Functional Imaging of the Bladder

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RENAL TRACT IMAGING

Functional imaging of the bladder

A SAHDEV, MRCP, FRCR

Barts and the London NHS Trust, St Bartholomew ’ s Hospital, London, UK

SummaryMain causes of bladder dysfunction can be categorised into:

• bladder outlet obstruction—prostatic enlargement, urethral strictures, bladdertumours

• poor sphincter relaxation—neurogenic causes or anxiety• detrusor weakness—long-term untreated bladder outlet• ineffective emptying—acontractile detrusor, bladder diverticulae or cystocoeles.

The common techniques and their roles are:• bladder uroflowmetry—assesses bladder voiding ability and pattern• ultrasound cystodynamogram—bladder wall thicknessandbladder andpelvic masses• intravenous urodynamogram—upper tract assessment and bladder emptying• cystometry and videocystometrography—bladder, urethral and sphincter pressures.

doi: 10.1259/imaging.20120017

© 2013 The British Institute of

Radiology

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

Abstract. The two primary functions of the bladder are storageof urine and initiating micturition. These functions requirecomplex coordination between the central and peripheral nervous

system, bladder muscles and urethral sphincter. There aremultiple disorders of the central nervous system, spinal cord and peripheral nervous system that affect and impair bladder andurethral function. Bladder dysfunction produces a variety of non-specific symptoms and signs requiring imaginginvestigations of the lower urinary tract. The mainstays of imaging functional disorders are ultrasound, urine flowmetry andurodynamics. Urodynamic imaging studies should always beinterpreted in combination with symptoms at clinical presentationand signs. Simple and routine urodynamics of the bladder includeultrasound assessment before and after micturition, intravenousurography and bladder flow rates. These simple techniques are

frequently performed in all imaging departments and will sufficein the majority of patients when assessing bladder dysfunction.

More complex techniques (including cystometry, videocystometryand videocystometrography) are only necessary for complex caseswith 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 articlewe review normal bladder anatomy and physiology, lower urinarytract innervation, and common disorders affecting the bladder andurethra. We discuss the role of imaging and urodynamic findingsin bladder outlet obstruction, urethral overactivity, detrusor

failure, incontinence and detrusor instability.

Bladder dysfunction produces a variety of non-specificsymptoms, which are investigated by lower tract urody-namics. These symptoms include frequency, dysuria, ur-

gency, incontinence, hesitancy and poor stream. Thesymptoms are caused by bladder disorders related to ab-normal storage of urine or abnormal bladder emptying,with a significant overlap. Urodynamics of the bladder isthe study of pressure and flow relationships during thestorage of urine and micturition. In routine practice, thisfocuses on the bladder and its sphincter mechanism to in-vestigate bladder filling and voiding, define bladder storagedisorders and assess the severity of voiding dysfunction.The basic principles of urodynamics require an un-derstanding of bladder anatomy and normal physiology.Urodynamic techniques allow an objective assessment of lower urinary tract disorders, but must be interpreted in thecontext of the patient’s clinical history and symptoms.

There are several clinically based simple techniques used toassess bladder dysfunction, such as volume voiding charts,pad testing and symptom monitoring, which will not bediscussed in this article. The discussion will be limited totechniques commonly involving the radiologist in thefunctional 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 layer—consisting of transitionalcells forming a barrier virtually impenetrable to anycomponent of urine.

2. Lamina propria—consisting mainly of dense connectivetissue, with many bundles of coarse collagenous fibres.

Address correspondence to: Dr Anju Sahdev, Barts and the LondonNHS Trust, St Bartholomew’s Hospital, West Smithfield, LondonEC1A 7BE, UK. E-mail: [email protected]

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3. Submucosa—consisting of a loose connective tissuethat supports the mucosa, contains blood vessels,nerves and lymphatics supplying the mucosa.

4. A smooth muscle layer consisting of an innerlongitudinal and outer circular layer of smooth musclecells with interlacing fibres. An additional outer layerof longitudinal fibres forms the detrusor muscle.

