Sleep-Disordered Breathing in Children: Symptoms, Causes & Treatment

What Is Sleep-Disordered Breathing in Children?

Sleep-disordered breathing (SDB) is a spectrum of conditions ranging from simple snoring to obstructive sleep apnea syndrome, where the airway becomes partially or completely blocked during sleep. In children, the most common cause is enlarged tonsils and adenoids, which obstruct the airway during the muscle relaxation that occurs during sleep.

Sleep-disordered breathing encompasses several related conditions that affect how children breathe during sleep. Understanding this spectrum is crucial for parents and caregivers, as the severity of the condition determines the urgency of treatment and the potential for complications. The term describes a continuum from mild breathing disturbances to severe obstructive sleep apnea that can significantly impact a child's health, development, and quality of life.

At its mildest, sleep-disordered breathing may present as primary snoring, where a child snores regularly but without significant breathing pauses or oxygen desaturation. Primary snoring affects approximately 10-12% of children and, while often considered benign, research increasingly suggests it may still impact sleep quality and daytime function in some children. Moving along the spectrum, upper airway resistance syndrome (UARS) involves increased effort to breathe that fragments sleep, even without frank apneas or significant oxygen drops.

The most concerning form is obstructive sleep apnea syndrome (OSAS), affecting 1-5% of children. In OSAS, the airway repeatedly collapses during sleep, causing breathing pauses (apneas) or significant reductions in airflow (hypopneas). These events lead to drops in blood oxygen levels and disrupted sleep architecture, with consequences that extend far beyond nighttime symptoms. Children with untreated OSAS may experience impaired growth due to disrupted growth hormone secretion, neurocognitive deficits affecting learning and memory, behavioral problems that mimic ADHD, and in severe cases, cardiovascular complications including pulmonary hypertension.

The pathophysiology in children differs significantly from adults. While adult obstructive sleep apnea is predominantly related to obesity and aging, pediatric SDB most commonly results from adenotonsillar hypertrophy – enlarged tonsils and adenoids that occupy a disproportionately large space in the child's relatively small airway. The peak incidence occurs between ages 2-8 years, corresponding to the age when lymphoid tissue (adenoids and tonsils) is largest relative to airway size. This anatomical basis explains why surgical removal of adenoids and tonsils is so effective in children, with cure rates of 80-90% in otherwise healthy children.

The Spectrum of Sleep-Disordered Breathing

Understanding where a child falls on the SDB spectrum helps guide appropriate evaluation and treatment. The spectrum includes several distinct but overlapping conditions, each with characteristic features and implications for management.

Primary snoring, the mildest form, involves habitual snoring (more than 3 nights per week) without apneas, hypopneas, frequent arousals, or gas exchange abnormalities. While often reassuring, primary snoring warrants monitoring as some children progress to more significant SDB. Recent research suggests that even primary snoring may affect some aspects of cognitive function and behavior, though findings are inconsistent.

Upper airway resistance syndrome sits between primary snoring and frank obstructive sleep apnea. Children with UARS experience increased respiratory effort during sleep that leads to frequent arousals and sleep fragmentation, even without meeting criteria for obstructive apnea. They may have significant daytime symptoms despite apparently normal polysomnography results when using standard scoring criteria.

Obstructive sleep apnea syndrome represents the severe end of the spectrum, characterized by repeated episodes of partial (hypopnea) or complete (apnea) upper airway obstruction during sleep. The American Academy of Sleep Medicine defines pediatric OSAS as an apnea-hypopnea index (AHI) of 1 or more events per hour, significantly lower than the adult threshold of 5 or more, reflecting the greater vulnerability of children to the effects of sleep disruption.

What Are the Symptoms of Sleep-Disordered Breathing in Children?

Symptoms of sleep-disordered breathing in children include loud snoring most nights, observed breathing pauses or gasping during sleep, restless sleep, mouth breathing, unusual sleeping positions, bedwetting, morning headaches, daytime fatigue, behavioral problems, and difficulty concentrating. Children may also show paradoxical hyperactivity rather than sleepiness.

