AUTHOR AND EDITOR INFORMATION

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• Medication
• Follow-up
• Miscellaneous
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INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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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. 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 addition, in contrast to adults, some children exhibit a variation of OSA 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 OSA 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 OSA. Adults with sleep apnea frequently present with hypersomnia, while children often demonstrate short attention spans, emotional lability, and behavior problems. 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. 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

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.

International

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 OSA 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. 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 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.

CLINICAL

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History

Not only do manifestations of OSA differ between children and adults, they also frequently vary from one child to another. Not every child with OSA has the exact same constellation of symptoms. Keeping this in mind, perform a careful interview to explore the following issues when OSA 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 OSA may describe choking sensations during the night.
• Enuresis: Bedwetting is common among children with OSA, although no well-controlled studies have been performed to date. Always consider the possibility of OSA in children who have histories of snoring and develop enuresis after they have already been successfully toilet trained. Older children need to be asked specifically 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: Adolescents and adults with OSA 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. Young children appear much less likely to develop excessive daytime sleepiness.
• Hyperactivity and/or behavior problems: Paradoxically, some children with OSA 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 OSA 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 any number of factors in addition to OSA. 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 suggestive of OSA syndrome are typically absent from children without OSA syndrome but poorly distinguish between OSA and primary snoring. Therefore, to differentiate between OSA syndrome and primary snoring, overnight polysomnography is essential.

Physical

Children with suspected OSA 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 and weight on a standard 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 OSA. Severe OSA 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 OSA.
• 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.
• 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 OSA. 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

Tonsil hypertrophy and adenoid hypertrophy account for most cases of OSA in children. However, any anomaly of the upper airway may spawn symptomatic intermittent obstruction with sleep. Facial, oral, and throat eccentricities occur in a number of 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 OSA include the following:

• Tonsillar and adenoid hypertrophy (This appears to be the most common cause of OSA. However, size of tonsils and adenoids does not predict the presence or severity of OSA.)
• 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
• 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

DIFFERENTIALS

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Other Problems to be Considered

OSA must be differentiated from simple snoring, which is a vibratory inspiratory noise that is usually not accompanied by oxygen desaturation, hypercarbia, or sleep disruption. Overnight polysomnography can be performed to differentiate pronounced snoring from true OSA in the pediatric age group.

Daytime somnolence is a common complaint among individuals with OSA. For teens and adults, this may be the presenting concern that brings them to medical attention. However, keep in mind that not all children with excessive daytime somnolence have OSA. Sleepiness during the day may be due to any number of factors in addition to sleep apnea. Many children are sleepy during the day simply because their parents do not have a clear idea as to how much sleep a child actually requires.

Chaotic sleep schedules with inconsistent bedtimes and rise times and with limited time allowed for sleep are major causes of daytime sleepiness and lassitude. Any evaluation for suspected sleep apnea must include a careful history with inquiries about sleep times, bedtime routines, and a description of the sleeping environment. Parents should be asked to complete a sleep diary for 1-2 weeks to evaluate whether a child is sleeping enough.

Narcolepsy is a disease characterized by irresistible sleeping attacks that occur intermittently throughout the day. It is included in the differential diagnosis of excessive daytime sleepiness. Patients with narcolepsy are tired throughout the day; thus, the disorder can be confused with OSA syndrome. A history of episodic sleep-onset paralysis, hypnagogic (sleep-onset) hallucinations, or daytime memory lapses with automatic behaviors may help differentiate between narcolepsy and OSA. Sleep paralysis is a frightening experience that lasts from a few seconds to several minutes, during which an individual can breathe and move the eyes but otherwise cannot speak or move.

Hypnagogic hallucinations are vivid lifelike dreams that occur just as one begins to fall asleep. These hallucinations often involve an awareness of another person or an animal in the room, bright colors, or unusual shapes. Often, other senses are involved during the experience, including touch, smell, and hearing. Older patients with narcolepsy may experience cataplexy, or the sudden brief loss of muscular tone without loss of consciousness. Multiple sleep latency testing (MSLT) following overnight polysomnography is necessary to confirm a diagnosis of narcolepsy and differentiate this from OSA.

Nocturnal gastroesophageal reflux may result in nocturnal restlessness, choking episodes during sleep, frequent awakenings, and labored breathing that resemble symptoms of OSA syndrome.

Periodic limb movement disorder, nocturnal seizures, rhythmic movement disorder, and a variety of parasomnias can be differentiated from OSA on the basis of polysomnography.

