Severe Acute Disseminated Intravascular Coagulation (DIC): Clinical Imporiance; Heparin Therapy; and Etiology

Abstract

We have reviewed 47 patients (pts.) with severe acute DIC (mean fibrinogen 100.5 mg/dl, platelets 45,700/μl, prothrombin time 19.4 sec, partial thromboplastin time 86.5 sec). Most pts. were critically ill. Predisposing conditions included infection (32), shock (32), and surgery or trauma (21). Routine treatment included aggressive therapy for underlying diseases and metabolic disturbances, vitamin K, folate, and blood conponents Twelve pts. were treated with heparin and 10 (83%) died. Heparin apparently benefited only 1 pt. and in 7 bleeding increased. Thirty (86%) of 35 pts. who did not receive heparin died. Analysis suggested that heparin would not have affected the outcome in any of them. in all pts. who died multiple potential causes were present. Thrombosis, ischemia, or hemorrhage were the apparent inmediate cause of death in only 2 pts. but were contributory causes in others. in most pts. with significant oonplications potentially attributable to DIC other causative pathology was present. Twenty-five pts. had autopsies. Microvascular thrombi were not found but large vessel thrombi were relatively common. VJe conclude that 1) Severe DIC is usually a preterminal event in critically ill pts. 2) Other pathology may be more important than DIC when death or significant ' thrombosis or bleeding occur. 3) Heparin is rarely beneficial and often increases bleeding. 4) Microvascular thrombi may not be the only mechanism responsible for DIC.