Porth's Essentials of Pathophysiology, 4e

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Kidney and Urinary Tract Function

U N I T 7

distention. This usually is accomplished through urinary catheterization. Long-term treatment is directed toward correcting the problem causing the obstruction.

Diverticulum

Cellulae

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

Benign prostatic hyperplasia

FIGURE 27-4. Destructive changes of the bladder wall with development of diverticulum caused by benign prostatic hyperplasia.

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

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 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 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 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 Increased filling and impaired sphincter control cause increased intravesicular pressure Bladder overfilling occurs owing to a loss of ability to perceive bladder filling

Stroke and advanced age

Basal ganglia or extrapyramidal tract

Parkinson disease

Pontine micturition center or communicating tracts in the spinal cord

Spinal cord injury

Sacral cord or nerve roots

Injury to sacral cord or spinal roots

Pelvic nerve

Radical pelvic surgery

Autonomic peripheral sensory pathways

Diabetic neuropathies, multiple sclerosis