To assess effects of anesthesia and opioids, we studied 13 children with obstructive sleep apnea (OSA, age 4.0 ± 2.2 yr, mean ± SD) and 24 age-matched control subjects (5.8 ± 4.0 yr). Apnea indexes of children with OSA were 29.4 ± 18 h⁻¹, median 30 h⁻¹. Under inhalational anesthetic, closing pressure at the mask was 2.2 ± 6.9 vs. −14.7 ± 7.8 cmH₂O, OSA vs. control ( P < 0.001). After intubation, spontaneous ventilation was 115.5 ± 56.9 vs. 158.7 ± 81.6 ml · kg⁻¹ · min⁻¹, OSA vs. control ( P = 0.02), despite elevated Pco ₂ (49.3 vs. 42.1 Torr, OSA vs. control, P < 0.001). Minute ventilation fell after fentanyl (0.5 μg/kg iv), with central apnea in 6 of 13 OSA cases vs. 1 of 23 control subjects ( P < 0.001). Consistent with the finding of reduced spontaneous ventilation, apnea was most likely when end-tidal CO₂ exceeded 50 Torr during spontaneous breathing under anesthetic. Thus children with OSA had depressed spontaneous ventilation under anesthesia, and opioids precipitated apnea in almost 50% of children with OSA who were intubated but breathing spontaneously under inhalational anesthesia.

Rationale: In adults, obstructive sleep apnea (OSA) is associated with metabolic dysfunction that improves with treatment of OSA. No equivalent studies exist in children. Objective: To examine the relationship between metabolic markers and OSA with time and treatment in children. Methods: Metabolic markers measured on a fasting morning blood sample at diagnostic polysomnography and follow-up 1.3 ± 0.6 yr later. Measurements and Main Results: Forty-five children (34 males), aged 6.9 ± 3.5 yr, and including 12 obese subjects, were in the final analysis. There were no differences in metabolic markers between children with and without OSA at initial study; however, obese children had significantly higher insulin (106.1 ± 72.1 vs. 66.7 ± 37.6 pmol/L; p = 0.028), insulin/glucose ratio (23.7 ± 14.3 vs. 14.7 ± 8.0; p = 0.02), and significantly lower high-density lipoprotein cholesterol (1.3 ± 0.2 vs. 1.6 ± 0.4 nmol/L; p = 0.005) than nonobese children. Twenty children underwent surgical removal of adenotonsillar tissue, whereas 12 children with OSA elected not to have treatment. OSA persisted after treatment in five children, and resolved in 27. Thirteen children did not have OSA on initial or follow-up studies. At follow-up, there was a small but significant improvement in total cholesterol in those children whose OSA was resolved (4.8 ± 0.8 to 4.7 ± 0.6 nmol/L; p = 0.005) and a trend for obese children with persisting OSA to have elevated insulin levels compared with obese children without OSA (p = 0.07). Conclusion: Obesity appears to be the major influence on metabolic dysfunction in children with OSA, but these preliminary data also suggest that resolution or persistence of OSA may affect changes in metabolic function over time.

Immunoreactive expression of three cell death markers was quantitatively analysed in the human infant brainstem medulla. We assessed active caspase-3, TUNEL and single-stranded DNA (ssDNA) in a cohort of 92 infants, and analysed for: (i) variations in the immunoreactive expression with development; (ii) comparison of infants diagnosed with the Sudden Infant Death Syndrome (SIDS, n = 67) to infants who died suddenly with another diagnosis (non-SIDS, n = 25); and (iii) correlations with known clinical risk factors for SIDS. Five nuclei from the brainstem medulla (caudal and rostral levels) were studied, including the hypoglossal (XII), dorsal motor nucleus of the vagus (DMNV), the dorsal column nuclei (gracile and cuneate) and the arcuate nucleus. Our main hypothesis was that neuronal cell death would be increased in SIDS compared to non-SIDS infants, and the increase would correlate with risk factors such as prone sleeping and cigarette smoke exposure. Comparing SIDS to non-SIDS, there was an increase in caspase-3 in the rostral DMNV (P = 0.01), and a trend to increased TUNEL in the arcuate nucleus (P = 0.1), which was statistically significant when comparing the male SIDS to male non-SIDS cohort (P = 0.04). No major changes for ssDNA immunoreactivity were found. Moreover, TUNEL expression was affected by post-conceptional age, by sleep-related risk factors (predominantly affecting the dorsal column nuclei), and by cigarette smoke exposure in the rostral DMNV and arcuate nucleus. Active caspase-3 was affected by post-conceptional age but only in the XII, while gender-related differences were seen in the arcuate nucleus. This study provides further evidence of increased apoptosis in the brainstem of SIDS infants, but shows for the first time that these changes are also affected by age and gender, and by clinical risk factors such as the sleep position and cigarette smoke exposure.

OBJECTIVES: It remains uncertain whether treatment with adenotonsillectomy for obstructive sleep apnea in children improves cognitive function. The Preschool Obstructive Sleep Apnea Tonsillectomy and Adenoidectomy study was a prospective randomized controlled study in which researchers evaluated outcomes 12 months after adenotonsillectomy compared with no surgery in preschool children symptomatic for obstructive sleep apnea. METHODS: A total of 190 children (age 3–5 years) were randomly assigned to early adenotonsillectomy (within 2 months) or to routine wait lists (12-month wait, no adenotonsillectomy [NoAT]). Baseline and 12-month assessments included cognitive and behavioral testing, medical assessment, polysomnography, and audiology. The primary outcome was global IQ at 12-month follow-up, measured by the Woodcock Johnson III Brief Intellectual Ability (BIA). Questionnaires included the Pediatric Sleep Questionnaire, Parent Rating Scale of the Behavioral Assessment System for Children–II, and Behavior Rating Inventory of Executive Function, Preschool Version. RESULTS: A total of 141 children (75.8%) attended baseline and 12-month assessments, and BIA was obtained at baseline and 12-month follow-up for 61 and 60 participants in the adenotonsillectomy versus NoAT groups, respectively. No cognitive gain was found after adenotonsillectomy compared with NoAT, adjusted for baseline; BIA scores at 12-month follow-up were as follows: adenotonsillectomy, 465.46 (17.9) versus NoAT, 463.12 (16.6) (mean [SD]). Improvements were seen for polysomnogram arousals and apnea indices and for parent reports of symptoms (Pediatric Sleep Questionnaire), behavior (Behavior Assessment System for Children behavioral symptoms, P = .04), overall health, and daytime napping. CONCLUSIONS: Structured testing showed no treatment-attributable improvement in cognitive functioning of preschool children 12 months after adenotonsillectomy compared with NoAT. Improvements were seen after adenotonsillectomy in sleep and behavior by using polysomnogram monitoring and parental questionnaires.