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Pathophysiology, Clinical Spectrum, and Management of Vasculotoxic Snake Envenomation: A Comprehensive Review
The term "vasculotoxic" is somewhat of a misnomer, as the venom primarily affects blood vessels and blood components. Key families include Viperidae (e.g., Daboia russelii , Echis carinatus , Bothrops atrox ) and some Colubridae. In India, Southeast Asia, Sub-Saharan Africa, and Latin America, viper bites account for the majority of vasculotoxic envenomations. The clinical syndrome is dominated by local tissue destruction, coagulopathy, and systemic vascular leakage. Without prompt intervention, patients succumb to intracranial hemorrhage, acute kidney injury (AKI), or hypovolemic shock. The vasculotoxic action is mediated by a complex mixture of enzymes and peptides. vasculotoxic snake bite
Unlike physiological thrombin, venom serine proteases (e.g., ancrod, batroxobin) cleave fibrinogen to fibrin without activating factor XIII. This produces unstable, loose fibrin clots that are rapidly lysed, leading to defibrination syndrome . Concurrently, venom activates factor X and prothrombin, leading to consumptive coagulopathy. The clinical syndrome is dominated by local tissue
[Generated for Academic Purposes] Affiliation: Department of Internal Medicine & Tropical Medicine Unlike physiological thrombin, venom serine proteases (e