5. An outer adventitial layer consisting of connectivetissue.

The detrusor muscle is controlled by the autonomicsystem; the parasympathetic system provides motor

control while the sympathetic system (found pre-dominantly in the bladder base) principally controls thevasculature. Additional sensorimotor nerves are foundin the bladder wall; their precise function is unclear.The spinal segments S2–S4 contain the efferent para-sympathetic supply, and T10–L2 nerves contain thesympathetic efferent nerves. After leaving the sacralforamina, the pelvic splanchnic nerves containing theparasympathetic neurones pass lateral to the rectum andenter the inferior pelvic plexus (hypogastric plexus).

These combine with the hypogastric nerve containing thesympathetic plexus and form the neural plexus at the

Figure 1. Normal anatomy of the bladder.

Figure 2. Innervation of the bladder.

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bladder base supplying the bladder trigone. Damage to

S2–S4 spinal segments abolishes the micturition reflex(Figure 2).

The flow of urine from the urinary bladder is con-trolled by the urethral sphincter. Both sexes have at leasttwo layers of muscle: the internal sphincter, or bladderneck; and the external, or distal, sphincter. In men, theseare the proximal bladder neck and the distal sphincter atthe apex of the prostate. In men both sphincters areequally important in maintaining continence. The bladderneck consists of an inner strong layer of circular musclesinnervated by adrenergic sympathetic nerves and anouter muscle layer contiguous with the detrusor muscle.In women, the bladder neck is weaker, with poorlydefined muscles, and continence is maintained mainly bythe urethral sphincter, which extends throughout theproximal two-thirds of the urethra. The striated muscle inthe urethral sphincter is innervated by autonomic nervesand somatic pudental nerves transmitting urethral mu-cosal sensation (Figures 2 and 3).

Symptoms of lower urinary tract dysfunction relateto disorders of the bladder or urethra. Symptoms re-lating to altered urine storage include frequency,

nocturia, urgency, incontinence and abnormal sensa-

tion. Symptoms relating to abnormal voiding are slowstream, straining and hesitancy. Post-micturition dis-orders are usually dribbling and incomplete bladderemptying.

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 volume–pressure relation-

ship is summarised in Figure 4. For normal function, in-tegrated coordination is necessary, for which the spinalcord has to be intact.

Storage of urine

The normal bladder should comfortably hold400–500 ml without any increase in the detrusor pressure

Figure 3. Muscle and sphincter complex.

Figure 4. Normal bladder pressure–volumerelationship.



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(,15mm H2O). Although there is an urge to void, thiscan be controlled. Two factors control the bladder’sability to store urine: bladder compliance and neuralcontrol.

Bladder complianceSmooth muscle in the bladder wall has elastic proper-

ties and the ability to maintain a constant tension overa wide range of distension, producing an intrinsic tone inthe bladder wall. As urine enters the bladder, the bladderwall relaxes, increasing the volume (but not pressure) inthe bladder. The change in volume (dV) in relation to thechange in intravesical pressure (dP) is called the bladdercompliance (dV/dP).

Neural control To aid urine storage and continence, as the bladder

distends with urine, afferent neural activity from thestretch receptors in the bladder wall send signals to the

spinal cord initiating the desire to void. The local spinalcord reflex increases the tone in the striated muscle of the sphincter, which tightens up thereby promotingcontinence. At rest the urethral tone keeps the urethralwalls in apposition to maintain continence. Equally,voluntary signals from higher centres, can inhibit thisspinal reflex when micturition is desired relaxing theurethral sphincter.

A decrease in the bladder’s ability to hold urine may bedue 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 mostcommon cause for this is increased bladder sensitivity,usually due to infection. In functional decreased

bladder capacity, there is no abnormality of detrusorpressures within the bladder. Small volume bladderpresents with frequency and occurs following partialcystectomy, bladder fibrosis (e.g. post radiotherapy,post bacillus Calmette-Guérin therapy) or due to ex-trinsic compression of the bladder. Bladder over-activity results in urgency and frequency caused by anunstable bladder due to non-neurological causes such

as recovery from long-term outflow obstruction.Sphincter incompetence is common, presenting withleakage and frequency. Bladder neck and pelvic floorweakness due to childbirth and age are the commonestcauses.

Normal micturition reflex and voiding mechanism

The micturition reflex involves impulses travellingfrom the bladder to the spinal cord and from the spinalcord back to the bladder. When the bladder wall isstretched afferent impulses travel to the spinal cord(S2–4). In response, parasympathetic impulses from the

spinal cord (S2–4) travel to the bladder, activate andcause smooth muscle contraction in the bladder wall.

