To describe the development of uroabdomen secondary to spontaneous bladder rupture in a dog with dystocia.
A 2-year-old intact female Boston Terrier was referred for prolonged labor of 72 hours. At presentation, the dog had delivered 8 puppies at home, with the last pup being stillborn. The dog was in hypovolemic shock and had free abdominal effusion. Abdominal radiographs showed no evidence of remaining fetuses. Abdominal fluid analysis revealed a fluid potassium that was 1.8 times higher than the peripheral blood potassium. Retrograde positive contrast cystography identified leakage of contrast into the abdomen, consistent with uroabdomen secondary to bladder rupture. Bloodwork abnormalities included a mild monocytic leukocytosis with a left shift, moderate azotemia, mild hyperbilirubinemia, mild increase of alkaline phosphatase activity, moderate hyponatremia, and moderate hypochloremia. The dog was resuscitated with IV fluids and received IV antimicrobials out of concerns for septic peritonitis and sepsis. An exploratory laparotomy revealed a moderate volume abdominal effusion, uterine enlargement with no identifiable fetuses, and a small rupture of the urinary bladder wall apex. The bladder wall defect was repaired, and the dog underwent an ovariohysterectomy. Perioperative systemic hypotension was treated with a norepinephrine constant rate infusion and resolved within 24 hours. The dog was discharged 5 days later. The combined peritoneal fluid and uterine fluid culture and sensitivity testing revealed Enterococcus spp. and Staphylococcus pseudintermedius, both susceptible to amoxicillin/clavulanic acid and enrofloxacin. Bladder wall histopathology revealed severe mural congestion, edema, and hemorrhage, without evidence of neoplasia, cystitis, or urolithiasis.
This is the first case report of a dog with uroabdomen secondary to a bladder wall rupture associated with dystocia. Early recognition of this rare phenomenon and vigilance in treatment is essential for a good prognosis and outcome.