| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
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.
References
Department of Anaesthetics, Royal Prince Alfred Hospital, Sydney, NSW, Australia
In Response:
We thank Dr. Belcher for his comments regarding our study (1). We would like to make only a few minor clarifications in response. Our objective was to determine whether the technique as described was effective in a large and homogenous group presumed at high-risk for bleeding and transfusion. We did not address mechanisms of effect in detail.
We agree that platelets would already be concentrated at intravascular sites of vessel wall damage. The topical application of autologous platelet gel to raw surfaces and wound edges was intended as an extravascular mechanical sealant along the lines of "tissue glue" rather than an attempt to correct for a local platelet deficiency. We noted in our introduction that the efficacy of this aspect of the technique had not been reported, but it was part of our established practice at the time (based on reports in conference proceedings (2) and personal communications), and was quick, easy, and safe to do. Recent publications in the orthopedic (3) and cosmetic (4) surgery literature support use of topical autologous platelet gel and fibrin glue to arrest capillary bleeding from bone and under skin flaps. Autologous platelet gel has also been reported to contain platelet-derived growth factor that may enhance wound healing.
Dr. Belcher lists several reasons for platelet dysfunction after cardiopulmonary bypass, all of which we recognized and attempted to prevent or minimize by our pheresis protocol. Therapeutic quantities of platelets were sequestered before heparinization and reinfused only after protamine reversal thus avoiding (in the sequestrate) the heparin and bypass induced plasma change(s) referred to by Dr. Belcher. The degree to which these plasma changes persist in the patient (if they do) after bypass and heparin reversal remains unquantified and deserving of further research. Autologous platelets prepared by whole blood centrifugation and stored for several hours before reinfusion exhibit less activation and greater responsiveness than allogeneic platelets (5). Our study of reoperative CABG patients showed only that therapeutic yield plateletpheresis did not improve the two clinical outcomes we measured. Mean chest tube drainage was close to obligate loss volumes in both groups, making further reduction unlikely. Allogeneic PRBC transfusion was also very low, averaging 1.2–1.5 units per patient. Up to 55% of patients in both groups received some allogeneic exposure, but this includes those patients receiving platelets and fresh frozen plasma as treatment for postoperative bleeding. Low rates of preoperative aspirin exposure, routine antifibrinolytic use, and minimal exposure of blood to nonbiologic surfaces are likely to have contributed to our low control group rates, and thus made a treatment difference less likely. We performed only routine measurements of hemostasis (platelet counts, INR, APTT—we did not measure bleeding times) perioperatively, and patients were transfused with platelets only if clinically bleeding with a count < 100 x 109/L.
We stand by our conclusion that while the technique was not beneficial in our unit, it may have a place in other institutions where baseline blood loss and transfusion rates are higher than ours. We agree with Dr. Belcher that platelet transfusions should be restricted to bleeding patients with significant thrombocytopenia, and not administered routinely after cardiopulmonary bypass surgery.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
