Year: 2026
Type: article
Study design: Case Report
Abstract: An elderly male in early 70s presented to the emergency room with breathlessness and unresponsiveness, following an unknown snake bite to the right lower limb (Fig. 1) 1 hour before. Initial PresentationOn examination, the patient had gurgling and pooling of secretions, and he was gasping with a heart rate of 100 bpm, blood pressure of 150/70 mm Hg, and a Glasgow Coma Scale (GCS) of 3/15.Bite marks IntroductIonSnakebites represent a significant cause of morbidity and mortality in India, with the highest burden in rural regions. 1 In Kerala, hemotoxic viper bites are the predominant cause. 2 Hemotoxins induce coagulopathy, endothelial damage, and inflammation, increasing the risk of ischemic and hemorrhagic cerebrovascular accidents (CVA).3-5 This case series highlights three patients who developed ischemic strokes following hemotoxic envenomation, emphasizing the clinical spectrum and importance of timely antisnake venom (ASV) administration.The presumed mechanisms for cerebral complications following snakebite envenoming involve the procoagulant and platelet aggregation properties of the venom.Snake-venom metalloproteinases (SVMPs), phospholipase A2 (PLA2), snake-venom serine proteases (SVSPs), L-amino-acid oxidase (LAAOs) and snake C-type lectin-like proteins (Snaclecs) are some of the key protein families in snake venom that contribute to hemorrhage, platelet aggregation/inhibition, and coagulation effects leading to intracranial hemorrhage and/or cerebral infarction.6 A pre-existing procoagulant state, deficiencies of protein C or S or antithrombin III, and antiphospholipid antibodies can increase the risk of thrombosis in large vessels.7 case descrIptIonThe following three cases highlight cerebrovascular complications observed after hemotoxic snakebites treated at Travancore Medical College.Kollam, Kerala.
Language: English
Subfield: Genetics
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7133234872