Disorders of Micturition
World Small Animal Veterinary Association World Congress Proceedings, 2011
Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN
Department of Surgical & Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA, USA

Micturition refers to both storage and voiding of urine, whereas urination refers only to voiding. Urinary incontinence is the involuntary passage of urine. Micturition disorders may cause both urinary incontinence and urine retention.

Non-Neurologic Causes of Incontinence

Urinary incontinence in young animals may be congenital, whereas the condition usually is acquired in older animals. Congenital abnormalities resulting in urinary incontinence include ectopic ureters, patent urachus, female pseudohermaphroditism, rectovaginal fistula, and vestibulovaginal stenosis.

Neurologic Causes of Incontinence

Urinary incontinence often is associated with neurologic disease. Neurologic abnormalities may disrupt function of the detrusor muscle, urethral sphincters, or both.

The location of a lesion in the nervous system dictates the nature of a micturition disorder. Additional concurrent neurologic abnormalities may be present. Neurologic incontinence may result from trauma, tumors, or herniated intervertebral discs.

Patients with UMN lesions (those affecting the spinal cord cranial to sacral spinal cord segments) lack voluntary control of micturition. Urination may be initiated by segmental (spinal) reflexes, but an absence of sensory perception and central control, and the sphincters' failure to relax, lead to interrupted, involuntary, and incomplete voiding. Manual bladder expression is difficult if sphincter tone is increased, but the urethra may be catheterized normally. Overflow of urine occurs when the bladder pressure exceeds sphincter resistance. The perineal reflex is intact.

Detrusor areflexia with decreased sphincter tone is a result of disease of the sacral spinal cord or bilateral lesions of the sacral spinal nerve roots (called LMN lesions). Voluntary control of urination is absent. Tail paresis/paralysis and fecal incontinence may be present. The perineal reflex and bulbcavernosus reflexes are absent. The bladder is easily expressed, and dribbling of urine occurs when intravesicular pressure exceeds urethral pressure.

Detrusor areflexia also can occur secondary to prolonged overdistention of the bladder. Tight junctions between detrusor muscle cells are disrupted, preventing spread of nerve impulses. The animal will attempt to void because sensory pathways are intact, but the atonic, flaccid bladder is unable to contract. Residual urine volume is large.

Reflex dyssynergia occurs with incomplete spinal cord lesions cranial to the sacral spinal cord segments. The detrusor reflex is normal to hyperactive, and the urethral sphincters are hyperactive. The patient voluntarily initiates urination, but the urine stream is abruptly stopped because there is lack of synchronization between bladder contraction and urethral relaxation, leading to incomplete voiding. Urethral obstruction can result in a similar abnormal pattern of micturition.

Cerebral lesions may result in the loss of voluntary control of micturition. Detrusor hyperreflexia rarely results from cerebellar disease. Urinary incontinence due to bladder atony may occur in cats with autonomic polygangliopathy (feline dysautonomia). Concurrent reduced tear production, pupillary dilation, and regurgitation are present.

Diagnostic Approach to Disorders of Micturition

Important historical information that should be obtained includes the following:

 The animal's age when incontinence first appeared

 The chronologic course of events

 When the incontinence is typically observed (at rest or with activity)

 Whether the animal can urinate normally

 Previous surgeries (such as neutering) and illness

 Use of medications that might stimulate polyuria (glucocorticoids, diuretics, anticonvulsants) or affect bladder and urethral tone

 Previous or current urinary tract disease or abnormalities

A physical examination should include observation of urination to assess voluntary initiation, volume of urine voided, and the diameter and continuity of the urine stream. Bladder size and tone should be assessed before and after urination.

