Sabulous cystitis marks neurologic injury to bladder

Sabulous cystitis marks neurologic injury to bladder

Mar 01, 2002
By staff

Though the equine species in general excretes urine with high mineral content, especially calcium carbonate, and despite a normally alkaline urine pH, which tends to favor formation of urinary tract stones, equine urinary tract lithiasis is relatively uncommon.

Equine urine production tends to be very turbid, due to high calcium carbonate content and to the secretion of mucoproteins from glands in the renal pelvis. Equine urine has a mucoid, tenacious content unique to the species that may help to lubricate and protect the luminal surfaces of the tract from scabrous damage from crystalluria.

Incontinence is the observation of unintended urine dribbling, intermittent or continuous, which is not linked to normal posturing and micturition. When chronic, prolonged contact of urine with the skin leads to scalding and dermatitis around the perineum and medial aspect of the hind limbs.

Incontinence diagnoses

Urolithiasis is one of the differential diagnoses for incontinence, along with cystitis; ectopic ureters; vaginal malformation; neurologic disease or injury to either the spinal cord or to the spinal nerves of the sacral segments; urethral incompetence; neoplasia, pyelonephritis, and hypoestrogenism.

As herbivores, normal urine pH in adult horses ranges from 7.0 to 9.0. Despite this alkaline milieu, the most important homeostatic scheme influencing freedom from calculus formation in the urinary tract appears to be the ability to posture and void the bladder at will frequently.

Incontinent horses due to neurologic dysfunction dribble urine because effective detrusor contraction is absent and bladder contents are not subject to muscle contraction and forced ejection from the body, as occurs in a normal state. The neurologic circuitry that mediates the micturition reflex is complex, and examples of disease processes that can interfere with various segments of the reflex loop include herpes myelitis, polyneuritis equi (cauda equine syndrome), and equine protozoal myeloencephalitis.

Bladders that become paralyzed because of these pathologic processes often show deposition of a sandy, crystalloid sediment, a condition called sabulous cystitis, instead of formed uroliths. Bladder paralysis permits settling of deposits onto the bladder floor, where the material's weight prevents it from being extruded during dribbling of urine from the incontinent bladder. The sediment contributes to inflammation and irritation of the mucosal lining, exacerbating cystitis and most likely, the discomfort of the horse. Analysis of the mineral content of sabulous sediment in horses has shown the main component to consist of calcium carbonate composed of calcite and vaterite, and magnesium, sodium, potassium, reduced iron, copper, manganese, and traces of phosphates, sulfates, and silicates.


Careful neurologic examination may help differentiate whether there are upper motor neuron or lower motor neuron signs affecting the bladder, although horses with this problem are typically presented for assessment well into the chronic stage of dysfunction,when clinical findings tend to blur.

Spinal cord disease affecting segments cranial to the sacral portion of the cord will elicit upper motor neuron signs and a bladder that may respond to detrusor stretching by partial voiding. Palpation of the bladder per rectum may reveal moderate distension, because the proximal urethral sphincter will be tonic. This means attempts to express the bladder through the rectal wall will be met with resistance.

Lower motor neuron signs result in bladder atony, and palpation per rectum typically demonstrates marked distension yet will be easily expressed manually.

Once the disease becomes chronic, however, clinical distinction between the original type of neurologic deficit becomes difficult to impossible, as the ongoing presence of sabulous sediment and attendant inflammation lead to progressive loss of detrusor function and eventual signs of complete bladder atony. Although some horses with paralytic bladders will show additional signs of neurologic injury such as ataxia, flaccid tail or anal tone, or denervation atrophy of hindquarter muscle groups, other horses may be presented for evaluation in which no additional neurologic deficits can be determined.


The presence of sabulous cystitis, then, is a symptom of underlying neurologic injury to the urinary bladder. The condition is diagnosed via cystoscopic visualization of the bladder interior following evacuation of urine from the lumen.

Cystic calculi can be palpated with transrectal ultrasound, but cystoscopy is preferred. Endoscopic imaging permits detection of findings such as hydroureter, and shows the volume of sediment present and degree of concomitant mucosal damage. The remainder of the urinary tract should be further examined.

Treatment methods

Treatment of the condition involves lavage of the bladder lumen with isotonic solutions to remove the sediment load, administration of systemic antibiotics chosen with regard for culture results and sensitivity testing of a catheterized urine sample, anti-inflammatories, and urine acidification. Lavage can be achieved through a catheter. Placement of an indwelling catheter for a brief initial period helps lower urine stasis and maintains the bladder in a fairly decompressed state, abating further detrusor damage. Adding acetic acid to decrease luminal pH during lavage is advocated. Acidification of equine urine is achievable with oral dosing with ammonium chloride(25-50 gm PO q 12 ­ 24 hrs), ammonium sulfate(175 mg/kg PO q 12 hours), and ascorbic acid(10-20 gm PO q 12 24 hours). Salt should be provided, to increase water consumption and fluid diuresis.

Pharmacologic options

In addition to those measures, pharmacologic manipulation to emulate the missing autonomic nervous system input may be attempted.

In all cases, provide owners with a guarded to negative prognosis for recovery of normal function in horses in which incontinence has been present for several months or longer. As for valuable horses, particularly broodmares, attempts to manage the problem have met with modest success, but a favorable response to treatment has been noted in some cases.

The parasympathomimetic drug bethanechol augments contractility of the detrusor smooth muscle, in an effect similar to its prokinetic actions on gastric musculature in cases of gastroparesis or delayed gastric emptying. Bethanechol (20-40 mg or 0.07 mg/kg SQ q 8 hours, 80 mg PO q 8 hours do not give I.V. or I.M.) is not currently available as a proprietary formulation but can be obtained from compounding pharmacies. Phenoxybenzamine, (0.2-0.7 mg/kg PO, q 6-8 hrs) is an adrenergic antagonist, and may be given to help relax the distal urethral sphincter in cases where the condition is determinedly due to upper motor neuron damage.

Phenazopyridine (4 mg/kg PO q 8-12 hours), an azo dye compound that acts to confer relief from irritation or spasm of the urinary tract mucosa via local anesthetic activity, may also be administered in the initial management of the cystitis caused by the sedimentary accumulation. This compound discolors urine. Owners should be warned that it will stain skin and textiles which inadvertently come into contact with the substance. In humans with urinary tract inflammation the agent alleviates symptoms of dysuria, frequency, burning, and the sensation of urgency.

Mares in which urinary incontinence is from hypoestrogenism may enjoy a better prognosis for response to treatment. Successful management of the condition in such mares has been observed in association with administration of estradiol cypionate or benzoate (5-10 _g/kg I.M. q 48 hours).

Dr. Sprayberry, dipl. ACVIM, is a 1988 graduate of the University of California, Davis, School of Veterinary Medicine. She presently works for Estrella Equine Clinic in California.


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