Medical and surgical management of uroperitoneum in a foal

Abstract

A 4-day-old, male, American paint foal was presented for abdominal distention, respiratory distress, and diarrhea. Bladder rupture and uroperitoneum were diagnosed following abdominal ultrasonography and abdominocentesis. The defect in the dorsocranial part of the bladder wall was surgically repaired.

A 4-day-old, intact male, American paint foal was referred to the Western College of Veterinary Medicine with a 1-day history of lethargy and labored breathing. Diarrhea and lack of nursing had also been noticed. The foal was apparently normal for the first 3 d of its life. Although normal urination was observed soon after birth, at 1 d of age, the foal was observed straining without passage of urine.

The foal was presented in lateral recumbency and in respiratory distress. On physical examination, the respiratory rate was 72 breaths/min with increased respiratory effort, and lung auscultation revealed wheezes and harsh lung sounds. The heart rate was 212 beats/min with an irregular rhythm and a Grade II systolic murmur. The foal was estimated to be 8% dehydrated and its mucous membranes were injected, and grey-pink. The capillary refill time was less than 2 s. The sclera were icteric and injected, and the distal part of the extremities were cool. A reducible umbilical hernia was also identified. A small amount of fecal material could be seen on the tail, and the abdomen was distended and painful on palpation.

The foal was treated with nasal insufflation of oxygen (5 L/min). Venous blood gas analysis (RapidLab 865; Bayer Diagnostics, Toronto, Ontario) revealed hyponatremia (sodium, 108.2 mmol/L; reference range 123 to 161 mmol/L), hypochloremia (chloride, 72 mmol/L; reference range 90 to 112 mmol/L), hyperkalemia (potassium, 7.18 mmol/L; reference range 3.4 to 6.2 mmol/L), and increased lactate concentration (6.28 mmol/L; reference range 0.55 to 1.11 mmol/L), consistent with uroperitoneum (Table 1). Blood samples were also submitted for a complete blood (cell) count (CBC) (Abbott Cell-Dyn 3500R; Abbott Laboratories, Saint-Laurent, Quebec) and a serum biochemical profile (Roche Hitachi 912; Montreal, Quebec). A mild leukocytosis (white blood cells, 12.8 × 10⁹/L; reference range 5.1 to 10.1 × 10⁹/L) with a mild left shift (bands, 0.384 × 10⁹/L; reference interval 0 × 10⁹/L) was attributed to a stress response. Biochemical analysis also revealed azotemia with an elevated urea concentration (15.3 mmol/L; reference 4.1 to 14.7 mmol/L) and a high creatinine concentration (347 mmol/L; reference 35 to 185 mmol/L), as well as hyperglycemia (glucose, 32.4 mmol/L; reference range 5.6 to 12.5 mol/L). The foal’s sepsis score was 11, according to the University of Florida system in which a score of 11 or higher correctly predicts sepsis 93% of the time (1).

Table 1.

Serum biochemical values at admission and at various intervals after initiation of treatment

	Serum electrolyte concentration(mmol/L)
	Na+	Cl−	K+
Normal	123–161	90–112	3.4–6.2
Admission 4 pm	108.2	72	7.18
8 pm	117.1	88	5.71
Preoperatively	121.6	91	5.07
Three days postoperatively	134	96	4.5

Na — sodium; Cl — chloride; K — potassium

Abdominal ultrasonography revealed large hypoechoic areas within the abdominal cavity, interpreted to be free fluid, and a collapsed bladder in the caudal part of the abdominal cavity. Abdominocentesis yielded 5 L of clear, yellow fluid with a urine-like odor, confirming uroabdomen. Intravenous fluids were administered (3 L of 0.9% saline/5% dextrose, 4 L of 0.9% saline, 1 L of 0.9% saline with 50 mL of 23% calcium gluconate, and 1 L of 0.9% saline with 50 mEq sodium bicarbonate over 22 h). Serum electrolytes were monitored repeatedly during the 1st evening after admission to monitor response to the fluid protocol (Table 1). The cardiac arrhythmia resolved following this fluid therapy.

