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Ann Thorac Surg 1999;68:2202-2208
© 1999 The Society of Thoracic Surgeons
a Departments of Cardiothoracic Surgery and Medical Neurochemistry and Institute of Laboratory Medicine, University Hospital Lund, Lund, Sweden
Address requests for reprints to Dr Jönsson, Department of Cardiothoracic Surgery, University Hospital Lund, SE-221 85 Lund, Sweden
e-mail: henrik.jonsson{at}thorax.lu.se
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Abstract |
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 Top Abstract IntroductionPatients and methodsResultsCommentReferences |
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Methods. Three groups of patients were investigated. All patients underwent coronary artery bypass surgery (CABG) with extracorporeal circulation. In group A, 110 patients had sampling of S100ß for the first 10 postoperative hours and also underwent neuropsychological testing. In group B, 14 patients were examined for the effect of autotransfusion on S100ß levels. Eight patients in group C had their intraoperative bleeding processed with a cell-saving device.
Results. Group A had a heterogeneous release pattern with several rapid elevations in S100ß concentration. In group B, high concentrations of S100ß were found in the autotransfusion blood (range 0.2 to 210 µg/L) with a concurrent elevation of serum S100ß levels after transfusion of shed blood. In group C, high levels of S100ß were found in the blood from the surgical field (12.0 ± 6.0 µg/L) and decreased (1.1 ± 0.64 µg/L) after wash. Group C had significantly lower S100ß values at the end of cardiopulmonary bypass compared to group A (0.53 ± 0.35 µg/L versus 2.40 ± 1.5 µg/L). S100ß values were corrected for extracerebral contamination with a kinetic model. With this correction, an association was found between adverse neuropsychological outcome and S100ß release in group A (r = 0.39, p < 0.02).
Conclusions. A significant amount of S100ß is found both in the blood from the surgical field and in the shed mediastinal blood postoperatively. Infusion of this blood will result in infusion of S100ß into the blood and interfere in the interpretation of early systemic S100ß values.
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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berg T. S-100 and memory function after cardiac surgery. Presented at the European Association of Cardiothoracic Surgery meeting, Prague 1996. Unpublished). As we and others have reported [6–8], virtually all patients undergoing CPB seem to release S100ß immediately after CPB. To date, this early release has not been associated with a postoperative neurological morbidity. It would therefore be most valuable to investigate whether this early release could be associated with a cognitive dysfunction after operation.
S100ß is a 21 kDa, calcium-binding protein and exists in several isoforms. The S100
ß and S100ßß forms are predominantly present in astroglial or microglial cells, are considered to be highly specific for the brain, and are commonly called S100ß [9].
The aim of the present study was to characterize the S100ß release in detail in a well-defined patient population undergoing coronary artery bypass grafting (CABG) as sole procedure and correlate it to cognitive dysfunction after surgery, measured with neuropsychological tests. During the early evaluation of the material an unexpected extracerebral source of S100ß was identified and the study was extended with two new groups to explain this extracerebral source of S100ß.
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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Clinical variables, such as angina score (Canadian Cardiovascular Society Classification of Angina Pectoris, CCS), ejection fraction, duration of cardiopulmonary perfusion, amount of postoperative bleeding, and reinfused shed mediastinal blood (autotransfusion) were retrospectively registered from patient records. The patients were examined for signs of neurological dysfunctions daily during the hospital stay by either experienced cardiac anesthesiologists or by experienced cardiac surgeons.
The patients were divided into three groups. Group A consisted of 110 patients, who underwent repeated neuropsychological tests the week before surgery and 2 times postoperatively. Blood for the analysis of S100ß protein was sampled from each patient before surgery, at the end of CPB (T0), and then hourly during the first 10 hours, thereafter at 15 (T15), 24 (T24), and finally 48 (T48) hours after the end of CPB.
After preliminary analysis of S100ß levels we found unexplained and transient increases in serum levels of S100ß and we designed two new groups. These groups were examined for the effects of all types of retransfused blood, ie, from the autotransfusion used postoperatively and from the cardiotomy suckers during operation, on serum S100ß levels.
Group B consisted of 14 patients. Blood samples were drawn both from the cardiotomy reservoir and from the patient before and after the retransfusion of the shed mediastinal blood. The amount of retransfused blood was recorded each time.
Group C consisted of 8 patients, where a cell-saving device was connected to the bypass circuit for the collection and washing of cardiotomy suction blood from the operating field during bypass. The washed blood was saved and retransfused 3 hours after termination of CPB. Thus, no blood directly from the operating field was retransfused during or after the operation. S100ß levels in the collected blood were measured both before and after wash, and from the patient at the end of CPB, 1, 2, 3, 5, 15, and 48 hours after termination of CPB.
