Therapy for feline secondary hypertriglyceridemia with fenofibrate.

OBJECTIVES: The aim of this study was to assess the short-term safety and efficacy of fenofibrate in controlling secondary hypertriglyceridemia in cats. METHODS: This was a prospective cohort study. Seventeen adult cats with hypertriglyceridemia (serum triglycerides [TG] >160 mg/dl) were enrolled. Cats received a median dose of 5 mg/kg (range 3.2-6) fenofibrate (q24h PO) for 1 month. Serum TG, total cholesterol (TC), creatine kinase and liver enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were evaluated before (t0) and after 1 month (t1) of fenofibrate treatment. RESULTS: The causes of secondary hypertriglyceridemia were diabetes mellitus (DM; 29.4%), obesity (29.4%), hyperadrenocorticism (HAC) and DM (11.7%), HAC without DM (5.9%), hypersomatotropism (HST) and DM (5.9%), hypothyroidism (5.9%), long-term treatment with glucocorticoids (5.9%) and chylothorax (5.9%). Serum TG (t0 median 920 mg/dl [range 237-1780]; t1 median 51 mg/dl [range 21-1001]; P = 0.0002) and TC (t0 median 278 mg/dl [range 103-502]; t1 median 156 mg/dl [range 66-244]; P = 0.0001) concentrations showed a significant decrease after 1 month of fenofibrate treatment. Fifteen cats normalized their TG concentration at t1 (88.2%). Of the eight cats that were hypercholesterolemic at t0, six (75%) normalized their TC concentrations at t1. One of 17 cats (5.9 %) presented with diarrhea; the remaining 16 did not show any adverse effects. CONCLUSIONS AND RELEVANCE: DM and obesity are the most common endocrine causes of secondary hyperlipidemia, although it can also be found in cats with HAC, HST or hypothyroidism. This study suggests that fenofibrate treatment was associated with reduction and normalization of TG and TC concentrations in cats with moderate and severe hypertriglyceridemia, regardless of the cause of secondary hypertriglyceridemia. Further work should focus on controlled studies with a greater number of cases.

Successful resolution of urothorax secondary to non-traumatic uroabdomen in a cat managed with peritoneal dialysis as a bridge to surgery.

CASE SUMMARY: A 9-year-old neutered male domestic shorthair cat was presented for evaluation of severe hemodynamic collapse and suspected lower urinary tract disease. On admission, severe metabolic acidosis, hyperkalemia and azotemia, and electrocardiographic findings consistent with cardiotoxicity were identified. The diagnosis of uroabdomen was made based on abdominal fluid to plasma concentration ratios of creatinine and potassium. A central line catheter was placed percutaneously into the abdomen for peritoneal drainage and used for peritoneal dialysis as a bridge to surgery. Retrograde contrast cystography confirmed rupture of the urinary bladder. Point-of-care ultrasound of the chest postoperatively revealed the presence of mild pleural effusion. Echocardiography was then performed showing no evidence of cardiac disease. Pleural fluid analysis revealed a transudate with a creatinine ratio of 2.38 ([Creatinine]pleural fluid/[Creatinine]plasma), consistent with the diagnosis of urothorax. The cat recovered uneventfully from surgery and was monitored for signs of respiratory distress during the rest of its stay in hospital. The cat was discharged 4 days later and the pleural effusion resolved without further medical intervention. RELEVANCE AND NOVEL INFORMATION: There is limited information on the causes of urothorax and uroabdomen management of feline patients. Pleural effusion is a complication observed in critically ill cats secondary to fluid overload, underlying cardiomyopathy, primary thoracic pathology or a combination of these. To our knowledge, this is the first report of urothorax in a cat secondary to non-traumatic uroabdomen. Careful monitoring of respiratory signs consistent with pleural space disease is recommended in cases of uroabdomen.

Caudal vena cava collapsibility index as a tool to predict fluid responsiveness in dogs.

OBJECTIVE: To evaluate the use of the caudal vena cava collapsibility index (CVCCI) as a predictor of fluid responsiveness in hospitalized, critically ill dogs with hemodynamic or tissue perfusion abnormalities. DESIGN: Retrospective observational study. SETTING: Private referral center. ANIMALS: Twenty-seven critically ill, spontaneously breathing dogs with compromised hemodynamics or tissue hypoperfusion. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The electronic medical records were searched for dogs admitted for any cause, from August 2016 to December 2017. We included dogs with ultrasound measurements of: CVCCI, performed at baseline; and velocity time integral (VTI) of the subaortic blood flow, carried out before and after a fluid load. CVCCI was estimated as: (maximum diameter-minimum diameter/maximum diameter) × 100. Dogs in which VTI increased ≥15% were considered fluid responders. The CVCCI accurately predicted fluid responsiveness with an area under the receiver operating characteristic curve of 0.96 (95% CI, 0.88 to 1.00). The optimal cut-off of CVCCI that better discriminated between fluid responders and nonresponders was 27%, with 100.0% sensitivity and 83.3% specificity. At baseline, fluid responders had lower VTI (5.48 [4.26 to 7.40] vs 10.61 [7.38 to 13.23] cm, P = 0.004) than nonresponders. The basal maximum diameter of the caudal vena cava adjusted to body weight was not different between responders and nonresponders (0.050 [0.030 to 0.100] vs 0.079 [0.067 to 0.140] cm/kg, P = 0.339). The increase in VTI was related to basal CVCCI (R = 0.60, P = 0.001). Bland-Altman analysis showed narrow 95% limits of agreement between measurements of CVCCI and VTI performed by different observers or by the same observer. CONCLUSIONS: The results of this small cohort study suggest that CVCCI can accurately predict fluid responsiveness in critically ill dogs with perfusion abnormalities. Further research is necessary to extrapolate these results to larger populations of hospitalized dogs.