incontinence, or bladder surgery. Injuries to the bladder and ureters are welldocumented during such procedures (68–71). For instance, incidence of ureteral
injury is as high as 11% after a high uterosacral colposuspension (69); whereas,
the incidence of cystotomy could be up to 5% after mid-urethral slings (68).
Identification of these injuries is relatively simple via the cystoscope, and
intraoperative or early treatment of the injury results in better long-term
outcomes. However, there is no consensus about performing cystoscopy
universally at the time of a hysterectomy (72–74). Rates of ureteral and bladder
injuries after hysterectomies for benign indications are reported to range between
0.02% and 1.8% and 0.85% to 2.9%, respectively (74,75).
Ultrasound and MRI of the Pelvis
Although pelvic ultrasound has been a gold standard diagnostic tool in many
areas of gynecology, its clinical utility in bladder control conditions has been
limited to research and experimental purposes. Imaging technologies such as the
pelvic ultrasound and MRI have enabled researchers to develop a better
understanding of the urinary continence mechanism, and the pathophysiology of
stress urinary incontinence (6). With the advancements of 3D and 4D imaging,
diagnostic ultrasound modalities have shown some promise in clinical practice
(76). They help in defining the morphology of the urethra and its sphincter where
women with stress urinary incontinence are noted to have shorter urethra and
smaller urethral sphincter volumes. Ultrasound can help assess changes in
morphology of the urethra, bladder neck mobility, pelvic support structures at rest
or with Valsalva, and to quantify these changes. These variations are accentuated
in women who have concomitant stress urinary incontinence and pelvic organ
prolapse. Moreover, it is possible to assess the integrity and strength of the levator
muscles during a pelvic floor contraction, and measure PVR bladder volume (77).
Other useful properties of the ultrasound include observation of urethral
coaptation after an injection of bulking agent for intrinsic sphincter deficiency,
identification of previous pubovaginal or mid-urethral sling location and
tightness, and detection of urethral diverticulum, foreign bodies or implants in the
urinary system.
MRI is another radiologic modality that has been used mostly in research to
better understand the anatomy of the pelvis and the organs within. It has played a
significant role in improving our understanding of the pathophysiology of pelvic
organ prolapse and stress urinary incontinence. Static MRI gives detailed
information of the urethral anatomy, the striated sphincter, and its surrounding
structures (78,79). Dynamic MRI can delineate compartments of the female
pelvis, including the urethra, with and without intra-abdominal straining to
1697characterize presence of prolapse (80). However, MRI is not routinely used in
clinical practice because of its expense and the availability of the simple pelvic
examination in the office that gives equally valuable information. Nonetheless,
one condition for which MRI is the diagnostic modality of choice is a urethral
diverticulum (81).
Neurophysiologic Testing
The function of the bladder, urethral sphincter, and pelvic floor are dependent on
the integrity of the nervous system, from the brain down to the terminal sensory
and motor nerve endings supplying the genitourinary system. Several imaging
and nerve conduction techniques are available to study the normal function and
pathophysiology of the neuromuscular system. These include modalities such as
functional CT and MRI scanning and somatosensory-evoked potentials (mostly
for urgency urinary incontinence), and pudendal or sacral nerve motor latency,
and EMG (mostly for stress urinary incontinence). These tests are usually
performed in specialized centers and are not routinely used in the clinical setting
during the workup of most women with urinary incontinence.
Prevention
Successful prevention and treatment strategies for all urinary incontinence
subtypes exist. Early detection is specially challenging because most patients do
not seek care, and specialists see only a small fraction of women with urinary
incontinence. Programs to mitigate onset and progression of disease should
start at the primary care level. Known risk factors that promote new-onset
urinary incontinence, such as age, BMI, and parity, have a long latent
period. There exists some evidence that early interventions may delay or
reduce risk of subsequent onset of urinary incontinence symptoms (46). One
such example is the effect of introduction of pelvic muscle training exercises
during pregnancy on prevention of urinary incontinence in the short term.
Large longitudinal population-based studies show that cesarean delivery, as
opposed to vaginal birth, may have a beneficial effect in reducing subsequent risk
of stress urinary incontinence. In the absence of other indications, promoting
elective cesarean section as the preferred method of delivery to prevent future
pelvic floor dysfunction, including stress urinary incontinence, is a topic of
debate. Other risk reduction interventions include: (a) weight loss in obese
women; (b) management of blood sugar control in diabetics; (c) reduced
consumption of high levels of alcohol and caffeine (46).
Conservative Nonpharmacologic Treatment
Conservative options should be offered to all patients as a first-line
1698treatment. To optimize treatment benefits, diagnosis should be made early during
the course of disease, and sometimes before onset of overt symptoms.
Conservative treatments are generally simple, noninvasive, readily available and
inexpensive, relatively effective and with little to no side effects. [3] Examples of
conservative nonpharmacologic interventions [4] include lifestyle
modification, counseling and patient education, bladder training (or
retraining), relaxation and urgency suppression, exercise training (e.g.,
pelvic floor muscle exercises), biofeedback, electric stimulation (E-stim),
pessaries, and urethral plugs (82).
Lifestyle Modification
This includes avoidance of risky behavior associated with urinary
incontinence, urgency, frequency, and nocturia such as smoking and alcohol
consumption. It includes staying healthy, developing an active lifestyle, being
physically fit and losing weight (if obese). In obese or overweight women, there
is ample evidence that weight loss improves both stress and urgency urinary
incontinence symptoms (83). A 10% weight loss leads to more than 50%
improvement in stress urinary incontinence symptoms (84). It requires that
women modify or alter their dietary habits, mostly the amount and type of fluid
intake. The recommended amount of fluid intake in a 24-hour period varies from
an individual to another depending on their activity level, their weight, and other
comorbidities. An assessment of a 24-hour bladder diary can help individualize
optimal amount, type, and timing of fluid intake for a particular patient. Caffeine
reduction is helpful in women with urgency and urgency urinary
incontinence (58).
Counseling and Education
This usually starts at the physician’s office, be it the patient’s primary care,
gynecologist, or female pelvic floor specialist. Patients can further be referred to a
dietician, physical therapist, counselor, or others to assist in establishing and
maintaining the health lifestyle modifications discussed above. Counseling and
education can take the form of different strategies such as supplying them with
educational material, motivational interviewing, empowering patients with tools
and coping strategies as it relates to their incontinence, and enabling patients to
take control of their condition and care for themselves (self-care or self-help).
Bladder Training
This intervention includes prompted voiding, and timed toileting and it aims
at assisting women with idiopathic OAB or urgency urinary incontinence to
minimize frequency of uncontrolled bladder urges and improve voluntary
control of urine. It is generally coupled with restricting fluids in women who
1699drink large quantities of liquid. Using her voiding diary as a guide, the
patient is asked to void at a fixed time interval that is comfortably long
enough (e.g., every 2 hours). Should she develop a strong desire to void
before the end of the time interval, she is asked to suppress the urge. Women
are instructed to double void. Here, the patient is asked to void normally in
the bathroom with a pelvic floor relaxation to allow the urine to flow; when
the flow of urine stops, the patient is instructed to voluntarily strain followed
by another relaxation period to allow additional unemptied urine to flow.
This regimented schedule of timed toileting and double voiding is continued
for a whole week and increased by an interval of 15 minutes every
subsequent week. The goal of bladder training is to prolong voiding and
improve bladder capacity while reducing urgency and incontinence episodes.
The whole intervention program usually takes up to 6 weeks and has been
shown to be effective when compared to medications (85).
Relaxation and Urgency Suppression
There are several maneuvers whereby a patient with a strong desire to void
can help mitigate the urgency sensation. One technique is to ask the patient
to do something that distracts her mind off the bladder urge, such as deep
breathing, singing silently, solving a simple mathematical problem, or
switching from the activity she was engaged in to a moment of inactivity.
