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Viper coagulopathy — DTM&H MCQ

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ModerateEnvironmental HealthViper coagulopathyDTM&H

A 35-year-old man bitten by a saw-scaled viper (Echis) in Pakistan develops bleeding from the bite site, gingival bleeding, and haematuria. His INR is >10 and fibrinogen is unmeasurably low. What is the mechanism of coagulopathy?

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Correct answer: CVenom procoagulant enzymes causing consumptive coagulopathy (DIC)

The correct answer is C, venom procoagulant enzymes causing consumptive coagulopathy (DIC). Saw-scaled viper (Echis) venom contains potent prothrombin-activating and factor X-activating enzymes that trigger widespread, inappropriate activation of the clotting cascade, rapidly consuming fibrinogen, factor V and prothrombin. This produces venom-induced consumption coagulopathy (VICC), clinically and biochemically indistinguishable from DIC, with an unrecordable or markedly prolonged INR, unmeasurable fibrinogen, and systemic bleeding (gum bleeding, haematuria, bite-site ooze) exactly as described in this patient. Recognition matters because the definitive treatment is prompt antivenom, which neutralises the circulating procoagulant toxins and allows clotting factor regeneration, not vitamin K or platelet transfusion. Why the other options are wrong: D. Direct hepatotoxicity causing coagulation factor deficiency: Echis venom is not primarily hepatotoxic; the coagulopathy arises from direct enzymatic activation of clotting factors in the circulation, not from impaired hepatic synthesis. A. Direct destruction of clotting factors by proteolysis: some viper venoms contain proteolytic components causing local tissue damage, but the systemic coagulopathy here is due to procoagulant activation and consumption, not proteolytic degradation of circulating factors. E. Venom-induced thrombocytopenia only: platelet counts can fall secondarily in VICC, but this is a consequence of the consumptive process, not the primary or sole mechanism, and does not explain the grossly deranged INR and unmeasurable fibrinogen. B. Inhibition of vitamin K metabolism: there is no vitamin K antagonism in viperid envenoming; the defect is procoagulant enzyme activity, not synthetic factor deficiency, so vitamin K has no therapeutic role. Key point: Unclottable blood after Echis bite reflects consumption of clotting factors by venom prothrombin/factor X activators (VICC), diagnosed at the bedside with the 20-minute whole blood clotting test and treated with specific antivenom.

Reference: World Health Organization, Guidelines for the Management of Snakebites, 2nd edition (2016), section on viperid envenoming and venom-induced consumption coagulopathy; used as core WHO/DTMH teaching reference, https://www.who.int/publications/i/item/9789290225300