Disseminated Intravascular Coagulation (Dic)

(DIC, Defibrinierungssyndrom)

The disseminated intravascular coagulation (DIC) is characterized by a pathological, excessive generation of thrombin and fibrin in the circulating blood. During this process it comes to increased platelet aggregation and consumption of clotting factors. DIC that develops quickly (over hours or days), primarily resulting in bleeding. Disseminated intravascular coagulation, which develops slowly (over weeks or months), mainly caused venous thrombotic and embolic events. A heavy, rapidly developing DIC is determined by the detection of thrombocytopenia, prolonged PTT and PT, increased levels of plasma D-dimer (or fibrin), and a reduced Fibrinogenplasmaspiegels diagnosed. The treatment includes the therapy of the cause and the replacement of platelets, coagulation factors (by fresh frozen plasma) and fibrinogen (by cryoprecipitates) to control heavy bleeding. In patients with a slowly evolving DIC, who are at risk for developing venous embolism, therapeutic (or prophylactic) heparin is used.

The disseminated intravascular coagulation (DIC) is characterized by a pathological, excessive generation of thrombin and fibrin in the circulating blood. During this process it comes to increased platelet aggregation and consumption of clotting factors. DIC that develops quickly (over hours or days), primarily resulting in bleeding. Disseminated intravascular coagulation, which develops slowly (over weeks or months), mainly caused venous thrombotic and embolic events. A heavy, rapidly developing DIC is determined by the detection of thrombocytopenia, prolonged PTT and PT, increased levels of plasma D-dimer (or fibrin), and a reduced Fibrinogenplasmaspiegels diagnosed. The treatment includes the therapy of the cause and the replacement of platelets, coagulation factors (by fresh frozen plasma) and fibrinogen (by cryoprecipitates) to control heavy bleeding. In patients with a slowly evolving DIC, who are at risk for developing venous embolism, therapeutic (or prophylactic) heparin is used.

