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CARDIOVASCULAR ANESTHESIA

Intraoperative Plateletpheresis and Autologous Platelet Gel Do Not Reduce Chest Tube Drainage or Allogeneic Blood Transfusion After Reoperative Coronary Artery Bypass Graft

Departments of Anaesthetics and Cardiothoracic Surgery, Royal Prince Alfred Hospital, Camperdown NSW, Australia

Address correspondence to Dr. Paul Wajon, MB, BS, FFARACS, FANZCA, P.O. Box 70, Gladesville NSW, Australia 1675. Address e-mail to pwajon{at}ozemail.com.au No reprints will be available from the author.

	Abstract

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Platelet-rich plasma (PRP) is postulated to decrease postoperative mediastinal chest tube drainage (MCTD) and allogeneic blood transfusions (ABT) after surgery with cardiopulmonary bypass. However, recent metaanalysis of the literature reveals that few good quality (therapeutic yield) trials that show a benefit have been published. The potential hemodynamic instability caused by plateletpheresis has not been emphasized. We studied the effect of plateletpheresis on MCTD, ABT, and hemodynamic stability in reoperative coronary artery bypass graft patients, a group perceived to be at high risk for ABT. Ninety patients were randomly assigned to Pheresis or Control groups. -Aminocaproic acid was given to all patients. Hemodynamic instability was assessed by degree of volume and inotrope resuscitation required. Part of the sequestered platelet volume was used to make autologous platelet gel, which was applied as a wound sealant. Mean pheresis yield was 30% ± 7% of the circulating platelet mass or 6.4 ± 2.2 allogeneic platelet unit equivalents. Total MCTD did not differ between the groups. There were no differences in mean packed red blood cell, platelet, and plasma transfusion rates. Overall, 52% of the Pheresis group received ABT, versus 55% of the Control group. Fifty-three percent of the Pheresis group patients exhibited significant hemodynamic instability, versus 27% of the Control group (P < 0.05). This study was unable to show any reduction in MCTD or ABT, although the plateletpheresis technique may offset platelet dysfunction caused by aspirin or increased blood exposure to nonbiologic surfaces, or it may compensate for lack of antifibrinolytic use. The significantly increased incidence of hemodynamic instability in the Pheresis group means that the risk/benefit ratio must be determined for individual cardiac surgical units.

IMPLICATIONS: This trial of plateletpheresis in reoperative coronary artery surgery was performed to assess its effect on allogeneic blood product transfusion. Routine antifibrinolytic usage, minimal aspirin, and nonbiologic surface exposure seem to negate any benefit of the technique in these patients. These findings differ from those of other recent reports. The study also emphasizes the potential hemodynamic disturbances related to the pheresis process.

	Introduction

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Surgery using cardiopulmonary bypass (CPB) still accounts for a significant proportion of all allogeneic blood transfusions (ABT) in most developed countries (1). Patients undergoing repeat coronary artery bypass graft (CABG) surgery are considered as particularly at risk for postoperative coagulopathy, blood loss, and ABT (2). Such patients made up to 10%–15% of the cardiac surgical caseload at the authors’ institution when this study was initiated. A major cause of impaired hemostasis after CPB is thrombocytopenia and platelet dysfunction caused by exposure to the extracorporeal circuit. Most investigators have found that the majority of ABTs are required after surgery, rather than during surgery. Hence, if reducing mediastinal bleeding by improving both platelet numbers and function can be achieved, the need for ABT could be decreased.

Prebypass sequestration of platelet-rich plasma (PRP) was first used in cardiac surgery by Harke et al. (3) in 1977, with a reported result of improved platelet function and decreased postoperative bleeding. This sequestered plasma is reinfused after CPB, thus avoiding some of the reduction in platelet number and function associated with CPB. An autologous platelet gel can be easily produced from some of the sequestered PRP and used as a topical wound sealant to further enhance hemostasis. There have been technological and methodological advances in the technique since its introduction and a considerable number of publications with differing outcomes (4). The interpretation and comparison of many of the earlier studies was difficult because of the lack of prospectivity and randomization, inadequate size of or nonhomogenous composition of patient groups, uncontrolled adjuvant drug administration, differences in plateletpheresis techniques and yields, and variable methods of reporting blood transfusion and laboratory data (5). The efficacy of adjunctive autologous platelet gel has not been reported in this patient group. The selective use of the technique in patients who are at greater risk of increased bleeding, such as reoperative CABG surgery patients, is more likely to be beneficial and cost-effective. Finally, the possibility of hemodynamic disturbances during the platelet harvest may influence the decision to use it when the benefit remains unproven.

We hypothesized that therapeutic yield intraoperative plateletpheresis and platelet gel should reduce blood loss and ABT in a homogenous high-risk group of patients undergoing repeat CABG. We also assessed prospectively the hemodynamic effect of the platelet harvesting process in this patient group.

