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.

[Generated for Academic Purposes] Affiliation: Department of Internal Medicine & Tropical Medicine vasculotoxic snake bite

PLA2 enzymes damage endothelial cell membranes directly and promote the release of inflammatory mediators (leukotrienes, prostaglandins). They also inhibit platelet aggregation through the hydrolysis of platelet membrane phospholipids, exacerbating the bleeding diathesis. Unlike physiological thrombin, venom serine proteases (e

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. with over 100