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 include both urinary incontinence and urine retention.

Anatomy and physiology of the lower urinary tract

To maintain urinary continence, the ureters must empty into the urinary bladder in the correct location, the bladder must expand to accommodate increasing volumes of urine, the urethra must exert tone greater than the resting pressure within the bladder, and neurologic pathways to and from the bladder and urethra must be intact. For normal urination to occur, the bladder must be able to contract, contraction must be coordinated with urethral sphincter relaxation, and neurologic pathways must be intact.

The urinary bladder is composed of smooth muscle collectively referred to as the detrusor muscle. Smooth muscle of the urethra is contiguous with the detrusor muscle and is referred to as the internal urethral sphincter, although it is not a true anatomic sphincter. Skeletal muscle surrounding the urethra is called the external urethral sphincter.

Innervation of the lower urinary tract is complex. Tight junctions between bladder smooth muscle cells allow for transmission of nerve impulses from cell to cell. The hypogastric nerve, originating from spinal cord segments of L1 through L4, supplies sympathetic innervation to the bladder and urethra. The pelvic nerve, originating from the spinal cord segments S1 through S3, supplies parasympathetic (cholinergic) innervation to the detrusor muscle and transmits sensory impulses from the bladder. Somatic innervation of the muscle of the external urethral sphincter is distributed via the pudendal nerve, originating from spinal cord segments S1 through S3. The pudendal nerve also innervates muscles of the anal sphincter and perineal region.

The storage phase of micturition is primarily controlled by the sympathetic and somatic nervous systems. Sympathetic stimulation of beta receptors in the detrusor muscle results in bladder relaxation to allow the bladder to fill. Sympathetic stimulation of alpha receptors in the neck of the bladder and internal urethral sphincter maintains continence. Sympathetic pathways also inhibit parasympathetic bladder innervation during storage. Stimulation of the pudendal nerve results in increased tone of the external urethral sphincter, contributing to continence. When the bladder is filled with urine, sensation is transmitted via the pelvic nerve to the sacral spinal cord, and subsequently to the brainstem. Voluntary control of urination originates from the cerebral cortex.

During the emptying phase of micturition, parasympathetic (cholinergic) stimulation of the detrusor muscle results in bladder contraction. Inhibition of sympathetic and somatic stimulation of the urethral smooth and skeletal muscle results in urethral relaxation. Following complete emptying of the bladder or voluntary cessation of urination, the storage phase begins again. External urethral sphincter tone can increase in response to sudden increases in abdominal pressure (during coughing or barking) to maintain continence.

Disruption of tight junctions between cells, peripheral nerves, spinal cord segments, or higher brain centers may alter micturition.

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Terms used to describe urinary incontinence

Overflow incontinence: A type of neurologic incontinence. Detrusor muscle function is abnormal or absent. The bladder fills until bladder pressure exceeds urethral resistance, and then urine is voided. This occurs at low pressures when the urethral sphincter tone is decreased (LMN) and at high bladder pressures when sphincter tone is increased (UMN).

Paradoxical incontinence: Occurs with mechanical or functional urethral obstruction. When bladder pressure exceeds pressure at the site of obstruction, urine leaks past the obstruction.

Stress incontinence: Leakage of urine when intra-abdominal pressure is increased. This occurs without detrusor contraction and is caused by an abnormally weak urethral sphincter.

Urge incontinence: Frequent, uncontrollable, involuntary voiding of urine associated with inflammatory lesions of the bladder or urethra, or with reduced bladder capacity.

Urethral sphincter incompetence: Decreased urethral sphincter tone leading to stress incontinence, urine leakage at rest, or urine leakage with activity. Hormone-responsive incontinence is one type of urethral sphincter incompetence.

Hormone-responsive incontinence: Occurs in neutered dogs and cats a variable length of time after neutering. Urine leakage occurs while at rest. Voluntary control is present when the animal is awake.

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Nonneurologic causes of incontinence

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

The most common congenital anomaly of the urinary tract is ectopic ureters. Siberian Huskies, Miniature Poodles, Labrador Retrievers, Collies, Welsh Corgies, Wire-haired Fox Terriers, and West Highland White Terriers have a higher prevalence of this abnormality than do other breeds. Although recognized primarily in female dogs, male dogs and cats of both sexes can be affected. The condition is rare in the cat, with a higher prevalence in males. If the condition is unilateral, the animal can urinate normally in addition to dribbling urine. If both ureters bypass the bladder, the animal may only dribble urine and not be able to urinate normally. The diagnosis of ectopic ureters may be made with contrast urography, contrast vaginourethrography, or direct visualization using cystoscopy/ vaginoscopy. Surgical correction can be curative, or the animal may remain incontinent despite surgery because of the presence of other anatomic congenital abnormalities of the lower urinary tract.

