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Intravenous fat emulsion as treatment for ivermectin toxicosis in three dogs homozygous for the ABCB1–1Δ gene mutation

Authors


  • The authors report no conflict of interest.

  • The results of this study were presented in part at the ACVIM Forum in Denver, Colorado on June 16, 2011.

Address correspondence and reprint requests to

Heather Wright, DVM, Veterinary Teaching Hospital, College of Veterinary Medicine, Washington State University, PO Box 647010, Pullman, WA 99164–7010.

Email: hwright@vetmed.wsu.edu

Abstract

Objective

To describe the outcome of 3 cases of ivermectin toxicosis in dogs homozygous for the ABCB1–1Δ gene mutation treated with intravenous fat emulsion (IFE).

Series Summary

One Australian Shepherd and 2 Miniature Australian Shepherds were treated for naturally occurring ivermectin toxicosis with IFE. All 3 dogs were homozygous for the ABCB1–1Δ gene mutation. Serum ivermectin concentrations confirmed ivermectin exposure in each case. All 3 dogs exhibited tremors, ptyalism, and central nervous system depression, which progressed over several hours to stupor in 2 dogs, and to a comatose state requiring mechanical ventilation in the remaining dog. A 20% formulation of IFEa was administered as an IV bolus (1.5 mL/kg) followed by a slow IV infusion (7.5–15 mL/kg [0.25–0.5 mL/kg/m], over 30 minutes). No change was observed in the neurologic status of any patient. Lipemia visible upon blood sampling persisted for 36 hours in 1 dog however, no other adverse effects were noted. Flumazenil (0.01 mg/kg IV), followed by a constant rate infusion(CRI) of 0.01 mg/kg/h IV was administered in 1 case, without any apparent clinical benefit or adverse effect.

New or Unique Information Provided

IFE was ineffective in the treatment of ivermectin toxicosis in these ABCB1–1Δ homozygous mutant dogs. Further investigation is necessary to determine why IFE treatment was unsuccessful in these cases and whether its use can be optimized to yield better results.

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