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211

PathoPhysiology of lowEr Urinary tract obstrUction

Table 16.1. Voiding and post-micturition symptoms as defined

suitable range, and is comparable to the typical

by the international continence society (ics) standardisation

voided volume on the individual’s frequency

committee in 200217,18

 

volume chart, is a means by which to ascertain

Voiding symptoms

 

that the flow rate test is representative and infor-

 

mative. Qmax is affected by VV, so nomograms

slow stream

the patient’s perception of

have been developed to aid interpretation,exem-

 

reduced urine flow, usually

plified by the Liverpool nomograms for men

 

compared to previous

and women22 and the Siroky nomogram for

 

performance or in

men.23,24 At low VV, the bladder has insufficient

 

comparison with others

 

volume to expel and Qmax may be reduced as a

intermittent stream

the urine flow stops and starts,

result; nonetheless, informative conclusions can

 

on one or more occasions,

sometimes be drawn regardless of low VV.25

 

during micturition

Above 550 mL, the bladder starts to overfill and

hesitancy

difficulty initiating micturition,

efficiency declines,26 again causing artefactual

 

resulting in a delay in the

reduction in Qmax. Failure of expulsion of the

 

onset of voiding after the

entire bladder contents, leading to a PVR, signi-

 

individual is ready to pass

fies inefficient bladder emptying; this suggests

 

urine

either reduced bladder contractility or outlet

straining

describes the muscular effort

obstruction, or both.

 

 

 

used to initiate, maintain, or

 

The normal flow curve should have a rapid

 

improve the urinary stream

upstroke, a clear Qmax, and decline quickly to

terminal dribble

the term used to describe a

end cleanly. Abnormal patterns include;

 

 

 

 

 

prolonged final part of

1.

Prostatic (men): Characterized by a slow

 

micturition, when the flow

 

 

upstroke, reduced Qmax, and prolonged down-

 

has slowed to a trickle/

 

 

dribble

 

stroke.

 

 

Post-micturition symptoms

2.

Urethral stricture (men): the pattern has a

 

“plateau” appearance.

 

 

feeling of incomplete

a self-explanatory term for a

 

 

 

3. Intermittent (men or women): several peaks

emptying

feeling experienced by the

 

in the flow curve can result if the patient

 

individual after passing urine

 

 

 

strains during voiding. Likewise, a poorly

Post micturition

involuntary loss of urine

 

 

sustained detrusor contraction causes the

dribble

immediately after he or she

 

 

stream to fluctuate.

 

 

 

has finished passing urine,

 

 

 

 

usually after leaving the

In men of the appropriate age group, a prostatic

 

toilet in men, or after rising

 

pattern with a reduced Qmax

when VV is ade-

 

from the toilet in women

 

 

quate is suggestive of BOO but accuracy is inad-

 

 

equate by itself.27 Where Q

max

is above the

 

 

expected range, outlet obstruction is unlikely.

is not so clear-cut,since relief of obstruction with

However, sensitivity of flow rate testing by itself

prostate resection surgery does not lead to reso-

as a diagnostic test for BOO is inadequate.

lution of storage urinary problems.21

Flow Rate and Post-void Residual

Flow rate machines measure flow volume over time and evaluate various parameters, of which the maximum flow rate (Qmax), flow pattern and post-void residual (PVR) volume are most widely used clinically. Findings have to be interpreted in the light of clinical circumstances; checking the voided volume (VV) falls into a

Voiding Cystometry

BOO is characterized by increased detrusor pressure and reduced urine flow rate.17 It is usually diagnosed by studying the synchronous values of flow rate and detrusor pressure, and is thus a urodynamic diagnosis.17

Consensus on what constitutes BOO in men has been achieved because of the relatively homogeneous nature of male BOO, reflecting

 

 

 

 

 

 

212

 

 

 

 

 

 

 

 

 

 

 

 

 

Practical Urology: EssEntial PrinciPlEs and PracticE

high prevalence of benign prostate enlargement

2. An alternative nomogram has been proposed

in older men, and the availability of transure-

by a different group.39

thral resection surgery to relieve obstruction.

3. The BOOI is applicable in men with benign

This provided suitable circumstances to derive

prostate enlargement and no relevant neuro-

urodynamic nomograms28; the nomogram of

logical problem. Nonetheless, the parameters

Abrams and Griffiths was adopted and adapted

of the BOOI have been evaluated in women,

by the International Continence Society as a

such that the BOOI evaluated in conjunction

standardized criterion for diagnosing male

BOO. Thus a plot of Qmax

against simultaneous

with Qmax could be a usable urodynamic

detrusor pressure (P

Q

) allows derivation of

parameter of female BOO.40 A separate study

 

 

det

max

 