Recognizing sleep-disordered breathing in children requires attention to both nighttime and daytime symptoms, as the manifestations differ substantially from adult presentations. Parents often first notice nighttime symptoms, but the daytime consequences may be equally or more impactful on the child's life. The symptoms can be subtle, and many parents initially dismiss snoring as normal or attribute behavioral problems to other causes.

Understanding the full range of symptoms is essential because sleep-disordered breathing often mimics other conditions. Children with untreated sleep apnea are frequently misdiagnosed with attention-deficit/hyperactivity disorder (ADHD) when their symptoms actually stem from chronic sleep deprivation. Similarly, growth failure may prompt extensive endocrine workups before the underlying sleep disorder is identified. Early recognition of the symptom pattern can expedite appropriate diagnosis and treatment.

Nighttime Symptoms

Snoring is the most recognizable symptom, present in virtually all children with obstructive sleep apnea. However, the quality and pattern of snoring provide important diagnostic clues. Snoring associated with significant SDB tends to be loud (often audible from another room), present most nights, and may have an irregular pattern with pauses followed by gasping or snorting sounds. Parents may describe the child as "struggling to breathe" during these episodes. It's important to note that snoring severity doesn't always correlate with apnea severity – some children with severe obstruction have relatively quiet snoring due to complete airway closure rather than vibration.

Observed apneas – witnessed breathing pauses during sleep – are highly specific for obstructive sleep apnea when reported by parents. These episodes may end with a gasp, snort, or body movement as the child partially arouses to resume breathing. Some parents describe hearing their child "stop breathing" followed by a loud intake of air. While parental observation of apneas has moderate sensitivity, its specificity makes it an important symptom to inquire about specifically.

Restless sleep and unusual sleeping positions reflect the child's unconscious attempts to maintain airway patency. Children with SDB often sleep in positions that help keep the airway open – with the neck hyperextended, propped up on pillows, or even sitting up. Some children adopt a knee-chest position. Frequent position changes, thrashing, and restlessness throughout the night suggest the sleep fragmentation characteristic of significant SDB.

Mouth breathing during sleep and when awake often accompanies adenoid hypertrophy, which obstructs the nasal airway. Chronic mouth breathing can lead to characteristic facial changes over time, including elongated facial structure, dental malocclusion, and orthodontic problems. The presence of mouth breathing should prompt evaluation of adenoid size.

Diaphoresis (sweating) during sleep results from the increased respiratory effort required to breathe against an obstructed airway. The autonomic activation associated with obstructive events can also contribute to night sweats. Parents may report needing to change pajamas or sheets due to sweating.

Secondary enuresis (bedwetting in a previously dry child) occurs more frequently in children with sleep apnea due to disrupted sleep architecture affecting normal arousal responses and alterations in hormone secretion including antidiuretic hormone. Resolution of bedwetting following treatment of sleep apnea provides evidence of this connection.

Daytime Symptoms

Behavioral problems are among the most common and impactful daytime manifestations of pediatric SDB. Unlike adults who typically become sleepy when sleep-deprived, children often exhibit paradoxical hyperactivity. They may be described as "always on the go," impulsive, easily frustrated, emotionally labile, or aggressive. These symptoms overlap substantially with ADHD, and studies suggest that 25-50% of children with ADHD symptoms may have underlying sleep-disordered breathing. Treatment of SDB often improves or resolves these behavioral concerns.

Cognitive and academic difficulties reflect the impact of chronic sleep fragmentation on brain function. Children with untreated SDB may have difficulty with attention, memory, and learning. School performance may suffer, with teachers reporting that the child seems unable to focus or complete tasks. Research has documented lower scores on neurocognitive testing and academic performance measures in children with sleep apnea compared to controls, with improvement following treatment.

Daytime sleepiness, while less prominent than in adults, does occur in some children with SDB. Parents may report difficulty waking the child in the morning, falling asleep during car rides or quiet activities, or needing naps beyond the age when peers have outgrown them. However, the absence of obvious sleepiness does not rule out significant SDB in children.

