Raj Ashok B, O'brien Louise M, Bertolone Salvatore J, Gozal David, Edmonds Harvey L
Department of Pediatrics, Division of Hematology, School of Medicine, University of Louisville, Louisville, Kentucky, USA.
Pediatr Pulmonol. 2006 Nov;41(11):1088-94. doi: 10.1002/ppul.20502.
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.
我们之前使用脑血氧饱和度测定法来识别患有镰状细胞病（SCD）的清醒儿童的低脑静脉血氧饱和度。由于SCD患者在睡眠期间动脉血氧血红蛋白去饱和很常见，本研究比较了患有和未患有SCD的儿童在清醒和睡眠状态下的全身动脉和脑静脉氧合动力学。将17名患有纯合子SCD的非裔美国（AA）儿童[8（4 - 15）岁；29%为男性；经颅多普勒速度正常]与一个由6名健康AA儿童组成的对照组（CON）[9（4 - 16）岁，33%为男性]进行比较。进行了标准的整夜多导睡眠图记录，包括通过脉搏血氧饱和度测定法（SpO₂）测量动脉血氧饱和度。使用脑血氧饱和度测定法无创测量局部脑血氧饱和度（rSO₂）。组内比较研究了睡眠对受试者SpO₂和rSO₂的影响。对SpO₂、rSO₂以及rSO₂/SpO₂比值进行组间比较，评估SCD对清醒和睡眠期间全身和脑氧合的影响。SpO₂在清醒或睡眠状态下的组间差异均无统计学意义。然而，仅在SCD组中，SpO₂变化的幅度具有统计学意义（P = 0.002）。相比之下，清醒和睡眠时rSO₂的组中位数确实存在显著差异[清醒时：CON为76（67 - 86），SCD为62（58 - 71），P = 0.01；睡眠时：CON为65（60 - 77），SCD为55（48 - 61），P = 0.01]。SCD组清醒时的rSO₂/SpO₂比值也显著更低[CON为0.78（0.68 - 0.88），SCD为0.66（0.61 - 0.72）；P = 0.015]。在睡眠期间，SCD组的该比值也显著更低[CON为0.71（0.66 - 0.81），SCD为0.59（0.52 - 0.65）；P = 0.011]。我们的研究结果表明，SCD患者在清醒和睡眠期间发生脑缺氧的风险可能都会增加。
