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Disorders of Micturition in Small Animals

By Scott A. Brown, VMD, PhD, DACVIM, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia

Disorders of micturition result from a dysfunction in the storage or voiding of urine and may be neurogenic or non-neurogenic in origin. Urinary incontinence is the failure of voluntary control of micturition, with constant or intermittent unconscious passage of urine. Incontinent animals may leave a pool of urine where they have been lying or may dribble urine while walking. The coat around the vulva or prepuce may be wet, and perivulvar or peripreputial dermatitis can result from urine scalding.

Failure of urine storage is characterized by inappropriate leakage of urine due to failure of bladder relaxation, urethral incompetence, anatomic defects, or overflow of stored urine. Urge incontinence is seen with detrusor irritability, usually associated with cystitis. The most common non-neurogenic incontinence is attributed to deficiency of sex hormones in neutered animals, particularly female dogs, and is referred to as hormonal-responsive urethral incompetence. Idiopathic urethral sphincter incompetence also is seen. Urinary incontinence associated with anatomic defects may be detected in animals at an early age. For example, an animal with a unilateral congenital ectopic ureter may void normally but “dribble” urine intermittently, whereas animals with bilateral ectopic ureters are less likely to void normally. Paradoxical urinary incontinence may develop when there is a partial obstruction of the urethra leading to bladder distention and overflow incontinence.

Failure of normal voiding is characterized by frequent attempts to urinate with stranguria and passage of only small amounts of urine. Inability to urinate can be due to mechanical obstruction of the urethra by calculi, neoplasms, or strictures; detrusor atony from overdistention of the bladder; or neurologic disease. Animals with abnormalities of the voiding phase may develop overflow incontinence due to dribbling of urine associated with bladder overdistention.

Neurologic causes of micturition disorders can be categorized as upper (UMN) or lower motor neuron (LMN) lesions. Lesions in the sacral spinal cord, pelvic nerve, and detrusor atony lead to LMN signs, which are often characterized by a distended, easily expressed bladder. Dysautonomia in cats is a multisystemic disease characterized by widespread disruption of autonomic system functions, including urinary incontinence of LMN origin. Damage to the thoracolumbar spinal cord or disease of the cerebrum, cerebellum, or brain stem can lead to UMN signs, characterized by a distended bladder that is difficult to express. Another neurologic cause of inability to urinate is functional obstruction (detrusor-sphincter reflex dyssynergia), which occurs when there is incoordination of the normal micturition reflex; this is believed to result from overdischarge of sympathetic nerve impulses to the urethral sphincter, resulting in a failure of urethral relaxation during detrusor contraction. Animals with neurogenic incontinence may leak urine (LMN) and/or develop overflow incontinence due to dribbling of urine associated with bladder overdistension (any neurogenic cause).

Diagnosis:

Clinical signs are usually suggestive of a micturition disorder. The history should include age of onset, whether the animal is intact or neutered, age at neutering, current medication, and history of previous urinary tract disorders. A thorough physical and neurologic examination is indicated, and the act of voiding should be observed, including estimation of initial and final bladder volume.

Animals with LMN lesions or an atonic bladder have a large, distended bladder that can be expressed with minimal pressure. Animals with mechanical or functional obstruction or with spinal lesions causing UMN signs also have a large distended bladder, but urine cannot be readily expressed. Caution must be exercised when attempting to express urine from these animals to avoid rupturing the bladder. Plain or contrast radiography, cystoscopy, or ultrasonography are necessary to determine the type and location of mechanical obstruction.

Animals with functional obstruction (reflex dyssynergia) generally exhibit pollakiuria with interrupted urine stream, distended urinary bladder, no identifiable structural cause of obstruction, and overflow incontinence; the neurologic examination is generally abnormal. A catheter can easily be passed into the bladder in animals with functional obstruction but will not pass in animals with mechanical obstruction.

Treatment:

Accurate diagnosis or localization of the lesion is essential for appropriate pharmacologic management. Animals with hormonal incontinence can be treated with the appropriate sex hormone (eg, diethylstilbestrol in females and testosterone in males). The dosage should be adjusted to the minimum required to maintain continence. Diethylstilbestrol may be difficult to obtain. Alternatively, an α-adrenergic agonist drug (eg, phenylpropanolamine, 2–4 mg/kg/day in divided doses) can be given to animals with urethral incompetence alone or in combination with an estrogenic compound. Although ephedrine is another α-agonist shown to be effective in the treatment of urinary incontinence in female dogs, its use is more often associated with adverse effects of anxiety and excitability. Pseudoephedrine is apparently not effective for this purpose. Urge incontinence (detrusor instability) is treated with anticholinergic drugs such as oxybutin chloride (0.5 mg/kg/day, PO) or propantheline (dogs <20 kg, 7.5 mg/day; dogs >20 kg, 15 mg/day; cats, 7.5 mg every 72 hr). Cholinergic drugs such as bethanechol are used in animals with detrusor atony. Functional obstruction is treated with sympatholytic drugs (eg, phenoxybenzamine, 2.5–10 mg, 1–3 times/day); cholinergic drugs may also be necessary.

Complete mechanical obstruction of the urethra is a medical emergency and should be relieved by catheterization and retropulsion of the obstructing material into the bladder or by surgery. Animals with detrusor atony from overdistention but without neurologic lesions benefit from decompression of the bladder by placement of an indwelling urinary catheter for 3–7 days. This may be done continuously or intermittently. Those with neurogenic atony, which usually does not respond to medical management, may require manual expression of the bladder or catheterization several times daily.