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Chang Gung Med J. 2009 May-Jun;32(3):247-57.

Sleep-disordered breathing in children.

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Department of Otolaryngology, Sleep Center, Chang Gung Memorial Hospital, Taipei, Chang Gung University College of Medicine, Taoyuan, Taiwan; Department of Sleep Medicine, Royal Infirmary Edinburgh, United Kingdom.


Children with sleep-disordered breathing (SDB) can manifest a continuum from simple snoring and upper airway resistance syndrome to obstructive sleep apnea (OSA) with secondary growth impairment, neurocognitive deficits, and less often cardiovascular sequelae. Most children who present with SDB are four to eight years old with variable clinical symptoms at different ages. In general, infants often present with noisy breathing and disturbed nocturnal sleep, toddlers and preschool-aged children with snoring and mouth breathing, and school-aged children with behavioral and dental problems. The pathogenesis of SDB in children remains incompletely understood. Adenotonsillar hypertrophy is the leading cause of OSA. Other risk factors include allergic rhinitis, craniofacial anomalies, cleft palate following pharyngeal flap surgery, neuromuscular diseases, laryngomalacia, and obesity. Polysomnography (PSG) is the gold standard diagnostic tool. However, great variation exists in the interpretation of PSG and criteria for the definition of pediatric OSA, even though consensus statements have been used to standardize the scoring of summary indices for the disorders. Adenotonsillectomy is the cardinal treatment for pediatric SDB. Rapid maxillary expansion is a useful approach in upper jaw contraction. Distraction osteogenesis has become an acceptable procedure in the treatment of severe maxillomandibular deficiency. Continuous positive airway pressure has been successful in treating intractable or severe OSA in children with other underlying medical disorders and has modified the indications for tracheotomy in pediatric patients with craniofacial anomalies and OSA. Follow-up in children treated for OSA reveals that underlying structural or neuromuscular abnormalities can decrease the response to treatment and obesity may lead to recurrence of OSA later during adolescence.

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