WITHIN the past few years it has become evident that disseminated intravascular coagulation is an intermediary mechanism of disease which occurs in many apparently divergent disease states.1 Although chronic forms of this process may be recognized, the most striking clinical syndromes are those presented by acute and massive clotting of the circulating blood. The immediate consequences are the sudden appearance of shock and the development of a hemorrhagic diathesis. Examination of the hemostatic mechanism during such an event usually reveals a depletion of many of the components of the blood coagulation system and ofen evidence of activation of plasma fibrinolysin. The majority of the clinical effects related to specific organs are mediated by ischemic necrosis caused by the obstruction of arterioles, capillaries, and venules by fibrin thrombi. Among the late sequelae of disseminated clotting are panhypopituitarism, acute renal failure, bilateral renal cortical necrosis, adrenal hemorrhage, acute hemorrhagic pancreatitis,
McKAY DG. Diseases of Hypersensitivity: Disseminated Intravascular Coagulation. Arch Intern Med. 1965;116(1):83–94. doi:10.1001/archinte.1965.03870010085011
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