• Martin Sillesen, Lars S Rasmussen, Guang Jin, Cecilie H Jepsen, Ayesha Imam, John O Hwabejire, Ihab Halaweish, Marc DeMoya, George Velmahos, Pär I Johansson, and Hasan B Alam.
• From the Division of Trauma, Emergency Surgery and Surgical Critical Care (M.S., C.H.J., A.I., J.O.H., M.D., G.V.), Department of Surgery, Massachusetts GeneralHospital/Harvard Medical School, Boston, Massachusetts; Department of Surgery (G.J., I.H., H.B.A.), University of Michigan, Ann Arbor, Michigan; and Department of Surgery (P.I.J.), University of Texas Medical School, Houston, Texas; and Department of Anesthesia (M.S., L.S.R.), Center of Head and Orthopedics, and Capital Region Blood Bank (C.H.J., P.I.J.), Copenhagen University Hospital, Rigshospitalet, Denmark.
• J Trauma Acute Care Surg. 2014 Jan 1;76(1):12-9; discussion 19-20.

BackgroundTraumatic brain injury (TBI) and hemorrhagic shock (HS) can be associated with coagulopathy and inflammation, but the mechanisms are poorly understood. We hypothesized that a combination of TBI and HS would disturb coagulation, damage the endothelium, and activate inflammatory and complement systems.MethodsA total of 33 swine were allocated to either TBI + HS (n = 27, TBI and volume-controlled 40% blood loss) or controls (n = 6, anesthesia and instrumentation). TBI + HS animals were left hypotensive (mean arterial pressure, 30-35 mm Hg) for 2 hours. Blood samples were drawn at baseline, 3 minutes and 15 minutes after injury, as well as following 2 hours of hypotension. Markers of coagulation, anticoagulation, endothelial activation/glycocalyx shedding, inflammation, complement, and sympathoadrenal function were measured.ResultsThe TBI + HS group demonstrated an immediate (3 minutes after injury) activation of coagulation (prothrombin fragment 1 + 2, 289 ng/mL vs. 232 ng/mL, p = 0.03) and complement (C5a, 2.83 ng/mL vs. 2.05 ng/mL, p = 0.05). Shedding of the endothelial glycocalyx (syndecan 1) was evident 15 minutes after injury (851.0 ng/ml vs. 715.5 ng/ml, p = 0.03) while inflammation (tumor necrosis factor α [TNF-α], 81.1 pg/mL vs. 50.8 pg/mL, p = 0.03) and activation of the protein C system (activated protein C, 56.7 ng/mL vs. 26.1 ng/mL, p = 0.01) were evident following the 2-hour hypotension phase.ConclusionThe combination of TBI and shock results in an immediate activation of coagulation and complement systems with subsequent endothelial shedding, protein C activation, and inflammation.

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