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Ann Thorac Surg 2004;78:54-59
© 2004 The Society of Thoracic Surgeons

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Original article: cardiovascular

Coronary surgery without cardiotomy suction and autotransfusion reduces the postoperative systemic inflammatory response

^a Department of Cardiothoracic Surgery, Sahlgrenska University Hospital, Gothenburg, Sweden
^b Department of Anesthesia and Intensive Care, Eastern Hospital, Gothenburg, Sweden

Accepted for publication December 10, 2003.

^* Address reprint requests to Dr Jeppsson, Department of Cardiothoracic Surgery, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden
e-mail: anders.jeppsson{at}vgregion.se

	Abstract

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
BACKGROUND: Cardiotomy suction and autotransfusion of mediastinal shed blood may contribute to the inflammatory response after cardiac surgery. We compared inflammatory activation, myocardial injury, bleeding, and hemoglobin levels in patients undergoing coronary surgery with or without retransfusion of cardiotomy suction blood and mediastinal shed blood.

METHODS: Twenty-nine patients were included in a prospective randomized study. Cardiotomy suction blood and mediastinal shed blood were either retransfused or discarded. Plasma concentrations of the cytokines tumor necrosis factor- and interleukin-6 and complement factor C3a were measured preoperatively and 10 minutes, 2 hours, and 24 hours after cardiopulmonary bypass. C-reactive protein, erythrocyte sedimentation rate, troponin-T, and hemoglobin levels were analyzed preoperatively, and 24 and 48 hours after cardiopulmonary bypass. Postoperative bleeding the first 12 hours was registered.

RESULTS: Baseline data did not differ between the groups. Plasma concentrations of tumor necrosis factor-, interleukin-6, and C3a increased after surgery in both groups but significantly less in the group without cardiotomy suction and autotransfusion. The peak delta values in the no-retransfusion group was 36% (tumor necrosis factor-), 47% (interleukin-6), and 75% (C3a) of the values in the retransfusion group. C-reactive protein, erythrocyte sedimentation rate, and troponin-T increased after surgery in both groups without intergroup differences. Postoperative bleeding and hemoglobin levels did not differ between the groups. No patient received homologous blood transfusion.

CONCLUSIONS: Coronary surgery without retransfusion of cardiotomy suction blood and mediastinal shed blood reduces the postoperative systemic inflammatory response.

	Introduction

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Cardiac surgery induces a pronounced systemic inflammatory response. The inflammatory response may contribute to organ dysfunction and complications, such as renal failure and bleeding, and has also been associated with myocardial injury [1, 2]. The inflammatory response is complex in its nature and a number of different factors may contribute. Historically, the inflammatory response was generally attributed to the use of cardiopulmonary bypass but in recent years a number of other factors, such as the operative trauma per se, regional ischemia/reperfusion injury, and endotoxin release have been suggested to be of importance [1–4].

Cardiotomy suction (CTS) during cardiopulmonary bypass and postoperative retransfusion of mediastinal shed blood (MSB) are used to maintain an appropriate hemoglobin concentration and to reduce the need for homologues blood transfusions. However, there is a pronounced activation of coagulation, fibrinolysis, and inflammation in CTS blood and MSB [5–9], and retransfusion of this blood has been suggested to contribute to the postoperative inflammatory response. No study has investigated how the postoperative inflammatory response is modulated if retransfusion of CTS blood and MSB is completely evaded. The aim of the present investigation was, therefore, to compare the inflammatory response, myocardial injury, and postoperative bleeding when cardiotomy suction blood and mediastinal shed blood are either discarded or retransfused. For this purpose, a randomized prospective study was performed in patients undergoing coronary artery surgery.

	Patients and methods

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Patients
Inclusion criteria were age 40 to 80 years, two- or three-vessel coronary artery disease with stable angina pectoris and appropriate coronary anatomy for coronary artery bypass grafting, left ventricular ejection fraction more than 40%, and no other significant disorders. Exclusion criteria were preoperative use of steroids or nonsteroidal anti-inflammatory drugs, perioperative myocardial infarction, postoperative low output heart failure, and reoperation for bleeding. As the local clinical routine at the time of the study was to retransfuse cardiotomy suction blood and mediastinal shed blood, the study protocol had a paragraph that excluded patients from the study if they had either more than 500 mL blood in the separate cardiotomy suction reservoir or a mediastinal shed bleeding more than 500 mL during the first 12 hours. If a patient reached any of these limits, the blood was retransfused and the patient excluded from the study.

