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Correspondence |
Duke University Medical Center, Durham, USA, E-mail: h.grocott{at}duke.edu
To the Editor:
Dr. Hall’s editorial1 in reference to the work by Kanbak et al.,2 eloquently outlines the pitfalls of using S100ß as a surrogate marker of postcardiac surgery neurologic dysfunction. He explains why S100ß, a glial protein long considered to be a specific marker of brain injury, may be elevated in the setting of cardiac surgery when no apparent neurologic injury (as described by Kanbak et al.)2 has occurred. The reason for this relationship (i.e., lack thereof) relates to apparent sources for S100ß. In addition to glial cells, it has been found in the mediastinal blood and when retransfused to the patient via the cardiotomy suction, subsequently leads to significant elevations in serum S100ß. However, to further clarify this point, one needs to elaborate why an erroneous relationship between S100ß and neurologic injury has repeatedly been made in the literature. It is commonly accepted that some of the particulate lipid-containing debris and blood aspirated by the cardiotomy suction from the mediastinum and pericardium during surgery makes its way back into the venous reservoir and passes through the cardiopulmonary bypass apparatus thus serving as a source of cerebral microemboli.3 In this regard, if the mediastinal drainage can cause injury by increasing cerebral embolization, and in an unrelated epiphenomenal manner also increases serum S100ß due to its apparent high S100ß content, an erroneous S100ß/cerebral injury relationship is realized.4 Importantly, however, further light has recently been shed on the source of this mediastinal S100ß. Fazio et al., have now demonstrated that there is in fact no extracerebral S100ß source in the mediastinum and that the error lies in the lack of S100ß specificity of conventional assays.5 These investigators have elegantly demonstrated that it is other large molecular weight protein contaminants (such as haptaglobin I precursor) that are falsely detected by conventional assays that are responsible for these elevated, although erroneous, S100ß levels. These recent publications reinforce how, at least in the setting of cardiac surgery, S100ß is clearly not ready yet for prime time as Dr. Hall states, and furthermore, likely never will be.6
References
1 Hall RI. Serum S-100ß protein and postoperative neurological dysfunction--ready for prime time? Can J Anesth 2004; 51: 645–8.
2 Kanbak M, Saricaoglu F, Avci A, Ocal T, Koray Z, Aypar U. Propofol offers no advantage over isoflurane anesthesia for cerebral protection during cardiopulmonary bypass: a preliminary study of S-100ß protein levels. Can J Anesth 2004; 51: 712–7.
3 Brooker RF, Brown WR, Moody DM, et al. Cardiotomy suction: a major source of brain lipid emboli during cardiopulmonary bypass. Ann Thorac Surg 1998; 65: 1651–5.
4 Grocott HP, Arrowsmith JE. Serum S100 protein as a marker of cerebral damage during cardiac surgery. Br J Anaesth 2001; 86: 289–90.
5 Fazio V, Bhudia SK, Marchi N, Aumayr B, Janigro D. Peripheral detection of S100beta during cardiothoracic surgery: what are we really measuring? Ann Thorac Surg 2004; 78: 46–52; discussion 52–3.
6 Grocott HP. Invited commentary. Ann Thorac Surg 2004; 78: 52–3.
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