Anesthesia
Anesthesia was induced with midazolam 3 to 5 mg iv (Dormicum, Roche, Basel, Switzerland) or propofol 10 mg/kg. It was subsequently maintained with fentanyl 10 µg/kg (Leptanal, Janssen Pharmaceutica, Beerse, Belgium), continuous infusion of propofol 3 to 6 mg/kg/h (Diprivan, Zeneca Ltd, Macclesfield, England) or isoflurane 0.5% to 1% (Abbott Laboratories, North Chicago, IL). Nitrous oxide (Aga Industries, Stockholm, Sweden) was used before but not during or after CPB.
Surgical technique
CABG was performed during aortic cross-clamping with the distal anastomosis preceding the proximal anastomosis. A tangential occluder replaced the cross-clamp during the proximal anastomosis. Antegrade cold St Thomas crystalloid cardioplegia was used (Cardioplegi, Pharmacia-Upjohn, Uppsala, Sweden) and administered in the ascending aorta and the anastomosed vein grafts intermittently.
Perfusion technique
Perfusion was performed with a roller pump (Cobe Industries, Denver, CO). The perfusion catheters and circuit were made of polyvinyl chloride in the catheter and silicon in the pump head. The arterial perfusion catheter was inserted in the ascending aorta. A two-stage venous cannula drained the heart through the right atrial appendage. All circuits contained a heparin-coated 40 µm arterial filter (Cobe Science, Cobe Industries) and a membrane oxygenator. In the first 27 patients the Cobe CMS oxygenator (Cobe Industries) was used, whereas the remaining 105 patients had the Cobe Duo oxygenator (Cobe Industries). The reason for this change was that the company took the CMS oxygenator out of production. The circuit was primed with approximately 1500 mL (CMS) or 1000 mL (Duo) of Ringer’s lactate (Pharmacia-Upjohn), 250 mL 15% mannitol (Pharmacia-Upjohn) and 75 mmol Addex tromethamine (Pharmacia-Upjohn). Perfusion flow was nonpulsatile with a flow rate of 2.4 L/min/m2 at normothermia or slight hypothermia. The perfusate was cooled to approximately 32°C. Heparin (3 mg/kg body weight) was given prior to cannulation and reversed with equal doses of protamine sulfate at decannulation. The mean arterial pressure (MAP) was maintained above 40 to 50 mm Hg with intermittent doses of norepinephrine if needed.
Postoperative care
After operation, the patients were moved to the intensive care unit for recovery and were extubated when they had regained normal body temperature and were able to breathe spontaneously. In groups A and B, the shed mediastinal blood was collected in the cardiotomy reservoir previously used during the operation, and retransfused to the patients by an autotransfusion system. Autotransfusions were given intermittently, usually after the collection of 200 to 300 mL, with a maximal interval of 4 hours. The transfusions were administered quickly, often during less than 30 minutes. The autotransfusion system was used no longer than 18 hours postoperatively. If clinically indicated, allogeneic blood transfusions were given.
Blood wash
In group C, a centrifugal cell-saving device (Electromedics AT-1000, Medtronics Inc, Anaheim, CA) was used to wash all blood from cardiotomy suckers. This blood was collected in a separate cardiotomy reservoir (Electromedics EL 240 with a 40 µm filter, Medtronics Inc) and it was primed with 50 mL of ACD solution (Baxter Healthcare, Thetford, England). The washing procedure was started after the termination of CPB, utilizing the cell-saving device with a 125-mL centrifuge bowl (Medtronics Inc). At each wash, 1000 mL of 0.9% saline was used at a speed of 200 mL/min.
Neuropsychological method
All patients in group A underwent repeated neuropsychological testing by the same trained psychologist in the same room. The test was performed one week before the operation and again at approximately 14 days and 2 months after the operation. The Wechsler Memory Scale (WMS-R) was used as a test battery [10]. The subtests included were Mental Control, Figural Memory, Logical Memory I, Verbal Paired Associates I, Visual Paired Associates I, Visual Reproduction I, Digit Span, Visual Memory Span, Logical Memory II, Visual Memory II, Verbal Paired Associates II, and Visual Reproduction II.
Differences for each subtest were first calculated and then standardized to Z values. All subtests were then aggregated to create two impairment indexes. The impairment indexes were continuous variables where a positive value reflected an improvement in neuropsychological test and a negative value reflected deterioration. The impairment index was dependent on age and preoperative test score, and these two factors were controlled for using multiple regression analysis. The final impairment indexes used were residuals from this analysis.
