Childhood Sleep Apnea 

Updated: Feb 13, 2019
Author: Mary E Cataletto, MD; Chief Editor: Denise Serebrisky, MD 

Overview

Practice Essentials

Obstructive sleep apnea (OSA) in children is characterized by episodic upper airway obstruction that occurs during sleep. The airway obstruction may be complete or partial.

Signs and symptoms

The clinical presentation of a child with obstructive sleep apnea (OSA) is nonspecific and requires increased awareness by the primary care physician. OSA symptoms in children can include the following:

  • Abnormal breathing during sleep

  • Frequent awakenings or restlessness

  • Frequent nightmares

  • Enuresis

  • Difficulty awakening

  • Excessive daytime sleepiness

  • Hyperactivity/behavior problems

  • Daytime mouth breathing

  • Poor or irregular sleep patterns

Complications of OSA in children can generally be divided into the 4 following immediate consequences of upper airway obstruction during sleep:

  • Sleep fragmentation

  • Increased work of breathing

  • Alveolar hypoventilation

  • Intermittent hypoxemia

See Clinical Presentation for more detail.

Diagnosis

Currently, the only available tool for definitive diagnosis of OSA is an overnight polysomnographic evaluation in the sleep laboratory (see the image below). Ideally, polysomnography should be performed overnight and during the patient's usual bedtime.

Example of an obstructive apnea and an obstructive Example of an obstructive apnea and an obstructive hypopnea recorded during polysomnography.

Polysomnography provides the following measures:

  • Sleep state (≥2 EEG leads)

  • Electrooculogram (right and left)

  • Submental electromyelogram (EMG)

  • Airflow at nose and mouth (thermistor, capnography, or mask and pneumotachygraph)

  • Chest and abdominal wall motion (impedance or inductance plethysmography)

  • Electrocardiogram (preferably with R-R interval derivation technology)

  • Pulse oximetry (including a pulse waveform channel)

  • End-tidal carbon dioxide (sidestream or mainstream infrared sensor)

  • Video camera monitor with sound montage (analog or digital)

  • Transcutaneous oxygen and carbon dioxide tensions (in infants and children < 8 y)

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 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.

See Workup for more detail.

Management

Surgical intervention

Although OSA has multiple etiologies in children, once the diagnosis has been established and its severity assessed, adenotonsillectomy is usually the first line of treatment. Tonsillotomy, rather than tonsillectomy, has been recently advocated as equally effective with less postoperative morbidity.

Adenotonsillectomy should be implemented along with weight normalization in obese children. Caloric intake limitation and dietary counseling are necessary if obesity complicates OSA. Children and adolescents with significant sleep apnea should avoid eating large amounts just before bedtime.

Continuous positive airway pressure

CPAP is the mainstay of therapy for most adults with OSA, as well as a large number of children and adolescents. However, it is often difficult for children to adhere to the therapy regimen.

CPAP devices can be uncomfortable and inappropriately fitting masks can leak, leading to the development of pressure sores on the bridge of the nose. Air leaks can also irritate the conjunctiva, causing increased lacrimation and eye discomfort. Also, midfacial hypoplasia may develop with long-term use, particularly in children with neuromuscular weakness.

See Treatment and Medication for more detail.

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 health care use in children.

Obstructive sleep apnea syndrome was described more than a century ago, but obstructive sleep apnea in children was first described in the 1970s. It is a common but underdiagnosed condition in children that may ultimately lead to substantial morbidity if left untreated.

The mechanisms of obstruction, adverse effects of obstructive sleep apnea, diagnostic criteria, and recommended treatment options are different in children from those in adults (see the image below). Important recent advances in the understanding of the underlying pathophysiological mechanisms of obstructive sleep apnea in children have been coupled with improved approaches to the diagnosis and management of obstructive sleep apnea.

Go to Obstructive Sleep Apnea for complete information on this topic.

Medical complications associated with obstructive Medical complications associated with obstructive sleep apnea 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 hypercapnia that occur in the absence of discrete respiratory events that fulfill the criteria for apnea or hypopnea.

Apneas and hypopneas

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. 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 into obstructive, central, and 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, and children have 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 being 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.

Upper airway obstruction

The ability to maintain upper airway patency during the normal respiratory cycle is the result of a delicate equilibrium between the forces that promote airway closure and dilation. This "balance of forces" concept was initially proposed by 2 independent groups and reflects the current line of thought regarding the underlying pathophysiological mechanisms that result in the clinical spectrum of obstructive apnea.

The 4 major predisposing factors for upper airway obstruction are the following:

  • Anatomic narrowing

  • Abnormal mechanical linkage between airway dilating muscles and airway walls

  • Muscle weakness

  • Abnormal neural regulation

Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including the 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 sleep apnea differs from adult obstructive sleep apnea in that adults with sleep apnea frequently present with hypersomnia, whereas children often demonstrate short attention spans, emotional lability, and behavioral problems. Obesity is a major risk factor in both adults and children.[1] 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.

Anatomic narrowing

At any point in life, a smaller cross-sectional area of the upper airway is associated with decreased ability to maintain upper airway patency. In adults, the upper airway behaves as predicted by the Starling resistor model. According to this model, under conditions of flow limitation, maximal inspiratory flow is determined by the pressure changes upstream (nasal) to a collapsible site of the upper airway, and flow is independent of downstream (tracheal) pressure generated by the diaphragm. Pressures at which the airway collapses have been termed critical closing pressures, or Pcrit. In other words, in the presence of a collapsible segment of the upper airway, such as the pharyngeal introitus, the overall resistance to airflow proximal to that segment is the major factor responsible for occlusion of the collapsible segment. This model explains why, for example, snoring and obstructive apnea worsen during a common cold (increased nasal-upstream resistance).

The validity of this model was also confirmed in children, and interestingly, the collapsibility of the upper airway in children was reduced when compared with that of adults. As predicted by the Starling resistor model, the collapsible segment of the upper airway in children displayed less negative (higher and, therefore, more collapsible) pressures in children with obstructive sleep apnea. Components that affect the upstream segment pressures or increase Pcrit are of major consequence to the ability to maintain airway patency. For example, a viral cold or allergic rhinitis that induces increased secretion in the nasal passages and mucosal swelling is associated with increased nasal resistance to airflow. Not surprisingly, the magnitude of snoring and the severity of obstructive apnea are increased during periods in which the upstream segment pressure has been adversely affected.

The contribution of the various anatomical nasopharyngeal structures to Pcrit and the interactions between these structures that lead to upper airway patency or obstruction during sleep are of obvious importance in increasing the understanding of the pathophysiology of obstructive sleep apnea in children. For most children, enlargement of the tonsils and/or adenoid is the proximate cause for the development of obstructive sleep apnea.

The static pressure and/or area relationships of the passive pharynx were endoscopically measured in 14 children with obstructive sleep apnea and in 13 healthy children under general anesthesia with complete paralysis,[2] and it was determined that children with obstructive sleep apnea closed their airways at the level of enlarged adenoids and tonsils at low positive pressures, whereas healthy children required subatmospheric pressures to induce upper airway closure. The cross-sectional area of the narrowest segment was significantly smaller in children with obstructive sleep apnea and particularly involved the retropalatal and retroglossal segments. Thus, both congenital and acquired anatomic factors clearly play a significant role in the pathogenesis of pediatric obstructive sleep apnea.

