16
Pathophysiology of Lower Urinary Tract
Obstruction
Marcus J. Drake and Ahmed M. Shaban
Introduction
Lower urinary tract obstruction signifies impedance of urine expulsion. It can give rise to symptoms, though some people who appear to have outlet obstruction do not complain of any symptomatic problem. Classically associated with benign prostate enlargement in men,obstruction is being increasingly recognized in women, and there is ongoing debate on how to diagnose the problem.In particular,symptoms similar to those of obstruction can derive from reduced expulsive ability associated with impaired bladder contractility, and the latter complicates the objective evaluation of outlet function. Mechanisms of obstruction can be either anatomical or functional, and the fundamental role of the central nervous system in regulating the phases of the micturition cycle and ensuring the synergic activity of the lower urinary tract means outlet obstruction in neurological disease is an important consideration.
The Normal Lower Urinary Tract
Anatomy
The lower urinary tract comprises the bladder and the bladder outlet. The bladder serves as the urine reservoir for storage and the expulsive organ for voiding. The muscle of the bladder wall is the detrusor, and the bladder lumen is
lined by functionally active urothelium, subjacent to which is a dense plexus of nerves and interstitial cells.
The bladder outlet comprises the urethra and urethral sphincters; it is anatomically complex and is different for men and women. In men, the urethra is of greater length and is subdivided into membranous, bulbar, and pendulous parts. At the start of the male urethra, the bladder neck serves as a genital sphincter, constricting at the time of seminal emission and ejaculation to ensure semen is propelled without passing retrogradely into the bladder. Just distal to the male bladder neck is the prostate, a secretory organ, which houses the ends of the ejaculatory ducts. The urethral sphincters are located just distal to the apex of the prostate, at the level of the pelvic floor. In women, the urethra is comparatively short (2–3 cm), and the bladder neck is anatomically poorly defined, probably serving no major functional role for continence. The urethral sphincters lie at the level of the pelvic floor, approximately at the midpoint of the urethra.
For both genders, the urethral sphincter comprises smooth muscle (leiosphincter), which provides the background continuous contraction, and an external skeletal muscle component (rhabdosphincter), for voluntary and reflex increases in urethral closure.The muscular component is distributed asymmetrically.1 In women, supportive anchoring to the pelvic floor and ligaments is a key aspect for normal function,2 along with a firm “back-plate0065” for urethral compression.3,4
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DOI: 10.1007/978-1-84882-034-0_16, © Springer-Verlag London Limited 2011 |
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Storage Function |
throughout the muscle, which binds to muscar- |
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inic receptors.13 In addition, intrinsic cellular |
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Urinary storage is dependent on relaxation of |
structures may provide the sustained contr- |
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the bladder to maximize reservoir capacity, |
action that maintains voiding until bladder |
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combined with simultaneous closure of the out- |
emptying is complete.14 Synchronously, outlet |
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let. The detrusor has some specific properties |
relaxation permits the easy flow of urine along |
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that allow it to elongate substantially without |
the urethra, with the peripheral nerves crucial |
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generating force during storage5; in addition, |
in ensuring active relaxation of the smooth |
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the muscle is inhibited by the sympathetic ner- |
muscle components of the outlet.15,16 |
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vous system. |
Voiding can be evaluated urodynamically, by |
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The nature of the sphincter activity can be |
simultaneously recording pressure within the |
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demonstrated by urethral pressure profilometry, |
bladder, the abdomen, and the urinary flow rate. |
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in which a catheter is drawn along the urethra, |
Subtraction of abdominal pressure allows esti- |
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while measuring the pressure needed to keep |
mation of the component of the bladder pres- |
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continuous perfusion of saline through holes in |
sure that is due to active detrusor contraction. |
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the side of the catheter.6 This technique provides |
In men, this detrusor pressure shows a clear |
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an indication of tonic background contraction, |
increase at the time of voiding (Fig. 16.1); the |
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additional superimposed voluntary contraction |
pressure rise is less clearly apparent in women, |
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and the tone of the non-sphincteric parts of the |
because the overall lower outlet resistance |
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urethra. |
results in pressure dissipation (Fig. 16.2). |
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In men, circular constriction by sphincter |
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activity is crucial for continence. In addition, the |
Neural Control |
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bladder neck is kept closed by sympathetic |
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innervation, acting through alpha-1 adrenergic |
The central nervous system (CNS) is responsible |
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receptors.7 Furthermore, tonic urethral contrac- |
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tion, sustained by intrinsic urethral cellular |
for regulating lower urinary tract function, |
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imposing several crucial properties which define |
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mechanisms,8 means that the greater length of |
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the male urethra renders men less prone to uri- |
normal function; |
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nary incontinence. Finally, the prostate provides |
1. During urine storage, activity in Onuf’s nuc- |
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both active (contractile) and passive (elastic) |
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leus in the ventral horn of the sacral part of |
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contributions to outlet resistance, which are |
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the spinal cord maintains outlet closure. |
