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Postoperative Bleeding After Coronary Artery Bypass Surgery with Cardiopulmonary Bypass

R. Belcher, Philip, MD, FRCS; Muriithi, Elijah W., MD, FRCS

doi: 10.1097/00000539-200211000-00086
LETTERS TO THE EDITOR: Letters & Announcements

Department of Cardiac Surgery

The Royal Infirmary

University of Glasgow

Glasgow, Scotland

To the Editor:

In their study of postoperative bleeding after coronary artery surgery with cardiopulmonary bypass, Wajon et al. observed that neither local application of the patients’ own platelets nor reinfusion of the platelets postoperatively either reduced postoperative blood loss or the transfusion of donor blood (1). Platelets were applied topically, we assume, to promote hemostasis by correcting for a deficiency of platelets at bleeding sites. A local platelet deficiency is unlikely because, during flow, platelets travel on the periphery of the blood stream (2). Furthermore, at areas where the vessel wall is damaged, platelets are activated by a number of stimuli, including shear stress and exposed collagen. Activated platelets secrete thromboxane A2and release ADP and serotonin; these mediators, which not only exert positive feedback on the activated platelets, but also recruit further platelets’ form microaggregates that coalesce to form macroaggregates. Thus platelets would already be concentrated at sites where the vessel wall is damaged. Regrettably, the hemostatic function of these platelets would be impaired as, during cardiopulmonary bypass, the ability of platelets to form macroaggregates is lost, although their ability to form microaggregates is well preserved (3–5). The process that transforms microaggregates into macroaggregates is essential for hemostasis, as it gives strength to a platelet plug, paving the way for clot retraction.

Regarding the reinfusion of autologous platelets after cardiopulmonary bypass, the intuitive notion that platelet transfusion will acutely improve hemostasis after cardiac surgery, not only fails to recognize that the function of platelets may be impaired by storage (6,7), but also assumes that platelet dysfunction is secondary to intrinsic platelet change. In recent studies we, among others, observed that extrinsic factors are major contributors to platelet dysfunction (8,9). Specifically, we demonstrated that a plasma change, induced by heparinization, was a major cause of platelet dysfunction (9). We further observed that platelets from normal individuals, and platelets obtained from patients before cardiopulmonary bypass, became dysfunctional when exposed to plasma obtained from blood sampled after heparinization or during cardiopulmonary bypass (9). These observations suggest that attempts to correct postcardiopulmonary bypass bleeding by transfusing donor platelets, or autologous platelets collected preoperatively, are unlikely to restore platelet function, unless efforts are also directed towards correcting (or preventing) the plasma change(s). Wajon et al. (1) and others (10–12) have observed that the postoperative reinfusion of autologous platelets, prepared preoperatively, does not improve bleeding times after surgery using cardiopulmonary bypass and is of (little or) no clinical benefit; other investigators have shown that donor platelets (13–15) are similarly ineffective. These findings also suggest that platelet transfusions may be ineffective in this context and should therefore be probably restricted to those patients who have significant thrombocytopenia.

Philip R. Belcher, MD, FRCS

Elijah W. Muriithi, MD, FRCS

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© 2002 International Anesthesia Research Society