Concurrently, the patient is asked to tighten her pelvic floor muscles, knee
and ankle flexion, sitting on a chair (if on her feet). Many of these can be
applied to women with history of stress urinary incontinence who anticipate
a urine loss episode with an imminent stress activity such as coughing or
sneezing.
Pelvic Floor Muscle Training
Historically, pelvic floor exercises were described by Arnold Kegel in 1948 as
a nonsurgical method to restore anatomy and function of genital relaxation
(86). Over time these exercises were structured into a physical therapy routine and
collectively termed pelvic floor muscle training (PFMT). There have been several
randomized trials demonstrating the benefits of PFMT (vs. placebo or no
treatment) in treating urinary incontinence, in general, and stress urinary
incontinence, in particular. A Cochrane review in 2015 showed that women
receiving PFMT reported improvement with fewer urine loss episodes or
cure, and a better QOL than controls. However, since most studies follow
patients up to a year or less, there is limited to no robust information on the longterm benefits of PFMT (87).
Commonly, during a PFMT program, women are encouraged to contract
1700their pelvic floor muscles for 3 seconds, 10 to 15 times per session, and 3
times a day. Helpful hints to contracting the right pelvic floor muscles
include: keeping the abdomen and hips relaxed; imagining that one is trying
to prevent passing of gas, tightening the rectum, or bringing the buttock
cheeks together. They should be done in a comfortable laying or sitting
position. It can be done while watching TV, in front of a computer on a desk,
or while driving a car. A common misconception is that women try to do
their Kegels in the bathroom every time they are voiding. However, this can
lead to voiding dysfunction and worsening OAB symptoms in the long run,
and Kegels are best done with an empty bladder.
Physical therapists often use adjunctive aids such as biofeedback and E-stim to
supplement the PFMT, especially when patients are not able to generate a good
squeeze during the physical therapy session. Biofeedback can be auditory or
visual and gives the patient a sensory feedback of the strength of her pelvic floor
squeeze. Electrical stimulation therapy delivers low levels of current via a probe
placed in the vagina or rectum. There is no evidence that biofeedback or E-stim
are superior to PFMT alone, especially when the latter are done regularly and
properly in women with stress urinary incontinence (87).
Mechanical Devices for Urinary Incontinence
Several devices are available to treat mostly women with stress urinary
incontinence (Fig. 29-12). These can be divided into two main groups:
urethral and vaginal. The urethral devices create a temporary occlusion of
the urethral meatus to prevent urine loss. One example of a urethral device is
the urethral insert FemSoft where a woman is instructed to place the insert into the
urethra and then remove it before urinating. These could be beneficial in female
competitive athletes who may have stress urinary incontinence episode only
during a sporting event (e.g., tennis). Although incontinence episodes are reported
to decrease, about one-third of women developed urinary tract infections in one
long-term follow-up study (88).
1701FIGURE 29-12 Vaginal incontinence pessaries: (clockwise from top): A: Suarez ring
(Cook Urological, Spencer, IN), B: PelvX ring (DesChutes Medical Products, Bend, OR),
C: Incontinence dish (Milex Inc., Chicago, IL), D: Incontinence dish with support (Mentor
Corp., Santa Barbara, CA), E: Introl prosthesis (was Johnson and Johnson; currently not
available), F: Incontinence ring with support (Milex Inc., Chicago, IL), (middle): G:
Incontinence dish with support (Milex Inc., Chicago, IL).
Vaginal devices consist of two categories. The first type of device is used as
an adjunct to PFMT such as vaginal weights or cones. These devices are
placed in the vagina by the patient for short periods of time in an effort to
improve the strength of the pelvic floor muscles. Alternatively, the second
type of a vaginal device is meant to be used long-term and throughout the
day to help support the bladder neck and assist in the urethral closure
mechanism of the urethral sphincter. These devices include pessaries, vaginal
sponges, or tampons. One randomized controlled trial comparing pessary use to
behavioral therapy to a combination treatment for stress urinary incontinence
showed that behavioral therapy produced greater patient satisfaction with fewer
incontinence symptoms that were bothersome at 3 months. By 12 months there
were no differences, and patient satisfaction persisted similarly in all three groups.
1702Single modality was similar to combination therapy (89). However, a recent
Cochrane review concluded that there is little evidence from controlled trials on
the role of mechanical devices on long-term sustained beneficial effects in the
management of urinary incontinence (90).
Other Treatment Options
Electric stimulation (E-stim) and magnetic stimulation (M-stim) are two
alternative conservative options that are available in specialized centers. Evidence
regarding those modalities in the management of urinary incontinence is not wellestablished and more research is needed to show whether they are more beneficial
than the traditional and less costly conservative options available.
Medications for Stress Urinary Incontinence
Historically, estrogen replacement therapy was used to treat women with
stress and urgency urinary incontinence. Based on large randomized trials
including the Women’s Health Initiative (WHI), estrogen (with or without
progesterone) has been shown to be associated with increased prevalence
(worsening incontinence) and incidence (new-onset incontinence), and with
the negative effect being more pronounced for stress than urgency urinary
incontinence (91). Similar results were found with the Heart Estrogen and
Progestin Replacement Study (HERS) comparing oral conjugated equine
estrogen and medroxyprogesterone acetate to placebo where 1,525 women
were followed for 4 years. More specifically, the HERS study showed that the
odds ratio for worsening incontinence was 1.5 among women with baseline
urinary incontinence; the odds ratio for developing new stress urinary
incontinence was 1.7, and new urgency urinary incontinence was 1.5 (92,93).
A Cochrane review on this topic confirmed these findings and concluded that
estrogen replacement therapy should not be offered to women as a treatment
for urinary incontinence, with the caveat that local (vaginal) use of estrogen
may improve symptoms of urgency and frequency in the short term (94).
Other medications have been used to treat stress urinary incontinence.
These are typically drugs that have a stimulating effect on the alphaadrenergic receptors present in the urethral sphincter. Examples include
epinephrine and norepinephrine, ephedrine and pseudoephedrine, and
phenylpropanolamine. These alpha-stimulating drugs are nonspecific and can
be associated with other systemic effects including on the heart, brain, and
blood pressure. They are not FDA approved and rarely, if ever, used purely for
stress urinary incontinence. Imipramine, a tricyclic antidepressant, has been used
with variable success, especially in women who have a coexisting stress and
urgency urinary incontinence. This may relax the bladder through its
1703anticholinergic effect, and constrict the urethra through its alpha-agonistic effect.
One other drug worthy of mention is duloxetine. It is an FDA-approved serotonin
and norepinephrine reuptake inhibitor drug to treat depression, chronic pain, and
anxiety, but not for stress urinary incontinence. Its mechanism of action on the
bladder is to increase bladder storage and improve urethral sphincter function via
its effect on the central nervous system. In one study, duloxetine was shown to be
equally effective as PFMT (95). But, but the presence of side effects (nausea,
fatigue, insomnia, somnolence, dizziness, and blurred vision) may preclude it
from being used as a first-line therapy for stress urinary incontinence.
Medications for Urgency Urinary Incontinence and Overactive Bladder
Medical treatment for urgency urinary incontinence and OAB is less
controversial than for stress urinary incontinence. Medications are usually
offered either when conservative treatment options have failed or in conjunction.
Their efficacy, however, is modest. One major medication class represents the
anticholinergic drugs. These include drugs that produce their effect by inhibiting
the stimulatory effect of the parasympathetic nervous system on the detrusor
muscle by blocking the cholinergic (acetylcholine or muscarinic) receptors.
Several of these drugs exist with similar efficacy profiles. These drugs differ
in duration of action (immediate release vs. long acting) and route of
administration (oral, patch, or gel) (Table 29-9) (58). In 2009, the Agency for
Healthcare Research and Quality published an evidence-based review of
over 230 publications on the medical treatment modalities for urgency
urinary incontinence and OAB (96). They showed that anticholinergic
medications reduced number of voids (and urinary incontinence episodes) by
1.5 to 2.2 per day, with the short-acting drugs being on the lower range, and
the long-acting drugs on the higher range. Interestingly, a relatively high
placebo effect exists in most randomized trials which is as high as 1.5 voids
per day reduction.
