Bleeding remains a complication of certain complex
surgical procedures, particularly those cardiac operations associated with long bypass times and profound
hypothermia. Clinical and novel experimental strategies to reduce
bleeding and the need for blood and blood-product transfusions are the focus of this review. Preoperative assessment of the patient will identify
drug-induced, acquired, or inherited coagulation defects that may contribute to this problem. The main attention is directed to the
perioperative period, and broad areas discussed include the preoperative use of
erythropoietin to increase red blood cell mass, autologous donation either preoperatively or before bypass,
autotransfusion/
hemofiltration, and acceptance of relative
anemia both during the operation and into the postoperative period. A further, often overlooked, management strategy in treating major coagulopathies is the consideration of the cost and half-lives of the
coagulation factors in individual blood components. Prevention of
bleeding has become possible both by manipulation of the control of coagulation and inflammatory processes and by the introduction of pharmacologic agents such as
aprotinin.
Aprotinin is widely used and has proven efficacy in the management of excess
bleeding. It is a
serine protease inhibitor and has several possible mechanisms of action, including inhibition of the plasma
enzyme systems activated by contact with the foreign surface of the bypass circuit and preservation of platelet function. Safety issues include the possibility of
hypersensitivity and
anaphylactic reaction on a second exposure. Concerns that
aprotinin may induce a prothrombotic or
coagulant state have no basis in theory or any good evidence in the current literature. A recent study specifically sought to identify the presence of disseminated microvascular platelet-
fibrin thrombi present at autopsy in patients who had received
aprotinin therapy. The study concluded that diffuse platelet-
fibrin thrombi were not a direct complication of
aprotinin therapy. Finally, modern molecular biology has led to the recent development of an inhibitor for
factor IXa that competitively replaced IXa in the intrinsic complex and blocked the conversion of
factor X to
factor Xa. This compound is under investigation in animal studies. These have so far shown efficacy in reducing blood loss after bypass in comparison with standard
heparin anticoagulation.