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Chapter category: Coagulation

DIC at the Intersection of the Thrombotic, Fibrinolytic and Inflammatory Axes

This chapter appears in the following book:

Molecular Mechanisms of Disseminated Intravascular Coagulation

Edited by: Hugo ten Cate
ISBN: 1-58706-058-2
» Get more information about this book at landesbioscience.com «

Chapter authors:
Sean P. Mazer, David J. Pinsky

Disseminated intravascular coagulation (DIC) is a common clinical syndrome with dichotomous presentations of hemorrhage and thrombosis with a common underlying pathophysiology. As a syndrome, DIC presents a spectrum of severity ranging from a chronic disorder with minimal hemolysis and coagulation to a fulminant disorder with uncontrollable hemorrhage and major organ failure from small vessel thrombosis. DIC occurs in many different diseases (Table 1). In its severest form it is one of the final steps leading to multi-system failure. In each case derangement of the normally dynamic complex balance between thrombosis and fibrinolysis results in either a dominant phenotype of microvascular clotting or hemorrhage. In the thrombotic phenotype, unregulated fibrin generation results in widespread coagulation, while in the hemorrhagic phenotype, unregulated plasmin generation results in fibrinolysis and proteolysis of all soluble clotting factors. Paradoxically, the hemorrhage associated with DIC is clinically more obvious, but the microvascular clotting is far more lethal. Several recent discoveries about prognosis and therapy in patients with DIC emphasize the fundamental importance of the microvascular clotting over that of hemorrhage. In DIC the diversity of causes makes a unifying description of its pathophysiology difficult. However, focussing on several of the more important cell types and enzymes clarifies how a group of diverse diseases causes this syndrome.

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