Urinary incontinence: A drippy problem (Proceedings)


Urinary incontinence: A drippy problem (Proceedings)

Apr 01, 2010

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).
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).

Physiology and pathophysiology

1 b
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 c
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.

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).