Problem Definition and Recognition
Urinary incontinence (UI) is loosely defined as the involuntary passage of urine. Technically, it is the involuntary escape of urine during the filling phase of the urinary cycle. Urinary incontinence is a frustrating and poorly tolerated problem for the pet owner, which sometimes results in abandonment or euthanasia of the affected pet. It must be differentiated from the problem of inappropriate urination, which is often a behavioral problem.
Pathophysiology
Normal micturition requires two steps to occur appropriately. The filling or storage phase is dominated by the sympathetic side of the nervous system, allowing the body of the bladder to distend with urine while constricting outflow from the neck of the bladder and proximal urethra. The parasympathetic branch of the nervous system takes over during the emptying or voiding phase of micturition, causing the detrusor muscle to contract and opening the bladder neck and proximal urethra to allow voiding of urine. A diagram of the two phases is shown in Figure 34-1, highlighting the innervation involved.
FIGURE 34-1. Diagram of phases of micturition.
Causes
The causes of urinary incontinence are summarized in Table 34-1. The diagnostic procedures for differentiating these causes are discussed in subsequent sections.
Diagnostic Plan
Athorough history and physical examination are the initial steps in determining the existence and causes of UI. Distinguishing neurogenic UI from nonneurogenic UI or from disorders associated with polyuria must be accomplished (see Figs. 34-2 and 34-3). Signalment can sometimes suggest the likelihood of a specific incontinence problem. Obtaining basic information about frequency, volume of urine produced, and urination habits in general will help in the diagnostic process. Past medical history, including drugs, diet, and previous trauma, should be evaluated. In performing the physical examination particular attention should be paid to the urogenital tract, evidence of urine staining/scalding, and the neurologic status of the patient. The urinary bladder should be palpated to assess bladder tone and ease of urine expression. A firm, distended bladder that is difficult to express is associated with urinary tract obstruction or upper motor neuron (UMN) lesions affecting the micturition reflex.Occasionally the bladder is atonic if urine retention has been prolonged and stretched the tight junctions of the detrusor muscle. An atonic, distended bladder can occur with neurologic lesions affecting the sacral spinal cord (lower motor neuron lesions), especially if the bladder is easily expressed.Measuring the volume of urine left in the bladder after voiding can help determine if excessive residual volume is present. Residual volume postmicturition should be ≤0.4 mL/kg normally in the dog or cat (Labato 2005). Amounts in excess of that support a neurogenic cause of incontinence or a bladder that has lost tone due to stretching of the detrusor muscle. Rectal examination should be performed as part of the physical examination to help evaluate the bladder, urethra, and prostate. Vaginal inspection, including palpation, should be carried out during the physical examination of the female dog to determine if anomalies or signs of infection are present. Assessing the neurologic status of the patient should include stroking the perineum (perineal reflex) and/or squeezing the base of the penis or clitoris (bulbocavernosus reflex) to determine if reflex contraction of the anus occurs since absence of this reflex is indicative of pudendal nerve dysfunction and lower motor neuron abnormalities.
Additional diagnostic procedures should include a routine database with urinalysis, urine culture, and imaging of the urogenital tract, if indicated. In cases where UI has been confirmed but the cause remains undiagnosed or unresponsive to treatment, a urethral pressure profile (UPP) and/or cystometrogram may be warranted, if available. The UPP uses special equipment to establish the adequacy of urethral sphincter pressure as well as the functional urethral length. Cystometrography helps determine the bladder threshold volume needed to trigger involuntary contraction of the detrusor muscle. The specialized equipment and training needed for interpretation of data generally make the use of UPPs and cystometrography practical only for select referral centers.
TABLE 34-1. Causes of urinary incontinence
Nonneurogenic Urinary Incontinence
Nonneurogenic causes of UI can be further categorized as continuous, intermittent, and variable as listed in Table 34-2. This subdivision of causes assists the practitioner in determining the specific origin of UI.
FIGURE 34-2. Algorithm for the diagnosis and localization of neurogenic urinary incontinence.
FIGURE 34-3. Algorithm for the diagnosis of nonneurogenic urinary incontinence.
TABLE 34-2. Causes of nonneurogenic urinary incontinence
| Continuous | Intermittent | Variable |
| Ectopic ureter | Obstruction related | Sphincter mechanism incompetence |
| Patent urachus | Urge | Congenital defects such as: |
| Fistula | Pseudohermaphroditism Underdeveloped urethra or bladder Vaginal stricture Pelvic bladder syndrome |
Continuous Urinary Incontinence
Causes of continuous UI are primarily congenital in origin. Patent urachus is a congenital anomaly that results in the newborn voiding urine through its umbilicus. Fistulas, abnormal communications between two internal organs or an internal organ and the body surface, can develop as congenital urinary tract defects, as a result of trauma, or as a surgical complication post-ovariohysterectomy. The most common congenital fistula resulting in UI is an urethrorectal fistula although this abnormality can also occur as an aftermath of trauma. Clinical signs related to urethrorectal fistula are recurring urinary tract infection (UTI) and passage of urine from the anus. Urovaginal fistula producing incontinence can result from iatrogenic ligature entrapment of the distal ureter with the vaginal stump, when performing an ovariohysterectomy. Although ultrasonography may be helpful in detecting fistulas, radiographic contrast studies are often needed to make a definitive diagnosis.
