- Mechanism of diphacinone rodenticide toxicosis in the dog and its therapeutic implications.
Mechanism of diphacinone rodenticide toxicosis in the dog and its therapeutic implications.
Vitamin K1 (5 mg/kg of body weight/day divided for several 5-day regimens) was effective in preventing bleeding diathesis in diphacinone-poisoned dogs. Diphacinone, a vitamin K-inhibiting rodenticide, was given 2.5 mg of diphacinone/kg of body weight orally in divided doses 2 times daily for 3 days. One dog was given 5.0 mg of warfarin/kg in 2 divided doses for 3 days. Hemograms and biochemical profiles were performed every other day. A pancreatic exocrine function test was performed before and after administration of diphacinone and warfarin. All dogs were monitored, using routine coagulation screening tests and assays of coagulation factors II, VII, IX, and X. When laboratory results or clinical illness indicated hemorrhage, diphacinone-treated dogs were given 5.0 or 2.5 mg of vitamin K1/kg in divided doses 3 times a day for 5 days. The warfarin-treated dog was given 2.5 mg of vitamin K1/kg of body weight in divided doses 3 times a day for 5 days. Of the diphacinone-treated dogs, 1 dog (given 2.5 mg of vitamin K1/kg) required 3 vitamin K regimens and 2 dogs (given 5.0 mg of vitamin K1/kg) required only 2 vitamin K regimens. The warfarin-treated dog required only 1 vitamin K1 regimen. Bleeding was observed in the diphacinone-treated dogs up to 2 weeks after treatment. The vitamin K-enzyme complex was inhibited in diphacinone-treated dogs for approximately 30 days, as indicated by routine coagulation screening tests and coagulation factor inhibition. Hepatic dysfunction was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)