Severe traumatic brain injury is associated with a unique coagulopathy phenotype

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 ACT30. 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 University of Colorado Denver, Department of General Surgery, Trauma Research Center Financial Disclosures: The authors appreciate research support from Haemonetics with shared intellectual property. Presentation history: portions of this manuscript was presented in the form of an oral presentation at the 13th Annual Academic Surgical Congress, January 30-February 1, 2018 in Jacksonville, Florida ** Member of Western Trauma Association Acknowledgments: "Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health (T32 GM008315 and P50 GM049222), The National Heart, Lung, and Blood Institute (UM 1HL 120877) and the Department of Defense (USAMRAA, W81XWH-12-2-0028). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health (or other sponsors of the project)." *Corresponding Author – Address: 13001 E. 17th Place, B119 Bldg 500, E3309 Aurora, CO 80045 Phone: (303) 724-2498, Email: angela.sauaia@ucdenver.edu © 2018 Lippincott Williams & Wilkins, Inc.

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