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Background: Childhood obstructive sleep apnea (OSA) syndrome is characterized by episodic upper airway obstruction that occurs during sleep. In contrast to simple snoring, OSA is accompanied by varying degrees of oxygen desaturation, hypercarbia, autonomic stimulation, and sleep fragmentation. Sleep disruption leaves some children with daytime somnolence, difficulty waking in the morning, and disturbed concentration. Other children develop paradoxical hyperactivity during the day rather than hypersomnolence; attention deficit hyperactivity disorder may be diagnosed. Common symptoms include restless sleep and loud nightly snoring, sometimes with audible pauses followed by gasping or snorting. Complaints of nocturnal enuresis, nightmares, and morning headaches may occur. Long-standing severe OSA may result in failure to thrive, neurobehavioral disorders, pulmonary hypertension, and, ultimately, cor pulmonale.

Pathophysiology: Disordered breathing during sleep is a hallmark of OSA syndrome. Breathing abnormalities include apnea (cessation of air flow) and hypopnea (decreased air flow). In contrast to adults, children with OSA often exhibit a pattern of obstructive hypoventilation or partial airway obstruction leading to hypoxemia and hypercarbia.

Physiologic recording methods can differentiate the types of apnea. During obstructive apnea, an individual makes respiratory efforts, but no airflow occurs because of upper airway obstruction. Central apnea is an interruption in both airflow and breathing effort. Mixed apneas have both central and obstructive components to them. A typical mixed event begins with a central apnea, which is followed immediately by one or more obstructed breaths.

Hypopneas are episodes of shallow breathing during which airflow is decreased by at least 50%. They are usually accompanied by some degree of oxygen desaturation, which can be minor and transient. Like apnea, hypopnea is subdivided as being obstructive, central, or mixed. Obstructive hypopneas are episodes of partial upper airway obstruction. Respiratory efforts occur, but airflow is reduced. In central hypopnea, breathing effort and airflow are both decreased. Mixed hypopneas have both central and obstructive components. Individuals with OSA syndrome have pathologic degrees of obstructive apnea, obstructive hypopnea, or both.

Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including nasopharynx (area from the nose to the hard palate), mouth, velopharynx (space behind the palate), retroglossal region (area behind the tongue), hypopharynx (region between the tongue base and larynx), and larynx.

The upper airway is a pliant tube whose sidewalls consist of muscle and other soft tissues. During wakefulness, neural input to a number of small muscle groups in the pharynx maintains muscle tone and airway patency. With sleep, an increased resistance to airflow normally accompanies muscular relaxation of these muscle groups. Although most people compensate for these changes, individuals with certain anatomic problems have repeated episodes of partial or complete upper airway obstruction when they sleep.

In adults, episodes of disordered breathing must last 10 or more seconds before being considered an apnea or hypopnea. Using this definition, most healthy adults have some degree of sleep-related disordered breathing. To help differentiate normal from pathologic apnea, the apnea index and hypopnea are determined. The apnea index is an average of the number of apneas occurring per hour during sleep. Apnea indices of fewer than 5 events per hour and hypopnea indices of fewer than 5 events per hour are generally considered to be within normal limits by adult standards. Healthy children have fewer episodes of sleep disordered breathing than adults, and adult criteria is inadequate for diagnosing OSA in a significant percentage of affected children. Most pediatric sleep centers view apneas or hypopneas that occur more than once per hour as abnormal.

Normal resting respiratory rates in children are faster than those in adults. The child has a smaller functional residual capacity and a more compliant chest wall. As a result, children undergo oxygen desaturation more rapidly than adults whenever airflow is interrupted. A definition of apnea or hypopnea requiring that an event last 10 seconds or more before it is considered significant is somewhat arbitrary and does not take the differences between adult and child physiology into account. Consequently, pediatric sleep centers use different duration criteria for labeling events such as apnea or hypopnea. In children, if obstruction occurs with 2 or more consecutive breaths, the event can be called an apnea or hypopnea, even if it lasts less than 10 seconds.

Other differences between childhood and adult OSA also exist. Among adults, obesity is a major risk factor for OSA. Fatty infiltration of the pharyngeal soft tissues narrows the caliber of the upper airway and contributes to airway resistance. Although obesity plays a role in some cases of childhood sleep apnea, the airway obstruction is usually related to tonsillar hypertrophy, adenoid hypertrophy, or craniofacial abnormalities.

Frequency:

    * In the US: Obstructive apnea is believed to affect approximately 4% of men and 2% of women in the United States. The disorder is most commonly recognized in middle-aged individuals, although symptoms usually predate diagnosis by years.

      Prevalence of OSA in US children is estimated to be 2%. In comparison, 7-9% of children snore habitually.

    * Internationally: In the United Kingdom, approximately 1.75-2.25% of children aged 4-5 years are thought to have OSA. Unfortunately, very few epidemiologic studies of childhood OSA exist.

Mortality/Morbidity: Major morbidities associated with childhood OSA include failure to thrive, difficulty concentrating and/or developmental delay, behavioral problems, hypertension, pulmonary hypertension, and, ultimately, cor pulmonale. Some pulmonologists theorize that chronic upper airway obstruction with labored breathing may result in the development of a pectus excavatum deformation in a compliant immature chest wall. Concomitant gastroesophageal reflux is likely to be exacerbated by OSA.

Children with severe OSA may develop postobstructive pulmonary edema within a few hours of surgery undertaken to relieve upper airway obstruction. Furthermore, such patients are at risk for postoperative respiratory compromise, which is characterized by severe upper airway obstruction and may require endotracheal intubation or the use of noninvasive respiratory support such as continuous positive airway pressure via a nasal mask. Surgical treatment of severe OSA warrants an overnight observation, especially if the child is younger than 3 years, has concomitant cardiopulmonary disease, morbid obesity, hypotonia, or craniofacial anomalies.

Obesity-related hypoventilation, commonly known as the pickwickian syndrome, occurs in some children who have obesity and OSA. These individuals respond abnormally to both hypercarbic and hypoxemic stimuli to breathe; they have repetitive obstructive events with sleep and marked daytime sleepiness, daytime hypoventilation, and hypercarbia.

The incidence of cor pulmonale and death due to OSA is unknown. Once pulmonary hypertension has developed, it is usually reversible if the underlying OSA is effectively treated.

Race: OSA occurs more commonly among African American and Hispanic individuals than among white adults and children. In patients younger than 18 years, African Americans are 3.5 times more likely to develop OSA than whites.

Sex: The male-to-female ratio of obstructive apnea in children is approximately 1:1. At puberty, the male-to-female ratio starts to increase. By adulthood, symptomatic men outnumber women by 2:1 or more.

Age: OSA is observed in children of all ages and may develop even in infancy. Retrospective studies note that a large number of parents with children in whom OSA is diagnosed recall that their child's snoring began within the first months of life. Most children with OSA are aged 2-10 years. Children with severe obstructive apnea are likely to present when aged 3-5 years. The mean age at diagnosis has been reported to be 14 months, plus or minus 12 months.