Sepsis is one of the major health problems all over the word. Its pathophysiological mechanisms are not completely understood, but coagulation alterations are a hallmark of this syndrome. There is a clear exacerbation of coagulation and a suppression of control mechanisms of this process, including a reduction in fibrinolysis with consequent impairment of fibrin removal. The leading cause of these alterations is the proinflammatory state of those patients, characterized by high cytokine levels, increase in adhesion molecules expression, endothelial and platelets activation, release of microparticles and other related phenomena. Moreover, coagulation and inflammation are linked in a variety of pathways with mutual activation that ultimately contributes for its maintenance. The components of this process will be herein discussed as well as therapeutical alternatives that have excessive coagulation as a target.
Keywords: Antithrombin, disseminated intravascular coagulation, inflammation mediators, protein c, sepsis, tissue factor pathway inhibitor
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