For a more general introduction to urolithiasis, see Noninfectious Diseases of the Urinary System in Small Animals: Urolithiasis in Small Animals.
Urolithiasis in Ruminants
Uroliths in cattle, sheep, and goats are common. Although uroliths can be found anywhere within the urinary tract, urethroliths are responsible for most clinical problems. Obstruction induced by urethroliths causes urine retention and leads to bladder distention, abdominal pain, and eventual urethral perforation or bladder rupture, with death from uremia or septicemia. It is an important disease of feeder animals but is also seen in mature breeding animals. Urolithiasis is seen most often during winter in steers and wethers on full feed, or on range during severe weather conditions with limited water intake, especially when the water has a high mineral content. Urolithiasis has no specific geographic distribution, and the different urolith types reflect the mineral distribution of the feed. Uroliths occur in either sex, but obstructive urolithiasis develops primarily in males because of anatomic differences.
Etiology and Pathogenesis
Ruminant urolithiasis is considered primarily a nutritional disease. The prevalence of urolithiasis in the USA is highest in calves, lambs, and kids castrated at an early age and fed high-grain diets with roughly a 1:1 calcium:phosphorus ratio or a diet high in magnesium. Ruminants fed high-grain diets with a low calcium:phosphorus ratio are at increased risk of developing struvite uroliths, while ruminants grazing on silica-rich soil are predisposed to form silica uroliths. Diets high in calcium (eg, subterranean clover) may result in calcium carbonate uroliths, while plants such as halogeton or tops from the common sugar beet may be a factor in calcium oxalate formation. The mineral composition of water, in concert with dietary mineral imbalances, probably contributes more to initiating urolith formation than does the lack of water itself. A definitive diagnosis of urolithiasis in a single animal suggests that all males in the population are at risk for the disease.
The distal aspect of the sigmoid flexure of cattle and the sigmoid flexure and urethral process of sheep and goats are the most common sites for uroliths to lodge. Irritation at the site of lodging causes inflammation and swelling that contributes to urethral occlusion. Castration of young males also predisposes to urolith-induced urethral obstruction by removing hormonal influences necessary for mature development of the penis and urethra.
Clinical signs may be associated with partial or complete urethral occlusion. Animals with partial obstruction dribble blood-tinged urine after prolonged, painful (stranguria) attempts at urination; before complete occlusion occurs, urine may dry on the preputial hairs and leave detectable mineral deposits. Animals with complete urethral obstruction exhibit tenesmus, tail twitching, weight shifting, and signs consistent with colic. Inappetence, bloat, depression, and rectal prolapse may also be seen. Affected steers may elevate the tail and show urethral pulsations just ventral to the rectum. Goats may vocalize.
Common sequelae of complete urethral obstruction include urethral perforation or urinary bladder rupture. Bladder rupture often results in death from uremia. The disease course may be 5–7 days. Although urethral perforation may also cause uremia and death, it is not uncommon for the ventral abdominal skin to necrose and slough, allowing the development of a pseudourethra.
Diagnosis based on the history, clinical signs, and physical examination is usually straightforward. Hypersensitivity in the region of the sigmoid flexure may be evident. Palpation may identify abnormal pulsations of the urethra and tissue swelling associated with the obstruction. Rectal palpation may reveal an enlarged, distended bladder, or the bladder may be nonpalpable, consistent with bladder rupture. Examination of the urethral process in sheep and goats may reveal the occluding urolith. If early clinical signs of obstructive uropathy are missed, the animal may show only inappetence, depression, subcutaneous swelling along the penis, or uroperitoneum; abdominal distention due to uroperitoneum must be differentiated from ruminal tympany, peritonitis, peritoneal tumors, uterine hydrops, and GI tract obstructions. Ballottement allows detection of the fluid, and when viewing the animal from behind, the abdomen appears symmetrically enlarged and pear-shaped. Ultrasound examination of the abdomen reveals a large amount of hypoechoic fluid.
Confirmation is obtained by examining fluid collected by abdominocentesis and finding that the creatinine in peritoneal fluid is 2 times or more that in plasma. Subcutaneous swellings along the prepuce and ventral abdomen due to a perforated urethra must be differentiated from traumatic injury, subcutaneous abscesses, and umbilical or ventral hernias. In breeding animals, preputial lacerations with prolapse and sheath infection, and hematoma of the penis must also be differentiated. In animals with clinical signs of acute colic, other causes of abdominal pain must be eliminated; these diseases include indigestion, stasis or obstruction of the GI tract, primary enteritis, abomasal ulcers, and coccidiosis.
