Disseminated intravascular coagulation
Disseminated intravascular coagulation, also called DIC, is an acquired disorder of diffuse activation of the coagulation cascade with resultant thrombotic and hemorrhagic clinical manifestations. This clinicopathologic syndrome is characterized by widespread intravascular fibrin formation in response to excessive blood protease activity that overcomes the natural anticoagulant mechanisms.
Disseminated intravascular coagulation (DIC) begins with excessive clotting. The excessive clotting is usually stimulated by a substance that enters the blood as part of a disease (such as an infection or certain cancers) or as a complication of childbirth, retention of a dead fetus, or surgery. In DIC, the body's natural ability to regulate blood clotting does not function properly. This causes the blood's clotting cells (platelets) to clump together and clog small blood vessels throughout the body. This excessive clotting damages organs, destroys blood cells, and depletes the supply of platelets and other clotting factors so that the blood is no longer able to clot normally. This often causes widespread bleeding, both internally and externally. Hence, patients with DIC have a loss of balance between the clot-forming activity of thrombin (enzyme that causes blood to clot) and the clot-lysing activity of plasmin (enzyme that dissolves blood clots).
DIC has several consistent components including activation of intravascular coagulation, depletion of clotting factors, and end-organ damage. Components of DIC include the following:
There are two types of Disseminated intravascular coagulation include acute DIC and chronic DIC. Acute DIC is a hemorrhagic disorder characterised by multiple bruises (ecchymoses), bleeding from mucosal sites (such as lips and genitals) and depletion of platelets and clotting factors in the blood. Purpura fulminans is a severe and rapidly fatal form of acute DIC. It is sometimes associated with symmetrical peripheral gangrene (tissue death affecting hands and feet).
chronic DIC reflects a compensated state that develops when blood is continuously or intermittently exposed to small amounts of tissue factor. Compensatory mechanisms in the liver and bone marrow are not overwhelmed, and there may be little obvious clinical or laboratory indication of the presence of DIC. Chronic DIC is more frequently observed in solid tumors and in large aortic aneurysms.
About half of DIC cases result from complications of pregnancy. DIC is most commonly observed in severe sepsis and septic shock. Although bacteremia, including both gram-positive and gram-negative organisms, is most commonly associated with DIC, other organisms including viruses, fungi, and parasites may cause DIC.
Trauma, especially neurotrauma, is also frequently associated with DIC. DIC is more frequently observed in those patients with trauma who develop the systemic inflammatory response syndrome. Evidence indicates that inflammatory cytokines play a central role in DIC in both trauma patients and septic patients.