Vasculotoxic Snake Bite !full! May 2026

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.

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.

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.

Pathophysiology, Clinical Spectrum, and Management of Vasculotoxic Snake Envenomation: A Comprehensive Review

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.