Long-acting
anticoagulant rodenticides (LAARs) inhibit
vitamin K epoxide reductase (VKOR). Related
bleeding may present a diagnostic challenge and require administration of blood component
therapy,
hemostatic agents, and
vitamin K. This article intends to provide the reader a comprehensive understanding of LAAR
poisoning. An exhaustive literature search of PubMed, Science Direct, US National Library of Medicine Toxicology Data Network, and Google Scholar yielded 174 reported cases of LAAR
poisoning from which clinical data were extracted and reviewed. In addition, 25 years of epidemiologic data from the American Association of Poison Control Centers was reviewed. In the United States, on average, there were 10413 exposures reported with 2750 patients treated annually. For 25 years, there were 315951 exposures reported with nearly 90% among children and more than 100000 patients treated in a health care facility. Fortunately, only 2% of all exposures result in morbidity or mortality. Inhalational, transcutaneous, and oral routes of exposure have been documented. Most exposures are unintentional. The most frequently reported
bleeding sites are mucocutaneous, with
hematuria being the most common feature. Deaths were most commonly associated with
intracranial hemorrhage. Long-acting
anticoagulant rodenticide-induced paradoxical
thrombosis and thrombotic complications accompanying
hemostatic therapy have also been observed. Most patients present with coagulation assay values beyond measurable limits. Long-acting
anticoagulant rodenticides have an extremely high affinity for VKOR compared with
warfarin, characterized by rebound coagulopathy and
bleeding after initial treatment and the need for high-dose, long-term
therapy with
vitamin K1. Treatment of acute hemorrhagic symptoms often required intravenous
vitamin K1 in excess of 50 to 100 mg; chronic maintenance with 100 mg PO
vitamin K1 daily was the most frequently used dose required to suppress coagulopathy. Treatment courses averaged 168 days. Adjunctive
hemostatic therapy with
recombinant factor VIIa and
prothrombin complex concentrate has been reported, and
phenobarbital has been used to expedite LAAR metabolism.