The bladder impulses from S2–4 also stimulate theascending pathways to the medulla, pons and cere-

brum, which influence a conscious decision to mictu-rate. Higher pathways return impulses to the spinalcord, either allowing or suppressing micturition,depending on convenience. Impulses from the spinalcord, via somatic nerve fibres (mainly S2–4 pudendalnerve), act on the striated muscle of the externalsphincter and pelvic floor. The external sphinctercontracts to inhibit micturition and relaxes to allowmicturition. When micturition is desired, the brainsends impulses to the bladder wall (via sympatheticand parasympathetic fibres) to contract the smoothmuscle, and to the external sphincter via the sympa-thetic 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 hyper-trophy in outflow obstruction) or altering the neuralfunction will result in poor bladder compliance anddetrusor instability. Complete peripheral denervationremoves all central nervous system control resulting inan atonic bladder and inactive sphincter. Voiding isachieved by voluntary contraction of the abdominal

muscles or manual bladder compression. Lesions in thespinal cord above the fifth lumbar vertebra result in lossof coordination between the detrusor contraction andsphincter relaxation (detrusor–sphicter dyssynergia).This results in intermittent voiding, but also urine retention[2]. Cerebral and basal ganglia lesions (Parkinson’s, stroke,multiple sclerosis) have a typical picture of involuntary

bladder contractions which can result in urge incontinencedue to the loss of inhibitory impulses from the cerebralcortex.

Abnormal voiding can be categorised into four maincategories:

• bladder outlet obstruction•

poor sphincter relaxation• detrusor weakness• ineffective emptying.

Bladder outlet obstruction presents mainly ashesitancy, poor stream and frequency, which is mostoften secondary to prostatic enlargement, urethralstrictures or bladder tumours. In clinical practice, menare most often affected and the degree of outlet obstruc-tion can be assessed clinically using the interna-tional prostate symptom score (Table 1), modifiedfrom the original symptom index. [3]. In po orsphincter relaxation, there is bladder neck and exter-nal sphincter dyssynergia, caused by neuropathic

causes or anxiety. Detrusor weakness results in poorstream, a long-term result of untreated bladder outlet

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obstruction. Ineffective emptying of the bladder in theform of residual post-micturition bladder volumesand pis en deux may be caused by acontractile detru-sor, bladder diverticulae or cystocoeles.

Urodynamic techniques

Urodynamics is a term that describes a series of di-

agnostic tests used to evaluate voiding and storage dis-orders. Prior to any urodynamics test, a concurrenturinary tract infection should be excluded as this inva-lidates any findings of the urodynamics and producesreversible detrusor instability or incompliance. Mostpatients can be assessed adequately using the simplerurodynamic investigations, but more complex studies areessential for:

patients with neuropathic disorderscomplex cases with equivocal resultsapparent failure to respond to previous surgicalprocedures.

Simple urodynamic tests

Bladder flow rate measurement (uroflowmetry)

Uroflowmetry is a non-invasive technique that is easilyperformed in the outpatient setting and is often used asa screening test for voiding problems, or for selectingpatients who may require more complex urodynamicstudies. This is the simplest and most commonly usedmeans of objectively assessing bladder voiding dysfunc-tion. When used in combination with measurement of post-micturition residual bladder volume, it provides anexcellent measure of outlet obstruction and identifiespatients requiring more detailed urodynamic studies[4, 5].

Urinary flow rate is measured by a flowmeter, whichusually measures volume of urine per unit time (ml s21).Patients should have a comfortably full bladder andprivacy is important to ensure the patient is comfortableto produce the most representative physiological mea-sure. The patient’s position (standing or sitting) should bedocumented. The total voided volume should be at least

150 ml, but volumes exceeding 600 ml produce false lowflow rates due to overstretching of the bladder. Thenormal flowmetric values for males and females is shownin Table 2. Normal and some common abnormal flowtrace patterns are shown in Figure 5.