Morning headaches can result from the elevated carbon dioxide levels and sleep disruption associated with obstructive events. These headaches typically improve within an hour of waking but may occur frequently in children with significant SDB.

Growth failure in severe cases reflects the disruption of growth hormone secretion, which normally occurs during deep sleep, as well as increased energy expenditure from labored breathing. Children with untreated severe sleep apnea may show failure to thrive or plot below expected growth curves, with catch-up growth following treatment.

What Causes Sleep-Disordered Breathing in Children?

The most common cause of sleep-disordered breathing in children is adenotonsillar hypertrophy – enlarged adenoids and tonsils that obstruct the airway during sleep. Other causes include obesity, craniofacial abnormalities (such as those in Down syndrome), neuromuscular disorders, and allergic rhinitis. Multiple factors often contribute to airway obstruction in any individual child.

Understanding the causes of pediatric sleep-disordered breathing is essential for appropriate treatment selection. Unlike adult obstructive sleep apnea, which is predominantly related to obesity and pharyngeal collapsibility, pediatric SDB has a more diverse etiology with adenotonsillar hypertrophy as the dominant factor. However, the increasing prevalence of childhood obesity has led to a rising proportion of cases with obesity as a primary or contributing cause, with implications for treatment approach and outcomes.

The upper airway is a complex structure that must remain patent during the muscle relaxation of sleep while still allowing the flexibility needed for speech and swallowing. In children, the airway is narrower than in adults, and any factor that further reduces airway caliber or increases its collapsibility can predispose to obstruction during sleep. The pathophysiology of pediatric SDB involves an interplay between anatomical factors (airway size, adenotonsillar tissue volume) and functional factors (neuromuscular control, ventilatory drive).

Adenotonsillar Hypertrophy

Enlarged tonsils and adenoids represent the most common cause of pediatric obstructive sleep apnea, accounting for the majority of cases in otherwise healthy children. The lymphoid tissue of the tonsils and adenoids grows throughout early childhood, typically reaching maximum size between ages 3-7 years before gradually involuting. During this period, the relative size of lymphoid tissue to airway space is at its highest, explaining the peak incidence of SDB in this age group.

The adenoids are located in the nasopharynx, where they can obstruct nasal airflow and contribute to mouth breathing even when awake. Enlarged adenoids force children to breathe through their mouths, altering airway dynamics and potentially contributing to upper airway collapsibility during sleep. The tonsils, located in the oropharynx, directly impinge on the airway and can cause obstruction particularly in the supine position when gravity allows them to fall posteriorly.

It's important to note that tonsil and adenoid size does not always correlate perfectly with sleep apnea severity. Some children with moderately enlarged tonsils have severe apnea, while others with very large tonsils may have minimal symptoms. This observation reflects the contribution of other factors to upper airway patency, including airway shape, neuromuscular tone, and ventilatory control mechanisms.

Obesity

Childhood obesity is an increasingly important cause of pediatric SDB, mirroring trends in adult populations. Fat deposition around the upper airway narrows its caliber and increases collapsibility. Additionally, central obesity with fat accumulation in the abdomen reduces lung volumes, which in turn affects upper airway stability through reduced tracheal tug. Obese children with SDB often have a combination of adenotonsillar hypertrophy and obesity-related factors.

The rising prevalence of childhood obesity has important implications for SDB treatment outcomes. While adenotonsillectomy is highly effective for non-obese children with SDB, cure rates are substantially lower in obese children, ranging from 25-75% depending on obesity severity. Obese children are more likely to have residual sleep apnea after surgery and may require additional interventions including weight management or CPAP therapy.

Craniofacial Abnormalities

Children with certain craniofacial conditions are at markedly increased risk for sleep-disordered breathing due to structural differences that narrow or predispose to collapse of the upper airway. Down syndrome is the most common genetic condition associated with pediatric OSA, with prevalence estimates ranging from 30-60%. Multiple factors contribute including midface hypoplasia, relative macroglossia, hypotonia, and increased susceptibility to respiratory infections. Children with Down syndrome often have more severe disease and lower cure rates with adenotonsillectomy alone.

