Lewis S Gall1, Ross A Davenport. 1. Centre for Trauma Sciences, Blizard Institute, Bart's and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Abstract
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: Improving the outcomes for bleeding traumapatients 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.
Authors: Ji Soo Kim; Il Jae Wang; Seok Ran Yeom; Suck Ju Cho; Jae Hun Kim; June Pill Seok; Seong Hwa Lee; Byung Gwan Bae; Mun Ki Min Journal: Acute Crit Care Date: 2018-08-31
Authors: Philip C Spinella; Kimberly A Thomas; Isaiah R Turnbull; Anja Fuchs; Kelly Bochicchio; Douglas Schuerer; Stacey Reese; Adrian A Coleoglou Centeno; Christopher B Horn; Jack Baty; Susan M Shea; M Adam Meledeo; Anthony E Pusateri; Jerrold H Levy; Andrew P Cap; Grant V Bochicchio Journal: Front Immunol Date: 2020-09-08 Impact factor: 7.561