Successful multimodal treatment of extreme hypertriglyceridemia in a juvenile diabetic dog.

OBJECTIVE: To describe the therapeutic protocol used to normalize severe hypertriglyceridemia in a dog. CASE SUMMARY: A 7-month-old, 1.2-kg female Pomeranian presented with acute polyuria, polydipsia, and ocular discoloration. Diagnoses included diabetic ketosis, severe hypertriglyceridemia (>225 mmol/L [>20,000 mg/dl]), lipemia retinalis, and bilateral uveitis. The triglyceride concentration was near normal within 2 days of initiating treatment with fenofibrate, regular insulin constant rate infusion (CRI), manual therapeutic plasma exchange (TPE), and a low-fat diet. All clinical signs resolved. The dog has had no relapse of hypertriglyceridemia at the time of writing the manuscript, 6 months later, with continued treatment of diabetes mellitus. NEW OR UNIQUE INFORMATION PROVIDED: This is the first case report documenting the combination of fenofibrate, insulin CRI, and manual TPE for treatment of severe hyperlipidemia in a dog. Detailed protocols for manual TPE and a novel insulin CRI are provided. A discussion of multiple spurious biochemical and hematologic errors associated with the severe hypertriglyceridemia is also provided.

Outcomes of 434 dogs with non-steroidal anti-inflammatory drug toxicosis treated with fluid therapy, lipid emulsion, or therapeutic plasma exchange.

BACKGROUND: Traditional management of non-steroidal anti-inflammatory drug (NSAID) intoxication includes gastrointestinal decontamination, intravenous administration of fluids (IVF), and gastroprotection. Intravenous administration of lipid emulsion (ILE) and therapeutic plasma exchange (TPE) are popular novel therapeutic strategies. HYPOTHESIS: Compare outcomes of dogs treated with IVF, ILE, and TPE for NSAID intoxications and evaluate outcome predictors for drug subgroups. ANIMALS: Four hundred thirty-four dogs with NSAID intoxications (2015-2020). METHODS: Multicenter retrospective study of ibuprofen, carprofen, and naproxen intoxication. An ordinal outcome was defined as mild gastrointestinal, moderate kidney, or signs of severe central nervous system disease. RESULTS: Signs of neurological disease were overrepresented and acute kidney injury underrepresented in the TPE group among dogs exposed to kidney- or CNS-toxic doses (P = .05), though all TPE dogs with signs of neurological disease had evidence of neurotoxicity at presentation. Dogs treated with IVF had a higher maximal creatinine concentration (median, 1.1 mg/dL; range, 0.4-8.44 mg/dL) compared with IVF + ILE (median, 0.9 mg/dL; range, 0.4-6.2 mg/dL; P = .01). Increased maximum time to presentation (P < .001), higher baseline creatinine (P < .001) and PCV (P = .007), and absence of induced emesis (P < .001) were associated with greater clinical severity. Ibuprofen toxicosis was associated with more severe clinical signs compared with carprofen (P = .03). Overall survival rate was 99%. CONCLUSIONS AND CLINICAL IMPORTANCE: NSAID toxicosis generally carries an excellent prognosis in dogs. Despite similar outcomes of lower incidence of AKI in the TPE group, and slightly lower maximal creatinine concentration in dogs treated with ILE vs IVF alone, ILE and TPE should be considered in the management of severe NSAID toxicosis.

Outcomes of nonsteroidal anti-inflammatory drug toxicosis treated with therapeutic plasma exchange in 62 dogs.

BACKGROUND: Therapeutic plasma exchange (TPE) is gaining popularity for the management of nonsteroidal anti-inflammatory drug (NSAID) overdose in dogs. HYPOTHESIS/OBJECTIVES: Describe a population of dogs treated with TPE for NSAID overdose. ANIMALS: Sixty-two dogs with NSAID overdose treated with TPE. METHODS: Multicenter retrospective study of dogs treated with TPE for ibuprofen, carprofen, or naproxen overdose. RESULTS: The median dose of ibuprofen, carprofen or naproxen ingested was 533 mg/kg (range, 36-4857 mg/kg), 217 mg/kg (range, 88-625 mg/kg) and 138 mg/kg (range, 26-3000 mg/kg), respectively. Based on previously established toxic ranges for each NSAID, 2 (3.2%), 14 (22.6%), and 46 (74.2%) dogs ingested a gastrointestinal, renal, and neurological toxic dose, respectively. The median time between ingestion and presentation was 4 hours (range, 1-20 hours). The median number of plasma volumes processed was 1.6 (range, 0.4-2.2). The median TPE session duration was 2 hours (range, 1-4.5 hours). Circuit clotting developed during 8 (12.9%) sessions. Patient adverse events reported during 21 (33.8%) sessions consisted of urticaria (12.9%), asymptomatic hypocalcemia (9.6%), and hypotension (9.6%). The median duration of hospitalization was 2.25 days (range, 1-11 days). Sixty-one (98.4%) dogs survived to discharge, and none were rehospitalized. Thirty-one (91.1%) of the 34 dogs with at least 1 follow-up visit were not azotemic at the time of reevaluation. CONCLUSIONS AND CLINICAL IMPORTANCE: This population of dogs managed with TPE had excellent outcomes, even in cases of high NSAID dose ingestion. When TPE is available and the time frame is appropriate, this extracorporeal modality should be considered for the management of NSAID overdose.