Anticoagulation in Hemorrhagic Snake Venom Poisoning

Abstract

High mortality in hemorrhagic snake venom poisoning continues to be an important problem in medicine. Nearly two centuries ago, hemorrhagic snake venoms were classified as coagulant and anticoagulant in their toxic action. In recent years, two major mechanisms causing the coagulation disorders of snake venom poisoning have been suggested. In crotalid venom, the typical coagulant effect has been attributed to its thrombinlike action (Macfarlane, 1961, 1967; Williams and Esnouf, 1962; Meaume, 1966), while in viperid venom, the prototype of Russell’s viper venom, an activation of factor X followed by conversion of prothrombin to thrombin in the presence of factor V, platelet, and Ca² is reported to be responsible for the toxic hemorrhagic manifestations (Macfarlane, 1961, 1967; Williams and Esnouf, 1962; Esnouf and Willliams, 1962; Nahas et al., 1964; Meaume, 1966; Schiffman et al., 1969). In either case, however, the pathogenesis of the hemorrhagic manifestation would be one of defibrination syndromes resulting in intravascular coagulation and a massive consumption of fibrinogen. Such a pathological state logically calls for a specific therapeutic approach to prevent intravascular clotting and rapid fibrinogen replacement in the treatment of the disorder.