[Coagulation deficits and hemorrhagic consequences after cardiac surgery under ECC].
I--A statistical study of the results of tests of hemostasis was carried out in patients who had undergone major cardiac surgery with extra-corporeal circulation. There were two series of patients (1.504 and 547 operated) suffering mainly from congenital cardiopathies, valvulopathies or coronaritis. Bearing in mind the hematocrit and the total protein level, the following was studied before and after ECC and 24 hours after the intervation: the blood platelet level, fibrinogen, prothrombin and its cofactors, antithemophilic factors A and B, FDP amd fibrinolytic activity. The fall in platelet stickiness is specifically pointed out, and also the fall in the level of fibrin stablizing factor (factor XIII) which is met with after ECC, and which can explain the persistence of certain hemorrhagies. Furthermore, the fall in antithrombin III level then its rise can contribute to the "heparine rebound" occurring in certain cases after neutralization of heparinemia with protamine. II--The deficits in the quantitatively and qualitatively variable hemostatic factors do not necessarily lead to hemorrhage. Hemorrhage, due to biological causes, are met with in 5 to 6 p. 100 of the cases. Most of the time they are provoked by a residual hemorrhage or a "heparine rebound", deficits in coagulation factors, a DIVC syndrome, difficult to diagnose and to treat, or fibrinolysis, much more rarely nowadays, owing to the almost routine use of antiproteases. Sometimes, the check up of coagulation can be barely disturbed and local abnormalities in biological hemostasis which are still not well understood, are invoked in order to explain the hemorrhage.
[Coagulation deficits and hemorrhagic consequences after cardiac surgery under ECC]. I--A statistical study of the results of tests of hemostasis was carried out in patients who had undergone major cardiac surgery with extra-corporeal circulation. There were two series of patients (1.504 and 547 operated) suffering mainly from congenital cardiopathies, valvulopathies or coronaritis. Bearing in mind the hematocrit and the total protein level, the following was studied before and after ECC and 24 hours after the intervation: the blood platelet level, fibrinogen, prothrombin and its cofactors, antithemophilic factors A and B, FDP amd fibrinolytic activity. The fall in platelet stickiness is specifically pointed out, and also the fall in the level of fibrin stablizing factor (factor XIII) which is met with after ECC, and which can explain the persistence of certain hemorrhagies. Furthermore, the fall in antithrombin III level then its rise can contribute to the "heparine rebound" occurring in certain cases after neutralization of heparinemia with protamine. II--The deficits in the quantitatively and qualitatively variable hemostatic factors do not necessarily lead to hemorrhage. Hemorrhage, due to biological causes, are met with in 5 to 6 p. 100 of the cases. Most of the time they are provoked by a residual hemorrhage or a "heparine rebound", deficits in coagulation factors, a DIVC syndrome, difficult to diagnose and to treat, or fibrinolysis, much more rarely nowadays, owing to the almost routine use of antiproteases. Sometimes, the check up of coagulation can be barely disturbed and local abnormalities in biological hemostasis which are still not well understood, are invoked in order to explain the hemorrhage.