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Imaging, 22 (2013), 20120017


Functional imaging of the bladder



Barts and the London NHS Trust, St Bartholomews Hospital, London, UK

Main causes of bladder dysfunction can be categorised into:
bladder outlet obstructionprostatic enlargement, urethral strictures, bladder

poor sphincter relaxationneurogenic causes or anxiety
detrusor weaknesslong-term untreated bladder outlet
ineffective emptyingacontractile detrusor, bladder diverticulae or cystocoeles.

The common techniques and their roles are:

bladder uroflowmetryassesses bladder voiding ability and pattern
ultrasound cystodynamogrambladder wall thickness and bladder and pelvic masses
intravenous urodynamogramupper tract assessment and bladder emptying
cystometry and videocystometrographybladder, urethral and sphincter pressures.

doi: 10.1259/imaging.
2013 The British Institute of

Cite this article as: Sahdev A. Functional imaging of the bladder. Imaging 2013;22:20120017.

Abstract. The two primary functions of the bladder are storage

of urine and initiating micturition. These functions require
complex coordination between the central and peripheral nervous
system, bladder muscles and urethral sphincter. There are
multiple disorders of the central nervous system, spinal cord and
peripheral nervous system that affect and impair bladder and
urethral function. Bladder dysfunction produces a variety of
non-specific symptoms and signs requiring imaging
investigations of the lower urinary tract. The mainstays of
imaging functional disorders are ultrasound, urine flowmetry and
urodynamics. Urodynamic imaging studies should always be
interpreted in combination with symptoms at clinical presentation
and signs. Simple and routine urodynamics of the bladder include
ultrasound assessment before and after micturition, intravenous
urography and bladder flow rates. These simple techniques are
frequently performed in all imaging departments and will suffice
in the majority of patients when assessing bladder dysfunction.
More complex techniques (including cystometry, videocystometry
and videocystometrography) are only necessary for complex cases
with mixed incontinence, prior to invasive treatment and in
patients with failed surgery, or in those where the clinical
presentation and simple urodynamics are equivocal. In this article
we review normal bladder anatomy and physiology, lower urinary
tract innervation, and common disorders affecting the bladder and
urethra. We discuss the role of imaging and urodynamic findings
in bladder outlet obstruction, urethral overactivity, detrusor
failure, incontinence and detrusor instability.

Address correspondence to: Dr Anju Sahdev, Barts and the London

NHS Trust, St Bartholomews Hospital, West Smithfield, London
EC1A 7BE, UK. E-mail:

Bladder dysfunction produces a variety of non-specific

symptoms, which are investigated by lower tract urodynamics. These symptoms include frequency, dysuria, urgency, incontinence, hesitancy and poor stream. The
symptoms are caused by bladder disorders related to abnormal storage of urine or abnormal bladder emptying,
with a significant overlap. Urodynamics of the bladder is
the study of pressure and flow relationships during the
storage of urine and micturition. In routine practice, this
focuses on the bladder and its sphincter mechanism to investigate bladder filling and voiding, define bladder storage
disorders and assess the severity of voiding dysfunction.
The basic principles of urodynamics require an understanding of bladder anatomy and normal physiology.
Urodynamic techniques allow an objective assessment of
lower urinary tract disorders, but must be interpreted in the
context of the patients clinical history and symptoms.
There are several clinically based simple techniques used to
assess bladder dysfunction, such as volume voiding charts,
pad testing and symptom monitoring, which will not be
discussed in this article. The discussion will be limited to
techniques commonly involving the radiologist in the
functional assessment of the lower urinary tract.

Normal anatomy and normal bladder function

The bladder is a hollow muscular organ histologically
(Figure 1) made up of:
1. An inner epithelial layerconsisting of transitional
cells forming a barrier virtually impenetrable to any
component of urine.
2. Lamina propriaconsisting mainly of dense connective
tissue, with many bundles of coarse collagenous fibres.
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Figure 1. Normal anatomy of the bladder.