Ectopic ureter (EcU) is one of the most common congenital anomalies resulting in continuous incontinence in the dog and cat. Occasionally the pet owner perceives the pet to have intermittent incontinence due to pooling of urine in the vagina and seemingly intermittent release. The female dog has the greatest incidence of EcU, accounting for at least 80% of all canine cases (Acierno and Labato 2006). Affected patients dribble urine but may also void urine in a normal manner. Clinical signs of concurrent UTI and/or vaginitis may temporarily shift the focus of the owner and veterinarian away from the primary underlying problem of incontinence.
Diagnosis of EcU has traditionally been accomplished by excretory urogram, retrograde contrast studies, and/or abdominal exploratory surgery.Helical computed tomography (CT) can identify over 90% of EcU cases (Samii et al. 2004), while transurethral cystoscopy has been reported to approach 100% accuracy in identification of this type of defect (Cannizzo et al. 2003). EcUs are surgically corrected, but UI is not always resolved completely due to the frequent presence of accompanying congenital defects.
Intermittent Urinary Incontinence
Intermittent UI of nonneurogenic origin falls primarily into the categories of obstructionrelated or urge incontinence. Obstruction-related, as the name implies, occurs as a consequence of obstruction to the lower urinary tract. As urine accumulates behind the obstruction, the pressure may eventually reach a point where it causes leakage around the obstruction. In most cases obstruction-related incontinence is diagnosed by the presence of lower urinary tract signs (e.g., pollakiuria and dysuria) and imaging. Relieving the obstruction will solve the obstruction-related incontinence, but depending on the length and severity of obstruction, it may leave the patient with a bladder that has impaired capability of contraction as a result of stretching of the muscle fiber-associated tight junctions.
Urge incontinence is the sudden urge to urinate accompanied by involuntary voiding of the bladder. Nonneurogenic urge incontinence is related to inflammation usually created by infection, uroliths, or neoplasia. Diagnosis is made by a combination of patient history, physical findings, urinalysis, urine culture, and abdominal imaging. Treatment is based on the nature of the underlying cause.
Intermittent incontinence has also been reported in cats positive for feline leukemia virus. The incontinence occurs primarily at rest and occurs in both sexes. The pathologic process by which the virus causes incontinence is unknown.
Variable Urinary Incontinence
Variable nonneurogenic causes of incontinence can result in either intermittent or continuous UI. One of these causes is the rare occurrence of pseudohermaphroditism, a congenital anomaly in which the gonads are of one sex but one or more contradictions exist in the morphologic criteria of sex. In the case where UI develops, pseudohermaphroditism may be found when looking for an underlying cause. Surgical intervention can sometimes result in correction of the associated UI. Other congenital problems such as an underdeveloped urethra or bladder or vaginal strictures can also contribute to incontinence in some cases. Underdevelopment of the urethra or bladder is generally detected in young patients by exclusion of other causes of incontinence and the use of UPP testing as well as cystometrography. Vaginal strictures, especially those distal to the urethral papilla, may cause pooling of urine, which later drips from the vagina. These abnormalities are most often detected by vaginoscopy and digital palpation.
Pelvic bladder is another congenital anomaly that can result in variable UI. Normally both the body and the neck of the bladder are situated within the abdomen. In patients with pelvic bladder, especially, large-breed, female dogs, the bladder is positioned with the neck and often part of the body within the pelvic canal. When the bladder is partially positioned within the pelvic canal, increased abdominal pressure is distributed unevenly along the length of the bladder, causing the normal mechanisms for maintaining continence to be disrupted. Although abdominal radiographs can indicate malpositioning of the bladder, contrast radiography is helpful in defining the problem further. Even more specific information can be obtained by utilizing a UPP and cystometrography measurements.