Large Bladder

 UMN disorders

 LMN disorders

 Reflex dyssynergia

 Outflow tract obstruction

Small or Normal Size Bladder

 Urethral sphincter incompetence

 Detrusor hyperrelexia

 Congenital abnormalities

Manual expression of the urinary bladder may aid in assessing urethral tone, although bladder expression in normal dogs of either gender may be difficult. The urethra may be palpated percutaneously in males and rectally in both sexes to identify urethral mass lesions. Passage of a urinary catheter will detect urethral obstruction. The volume of residual urine following voiding should be determined by catheterization. Normal residual volume following complete voiding is less than 0.2 to 0.4 ml/kg body weight. Territorial marking of male dogs makes it difficult to assess residual volume.

Following urination, the bladder should be palpated to assess bladder wall thickness or detect calculi or soft tissue masses. In male dogs, the prostate gland should be palpated rectally, abdominally, or by both methods. Urethral discharges should be compared with urine through gross examination, dipstick testing, and sediment examination. A complete neurologic examination should be performed if the incontinence is suspected to be neurogenic. The perineal reflex and bulbocavernosus reflex can be used to evaluate the sacral spinal cord segments and pudendal nerves. The perineal reflex is initiated by stimulating the perineum with a needle. The bulbocavernosus reflex is obtained by squeezing the penis or vulva. Both of these reflexes depend upon an intact pudendal nerve (sensory & motor) and intact sacral spinal cord segments. The response to both reflexes should be constriction of the anal sphincter muscle and flexion of the tail.

Laboratory evaluation should include a urinalysis and a CBC, which might reflect an infection that involves the kidneys. A serum chemistry analysis will assess the presence and magnitude of postrenal azotemia and hyperkalemia in patients with mechanical or functional urethral obstruction. If urinalysis results are consistent with urinary tract infection, urine culture and sensitivity testing are indicated. Survey and contrast radiography may be necessary to evaluate anatomic urinary tract abnormalities.

Additional diagnostic tests that can be performed at many referral institutions include cystometrography, measurement of urethral pressures, and urethral or anal sphincter electromyography and evoked responses. A cystometrogram evaluates bladder capacity, detrusor muscle tone, and the detrusor muscle reflex. Urethral pressure profiles record resting urethral pressures along the length of the urethra and will identify areas of reduced or excessive urethral tone. Electromyography of the urethra and anus aids in evaluation of partial denervation that can be difficult to assess during a neurologic exam. Spinal evoked responses evaluate sensory and motor pathways that mediate the detrusor reflex. Neurogenic abnormalities of micturition may be further evaluated using vertebral column radiography, myelography, computed tomography, magnetic resonance imaging, and cerebrospinal fluid analysis. Direct visualization of the urethra, bladder and vagina can be performed using a rigid cystoscope in female dogs and some cats.

Treatment of Urinary Incontinence

Specific treatment of an underlying disease may resolve incontinence; for example, surgery can be used to correct anatomic defects or remove obstructive calculi. Inappropriate urination due to behavioral problems may be corrected with training that modifies the pet's behavior.

Patients With Neuromuscular Dysfunction

These patients may benefit from temporary drug therapy that assists micturition until neuromuscular function is restored. Rational drug therapy depends on defining the micturition disorder since drugs are selected to produce a specific response (increase or decrease detrusor activity; increase or decrease the tone of the internal or external urethral sphincters). Patients with small bladder capacity due to detrusor hyperactivity may benefit from anticholinergic drugs or smooth muscle relaxants. Atropine is generally ineffective for this purpose and has a substantial risk of adverse effects. Detrusor atony is treated with cholinergic agents. Care must be taken to ensure urethral patency when using cholinergic agents. If the bladder were to contract against a urethral obstruction or in the presence of sphincter hypertonia, the result might be a ruptured bladder or urine reflux into the renal pelves that may result in pyelonephritis.

