BackgroundGallbladder mucocele (GBM) is an increasingly recognized extrahepatic biliary disease in dogs.ObjectivesTo investigate cases of GBM and identify variables associated with survival and the sensitivity and specificity of ultrasonography to identify gallbladder rupture.AnimalsTwo hundred and nineteen client‐owned dogs with GBM.MethodsMulticenter, retrospective study of dogs with GBM, presented from January 2007 to November 2016 to 6 academic veterinary hospitals in the United States. Interrogation of hospital databases identified all cases with the inclusion criteria of a gross and histopathologic diagnosis of GBM after cholecystectomy and intraoperative bacteriologic cultures of at least 1 of the following: gallbladder wall, gallbladder contents, or abdominal effusion.ResultsTwo hundred and nineteen dogs fulfilled the inclusion criteria. Dogs with GBM and gallbladder rupture with bile peritonitis at the time of surgery were 2.7 times more likely to die than dogs without gallbladder rupture and bile peritonitis (P = 0.001; 95% confidence interval [CI], 1.50–4.68; n = 41). No significant associations were identified between survival and positive bacteriologic cultures, antibiotic administration, or time (days) from ultrasonographic identification of GBM to the time of surgery. The sensitivity, specificity, positive, and negative likelihood ratios for ultrasonographic identification of gallbladder rupture were 56.1% (95% CI, 39.9–71.2), 91.7% (95% CI, 85.3–95.6), 6.74, and 0.44, respectively.Conclusion and Clinical ImportanceDogs in our study with GBM and intraoperative evidence of gallbladder rupture and bile peritonitis had a significantly higher risk of death. Additionally, abdominal ultrasonography had low sensitivity for identification of gallbladder rupture.

Gallbladder mucocele (GBM) is a common extra-hepatic biliary syndrome in dogs with death rates ranging from 7-45%. Therefore, the aim of this study was to identify the association of survival with variables that could be utilized to improve clinical decisions. A total of 1194 dogs with a gross and histopathological diagnosis of GBM were included from 41 veterinary referral hospitals in this retrospective study. Dogs with GBM that demonstrated abnormal clinical signs had significantly greater odds of death than subclinical dogs in a univariable analysis (OR, 4.2; 95% CI, 2.14-8.23; P<0.001). The multivariable model indicated that categorical variables including owner recognition of

A juvenile male mixed breed dog was presented for lethargy, exercise intolerance, and aggression when touched on the head. Cyanosis, tachycardia, and tachypnea were observed and persisted during oxygen supplementation. Arterial blood gas analysis by co‐oximetry identified an increased methemoglobin concentration (27%; normal, <2%) with normal arterial oxygen tension. The methemoglobinemia and associated clinical signs resolved after administration of methylene blue (1 mg/kg) IV, and the dog was discharged. The affected dog's whole‐genome sequence contained 2 potentially causal heterozygous CYB5R3 missense mutations suggesting that cytochrome b5 reductase deficiency was responsible for the methemoglobinemia. This hypothesis was confirmed by enzyme analysis that identified cytochrome b5 reductase activity in the affected dog's erythrocytes to only approximately 6% of that in a control sample. Clinical signs recurred 11 days after discharge but normalized and the methemoglobin concentration decreased with methylene blue administration PO (1.5 mg/kg, initially daily and then every other day).