Thirty-five patients were originally included in the study and randomly allocated before surgery after informed consent. Six patients were excluded from the study after surgery, 4 because of cardiotomy suction blood volume or postoperative bleeding more than 500 mL and 2 because of electrocardoigraphic signs of perioperative myocardial infarction. The study group therefore consists of 29 patients with a mean age of 65.8 ± 1.6 years; 86% were men. Patient characteristics are given in Table 1. The study protocol was approved by the Research Ethics Committee of the Medical Faculty, University of Gothenburg.

The operations were performed with standard nonpulsatile CPB technique with moderate hypothermia (nasopharyngeal temperature 34°C) and hemodilution (hematocrit 20% to 30%). No topical cooling was used. Cardioprotection was achieved with cold blood cardioplegia. Weaning off CPB was performed after rewarming to a rectal temperature of at least 36°C. Patients were weaned from respirator when their body temperature was 37°C, no abnormal bleeding, and a stable circulatory and respiratory situation was present.

Study protocol
The patients were randomly allocated into two groups: in the retransfusion group (n = 12), CTS blood during CPB and mediastinal shed blood during the first 12 postoperative hours were retransfused. The CTS blood was collected during CPB and retransfused immediately before weaning CPB. In the no-retransfusion group (n = 17), all cardiotomy suction blood and mediastinal shed blood were discarded.

Plasma concentrations of the proinflammatory cytokines tumor necrosis factor- (TNF-) and interleukin-6 (IL-6) and complement factor C3a were measured preoperatively and 10 minutes after CPB discontinuation (before protamine administration), and 2 hours and 24 hours after CPB. Autotransfusion of mediastinal shed blood in the transfusion group started after the 2-hour sampling. All samples were collected from a radial or femoral arterial line. Samples were also collected from the separate cardiotomy suction reservoir before retransfusion.

C-reactive protein, erythrocyte sedimentation rate, troponin-T, and hemoglobin were analyzed preoperatively, and 24 hours and 48 hours after CPB. Postoperative bleeding during the first 12 postoperative hours and time on ventilator was registered.

Analyses
Samples for cytokine and complement analyses were collected into tubes with ethylenediaminetetraacetic acid and placed immediately on ice. The aliquots were centrifuged immediately and the resultant plasma was stored at –70°C until analysis. The C3a, TNF-, and IL-6 were determined with commercially available enzyme-linked immunosorbent assay (ELISA) kits using double antibody ELISAs according to the manufacturer's instructions. The following assays were used: C3a (Quidel, San Diego, CA); IL-6 and TNF- (R&D systems, Minneapolis, MN). Troponin-T, C-reactive protein, erythrocyte sedimentation rate, serum creatinine, and hemoglobin levels were analyzed with standard clinical methods.

Calculations
Hematocrit varied substantially between the measurement points during the first 24 hours. Plasma concentrations of TNF-, IL-6, and C3a were therefore corrected for hematocrit by relating every measurement to a standard hematocrit value of 40% according to the following formula: corrected concentration = measured concentration x (standard hematokrit/measured hematocrit). Changes in serum concentrations of the proinflammatory mediators from the preoperative measurements were calculated according to the formula: delta concentration = measured concentration – baseline concentration.

Statistics
The nonparametric Mann-Whitney U test (continuous variables) or ² test (categorical variables) was used to establish whether the randomization process had provided groups that were comparable, and to compare postoperative bleeding and time on ventilator between the two groups. The nonparametric Wilcoxon paired test was used to compare inflammatory mediators at baseline and in cardiotomy suction blood. Two-way analysis of variance (ANOVA) with correction for repeated measurements was used to evaluate differences in concentrations of TNF-, IL-6, C3a, C-reactive protein, erythrocyte sedimentation rate, troponin-T, serum creatinine, and hemoglobin levels between the groups, followed by Student's t test if group or interaction between group indicated a significant difference. Correlation was analyzed with Spearman's rank-sum test. Statistical significance was defined as p less than 0.05. All the results are expressed as the mean ± standard error of the mean (SEM).

	Results

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Clinical course
All patients recovered normally after surgery and were discharged from the hospital within seven days. None of the patients received any homologous or predonated autologous blood or blood product transfusion.

Baseline characteristics
There were no statistically significant differences between the groups with respect to age, sex, or number of grafts (Table 1). Cardiopulmonary bypass time was longer in the no-retransfusion group (59 ± 3 versus 48 ± 3 minutes, p = 0.030 and aortic clamp time tended to be longer (p = 0.051). Mean volume of cardiotomy suction blood was 267 ± 37 mL in the retransfusion group and 204 ± 24 mL in the no-retransfusion group (p = 0.20). In the retransfusion group, the mean volume of retransfused mediastinal shed blood was 218 ± 24 mL. In the no-retransfusion group 360 ± 21 mL mediastinal shed blood was discarded.

