Delayed impairment of cerebral oxygenation after deep hypothermic circulatory arrest in children

Background. Clinical studies of deep hypothermic circulatory arrest (DHCA) have focused only on the immediate postoperative period. However, experimen tal findings suggest impairment of cerebral oxygenation at 2 to 8 hours aft er reperfusion. Methods, In 10 children who had DHCA for heart operations, transcerebral di fferences of hemoglobin oxygen saturation and plasma hypoxanthine, xanthine , and lactoferrin concentrations were measured in concurrently obtained cer ebral venous, arterial, and mixed venous samples up to 10 hours postoperati vely. Results. Compared with preoperative levels (57% +/- 7%), cerebral venous ox ygen saturation was not significantly reduced until 2 hours (44% +/- 6%) an d 6 hours (42% +/- 5%) after DHCA (p < 0.05). A statistically significant t ranscerebral (ie, cerebral vein versus artery) concentration difference of hypoxanthine was observed at 30 minutes (3.6 +/- 0.9 mu mol/L), 1 hour (3.4 +/- 1.1 mu mol/L), and 2 hours (3.1 +/- 0.8 mu mol/L) after DHCA but not p reoperatively (0.4 +/- 0.2 mu mol/L). A transcerebral concentration differe nce of lactoferrin occurred 30 minutes after DHCA (196 +/- 70 mu g/mL) but not preoperatively (16 +/- 20 mu g/mL). Conclusions. Cerebral venous oxygen saturation of hemoglobin decreased as l ate as 2 to 6 hours after DHCA, in association with impaired cerebral energ y status. Neutrophil activation in the cerebral circulation occurred 30 min utes after reperfusion. (C) 1999 by The Society of Thoracic Surgeons.