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Ann Thorac Surg 2000;69:847-850
© 2000 The Society of Thoracic Surgeons

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Original Articles

The effect of cardiotomy suction on the brain injury marker S100ß after cardiopulmonary bypass

^a Department of Cardiothoracic Anaesthetics and Intensive Care, Karolinska Hospital, Stockholm, Sweden
^b Department of Clinical Chemistry, Karolinska Hospital, Stockholm, Sweden
^c Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden

Address reprint requests to Dr Anderson, Department of Cardiothoracic Anaesthetics and Intensive Care, Karolinska Hospital, S-171 76 Stockholm, Sweden
e-mail: russell.anderson{at}kirurgi.ki.se

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. An increase of S100ß in serum during cardiopulmonary bypass (CPB) has been interpreted as a sign of brain injury. Cardiotomy suction may cause fat embolization, and its role in the S100ß increase was examined.

Methods. Twenty coronary artery operation patients were randomly assigned to two groups, 10 with suction during CPB to cardiotomy reservoir (CR), 10 to cell saving device (CS). S100ß was measured (immunoassay) in blood from the patients and from cell saving device after processing. In 7 additional patients S100ß was measured in the cell saving device before processing and directly from the wound at sternotomy.

Results. Before anesthesia, serum S100ß was 0.03 ± 0.06 µg/L. At the end of CPB it was 2.47 ± 1.31 µg/L and 0.44 ± 0.27 µg/L (CR vs CS; p < 0.001). S100ß was 33 ± 12 µg/L in CS reservoir and 42 ± 18 µg/L in blood from the wound.

Conclusions. Most serum S100ß after CPB with cardiotomy suction may be of extracerebral origin. S100ß after CPB with cell saving device was the same as after off-pump operation. The interpretation that an increase in S100ß during CPB in patients reflects cerebral injury must be questioned.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Postoperative neurologic deficits after cardiac operation with cardiopulmonary bypass (CPB) range from strokes in a few percent to subtle neurobehavioral dysfunction in a majority of patients [1–4]. Both macroembolization and microembolization have been implicated in these deficits [5–7].

Moody and associates [8] demonstrated the presence of small capillary and arterial dilatations (SCADs) in the brains of patients after operation with CPB, but not after other types of surgical procedures. The capillary dilatations are believed to be the result of lipid microemboli. During histologic preparation, the embolized fat is dissolved and the resulting histologic finding is a SCAD. In a recent study with dogs on CPB, Brooker and colleagues [9] demonstrated 10 times more SCADs in microvasculature of the brains when cardiotomy suction was used than when it was not. They argued that the dilatations to a great extent are footprints of lipid microembolization from blood aspirated from the surgical field and reinfused through the aortic cannula. The clinical significance of these dilatations is not known. There is no proved connection with either the neurobehavioral deficits demonstrated after CPB or to the increased blood concentrations of biochemical markers of brain damage like S100.

S100 is a family of proteins, two of which originate from astroglial and Schwann cells in the brain [10]. With present methods, these two proteins are analyzed together because of a common ß-subunit, and they are therefore collectively designated S100ß. Damaged brain cells release S100ß into the cerebral spinal fluid, but S100ß will only appear in serum if there is a concomitant increase in blood brain barrier permeability [11]. Serum concentration of S100ß has been shown to increase after stroke [12].

S100ß increases 50–100 fold after cardiac operation [13–15], and these findings have supported the association between CPB, microembolization, and brain damage. The postoperative serum concentration increases with duration of CPB and with the number of cerebral emboli detected with transcranial Doppler [5], whereas it decreases if an arterial filter is used in the extracorporeal circuit [16]. A recent study [15] compared the serum S100ß concentration after coronary bypass grafting (CABG) with and without (off-pump) the use of CPB. Compared to off-pump operation, S100ß increased 10 fold after CABG with CPB. The difference was interpreted as a consequence of CPB causing cerebral impairment.

The present work is an extension of Brooker’s study [9], which associated cerebral fat embolization (SCADs) with the use of cardiotomy suction during CPB. The purpose was to determine if the use of the cardiotomy suction contributes to the increase in serum S100ß seen after CABG with CPB. Serum S100ß was determined in two groups of patients undergoing CABG with CPB, one group using conventional cardiotomy suction and the other using a cell saving device.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Patients undergoing elective CABG were studied after informed consent and approval from the local ethics committee. Only patients with normal hemoglobin content and without cerebrovascular, carotid, or other complicating diseases were included. None had a history of heart failure or severely reduced myocardial function. All patients had sinus rhythm and received their normal antianginal medications on the morning of operation. Patient data are presented in Table 1.

