662
U N I T 7
Kidney and Urinary Tract Function
as burning on urination and cloudy urine. With progres-
sive decompensation, the bladder may become severely
overstretched, with a residual urine volume of 1000 to
3000 mL.
10
At this point, it loses its power of contrac-
tion and overflow incontinence occurs.
The immediate treatment of lower urinary tract
obstruction and stasis is directed toward relief of bladder
distention. This usually is accomplished through urinary
catheterization. Long-term treatment is directed toward
correcting the problem causing the obstruction.
Neurogenic Bladder Disorders
The urinary bladder is unique in that it is probably the
only autonomically innervated visceral organ that is
under CNS control. The neural control of bladder func-
tion can be interrupted at any level. It can be interrupted
at the level of the peripheral nerves that innervate the
bladder, the sacral cord reflex center, the ascending and
descending tracts in the spinal cord, the pontine mictu-
rition center, or the cortical centers that are involved in
voluntary control of micturition
7,11,12
(see Fig. 27-3).
Neurogenic disorders of bladder function commonly
are manifested in one of two ways: bladder overactivity
with a failure to relax and store urine; or areflexic blad-
der dysfunction, with a failure to contract and empty.
Neurogenic detrusor overactivity usually results from
neural lesions located above the level of the sacral mictu-
rition reflexes; in contrast, failure to contract (areflexic
bladder dysfunction) results from lesions at the level of
the sacral micturition center or the peripheral nerves
that innervate the bladder. Less commonly, disorders of
micturition occur when the neural control of external
sphincter function is disrupted. Table 27-2 describes the
characteristics of neurogenic bladder according to the
level of the lesion.
Neurogenic Overactive Bladder: Failure to
Store Urine
Neurogenic detrusor overactivity, or spastic bladder,
is usually characterized by reflex bladder spasms and
a decrease in bladder volume. It commonly is caused
by conditions that produce partial or extensive neural
damage above the level of the micturition reflex center
Diverticulum
Cellulae
Benign
prostatic
hyperplasia
FIGURE 27-4.
Destructive changes of the bladder wall with
development of diverticulum caused by benign prostatic
hyperplasia.
TABLE 27-2
Types and Characteristics of Neurogenic Bladder
Level of Lesion
Change in Bladder Function
Common Causes
Sensory cortex, motor cortex,
or corticospinal tract
Loss of ability to perceive bladder filling; low-volume,
physiologically normal micturition that occurs suddenly and is
difficult to inhibit
Stroke and advanced age
Basal ganglia or
extrapyramidal tract
Detrusor contractions are elicited suddenly without warning
and are difficult to control; bladder contraction is shorter than
normal and does not produce full bladder emptying
Parkinson disease
Pontine micturition center or
communicating tracts in the
spinal cord
Storage reflexes are provoked during filling, and external
sphincter responses are heightened; uninhibited bladder
contractions occur at a lower volume than normal and do not
continue until the bladder is emptied; antagonistic activity
occurs between the detrusor muscle and the external sphincter
Spinal cord injury
Sacral cord or nerve roots
Areflexic bladder fills but does not contract; loss of external
sphincter tone occurs when the lesion affects the
α
-adrenergic
motor neurons or pudendal nerve
Injury to sacral cord or
spinal roots
Pelvic nerve
Increased filling and impaired sphincter control cause increased
intravesicular pressure
Radical pelvic surgery
Autonomic peripheral sensory
pathways
Bladder overfilling occurs owing to a loss of ability to perceive
bladder filling
Diabetic neuropathies,
multiple sclerosis
