High-dose FXIII Administration Induces Effective Hemostasis for Trauma Associated Coagulopathy (TAC) both in vitro and in Rat Hemorrhagic Shock in vivo Models

Background Trauma associated coagulopathy (TAC) is an early and primary complication in severe trauma patients. FXIII is reported to stabilize a clot in the late phase of the coagulation cascade. The goal of this study was to investigate whether the administration of FXIII improves the condition of TAC both in vitro and in vivo. Methods We evaluated the effects of different doses, including a very high dose of FXIII (3.6- 32.4 IU/ml) on tissue-plasminogen activator (t-PA) induced hyperfibrinolysis and the combined condition of dilutional coagulopathy and t-PA induced hyperfibrinolysis in vitro. The coagulation status was analyzed by thromboelastometry (ROTEM) and Sonoclot. Then, we evaluated the effect of high dose FXIII (300 IU/kg) for severe coagulopathy in vivo using a rat liver trauma model in which coagulopathy similar to TAC was observed. Survival time and the amount of intra-abdominal bleeding of rats were measured and a coagulation test was also performed. Histological evaluations of rats’ lung and kidney after FXIII administration were completed. Results High-dose FXIII significantly improved clot strength as well as increased resistance to hyperfibrinolysis in vitro which was confirmed by ROTEM. Platelet function (PF) on Sonoclot was significantly increased by FXIII in a dose dependent manner. FXIII significantly decreased the total amount of bleeding and prolonged the survival time compared to control (control vs FXIII: 108.9±11.4 vs 32.6±5.5 ml/kg; p

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