• K M Taylor.
• Cardiac Surgical Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, England.
• Ann. Thorac. Surg. 1993 Nov 1;56(5 Suppl):S78-82.

AbstractCardiac surgical procedures are known to be associated with coagulation defects and disordered hemostasis. Excessive perioperative and postoperative bleeding and the need for considerable volumes of blood and blood product transfusions are well recognized. The risks of blood transfusion with high donor-exposure levels have focused attention on blood conservation as a priority in reducing the complications of cardiac operations. Hemostatic defects may be related to patient-inherent coagulopathies, preexisting associated pathology, and preoperative drug therapy. In addition, hemostatic defects are induced during the operation itself. Two principal therapeutic approaches to this complex problem have evolved. Although different, these approaches are not mutually exclusive and may be used complementarily. The first is autotransfusion and the second is hemostatic drug therapy. Although many drugs have been tried, including antifibrinolytic agents (epsilon-aminocaproic acid, tranexamic acid), platelet-preserving agents (prostacyclin, dipyridamole), and desmopressin, the only drug that has shown significant and consistent efficacy in reducing bleeding in cardiac surgery patients is the serine protease inhibitor aprotinin. Aprotinin has been shown to be highly effective in reducing blood loss and blood and blood product transfusion requirements in high-risk patients. Clinical experience with aprotinin therapy in cardiac patients and specific issues such as dosage regimens and the target automated clotting time levels in patients on high-dose aprotinin therapy are outlined. Indications for the use of aprotinin and the balance between risk and benefit are discussed.

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