Micturition Disorders
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.
| Desired
effect |
Drug |
Mechanism of action |
| Stimulate detrusor activity |
Bethanechol (Urecholine) |
Cholinergic stimulation |
| Reduce detrusor activity |
Propantheline (Pro- Banthine) |
Anticholinergic, antispasmodic effect on smooth muscle |
|
|
Oxbutynin |
Direct antispasmodic effect on smooth muscle, anticholinergic
|
| Increase urethral tone |
Pseudophedrine |
Alpha-adrenergic stimulation |
| |
Phenylpropanolamine |
Alpha-adrenergic stimulation |
| |
Imipramine |
Alpha- and beta- adrenergic stimulation |
| Increased urethral tone (hormone-responsive incontinence) |
Diethylstilbestrol |
Unknown, may increase internal sphincter sensitivity to
catecholamines |
| |
Testosterone |
Unknown |
| Reduce urethral tone |
Phenoxybenzamine |
Alpha-adrenergic antagonism |
| |
Diazepam (Valium) |
Central-acting skeletal muscle relaxation |
| |
Baclofen |
Skeletal muscle relaxation |
| |
Dantrolene |
Direct-acting skeletal muscle relaxation |
Last Edited: Jul 26, 2007 3:04 PM