Abnormal mechanical linkage between airway dilating muscles and airway walls

Malposition or malinsertion of specific dilating muscles is likely to have major consequences on the mechanical dilating efficiency. Therefore, even if a major weakness is not present, the mechanical disadvantage imposed by muscle shortening or by displacement of the muscle insertion on the pharyngeal wall undoubtedly results in diminished ability to stiffen the airway, thus leading to increased collapsibility or elevation of Pcrit.

Control of the upper airway size and stiffness depends on the relative and rhythmic contraction of a host of paired muscles, which include the palatal, pterygoid, tensor palatini, genioglossus, geniohyoid, and sternohyoid muscles. These muscles tend to promote a patent pharyngeal lumen and receive phasic activation in synchrony with phrenic nerve activation. Upon contraction, these muscles promote motion of the soft palate, mandible, tongue, and hyoid bone. Although the coordinated action of these muscles during the respiratory cycle has yet to be deciphered, a reasonable generalization is that inspiratory muscle output stiffens the pharynx and related structures and enlarges the lumen.

The optimal activity of these muscles depends on their anatomic arrangement; for example, airway patency is compromised during increased neck flexion by changing the points of attachment of muscles acting on the hyoid bone, such that the resulting vector of their forces may be nullified. The activity of pharyngeal muscles greatly depends on various factors within the CNS and, more particularly, on the brainstem respiratory network. Wakefulness conveys a supervisory function that ensures airway patency, and sedative agents, which compromise genioglossal muscle activity, may result in significant upper airway compromise.

Mechanoreceptor-mediated and chemoreceptor-mediated genioglossal activity is critical for maintenance of upper airway patency in healthy and micrognathic infants. Changes in genioglossal activity during transitions, from oral to nasal breathing and relative to Pcrit, suggest that genioglossus activation is critical for airway patency in micrognathic infants.

Muscle weakness

Little evidence suggests that intrinsic muscle weakness is a major contributor to upper airway dysfunction in conditions other than those associated with neuromuscular disorders. However, in neuromuscular disorders, upper airway obstruction is frequently observed during sleep, further reinforcing the validity of the balance-of-pressures concept.

Abnormal neural regulation

Abnormal respiratory control does not appear to play a significant role in upper airway obstruction during sleep in children with obstructive sleep apnea. In one study, the ventilatory response to hyperoxic hypercapnic challenge in children and adolescents with obstructive sleep apnea was similar to that measured in age-matched and sex-matched controls.[3] Similarly, no differences were found in the ventilatory response to isocapnic hypoxia. Blunting in central chemosensitivity was reported in some children with obstructive sleep apnea undergoing surgery; however, despite such reports, central chemosensitivity during sleep in children with obstructive sleep apnea was similar to that in matched controls. However, arousal to hypercapnia was blunted, suggesting that subtle alterations in the central chemosensitive arousal network may have occurred in these children.

These subtle changes have been further substantiated by examining the ventilatory response to repeated hypercapnia, whereby reciprocal changes in respiratory frequency and tidal volume occur. In addition, children with obstructive sleep apnea demonstrate impaired arousal responses to inspiratory loads during rapid eye movement (REM) and non-REM sleep, compared to controls. Neural responses to hypoxia and hypercapnia have not been well studied in children with obstructive sleep apnea and underlying syndromes.

In addition to the aforementioned considerations, diminished laryngeal reflexes to mechanoreceptor and chemoreceptor stimulation, with reduced afferent inputs into central neural regions underlying inspiratory inputs, can be present. For example, chemoreceptor stimuli, such as increased PaCO2 or decreased PaO2, stimulate the airway, dilating muscles in a preferential mode (ie, upper airway musculature is more stimulated than the diaphragm).

This preferential recruitment tends to correct an imbalance of forces acting on the airway and, therefore, maintains airway patency. Similarly, stimuli that result from suction pressures in the nose, pharynx, or larynx rapidly stimulate the activity of upper airway dilators. This effect is also preferential to the upper airway, causing some degree of diaphragmatic inhibition and, thus, compensating for increases in upstream resistance. The function of these upper airway receptors in children with adenotonsillar hypertrophy with and without obstructive sleep apnea is not known.

Etiology

Obesity and hypertrophy of tonsils and/or adenoids account for most cases of obstructive sleep apnea in children.[1] 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 sleep 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. Persons 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, which is the most common cause of obstructive sleep apnea in children (however, 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

  • Cerebral palsy

  • Sickle cell diseases

  • Hypothyroidism

  • Hallermann-Streiff syndrome

  • Osteopetrosis

  • Oropharyngeal papillomatosis

Epidemiology

In nonobese and otherwise healthy children younger than 8 years, the prevalence of obstructive sleep apnea is estimated to be 1-3%. Habitual snoring is common during childhood and 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.

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.

Racial distribution

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.

The high frequency of obstructive sleep apnea in adult Asian populations indicates that the anthropometric characteristics of the craniofacial structures in this racial group also predispose to higher obstructive sleep apnea rates in children. The frequency of obstructive sleep apnea in Hispanic children is equal to that of white children.

Sex distribution

The male-to-female ratio of obstructive sleep apnea in children is approximately 1:1. At puberty, the male-to-female ratio starts to increase. In older adolescents, a male preponderance emerges that essentially reflects the typical male predominance observed in the adult population. By adulthood, symptomatic men outnumber symptomatic women by 2:1 or more.

Age distribution

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. Preterm babies are at risk for more obstructive events while supine, but some have suggested that they are still at a lower risk of death from sudden infant death syndrome. However, Moon et al, citing 3 studies, report that premature infants may be at 4 times increased risk for sudden infant death syndrome compared with term infants, with the risk increasing at lower gestational age and birthweight.[4]

Most children with obstructive sleep apnea are aged 2-10 years (coinciding with adenotonsillar lymphatic tissue growth). 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.

Prognosis

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 hypercapnia contribute to dysfunction in the prefrontal areas of the brain.[5] 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.

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 hypercapnic and hypoxemic stimuli to breathe; they have repetitive obstructive events with sleep and marked daytime sleepiness, daytime hypoventilation, and hypercapnia.

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.

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.

Prognosis after surgery

Surgical treatment of severe obstructive sleep apnea warrants an overnight observation, especially if the child is younger than 3 years or has concomitant cardiopulmonary disease, morbid obesity, hypotonia, or craniofacial anomalies.

The major determinants of surgical outcome include the apnea hypopnea index (AHI) and obesity at the time of diagnosis. The AHI is the total number of apneas and hypopneas that occur divided by the total duration of sleep in hours. An AHI of 1 or less 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.

In children with enlarged tonsils and adenoids that lead to obstructive sleep apnea, an adenotonsillectomy usually results in complete cure, although no definitive studies have clearly demonstrated this issue.

The outcome of patients who require extensive surgical management obviously depends on the severity of the condition that leads to upper airway compromise. With the emergence of noninvasive ventilation as an alternative option for these children, upper airway obstruction during sleep can be conservatively and successfully managed in most children.

