Disseminated intravascular coagulation | |
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Synonyms | Disseminated intravascular coagulopathy, consumptive coagulopathy |
Micrograph showing an acute thrombotic microangiopathy, the histologic correlate of DIC, in a kidney biopsy. A thrombus is present in the hilum of the glomerulus (center of image). PAS stain. | |
Specialty | Haematology |
Classification |
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External resources |
Disseminated intravascular coagulation (DIC) is a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body. This leads to compromised tissue blood flow and can ultimately lead to multiple organ damage. In addition, as the coagulation process consumes clotting factors and platelets, normal clotting is disrupted and severe bleeding can occur from various sites.
DIC does not occur by itself but only as a complicating factor from another underlying condition, usually in those with a critical illness. The combination of widespread loss of tissue blood flow and simultaneous bleeding leads to an increased risk of death in addition to that posed by the underlying disease. DIC can be overt and severe in some cases, but milder and insidious in others. The diagnosis of DIC depends on the findings of characteristic laboratory tests and clinical background. Treatment is mainly geared towards the underlying condition.
In DIC, the underlying cause usually leads to symptoms and signs, and DIC is discovered on laboratory testing. The onset of DIC can be sudden, as in endotoxic shock or amniotic fluid embolism, or it may be insidious and chronic, as in cancer. DIC can lead to multiorgan failure and widespread bleeding.
DIC can occur in the following conditions:
Liver disease, HELLP syndrome, thrombotic thrombocytopenic purpura/Haemolytic uremic syndrome, and malignant hypertension may mimic DIC but do not occur via the same pathways.
Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.