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SUMMARY

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SUMMARY

When procoagulants are produced or introduced into the blood and overcome the anticoagulant mechanisms of coagulation, intravascular thrombin is generated systemically, which can lead to disseminated intravascular coagulation (DIC). The clinical manifestations of intravascular coagulation include (1) multiorgan dysfunction caused by microthrombi; (2) bleeding caused by consumption of platelets, fibrinogen, and other coagulation factors; and (3) secondary fibrinolysis. Exposure of blood to tissue factor is the most common trigger. This event can occur when mononuclear cells and endothelial cells are induced to generate and express tissue factor during the systemic inflammatory response syndrome (e.g., Gram-negative and Gram-positive infections, fungemia, burns, severe trauma), or when contact is established between blood and tissue factor constitutively present on membranes of cells foreign to blood (e.g., malignant, placental, brain, adventitial cells, or traumatized tissues). Laboratory features include thrombocytopenia, reduced levels of fibrinogen and other coagulation factors (leading to prolonged partial thromboplastin, prothrombin, and thrombin times), and elevated levels of D-dimer and fibrin(ogen) degradation products. Several underlying disorders affect these hemostatic parameters and can lead to a false-positive diagnosis of DIC (e.g., liver disease–related coagulation abnormalities and thrombocytopenia) or to a false-negative diagnosis (e.g., pregnancy-related high fibrinogen levels). Reexamining these variables every 6 to 8 hours may permit a specific diagnosis. Early detection, vigorous treatment of the underlying disorder, and support of vital functions are essential for survival of affected patients. Blood component therapy is effective in patients who bleed excessively, whereas heparin administration is indicated in a limited number of circumstances. Intravascular coagulation and the underlying disorders causing it contribute to a high rate of mortality. The severity of the organ dysfunction and extent of hemostatic failure, as well as increasing patient age, have been associated with a grave prognosis.

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Acronyms and Abbreviations:

APACHE, Acute Physiology and Chronic Health Evaluation; APC, activated protein C; APL, acute promyelocytic leukemia; aPTT, activated partial thromboplastin time; ARDS, acute respiratory distress syndrome; AT, antithrombin; DIC, disseminated intravascular coagulation; EPCR, endothelial protein C receptor; FDP, fibrinogen degradation product; HDL, high-density lipoprotein; HELLP, hemolysis, elevated liver enzymes, low platelet count; IL, interleukin; LCAD, long-chain acyl-coenzyme A dehydrogenase; LPS, lipopolysaccharide; NET, neutrophil extracellular trap; PAI, plasminogen-activator inhibitor; PAR, protease-activated receptor; rHDL, recombinant high-density lipoprotein; TAFI, thrombin-activatable fibrinolysis inhibitor; TAT, thrombin–antithrombin; TF, tissue factor; TFPI, tissue factor pathway inhibitor; TNF, tumor necrosis factor; t-PA, tissue-type plasminogen activator.

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DEFINITION AND HISTORY

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Disseminated intravascular coagulation (DIC) is a clinicopathologic syndrome in which widespread intravascular coagulation occurs as a result of exposure or production of procoagulants insufficiently balanced by natural anticoagulant mechanisms and endogenous fibrino­lysis. Perturbation of the endothelium in the microcirculation, along with stimulated inflammatory cells and release of inflammatory mediators, plays a key role in this mechanism. DIC may cause tissue ischemia from occlusive microthrombi, bleeding from the consumption of platelets and coagulation factors, and, in some cases, an excessive fibrinolytic response. DIC complicates a variety of disorders, and the complexity of its pathophysiology ...

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