The endothelium

Trauma patients develop coagulopathy (TIC) that is linked to shock and injury severity with a progressive change in whole blood hemostasis from normal to hypercoagulability, hypocoagulability, and hyperfibrinolysis with increasing injury severity. Hemostasis occurs in a vascular system comprising whole blood and blood vessels in a delicate balance with each other and coagulopathy should be interpreted with emphasis on balance and interaction between the flowing blood (the fluid phase of the vascular system) and the endothelium (the solid phase of the vascular system). Excessive sympathoadrenal activation is a hallmark of acute critical illness, and trauma and shock induce an instantaneous increase in circulating catecholamines that exert widespread dose-dependent effects on metabolism and the vascular system. Importantly, catecholamines influence the endothelium and flowing blood in opposite directions with an overall aim to induce local hemostasis while at the same time preserving perfusion/oxygen delivery and minimizing the risk of systemic intravascular coagulation. Hereby, the catecholamine-induced switch from hyper- to hypocoagulability in the flowing blood may represent an evolutionary adaptation rendering the trauma patient with optimal ability to survive. Thus, though coagulopathy is bad, the alternative may be worse. We provide evidence that TIC is critically linked to excessive sympathoadrenal activation and endothelial damage.