Abstract
Severe infection and inflammation almost invariably lead to hemostatic abnormalities,
ranging from insignificant laboratory changes to gross activation of coagulation that
may result in localized thrombotic complications or systemic intravascular fibrin
deposition. Systemic inflammation results in activation of coagulation, due to tissue
factor-mediated thrombin generation, downregulation of physiological anticoagulant
mechanisms, and inhibition of fibrinolysis. Proinflammatory cytokines, immune cells,
and the endothelium play a central role in the differential effects on the coagulation
and fibrinolysis pathways. Vice-versa, activation of the coagulation system may importantly
affect inflammatory responses by direct and indirect mechanisms. Similar mechanisms
appear to play a role in the development of atherosclerosis and related arterial thrombosis.
Apart from the general coagulation response to inflammation associated with severe
infection, specific infections may cause distinct features, such as hemorrhagic fever
or thrombotic microangiopathy.
Keywords
infection - inflammation - thrombosis - atherosclerosis - coagulation - endothelium
- cytokines
