Managing urolithiasis (Proceedings)

Pathophysiology

Obstructive urolithiasis is a common problem encountered in small ruminant practice. It can be debilitating and life-threatening, so needs to be recognized early, and treated promptly. Obstructive urolithiasis is almost exclusively a disease of males. It occurs in both castrated and intact males. In males castrated early, the preputial attachment to the penis may not break down, preventing the sigmoid flexure from completely straightening. This may predispose to obstructions at the sigmoid flexure. Obstructive urolithiasis can be caused by one large stone or many small, sandlike stones, depending on the makeup of the stones.

Calculus formation begins when bacteria, cells, casts, mucoprotein or other urinary tract debris act as a nidus upon which crystals can form. Deficiencies in Vitamin A can lead to increased desquamation of epithelial cells and increased nidus formation. If urine then becomes supersaturated, calculogenic crystals precipitate and build upon a nidus, eventually forming calculi. The degree of urine supersaturation depends mainly on diet, urine pH, and water intake. Increased mucoprotein in urine from pelleted rations and/or estrogenic compounds (white clover, growth-promoting implants) can also predispose to the formation of calculi. High concentrate diets and diets high in calcium, magnesium and/or phosphorus (feedlot rations) and/or having a low Ca:P ratio can predispose to magnesium ammonium phosphate or calcium phosphate calculi. Pelleted rations also predispose to magnesium ammonium phosphate calculi. Pelleted rations require less saliva to ingest than other feeds, causing decreased phosphorus excretion in saliva and increased urinary excretion of phosphorus. Calcium carbonate and calcium oxalate calculi occur more frequently in animals consuming legumes (alfalfa, clover, kudzu).

Calculi form more readily in alkaline urine pH, which is common in herbivores. High protein diets and urinary tract infections can also alter urinary pH and predispose to calculi formation.

Decreased water intake is a very important predisposing factor for calculi formation. Decreased water intake can occur if clean water is not provided, or during cold weather. Other illnesses may also cause decreased water intake. A common historical finding in animals presented for obstructive urolithiasis is a recent illness.

The most common site of lodging of calculi in small ruminants is the urethral process and/or the distal sigmoid flexure. Three clinical syndromes occur: urethral obstruction; rupture of the urethra; and rupture of the bladder. If urethral obstruction goes undetected, and untreated, the urethra and/or the bladder can rupture. If bladder distension is severe and/or prolonged the bladder wall can be damaged, and normal emptying may not occur even after relief of the obstruction. Damage to the urethral wall can lead to stricture formation, increasing the likelihood of recurrence even if preventive measures are instituted.

Clinical Signs

The clinical signs of urethral obstruction are restlessness, tail switching, colic signs, dribbling of urine or anuria, urethral pulsations without normal urine flow, urethral swelling at the sight of obstruction, crystal and/or blood on the preputial hairs, and an enlarged bladder on abdominal palpation or ultrasound. Goats may become very vocal from pain. Posturing and straining to urinate are often mistaken for straining to defecate by owners, and straining to urinate can lead to rectal prolapse, further confusing the diagnosis. Increased a respiratory rate from pain and possibly metabolic abnormalities should not be confused with pneumonia. Neurologic disease, especially polioencephalomalacia in goats, can cause animals to behave strangely, and vocalize, and should be ruled out as a cause of clinical signs. Urine leaking into the subcutaneous tissues around the rupture accumulates, and ventral and preputial edema is evident ("water belly"). After several days, the skin and subcutaneous tissues will begin to necrose and slough. Preputial prolapse may also occur secondarily and penile adhesions to the prepuce can occur chronically. Pain is decreased when the bladder ruptures, so clinical signs may be delayed until abdominal distension is evident, or uremia causes depression and anorexia. If distension is severe, fluid may be balloted in the abdomen and respiratory distress may be evident.

Clinicopathology

Clinicopathology may be normal in early cases of complete urethral obstruction. However, with chronic partial obstruction, or rupture of the urethra or bladder, elevated serum creatinine, hyponatremia, and hypochloremia are usually present. Due to salivary excretion and recycling, BUN and potassium aren't always elevated as classically seen in other species. Hyperphosphatemia and hypocalcemia are also possible. Other abnormalities may be hemoconcentration from dehydration, and evidence of an inflammatory process.

Diagnosis

A diagnosis of obstructive urolithiasis is usually based on clinical signs. Abdominal radiographs may reveal calcium carbonate or oxalate stones. Contrast radiography is difficult in most cases, especially in early castrated males, and should be performed with caution to avoid rupturing the urethra. If the urethra or bladder is ruptured, aspiration of the fluid from the subcutaneous tissues or abdomen, respectively, yields clear fluid that smells like urine when heated. A creatinine of subcutaneous or abdominal fluid that is 1.5-2X that of serum creatinine is diagnostic. Abdominal ultrasound shows a honeycombed appearance to the subcutaneous tissues with urethral rupture and free fluid in the abdomen with ruptured bladder.

