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J Thorac Cardiovasc Surg 1996;111:272-275
© 1996 Mosby, Inc.

BRIEF COMMUNICATIONS

RETRANSFUSION OF THORACIC WOUND BLOOD DURING HEART SURGERY OBSCURES BIOCOMPATIBILITY OF THE EXTRACORPOREAL CIRCUIT

Groningen, The Netherlands

Accepted for publication May 31, 1995. To minimize blood trauma and postoperative pathologic outcomes, it is of great concern to improve the biocompatibility of extracorporeal circuits. ¹ Worldwide, many comparative studies have been performed to select the most biocompatible extracorporeal circuit. In many of these studies, however, a systematic error was made. Retransfusion of heparinized blood from the wound area is an established method to attenuate excessive blood loss during cardiopulmonary bypass (CPB). Retransfusion of this wound blood is feasible by suction from the thoracic cavity and recirculation through the cardiotomy reservoir. Because wound blood is highly traumatized, as we demonstrated in recent studies, ^2,3 there are likely to be significant effects of wound blood retransfusion on the systemic blood, depending on the amount of retransfused wound blood. Particularly, retransfusion of the damaged wound blood could obscure possible improvements in biocompatibility of extracorporeal circuits. ⁴ In this study, wound blood was retained during CPB in one group of 14 patients and retransfused only at the end of bypass. The control group consisted of 20 other patients, who were subjected to immediate and continuous retransfusion of wound blood during the operation. Blood damage and activation during operation were assessed by measuring the plasma levels of variables indicative of hemolysis (Fig. 1), clotting (Fig. 2), platelet degranulation (Fig. 3), and complement activation (Fig. 4). The validity of these variables in reflecting extracorporeal related blood damage could thus be evaluated.

View larger version (35K): [in this window] [in a new window]   Fig. 1. The degree of hemolysis during CPB is reflected by plasma levels of hemoglobin (Free Plasma Hb). Mean values of the patient group with continuous retransfusion of wound blood are indicated by the white bars; mean values of the patient group with retainment of wound blood are indicated by gray bars. The sample points indicate 5 minutes after heparinization and before start of CPB (-5'), before release of the aortic crossclamp (pre-X), after release of the aortic crossclamp (post-X), and at the end of CPB (end CPB). The wound blood bar indicates the concentration of free hemoglobin in the wound blood during retention. Error bars indicate the standard error of the mean. An asterisk indicates a significant difference (p < 0.01 by unpaired Student's t test) between both groups at a specific sample point.

View larger version (38K): [in this window] [in a new window]   Fig. 2. The degree of clotting activation during CPB is reflected by plasma levels of TAT III (TAT). All other graph specifications are the same as those in Fig. 1.

View larger version (38K): [in this window] [in a new window]   Fig. 3. The degree of platelet degranulation during CPB is reflected by plasma levels of ß-TG. All other graph specifications are the same as those in Fig. 1.

View larger version (33K): [in this window] [in a new window]   Fig. 4. The degree of complement activation during CPB is reflected by plasma levels of complement factor c3adesArg (C3a). All other graph specifications are the same as those in Fig. 1.

The effect of retransfusing wound blood on circulating concentrations of products such as free hemoglobin and TAT III was demonstrated by the immediate increase in the blood retention group after the retransfusion and the more gradual and lesser increase in patients with continuous retransfusion. Furthermore, the lack of any noticeable increase of these variables before retransfusion endorses the dominating effect of wound blood retransfusion on free hemoglobin and TAT III levels. Moreover, the high concentrations of free hemoglobin and TAT III in the wound blood explain the observed increases satisfactorily.

Concentrations of ß-TG also increased, in particular after the retransfusion of wound blood. A significant increase of ß-TG in the retainment group was also observed, however, during the first phase of CPB before release of the aortic crossclamp and before any retransfusion of wound blood. This increase, independent of retransfusion, strongly suggests that the extracorporeal circuit contributes significantly to platelet damage. Finally, the complement system was activated in both groups of patients, as indicated by the increasing C3a concentrations after the start of CPB, although to a much lesser extent in the blood retention group than in patients who underwent continuous retransfusion. The common C3a generation indicates complement activation by the extracorporeal circuit in all patients. ⁶ The differences between groups is explainable by the method of wound blood retransfusion. It is likely that blood complement in the wound is activated through the classic pathway, resulting in C3a levels similar to the levels in circulation. The increase in systemic C3a level after continuous retransfusion or retransfusion of retained wound blood suggests that infusion of denatured or substances unfamiliar to blood is triggering an additional systemic complement activation response. ⁷

In conclusion, our study demonstrates that data obtained in previous clinical studies that focused on biocompatibility assessment of extracorporeal circuits were biased when substantial amounts of wound blood were retransfused during the procedure. Blood activation related to clotting, platelet degranulation, complement activation, and hemolysis by the extracorporeal circuit during CPB—as indicated by TAT III, ß-TG, C3a, and free hemoglobin—is vastly influenced by the retransfusion of wound blood. Moreover, free hemoglobin and TAT III generation related to the extracorporeal circuit were found insignificant. Variables such as TAT III and hemolysis are therefore unfit to analyze and quantify the biocompatibility of extracorporeal circuits. Furthermore, biocompatibility of extracorporeal circuits, as analyzed by variables such as C3a and ß-TG, cannot be evaluated with the presently used technique for heart operations of continuously retransfusing wound blood. We suggest that the wound blood be retained during assessment of the biocompatibility of extracorporeal circuits or that the wound blood be washed by cell-saving techniques, to wash out the disturbing plasma factors before retransfusion.

Footnotes

From the Blood Interaction Research Division^a and the Department of Cardiothoracic Surgery, University Hospital Groningen, The Netherlands.

J THORAC CARDIOVASC SURG 1996;111:272-5

References

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This Article Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Piet W. Boonstra Tjark Ebels Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by de Haan, J. Articles by Ebels, T. Search for Related Content PubMed PubMed Citation Articles by de Haan, J. Articles by Ebels, T.