H. B. Moore1, B. Huebner1, T. L. Nydam1, G. Settler1, G. Nunns1, C. C. Silliman1, A. Sauaia1, E. E. Moore1 1University Of Colorado Denver,Surgery,Aurora, CO, USA
Introduction: Utilization of tranexamic acid (TXA) in trauma remains debated. While European guidelines recommend empiric TXA in hypotensive trauma patients, many trauma centers in the United States question this practice. Recent appreciation of the spectrum of fibrinolysis acutely after injury has identified an associated protective effect of a moderate level of fibrinolysis. There are concerns that TXA may harm this patient population. TXA administration at our trauma center is goal directed on rapid thrombelastography (rTEG) LY30 results, although clinicians can empirically administer TXA if they believe it is indicated. We hypothesize that this is a futile intervention and poses the risk of increased mortality in patients with physiologic fibrinolysis levels.
Methods: Trauma activations from 2015-2016 with blood samples obtained in the ambulance or emergency department were analyzed with rTEG. Patients included in the analysis had an LY30 between 0.8 and 2.9 (previously defined as physiologic fibrinolysis). Demographics, clinical variables, and blood product utilization were collected by prospectively by trained research assistants. The primary outcome of interest was in hospital mortality contrasted between patients who received TXA and no TXA. Confounders(age, NISS, systolic blood pressure(SBP), Glasgow Coma Score(GCS), RBC transfusion in the first 2 hours from injury) were adjusted with multivariate logistic regression and cox regression analysis.
Results: Fourtny nine percent of patients (141/291) were identified to have physiologic levels of fibrinolysis The median NISS was 27 and mortality rate was 6% (significantly less than hyperfibrinolysis 20% and shutdown 16% p=0.004). Patients with physiologic phenotype were given TXA 5% of the time and delayed delivery(>3 hours) occurred in 38% of patients. NISS was higher but not significant in patients given TXA (48 vs 27p=0.334), while SBP (108 vs 118 p=0.325) and GCS were similar (15 vs 15 p=0.779). TXA patients received more RBC units at hour 1 and 2 during resuscitation (1 vs 0 p<0.001 and 2 vs 0 p=0.001). Mortality was significantly higher in the TXA group 38% vs 4% (p=0.004). After adjusting for confounders TXA was significantly associated with increased mortality in logistic regression analysis (p=0.024) and cox regression (HR 14.5 p=0.042). In patients with hyperfibrinolysis there was no differnce in survival with TXA use before (p=0.521) and after adjustment (p=0.531).
Conclusion:Patient's with physiologic levels of fibrinolysis that receive TXA have increased mortality compared to patients who did not receive this medication. While the TXA patients had an overall higher requirement of blood products and were given this medication based on clinician gestalt, there was no observed benefit. These data support the continued concerns of empiric utilization of TXA, and has identified a potential danger of giving this medication to patients who present to the hospital with physiologic levels of fibrinolysis.