Background Supplementary oxygen is often administered when preterm neonates experience desaturations i.e. after apnea, sometimes resulting in cerebral hyperoxia during recovery. Whether this post-hypoxic cerebral hyperoxia is induced by the supplementary oxygen, remains unknown.

Aim To compare the regional cerebral oxygen saturation (rcSO₂) and cerebral fractional oxygen extraction (cFTOE) following a desaturation, between preterm neonates who did and did not receive supplementary oxygen.

Methods As part of a larger prospective cohort study, near infrared spectroscopy (NIRS) was used to measure rcSO₂ during days 2 to 5 after birth. We collected 50 consecutive desaturations (SpO₂ <80%). CFTOE was calculated: [(SpO₂–rcSO₂)/SpO₂]. We used a Wilcoxon signed rank test to compare mean rcSO₂ and cFTOE ten minutes before to ten minutes after desaturation. The Mann-Whitney U test was used to compare these values in neonates who did and did not receive supplementary oxygen.

Results We included 50 desaturations in 16 preterm neonates (median GA 28+4/7 (range 25+0/7–30+0/7) weeks; birth weight 1144 (800–1630) grams). Supplementary oxygen was administered in 60% of the events. We found higher rcSO₂ values following desaturation (mean 76.9%) compared to before desaturation (mean 70.2%, p = 0.001). There was no difference in rcSO2-increase between neonates who did and who did not receive supplementary oxygen (p = 0.79). CFTOE was lower after desaturation (0.17%) compared to cFTOE before desaturation (0.22%, p < 0.001).

Conclusion Cerebral hyperoxia after desaturation in preterm neonates indeed occurs, but is not induced by supplementary oxygen administration. The decrease of cFTOE after desaturation supports the hypothesis that post-hypoxic reperfusion might cause cerebral hyperoxia after desaturation.