A model for venom-induced consumptive coagulopathy in snake bite

Toxicon. 2008 Dec 1;52(7):769-80. doi: 10.1016/j.toxicon.2008.08.013. Epub 2008 Sep 12.


Many snake venoms contain procoagulant toxins that activate the coagulation cascade and cause venom-induced consumptive coagulopathy (VICC). We developed a semi-mechanistic model of the clotting cascade in order to explore the effects of the procoagulant toxin from taipan venom on this system as well as the effects of antivenom. Simulations of the time course in the change of clotting factors were compared to data collected from taipan envenomed patients. The model accurately predicted the observed concentration of clotting factors over time following taipan envenomation. Investigations from the model indicated that the upper limit of the half-life of the procoagulant toxin was 1h. Simulations from the model also suggest that antivenom for Australasian elapids has negligible effect on reducing the recovery time of the coagulation profile unless administered almost immediately after envenomation. The model has generality to be expanded to describe the effects of other venoms and drugs on the clotting cascade.

MeSH terms

  • Antivenins / pharmacology*
  • Blood Coagulation / drug effects*
  • Blood Coagulation / physiology
  • Disseminated Intravascular Coagulation / chemically induced*
  • Elapid Venoms / chemistry
  • Elapid Venoms / toxicity*
  • Half-Life
  • Models, Biological*
  • Time Factors


  • Antivenins
  • Elapid Venoms