Urolithiasis is the most widespread and economically important urinary disease of ruminant species.
Urolithiasis is the most widespread and economically important urinary disease of ruminant species. Clinical urolithiasis is more common in males and castrated males. Particularly those castrated prior to 2 months of age. It is more common in young animals and may reflect both population and feed bias. Disease predominates in late fall or winter and the arid months of summer, likely due to fluctuations in water supply and intake.
Silica, magnesium ammonium phosphate (phosphatic, struvite), calcium carbonate, and calcium oxylate are the most common types of crystals found in ruminants. Silica urolithiasis typically occurs in the western United States in animals that are grazing pastures or eating feeds harvested from pastures with high silicate concentrations. The stones are single, hard, and damage urethral mucosa during passage. High dietary Ca may predispose to the development of these uroliths. Magnesium ammonium phosphate uroliths are often referred to as phosphatic or struvite stones. These are most common in feedlot animals and others on high concentrate rations. Animals with Magnesium ammonium phosphate stones generally have multiple small, soft, amorphous stones or sludge in the urinary tract. Crystals are often present on the preputial orifice in affected animals. Calcium carbonate and calcium oxalate urolithiasis is less common and seen primarily in sheep grazing lush clover or legume pastures. High dietary calcium and oxalate may predispose to carbonate and oxylate urolithiasis.
Formation or urinary calculi is dependent on the supersaturation of urine with soluble ionized minerals. Crystal formation occurs when the inhibitory capacity of mucopolysaccharides, ions, and organic acids is exceeded. A variety of risk factors exist for the development of uroliths in ruminant species. Decreased salt or water intake, urinary stasis, urinary tract infection, high urine pH (struvite, calcium phosphate, and calcium carbonate stones), vitamin A deficiency, and high estrogen intake have all been implicated as risk factors. In addition, the anatomy of the male ruminant urinary tract also contributes due to the potential narrowness of the passage and tortuous route. The sigmoid flexure is a common site for uroliths to lodge in all ruminant species. Uroliths may also be fount on lesser occasion at the ischial arch. In small ruminants the urethral process is an extremely common site for uroliths to lodge.
If left untreated, obstruction of the urinary tract may result in urethral rupture or urinary bladder rupture. Even with appropriate treatment urethral stricture or hydronephrosis may present long term complications. Clinical signs will vary depending on the duration of obstruction, the site of obstruction, and whether a rupture has occurred. Early clinical signs associated with obstruction include signs of colic. Animals may have an arched stance, tread their feet, swish the tail, or kick at their belly. Urolithiasis should always be near the top of the differential list in male ruminants with signs of colic, particularly in sheep and goats. Stranguria, anuria, oliguria, hematuria, mineral deposits on the urethral hairs, uremic odor to the breath, urinary bladder distention and pulsations of the pelvic urethra may also be present. Less specific signs include rectal prolapse, rumen stasis, tachycardia, and tachypnea.
After rupture has occurred animals generally have a short reprieve from the pain associated with the distention. At this time they may appear to be clinically normal to the producer. However, depression, lethargy, and anorexia will soon set in. In cases of urethral rupture swelling, edema, cellulitis, and necrosis of the subcutaneous tissue caudal to the preputial orifice will occur. In some animals this process may be protracted and large quantities of subcutaneous urine may result. In cases with a rupture of the urinary bladder, progressive abdominal distention and the presence of a fluid wave within the abdomen will be detectable.
Complete blood count and serum chemistry results in animals with obstructive urolithiasis may vary based on the severity and progression of disease. A stress leukogram with hyperglycemia, hemoconcentration, azotemia, hematuria, proteinuria, and crystalluria is characteristic of animals with a obstruction. Potassium may be elevated, but a normal potassium concentration does not rule out obstruction in ruminants. Once urinary bladder rupture has occurred increased packed cell volume and total protein, azotemia, hyponatremia, and hypochloridemia are generally are generally present. Peritoneal fluid creatinine concentration will be greater than 2 times serum levels. Potassium concentration and acid base status are variable. Hyperphosphatemia and hypocalcemia may also be present. Abdominal ultrasound may be useful in the detection of abdominal fluid and uroliths. In the hands of a skilled sonographer assessment of the bladder, ureters, and kidneys can be made.