In children with failure to thrive (FTT), treatment of obstructive sleep apnea leads to resolution of the somatic growth disturbance. Similarly, pulmonary hypertension resolves. Although major improvements in neurobehavioral outcomes are expected, data are currently insufficient to support a complete recovery in some of the cognitive abilities affected by obstructive sleep apnea.

Tauman et al reported that only 25% of children treated for obstructive sleep apnea with adenotonsillectomy had complete postoperative normalization of symptoms.[6]

Patient Education

Patients receiving continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea 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.

Obesity is increasing in children; 16-33% of children and adolescents are obese. Primary care providers should provide basic weight loss information and support and readily refer patients to a pediatric weight loss program. A pediatric sleep disorders clinic should work closely with a weight loss program and can be a portal of entry for a patient into such care systems.

Compliance issues are of particular importance in patients treated with noninvasive ventilation. Weight loss through an appropriate program of diet and exercise is clearly beneficial for patients with obstructive sleep apnea who are obese.

Avoidance of certain drugs and alcohol

Patients should avoid alcohol and other depressant recreational drugs, which may worsen their sleep apnea. They should avoid sedating medications when possible; if necessary appropriate monitoring and medical supervision is required.

Infants and children with obstructive sleep apnea may have serious respiratory embarrassment when given any sedative medication. Caution is necessary during any medical or dental procedures requiring conscious sedation.

For patient education resources, see the Sleep Disorders Center, as well as Disorders That Disrupt Sleep (Parasomnias).

 

Presentation

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.

Although no specific prevention has been reported, a high index of suspicion in patients with predisposing conditions or suggestive history is necessary for early detection. The need for increased awareness of and screening for obstructive sleep apnea among primary care providers is significant. History obtained during preventive health visits should include questions regarding snoring (frequency, quality), obvious nocturnal airway obstruction or apnea, restless sleep, mouth breathing, daytime inattention, hyperactivity or hypersomnolence, and family history of obstructive sleep apnea. Loud snoring 3 or more nights per week warrants further investigation.

The clinical presentation of a child with obstructive sleep apnea (OSA) syndrome is nonspecific and requires increased awareness by the primary care physician. Indeed, the medical history is usually normal, unless the pathophysiology of sleep-associated airway obstruction is related to one of the various conditions delineated in Etiology.

Clinical findings of tonsillar enlargement or obesity should prompt questioning regarding snoring. Family history of snoring, allergies, and exposure to environmental tobacco smoke are all strongly related to snoring. In the otherwise healthy child, parents principally report snoring during sleep. History of loud snoring 3 or more nights per week should increase suspicion of obstructive sleep apnea.

Parents occasionally comment on breathing difficulties during sleep (eg, gasps or heroic snorts), unusual sleeping positions, morning headaches, daytime fatigue, irritability, poor growth and weight gain, and behavioral problems. Nevertheless, even in cases in which a sleep specialist conducts the diagnostic interview, the accuracy of obstructive sleep apnea prediction is poor and does not exceed a sensitivity and specificity of 50-60%, particularly in distinguishing obstructive sleep apnea from benign snoring.

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.[7]

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 Examination

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.

Height and weight

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.

Face, neck, nose, and mouth

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 is abnormally small (micrognathia) or the jaw is 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. Carefully examine the nasal passages for mucosal swelling, cobblestone pattern of the mucosa, and reduced nasal airflow. Carefully evaluate the size and position of tonsils and uvula, particularly noting hypertrophy or malformation. Unfortunately, although tonsillar hypertrophy may contribute to the severity of obstructive sleep apnea, the data available to date have not established a clear relationship between tonsillar size and frequency or severity of apneic events. Furthermore, although more prevalent in patients with obstructive sleep apnea, tonsillar hypertrophy is also common in healthy children without obstructive sleep apnea, with a prevalence as high as 57%.

Document the width and height of the hard palate, as well as the overall appearance of the soft palate, looking for evidence of cleft or pharyngeal narrowing or compression.

Although not extensively evaluated in children, the Mallampati classification may help quantify the degree of oropharyngeal anatomical obstruction. This classification is based on the structures visualized with maximal mouth opening and the tongue extended. The classes are determined by the visible structures. In class I, the soft palate, fauces, uvula, and pillars are visible. In class II, the soft palate, fauces, and a portion of uvula are visible. In class III, the soft palate and base of uvula are visible. In class IV, only the hard palate is visible. The higher the Mallampati classification, the greater the likelihood of oropharyngeal obstruction, and the greater the risk of persistent obstruction following tonsillectomy and adenoidectomy.[8]

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 distention 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.

Chest and back

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.

Pulmonary

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.

Complications of Childhood Sleep Apnea

Morbidities can generally be divided into the 4 following immediate consequences of upper airway obstruction during sleep:

  • Sleep fragmentation

  • Increased work of breathing

  • Alveolar hypoventilation

  • Intermittent hypoxemia

Sleep fragmentation

Healthy adults who were awakened at various intervals during the night demonstrated performance decrements and increased sleepiness on the following day.[9] This was also true when EEG arousals, rather than behavioral arousals, were induced.

The physiological and behavioral effects of partial and total sleep loss due to obstructive sleep apnea in adults have been extensively investigated. Daytime tiredness or fatigue is a common symptom, although sleepiness, which is a subjective notion, may not be directly reported. Significant deterioration in functions that require concentration or dexterity, as well as automatic behavior with retrograde amnesia, disorientation, and morning confusion, have all been reported in patients with sleep fragmentation and has led to the term sleep drunkenness. In addition, personality changes and abnormal behavioral outbursts follow sleep fragmentation. Aggressiveness, irritability, anxiety attacks, and depression may occur.

Sleep fragmentation in adults affects neuropsychological and cognitive performance. No evidence suggests such impairments are absent in children, and such deleterious effects may be worse, given that the child's brain is undergoing active developmental changes. Reports of decreased intellectual function in children with tonsillar and adenoidal hypertrophy date from 1889 when Hill reported on "some causes of backwardness and stupidity in children." Schooling problems have been repeatedly reported in case studies of children with obstructive sleep apnea and, in fact, may underlie more extensive behavioral disturbances, such as restlessness, aggressive behavior, excessive daytime sleepiness, and poor test performances.

The neurocognitive and behavioral consequences of disrupted sleep architecture and hypoxemia caused by sleep-disordered breathing in children with obstructive sleep apnea have only recently been defined by appropriate scientific methodology in the pediatric population. However, some studies have documented that children with sleep disorders tend to have behavioral problems similar to those observed in children with attention deficit hyperactivity disorder (ADHD). A survey study of 782 children documented daytime sleepiness, hyperactivity, and aggressive behavior in children who snore.[10] Inverse correlations between memory and learning performance and the severity of obstructive sleep apnea were also found, and other studies have clearly demonstrated significant improvements in school performance after treatment of obstructive sleep apnea.

In a study of 19 preschool-aged children with obstructive sleep apnea, prior to tonsillectomy and adenoidectomy, cognitive scores were significantly lower in children with obstructive sleep apnea versus control subjects.[11] Following tonsillectomy and adenoidectomy, the scores of the children with obstructive sleep apnea improved compared with preoperative scores and did not differ from those of the matched controls. This underscores the importance of diagnosis and treatment, insofar as the cognitive impairments of children, unlike adults, take place in the developing brain.