3. Submucosaconsisting of a loose connective tissue

that supports the mucosa, contains blood vessels,
nerves and lymphatics supplying the mucosa.
4. A smooth muscle layer consisting of an inner
longitudinal and outer circular layer of smooth muscle
cells with interlacing fibres. An additional outer layer
of longitudinal fibres forms the detrusor muscle.
5. An outer adventitial layer consisting of connective
The detrusor muscle is controlled by the autonomic
system; the parasympathetic system provides motor

control while the sympathetic system (found predominantly in the bladder base) principally controls the
vasculature. Additional sensorimotor nerves are found
in the bladder wall; their precise function is unclear.
The spinal segments S2S4 contain the efferent parasympathetic supply, and T10L2 nerves contain the
sympathetic efferent nerves. After leaving the sacral
foramina, the pelvic splanchnic nerves containing the
parasympathetic neurones pass lateral to the rectum and
enter the inferior pelvic plexus (hypogastric plexus).
These combine with the hypogastric nerve containing the
sympathetic plexus and form the neural plexus at the

Figure 2. Innervation of the bladder.

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Functional imaging of the bladder

Figure 3. Muscle and sphincter complex.

bladder base supplying the bladder trigone. Damage to

S2S4 spinal segments abolishes the micturition reflex
(Figure 2).
The flow of urine from the urinary bladder is controlled by the urethral sphincter. Both sexes have at least
two layers of muscle: the internal sphincter, or bladder
neck; and the external, or distal, sphincter. In men, these
are the proximal bladder neck and the distal sphincter at
the apex of the prostate. In men both sphincters are
equally important in maintaining continence. The bladder
neck consists of an inner strong layer of circular muscles
innervated by adrenergic sympathetic nerves and an
outer muscle layer contiguous with the detrusor muscle.
In women, the bladder neck is weaker, with poorly
defined muscles, and continence is maintained mainly by
the urethral sphincter, which extends throughout the
proximal two-thirds of the urethra. The striated muscle in
the urethral sphincter is innervated by autonomic nerves
and somatic pudental nerves transmitting urethral mucosal sensation (Figures 2 and 3).
Symptoms of lower urinary tract dysfunction relate
to disorders of the bladder or urethra. Symptoms relating to altered urine storage include frequency,

nocturia, urgency, incontinence and abnormal sensation. Symptoms relating to abnormal voiding are slow
stream, straining and hesitancy. Post-micturition disorders are usually dribbling and incomplete bladder

Normal bladder function

The main functions of the bladder are:
to collect and store urine at low pressure
to void urine efficiently and appropriately.

These are two distinct but interrelated functions of the

bladder. The normal bladder volumepressure relationship is summarised in Figure 4. For normal function, integrated coordination is necessary, for which the spinal
cord has to be intact.

Storage of urine
The normal bladder should comfortably hold
400500 ml without any increase in the detrusor pressure

Figure 4. Normal bladder pressurevolume


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(,15 mm H2O). Although there is an urge to void, this

can be controlled. Two factors control the bladders
ability to store urine: bladder compliance and neural

Bladder compliance
Smooth muscle in the bladder wall has elastic properties and the ability to maintain a constant tension over
a wide range of distension, producing an intrinsic tone in
the bladder wall. As urine enters the bladder, the bladder
wall relaxes, increasing the volume (but not pressure) in
the bladder. The change in volume (dV) in relation to the
change in intravesical pressure (dP) is called the bladder
compliance (dV/dP).
Neural control
To aid urine storage and continence, as the bladder
distends with urine, afferent neural activity from the
stretch receptors in the bladder wall send signals to the
spinal cord initiating the desire to void. The local spinal
cord reflex increases the tone in the striated muscle of
the sphincter, which tightens up thereby promoting
continence. At rest the urethral tone keeps the urethral
walls in apposition to maintain continence. Equally,
voluntary signals from higher centres, can inhibit this
spinal reflex when micturition is desired relaxing the
urethral sphincter.
A decrease in the bladders ability to hold urine may be
due to:

reduced functional bladder volume

small volume bladder
bladder overactivity
sphincter incompetence.

