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.
Though the equine species in general excretes urine with high mineralcontent, especially calcium carbonate, and despite a normally alkaline urinepH, which tends to favor formation of urinary tract stones, equine urinarytract lithiasis is relatively uncommon.
Equine urine production tends to be very turbid, due to high calciumcarbonate content and to the secretion of mucoproteins from glands in therenal pelvis. Equine urine has a mucoid, tenacious content unique to thespecies that may help to lubricate and protect the luminal surfaces of thetract from scabrous damage from crystalluria.
Incontinence is the observation of unintended urine dribbling, intermittentor continuous, which is not linked to normal posturing and micturition.When chronic, prolonged contact of urine with the skin leads to scaldingand dermatitis around the perineum and medial aspect of the hind limbs.
Urolithiasis is one of the differential diagnoses for incontinence, alongwith cystitis; ectopic ureters; vaginal malformation; neurologic diseaseor injury to either the spinal cord or to the spinal nerves of the sacralsegments; 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 influencingfreedom from calculus formation in the urinary tract appears to be the abilityto posture and void the bladder at will frequently.
Incontinent horses due to neurologic dysfunction dribble urine becauseeffective detrusor contraction is absent and bladder contents are not subjectto muscle contraction and forced ejection from the body, as occurs in anormal state. The neurologic circuitry that mediates the micturition reflexis complex, and examples of disease processes that can interfere with varioussegments of the reflex loop include herpes myelitis, polyneuritis equi (caudaequine syndrome), and equine protozoal myeloencephalitis.
Bladders that become paralyzed because of these pathologic processesoften show deposition of a sandy, crystalloid sediment, a condition calledsabulous cystitis, instead of formed uroliths. Bladder paralysis permitssettling of deposits onto the bladder floor, where the material's weightprevents it from being extruded during dribbling of urine from the incontinentbladder. The sediment contributes to inflammation and irritation of themucosal lining, exacerbating cystitis and most likely, the discomfort ofthe horse. Analysis of the mineral content of sabulous sediment in horseshas shown the main component to consist of calcium carbonate composed ofcalcite 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 areupper motor neuron or lower motor neuron signs affecting the bladder, althoughhorses with this problem are typically presented for assessment well intothe chronic stage of dysfunction,when clinical findings tend to blur.
Spinal cord disease affecting segments cranial to the sacral portionof the cord will elicit upper motor neuron signs and a bladder that may respond to detrusor stretching by partial voiding. Palpation of the bladderper rectum may reveal moderate distension, because the proximal urethralsphincter will be tonic. This means attempts to express the bladder throughthe rectal wall will be met with resistance.
Lower motor neuron signs result in bladder atony, and palpation per rectumtypically demonstrates marked distension yet will be easily expressed manually.
Once the disease becomes chronic, however, clinical distinction betweenthe original type of neurologic deficit becomes difficult to impossible,as the ongoing presence of sabulous sediment and attendant inflammationlead to progressive loss of detrusor function and eventual signs of completebladder atony. Although some horses with paralytic bladders will show additionalsigns of neurologic injury such as ataxia, flaccid tail or anal tone, ordenervation atrophy of hindquarter muscle groups, other horses may be presentedfor evaluation in which no additional neurologic deficits can be determined.
The presence of sabulous cystitis, then, is a symptom of underlying neurologicinjury to the urinary bladder. The condition is diagnosed via cystoscopicvisualization of the bladder interior following evacuation of urine fromthe lumen.
Cystic calculi can be palpated with transrectal ultrasound, but cystoscopyis preferred. Endoscopic imaging permits detection of findings such as hydroureter,and shows the volume of sediment present and degree of concomitant mucosaldamage. The remainder of the urinary tract should be further examined.
Treatment of the condition involves lavage of the bladder lumen withisotonic solutions to remove the sediment load, administration of systemicantibiotics chosen with regard for culture results and sensitivity testingof a catheterized urine sample, anti-inflammatories, and urine acidification.Lavage can be achieved through a catheter. Placement of an indwelling catheterfor a brief initial period helps lower urine stasis and maintains the bladderin a fairly decompressed state, abating further detrusor damage. Addingacetic acid to decrease luminal pH during lavage is advocated. Acidificationof equine urine is achievable with oral dosing with ammonium chloride(25-50gm PO q 12 24 hrs), ammonium sulfate(175 mg/kg PO q 12 hours), andascorbic acid(10-20 gm PO q 12 24 hours). Salt should be provided, to increasewater consumption and fluid diuresis.
In addition to those measures, pharmacologic manipulation to emulatethe missing autonomic nervous system input may be attempted.
In all cases, provide owners with a guarded to negative prognosis forrecovery of normal function in horses in which incontinence has been presentfor several months or longer. As for valuable horses, particularly broodmares,attempts to manage the problem have met with modest success, but a favorableresponse to treatment has been noted in some cases.
The parasympathomimetic drug bethanechol augments contractility of thedetrusor smooth muscle, in an effect similar to its prokinetic actions ongastric 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 donot give I.V. or I.M.) is not currently available as a proprietary formulationbut can be obtained from compounding pharmacies. Phenoxybenzamine, (0.2-0.7mg/kg PO, q 6-8 hrs) is an adrenergic antagonist, and may be given to helprelax the distal urethral sphincter in cases where the condition is determinedlydue to upper motor neuron damage.
Phenazopyridine (4 mg/kg PO q 8-12 hours), an azo dye compoundthat acts to confer relief from irritation or spasm of the urinary tractmucosa via local anesthetic activity, may also be administered in the initialmanagement of the cystitis caused by the sedimentary accumulation. Thiscompound discolors urine. Owners should be warned that it will stain skinand textiles which inadvertently come into contact with the substance. Inhumans with urinary tract inflammation the agent alleviates symptoms ofdysuria, frequency, burning, and the sensation of urgency.
Mares in which urinary incontinence is from hypoestrogenism may enjoya better prognosis for response to treatment. Successful management ofthe condition in such mares has been observed in association with administrationof estradiol cypionate or benzoate (5-10 _g/kg I.M. q 48 hours).
Dr. Sprayberry, dipl. ACVIM, is a 1988 graduate of theUniversity of California, Davis, School of Veterinary Medicine. She presentlyworks for Estrella Equine Clinic in California.
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