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Ann Thorac Surg 2002;74:986-987
© 2002 The Society of Thoracic Surgeons
a Department of Anesthesiology, Virginia Commonwealth University/Medical College of Virginia, Richmond, Virginia, USA
* Address reprint requests to Dr Spiess, Department of Anesthesiology, VCU/MCV, 1200 East Broad Street, Richmond, VA, USA
e-mail: bdspiess{at}hsc.vcu.edu
Blood transfusion is given with the intent of increasing oxygen carrying capacity to tissue, thereby prophylaxing against ischemic tissue damage. Physicians have the best of intentions in applying the therapy, but the decision to transfuse is driven by fear (ie, of not acting, lawsuit, or adverse outcome) and emotion. The transfusion trigger, a particular hemoglobin level of discomfort in the prescribing physician, is not defined by clear physiologic parameters. To date, we do not have a real time monitor of oxygen supply and demand to the microcirculation of the whole body or individual organs. Therefore, physicians make transfusion decisions based upon their past teaching and enculturation. We are encultured to believe that giving blood saves lives, yet there is little data published to support such a conclusion. As a result of the lack of evidence based medicine supporting the transfusion decision, the use of blood products during coronary artery bypass grafting (CABG) surgery varies widely. In one series of over 2000 cases, only 3% of patients were transfused, whereas in others 83% of patients received blood [1, 2]. Which practice is the best, has the better outcomes, least costly, etc.?
In the present issue of The Annals, a pioneering article appears and for the first time examines the long-term consequences of blood transfusion. Over 3000 articles are in the literature delineating the risks of blood transfusion. Some recent and well-done studies have been randomized trials of transfusion in critically ill or CABG patients [3, 4]. In such studies, patients transfused had no better and most often worse outcomes within 30 days of surgery. To my knowledge, the article by Engoren and associates in this issue is the first time that medium to long-term mortality associated with transfusion has been examined in CABG surgery. The findings are sobering and should be studied in depth by every cardiovascular surgeon and anesthesiologist. Those patients transfused during elective CABG surgery were twice as likely to die as those not transfused. The authors are to be congratulated for doing exhaustive and appropriate multivariate analysis to examine the effects of covariates. The conclusion that transfusion in CABG surgery is associated with increased mortality withstands such scrutiny and is a significant independent predictor of death. Databased research cannot prove cause and effect, yet the data from a number of such databased examinations are compelling and consistent. Our prior work in over 2200 patients showed that when transfusion was taken into account, lower hematocrit on entry to the intensive care unit was associated with fewer myocardial infarctions and congestive heart failure [5]. Other databased studies have examined outcomes and lowest hematocrit at various times during and after surgery [6–8]. These lowest hematocrit studies have sent a message that low hematocrit may be associated with bad outcome yet low hematocrit is a marker for transfusion and the authors neglected to examine transfusion in their analyses. Perhaps they have actually done a disservice by encouraging more transfusion. Recent examination of a database from the accumulated trials of aprotinin prior to FDA approval agrees with Engoren and associates that transfusion is independently associated with a number of adverse outcomes [9]. Long-term outcome and transfusion has been investigated in colon and prostate cancer [10–12]. Although some controversy still exists, considerable literature suggests that the risk of metastatic disease increases if a patient is transfused during resection of tumor. A paucity of literature exists demonstrating that patients transfused do as well or better than those not transfused. One recently published study examining transfusion in elderly patients actively undergoing myocardial infarction claims to be able to show that patients entering the emergency department already anemic can benefit from a transfusion [13]. However, bias is present in this study as those who were already anemic were twice as likely to be in the "do not resuscitate" (DNR) category. These patients (anemic with myocardial infarction) underwent interventions (angioplasty, surgery, or thrombolysis) half as often as those who were not anemic. The authors of this study ignore the fact that those patients transfused who were not anemic had a higher mortality rate than those not transfused.
Red blood cells stored for a period of time (28 days or longer) in the blood bank do not perform as fresh whole blood. They are depleted of 2,3 diphosphoglycerate (DPG), are fragile nondistensable and have a dramatically left shifted oxy-hemoglobin dissociation curve [14, 15]. Fresh whole blood can donate up to 23% of its carried oxygen whereas 28-day old blood only 6%. Because the oxy-hemaglobin curve is so left shifted in stored blood it is possible that bank blood may actually draw oxygen out of the tissues or microcirculation. In animal models of transfusion and trauma, transfused blood does not restore blood flow to vital organs, whereas whole blood is capable of fully restoring flow. Therefore, stored blood has major performance limitations in delivery of oxygen. This again calls into question the basic premise of transfusion.