A reduced functional volume, leads to symptoms of

frequency, urgency and urge incontinence. The most
common cause for this is increased bladder sensitivity,
usually due to infection. In functional decreased
bladder capacity, there is no abnormality of detrusor
pressures within the bladder. Small volume bladder
presents with frequency and occurs following partial
cystectomy, bladder fibrosis (e.g. post radiotherapy,
post bacillus Calmette-Guerin therapy) or due to extrinsic compression of the bladder. Bladder overactivity results in urgency and frequency caused by an
unstable bladder due to non-neurological causes such
as recovery from long-term outflow obstruction.
Sphincter incompetence is common, presenting with
leakage and frequency. Bladder neck and pelvic floor
weakness due to childbirth and age are the commonest

Normal micturition reflex and voiding mechanism

The micturition reflex involves impulses travelling
from the bladder to the spinal cord and from the spinal
cord back to the bladder. When the bladder wall is
stretched afferent impulses travel to the spinal cord
(S24). In response, parasympathetic impulses from the
spinal cord (S24) travel to the bladder, activate and
cause smooth muscle contraction in the bladder wall.
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The bladder impulses from S24 also stimulate the

ascending pathways to the medulla, pons and cerebrum, which influence a conscious decision to micturate. Higher pathways return impulses to the spinal
cord, either allowing or suppressing micturition,
depending on convenience. Impulses from the spinal
cord, via somatic nerve fibres (mainly S24 pudendal
nerve), act on the striated muscle of the external
sphincter and pelvic floor. The external sphincter
contracts to inhibit micturition and relaxes to allow
micturition. When micturition is desired, the brain
sends impulses to the bladder wall (via sympathetic
and parasympathetic fibres) to contract the smooth
muscle, and to the external sphincter via the sympathetic and somatic fibres to relax the sphincter [1].
Therefore, during voiding:
urethral relaxation precedes detrusor contraction
pelvic floor muscles relax
increased parasympathetic activity contracts the detru-

sor muscle
voiding is initiated under brain stem control
end of voiding, the proximal urethra closes in a

retrograde manner
once complete, sacral centres re-inhibit the cerebral

cortex and the bladder fills again.

Any conditions altering the morphology of the
bladder wall (e.g. collagen disorders, muscular hypertrophy in outflow obstruction) or altering the neural
function will result in poor bladder compliance and
detrusor instability. Complete peripheral denervation
removes all central nervous system control resulting in
an atonic bladder and inactive sphincter. Voiding is
achieved by voluntary contraction of the abdominal
muscles or manual bladder compression. Lesions in the
spinal cord above the fifth lumbar vertebra result in loss
of coordination between the detrusor contraction and
sphincter relaxation (detrusorsphicter dyssynergia).
This results in intermittent voiding, but also urine retention
[2]. Cerebral and basal ganglia lesions (Parkinsons, stroke,
multiple sclerosis) have a typical picture of involuntary
bladder contractions which can result in urge incontinence
due to the loss of inhibitory impulses from the cerebral
Abnormal voiding can be categorised into four main

bladder outlet obstruction

poor sphincter relaxation
detrusor weakness
ineffective emptying.

Bladder outlet obstruction presents mainly as

hesitancy, poor stream and frequency, which is most
often secondary to prostatic enlargement, urethral
strictures or bladder tumours. In clinical practice, men
are most often affected and the degree of outlet obstruction can be assessed clinically using the international prostate symptom score (Table 1), modified
from the original symptom index. [3]. In poor
sphincter relaxation, there is bladder neck and external sphincter dyssynergia, caused by neuropathic
causes or anxiety. Detrusor weakness results in poor
stream, a long-term result of untreated bladder outlet
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Functional imaging of the bladder

Table 1. International prostate symptom score

Not at all

<once in 5

<50% of
the time

About 50%
of the time

>50% of
the time


Over the past month, how often have

you had a sensation of not emptying
your bladder completely after you
finish urinating?
Over the past month, how often have
you had to urinate again less than
two hours after you have urinated?
Over the past month, how often have
you stopped and started, several
times when you urinated?
Over the past month, how often have
you found it difficult to postpone
Over the past month, how often have
you had a weak urinary stream?
Over the past month, how often have
you had to push or stain to urinate?
Over the past month, how many times
did you most typically get up to urinate
from the time you went to bed at night
until the time you got up in the morning?




3 times

4 times

More than
5 times


Indications from total scores: 07, mildly symptomatic; 819, moderately symptomatic; 2035, severely symptomatic.

obstruction. Ineffective emptying of the bladder in the

form of residual post-micturition bladder volumes
and pis en deux may be caused by acontractile detrusor, bladder diverticulae or cystocoeles.

