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Ann Thorac Surg 1999;68:2013-2014
© 1999 The Society of Thoracic Surgeons
a Department of Cardiothoracic Anesthesia, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
Address reprint requests to Dr Bokesch, Department of Cardiothoracic Anesthesia, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195
e-mail: bokescp{at}ccf.org
Unexpected neurologic dysfunction, be it a stroke, seizures, or even insidious neurobehavioral dysfunction, when associated with a successful cardiac operation is devastating. Very little progress has been made toward reducing neurologic injury from cardiopulmonary bypass despite arterial filters, advances in monitoring, acid–base management, and methods to decrease the embolic load. Recent findings during a multicenter study by Roach and colleagues [1] showed that the present practice is still associated with a 50% incidence of neurologic injury. Neurologic and developmental abnormalities occur in 30% of infants and children undergoing cardiopulmonary bypass [2]. The search for an accurate, rapid, bedside biochemical marker of brain injury is justified not only for diagnosis, but also for the evaluation of strategies for prevention and treatment.
S100ß is a calcium-binding protein found predominantly in glial and Schwann cells in the brain, that regulates intracellular, calcium-mediated, protein phosphorylation [3]. S100ß has been shown to modulate glial cell growth and differentiation, energy metabolism, and the secretory functions of the pituitary gland [4]. Overexpression of S100ß has been proposed as a factor in the pathogenesis of Alzheimer’s disease, Down’s syndrome, multiple sclerosis, and apoptosis [5]. S100ß is normally detected at low concentrations in the serum. Increases in S100ß are believed to occur if, and only if, there is both damage to the glia or Schwann cells and also damage to the blood–brain barrier. Therefore, increased serum concentrations of S100ß can be an early marker of brain damage after stroke, traumatic brain injury, global ischemia, and cardiac surgery with cardiopulmonary bypass [6–8]. Cardiopulmonary bypass is included in the cerebral ischemia category because of the presumed effects of emboli and hypoperfusion disrupting the blood–brain barrier.
Although S100ß may be useful as an indicator of stroke, can it be used during cardiac surgery as a warning of ischemic injury in progress? Muddying the waters (and serum) of S100ß detection are the extracerebral sources of the protein. Besides glial and Schwann cells, S100ß is found in cells of mesenchymal origin that includes fat cells, testes, and the thymus of the newborn [9,10]. Tissue trauma and exposure to epinephrine can release S100ß from fat cells [11]. Indeed, as reported by Jonsson and colleagues [12] in this issue of The Annals of Thoracic Surgery, traumatized tissues from cardiotomy suction during cardiopulmonary bypass is a significant source of S100ß. They found elevated S100ß levels, at concentrations usually associated with brain injury, in the blood returning to the pump (and subsequently to the patient) from the cardiotomy suction as well as from the reinfused blood from the chest tubes. Elimination of S100ß is through the kidneys; therefore, variations in kidney function, common after cardiopulmonary bypass, could also delay the decrease in serum concentrations. Just as elevated troponin T and creatinine kinase-MB can misdiagnose a myocardial infarction after noncardiac operation, falsely elevated S100ß can misdiagnose a cerebral infarction during cardiac operation [13].
Although it is unlikely that reinfused S100ß is crossing back through the blood–brain barrier into the brain and causing neurologic dysfunction, other reinfused mysterious proteins and bad humors from the pump suckers and chest tubes could be contributing to organ dysfunction in the heart, lungs, and kidneys. Indeed, cardiotomy suction has been found to be a major source of lipid microembolization to the brain during cardiopulmonary bypass [14]. We may come to accept that direct transfusion of traumatized tissue and blood back into the patient from the cardiotomy suction or chest tubes is as distasteful as drinking one’s own dirty bath water. This study supports using off-pump surgery whenever possible as suggested recently by Anderson and associates [15].
Traditional methods to assay serum concentrations of S100ß take approximately 3 to 4 hours to perform and require a luminator or scintillation counter for quantitation. Ettinger and colleagues [16] report in this issue of The Annals of Thoracic Surgery a new optical immunoassay to quantitate S100ß in whole blood in less than 20 minutes. This rapid assay allows for prompt evaluation of whole blood for cerebral damage in the operating room or at the bedside in the postoperative intensive care unit. Unfortunately, even rapid assays of S100ß in the operating room during cardiac operation could be misleading. How does one differentiate brain injury from cardiotomy suction-induced release of S100ß in the operating room? Although Jonsson and colleagues [12] attempt to sort out the sources of S100ß in the operating room using computer modeling, the lack of specificity for the brain during operation makes the assay uninterpretable. Fortunately, the biological half-life of S100ß is less than 1 hour. Therefore, secondary release of S100ß in the postoperative period is an ominous sign of further neurologic injury, unless there is ongoing autotransfusion from the chest tubes. Blomquist and coworkers [8] reported an abrupt increase in S100ß 48 hours after cardiopulmonary bypass in a patient who developed confusion postoperatively and was subsequently found to have fresh infarctions on computed tomographic scan.
S100ß may not be the magic marker for intraoperative detection of doomed neurons during cardiac surgery as currently performed, but neither should it be thrown out with the pump prime. When extracerebral contamination is controlled, S100ß correlates nicely with neuropsychologic dysfunction confirming cerebral injury and adding credibility to what some surgeons consider to be "soft" data. A rapid, bedside assay could identify brain-damaged neonates with congenital heart disease before operation. Monitoring the cerebrospinal fluid for changes in S100ß during thoracoabdominal aortic procedures may be helpful to prevent damage from the aortic cross-clamp. S100ß may also be useful to evaluate therapeutic interventions to protect the brain preemptively from cardiopulmonary bypass and follow patients postoperatively. In the meantime, brain injury remains a feared complication in all patients undergoing cardiac operations requiring cardiopulmonary bypass.
References
This article has been cited by other articles:
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  E. B. Mossad Introduction Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 185 - 186. [PDF]
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E. Appachi and E. B. Mossad Inflammatory Mediators and S-100{beta} Protein Concentrations in Neonates and Infants With Congenital Heart Disease Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 256 - 261. [Abstract] [PDF]
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 S. A. LeMaire, J. K. Bhama, Z. C. Schmittling, P. J. Oberwalder, C. Koksoy, S. A. Raskin, P. E. Curling, and J. S. Coselli S100{beta} correlates with neurologic complications after aortic operation using circulatory arrest Ann. Thorac. Surg., June 1, 2001; 71(6): 1913 - 1919. [Abstract] [Full Text] [PDF]
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