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Summary of the CRASH 2 Trial
Tranexamic acid reduced all-cause mortality in a broad population of trauma patients without an increase in vascular occlusion complications.
Key Points from CRASH 2
- Included 20,211 trauma patients with significant hemorrhage (or at risk) who were within 8 hours of initial injury and at least 16 years old
- Randomized to receive tranexamic acid (1 gm loading dose over 10 minutes, then 1 gm infusion over 8 hrs) or placebo
- Tranexamic acid is a lysine derivative that blocks the lysine site on plasminogen (thus inhibiting fibrinolysis)
- Primary endpoint (hospital mortality within 4 weeks of injury) was reduced with tranexamic acid (14.5% vs. 16.0%, p=0.0035, NNT 66)
- Death due to hemorrhage was also reduced with tranexamic acid (4.9% vs. 5.7%, p=0.0077, NNT 125)
- Interestingly, there was no difference in blood transfusions (50.4% vs. 51.3%, p=0.21) or the median number of blood products transfused (3 vs. 3 units, p=0.59). This lack of difference in transfusion brings the beneficial mechanism of tranexamic acid into question
- Safety analysis did not reveal an increase in vascular occlusion (MI, CVA, PE) between tranexamic acid and placebo (1.7% vs. 2.0%, p=0.084)
Citation
CRASH-2 trial collaborators, Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010 Jul 3;376(9734):23-32. PMID 20554319