Clinical and pathophysiological aspects of disseminated intravascular coagulation

Disseminated intravascular coagulation (DIC) is a complex process, the course and outcome of which is determined by triggering mechanisms, the reactivity of the body and a number of related conditions. As a result of these interactions, the clinical and laboratory manifestations of DIC vary greatly, making it difficult to diagnose and correct it. With DIC, there are no standard, especially pathognomonic, clinical symptoms, there are no generally accepted laboratory diagnostic criteria, as well as specific therapy. The development of methods for treating DIC and assessing their effectiveness is hampered by the fact that, firstly, the outcome of DIC depends more on its immediate cause than on treatment; secondly, the usually recommended therapeutic effects (heparin therapy, infusion of antithrombin III concentrates, protein C, etc.) have never been the subject of objective randomized follow-up studies, with the exception, perhaps, of the use of antithrombin III drugs [4]. Undoubtedly, advances in the prevention, diagnosis and treatment of DIC directly depend on the depth of understanding of its pathogenetic mechanisms that unfold at the molecular and cellular levels. Modern ideas about the pathogenesis of DIC syndrome are, in one way or another, a development of the idea of ​​continuous intravascular coagulation [5], which under some conditions from latent physiological becomes massive pathological with distinct clinical and laboratory manifestations [1, 2, 7].