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Abstract
Bleeding is one of the major complications after cardiopulmonary bypass (CPB).
In the earlier days of cardiopulmonary bypass, the cellular and molecular elements of blood sustained significant mechanical trauma during perfusion, resulting in destruction of red cells, platelets and denaturation of plasma proteins.
Post-CPB platelet dysfunction, dilutional coagulopathy and abnormal fibrinolysis contribute to this bleeding tendency and increase the need for homologous blood products transfusion.
The beneficial effect of each unit of blood or blood components transfused is accompanied by the possibility that the patients may experience an adverse reaction to the transfusion.
Because of the multifactorial etiology of the CPB-induced hemostatic defect, a multimodal approach to blood conservation and hemostasis must be employed throughout the entire perioperative period.
Blood conservation in open heart surgery can be achieved by different methods:
•Antifibrinolytic therapy (aminocaproic acid “EACA”, tranexamic acid, and aprotinin) has been shown to reduce bleeding and transfusion requirement through inhibiting fibrinolylic process.
•Desmopressin acetate increases Von Willebrand Factor and cause a non-specific enhancement of platelet function.
•Acute normovolemic hemodilution provides a source of fresh blood for autologous re-infusion after cardiopulmonary bypass (CPB).
•Autologous platelet rich plasma sequestration decreases homologous transfusion by attenuating or eliminating the hemostatic defects.