It remains debated whether traumatic brain injury (TBI) induces a different coagulopathy compared to non-TBI. This study investigated traditional coagulation tests, biomarkers of coagulopathy and endothelial damage in trauma patients with and without TBI. Blood from 80 adult trauma patients were sampled (median of 68 min (IQR 48-88) post-injury) upon admission to our trauma centre. Plasma/serum were retrospectively analysed for biomarkers reflecting sympathoadrenal activation (adrenaline, noradrenaline), coagulation activation/inhibition and fibrinolysis (protein C, activated protein C, tissue factor pathway inhibitor, antithrombin, prothrombinfragment 1+2, thrombin/antithrombin complex, von Willebrand factor, factor XIII, d-dimer, tissue-type plasminogen activator, plasminogen activator inhibitor-1), immunology (IL6), endothelial cell/glycocalyx damage (soluble thrombomodulin, syndecan-1) and vasculogenesis (angiopoietin-1, -2). Patients were stratified according to: 1) isolated severe head/neck injuries (AIS-head/neck≥3, AIS-other3) (sTBI+other) and 3) injuries without significant head/neck injuries (AIS-head/neck 35 sec. and > 1.2, was found in 13%, 47% and 5%, respectively (p=0.000). STBI+other had significantly higher plasma levels of adrenaline, noradrenaline, annexinV, d-dimer, IL6, syndecan-1, solubel thrombomodulin, and reduced protein C and factor XIII levels (all p