	Methods

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After Ethics Review Committee approval and written informed consent, 90 adult patients undergoing repeat CABG surgery were randomly assigned by using a random-number table to an experimental (plateletpheresis of PRP, Pheresis) group or a Control group. Primary exclusion criteria for the study were thrombolytic therapy within 48 h of surgery, significant renal impairment (plasma creatinine >200 mmol/L), thrombocytopenia (platelet count <100 x 10⁹/L), abnormal platelet aggregation studies or coagulation profile, preoperative intraaortic balloon pump use, concomitant valvular surgery, and patient refusal of blood products. Secondary exclusion criteria were failure to achieve therapeutic platelet yield (defined as a minimum of four platelet unit equivalents), nonhemorrhagic death within 24 h after surgery, postoperative surgical bleeding confirmed at mediastinal reexploration, and intraoperative placement of a ventricular assist device.

Our standard anesthetic techniques were used. General anesthesia was induced with fentanyl or thiopentone and maintained with isoflurane or halothane with N₂O or supplemental doses of fentanyl. Pancuronium was used for muscle relaxation. In addition to the standard venous, radial arterial, and pulmonary artery catheters, an 8F catheter (Gamcath; Gambro/JOKA GmbH, Hechinger, Germany) was inserted into the right internal jugular or subclavian vein for the plateletpheresis in the Pheresis group. All patients received a glyceryl trinitrate infusion.

Plateletpheresis was commenced after induction by use of the Electromedics AT 1000 cell saver (Electromedics Inc., Eaglewood, CO). The blood was separated into three components by using the direct-draw modified buffy coat method of plateletpheresis. Blood was initially withdrawn from the patient at 100 mL/min into a 225-mL bowl at 5600 rpm and the platelet-poor plasma (PPP) separated. The centrifuge was then slowed to 2400 rpm and the draw rate reduced to 50 mL/min, allowing the PRP in the buffy coat and upper red cell layer to be collected. Between 2500 and 3000 mL of blood was processed in three to six such passes, each taking approximately 10 min. Citrate (Anticoagulant Citrate Dextrose-A; Baxter Healthcare, Toongabbie, NSW, Australia) was used as the anticoagulant (12%–15% by volume). The majority of the PPP and the red cells were returned to the patient immediately. The hemodynamic status of the patient was invasively monitored continuously during the pheresis process, and crystalloid (saline) or colloid (Hemaccel; Hoechst, Marburg, W. Germany) fluid replacement was given to maximum volumes of 4 and 1 L, respectively. Hemodynamic instability was considered significant if mean arterial blood pressure could be maintained >60 mm Hg only by transfusion of 4 L saline, 1 L Hemaccel, and the use of inotrope or vasopressor infusion. Myocardial ischemia was diagnosed by the standard ST segment trend changes in leads II or V₅ of the electrocardiogram. If necessary, the process could be terminated or regulated at any time by the supervising anesthetist on clinical grounds. Before CPB, all patients received an initial dose of porcine heparin (Delta West, Bentley, WA, Australia) 400 U/kg and -aminocaproic acid (EACA, Amicar; Lederle Laboratories Division, Cyanamid Australia Pty Ltd, Baulkham Hills, NSW, Australia) 10 g. Supplemental doses of heparin were given as required to achieve and maintain the activated clotting time of longer than 400 s before and during CPB. The cell saver was not used after the onset of CPB.

CPB was performed with our standard equipment and operational procedures. This included the use of a nonpulsatile roller pump, membrane oxygenator, crystalloid prime, and cold crystalloid cardioplegia. Moderate systemic hypothermia was used (25°C–30°C nasopharynx). Heparin 10,000 U was routinely added to the pump prime before CPB. Protamine sulfate 5 mg/kg was given to all patients after termination of CPB. The PRP and any remaining PPP and red cells were transfused before patient transfer to the cardiothoracic surgical intensive care unit (CICU). Approximately 50 mL of PRP from the first pass (P_con) was reserved to produce the platelet gel, which was prepared just before placement of the sternal wires. Ten-thousand units of topical thrombin (Thrombostat; Parke-Davis Pty Ltd, Caringbah, NSW, Australia) were dissolved in 10 mL of 10% CaCl₂. This calcified thrombin solution was then mixed in a 1:6 ratio with the P_con, producing in 10–15 s a firm gel that acts as a wound sealant. It was applied to suture lines, raw areas, and sternal edges just as it began to set. Shed mediastinal blood was reinfused via a closed system by using the oxygenator reservoir. All patients had a 50-mg bolus of protamine administered upon arrival in CICU and repeated 1 h later.

