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Diagnosis and management of canine urinary incontinence.

Urinary incontinence is defined as a loss of voluntary control of urination leading to inappropriate

voiding of urine. It is caused an imbalance between the normal storage capacity of the bladder

and urethral tone, or anatomical disorders which bypass normal urine storage mechanisms.

Although urethral sphincter mechanism incompetence (USMI) is the most common cause of

urinary incontinence in dogs, other conditions must be excluded. Successful management of

incontinence relies upon accurate diagnosis of the cause and choosing the most appropriate form

of therapy.

Pathophysiology:

The bladder and urethra are supplied by both somatic (voluntary) and autonomic innervation

(Figure 1, Table 1).

Figure 1. Innervation of the bladder and urethra


Nerve Origin Site of action Effect

Pudendal nerve S1-S3 External urethral sphincter Contraction of external urethral

(somatic) (striated muscle) sphincter

Pelvic S1-S3 Bladder detrusor muscle Contraction of detrusor muscle

(parasympathetic)

Sensory fibres from stretch Sensation of bladder fullness

receptors in bladder wall

Hypogastric L1-L4 Bladder detrusor muscle Relaxation of detrusor muscle

(sympathetic)

Internal urethral sphincter Contraction of internal urethral

(smooth muscle) sphincter

During micturition, stretch receptors in the bladder wall send impulses via the pelvic nerve and

spinal cord to the brain. Information is co-ordinated to allow for voluntary relaxation of the

external urethral sphincter (pudendal nerve), activation of the bladder detrusor muscle (pelvic

nerve) and inhibition of sympathetic innervation (hypogastric nerve).

During the storage phase, sympathetic innervation predominates, resulting in detrusor muscle

relaxation and internal urethral sphincter stimulation. Voiding is also inhibited by somatic

stimulation of the external urethral sphincter.

Any condition associated with either increased intravesical pressure or decreased urethral tone

may be associated with incontinence. In addition, external factors may be important: the position

of the bladder neck may affect urethral pressure, and increased intra-abdominal pressure (e.g.

with coughing or barking) may increase intravesical pressure and result in urine leakage.

Increased intravesical pressure may be due to increased detrusor activity or increased bladder

volume. Increased detrusor activity may be a result of urge incontinence (inflammation

associated with infection, urolithiasis or neoplasia) or idiopathic detrusor instability. Detrusor


instability is the term used when clinical signs of urge incontinence are detected, but an

underlying cause cannot be identified.

Increased bladder volume is most often associated with neurologic disorders, leading to overflow

incontinence. Lesions above the fifth lumbar vertebra lead to upper motor neuron disease of the

bladder, characterized by a distended bladder that is difficult to express. This is due to a lack of

voluntary control of urination and hyperexcitability of the external urethral sphincter. When the

intravesical pressure exceeds the urethral pressure overflow incontinence occurs. Lesions

affecting the sacral segments of the spinal cord are characterised by a distended bladder that is

easily expressed, due to both detrusor and sphincter hyporeflexia. Detrusor paralysis is the term

used to describe bladder atony which develops following prolonged accumulation of large

volumes of urine.

Decreased urethral tone may be caused by neurological or structural abnormalities of the urethra.

The most common condition is urethral sphincter mechanism incompetence, for which the

pathogenesis remains obscure.

Finally, incontinence may be due to anatomical conditions which bypass the normal urinary

structures (e.g. ectopic ureters). Conditions associated with pooling of urine beyond the urethral

sphincter (e.g. vaginal stricture) may also lead to pooling and leakage of urine following urination.

History and signalment:

The first questions should ascertain whether urinary incontinence is the likely cause of the signs

described by the owner. Differentials other than incontinence include polyuria, reproductive tract

discharges (e.g. endometrial and prostatic disease) or inappropriate urination because of

behavioural or mobility disorders.

Urethral sphincter mechanism incompetence typically results in no signs other than incontinence,

often with bed wetting at night. It is unusual for dogs with voluntary control of urination to urinate

in their lying areas. Neurological disorders are usually accompanied by defaecation

abnormalities or hind limb neurological deficits. Urge incontinence may be associated with

dysuria, pollakiuria and urinary tenesmus.


The signalment may also provide useful information. For example, ectopic ureters are more

commonly detected in young, female dogs. Acquired urethral sphincter mechanism

incompetence is more common in young to middle aged, female, spayed, large breed dogs.

Lumbosacral and neoplastic disorders are more common in older animals.

Differential diagnosis:

The differential diagnoses may be divided into those conditions resulting in bladder distension,

and those resulting in a normal or small sized bladder (Table 2).

Table 2. Causes of urinary incontinence.

