Obstructive Sleep Apnea in Infants

Abstract

Obstructive sleep apnea in infants has a distinctive pathophysiology, natural history, and treatment compared with that of older children and adults. Infants have both anatomical and physiological predispositions toward airway obstruction and gas exchange abnormalities; including a superiorly placed larynx, increased chest wall compliance, ventilation-perfusion mismatching, and ventilatory control instability. Congenital abnormalities of the airway, such as laryngomalacia, hemangiomas, pyriform aperture stenosis, choanal atresia, and laryngeal webs, may also have adverse effects on airway patency. Additional exacerbating factors predisposing infants toward airway collapse include neck flexion, airway secretions, gastroesophageal reflux, and sleep deprivation. Obstructive sleep apnea in infants has been associated with failure to thrive, behavioral deficits, and sudden infant death. The proper interpretation of infant polysomnography requires an understanding of normative data related to gestation and postconceptual age for apnea, arousal, and oxygenation. Direct visualization of the upper airway is an important diagnostic modality in infants with obstructive apnea. Treatment options for infant obstructive sleep apnea are predicated on the underlying etiology, including supraglottoplasty for severe laryngomalacia, mandibular distraction for micrognathia, tonsillectomy and/or adenoidectomy, choanal atresia repair, and/or treatment of gastroesophageal reflux.Keywords: sleep-disordered breathing; adenotonsillar hypertrophy; craniofacial; micrognathia; laryngomalacia Infants experience a wide range of sleep-disordered breathing patterns, including periodic breathing (1), apnea of prematurity (2), and central apnea, but little attention has been given to obstructive sleep apnea (OSA). Infants are particularly vulnerable to obstructive sleep-disordered breathing related to their upper airway structure (3), adverse pulmonary mechanics (4), ventilatory control (5), arousal threshold (6), laryngeal chemoreflex (7), and an REM-predominant sleep state distribution (8). The anatomical and physiological predispositions toward airway obstruction in infants are summarized in Table 1. Airway collapse may occur passively related to the balance between the viscoelastic properties of the pharynx, pharyngeal dilators, and the transmural pressure. Alternatively, obstructive apnea may result from active glottic closure, termed the laryngeal chemoreflex. The diagnosis of OSA in infants is confirmed by polysomnography and the etiology is often determined via direct endoscopic visualization of the airway. Infants with severe OSA will often have marked hypoxemia or sleep fragmentation, which is likely to result in considerable morbidity. As such, successful therapy is mandatory, even if this requires invasive treatment including nasopharyngeal tubes, continuous positive airway pressure (CPAP), supraglottoplasty, or even tracheostomy. This review focuses on the clinical features, polysomnographic patterns, pathogenesis, diagnosis, and mana...

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