In clinical practice, the features to assess and report onflowmetry are:

• Voided 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)

Table 1. International prostate symptom score

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Table 2. Normal flow rate measurements

Measure Male Female

Bladder capacity 500 ml 500 mlMaximum flow rate Under 40 years .25m l s21 25–50m l s21

Over 60 years .15m l s21

Voiding pressure 40–50cm H2O 30–40cm H2OTime to maximum flow ,1/3 of total flow time and within 3–10 s from

start of flow

,1/3 of total flow time and within 3–10 s from

start of flowThe shape of the normal flow pattern is unimodal (“bell shaped”). Flow rate measurements are inaccurate if the voided volume is

less than 125–150 ml. Urine flow rate is highly dependent on the volume voided. Flow rates are highest and most predictabledue to optimal detrusor muscle stretch with 200–400 ml voided volume. Volumes greater than 500 mls voided volume causesexcessive detrusor stretch with a false reduction in maximal flow rate. The final phase of a normal flow trace shows a rapid fallfrom 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 squeezingartefact secondary to penile squeezing to im-prove the stream).

A flow test provides the sum of interaction betweendetrusor function and outlet resistance, and consequentlycannot determine the cause of voiding dysfunction. Forinstance, reduced flow on flowmetry could be either

bladder outflow obstruction or detrusor hypocon-tractility, whereas “supranormal” flow may be due toeither detrusor over activity or following reversal of

bladder outlet obstruction.

Ultrasound cystodynamogram

This combines ultrasound of the bladder with flowrate measurement to provide more detailed informationon bladder function. Ultrasound is an important toolfor assessing bladder wall thickening, trabeculation,

masses, calculi, diverticulae and urinary volumes. Acomfortably full bladder is imaged on ultrasound todocument the full bladder capacity, bladder wallthickness and bladder wall trabeculation or diverticularformation. The patient then voids into a flowmeter.Post-void images of the bladder should be done as soonas possible after voiding to document true bladder residualvolume. Suprapubic transabdominal ultrasound is wellsuited for the measurement of residual volume and hasreplaced invasive catherisation for this purpose. In patientswith a significant residual volume, the patient should beasked to void again and the second post-voided residualvolume documented. There is no evidence-based agreedspecific maximum or a minimum post-void residualvolume that is considered abnormal. An ultrasoundcystodynamogram (USCD) is of particular value in post-operative patients with hypocontractile detrusor dys-function and after failed repair procedure for stressincontinence.

Intravenous urodynamogram

This provides upper tract IVU images, includesa voiding flow rate measured when the patient feels a full

bladder and a subsequent post micturition film whichallows assessment of the residual bladder volume. In-travenous urodynamogram (IVUD) provides a compre-

hensive assessment of patients with outflow obstruction,and is particularly useful as it can be integrated into theroutine radiology department without additional equip-ment or staff training. USCD has almost entirely replacedIVUD as the latter carries a radiation burden that can beavoided with ultrasound.

Complex urodynamic tests

Cystometry and videocystometrography

These are detailed urodynamic investigations neces-sary for complex urological cases, patients with failed

surgery, or patients where the symptoms or simple uro-dynamics are equivocal [5]. Cystometery measures the

bladder pressure–volume relationship by measuring thedetrusor pressure during controlled bladder filling andduring voiding with measurement of the flow rate. Itcharacterises bladder

• compliance• sensation• stability

• capacity.

The normal pressure–volume relationship is shown inFigure 4. In simple cystometry, the intravesical pressureis 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 intra-abdominal, detrusor pressure is influenced by intra-abdominal pressure. In subtracted cystometry, thisproblem is overcome by measuring intravesical andintra-abdominal pressure simultaneously. The detrusorpressure (dD) is obtained by subtracting intra-abdominal pressure (dA) from intra-vesical pressure(dV); dD5dV–dA. The normal bladder is compliant anddetrusor pressure should not increase during fillingunless overfilled to discomfort.

Videocystometrography

Videocystometrography (VCMG) has gained popular-ity since its introduction in the 1970s. In this technique the

bladder is filled with contrast medium and the urinarytract is screened during bladder filling and voiding.Visualisation of the bladder and bladder neck duringfilling, and the urethra during voiding, has added in-formation in integrating various aspects of lower urinarytract function and characterising abnormalities. Screening

provides additional information on the presence of vesico-ureteric reflux, level of outflow obstruction inthe lower urinary tract, sphincter competence andpelvic floor support during straining. Pressure flowtraces are obtained and recorded on videotape,allowing subsequent review. The normal appearanceof a contrast-filled bladder at maximal distension andfollowing micturition is shown in Figure 6.

