eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Sleep Apnea

Author: Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Contributor Information and Disclosures

Updated: Feb 27, 2009

Introduction

Background

Childhood obstructive sleep apnea (OSA) syndrome is characterized by episodic upper airway obstruction that occurs during sleep. The airway obstruction may be complete or partial. Three major components of obstructive sleep apnea have been identified: episodic hypoxia, intermittent hypercapnia, and sleep fragmentation. Habitual snoring without obstructive sleep apnea is more common and may also lead to sleep fragmentation. Both primary snoring and obstructive sleep apnea have been associated with poor quality of life and increased healthcare use in children.

Pathophysiology

Disordered breathing during sleep is a hallmark of obstructive sleep apnea syndrome. Breathing abnormalities include apnea (cessation of air flow) and hypopnea (decreased air flow). In addition, in contrast to adults, some children exhibit a variation of obstructive sleep apnea termed obstructive hypoventilation (OH). Children with obstructive hypoventilation demonstrate periods of hypercarbia that occur in the absence of discrete respiratory events that fulfill criteria for apnea or hypopnea.

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.

In adults, episodes of disordered breathing must last 10 seconds or more before being considered an apnea or hypopnea. 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 into account the physiologic differences between adults and children. 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.

Individuals with obstructive sleep apnea syndrome have pathologic degrees of obstructive apnea, obstructive hypopnea, or both. Severity is quantified using a polysomnographic-derived index known as the apnea hypopnea index (AHI). The AHI is the total number of apneas and hypopneas that occur divided by the total duration of sleep in hours. An AHI of less than or equal to 1 is considered to be normal by pediatric standards. An AHI of 1-5 is very mildly increased, 5-10 is mildly increased, 10-20 is moderately increased, and greater than 20 is severely abnormal.

OH in children is a sleep-related breathing disorder that is considered a variation of obstructive sleep apnea. Children with OH may have a normal ranged AHI, but they have episodic periods of hypercarbia, as identified based on end-tidal (ET) CO₂ monitors. Peak ET CO₂ measurements of greater than 53 mm Hg are considered abnormal. The percentage of sleep time spent with ET CO₂ measurements greater than 50 mm Hg should not be more than 9%.

Most physicians who treat children with sleep apnea generally recommend specific interventions when the AHI is greater than 5 or respiratory events are associated with oxygen desaturations of less than 85%. When the AHI falls between 1 and 5, other clinical factors must be taken into account to determine whether to pursue adenotonsillectomy or other therapy.

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.

Childhood differs from adult obstructive sleep apnea. Adults with sleep apnea frequently present with hypersomnia, whereas children often demonstrate short attention spans, emotional lability, and behavior problems. Among adults, obesity is a major risk factor for obstructive sleep apnea. 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. Children with some types of neuromuscular disease (eg, Duchenne muscular dystrophy, spinal muscular atrophy, cerebral palsy) may also have a higher risk of developing sleep apnea.

Frequency

United States

In nonobese and otherwise healthy children younger than 8 years, the prevalence of obstructive sleep apnea is estimated at 1-3%. Habitual snoring is common during childhood affects approximately 10% of children aged 2-8 years; the frequency decreases after age 9-10 years. Obesity confers 4-fold to 5-fold added risk for sleep-disordered breathing.

International

In the United Kingdom, approximately 1.75-2.25% of children aged 4-5 years are thought to have obstructive sleep apnea. Unfortunately, very few epidemiologic studies of childhood obstructive sleep apnea are available.

Mortality/Morbidity

Major morbidities associated with childhood obstructive sleep apnea 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 obstructive sleep apnea.

Children with obstructive sleep apnea syndrome, as well as children with a history of loud habitual snoring, appear to be at risk for developing deficits of executive function. According to the model by Beebe and Gozal, sleep fragmentation, intermittent hypoxemia, and hypercarbia contribute to dysfunction in the prefrontal areas of the brain.¹ Executive functions include behavioral inhibition, regulation of affect and arousal, ability to analyze and synthesize, and memory. Executive dysfunction interferes with cognitive abilities and learning.

Children with severe obstructive sleep apnea 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 obstructive sleep apnea 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 obstructive sleep apnea. 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 obstructive sleep apnea is unknown. Once pulmonary hypertension has developed, it is usually reversible if the underlying obstructive sleep apnea is effectively treated.

