Dervan Leslie A, Wrede Joanna E, Watson R Scott
Division of Pediatric Critical Care Medicine, Department of Pediatrics, University of Washington, Seattle, Washington, United States.
Center for Clinical and Translational Research, Seattle Children's Research Institute, Seattle, Washington, United States.
J Pediatr Intensive Care. 2020 Nov 19;11(1):32-40. doi: 10.1055/s-0040-1719170. eCollection 2022 Mar.
This single-center prospective observational study aimed to evaluate sleep architecture in mechanically ventilated pediatric intensive care unit (PICU) patients receiving protocolized light sedation. We enrolled 18 children, 6 months to 17 years of age, receiving mechanical ventilation and standard, protocolized sedation for acute respiratory failure, and monitored them with 24 hours of limited (10 channels) polysomnogram (PSG). The PSG was scored by a sleep technician and reviewed by a pediatric sleep medicine physician. Sixteen children had adequate PSG data for sleep stage scoring. All received continuous opioid infusions, 15 (94%) received dexmedetomidine, and 7 (44%) received intermittent benzodiazepines. Total sleep time was above the age-matched normal reference range (median 867 vs. 641 minutes, = 0.002), attributable to increased stage N1 and N2 sleep. Diurnal variation was absent, with a median of 47% of sleep occurring during night-time hours. Rapid eye movement (REM) sleep was observed as absent in most patients ( = 12, 75%). Sleep was substantially disrupted, with more awakenings per hour than normal for age (median 2.2 vs. 1.1, = 0.008), resulting in a median average sleep period duration (sleep before awakening) of only 25 minutes (interquartile range [IQR]: 14-36) versus normal 72 minutes (IQR: 65-86, = 0.001). Higher ketamine and propofol doses were associated with increased sleep disruption. Children receiving targeted, opioid-, and dexmedetomidine-based sedation to facilitate mechanical ventilation for acute respiratory failure have substantial sleep disruption and abnormal sleep architecture, achieving little to no REM sleep. Dexmedetomidine-based sedation does not ensure quality sleep in this population.
这项单中心前瞻性观察性研究旨在评估接受程序化浅镇静的机械通气儿科重症监护病房（PICU）患者的睡眠结构。我们纳入了18名6个月至17岁接受机械通气且因急性呼吸衰竭接受标准程序化镇静的儿童，并对他们进行了24小时有限（10通道）多导睡眠图（PSG）监测。PSG由一名睡眠技师评分，并由一名儿科睡眠医学医生审核。16名儿童有足够的PSG数据用于睡眠阶段评分。所有儿童均接受持续阿片类药物输注，15名（94%）接受右美托咪定，7名（44%）接受间歇性苯二氮䓬类药物。总睡眠时间高于年龄匹配的正常参考范围（中位数867分钟对641分钟，P = 0.002），这归因于N1期和N2期睡眠增加。不存在昼夜变化，中位数为47%的睡眠发生在夜间。大多数患者（n = 12，75%）未观察到快速眼动（REM）睡眠。睡眠受到严重干扰，每小时觉醒次数高于同年龄正常水平（中位数2.2次对1.1次，P = 0.008），导致平均睡眠周期持续时间（觉醒前睡眠）中位数仅为25分钟（四分位间距[IQR]：14 - 36），而正常为72分钟（IQR：65 - 86，P = 0.001）。较高剂量的氯胺酮和丙泊酚与睡眠干扰增加有关。接受以阿片类药物和右美托咪定为基础的靶向镇静以促进急性呼吸衰竭机械通气的儿童存在严重的睡眠干扰和异常睡眠结构，几乎没有REM睡眠。以右美托咪定为基础的镇静并不能确保该人群的优质睡眠。