Sleep deprivation, sleep disruption, and intermittent hypoxia independently may be sufficient to cause daytime effects in vulnerable children. Preliminary evidence suggests that, if left untreated, sleep-disordered breathing may impose long-term decrements in academic performance and that the combination of 2 or more of these factors can result in particularly impaired daytime functioning.

Increased work of breathing

A major cardiovascular consequence of obstructive sleep apnea in adults is arterial hypertension. Although the pathophysiological mechanisms of elevation in arterial tension are still under debate, intermittent arousal, hypoxemia, and increases in cardiac afterload during the obstructive apneic event apparently lead to enhanced sympathoadrenal discharge and heightened sympathetic tone, even during waking hours. Significant alterations in autonomic nervous system tone have been documented in children with obstructive sleep apnea, and modest diurnal elevations in arterial blood pressure have also been reported.

Sleep-disordered breathing is associated with higher systolic blood pressures in children aged 5-12 years and supports the use of an apnea hypopnea index (AHI) threshold of 5 for initiating treatment.[12] The long-term effects of this process in childhood and the effect on adult health are unknown.

A prominent clinical manifestation of increased work of breathing in children with obstructive sleep apnea is failure to thrive (FTT). Indeed, reports from the early 1980s found more than a 50% prevalence of FTT in patients with pediatric obstructive sleep apnea, and significant catch-up growth patterns have been reported after tonsillectomy and adenoidectomy, even in children with obesity and obstructive sleep apnea. The causes of poor growth include anorexia and dysphagia due to tonsillar and adenoid hypertrophy, diminished or altered patterns of nocturnal growth hormone secretion, hypoxemia, acidosis, and increased work of breathing during sleep.

In one study, a substantial reduction in resting energy expenditure was reported after adenotonsillectomy in children with obstructive sleep apnea and FTT with concomitant gains in body weight.[13] Another study demonstrated significant recovery in the insulin growth factor 1 axis.[14] These findings suggest that an important factor that mediates FTT in pediatric obstructive sleep apnea involves the combination of increased energy expenditure caused by increased respiratory effort and disruption of the pathways of the growth hormone somatomedin.

Alveolar hypoventilation

Intermittent hypercapnia frequently occurs among patients with various respiratory disorders, becomes more prominent or sustained during sleep, and is minimal or absent during wakefulness.

Children with obstructive sleep apnea who snore exhibit classic intermittent alveolar hypoventilation, which is elicited by increased upper airway resistance, concurrent with diminished or insufficient compensatory mechanisms developing during sleep.

In adults with obstructive sleep apnea, blunted ventilatory drive to hypercapnia during wakefulness develops and may potentially contribute to the pathophysiology of upper airway obstruction. In contrast, waking and sleeping ventilatory responses to hypercapnia in children with obstructive sleep apnea are similar to those measured in healthy children. However, arousal responses are attenuated during sleep, suggesting that long-standing interactions between sleep and upper airway resistance in these children primarily affect arousal mechanisms during sleep. Another potential contribution of alveolar hypoventilation and hypercapnia during sleep may relate to exacerbation of the effect of intermittent hypoxia on the vasomotor tone of the pulmonary circulation.

Intermittent hypoxemia

A serious consequence of intermittent hypoxia is elevation of pulmonary artery pressure due to pulmonary vasoconstriction, such that chronic intermittent nocturnal hypoxemia leads to development of pulmonary hypertension and cor pulmonale. In 27 pediatric patients with moderate-to-severe obstructive sleep apnea, radionuclide assessment of right ventricular function revealed reduced ejection fraction in 37% of these children and wall motion abnormality in 45%.[15] Another potentially serious consequence of intermittent hypoxia may involve its long-term deleterious effects on neuronal and intellectual function. Indeed, in a study on an animal model developed in the coauthor's laboratory, intermittent hypoxia was associated with significant increases in neuronal apoptosis and reduced functionality within brain regions that mediate learning and memory.

Because the peak age for obstructive sleep apnea coincides with that of a critical period for brain development, delayed diagnosis and treatment of obstructive sleep apnea possibly imposes a greater burden on vulnerable brain structures and ultimately hampers the overall neurocognitive potential of children with obstructive sleep apnea.

Neurobehavioral disturbances and diminished learning capabilities, stunted growth, altered respiratory load response patterns, and pulmonary hypertension are major consequences of obstructive sleep apnea in childhood. Early diagnosis and prevention of such morbidities are fundamental aspects of adequate pediatric care in the community.

Inflammation

The association of inflammation with obstructive sleep apnea is uncertain.

Markers of systemic inflammation such as interleukin (IL)–6[16] and C-reactive protein[17, 18, 19] are elevated in obstructive sleep apnea and decrease following adenotonsillectomy, suggesting that the elevation was due to the obstructive sleep apnea.

An increased inflammatory response may be associated with infectious diseases associated with tonsillar and adenoidal hypertrophy; thus, the issue of cause and effect can be difficult to ascertain.

 

 

DDx

Diagnostic Considerations

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

Go to Upper Airway Evaluation in Snoring and Obstructive Sleep Apnea for complete information on this topic.

Daytime somnolence

Daytime somnolence is a common complaint among individuals with obstructive sleep apnea. 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 obstructive sleep apnea. Sleepiness during the day may be due to numerous 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

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 obstructive sleep apnea 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 obstructive sleep apnea. 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

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 obstructive sleep apnea.

Nocturnal gastroesophageal reflux

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

Other disorders

Periodic limb movement disorder, nocturnal seizures, rhythmic movement disorder, and various parasomnias can be differentiated from obstructive sleep apnea on the basis of polysomnography.

Differential Diagnoses

 

Workup

Approach Considerations

Compared with the adult literature, the available normative data for sleep and cardiorespiratory parameters are rather sparse in the pediatric literature, such that most pediatric sleep laboratories use individually established reference ranges rather than referring to an authoritative text. Nevertheless, the general consensus criteria for a normal finding on sleep study are presented below and have been derived from the published literature on this subject and the authors' experience.

Reference-range parameters for sleep gas exchange and gas exchange in children are as follows (see also the image below):

  • Sleep latency - More than 10 minutes

  • Total sleep time (TST) - More than 5.5 hours

  • Percentage of rapid eye movement (REM) sleep - More than 15% of TST

  • Percentage of stage 3-4 non-REM sleep - More than 25% of TST

  • Respiratory arousal index (number per hour of TST) - Less than 5

  • Periodic leg movements (number per hour of TST) - Less than 1

  • Apnea index (number per hour of TST) - Less than 1

  • Hypopnea index (nasal/esophageal pressure catheter; number per hour of TST) - Less than 3

  • Nadir oxygen saturation - More than 92%

  • Mean oxygen saturation - More than 95%

  • Desaturation index (>4% for 5 s; number per hour of TST) - Less than 5

  • Highest carbon dioxide level - 52 mm Hg

  • Carbon dioxide level of more than 45 mm Hg - Less than 20% of TST

    Normal parameters for sleep gas exchange and gas e Normal parameters for sleep gas exchange and gas exchange in children.