Urodynamic techniques
Urodynamics is a term that describes a series of diagnostic tests used to evaluate voiding and storage disorders. Prior to any urodynamics test, a concurrent
urinary tract infection should be excluded as this invalidates any findings of the urodynamics and produces
reversible detrusor instability or incompliance. Most
patients can be assessed adequately using the simpler
urodynamic investigations, but more complex studies are
essential for:
patients with neuropathic disorders
complex cases with equivocal results
apparent failure to respond to previous surgical

Simple techniques
Urine flow rate measurements.
Pre- and post-micturition suprapubic transabdominal
Intravenous urogram1flow rate.

Complex techniques
Cystometry and cystometrography.

Simple urodynamic tests

Bladder flow rate measurement (uroflowmetry)
Uroflowmetry is a non-invasive technique that is easily
performed in the outpatient setting and is often used as
a screening test for voiding problems, or for selecting
patients who may require more complex urodynamic
studies. This is the simplest and most commonly used
means of objectively assessing bladder voiding dysfunction. When used in combination with measurement of
post-micturition residual bladder volume, it provides an
excellent measure of outlet obstruction and identifies
patients requiring more detailed urodynamic studies
[4, 5].
Urinary flow rate is measured by a flowmeter, which
usually measures volume of urine per unit time (ml s21).
Patients should have a comfortably full bladder and
privacy is important to ensure the patient is comfortable
to produce the most representative physiological measure. The patients position (standing or sitting) should be
documented. The total voided volume should be at least
150 ml, but volumes exceeding 600 ml produce false low
flow rates due to overstretching of the bladder. The
normal flowmetric values for males and females is shown
in Table 2. Normal and some common abnormal flow
trace patterns are shown in Figure 5.
In clinical practice, the features to assess and report on
flowmetry are:

volume: whether representative (usually

.150 ml)
Maximum flow rate (Qmax)
Voiding time
The shape of the curve

Overall configuration
Amplitude variations within the flow
Any return to baseline (interruptions)
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Table 2. Normal flow rate measurements


Bladder capacity
Maximum flow rate

500 ml
Under 40 years .25 ml s21
Over 60 years .15 ml s21
Voiding pressure
4050 cm H2O
Time to maximum flow ,1/3 of total flow time and within 310 s from
start of flow


500 ml
2550 ml s21
3040 cm H2O
,1/3 of total flow time and within 310 s from
start of flow

The shape of the normal flow pattern is unimodal (bell shaped). Flow rate measurements are inaccurate if the voided volume is
less than 125150 ml. Urine flow rate is highly dependent on the volume voided. Flow rates are highest and most predictable
due to optimal detrusor muscle stretch with 200400 ml voided volume. Volumes greater than 500 mls voided volume causes
excessive detrusor stretch with a false reduction in maximal flow rate. The final phase of a normal flow trace shows a rapid fall
from high flow, with a sharp cut-off at the termination.

Figure 5. Cytometry and flow patterns in bladder disorders.

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- Post-void dribble
- Artifacts (e.g. cruising artefact due to patient
voiding at the edge of the funnel or squeezing
artefact secondary to penile squeezing to improve the stream).
A flow test provides the sum of interaction between
detrusor function and outlet resistance, and consequently
cannot determine the cause of voiding dysfunction. For
instance, reduced flow on flowmetry could be either
bladder outflow obstruction or detrusor hypocontractility, whereas supranormal flow may be due to
either detrusor over activity or following reversal of
bladder outlet obstruction.

Ultrasound cystodynamogram
This combines ultrasound of the bladder with flow
rate measurement to provide more detailed information
on bladder function. Ultrasound is an important tool
for assessing bladder wall thickening, trabeculation,
masses, calculi, diverticulae and urinary volumes. A
comfortably full bladder is imaged on ultrasound to
document the full bladder capacity, bladder wall
thickness and bladder wall trabeculation or diverticular
formation. The patient then voids into a flowmeter.
Post-void images of the bladder should be done as soon
as possible after voiding to document true bladder residual
volume. Suprapubic transabdominal ultrasound is well
suited for the measurement of residual volume and has
replaced invasive catherisation for this purpose. In patients
with a significant residual volume, the patient should be
asked to void again and the second post-voided residual
volume documented. There is no evidence-based agreed
specific maximum or a minimum post-void residual
volume that is considered abnormal. An ultrasound
cystodynamogram (USCD) is of particular value in postoperative patients with hypocontractile detrusor dysfunction and after failed repair procedure for stress

Intravenous urodynamogram
This provides upper tract IVU images, includes
a voiding flow rate measured when the patient feels a full
bladder and a subsequent post micturition film which
allows assessment of the residual bladder volume. Intravenous urodynamogram (IVUD) provides a comprehensive assessment of patients with outflow obstruction,
and is particularly useful as it can be integrated into the
routine radiology department without additional equipment or staff training. USCD has almost entirely replaced
IVUD as the latter carries a radiation burden that can be
avoided with ultrasound.

