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