Disseminated intravascular coagulation (DIC) is a loosely defined syndrome that is reflective of serious underlying disease. Patients who have severe DIC have a mortality rate of up to 85 percent. DIC can be triggered by a wide variety of disorders ( T.a.b.!.e...21...1.,:Z) and can be acute and life-threatening or chronic and compensated. The most common trigger of DIC is the liberation of tissue factor. Tissue factor is usually confined within the extravascular space; when it is released, the coagulation system is activated (Fig.. . 2.1.1:1). Small fibrin clots are formed and deposited as thrombi or emboli in the microcirculation. Fibrinolysis then occurs and can be massive. FDPs are released and further inhibit hemostasis. The usually tightly regulated system of coagulation and fibrinolysis becomes unbalanced. Because of clot formation, coagulation factors and platelets are consumed. Microthrombi in the circulation can lead to tissue hypoxia, and the red blood cells are damaged trying to pass through the microcirculation. The severity of DIC that develops depends on the synthetic function of the liver, the integrity of the vascular endothelium, and the capacity of the bone marrow to replace platelets. Chronic, compensated DIC occurs when the rate of consumption of clotting factors and platelets does not exceed their rate of production.
TABLE 211-7 Common Causes of Disseminated Intravascular Coagulation
FIG. 211-1. Pathophysiology of disseminated intravascular coagulation. Refer to text for details. FDPs, fibrin/fibrinogen degradation products.
T§ble..,2..1...1:7 lists the more common causes of DIC, particularly as encountered in the emergency setting. The reader is referred to a standard text for a complete list of causes. DIC occurs in its most extreme form in Neisseria meningitidis sepsis and acute myelogenous leukemia, promyelocytic (M3) type.
The clinical complications of DIC are bleeding, thrombosis, and purpura fulminans. Although hemorrhage and thrombosis may occur simultaneously, in an individual patient, one may predominate. Bleeding occurs in up to 75 percent of patients with DIC. Bleeding from the skin and mucous membranes is most common; usually there is bleeding from several sites, including venipuncture sites, surgical wounds, epistaxis, petechiae, and ecchymoses. Hematuria and gastrointestinal bleeding are seen; intracerebral bleeding carries a very poor prognosis. Thromboses (usually microthrombi) predominate in some patients. Clinical signs of this include mental status changes, focal ischemia or gangrene, oliguria, renal cortical necrosis, and adult respiratory distress syndrome (ARDS). Purpura fulminans occurs when there are widespread arterial and venous thromboses. Gangrene develops in the digits or extremities and there is hemorrhagic infarction of the skin. Purpura fulminans is most commonly seen with high-grade bacteremia (Streptococcus pneumoniae or N. meningitidis).
The diagnosis of DIC is based on the clinical setting and characteristic laboratory abnormalities. The typical laboratory results in DIC are outlined in T§b.!e,.2.11-8. Patients with chronic DIC have laboratory evidence of the disorder but no clinical evidence of hemorrhage or thrombosis.
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