The adult criteria usually used around the world for the diagnosis of obstructive sleep apnea do not apply to children. In fact, the finding of 10-15 obstructive apneic events per hour of sleep, which represents mild obstructive sleep apnea in an adult patient in whom treatment may not even be contemplated, represents a sleep-related respiratory disturbance corresponding to a severely affected child definitely in need of therapeutic intervention. Thus, an apnea hypopnea index (AHI) of more than 5 events per hour clearly represents an indication for treatment in children. An AHI of fewer than 3 events per hour does not require any intervention, and, in children with an AHI of more than 3 but fewer than 5 events per hour, the benefit of treatment remains to be determined.

Other diagnostic studies may be warranted to evaluate for complications of obstructive sleep apnea or to better assess the contribution of an underlying condition. In patients with severe obstructive sleep apnea, electrocardiography and echocardiography are particularly important to assess for pulmonary hypertension and cor pulmonale.

Currently, the only available tool for definitive diagnosis of obstructive sleep apnea is an overnight polysomnographic evaluation in the sleep laboratory. An overnight polysomnographic study usually includes multiple channels that aim to monitor sleep state, as well as cardiac and respiratory parameters (see the images below).

Nasopharyngoscopy or direct laryngoscopy and bronchoscopy may be required to determine anatomy prior to contemplated otolaryngologic surgery.

Compressed overnight polysomnography tracing of a Compressed overnight polysomnography tracing of a 6-year-old boy who snores, showing multiple events of obstructive apnea (green-shaded areas) associated with oxyhemoglobin desaturation (yellow-shaded areas) and EEG arousals (red-shaded areas).
Parameters monitored during an overnight pediatric Parameters monitored during an overnight pediatric sleep study.

Polysomnography

Polysomnography remains the criterion standard for establishing the diagnosis of obstructive sleep apnea (OSA) in infants, children, and adults. Ideally, polysomnography should be performed overnight and during the patient's usual bedtime.

Polysomnography provides the following measures:

  • Sleep state (≥2 EEG leads)

  • Electrooculogram (right and left)

  • Submental electromyelogram (EMG)

  • Airflow at nose and mouth (thermistor, capnography, or mask and pneumotachygraph)

  • Chest and abdominal wall motion (impedance or inductance plethysmography)

  • Electrocardiogram (preferably with R-R interval derivation technology)

  • Pulse oximetry (including a pulse waveform channel)

  • End-tidal carbon dioxide (sidestream or mainstream infrared sensor)

  • Video camera monitor with sound montage (analog or digital)

  • Transcutaneous oxygen and carbon dioxide tensions (in infants and children < 8 y)

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 (ET) CO2 measurements 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 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.

See the related polysomnographic image below.

Example of an obstructive apnea and an obstructive Example of an obstructive apnea and an obstructive hypopnea recorded during polysomnography.

Polysomnography is necessary to document obstructive sleep apnea and gauge its severity. A history of snoring alone is not adequate for making a diagnosis of obstructive sleep apnea or for determining its seriousness.

Some children with obstructive sleep apnea have primarily obstructive hypoventilation in which repetitive partial obstructions occur with some degree of relative oxygen desaturation and hypercapnia. Because of this, pediatric polysomnographic testing should include some means of determining CO2 levels, such as end-tidal (ET) CO2 monitoring or transcutaneous CO2 monitoring.

PSG, continuously monitored by appropriately trained technical personnel, may be difficult to arrange due to relative unavailability, with long waiting periods between referral and testing times. For these reasons, attempts have recently been made to evaluate the role of outpatient overnight studies to provide more accessible and practical approaches to the diagnosis of pediatric obstructive sleep apnea. However, these outpatient studies are not well validated yet or covered by third party payers and, thus, remain largely available only as research tools.

Apnea Hypopnea Index

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 1 or less 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.

Obstructive hypopnea (OH) in children is a sleep-related breathing disorder that is considered a variation of obstructive sleep apnea. Children with OH may have an AHI in the normal range, but they have episodic periods of hypercapnia, as identified on the basis of 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 to between 1 and 5, other clinical factors must be taken into account to determine whether to pursue adenotonsillectomy or other therapy.

Daytime Nap Studies

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 obstructive sleep apnea who have normal nap study findings must undergo nocturnal polysomnography to exclude the diagnosis. Sleep studies should be performed without sedation.

Overnight Oximetry

Unattended home overnight oximetry has been proposed as a screening study. However, it may miss the child with significant obstructive sleep apnea who does not have marked episodes of oxygen desaturation.

Overnight pulse oximetry by itself is not adequate for establishing the diagnosis or excluding obstructive sleep apnea in children because it provides no information concerning sleep staging/sleep fragmentation or carbon dioxide.

The results of initial studies indicate that, although home audio tape recordings appear relatively insensitive, oximetry trend analysis with or without additional measures may provide a useful alternative in establishing the definitive cases that require intervention. However, despite high specificity, home oximetry has low sensitivity, and children with negative findings on studies still require complete nocturnal polysomnography.

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.

Assessment of tonsillar size usually does not require any type of imaging; however, lateral neck radiographs can be used to determine adenoid size. Although MRI can provide very detailed images of soft tissues and bony structures underlying the nasopharynx, such images are not usually required, except in cases of suspected aberrant anatomy.

Cine MRI

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.

Thyroid-Stimulating Hormone and Thyroxine

Thyroid function studies are useful to exclude hypothyroidism, which is associated with tongue enlargement, weight gain, and obstructive sleep apnea.

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 echocardiography are helpful in assessing ventricular thickness and function and to check for evidence of pulmonary hypertension.

Multiple Sleep Latency Test (MSLT)

If the clinical history suggests the possibility of narcolepsy, the MSLT should be ordered in conjunction with overnight polysomnography.

MRI 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.

Other Studies

Additional studies include the following:

  • CBC count may be useful because chronic hypoxia related to recurrent airway obstruction may lead to polycythemia

  • Cephalometric radiography and 3-dimensional CT reconstruction imaging are rarely, if ever, necessary in the pediatric age group

  • Multichannel studies lack reliable assessment of sleep disruption

Emerging Studies

The following sleep study parameters are under investigation:

  • Nasal pressure–flow measurements

  • Esophageal manometry

  • Continuous noninvasive blood pressure monitoring

  • Autonomic nervous system tone using finger tonometry

 

Treatment

Approach Considerations

Adenotonsillectomy

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

Adenotonsillectomy, along with weight normalization, is considered the first line of therapy in children and adolescents with obstructive sleep apnea. Surgically removing the tonsils and adenoids increases cross-sectional airway caliber in patients, although 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 obstructive sleep apnea 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.

Children with severe obstructive sleep apnea require overnight hospital observation following adenotonsillectomy, especially if they fall into one of the high-risk groups.

Absence of snoring following surgery does not equal an absence of obstructive apnea.

Dietary restrictions

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

Introduce an appropriate diet in patients who are obese to facilitate weight reduction.

Weight reduction is most successful with the aid of a nutritionist or an established weight reduction program. However, such programs have a low success rate, and surgical intervention for severe obesity is increasingly considered in older children.

Although bariatric surgery is primarily thought of as a treatment option for adults, it is increasingly being considered in adolescents.

Activity restrictions

Many individuals with obstructive sleep apnea 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. Numerous epidemiologic studies link obstructive sleep apnea to motor vehicle accidents.[20]

Avoidance of certain drugs and alcohol

Patients should avoid alcohol and other depressant recreational drugs, which may worsen their sleep apnea. They should avoid sedating medications when possible; if necessary appropriate monitoring and medical supervision is required.

