Citation

Samuels JM, Moore EE, Silliman CC, Banerjee A, Cohen MJ, Ghasabyan A, Chandler J, Coleman JR, Sauaia A. J. Trauma Acute Care Surg. 2019; 86(4): 686-693.

Affiliation

University of Colorado Denver, Department of Surgery, Aurora CO, U.S., Jason.Samuels@ucdenver.edu Denver Health Medical Center, Department of Surgery, Denver CO, U.S., Ernest.Moore@dhha.org** University of Colorado Denver. Department of Pediatrics, Aurora CO, U.S., Christopher.Silliman@ucdenver.edu University of Colorado, Department of Surgery, Aurora CO, U.S., Anirban.Banerjee@ucdenver.edu Denver Health Medical Center, Department of Surgery, Denver CO, U.S., Mitchell.Cohen@dhha.org Denver Health Medical Center, Department of Surgery, Denver CO, U.S., Arsen.Ghasabyan@dhha.org Denver Health Medical Center, Department of Surgery, Denver CO, U.S. James.Chandler@dhha.org University of Colorado Denver, Department of Surgery, Aurora CO, U.S. Julia.Coleman@UCDenver.edu University of Colorado School of Medicine Department of Surgery, Aurora, CO; University of Colorado School of Public Health, Aurora, CO., U.S., Angela.Sauaia@ucdenver.edu.

Copyright

(Copyright © 2019, Lippincott Williams and Wilkins)

DOI

10.1097/TA.0000000000002173

PMID

30601456

Abstract

BACKGROUND: Traumatic brain injury (TBI) patients present on a spectrum from hypo- to hypercoagulability, depending on the injury complexity, severity, and time since injury. Prior studies have found a unique coagulopathy associated with TBI utilizing conventional coagulation assays such as INR; however, few studies have assessed the association of TBI and coagulopathy employing viscoelastic assays that comprehensively evaluate the coagulation in whole blood. This study aims to reevaluate the TBI-specific trauma-induced coagulopathy utilizing arrival thrombelastography (TEG). Because brain tissue is high in key pro-coagulant molecules, we hypothesize that isolated TBI is associated with pro-coagulant and hypofibrinolytic profiles compared to injuries of the torso, extremities and polytrauma including TBI.

METHODS: Data are from the prospective Trauma Activation Protocol (TAP) study. Activated clotting time (ACT), angle, maximum amplitude (MA), 30-minute percent lysis after MA (LY30), and functional fibrinogen levels (FFLEV) were recorded. Patients were categorized into isolated severe TBI (I-TBI), severe TBI with torso and extremity injuries (TBI+TORSO/EXTREMITIES), and isolated torso and extremity injuries (I-TORSO/EXTREMITIES). Poisson regression was used to adjust for multiple confounders.

RESULTS: Overall, 572 patients (48 I-TBI, 45 TBI+TORSO/EXTREMITIES, 479 I-TORSO/EXTREMITIES) were included in this analysis. The groups differed in INR, ACT, angle, MA, and FFLEV but not in LY30. When compared to I-Torso/Extremities, after adjustment for confounders, severe I-TBI was independently associated with ACT<128 seconds (RR= 1.5; 95% CI 1.1-2.2), angle<65 (RR=2.2; 95% CI 1.4-3.6), FFLEV<356 (RR=1.7; 1.2-2.4) but not MA<55mm, hyperfibrinolysis, fibrinolysis shutdown, or PTT>30.

CONCLUSION: Severe I-TBI was independently associated with a distinct coagulopathy with delayed clot formation but did not appear to be associated with fibrinolysis abnormalities. Low fibrinogen and longer ACT values associated with I-TBI suggest that early coagulation factor replacement may be indicated in I-TBI patients over empiric antifibrinolytic therapy. Mechanisms triggering coagulopathy in TBI are unique and warrant further investigation. LEVEL OF EVIDENCE: Level III, retrospective cohort study, prognostic.

Language: en