Urinary incontinence: A drippy problem (Proceedings)

Urinary incontinence: Urinary incontinence is a frustrating disorder in horses because establishing a definitive diagnosis for the cause, in the absence of other lower urinary tract or neurological signs, is difficult and substantial nursing care by the client is required to minimize urine scalding of the hind limbs (Figure 1 a). Further, horses with detrusor dysfunction typically develop sabulous urolithiasis, accumulation of a large amount of urine sediment in the ventral aspect of the bladder. Because horses normally excrete large amounts of crystalloid material in urine daily, sabulous urolithiasis is usually a consequence, not the cause, of urinary incontinence. However, accumulated sediment can exacerbate bladder distension and likely contributes to further loss of detrusor function and eventual complete bladder paralysis (Figure 1a, 1b & 1c).

Figure 1. a Urine scalding of the perineum of a mare that developed urinary incontinence following a dystocia (left); an enlarged bladder filled with a "urolith" of sabulous urine sediment at post-mortem (1 b); the mass of urine sediment (sabulous urolith) from the bladder in the middle image weighed 5 kg and could be cut rather easily with a knife (1 c).

Physiology and pathophysiology

Urinary incontinence develops when intravesicular pressure, increased by detrusor contraction or by contraction of abdominal musculature, exceeds outflow resistance, generated by the urethral sphincter, and results in involuntary passage of urine. This may occur with both neurological and non-neurological disorders. The classic example of neurological incontinence is that associated with equine herpes virus-1 myelitis (likely affecting both detrusor and sphincter function) while ectopic ureter and urolithiasis are non-neurological disorders that may have urinary incontinence as a presenting complaint.

1 b

Classically, neurological bladder dysfunction and associated incontinence has been categorized by disorders affecting gray matter of the sacral segments, resulting in loss of lower motor neuron function (a lower motor neuron bladder) and disorders affecting the lumbar or higher portions of the spinal cord, resulting in loss of upper motor neuron function (an upper motor neuron bladder). Lower motor neuron damage leads to loss of detrusor function and overflow incontinence and a large, easily expressed bladder is found on rectal palpation. Detrusor arreflexia (DA) is the term used to describe this type of dysfunction in affected human patients. Injury to the spinal cord above the sacral segments can lead to detrusor hyperreflexia (DH) and detrusor-external sphincter dyssynergia (DESD), a lack of coordination between detrusor and urethral sphincter activity. With upper motor neuron disease increased urethral resistance, requiring greater intravesicular pressure before voiding can occur and may initially be observed as short bursts of urine passage with incomplete bladder emptying. Rectal examination may reveal a turgid bladder that is small, normal, or large in size.

1 c

Although this classical separation of lower from upper motor neuron bladder may be useful for neuroanatomical localization of spinal cord disease, it is important to recognize that the separation is not absolute. For example, in a report of urodynamic findings in 284 people with cervical spinal cord injuries, 85% had DH with or without DESD while 15% had DA. Similarly, the reverse was found with sacral cord injuries: 64% had DA as expected while the remainder either had no bladder dysfunction or had DH with or without DESD. In human patients with incontinence, differentiation of DH, DESD, and DA generally requires urodynamic and electromyographic studies that are rarely pursued in horses with urinary incontinence. Further, upper motor neuron signs of bladder dysfunction may be missed in horses until overflow incontinence develops as a result of accumulation of urine sediment (sabulous urolithiasis) and progressive loss of detrusor function. For these reasons bladder paralysis and overflow incontinence, consistent with lower motor neuron disease, may occasionally be found in horses with neurological diseases that typically do not affect the gray matter of the sacral segments (cervical stenotic myelopathy or equine degenerative myelopathy).

Causes of urinary incontinence

Urinary incontinence has several causes and it is logical to categorize them as non-neurological, neurological, or idiopathic. Non-neurological causes of incontinence can be further divided into anomalies of development, cystolithiasis, or a consequence of pregnancy and parturition. The most common developmental defect is ectopic ureter but a variety of other anomalies have also resulted in incontinence. Unlike cystolithiasis in male horses that usually results in dysuria and post-exercise hematuria, incontinence has been one of the more common presenting complaints for female horses with cystoliths in the author's experience.

Sphincter incontinence (and bladder paresis) can develop in multiparous mares with repeated foaling trauma. The problem may initially be recognized as urine pooling in the vagina, rather than sphincter incontinence. During pregnancy the lower urinary tract in women undergoes anatomical and functional changes to minimize the risk of incontinence. Nevertheless, 30-40% of pregnant women experience some degree of urinary incontinence during pregnancy. Coupled with pelvic canal trauma during childbirth, incontinence may persist after parturition and multiple vaginal deliveries are a well-recognized risk factor for chronic incontinence in women. Although changes in lower urinary tract anatomy and physiology have not been studied in mares, it is likely that pregnancy and parturition may be an important, and perhaps under-recognized, cause of urinary incontinence in multiparous mares. A history of dystocia, even several years previously, should be considered a potential inciting cause in mares presenting for evaluation of incontinence.