Complex urodynamic tests

Cystometry and videocystometrography
These are detailed urodynamic investigations necessary for complex urological cases, patients with failed
surgery, or patients where the symptoms or simple urodynamics are equivocal [5]. Cystometery measures the

bladder pressurevolume relationship by measuring the

detrusor pressure during controlled bladder filling and
during voiding with measurement of the flow rate. It
characterises bladder


The normal pressurevolume relationship is shown in

Figure 4. In simple cystometry, the intravesical pressure
is measured while the bladder is filled via a catheter.
This assumes the detrusor pressure is equivalent to the
bladder pressure. However, as the bladder is intraabdominal, detrusor pressure is influenced by intraabdominal pressure. In subtracted cystometry, this
problem is overcome by measuring intravesical and
intra-abdominal pressure simultaneously. The detrusor
pressure (dD) is obtained by subtracting intraabdominal pressure (dA) from intra-vesical pressure
(dV); dD5dVdA. The normal bladder is compliant and
detrusor pressure should not increase during filling
unless overfilled to discomfort.

Videocystometrography (VCMG) has gained popularity since its introduction in the 1970s. In this technique the
bladder is filled with contrast medium and the urinary
tract is screened during bladder filling and voiding.
Visualisation of the bladder and bladder neck during
filling, and the urethra during voiding, has added information in integrating various aspects of lower urinary
tract function and characterising abnormalities. Screening
provides additional information on the presence of
vesico-ureteric reflux, level of outflow obstruction in
the lower urinary tract, sphincter competence and
pelvic floor support during straining. Pressure flow
traces are obtained and recorded on videotape,
allowing subsequent review. The normal appearance
of a contrast-filled bladder at maximal distension and
following micturition is shown in Figure 6.

Technique of videocystometrography
In the study, notes are made of initial bladder residual volume, bladder volume at the time of patients
first sensation of filling, final tolerated bladder volume
and final residual volume after voiding. Patients are
asked at the start of the study to void into a flowmeter
to allow assessment of free flow rate. They are then
asked to lie in a supine position on a screening table
while a saline-filled catheter (2 mm diameter) is introduced into the rectum to measure abdominal pressures. The end of the tube is covered to prevent faecal
blockage, but a slit is made in the cover to prevent
tamponade artefacts. A 10 F filling catheter linked to a
1 mm diameter saline-filled pressure catheter is inserted
into the bladder and then disassociated. Alternatively
a 68 F biluminal catheter can be used. The bladder is
drained of urine, providing the measure of resting initial residual volume. The two pressure measurement
lines, bladder and rectal, are zeroed at atmospheric
pressure, connected to the transducers of the
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urodynamics apparatus and then flushed through with

saline, avoiding air bubbles. Contrast medium at room
temperature is then instilled into the bladder, using
a peristaltic pump, at a slow physiological rate of
1020 ml min21. Bladder filling continues in the supine
position until the first sensation of filling occurs and the
volume instilled is documented. The patient is then
tipped towards a standing position and bladder filling
continued until maximum tolerated capacity. During
this filling phase the patient is asked to suppress voiding. The filling rate should be slow and physiological
(,10 ml s21). The faster the bladder is filled, the lower
the bladder compliance, and this may not be representative physiologically. The normal detrusor should be
quiescent in the filling phase, with a maximum end
filling pressure of 10 mm H2O. Phasic involuntary
spontaneous or provoked detrusor contractions are
only considered significant if symptomatic. The first
sensation to void should occur at 50%, normal desire to
void at 75% and a strong desire to void should occur
at 90% of functional bladder capacity. Once filling is
complete, the patient is turned to a vertical position and
the bladder base screened while coughing for sphincter
weakness. The pressure trace is also evaluated for
postural detrusor instability. The patient then voids into
a flowmeter. Throughout the study, rectal pressure,
bladder pressure and subtracted detrusor pressure are
sampled at a predetermined rate (usually 1 Hz) and the
results displayed and/or recorded on video display or
paper charts. This arrangement and results of a normal
study are shown in Figures 79.


