J. Samuels1, E. Moore2, A. Banerjee1, C. Silliman3, J. Coleman1, G. Stettler1, G. Nunns1, A. Sauaia1 1University Of Colorado Denver,Department Of General Surgery,Aurora, CO, USA 2Denver Health Medical Center,Department Of Surgery,Aurora, CO, USA 3Children’s Hospital Colorado,Pediatrics-Heme Onc And Bone Marrow Transplantation,Aurora, CO, USA
Introduction:
While trauma-induced coagulopathy (TIC) contributes to mortality in seriously injured patients, the additive effect of Traumatic Brain Injury (TBI) remains unclear. Prior studies have suggested TBI initiates an exaggerated bleeding diathesis with decreased clot formation and increased clot degradation in the initial post-injury phase. However, this coagulation phenotype has not been assessed using comprehensive coagulation assays, such as thrombelastography (TEG). This is desperately needed with the growing practice of empiric anti-fibrinolytic therapy. Therefore, the purpose of this study is to define the coagulation phenotypes of patients with TBI compared to other injury patterns as measured by TEG as well as conventional coagulation tests (CCT).
Methods:
The TAP (Trauma Activation Protocol) database is a prospective assessment of TIC in all patients meeting criteria for trauma activation at a level I trauma center. Patients were categorized into three groups: 1) Isolated TBI (I-TBI): AIS head ≥3 and ED GCS≤8 and AIS ≤2 for all other body regions; 2) TBI with polytrauma (TBI+Torso): AIS head≥3 and at least one AIS≥3 for other regions; and 3) Non-TBI (I-Torso): AIS head <3 and at least one AIS≥3 for other regions. Phenotype frequency was compared using the Chi-square test. Significance was declared at P<0.05.
Results:
There were 186 qualified patients, 38 with I-TBI, 55 with TBI+Torso, and 93 non-TBI patients enrolled between 2013 and 2016. Arrival SBP was higher for I-TBI (138 mmHg) compared to I-Torso (108 mmHg), but there were no significant differences in signs of shock (lactate, base deficit). Also, no differences existed between the three groups’ INRs, PTTs, or TEG measurements (ACT, Angle, and MA).
The distribution of fibrinolysis phenotypes is depicted in Figure 1. I-TBI and TBI+Torso had significantly higher incidence of fibrinolysis shutdown (rTEG Ly30 <0.9%) compared to I-Torso (p=0.045), and this persisted when only comparing patients in shock (Base Deficit ≥6) with a third of patients in the I-TBI group demonstrating shutdown, (p <0.01). Hyperfibrinolysis occurred in a minority of phenotypes (≤ 33%) in all three groups. Nearly 50% of patients with shock demonstrated shutdown after experiencing a TBI with other injuries.
Conclusion:
Historically, TBI has been associated with a coagulopathy characterized by hyperfibrinolysis. In contrast, this study found that TBI (isolated or with other injuries) was associated with fibrinolysis shutdown rather with a minority of patients demonstrating hyperfibrinolysis. With the growing use of empiric tranexamic acid (TXA), these data suggest that TXA should be given only when indicated by point of care testing.