The prevalence of OSAS in children with SCA is higher than in the general pediatric population.
We found that the institution of pediatric adenotonsillectomy guidelines for patients undergoing adenotonsillectomy significantly decreased the rate of unanticipated admission.
Children who are otherwise well with mild to moderate OSA have a sufficiently low risk of respiratory complications following adenotonsillectomy to permit day-stay surgery in the setting of appropriate facilities with careful post-operative monitoring for the first 6h to identify a small sub-group who require overnight observations.
Nuclear factor kappa B is locally and systemically activated in children with obstructive sleep apnea syndrome. This observation may motivate the search for new anti-inflammatory strategies for controlling nuclear factor kappa B activation in obstructive sleep apnea syndrome.
Oximetry studies evaluated with the McGill Oximetry Score expedite diagnosis and treatment of children with adenotonsillar hypertrophy referred for suspected sleep-disordered breathing.
Our findings suggest that depressive symptoms are higher among children with OSA. Therefore, patients with depressive symptomatology should receive screening for sleep disordered breathing.
Our study confirms the high prevalence of interictal epileptiform discharges in children with SDB. Follow-up data indicate that they may recede over time, accompanied by an improvement of sleep respiratory parameters.
Among the four salivary cortisol parameters, r-sCor was negatively associated with OSAS severity, ODI, and QOL (KOSA-18), which may indicate a chronically stressed HPA axis. These results demonstrate that salivary cortisol may be a useful biomarker of OSAS.
Children with moderate-to-severe obstructive sleep apnea and the phenotype of hypertrophic tonsils have reduced morning serum cortisol levels and potentially decreased glucocorticoid inhibitory effects on tonsillar growth.
We postulate that disrupted sleep and other factors facilitating obesity such as a high-fat diet may disrupt the gut microbiome and lead to increased systemic LPS levels with resultant inflammation, promoting downstream metabolic dysfunction.