Hemostasis in Sepsis

Septic shock is frequently complicated by massive activation of the coagulation system. This can occur concomitantly with biphasic change in the fibrinolytic system, involving both activation and inhibition of plasminogen activation. The net result of the altered hemostatic state in sepsis is widespread microvascular trom-bosis. The early events leading to these disturbances are incompletely understood, 

The Role of Plasma Cascade Systems in Sepsis 4.1.1. The Coagulation System 

Pathological findings frequently observed in organs of patients who have died of sepsis include disseminated intravascular coagulation (DIC), manifested as diffuse thrombotic occlusions in the entire microvascular system, associated with alterations in the hemostatic mechanism and clinical signs of hemorrhagic diathesis. Many observations indicate that DIC contributes to the major symptoms of the systemic inflammatory response syndrome (SIRS), which frequently complicate sepsis (HI, H2, H3, T6). 

Activation of the coagulation system may start after activation of the contact factors (intrinsic system) or after release of tissue factor (extrinsic system). 

At present, the activation of the extrinsic coagulation system is considered to be of more importance in the initiation of DIC than the activation of the contact system (LI2, Cl 3). The activation of the extrinsic system starts with the release of tissue factor (TF) from endothelial cells. TF is a macromolecule, composed of a protein and a lipid fraction, that is synthesized by endothelial cells and monocytes. TF 

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