Aprotinin and bleeding in profoundly hypothermic perfusion

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Abstract
Clinical observation led us to believe that aprotinin fails to preservehaemostatic function in patients undergoing deep hypothermic perfusion withor without circulatory arrest. A retrospective study was made of blood lossin 80 consecutive acute Type A dissection patients before and during theaprotinin era (1987-1992). After 1988 all patients were cooled below 20degrees C pending circulatory arrest. Fourteen patients underwent aorticroot replacement and 66 replacements of the ascending aorta. Agedistribution (range 22-79 years) and type of operation were similar in theaprotinin and control groups. The impervious Hemashield (Meadox) graft wasused for all but five patients. These underwent aortic root replacementwith preclotted, valved conduits. Overall the mean blood loss for 27patients operated without aprotinin was 837 ml per 24 h (standard error +/-90) and for 53 patients with aprotinin 1,929 ml per 24 h (standard error+/- 90). There was a significant difference between the two groups whenprofoundly hypothermic perfusion was used, with greater bleeding inaprotinin-treated patients. There were six re-entries in the aprotiningroup and none in the control patients. There were ten hospital deaths(11.1%). A greater incidence of bleeding and thrombosis-related deaths wasrecorded for the aprotinin-treated patients. In addition, four survivingaprotinin patients suffered severe coagulation defect with blood lossgreater than 4,500 ml and platelets less than 50 x 10(6). We suggest thataprotinin inhibits the protease enzymes which maintain the fluid state ofblood during hypothermic low flow and arrest states. Disseminatedintravascular coagulation may consume platelets thereby predisposing toabnormal bleeding and potentially fatal thrombotic events. The use ofaprotinin in profoundly hypothermic perfusion should be adoptedcautiously.

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