Treatment

Obstructive urolithiasis should be treated as an emergency. Immediate slaughter should be considered in feedlot or grade animals if rupture of the bladder or urethra has not occurred. If surgery is indicated, it should not be delayed. Dehydration and electrolyte abnormalities should be corrected with isotonic sodium chloride during surgery. If hyperkalemia is severe, adding dextrose or sodium bicarbonate to fluids may help decrease potassium. Calcium may also be needed. Nonsteroidal anti-inflammatory drugs are an important part of therapy. Not only do they help with pain, shock, and urethral swelling in the acute stages of the disease, they may also help decrease the amount of urethral stricture formation chronically. Broad-spectrum antibiotics should be administered prophylactically.

In cases of urethral obstruction, if the penis can be exteriorized, the urethral process can be removed with sharp scissors or a scalpel blade if it has not already necrosed off. Antibiotic and/or steroid cream can be applied to the penis. Removal of the urethral process may relieve the obstruction initially, but obstruction at the sigmoid flexure commonly occurs secondarily, so careful monitoring for recurrence is necessary. Sedation and/or caudal epidural may facilitate exteriorization of the penis. Acepromazine is the sedative of choice as it may also have antispasmodic effects on the urethra. Xylazine should be avoided due to its diuretic effects. Urethral catheterization is difficult to perform and should be performed with extreme caution to prevent rupture of the urethra. A mixture of 1 part 2% lidocaine and 3 parts saline may relieve some urethral spasms and facilitate flushing.

A more acceptable alternative to urethral catheterization if removing the urethral process fails to relieve the obstruction or the obstruction recurs is chemical dissolution of the calculi. Under general anesthesia, the bladder is located with ultrasound, and an 18 gauge 4 inch needle is inserted into the trigone of the bladder. Urine is aspirated until the bladder is small, and 30-60 mls of Walpole's solution is placed in the bladder and removed again until the turbidity of the urine is decreased. Then another 30 to 50 mls of Walpole's solution is infused into the bladder and the needle removed. Urine flow is usually seen in 24-36 hours, and is normal in 3-5 days. A second infusion of Walpole's may be needed in some cases.

Several surgical procedures are available for urethral obstruction. If the animal is destined for slaughter, temporary measures such as perineal or ischial urethrostomy or penile amputation can be performed. Urethrostomy can be difficult to perform in small ruminants, and stricture formation with obstruction at the surgical sight usually occurs in a few weeks to a few months. If the stones can be palpated in the urethra, a urethrotomy can be performed at this sight. However, stricture formation and reobstruction can still occur. For cases in which breeding is important, or in pets in which long term survival is important, a tube cystostomy or bladder marsupialization is recommended.

If the tube cystostomy fails (estimated to fail in about 20% of cases), or the animal is a pet and breeding is not desired, the bladder can be marsupialized. A stoma is made lateral to the prepuce and as cranial as the bladder will allow. Note that this surgery can be difficult to perform following a failed tube cystostomy due to intra-abdominal adhesions. Although breeding success rates following marsupialization have not been reported, the author is aware of one animal that successfully bred females following bladder marsupialization.

The prognosis for urethral rupture is poor compared to simple obstruction or bladder rupture if these are treated appropriately. With urethral rupture, urine still needs an outlet, so a urethrostomy or penile amputation should be performed. Tube cystostomy or bladder marsupialization may not be able to be performed due to the severe ventral accumulation of urine, and tissue necrosis. Multiple incisions in the skin to allow drainage, and debridement of necrotic tissue is necessary. Severe adhesions of the prepuce and penis may interfere with subsequent breeding.

Prevention

Because preventive measures are dependent on the type of stone present, which is difficult to predict in small ruminants, it is important to have calculi analyzed. A thorough dietary history is necessary to determine any predisposing dietary factors. Castration of pet animals should be delayed as long as possible, preferably until the preputial attachment to the penis has broken down.

Increased water intake is indicated with any type of stone. This can be accomplished by adding salt to the diet at 4% to 5%. If free choice trace mineralized salt is the source of minerals, intake of these may drop when salt is added to the ration. Therefore, adequate minerals should be added to the ration. Clean water should be provided at all times. In winter, warm water can be provided to pet animals to keep intake up.

Pet small ruminants not used for breeding tend toward obesity, and can usually be maintained on good quality grass hay. Concentrate supplements should be reserved for breeding or feedlot animals. The concentrate in the diet should be limited to 25% of the ration (feedlot rations may be the exception). A 1.5 to 2:1 Ca:P ratio should be maintained in the entire diet. The total recommended amounts of calcium and phosphorus should not be exceeded, and magnesium should not be in excess. Adequate vitamin A should be included in the ration, especially if dry forages are the majority of the ration. Legume hay should be avoided, or limited to only what is needed if certain production systems require them.

Acidification of the urine can be accomplished several ways. For large numbers of animals, an anionic ration similar to that fed to dairy cattle to prevent hypocalcemia can be fed. Also, ammonium chloride can be added at 0.5% to 1% of the total ration, or 2% of the concentrate. For individual animals 5-10 grams/head/day should maintain the urine pH at approximately 6.5. This can be checked weekly by the owner with pH paper. Ammonium chloride is highly unpalatable, and should be mixed with syrup or put in gelcaps for administration (avoid molasses since it is high in cations). Vitamin C has to be administered several times per day in ruminants to be effective so is impractical.