Inflammatory response: cardiotomy reservoir
Plasma concentrations of TNF-, IL-6 and C3a were significantly elevated in cardiotomy suction blood compared with systemic plasma concentrations at baseline (TNF-: 5.7 ± 1.0 versus 2.8 ± 1.0 pg/mL, p = 0.005; IL-6: 45.0 ± 7.8 versus 4.5 ± 1.0 pg/mL, p < 0.001; and C3a: 3,300 ± 445 versus 579 ± 64 ng/mL, p < 0.001, all patients). There were no differences in cytokine and complement concentrations in cardiotomy suction blood between the retransfusion and no-retransfusion groups (data not shown).

Plasma
At baseline, plasma concentrations of TNF-, IL-6, and C3a did not differ significantly between the retransfusion group and the no-retransfusion group (TNF-: 1.6 ± 0.7 pg/mL versus 3.6 ± 1.6 pg/mL, p = 0.67; IL-6: 5.4 ± 1.3 pg/mL versus 4.0 ± 1.5 pg/mL, p = 0.13; and C3a: 525 ± 82 ng/mL versus 613 ± 92 ng/mL, p = 0.65).

Plasma concentrations of TNF-, IL-6, and C3a increased after surgery in both groups (Table 2). The increases in IL-6 and C3a differed significantly between the groups with a more pronounced inflammatory response in patients operated on with retransfusion of cardiotomy suction and mediastinal shed blood. Tumor necrosis factor- tended to be higher in the retransfusion group but the difference did not reach statistical significance (p = 0.063; Table 2).

View this table: [in this window] [in a new window]   Table 2. Changes From Baseline in TNF-, IL-6, and C3a Concentration in Retransfusion and No-Retransfusion Groups

View larger version (13K): [in this window] [in a new window]   Fig 1. Volume of retransfused cardiotomy suction blood versus absolute tumor necrosis factor (TNF-) concentrations 24 hours after surgery in the retransfusion group. There was a significant correlation (Spearman's test) between the two variables (n = 12, r = 0.63, r2 = 0.40, p = 0.027, regression equation: y = –1.3 + 0.01x). (CPB = cardiopulmonary bypass.)

View this table: [in this window] [in a new window]   Table 4. Correlation (Spearman's Test) Between Amount of Retransfused Cardiotomy Suction Blood and TNF-, IL-6, and C3a Concentrations Corrected for Hematocrita

View larger version (13K): [in this window] [in a new window]   Fig 2. Volume of retransfused cardiotomy suction blood versus hemoglobin levels 48 hours after surgery in the retransfusion group. There was a significant negative correlation (Spearman's test) between the two variables (n = 11, r = –0.79, r2 = 0.62, p = 0.004, regression equation: y = 128 – 0.08x). (CPB = cardiopulmonary bypass.)

	Comment

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

The influence of CTS and autotransfusion of MSB on postoperative systemic inflammatory response is not fully understood. Practically all studies on the subject have demonstrated elevated levels of inflammatory mediators in CTS and MSB and therefore concluded that retransfusion of CTS and MSB contributes to the postoperative response [5–9]. However, the studies do not clarify the magnitude of the contribution. If the retransfused volume is small (compared with the total blood volume), the contribution to the total postoperative inflammatory response could be insignificant even if the concentrations are high. On the other hand, the amount of retransfused blood may be irrelevant since a small amount of highly activated blood may trigger pathways within the systemic circulation.

The impact of CTS has recently been investigated in two prospective randomized studies with contradictory results. Aldea and associates [5] investigated inflammatory response in patients undergoing coronary artery bypass grafting with heparin-bonded circuits and found that postoperative inflammatory indicators were generally reduced in the group where CTS was eliminated, whereas Svenmarker and associates [6] could not detect any differences. The present investigation differs from these two studies in two important aspects. First, the control group in both these studies received cell-saving device processed CTS blood, in contrast to the present study in which CTS blood was completely discarded. It has been demonstrated that inflammatory mediators remain above the reference levels after cell-saving device processing [10, 11], and it is therefore unclear to what extent cell-saver devices reduces key inflammatory mediators in CTS blood and, accordingly, whether a cell-saving device group is an appropriate control group. Second, in the present study, cytokine and complement measurements were corrected for hemodilution [12] owing to the large intraindividual and interindividual variation seen in hematocrit at baseline and during the first 24 hours (range in this study, 24% to 46%).