The immediate-release oxybutinin was the first FDA-approved
anticholinergic drug, but it has a short half-life and is taken three times a
day to be optimally effective. Extended-release medications tend to be better
tolerated because of their once daily administration, and a lower side-effect
profile (97). In general, anticholinergics are administered at a low dose, with
subsequent increase in dosage after a period of 4 to 6 weeks should there be
no significant improvement. In the presence of side effects, it is reasonable to
try another anticholinergic. Because anticholinergics are not purely specific
to the bladder muscarinic receptors, they all produce side effects with a
varying degree on other tissues or organs These include the salivary glands
resulting in dry mouth, the iris and ciliary muscles of the eyes resulting in
1704blurry vision, the gastrointestinal system resulting in constipation, the heart
resulting in altered heart rate, and the brain resulting in memory problems.
One exception may be trospium chloride, a quaternary amine anticholinergic,
which is hydrophilic with a large molecular size limiting its distribution into
the central nervous system and reducing its effect on cognition.
Table 29-9 Pharmacologic Therapies Indicated for Overactive Bladder with or
without Urgency Incontinence
Compound Usual Dose
Oxybutynin chloride (Ditropan, Ortho-McNeil–Janssen
Pharmaceuticals and available as generic formulation)
5 mg by mouth
3–4 times daily
Oxybutynin chloride extended release (Ditropan XL, OrthoMcNeil–Janssen Pharmaceuticals and available as generic
formulation)
5, 10, or 15 mg
by mouth once
daily
Oxybutynin transdermal patch (OxytroI, Watson Pharmaceuticals) One patch
applied twice
weekly
Oxybutynin gel 10% (Gelnique, Watson Pharmaceuticals) One sachet
applied daily
Tolterodine tartrate (Detrol, Pfizer) 2 mg by mouth
twice daily
Tolterodine tartrate long acting (Detrol LA, Pfizer) 4 mg by mouth
once daily
Fesoterodine fumarate (Toviaz, Pfizer)a 4 or 8 mg by
mouth once daily
Solifenacin succinate (Vesicare, Astellas Pharmaceuticals) 5 or 10 mg by
mouth once daily
Trospium chloride (Sanctura, Allergan) 20 mg by mouth
twice daily
Trospium chloride extended release (Sanctura XR, Allergan) 60 mg by mouth
once daily
Darifenacin (Enablex, Novartis Pharmaceuticals) 7.5 or 15 mg by
1705mouth once daily
aTolterodine is the active metabolite of fesoterodine.
Nygaard I. Clinical practice. Idiopathic urgency urinary incontinence. N Engl J Med
2010;363:1156–1162; Table 1, need permission.
There has been increased concern regarding the cumulative effect of
anticholinergics on cognition, dementia, and onset of Alzheimer’s disease. In
one review study of patients prescribed anticholinergic medications over a
follow-up period of 7 years, 797 participants (23%) developed dementia (of
whom, 637 developed Alzheimer’s). There was a significant 10-year
cumulative dose–response relationship for dementia and Alzheimer disease
(98). Based on this and other evidences, AUGS published a consensus
statement in 2017 recommending behavioral therapies as a first-line
treatment for urgency urinary incontinence, followed by medical
interventions. More specifically, AUGS recommends “ . . . caution in
prescribing anticholinergic medications in frail or cognitively impaired
patients” and that “ . . . providers should counsel on the associated risks,
prescribe the lowest effective dose, and consider alternative medications in
patients at risk” (99).
A second class of medications to treat urgency urinary incontinence
includes the beta agonists. This class currently includes only one FDAapproved (2012) medication known as mirabegron, which is a specific beta-3
receptor agonist. It produces its effect via the sympathetic system by stimulating
the beta receptors on the bladder, leading to relaxation of the detrusor muscle
(100). Unlike anticholinergics, it does not have dry mouth, constipation or
blurred vision as side effects, but it ought to be used with caution in women
with uncontrolled hypertension (it increases blood pressure), renal or hepatic
impairment and urinary retention. It can be used in women with cognitive
impairment. In one recent randomized trial comparing mirabegron to tolterodine,
patient tolerability for mirabegron was higher than tolterodine which was
associated with more side effects, but patient preference and OAB symptom
improvements were similar between the two drugs (101).
Medications for Nocturia and Enuresis
Nocturia, especially in the elderly, may be multifactorial. Waking up to go to
the bathroom one or more times during the night may be the consequence of
increased fluid intake, caused by bladder storage conditions like OAB, or
other comorbidities unrelated to the bladder, such as vascular insufficiency,
heart disease, or others. Desmopressin, a medication used to treat nocturia or
enuresis, is effective mostly through its central inhibitory action on reducing
1706urine production. It is available as a nasal spray and as an oral preparation.
Caution is recommended in the elderly or in women with hypertension; it
requires periodic measurement of sodium levels. Imipramine, may work
centrally to improve sleep, and peripherally on the bladder and urethra to improve
bladder storage. Anticholinergics can be used to help with nocturia, especially in
women with OAB. Diuretics like furosemide, can be helpful, especially in the
presence of vascular insufficiency and peripheral edema.
Medications to Treat Overflow Urinary Incontinence or Urinary Retention
Overflow urinary incontinence or urinary retention is a condition more
prevalent in men, and commonly occurs as a result of benign prostatic
hyperplasia. In women, in the absence of an anatomic obstruction, such as a
urethral stricture, previous anti-incontinence surgery or advanced prolapse,
overflow incontinence can occur because of bladder detrusor muscle
underactivity, diabetic neuropathy, or central nervous system conditions.
Different drugs have been used, albeit with limited success, to either stimulate the
detrusor muscle or to reduce urethral sphincter resistance, and therefore improve
voiding (102). Examples of detrusor muscle stimulants include muscarinic
receptor agonists, such as bethanechol, or cholinesterase inhibitors, such as
distigmine. There is no evidence from controlled clinical studies that these
medications offer substantial benefit, and these drugs may be associated with
significant side effects (103). A hypoactive or atonic bladder is generally not
responsive to medical treatment. Alpha-receptor blockers such as alfuzosin have
been shown to be beneficial in men by reducing the resistance in the bladder neck
and urethra to facilitate bladder emptying. Although these medications have been
used in women with urinary retention, they have produced variable results
(104,105).
Surgical Treatment of Urinary Incontinence
Pubovaginal Slings
At the turn of the 20th century, one of the earliest described surgeries reported in
Europe for stress urinary incontinence involved placing an organic sling at the
bladder neck (106). These operations, presently referred to as traditional slings,
are performed through two incisions, one in the vagina to pass the sling around
the urethra, and one through the abdomen to gain access around the space of
Retzius. The two free ends of the sling material are passed up from the vagina and
then attached commonly to the fascia of the rectus muscle (or other pelvic
structures) to create a fixed loop around the bladder neck and proximal urethra
(Fig. 29-13). This provides support to the urethral closure mechanism at times of
increased abdominal pressure (107). Over the years, use of different sling
1707materials has been described including autologous (e.g., fascia lata, rectus muscle,
or fascia harvested from the patient), allografts obtained from donors (e.g.,
cadaveric fascia lata), heterologous obtained from other species (e.g., bovine or
porcine), or synthetic (e.g., prolene or Gore-Tex) (108).
FIGURE 29-13 A completed traditional suburethral sling procedure with the fascia
located at the bladder neck with the ends of the sling tied to or above the rectus fascia. The
classic procedure uses autologous fascia; however, some surgeons use allograft or
xenograft tissue performed in a similar fashion. (Redrawn from original by Jasmine Tan.)
