A model of coagulation disturbances in snake bites

Background: A procoagulant toxin (group C) is found in taipan (Oxyuranus genus) venom, which activates the coagulation cascade and causes venom induced consumptive coagulopathy (VICC).


  1. To explore the turnover of the clotting factors in the coagulation cascade using a mathematical model and the effects of the procoagulant toxin on this system
  2. Evaluate the performance of the model 3. Investigate the influence of interventions based on the model. 

Methods: a semi-mechanistic turnover model of the coagulation cascade was developed from the literature. Simulations following the effects of a prothrombinase-like enzyme were compared with data collected from taipan envenomed patients and the final model was assessed for sensitivity. The model was then used to investigate clinical questions such as the likely half-life of the venom and effects of antivenom. 

Results: The model performed well in predicting the concentration of clotting factors over time following taipan envenoming. The upper limit half-life of the toxin in the blood was found to be approximately 1 hour although it is likely that the real value is closer to 10-15 minutes. The model also suggests that unless given almost immediately, antivenom is likely to be limited in reducing the recovery time of the coagulation profile. 

Conclusions: The developed model is a useful way of exploring changes that occur in the coagulation cascade upon stimulation.  The model predicts the use of antivenom, although accepted as the therapy of choice, may have a more limited role in the treatment of VICC caused by taipans than previously believed.