In the present investigation significantly lower IL-6 and C3a concentrations and a tendency toward lower TNF- levels (p = 0.063) were detected in patients operated without retransfusion of cardiotomy suction blood and mediastinal shed blood. Tumor necrosis factor-, IL-6, and C3a are not only markers of inflammation but have important pathophysiologic effects [13, 14]. Tumor necrosis factor- increases stress hormone release and neutrophil adhesion, causes myocardial depression and stimulates production of other cytokines such as IL-6 and IL-8. Interleukin-6 mediates vasodilation and impairs cardiac function while C3a contracts smooth muscle and increases vascular permeability. Complement factor C3a is also myocardial depressive. Therefore, it is advantageous if these proinflammatory factors in the circulation could be eluded, and our results show that this could be achieved by avoiding retranfusion of CTS blood and MSB. Further evidence for the importance of CTS for the postoperative inflammatory response is the correlation between the amount of retransfused blood and TNF- levels after surgery in the retransfusion group (Fig 1).

One side effect of avoiding perioperative and postoperative retransfusion of autologous blood could be an increased need for homologous blood transfusions. In the present study did the retransfusion group receive approximately 500 mL more autologous blood than the no-retransfusion group, but this difference was not reflected in postoperative hemoglobin levels, which did not differ significantly between the two groups 24 and 48 hours after surgery. In fact, there was a negative correlation between the amount of retransfused CTS blood and hemoglobin levels both at 24 and 48 hours after surgery in the retransfusion group (Fig 2). Even if correlation data should be interpreted with caution, the results indicate that it may be advantageous to refrain from retransfusion of the traumatized CTS blood if the volumes are small to moderate. The results are also in accordance with the study by de Haan and associates [15] in which retransfusion of suctioned blood during cardiopulmonary bypass impaired hemostasis and exacerbated postoperative bleeding, although postoperative bleeding did not differ between the groups in our study. However, one must consider that our study was powered to detect differences in the release of early inflammatory markers and a study with clinical end-points would require a substantially larger patient population.

The cease of CTS may also have another advantage. The CTS blood contains lipids, and experimental data suggest that the CTS lipids represent a significant source for microembolization [16, 17], which subsequently has been associated with diffuse brain injury after cardiac surgery [18]. The importance of CTS for postoperative neurologic dysfunction needs to be investigated in clinical studies.

The present study has important limitations. First, since both CTS and MSB were discarded in the no-retransfusion group, we cannot discriminate between the effects of either component after the 2 hours after CPB sampling. The sampling at 10 minutes and 2 hours after CPB were performed before autotransfusion was started and can therefore be regarded as representative for CTS. Second, despite the randomization process, the groups were not completely comparable, as CPB time was longer in the no-retransfusion group. Operation time may increase the magnitude of the inflammatory response. In the present investigation, however, the group with the longest operation time (no-retransfusion group) had a lesser inflammatory response. This finding suggests that the demonstrated difference in inflammatory response may be even more pronounced if the groups had been comparable. Furthermore, the investigation was performed in low-risk patients undergoing standard coronary artery bypass grafting with short operation times (Table 1) with a small to moderate perioperative and postoperative bleeding, and we analyzed only a few markers of inflammation. The inflammatory response is extremely complex, and other markers and mediators may react different to CTS and autotransfusion. It should, therefore, be emphasized that the conclusions of this study are limited to the investigated population and the analyzed markers only, and different results may be yielded in a study performed in high-risk patients undergoing longer operations. In addition, as mentioned above, the study was designed to detect differences in cytokine concentrations after coronary artery bypass grafting and lacks therefore statistical power in clinical endpoints.

In summary, the results suggest that coronary surgery, without retransfusion of small to moderate volumes of cardiotomy suction blood and mediastinal shed blood, significantly reduces inflammatory response after cardiac surgery without influencing postoperative hemoglobin levels. The importance of this suggestion needs to be evaluated in larger studies with clinical endpoints.

	Acknowledgments

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
The authors are grateful for the skillful assistance in data collection and laboratory analyses from Marie Jungbeck, Christina Edvinsson, Ola Eidem, and Maria Tylman. The study was supported by the Gothenburg Medical Association.

	References

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 

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This Article Abstract Full Text (PDF) 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): Anders Jeppsson Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Westerberg, M. Articles by Jeppsson, A. Search for Related Content PubMed PubMed Citation Articles by Westerberg, M. Articles by Jeppsson, A. Related Collections Extracorporeal circulation