Technique of videocystometrography

In the study, notes are made of initial bladder re-sidual volume, bladder volume at the time of patient ’sfirst sensation of filling, final tolerated bladder volume

and final residual volume after voiding. Patients areasked at the start of the study to void into a flowmeterto allow assessment of free flow rate. They are thenasked to lie in a supine position on a screening tablewhile a saline-filled catheter (2 mm diameter) is in-troduced into the rectum to measure abdominal pres-sures. The end of the tube is covered to prevent faecal

blockage, but a slit is made in the cover to preventtamponade artefacts. A 10 F filling catheter linked to a1 mm diameter saline-filled pressure catheter is insertedinto the bladder and then disassociated. Alternativelya 6–8 F biluminal catheter can be used. The bladder isdrained of urine, providing the measure of resting ini-tial residual volume. The two pressure measurement

lines, bladder and rectal, are zeroed at atmosphericpressure, connected to the transducers of the





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urodynamics apparatus and then flushed through withsaline, avoiding air bubbles. Contrast medium at roomtemperature is then instilled into the bladder, usinga peristaltic pump, at a slow physiological rate of 10–20ml min21. Bladder filling continues in the supineposition until the first sensation of filling occurs and the

volume instilled is documented. The patient is thentipped towards a standing position and bladder fillingcontinued until maximum tolerated capacity. Duringthis filling phase the patient is asked to suppress void-ing. The filling rate should be slow and physiological(,10mls21). The faster the bladder is filled, the lowerthe bladder compliance, and this may not be represen-tative physiologically. The normal detrusor should bequiescent in the filling phase, with a maximum endfilling pressure of 10 mm H2O. Phasic involuntaryspontaneous or provoked detrusor contractions areonly considered significant if symptomatic. The firstsensation to void should occur at 50%, normal desire tovoid at 75% and a strong desire to void should occurat 90% of functional bladder capacity. Once filling iscomplete, the patient is turned to a vertical position andthe bladder base screened while coughing for sphincterweakness. The pressure trace is also evaluated forpostural detrusor instability. The patient then voids intoa flowmeter. Throughout the study, rectal pressure,

bladder pressure and subtracted detrusor pressure aresampled at a predetermined rate (usually 1 Hz) and theresults displayed and/or recorded on video display orpaper charts. This arrangement and results of a normalstudy are shown in Figures 7–9.

Use and interpretation of urodynamics incommon disorders

Voiding difficulty

Prostatic outflow obstructionThis is the most common presentation in men due to

the common prevalence of prostatic outflow obstruction.Other causes include urethral strictures and primary orsecondary detrusor failure. Females rarely present withvoiding difficulty, and the commonest cause in women isa neuropathic disorder.

Urethral strictures present with a diminished urine

stream and a prolonged slow flow rate. These are bestinvestigated and demonstrated by urethrography.

Patients with prostatic and detrusor failure presentwith lower urinary tract symptoms (LUTS) and 60–70%have urodynamically confirmed bladder outflow ob-struction (BOO). The symptoms include symptoms sug-gestive of overactive bladder (frequency, nocturia,urgency and rarely urge incontinence) or voiding symp-

toms (hesitancy, poor stream, incomplete bladder emp-tying). The objective severity of LUTS is assessed by theinternational prostate symptom score (I-PSS), summar-ised in Table 1. Physical examination includes digitalrectal examination, pelvic examination and focused neu-rological examination to exclude extrinsic pelvic andneurological causes. On flowmetry, patients with BOOhave a typical flow pattern. They have a delayed andreduced flow rate (,10mls21). Bladder outlet obstruc-tion is unlikely if the flow rate is more than 15 ml s21. Anultrasound of the bladder may demonstrate a thickened

bladder wall, trabeculation and diverticular formationsecondary to the increased voiding pressure, and reducedflow rate in BOO (Figures 10 and 11) [6]. Post-micturition

(a) (b)

Figure 6. (a) Pre-micturition malebladder on VCMG. Normal bladdercontour with a smooth wall andnormal bladder neck and urethra.(b) Post-micturition male bladderon VCMG. There i s compl etebladder emptying with no measur-able residual volume. VCMG,videocystometrography.

Figure 7. Schematic diagram of urodynamic apparatus.

