Cerebral oximetry improves detection of sickle cell patients at risk for nocturnal cerebral hypoxia.

We previously used cerebral oximetry to identify low cerebral venous oxygen saturation in waking children with sickle cell disease (SCD). Because arterial oxyhemoglobin desaturation is common during sleep in SCD patients, this study compared both waking and sleeping systemic arterial and cerebral venous oxygenation dynamics in children with and without SCD. Seventeen African-American (AA) children with homozygous SCD [8 (4-15) years; 29% male; normal transcranial Doppler velocities] were compared with a control cohort (CON) comprised of six healthy AA children [9 (4-16) years, 33% male]. Standard all-night polysomnographic recordings were performed, including measurement of arterial oxygen saturation by pulse oximetry (SpO(2)). Regional cerebral oxygen saturation (rSO(2)) was measured non-invasively with cerebral oximetry. Intra-cohort comparisons examined the influence of sleep on SpO(2) and rSO(2) in the subjects. Inter-cohort comparisons of SpO(2), rSO(2,) and the rSO(2)/SpO(2) ratio assessed the impact of SCD on systemic and cerebral oxygenation during wakefulness and sleep. Cohort differences in SpO(2) were not statistically significant in either wakefulness or sleep. However, only in the SCD cohort was the magnitude of SpO(2) change statistically significant (P = 0.002). In contrast, both waking and sleep rSO(2) cohort median values did differ significantly [awake: CON 76 (67-86) vs. SCD 62 (58-71), P = 0.01; sleep: CON 65 (60-77) vs. SCD 55 (48-61), P = 0.01)]. The waking rSO(2)/SpO(2) ratio was also significantly lower in the SCD group [CON 0.78 (0.68-0.88) vs. SCD of 0.66 (0.61-0.72); P = 0.015]. During sleep, the ratio was also significantly lower in the SCD group [CON 0.71 (0.66-0.81) vs. SCD 0.59 (0.52-0.65); P = 0.011]. Our findings suggest that SCD patients may be at increased risk of cerebral hypoxia during both wakefulness and sleep.