(See also coagulation disorders overview.) The disseminated intravascular coagulation (DIC) is characterized by a pathological, excessive formation of thrombin and fibrin in the circulating blood. During this process it comes to increased platelet aggregation and consumption of clotting factors. DIC that develops quickly (over hours or days), primarily resulting in bleeding. Disseminated intravascular coagulation, which develops slowly (over weeks or months), mainly caused venous thrombotic and embolic events. A heavy, rapidly developing DIC is determined by the detection of thrombocytopenia, prolonged PTT and PT, increased levels of plasma D-dimer (or fibrin), and a reduced Fibrinogenplasmaspiegels diagnosed. The treatment includes the therapy of the cause and the replacement of platelets, coagulation factors (by fresh frozen plasma) and fibrinogen (by cryoprecipitates) to control heavy bleeding. In patients with a slowly evolving DIC, who are at risk for developing venous embolism, therapeutic (or prophylactic) heparin is used. Etiology Disseminated intravascular coagulation is usually the result of exposure of tissue factor to blood, through which the coagulation cascade is triggered. In addition, DIC activates the fibrinolytic pathway (fibrinolysis). Stimulation of endothelial cells by cytokines and impaired microvascular blood flow cause the release of tissue plasminogen activator (tPA) from endothelial cells. Both tPA and plasminogen adhere to fibrin, and plasmin (generated by cleavage of plasminogen tPA) cleaves fibrin in U-dimers and other degradation products of fibrin). therefore DIC causes both thrombosis and bleeding. Fibrinolysis A DIC in the following clinical situations is most common: complications in obstetrics (eg placental abruption, induced by saline therapeutic abortion, fetal death, intrauterine retention of contraceptives, amniotic fluid embolism.): Placental tissue with tissue factor activity passes into the maternal circulation or come into contact with him. Infection, especially with gram-negative organisms: gram-negative endotoxins cause the formation of tissue factor activity or the phagocytic and exposure through endothelial cells and tissue cells. Malignant tumors, particularly mucin-secreting adenocarcinomas of the pancreas and adenocarcinoma of the prostate and acute promyelocytic leukemia: expressing tumor cells or tissue factor activity set free. Any kind of shock that leads to an ischemic tissue damage and so the release of tissue factor. Less common causes of DIC severity tissue damage caused by head injuries, burns, frostbite, or gunshot wounds complications of prostate surgery that allow that prostate material with tissue factor activity passes (along with plasminogen activators) in the circulation Poisonous snake bites in which enzymes enter the circulation, activate one or generate a plurality of clotting factors and either thrombin or directly convert fibrinogen to fibrin depth of intravascular hemolysis aortic aneurysms or cavernomas (Kasabach-Merritt syndrome) with vessel wall damage and parts of blood stasis disseminated intravascular coagulation, slowly developed, typically results from cancer, aneurysm or cavernous hemangiomas. Pathophysiology slowly evolving DIC (subacute form) mainly results in venous thromboembolic events (eg. As deep vein thrombosis, pulmonary embolism), although occasionally vegetations occur on the heart valves. Abnormal bleeding here are unusual. However, the severe, rapidly evolving DIC leads (fulminant form) of thrombocytopenia and a decrease of coagulation factors and fibrinogen, it comes as a consequence bleeding. Bleeding into organs perform along with microvascular thrombosis to dysfunction and failure of multiple organs. Delayed dissolution of fibrin by fibrinolysis can lead to mechanical destruction of red blood cells, formation of schistocytes and a slight intravascular hemolysis lead (thrombotic thrombocytopenic purpura and hemolytic uremic syndrome. Symptoms and signs In the subacute DIC can be symptoms of venous thrombosis and / or symptoms of pulmonary embolism are present. In the fulminant DIC punctures the skin to bleed (eg., intravenous or arterial punctures) permanently on. At the site of parenteral injections is bruising form, and it can cause serious gastrointestinal bleeding. diagnosis platelet count, PT, PTT, plasma fibrinogen , plasma D-dimer De r suspected disseminated intravascular coagulopathy, patients with unexplained bleeding or venous thromboembolic events, especially in the presence of an additional predisposing factor. In case of doubt, the platelets are counted and PT, PTT, Plasmafibrinogenwerte and plasma D-dimer levels determined (an indication of fibrin and degradation in serum). The subacute DIC results in a slight thrombocytopenia with a normal to geringgradig prolonged PT (PT is usually represented as INR) and PTT, normal to slightly reduced fibrinogen and elevated plasma D-dimer levels. As various disturbances to the increased synthesis of fibrinogen, as an acute phase protein, the reduction in fibrinogen in two successive measurements may be helpful in the diagnosis of DIC. Presumably because of activated clotting factors in the plasma, the initial PTT values ??can be reduced in the subacute DIC. The fulminant DIC has a much heavier thrombocytopenia with more prolonged PT and PTT, rapidly decreasing plasma fibrinogen levels and high plasma D-dimer levels result. The determination of factor VIII levels can sometimes be helpful to distinguish the severe acute DIC by a massive liver necrosis, which can lead to similar changes in coagulation parameters. In hepatic necrosis factor VIII levels are elevated because Factor VIII synthesized in the hepatic endothelial cells and is released by their destruction. In Vorligen DIC factor VIII, however, is reduced because its activated form is cleaved by thrombin-induced formation of activated protein C. has treatment treating the cause may replacement therapy (eg. B. platelets, cryoprecipitates, fresh frozen plasma) Occasionally, heparin, the immediate treatment of the cause of the highest priority (z. B. broad-spectrum antibiotics in suspected gram-negative sepsis, induction of labor in case of premature detachment of the placenta). Is this treatment effectively, there should be a rapid improvement of disseminated intravascular coagulopathy. Severe bleeding If the bleeding is strong or a critical point concerns (eg., Brain, GI tract), or when an urgent need for an operation, then an additional replacement therapy is indicated. Replacement may consist of platelet concentrates to correct thrombocytopenia (with rapidly declining number of platelets or platelets <10,000 to 20,000 / ul) cryoprecipitate to replace fibrinogen (and Factor VIII), when the fibrinogen level falls quickly or <100 mg / dl. Brush up on frozen plasma in order to increase the levels of other coagulation factors and natural anticoagulants (antithrombin, protein C, S and Z) It is unclear whether the infusion of Antithrombinkonzentraten with fulminant DIC is effective. Volume resuscitation if hypotension is present, is essential to the DIC to verhaften.sich slowly evolving DIC heparin is useful in the treatment of subacute disseminated intravascular coagulopathy with venous thrombosis or pulmonary embolism. Treatment with heparin is not indicated in the fulminating DIC with bleeding, or increased risk of bleeding in general. An exception is women who are conditionally developed by intrauterine death DIC with increasing drop of platelets, fibrinogen and clotting factors. In these patients, heparin for several days must be administered to control the DIC to increase fibrinogen and platelet counts and reduce the excessive consumption of clotting factors. Heparin is then deposited and empties the uterus. Important points in disseminated intravascular coagulation (DIC), the coagulation cascade is activated when blood is exposed to tissue factor. In connection with the coagulation system of the fibrinolytic pathway is also activated. DIC starts usually fast and cause bleeding and microvascular occlusion, leading to organ failure. DIC sometimes starts slowly, causing thromboembolic phenomena rather than bleeding. The severe and rapid onset of DIC caused a significantly more severe thrombocytopenia with very prolonged PT and PTT, rapidly decreasing plasma fibrinogen levels and high plasma D-dimer levels result. The immediate correction of the cause has priority; heavy bleeding may also require replacement therapy with platelet concentrate, cryoprecipitate and fresh frozen plasma. However, heparin is useful in slow onset of DIC, rare in the rapid onset of DIC (especially in women with a dead fetus in the womb).

Health Life Media Team

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