 

the bladder outlet obstruction index (BOOI),

came to similar conclusions, but cut-off val-

from which a definite diagnosis of BOO, equivo-

ues were different.41

cal BOO or unobstructed can be made, as illus-

4. An alternative compared women with ana-

trated in Fig. 16.1. The concept superseded the

tomical BOO against women with stress uri-

earlier concept of a urethral resistance factor,

nary incontinence,42 with revisions using a

which originated from rigid tube hydrodyn-

amics. Since the urethra is an irregular and

larger study group in 2000,43 and a control

distensible conduit, whose walls and surround-

group without stress incontinence in 2004.44

ings have active and passive elements which

5. A panel of criteria derived during videouro-

influence the flow, a resistance factor does not

dynamic evaluation has been proposed based

reliably provide a valid

comparison

between

on study of a group of women clinically felt

patients.29

 

 

 

 

 

 

 

 

to have BOO.45

While measurements to derive a BOOI are

6. Area under the curve of detrusor pressure

generally made by invasive urodynamic testing,

during voiding, adjusted for voided volume, is

noninvasive techniques are now emerging30,31

which may be able to derive an estimate of the

a proposed parameter for diagnosing female

detrusor pressure generating maximum flow

BOO, though more work is needed.46

(i.e., with no catheter within the bladder lumen

7. Abnormalities of free flow pattern are seen in

to measure pressure). Penile cuff intermittent

a greater proportion of women subsequently

urethral compression32 is one approach and a

concluded to be obstructed on urodynamic

nomogram has been developed for the tech-

evaluation.47

nique.33 Similar noninvasive pressure measure-

ment can be derived from a modified condom

 

collecting device.34 Detrusor wall thickness is

Causes of Bladder Outlet

another parameter which may also indirectly

signify the presence of BOO.35,36

 

Obstruction

Diagnosis of BOO in women has not been

standardized and remains an area of ongoing

 

discussion.37 Proposals for urodynamic diagno-

Male

sis of BOO have been made as follows;

 

The additional anatomical structure of the male

1. Female BOO nomogram38; derived a nomo-

bladder outlet is the prostate gland, which

gram based on study of several hundred

encompasses the urethra between the genital

women defined as obstructed on clinical

and urethral sphincters. With aging, the gland

grounds, with quite a heterogeneous group of

undergoes benign prostate enlargement (BPE),

causative pathologies. The study estimated

which can typically be shown to be a conse-

the prevalence of female BOO at 6.5%. The

quence of benign prostate hyperplasia (BPH);

BPH can only be diagnosed where pathological

nomogram

employs

somewhat

different

specimens by biopsy or resection are available.48

parameters from the male BOOI, using the

The prevalence of BPH determined from autopsy

maximum

detrusor

pressure ascertained

studies shows that it does not occur below the

during invasive urodynamics and the maxi-

age of 30 years and that almost 90% of men have

mum flow rate on free flow testing.

 

developed BPH by their ninth decade.49 Likewise,

213

PathoPhysiology of lowEr Urinary tract obstrUction

Figure 16.3. Left panel; a urethroscopic view of the intrusion of the lateral lobes and median lobe of a benignly enlarged prostate gland. Right panel; urethroscopic view of a dense fibrotic urethral stricture.

there is a steady increase in both LUTS50 and

placebo, the alpha-blocker terazosin, the 5-alpha

BPE,51 and all three processes are clearly inter-

reductase inhibitor finasteride and combination

related with ageing in men.52

therapy, suggested that factors other than BOO

Implicitly, the intrusion of the prostate into

alone almost certainly contribute to LUTS in

the urethral lumen in BPE (Fig. 16.3) can be

BPH. Recent studies using botulinum injections

expected to provide a degree of anatomical

within the prostate suggest that afferent nerve

impedance to urine flow during voiding by

activity may also be an element of LUTS in

direct flow impedance, and by distortion of the

BPE.58 Furthermore, the persistence of LUTS

bladder outlet. Thus, flow rate does decline with

after effective surgical management of BPE21

ageing in a population of men with BPE.25 The

strongly suggests that age-related changes in

role of anatomical impedance to flow is sup-

bladder function contribute to male LUTS as a

ported clinically by the response to treatment

codependent variable alongside BPE.59 The

aimed at reducing male sex hormones, which

inherent difficulties of controlling for the range

reduces the trophic factors giving rise to BPH

of contributory variables means that the

and thereby can partly reverse the enlargement.

pathophysiology of male LUTS will remain a

Within the prostate, the conversion of andro-

source of considerable scientific debate for the

gens to dihydrotestosterone by 5-alpha reductase

foreseeable future.

is a means by which this can be achieved.53 A

Urethral strictures are another mechanism

second contribution to BOO in BPE is the active

giving rise to BOO in men. They comprise an

contraction of smooth muscle in the prostate

inelastic circumferential fibrous constriction

stroma. The smooth muscle of the prostate

(Fig. 16.3), and thereby differ from BPE in that

expresses alpha-adrenergic receptors, falling

there is not contribution of active muscle con-

into at least two subtypes in the human pros-

traction to the BOO. They can be present at any

tate.54 Clinically, alpha-adrenergic antagonists

point along the urethra; postsurgical bladder

relax prostate smooth muscle, indicating a con-

neck stenosis is a related situation. Strictures

tribution of functional prostate muscle activity

have comparatively little effect on lower urinary

in BOO.55 On this basis, alpha-adrenergic antag-

tract function until they cause significant con-

onists and hormonal therapy may respectively

striction of the lumen. Characteristically, the pat-

decrease BOO by relaxing or shrinking the pros-

tern of urine flow differs from that seen in BPE.

tate. These clinical observations support the

Strictures usually arise as a consequence of ure-

hypothesis that there are both dynamic and

thral trauma,which can be iatrogenic.Congenital

static components of BOO associated with BPE.

male urethral strictures have been described.