Animals that submissively urinate may present with the complaint of incontinence. Submissive urination occurs more frequently in young animals, but the problem may continue into adulthood. The animals can urinate normally. This is a behavioral trait rather than a problem of the urinary tract.

Several acquired disorders of the urinary tract can result in incontinence. Chronic cystitis resulting in fibrosis, partial cystectomy, or postsurgical adhesions to the bladder can reduce bladder capacity, resulting in urge incontinence. A frequent, uncontrollable desire to void may be confused with urethral incontinence. Severe urethral inflammation can decrease sphincter tone and result in incontinence. Urethral calculi or luminal or extraluminal masses can interfere with normal urination and cause incontinence when intravesicular pressure exceeds urethral pressure at the site of the obstruction. This is called paradoxical incontinence.

Reproductive-hormone-responsive incontinence occurs in neutered dogs of both sexes and spayed female cats. The animals can urinate normally, but they passively leak urine while resting. Physical, neurologic, and laboratory evaluations are generally normal. The definitive cause of hormone-responsive incontinence is uncertain. One theory is that testosterone or estrogen contributes to the maintenance of urethral muscle tone and function of the mucosal epithelium.

Dogs with prostatitis may develop concurrent infection of the lower urinary tract that may result in incontinence if inflammation is chronic or severe. Urethral discharge may be observed in patients with prostatic disease and an owner may incorrectly identify the discharge as urine. Prostatic disease infrequently results in obstruction to urine flow and when obstruction is present, the prostatic disease is usually neoplastic. Iatrogenic incontinence can occur following prostatectomy due to neurologic damage.

Polyuria can contribute to the development of urinary incontinence. If urethral sphincter tone or bladder capacity are reduced, incontinence may develop because of an inability to retain increased volumes of urine. The causes of polyuria are numerous.

Some dogs with the neck of the bladder positioned caudal to the pubis on radiographic examination (pelvic bladder) have been noted to have urinary incontinence. This can be either a congenital disorder or an acquired disorder. The relationship between a pelvic bladder and incontinence is speculative since pelvic bladders may be present in continent dogs as well.

Intermittent incontinence, primarily at rest, has been reported in FeLV-positive cats of both sexes. Concurrent anisocoria may be present. The association between FeLV and incontinence is uncertain. Speculated mechanisms of incontinence include urethral incompetence or virus-related detrusor muscle hyperactivity.

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Neurologic causes of incontinence

Urinary incontinence is often associated with neurologic disease. Neurologic abnormalities may disrupt function of the detrusor muscle, urethral sphincters, or both. Neurologic incontinence may result from trauma, tumors, or herniated intervertebral discs. The location of the lesion will dictate the type of micturition disorder and other concurrent neurologic abnormalities. Upper motor neuron (UMN) lesions are those above the sacral spinal cord segments (L5 in the dog and L7 in the cat); lower motor neuron (LMN) lesions involve the sacral segments.

Patients with UMN lesions lack voluntary control of micturition. Urination may be initiated by spinal reflexes, but an absence of sensation 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 can 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 (LMN lesions). Voluntary control of urination is absent. Tail paralysis and fecal incontinence may be present. The perineal reflex and bulbospongiosus reflexes are absent. The bladder is easily expressed, and dribbling of urine occurs when intravesicular pressure exceeds urethral pressure.

Detrusor areflexia can occur secondary to prolonged overdistention of the bladder. Tight junctions between 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 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 rear production, pupillary dilation, and regurgitation are present.

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A diagnostic approach to the incontinent patient

Important historical information that should be obtained:

• 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 can be difficult. The urethra can 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 make it difficult to assess residual volume.

Following urination, the bladder should be palpated to asses 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 which 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 asses 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 skill or spinal 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.

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Treating the incontinent patient

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 may benefit from temporary drug therapy that assists micturition until neuromuscular functions are 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 side 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 which can result in pyelonephritis.

Patients with decreased urethral tone are treated with drugs that stimulate sympathetic alpha receptors in the smooth muscle of the urethra. Patients with increase 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 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 are often empirical, established by clinical observation or extrapolation from human medical data. You may locate 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.