Anicteric Gallbladder Rupture with Elevated Bile Acids in Abdominal Effusion in a Dog with Cholecystitis.

Anicteric gallbladder rupture has been rarely described in veterinary medicine, and, generally, it has been related to gallbladder wall necrosis secondary to gallbladder mucocele. A 5 yr old, male, neutered Labrador retriever presented for acute onset anorexia, lethargy, and vomiting. Cholecystitis was diagnosed based on the ultrasonographic findings and bactibilia, and, consequently, medical treatment was established. Despite improvement of the patient, a focal ultrasound of the hepatobiliary tract was performed 72 hr after admission for reassessment, revealing gallbladder wall thickening and abdominal effusion. Intracellular bacteria were present in nondegenerated neutrophils, and the effusion was categorized as septic exudate, compatible with septic peritonitis. Exploratory laparotomy confirmed an anicteric gallbladder rupture potentially secondary to cholecystitis and/or previous cholecystocentesis. The patient was not icteric the day of the surgery, serum bilirubin was within normal limits, abdominal fluid bilirubin concentration was below that of serum, and no bile pigment was detected; however, bile acids were significantly higher in the abdominal effusion compared with the serum concentration. This case describes an anicteric gallbladder rupture in a dog with concomitant cholecystitis and raises the question about the sensitivity of bile acid evaluation as a tool for diagnosis of gallbladder rupture and bile peritonitis in dogs.

Cerebral gliosarcoma with perivascular involvement in a cat.

CASE SUMMARY: A 5-year-old neutered male domestic shorthair cat presented with an 18-month history of facial tics, and progressive general ataxia, weakness, lethargy and anorexia of 2 weeks' duration. MRI of the brain showed a well-defined heterogeneous hyperintense mass on T1-weighted and T2-weighted images, with central hypointensity in the rostral commissure and septum pellucidum, and perilesional hyperintensity in fluid-attenuated inversion recovery, suggestive of perilesional oedema. Gross examination in a transverse section of the brain at the level of the septum pellucidum revealed a 0.2 cm brown soft mass. Histopathological examination identified a biphasic neoplastic proliferation of mesenchymal and neuroepithelial cell populations. Fusiform cells were predominately distributed in bundles showing a high degree of anisocytosis and marked immune-positive reaction to vimentin immunochemistry, confirming a sarcomatous origin. Additionally, high numbers of astrocytic cells were identified by an intense immunopositive reaction to glial fibrillary acidic protein and negative reaction to oligodendrocyte transcription factor 2 immunochemistry. Vascular invasion of the neoplasia into the wall of a medium branch of the rostral cerebral artery was present (secondary Scherer structures). Based on these characteristics, the tumour was defined as a gliosarcoma. Gliosarcoma is a recognised astrocytoma grade IV anaplastic glial cell tumour with sarcomatous differentiation. RELEVANCE AND NOVEL INFORMATION: To our knowledge, this is the first report describing a cerebral gliosarcoma in a cat including clinical, MRI, macroscopic and histopathological features and immunolabelling characteristics.