Patients with Decreased Urethral Tone

These patients are treated with drugs that stimulate sympathetic alpha receptors in the smooth muscle of the urethra. Patients with increased urethral tone are treated with sympathetic alpha-blocking agents or direct-acting smooth muscle relaxants to reduce activity of the internal urethral sphincter. These patients can also be given skeletal muscle relaxants to reduce activity of the external urethral sphincter. A combination of drugs may be required to alter the function of both the detrusor muscle and urethral sphincters. One example is the use of a cholinergic drug to increase detrusor activity and a sympathetic alpha-blocking agent to reduce urethral tone in patients with UMN lesions and sphincter hypertonia. Hormone-responsive incontinence in females or males often responds to administration of estrogen or testosterone, respectively. These patients may also respond to sympathetic alpha-stimulating drugs, and females may respond to a combination of estrogens and alpha-agonist drugs.

Drug doses often are "empirical", established by clinical observation or extrapolation from human medical data. Several dose ranges for the same drug from different references. Pharmacological manipulation of urination is often through trial and error. Drug doses on the lower end of the range should be used initially, and the doses should be raised in small increments until the response is adequate. Clinical response to some drugs such as phenoxybenzamine may be slow, taking a week or longer. As long as there are no undesirable side effects, a drug trial should continue for several weeks before the drug is considered ineffective.

The duration of drug therapy is determined by the reversibility or irreversibility of the disease causing the micturition disorder. When long-term pharmacologic manipulation is necessary, the lowest dose and the least frequent dosing interval needed to achieve the desired response should be used. Patients should be monitored closely for adverse side effects, some of which may be life-threatening if not recognized early (profound hypotension subsequent to the administration of sympathetic alpha-blocking agents).

Patients with distended bladders often require expression of the bladder or catheterization in addition to drug therapy. Urinary tract infections occur frequently in patients that cannot completely empty their bladders. Infections should be identified and treated appropriately based on the results of culture and sensitivity tests.

Drugs Affecting the Urinary System

Drugs used to treat neurologically caused urinary incontinence:

 Cholinergic agonists treat animals with damage to the nerves that control relaxation of the urinary bladder

 Promote voiding of urine from the urinary bladder

 An example is bethanechol

 Anticholinergics treat urinary incontinence by promoting urine retention in the urinary bladder

 Block binding of ACh to its receptor site, causing muscle relaxation

 Examples include propantheline, dicyclomine, and butylhyoscine

 Alpha-adrenergic antagonists decrease the tone of internal urethral sphincters and are used to treat urinary incontinence due to decreased urinary tone as a result of over-distention of the urinary bladder

 Examples include phenoxybenzamine, prazosin, and nicergoline

Drugs used to treat non-neurologically caused urinary incontinence:

 Estrogen treats hormone-responsive urinary incontinence seen mainly in F/S dogs. An example is diethylstilbestrol (DES)

 Testosterone treats hormone-responsive urinary incontinence seen mainly in M/C dogs. Examples include testosterone cypionate and testosterone propionate

 Alpha- and beta-adrenergic agonists stimulate these receptors, which increases urethral tone; examples include phenylpropanolamine and ephedrine

 Skeletal muscle relaxants treat urge incontinence or urethral obstructions due to increased external urethral sphincter tone; examples include dantrolene, aminopropazine, and diazepam

Desired effect


Mechanism of action

Stimulate detrusor activity

Bethanechol (Urecholine)

Cholinergic stimulation

Reduce detrusor activity

Propantheline (Pro- Banthine)

Anticholinergic, antispasmodic effect on smooth muscle



Direct antispasmodic effect on smooth muscle, anticholinergic

Increase urethral tone


Alpha-adrenergic stimulation



Alpha-adrenergic stimulation



Alpha- and beta- adrenergic stimulation

Reduce urethral tone


Alpha-adrenergic antagonism


Diazepam (Valium)

Central-acting skeletal muscle relaxation



Skeletal muscle relaxation



Direct-acting skeletal muscle relaxation


Speaker Information
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Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN
Department of Surgical & Radiological Sciences, School of Veterinary Medicine
University of California
Davis, CA, USA

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