Obstructive Sleep Apnea in Children

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Symposium on Adult Diseases in Children - February 2009  


Tex Med. 2009;105(2):47-50.  

By Daina Dreimane, MD  

Obstructive sleep apnea (OSA) did not receive attention until the mid-1900s. The first report of adult OSA in the medical literature appeared in 1966. In 1976, Guilleminault et al reported on pediatric OSA. 1

The American Thoracic Society defines OSA as "a disorder of breathing during sleep characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction (obstructive apnea) that disrupts normal ventilation during sleep and normal sleep patterns."

OSA lies on a continuum of sleep-disordered breathing (SDB) that ranges from mild habitual snoring to hypopnea to OSA with significant clinical sequelae. Children with habitual snoring lack apnea, hypopnea, respiratory effort-related arousals, and abnormal pulmonary gas exchange because of an adequate neuromuscular compensation. The upper-airway resistance syndrome typically involves brief, repetitive, respiratory effort-related arousals in the absence of apnea, hypopnea, or abnormal gas exchange. Obstructive hypopnea is defined as a decrease in airflow by 50 percent despite effort during the same time of breathing cycles, associated with a desaturation or arousal. 2

Children with OSA will have recurrent episodes of variable-degree airway obstruction. Despite the fact that the disorder is common in adults, many of the clinical characteristics of pediatric OSA and the determinants of its epidemiology differ from those of adult OSA. Most of the children with OSA have mild symptoms, and many outgrow the condition. OSA often is the result of adenotonsillar hypertrophy, neuromuscular disease, and craniofacial abnormalities.

The effects of OSA are pervasive, including decreased cognitive   function, cardiovascular complications such as cor pulmonale,   and, rarely, overt congestive heart failure. Moreover, infants younger than 1 year with OSA may be at increased risk of sudden infant   death syndrome ( Table 1 ). 3   


The peak incidence of childhood OSA is between ages 2 and 6 years, when lymphoid tissue growth is at its peak. The prevalence of SDB by varying constellations of parent-reported symptoms on questionnaire is estimated at 4 to 11 percent.

The prevalence of OSA diagnosed by varying criteria on diagnostic studies has ranged widely from 0.1 to 13 percent, but most studies report a prevalence between 1 and 4 percent. The incidence of obstructive sleep apnea in children, which is increasing, has been attributed to the increasing prevalence of overweight in children. 


Increased upper-airway resistance is the main factor in developing OSA. Multiple mechanisms are involved in maintaining an adequate airway patency: anatomic (soft tissue and skeletal) structure, neuromuscular function, ventilatory control, and arousal. 4

Craniofacial skeletal abnormalities most frequently reported in children with OSA include narrow maxilla, mandibular retrognathia, long lower facial height, and caudal placement of hyoid bone; however, the frequency of these abnormalities in the healthy pediatric population is unknown. Craniofacial development and growth are genetically determined, but the environment and breathing abnormalities such as upper-airway obstruction and mouth breathing may affect the final anatomy. Children with OSA are often found to have tonsillar and adenoid hypertrophy and a larger soft palate, resulting in a smaller pharyngeal airway. An increased negative airway pressure is required to continue ventilation; this contributes to airway collapse.

Obesity is associated with large tonsils and adenoids in young children, as well as adults and older children, with increased size of the pharyngeal fat pads near and within the soft palate. Pulmonary gas exchange is worse in children with abdominal or visceral obesity because of impaired chest bellows, particularly when in the supine position.

Neuromuscular compensation involves activation of upper-airway muscles. Muscles involved in dilation of the airway are the genioglossus, styloglossus, and hyoglossus. Airway muscle activity in children with OSA is reduced at sleep onset, and ventilation becomes variable, with an apneic threshold slightly below eupneic in non-rapid eye movement (REM) sleep. In response, pharyngeal dilator activity increases as a result of hypercapnia and negative luminal pressure (negative pressure reflex). Hyperpnea causes a ventilatory overshoot, which in turn results in sudden reduction in airway muscle activation contributing to obstruction in non-REM sleep. REM-sleep-associated atonia eliminates contractions of the accessory respiratory muscles and abdominal muscles, and the diaphragm position is further flattened, worsening the gas exchange. Paroxysmal reductions in pharyngeal dilator activity in REM sleep likely account for the disproportionate severity and increased frequency of OSA in REM sleep.

