LETTERS TO THE EDITOR: Letters & Announcements
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
1. Wajon P, Gibson J, Calcroft R, et al. Intraoperative plateletpheresis and autologous platelet gel do not reduce chest tube drainage or allogenic blood transfusion after reoperative coronary artery bypass graft. Anesth Analg 2001; 93: 536–42.
2. Aarts PA, van den Broek SA, Pins GW, et al. Blood platelets are concentrated near the wall and red blood cells, in the center in flowing blood. Arteriosclerosis 1988; 8: 819–24.
3. Menys VC, Belcher PR, Noble MIM, et al. Macroaggregation of platelets in plasma, as distinct from microaggregation in whole blood (and plasma), as determined using optical aggregometry and platelet counting respectively, is specifically impaired following cardiopulmonary bypass in man. Thromb Haemostas 1994; 72: 511–8.
4. Belcher PR, Muriithi EW, Milne EM, et al. Heparin, platelet aggregation, neutrophils and cardiopulmonary bypass. Thromb Res 1999; 98: 249–56.
5. Kawahito K, Kobayashi E, Iwasa H, et al. Platelet aggregation during cardiopulmonary bypass evaluated by a laser light-scattering method. Ann Thorac Surg 1999; 67: 79–84.
6. Silver WP, Keller MP, Teel R, Silver D. Effects of donor characteristics and platelet in vitro time and temperature on platelet aggregometry. J Vasc Surg 1993; 17: 726–33.
7. Rosenfeld BA, Herfel B, Faraday N, et al. Effects of storage time on quantitative and qualitative platelet function after transfusion. Anesthesiology 1995; 83: 1167–72.
8. Kestin AS, Valen CR, Khuri SF, et al. The platelet function defect of cardiopulmonary bypass. Blood 1993; 82: 107–17.
9. Muriithi EW, Belcher PR, Day SP, et al. Heparin-induced platelet dysfunction and cardiopulmonary bypass. Ann Thorac Surg 2000; 69: 1827–32.
10. Tobe CE, Vocelka C, Sepulvada R, et al. Infusion of autologous platelet rich plasma does not reduce blood loss and product use after coronary artery bypass: a prospective, randomized, blinded study. J Thorac Cardiovasc Surg 1993; 105: 1007–13.
11. Ereth MH, Oliver WC Jr, Beynen FM, et al. Autologous platelet-rich plasma does not reduce transfusion of homologous blood products in patients undergoing repeat valvular surgery. Anesthesiology 1993; 79: 540–7.
12. Shore-Lesserson L, Reich DL, DePerio M, et al. Autologous platelet-rich plasmapheresis: risk versus benefit in repeat cardiac operations. Anesth Analg 1995; 81: 229–35.
13. Harding SA, Shakoor MA, Grindon AJ. Platelet support for cardiopulmonary bypass surgery. J Thorac Cardiovasc Surg 1975; 70: 350–3.
14. Simon TL, Aki BF, Murphy W. Controlled trial of routine administration of platelet concentrates in cardiopulmonary bypass surgery. Ann Thorac Surg 1984; 37: 359–64.
15. Premaratne S, Razzuk AM, Premaratne DR, et al. Effects of platelet transfusion on post cardiopulmonary bypass bleeding. Jpn Heart J 2001; 42: 425–33.