The Leakers: Disorders of Micturition and Continence
Melissa S. Wallace, DVM, Dipl. ACVIM
Definition & Overview
A disorder of micturition is a lack of voluntary control over the elimination of urine. Disorders of micturition include disorders of urine retention (incontinence) and disorders of bladder emptying, which may or may not be accompanied by incontinence. True incontinence must be differentiated from inappropriate voiding of urine (i.e. behavior problems), lower urinary tract diseases causing pollakiuria, and from polyuria/polydipsia resulting in voluntary voiding in inappropriate places.
Normal Micturition (i.e. Neurology for Dummies)
There are two phases of normal micturition; the storage phase and the bladder-emptying phase. During the storage phase, the detrusor muscle progressively relaxes while the urethral sphincter tone remains high, which allows the bladder to hold a gradually increasing volume of urine. During the emptying phase, the detrusor muscle contracts while the urethral sphincter relaxes, allowing the urine to be eliminated.
The bladder muscle (detrusor) is smooth muscle that is supplied by both sympathetic (beta-adrenergic) and parasympathetic (cholinergic) receptors. Sympathetic stimulation causes relaxation, and parasympathetic stimulation causes contraction. The internal urethral sphincter is composed of smooth muscle fibers in the trigone and proximal urethra, and contains sympathetic (alpha-adrenergic) receptors. When these receptors are stimulated, increased urethral tone is achieved, which is the normal 'resting' state. The external urethral sphincter is striated muscle, and is supplied by somatic neurons via the pudendal nerve.
Normal micturition requires stimulation of the parasympathetic receptors in the detrusor, with a simultaneous decrease in sympathetic and somatic tone to relax the urethra and allow complete contraction of the bladder. Any imbalance in the coordination of these 'arms' of the nervous system can result in a micturition disorder. The parasympathetic and somatic control arises from the sacral spinal cord segments (S1 - S3) and travels via the pelvic and pudendal nerves, respectively. The sympathetic nerves leave the spinal cord at segments L1-L4 via the hypogastric nerve. Higher centers in the cerebral cortex, brainstem, cerebellum, and thalamus modify the reflex through the spinal cord. This complex system can be interrupted at many points from the brain to the bladder.
Causes of Incontinence
Incontinence is categorized for diagnostic evaluation based on history, observance of the animal's micturition, and physical examination findings. No other aspect of internal medicine is so dependent on these basic skills and less dependent on diagnostic testing. This is why these cases are often so frustrating to inexperienced clinicians or to those who do not routinely evaluate urologic patients.
An animal that can eliminate urine normally and has a small bladder after voluntarily voiding, but is incontinent during what should be the storage phase characterizes a disorder of urine storage. A disorder of bladder emptying is characterized by incomplete voiding, so that the animal maintains a large bladder, and the incontinence is usually an overflow problem. A normal dog or cat should have < 0.2 - 0.5 ml/kg of urine in the bladder after voluntarily voiding. Once the disorder is divided into either a disorder of storage vs. emptying, the search for an underlying cause can often be narrowed. There are neurogenic and non-neurogenic causes, as described below.
1. Neurogenic Origin - Upper Motor Neuron
A lesion cranial to the sacral spinal cord segments causes disruption of the inhibitory control by the higher centers, so that sympathetic tone remains inappropriately high during the micturition reflex. If the pelvic nerve is intact the detrusor will contract, but the urethral sphincter fails to relax, resulting in a poor urine stream and incomplete emptying of the urinary bladder. Over time, increased urine volume will cause bladder distention and an atonic detrusor muscle. When this becomes chronic, it is irreversible, which is why aggressive bladder management is so critical in cases of UMN bladder dysfunction.
An incoordination of the sympathetic with the parasympathetic actions of voluntary micturition is often termed reflex dyssynergia, and in some cases this can occur as an idiopathic condition without other apparent neurologic deficits.
2. Neurogenic Origin - Lower Motor Neuron
Lesions of the sacral spinal cord segments, pelvic nerve, and/or pudendal nerve cause reduced or absent pelvic sensation and loss of detrusor contraction. The bladder muscle will be flaccid and overdistended, which will lead to damage of the tight junctions of the detrusor and permanent bladder atony. As increased intravesicular pressure exceeds urethral outflow resistance, overflow incontinence will result.
3. Nonneurogenic Conditions
Anatomic abnormalities can result in incontinence, and these are often congenital conditions. Examples are ectopic ureter, urethral hypoplasia, pelvic bladder, urethrovaginal fistula, and congenital urethral sphincter mechanism incompetence. Acquired anatomic defects of the urethra or bladder can result from infiltrative disease, prostatic disease, uroliths, trauma or surgery.
