American Journal of Veterinary Research · 1983 · 45 citations · 0 references
Veterinary MedicinePharmacologyToxicologyDiagnostic ToxicologyPharmaceutical ToxicologyRodent MedicineAnticoagulant ToxicityRodent ToxicologyRodenticide PoisoningRodenticide ToxicologyVitamin K TherapyAnticoagulant Rodenticide ToxicityCoagulationPancreatic Exocrine FunctionPancreatic Exocrine InteractionRodenticide AntidotesToxicity In AnimalsToxicology Of Veterinary Drugs
SUMMARY Vitamin K 1 (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 K 1 /kg in divided doses 3 times a day for 5 days. The warfarin-treated dog was given 2.5 mg of vitamin K 1 /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 K 1 /kg) required 3 vitamin K regimens and 2 dogs (given 5.0 mg of vitamin K 1 /kg) required only 2 vitamin K regimens. The warfarin-treated dog required only 1 vitamin K 1 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. There was a significant reduction ( P < 0.001) in pancreatic exocrine function although the final values were within the values established for 24 clinically normal dogs. Amount and duration of vitamin K 1 therapy were important aspects of therapy for diphacinone-induced toxicosis in dogs. Therapy effective for warfarin toxicosis was ineffective against diphacinone toxicosis due to inadequate vitamin K dosage and duration of therapy.