1708Although successful, the pubovaginal slings can result in urinary retention
requiring further surgery to resolve ensuing voiding dysfunction. Synthetic
slings can be associated with risk of erosion (109). In a large randomized
surgical study, women with stress urinary incontinence who underwent
fascial pubovaginal sling had a higher success rate than a Burch
colposuspension at 2-year follow-up (47% vs. 38%; P = 0.01). However, there
was a higher rate of complications in the pubovaginal sling group, including
voiding dysfunction, urinary tract infections, and new-onset urgency urinary
incontinence (110). Of the original 655 women in the initial randomized
clinical trial, 482 (75%) were enrolled in a follow-up study up to 7 years. The
vigorously defined composite success rate decreased from 42% to 13% in the
Burch group and 52% to 27% in the sling group (111). When success was
defined using only one criterion (e.g., 1-hour pad test), reported rates were
much higher and similar between the two groups (84% for the Burch group
and 85% for the sling group) (110). Based on this and other evidences, the
pubovaginal sling using autologous fascia remains a viable option to treat
women with predominant stress urinary incontinence (64).
Anterior Vaginal Wall Repair
A few years after the publication of the initial pubovaginal sling procedures to
treat stress urinary incontinence, Kelly reported on the anterior vaginal repair (or
anterior colporrhaphy) in 1914 (112). This operation was a simple procedure and
based on case series, it was initially thought to be a very successful surgery, and
therefore became quite popular for over half a century. The key concept of the
anterior vaginal repair is to plicate the pubovesical fascia around the bladder neck
and proximal urethra to give it the necessary support and to assist in the
sphincteric closing mechanism by preventing urine loss. Randomized controlled
trials comparing the anterior vaginal wall repair to alternative procedures revealed
that the former’s long-term success was suboptimal (113,114). The Kelly
plication (anterior vaginal wall repair) is not recommended to treat women with
stress urinary incontinence (64,109).
Needle Suspension Surgeries
One of the earliest needle suspension procedures was introduced by Pereyra in
1959 (115). The technique of this surgery and several of its subsequent
modifications involved passage of a special needle carrier introduced bilaterally
through an abdominal incision down into the vagina. Sutures were placed on both
sides of the urethra within the vaginal and underlying connective tissue, brought
up and then attached to the rectus fascia. It was presumed that this suspension
would provide lasting bladder neck support and help mitigate stress urinary
1709incontinence episodes. However, similar to the Kelly plication, long-term success
of needle suspension procedures failed to withstand the test of time in randomized
controlled trials (109,114), and they are no longer recommended for the treatment
of stress urinary incontinence (64).
Retropubic Colposuspension Surgeries
Because most women with stress urinary incontinence have hypermobility of the
bladder neck, DeLancey’s Hammock Theory made clinical sense (30). As a result,
retropubic colposuspensions (urethropexies), where the endopelvic fascia around
the bladder neck and proximal urethra is suspended to structures on the anterior
pelvis, were shown to be good surgeries to treat stress urinary incontinence (Fig.
29-14). The two most commonly performed retropubic urethropexies are the
Marshall–Marchetti–Krantz (MMK) and Burch procedures (116,117). The
procedures are similar in that the approach is abdominal, requiring entry
into the retropubic space. The MMK was initially described in a man with
urinary incontinence following prostatectomy where the endopelvic fascia
was attached to the pubic bone (116). With the Burch retropubic
urethropexy, the periurethral tissue was fixed to Cooper ligament (117).
Burch followed 143 of his patients up to 9 years and reported a success rate
of 82% (118).
FIGURE 29-14 Points of reattachment of the endopelvic fascia during retropubic bladder
neck suspensions. A: Arcus tendineus fascia pelvis (for paravaginal repair). B: Periosteum
of pubic symphysis (for Marshall–Marchetti–Krantz procedure). C: Ileopectineal, or
Cooper, ligament (for Burch colposuspension). D: Obturator internus fascia (also used for
paravaginal, or obturator shelf, repair).
1710In a randomized trial comparing the open Burch urethropexy to the midurethral sling procedure, success rate (reported as a negative 1-hour pad test) was
44/49 (90%) versus 58/72 (81%), respectively (P = 0.21) at 5 years (119).
Retropubic urethropexies can be performed laparoscopically, but there are limited
data on their long-term efficacy (120). In one randomized trial, patients were
followed for a median of 65 months (range 12 to 88 months). Here, 58% of
women reported any urinary incontinence after a laparoscopic Burch compared
with 48% after a mid-urethral sling, with no statistically significant difference
between the two groups; stress urinary incontinence bother symptoms were
reported in only 11% and 8% of women, respectively (121). Using strict criteria
to define urinary incontinence yields a higher failure rate, but most women report
significant improvement in bother symptoms and impact on QOL after
colposuspension procedures. A recent 2017 Cochrane review showed that the
open Burch and other retropubic colposuspension procedures remain very
successful operations to treat stress urinary incontinence, with long-term (5 years
or more) success rates of around 70% (120). Compared to pubovaginal slings,
open colposuspension is associated with a lower risk of voiding dysfunction,
but with a higher risk of subsequent pelvic organ prolapse (110,119).
Mid-Urethral Slings
The mid-urethral slings were developed as a direct consequence of the
integral theory that was promoted by Petros et al. (31). The polypropylene
tension-free vaginal tape (TVT) was the original mid-urethral sling described
by Ulmsten in 1996 as a simple minimally invasive outpatient procedure
under local or regional anesthesia (122). With this procedure, a synthetic
sling is placed under the mid-urethra (in contrast to pubovaginal slings that
are placed at the bladder neck) in a tension-free manner. The two ends of the
sling are not attached or sutured to a pelvic structure, but rather the urethra
is free of any tension upon placement of the sling. The TVT is commonly
placed in a bottom-up direction through a small 1 to 2 cm mid-urethral
vaginal incision, and the two free ends are passed up and behind the pubic
bone through the space of Retzius and out through two suprapubic incisions
(Fig. 29-15). As each side of the sling is advanced around the urethra using a
trocar, the bladder is deviated to the contralateral side via a guide wire placed
through a Foley catheter to minimize the risk of a cystotomy. Cystoscopy is
performed to confirm the integrity of the bladder. Although mid-urethral slings
were initially received with skepticism, over time they have proven to be very
effective surgeries with low rates of complications replacing all other procedures
as the gold standard to treat stress urinary incontinence (123,124). Of the original
90 women who underwent the TVT procedure, 78% were followed-up to 17
1711years. Of those evaluated either by a clinic visit or by phone, about 90% had
objective and 87% had subjective cure or significant improvement (125).
FIGURE 29-15 Midurethral synthetic slings involve the use of large pore, monofilament
polypropylene mesh placed after minimal dissection at the midurethra followed by
placement of a trocar through the retropubic route. A: The trocar is guided into the
previously performed midurethral incision with care to place the trocar against the pubic
bone to avoid entry into the peritoneal cavity. The trocar handle has been removed in this
view after perforation through the abdominal incision. B: The synthetic sling should rest in
the midurethra location and is brought through two stab incisions above the pubic
symphysis. (Redrawn from original by Jasmine Tan.)
In 2001, Delorme reported on the transobturator tape (TOT) where the
sling position is still mid-urethral, however its general direction is through
the ischiorectal fossa and the free ends exit via the obturator canal and out
through the genitofemoral creases bilaterally (126). The TOT sling can be
placed in an outside-in or inside-out direction. The TOT mid-urethral slings
were developed in an attempt to reduce complications associated with the
TVT procedure, including bowel, bladder, and vascular injury. Subsequent
studies have shown that women undergoing TOT procedures are still at risk
of vascular and bladder injuries, although rare. Over the past two decades,
there has been an accumulation of a large body of evidence on mid-urethral slings
from randomized controlled trials, including several meta-analyses and Cochrane
reviews (120,123,124,127,128). The overarching summary is that mid-
1712urethral slings have become the procedure of choice in treating women with
stress urinary incontinence. They have a good safety profile with a significant
improvement of QOL measures, and irrespective of route of placement, they are
highly effective in the short, medium, and long term. There is evidence to suggest
that the mid-urethral slings are more effective than the Burch colposuspension
procedure, and as effective as the autologous pubovaginal sling (123).
