Normal urinary continence. Micturition may be defined as function of the lower urinary tract that encompasses both a storage phase and a voiding phase. During the storage phase of micturition, the urinary bladder, acting as a low-pressure reservoir, is relaxed and fills with urine.
Micturition may be defined as function of the lower urinary tract that encompasses both a storage phase and a voiding phase. During the storage phase of micturition, the urinary bladder, acting as a low-pressure reservoir, is relaxed and fills with urine. Even though pressure in the urinary bladder gradually increases, urine remains contained within the bladder lumen because of resistance generated primarily by smooth muscle in the bladder neck and striated muscle in the urethra which function as high-pressure, unidirectional valves.
Low pressure in the bladder lumen is maintained by activity in beta-adrenergic (sympathetic) receptors via the hypogastric nerve and central inhibition of cholinergic (parasympathetic) activity. High pressure in the bladder neck and preprostatic urethra is maintained primarily by activity of alpha-adrenergic (sympathetic) receptors via the hypogastric nerve.
High pressure in the postprostatic urethra is sustained primarily by skeletal (urethralis) muscle activated by the pudental nerve.
During the voiding phase of micturition, the parasympathetic innervation (via the pelvic nerve) of the bladder muscle (detrusor muscle) is activated. As a result of contraction of the detrusor muscle, the bladder becomes a high-pressure pump, expelling urine through the urethral lumen. Simultaneously, the urethra becomes a low-pressure conduit for urine being voided from the bladder because of inhibition of alpha adrenergic innervation to smooth muscle of the bladder neck and urethra, and inhibition of innervation to the striated urethralis muscle.
Urinary incontinence
is defined as involuntary leakage of urine. Therefore, it is different from behavioral periuria characterized by normal voluntary elimination of urine in the wrong place (sites other than the litter box or outdoors) or the wrong time (nocturia) as defined by the owner. There are a variety of types of urinary incontinence.
Urge incontinence is defined as frequent uncontrollable contraction of the detrusor muscle when the bladder is minimally distended with urine. It is intermittent in nature, and is often associated with pollakiuria, dysuria and sometimes hematuria. It is typically associated with inflammation of the lower urinary tract. Urge incontinence may also be associated with reduced bladder capacity secondary to diffuse neoplasia of the bladder wall, chronic inflammatory fibrosis of the bladder wall or partial cystectomy. Refer to the sections on bacteria UTI and neoplasia for additional information.
Urethral sphincter incompetence may result in urinary incontinence due to decreased urethral tone during the storage phase of micturition. Incontinence may be more noticeable during periods of rest, or during events associated with increased abdominal pressure such as coughing. It may also develop or become more evident if the patient develops polyuria. Incontinence due to urethral sphincter incompetence is often an exclusion diagnosis.
Overflow incontinence is a type of neurogenic incontinence associated with impaired detrusor muscle function such that the bladder lumen continues to fill until intravesicular pressure exceeds urethral resistance. With lower motor neuron disorders involving sphincters, overflow of urine into the urethra occurs at low intravesicular pressures. In contrast, with upper motor neuron disorders, incontinence occurs at higher intravesicular pressures due to reflex sphincter resistance.
Paradoxical incontinence occurs when mechanical (e.g. uroliths or urethral plug) or functional (e.g. reflex dyssynergia) obstruction of the urethra impairs the voiding phase of micturition. When intravesicular pressure exceeds the pressure at the site(s) of urethral obstruction, urine escapes around the obstruction through the remaining unobstructed portions of the urethra. The name paradoxical incontinence is derived from the fact that incontinence occurs in association with obstruction.
Most causes of urinary incontinence may be classified as disorders of the storage phase of micturition. The exception is overflow (including paradoxical) urinary incontinence, which is a disorder of the voiding phase of micturition. Urinary incontinence may be: 1) congenital or acquired, 2) neurogenic or non-neurogenic, and 3) constant or intermittent.
See Table 1 for suggestions regarding the initial diagnostic evaluation of patients with urinary incontinence. In some patients, a functional diagnosis may require urodynamic studies, including cystometry, urethral pressure measurements and electromyography. Even then, the underlying cause may not be detected.
Although frequently cited in textbooks, the safety and efficacy of many drugs commonly used to treat urinary incontinence and other disorders of micturition in cats have not been evaluated by blinded controlled clinical trials using patients with naturally occurring disease (Table 2, p. 8S). Many dosages have been extrapolated from recommendations derived for other species and personal experience.
Therefore, they should be used only after informed consent of clients and with compassionate precautions. This includes review of the manufacturer's description of indications, contraindications, adverse events and contacting the manufacturer for additional information about unpublished studies in the feline species.
If significant side effects are associated with use of these drugs, then they may be minimized by reducing the dose and/or frequency of administration. In this context client education is important. Undesirable side effects are often associated with less frustration if clients can 1) anticipate them, 2) recognize the difference between nuisance side effects and significant adverse reactions, and 3) be taught how to deal with them if they occur.
Idiopathic urethral sphincter incompetence following neutering is less commonly observed in cats than dogs. A diagnosis of idiopathic urethral incompetence is based on exclusion of other known causes.
Estrogens should not be empirically administered to cats with idiopathic urethral sphincter incompetence based on the premise that they might help, but can do no harm. They may induce estrus, and high doses have the potential to cause bone marrow suppression and blood dyscrasias. Phenylpropanolamine, a nonselective alpha and beta adrenergic agonist, may be a safer alternative. The suggested oral dose is 1.5 to 2.2 mg/kg given every eight hours (Table 2, p. 8S).
Sustained release capsules of phenylpropanolamine may be considered to reduce dosage frequency provided they are properly compounded by a reputable pharmacy. Adverse events that may be associated with phenylpropanolamine include tachycardia, hypertension and restlessness. Caution should be used if these drugs are being considered for incontinent cats that are hypertensive or have cardiovascular dysfunction.
Testosterone administered intramuscularly was reported to be associated with improvement in urinary incontinence in only one of three male cats with urinary incontinence.
One therapeutic option consists of trial therapy with bethanachol, a parasympathomimetic (muscarinic) agent. This drug may enhance detrusor contractility. The recommended oral dosage for cats is 1.25 to 2.5 mg given every eight hours (Table 2). If the desired effect does not occur within a few days, the dose may be increased incrementally up to 5 mg to 7.5 mg every eight hours, provided harmful side effects do not occur (e.g. excessive salivation, abdominal cramping, vomiting and/or diarrhea).
Since bethanachol can also increase urethral resistance by its nicotinic effects on smooth muscle in the proximal urethra, it may be given with phenoxybenzamine. Phenoxybenzamine is an alpha adrenergic antagonist which facilitates relaxation of smooth muscle in the proximal urethral (oral dose = 0.25 mg/kg every 12 hours). Alternatively, an indwelling catheter whose tip is located within the bladder lumen may be used. Periodic attempts to induce voiding by manual compression of the urinary bladder may also be considered, provided they do not result in a marked increase in intraluminal pressure.
If an indwelling urinary catheter is used to minimize accumulation of urine within the bladder, precautions designed to prevent catheter-induced injury should be considered.
Dysfunction of the lower urinary tract is related to impaired ability of the detrusor muscle to contract. Voiding may be easily induced by manual compression of the urinary bladder. Management consists of supportive and symptomatic treatment.
For patients that have an unacceptable degree of incontinence that is not responsive to symptomatic use of drugs, chemotherapy has been suggested. We have no experience with use of chemotherapy in this clinical setting.