Arousal as a part of ventilatory control is triggered by hypercapnia and increased respiratory effort, and it immediately restores the airway and normalizes the gas exchange. Arousal threshold is lowest in REM, but highest in stage 4 sleep. In children with OSA, the degree of arousal varies. In OSA, arousal may contribute to abnormal sleep homeostasis. It has a destabilizing effect on ventilation during sleep and potentiates abnormal obstructive cycling. Some studies indicate that spontaneous arousals are decreased in OSA. 

Impact on Health  

Untreated OSA can lead to significant neurocognitive sequelae. Poor quality and reduced nighttime sleep have been associated with impaired learning ability and daytime sleepiness in children and adolescents. 5 Of those children with OSA, 20 to 30 percent suffer from hyperactivity and attention deficit and have problems with working memory, self-regulation, motivation, and affect.

Complications related to chronic hypoxemia are pulmonary hypertension and cor pulmonale, which are major sources of morbidity. Less commonly, arrhythmias and sudden death have been described. Failure to thrive and growth failure, which may be related to increased energy expenditure during sleep, improve after adenotonsillectomy.

Obesity is a well-known risk factor for OSA. (See " Childhood Obesity: The Scope of the Problem .") Behavioral problems associated with OSA, however, are also associated with obesity in children and adolescents, suggesting a causal relationship between OSA and obesity. Childhood tantrums, anger, child temperament, and frustration over food are among the primary factors contributing to disordered eating and obesity. 6

In adults, obesity is exacerbated by reduced physical activity caused by OSA. This may be true in children, as well; to date, no studies have been conducted to prove this hypothesis.

Childhood obesity carries a risk for obesity in adulthood, along with a number of health problems such as diabetes and cardiovascular disease. Adipose-tissue-altering levels of inflammatory cytokines, growth factors, and sex steroid levels adversely affect endothelial function. In adults, OSA leads to a similar pattern of metabolic and inflammatory processes, perhaps due to chronic intermittent hypoxemia and oxidative stress. Studies in children with OSA demonstrate a similar elevation in inflammatory cytokines and presence of insulin resistance. 7 Over many years, this may result in significant morbidity. Most susceptible are children from ethnic minorities and from households with low socioeconomic status. 


Most children with OSA do not have symptoms while awake. The diagnosis begins with a thorough sleep-based history and physical examination. The most common complaints reported by parents and children are snoring, restless sleep, and daytime sleepiness. Physical examination is aimed at identifying conditions that commonly predispose children to OSA, such as adenotonsillar hypertrophy, obesity, neuromuscular disease, and craniofacial abnormalities ( Table 2 ).

Other conditions causing disordered sleep such as asthma, allergic rhinitis, seizures, gastroesophageal reflux disease, and parasomnias should be ruled out. Specific questionnaires and home videotaping are used, but may not be specific enough. The Pediatric Daytime Sleepiness Scale is a validated measure to assess the degree of sleepiness in children and to predict their academic failure.

Polysomnography is the most comprehensive laboratory test used to diagnose OSA and to monitor treatment in adults. Because the test has not been well standardized for use in children younger than 7 years and because few pediatric sleep laboratories are available, its usefulness in children is limited. However, polysomnography remains a valuable tool and may be used to exclude other causes of disordered sleep such as seizures or narcolepsy. The test must monitor sleep-wake states through electroencephalography, electrooculography, chin and leg electromyography, electrocardiography, body position, and appropriate monitoring of breathing by use of nasal cannula-pressure transducer, oral thermistor, chest and abdominal belts, and a neck microphone. It provides the apnea-hypopnea index, the respiratory disturbance index, and the number of respiratory-effort-related arousals per hour of sleep, and documents oxygen desaturations, carbon dioxide retention, and overall sleep cycling. 8   

Surgical Treatment  

Otolaryngological evaluation and adenotonsillectomy are indicated in all children with OSA, with or without adenotonsillar hypertrophy. Independent of the size of the tonsils or adenoids, surgery will improve the airway space. After surgery, 70 to 100 percent of children will show a tremendous improvement in snoring, behavior, attention, enuresis, growth, and overall quality of life. 

