抄録
Disseminated intravascular coagulation (DIC) is a pathological syndrome resulting from formation of thrombin and consumption of coagulation factors and platelets with associated activation of secondary fibrinolysis, encountered in numerous underlying diseases with varying degrees of severeity. The differences of manifestations are dependent upon the rate, the amount and continuance of thrombin formation as well as the level of functioning of the fibrinolytic system, liver, bone marrow, and reticuloendothelial system.
DIC has been tried to be classified into many types, based on the pattern of laboratory data and on somewhat theoretical explanations.
But right now, I think it is simple and best to classify DIC into acute and chronic type accoring to the clinical conditions and the severity of the laboratory manifestation.
Cooper et al defined compensated DIC, in which most of the criteria for DIC are met but one or two of the usually depressed constituents are normal.
Observing the cases of chronic DIC, we can say that there may be compensatory mechanism in regulation of coagulation and fibrinolytic system.
However, addition of this new philosophical definition may make us confused in diagnosis and treatment of DIC. We had better clarify the meaning of compensation by the more scientific language.
I tried to analyze the regulation of the number of platelets in DIC patients by observing the megakaryocytic colony formation according to the method of Messner. Fibrinogen and fibrin degradation products encountered in the patients who had ascites or pleural fluid with conformative DIC according to other laboratory data and clinical conditions and without were also tried to be evaluated.