One of the most frequent causes of variable UI is urethral sphincter mechanism incompetence (SMI), which includes the category of hormone-responsive incontinence. This type of incontinence most commonly develops in adult spayed female dogs, with an incidence of approximately 20% in that population and a slightly higher incidence in large-breed, spayed female dogs, especially the Doberman pinscher, Old English sheepdog, Irish setter, and Rottweiler (Hoelzler and Lidbetter 2004). Affected dogs frequently dribble urine, especially when sleeping. It has been theorized that the lack of estrogen results in decreased urethral sphincter tone by decreasing the responsiveness of the internal sphincter α-receptors to sympathetic stimulation (Acierno and Labato 2006). Intact female dogs, male dogs, and spayed cats occasionally develop a similar type of SMI, but the role of hormones in its development is not clearly understood. Hormone-responsive incontinence is frequently diagnosed by exclusion of other causes and response to appropriate therapy. Definitive diagnosis of SMI presumed to be hormonal related can only be made by obtaining a UPP although most diagnoses are made from historical, physical, and imaging findings. Therapy of hormone-responsive incontinence and associated SMI consists of hormone replacement therapy and/or the administration of α-adrenergic agonists. Although adult pets are the population most commonly affected by SMI, a congenital, juvenile version of SMI exists in dogs. It has been estimated that 50% of dogs with juvenile SMI will become continent following their first estrus (Holt and Thrusfield 1993).
Neurogenic Urinary Incontinence
Recognition of urinary incontinence as neurogenic and localization of potentially associated lesions require that the patient be evaluated with a complete neurologic examination. Radiography is often indicated and special diagnostic procedures such as cerebrospinal fluid taps, myelograms, CT, and magnetic resonance scans may be required to identify or confirm a suspected cause.
Neurogenic UI usually occurs as a result of abnormalities of the detrusor reflex, urethral sphincter control, or reflex integration of the two mechanisms (Oliver and Lorenz 1993).
Detrusor Areflexia—Normal or Hypertonic Urethral Sphincter
One of the most common presentations identified with neurogenic UI consists of detrusor areflexia with a normal or hypertonic sphincter. In this situation the bladder is usually firmly distended with urine but resistant to expression. Causes of this type of presentation might be bilateral pelvic nerve damage (rare), bladder overdistention due to urethral obstruction, or, the most common cause, a lesion of the spinal cord cranial to L4 (UMN disorder). With UMN lesions varying degrees of hyperreflexia, paresis, and proprioceptive deficits of the front and/or hind limbs may be seen. Urine retention is more common than UI with UMN disorders. However, overflow incontinence (urine leaking from a grossly distended bladder) and spastic release of urine from reflex emptying of the bladder may be found in some patients. Treatment is directed at the underlying cause but may also include manual expression or catheterization of the bladder, monitoring for signs of UTI, and prevention of urine scalding.
Detrusor Areflexia—Urethral Sphincter Areflexia
Detrusor areflexia is also found in combination with urethral sphincter areflexia. Causes of this combination of abnormalities are related to lesions of the sacral spinal cord (S1–S3), sacral nerve roots, or bilateral dysfunction of both the pelvic and pudendal nerves. Patients in this category are considered to have lower motor neuron disorders and generally have an overdistended bladder that is atonic and easily expressed. Additional clinical signs may include tail paralysis, loss of sensation to the perineum, fecal incontinence and loss of anal tone, and varying degrees of deficits to the flexor muscles of the pelvic limbs, resulting in hind limb paresis and hyporeflexia. Lower motor neuron signs resulting in dysuria with overflow incontinence can also be found in dogs and cats affected by dysautonomia. Dysautonomia is an uncommon disorder of the autonomic nervous system that can affect multiple organ systems through disruption of parasympathetic and sympathetic innervation.
Detrusor Hyperreflexia
Idiopathic detrusor instability and hyperreflexia can be present in some dogs, especially middle-aged female dogs. This condition is characterized by a sudden urge to urinate followed by involuntary bladder contractions. Clinical signs include nocturia, pollakiuria, urgency, and incontinence. Idiopathic detrusor instability must be distinguished from urge incontinence due to inflammatory disease. The neurologic examination is generally normal; however, cerebellar disease with loss of its inhibitory influence on micturition can also result in detrusor instability and accompanying incontinence. Other signs of cerebellar disease would be expected to be present if detrusor instability is cerebellar related. In addition to establishing that the neurologic examination is normal, diagnosis of idiopathic detrusor instability requires ruling out other underlying causes through urinalysis, urine culture, and ultrasonography of the urinary tract. Cystometrography is needed for definitive diagnosis. Treatment of patients with idiopathic detrusor instability usually requires administration of anticholinergic drugs.
Detrusor–Urethral Dyssynergia
Although uncommon and largely undocumented, detrusor–urethral dyssynergia should be considered in patients that initiate voiding but have the urine stream suddenly interrupted. Urination may continue in small spurts. Detrusor–urethral dyssynergia may be the result of lesions of the spinal cord or of autonomic ganglia, resulting in an incoordination between detrusor contraction and sphincter relaxation in the act of micturition. Urethral stricture or obstruction should be ruled out.
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