Neurological causes of incontinence include equine herpes virus-1 myelitis, cauda equine neuritis, intoxications, and sacral trauma. However, the spectrum of neurological diseases that may be accompanied by incontinence appears to be wider than previously thought and may include horses afflicted with equine protozoal myeloencephalitis (EPM), cervical stenotic myelopathy, and equine degenerative myelopathy. Although the latter two diseases do not directly affect the sacral segments, bladder paralysis, overflow incontinence, and sabulous urolithiasis can develop in some affected horses. This recognition calls into question the traditional neurological categorization of incontinence described above as an upper motor neuron bladder or a lower motor neuron bladder. One explanation for finding DA in horses that have no apparent damage to sacral segments (i.e., with cervical cord compression) is that the earlier signs of an upper motor neuron bladder (DH-DESD) may have been overlooked. Incontinence does not become a complaint until weeks or months into the disease process after prolonged detrusor dysfunction ultimately leads to DA. Another explanation may be that control of bladder and urethral sphincter function may be more complex than currently understood; thus, neural lesions may have variable effects on lower urinary tract function.

Finally, idiopathic bladder paralysis syndrome, complicated by incontinence and sabulous urolithiasis, remains an important contributor to the overall number of horses presented for evaluation of urinary incontinence. Although the cause remains elusive, either historical neurological disease or more subtle neurological disease for which gait deficits are not apparent may be the cause in some horses. As an example of historical neurological disease, a clinical diagnosis of equine protozoal myelitis (EPM) was established in a horse with hind limb ataxia and weakness and urinary incontinence seen by the author. Treatment included an indwelling bladder catheter and anti-protozoal drugs. Both gait deficits and incontinence resolved within a month's time yet the horse presented again 4 years later for urinary incontinence due to bladder paralysis. Although gait remained normal, it is likely that detrusor dysfunction never fully recovered and eventually led to complete bladder paralysis. In support of subtle neurological disease as a potential cause of idiopathic bladder paralysis, bladder dysfunction has been reported in human patients with thoracolumbar spinal cord injury that are neurologically intact on clinical examination. Another speculated cause of idiopathic bladder paralysis syndrome is chronic pain in the lumbosacral area. Pain that prevents affected horses from assuming a normal posture for urination could lead to incomplete emptying of the bladder. Over time, urine sediment can accumulate and lead to irritation of the bladder mucosa and underlying detrusor muscle. In this scenario sabulous urolithiasis could actually cause progressive loss of detrusor function leading to complete paralysis. This pathogenesis has been termed myogenic bladder paralysis but this syndrome remains largely speculative at the present time.

In a series of 34 horses with urinary incontinence as a presenting complaint evaluated by the author, two female foals had urinary tract anomalies (ectopic ureter), five had cystolithiasis (four of five were mares), 10 were multiparous mares (some with a history of dystocia), 10 had neurological disease accompanied by incontinence (six geldings and four mares), and seven geldings had "idiopathic" incontinence complicated by sabulous urolithiasis. The latter cases were termed idiopathic because no primary neurological disease was identified to explain bladder dysfunction and other neurological deficits were not apparent. Of the 10 horses with neurological disease and incontinence, three were attributed to EPM, three had cervical spinal cord compression, cauda equine neuritis was suspected in two, equine degenerative myelopathy was found in one, and one surviving horse had an undiagnosed neurological disorder. In addition to illustrating the variety of problems that may lead to incontinence, this series revealed that incontinence with bladder stones is more common in mares, that multiple foalings and dystocia may be an under-recognized cause of incontinence, and that multiple neurological diseases may be accompanied by incontinence.

Figure 2. a Cytoscopic images revealing sabulous urolithiasis, accumulation of urine sediment in the ventral aspect of the bladder, and dilation of the ureteral orifices (2 b) in two horses with long-standing urinary incontinence.

Diagnostic evaluation

In addition to complete physical and neurological examinations, a careful history should be collected during evaluation of affected horses because the initiating cause of bladder dysfunction and incontinence may have occurred months to years before incontinence actually became a problem. Owners should be carefully questioned about when incontinence is observed and whether or not and how often the horse assumes a posture to urinate. For example, involuntary urine passage that is limited to exercise may indicate decreased sphincter tone, rather than detrusor dysfunction, as the cause of incontinence. Similarly, horses that posture to urinate are assumed to have intact sensation of bladder fullness while those that never posture have likely lost bladder sensation as well as motor function. Because one of the major complications of incontinence is ascending urinary tract infection (UTI), collection of a urine sample for urinalysis and quantitative culture should be included in the minimum data base for affected horses. Further, endoscopic evaluation of the lower urinary tract is indicated to exclude congenital or acquired anatomical defects that may interfere with urine storage as well as for assessment of integrity of the ureteral orifices. With long-standing incontinence and detrusor dysfunction, the ureteral openings may become dilated due to chronic distension and a loss of bladder compliance. Endoscopic visualization of open ureteral orifices would imply vesiculoureteral reflux and increased risk of upper tract infection (Figure 2).

