Porth's Essentials of Pathophysiology, 4e

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Disorders of the Bladder and Lower Urinary Tract

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in the sacral cord (see Fig. 27-3). As a result, bladder function is regulated by segmental reflexes, without control from higher brain centers. The degree of blad- der spasticity and dysfunction depends on the level and extent of neural dysfunction. Usually, both the ANS neurons controlling bladder function and the somatic neurons controlling the function of the striated muscles in the external sphincter are affected. The most common causes of neurogenic detrusor overactivity are spinal cord lesions such as spinal cord injury, vascular lesions, tumors, or herniated intervertebral disk, and multiple sclerosis. Bladder Dysfunction Caused by Spinal Cord Injury. Bladder dysfunction is a common problem in persons with spinal cord injury (see Chapter 36). The immediate and early effects of spinal cord injury on bladder func- tion are quite different from those that follow recovery from the initial injury. 7,13 During the period immedi- ately after spinal cord injury, a state of spinal shock develops in which all reflexes, including the micturi- tion reflex, are depressed. During this stage, the bladder becomes atonic and cannot contract. Catheterization is necessary to prevent injury to urinary structures associ- ated with overdistention of the bladder. Depression of reflexes lasts from a few weeks to 6 months (usually 2 to 3 months), after which the spinal reflexes return and become hyperactive. After the acute stage of spinal cord injury, the mictu- rition response changes to a segmental reflex. Because the sacral reflex arc remains intact, stimuli generated by bladder stretch receptors during filling produce frequent spontaneous contractions of the detrusor muscle. This creates a small, hyperactive bladder subject to high-pres- sure and short-duration uninhibited bladder contrac- tions. Voiding is interrupted, involuntary, or incomplete. Dilation of the internal sphincter and spasticity of the external sphincter and perineal muscles occurs, produc- ing resistance to bladder emptying. Overdistention of the bladder with hypertrophy of the trigone area devel- ops, often leading to vesicoureteral reflux and risk for renal damage. Overactive bladder due to spinal cord injuries at the cervical level is often accompanied by a condition known as autonomic hyperreflexia (see Chapter 36). Because the injury interrupts CNS control of sympathetic reflexes in the spinal cord, severe hypertension, bradycardia, and sweating can be triggered by even mild overdistention of the bladder or by insertion of a catheter. Uninhibited Neurogenic Bladder. A mild form of reflex neurogenic bladder, sometimes called uninhibited bladder , can develop after a stroke, during the early stages of multiple sclerosis, or as a result of lesions located in the inhibitory centers of the cortex or associ- ated structures. 13 With this type of disorder, sacral reflex motor function and sensation are retained, the urine stream is normal, and there is no residual urine. There usually is reduced awareness of bladder fullness and a low bladder capacity due to reduced inhibition by the pontine micturition center or cortical centers.

Detrusor–Sphincter Dyssynergia. Lesions that affect the micturition center in the pons or impair communi- cation between the micturition center and spinal cord centers interrupt the coordinated activity of the detru- sor muscle and the external sphincter. 13 This is called detrusor – sphincter dyssynergia . Instead of relaxing dur- ing micturition, the external sphincter becomes more constricted. This condition can lead to elevated intraves- ical pressures, vesicoureteral reflux, and kidney damage. Detrusor muscle areflexia, or flaccid neurogenic bladder, occurs when there is injury to nerves in the micturition center of the sacral cord, the cauda equina, or periph- eral nerves that supply the bladder. Atony of the detru- sor muscle and loss of the perception of bladder fullness permit overstretching of the detrusor muscle; which in turn, leads to weak and ineffective bladder contrac- tions. External sphincter tone and perineal muscle tone are diminished. Voluntary urination does not occur, but fairly efficient emptying usually can be achieved by increasing the intra-abdominal pressure or applying manual suprapubic pressure. Among the causes of are- flexic neurogenic bladder are trauma, tumors, and con- genital anomalies (e.g., spina bifida, meningomyelocele). Bladder Dysfunction Caused by Peripheral Neuropathies. Disorders of the peripheral (pelvic, pudendal, and hypogastric) nerves that supply the muscles of micturition can selectively interrupt sensory or motor pathways for the bladder or involve both pathways. Bladder atony with dysfunction is a frequent com- plication of diabetes mellitus. 14,15 The disorder ini- tially affects the sensory nerves of the bladder without involvement of the pudendal nerve. This leads to large residual volumes after micturition, sometimes compli- cated by infection. There frequently is a need for strain- ing, accompanied by hesitation, weakness of the urinary stream, dribbling, and a sensation of incomplete bladder emptying. 15 The most common complications are vesi- coureteral reflux and ascending urinary tract infection. Because persons with diabetes are already at risk for development of kidney disease, urinary stasis and reflux can have serious effects on renal function. Nonrelaxing External Sphincter Another condition that affects micturition and bladder function is the nonrelaxing external sphincter. This con- dition usually is related to a delay in maturation, devel- opmental regression, psychomotor disorders, or locally irritative lesions. Inadequate relaxation of the external sphincter can also result from anxiety or depression. Any local irritation, including vaginitis or perineal irri- tation, can produce spasms of the sphincter through afferent sensory input from the pudendal nerve. In men, chronic prostatitis contributes to impaired relaxation of the external sphincter. Neurogenic Areflexic Bladder: Failure to Empty Urine