WORKUP

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Lab Studies

• Polysomnography remains the criterion standard for establishing the diagnosis of OSA in infants, children, and adults. Ideally, polysomnography should be performed overnight and during the patient's usual bedtime.
• Daytime nap studies are specific, but not sensitive, in detecting sleep apnea. This is because obstructive events are more likely to occur during rapid eye movement (REM) sleep than during other sleep stages, and very little (if any) REM sleep occurs during daytime naps in noninfants. Therefore, children with symptoms of OSA who have normal nap study findings must undergo nocturnal polysomnography to exclude the diagnosis. Sleep studies should be performed without a sedative, if possible.
• • Multiple physiologic parameters are monitored during polysomnography, although the specific montage may vary slightly between sleep laboratories. Generally, electrooculography, chin and leg surface electromyography (EMG), and at least 2 EEG channels are included to confirm sleep and assess sleep architecture. Breathing is assessed using nasal/oral airflow sensors, pulse oximetry, and end-tidal carbon dioxide monitoring and by placing piezo crystal belts across the chest and abdomen to detect respiratory efforts. At least one ECG channel is necessary to determine heart rate and rhythm. Occasionally, other channels are incorporated into the study as needed. These might include additional EEG leads to better detect seizure activity, esophageal pH measurements, or transcutaneous carbon dioxide monitoring.
  • Polysomnographic normal standards differ between children and adults. In the pediatric age range abnormalities include oxygen desaturation under 92%, more than one obstructive apnea per hour, and elevations of end-tidal (ET) CO₂ measurements of more than 50 mm Hg for more than 9% of sleep time or a peak level of greater than 53 mm Hg.

Imaging Studies

• Anteroposterior and lateral neck radiography: Neck radiography for soft tissue detail help define upper airway anatomy and adenoid size and exclude the possibility of rare nasal pharyngeal neoplasms.
• Cephalometric radiography and 3-dimensional CT reconstruction imaging are rarely, if ever, necessary in the pediatric age group.
• Cine MRI during sleep may be helpful in identifying specific sites of airway obstruction in the complicated patient being evaluated for surgical interventions. This technique is currently only available at a handful of specialized tertiary care facilities.

Other Tests

• Highly sensitive thyroid stimulating hormone and thyroxine: Thyroid function studies are useful to exclude hypothyroidism, which is associated with tongue enlargement, weight gain, and OSA.
• Complete blood count: Chronic hypoxia related to recurrent airway obstruction may lead to polycythemia.
• Electrocardiography and echocardiography: These studies are not necessary in all children with suspected sleep apnea. However if very severe long-standing obstruction is suspected, an ECG and echocardiogram are helpful in assessing ventricular thickness and function and to check for evidence of pulmonary hypertension.
• Multiple sleep latency test: If the clinical history suggests the possibility of narcolepsy, the MSLT should be ordered in conjunction with overnight polysomnography.
• Magnetic resonance imaging of the brain and brainstem: A history of severe snoring, headaches, neck pain, urinary frequency, or swallowing problems raises the suspicion of Chiari malformation. Chiari malformations may occur in otherwise normal children and in association with congenital myelomeningocele. If brainstem dysfunction is suspected, MRI is necessary. Cranial CT imaging is not adequate to assess for brainstem and upper cervical cord lesions.

Procedures

• Polysomnography is necessary to document OSA and gauge its severity. A history of snoring alone is not adequate for making a diagnosis of OSA or for determining its seriousness.
• Some children with OSA have primarily obstructive hypoventilation in which repetitive partial obstructions occur with some degree of relative oxygen desaturation and hypercarbia. Because of this, pediatric polysomnographic testing should include some means of determining carbon dioxide levels, such as end-tidal carbon dioxide monitoring or transcutaneous carbon dioxide monitoring.
• Overnight pulse oximetry by itself is not adequate for establishing the diagnosis or excluding OSA in children because it provides no information concerning sleep staging/sleep fragmentation or carbon dioxide.

Histologic Findings

Little consistent difference in tonsil and adenoid weights and volumes is seen in individuals with OSA compared with patients whose tonsils and adenoids were removed for other reasons. No distinct histologic findings exist to separate adenoid and/or tonsillar hypertrophy from hypertrophy associated with OSA.

TREATMENT

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Medical Care

Obstructive sleep apnea in pediatric patients generally responds to adenotonsillectomy. However, not all children with obstructive sleep apnea (OSA) are surgical candidates.

Children with OSA due to tonsillar or adenoid hypertrophy are best treated with adenotonsillectomy.

