Our understanding of the coagulation system defects associated with injury continues to evolve. Hyperfibrinolysis has been identified as one of these coagulation abnormalities. Recently, the therapeutic impact of the antifibrinolytic tranexamic acid was examined in the CRASH-2 study.1 Despite a subtle but significant outcome benefit, direct application of these results to clinical practice was made challenging by several factors, including the inclusion criteria that effectively diluted out those patients who were actually bleeding. These results became even more difficult to interpret when an analysis of the time from injury to treatment demonstrated an increase in the risk of death due to bleeding2 if the antifibrinolytic was administered beyond 3 hours.
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