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affected by ongoing prostate growth.9 None- |
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theless, while the bladder neck, prostate, and |
2. During urine storage, the sympathetic neu- |
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rones in the intermediolateral horn of the |
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urethra provide some additional outlet closure, |
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their removal by standard prostate surgery does |
thoracolumbar spinal cord inhibit detrusor |
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not normally result in incontinence. |
activity and maintain bladder neck closure. |
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In women, sphincteric contraction serves |
3. The pontine part of the brainstem (“pontine |
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both to elongate the urethra10 and to “kink” it.11 |
micturition center”) and parts of the mid- |
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Additionally, the closure of the urethra is main- |
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brain ensure the synergic function of the |
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tained by coaptation of the lining urothelium. |
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bladder outlet and detrusor, such that only |
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Overall, continence is maintained by numerous |
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one element is actively contracting at any |
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factors.12 |
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given moment. During voiding, the PMC |
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actively relaxes the outlet by inhibition of |
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Voiding Function |
Onuf’s nucleus, while the parasympathetic |
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Voiding represents a reversal of the bladder and |
neurones in the intermediolateral horn of the |
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sacral spinal cord are activated to drive detru- |
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outlet roles from that during storage, with global |
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sor contraction. |
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contraction of the detrusor muscle providing |
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4. The frontal cortex allows volitional control, |
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expulsive pressure, and synchronous outlet |
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so an individual has executive control on |
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relaxation to permit flow. Detrusor contraction |
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timing of micturition, which is thereby pos- |
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is achieved by widespread release of acetylcho- |
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line from the parasympathetic nerves ramifying |
sible regardless of extent of bladder filling. |
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PathoPhysiology of lowEr Urinary tract obstrUction
Figure 16.1. Male voiding cystometrogram; simultaneous pressure recordings have been made from a catheter in the rectum (red line) as a measure of abdominal pressure, and another catheter in the bladder (blue line). since the bladder is an intraabdominal organ, abdominal pressure change is visible in the bladder; subtracting the abdominal pressure allows the investigator to see when the bladder itself is contracting, which is plotted as the “subtracted detrusor pressure” (green line). flow rate is shown in black.the top panel shows a normal male; at the time
5.Additional CNS functions include sensory awareness of bladder filling, emotional aspects, and coordination with other vegetative functions such as bowel opening and blood pressure
100 Pves
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177 Ÿ
0 cm H20
100 Pabd
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179 Ÿ
0 cm H20
100 Pdet
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149 Ÿ
0 cm H20
25 Flow
0
15 Ÿ
0 mL/s
600 VH20
140 Pves
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593 Ÿ
0 cm H20
100 Pabd
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142 Ÿ
0 cm H20
140 Pdet
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563 Ÿ
0 cm H20
25 Flow
0
4Ÿ
0 mL/s
600 VH20
of the maximum flow of 14.6 ml/s, the subtracted detrusor pressure is 43.4. from the equation PdetQmax − 2Qmax, this gives a booi of 14.2; anything below 20 is defined as not obstructed. in the lower panel, the study is of a man with bladder outlet obstruction.
PdetQmax is 122, and Qmax is 2.5, giving a booi of 117; anything above 40 is taken as unequivocally obstructed. this man is also
straining in an attempt to improve his flow rate, shown by the simultaneous intermittent increases in both abdominal and bladder pressure during the time of urine flow.
Diagnosing Bladder Outlet
Obstruction
Symptoms
The complexity of CNS control means that lower urinary tract dysfunction is a common consequence of clinical neurological disease.
Bladder outlet obstruction (BOO) represents a problem whereby some impedance, whether functional or anatomical, prevents the free flow
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Figure 16.2. female voiding cystometrogram; both women in this figure have previously had stress incontinence surgery. in the top trace, a lady who previously had had a colposuspension; the urine flow rate is fairly good (Qmax 12.2 ml/s), and associated increase in detrusor pressure to achieve this is very small (which
of urine from the bladder. This may be asymptomatic if the detrusor contractility increases the pressure of expulsion. Nonetheless, in many patients there will be lower urinary tract symptoms (LUTS),including“voiding symptoms”experienced during voiding, and post-micturition symptoms immediately afterward (Table 16.1). A combination of BOO and reduced contractility can result in a post-void residual and chronic urinary retention. Ultimately, complete inability to void can arise from severe BOO, culminating as acute urinary retention – a painful bladder distension which presents as an emergency to
is common in women). in the lower panel, from a lady with outlet obstruction after tVt, there is a greater increase in detrusor pressure,flow fails to start for some time,flow is intermittent,and the patient is straining. there was a significant post-void residual in the tVt patient, and no residual in the colposuspension patient.
relieve the obstruction. Any of the symptoms listed in Table 16.1 suggests the possibility of BOO. However, very similar symptoms arise in people with reduced bladder contractility; thus, symptoms alone are inadequate for diagnosing BOO.19 A complicating factor is the high prevalence of storage phase symptoms in people with BOO. It is unclear whether BOO gives rise to secondary bladder changes predisposing to storage LUTS. Certainly, BOO in the experimental setting leads to detrusor hypertrophy and abnormal detrusor contractions during bladder filling.20 However, in the clinical setting, the relationship