LAUSR

H yperfibrinolysis (HF) is a highly lethal phenotype of traumainduced coagulopathy characterized by accelerated fibrin breakdown causing increased clot dissolution and reduced hemostasis. It is postulated to be due to a pathological upregulation of the normal fibrinolysis system responsible for maintaining vascular patency, driven by overwhelming endothelial tissue plasminogen activator release, and a reduction in circulating plasminogen activator inhibitor-1 during shock. Clinically, HF manifests as diffuse bleeding, often from uninvolved sites, and is an independent predictor for massive transfusion (MT) and early death from exsanguination, with a mortality greater than 40%. Using viscoelastic assays such as thrombelastography (TEG), HF can be measured by an elevated clot lysis 30 minutes after maximum clot strength (LY30). Although TEG has the ability to quantify the level of fibrinolysis occurring in a trauma patient, the pathologic LY30 threshold remains a source of debate. Various studies in healthy volunteers and trauma patients have set a wide range of LY30 thresholds. Indeed, our group was, to our knowledge, the first to publish that an LY30 threshold of 3% was the critical value for initiation of antifibrinolytics in severely injured patients. On a subsequent study, we observed that a higher LY30 level of 7.6% was associated with adverse outcomes. Recently, a European study of trauma-induced coagulopathy noted that for rapid TEG detection of HF, there was an increase in mortality and in red blood cell (RBC) transfusions at LY30 values greater than 10%. We also noted that these studies had substantial differences in median injury severity scores (ISS) (30 vs 16 vs 13) and degrees of shock. Thus, we conducted a multicenter study to determine whether HF LY30 thresholds were dependent on levels of injury severity and