Infants and children with obstructive sleep apnea may have serious respiratory embarrassment when given any sedative medication. Caution is necessary during any medical or dental procedures requiring conscious sedation.

Drug therapy

In general, medical therapy is of limited value in the typical pediatric patient with obstructive sleep apnea (OSA). Oxygen therapy should not be prescribed as the primary therapy for OSA.

Antihistamine or antimuscarinic therapy may lead to relief in cases of nasal congestion, although sustained benefit is uncertain. For allergic rhinitis or conditions associated with decreased nasal airflow, efforts to improve nasal patency may be beneficial.

An oral leukotriene modifier may eliminate residual obstructive sleep apnea following surgery, and these agents may have a role in improving clinical outcomes without surgery. Although systemic steroids do not improve obstructive sleep apnea, topical budesonide used for 6 weeks has been demonstrated to lead to a sustained improvement in mild obstructive sleep apnea. Such preparations are unproven as therapy for severe obstructive sleep apnea. Topical therapy as a primary treatment for obstructive sleep apnea remains largely investigational.

In recent years, positive-pressure ventilation administered via a noninvasive interface (nasal mask) has become a safe, efficient, and viable alternative to further surgery or tracheotomy in children and infants with unresolved obstructive sleep apnea after tonsillectomy and adenoidectomy.

Positive-Pressure Ventilation

An important distinction must be made between continuous positive airway pressure (CPAP) and bilevel (or biphasic) positive airway pressure (BiPAP). In CPAP, airway pressure is maintained above atmospheric pressure throughout the respiratory cycle. CPAP is the mainstay of therapy for most adults with obstructive sleep apnea, 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. BiPAP or noninvasive ventilation is the preferred form of treatment over CPAP in children with OSA due to neuromuscular disease.[29]

Marcus et al demonstrated improvements in daytime sleepiness, ADHD symptoms, internalizing behaviors and overall quality of life in children with OSA as early as 3 months following the initiation of CPAP therapy. The findings held true in a heterogeneous group of children with OSA and were present even with a mean use of 3 hours/night. These authors suggest that despite the challenges of adherence in young or developmentally delayed children with OSA, clinicians should encourage use of CPAP therapy in appropriate children.[21]

Various 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.

In BiPAP, pressure is delivered during the inspiratory cycle; exhalation then occurs at either atmospheric pressure or at a preset positive airway pressure, such that differences between inspiratory and expiratory pressures are usually greater than 10 cm H2 O. The BiPAP device may be set to control ventilation entirely (control mode), to deliver breaths only when triggered by a threshold negative pressure or nasal flow generated by the patient (assist mode), or both (assist/control mode).

Because CPAP does not involve a respiratory phase change in pressure, no control or assist modes are available.

Another important aspect of these interventions involves the patient-machine interface. The use of nasal prongs, nasal masks, or facemasks requires individualized case-by-case consideration. However, when a silicone mask is selected, particular care to ensure that the mask fits snugly and is comfortable to the patient is essential for ensuring successful intervention. Pediatric masks are currently available in several sizes and for particular clinical conditions, such as craniofacial syndromes. Custom-made masks can be ordered to fit the facial contours.

Inappropriately fitting masks inevitably leak, and efforts to seal these leaks frequently result in pressure sores on the bridge of the nose. Bubble-cushioned masks have been developed and sometimes palliate the severity of the air leak while adding to the patient's comfort. In addition, air leaks are more frequently directed upward and may irritate the conjunctiva, leading to increased lacrimation and eye discomfort. Tolerance of CPAP or BiPAP may be greatly increased by devoting time to condition the patient to use the mask during waking hours, particularly in young or developmentally delayed patients.

Pay attention to the mask manifold to ensure that no pressure vectors are generated. Multiple techniques may be used to secure the mask and primarily include Velcro, elastic straps, or a tissue cap. Again, the importance of the patient's comfort cannot be overemphasized. Finally, implement adequate parental training and behavioral techniques designed to improve the acceptance and tolerance of these devices in order to increase patient and family compliance. Over the last decade, CPAP has been increasingly used in children as a successful alternative to upper airway surgery or tracheotomy. However, midfacial hypoplasia may develop with long-term use, particularly in children with neuromuscular weakness. In other situations, temporary palliation using supplemental oxygen may be implemented until surgery, provided that sufficient attention is given to the possibility that severe hypercapnia may develop.

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

Oral Appliances

Numerous commercially available oral (PO) appliances assist in bringing the lower jaw and tongue forward during sleep, thus improving obstructive sleep apnea. 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, PO appliances have extremely limited usefulness, if any, in pediatric patients.

Go to Oral Appliances in Snoring and Obstructive Sleep Apnea for complete information on this topic.

Nasal Strips

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.

Sleeping Position

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

Nasal fluticasone administered daily for 6 weeks is shown to ameliorate the frequency of obstructive events in children with mild-to-moderate obstructive sleep apnea due to tonsil or adenoid hypertrophy by about one half.

Nasal Steroids

Nasal steroids offer an opportunity to reduce obstructive events pending surgery or can be an alternative remedy for children with mild disease whose parents are reluctant to pursue surgical treatment.[22]

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 tonsillar hypertrophy or moderate-to-severe obstructive sleep apnea.

No studies have assessed the efficacy of topical steroid therapy in children with craniofacial abnormalities and obstructive sleep apnea.

Short courses of systemic steroids (prednisone, 1 mg/kg/d PO for 5 d) have been shown to be ineffective in the treatment of childhood obstructive sleep apnea due to tonsil or adenoid hypertrophy.

Adenotonsillectomy

In the pediatric population, most obstructive sleep apnea is related to tonsillar hypertrophy or adenoid hypertrophy. Adenotonsillectomy is curative in most instances. Children with obstructive sleep apnea 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%).

Although obstructive sleep apnea has multiple etiologies in children, once the diagnosis of obstructive sleep apnea has been established and its severity assessed, adenotonsillectomy is usually the first line of treatment. Tonsillotomy, rather than tonsillectomy, has been recently advocated as equally effective with less postoperative morbidity. Most of these surgical procedures can be performed safely on an outpatient basis.

Notwithstanding the surgery being planned, carefully consider the existence of risk factors for perioperative morbidity and adverse outcomes in the surgical planning. Children with severe obstructive sleep apnea, children younger than 2 years, and children with craniofacial syndromes or other conditions that contribute to the pathophysiology of obstructive sleep apnea are at a higher risk for surgical complications. For example, in children with severe obstructive sleep apnea, the existence of pulmonary hypertension and right ventricular dysfunction has been linked to the onset of cardiac arrhythmias during the process of anesthesia induction. Thus, preoperative echocardiographic assessment is indicated in these patients.

Similarly, for all of the risk categories mentioned above, an obtunded patient in whom the anesthetic effects on upper airway tone and reflexes are still compromised has a high risk of postsurgical upper airway obstruction.

Finally, the development of idiopathic pulmonary edema following the relief of upper airway obstruction has also been noted. Therefore, in this high-risk group of patients, pursue overnight cardiorespiratory monitoring in the intensive care unit.

