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Childhood Sleep Apnea Clinical Presentation

  • Author: Mary E Cataletto, MD; Chief Editor: Girish D Sharma, MD, FCCP, FAAP  more...
Updated: Apr 21, 2016


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.


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.


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.


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] 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.

Contributor Information and Disclosures

Mary E Cataletto, MD Professor of Clinical Pediatrics, State University of New York at Stony Brook

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians

Disclosure: Nothing to disclose.


Timothy D Murphy, MD Consulting and Attending Staff, Pediatric Pulmonary and Sleep Medicine, Mary Bridge Children's Hospital

Timothy D Murphy, MD is a member of the following medical societies: American Thoracic Society, American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Andrew J Lipton, MD MPH and TM, Staff Pediatric Pulmonologist, Assistant Professor of Pediatrics, Department of Pediatrics, Walter Reed Army Medical Center

Andrew J Lipton, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Girish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush Children's Hospital, Rush University Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Additional Contributors

Susanna A McColley, MD Professor of Pediatrics, Northwestern University, The Feinberg School of Medicine; Director of Cystic Fibrosis Center, Head, Division of Pulmonary Medicine, Children's Memorial Medical Center of Chicago

Susanna A McColley, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Sleep Disorders Association, American Thoracic Society

Disclosure: Received honoraria from Genentech for speaking and teaching; Received honoraria from Genentech for consulting; Partner received consulting fee from Boston Scientific for consulting; Received honoraria from Gilead for speaking and teaching; Received consulting fee from Caremark for consulting; Received honoraria from Vertex Pharmaceuticals for speaking and teaching.


Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

David Gozal, MD Vice-Chairman of Research and Director, Comprehensive Sleep Medicine Center, Kosair Children's Hospital; Professor, Department of Pediatrics, University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Michael Steffan, MD Director of Pediatric Sleep Center, Department of Pediatrics, Department of Pediatrics, Children's Medical Center; Associate Professor, Wright State University School of Medicine

Disclosure: Nothing to disclose.

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Palate appearance following uvulopalatopharyngoplasty (UPPP) surgery.
Example of an obstructive apnea and an obstructive hypopnea recorded during polysomnography.
Medical complications associated with obstructive sleep apnea in children.
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 sleep study.
Normal parameters for sleep gas exchange and gas exchange in children.
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