Why might blood transfusion actually lead to an increased mortality rate? If red cell transfusions do not actually increase tissue oxygen delivery that may well be part of the explanation. The endothelium of patients after cardiopulmonary bypass is dysfunctional, pro-inflammatory, and pro-thrombotic. Endothelial cell biology and reactivity with platelets and white cells probably has a lot to do with early graft thrombosis, accelerated atheroma, and other cellular events shortening lifespan. Blood circulating systemically after CPB has been filled with inflammatory mediators such as cytokines and activated white cells. Blood transfusion carries a large inflammatory load and increases the already inflammatory state after CPB [16, 17]. The levels of cytokines can reach very high levels in nonleukocyte reduced, red cell transfusion and may be up to 1000 times baseline in platelet transfusions. Cytokine levels in post CPB patients show a 15-fold rise with a single red cell transfusion [18]. Anesthesiologists and surgeons underappreciate these facts. To date, the inflammatory nature of the bypass machine has not been separated from the transfusion behavior of physicians. Perhaps a great deal of the inflammation attributed to CPB has been caused by transfusion. One of the advantages of "blood substitute" technologies now undergoing trial is that they will allow a scientific comparison of outcome with and without transfusion of allogeneic red cells. There is ample data to show that anemia is well tolerated, transfusion is pro-inflammatory, and carries risks far beyond hepatitis and HIV transmission. Data is gathering, in support of the idea that patients have a better outcome with less transfusion (perhaps counterintuitive and contradictory to classical teaching). Transfusion for cardiac surgery still utilizes approximately 20% of the blood supply of the United States. Approximately 2.5 million units are utilized for heart surgery. Shortages of blood are common and will become more acute in the next few years. Costs are also increasing dramatically. A change in transfusion behavior by a large segment of physicians caring for CABG patients will be healthy. Such a reduction in transfusion utilization will save medical care dollars (20–35 million dollars/year), increase the availability of blood, and ultimately improve outcome and longevity for our patients.
References
This article has been cited by other articles:
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  F. W. Maddux, T. A. Dickinson, D. Rilla, R. W. Kamienski, S. P. Saha, F. Eales, A. Rego, H. W. Donias, S. L. Crutchfield, and R. A. Hardin Institutional Variability of Intraoperative Red Blood Cell Utilization in Coronary Artery Bypass Graft Surgery American Journal of Medical Quality, September 1, 2009; 24(5): 403 - 411. [Abstract] [PDF]
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 J. Brevig, J. McDonald, E. S. Zelinka, T. Gallagher, R. Jin, and G. L. Grunkemeier Blood transfusion reduction in cardiac surgery: multidisciplinary approach at a community hospital. Ann. Thorac. Surg., February 1, 2009; 87(2): 532 - 539. [Abstract] [Full Text] [PDF]
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 A. F. Merry Focus on Thrombin: Alternative Anticoagulants Seminars in Cardiothoracic and Vascular Anesthesia, December 1, 2007; 11(4): 256 - 260. [Abstract] [PDF]
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 C. R. Bridges Valid Comparisons of Antifibrinolytic Agents Used in Cardiac Surgery Circulation, June 5, 2007; 115(22): 2790 - 2792. [Full Text] [PDF]
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J. R. Brown, N. J.O. Birkmeyer, and G. T. O'Connor Meta-Analysis Comparing the Effectiveness and Adverse Outcomes of Antifibrinolytic Agents in Cardiac Surgery Circulation, June 5, 2007; 115(22): 2801 - 2813. [Abstract] [Full Text] [PDF]
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 K. G. Shann, D. S. Likosky, J. M. Murkin, R. A. Baker, Y. R. Baribeau, G. R. DeFoe, T. A. Dickinson, T. J. Gardner, H. P. Grocott, G. T. O'Connor, et al. An evidence-based review of the practice of cardiopulmonary bypass in adults: A focus on neurologic injury, glycemic control, hemodilution, and the inflammatory response. J. Thorac. Cardiovasc. Surg., August 1, 2006; 132(2): 283 - 290.e3. [Full Text] [PDF]
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A. DeAnda Jr, K. M. Baker, S. D. Roseff, J. A. Green, H. Mccarthy, T. Aron, and B. D. Spiess Developing a Blood Conservation Program in Cardiac Surgery American Journal of Medical Quality, July 1, 2006; 21(4): 230 - 237. [Abstract] [PDF]
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 M. Kuduvalli, A. Y. Oo, N. Newall, A. D. Grayson, M. Jackson, M. J. Desmond, B. M. Fabri, and A. Rashid Effect of peri-operative red blood cell transfusion on 30-day and 1-year mortality following coronary artery bypass surgery Eur. J. Cardiothorac. Surg., April 1, 2005; 27(4): 592 - 598. [Abstract] [Full Text] [PDF]
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J. J. Andreasen and C. Nielsen Prophylactic tranexamic acid in elective, primary coronary artery bypass surgery using cardiopulmonary bypass Eur. J. Cardiothorac. Surg., August 1, 2004; 26(2): 311 - 317. [Abstract] [Full Text] [PDF]
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