Trauma-induced acute coagulopathy predicts a poor outcome. Although its pathophysiology is unclear, severe injury and shock(hypoperfusion) are proposed drivers. This study investigated the association between sympathoadrenal activation (circulating catecholamines) and biomarkers of coagulopathy.
Prospective study of 75 adult trauma patients admitted to a Level I trauma center directly from the scene of accident. Patients were selected blinded post hoc from three predefined Injury Severity Score groups (27) and had available blood samples on arrival. We measured activated partial thromboplastin time, international normalized ratio, hematology, biochemistry, circulating adrenaline and noradrenaline, 11 biomarkers of tissue and endothelial damage, glycocalyx degradation, natural anticoagulation and fibrinolysis (histone-complexed DNA fragments, high-mobility group box 1, syndecan-1, von Willebrand factor, soluble thrombomodulin, protein C, tissue factor pathway inhibitor, antithrombin, tissue-type plasminogen activator, plasminogen activator inhibitor-1,D-dimer) and registered 30-day mortality. Biomarkers were compared between survivors and nonsurvivors.
The adrenaline level was increased in nonsurvivors (p = 0.026), it was independently associated with increased activated partial thromboplastin time (p = 0.034) and syndecan-1 (p = 0.007), a marker of glycocalyx degradation, and it correlated with biomarkers of tissue and endothelial damage (histone-complexed DNA, high-mobility group box 1, soluble thrombomodulin) and hyperfibrinolysis (tissue-type plasminogen activator, D-dimer). Furthermore, nonsurvivors had higher syndecan-1, tissue factor pathway inhibitor, and D-dimer levels (all p 3; p = 0.011).
The trauma-induced catecholamine surge is closely associated with biomarkers of tissue and endothelial damage, glycocalyx degradation,coagulopathy including hyperfibrinolysis and independently predicts mortality.