Figure 6. (a) Pre-micturition male

bladder on VCMG. Normal bladder
contour with a smooth wall and
normal bladder neck and urethra.
(b) Post-micturition male bladder
on VCMG. There is complete
bladder emptying with no measurable residual volume. VCMG,

Patients with prostatic and detrusor failure present

with lower urinary tract symptoms (LUTS) and 6070%
have urodynamically confirmed bladder outflow obstruction (BOO). The symptoms include symptoms suggestive of overactive bladder (frequency, nocturia,
urgency and rarely urge incontinence) or voiding symptoms (hesitancy, poor stream, incomplete bladder emptying). The objective severity of LUTS is assessed by the
international prostate symptom score (I-PSS), summarised in Table 1. Physical examination includes digital
rectal examination, pelvic examination and focused neurological examination to exclude extrinsic pelvic and
neurological causes. On flowmetry, patients with BOO
have a typical flow pattern. They have a delayed and
reduced flow rate (,10 ml s21). Bladder outlet obstruction is unlikely if the flow rate is more than 15 ml s21. An
ultrasound of the bladder may demonstrate a thickened
bladder wall, trabeculation and diverticular formation
secondary to the increased voiding pressure, and reduced
flow rate in BOO (Figures 10 and 11) [6]. Post-micturition

Use and interpretation of urodynamics in

common disorders
Voiding difficulty
Prostatic outflow obstruction
This is the most common presentation in men due to
the common prevalence of prostatic outflow obstruction.
Other causes include urethral strictures and primary or
secondary detrusor failure. Females rarely present with
voiding difficulty, and the commonest cause in women is
a neuropathic disorder.
Urethral strictures present with a diminished urine
stream and a prolonged slow flow rate. These are best
investigated and demonstrated by urethrography.
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Figure 7. Schematic diagram of urodynamic apparatus.

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Figure 8. Normal urodynamic pressures.

residual volume is performed routinely. An increase in

residual urine volume is a sign of increasing bladder
decompensation rather than obstruction alone. Although
flow rate studies alone will not distinguish between high
pressurelow flow (BOO) and low pressurelow flow
(detrusor failure) pathologies, invasive urodynamics (including cystometry and VCMG) are not routinely performed in all patients. These are limited to younger
patients, who have predominantly filling symptoms or
underlying neuropathology, or those who have previous
failed prostate surgery to determine detrusor function. In

Figure 9. Normal flow pattern.

BOO alone, intravesical and subtracted detrusor pressure

is high in the presence of a low flow rate. In detrusor
failure intravesical pressure and detrusor pressures are
unstable and irregular with low urinary flow.

Detrusor overactivity
In normal voiding, the urethra relaxes and the bladder detrusor muscle contracts simultaneously. In dysfunctional voiding, this co-ordination is lost and there is
premature activation of the micturition reflex. This
condition can be further subdivided into detrusorbladder neck dyssynergia and detrusorsphincter dyssynergia. Detrusorbladder neck dyssynergia is also
known as idiopathic detrusor overactivity or detrusor
instability, and is the commonest cause of detrusor
overactivity. It presents in the third decade of life
with a lifelong history of diminished urinary steam.
Detrusorsphincter dyssynergia is also known as neurogenic detrusor hyper-reflexia and is a result of disturbance of nervous control mechanisms. This occurs in
younger women and is often associated with hormonal
disturbances such as SteinLeventhal syndrome, and
rarely complicates neurological disorders such as multiple
sclerosis and Parkinsons disease. In detrusorsphincter
dyssynergia the intravesical pressure is characteristically
unstable, producing intermittent straining and detrusor
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hyperactivity flowmetry patterns, and high-pressure,

low-flow voiding parameters. The bladder has features
of a high-pressure system, and is thick-walled and trabeculated with diverticulae. The aetiology of detrusor
instability is poorly understood. Altered responsiveness
of the smooth muscle, nerves and urothelium have all
been implicated in its pathogenesis.
In detrusor instability with incontinence:

Figure 10. Severe bladder outflow.