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residual volume is performed routinely. An increase inresidual urine volume is a sign of increasing bladderdecompensation rather than obstruction alone. Althoughflow rate studies alone will not distinguish between highpressure–low flow (BOO) and low pressure–low flow(detrusor failure) pathologies, invasive urodynamics (in-cluding cystometry and VCMG) are not routinely per-formed in all patients. These are limited to youngerpatients, who have predominantly filling symptoms orunderlying neuropathology, or those who have previousfailed prostate surgery to determine detrusor function. In

BOO alone, intravesical and subtracted detrusor pressureis high in the presence of a low flow rate. In detrusorfailure intravesical pressure and detrusor pressures areunstable and irregular with low urinary flow.

Detrusor overactivity In normal voiding, the urethra relaxes and the blad-

der detrusor muscle contracts simultaneously. In dys-functional voiding, this co-ordination is lost and there ispremature activation of the micturition reflex. This

condition can be further subdivided into detrusor–

- bladder neck dyssynergia and detrusor–sphincter dys-synergia. Detrusor– bladder neck dyssynergia is alsoknown as idiopathic detrusor overactivity or detrusorinstability, and is the commonest cause of detrusoroveractivity. It presents in the third decade of lifewith a lifelong history of diminished urinary steam.Detrusor–sphincter dyssynergia is also known as neu-rogenic detrusor hyper-reflexia and is a result of dis-turbance of nervous control mechanisms. This occurs inyounger women and is often associated with hormonaldisturbances such as Stein–Leventhal syndrome, andrarely complicates neurological disorders such as multiplesclerosis and Parkinson’s disease. In detrusor–sphincter

dyssynergia the intravesical pressure is characteristicallyunstable, producing intermittent straining and detrusor

Figure 8. Normal urodynamic pressures.

Figure 9. Normal flow pattern.





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hyperactivity flowmetry patterns, and high-pressure,low-flow voiding parameters. The bladder has featuresof a high-pressure system, and is thick-walled and tra-

beculated with diverticulae. The aetiology of detrusorinstability is poorly understood. Altered responsivenessof the smooth muscle, nerves and urothelium have all

been implicated in its pathogenesis.In detrusor instability with incontinence:

• There is increased bladder pressure, which overcomesthe combined resistance of urethral and externalsphincters.

• The urethra may relax with increased bladder pressureas part of the premature micturition reflex.

In detrusor instability without incontinence:

The external sphincter is effective enough to preventurinary leak. It does so by increasing the outflowresistance above the bladder pressure. Increasedexternal sphincter/pelvic floor activity triggers areflex inhibition of micturition reflex. These findingsare especially prominent in nulliparous womenwith detrusor instability. These women do notpresent with incontinence as they are able to preventurinary leak with the help of good pelvic floormusculature.

Detrusor instability is said to be present if the urody-namics show involuntary phasic detrusor contractions,producing a rise and fall in detrusor pressure during fillingphase. Previously this was diagnosed only if detrusorpressure increased by greater than 15 cm H2O duringfilling phase. However, the International Continence So-ciety (ICS) Standardisation Steering Committee makes itclear that any phasic contraction with rise and fall inpressure is diagnostic of instability. The ICS definitiondoes not specify a minimum change in pressure, althoughwaves less than 5 cm H2O are difficult to detect [7].Detrusor instability seen on urodynamics is not alwaysclinically significant. Clinically significant instability is onethat produces symptoms of urgency or incontinence.

Detrusor failureDetrusor failure should be considered in elderly male

patients presenting with incontinence, in whom thediagnosis may be chronic retention with overflow in-continence. The chronic retention is usually due tolong-standing prostatic obstruction, urethral strictureor lower motor neurone lesion affecting the bladder.Urodynamics, particularly cystometry, demonstrates anunderactive detrusor with chronic retention. The detrusorpressure remains low and unchanging despite increasingtotal bladder and abdominal pressure. No significant

(a) (b) Figure 10. Severe bladder outflow.

(a) (b)

Figure 11. (a) VCUG and (b) trans-abdominal ultrasound. Bladder di-verticulum (solid arrows) due tobladder outlet obstruction in a pa-tient with a short membranousstricture (dashed arrow).

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urine flow is demonstrated and there remains a largeresidual volume in the bladder.