Standard nonpulsatile CPB with centrifugal pumps was used for both groups. The extracorporeal system was primed with Ringer acetate and a Maxima Forte (Medtronic Inc, Minneapolis, MN) membrane oxygenator was used with no arterial filters. Blood cardioplegia was used in all patients. The core temperature was cooled, or was allowed to drift to 34°C. Distal anastomoses were made during cardioplegic arrest, whereas proximal anastomoses were sutured with resumed perfusion and a side-biting clamp. All patients received the left interior thoracic artery grafted to the left anterior descending coronary artery. Other vessels were bypassed by saphenous vein grafts (Table 1). Noradrenaline or nitroprusside infusions were used to strive for a mean arterial pressure during CPB of 70 mm Hg.

In the first part of the study, patients were randomly assigned to either a control group, in which standard procedures, including cardiotomy suction were used, or to a study group. In the study group all blood from the surgical field, from skin incision to skin closure, was collected in a cell saving device (Shiley Therapeutic Autotransfusion System; Dideco Shiley SpA, Modena, Italy). After skin closure, it was centrifuged, washed (1000 mL Ringer acetate per 500 mL suctioned blood), recentrifuged to a hematocrit of about 60, and returned to the patient 1 hour after skin closure. Other than this exception, the same equipment and procedures were used.

Protocol for blood sampling
Arterial blood samples were drawn on 9 occasions: before induction of anesthesia, 3 to 4 minutes after heparin administration, at the end of CPB, at skin closure, and at 1, 2, 3, 6, and 20 hours after skin closure. An additional sample was drawn from the washed erythrocyte concentrate in the cell saving device group. The samples were immediately sent for centrifugation, freezing (-20°C), and blinded analysis. S100ß was analyzed by immunoassay Sangtec 100 LIA (Sangtec Medical, Bromma, Sweden). The functional detection limit of the assay is 0.02 µg/L.

The second part of this study was initiated after analysis of the initial two groups of patients. Cell saving device suction was used in this group (n = 7), but only during the period when the cardiotomy suction would have been used (from heparinization until heparin was reversed with protamine). Arterial blood samples were drawn preoperatively and at the end of operation. Blood was also aspirated into 10 mL syringes directly from accumulations in the midline incision before sternotomy, and from the sternal marrow after sternotomy. In addition, a sample was drawn from the suction reservoir before washing and centrifuging. Analysis was as described above.

Statistics
Results are presented as mean ± standard deviation (range). S100ß data were compared using 2-way analysis of variance or Student’s t-test where appropriate. The criterion for significance throughout was p less than 0.05.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
The peak serum value of S100ß was six-fold reduced in the cell saving device group compared to the cardiotomy suction group (Fig 1). The S100ß levels did not differ for the two groups preoperatively, nor after heparinization. S100ß increased slightly (6-fold; p < 0.001) and equally with operation before heparinization, and both groups reached their maxima at end-CPB or postoperatively (the groups’ maximal concentrations differed 5-fold; p < 0.001). S100ß in the washed and centrifuged cell saving device blood (n = 10) was 1.97 ± 0.78 (0.81 to 2.9) µg/L. It was returned to the patient (615 ± 168 mL) immediately after blood sampling 1 hour postoperatively, but did not noticeably affect the level of serum S100ß.

View larger version (14K): [in this window] [in a new window]   Fig 1. Serum S100ß concentration postoperatively with cardiopulmonary bypass during which cardiotomy (n = 10, solid squares) or cell saving device (n = 10, solid diamonds) suction was used. Sampling shown at number of hours postoperatively. (Error bars are standard deviation. *p < 0.001 relative to before operation; **p < 0.001 between groups).

Patients in all 3 groups completed operation without any myocardial infarctions or clinically apparent cerebral incidents. One patient died 3 days postoperatively of arrhythmia and graft occlusion. All patients retained their sinus rhythm and no inotropic support was required. The groups did not differ in age, duration of aortic occlusion, or CPB duration (Table 1).

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
The current study was designed to determine if the experimentally demonstrated reduction of the number of SCADs in dog brains when cardiotomy suction was not used during CPB [9], would be paralleled in patients by a lower increase of the biochemical marker of damaged brain tissue, S100ß. The assumed mechanism would be that by not immediately reinfusing blood from the surgical field through the aortic cannula, there would be less fat microembolization, and consequently less brain damage and a lower serum concentration of S100ß after CPB.

As expected, not using the cardiotomy suction during CABG with CPB reduced by six-fold the serum S100ß concentration seen after conventional CABG with a cardiotomy suction. These results, summarized in Figure 1, show that it is the cardiotomy suction, and not CPB as such, which results in most of the S100ß observed after conventional CABG. The unexpected result of extremely high concentrations of S100ß in the cell saving device reservoir, however, requires a different interpretation than the hypothesis of this study. The increase in serum S100ß seen during and after conventional CABG must largely originate from extracerebral sources. Furthermore, the observation that the small increase in serum S100ß seen after CPB without cardiotomy suction is identical to the small increase seen after off-pump CABG [15], indicates that CPB as such contributes nothing or only negligibly to the increased S100ß seen after CABG.

