Published online by Cambridge University Press: 04 May 2010
Disseminated intravascular coagulation (DIC) is a syndrome characterized by the systemic activation of coagulation, leading to the intravascular deposition of fibrin in the (micro)vasculature and the simultaneous consumption of coagulation factors and platelets (1). DIC may result in the formation of microvascular thrombi and thereby compromise an adequate blood supply to various organs, which may contribute to organ failure. Simultaneous exhaustion of coagulation factors, protease inhibitors, and platelets, due to ongoing coagulation activation, may lead to serious bleeding. It is important to emphasize that DIC is not a disease in itself but is always secondary to an underlying disorder, for example sepsis, severe trauma, some forms of cancer, or serious immunologic or toxic reactions. A diagnosis of DIC can only be made when one of these underlying disorders is present and is further based on a scoring system, using laboratory results (platelet count, prothrombin time, and fibrin degradation products). Although the pathophysiology of DIC may vary according to the underlying clinical disorder, certain pathogenic mechanisms are common to most if not all cases, including the mediatory role of inflammatory cytokines, the tissue factor–dependent initiation of intravascular coagulation, and the attenuation of natural anticoagulants and fibrinolysis.
The endothelium plays a central role in all major pathways involved in the pathogenesis of DIC. Endothelial cells (ECs) release and respond to myriad proinflammatory mediators, resulting in the induction of tissue factor expression and downregulation of important physiological anticoagulant pathways (2). However, rather than being a unidirectional relationship, the interaction between inflammation and coagulation involves significant cross-talk in which the endothelium appears to play a pivotal role (3).