These common patterns and their respective findingson cystometry and flow rate are summarised in Figure 5.

Incontinence

Urinary incontinence is defined as the involuntary

leakage of urine through the urethral or an extra-urethral route, which can be objectively demonstrated.Extra-urethral incontinence may be due to ectopicureteric insertion, vesico-vaginal fistulae or iatrogenic.This condition is more common in women and it isestimated that up to one in four women experienceurinary incontinence at some time in their lives. Thereare mainly four types of incontinence:

• stress• urge• overflow• unconscious or total incontinence.

Stress incontinence is associated with activities in-creasing intra-abdominal pressure, such as coughing orsneezing. In women, descent of the bladder neck andproximal urethra due to poor pelvic support is the maincause. In men this is most frequently seen after radicalprostatectomy. The descent of the bladder neck results inunequal pressure distribution to the bladder, prematurelyelevating the bladder pressure above the urethralsphincter pressure, resulting in stress incontinence. Sur-gery remains the mainstay of treatment for stress in-continence. This is sling surgery, either using syntheticmesh or tissue (cadaveric, stem cell or porcine), whichconceptually tightens the bladder neck. Urge incontinenceis associated with a strong desire to void without elevationof abdominal pressures, frequency and often with noctu-ria. This can be a difficult condition to demonstrate and upto 30% of patients have a normal cystometrogram. Patientsdemonstrate an involuntary increase in intravesical pres-sure (unstable bladder contraction) during bladder filling.Others have poor bladder compliance, resulting in a smallfunctional bladder capacity. Conservative urge suppres-sion exercises, timed voiding and medical treatmentwith anticholinergic drugs are used to treat urge in-continence. Overflow incontinence is associated withoverdistension of the bladder due to inefficient empty-ing. This is more common in men and is usuallya complication of bladder outlet obstruction or detrusor

failure. Removal of the cause of bladder outlet ob-struction improves overflow incontinence. Unconsciousor total incontinence occurs when the patient’s firstsensation is wetness without urge or stress. This usu-ally represents at end-stage bladder dysfunction due tosevere sphincter deficiency, bladder instability, overflowincontinence, or vesico-vaginal or recto-vesical fistulae.

Urodynamic evaluation is important in investigatingall forms of incontinence, but may not be necessary wherehistory and examination reveal straightforward lowerurinary tract infection or stress incontinence. When pri-mary therapy fails, diagnosis is unclear, or symptomsand/or signs are complex/severe, more elaborate as-sessment is generally required, including imaging, en-

doscopy and urodynamics [8–10]. The main role of urodynamic investigations is to identify patients with

mixed urge and stress incontinence, large residual blad-der volumes, failed surgery or medical treatment, andevidence of neurological disorders. With VCMG, fluo-roscopy during bladder filling may reveal opening of the

bladder neck, descent of the bladder base and leakage inthe supine or standing positions (Figure 12). VCMGallows differentiation of the relative contributions of

bladder base prolapse and intrinsic sphincter deficiency, because cystometry defines function, cystography showsanatomy, and screening demonstrates the dynamics of the bladder neck, prolapse and demonstrable leakage. Instress incontinence the bladder pressure should not riseabove baseline during filling, with low voiding pressuredue to reduced outflow resistance. Voiding is rapid andcomplete, and cough leakage is almost always de-monstrable, and associated with bladder base descent.Patients are generally unable to interrupt micturition dueto weakness of the voluntary sphincter mechanism.Complex patients suspected of bladder fistula or urethraldiverticulum 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 in-continence. Primary detrusor instability is a diagnosis of exclusion; its aetiology is poorly understood and is de-fined as instability that is not secondary to outflow ob-struction. Secondary detrusor instability may beassociated with Parkinson’s disease, spinal cord injury,diabetic neuropathy, multiple sclerosis, dementia orstroke; however, most cases have no specific cause.

On urodynamics, there are two main types of detrusorinstability:

• phasic

• hypocompliant.

Figure 12. Videocystometrography. Wide open bladder neck(arrow) with leakage of urine during coughing seen ina patient with stress incontinence.