Adenotonsillectomy, along with weight normalization, is considered the first line of therapy in children and adolescents with OSA. Surgically removing the tonsils and adenoids increases cross-sectional airway caliber in patients, even though it does not directly affect the fatty infiltration of the soft tissues of the velopharynx and hypopharynx that occurs in children who are obese. Children with OSA who are obese generally require follow-up polysomnography 8-12 weeks following adenotonsillectomy to assess for residual sleep apnea and determine whether other interventions (eg, continuous positive airway pressure [CPAP]) are needed.

Some children have profound craniofacial deformities that are not easily remedied. Occasionally, surgical procedures undertaken to remedy OSA only help the problem but do not completely eliminate it. In these situations, therapy is usually best accomplished with devices that deliver CPAP.

• CPAP is the mainstay of therapy for most adults with OSA, as well as a large number of children and adolescents. Continuous distending airway pressure is applied during sleep using a nasal mask and small compressor. CPAP acts as a pneumatic splint to maintain airway patency. By simultaneously increasing the functional residual capacity, this pressure also helps prevent oxygen desaturation even if airway obstruction breaks through.
• A variety of patient interfaces are available, including nasal masks, facemasks, gel masks, and nasal pillows to help facilitate a comfortable fit and adherence to therapy. The amount of CPAP pressure must be individualized for each patient and is determined during a CPAP titration study in the sleep laboratory. The goal is to find an optimal pressure that eliminates apnea and minimizes snoring but is still comfortable and does not lead to excessive air swallowing, gastric distention, and air leak around the mask or through the mouth. Long-term effects of nasal CPAP therapy on maxillofacial structure development in children are unknown.
• A number of commercially available oral appliances assist in bringing the lower jaw and tongue forward during sleep, thus improving OSA. These devices are expensive, require special dental expertise, and are associated with frequent adverse effects such as jaw pain and temporal mandibular joint dysfunction. Small growing children are likely to outgrow appliances, necessitating refitting and replacement. In general, oral appliances have extremely limited usefulness, if any, in pediatric patients.
• Over-the-counter, disposable, adhesive covered nasal strips purported to decrease nasal airflow resistance have been promoted as a treatment for snoring and obstructive apnea. These have not been proven to be effective in pediatric sleep apnea, and their use should be discouraged.
• Obstructive apnea is generally worse in supine sleeping than in prone sleeping. Measures to encourage patients to sleep prone, such as sewing a pocket to the back of the pajama shirt and putting a tennis ball into it, have some minimal success among adults who snore or have very mild obstructive apnea. This strategy is generally not helpful in managing significant childhood sleep apnea.
• Nasal fluticasone administered daily for 6 weeks is shown to ameliorate the frequency of obstructive events in children with mild-to-moderate OSA due to tonsil or adenoid hypertrophy by about one half. Nasal steroids offer an opportunity to reduce obstructive events pending surgery, or they can be an alternative remedy for children with mild disease whose parents are reluctant to pursue surgical treatment. Steroids are not shown to decrease obstructive symptoms, eliminate the need for surgery, prevent oxygen desaturation, or shrink tonsil or adenoid tissue. No long-term studies are available to assess the duration of steroid effect, and whether beneficial aspects persist even if therapy is continued is unknown. A trial of topical steroid therapy should not delay surgical treatment of obstructive apnea in children with severe tonsil hypertrophy (>4 tonsils) or moderate-to-severe OSA. No studies have assessed the efficacy of topical steroid therapy in children with craniofacialabnormalitiesandOSA.
• Short courses of systemic steroids (prednisone, 1 mg/kg/d orally [PO] for 5 d) are shown to be ineffective in the treatment of childhood OSA due to tonsil or adenoid hypertrophy.

Surgical Care

• In the pediatric population, most OSA is related to tonsillar hypertrophy or adenoid hypertrophy. Adenotonsillectomy is curative in most instances. Children with OSA who undergo adenotonsillectomy demonstrate improvement in measures of neurocognitive function.
• Certain children who are known to have a high risk of postoperative complications should only undergo surgery at institutions that possess pediatric intensive care facilities (PICUs). This high-risk group includes children younger than 3 years and those with craniofacial abnormalities, failure to thrive, hypotonia, morbid obesity, a history of previous airway trauma, and severe abnormalities on polysomnography (respiratory disturbance index [RDI] >40 or oxygen desaturations <70%).
• Uvulopalatopharyngoplasty (UPPP [ie, UP3]) is the major surgical intervention for adults with OSA but is not commonly performed in children. During the procedure, the uvula, posterior margins of the soft palate, and lateral pharyngeal wall mucosa are removed via scalpel or laser ablation. UPPP surgery is likely to be successful in relieving OSA only if the major site of obstruction is localized to the soft palate. This surgery carries a risk of velopharyngeal insufficiency, which may be increased among pediatric patients. Although UPPP may effectively eliminate most snoring, the procedure does not always cure OSA. Follow-up polysomnography 2-3 months after surgery is warranted to reassess for residual apnea.
• Tongue reduction procedures (midline partial glossectomy) may have some utility in small number of carefully selected pediatric patients.
• Tracheotomy remains an effective surgical option for life-threatening obstructive apnea that is not amenable to other therapies.

