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, Snakebite, Viperidae, Coagulopathy, Antivenom, Acute Kidney Injury. 1. Introduction Snakebite envenomation is a neglected tropical disease (NTD) responsible for an estimated 1.8 to 2.7 million envenomations annually, with over 100,000 deaths and 400,000 permanent disabilities (WHO, 2019). The pathophysiological effects of snake venom are broadly classified into three categories: neurotoxic (elapids), myotoxic (sea snakes), and vasculotoxic (vipers). Vasculotoxic snake bites are characterized by their predilection for the vascular endothelium and hemostatic system. vasculotoxic snake bite
SVMPs degrade the basement membrane of capillary endothelial cells. By cleaving type IV collagen, laminin, and fibronectin, they increase vascular permeability, leading to local edema, blistering, and systemic capillary leak syndrome. This directly causes petechiae, ecchymosis, and spontaneous systemic hemorrhage. The term "vasculotoxic" is somewhat of a misnomer,
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
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, Snakebite, Viperidae, Coagulopathy, Antivenom, Acute Kidney Injury. 1. Introduction Snakebite envenomation is a neglected tropical disease (NTD) responsible for an estimated 1.8 to 2.7 million envenomations annually, with over 100,000 deaths and 400,000 permanent disabilities (WHO, 2019). The pathophysiological effects of snake venom are broadly classified into three categories: neurotoxic (elapids), myotoxic (sea snakes), and vasculotoxic (vipers). Vasculotoxic snake bites are characterized by their predilection for the vascular endothelium and hemostatic system.
SVMPs degrade the basement membrane of capillary endothelial cells. By cleaving type IV collagen, laminin, and fibronectin, they increase vascular permeability, leading to local edema, blistering, and systemic capillary leak syndrome. This directly causes petechiae, ecchymosis, and spontaneous systemic hemorrhage.
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.