Paradoxical incontinence is caused by partial or intermittent obstruction of the urethra that allows leakage around the obstruction when the bladder is full. Sometimes these animals leak urine at rest, but are obstructed when they attempt to voluntarily void. Examples are urethral calculi, neoplasia, and prostatitis/urethritits.
Urge incontinence is caused by severe irritation or inflammation of the urinary bladder. This causes a sensation of fullness and initiates a micturition reflex at a low filling volume. Cats with severe FLUTD often exhibit this type of incontinence, as do some dogs with cystic calculi or severe bacterial cystitis. The pet may act suddenly anxious, because he feels an urgency to urinate that he can not control. Detrusor instability (detrusor hyperreflexia) is an idiopathic functional disorder in which the bladder contracts at a very low filling volume, but the pet usually does not feel a sense of urgency. This condition is uncommon in veterinary patients, and results in frequent small volumes of urine being involuntarily voided.
Stress incontinence is the most common form of incontinence in dogs, and is more appropriately termed urethral sphincter mechanism incompetence. It is also called spay incontinence or hormone-responsive incontinence. The bladder emptying part of the micturition reflex is normal, but when the dog is at rest and the bladder is full, the internal sphincter tone is insufficient to prevent leakage of urine. The incontinence is typically at night or when the dog is relaxed, and is usually several hours after the dog has voided. This problem is most commonly seen in middle-aged spayed female dogs, but can be seen with other signalments. Causes are multifactorial, but individual anatomy, a pelvic location of the internal urethral sphincter due to removal of the broad ligaments during OHE, and lack of estrogenic stimulation to the receptors in the internal sphincter are all possible contributing factors. A dog with marginal internal urethral sphincter tone that becomes PU/PD may exhibit this type of incontinence as well.
Detrusor areflexia (atonic bladder) is a large flaccid bladder that can not contract, resulting in overflow incontinence. A lower motor neuron disorder may cause this, but so can any condition that causes chronic physical or functional urethral obstruction, which results in damage to the tight junctions of the smooth muscle of the detrusor. Urine retention with a large bladder is always considered a medical emergency, and should be managed by indwelling or intermittent urethral catheterization while a diagnosis of the underlying cause is being sought. Urinary retention is often accompanied by secondary bacterial infection.
Diagnostic Approach to Incontinence
This is the most important and difficult aspect of a micturition disorder evaluation. Terms like incontinence are often misunderstood by the client, and should be avoided. Try to find out what the owner is actually observing the pet doing that is abnormal or different than before. The owner should be questioned about any straining or interruption of the urine stream. The description of how and when the pet leaks urine is very important. Incontinence must be differentiated from pollakiuria or polyuria. Leakage of urine only at rest or during sleep is very suggestive of urethral sphincter mechanism incompetence. The pet's age may suggest the cause, as young dogs and cats are more likely to have congenital abnormalities. Geriatric pets are more prone to prostatic diseases or neoplasia, and young adult to middle-aged pets are more commonly affected with uroliths. A history of trauma or surgery may suggest the cause. Other signs such as fecal incontinence, changes in tail movement and/or lameness may suggest a neurologic problem.
In micturition disorders careful attention should be paid to the size and position of the urinary bladder. A rectal examination and digital vaginal examination or preputial examination should be performed. A neurologic examination with particular attention to perineal reflex, anal tone, perineal sensation, tail movement, and conscious proprioception in the rear legs is important. After the P.E., it is helpful to observe the animal's micturition behavior. Palpation of the urinary bladder after voiding will help to distinguish whether the disorder is of storage vs. elimination. If the bladder size is difficult to palpate, measuring residual urine volume by passing a urethral catheter is advised. This will also help in ruling out partial urethral obstructions.
Minimum Data Base
The initial evaluation will include a CBC, chemistry profile, urinalysis and urine culture. Survey abdominal radiographs are necessary in most cases. These initial tests are useful to rule out urinary tract infection, urolithiasis, many causes of PU/PD and metabolic diseases.
Case-based Diagnostic Testing
Depending on the results of the history, P.E. and minimum database, the work-up can be tailored to the most likely causes. If the pet has evidence of a neurogenic cause, then a neurologic work-up or referral is indicated (e.g. spinal radiographs, myelography, epidurography, MRI, etc.).
If the neurologic examination is normal, then an evaluation of the lower urinary tract for structural disease is indicated, and the approach will depend on the age of the pet and the type of incontinence or voiding abnormality. For ectopic ureter evaluation, both an IVP and a complete lower urinary tract study (double and positive contrast cystogram plus vaginourethrogram) are often necessary. Finding evidence of hydronephrosis, hydroureter and pyelonephritis in a young dog (e.g. with ultrasound) is strong evidence that an ectopic ureter may be present. Cystoscopy and/or abdominal exploratory with cystotomy are often needed to complete the evaluation if structural disease is suspected from the contrast studies; these evaluations are often done by a soft tissue surgical specialist who can repair the defect at the same time.
