Sleep Apnea

Sam Goldstein and Jack A. NaglieriEncyclopedia of Child Behavior and Development10.1007/978-0-387-79061-9_2663
© Springer Science+Business Media, LLC 2011

Sleep Apnea

David J. Lozano 
Pediatric Pulmonary Division, Children’s Hospital of Alabama, Birmingham, AL, USA
David J. Lozano
Without Abstract


Childhood obstructive sleep apnea is characterized by repeated episodes of partial or complete upper airway obstruction that occur during sleep that are usually associated with disruption in gas exchange and/or sleep fragmentation.



Sleep disordered breathing (SDB) is a spectrum that encompasses primary snoring at the mild end of severity to classic obstructive sleep apnea syndrome (OSAS) at the more severe end. Upper airway resistance and obstructive sleep hypoventilation are part of this spectrum and are felt to be less severe than outright obstructive sleep apnea syndrome. OSAS is characterized by repeated episodes of upper airway resistance along with partial or complete airway obstruction during sleep. These episodes can be associated with ventilation and/or oxygenation disturbances. A degree of sleep fragmentation can be seen with these patients as well.
Sleep disordered breathing can occur in a child of any age ranging from neonates to adolescents. OSAS occurs in approximately 1–3% of the pediatric population. More specifically, OSAS affects up to 3% of children between the ages of 2 and 8 years old.


Obstructive sleep apnea syndrome occurs when the upper airway collapses or when the luminal cross section is reduced during inspiration. Collapsibility of the upper airway is a dynamic process that involves multiple factors such as sleep state, anatomy, respiratory drive, and neuromotor tone. The airway of the child is inherently smaller than that of an adult. As a result, size of the pharynx which includes the size of the adenoids and tonsils has long been implicated in pediatric obstructive sleep apnea. It has been shown that the site of upper airway obstruction in children with obstructive sleep apnea is at the level of the tonsils and adenoids. In normal children, it occurs at the level of the soft palate. Tonsils and adenoids increase in size from birth to 12 years of age with maximal growth appearing between the 2 and 7 years of age. However, multiple studies have not shown a strong correlation between increased adenotonsillar size and obstructive sleep apnea. Thus, pediatric obstructive sleep apnea may not be caused by adenotonsillar hypertrophy alone. Obesity can be a contributing factor in OSAS. Adipose tissue within the muscles and soft tissue surrounding the airway can narrow the pharynx. Thus, the likelihood of airway collapse is increased. Children with craniofacial abnormalities are at high risk for OSAS. Examples of conditions associated with craniofacial abnormalities include Down syndrome, achondroplasia, Pierre Robin syndrome, and Aperts’ syndrome.

History and Physical Examination

Nightly loud snoring is almost universal with pediatric OSAS. In many patients, the snoring is accompanied by pauses in breathing, choking/gasping for breath, and neck hyperextension. Other associated symptoms can include sweating, restless sleep, and dry mouth. It should be noted that snoring itself is not always an accurate predictor of polysomnographic OSAS. Daytime sleepiness can be a manifestation of pediatric OSAS. However, daytime sleepiness is much more prominent with adult OSA as compared to pediatric OSAS. Physical examination of a child with OSAS is usually normal. However, children may present with adenotonsillar hypertrophy and craniofacial abnormalities which should alert a clinician to the possibility of OSAS. Obesity and failure to thrive can be seen as well. In rare instances, cardiovascular consequences of cor pulmonale and congestive heart failure can be seen in children with OSAS.


Nocturnal polysomnography (sleep study) is felt to be the gold standard for diagnosis of OSAS. It is the diagnostic test that should be ordered in any child with suspected SDB. The nocturnal polysomnogram should be performed in a pediatric sleep laboratory. Adult oriented laboratories attempt to perform sleep studies in children with limited success. Other diagnostic studies have been looked at to evaluate OSAS which include symptom questionnaires and video/audio recordings. These individual studies have not shown adequate sensitivity or specificity in diagnosing pediatric OSAS.


Tonsillectomy and adenoidectomy is first line treatment for pediatric OSAS. It is felt to be curative in approximately 80–85% of children with this diagnosis. However, a percentage of children have symptoms that persist despite adenotonsillectomy especially in children with obesity, craniofacial abnormalities, and cerebral palsy. Continuous positive airway pressure (CPAP) has been shown to be an effective therapy for OSAS in children who have either failed surgical intervention or are not good surgical candidates. Other treatment modalities include weight loss, oral appliances, supplemental oxygen, and tracheostomy.
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