Acute Traumatic Endotheliopathy in Isolated Severe Brain Injury and Its Impact on Clinical Outcome.

摘要: Study design: Prospective observational cohort. Objective: To investigate the difference in plasma levels of syndecan-1 (due to glycocalyx degradation) and soluble thrombomodulin endothelial damage) isolated severe traumatic brain injury (TBI) patients with/without early coagulopathy. A secondary objective was compare effects degree TBI endotheliopathy on hospital mortality among with TBI-associated coagulopathy (TBI-AC). Methods: Data prospectively collected (sTBI) Glasgow Coma Scale (GCS) ≤8 less than 12 h after admitted a level I trauma centre. Isolated sTBI samples withdrawn prior blood transfusion were stratified by conventional coagulation tests as coagulopathic (prothrombin time (PT) ≥ 16.7 s, international normalized ratio (INR) 1.27, activated partial thromboplastin (aPTT) 28.8 s) non-coagulopathic. Twenty healthy controls also included. Plasma estimated ELISA. With receiver operating characteristic curve (ROC) analysis, we defined cut-off that maximized sum sensitivity specificity for predicting TBI-AC. Results: Inclusion criteria met 120 cases, subjects aged 35.5 ± 12.6 years (88.3% males). TBI-AC identified 50 (41.6%) patients, independent age, gender, GCS, but there an association acidosis (60%; p = 0.01). Following sTBI, found insignificant changes (sTM) between controls, sTM lower compared non-coagulopathic patients. Elevations (ng/mL) seen control (31.1(21.5–30.6) vs. 24.8(18.5–30.6); 0.08). Syndecan-1(ng/mL) significantly elevated (33.7(21.6–109.5) 29.9(19.239.5); 0.03). Using ROC analysis (area under 0.61; 95% Confidence Interval (CI) 0.50 0.72), established cutoff ≥30.5 ng/mL (sensitivity % 55.3, 52.3), significant Conclusion: Subsequent injury, shedding may be associated abnormalities. TBI-AC, importance guiding management clinical decision-making.