A 35-year-old farmer is bitten by a Russell's viper (Daboia russelii) on the right ankle. Six hours later he develops swelling of the entire limb, gum bleeding, haematuria, and his coagulation screen shows unclottable blood. The mechanism of this coagulopathy is:

• A Inhibition of fibrinogen synthesis in the liver by a metalloprotease
• B Venom factor X activator and thrombin-like enzyme causing consumption coagulopathy (venom-induced consumptive coagulopathy, VICC) ✓
• C Direct platelet membrane lysis by phospholipase A2, causing isolated thrombocytopenia
• D IgE-mediated mast cell degranulation releasing histamine that dilutes clotting factors

Explanation

Russell's viper venom (RVV) contains a factor X activator and RVV-V (a serine protease) that directly activate the coagulation cascade, leading to defibrination — massive consumption of fibrinogen, factors V, VIII, and platelets. This produces venom-induced consumptive coagulopathy (VICC), characterised by unclottable blood, 20-minute whole blood clotting test (WBCT-20) positivity, haematuria, and bleeding. The treatment is polyvalent anti-snake venom (ASV). Phospholipase A2 contributes to local tissue necrosis and myotoxicity but is not the primary mechanism of VICC.

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

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Written and medically reviewed by the StethoPrep medical team.