Disseminated intravascular coagulation (DIC) is a syndrome that is characterized by systemic intravascular activation of coagulation, leading to fibrin deposition in the microvasculature and small- and mid-size vessels, thereby contributing to organ dysfunction. Simultaneously, ongoing consumption of platelets and coagulation factors leads to thrombocytopenia and impaired coagulation and may result in serious bleeding complications.
DIC never occurs by itself but is always secondary to an underlying cause. Table 85–1 lists the most frequently occurring disorders know to be associated with DIC.
TABLE 85–1CLINICAL CONDITIONS THAT MAY BE COMPLICATED BY DISSEMINATED INTRAVASCULAR COAGULATION |Favorite Table|Download (.pdf) TABLE 85–1 CLINICAL CONDITIONS THAT MAY BE COMPLICATED BY DISSEMINATED INTRAVASCULAR COAGULATION
Infectious diseases: purpura fulminans
Severe allergic/toxic reactions
Other vascular malformations
Severe immunologic reactions (eg, transfusion reaction)
Amniotic fluid embolism
HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome
Sepsis during pregnancy
Acute fatty liver
The pathogenesis of DIC is diagrammed in Figure 85–1.
Exposure of blood to tissue factor appears to be the principal mechanism of activation of coagulation. Tissue factor may be expressed by mononuclear cells or by the endothelium.
Other stimuli include activation of factor Xa by a cancer procoagulant, snake envenomation, and tissue/cellular debris in patients with massive trauma or pancreatitis.
Activation of coagulation is insufficiently balanced by physiologic anticoagulant pathways (eg, antithrombin, protein C system) and a downregulation of endogenous fibrinolysis due to high levels of the fibrinolysis inhibitor plasminogen activator inhibitor type 1 (PAI-1).
Schematic presentation of pathogenetic pathways involved in the activation of coagulation in disseminated intravascular coagulation (DIC). In DIC, both perturbed endothelial cells and activated mononuclear cells may produce proinflammatory cytokines that mediate coagulation activation. Activation of coagulation is initiated by tissue factor expression on activated mononuclear cells and endothelial cells. In addition, downregulation of physiologic anticoagulant mechanisms and inhibition of fibrinolysis by endothelial cells further promote intravascular fibrin deposition. PAI-1, plasminogen-activator inhibitor type 1. (Source: Williams Hematology, 9th ed, Chap. 129, Fig. 129–1.)
Clinical features are related to the underlying disorder, to the DIC, or both.
Bleeding manifestations have been observed in about 25% of cases in several series.
Persistent bleeding from venipuncture sites or other skin wounds occurs frequently.
Hemorrhage may be life-threatening.
Extensive organ dysfunction may be induced by microvascular thrombi, or by venous and/or arterial thromboembolism.
Organ dysfunction may manifest as acute renal failure (renal cortical ischemia and acute tubular necrosis occur frequently), hepatic dysfunction, and respiratory insufficiency due to acute respiratory distress syndrome.
Coma, delirium, focal neurologic symptoms, and ...
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