S100ß-protein analysis
Blood samples, both arterial and venous samples, were cooled and centrifuged within 5 hours. All samples were measured by a monoclonal two-site immunoradiometric assay (Sangtec 100, AB Sangtec Medical, Bromma, Sweden). The method is defined by three monoclonal antibodies: SMST 12, SMSK 25, and SMSK 28. The serum samples were diluted with phosphate buffer and incubated with a plastic bead coated with monoclonal S100ß antibodies. During incubation S100ß is bound to the antibody-coated bead. After 1 hour of incubation, these beads were washed and incubated with iodine-125-labeled anti-100ß antibody. After a 2-hour incubation and subsequent washing, the amount of radioactive label bound to immobilized S100ß was measured by gamma counter. The precision was 7.0 CV% (coefficient of variation) and sensitivity was 0.2 µg/L.
Adjusted s100ß release
Based on the information presented later on an extracerebral contamination, a kinetic model was formulated that could approximate the true cerebral release. Three assumptions had to be made concerning the kinetics of S100ß release and elimination to achieve an indirect value of true cerebral release of S100ß in group A: (1) The release measured in patients operated with cell-saving device (group C) is of cerebral origin; (2) Clearance of S100ß from blood in our patients is the same for all patients. As a consequence, a prolonged biological elimination rate for the individual would depend on a novel release. In our material, all patients had a S-creatinine less than 2.0 mg/dL. So far, no publications have shown that a limited renal dysfunction influences the elimination rate of S100ß, and we therefore assumed that the clearance from plasma was constant; (3) 22 kDa protein follows the same pattern of kinetics as albumin after operation and does not undergo any substantial redistribution to other compartments besides the plasma [11].
Cerebral s100ß calculations
According to Rang and Dale [12], the individual elimination rate for the first 4 postoperative hours was calculated as follows:
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Accepting the above mentioned assumptions, this rate could be used as an indirect measurement of the cerebral S100ß release. To explain this kinetic model, elimination curves were constructed for three different scenarios, as presented in Figure 1.
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Results |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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The release pattern of S100ß is illustrated in Figure 2. The mean S100ß concentration peaked at (T0), 2.40 ± 1.5 µg/L. Thereafter, a continuous decrease in mean values was seen. The lowest mean value, 0.23 ± 0.13 µg/L, was seen at the end of the study period 48 hours after surgery.
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Cp, where Vd = volume of distribution, QA = amount S100ß given with autotransfusion, and Cp = shift in serum concentration of S100ß). Two extreme outliers were found (Vd = 3.5L and Vd = 240L) and excluded since their calculations were based on very low levels of S100ß, either close to or below the detection limit. The mean distribution volume for S100ß was 8.8 L (SD 1.5 L).
Cell-saving device group (C)
The mean release pattern in this group is showed in Figure 2 (open circles). The blood collected from the operating field had a mean volume of 932 mL (SD 406 mL) and a mean S100ß concentration of 12.0 µg/L (SD 6.0 µg/L). After processing in the cell-saving device, the mean volume decreased to 210 mL (SD 156 mL) and the mean S100ß concentration was 1.14 µg/L (SD 0.64 µg/L). The group had overall lower postoperative S100ß-values as compared to patients without blood wash and with autotransfusion (Fig 2). The peak S100ß concentration occurred in all patients 1 hour after the termination of CPB, which differed from the patients in group A, who had their peak value at the termination of CPB, as illustrated in Figure 3.
Neuropsychological test results
The 90 patients in group A that completed both the preoperative test and the first of the postoperative tests were used in the final analysis. Eighty-eight of these had also completed the second postoperative test.
In multiple regression analysis of the 2-week follow-up, there was a significant correlation (r = 0.39, p = 0.02, Table 2 ) between the neuropsychological impairment index (dependent variable) and the S-100 elimination rate during the first 4 hours (independent variable). This correlation did not persist at the 2-month neuropsychological test.
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Comment |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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berg T. S-100 and memory function after cardiac surgery. European Association of Cardiothoracic Surgery meeting, Prague, 1996. Unpublished). When autotransfusion is part of the postoperative routine, it is usually discontinued after 5 to 10 hours. Therefore, the addition of S100ß from shed mediastinal blood during this period obscures possible cerebral release of S100ß and explains the contradictory findings of the significance of the S100ß values at the end of CPB [1, 8]. The very early samples reflect more the extracerebral contamination from autotransfusion and from cardiotomy suckers rather than the true release from the brain. In the present study, the difference in mean S100ß values for the washed group (group C) as compared to the main group (group A) was almost fivefold, implicating that the S100ß protein detected in systemic blood directly after the termination of CPB is due largely to contamination.