The simplest proof of the existence of extracerebral sources of S100ß is that blood aspirated from the midline incision before sternotomy contains 200 times more S100ß than preoperative serum. Even larger amounts are seen in sternal bleeding after the sternotomy. The high S100ß content in the cell saving device reservoir confirms the conclusion that the six-fold greater increase in serum S100ß, seen when the cardiotomy suction is used, results from the admixing of extracerebral S100ß from blood aspirated from the surgical field.

Although many studies have supported the hypothesis that microemboli were the etiology of the S100ß increase observed after CPB, in retrospect many of these finding can be instead correlated with the use of cardiotomy suction. These include the correlation of S100ß with duration of CPB and aortic occlusion [13, 15] and even the smaller increase associated with the use of a heparinized CPB system [17]. Similarly, our recent study showing a six-fold smaller difference in S100ß after pump and off-pump (with sternotomy) CABG [15], can be explained by the cardiotomy suction without implicating CPB as such. Similarly, our correlation of the number of anastomoses and serum S100ß [15] could also be explained simply by the time and extent of suction. More difficult to explain, however, is the correlation of S100 with the number of emboli counted with transcranial Doppler during the period between aortic cannulation and cross-clamp onset [18], or the lesser increase in S100ß associated with the use of a CPB arterial line filter [16]. Perioperative strokes result in prolonged S100ß release [14].

Other puzzling questions remain. The same small increase in S100ß was seen in the cell saving device group in the present study and in the off-pump group with sternotomy in our previous study [15]. That is, the surgical procedure itself causes an increase in serum S100ß of unknown origin. Furthermore, those off-pump patients in that study having a sternotomy had almost twice the serum S100ß seen after a minithoracotomy, perhaps reflecting larger amounts of surgically released from the larger wound. Although the present study cannot exclude a cerebral origin, the extracerebral sources of S100ß are probably overwhelming in comparison.

As the currently used assay measures at least two different forms of S100 proteins, this study and present methods of analysis cannot even determine if the S100ß in blood aspirated from the surgical field is the same protein(s) as that appearing in serum because of the surgical procedure itself. The commercial immunoassay used in this study uses three different monoclonal antibodies directed against the ß-subunit of these dimeric proteins, and it will therefore detect any S100 protein that contains at least one ß-subunit. Other members of the S100 family, which do not contain any ß-subunit, are found in striated muscle, heart, and kidney and should not be detected by present methods of analysis [10]. The two dimers that are known to be analyzed together as S100ß consist of a protein containing only a single ß-subunit (plus an -subunit) and one with (designated S100B) two ß chains. Both should only originate from glia and Schwann cells, and S100B with two ß-subunits dominates 30 to 100 fold [19]. The literature often uses S100ß and S100B interchangeably, as all contributions to S100ß other than S100B have been assumed to be negligible. The literature is now cluttered with artifacts because of this methodological problem.

The original study design was flawed by neglecting to determine the S100ß concentration in the cell saving device reservoir before processing. S100ß in the processed cell saving device blood was incorrectly assumed to be very low and was measured only to be able to determine how much S100ß was returned to the patients 1 hour postoperatively. As S100ß is washed away in the cell saving device processing, the finding of high S100ß in the concentrate was sufficient to conclude that the reservoir concentration was at least 10 times higher. For confirmation, however, the 7 extra cell saving device patients, in whom S100ß was measured in the reservoir and directly from the initial skin incision and sternal marrow bleeding, were studied after the first two groups were analyzed. The serum values of S100ß did not change from part 1 to part 2 of the study.

The plot of S100ß concentration does not show any positive inflection when the patients are autotransfused with cell saving device blood between the sampling at 1 and 2 hours postoperatively. Although this blood had a relatively high S100ß concentration, it was only about 10% of the total blood volume and contributed little to the net serum concentration.

The original hypothesis of this study of fat microembolization from the cardiotomy suction, can neither be supported nor refuted by the data reported here. However, this study has demonstrated that CPB itself does not cause an increased release of serum S100ß detectable with present methods. The dominant increase in S100ß previously ascribed to CPB is an artifact mainly because of S100ß from extracerebral origins, which is returned to the circulation through the cardiotomy suction. Until methodologic problems are solved, S100ß should be used with caution as a serum marker of brain damage after operation with CPB, and the cardiotomy suction absolutely avoided in such investigations.

	Acknowledgments

 
We gratefully acknowledge the technical assistance of Gunilla Barr and Rumjana Dijlai-Merzoug. This study has been supported by the Swedish Heart Lung Foundation and the Swedish Medical Research Council (grant no. 11235).

	References

Top Abstract Introduction Patients and methods Results Comment References

 

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