Demographic, operative, and bypass variables, cumulative mediastinal chest tube drainage (MCTD) volumes, baseline and interval hematologic values, blood product transfusions, and length of postoperative hospital stay were measured in all patients. Also recorded in the Pheresis group were 19 variables associated with the plateletpheresis performance and complications.

Our established criteria for transfusion were used. Red blood cells were transfused to maintain the hemoglobin concentration at >7 g/dL during CPB and >8 g/dL after CPB and before hospital discharge. Fresh frozen plasma and platelets were transfused if the patient was bleeding (>2 mL · kg^-1 · h^-1 chest tube drainage) or if the patient was clinically coagulopathic and laboratory tests indicated their use (i.e., fresh frozen plasma if the international normalized ratio was >1.5, if the activated partial thromboplastin time was >45 s, or both of these; platelets if the count was <100 x 10⁹/L).

Before beginning the study, we performed a power analysis based on a retrospective review of 70 patients who had undergone repeat CABG surgery in the preceding 12 mo and on our experience with the same plateletpheresis technique in patients having ascending aorta replacement surgery (Bentall’s procedure) (6). This revealed that the detection of a 60% decrease in the number of repeat CABG patients requiring any ABT with 80% power, = 0.05, required 45 patients in each arm of the study. Parametric data were compared by means of unpaired Student’s t-tests. Discrete variables were compared with ² analysis or Fisher’s exact test, as appropriate. The Mann-Whitney U-test was used to compare nonparametric data. All data were expressed as mean ± SD unless otherwise noted, and differences were considered significant when P < 0.05.

	Results

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Between June 1, 1995, and December 15, 1996, 90 adult patients presenting for repeat CABG surgery were enrolled in the study. Six patients were excluded from data analysis by secondary exclusion criteria. The specific reasons for this were failure to achieve therapeutic platelet yield (three patients, Pheresis group), surgical bleeding confirmed at mediastinal reexploration (one patient, Pheresis group), intraoperative placement of left ventricular assist device (one patient, Control group), and nonhemorrhagic postoperative death within 24 h (one patient, Pheresis group, intractable ventricular arrhythmias at 60 min after intensive care unit arrival). Forty Pheresis group and 44 Control group patients completed the study.

There were no significant differences in patient demographic characteristics and operative details between the Control and Pheresis groups. In particular, the preoperative aspirin exposure incidence, CPB and cross-clamp times, and frequency of use of the internal mammary artery did not differ between the groups. These data are summarized in Table 1. The average PRP volume was 628 ± 126 mL (platelet count, 586 ± 213 x 10⁹/L), equivalent to 30% ± 7% of the circulating platelet mass or 6.4 ± 2.2 allogeneic platelet units. Total cumulative MCTD was not significantly different between the groups, nor were there any significant differences in allogeneic red blood cell, platelet, or plasma transfusion rates. These data are shown in Table 2. With the exception of the hemoglobin level at admission to the CICU, there were no statistically significant differences in hemoglobin concentrations, platelet counts, or coagulation variables between the groups (Table 3). Fifty-three percent of the Pheresis group patients exhibited significant hemodynamic instability versus 27% of the Control group (P < 0.05). There was no significant difference between the groups in the incidence of new ST segment changes before CPB (10% Pheresis group versus 14% Control group). The length of hospital stay did not differ significantly (median, 7.5 days; mean, 10.0 ± 8.9 days in the Pheresis group versus 8.0, 10.7 ± 8.1 in the Control group).

	Discussion

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We found no statistically significant reduction in MCTD or ABT despite achievement of a therapeutic yield of PRP and the use of autologous platelet gel. The obligate blood loss associated with procedures involving CPB implies that a clinically important reduction in total MCTD to <600 mL (the level of our Control group) cannot be expected. More important is the effect of PRP on ABT. Although we found no difference in the percentages of treatment group patients transfused and in the mean number of allogeneic units transfused, there seemed to be a trend toward a significant difference in platelet transfusion. Only one Pheresis group patient received platelet transfusion (4 U), compared with five Control group patients (mean, 7 U). Our sample size was determined with a power calculation based on total allogeneic unit exposures. One based on platelet transfusions may have led us to adopt a larger sample size and allowed this trend to reach statistical significance.

The single hematologic difference between the groups in our study was a lower hemoglobin level in the Pheresis group on admission to the CICU (9.0 ± 1.1 g/dL versus 9.9 ± 1.3 g/dL in the Control group, P = 0.001). The likely explanation for this is hemodilution from the increased fluid resuscitation required during plateletpheresis in the Pheresis group. This trend persisted to eight hours after admission to the CICU but was not statistically significant then, and thereafter there was no difference clinically or statistically. Although the fluid resuscitation was according to predetermined protocol, no volume data were collected prospectively, and thus we cannot confirm our supposition.

