Fibrinolysis and antifibrinolytic treatment in the trauma patient.

Abstract

The role of antifibrinolytics in trauma haemorrhage and early coagulopathy remains controversial with respect to patient selection, dosage, timing of treatment, and risk of thrombotic complications. This review presents our current understanding of the mechanisms of fibrinolysis in trauma, diagnostic evaluation, and the evidence base for treatment. Excessive fibrinolysis following severe injury is a major component of acute traumatic coagulopathy and contributes to the high mortality from trauma haemorrhage. The protein C pathway, endothelial dysfunction, platelet activity, shock, and tissue injury are key to the development of hyper fibrinolysis in trauma. D-dimer and viscoelastic haemostatic assays (rotational thromboelastometry, TEG) remain the best available diagnostic modalities but have a number of limitations compared with plasma biomarkers of fibrinolytic activation, for example, plasmin-α2-antiplasmin complex. Current evidence supports the continued empiric use of tranexamic acid in major trauma haemorrhage. Improving the outcomes for bleeding trauma patients requires a deeper understanding of the mechanisms driving hyperfibrinolysis and the subsequent switch toward a prothrombotic state. Discovering the interplay between platelet activity, fibrinogen utilization, the immune response, and the fibrinolytic system may lead to development of novel therapeutics.