Ioana Iovănescu, Ioana Robitu, Elisabeta Bălăiţă, C. Apostolescu, Cleo Roşculeţ, Monica Ivan
Secţia ATI, Institutul Naţional de Boli Infecţioase „Matei Balş”, Bucureşti
Abstract
Sepsis is an infection-induced inflammatory syndrome that results in a complex network of adaptive and maladaptive alterations in homeostatic mechanisms. Severe sepsis, defined as sepsis associated with acute organ failure, is a serious disease with a mortality rate of 30-50%. The coagulation system, through complex interactions, has an important role in the final outcome of the sepsis-induced inflammatory cascade. A fine and delicate balance that normally exists between anticoagulant mechanisms and the procoagulant response is altered in sepsis. Evidence suggesting that activation of the coagulation system may contribute to sepsis-related morbidity and mortality has led to extensive research attempting to correct the hemostatic defects seen in septic patients.