Detrusor instability is said to be present if the urodynamics show involuntary phasic detrusor contractions,
producing a rise and fall in detrusor pressure during filling
phase. Previously this was diagnosed only if detrusor
pressure increased by greater than 15 cm H2O during
filling phase. However, the International Continence Society (ICS) Standardisation Steering Committee makes it
clear that any phasic contraction with rise and fall in
pressure is diagnostic of instability. The ICS definition
does not specify a minimum change in pressure, although
waves less than 5 cm H2O are difficult to detect [7].
Detrusor instability seen on urodynamics is not always
clinically significant. Clinically significant instability is one
that produces symptoms of urgency or incontinence.

There is increased bladder pressure, which overcomes

the combined resistance of urethral and external

The urethra may relax with increased bladder pressure
as part of the premature micturition reflex.
In detrusor instability without incontinence:

Detrusor failure
Detrusor failure should be considered in elderly male
patients presenting with incontinence, in whom the
diagnosis may be chronic retention with overflow incontinence. The chronic retention is usually due to
long-standing prostatic obstruction, urethral stricture
or lower motor neurone lesion affecting the bladder.
Urodynamics, particularly cystometry, demonstrates an
underactive detrusor with chronic retention. The detrusor
pressure remains low and unchanging despite increasing
total bladder and abdominal pressure. No significant

The external sphincter is effective enough to prevent

urinary leak. It does so by increasing the outflow
resistance above the bladder pressure. Increased
external sphincter/pelvic floor activity triggers a
reflex inhibition of micturition reflex. These findings
are especially prominent in nulliparous women
with detrusor instability. These women do not
present with incontinence as they are able to prevent
urinary leak with the help of good pelvic floor

Figure 11. (a) VCUG and (b) trans-


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abdominal ultrasound. Bladder diverticulum (solid arrows) due to

bladder outlet obstruction in a patient with a short membranous
stricture (dashed arrow).

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Functional imaging of the bladder

urine flow is demonstrated and there remains a large

residual volume in the bladder.
These common patterns and their respective findings
on cystometry and flow rate are summarised in Figure 5.

Urinary incontinence is defined as the involuntary
leakage of urine through the urethral or an extraurethral route, which can be objectively demonstrated.
Extra-urethral incontinence may be due to ectopic
ureteric insertion, vesico-vaginal fistulae or iatrogenic.
This condition is more common in women and it is
estimated that up to one in four women experience
urinary incontinence at some time in their lives. There
are mainly four types of incontinence:

unconscious or total incontinence.

Stress incontinence is associated with activities increasing intra-abdominal pressure, such as coughing or
sneezing. In women, descent of the bladder neck and
proximal urethra due to poor pelvic support is the main
cause. In men this is most frequently seen after radical
prostatectomy. The descent of the bladder neck results in
unequal pressure distribution to the bladder, prematurely
elevating the bladder pressure above the urethral
sphincter pressure, resulting in stress incontinence. Surgery remains the mainstay of treatment for stress incontinence. This is sling surgery, either using synthetic
mesh or tissue (cadaveric, stem cell or porcine), which
conceptually tightens the bladder neck. Urge incontinence
is associated with a strong desire to void without elevation
of abdominal pressures, frequency and often with nocturia. This can be a difficult condition to demonstrate and up
to 30% of patients have a normal cystometrogram. Patients
demonstrate an involuntary increase in intravesical pressure (unstable bladder contraction) during bladder filling.
Others have poor bladder compliance, resulting in a small
functional bladder capacity. Conservative urge suppression exercises, timed voiding and medical treatment
with anticholinergic drugs are used to treat urge incontinence. Overflow incontinence is associated with
overdistension of the bladder due to inefficient emptying. This is more common in men and is usually
a complication of bladder outlet obstruction or detrusor
failure. Removal of the cause of bladder outlet obstruction improves overflow incontinence. Unconscious
or total incontinence occurs when the patients first
sensation is wetness without urge or stress. This usually represents at end-stage bladder dysfunction due to
severe sphincter deficiency, bladder instability, overflow
incontinence, or vesico-vaginal or recto-vesical fistulae.
Urodynamic evaluation is important in investigating
all forms of incontinence, but may not be necessary where
history and examination reveal straightforward lower
urinary tract infection or stress incontinence. When primary therapy fails, diagnosis is unclear, or symptoms
and/or signs are complex/severe, more elaborate assessment is generally required, including imaging, endoscopy and urodynamics [810]. The main role of
urodynamic investigations is to identify patients with

