Urinary Incontinence
Loss of voluntary control of micturition, usually observed as involuntary urine leakage.
PATHOPHYSIOLOGY
Usually, a disorder of the storage phase of micturition. Urine storage failure is caused by impaired urinary bladder accommodation, failure of urethral continence mechanisms, or anatomic bypass of urinary storage structures. Partial outlet obstruction and other causes of urinary bladder overdistension may cause paradoxical, or overflow, urinary incontinence.
SYSTEMS AFFECTED
Renal/Urologic.
Nervous.
Skin/Exocrine—urine scald and perineal and ventral dermatitis, recessed vulva.
INCIDENCE/PREVALENCE
Urinary incontinence may affect ∼ 20% of spayed female dogs, especially large-breed dogs.
SIGNALMENT
Dog and (rarely) cat.
Most common in middle-aged to old neutered female dogs; also observed in juvenile females and (rarely) neutered males.
Medium- to large-breed dogs most often affected.
CAUSES
Neurologic
Disruption of local neuroreceptors, peripheral nerves, spinal pathways, or higher centers involved in the control of micturition can disrupt urine storage. Generalized peripheral lower motor neuron disorders or autonomic disorders also can cause urinary incontinence.
Lesions of the sacral spinal cord, such as a congenital malformation, cauda equina compression, lumbosacral disc disease, or traumatic fractures or dislocation, can result in a flaccid, overdistended urinary bladder with weak outlet resistance. Urine retention and overflow incontinence develop.
Lesions of the cerebellum or cerebral micturition center affect inhibition and voluntary control of voiding, usually resulting in frequent, involuntary urination or leakage of small volumes of urine.
Urinary Bladder Storage Dysfunction
Poor accommodation of urine during storage or urinary bladder overactivity (detrusor instability) leads to frequent leakage of small amounts of urine.
Urinary tract infections, chronic inflammatory disorders, infiltrative neoplastic lesions, external compression, and chronic partial outlet obstruction are potential causes.
Congenital urinary bladder hypoplasia may accompany ectopic ureters or other developmental disorders of the urogenital tract.
Idiopathic detrusor instability has been associated with feline leukemia virus infection in cats and unknown causes in dogs.
Urethral Disorders
If urethral closure provided by urethral smooth muscle, striated muscle, and connective tissue does not prevent leakage of urine during storage, intermittent urinary incontinence is observed.
Examples—congenital urethral hypoplasia or incompetence, acquired urethral incompetence (i.e., reproductive hormone-responsive urinary incontinence), urinary tract infection or inflammation, prostatic disease or prostatic surgery.
Anatomic
Developmental or acquired anatomic abnormalities that divert urine from normal storage mechanisms or interfere with urinary bladder or urethral function.
Ectopic ureters can terminate in the distal urethra, uterus, or vagina.
Patent urachal remnants divert urine outflow to the umbilicus.
Vestibulovaginal anomalies, congenital urocystic hypoplasia, or urethral hypoplasia.
Intrapelvic bladder neck location may contribute to urine leakage due to urethral incompetence.
Vulvar and perivulvar conformation abnormalities may contribute to urine pooling and intermittent urine leakage.
Urine Retention
Overflow observed when intravesicular pressure exceeds outlet resistance.
Mixed Urinary Incontinence
Mixed or multiple causes may occur in dogs and cats, e.g., combinations of urethral and bladder storage dysfunction and combinations of anatomic and functional disorders.
RISK FACTORS
Neutering increases the risk of development of urethral incompetence, especially in large dogs (> 20 kg).
Early neutering (< 3 months) increases the risk of urinary incontinence in female dogs.
Conformational characteristics such as bladder neck position, urethral length, and concurrent vaginal anomalies may increase the risk of urinary incontinence in female dogs.
Obesity may increase the risk of urinary incontinence in neutered female dogs.
Other possible risk factors for urethral incompetence include breed, large body size, polyuria, and early tail docking.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
Differentiating Similar Signs
Voluntary but inappropriate urination (usually behavioral).
Urethral discharges, often associated with prostatic disease in male dogs and vaginal disorders in female dogs.
Urine spraying or inappropriate urination in cats can be confused with urinary incontinence.
Polyuria—may precipitate or exacerbate urinary incontinence or lead to nocturia and inappropriate urination; a urine specific gravity may rule in or out clinically important polyuria.
Differentiating Causes
Neurogenic causes of urinary incontinence—usually cause a large, distended urinary bladder and other neurologic deficits such as weak anal or tail tone, depressed perineal sensation, and proprioceptive deficits.
Dogs with urethral incompetence typically exhibit intermittent occurrences of urinary incontinence, observed most often at night or while the animal is sleeping. Physical examination reveals a small urinary bladder and no other defects.
Urine pooling—affected dogs may leak small amounts of urine after voiding.
Historical and physical findings in patients with urinary bladder storage dysfunction resemble those observed in patients with urethral incompetence, although increased frequency of urination or apparent urgency may be additional clinical signs.
Historical signs in male dogs with prostatic disease include tenesmus, hind limb weakness, dysuria, and pollakiuria. Physical findings include prostatomegaly, lumbosacral pain, pain on prostatic palpation, and hind limb trembling or weakness.
Recessed or juvenile vulvar conformation may contribute to urine pooling.
CBC/BIOCHEMISTRY/URINALYSIS
Hematologic and biochemical analyses may be indicated in patients with polyuric disorders (see Polyuria and Polydipsia).
Urinalysis may reveal evidence of urinary tract infection (e.g., pyuria, hematuria, and bacteria) or polyuria (e.g., low urine specific gravity).
