Disseminated intravascular coagulation
    Disseminated intravascular coagulation (DIC) is the term most commonly used for a clinicopathologic syndrome in which widespread intravascular coagulation is induced by procoagulants that are introduced or produced in the blood circulation and overcome the natural anticoagulant mechanisms. DIC may cause tissue ischemia from occlusive microthrombi and bleeding from both the consumption of platelets and coagulation factors and the anticoagulant effects of products of compensatory or secondary fibrinolysis.
[Etiology]
Numerous disorders can provoke DIC: ① Infections (Viral, bacterial, rickettsial, mycotic, protozoal); ② Malignant diseases; ③ Obstetric complications (Abruptio placentae, septic abortion and chorioamnionitis, amniotic fluid embolism, intrauterine fetal death, miscellaneous); ④ Surgery and trauma ; ⑤ Miscellaneous diseases.
[Pathogenesis]
The mechanisms that activate or “trigger” DIC act on processes that are involved in normal hemostasis; namely, the processes of platelet adhesion and aggregation and the contact-activated (intrinsic) and tissue-activated (extrinsic) pathways of coagulation.
1. Activation of the extrinsic coagulation system by tissue factor expressed on cell surfaces: trauma, cancer, obstetric events, ascites (shunt) etc;
2. Activation of intrinsic coagulation system by causing injury to endothelial cells: hypotension, endotoxin, heat stroke, vasculitis, aneurysm, hemangioma etc;
3. Activation of coagulation factors, e.g., factor Ⅹ by cancers, factor Ⅱ by snake venoms;
    All of these lead to thrombin generation that in the presence of failure of the control mechanisms results in intravascular coagulation. This in turn, can lead to thrombosis and consumption of platelets, fibrinogen, and other coagulation factors. Bleeding can be caused by depletion of these essential hemostatic components; by the anticoagulant effects of fibrinogen/fibrin degradation products; and by further depletion of fibrinogen, facto
r Ⅴ, and factor Ⅷ by plasmin if generated in excess by the secondary fibrinolysis or if uninhibited due to diminished antiplasmin levels.
documented evidence[Clinical features]
The manifestations of DIC depend on the magnitude and rate of exposure to the DIC trigger. For example, the dramatic cases of “acute” DIC, characterized by severe bleeding due to excessive consumption of hemostatic components, may develop when blood is exposed to large amounts of tissue factor over a brief period of time. Alternatively, “chronic” DIC develops when blood is continuously or intermittently exposed to small amounts of tissue factor. Under these circumstances, clinical signs may be minimal or altogether absent, and most coagulation tests will be only slightly impaired.
1. Bleeding
Acute DIC is frequently heralded by hemorrhage into the skin at multiple sites. Petechiae, ecchymosis, and oozing from veni-punctures, arterial lines, catheters, and injured tissues a
re common. Bleeding may also occur on mucosal surfaces. Hemorrhage may be life-threatening, with massive bleeding into the gastrointestinal, lungs, central nervous system, or orbit. Patients with chronic DIC usually exhibit minor skin and mucosal bleeding.
2. Thromboembolism
Extensive organ dysfunction can result from microvascular thrombi or from venous and/or arterial thromboembolism. For example, involvement of the skin can cause hemorrhage bullae, acral necrosis, and gangrene; involvement of the lungs can cause acute respiratory distress syndrome, hypoxemia, edema, hemorrhage; involvement of liver can cause jaundice, parenchymal damage; involvement of gastrointestinal can cause bleeding, mucosal necrosis, and ulceration; involvement of central nervous system can cause stupor, coma, convulsions, focal lesions and intracranial bleeding.
3. Circulatory disturbance, shock
Both the diseases underlying DIC and DIC itself can cause shock. For example, septicemia
or excessive blood loss to trauma or to obstetric complications can by themselves cause shock.
4. Microangiopathic hemolytic anemia
Erythrocytes are injured mechanically during passage through fibrin networks in the microcirculation. Such microangiopathic hemolysis leads to the production or schistocytes and microspherocytes.
[Laboratory features]
1. Basic blood examinations
(1) Platelet count: thrombocytopenia is an early and consistent sign of DIC.
(2) Peripheral blood smear: Examination of the blood smear reveals schistocytes in approximately 50% of cases.
2. The coagulation defect
(1) Partial thromboplastin time (PTT), Prothrombin time, and thrombin time: The PTT, PT, TT are prolonged in most patients with acute DIC. Early in the course of the disorder, and in chronic DIC, the PTT may be normal, or even shorter than normal, which may be the result of the procoagulant effects of activated coagulation factors.

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