Rooney S J, Pagano D, Bognolo G, Wong C, Bonser R S
Cardiothoracic Surgical Unit, Queen Elizabeth Hospital, Birmingham, UK.
Eur J Cardiothorac Surg. 1997 Feb;11(2):373-8. doi: 10.1016/s1010-7940(96)01033-0.
The use of aprotinin in cardiac surgery to improve haemostasis and reduce blood loss particularly in patient groups at increased risk of bleeding is well established. Previous retrospective studies in profound hypothermic surgery have highlighted concerns that in this circumstances aprotinin may paradoxically cause increased bleeding and intravascular thrombosis. We therefore adopted a modified protocol for administering aprotinin, which was not started until cardiopulmonary bypass had been reinstituted after circulatory arrest.
Between April 1993 and June 1995, 45 patients underwent 46 thoracic aortic procedures which required hypothermic circulatory arrest; 25 of these were emergencies. All of these patients received aprotinin.
There were five deaths (10.8%) in hospital. Two patients with preoperative oliguric renal failure required postoperative dialysis, and a further six (13%) developed transient renal dysfunction with complete recovery. Two patients suffered postoperative stroke; one from embolisation of a severely diseased aorta, while the other had signs of an acute evolving stroke before surgery. None of the patients suffered acute Q-wave perioperative myocardial infarction. The mean blood loss was 575 ml in the first 12 h, with a mean postoperative transfusion requirement of 1 U blood.
We cannot implicate aprotinin in increased postoperative blood loss, renal dysfunction or mortality when used with hypothermic circulatory arrest according to this protocol. Elucidating the role of aprotinin in hypothermic circulatory arrest requires a randomised prospective study.