The Olmstead County Study of Urinary

Cobb’s collar is a congenital narrowing in the

Symptoms and Health Status56 studied 2,115

male urethral bulb of uncertain etiology.60

men between 40 and 79 years of age and showed

BPE and urethra stricture are by far the most

that the severity of LUTS, peak flow rate, and

common causes of BOO in men. Rare causes of

extent of prostate enlargement were all age-

obstruction in men include congenital urethral

dependent and interrelated. However, the

abnormalities,61,62 foreign bodies,63 uretero-

Veterans Affairs Cooperative Study57 comparing

coele,64 adult onset voiding dysfunction.65

214

Practical Urology: EssEntial PrinciPlEs and PracticE

Female

 

 

 

2.

BOO caused by stress incontinence surgery is

In women, several factors can contribute to BOO

 

symptomatic of

the conflicting roles of the

 

lower urinary tract in being responsible both

(Table 16.2), which consequently represents a

 

 

for urinary storage and intermittent expulsion

more diverse

situation

pathophysiologically

 

 

of the urine. In women with incontinence, the

than is the case in men. As discussed above,

 

 

need to improve urine storage surgically car-

this renders formal standardized diagnosis

 

 

ries an implicit risk that voiding may be

problematic.

 

 

 

 

1. Pelvic Organ Prolapse (POP). Deficiency of

 

impaired.For most women,voiding function is

 

satisfactorily preserved, but a minority do suf-

ligamentous support of the pelvic floor and

 

 

fer impaired voiding, taking the form of void-

weakness of the musculature results in pro-

 

 

ing symptoms, an increased post-void residual

lapse of pelvic and abdominal organs. Where

 

 

or acute urinary retention. This is recognized

the anterior vaginal compartment is affected,

 

 

for the main surgical options available, includ-

the altered configuration may distort the ure-

 

 

ing midurethral slings,74 other forms of sling75

thra, which can impair voiding.Where middle

 

and colposuspension,76 along with techniques

compartment prolapse to the level of the vag-

 

no longer in general use such as the Stamey

inal introitus is present, a direct compression

 

 

procedure77 and bone-anchored slings.78

 

effect on the urethra could also

occur.

3.

Functional causes; the lower urinary

tract

Obstructive voiding, LUTS, in general, and

 

musculature and the range of CNS structures

occult stress incontinence can all coexist.72

 

 

contributing

to

their regulation requires

Some women with prolapse find that voiding

 

 

coordinated activity to achieve normal func-

is impeded during the daytime, as a conse-

 

 

tion. Some women manifest voiding abnor-

quence of upright posture, and complain of

 

 

malities,

which

appear

to

derive

from

incontinence

overnight, when the

supine

 

 

excessive

activity, failure

of

relaxation, or

position reduces the

prolapse. The

precise

 

 

impaired coordination of some of these com-

effect can be hard to evaluate urodynami-

 

 

plex components. In part, this can derive

cally,73 since effects on voiding are dependent

 

 

from failure to acquire normal toileting hab-

on the patient’s position, which will affect the

 

 

its in childhood, or acquired in adulthood,65

anatomical relationship between the abnor-

 

leading

to

dysfunctional

voiding79

and

mally mobile structures and markedly influ-

 

“pseudo-dyssynergia.” Fowler’s syndrome is

ence their function.

 

 

 

 

 

 

an acute onset condition arising in adult

 

 

 

 

 

 

 

 

 

 

women, characterized by painless retention,

Table 16.2. causes of female bladder outlet obstruction

 

and diagnosed by high urethral closure pres-

 

sures and abnormal urethral sphincter EMG

Anatomical

 

Functional

 

 

 

 

 

activity 80 (Fig. 16.4).

 

 

 

 

 

 

 

 

 

 

 

gynecological; pelvic organ

bladder neck obstruction

prolapse, fibroids, lichen

 

sclerosus66

 

Postsurgical

Pseudodyssynergia

Urethral abnormalities,

fowler’s syndrome

such as diverticulum,67

 

stenosis68

 

Mass lesions such as

 

uterine fibroids,69 other

 

intra-abdominal

 

lesions70

 

Ureterocoele71

 

Neurourology

Impaired voiding function is common in patients with neurological disease, resulting from reduced bladder contractility (Fig. 16.4), BOO, or both. In lower motor neurone neurological lesions, BOO can be a consequence of pelvic floor denervation, leading to pelvic organ prolapse and urethral distortion. For upper motor neurone neurological lesions, the problem is one of failure of the urethral sphincter to relax appropriately at the time of voiding. This can