disseminated intravascular coagulation

1. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation or hotocoagulation.

2. in colloid chemistry, solidification of a sol into a gelatinous mass.

blood coagulation clotting.

diffuse intravascular coagulation (disseminated intravascular coagulation (DIC)) see disseminated intravascular coagulation.

coagulation factors factors essential to normal blood clotting, whose absence, diminution, or excess may lead to abnormality of the clotting. Twelve factors, commonly designated by Roman numerals, have been described (I–V and VII–XIII; VI is no longer considered to have a clotting function). (See table 6.)

Factor I is a high-molecular-weight plasma protein that is converted to fibrin through the action of thrombin; deficiency conditions are called afibrinogenemia and hypofibrinogenemia. Called also fibrinogen. Factor II is a glycoprotein present in the plasma that is converted into thrombin in the common pathway of coagulation; deficiency is called hypoprothrombinemia. Called also prothrombin. Factor III is involved in the extrinsic pathway of coagulation, activating factor X; called also tissue thromboplastin or factor.

Factor IV is calcium, required in many stages of blood clotting. Factor V is a heat- and storage-labile material, present in plasma and not in serum and is involved in the intrinsic and extrinsic pathways of coagulation, causing the cleavage of prothrombin to the active thrombin. Deficiency causes parahemophilia. Called also accelerator globulin or factor and proaccelerin. Factor VI is no longer considered in the scheme of hemostasis, and hence is assigned neither a name nor a function.

Factor VII is a heat- and storage-stable material, present in serum and in plasma and participating in the extrinsic pathway of coagulation, acting with factor III to activate factor X. Deficiency, either hereditary or acquired (vitamin k deficiency), leads to hemorrhagic tendency. Called also proconvertin and serum prothrombin conversion accelerator (SPCA). Factor VIII is a relatively storage-labile material that participates in the intrinsic pathway of coagulation, acting as a cofactor in the activation of factor X. Deficiency, an X-linked recessive trait, results in hemophilia a (classical hemophilia). Called also antihemophilic factor (AHF) and antihemophilic globulin (AHG). Factor IX is a relatively storage-stable substance involved in the intrinsic pathway of coagulation, acting to activate factor X. Deficiency of this factor results in a hemorrhagic syndrome called hemophilia b (or Christmas disease), which is similar to classical hemophilia A. It is treated with purified preparations of the factor, derived from human plasma or recombinant, or with factor IX complex. Called also plasma thromboplastin component (PTC) and antihemophilic factor B.

Factor X is a heat-labile material with some storage stability, which is involved in both intrinsic and extrinsic pathways of coagulation, uniting them to begin the common pathway. Once activated, it complexes with calcium, phospholipid, and activated factor V to form prothrombinase, which cleaves and activates prothrombin to thrombin. Called also Stuart or Stuart-Prower factor. Factor XI is a stable factor involved in the intrinsic pathway of coagulation, activating factor IX. Deficiency results in hemophilia c. Called also plasma thromboplastin antecedent (PTA) and antihemophilic factor C. Factor XII is a stable factor activated by contact with glass or other foreign substances, which initiates coagulation through the intrinsic pathway by activating factor XI; called also Hageman factor. Factor XIII is a factor that polymerizes fibrin monomers, enabling fibrin to form a firm blood clot. Deficiency causes a clinical hemorrhagic diathesis. Called also fibrin-stabilizing factor.

disseminated intravascular coagulation (DIC) a bleeding disorder characterized by abnormal reduction in the elements involved in blood clotting due to their use in widespread intravascular clotting. It may be a secondary complication of any of numerous obstetrical, surgical, infectious, hemolytic, and neoplastic disorders, all of which activate in some way the intrinsic coagulation sequence. Paradoxically, the intravascular clotting ultimately produces hemorrhage because of rapid consumption of fibrinogen, platelets, prothrombin, and coagulation factors V, VIII, and X. Because of this pathology, the condition is sometimes called defibrination syndrome or consumption coagulopathy.

There may be signs and symptoms related to tissue hypoxia and infarction caused by the many microthrombi, but DIC is more often seen as an acute or chronic hemorrhagic disorder related to excessive and diffuse depletion of the elements needed for hemostasis. DIC should be suspected in any patient who has an unexplained tendency toward bleeding, and is suffering from one of the following types of clinical conditions: (1) those that introduce coagulation-promoting factors into the circulation, as in abruptio placentae, retained dead fetus, amniotic fluid embolism, metastatic carcinoma of the pancreas, lung, stomach, or prostate, and acute promyelocytic leukemia; (2) those that lead to stagnant blood flow, as in hypotension and polycythemia; (3) those accompanied by widespread endothelial injury, as in severe burns, trauma, heat stroke, and surgery, particularly surgery involving extracorporeal circulation; (4) various types of infections and bacteremias; and (5) snake bite and fat embolism.

The tendency toward excessive bleeding can appear suddenly and, with little warning, rapidly progress to severe or even fatal hemorrhage. Signs of DIC include continued bleeding from a venipuncture site, occult and internal bleeding, and, in some cases, profuse bleeding from all orifices. Other less obvious and more easily missed signs are generalized sweating, cold and mottled fingers and toes (due to capillary thrombi and hypoxia), and petechiae.

The diagnosis of DIC is confirmed by laboratory tests that show prolonged thrombin time, prothrombin time, and partial thromboplastin time; depressed platelet count and fibrinogen count; elevated fibrin split products (FSP); and a strongly positive protamine sulfate test. Assays for coagulation factors are commonly done to diagnose DIC; if the condition is present, the levels of these factors are reduced.

Extreme care must be taken to prevent complications related to bleeding. Injections should be avoided. Venipunctures should be limited whenever possible.

Treatment of DIC consists of replacement of the inadequate blood products and correction, when possible, of the underlying cause. When the primary disease cannot be treated, intravenous injections of heparin may inhibit the clotting process and raise the level of the depleted clotting factors. However, heparin therapy remains controversial as it can itself cause bleeding.

A serious medical condition that develops when the normal balance between bleeding and clotting is disturbed. Excessive bleeding and clotting injures body organs, and causes anemia or death.