Uroperitoneum is defined as urine leakage into the peritoneal space. In foals, this most commonly results from tearing of the bladder during parturition, prolonged recumbency while being treated for a neonatal illness, or rupture of the urachus secondary to umbilical abscessation. Ureteral or urethral tears are rare. Some studies indicate a higher incidence of bladder rupture in males than in females, possibly because the narrower pelvis and the longer, narrower urethra of colts is a predisposing factor. Urachal rupture occurs both in males and females. Traumatic bladder rupture is thought to be caused by uterine contractions on a full bladder as the foal passes through the birth canal. Although most ruptured bladders at birth are thought to be traumatic, the presence of smooth edges and absence of hemorrhage around the tear in some foals might suggest a congenital origin (developmental defect of the bladder wall). Most bladder tears are located on the dorsum of the bladder. In the case of a ruptured urachus, infection in the umbilical stump can weaken the urachal wall and result in leakage of urine into the abdomen or subcutaneously near the umbilicus. Prematurity, neonatal encephalopathy, cystitis, ascending infection, abdominal trauma, failure of passive transfer, and sepsis may predispose the foal to bladder rupture.
Foals generally appear normal at birth but progressively become lethargic, tachycardic, and tachypneic throughout 24–48 hr. Signs may not appear for a longer period in foals with a ruptured urachus. As the condition progresses, the abdomen becomes noticeably distended, and ballottement may produce a fluid wave. Most foals attempt to urinate often, with small amounts of urine being produced. This stranguria is often misinterpreted as straining to defecate. Other foals may be anuric or urinate normally.
Ultrasonographic abdominal examination and blood and peritoneal fluid analysis can be helpful in diagnosis. Foals usually have a neutrophilic leukocytosis. Serum hyperkalemia combined with hyponatremia and hypochloremia are seen because of the high concentration of potassium and low levels of sodium and chloride in the urine, which rapidly equilibrate across the peritoneum. An ECG may show broad QRS complexes and very tall T waves due to hyperkalemia. The increased serum potassium predisposes the foal to bradycardia and cardiac arrhythmias (AV block, atrial standstill, and cardiac arrest) if not corrected. Serum BUN and creatinine values can be normal but usually are increased. Blood gas analysis may also be normal or reveal a metabolic acidosis. Abdominal fluid is pale yellow and copious and can easily be detected on ultrasonographic evaluation. The creatinine level in the peritoneal fluid is at least double that in the serum. This test is the most accurate in diagnosing the problem. If laboratory testing is not available, 10 mL of methylene blue can be injected into the bladder via a urinary catheter. If the bladder is patent to the peritoneal space, dye should be seen in the peritoneal fluid within 15 min.
The clinical signs of progressive depression and stranguria can confuse the diagnosis. Differential diagnoses include septicemia (see Sepsis in Foals), hypoxic ischemic encephalopathy/neonatal encephalopathy (see Neonatal Encephalopathy), persistent meconium impaction (see Perinatal Mare and Foal Care), or colic (see Colic in Horses) for other reasons.
In the case of a urachal rupture, abdominal ultrasonography may be helpful to establish an etiologic diagnosis. Ultrasonography of the umbilical remnants may suggest the presence of infection or abscessation. A large amount of fluid in the abdomen is also seen. Rarely, neonatal foals may become azotemic because of rupture of one or both ureters. Accumulation of urine in the retroperitoneal area can be seen via ultrasound.
Surgery is necessary to correct the defect and, in uncomplicated cases, is very successful. The foal should be stabilized before surgery. Potassium >6 mEq/L should be lowered preoperatively by either 500 mL of normal saline, sodium bicarbonate plus 10% dextrose throughout 30–40 min, or sodium bicarbonate administration alone. All of these treatments help drive potassium into cells. If the potassium is >8 mEq/L or the above treatments are unsuccessful, administration of insulin at 0.1 mg/kg, IV, in dextrose and saline and/or peritoneal fluid drainage can be considered.
The bladder should be repaired using absorbable sutures. Because surgical staples have migrated into the bladder and become the nidus for stone formation at a later date, they should not be used. If the umbilical structures are enlarged (indicating infection), they should be removed at the time of surgery and cultured. After surgical correction of the bladder, an indwelling urinary catheter may be placed for 48 hr to decrease bladder distention and leakage of urine at the repair site; however, this is rarely done on a first repair.
If a bladder rupture is recognized early in an otherwise healthy foal and the foal is stabilized appropriately beforesurgery, the prognosis for recovery is good to excellent, with success rates as high as 95%. In septic or premature foals, in which complications such as peritonitis, incisional complications, adhesions, and anesthetic death are encountered more frequently, the prognosis is fair. All recumbent foals should be considered at high risk of bladder rupture and may require prophylactic indwelling catheterization.
Last full review/revision July 2013 by Thomas J. Divers, DVM, DACVIM, DACVECC