Pierre Robin sequence, characterized by micrognathia, glossoptosis, and often cleft palate, can cause significant airway obstruction from birth. These infants may require specialized positioning, airway interventions, or surgical procedures to maintain adequate breathing. Achondroplasia, Treacher Collins syndrome, and other craniofacial dysostoses also predispose to SDB through various mechanisms affecting airway size and shape.

Other Contributing Factors

Allergic rhinitis and chronic nasal congestion contribute to SDB by increasing nasal resistance and promoting mouth breathing. The resulting oral breathing alters upper airway dynamics and may worsen obstruction during sleep. Treatment of allergies with nasal corticosteroids or antihistamines may improve mild SDB or serve as adjunctive therapy.

Neuromuscular disorders predispose to SDB through reduced upper airway muscle tone. Conditions such as muscular dystrophy, cerebral palsy, and other hypotonic states are associated with increased risk of both obstructive and central sleep apnea. These children often require specialized evaluation and management.

Laryngomalacia and other laryngeal abnormalities can contribute to airway obstruction, particularly in infants and young children. While laryngomalacia typically improves by age 2, some children have persistent or recurrent symptoms that warrant evaluation for sleep-disordered breathing.

When Should You Take Your Child to the Doctor?

Take your child to the doctor if they snore loudly most nights, you observe breathing pauses during sleep, they have excessive daytime sleepiness or behavioral problems, school performance is declining, bedwetting has developed after previously being dry, or they have morning headaches. Seek immediate evaluation for prolonged breathing pauses or color changes during sleep.

Parents often wonder whether their child's snoring warrants medical attention or represents a normal variation. While mild, occasional snoring can be benign, certain patterns and associated symptoms should prompt evaluation. Early identification and treatment of significant sleep-disordered breathing can prevent complications affecting growth, development, behavior, and cardiovascular health.

The American Academy of Pediatrics recommends that all children be screened for snoring as part of routine health supervision visits. Children who snore regularly should be evaluated further for symptoms and signs of obstructive sleep apnea. However, symptoms may develop gradually, and parents may not recognize problems that have evolved slowly over time. Being aware of the specific symptoms that warrant concern can help parents seek timely evaluation.

Signs That Warrant Medical Evaluation

Consultation with your child's pediatrician is recommended if you observe any of the following patterns:

• Habitual snoring: Snoring that occurs most nights (three or more nights per week) rather than only when congested with a cold
• Loud snoring: Snoring audible from outside the child's room or described as "like a train"
• Witnessed breathing pauses: Any observed episodes where the child appears to stop breathing during sleep, especially if followed by gasping or choking
• Labored breathing during sleep: Visible effort to breathe, use of accessory muscles, or chest retractions during sleep
• Unusual sleeping positions: Consistently sleeping with neck hyperextended, propped up, or in other positions that suggest airway compromise
• Mouth breathing: Chronic mouth breathing during sleep and wakefulness
• Secondary enuresis: Bedwetting that develops after the child had been reliably dry
• Behavioral problems: New or worsening hyperactivity, aggression, attention problems, or emotional dysregulation
• School difficulties: Declining academic performance, difficulty concentrating, or reports of inattention from teachers
• Excessive daytime sleepiness: Difficulty waking, falling asleep during activities, or needing naps beyond age-appropriate patterns
• Morning headaches: Regular headaches upon waking that improve within an hour
• Growth concerns: Failure to follow expected growth curves or falling off the growth chart

How Is Sleep-Disordered Breathing Diagnosed in Children?

Diagnosis of sleep-disordered breathing in children involves clinical history, physical examination focusing on tonsil and adenoid size, and polysomnography (overnight sleep study) as the gold standard test. The sleep study measures brain waves, oxygen levels, breathing patterns, and body movements to determine the severity of obstruction. Home sleep testing may be used in select cases.

Accurate diagnosis of pediatric sleep-disordered breathing requires a systematic approach combining clinical assessment with objective sleep testing. While symptoms and physical examination findings can suggest the diagnosis, neither clinical prediction models nor questionnaires alone are sufficiently accurate to definitively diagnose or exclude obstructive sleep apnea. Polysomnography remains the gold standard for confirming the diagnosis and determining severity, which guides treatment decisions.