An estimation of the elimination of S100ß after autotransfusion can be made from the concentration curves shown in Figure 3. The concentration decreases more than 50% during 1 hour indicating that the biological half-time for S100ß is well below 60 minutes, as compared to the 113 minutes that have been reported for the S-100 form [13].
These findings have direct implications for the use of S100ß as a marker for cerebral injury in clinical practice. If autotransfusion is used, S100ß measurements can hardly be used with any accuracy until a couple of hours after the termination of the autotransfusion. However, if no autotransfusion is given, the S100ß from the cardiotomy suckers will be excreted within a couple of hours after the end of surgery. Therefore, high levels of S100ß after 2 to 3 hours post-CPB may reflect an increased release from cerebral sources. Future studies should consider this interference and select the sampling interval accordingly.
However, if a blood-washing system is used, the interference is substantially reduced and possibly negligible in comparison to the true release, as seen in the release curves from group C (Fig 2). About 2 hours after the possible cerebral insult, all patients reached their peak S100ß-levels with a slow decrease of S100ß levels during the next few hours. This release pattern resembles that of other serum markers for cellular damage (eg, CK, CK-BB, troponin) as compared to the uneven release pattern seen in group A. The time from the onset of the insult, ie, the start of perfusion, to the maximum release does not indicate whether this is a release of intracellular deposits, a new synthesis due to an upregulation of the S100ß gene, or diffusion of extracellular S100ß in conjunction with a permeability shift of the blood-brain barrier.
Our finding that S100ß concentration is high in mediastinal blood raises the question of the cellular origin of this S100ß. The protein is found in cells of mesenchymal origin (eg, in adipocytes as well as in glial and Schwann’s cells). The concentration in adipocytes is, however, small compared to the concentration in brain cells [14, 15]. Suzuki and associates [16] found S100ß release when adipocytes were placed in a medium containing epinephrine. S100ß has also been found in the thymus of newborn, which may be yet another source for the extracerebral S100ß [17].
Another explanation for the high levels found in autotransfusion would be a lack of sensitivity of the radiometric method used to analyze the S100ß isomer. However, this issue was intensely discussed with the manufacturer (Sangtec AB) and they controlled their assay and verified that it is specific for S100ß in both autotransfusion and blood.
A kinetic model, for the evaluation of S100ß release and neuropsychological test results, was introduced. Despite the limitations of this model a possible connection between adverse neuropsychological outcome and increased S-100-release during the first 1 to 4 hours was found. We suggest that this finding is of great importance to anyone interested in neurological complications after cardiac operation. An increased knowledge of how S100ß values should be interpreted will help us to understand some of the mechanisms behind cognitive dysfunction after cardiac surgery. However, methodological problems with our kinetic model for S100ß release must still be considered. The elimination rate could vary with other factors such as redistribution of the protein, renal function, and the uncontrolled infusion of extracerebral S100ß from autotransfusion the first hours.
After correction of the extracerebral contamination by a kinetic model, measured S100ß values were found to correlate with neuropsychological test results. This finding implies that the early S100ß is of value for the evaluation of cerebral dysfunction and indirectly suggests cerebral origin of the early S100ß.
Furthermore, it must be emphasized that we are not measuring S100ß with neuropsychological tests or vice versa; but attempting to quantify a diffuse cerebral trauma with two completely different methods. Given these circumstances, we could not expect to find a high degree of correlation between S100ß release and neuropsychological tests.
The biological role of S100ß is still unclear, but it seems to be involved in dual and conflicting mechanisms. S100ß in low concentrations has neurotrophic qualities, whereas in high concentrations it induces neuronal apoptosis [18]. In rats S100ß has been used to induce experimental autoimmune encephalomyelitis [17].
In view of these findings of detrimental effects of S100ß, our results raise the intriguing question of whether S100ß derived from mediastinum and retransfused by autotransfusion could in any way be harmful to the patient.
In summary, our results show heterogeneous release of S100ß after cardiac operation due to contamination from shed mediastinal blood. The results from neuropsychological test suggest that S100ß could be used as a marker for cerebral dysfunction if the extracerebral contamination could be controlled. These findings implicate the need for further studies on the relation between S100ß release and postoperative cerebral injury.
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Acknowledgments |
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References |
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(alpha alpha) protein is mainly located in the heart and striated muscles. Biochim Biophys Acta 1985;842:146-150.[Medline]
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