Race

Obstructive sleep apnea occurs more commonly among black and Hispanic individuals than among white adults and children. In patients younger than 18 years, blacks are 3.5 times more likely to develop obstructive sleep apnea 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

Obstructive sleep apnea 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 obstructive sleep apnea is diagnosed recall that their child's snoring began within the first months of life. Most children with obstructive sleep apnea 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.

Clinical

History

Not only do manifestations of obstructive sleep apnea (OSA) differ between children and adults, they also frequently vary from one child to another. Not every child with obstructive sleep apnea has the exact same constellation of symptoms. Keeping this in mind, perform a careful interview to explore the following issues when obstructive sleep apnea is suspected:

• Abnormal breathing during sleep: Parents should describe their child's breathing in detail. Some children snore loudly and have audible intermittent gasps. Some demonstrate paradoxical chest and abdominal wall movements, labored breathing with retractions, cyanosis, sweating, and restlessness. Often, children prefer sleeping in unusual positions, with their head and neck extended and their mouth wide open.
• Frequent awakenings or restlessness: Recurrent obstruction leads to restlessness, and parents may report that the child wakes frequently or falls out of bed. Ask families about the child's sheets and blankets. Constant tossing and turning during the night often causes the child's bedcovers to be in wild disarray by morning.
• Frequent nightmares: Obstructive apnea and hypopnea tend to worsen during rapid eye movement (REM) sleep, which is associated with dreaming. Frequent wakening with nightmares or vivid dreams is common in children. Occasionally, the dreams may include imagery about suffocation or drowning. Adults or children with obstructive sleep apnea may describe choking sensations during the night.
• Enuresis: Bedwetting is common among children with obstructive sleep apnea, although no well-controlled studies have been performed to date. Always consider the possibility of obstructive sleep apnea in children who have histories of snoring and develop enuresis after they have already been successfully toilet trained. Older children need to be specifically asked about whether they wet the bed because often they are too embarrassed to bring up the subject on their own. In addition to questioning the family about enuresis, ask about nocturia. Many children and adults with obstructive apnea report frequent awakenings to use the bathroom at night.
• Difficulty getting up in the morning: Morning complaints may include dry mouth, grogginess, disorientation, fatigue, and an unrefreshed feeling after an overnight sleep. Some children are very difficult to arouse in the morning and require multiple interventions by the family before they get out of bed.
• Excessive daytime sleepiness (EDS): Adolescents and adults with obstructive sleep apnea frequently report feeling sleepy during the day and may fall asleep at inappropriate times. They have difficulty staying awake in quiet situations and can have problems focusing their attention. Ask children whether they struggle to stay awake in class or while watching television, reading, or sitting in a car. Daytime somnolence may lead to falling grades, mood changes, and inattentiveness. Prepubertal children who are obese are more likely to have EDS compared with their nonobese counterparts at any given level of obstructive sleep apnea severity.²
• Hyperactivity and/or behavior problems: Paradoxically, some children with obstructive sleep apnea develop signs of hyperactivity rather than daytime somnolence. Patients may exhibit aggressive behavior, discipline problems, decreased attention span, emotional withdrawal, and bizarre behaviors.
• Daytime mouth breathing: Most children with obstructive sleep apnea have tonsillar hypertrophy, adenoid hypertrophy, or both. Parents frequently describe these children as mouth breathers, even during the day while they are awake.
• Sleep patterns: Daytime somnolence may be due to numerous factors in addition to obstructive sleep apnea. Many children and teenagers have poor sleep habits, irregular sleep schedules, and unrealistic views regarding how much sleep they need. Often, having families keep a sleep diary for 2 weeks to document bedtimes, rise times, and naps can be very informative to both the physician and the family.
• Historical features: Historical features suggestive of obstructive sleep apnea syndrome are typically absent from children without obstructive sleep apnea syndrome but poorly distinguish between obstructive sleep apnea and primary snoring. Therefore, to differentiate between obstructive sleep apnea syndrome and primary snoring, overnight polysomnography is essential.

Physical

Children with suspected obstructive sleep apnea should undergo a complete physical examination with special attention to structures of the upper airway. Obtain accurate vital signs, including measurement of blood pressure; plot the child's height, weight, and body mass index (BMI) by age on a gender-specific growth chart.