Additional surgical options may include uvulopalatopharyngoplasty (see below), epiglottoplasty, and mandibular advancement procedures. However, most facilities lack extensive experience with these procedures in children, and the overall outcomes from these interventions have not been appropriately documented in the pediatric population. Extensive surgical intervention in the upper airway of the child may lead to decreased oral-motor functioning (ie, increased risk of aspiration) and, thus, multiple long-term complications. Therefore, seriously consider nonsurgical alternatives before recommending additional surgery.

A study by Mukhatiyar et al compared polysomnography outcomes of extracapsular tonsillectomy and adenoidectomy (ETA) and intracapsular tonsillectomy and adenoidectomy (ITA) in a cross-sectional study of 89 children with obstructive sleep apnea syndrome. The study found that both ETA and ITA are effective modalities to treat children with obstructive sleep apnea syndrome, with comparable surgical outcomes on short-term follow-up. However, the study added that when comorbid diagnoses of both asthma and obesity exist, children with obstructive sleep apnea syndrome are likely to be resistant to treatment with ITA compared with ETA.[23]

Another study sought to determine the prognosis for children with obstructive sleep apnea not treated with adenotonsillectomy who undergo watchful waiting instead. The study found that many candidates for adenotonsillectomy no longer have childhood obstructive sleep apnea syndrome on polysomnography after 7 months of watchful waiting. In this study, 42% of the children resolved and no longer met polysomnographic criteria for OSAS. In practice, a baseline low apnea/hypopnea index (AHI) and normal waist circumference, or low Pediatric Sleep Questionnaire (PSQ), and snoring score, may help identify an opportunity to avoid adenotonsillectomy.[24]

A study by Taylor et al investigated effects of adenotonsillectomy on cognitive test scores in children with obstructive sleep apnea reported small and selective effects on nonverbal reasoning, fine motor skills, and selective attention.[25]  Another study by Lee et al that included 240 nonobese children with OSA reported that adenotonsillectomy led to significant improvement in blood pressure in hyperintensive children with OSA.[26]

 

Go to Surgical Approach to Snoring and Obstructive Sleep Apnea for complete information on this topic.

Uvulopalatopharyngoplasty

Uvulopalatopharyngoplasty (UPPP [ie, UP3]) 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 obstructive sleep apnea 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 obstructive sleep apnea. Follow-up polysomnography 2-3 months after surgery is warranted to reassess for residual apnea.

Palate appearance following uvulopalatopharyngopla Palate appearance following uvulopalatopharyngoplasty (UPPP) surgery.

Go to Surgical Approach to Snoring and Obstructive Sleep Apnea for complete information on this topic.

Tongue Reduction

Tongue reduction procedures (midline partial glossectomy) may have some use in a small number of carefully selected pediatric patients (eg, Beckwith-Wiedemann syndrome).

Tracheotomy

Tracheotomy remains an effective surgical option for life-threatening obstructive apnea that is not amenable to other therapies.

In the past, when surgery did not relieve the degree of sleep-associated respiratory disturbance, a tracheotomy was frequently performed. Currently, this alternative is rarely needed because of the development of noninvasive approaches to maintain upper airway patency during sleep.

Bariatric Surgery

Although bariatric surgery is primarily performed in patients who are obese, the associated weight loss may be of value in reducing obstructive sleep apnea because obesity predicts a lower success rate in treatment of obstructive sleep apnea by adenotonsillectomy.

The effects of weight loss surgery on health problems associated with morbid obesity include decreases in severity or incidence of obstructive sleep apnea, diabetes, asthma, hypertension, infertility, arthritis, heart disease, reflux, stress incontinence, and pseudotumor cerebri.

Go to Surgical Approach to Snoring and Obstructive Sleep Apnea for complete information on this topic.

Complications

Children with severe obstructive sleep apnea 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 a respiratory disturbance index (RDI) of more than 40 events per hour or oxygen desaturations less than 70%

  • Patients undergoing uvulopalatopharyngoplasty (UPPP) in addition to tonsillectomy or adenoidectomy

  • Complicating cardiac or pulmonary disease

Consultations

Teams of pediatric specialists often collaborate in the care of infants and children with sleep apnea. Members of the following specialty groups have specific expertise that may help the primary care physician coordinate the care of their patient with sleep apnea:

  • Pediatric sleep medicine

  • Pediatric otolaryngology

  • Pediatric plastic surgery

  • Orthognathic surgery

  • Pediatric neurosurgery

  • Pediatric anesthesia

  • PICU

  • Pediatric endocrinology

  • Pediatric pulmonology

  • Pediatric cardiology

For the otherwise healthy child with enlarged tonsils and adenoids, consultation with a pediatric sleep specialist and referral to a pediatric sleep laboratory for diagnosis are usually sufficient.

When findings support the existence of obstructive sleep apnea, refer the patient to a pediatric otolaryngologist for adenotonsillectomy and take appropriate perioperative and postoperative precautions in higher-risk groups. When obesity is present, refer the patient to a nutritional intervention program. Similarly, pursue echocardiography and input from a pediatric cardiologist when pulmonary hypertension is clinically suspected.

When craniofacial syndromes or neuromuscular disorders are the major cause of obstructive sleep apnea, a multidisciplinary approach is mandatory for improved outcomes.

Long-Term Monitoring

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

In most otherwise healthy children with obstructive sleep apnea, adenotonsillectomy results in complete resolution of the problem, and a postsurgical evaluation in the sleep laboratory is usually not recommended. However, residual mild sleep-disordered breathing is found in more than one third of these patients after adenotonsillectomy, particularly those included in the high-risk category. Thus, adenotonsillectomy alone may not suffice, and polysomnographic evaluation 6-8 weeks after adenotonsillectomy may confirm the need for additional treatment, including the use of intranasal steroids and oral leukotriene modifier therapy or CPAP and/or bilevel positive airway pressure (BiPAP).

Individuals undergoing surgical treatment for moderate-to-severe obstructive sleep apnea should have follow-up polysomnography 2-3 months after their operations to ensure 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 true for individuals who undergo uvulopalatopharyngoplasty (UPPP) alone.

Daytime fatigue and somnolence may persist after successful treatment for obstructive sleep apnea 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.

Patients should maintain a healthy weight with good eating habits and appropriate exercise. Although numerous factors influence the development of obstructive sleep apnea, obesity has been associated with a 4-fold to 5-fold risk in children aged 2-18 years.

Patients treated with noninvasive ventilation require close follow-up by a pediatric pulmonologist and may periodically require a repeat polysomnographic evaluation. Treat patients who are found to have significant hypoxemia during polysomnography as soon as possible with overnight supplemental oxygen until adenotonsillectomy can be performed. Carefully assess the patient when using oxygen because of the rare possibility that significant hypercapnia may develop during the night

 

Medication

Medication Summary

No effective pharmacologic therapy for childhood obstructive sleep apnea is recognized. Individuals with obstructive sleep apnea 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 obstructive sleep apnea. 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 obstructive sleep apnea 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.

Preliminary studies suggest an oral leukotriene modifier therapy may reduce the severity of obstructive sleep apnea; however, this intervention is currently considered investigational. Intranasal budesonide used for 6 weeks has been demonstrated to lead to a sustained improvement in mild obstructive sleep apnea but is unproven as therapy for severe obstructive sleep apnea.[27]

 

Questions & Answers

Overview

How is childhood obstructive sleep apnea (OSA) characterized?