Consultations

• Most childhood obstructive apnea involves adenotonsillar hypertrophy, which is curable with surgery. Children with congenital craniofacial abnormalities may require reconstructive surgeries that often are performed jointly by an ear, nose, and throat (ENT) specialist and plastic surgeon.
• Consultation with a neurosurgeon is occasionally required if OSA is related to symptomatic Chiari malformation.

Diet

OSA may aggravate gastroesophageal reflux. Children and adolescents with significant sleep apnea should avoid eating large amounts just before bedtime. This is especially the case if children are being treated with CPAP, which can lead to air swallowing and gastric distention.

Caloric intake limitation and dietary counseling are necessary if obesity complicates obstructive apnea.

Activity

Many individuals with OSA have daytime sleepiness with reduced attention span and difficulty focusing their concentration. Warn teenagers who drive about the potential danger of falling asleep at the wheel; advise them to avoid driving long distances without a break or driving when they are unusually tired. A number of epidemiologic studies link OSA to motor vehicle accidents.

MEDICATION

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

No effective pharmacologic therapy exists for childhood OSA. Individuals with OSA and hypersomnolence should have the underlying cause of their obstructive apnea addressed, rather than use stimulant medication during the day in an attempt to help stay alert.

Nocturnal supplemental oxygen is generally not advised as a primary treatment for OSA. Although oxygen may blunt the degree of hemoglobin desaturation during sleep, it does not prevent sleep fragmentation, sleep deprivation, or associated autonomic stimulation during the obstructive episodes. Preoperative supplemental oxygen treatment has been reported to worsen obstructive hypoventilation in some children. Therefore, if oxygen is used as a bridge to more definitive therapy, the effect of supplemental oxygen should be documented during nocturnal polysomnography.

Intranasal fluticasone propionate (Flonase) administered daily for 6 weeks has been shown to ameliorate the frequency of obstructive events in children with documented mild-to-moderate OSA caused by tonsil and/or adenoid hypertrophy by about one half. Intranasal corticosteroids have not been shown to decrease obstructive symptoms, eliminate the need for surgery, prevent oxygen desaturation, or shrink tonsil or adenoid tissue; therefore, if intranasal corticosteroids are used, the treatment is only temporary pending a more permanent solution. Systemic corticosteroids have not been shown effective and have no role in treatment.

FOLLOW-UP

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Further Inpatient Care

• Some children with severe obstructive apnea continue to have apneas in the immediate postoperative period until surgery-related edema subsides. For these children, CPAP therapy can serve as a bridge treatment after surgery until operative swelling subsides.

Further Outpatient Care

• Individuals undergoing surgical treatment of moderate-to-severe OSA should have follow-up polysomnography 2-3 months after their operations to assure that the surgery successfully eliminated their obstructive apnea. Some patients continue to have significant obstructive apnea after surgery even though their snoring improves dramatically or disappears altogether. This is especially the case for individuals who undergo UPPP alone.
• Daytime fatigue and somnolence may persist after successful treatment for OSA if the patient continues to follow a chaotic sleep schedule at home. Use outpatient contacts as an opportunity to reinforce good sleep hygiene, which is the phrase used to describe the conditions and habits that foster effective satisfying sleep. Stress the importance of maintaining a regular bedtime and rise time and of allowing an adequate period for overnight sleep.

Complications

• Children with severe OSA may develop postobstructive pulmonary edema within a few hours of surgery to relieve upper airway obstruction. Risk factors for postoperative pulmonary edema include the following:
• • Age younger than 3 years
  • Craniofacial anomalies affecting the pharyngeal airway, especially midfacial hypoplasia, micrognathia, or retrognathia
  • Failure to thrive
  • Hypotonia
  • Morbid obesity
  • Previous upper airway trauma
  • Severe abnormalities on polysomnography, with an RDI more than 40 events per hour or oxygen desaturations less than 70%
  • Patients undergoing UPPP in addition to tonsillectomy or adenoidectomy
  • Complicating cardiac or pulmonary disease

Prognosis

• Adenotonsillectomy is curative in most individuals. However, long-term follow-up studies that address the risk of recurrence are not available. The prognosis for OSA in children with congenital craniofacial syndromes varies with the degree of involvement and response to reconstructive surgery.
• Long-term studies involving CPAP therapy in children have not been published to date, but data from adult studies should be considered encouraging.

