Background: Gallbladder mucocele (GBM) is an increasingly recognized extrahepatic biliary disease in dogs. Objectives: To investigate cases of GBM and identify variables associated with survival and the sensitivity and specificity of ultrasonography to identify gallbladder rupture. Animals: Two hundred and nineteen client-owned dogs with GBM. Methods: Multicenter, 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. Results: Two 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 Importance: Dogs 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.

Hypovitaminosis D has been extensively documented in critically ill humans. However, whether or not critically ill dogs have alterations in vitamin D concentrations remains unconfirmed. The primary aims of our study were to compare serum 25-hydroxycholecalciferol [25(OH)D] concentrations in critically ill dogs with healthy control dogs, determine the prognostic utility of serum 25(OH)D concentration as a biomarker in critically ill dogs, and to assess if serum 25(OH)D concentrations in critically ill dogs are associated with length of stay in the intensive care unit or illness severity. Serum concentrations of 25(OH)D together with a range of other clinical, biochemical, and hematological parameters, were measured in 99 dogs within 24 hours of admission to the Intensive Care Unit (ICU). Critically ill dogs (P = 0.001) and dogs with sepsis (P = 0.002) had significantly lower serum 25(OH)D concentrations compared to healthy control dogs. In addition, serum 25(OH)D concentration was an independent predictor of in-hospital and 30 day survival. Using a cut-off of 33 ng/mL, serum 25(OH)D concentrations had excellent sensitivity (0.94; 95% CI, 0.71–1.00), but poor specificity (0.41; 95% CI, 0.31–0.53) for detection of survival. Serum 25(OH)D concentrations were inversely associated with acute patient physiologic and laboratory evaluation (APPLE) fast score but were not associated with ICU length of stay. Hospitalized dogs with critical illness have decreased serum 25(OH)D concentrations compared to healthy dogs and can be used to predict survival in this cohort.

Background: Clinicians alter dosing for desoxycorticosterone pivalate (DOCP) to mitigate costs, but this practice has not been critically evaluated in a prospective clinical trial. Hypothesis/Objectives: The duration of action of DOCP is longer than 30 days in dogs with primary hypoadrenocorticism (PH). Animals: A total of 53 client-owned dogs with PH. Twenty-four dogs with newly diagnosed PH (Group 1) and 29 dogs with treated PH (Group 2). Methods: Prospective, multicenter, clinical trial. For phase I, DOCP was administered and plasma sodium and potassium concentrations were measured until the dog developed hyponatremia or hyperkalemia at a planned evaluation, or displayed clinical signs with plasma electrolyte concentrations outside of the reference interval independent of a planned evaluation, thus defining DOCP duration of action. Plasma electrolyte concentrations then were assessed at the end of the individualized dosing interval (IDI; i.e., DOCP duration of action minus 7 days, phase II and at least 3 months after concluding phase II, phase III). Results: The duration of action of DOCP in dogs in phase I with naïve PH (n = 24) ranged from 32 to 94 days (median, 62 days; 95% confidence interval [CI], 57, 65) and previously treated PH (n = 29) from 41 to 124 days (median, 67 days; CI, 56, 72). Overall, the final DOCP dosing interval for all dogs that completed phase II (n = 36) ranged from 38 days to 90 days (median, 58 days; CI, 53, 61). No dog that completed phase III (n = 15) required reduction in the IDI. The DOCP duration of action, independent of group, was not significantly associated with several baseline variables. The median drug cost reduction using IDI was approximately 57.5% per year. Conclusion and Clinical Importance: The duration of action of DOCP in dogs with PH is >30 days, and plasma sodium and potassium concentrations can be maintained with an IDI >30 days long term.