It is often particularly apparent after on-pump cardiac surgery, during which surgi- cal trauma, contact of blood with nonphysiological surfaces (eg, pump tubing, oxygenator surfaces), myocardial ischemia and reperfusion, and hypothermia combine to cause a dra- matic release of cytokines (eg, interleukin [IL] 6 and IL8) and other mediators of inflammation.55 Some investigators have used serum concentrations of S100 beta as a marker of brain injury56 and have correlated increased serum levels with the number of microemboli exiting the CPB circuit during CABG. In contrast, others have noted the increased incidence of microemboli with on-pump CABG (relative to off-pump CABG) but have failed to show a corresponding worsening of neurocognitive function 1 week to 6 months postopera- tively.57,58 Blood retrieved from the operative field during on-pump CABG contains lipid material and particulate mat- ter, which have been implicated as possible causes of post- operative neurocognitive dysfunction. Although a study59 reported that CPB-associated neurocognitive dysfunction can be mitigated by the routine processing of shed blood with a cell saver before its reinfusion, another study60 failed to show such an improvement. It has been suggested that CPB leads to an increased incidence of postoperative renal failure requiring dialysis, but a large RCT comparing on-pump and off-pump CABG showed no difference in its occurrence.61 Of interest, this study failed to show a decreased incidence of postoperative adverse neurological events (stroke, coma, or neurocognitive deficit) in those undergoing off-pump CABG. The occurrence of SIRS in patients undergoing CPB has led to the development of strategies designed to prevent or to minimize its occurrence. 