The diagnostic evaluation serves multiple purposes: confirming the presence of sleep-disordered breathing, determining its severity, identifying contributing anatomical or medical factors, and establishing baseline measurements for comparison after treatment. This comprehensive assessment informs treatment selection, predicts outcomes, and identifies children who may need additional interventions or closer monitoring.

Clinical Evaluation

The diagnostic process begins with a thorough history focusing on sleep-related symptoms (snoring characteristics, witnessed apneas, sleep quality, sleeping positions), daytime symptoms (sleepiness, behavioral problems, school performance), and relevant medical history (recurrent throat infections, allergies, previous surgeries). Questions about developmental milestones, growth patterns, and family history of sleep disorders provide additional context.

Physical examination focuses on factors that may predispose to or worsen sleep-disordered breathing. Assessment of tonsil size (graded 0-4+ based on how much of the airway they occupy), evaluation of the adenoid facies (chronic mouth breathing appearance), examination of the nasal passages for obstruction, assessment of craniofacial structure, and documentation of height and weight for growth curve evaluation are all important components. The presence of obesity, hypotonia, or features of underlying syndromes guides further evaluation and treatment planning.

Questionnaires and screening tools, such as the Pediatric Sleep Questionnaire (PSQ) and Sleep-Related Breathing Disorder scale of the Pediatric Sleep Questionnaire (SRBD), can help identify children at higher risk for OSA. However, these tools have limited accuracy and cannot replace polysomnography for definitive diagnosis. They are most useful for screening and prioritizing which children need urgent evaluation.

Polysomnography

Polysomnography (PSG), commonly called a sleep study, is the definitive test for diagnosing and grading the severity of obstructive sleep apnea in children. During an overnight study in a sleep laboratory, multiple physiological parameters are continuously monitored and recorded by trained technicians.

The study measures brain activity (EEG) to determine sleep stages and identify arousals, eye movements (EOG) to help with sleep staging, muscle activity (EMG) to detect movement and REM sleep, airflow at the nose and mouth, respiratory effort using chest and abdominal sensors, oxygen saturation via pulse oximetry, heart rate and rhythm (ECG), body position, and often video recording. Analysis of this comprehensive data allows precise quantification of sleep architecture, respiratory events, and their consequences.

The apnea-hypopnea index (AHI) – the number of apneas and hypopneas per hour of sleep – is the primary metric for grading severity. In children, an AHI of 1-5 is considered mild OSA, 5-10 is moderate, and greater than 10 is severe. However, the AHI alone doesn't capture all relevant information; oxygen desaturation nadir, arousal index, sleep architecture, and other parameters also inform clinical decision-making.

Pediatric sleep studies have special considerations compared to adult studies. Children may need time to acclimate to the sleep laboratory environment, and a parent typically stays overnight with the child. The scoring criteria for pediatric respiratory events differ from adult criteria, reflecting developmental differences. Pediatric sleep specialists or appropriately trained technicians should interpret these studies.

Alternative Diagnostic Approaches

Home sleep apnea testing using portable monitors is increasingly available but has important limitations in pediatric populations. These devices typically measure fewer parameters than in-laboratory polysomnography and may underestimate disease severity. Current guidelines suggest home testing may be appropriate in select situations for otherwise healthy children with a high pretest probability of moderate-to-severe OSA, when access to laboratory polysomnography is limited. However, negative or inconclusive home studies often require follow-up laboratory PSG.

Drug-induced sleep endoscopy (DISE) involves performing flexible laryngoscopy while the child is sedated to simulate sleep. This allows direct visualization of the level(s) of airway obstruction, which can be helpful for surgical planning, particularly in children with complex anatomy or those who have persistent symptoms after initial surgery.

Lateral neck radiograph or flexible nasal endoscopy can assess adenoid size when adenoid hypertrophy is suspected. These tests are often performed as part of ENT evaluation to determine candidacy for adenotonsillectomy.