Functional evaluation of the lower urinary tract requires urodynamic studies, such as a cystometrogram and/or a urethral pressure profile. A cystometrogram records the intravesicular pressure during bladder filling and detrusor contraction. A urethral pressure profile measures the intraluminal pressure over the length of the urethra during the filling phase. Simultaneous cystometry and uroflowmetry evaluates the micturition reflex during both the storage and voiding phase, but is technically more difficult and invasive. Because these studies are not routinely available to most clinicians, it is common to estimate the micturition dynamics based on astute observation, meticulous history and physical examination skills, and ruling out structural disease by ultrasonography and contrast radiography. Sometimes, response to pharmacological manipulation can further help to elucidate the disorder.
Therapy of Incontinence and Micturition Disorders
Urethral Sphincter Mechanism Incompetence
1. Diethylstilbestrol (DES); a synthetic estrogen, this may increase internal urethral sphincter sensitivity to catecholamines, or stimulate estrogen receptors within the sphincter. The dose is 0.1 - 1 mg PO SID x 5 days, then 1 - 3 times weekly. Small dogs receive 0.1 mg. size. Large and giant breed dogs receive 1 mg size. Medium sized dogs 0.25 mg size. Dosing is somewhat empirical; use caution to avoid estrogen toxicity (bone marrow suppression).
2. Phenylpropanolamine (PPA); this alpha-agonist stimulates the alpha-adrenergic receptors within the internal urethral sphincter, increasing resting urethral tone. The dose is 1 - 1.5 mg/kg PO BID - TID. Side effects are hyperactivity and hypertension. This drug may work in conjunction with DES in refractory cases. Down-regulation of the receptors may occur with time, but with cessation of the drug the receptors will become sensitive again.
3. Ephedrine; this is an alpha-agonist similar to PPA, but has more side effects such as tachycardia and dry mouth. It is commonly used in countries where PPA is unavailable. The dose is 2 - 4 mg/kg PO BID.
4. Imipramine; This tricyclic antidepressant has anticholinergic and alpha-agonist effects. It may be useful in some cases for urethral sphincter mechanism incompetence and for detrusor instability. Side effects are hyperexcitability, seizures, tremors and tachycardia. The dose is 5 -15 mg PO BID (dogs) and 2.5 - 5 mg PO BID (cats). I have not had good success with this therapy.
5. Estradiol cypionate (ECP); this potent and long-acting injectable estrogen should never be used for incontinence due to the very real risk of estrogen toxicity.
6. Testosterone cypionate; a respositol form of testosterone, which is sometimes useful in castrated male dogs or cats with urethral sphincter mechanism incompetence (a rare disorder). Side effects are prostatic hyperplasia and unwanted male behaviors.
Urge Incontinence and Detrusor Instability
1. Propantheline; an anticholinergic that reduces detrusor contractions. Side effects are dry mucous membranes, constipation and urinary retention with bladder overdistention. The doe is 7.5 - 15 mg PO BID - TID (dog) and 5 - 7.5 mg PO TID (cat).
2. Oxybutynin; this drug has both anticholinergic and antispasmodic (smooth and skeletal muscle relaxing) effects. The dose is 0.1 - 0.2 mg/kg PO BID. A side effect is ileus.
Disorders of Bladder Emptying with Increased Urethral Tone
1. Phenoxybenzamine; this is an alpha-adrenergic blocking agent, which relaxes the internal urethral sphincter. A side effect is hypotension. The dose is 0.25 mg/kg PO TID (dog) and 0.5 mg/kg PO BID (cat). This drug takes 3 - 5 days to reach therapeutic levels. Other alpha-blocking agents with a similar effect on the internal sphincter but more side effects are acepromazine (hypotension, sedation) and prazocin (hypotension). Be cautious when using these drugs simultaneously.
2. Diazepam; this is a centrally acting skeletal muscle relaxant, which decreases external urethral sphincter tone and spasm. Side effects are sedation and incoordination. Hepatotoxicity occurs in cats with repeated oral administration. Other drugs with a similar mechanism are dantrolene and baclofen.
Decreased Detrusor Contractility (e.g. atonic bladder)
1. Bethanecol; this is a cholinergic agent which stimulates detrusor contractions. Side effects are abdominal cramping and gastrointestinal effects. This drug has a weak effect on nicotinic receptors in the internal urethral sphincter, and is therefore best when used in combination with an alpha-adrenergic blocker like phenoxybenzamine. The dose is 2.5 - 10 mg PO BID to TID (dog) and 2.5 mg PO BID (cat). Other agents suggested to increase detrusor tone include metoclopramide and prostaglandin E2.
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