Fibrinolysis greater than 3% is the critical value for initiation of antifibrinolytic therapy

The acute coagulopathy of trauma (ACOT) is established in up to one third of patients by the time they reach the hospital.1–5 Two thirds of patients who die of hemorrhage will do so within the first 6 hours after injury, and up to 80% of the blood products transfused will be given with these first 6 hours as well.6,7 Thus, an urgent need exists for the rapid diagnosis and treatment of ACOT. The development and widespread adoption of point-of-care viscoelastic coagulation assays, for example, thromboelastography (TEG) and rotational thromboelastometry (ROTEM), have answered this need and opened new doors both scientifically and clinically for the study of ACOT.8–10 ACOT is multifactorial, and we now have the analytic tools to untangle the multiple factors contributing to an individual patient’s coagulopathy. Clinical application of these assays has now identified hyperfibrinolysis as a significant contributor to ACOT.2,11,12 Moreover, the recent CRASH-2 and MATTERs trials have shown the spotlight on hyperfibrinolysis and focused worldwide attention on the presumptive treatment of coagulopathic bleeding with antifibrinolytic agents.13–16 However, a scientific basis for defining a threshold for instituting therapy is lacking.17 Clot lysis at 30 minutes after maximum clot strength (LY30) is the standard measure of fibrinolysis by TEG. LY30 offers a rapid measure of fibrinolysis and, as a predictor of this critical component of ACOT, may be a vital early prognostic indicator for the risk of massive hemorrhage. However, it is unclear whether the accepted normal upper bound of LY30 (7.5%, as stated in the TEG instrument reference range documentation, Haemonetics, Niles, IL) is appropriate for guiding therapy in trauma.18,19 Recent data suggest that the risk of death rises at a much lower level of clot lysis than 7.5%, but more detailed investigation is required to establish the utility of TEG LY30 as a test for hyperfibrinolysis and how to use this tool to guide antifibrinolytic therapy.17,19,20 As one of the objectives of a prospective study to characterize ACOT, we sought to determine the clinically relevant threshold for fibrinolysis in the population of severely injured patients who prompt the activation of our massive transfusion protocol (MTP). Specifically, we hypothesized that even small elevations of LY30 would predict massive transfusion requirement and hemorrhage-related death and should therefore serve as a trigger for antifibrinolytic therapy.11,21–26