Concerning the choice of mid-urethral sling (retropubic vs. transobturator), data
show that the retropubic approach may be favored in terms of long-term efficacy,
but with the risk of higher overall complication rates (123,127,129). In a large
national cohort of more than 8,600 women undergoing mid-urethral slings in
Denmark over a 10-year span, the reoperation rate at 5 years was 6% for the TVT
and 9% for the TOT. In the adjusted model, the TOT sling was associated with a
twofold higher risk of reoperation (HR, 2.1; 95% CI, 1.5–2.9) than the TVT sling.
In terms of complications, urinary tract infections occur in up to 10% after midurethral slings (130). Bladder perforation is another complication that can occur
with both approaches but more commonly with the TVT. Of note is that bladder
perforations are mostly inconsequential. With universal cystoscopy at the time of
sling placement, the cystotomy, typically at the dome of the bladder, is easily
identified. Repositioning of the sling, and ensuring subsequent proper placement
is generally sufficient. In certain cases, keeping the Foley catheter in for up to a
week may be necessary. Other complications that are more common with the
TVT include bleeding (intra and postoperative), and postoperative voiding
dysfunction necessitating sling revision; in contrast, the TOT has a higher rate of
mesh erosion, and postoperative groin and leg pain (123,130). Rare complications
include bowel injuries, and patient deaths after retropubic slings, and severe
infections after transobturator slings (131).
1713FIGURE 29-16 Sling erosion into the bladder. (Bieniek JM, Holste TL, Platte RO, et al.
Cystoscopic removal of intravesical synthetic mesh extrusion with the aid of Endoloop
sutures and endoscopic scissors. Int Urogynecol J 2012;23:1137–1139; Figure 1, need
permission.)
A unique complication associated with mid-urethral slings is erosion of the
sling material (130). Although uncommon, sling erosion into the vagina
generally requires surgical repair which involves resection of the segment eroding
into the vagina and repairing the vaginal mucosa over the involved site. When the
sling erodes into the bladder (and uncommonly into the urethra), this requires
more complicated surgery to resect the eroded segment (Fig. 29-16). Rarely, the
whole sling material (TVT or TOT) may need to be removed typically because of
chronic pain resulting from placement of the sling.
Certain mid-urethral sling characteristics and indications worthy of
mention include the following: (a) with retropubic slings, the bottom-up
route may be more effective than top-down route; (b) with the exception of
leg and groin pain, fewer adverse events occur with the transobturator than
1714the retropubic approach; (c) the transobturator may be more cost-effective
compared with the retropubic sling, although studies looking at cost do not
take into account the potential impact of repeat surgery to address
recurrence of incontinence on overall cost; (d) the retropubic sling is favored
over the transobturator sling in cases of fixed immobile urethra (intrinsic
sphincter deficiency) and mixed urinary incontinence; and (e) the
transobturator approach may be favored in cases where there is previous
significant bowel or pelvic adhesive disease.
Single incision (mini) slings have been introduced with the goal of further
minimizing surgical complications while maintaining efficacy. A mid-urethral
incision is made to introduce the sling while fixing (or anchoring) the two shorter
arms to the fascia in the obturator or retropubic space. However, their short- to
mid-term results are not very promising. In a recent Cochrane review, minislings were reported to be either inferior, or they lacked enough evidence to
support their endorsement over the retropubic or transobturator slings
(132). More studies with longer-term follow-up are needed to establish their
safety profile in treating women with stress urinary incontinence without
compromising surgical success. When a mid-urethral sling is chosen as a
treatment option, the AUA guidelines recommend either a retropubic or
transobturator sling as a first choice, and if a mini-sling is to be used, patients are
to be informed that not enough short-, medium- and long-term data exist in its
support (64).
Over the past century, surgical standards of care for stress urinary incontinence
have made a full circle from slings (mostly pubovaginal) to bladder neck and
retropubic suspensions and back to slings (mostly mid-urethral). These transitions
in surgical care have occurred mostly on the heels of an in-depth understanding of
the anatomy of the pelvic floor and rigorous evidence-based epidemiologic and
clinical research.
Bulking Agents
Urethral bulking agents are an accepted treatment option for women with
stress urinary incontinence. They are typically injected around the proximal
urethra submucosally to give it bulk, either transurethrally or periurethrally,
using an operative cystoscope. When compared to the mid-urethral slings,
the colposuspension, and pubovaginal slings, there exist little data evaluating
their long-term success. Repeat operations are common after bulking agent
therapy. However, they are appropriate procedures for patients who are poor
surgical candidates, on anticoagulation therapy, with high PVRs, or in older
women with high surgical anesthesia risk (133). The advantage of injectable
agents is that they are less invasive and they can potentially be done in a clinic
1715setting without the need for general or regional anesthesia.
Available and FDA-approved bulking agents for stress urinary incontinence
treatment include pyrolytic carbon–coated zirconium oxide spheres (beads)
(Durasphere), cross-linked polydimethylsiloxane (Macroplastique), and spherical
particles of calcium hydroxylapatite (Coaptite). The glutaraldehyde cross-linked
bovine collagen (Contigen) is not being produced by its manufacturer and is no
longer available in the United States market. Injection of the bulking agent into
the urethral submucosa produces its coaptation to help maintain continence in the
presence of an increased abdominal pressure (134–136). In one review article, it
was noted that subjective success rates ranged from 66% to 90% at 12-months
follow-up, whereas objective improvement ranged from 25% to 73% (137). A
2017 Cochrane review showed that limited data exist beyond 2 years
posttreatment with urethral bulking agents. Short-term data are suggestive
of an improvement, but they lack the robust success or cure rates associated
with mid-urethral slings (138). Reported complications of the urethral
bulking agents include urinary tract infections, urinary retention, erosion
and migration of the implanted material (139).
Other Potential Future Therapies
Autologous stem cells have been used experimentally to help regain bladder
control. Most studies have used stem cells derived from muscle or adipose tissue.
The stem cells can be injected periurethrally or into the pelvic floor to regenerate
damaged urethral sphincter or repair/reconstruct pelvic support structures using
tissue engineering techniques. Although preclinical and early clinical trials have
demonstrated safety, efficacy of those techniques to treat stress urinary
incontinence is still in question (140,141). Radiofrequency applied transurethrally
to promote collagen denaturation is another modality that has been proposed as a
nonsurgical procedure to treat stress urinary incontinence. However, a Cochrane
review demonstrated no benefit (or insufficient evidence) of radiofrequency when
compared with sham treatment (142). Vaginal laser therapy is another technique
that is being marketed as a safe and office-based treatment modality for female
stress urinary incontinence. There is no evidence to support this use in clinical
practice over conventional treatment options (143).
Procedures for Urgency Urinary Incontinence
When conservative and pharmacologic options fail, second-line treatments
for urgency urinary incontinence include injection of onabotulinumtoxinA
(Botox) in the bladder, percutaneous tibial nerve stimulation (PTNS), and
sacral neuromodulation (Interstim) (144).
Botox Injections
1716OnabotulinumtoxinA (Botox) is a neurotoxin that produces its paralytic
effect on the detrusor muscle of the bladder by blocking the calcium channels
and inhibiting release of acetylcholine at the presynaptic neuromuscular
junction. Its use was initially FDA-approved in women with neurogenic detrusor
overactivity with a typical injected dose being 200 units (U) (145). In 2013, its
use was approved for idiopathic OAB and urgency urinary incontinence. The
typical dose for nonneurogenic OAB is 100 U where injection of
onabotulinumtoxinA is performed cystoscopically with about 20 injection
points within the detrusor muscle sites and mostly supratrigonal (Fig. 29-17).
When successful, the effect of the injection typically lasts for 6 months to 2
years with repeat injections needed in 50% of women within 12 months
(146).