Treatment and Control
Treatment of obstructive urolithiasis generally involves establishing a patent urethra and correcting fluid and electrolyte imbalances. In many instances, surgical management of the obstruction is all that is necessary; however, severely uremic and depressed animals require rehydration and correction of acid-base and electrolyte abnormalities. If a rupture of the urinary tract has occurred, hyponatremia, hypochloremia, hyperphosphatemia, and metabolic alkalosis with variable potassium concentrations are found. Treatment with IV normal saline is indicated. The volume of fluid administered should be calculated to correct clinical dehydration. Once the animal is rehydrated and any rupture repaired, fluid therapy may be continued to encourage diuresis.
Animals with an intact urethra and bladder that have early clinical signs of obstructive urethral disease may benefit from conservative therapy using antispasmodics and tranquilizers. This is believed to relax the retractor penis muscles with straightening of the sigmoid flexure. However, conservative therapy is only rarely beneficial in small ruminants, and is warranted only in cases of acute or partial obstruction without evidence of urethral or bladder damage; it should not be used in complicated or advanced cases. Uroliths trapped within the urethral process of sheep and goats may be removed by gentle manipulation or by amputation of the urethral process. Proper restraint, tranquilization, and a regional anesthetic are necessary. The techniques vary, but the typical procedure requires exteriorization of the penis. Although amputation may be effective, relief is typically temporary (<2 days) in most animals because obstruction recurs due to the presence of multiple uroliths.
Perineal urethrostomy has also been recommended as an effective surgical technique in castrated males. Short-term complications associated with perineal urethrostomy may include postoperative hemorrhage, surgical wound dehiscence, and subcutaneous urine accumulation. Urethral stricture is a common longterm complication. In addition, perineal urethrostomy is associated with loss of breeding ability in intact males. In more complicated cases, such as those with urethral perforation, amputation of the penis proximal to the sigmoid flexure or near the perineal area may be necessary as a salvage procedure. Animals that develop urethral perforation also require drainage of accumulated subcutaneous urine; this is accomplished by lancing the skin overlying the area of accumulated urine. Topical antiseptics and fly repellents may be applied to these ventral lacerations, and parenteral antibiotics are recommended to prevent infection.
Cystotomy followed by dietary management is believed to be a more effective longterm solution to urolithiasis in sheep and goats than is perineal urethrostomy. Cystotomy allows removal of multiple urocystoliths, permits bidirectional urethral flushing, and poses less risk for urethral stricture. Tube cystotomy is generally considered the treatment of choice, allowing time for the calculi to be expelled spontaneously. An intact urethral process, absence of abdominal fluid, and serum potassium concentration <5.2 mEq/L have all been associated with improved survival after tube cystotomy in small ruminants.
If the bladder is ruptured, the ability to urinate must be restored and uremia corrected. In animals with substantial uroperitoneum, the peritoneal cavity should be slowly drained using a teat tube or trocar. Urine removal may also reduce the severity of peritonitis and make the animal more comfortable. Fluid, electrolyte, and acid-base homeostasis normally returns within 24 hr after restoration of a patent urinary system. Persistent uremia indicates the possibility of hydronephrosis or ascending pyelonephritis, or both. A urethrostomy should be performed to provide unobstructed passage of urine. Attempts to surgically repair the ruptured bladder have been largely unsuccessful due to the chronic distention prior to rupture. The bladder may heal spontaneously after urethrostomy and removal of abdominal fluid; however, these animals are best salvaged within 3–4 mo to avoid further complications. Despite treatment, some animals fail to pass urine effectively and the uroperitoneum recurs. These animals may be treated by performing tube cystotomy, followed by appropriate antibiotic and fluid therapy.
Several measures to prevent the formation of urethral calculi have been recommended. The most important is to provide a calcium:phosphorus ratio of 2:1 in the complete ration. Intensive concentrate feeding, such as in many finishing programs, frequently leads to urolith formation and urethral obstruction. Thus, any feeding program incorporating concentrate feeding must include appropriate calcium supplementation. Adjunct measures to minimize the formation of urethral calculi include adding sodium chloride up to 4% of the total ration. This promotes increased sodium and chloride concentration in the urine, water intake, and urine dilution, which increases the mineral solubility. Ammonium chloride can be used as a urinary acidifying agent (7–10 g/head/day for a 30-kg lamb or kid; 50–80 g/head/day for a 240-kg steer). Urine acidification antagonizes magnesium-ammonium-phosphate crystal formation and has been shown empirically to be a useful preventive measure.