How Is Sleep-Disordered Breathing Treated in Children?

Treatment for sleep-disordered breathing in children depends on the cause and severity. Adenotonsillectomy (surgical removal of tonsils and adenoids) is the first-line treatment for most children, with 80-90% cure rates in otherwise healthy children. Other treatments include CPAP therapy, weight management for obese children, nasal corticosteroids for mild cases, and orthodontic interventions. Many children benefit from a combination approach.

The treatment of pediatric sleep-disordered breathing aims to eliminate obstruction, normalize sleep quality, resolve symptoms, and prevent complications. Treatment selection depends on the underlying cause(s), severity of disease, presence of contributing factors like obesity, and individual patient and family considerations. For most children with SDB caused by enlarged tonsils and adenoids, adenotonsillectomy is the primary treatment and is often curative. However, a significant minority of children, particularly those with obesity or craniofacial abnormalities, may require additional or alternative interventions.

The treatment approach should be individualized based on comprehensive evaluation. Factors influencing treatment selection include the severity of sleep apnea (AHI and oxygen nadir on polysomnography), anatomical contributors identified on examination, presence of obesity, comorbid conditions, family preferences, and access to various treatment options. A shared decision-making approach involving families in treatment planning leads to better adherence and outcomes.

Adenotonsillectomy

Adenotonsillectomy (AT) – surgical removal of the tonsils and adenoids – is the first-line treatment for pediatric obstructive sleep apnea in children with adenotonsillar hypertrophy. This procedure has been performed for over a century and has extensive safety and efficacy data in the pediatric population. For otherwise healthy children with moderate-to-severe OSA and enlarged tonsils/adenoids, adenotonsillectomy results in cure (normalization of AHI) in approximately 80-90% of cases.

The surgery is typically performed as an outpatient procedure under general anesthesia, with children going home the same day unless they have risk factors requiring overnight observation (severe OSA, age under 3, significant comorbidities). Several surgical techniques exist, including traditional complete tonsillectomy, intracapsular tonsillectomy (tonsillotomy), and various energy-based approaches. The choice of technique may affect postoperative pain and bleeding risk but appears to result in similar sleep outcomes.

Recovery typically takes 1-2 weeks, during which children experience throat pain that is managed with analgesics. Potential complications include pain, bleeding (1-4% risk, typically within the first two weeks), dehydration, and anesthetic risks. Serious complications are rare but include severe bleeding requiring return to surgery, airway compromise, and very rarely, death (estimated at 1 in 30,000 procedures).

Outcomes following adenotonsillectomy are generally excellent in appropriately selected patients. Studies document improvements in sleep parameters (AHI, oxygen saturation, sleep efficiency), symptoms (snoring, observed apneas, daytime sleepiness), quality of life, behavior, and in some studies, cognitive function and school performance. Growth improvement, including catch-up growth, is commonly observed following successful treatment of severe OSA.

However, certain groups have lower cure rates with adenotonsillectomy alone. Obese children have residual OSA in 25-75% of cases depending on obesity severity and should have postoperative polysomnography to assess outcomes. Children with Down syndrome and other craniofacial conditions also have higher residual disease rates. Children with severe OSA (AHI > 10) are more likely to have residual disease. These groups warrant postoperative sleep testing and may require additional interventions.

CPAP and BiPAP Therapy

Continuous positive airway pressure (CPAP) delivers a constant stream of pressurized air through a mask to splint the airway open during sleep. It is highly effective when used consistently but requires nightly use and ongoing management. CPAP is indicated for children with persistent OSA after adenotonsillectomy, those who are not surgical candidates, or those with predominantly central or complex sleep apnea.

The main challenge with CPAP in children is adherence. Many children have difficulty tolerating a mask interface every night, and families may struggle with the logistics of nightly therapy. Success with pediatric CPAP requires careful mask fitting (with multiple size and style options), gradual acclimatization, family education and support, and often behavioral interventions. Despite challenges, many children successfully use CPAP with appropriate support, and adherence improves with age and maturity.