Rigorous attention to the cessation of aspirin for elective cases meant that only 17% overall of our patients had been exposed to aspirin within the previous seven days (compared with 85% of those in the Christenson et al. study and 55% in the Stover et al. report) (20, 21). Whether plateletpheresis has a protective effect on aspirin-treated platelets is unknown. Concomitant antifibrinolytic therapy (EACA) was used in our study and that of Stover et al., and this may have contributed to the inability to show a reduction in the already low MCTD reported in these two studies. A recent metaanalysis concluded that the efficacy of EACA was significant and comparable to that of aprotinin (22).

Use of intraoperative cell salvage, ultrafiltration or hemoconcentration devices, or full-flow normothermic bypass results in an increase in exposure to nonbiological surfaces and additional trauma to the formed elements of the blood during CPB. Plateletpheresis may exert a beneficial effect by protecting a significant number of platelets from such additional CPB-related trauma. The fact that we did not use any of these techniques may have made it more difficult to show a benefit from plateletpheresis in our study.

Differences in the transfusion algorithms must also be noted. The algorithm used by Stover et al. (21) was essentially identical to ours and most others reported in the literature. Christenson et al. (20) used much more stringent criteria for both packed red blood cells (hematocrit <20%) and platelet (count <50 x 10⁹/L) transfusions. This would obviously result in less ABT and makes direct comparison of their study with ours and that of Stover et al. difficult. Despite these strict criteria, the Control group of Christenson et al. had a 70% incidence of ABT, compared with 45% and 55% in the Stover et al. study and our trials, respectively.

Only one other study has addressed in detail the issue of risk/benefit in the application of the plateletpheresis technique. Shore-Lesserson et al. (23) commented on the high incidence of hypotension (60%) during reinfusion of the PRP, compared with 16% in their Control group (23). They postulate citrate-induced hypocalcemia or perhaps the "salvaged blood syndrome" as possible causes for this. We did not specifically measure the incidence of hypotension after CPB, because it is a common event for a variety of reasons (surgical handling of the heart, rapid vasodilation, adjustment of vasoactive support), but we were not impressed by any particular susceptibility of the Pheresis group. The PRP reinfused by Shore-Lesserson et al. contained an average of only 2.4 platelet unit equivalents in 15 mL/kg (our calculation from their data, compared with 6.4 U in 8 mL/kg in our PRP) and may thus have contained relatively more citrate anticoagulant than our product. We did, however, prospectively measure the frequency and degree of hypotension during the plateletpheresis process. Although our Pheresis patients had a significantly increased frequency of hypotension than Controls and required additional fluid and vasoactive drug intervention, we were able to complete the planned number of pheresis passes in all patients. The liberal fluid replacement protocol used suggests that significant hypovolemia was unlikely to be the major cause of the observed hypotension, but quantitative data were not collected. Variable surgical stimulation and anesthetic or other drug effect in the presence of ventricular dysfunction could easily potentiate the effect of even relatively minor transient hypovolemia induced by the pheresis process. This hemodynamic instability did not manifest before CPB as an increased incidence of myocardial ischemia (new ST segment changes). Quigley et al. (24) describe a method of low-yield plateletpheresis during CPB in an effort to avoid pheresis-related hemodynamic instability, and of all the trials achieving therapeutic PRP yield, both Stover et al. (21) and Christenson et al. (20) comment only that no PRP collection was aborted for hemodynamic instability. Another author acknowledges the need for vasoactive intervention during pheresis but gives no details (25). We conclude that hypotension is more likely during the pre-CPB period of repeat CABG surgery when withdrawal of blood for therapeutic yield plateletpheresis is performed.

In conclusion, we have shown no reduction in MCTD or ABT in this randomized, controlled, prospective trial of therapeutic yield plateletpheresis in a sufficiently large high-risk group of reoperative CABG surgical patients. Further, we have documented a significant incidence of hemodynamic instability during the plateletpheresis in the treatment group. Our findings differ from some of the other recently published comparable trials, but, because of methodologic differences, the reasons for this cannot be clearly established. We acknowledge that the technique may be of benefit in some institutions and could be considered as one of several strategies available to reduce blood loss and transfusion requirements in cardiac surgery. Where it is used, the efficacy of the technique should be monitored as part of continuing quality assurance, because the cost/benefit may vary among institutions.

	Acknowledgments

 
Financial support for the nonroutine hematologic investigations was provided by Medtronic Australasia Pty Ltd., Northbridge NSW, Australia.

We thank Medtronic Australasia Pty Ltd, Northbridge, NSW, Australia for funding the nonroutine hematologic investigations performed.

	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 Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Wajon, P. Articles by Thrift, B. Search for Related Content PubMed PubMed Citation Articles by Wajon, P. Articles by Thrift, B. Related Collections Blood Heart

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999