Role of DIC in multiple organ failure

Disseminated intravascular coagulation (DIC) is a severe and complex coagulopathy resulting from excessive thrombin formation. Although there is a final common pathway, consumption coagulopathy and multiple organ failure (MOF), the early pathophysiology differs depending on the underlying disease.

The aim of this study is to elucidate the pathophysiology of septic DIC, and also to assess logical diagnostic and therapeutic procedure.

Blood samples were collected from septic patients. Coagulant, fibrinolytic and vascular markers were analyzed.

Damaged vascular endothelial cells overproduce plasminogen activator inhibitor 1, which, with excess production of thrombin, leads to fibrnolysis-suppressive DIC and fibrin formation in the microvasculature. These changes characterize the septic coagulopathy, which is often complicated by MOF; however, a bleeding tendency is relatively rare. The platelet count and fibrinogen/fibrin degradation products are most useful for the diagnosis of septic DIC. However, since the specificity is not sufficient with these screening tests, other tests including molecular markers should be added. Since endothelial damage plays an important role in the pathophysiology in septic DIC, treatment should be focused not only on abnormal coagulopathy but also on vascular damage. Protease inhibitors and antithrombin III are both effective treatments for DIC. Although heparin is a standard drug for the treatment of DIC, the use of heparin is not recommended in case of septic DIC.