The FDA approval decision was mostly based on a multicenter double-blind,
randomized controlled trial comparing one intradetrusor injection of 100 U of
onabotulinumtoxinA to daily oral anticholinergic medication (solifenacin or
trospium) in 249 women with urgency urinary incontinence over a period of 6
months. This study demonstrated similar reductions in daily urgency, frequency,
and urgency urinary incontinence episodes between the two groups. Complete
resolution of urgency urinary incontinence occurred in more than twice of the
onabotulinumtoxinA (27%) than the anticholinergic (13%) group, P = 0.003. Side
effects with the injection group included catheter use up to 2 months (5%) and
urinary tract infections (33%) (147).
A meta-analysis of 56 randomized controlled trials showed that patients
receiving onabotulinumtoxinA (100 U) had improvements in urgency, frequency,
and incontinence episodes similar or better than medications, and significantly
better than placebo (146). The AUA currently recommends intradetrusor
onabotulinumtoxinA (100 U) when conservative and medical treatments have
failed in women with OAB. It is noteworthy that the patient must be taught and be
willing to perform self-catheterization, if needed, after the injection. In addition to
urinary tract infections and retention, side effects include gross hematuria, dry
mouth, dysphagia, impaired vision, and muscle weakness (144).
Percutaneous Tibial Nerve Stimulation
PTNS was approved by the FDA in 2000 for OAB. PTNS involves
introducing an acupuncture-type needle electrode (34-gauge) at a 60-degree
angle around the ankle, about 3 fingerbreadths above the medial malleolus
and posterior to the tibia. The electrode is connected to a battery-charged
stimulator, and treatment involves 30-minute weekly sessions for 12 weeks. If
successful, maintenance involves once monthly sessions thereafter. A
multicenter trial of 220 women with OAB symptoms randomized to 12 weeks
1717of treatment with PTNS versus sham therapy resulted in marked
improvement of symptoms in 55% compared to 21% in the respective
groups (148).
FIGURE 29-17 Injection of onabotulinumtoxinA into the detrusor muscle. (Ginsberg D,
Gousse A, Keppenne V, et al. Phase 3 efficacy and tolerability study of
onabotulinumtoxinA for urinary incontinence from neurogenic detrusor overactivity. J
Urol 2012;187:2131–2139; Figure 1, need permission.)
PTNS has been compared to anticholinergic medications including longacting toleterodine and oxybutynin in different studies (149). Similar
improvements have been shown in urinary frequency, incontinence,
nocturia, bother, and QOL scores in the short term (12 weeks) between the
two treatment modalities (150). At 2- to 3-years follow-up, the medication
group reported worsening symptoms especially that many women on
anticholinergics are not compliant with taking medications long term
because of side effects (149,151). PTNS is considered an acceptable
1718alternative to medical treatment, in the short term in patients who cannot
tolerate anticholinergic side effects, or in the long term in patients who show
signs of impaired cognition and memory loss. It is important to emphasize to
patients that for optimal results, treatment sessions are administered weekly for
the initial 12 weeks, and women should have the appropriate resources to make
frequent clinic visits. Side effects of PTNS are limited and they include minor
bleeding, pain, or tingling sensation at the needle site.
Neuromodulation
Sacral nerve stimulation (also known as neuromodulation) is another FDAapproved treatment modality for refractory OAB, urgency urinary
incontinence, and voiding dysfunction in women who have failed
conventional treatment options. Sacral nerve stimulation involves an initial
phase with a 1- to 2-week trial lead placed percutaneously to evaluate
response to treatment. Those reporting at least 50% improvement in their
OAB symptoms move on to phase two where a permanent electrode lead is
introduced through the back and placed around the third sacral nerve root.
This electrode is connected to a pulse generator that is implanted in the
patient’s buttock. Unlike PTNS and onabotulinumtoxinA, sacral nerve
stimulation is a more complex procedure that generally requires fluoroscopy
in an operating room setting and is associated with a different adverse event
profile (152). It is contraindicated to perform an MRI in women with an
implanted neurostimulator.
A randomized controlled trial of 147 women compared medical treatment to
sacral nerve stimulation over a period of 6 months. At baseline, women reported
bothersome symptoms of OAB with more than two urgency incontinence
episodes within 3 days and more than eight voids per day. Results showed that
women who received the neurostimulator (61%) had significantly higher
treatment success than women receiving medical treatment (42%) (P = 0.02).
Adverse events were similar between the two group at 31% and 27%, respectively
(153). In another prospective multicenter study, 272 patients implanted with the
sacral nerve stimulation were followed for a year. Using diary data at 12 months
showed a therapeutic improvement rate of 85% including a mean reduction of
urgency incontinence episodes of 2.2 leaks/day (down from 3.1) and urinary
frequency of 5.1 voids/day (down from 12.6), both P <0.0001. Women reported
significant improvement in their QOL measures and decreased interference of
urinary symptoms with their daily activities (154). Device-related adverse events
occurred in 30% (82/272) of women with an implanted neurostimulator at 12
months. These included undesirable change in stimulation (12%), implant site
pain (7%), and implant site infection (3%). Of the 26 women with implant site
1719pain, 13 underwent surgical intervention, and two had removal of the stimulator.
Of the 13 cases with implant site infection, five received antibiotics and eight
required removal (155).
A randomized controlled trial compared 364 women with OAB who underwent
treatment either with onabotulinumtoxinA or sacral nerve stimulation. Women
who received onabotulinumtoxinA reported greater reduction in 6-month mean
number of urgency incontinence episodes per day than those who received sacral
neuromodulation (–3.9 vs. –3.3; P = 0.01). Participants treated with
onabotulinumtoxinA showed greater improvement in symptom bother (–46.7 vs.
–38.6; P = 0.002) and treatment satisfaction (68 vs. 60; P = 0.01) than those
receiving sacral neuromodulation. There were no differences in treatment
preference (92% vs. 89%; P = 0.49) or adverse events, except for urinary tract
infections which were more frequent in the onabotulinumtoxinA group (35% vs.
11%; P < 0.001). Urinary retention requiring self-catheterization was 2% at 6
months in the onabotulinumtoxinA group, and stimulator device revisions or
removals occurred in 3% (156).
Augmentation Cystoplasty and Urinary Diversion
Augmentation cystoplasty and urinary diversion, typically using segments of the
patient’s intestine, are procedures that are rarely performed to treat urinary
incontinence, and typically fall in the advance urology domain. They have been
reported in women with chronic and debilitating detrusor overactivity
unresponsive to second or third-line treatment options (157). A 2012 updated
Cochrane review found a handful of small studies with limited information to
guide clinical practice (158). As neuromodulation and cystoscopic injection with
onabotulinumtoxinA become more prevalent and better studied, there will be
limited, if any, role for augmentation cystoplasty and urinary diversion to treat
women with urgency urinary incontinence.
Surgery for Fistula Repair
Genitourinary fistula repair is commonly performed vaginally, but can be
repaired through an abdominal access, either open, laparoscopic, or
robotically. For very small pinpoint fistulae, there may be a role for
conservative options with an attempt of 10 to 14 days of transurethral
catheterization and to allow the fistula to close spontaneously. If that fails, or
for larger fistulae, surgery is the mainstay (Fig. 29-18). Proper surgical
technique involves: (a) identification of fistula (ae); (b) getting adequate
access and exposure (e.g., if a vaginal approach is preferred, a pediatric
Foley catheter can be placed vaginally and the balloon inflated to put
downward traction on the fistula for better visualization); (c) debridement of
1720nonviable tissue; (d) mobilization of fresh and viable tissue (1 to 2 cm)
around and all along the fistulous tract; (e) repair of the fistula in several
layers starting at the bladder end and going out to the vagina; (f) minimal
tension on the repaired layers; (g) 7 to 14 days of postoperative
catheterization; (h) use of tissue grafts (e.g., Martius labial fat-pad) as
needed for larger or recurrent fistulae.
