Abstract

The accident of incompatible blood transfusion is not infrequent in practical medicine. The acute hemolytic transfusion reaction sometimes results severe complications. In authors' experience in the treatment and clinical analysis of this disorder during last one decade, there were some evidences that disseminated intravascular coagulation attributed in considerable extent to the development of such complications as shock, hemorrhagic tendencies and acute renal failure. In this paper, six patients received incompatible blood transfusion are reviewed and some therapeutic approaches are presented.On the hypothesis that DIC is a primary pathogenetic mechanism involved in these hemolytic reaction, authors have learned that the heparin therapy would be the best at interfering with these pathophysiologic pathways, and have been getting the benifits in prevention of severe complications or of exaggeration of signs and symptoms developed. Of 6 cases presented, five of the incompatibilities were in ABO system and one in Rh system. A 26-year-old female, blood group 0, Rh positive, was given a transfusion with 0 positive blood but she was positive in anti-E antibody. The amount of blood transfused were 50-350ml in ABO incompatibilities and 1, 000ml of E-positive blood in a Rh-incompatible case.Hemostatic studies were done in 3 patients. One patient received ABO incompatible blood revealed clotting abnormalities even 2 days after the heparin administration. The case with positive E-antibody developed acute renal failure. Severe bleeding tendency was observed at the Cesarian section when she was given more than 1, 500ml of blood. Thrombocytopenia, positive tests in FDP and protamine sulfate test and prolongation of thrombin time and serial thrombin time were seen in these 2 cases. Remaining one patient who was given heparin just after the accident showed no coagulation disturbance when tested during heparin therapy. Five patients received mismatched blood in ABO system were all given heparin as soon as possible after the accident to prevent severe reactions due to DIC. All were symptomatically uneventful, however, the elevation of FDP and thrombocytopenia were noted in one as mentioned above and moderate increase of blood urea nitrogen in three clinical courses. These findings seem to represent the subclinical participation of clotting episodes in mismatched transfusion reactions even after the heparin administration. Therefore, the occurrence of DIC may be more frequent that has been appreciated and prompt treatment with heparin prior to the recognition of signs and symptoms may decrease the morbidity and mortality from incompatible transfusion reactions.

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