Tranexamic Acid Use in Trauma

18 Feb


inhibits plasminogen activation thereby decreasing plasmin activity

Inhibits clot breakdown as opposed to new clot formation

-Excreted in urine

Half-life of 2 hours



1g loading dose over 10 minutes, followed by 1g over 8 hours


Data Behind its Use:

CRASH-2 Study

-looked at 20,211 trauma patients in 40 countries

-randomized double blinded placebo controlled multicenter study

-Primary outcome looked at was in hospital mortality

-Secondary outcomes included vascular occlusive events, transfusions, surgical interventions


Reduction in relative risk of all cause mortality (14.5% vs. 16%; p=0.0035) with a NNT of 67 trauma patients

Reduction in RR of death from bleeding of 15% (4.9% vs. 5.7%; p=0.0077)

-Benefits of TXA increased with administration within 3 hours and in hypotensive patients

-Death from head injury the same in both groups (previous studies showed not beneficial in SAH patients)

No significant difference in rate of vascular occlusive events (1.7% vs. 2.0%; p=0.084)


 Submitted by Joey Grover. 


Sources: Cap AP, Baer DG, Orman JA, Aden J, Ryan K, Blackbourne LH.  “Tranexamic Acid for Trauma Patients:  A Crticial Review of the Literature.” J Trauma.  2011;71:S9-S14.; CRASH-2 Trial Collaborators.  “Effect of Traneamic Acid on Death, Vascular Occlusive Events, and Blood Transfusion in Trauma Patients with Significant Haemorrhage (CRASH-2):  A Randomised Placebo-Controlled Trial.”  Lancet.   2010;376:23-32.; picture


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