Patient Education

• Patients receiving CPAP therapy for OSA must understand that they need to use their machines every night and each time they nap.
• Educate families of children and adolescents who have obesity and obstructive apnea about nutrition and weight loss.
• For excellent patient education resources, visit eMedicine's Sleep Disorders Center. Also, see eMedicine's patient education article Disorders That Disrupt Sleep (Parasomnias).

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Sleeping pills should rarely, if ever, be prescribed for individuals with significant OSA.
• Oxygen therapy should not be prescribed as the primary therapy for OSA.
• Adolescents must be warned that sleep apnea may lead to decreased attention span and vigilance. They should not drive when tired, they should not drive long distances without a taking a break, and they should avoid alcohol and other depressant recreational drugs, which may worsen their sleep apnea.
• Children with severe OSA require overnight hospital observation following adenotonsillectomy, especially if they fall into one of the high-risk groups noted in Complications.
• Children undergoing surgery for severe obstructive apnea require follow-up polysomnography to reassess for residual apnea. Absence of snoring following surgery does not equal an absence of obstructive apnea.

Special Concerns

• Infants and children with OSA may have serious respiratory embarrassment when given any sedative medication. Caution is necessary during any medical or dental procedures requiring conscious sedation.
• Please see the companion article Obstructive Sleep Apnea Syndrome for additional reading.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Palate appearance following uvulopalatopharyngoplasty (UPPP) surgery.
	View Full Size Image
Media type:  Photo

Media file 2:  Example of an obstructive apnea and an obstructive hypopnea recorded during polysomnography.
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Media type:  Image

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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• Barbe, Pericas J, Munoz A, et al. Automobile accidents in patients with sleep apnea syndrome. An epidemiological and mechanistic study. Am J Respir Crit Care Med. Jul 1998;158(1):18-22. [Medline].
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• Ferber R, Kryger M. '. Principles and Practice of Sleep Medicine in the Child. 1995;155-216.
• Friedman BC, Hendeles-Amitai A, Kozminsky E, et al. Adenotonsillectomy improves neurocognitive function in children with obstructive sleep apnea syndrome. Sleep. Dec 15 2003;26(8):999-1005. [Medline].
• Goodwin JL, Kaemingk KL, Mulvaney SA et al. Clinical screening of school children for polysomnography to detect sleep disordered breathing-the Tucson Children's Assessment of Sleep Apnea Study (TuCASA). J Clin Sleep Med 2005. 2005;1(3):247-254.
• Kennedy JD, Blunden S, Hirte C, et al. Reduced neurocognition in children who snore. Pediatr Pulmonol. Apr 2004;37(4):330-7. [Medline].
• Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med. Apr 1998;157(4 Pt 1):1098-103. [Medline].
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• McNamara F, Sullivan CE. Obstructive sleep apnea in infants and its management with nasal continuous positive airway pressure. Chest. Jul 1999;116(1):10-6. [Medline].
• Mindell JA, Owens JA. '. A Clinical Guide to Pediatric Sleep. Diagnosis and Management of Sleep Problems. 2003;106-121.
• Redline S, Tishler PV, Schluchter M, et al. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med. May 1999;159(5 Pt 1):1527-32. [Medline].
• Redline S, Tishler PV, Hans MG, et al. Racial differences in sleep-disordered breathing in African-Americans and Caucasians. Am J Respir Crit Care Med. Jan 1997;155(1):186-92. [Medline].
• Rosen CL, D''Andrea L, Haddad GG. Adult criteria for obstructive sleep apnea do not identify children with serious obstruction. Am Rev Respir Dis. Nov 1992;146(5 Pt 1):1231-4. [Medline].
• Rosen GM, Muckle RP, Mahowald MW, et al. Postoperative respiratory compromise in children with obstructive sleep apnea syndrome: can it be anticipated?. Pediatrics. May 1994;93(5):784-8. [Medline].
• Strohl KP, Redline S. Recognition of obstructive sleep apnea. Am J Respir Crit Care Med. Aug 1996;154(2 Pt 1):279-89. [Medline].
• Woodson BT. Predicting which patients will benefit from surgery for obstructive sleep apnea: the ENT exam. Ear Nose Throat J. Oct 1999;78(10):792-5, 798-800. [Medline].

Article Last Updated: May 17, 2006