OTHER LABORATORY TESTS
Test cats for feline leukemia virus infection
Urine culture in dogs with urethral incompetence
IMAGING
Radiographic Findings
Contrast radiography is indicated in juvenile animals and animals exhibiting urinary incontinence shortly after surgical procedures or traumatic incidents.
Excretory urography, contrast tomography, or magnetic resonance nephrography allows visualization of the kidneys, ureteral terminations, and urinary bladder.
Retrograde vaginourethrography allows visualization of the vaginal vault, urethra, and urinary bladder. Ectopic ureters usually fill with contrast media in these retrograde studies.
Double-contrast cystography may be required for full visualization of bladder structure and identification of urinary bladder lesions.
Ultrasonographic Findings
Can use for evaluation of the kidneys, ureters, and urinary bladder to identify uroliths, masses, hydronephrosis or hydroureter, or evidence of pyelonephritis.
DIAGNOSTIC PROCEDURES
Neurologic examination—examination of anal tone, tail tone, perineal sensation, and bulbospongiosus reflexes.
Urethral catheterization—may be required to assess patency of the urethra if urine retention is observed.
Cystoscopy—may visualize bladder, urethra, and ectopic ureteral terminations.
TREATMENT
APPROPRIATE HEALTH CARE
Usually as outpatient.
Address partial obstructive disorders and primary neurologic disorders specifically if possible.
Identify urinary tract infection and treat appropriately.
Ectopic ureters and congenital urethral hypoplasia can often be surgically corrected; endoscopic-guided laser ablation has been utilized for intramural ectopic ureters. Functional abnormalities of urethral competence or urinary bladder storage may accompany the anatomic disorder and require ancillary medical treatment.
Teflon or collagen bulking agents can be injected into urethral submucosa to control incontinence.
Surgical procedures such as colposuspension, cystourethropexy, and prosthetic sphincter implantation have been described for the treatment of refractory incontinence.
MEDICATIONS
DRUG(S) OF CHOICE
Urethral Incompetence
Manage with α-adrenergic agonists (e.g., phenylpropanolamine 1–1.5 mg/kg PO q8–12h or 1.5 mg/kg PO q24h, ephedrine 1–4 mg/kg PO q8–12h) or reproductive hormones (e.g., conjugated short-acting estrogens, estriol 1–2 mg/dog PO q24h for 7 days, then 0.5–1 mg/dog q24–48h if required, and testosterone or diethylstilbestrol 0.1–1 mg/dog PO q24h for 5–7 days then 0.1–1 mg/dog PO q4–7 days PRN).
α-adrenergics and reproductive hormones can be co-administered for a synergistic therapeutic effect.
Depot deslorelin, a gonadotropin-releasing hormone analogue (5–10 mg/dog, or dogs ≤ 30 kg use a 4.7 mg implant, for dogs > 30 kg use a 9.4 mg implant) or depot leuprolide (1 mg/kg or 11–25 mg/dog) have also been used in refractory cases.
Imipramine (5–15 mg/dog PO q12h), a tricyclic antidepressant with anticholinergic and α-agonist actions, provides an alternative method of treatment especially if there may be inappropriate voiding with a suspected behavioral origin.
Detrusor Instability
Manage with anticholinergic or antispasmodic agents (e.g., oxybutynin, approximately 0.2 mg/kg PO q8–12h, up to 5 mg total dose q8–12h).
Prostatic Disease
CONTRAINDICATIONS
Estrogen in immature bitches with congenital USMI (urethral sphincter mechanism incompetence), intact bitches, or male dogs.
Adrenergic agonists in patients with cardiac disease, renal disease, and hypertensive disorders.
Anticholinergic agents in patients with glaucoma or cardiac disease.
PRECAUTIONS
Long-acting estrogen compounds rarely cause signs of estrus and bone marrow suppression, and exacerbate immune-mediated disease. However, bone marrow suppression due to estrogen therapy is usually fatal. Therefore, use the minimum effective dose for the minimum amount of time.
Testosterone administration can cause signs of aggression or libido, exacerbate prostatic disease, and contribute to the development of perineal hernia or perianal adenoma.
Adrenergic agonists can cause restlessness, tachycardia, and hypertension.
Anticholinergic agents can cause nausea, vomiting, and constipation.
POSSIBLE INTERACTIONS
Do not administer tricyclic antidepressants concurrently with monoamine oxidase inhibitors (e.g., selegiline).
The risk of hypertension increases if α-adrenergic agonists are administered concurrently with tricyclic antidepressants.
FOLLOW-UP
PATIENT MONITORING
Patients receiving α-adrenergic agents—observe during the initial treatment period for adverse effects.
Patients receiving long-term estrogen—initial, 1 month, and periodic hemograms.
Periodic urinalysis and urine culture.
Expect excellent response to medical treatment in 60–90% of treated patients.
Once a therapeutic effect is achieved, slowly reduce the dose and frequency of drugs to the minimum required.
Consider combination treatment (α-adrenergic agonist with reproductive hormones or anticholinergic agents), deslorelin or surgical options if poor response to single-agent medication.
POSSIBLE COMPLICATIONS
Recurrent and ascending urinary tract infection
Urine scald and perineal and ventral dermatitis
Refractory and unmanageable incontinence.
MISCELLANEOUS
ASSOCIATED CONDITIONS
Urinary tract infection
Vaginitis
PREGNANCY/FERTILITY/BREEDING
Although urinary incontinence is rare in pregnant animals, the use of estrogens or anticholinergic agents is not advised.
SYNONYMS
Enuresis
Visit your veterinarian as early recognition, diagnosis, and treatment are essential.