CONICET | Buscador de Institutos y Recursos Humanos

Introduction: Superwarfarins are anticoagulant rodenticides, nearly 100 times more potent than warfarins. Accidental and intentional poisoning cases have been reported. The differential diagnosis includes all causes of vitamin K (VK) deficiency, factor deficiencies or inhibitor, disseminated intravascular coagulation, and liver disease. We describe 4 cases with poisoning with superwarfarinsSuperwarfarins are anticoagulant rodenticides, nearly 100 times more potent than warfarins. Accidental and intentional poisoning cases have been reported. The differential diagnosis includes all causes of vitamin K (VK) deficiency, factor deficiencies or inhibitor, disseminated intravascular coagulation, and liver disease. We describe 4 cases with poisoning with superwarfarins Methods: Four patients (pts.), 2 females, mean age: 39 years (range: 22-64), were evaluated. The symptoms included muco-cutaneous bleeding and menorrhage. Two cases had confirmed rodenticide exposition. They had prothrombin activity less than 10%, with VK coagulation factor deficiencies and normal liver function. Malabsorption was excluded in all cases.Four patients (pts.), 2 females, mean age: 39 years (range: 22-64), were evaluated. The symptoms included muco-cutaneous bleeding and menorrhage. Two cases had confirmed rodenticide exposition. They had prothrombin activity less than 10%, with VK coagulation factor deficiencies and normal liver function. Malabsorption was excluded in all cases. Results: They received high intravenous (i.v.) doses of VK (30-100 mg/d). In two cases, after 8 and 11 months of therapy, phenobarbital was indicated. In three pts., the accumulation of large amounts of VK 1 epoxide in the blood suggested severe poisoning with a VK antagonist by inhibition of VK epoxide enzyme. In one case, brodifacoum was detected. Three pts. showed a VK dependency for 7 to 12 months: one patient (pt.) is currently on VK after 10 months of treatment, another discontinued her treatment and the older pt. died for bleeding complications. The fourth pt., with brodifacoum poisoning, had complete recovery after 7 months.They received high intravenous (i.v.) doses of VK (30-100 mg/d). In two cases, after 8 and 11 months of therapy, phenobarbital was indicated. In three pts., the accumulation of large amounts of VK 1 epoxide in the blood suggested severe poisoning with a VK antagonist by inhibition of VK epoxide enzyme. In one case, brodifacoum was detected. Three pts. showed a VK dependency for 7 to 12 months: one patient (pt.) is currently on VK after 10 months of treatment, another discontinued her treatment and the older pt. died for bleeding complications. The fourth pt., with brodifacoum poisoning, had complete recovery after 7 months. Conclusions: It is usually difficult to prove the poisoning with superwarfarin. The diagnosis depends either on the superwarfarin detection or on the VK 1 epoxide measurement. In our experience, when brodifacoum was identified, we observed favourable outcome. When the toxic agent could not be identified, evolution was torpid, with prolonged requirement of i.v. VK.It is usually difficult to prove the poisoning with superwarfarin. The diagnosis depends either on the superwarfarin detection or on the VK 1 epoxide measurement. In our experience, when brodifacoum was identified, we observed favourable outcome. When the toxic agent could not be identified, evolution was torpid, with prolonged requirement of i.v. VK.