What are the signs and symptoms of childhood obstructive sleep apnea (OSA) in children?

How are the complications of childhood obstructive sleep apnea (OSA) categorized?

What is the only available tool for definitive workup of childhood obstructive sleep apnea (OSA)?

Which measures are provided by polysomnography in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of surgery in the treatment of obstructive sleep apnea (OSA)?

What is the role of CPAP in childhood obstructive sleep apnea (OSA) treatment?

What is childhood obstructive sleep apnea (OSA)?

What is the pathophysiology of childhood obstructive sleep apnea (OSA)?

What is the pathophysiology of apneas and hypopneas in childhood obstructive sleep apnea (OSA)?

What is the pathophysiology of upper airway obstruction in childhood obstructive sleep apnea (OSA)?

How does the pathophysiology of obstructive sleep apnea (OSA) differ between children and adults?

What is the role of anatomic narrowing in the pathophysiology of childhood obstructive sleep apnea (OSA)?

What is the role of mechanical dilating in the pathophysiology of childhood obstructive sleep apnea (OSA)?

What is the role of muscle weakness in the pathophysiology of childhood obstructive sleep apnea (OSA)?

What is the role of neural regulation in the pathophysiology of childhood obstructive sleep apnea (OSA)?

What causes childhood obstructive sleep apnea (OSA)?

Which disorders are associated with childhood obstructive sleep apnea (OSA)?

What is the prevalence of childhood obstructive sleep apnea (OSA)?

What are the racial predilections of childhood obstructive sleep apnea (OSA)?

What are the sexual predilections of childhood obstructive sleep apnea (OSA)?

Which age groups have the highest prevalence of childhood obstructive sleep apnea (OSA)?

What is the prognosis of obstructive sleep apnea (OSA)?

What is the postsurgical prognosis of childhood obstructive sleep apnea (OSA)?

What is included in patient education about childhood obstructive sleep apnea (OSA)?

Presentation

Which clinical history findings are characteristic of childhood obstructive sleep apnea (OSA)?

Which clinical history findings are characteristic of abnormal breathing during sleep in childhood obstructive sleep apnea (OSA)?

Which clinical history findings of restlessness suggest childhood obstructive sleep apnea (OSA)?

Which clinical history findings related to dreaming suggest childhood obstructive sleep apnea (OSA)?

Which clinical history findings related to enuresis suggest childhood obstructive sleep apnea (OSA)?

Which clinical history findings related to morning awakening suggest obstructive sleep apnea (OSA)?

Which clinical history findings are characteristic of excessive daytime sleepiness (EDS) in obstructive sleep apnea (OSA)?

Which behavior problems may suggest childhood obstructive sleep apnea (OSA)?

What causes daytime mouth breathing in obstructive sleep apnea (OSA)?

How are other causes of excessive daytime sleepiness differentiated from childhood obstructive sleep apnea (OSA)?

How is primary snoring differentiated from childhood obstructive sleep apnea (OSA)?

Which oral and maxillofacial findings are characteristic of childhood obstructive sleep apnea (OSA)?

What is included in the physical exam to evaluate childhood obstructive sleep apnea (OSA)?

Which height and weight findings are characteristic of childhood obstructive sleep apnea (OSA)?

Which chest and back findings are characteristic of childhood obstructive sleep apnea (OSA)?

Which pulmonary findings are characteristic of childhood obstructive sleep apnea (OSA)?

What are the common morbidities of childhood obstructive sleep apnea (OSA)?

What are the adverse effects of sleep fragmentation due to childhood obstructive sleep apnea (OSA)?

What are the adverse effects of the increased work of breathing due to childhood obstructive sleep apnea (OSA)?

What are the adverse effects of alveolar hypoventilation due to childhood obstructive sleep apnea (OSA)?

What are the adverse effects of intermittent hypoxemia due to childhood obstructive sleep apnea (OSA)?

What is the role of inflammation in obstructive sleep apnea (OSA)?

DDX

How do the symptoms of simple snoring differ from childhood obstructive sleep apnea (OSA)?

How is daytime somnolence differentiated from childhood obstructive sleep apnea (OSA)?

How is narcolepsy differentiated from childhood obstructive sleep apnea (OSA)?

How are hypnagogic hallucinations differentiated from childhood obstructive sleep apnea (OSA)?

How is nocturnal gastroesophageal reflux differentiated from childhood obstructive sleep apnea (OSA)?

Which sleep disorders are differentiated from childhood obstructive sleep apnea (OSA) on the basis of polysomnography?

What are the differential diagnoses for Childhood Sleep Apnea?

Workup

What are the reference-range parameters for sleep study findings in children with obstructive sleep apnea (OSA)?

How are pulmonary hypertension and cor pulmonale assessed in childhood obstructive sleep apnea (OSA)?

Which tests are performed in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of polysomnography in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of the apnea hypopnea index (API) in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of daytime nap studies in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of overnight oximetry in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of radiography in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of cine MRI in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of thyroid function tests in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of ECG and echocardiography in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of multiple sleep latency test (MSLT) in the workup of childhood obstructive sleep apnea (OSA)?

What is the role of MRI of the brain in the workup of childhood obstructive sleep apnea (OSA)?

Which clinical studies may be beneficial in the workup of childhood obstructive sleep apnea (OSA)?

Which sleep study parameters are under investigation for assessment of childhood obstructive sleep apnea (OSA)?

Treatment

What is the role of adenotonsillectomy in childhood obstructive sleep apnea (OSA) treatment?

Which dietary modifications are used in the treatment of children with obstructive sleep apnea (OSA)?

Which activity modifications are used in the treatment of children with obstructive sleep apnea (OSA)?

Why should patients with obstructive sleep apnea (OSA) avoid certain drugs and alcohol?

Which medications are used in the treatment of childhood obstructive sleep apnea (OSA)?

What is the role of positive-pressure ventilation in childhood obstructive sleep apnea (OSA) treatment?

What is the role of oral appliances in childhood obstructive sleep apnea (OSA) treatment?

What is the role of nasal strips in childhood obstructive sleep apnea (OSA) treatment?

What is the role of sleeping position in the treatment of childhood obstructive sleep apnea (OSA)?

What is the role of nasal fluticasone in childhood obstructive sleep apnea (OSA) treatment?

What is the role of nasal steroids in childhood obstructive sleep apnea (OSA) treatment?

What is the role of adenotonsillectomy in the treatment of childhood obstructive sleep apnea (OSA)?

What is the role of uvulopalatopharyngoplasty (UPPP) in childhood obstructive sleep apnea (OSA) treatment?

What is the role of tongue reduction in childhood obstructive sleep apnea (OSA) treatment?

What is the role of tracheotomy in childhood obstructive sleep apnea (OSA) treatment?

What is the role of bariatric surgery in childhood obstructive sleep apnea (OSA) treatment?

What are the risk factors for postoperative pulmonary edema in children with obstructive sleep apnea (OSA)?

Which specialist consultations are beneficial to patients with childhood obstructive sleep apnea (OSA)?

What is included in long-term monitoring of childhood obstructive sleep apnea (OSA)?

Medications

What is the role of medications in childhood obstructive sleep apnea (OSA) treatment?