From hematuria to perineal scalding: Urinary tract disorders (Proceedings)
Urinary tract disorders occur infrequently in horses but represent significant diagnostic and therapeutic challenges. In this article, we will discuss identification and management of urinary incontinence and bladder dysfunction, urolithiasis, and hematuria.
Three types of problems can lead to disorders of micturition: 1) the reflex or upper motor neuron bladder, 2) paralytic or lower motor neuron bladder, and 3) the myogenic bladder. The last two conditions result in an overflow bladder. The upper motor neuron bladder commonly not recognized in horses until it progresses to an overflow bladder.
Bladder function can be most simply described by considering the events during bladder filling and bladder emptying. During filling of the bladder, sympathetic nerves stimulate alpha receptors in the urethra which increase urethral tone to prevent urine flow. At the same time, sympathetic receptors in the bladder wall (Beta receptors) relax the bladder detrusor muscle allowing filling. Increasing stretch of the bladder wall sends impulses to the brain where bladder fullness is sensed and micturition is initiated. Impulses are sent via parasympathetic nerves to contract the detrusor muscle. Simultaneously inhibition of sympathetic nerves relaxes the urethral sphincters and removes the sympathetic relaxation affect on the detrusor. Thusly, urethra relaxation is coordinated with detrusor contraction creating bladder emptying.Upper motor neuron disease of the bladder usually is associated with extensive spinal cord lesions (EPM, Herpes Virus, West Nile Virus) creating a high degree of neurologic deficits. An upper motor neuron bladder is manifest as periodic dribbling of urine that is exacerbated by exercise, coughing, etc. Examination only rarely reveals urine scalding. Rectal examination reveals a distended bladder and high urethral tone that prevents bladder evacuation by the examiner. In chronic situation reflex bladder emptying develops that leads to reflex micturition. Residual urine is left in the bladder after this reflex voiding and can lead to secondary bacterial infection.
Lower motor neuron bladder results from lumbosacral trauma, herpes virus, cauda equina neuritis, sorghum cystitis, and iatrogenic due to epidural administration of alcohol. Loss of anal sphincter tone, perineal hypalgesia, and tail paralysis commonly accompany the lower motor neuron bladder with many of these diseases. Perineal scalding is common. Rectal examination reveals that the bladder is distended and easily expressed.
Myogenic problems occur as a result of cystic calculi, cystitis, and accumulation of sabulous or mucoid urinary sediment (sludge) in the bladder. The most common form is with sludge accumulation in geldings. The weight of this material stretches the detrusor muscle over time preventing normal contraction and micturition. Severe distentions can breakdown tight junctions preventing depolarization waves from travelling across the detrusor muscle. As the disease progresses and secondary cystitis and urethritis (ammonia and bacteria) ensue, urethral dysfunction leads to incontinence. This can occur with no other signs of neurologic disease. Urine dribbling and perineal scalding are noted. Rectal examination reveals bladder distention. Earlier in the disease, there is urethral resistance to manual expression of urine. As the disease progresses, the urethral can be involved and the bladder easily expresses.
Cystitis and urethritis can lead to clinical signs of incontinence. Sometimes these diseases complicate upper motor neuron, lower motor neuron, and myogenic bladder disease as urinary retention leads to cystitis. Cystitis can also occur rarely as a primary disease and can lead to irritation of stretch receptors in the bladder wall causing regular stimulation of micturition. This can lead to frequent urination (pollakiuria). Horses commonly frequently posture to urinate as a result of abdominal pain so this must be differentiated from colic.
Diagnosis of these conditions is most commonly based on careful observation of clinical signs and examination of the bladder on rectal exam. Pressure testing can be performed to determine the amount of function of the urethra and detrusor in cases where adequate assessment via rectal examination is not possible. Identification of other neurologic signs, cerebrospinal fluid cytology and antibody testing (EPM), herpes virus PCR and serology, and West Nile Virus Capture ELISA can help differentiate etiologies of neurologic disease. Therapy should be directed at the specific etiology and at avoiding urine retention via intermittent or indwelling catheters. Antimicrobial therapy becomes important for secondary bacterial cystitis.
Urolithiasis and sabulous cystitis can often be identified via rectal examination or via rectal examination. Catheterization and removal of urine may facilitate palpation of urolithiasis. Endoscopic examination of the bladder can confirm rectal examination findings and estimate the size of the stones for planning removal.
Pharmacologic support of bladder function can improve bladder function. The alpha-adrenergic blocker phenoxybenzamine (0.7 mg/kg per os every 6 hours) helps to reduce urethral resistance facilitating emptying of the upper motor neuron bladder. Bethanochol chloride (0.25 to 0.75 mg/kg subcutaneously 3 times daily; 80 mg PO 3 times daily) is a parasympathomimetic agent that mimics the action of acetylcholine to increase the tone of the detrusor muscle. If the bladder is completely paralyzed, bethanechol will not generate contractions.