• Determine whether the child's growth is normal. Recent rapid weight gain or obesity may predispose a school-aged child or adolescent to developing obstructive sleep apnea. Severe obstructive sleep apnea in the younger child may lead to failure to thrive and stunted growth.
• Determine if the child's face appears normal, or if craniofacial anomalies are present. Inspect for midfacial hypoplasia, a flat nasal bridge, or facial asymmetry. Determine if the jaw abnormally small (micrognathia) or jaw recessed (retrognathia). Look for adenoid facies with mouth breathing, nasal speech, and periorbital swelling, which may be present in as many as 15-20% of younger children with obstructive sleep apnea.
• Assess nasal patency. Evaluate for signs of allergic rhinitis, nasal polyps and growths, and septal deviation. Determine if the child can breathe through the nose.
• Assess whether the child can open his or her mouth fully or if jaw movement is limited. Assess the size of the oral pharynx and note whether it seems crowded by a large tongue, tonsil hypertrophy, a redundant soft palate, or by the dentition. Determine if space is present between the end of the soft palate and the posterior pharyngeal wall or if the palate and uvula abut the back of the throat. Often, repetitive episodes of obstructive apnea lead to painless edema of the uvula, which is worse in the morning and subsides as the day goes on. Listen to the voice for weakness or hoarseness, suggesting vocal cord problems. Obstructive sleep apnea is most commonly associated with adenotonsillar hypertrophy in children.
• Look at the shape of the neck. Short thick necks predispose adults and older adolescents to obstructive apnea. Palpate for masses and thyromegaly, keeping in mind that obstructive apnea is more common in patients with hypothyroidism. Assess for jugular venous distension that might accompany heart failure. Look for head and neck swelling; obstruction of venous return from the head as seen in superior vena caval obstruction predisposes individuals to obstructive apnea.
• Pectus excavatum is sometimes seen in younger children with obstructive sleep apnea. Severe scoliosis or abnormally narrow chests can lead to restrictive pulmonary limitation and place individuals at a higher risk of desaturating with sleep. Barrel-shaped chests are seen in patients with chronic obstructive lung disease.
• Obtain blood pressure measurements to assess for hypertension. Listen to the pulmonic valve closure component of S₂. Unlike in adults, in healthy young children, the pulmonary valve closure sound in the left second interspace can be a little louder than the aortic closure sound heard over the right second interspace. Listen for an unusually loud snappy pulmonary closure sound, which may indicate pulmonary hypertension. Assess for evidence of heart failure.

Causes

Hypertrophy of tonsils and/or adenoids account for most cases of obstructive sleep apnea in children. However, any anomaly of the upper airway may produce intermittent obstructive symptoms during sleep. Facial, oral, and throat eccentricities occur in numerous congenital syndromes. Certain storage diseases, hypothyroidism, and Down syndrome result in upper airway crowding due to a relative increase in tongue mass compared to mouth size.

Neuromuscular diseases contribute to obstructive apnea because of abnormal muscle tone in the pharyngeal constrictors, which are responsible for maintaining airway patency. Children with Chiari malformations are usually not weak but may develop obstructive apnea due to dysfunction of the same pharyngeal muscle groups. Individuals with obesity typically have fatty infiltration of the soft tissues of the throat, limiting airway caliber and predisposing them to obstructive apnea. People with sickle cell anemia have a tendency toward obstructive apnea for reasons that are still unclear.

Disorders associated with childhood obstructive sleep apnea include, but are not limited to, the following:

• Adenotonsillar hypertrophy: This is most common cause of obstructive sleep apnea in children. The size of the tonsils and adenoids alone does not predict the presence or severity of obstructive sleep apnea.
• Chronic nasal obstruction, including choanal stenosis, severe septal deviation, allergic rhinitis, nasal polyps, and rare nasal and/or pharyngeal tumors
• Down syndrome
• Pierre Robin anomaly
• Crouzon syndrome
• Treacher Collins syndrome
• Klippel-Feil syndrome
• Beckwith-Wiedemann syndrome
• Apert syndrome
• Prader Willi syndrome
• Morbid obesity
• Marfan syndrome
• Achondroplasia
• Laryngomalacia
• Mucopolysaccharidoses
• Conditions involving neuromuscular weakness, including Duchenne muscular dystrophy, Werdnig-Hoffman disease, late onset spinal muscular atrophy, Guillain Barré syndrome, myotonic dystrophy, and myotubular myopathy
• Chiari malformation

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