Uroperitoneum is defined as urine leakage into the peritoneal space. In foals, this most commonly results from tearing of the bladder or urachus during parturition, prolonged recumbency while being treated for a neonatal illness, or less commonly from rupture of the urachus secondary to umbilical abscessation. Ureteral or urethral tears are uncommon causes of uroperitoneum.
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. Regardless, 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 Neonatal Encephalopathy Neonatal encephalopathy (NE) is a common, noninfectious CNS disorder of neonatal foals, resulting in clinical signs such as lethargy, inappropriate behavior, seizures, and other neurologic deficits... read more , prolonged recumbency, cystitis, ascending infection, abdominal trauma, failure of passive transfer Failure of Passive Transfer Large animal neonates are born with limited energy reserves and are considered immunocompetent but immunologically naive at birth (ie, agammaglobulinemic). Thus, ensuring the provision of good-quality... read more , and sepsis may predispose the foal to bladder rupture.
Foals with uroperitoneum generally appear normal at birth but progressively become lethargic, tachycardic, and tachypneic throughout 24–72 hours after the rupture. 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, but some continue to urinate normally.
History, clinical findings, laboratory tests, and ultrasonography
Ultrasonographic abdominal examination and blood and peritoneal fluid analysis are crucial to confirming a diagnosis of uroperitoneum. Serum hyperkalemia combined with hyponatremia and hypochloremia are observed in most cases because of the high concentration of potassium and low levels of sodium and chloride in the urine, which rapidly equilibrate across the peritoneum into the plasma and other extracellular fluid sites.
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 as hypoechoic-appearing fluid on ultrasonographic evaluation Ultrasonography in Animals Ultrasonography is the second most commonly used imaging format in veterinary practice. It uses ultrasonic sound waves in the frequency range of 1.5–15 megahertz (MHz) to create images of body... read more . 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 minutes. This test is rarely necessary to make the diagnosis and therefore rarely performed.
The clinical signs of progressive depression and stranguria can confuse the diagnosis with meconium impaction (see Meconium Impaction Meconium Impaction Meconium is the earliest feces of newborn foals. It is composed of intestinal secretions, swallowed amniotic fluid, and cellular debris; it has a sticky, caramelized appearance. Most foals pass... read more ). Other differential diagnoses for uroperitoneum are listed (see Table: Differential Diagnoses for Clinical Signs Associated with Uroperitoneum in Foals Differential Diagnoses for Clinical Signs Associated with Uroperitoneum in Foals Uroperitoneum is leakage of urine into the peritoneal space and is caused most often by rupture of the urinary bladder or urachus. Signs, including lethargy, tachycardia, frequent attempts to... read more ). Detrusor sphincter dyssynergia generally resolves within 2–4 days if a catheter is placed in the bladder to prevent rupture. This may be a form of neonatal encephalopathy.
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 if the urachal defect is within the abdomen. Subcutaneous urachal ruptures may also occur, causing an accumulation of urine in that area and marked stranguria. Rarely, neonatal foals may become azotemic because of rupture of one or both ureters. With rupture of a ureter, accumulation of urine in the retroperitoneal area can be seen via ultrasound until the retroperitoneal membrane ruptures, at which time the abdominal ultrasound findings and laboratory findings are identical to those with ruptured bladder.
Surgery is necessary to correct the uroperitoneal defect and, in uncomplicated cases, is very successful. The foal should be stabilized with IV fluids and by draining the urine from the peritoneal space when needed to correct electrolyte abnormalities, fluid deficits, and pressure on the diaphragm before surgery. Potassium >6 mEq/L should be lowered preoperatively by either 500 mL of isotonic sodium bicarbonate plus 10% dextrose given over 30–40 minutes, 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. If the tear is in the urachus, it is surgically removed. If the umbilical structures are enlarged (indicating infection), they should be removed at the time of surgery and cultured. After surgical correction of the ruptured bladder or urachal tear, an indwelling urinary catheter may be placed for 48 hours 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 before surgery, the prognosis for recovery is 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.
Ruptured bladder or urachus leading to uroperitoneum is common in neonatal foals.
The earlier that surgical correction can be done, the less severe are plasma electrolyte abnormalities and volume of urine accumulating in the peritoneal space, both of which make successful preoperative medical management easier.
Sick neonatal foals that are persistently recumbent are also at risk of developing a ruptured bladder, and an indwelling urinary catheter may be needed to prevent this complication.
For More Information
Schott HC, Waldridge B, and Bayly WM. Disorders of the Urinary System, in Equine Internal Medicine 4th ed. Reed SM, Bayly WM, and Sellon DC (eds), pp 895–898, Elsevier, 2018.