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  Vol. 116 No. 1, July 1965 TABLE OF CONTENTS
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Diseases of Hypersensitivity

Disseminated Intravascular Coagulation

DONALD G. McKAY, MD

Arch Intern Med. 1965;116(1):83-94.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

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, . . . [Full Text PDF of this Article]


Author Affiliations

NEW YORK

From the College of Physicians and Surgeons of Columbia University, New York. Delafield Professor and Chairman, Department of Pathology.


Footnotes

Received for publication Dec 30, 1964; accepted Jan 1, 1965.

Reprint requests to 630 W 168th St, New York, NY 10032 (Dr. McKay).



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