Treatment options for obstructive urolithiasis are varied, but resolution usually requires surgical intervention. Partial obstructions may be cured by diuresis, diet change, and urine acidification. Analgesics and antibiotics are often indicated in these cases. In addition, monitoring is imperative as a stone may lodge during this process causing a complete obstruction. This can rapidly lead to urinary bladder rupture in animals undergoing diuresis. Due to the anatomy of male ruminants, urethral catheterization & flushing are often unrewarding. Once recent study describes an 80% success rate treating obstructive urolithiasis in goats using ultrasound guided cystocentesis and percutaneous infusion of Walpole's solution.
Complete obstructions and urinary bladder ruptures require surgery. Obstruction at the urethral process may be resolved by amputation of the process. However, small ruminants often have multiple stones and they should be monitored closely for additional obstruction even if urine flow is reestablished by urethral process amputation. Amputation of the urethral process is best accomplished by rolling the animal on his rump and exteriorizing the penis. Some animals will require sedation for this. Either acepromazine maleate (0.01 mg/kg IV) or xylazine hydrochloride (0.05 mg/kg IV) may be used. Salvage is a viable option, particularly in production animals, prior to the onset of uremia. Recurrence is common particularly if management changes are not instituted. This is particularly critical when dealing with pet animals.
Perineal urethrostomy
o ***urethrostomy should be 10-15 mm in bulls and 3-6 mm in small ruminants
o Not for breeding males
o Does not address multiple stones in bladder
o Stricture common
o Does not address uroabdomen if bladder is ruptured
Urethrotomy
Laparotomy
o Other layers should be incised on ventral midline caudal to the umbilicus
o With cystotomy
o Perform at the cranial edge of the bladder
o If a thin spot is present cystotomy can be done at that site (prior to rupture)
o Remove all stones
o Catheterize urethra to ensure patency
o With tube cystotomy
o Intermittently occlude to ensure patency of the urethra
o With bladder marsupialization
o Last ditch surgical repair
o This should be used when all other options are exhausted
o Sew bladder wall to skin just lateral to the teats
o Marsupialization hole should be 1-2 cm in length
Surgical salvage procedures
o Performed like PU except penis is exteriorized and fixed to the skin
o Performed as a salvage procedure on animals with a ruptured bladder
o Urethra is incised and an indwelling catheter is introduced into the bladder
o An indwelling catheter is placed and the bladder is allowed to heal spontaneously. This only works if the rupture is dorsal.
Dietary manipulation is the cornerstone to prevention of obstructive urolithiasis. Short term urine acidification in the face of an obstruction can be accomplished by individual administration of ammonium chloride (feedlot steers - 28.4-42.5 g/day; wethers - 10 g/day). Ammonium chloride is bitter and poorly palatable. High doses often require individual administration as opposed to top dressing feed. Adding ammonium chloride to the feed at 0.5-1.0% of ration dry matter has been advocated, but long term dosing may allow the kidneys to acclimate and reestablish a normal urine pH. Short term DCAD studies have shown promise for decreasing urinary pH in goats. Sodium chloride can be administered at 1-4% of ration dry matter to stimulate thirst and promote chloriduria. It is imperative to provide fresh, clean water as limited intake may promote the development of salt toxicity at higher sodium chloride intakes. Delaying castration until animals are a minimum of 2 months of age has been advocated to allow for increased urethral diameter.
Urolith specific therapy for struvite uroliths focuses on phosphorus concentrations. Maintaining animals on a low P ration (≤0.23% DM) and adjusting the ration for a Ca:P ratio ≥ 2:1 will limit phosphatic based urolith development. Pelleted feeds should also be avoided when phosphatic urolith are suspected. For other types of uroliths (Silica and Calcium based) animals should be removed from offending pasture and provided supplemental feed. In cases of calcium based stones, reduction of the Ca:P ratio of ration will limit urolith development.
1. Janke JJ, Osterstock JB, Washburn KE, et al. Use of Walpole's solution for treatment of goats with urolithiasis: 25 cases (2001-2006). J Am Vet Med Assoc 2009;234:249–252.
2. George JW, Hird DW, and George LW. Serum biochemical abnormalities in goats with uroliths: 107 cases (1992–2003). J Am Vet Med Assoc 2007;230:101–106.
3. Fortier LA, Gregg AJ, Erb HN, and Fubini SL. Caprine Obstructive Urolithiasis: Requirement for 2nd Surgical Intervention and Mortality After Percutaneous Tube Cystostomy, Surgical Tube Cystostomy, or Urinary Bladder Marsupialization. Vet Surg 2004;33:661-667.
4. Jones ML, Streeter RN, Goad CL. Use of dietary cation anion difference for control of urolithiasis risk factors in goats. Am J Vet Res 2009;70:149–155.
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