Pathology - Disseminated Intravascular Coagulation (DIC)
DIC may occur secondary to gram-negative bacterial septic shock. DIC is a thrombohemorrhagic illness that develops from activation of the coagulation cascade and consumption of coagulation factors as a complication of a number of disorders. Gram-negative organisms (such as N. meningitidis as in this case or most commonly E. coli), trauma, obstetric complications, malignancy or other causes of vascular damage, and inflammatory mediators result in the release or exposure of tissue factor, the most fibrogenic substance known, initiating coagulation. Fibrin thrombi form in the microcirculation, consuming coagulation factors, trapping platelets, and restricting blood flow (producing ischemic tissue damage). Excess thrombin from coagulation results in conversion of plasminogen to plasmin, which cleaves the fibrin thrombi (fibrinolysis) creating fibrin split products and promotes proteolysis of clotting components. The fibrin degradation products (FDPs) in turn exhibit anticoagulant properties, including preventing thrombin production. The net outcome is uncontrollable bleeding. Patients may bleed from any breaks in the skin or mucous membranes. Laboratory results will demonstrate increased PT and PTT, decreased fibrinogen, thrombocytopenia, prolonged bleeding time, increased D-dimer, and presence of FDPs. Fibrin thrombi cause damage to RBC membranes producing a normocytic anemia with schistocytes and reticulocytosis (microangiopathic hemolytic anemia).
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