Abstract
Nine out of 319 patients who underwent open heart surgery from March 1977 to July 1978 at the University Hospital developed the laboratory evidence of DIC and were administrated heparin. Among the 9 patients, 6 cases were tetralogy or pentalogy of Fallot. (27 of 319 patients were Fallot's disease.) Other cases were endocardial cushion defect, annuloaortic ectasia and ventricular septal defect with pulmonary hypertension.
Laboratory evidence of DIC was found within 3 days after surgery. They had many etiologic factors contributing to the production of DIC following cardiopulmonary bypass, i. e. a long term bypass, hemolysis, shock or low cardiac output, polycythemia and severe infection. Eight out of 9 patients were associated with shock or low cardiac output and 5 of them had a hematocrit greater than 50 per cent. We suggest that low cardiac output and polycythemia may be main factors to develop DIC.
When diagnosis of DIC was established, all patients had a bleeding tendeney. One patient had acute renal failure. During heparin therapy, 2 patients had renal dysfunction and one of them developed acute renal failure. In this series of 9 patients, 2 who had renal failure ultimately died. In other cases, there were recovery from the bleeding tendency and improvement in coagulation findings.
In coagulation studies, platelet count, prothrombin time, FDP and thrombelastograph were useful for diagnosis and judgement of recovery or progress of DIC.
Early diagnosis is important because early administration of heparin may inhibit progress of DIC and dysfunction of organ, such as renal failure.
