Uroabdomen secondary to spontaneous bladder rupture in a dog with dystocia.

OBJECTIVE: To describe the development of uroabdomen secondary to spontaneous bladder rupture in a dog with dystocia. CASE SUMMARY: 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. UNIQUE INFORMATION PROVIDED: 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.

Electrocardiographic abnormalities are associated with seropositive Trypanosoma cruzi infection status using a simplified cardiac diagnostic evaluation in dogs.

OBJECTIVE: To describe associations between cardiac abnormalities and Trypanosoma cruzi serostatus by use of a simplified diagnostic evaluation in dogs at risk for T cruzi infection. METHODS: A prospective, cross-sectional study was performed using a simplified diagnostic evaluation including high-sensitivity cardiac troponin I, 30-second ECG, and echocardiogram with 7 variables in 46 client-owned dogs from high-risk environments. Dogs were categorized as serologically positive (SP), negative (SN), or discordant (SD) by use of 2 antibody tests. Functional evaluation of cardiac health scores and blood PCR were obtained. RESULTS: Dogs were SP (n = 19), SN (17), and SD (10), with 9 PCR positive (7 SP, 1 SN, 1 SD). Troponin was above reference range in 6 of 46 (4 SP, 1 SN, 1 SD), and functional evaluation of cardiac health scores were 0 in all dogs. Conduction system abnormalities (prolonged interval durations, second-degree atrioventricular block, splintered QRS complex) and ventricular arrhythmias were documented in 8 (7 SP, 0 SN, 1 SD). Twenty-six (12 SP, 8 SN, 6 SD) had echocardiographic abnormalities, most often myxomatous mitral valve disease (MMVD) and left ventricular enlargement. Seropositive dogs were significantly older and had a higher likelihood of MMVD. Conduction system abnormalities were associated with positive serostatus. CONCLUSIONS: Echocardiographic abnormalities were complicated by MMVD and did not distinguish between serostatus. An ECG with assessment and detailed measurement of complexes and cardiac troponin I are simple tests to perform with abnormalities detected in seroreactive dogs. CLINICAL RELEVANCE: Electrocardiographic abnormalities in high-risk or seroreactive dogs should prompt further evaluation and monitoring of T cruzi infection.

Positive clinical outcome using a modified dosing regimen of benznidazole in dogs at high risk for infection or acutely infected with Trypanosoma cruzi.

Trypanosoma cruzi infection in dogs can cause heart failure and sudden death with few treatment options available. A litter of 4 dogs living in a T cruzi endemic area were randomized to prophylaxis and nonprophylaxis groups as part of a study evaluating a modified benznidazole dosing regimen administered twice weekly to prevent T cruzi infection during a vector transmission season. The 2 dogs that received prophylaxis remained healthy without T cruzi infection or cardiac disease for >2 years. One dog that did not receive prophylaxis died unexpectedly with acute T cruzi-induced pancarditis, and the second dog tested positive for T cruzi and developed complex arrhythmias with markedly increased cardiac troponin I and improved with a higher benznidazole treatment dose. Although the small sample size precludes definitive conclusions, we describe the potential clinical benefit of prophylactic and early treatment with modified benznidazole dosing regimens for dogs with T cruzi infection.