Fibrinolysis activation occurs almost universally after severe trauma. Systemic hyperfibrinolysis is a key component of acute traumatic coagulopathy and associated with poor clinical outcomes, although controversy exists over optimal treatment strategies. The mechanistic drivers and dynamics of fibrinolytic activation in response to injury and trauma resuscitation are currently unclear. Furthermore, therapeutic triggers are compounded by the lack of a sensitive and rapid diagnostic tool, with discrepancy between hyperfibrinolysis diagnosed by viscoelastic hemostatic assays versus biomarkers for fibrinolysis. Rotational thromboelastometry and thromboelastography appear capable of detecting the severest forms of hyperfibrinolysis but are relatively insensitive to moderate, yet clinically significant fibrinolytic activation. Rapid evaluation of the current status of the fibrinolytic system remains a challenge and therefore the decision whether to administer an antifibrinolytic agent should be based on available evidence from clinical trials. In line with current European guidelines, we recommend that all bleeding trauma patients, and in particular, severely injured patients with evidence of hemorrhagic shock, should receive early empiric tranexamic acid. This review explains our current knowledge of the pathophysiological pathways which induce hyperfibrinolysis in trauma hemorrhage, evaluates the available diagnostic modalities, and describes current treatment strategies.
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