Obstructive sleep apnea and fractures in children and adolescents.

STUDY OBJECTIVES: To examine, among girls and boys, associations between site-specific extremity fracture and sleep apnea diagnosis or treatment. METHODS: A cross-sectional analysis of claims data from 2016 to 2018 for children aged 2-18 years. Children with sleep apnea, continuous positive airway pressure, adenotonsillectomy, and fracture were identified using International Classification of Diseases, 10th Revision, Current Procedural Terminology, and Healthcare Common Procedure Coding System codes. We examined sex-stratified associations between site-specific fracture, sleep apnea, and sleep apnea treatment. RESULTS: Among 2,327,104 children, 9,547 (0.41%) had sleep apnea and nearly 61% were treated. Girls with sleep apnea, treated or untreated, had increased odds of lower, but not upper, extremity fracture compared to those without sleep apnea (treated 1.56, 95% confidence interval 1.11, 2.21; untreated odds ratio 1.63, 95% confidence interval 1.09, 2.44). Only boys untreated for sleep apnea had increased odds of lower extremity fracture in comparison to those without a diagnosis of sleep apnea (odds ratio 1.65, 95% confidence interval 1.20, 2.27). Interestingly, boys treated for sleep apnea but not those untreated, in comparison to boys without sleep apnea, had different (reduced) odds of upper extremity fracture (odds ratio 0.74, 95% confidence interval 0.59, 0.95). CONCLUSIONS: These large datasets provide evidence that both boys and girls with untreated sleep apnea have higher odds of lower extremity fractures. However, treatment for sleep apnea was associated with improved odds of lower extremity fracture only in boys. Upper extremity data were less clear. These data are cross-sectional and cannot show causality, but they suggest that treatment for sleep apnea may lower risk for extremity fractures in boys. CITATION: Matlen LB, Whitney DG, Whibley D, Jansen EC, Chervin RD, Dunietz GL. Obstructive sleep apnea and fractures in children and adolescents. J Clin Sleep Med. 2021;17(9):1853-1858.

Associations between age and sleep apnea risk among newborn infants.

OBJECTIVE: Among older children, sleep-disordered breathing (SDB) is associated with measurable neurocognitive consequences. However, diagnostic SDB thresholds are lacking for infants < 12 months. We sought to evaluate the relationship between SDB indices, gestational age (GA), and postmenstrual age (PMA) for infants who underwent clinically-indicated polysomnograms at a tertiary care center. METHODS: Every infant < 3-months chronological age whose first clinically-indicated polysomnogram was between 2/2012 and 2/2017 was included. Linear regression was used to evaluate associations between apnea-hypopnea index (AHI), obstructive-apnea index (OAI), and GA and PMA for infants with and without obvious clinical risk factors for SDB (eg, micrognathia and cleft palate). RESULTS: For 53 infants without obvious SDB risk factors (GA 35.6 ± 4.5 weeks; PMA 41.2 ± 4.0 weeks), mean AHI was 27 ± 18 and OAI 2.9 ± 4.5. There was a weak inverse relationship between AHI and PMA (r 2 = 0.12, P = 0.01), but AHI was not predicted by GA (r 2 = 0.04, P = 0.13). Conversely, OAI was more strongly associated with GA (r 2 = 0.33, P < 0.0001) than PMA (r 2 = 0.08, P = 0.036). For 28 infants with congenital structural anomalies that predispose to SDB (GA 38.0 ± 3.1 weeks, PMA 43.1 ± 3.3 weeks, AHI 37.7 ± 30, OAI 8.2 ± 11.8), neither AHI nor OAI were related to PMA or GA. CONCLUSIONS: Among infants who received clinically-indicated polysomnograms but did not have obvious structural risk for SDB, AHI declined with advancing PMA, but obstructive-apnea was best predicted by prematurity. In contrast, the SDB risk did not improve with increasing GA or PMA for infants with congenital structural risk factors; such infants may not outgrow their risk for SDB.

Isoflurane anesthesia does not satisfy the homeostatic need for rapid eye movement sleep.

BACKGROUND: Sleep and general anesthesia are distinct states of consciousness that share many traits. Prior studies suggest that propofol anesthesia facilitates recovery from rapid eye movement (REM) and non-REM (NREM) sleep deprivation, but the effects of inhaled anesthetics have not yet been studied. We tested the hypothesis that isoflurane anesthesia would also facilitate recovery from REM sleep deprivation. METHODS: Six rats were implanted with superficial cortical, deep hippocampal, and nuchal muscle electrodes. Animals were deprived of REM sleep for 24 hours and then (1) allowed to sleep ad libitum for 8 hours or (2) were immediately anesthetized with isoflurane for a 4-hour period followed by ad libitum sleep for 4 hours. The percentage of REM and NREM sleep after the protocols was compared with similar conditions without sleep deprivation. Hippocampal activity during isoflurane anesthesia was also compared with activity during REM sleep and active waking. RESULTS: Recovery after deprivation was associated with a 5.7-fold increase (P = 0.0005) in REM sleep in the first 2 hours and a 2.6-fold increase (P = 0.004) in the following 2 hours. Animals that underwent isoflurane anesthesia after deprivation demonstrated a 3.6-fold increase (P = 0.001) in REM sleep in the first 2 hours of recovery and a 2.2-fold increase (P = 0.003) in the second 2 hours. There were no significant differences in REM sleep rebound between the first 4 hours after deprivation and the first 4 hours after both deprivation and isoflurane anesthesia. Hippocampal activity during isoflurane anesthesia was not affected by REM sleep deprivation, and the probability distribution of events during anesthesia was more similar to that of waking than to REM sleep. CONCLUSION: Unlike propofol, isoflurane does not satisfy the homeostatic need for REM sleep. Furthermore, the regulation and organization of hippocampal events during anesthesia are unlike sleep. We conclude that different anesthetics have distinct interfaces with sleep.