Author + information
- Steven Fruchtman, MD and
- Louis M. Aledort, MDa
- ↵aAddress for reprints: Louis M. Aledort, MD, Mount Sinai School of Medicine, One Gustave Levy Place, New York, New York 10029.
Known variously as disseminated intravascular coagulation, defibrination consumption coagulopathy or, more simply, as defibrination, disseminated intravascular coagulation is a serious epiphenomenon that occurs most often as a complicating factor of an underlying disease process. Although frequently triggered by underlying disease such as infection or tumor, if not recognized and treated appropriately, disseminated intravascular coagulation alone may lead to the patient's death as a result of hemorrhage or thrombosis, or both, of vital organs. Frequently, it may only manifest itself as an abnormality of coagulation tests, causing no immediate problem for the patient, and potentially normalizing when the inciting cause is appropriately managed.
The central process that marks disseminated intravascular coagulation is the generation of thrombin in the circulating blood by means of the activation of the coagulation mechanism, leading to the conversion of fibrinogen to fibrin, which, in turn, may lead to thrombosis mainly of the microcirculation. Because platelets and coagulation factors are consumed and fibrinolysis is enhanced during the coagulation process, hemorrhage may also ensue.
Although disseminated intravascular coagulation is frequently encountered in medical and obstetric patients, the difficulty in diagnosis and controversy regarding optimal therapy are frustrating for both patient and physician. By understanding the pathophysiology of disseminated intravascular coagulation and combining clinical observation and laboratory data, one can arrive at the appropriate diagnosis. Therapy must be individualized, and assessment of the benefit versus risk ratio of intervention must be made. Early recognition of acute and life-threatening disseminated intravascular coagulation can be lifesaving with appropriate supportive measures.
This study was supported in part by a contract from the National Heart, Lung, and Blood Institute, Bethesda, Maryland; Health Services Administration Grant MCB-360001-04-01; Health and Human Services Grant HL-30567-02; the Regional Comprehensive Hemophilia Diagnostic and Treatment Center; the Margie Boas Fund; the International Hemophilia Training Center of the World Federation of Hemophilia and the Polly Annenberg Levee Hematology Center, Department of Medicine, Mount Sinai School of Medicine of the City University of New York, New York, New York.
- American College of Cardiology Foundation