Traumatic rupture of the urinary bladder in a horse.

An 18-months-old Thoroughbred filly weighing 400 kg presented at the Rural Veterinary Centre 12 h after running through a fence. Two hours before presentation the filly showed signs of depression and reluctance to move. Physical examination revealed an increased heart rate (80 beats/min) and respiratory rate (40 breaths /min) and reduced gastrointestinal motility on auscultation of the abdomen. Moderate soft tissue swelling of the musculature of the left flank was associated with superficial skin abrasions. The ascending colon was moderately distended on transrectal palpation and there was 5 L of spontaneous reflux after passage of a nasogastric tube. Apart from an increased haematocrit (0.52 LA), other haematological values were within normal limits. Serum biochemical analysis indicated a hyperkalaemia (6.81 mmoWL) and increased creatinine (188 pol /L) and blood urea nitrogen (10.35 mmoVL) concentrations and creatinine kinase activity (1216 UL). Abdominocentesis yielded a large volume of slightly turbid, yellow fluid with an increased creatinine concentration (1 134 pmoYL). The protein concentration (1 .O g/L) and total nucleated cell count (420 cells/$) were within normal limits. A transabdominal ultrasoundexamination confirmed the presence of a large volume of fluid in the abdominal cavity. On the basis of the clinical findings, uroperitoneum secondary to rupture of the urinary tract was suspected. The filly was sedated and the vulva and the caudal vaginal vault aseptically prepared. A 1 m videoendoscope that had been chemically sterilised with dialdehyde' and rinsed with sterile sodium chloride was passed through the external urethral orifice into the bladder. A full thickness tear approximately 3 cm long could be seen at the apex of the bladder. The endoscope was passed through the tear into the abdominal cavity and the parietal peritoneum underlying the skin abrasions on the left flank was inspected. There was a laceration in the parietal peritoneum with separation from the deep abdominal musculature at the ventral aspect of this laceration. Surgical repair of the bladder defect through a ventral midline coeliotomy was recommended. Because of financial constraints the owner declined surgery in preference to medical management. Initially intravenous fluid therapy consisted of 50 L of 0.45% sodium chloride and 5% dextrose administered over the first 24 h of hospitalisation. The ventral midline of the anterior abdomen was aseptically prepared and a sump draint placed transabdominally under local anaesthesia and sutured in place. Approximately 10 L of urine was drained from the abdominal cavity. A 14 gauge Foley balloon tipped catheter with a one-way valve was passed through the urethra and secured in the bladder by inflation of the balloon. Antimicrobial therapy was commenced with procaine penicillin (15 OOO IU/kg, intramuscularly, every 12 h), and gentamicin sulphate (3.3 mgkg, intravenously, every 12 h). Additionally the filly was given flunixin meglumine (0.25 mgkg, intravenously every 8 h) as prophylaxis for endotoxaemia. These agents were administered throughout hospitalisation. Serial blood samples collected during the following 24 h indicated that the serum potassium, creatinine and blood urea nitrogen concentrations and the abdominal fluid creatinine concentration (174 mmoVL) had returned to within normal limits. There was an increase