Voiding Dysfunction
Definition
The mechanism of normal bladder emptying is a coordinated effort that is
initiated by the individual. It involves a detrusor muscle contraction
associated with urethral sphincter relaxation. The pressure generated by the
detrusor muscle contraction should be of an appropriate duration and a magnitude
that is higher than the pressure in the urethra to produce the desired effect of
completely emptying the bladder. The neurophysiology of micturition has
previously been described. In addition to an intact neuromuscular control and
support, voiding is dependent on the volume of urine within the bladder and
intravascular volume that gets filtered through the kidneys. One study of 165
women with no history of urologic diseases and/or pelvic surgery showed a
significant difference in the frequency and volume of urine produced in 24 hours
(range between 437 and 3,861 mL) (159). In addition to the bladder volume at the
time of voiding, the maximum urine flow rate (range between 16 and 37mL/s) is
variable and dependent on patient position, age, and menopausal status among
other factors (160).
[6] Voiding dysfunction occurs when a woman loses the ability to empty her
bladder effortlessly and completely within a limited time frame (usually
within 60 seconds or less). Objectively, voiding dysfunction can be identified
on a uroflow when the voiding time is prolonged, the flow pattern is
interrupted (see Fig. 29-8 above), or the maximum flow rate is diminished.
During complex urodynamics, additional objective measures of voiding
dysfunction include increased urethral pressure (resistance) with an increased
detrusor pressure (detrusor–sphincter dyssynergia), or a low detrusor pressure
with a normal or low urethral pressure (detrusor underactivity) at the time of
urination (65). [6] Patients with voiding dysfunction may express a host of
sensory and abnormal bladder emptying symptoms including hesitancy, slow
or intermittent urinary stream, straining on urination, feeling of incomplete
bladder emptying, reduced bladder sensation and others (Table 29-10).
Etiology
1721Acute urinary retention is a sudden and often painful inability to void despite
the sensation of a full bladder and desire to urinate. It is mostly iatrogenic
resulting from neurologic injury after radical pelvic surgery (radical
hysterectomy, radical perineal resection, colorectal extensive resections),
neurologic injury during spinal surgery or commonly after female pelvic
reconstructive surgery, and incontinence surgery (e.g., mid-urethral sling).
Rarely, and uniquely in pregnant patients, especially in the peripartum period, the
bladder is vulnerable to urinary retention; if undetected, this can lead to bladder
underactivity, recurrent urinary tract infection, and incontinence (161).
Chronic urinary retention may be caused by neurogenic (e.g., multiple
sclerosis, diabetic neuropathy) or nonneurogenic conditions (e.g., advanced
prolapse) (162). This can lead to serious conditions like hydronephrosis and
chronic renal insufficiency, but is more commonly associated with conditions
that impair an individual’s daily activities like recurrent urinary tract
infections, feelings of incomplete bladder emptying, and overflow
incontinence. Chronic urinary retention is defined as PVR of more than 300
mL persisting for more than 6 months which has been documented in two
separate occasions (162). Common conditions associated with incomplete
bladder emptying and retention in women are outlined below (Table 29-11).
1722FIGURE 29-18 Repair of apical vesicovaginal fistula. A: The fistula at the vaginal apex is
exposed with adequate retraction. A pediatric Foley can be placed into the fistula tract to
aid in traction and dissection. B: The vaginal epithelium is dissected from the fistula to
mobilize the tissue to allow for tension-free closure. In the classic Latzko procedure, the
vaginal epithelium 2 cm around the opening of the fistula is removed. C: The fistula tract
may either be completely excised, or in the Latzko procedure, the fistula edge may
freshened up slightly but is not excised. D: Interrupted absorbable sutures are placed in an
1723extramucosal location in an interrupted fashion. An additional layer of interrupted sutures
is often placed to invert the initial suture line. The vaginal epithelium is then closed over
the repair. In the classic Latzko procedure, the initial layer involves closure of the vagina
over the fistula tract, then two additional layers with the vaginal epithelium result in an
apical colpocleisis. (Redrawn from original by Jasmine Tan.)
Evaluation
Evaluation starts with a careful medical history to eliminate possible conditions
associated with voiding dysfunction (e.g., multiple sclerosis, diabetes, psychiatric
disorders) and concomitant medications. Should medical history reveal previous
surgical treatment for urinary incontinence, it is important to obtain medical
records or operative reports to determine the exact nature of the surgery. A careful
pelvic examination is conducted with special attention to urethral orifice and
anterior wall of vagina to rule out possible pelvic or vaginal masses causing
urethral obstruction. Abdominal palpation or suprapubic percussion may indicate
a full bladder. Cystoscopy can help diagnose the presence of urethral polyps or
bladder tumors, stones, or foreign bodies causing obstruction. Evaluation of the
strength of the detrusor muscle contraction during voiding and urethral outlet
relaxation, or lack thereof (i.e., urethral resistance) can be undertaken at the time
of urodynamics, including measurement of PVR.
Table 29-10 Classification and Definition of Lower Urinary Tract Symptoms in
Women
II. Abnormal Sensory Symptoms
Increased
bladder
sensation
Desire to void during bladder filling occurs earlier or is more
persistent from that previous experienced (differs from urgency by
the fact that micturition can be postponed despite the desire to void)
Reduced
bladder
sensation
Definite desire to void occurs later than that previously experienced,
despite an awareness that the bladder is filling
Absent bladder
sensation
Absence of the sensation of bladder filling and a definite desire to
void
III. Abnormal Emptying
Hesitancy Delay in initiating micturition
Straining to
void
Need to make an intensive effort (by abdominal straining, Valsalva
or suprapubic pressure) to initiate, maintain, or improve urinary
stream
1724Slow stream Urinary stream perceived as slower compared to previous
performance or in comparison with others
Intermittency Urine flow that stops and starts on one or more occasions during
voiding
Feeling of
incomplete
bladder
emptying
Bladder does not feel empty after micturition
Postmicturition
leakage
Involuntary passage of urine following the completion of
micturition
Spraying of
urinary stream
Urine passage is a spray or split rather than a single discrete stream
Positiondependent
micturition
Requiring specific positions to be able to micturate spontaneously
or to improve bladder emptying, for example, leaning forward or
backward on the toilet seat or voiding in a semi-standing position
Urinary
retention
Inability to pass urine despite persistent effort
From Haylen BT, de Ridder D, Freeman RM, et al. An International Urogynecological
Association (IUGA)/International Continence Society (ICS) joint report on the
terminology for female pelvic floor dysfunction. Neurourol Urodyn 2010;29:4–20, with
permission.
Treatment
Prior to treatment initiation for chronic urinary retention, the AUA
guidelines recommend evaluation of the upper tracts to assess the functional
integrity of the kidneys (creatinine clearance) and rule out hydronephrosis
(renal ultrasound or CT urogram) (162). Low-risk, asymptomatic individuals
can be surveilled with yearly urinalysis and urine culture with no unnecessary
treatment. [6] In symptomatic patients (e.g., recurrent urinary tract infections),
treatment is symptom driven. Patients are encouraged to double void and have
frequent trips to the bathroom (162). Patients can be referred to pelvic floor
physical therapy for bladder retraining.
Table 29-11 Conditions Associated with Voiding Dysfunction and Urinary Retention
Effect on Bladder Muscle CONTRACTION Effect on Urethra OUTFLOW
1725• Medications (anticholinergics, opioids, beta
adrenergic agonists, Ca channel blockers,
NSAIDs, tricyclic antidepressants,
benzodiazepines, antipsychotics)
• Urethral or bladder neck
stricture (post-incontinence
surgery, prior vaginal or
reconstructive surgery)
• Diabetes mellitus • Urethral narrowing, swelling or
obstruction due to sling,
urethral bulking agent or other
• Long-standing outlet obstruction • Pelvic organ prolapse (high
grade)
• Constipation • Urethral diverticulum, stones,
or tumor
• Neurologic diseases (MS) • Primary bladder neck
obstruction
• Aging • Extrinsic compression (tumors)
• Fowler syndrome • Neurologic disorders
• Acontractile bladder (Detrusor sphincter
dyssenergia)
[6] In high-risk patients, intermittent catheterization is recommended.
