The Impact of Prehospital Tranexamic Acid on Blood Coagulation in Trauma Patients.

Stein, Philipp; Studt, Jan-Dirk; Albrecht, Roland; Müller, Stefan; von Ow, Dieter; Fischer, Simon; Seifert, Burkhardt; Mariotti, Sergio et al. · Anesth Analg · 2018

prospective_cohort · Level II

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Abstract

There is limited data on prehospital administration of tranexamic acid (TXA) in civilian trauma. The aim of this study was to evaluate changes in coagulation after severe trauma from on-scene to the hospital after TXA application in comparison to a previous study without TXA. The study protocol was registered at ClinicalTrials.gov (NCT02354885). A prospective, multicenter, observational study investigating coagulation status in 70 trauma patients receiving TXA (1 g intravenously) on-scene versus a control group of 38 patients previously published without TXA. To account for potential differences in patient and trauma epidemiology, crystalloid and colloidal resuscitation fluid, 2 propensity score matched groups (n = 24 per group) were created. Measurements included ROTEM, standard coagulation tests and blood gas analyses on-scene and emergency department admission. Presented values are mean and [standard deviation], and difference in means and 95% confidence intervals. Patient epidemiology was not different between groups. Coagulation assays on-scene were comparable between the TXA and C. Prehospital hyperfibrinolysis was blunted in all 4 patients in the TXA group. Viscoelastic FIBTEM maximum clot firmness (MCF), representing functional fibrinogen levels, did not change from on-scene to the emergency department in the TXA group, whereas MCF decreased -3.7 [1.8] mm in the control group. Decrease of MCF was significantly reduced in the TXA group in EXTEM by 9.2 (7.2-11.2) mm (P < .001) and INTEM by 6.8 (4.7-9.0) mm (P < .001) in favor of the TXA group. Production of fibrinogen fragments (represented by D-dimers) was significantly lower in the TXA group compared to group C. Early prehospital administration of TXA leads to clot stabilization and a reduction of fibrinolytic activity, causing a decrease in fibrin degradation products buildup (D-dimer).

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