CIVD et défaillance d’organes : arguments expérimentaux et cliniques

Abstract

Disseminated intravascular coagulation (DIC) is thought to contribute to multiple organ failure in a variety of underlying conditions for several reasons. First, clinical studies have found that, in patients with severe sepsis or septic shock, those with DIC exhibited more acquired organ failures than those without DIC, and their mortality rate was higher. Second, experimental studies of DIC associated with sepsis or low-grade activation of coagulation have repeatedly indicated that effective inhibition of DIC can indeed reduce organ failures and mortality. The mechanisms by which this role could be effectuated, however, are not clearly understood. The repeatedly demonstrated microvascular fibrin deposition in tissues of patients who have died from an illness with evidence of DIC may deprive downstream cells of oxygen, and cellular hypoxia could be a mechanism by which cells are damaged. In contrast, many investigators currently believe that it is not fibrin formation itself that is harmful, but rather is the generation of serine proteases and their interactions with pro-inflammatory mediators that contributes to organ failure and death. With the emergence of powerful anticoagulant strategies, aspects involving ischemia-reperfusion damage and organ recovery become important to investigate.