Urinary Incontinence in 37 Horses

Urinary incontinence can be a sign of primary lower urinary tract disease, can accompany a variety of neurological diseases, or can be a complication of dystocia or multiple births. In addition, a syndrome of idiopathic incontinence, usually complicated by sabulous urolithiasis, occurs in geldings. Although a complete diagnostic evaluation may establish the cause in ~80% of affected horses, only ~20% can be treated successfully. Long-term management includes limiting infection and nursing care to minimize urine scalding of the hind limbs.

1. Introduction

Urinary incontinence is a frustrating problem in horses, because establishing a definitive diagnosis for the cause, in the absence of other lower urinary tract problems (e.g., developmental anomalies, cystolithiasis, urethral sphincter dysfunction) or neurological deficits, can be challenging [1,2]. Furthermore, because overflow incontinence may require months or years to become clinically recognized in horses with detrusor dysfunction, a careful history must be obtained to implicate dystocia, musculoskeletal injury, or prior neurological disease as a potential inciting cause. When detrusor dysfunction is recognized, affected horses have also usually developed sabulous urolithiasis, an accumulation of a large amount of urine sediment in the ventral aspect of the bladder [3]. This problem further prevents complete bladder emptying and contributes to further loss of detrusor function. The end result is complete bladder paralysis that can be complicated by ascending infection. Introduction of the term sabulous urolithiasis into the equine veterinary literature seems to have had the unfortunate effect of focusing practitioners’ attention on removing the sabulous debris, often initially confused with a large cystolith, rather than on investigating the cause of detrusor dysfunction. As a consequence, unnecessary cystotomies have been performed on many affected patients only to have the problem reoccur weeks or months later.

The purpose of this report is to describe a series of 37 horses with urinary incontinence. Complete diagnostic evaluation of the neurological and urinary systems was used to determine a cause of incontinence in ~80% of affected horses. Unfortunately, only ~20% of affected horses were treated successfully, and long-term management of the horses that were not subjected to humane euthanasia included intermittent antibiotic treatment to limit ascending infection and daily hygiene by the client to minimize urine scalding of the hind limbs.

2. Materials and Methods

The case records of 37 horses with urinary incontinence at Michigan State University (n = 31) and Washington State University (n = 6) from 1995 to 2003 were reviewed.

3. Results

In 37 horses with urinary incontinence, 2 female foals had urinary tract anomalies, 1 mare had estrogen-responsive urethral sphincter dysfunction, 7 had cystolithiasis (6 of 7 were mares), 9 were multiparous mares (some with a history of dystocia), 11 had neurological disease accompanied by incontinence (7 geldings and 4 mares), and 7 geldings had "idiopathic" incontinence with bladder paresis/paralysis. The latter cases were termed idiopathic because primary neurological disease was not identified to explain bladder dysfunction. Additionally, other neurological deficits were not apparent at the time of presentation (although prior neurological disease could not be ruled out with complete confidence). All in all, detrusor function was normal in 10 horses (foals with anomalies, mare with urethral sphincter dysfunction, and 7 horses with bladder stones). In the multiparous mares, birth trauma to the urethral sphincter was considered the primary cause of incontinence; however, detrusor dysfunction and sabulous urolithiasis were also found in several mares. Of the 11 horses with neurological disease and incontinence, 3 of the cases were attributed to equine protozoal myeloencephalitis (EPM), 3 had cervical spinal cord compression, 3 had cauda equina syndrome, 1 had equine degenerative myelopathy, and 1 surviving horse had an undiagnosed neurological disorder from which it fully recovered. Of interest, signs of an "upper motor neuron bladder" (characterized by a turgid bladder, increased urethral sphincter tone, and uncontrolled "squirts" of urine) were observed in only one horse, the mare with the undiagnosed neurological disorder.