Differential diagnosis
Distended bladder:
Neurologic disorders
Upper motor neuron lesions
Lower motor neuron lesions
Detrusor paralysis
Functional or anatomical urethral obstruction
Normal or small sized bladder:
Decreased bladder compliance
Urge incontinence (inflammation, urolithiasis, neoplasia)
Idiopathic detrusor instability
Decreased urethral pressure
Urethral sphincter mechanism incompetence
Primary
Secondary
Anatomical disorders (congenital / acquired)
Ectopic ureters
Ureterocoele
Intrapelvic bladder
Vaginal strictures/ masses
Ureterovaginal or vesicovaginal fistulation
Urachal diverticula
Pseudohermaphroditism
Diagnosis:

Physical examination:

A complete physical examination should be performed. Urine scalding of the skin may be

apparent. The urinary bladder should be palpated to assess size and the effort necessary for

expression. In addition, masses or calculi may be palpable. Rectal examination should be

performed to assess the prostate and the proximal urethra. Vaginal palpation should be

performed in female dogs to assess strictures and urethral masses. Neurological examination

should be performed to assess anal tone, perineal sensation and the bulbospongiosus reflex. If

reduced, this suggests lower motor neuron disease. Hind limb neurological deficits may also be

observed.

Clinicopathological testing:

Routine haematology and biochemistry should be performed to further investigate potential

causes of polyuria and polydipsia. Additional testing may be necessary. Urinalysis and urine

bacteriological culture should be performed to exclude urinary tract infection, or to determine the

most ideal antimicrobial therapy. Whilst urinary tract infections are common in incontinent

animals, urge incontinence associated with inflammation may also be detected.

Diagnostic imaging:

Radiography and ultrasonography are useful when an anatomical or structural cause of

incontinence is suspected. Plain radiography is of limited value, other than in the detection of

radio-opaque uroliths (calcium oxalate, struvite and silicate) and determination of the size and

position of the urinary bladder. Spinal radiography (+/- myelography or more advance imaging)

may confirm spinal cord disease. Contrast studies are often more informative. Positive contrast

urethrocystography and vaginography may be performed using water-soluble organic iodide

contrast media. Double contrast cystography may provide additional information with bladder

disorders. Intravenous urography may be used to identify renal and ureteral abnormalities.
Computed tomography has recently been shown to be more useful than other established

diagnostic imaging techniques for the diagnosis of ectopic ureters.

Ultrasonography can be used to assess the kidneys, bladder, proximal urethra, reproductive tract

and ureters (if distended). This is particularly important to document structural abnormalities such

as neoplasia, urinary calculi, hydroureter or hydronephrosis. Given the high incidence of

concurrent urinary tract abnormalities in animals with ectopic ureters, such imaging is

recommended prior to surgery. Ultrasound guided biopsies may also be obtained.

Endoscopy:

Anatomical and structural causes of incontinence may also be assessed by endoscopy. It is one

of the most sensitive methods of detecting ectopic ureters in dogs, and can also be used to obtain

biopsies when neoplasia and/or inflammatory lesions are suspected.

Urodynamic testing:

These techniques may be used to assess urethral pressure profiles (UPP) and bladder detrusor

muscle function (cystometrography (CMG)). UPP is the test of choice for the confirmation of

urethral sphincter mechanism incompetence, and may allow prediction of the response to

therapy. CMG may allow confirmation of detrusor instability or to provide an assessment of the

degree of bladder atony in animals with neurologic bladder dysfunction. Unfortunately, it is not

widely available.

Treatment:

Underlying disorders should initially be treated. In general, surgical treatment is necessary for

anatomical and congenital disorders. Urolithiasis can be managed surgically or medically,

depending on the severity and type of calculi present. If urinary tract infection is present, this

should be managed with appropriate antibiotic therapy. Neoplasia may be treated surgically or

medically with drugs such as piroxicam if transitional cell carcinoma is diagnosed.


Neurologic disorders may be managed medically with drugs chosen to increase or decrease

urethral tone, or alter detrusor activity. The choice of drug is dependent on the specific disorder

(Table 2).

The treatment of urethral sphincter mechanism incompetence is complex and detailed below.

Table 2. Drugs used for the treatment of urinary incontinence.

Drug Dose Action / considerations


Phenylpropanolamine* 1.5mg/kg BID or 1mg/kg -adrenergic agonist. Increases
TID internal urethral sphincter tone.
Estriol* Initial dose 1mg/dog SID, Increases density and responsiveness
adjusting from 0.5mg EOD of -adrenergic receptors, thereby
to 2mg SID as required increasing urethral sphincter tone.
Diethylstilboestrol 1mg once weekly As estriol. Not used because estriol is
licensed in Ireland.
Diazepam 0.2mg/kg TID Decreases external urethral sphincter
tone.
Phenoxybenzamine 10mg SID Decreases internal urethral sphincter
tone
Bethanechol 5-25mg/kg TID Increases detrusor activity
*Only estriol and phenylpropanolamine are licensed for use in dogs in Ireland.

Urethral sphincter mechanism incompetence (USMI).


1,2
USMI reportedly effects between 9.7 and 20.1% of spayed female dogs . 90% of female dogs

with USMI are spayed. Approximately 75% of affected dogs develop signs of urinary
3
incontinence within one year of ovariohysterectomy, but it may occur at a later stage . It is more

common in large than small breed dogs (30.9% incontinence post ovariohysterectomy in dogs >
2
20kg, 9.3% incontinence in dogs < 20kg) . Early age (<3 months) neutering has been associated
4
with an increased incidence of incontinence in one study .

