Abstract
The incursion of pathogens into a living body causes inflammation as a result of innate immune reactions. The inflammation activates the coagulation cascades and accelerates intravascular clot formation. The intravascular clot formation is “immunothrombosis,” which develops to confine the pathogen in the local site. However, strong invasion and the subsequent excessive reactions cause dissemination of the inflammation and coagulation in the systemic circulation, thus resulting in disseminated intravascular coagulation (DIC). Septic DIC is characterized by the suppression of anti-coagulation and fibrinolytic functions, as well as the activation of coagulation. These characteristics of septic DIC lead to the consumption of platelets and coagulation factors, and induce multiple organ dysfunction.