In operations with a significant problem of urolith formation, evaluation of the ration is the most important measure that can be taken to reduce the incidence. Commercial anionic dietary supplements are available for small ruminants.
Urolithiasis in Horses
Urolithiasis is a less common condition in horses than in small ruminants or steers. The disease can affect immature horses but is seen most frequently in adults. There is no breed predilection. Urolithiasis is seen more frequently in males than females, which has been attributed to anatomic differences between the male and female urethra.
Equine uroliths have a diameter of 0.5–21 cm, weigh as much as 6.5 kg, and are found most often within the bladder. Most equine uroliths are composed of calcium carbonate, in various hydrated forms, with either calcium phosphate or struvite uroliths occasionally noted. Calcium carbonate uroliths have 2 separate clinical forms. The first form is a concretion of salts and mucoproteins that varies in consistency from friable to firm. These uroliths are usually yellow and oval or irregularly shaped; they frequently have a rough or spiculated surface and are generally soft enough to be fragmented during surgery. The second calcium carbonate form is a firm concretion that is hard and resistant to fragmentation and is typically smooth and white. There appears to be no difference in chemical composition between these forms.
The mechanism of urolith formation in horses is unknown, although the alkaline pH and high mineral content of normal equine urine may favor crystal formation and precipitation. Normal equine urine also contains large amounts of mucoproteins, which may serve as a cementing substance to adhere crystals. Consumption of feed and water high in mineral content may increase urinary solute concentrations and thereby promote crystallization and precipitation. Multiple nephroliths may develop in horses with renal papillary necrosis (associated with NSAID administration while dehydrated) and mineralization of the papillae.
Clinical signs depend on the urolith location. Most uroliths are located in the bladder and cause dysuria, pollakiuria, and hematuria. Hematuria is most evident after exercise and toward the end of a voided urine stream. Affected horses frequently stretch out to urinate and may maintain this posture for variable periods before and after micturition. Additional signs may include scalding of the perineum in females or of the medial aspect of the hindlimbs in males. Geldings and stallions may protrude the penis flaccidly for prolonged periods while intermittently dribbling urine. Affected horses may occasionally exhibit recurrent bouts of colic or an altered hindlimb gait. Urethral obstruction may also develop as the result of a trapped urolith and is typically accompanied by restlessness, sweating, varying degrees of colic, and frequent attempts to urinate. The bladder is distended on rectal examination. In most fatal cases, a single large urolith, occasionally accompanied by smaller ones, is found in the bladder; less frequently, the urolith may be found lodged at the bladder neck or the ischial arch. Nephroliths are occasionally found via ultrasonography in horses with cystic calculi; owners of such horses should be informed that obstruction may recur.
Bilateral nephroliths are not uncommon in adult horses that have been used for performance. Intermittent chronic obstruction of ureters will eventually cause renal failure, resulting in weight loss and anorexia.
Tentative diagnosis of urolithiasis is usually based on the history and clinical signs and confirmed most easily by rectal palpation of a firm, ovoid, intravesicular mass at or near the neck of the bladder. In most cases, urolith palpation is not difficult because clinical signs are rarely evident until the stone is several centimeters in diameter. Transrectal ultrasonography with a 7.5 mHz linear probe allows visualization of the stone. If ultrasound examination cannot be performed, the distended bladder should be catheterized to facilitate palpation and eliminate the possibility of urethroliths, urethral stricture, or smegma impaction of the urethral sinus. Urinalysis frequently reveals RBC, neutrophils, calcium carbonate crystals, and proteinuria. Cystoscopy, ultrasonography, and radiology are not essential for detection of urocystoliths in horses but may provide additional diagnostic or prognostic information. Ultrasonography is necessary to identify nephroliths. Ureteroliths and cystic calculi can usually be palpated during rectal examination.
Several surgical procedures have been described for urocystolith removal. The surgical options include midline or paramedian laparotomy and cystotomy, pararectal cystotomy, subischial urethrostomy, urethral sphincterotomy, and laser or shock wave lithotripsy. The selection of a procedure is dictated by the size, location, and number of uroliths; the sex and physiologic status of the horse; and the availability of surgical facilities. Bladder rupture, although uncommon in adult horses, may occur due to urethral obstruction or recumbency, or after foaling in mares.
Last full review/revision July 2011 by Thomas J. Divers, DVM, DACVIM, DACVECC