USMI rarely affects entire female and male dogs. It can be congenital (juvenile USMI).
5
Approximately 50% of bitches with juvenile USMI may recover continence after their first oestrus .
The pathogenesis of this disorder is not fully understood. Reduced urethral length, possible

oestrogen deficiency, intrapelvic bladder, reduced vesicourethral support, urethral smooth muscle

abnormalities and obesity have been postulated.

USMI is diagnosed by exclusion of other causes. If available, UPP may be performed to confirm

reduced urethral pressures.

Treatment:

Medical and surgical therapies may be attempted. Surgery may be successful in animals in

which medical therapy has been unrewarding. If successful, it also negates the need for long term

medical management.

Medical management:

Estriol (Table 2) Estriol increases urethral tone by increasing the density and responsiveness of

-adrenergic receptors in urethral smooth muscle. Studies have reported complete urinary

continence in approximately 65% of treated dogs. Mild and transient oestrogenic effects (vulval

swelling and attractiveness to male dogs) have been observed at higher dose rates (incidence 5-

9%). Side effects are reversed by dose reduction. Bone marrow suppression has not been

reported at recommended doses (unlike other forms of oestrogen therapy).

Phenylpropanolamine (Table 2) -adrenergic drugs exert their effect by direct stimulation of the

smooth muscle of the internal urethral sphincter. Approximately 85% of treated dogs have

complete urinary continence. Side effects include are rare, and are typically mild and transient.

Aggressiveness and restlessness in dogs are rarely described following treatment.

Combination therapy with both estriol and phenylpropanolamine is often suggested. In theory,

administration of estriol increases the responsiveness to phenylpropanolamine, and may be

effective when either therapy alone has been unsuccessful. However, one recent study showed

that the administration of both estriol and phenylpropanolamine did not increase urethral
6
resistance more than estriol alone .

Surgical management:
7
The two most commonly performed surgical techniques are colposuspension and urethropexy .

Colposuspension results in relocation of the bladder neck from an intrapelvic to an intra-

abdominal location. It has been reported to be completely successful in approximately 40-56% of

bitches, with a further 40-42% showing significant improvement. 10-18% fail to respond to this

treatment. However, incontinence may redevelop in some animals despite initial improvement.

Complications are uncommon, and include postoperative straining to urinate, inability to urinate,

tearing of sutures from the vagina and recurrence of incontinence. Dyssynergia is often

responsive to diazepam. Pre-operative oestrogen administration may contribute in some cases.

Urethropexy has comparable success rates, with 56% of dogs showing complete continence and

improvement in a further 27%. Incontinence also recurs in a proportion of these dogs when

followed long term. Similar complications to those seen following colposuspension may occur.

Medical therapy may be re-attempted following surgery if surgery alone has been unsuccessful.

Other treatment options:

Endoscopic periurethral injections of glutaraldehyde cross-linked collagen or Teflon may be used

to narrow the urethral lumen and increase urethral resistance. It has been shown to resolve

urinary incontinence in approximately 53-68% of dogs.

USMI in male dogs may be managed medically with phenylpropanolamine, or surgically with vas

deferentopexy or prostatopexy.

References:

1. Stocklin-Gautschi, N.M., Hassig, M., Reichler, I.M., Hubler M. & Arnold S. (2001) The relationship
of urinary incontinence to early spaying in bitches. J Reprod Fertil Suppl 57, 233-236
2. Arnold, S., Arnold, P., Hubler, M., Casal, M. & Rusch P. (1989) Urinary incontinence in spayed
female dogs: frequency and breed disposition. Schweiz Arch Tierheilkd 131, 259-263
3. Marchevsky, A. Edwards, G.A., Lavelle, R.B. & Robertson, I.D. (1999) Colposuspension in 60
bitches with incompetence of the urethral sphincter mechanism. Aust Vet Pract 29, 2-8
4. Spain, C.V., Scarlett, J.M. & Houpt, K.A. (2004) Long-term risks and benefits of early-age
gonadectomy in dogs. J Am Vet Med Assoc 224, 380-387
5. Holt, P.E. & Thrusfield, M.P. (1993) Association in bitches between breed, size, neutering and
docking and acquired urinary incontinence due to incompetence of the urethral sphincter
mechanism. Vet Rec 133, 177-180
6. Hamaide, A.J., Grand, J.G., Farnir, F., Le Couls, G., Snaps, F.R., Balligand, M.H. & Verstegen, J.P.
(2006) Urodynamic and morphologic changes in the lower portion of the urogenital tract after
administration of estriol alone and in combination with phenylpropanolamine in sexually intact and
spayed female dogs. Am J Vet Res 67, 901-908
7. Hoelzler, M.G. & Lidbetter, D.A. (2004) Surgical management of urinary incontinence. Vet Clin
North Am Small Anim Pract 34, 1057-1073

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