Although there is lack of evidence comparing intermittent selfcatheterization to indwelling catheters, expert opinion, favors intermittent
catheterization for better long-term outcomes (163). Either the patient or her
caregiver can be instructed to perform bladder self-catheterization. In the
presence of advanced prolapse, a trial of pessary can be performed with the goal
of reducing the prolapse to relieve the obstruction on the urethra resulting in
improved voiding and decreased retention (162).
[6] Acute urinary retention is addressed according to the specific situation
causing the retention. This may take the form of expectant management with an
indwelling catheter for postradical hysterectomy, pelvic reconstructive, or
incontinence surgery. The catheter can be plugged after a week of retention and
continued voiding dysfunction to allow the bladder to recover filling sensation.
When a full bladder in sensed by the patient, she is instructed to remove the plug
and drain the bladder. Alternatively, patients can be instructed to self-catheterize
until resolution of the retention (usually a PVR of volume of 100 mL or less is
acceptable). Should the patient continue to have voiding dysfunction for several
weeks after surgery, a sling revision and/or urethrolysis may be necessary (164).
[6] In the absence of an obstruction, medications can be used for urinary retention
1726caused by either detrusor underactivity or increased resistance in urethral
sphincter. These include alpha blockers or beta agonists, however these drugs
have proven to be generally ineffective and there is lack of clear evidence to
support their routine use (104,105,165).
Neuromodulation and intravesical electrical stimulation may be effective in
select patients (166). In addition to urgency, frequency, and urgency urinary
incontinence, sacral neuromodulation has been used to treat nonobstructive
voiding dysfunction in women (167). Long-term follow-up shows promising
results in idiopathic retention (Fowler syndrome, patients with multiple sclerosis
and painful bladder syndrome) with a success rate of as high as 73% (168).
Bladder Pain Syndrome
The recent IUGA/ICS report on management of pelvic floor dysfunction defines
acute pain as that related to recent trauma, infection or other disease and chronic
pain as either persistent or recurring pain for at least 6 months (82). It is important
to differentiate pain which is a sensation expressed subjectively by the individual
from tenderness which is a sensation of discomfort, with or without pain, and that
may be elucidated by palpation on a physical examination.
Definition
[6] Bladder pain syndrome is challenging to diagnose, prevent, and treat
because its basic science and pathophysiology is poorly understood. Bladder
pain is defined as the complaint of suprapubic or retropubic pain, pressure,
or discomfort related to the bladder. It usually increases in intensity with
bladder filling and may persist or disappear after voiding (8). Women with
bladder pain syndrome usually have other associated urinary symptoms,
such as urinary urgency or frequency; the pain is of a duration of at least 6
weeks or more in the absence of urinary tract infections or other identifiable
causes (169). The prevalence of bladder pain syndrome varies widely, based
on definitions used, from less than 1% to as high as 20% (170,171). Some
authors have developed an interstitial cystitis/bladder pain syndrome
questionnaire for use in epidemiologic studies (172). Based on this questionnaire,
the prevalence in adult U.S. females ranges between 3% and 7% with the peak
prevalence being in the 50’s (173).
The terms “bladder pain syndrome” and “interstitial cystitis” have been
used interchangeably in the literature, where the latter was first described as
an inflammatory bladder condition, sometimes associated with ulceration of
the bladder wall, named Hunner lesion (174). Interstitial cystitis is believed to
be associated with a defective glycosaminoglycan sulfate layer that covers the
bladder mucosa. To standardize definitions and enable comparative research, the
1727National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK)
developed strict criteria for interstitial cystitis; however, these definitions have
been shown to be too restrictive to use in clinical practice. NIDDK criteria
include the presence of pain and urgency associated with objective findings of
glomerulations or Hunner ulcers during cystoscopy and hydrodistention of the
bladder, including a small bladder capacity and terminal hematuria (175). Most
clinicians prefer to use Looser criteria when treating women with bladder pain
syndrome. The understanding of bladder pain syndrome is that it is not limited to
an inflammatory mechanism but may encompass a spectrum of conditions
including OAB, other chronic pain conditions, somatization disorders, and
neurologic diseases (176).
Diagnosis
Basic assessment in a woman with bladder pain syndrome consists of
obtaining a detailed medical history, physical examination, bladder diary
(frequency/volume chart) and urinalysis with culture (177). The workup
should be supplemented with urine cytology in older women, especially those
who report history of smoking or prior exposure to chemical. Bladder pain
syndrome is a diagnosis of exclusion. A differential diagnosis includes chronic or
recurrent urinary tract infections, urethral diverticulum, vulvovaginal atrophic,
inflammatory, allergic, or infectious conditions, chronic pelvic pain related to
endometriosis, inflammatory bowel conditions, myofascial pain, and others.
Exclusion of these diseases may require further imaging, cystoscopy,
urodynamics, and even laparoscopy.
Treatment
The initial management of bladder pain syndrome relies on patient
education, dietary modification, stress reduction, and pelvic floor relaxation
techniques (177). Women are encouraged to avoid bladder irritants such as
caffeinated beverages, alcohol, carbonated drinks, acidic drinks, and spicy foods.
When the conservative approach fails, medication, physical therapy or
intravesical treatment are implemented. Referral to a pain specialist can be
beneficial. Effectiveness of medical therapy is not well-proven, and long-term
follow-up is not well-studied. One study reviewed treatments received by 581
women enrolled in the interstitial cystitis database study group between 1993 and
1997. A total of 183 different types of treatments were reported, with the most
commonly prescribed being cystoscopy and hydrodistention, amitriptyline,
phenazopyridine, special diet, and intravesical heparin (178).
Urinary analgesics like phenazopyridine and Prosed DS have been offered to
patients with painful bladder syndrome for pain or bladder spasm relief. The latter
1728is a mixture of methenamine, methylene blue, phenyl salicylate, benzoic acid, and
hyoscyamine. Amitryptyline, a tricyclic antidepressant, has been studied for
symptom relief in women with painful bladder syndrome, and it has been shown
to be beneficial only when a dose of 50 mg or more is achieved (179).
Antihistamines have been proposed as potentially being helpful for bladder pain
syndrome since pain may be the consequence of histamine release. Hydroxyzine
is a commonly used antihistamine; however, a multicenter, randomized clinical
trial showed only a 30% versus 20% response for those who were treated with
hydroxyzine versus placebo, respectively (180). Another antihistamine includes
cimetidine; but studies on its use have included a very small number of patients
with inconclusive results (181,182).
Pentosan polysulfate (elmiron) is an FDA-approved heparinoid medication
to treat women with bladder pain syndrome/interstitial cystitis. The
recommended dose is 100 mg three times per day and symptom relief may
not be achieved for at least 3 months. The efficacy of pentosan polysulfate
has been brought to question by a placebo-controlled randomized trial
showing similar symptom relief between the two groups (183). As an
alternative to oral medications, intravesical treatment may be offered to patients
with bladder pain syndrome. Dimethylsulfoxide (DMSO) is the only FDAapproved intravesical treatment. This involves instilling the bladder with 50 mL
of 50% solution of DMSO for 20 to 30 minutes, and to be repeated weekly or
every other week for six sessions. It is believed to reduce inflammation, relax
muscles, and alleviate pain. As side effects, patients report garlic odor and
transient bladder irritation (177). Alternative intravesical instillations that have
been investigated include hyaluronic acid, chondroitin sulfate, cyclosporine A,
bacillus Calmette–Guerin, oxybutynin, bupivacaine/heparin/steroid (mix), and
others (184–188). Other treatment options include cystoscopy under anesthesia
with hydrodistention, neuromodulation, transcutaneous electrical stimulation
(TENS), and intradetrusor botulinum toxin A injection (189–191).
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