A victim of snakebite by Daboia russelii (Russell's viper) develops severe local swelling, spontaneous bleeding from gums, haematuria, and passes into acute renal failure. The primary mechanism of coagulopathy in Russell's viper envenomation is:

• A Inhibition of thrombin formation by blocking factor Xa
• B Direct fibrinolysis by viper metalloproteinases without coagulation cascade involvement
• C Complement-mediated platelet destruction causing isolated thrombocytopaenia
• D Venom factor V activator causing consumption coagulopathy and DIC via prothrombin activation ✓

Explanation

Daboia russelii venom contains RVV-X (a factor X activator) and RVV-V (a factor V activator), which bypass normal coagulation cascade steps to directly activate prothrombin. This generates excess thrombin, consuming fibrinogen, clotting factors, and platelets — producing disseminated intravascular coagulation (DIC). Clinically this manifests as a consumption coagulopathy with spontaneous haemorrhage. Venom metalloproteinases also cause local tissue destruction and haemorrhage, but the systemic coagulopathy is primarily due to prothrombin activation.

Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.