mixed urge and stress incontinence, large residual bladder volumes, failed surgery or medical treatment, and
evidence of neurological disorders. With VCMG, fluoroscopy during bladder filling may reveal opening of the
bladder neck, descent of the bladder base and leakage in
the supine or standing positions (Figure 12). VCMG
allows differentiation of the relative contributions of
bladder base prolapse and intrinsic sphincter deficiency,
because cystometry defines function, cystography shows
anatomy, and screening demonstrates the dynamics of
the bladder neck, prolapse and demonstrable leakage. In
stress incontinence the bladder pressure should not rise
above baseline during filling, with low voiding pressure
due to reduced outflow resistance. Voiding is rapid and
complete, and cough leakage is almost always demonstrable, and associated with bladder base descent.
Patients are generally unable to interrupt micturition due
to weakness of the voluntary sphincter mechanism.
Complex patients suspected of bladder fistula or urethral
diverticulum will also require cystoscopy.
Detrusor instability is the second commonest cause of
female urinary incontinence and increases with age.
There is an involuntary increase in detrusor pressure,
which causes symptoms of urgency and urge incontinence. Primary detrusor instability is a diagnosis of
exclusion; its aetiology is poorly understood and is defined as instability that is not secondary to outflow obstruction. Secondary detrusor instability may be
associated with Parkinsons disease, spinal cord injury,
diabetic neuropathy, multiple sclerosis, dementia or
stroke; however, most cases have no specific cause.
On urodynamics, there are two main types of detrusor

Figure 12. Videocystometrography. Wide open bladder neck

(arrow) with leakage of urine during coughing seen in
a patient with stress incontinence.

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A Sahdev
Table 3. Commonest types and causes of incontinence
Incontinence type




Primary detrusor instability or secondary causes

(e.g. neurogenic and BPH)
Bladder neck weakness due to surgery, childbirth,
Urge and stress causes
Long-standing BPH

Urgency and frequency day or night


Small volumes of urinary leakage with raised

abdominal pressures (e.g. cough, sneeze)
Urge and stress symptoms
Poor stream, incomplete voiding, urgency

BPH, benign prostatic hyperplasia.

The hypocompliant bladder is more often associated

with bladder fibrosis and neuropathic bladder. In phasic
overactivity, the pressure increases in a waveform while
in a hypocompliant bladder the pressure increases linearly related to the filling volume. On VCMG, the bladder
is characteristically trabeculated without a residual volume, and vesico-ureteric reflux is common. During filling, the bladder and detrusor pressure increases above
physiological baseline, and at this point the patient usually complains of urgency and impending incontinence.
Regular detrusor contractions result in a phasic pattern,
while a linear increase is associated with a hypocompliant bladder. The urinary flow rate is high, the time to
maximum flow is short (often ,2 s) and the voiding
pressures are normal (Figure 5). Opening of the bladder
neck occurs when the bladder pressure exceeds the urethral pressure, and usually large volumes of urine are
leaked [8]. The main types of incontinence, their symptoms and common causes are summarised in Table 3.
In patients with incontinence, the indications for urodynamics are:
history of mixed urge and stress incontinence
prior to invasive treatment
in previously failed incontinence surgery and where

resurgery is contemplated
associated obstructive voiding pattern or abnormal

post-void residual volume

associated neurologic disorders.

Urodynamics prior to invasive treatment should provide the following information:

confirmation of incontinence and its cause
definition of detrusor activity during filling and

during voiding to rule out obstruction or detrusor

assessment of degree of sphincter weakness.

Simple urodynamic techniques such as flow rate
measurements combined with ultrasound of the bladder
are frequently performed in radiology departments,
largely due to their simplicity, ease of use, affordability
and wide availability. Their interpretation requires the
application of basic bladder anatomy and physiology,

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and, in combination with the patients symptoms,

usually suffice in identifying the correct cause of
bladder dysfunction. However, it is not without its
pitfalls, which the clinician should keep in mind when
interpreting results. More complex urodynamics are
reserved for select patients with bladder outlet obstruction, mixed incontinence or failed surgery, or
where differentiation between detrusor and urethral
dysfunction is required.

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Imaging 2013, 22, 20120017