The foal developed intermittent focal seizures (facial grimacing), which progressed to brief generalized seizures and recumbency 2 h postadmission. The seizures were controlled with diazepam (Valium; Sandoz, Boucherville, Quebec), 0.1 mg/kg bodyweight (BW), IV. Antibiotic therapy was initiated with ceftiofur (Excenel; Pharmacia Animal Health, Orangeville, Ontario), 5 mg/kg BW, IV, q6h, and tetanus antitoxin (Fort Dodge Animal Health, Fort Dodge, Iowa), 1500 units, SC, were administered prophylactically.

Six hours after presentation, the foal was brighter and began nursing, the seizure activity had ceased, and respiratory effort was decreased. A total of 18 L of fluid were removed from the peritoneal cavity over the next 22 h. However, as the foal’s abdomen continued to distend rapidly, despite drainage of fluid, and the fluid therapy was not normalizing the serum sodium concentration (Table 1), surgery was recommended. The foal was premedicated with diazepam (Valium), 0.2 mg/kg BW, IV, and butorphanol (Torbugesic; Wyeth Animal Health, Saint Laurent, Quebec), 0.05 mg/kg BW, IV. Anesthesia was induced with ketamine (Ketalean; Biomeda-MTC Animal Health Inc, Cambridge, Ontario), 2.0 mg/kg BW, IV, and maintained with 1.5% isoflurane (Aerrane; Baxter Corporation, Mississauga, Ontario) in 3 L/min oxygen. The foal was placed in dorsal recumbency, the ventral aspect of the abdominal wall was aseptically prepared for surgery, and a sterile Foley catheter was placed in the urethra. Palpation confirmed a 4-cm diameter umbilical hernia. A fusiform incision was centered on the umbilicus, and blunt dissection exposed the defect in the abdominal wall. Suction drainage removed 6 L of urine from the peritoneal cavity, and the umbilical remnants and a small segment of hemorrhagic omentum were resected. Upon exposure of the bladder, a 3-cm tear in its dorsocranial margin was evident (Figure 1). The margins of the tear were debrided and the defect was closed with a routine 2-layer closure (simple continuous with Lembert oversew). The bladder was then distended via the urethral catheter with sterile saline (approximately 200 mL) to which a few drops of methylene blue had been added to test the adequacy of the bladder wall repair; leakage was not observed. The peritoneal cavity was then lavaged with 2 L of sterile saline. The abdominal wall was suture-closed routinely, including the hernia.

Figure 1.

Three centimeter defect in the dorsocranial margin of bladder wall.

Postoperatively, treatment with ceftiofur, 5 mg/kg BW, IV, q6h, was continued; however, the frequency of administration was decreased to q24h as the foal’s condition improved. The ceftiofur was administered, IV, for 1 d, after which the IV catheter was removed and the antibiotic was given, IM, for 2 d. The foal was treated with vedaprofen (Quadrisol; Intervet, Whitby, Ontario), 1 mg/kg BW, PO, q12h for 2 d to reduce pain and inflammation associated with the surgical site. Seven hours after surgery, the blood gas value had improved significantly (sodium, 121.6 mmol/L; reference range 123 to 161 mmol/L). The foal was observed urinating normally the day after surgery. Three days postoperatively, the CBC and blood chemical values were within normal limits and the foal was discharged 1 wk after admission with instructions for confinement and daily monitoring of the incision, nursing behavior, urination, and attitude. The skin staples were removed in 10 to 14 d. Communication with the owners revealed that the foal was doing well at 8 mo of age.

Uroperitoneum is reported in neonatal foals (2). The condition may be more common in males (3). The most frequent cause of urine accumulation in the peritoneal cavity is leakage from a bladder defect (4,5), typically in the dorsal aspect of the bladder wall (2), although urachal and ureteral defects have also been identified (3,4,6). Proposed causes for neonatal bladder rupture include congenital defects within the bladder, parturient or external trauma, strenuous exercise, and urachal infection (4). Sepsis and urinary tract infections have been implicated in the development of uroperitoneum in critically ill, hospitalized patients, presumably due to focal ischemia induced by the infectious processes (3,6,7). Foals that develop uroperitoneum during hospitalization and are receiving fluid therapy for other conditions can remain subclinical, as the serum chemical values associated with uroperitoneum may be masked (6,7). History regarding micturition varies (4,6); however, affected foals usually appear normal at birth. Clinical manifestations include depression, weakness, tachycardia, tachypnea, diarrhea, injected mucous membranes, abdominal distention, colic, progressive anorexia, urine dribbling, or stranguria (2,4). Respiratory distress is usually attributed to compression of the thorax by the uroperitoneum, although fluid may also accumulate within the pleural cavity (1).