A cause of incontinence was diagnosed, or highly incriminated, in 30 of 37 horses (81%), but the diagnosis remained open (idiopathic) in the remaining 7 geldings. Of the 37 horses, 25 (68%) were discharged alive (2 foals, 1 mare with estrogen-responsive urethral sphincter dysfunction, 6 horses with cystolithiasis, 7 multiparous mares, 6 horses with primary neurological disease, and 3 horses with idiopathic bladder paralysis). Incontinence prompted either an immediate decision for euthanasia in four horses (two multiparous mares and two geldings with idiopathic bladder paralysis) or a decision for euthanasia was made after several days or weeks of hospital treatment for persisting incontinence (four horses), combined problems of neurological disease and incontinence (three horses), and development of osteomyelitis after resolution of incontinence attributed to transient cauda equine neuritis (one horse). In addition, euthanasia was subsequently performed on 7 of 25 horses that were initially discharged because of persistent incontinence.

All in all, incontinence was an important factor leading to a decision for euthanasia in 18 horses. Of 18 surviving horses, incontinence completely resolved in 7 horses (3 mares with cystoliths, 2 foals with developmental anomalies, 1 mare with neurological disease, and 1 gelding with transient idiopathic bladder paresis). In addition, incontinence in the mare with urethral sphincter dysfunction has been successfully managed with estrogen treatment, leading to an overall treatment success in 8 of 37 horses (21%). Of the remaining 10 horses, incontinence persists in 7 horses (2 multiparous mares, 2 horses that had EPM, 2 geldings with idiopathic bladder paralysis, and 1 mare with cystolithiasis), and 3 horses have been lost to follow-up.

4. Discussion

In addition to illustrating the variety of problems that may lead to urinary incontinence, this case series reveals that incontinence may be a presenting complaint for bladder stones in mares and that multiple births with or without dystocia may be an under-recognized cause of incontinence. Although neurological disease has long been recognized as a cause of incontinence, this series also reveals that spinal cord lesions cranial to the sacral segments (e.g., cervical spinal cord compression) can result in incontinence. The latter finding should not really be surprising as both "upper motor neuron" and "lower motor neuron" bladder signs are recognized in human patients with spinal cord injury at all levels of the cord. Despite providing aggressive supportive care in several horses in this series, the results further indicate that a guarded to poor prognosis should be issued for horses with detrusor dysfunction leading to a large atonic bladder and sabulous urolithiasis. Again, this relatively poor prognosis can likely be attributed to a long-standing (months to years) detrusor dysfunction before overflow incontinence becomes a recognizable problem.

The cause of idiopathic incontinence in geldings remains unknown. However, suggested causes include historical neurological disease or neurological disease in which other deficits may be subtle or absent. Although not definitively documented in any of these cases, a potential cause of idiopathic incontinence is musculoskeletal disease that results in lower back, sacral, or hind limb pain. If a painful musculoskeletal condition limits a horse’s ability to posture to urinate, bladder emptying may be incomplete during micturition. Incomplete bladder emptying could lead to sabulous urolithiasis, myogenic detrusor dysfunction, and eventual bladder paralysis. Thus, a careful history should be taken in affected geldings, including questioning about urination, before the problem is misdiagnosed as a cystolith and an unnecessary cystotomy is pursued. Careful palpation of the bladder per rectum is usually helpful in discriminating between the two problems; cystoliths are usually found in small bladders (incontinence often accompanied by stranguria), whereas sabulous accumulations are found in large atonic bladders and the urine sediment can typically be indented during palpation. When a diagnosis of idiopathic incontinence with sabulous urolithiasis is detected, bladder lavage is usually successful in removing the accumulated urine sediment, although the procedure often must be repeated at regular intervals. Intermittent use of antibiotics and feeding a forage low in calcium are other treatment recommendations.

In summary, in horses with an underlying disorder that can be corrected (e.g., congenital anomaly or cystolith), the prognosis for correction of incontinence is generally favorable. With acute onset of incontinence caused by neurological disease, the prognosis may also be favorable as long as evidence of detrusor and sphincter function returns within 10 - 14 days after onset. However, the prognosis for recovery from long-standing incontinence caused by bladder paralysis is generally poor, and patient management is complicated by sabulous concretions and urinary tract infections. Urine scalding is an added problem for horses; thus, maintenance of horses with bladder paresis or paralysis requires a client dedicated to nursing care and may further require intermittent bladder lavage to remove accumulation of urine sediment.