Determining the age at which a child should have the surgery is somewhat controversial. Typically, adenotonsillectomy is performed after 24 months of age but, if necessary, can be done in a child as young as 6 months. Rarely, a more complex surgical treatment is indicated, such as radiofrequency treatment of nasal turbinates, uvuloplasty, removal of nasal polyps, tongue base reduction, or orthognathic surgery. Orthodontic procedures can be used to widen the nose and palate. 

Medical Treatment  

If symptoms continue after adenotonsillectomy, home nasal continuous positive airway pressure (CPAP) and bidirectional positive airway pressure (BiPAP) application are used to supply external pressure to the upper airway to maintain patency during sleep. Both modalities require thorough training to ensure compliance and optimal fit of the nasal interface. Children are monitored and reevaluated at least every six months in light of the rapid growth of their craniofacial structures.

No pharmaceutical agents are available specifically for the treatment of OSA; however, antihistamines, decongestants, and nasal steroids should be used to treat allergic rhinitis if present. Allergy testing may be indicated to identify the provoking allergen. Antibacterial therapy may offer temporary improvement if OSA is associated with recurrent tonsillitis and sinusitis.

In children and adolescents whose OSA is caused by obesity, an aggressive weight management plan should be implemented. 


OSA is a common childhood disorder. With the recent increase in childhood obesity, the incidence of OSA has increased significantly. If left untreated, it may result in significant morbidity. Primary care physicians should routinely screen patients for OSA. A good health and sleep history in the presence of common risk factors may be sufficient for making the diagnosis. Polysomnography is frequently performed, but it is not well standardized for use in children. The main and most effective treatment modality of OSA in pediatric patients is adenotonsillectomy. Nonsurgical methods are available and should be tailored to fit individual needs. Appropriate nutrition, exercise, and weight control may prevent the development of obesity and OSA in older children and adolescents.




  1. Guilleminault C, Eldridge FL, Simmons FB, dement WC. Sleep apnea in eight children. Pediatrics.  1976;58:23-30.
  2. Guilleminault C,  Lee JH, Chan A. Pediatric obstructive sleep apnea syndrome. Arch Pediatr Adolesc Med . 2005;159(8);775-785.
  3. Ward SL, Marcus CL. Obstructive sleep apnea in infants and young children. J Clin Neurophysiol . 1996;13(3):198-207.
  4. Katz ES, D'Ambrosio CM. Pathophysiology of pediatric obstructive apnea. Proc Am Thorac Soc . 2008;5(2):253-262.
  5. Perez-Chada D, Perez-Lloret S, Videla AJ, et al. Sleep disordered breathing and daytime sleepiness are associated with poor academic performance in teenagers. A study using the Pediatric Daytime Sleepiness Scale (PDSS). Sleep . 2007;30(12):1698-1703.
  6. Ievers-Landis, CE, Redline S. Pediatric sleep apnea, implications of the epidemic of childhood overweight. Am J Respir Crit Care Med . 2007;175(5):436-441.
  7. Gozal D, Capdevila OS, Kheirandish-Gozal L. Metabolic alterations and systemic inflammation in obstructive sleep apnea among nonobese and obese prepubertal children. Am J Respir Crit Care Med . 2008;177(10):1142-1149.
  8. Muzumdar H, Arens R. Diagnostic issues in pediatric obstructive sleep apnea. Proc Am Thorac Soc . 2008;5:263-273.




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Dr. Dreimane is an associate professor in the Department of Pediatrics at Texas Tech University Health Sciences Center in Lubbock.  



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