2 b

Treatment

Treatment is always directed toward correction of the underlying cause. Thus, horses with anomalies of development or cystoliths as the cause of incontinence will usually respond favorably to correction of the primary problem. Unfortunately, horses with subtle neurological deficits accompanied by incontinence or with idiopathic incontinence are often not presented until months or years after the damage initially occurred. By that time, most horses have developed irreversible detrusor dysfunction regardless of the initiating cause and a successful response to treatment should not be expected. It is not uncommon, however, for geldings with incontinence and sabulous urolithiasis to be presented for suspected cystolithiasis. These patients should be carefully evaluated before an unnecessary cystotomy is performed because thick urine sediment can generally be removed by bladder lavage (via a urethral catheter) and rectal manipulation of the bladder. Careful rectal palpation is usually rewarding in discriminating between accumulation of urine sediment (which can be indented with firm digital pressure) and a true cystolith. Further, that latter problem should not demonstrate overflow incontinence during palpation of the bladder. In addition to having clients provide daily care to minimize urine scalding, reduction of dietary calcium intake is recommended in an attempt to limit recurrence of sabulous urolithiasis. Appropriate oral antibiotic treatment is also recommended if UTI is detected and many, if not most, affected horses may need to remain on antimicrobial treatment indefinitely.

Administration of cholinergic drugs has been advocated to stimulate detrusor function in horses with bladder paralysis. Subcutaneous administration of bethanechol chloride is sometimes used as a diagnostic test of residual detrusor function because the drug causes rather rapid detrusor contraction. The drug should never be given intravenously or intramuscularly because loss of muscarinic receptor selectivity when given by these routes causes serious adverse effects on the cardiovascular and respiratory systems. No pharmacokinetic data for bethanechol chloride exist in horses; however, the drug has been used subcutaneously at doses of 0.025-0.075 mg/kg two or three times a day. Although there are anecdotal reports of efficacy (observation of more vigorous voiding activity after administration), this drug is unlikely to have any beneficial effect when the bladder is completely atonic or arreflexic. If the detrusor is capable of generating weak contractions, then bethanechol treatment may be useful. Although oral administration of bethanechol (0.25-0.75 mg/kg two to four times a day) has been described, a favorable response to treatment has not been reported or observed by the author. Disappointing results are more likely a consequence of long-standing detrusor dysfunction rather than poor intestinal absorption of the drug.

Mares may develop overflow incontinence in the immediate post-partum period. This condition is associated with bladder and urethral trauma during delivery. Early recognition of this complication and temporary placement of an indwelling catheter to decompress the bladder in combination with anti-inflammatory drugs is the treatment of choice for this condition. Prophylactic administration of antimicrobial drugs, typically a trimethoprim-sulfonamide combination, is also indicated. Despite aggressive post-partum management, some affected mares may never fully recover. When the condition is not recognized in the immediate post-partum period, mares may progress to end stage bladder paresis and incontinence months to years later. Aggressive decompression of the bladder, with an indwelling urinary catheter, is also the treatment of choice for horses with acute onset of bladder paresis and incontinence attributable to neurological disease. While catheterized, horses should again be treated with prophylactic antibiotics in order to decrease the risk of UTI.

In horses that have decreased urethral sphincter tone with normal detrusor function or that have DESD, use of the α-adrenergic agonist phenylpropanolamine (0.5-1.0 mg/kg orally 1-3 times a day) to increase sphincter tone has been recommended but a successful response has not been reported. As with bethanecol, dosing regimens for many of the autonomic drugs used in incontinent small animals have been extrapolated from use in these species because no pharmacokinetic data in horses is available. On a more positive note, treatment of a few mares with estradiol cypionate (4-10 µg/kg IM, daily for three days then every other day) has improved, but not cured, urinary incontinence. Estrogen receptors are present in the bladder neck and the hormone appears to modulate the effect of norepinephrine on α-adrenergic receptors in the urethral sphincter, thereby improving urethral sphincter tone.

Prognosis

In horses with an underlying disorder that can be corrected surgically (congenital anomaly or cystolith), the prognosis is generally favorable. With acute onset of incontinence due to neurological disease, the prognosis can also be favorable as long as evidence of detrusor and sphincter function returns within 10-14 days after onset. In contrast, the prognosis for recovery from long-standing incontinence due to bladder paralysis is generally poor and patient management is complicated by urine scalding, sabulous concretions, and UTI. Maintenance of horses with bladder paresis and urinary incontinence requires a client dedicated to nursing care and may further require intermittent bladder lavage to remove accumulation of urine sediment.

Supplemental readings available on request to the author