Urolithiasis: The process of forming stones in the kidney, bladder, and/or urethra (urinary tract).
Kidney stones are a common cause of blood in the urine and pain in the abdomen, flank, or groin. Kidney stones occur in 1 in 20 people at some time in their life.
The development of the stones is related to decreased urine volume or increased excretion of stone-forming components such as calcium, oxalate, urate, cystine, xanthine, and phosphate. The stones form in the urine collecting area (the pelvis) of the kidney and may range in size from tiny to staghorn stones the size of the renal pelvis itself.
The cystine stones (below) compared in size to a quarter (a U.S. $0.25 coin) were obtained from the kidney of a young woman by percutaneous nephrolithotripsy (PNL), a procedure for crushing and removing the dense stubborn stones characteristic of cystinuria.
The pain with kidney stones is usually of sudden onset, very severe and colicky (intermittent), not improved by changes in position, radiating from the back, down the flank, and into the groin. Nausea and vomiting are common.
Factors predisposing to kidney stones include recent reduction in fluid intake, increased exercise with dehydration, medications that cause hyperuricemia (high uric acid) and a history of gout.
Treatment includes relief of pain, hydration and, if there is concurrent urinary infection, antibiotics.

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.
Obstructive uroliths are common in male goats, regardless of feed, season, or other risk factors. 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 highgrain diets with a low calcium:phosphorus ratio are at increased risk of developing struvite uroliths, whereas 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 of the disease.

Struvite calculi have the apperance of sand, whereas calcium
carbonate calculi and calcium oxalate are distinct, round stones.
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 Findings:
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 also may 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, hydronephrosis, 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 a pseudourethra to develop.


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. In small ruminants, the distended bladder
can be felt by abdominal palpation and visualized on ultrasound examination.
Calcium carbonate and calcium oxalate calculi can be seen on radiographs of the urethra in small ruminants; struvite calculi are not seen on radiographs. 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.

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, especially hyperkalemia or hyperammonemia. 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.

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 long-term complication. Transection of penile attachments to the pelvis may decrease risk of postoperative stricture. 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.
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. An urethrostomy should be performed to provide unobstructed passage of urine. Attempts to surgically repair the ruptured bladder have been largely unsuccessful because of the chronic distention before the rupture. The bladder may heal spontaneously after urethrostomy and removal of abdominal fluid; however, these animals are best salvaged within 3–4 months to avoid further
Several measures to prevent the formation of urethral calculi have been recommended. Most important for struvite calculi prevention are to increase urinary chloride excretion, decrease urine pH, and 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 that incorporates 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). Complete rations with
dietary cation-anion difference (DCAD) are also used to prevent struvite calculi; these rations are high in chloride. Urine acidification antagonizes magnesium-ammonium-phosphate crystal formation and has been shown
empirically to be a useful preventive measure. Lower calcium diets should be used if calcium carbonate or calcium oxalate is a concern.

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