H. Fisher; R. Dörfelt
Signalement: 2 year old, female Jack Russell Terrier.
History: The patient was presented for suspected ingestion of 310 mg/kg of naproxen, which is 12 times the reported nephrotoxic dose, 1–3 hours before presentation. Clinical examination revealed no abnormalities.
Diagnostic investigations: Complete bloodwork comprised of automated complete blood count with differentiation, blood gas analysis, coagulation profile, serum biochemistry and blood group were obtained at the time of presentation. The dog had a mild lymphocytosis (3.95x109/l), hyperglycemia (6.8 mmol/l) and hypoproteinemia (55.4 g/l). Albumin (42.2 g/l), creatinine (90 µmol/l) and urea (5.8 mmol/l) were within reference range.
Therapy: After inducing emesis, the dog was treated with IV fluids, esomeprazole, misoprostol, antiemetics, plasmapheresis and repeated activated charcoal application.
Plasmapheresis was performed applying the VETSmart® machine and the PEX 100 tubing and filter system. Heparin was used for systemic anticoagulation. During the 2 hours of treatment time, 1.8 times plasma volume was removed. Plasma was replaced with ½ fresh frozen plasma and ½ HES 6% (130 KDa/0.42) solution. Blood samples to analyze naproxen concentration were obtained before, during and after plasmapheresis, frozen at -80°C and sent for batch analysis via high-pressure liquid chromatography.
Naproxen plasma concentration was 110 µg/ml at presentation, 52 µg/ml after 1 hour and 47 µg/ml after 2 hours of plasmapheresis. Twenty hours after plasmapheresis, naproxen plasma concentration had increased to 97 µg/ml. At day 6, naproxen concentration was 5 µg/l. The dog was discharged with omeprazole and misoprostol the day after plasmapheresis. Creatinine values did not increase, but mild, self-limiting, gastrointestinal signs occurred during the next 5 days.
Discussion: Plasmapheresis has been described as potential treatment option in several NSAID intoxications, though none described naproxen. Plasma concentrations of naproxen were reduced by 50% during the course of plasmapheresis. As plasmapheresis was started early in the disease process, increase in naproxen serum concentrations on the day after plasmapheresis could have been caused by additional naproxen resorption or redistribution.