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The hypocompliant bladder is more often associatedwith bladder fibrosis and neuropathic bladder. In phasicoveractivity, the pressure increases in a waveform whilein a hypocompliant bladder the pressure increases line-arly related to the filling volume. On VCMG, the bladderis characteristically trabeculated without a residual vol-ume, and vesico-ureteric reflux is common. During fill-ing, the bladder and detrusor pressure increases abovephysiological baseline, and at this point the patient usu-

ally complains of urgency and impending incontinence.Regular detrusor contractions result in a phasic pattern,while a linear increase is associated with a hypocom-pliant bladder. The urinary flow rate is high, the time tomaximum flow is short (often ,2 s) and the voidingpressures are normal (Figure 5). Opening of the bladderneck occurs when the bladder pressure exceeds the ure-thral pressure, and usually large volumes of urine areleaked [8]. The main types of incontinence, their symp-toms and common causes are summarised in Table 3.

In patients with incontinence, the indications for uro-dynamics 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 pro-vide the following information:

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

during voiding to rule out obstruction or detrusorunderactivity

• assessment of degree of sphincter weakness.

Conclusion

Simple urodynamic techniques such as flow ratemeasurements combined with ultrasound of the bladderare frequently performed in radiology departments,largely due to their simplicity, ease of use, affordabilityand wide availability. Their interpretation requires theapplication of basic bladder anatomy and physiology,

and, in combination with the patient’s symptoms,usually suffice in identifying the correct cause of

bladder dysfunction. However, it is not without itspitfalls, which the clinician should keep in mind wheninterpreting results. More complex urodynamics arereserved for select patients with bladder outlet ob-struction, mixed incontinence or failed surgery, orwhere differentiation between detrusor and urethraldysfunction is required.

References

1. Sutton D, ed. Textbook of radiology and imaging. 7th edn.Edinburgh, UK: Elsevier Science.

2. Dorkin TJ, Leonard AS, Pickard RS. Can bladder outflowobstruction be diagnosed from pressure flow analysis of voiding initiated by involuntary detrusor overactivity? JUrol 2003;170:1234–6.

3. Barry MJ, Fowler FJ Jr, O’Leary MP, Bruskewitz RC,Holtgrewe HL, Mebust WK, et al; The American UrologicalAssociation symptom index for benign prostatic hyperpla-sia. The Measurement Committee of the American Urolog-ical Association. J Urol 1992;148:1549–57.

4. Gacci M, Del Popolo G, Artibani W, Tubaro A, Palli D,Vittori G, et al. Visual assessment of uroflowmetry curves:description and interpretation by urodynamists. World JUrol 2007;25:333–7.

5. Steele GS, Sullivan MP, Sleep DJ, Yalla SV. Combination of symptom score, flow rate and prostate volume for predict-ing bladder outflow obstruction in men with lower urinarytract symptoms. J Urol 2000;164:344–8.

6. Szabó L, Lombay B, Borbás E, Bajusz I. Videourodynamicsin the diagnosis of urinary tract abnormalities in a singlecenter. Pediatr Nephrol 2004;19:326–31.

7. Rowan D, James ED, Kramer AE, Sterling AM, Suhel PF.Urodynamic equipment: technical aspects. Produced by theInternational Continence Society Working Party on Urody-namic Equipment. J Med Eng Technol 1987;11:57–64.

8. Thüroff JW, Abrams P, Andersson KE, Artibani W, ChappleCR, Drake MJ, et al. EAU guidelines on urinary in-continence. Eur Urol 2011;59:387–400.

9. O’Dowd A. NICE issues new guidance on urinary in-continence in women. BMJ 2006;333:876.

10. Porru D, Jallous H, Cavalli V, Sallusto F, Rovereto B.Prognostic value of a combination of IPSS, flow rate andresidual urine volume compared to pressure-flow studies inthe preoperative evaluation of symptomatic BPH. Eur Urol2002;41:246–9.

Table 3. Commonest types and causes of incontinence

Incontinence type Causes Symptoms

Urge Primary detrusor instability or secondary causes(e.g. neurogenic and BPH)

Urgency and frequency day or night

Stress Bladder neck weakness due to surgery, childbirth,age

Small volumes of urinary leakage with raisedabdominal pressures (e.g. cough, sneeze)

Mixed Urge and stress causes Urge and stress symptoms

Overflow Long-standing BPH Poor stream, incomplete voiding, urgencyBPH, benign prostatic hyperplasia.

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