Mechanisms of Traumatic Hyperfibrinolysis and Implications for Antifibrinolytic Therapy
Author:
Publisher
Springer Science and Business Media LLC
Subject
Rehabilitation,Orthopedics and Sports Medicine,Surgery
Link
http://link.springer.com/content/pdf/10.1007/s40719-019-00175-5.pdf
Reference41 articles.
1. Taylor JR 3rd, Fox EE, Holcomb JB, Rizoli S, Inaba K, Schreiber MA, et al. The hyperfibrinolytic phenotype is the most lethal and resource intense presentation of fibrinolysis in massive transfusion patients. J Trauma Acute Care Surg. 2018;84(1):25–30.
2. Cotton BA, Harvin JA, Kostousouv V, Minei KM, Radwan ZA, Schochl H, et al. Hyperfibrinolysis at admission is an uncommon but highly lethal event associated with shock and prehospital fluid administration. J Trauma Acute Care Surg. 2012;73(2):365–70 discussion 370.
3. Raza I, Davenport R, Rourke C, Platton S, Manson J, Spoors C, et al. The incidence and magnitude of fibrinolytic activation in trauma patients. J Thromb Haemost. 2013;11(2):307–14.
4. Cardenas JC, Matijevic N, Baer LA, Holcomb JB, Cotton BA, Wade CE. Elevated tissue plasminogen activator and reduced plasminogen activator inhibitor promote hyperfibrinolysis in trauma patients. Shock. 2014;41(6):514–21.
5. Chapman MP, Moore EE, Moore HB, Gonzalez E, Gamboni F, Chandler JG, et al. Overwhelming tPA release, not PAI-1 degradation, is responsible for hyperfibrinolysis in severely injured trauma patients. J Trauma Acute Care Surg. 2016;80(1):16–23 discussion 23-15.
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