Uroperitoneum is a medical emergency and the immediate goals of treatment are to improve cardiovascular and respiratory status by drainage of the peritoneal cavity and to correct electrolyte imbalances. The high levels of potassium and low levels of sodium in mare’s milk (2) exacerbate the electrolyte abnormalities (hyponatremia, hypochloremia, hyperkalemia).

In the case reported here, the hyponatremia on presentation was the most likely cause of the seizures. Other differential diagnoses for seizure activity in a neonatal foal include hypoglycemia, neonatal maladjustment syndrome, hypocalcemia, hypomagnesemia, intracranial trauma, septic encephalopathy, and severe anemia (1,2); they were less likely in this case, given the history, clinical signs, laboratory findings, and response to therapy. Hyponatremia decreases the osmolality of extracellular fluid, resulting in movement of water into cells, elevated intracellular volume, and edema. Within the bony calvarium of the skull, edema increases intracranial pressure and incites neurological dysfunction, including seizure activity (8). If hyponatremia is chronic, the brain adapts by altering the osmolality of cells in the brain through loss of intracellular potassium and organic osmolytes (8). For this reason, chronic hyponatremia should be corrected slowly to avoid central pontine myelinosis that may result from a rapid rise in serum sodium levels and the creation of a reverse osmotic gradient (1,8). In this foal, the relatively rapid correction of serum sodium concentrations (Table 1) did not result in any adverse neurological effects, suggesting a short duration of severe hyponatremia, and the rapid improvement precluded treatment of cerebral edema with mannitol.

An electrocardiogram (ECG) would have been useful in this case to characterize the arrhythmia, but this was not completed. Hyperkalemia was the likely cause for the arrhythmia. Electrocardiographic findings consistent with hyperkalemia include broadening, flattening, or absence of P waves, peaked T waves, widening of QRS complexes, and atrial standstill (2,9). If hyperkalemia is severe, ventricular fibrillation or asystole can be observed (9).

Elevated serum potassium levels are variously treated, including sodium replacement with potassium-poor fluids, usually physiologic saline with or without dextrose (1,2). Dextrose reduces serum potassium concentration by inducing endogenous insulin release, as insulin drives potassium from the serum into cells. Exogenous insulin administration is occasionally required as an adjunct treatment (1). Sodium bicarbonate lowers serum potassium concentration by increasing the serum pH and liberating hydrogen ions from intracellular locations (2). As hydrogen ions exit cells, potassium ions from serum enter cells in exchange to maintain electroneutrality. Administration of sodium bicarbonate, however, must be undertaken cautiously, as hypocalcemia may be induced. Finally, calcium gluconate is considered cardioprotective. Increasing extracellular-free calcium increases the threshold potential of excitable cells. This counteracts the increased excitability that accompanies hyperkalemia (2). In this foal, the cardiac arrhythmia resolved after serum potassium was reduced, suggesting that the arrhythmia may have been secondary. Although hyponatremia and hypochloremia were also corrected with the fluid therapy, these abnormalities are not generally associated with arrhythmias (9). Other electrolyte disturbances associated with abnormal cardiac rhythms (altered serum calcium or magnesium concentrations) were not observed in this foal.

Although medical treatment (closed urinary drainage system, fluid, and antimicrobial therapy) has been described in critically ill foals that cannot be adequately stabilized (10), surgical correction is advised in most cases.

Prognosis following surgical repair is good (3,4). The outcome is often less favorable if leakage occurs from areas other than the bladder, such as the ureters (4). In septic foals with lower urinary tract involvement that develop uroperitoneum secondarily, prognosis for successful repair of bladder defects is more guarded due to their comprised immune function and diffuse involvement of the bladder (3). CVJ