• Alex P Di Battista, Sandro B Rizoli, Brandon Lejnieks, Arimie Min, Maria Y Shiu, Henry T Peng, Andrew J Baker, Michael G Hutchison, Nathan Churchill, Kenji Inaba, Bartolomeu B Nascimento, Airton Leonardo de Oliveira Manoel, Andrew Beckett, and Shawn G Rhind.
• *Defence Research and Development Canada, Toronto Research Centre, Toronto, Ontario, Canada †Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada ‡Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada §Department of Critical Care, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada ¶Department of Anesthesia and Surgery, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada ||Faculty of Kinesiology and Physical Education, University of Toronto, Toronto, Ontario, Canada **Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada ††Division of Trauma and Critical Care, University of Southern California, Los Angeles, California ‡‡LA County and USC Medical Center, Los Angeles, California §§Department of Surgery, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada ¶¶Canadian Forces Health Services, The 1 Canadian Field Hospital, Petawawa, Ontario, and The Trauma Program, McGill University Health Centre, Montréal, Quebec, Canada.
• Shock. 2016 Sep 1; 46 (3 Suppl 1): 96-103.

BackgroundAcute coagulopathy after traumatic brain injury (TBI) involves a complex multifactorial hemostatic response that is poorly characterized.ObjectivesTo examine early posttraumatic alterations in coagulofibrinolytic, endothelial, and inflammatory blood biomarkers in relation to sympathetic nervous system (SNS) activation and 6-month patient outcomes, using multivariate partial least-squares (PLS) analysis.Patients And MethodsA multicenter observational study of 159 adult isolated TBI patients admitted to the emergency department at an urban level I trauma center, was performed. Plasma concentrations of 6 coagulofibrinolytic, 10 vascular endothelial, 19 inflammatory, and 2 catecholamine biomarkers were measured by immunoassay on admission and 24 h postinjury. Neurological outcome at 6 months was assessed using the Extended Glasgow Outcome Scale. PLS-discriminant analysis was used to identify salient biomarker contributions to unfavorable outcome, whereas PLS regression analysis was used to evaluate the covariance between SNS correlates (catecholamines) and biomarkers of coagulopathy, endotheliopathy, and inflammation.ResultsBiomarker profiles in patients with an unfavorable outcome displayed procoagulation, hyperfibrinolysis, glycocalyx and endothelial damage, vasculature activation, and inflammation. A strong covariant relationship was evident between catecholamines and biomarkers of coagulopathy, endotheliopathy, and inflammation at both admission and 24 h postinjury.ConclusionsBiomarkers of coagulopathy and endotheliopathy are associated with poor outcome after TBI. Catecholamine levels were highly correlated with endotheliopathy and coagulopathy markers within the first 24 h after injury. Further research is warranted to characterize the pathogenic role of SNS-mediated hemostatic alterations in isolated TBI.

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