Bilevel positive airway pressure (BiPAP) provides different pressures for inhalation and exhalation and may be better tolerated by some children or indicated for those with hypoventilation syndromes.

Medical Therapy

Intranasal corticosteroids (such as fluticasone or mometasone) reduce inflammation and lymphoid tissue size in the nasopharynx. They are most effective for mild OSA and may provide sufficient improvement to avoid surgery in some cases. They can also serve as adjunctive therapy before or after surgery, or while awaiting surgical intervention. Treatment is typically given for several weeks to months, with periodic reassessment.

Montelukast, a leukotriene receptor antagonist typically used for asthma and allergies, has also shown benefit in some children with mild SDB, possibly through anti-inflammatory effects on lymphoid tissue. Some studies suggest combination therapy with intranasal steroids and montelukast may be more effective than either alone for mild OSA.

Weight management is essential for obese children with SDB. While weight loss alone may not cure OSA, it improves outcomes when combined with other treatments and reduces the risk of residual disease after adenotonsillectomy. Comprehensive weight management involving dietary modification, increased physical activity, and behavioral strategies should be incorporated into the treatment plan for obese children.

Other Treatment Approaches

Rapid maxillary expansion and other orthodontic interventions can enlarge the nasal cavity and upper airway in selected children with narrow maxillary arches or other dental/skeletal abnormalities. These treatments are typically managed by pediatric dentists or orthodontists with expertise in sleep-related breathing disorders and may be used as primary or adjunctive therapy.

Myofunctional therapy involves exercises to strengthen oropharyngeal muscles and improve tongue posture. While evidence in children is still developing, some studies suggest benefit as adjunctive therapy, particularly for residual disease after adenotonsillectomy.

Additional surgical procedures may be considered for children with persistent OSA after adenotonsillectomy or those with specific anatomical contributions. Options include tongue base reduction, supraglottoplasty, maxillomandibular advancement, or hypoglossal nerve stimulation (currently under investigation in pediatric populations). These are typically reserved for complex cases managed by multidisciplinary teams.

What Are the Complications of Untreated Sleep-Disordered Breathing?

Untreated sleep-disordered breathing in children can lead to growth problems due to disrupted growth hormone release, behavioral and cognitive difficulties including ADHD-like symptoms and learning problems, cardiovascular complications such as pulmonary hypertension and heart strain, and reduced quality of life. Early treatment can prevent or reverse many of these complications.

The consequences of untreated sleep-disordered breathing extend far beyond poor sleep quality. Chronic intermittent hypoxia, sleep fragmentation, and increased respiratory effort have wide-ranging effects on multiple organ systems, particularly in the developing child. Understanding these potential complications emphasizes the importance of timely diagnosis and treatment and provides motivation for families navigating treatment decisions.

Fortunately, many complications are reversible with appropriate treatment, particularly when intervention occurs before long-standing damage accumulates. Studies document improvements in growth, behavior, cognition, cardiovascular parameters, and quality of life following successful treatment of pediatric OSA. However, some evidence suggests that prolonged untreated disease may result in deficits that don't fully normalize, emphasizing the value of early intervention.

Growth and Development

Growth impairment is a well-recognized complication of severe pediatric OSA. Multiple mechanisms contribute: disrupted sleep architecture impairs the pulsatile nocturnal release of growth hormone, which is essential for normal growth; increased work of breathing raises caloric expenditure; and severe disease may be associated with reduced appetite and caloric intake. Children with severe untreated OSA may fall off their growth curves, and failure to thrive may be a presenting concern.

The good news is that catch-up growth typically occurs following successful treatment. Studies consistently document improved growth velocity and normalization of growth trajectories after adenotonsillectomy for OSA. This growth acceleration supports the causal relationship between OSA and growth impairment.

Behavioral and Cognitive Effects

Behavioral problems are among the most common and impactful consequences of pediatric SDB. The relationship between sleep deprivation and behavior in children differs from adults – rather than becoming obviously sleepy, children often manifest hyperactive, impulsive, and emotionally dysregulated behavior. Studies suggest that 25-50% of children diagnosed with ADHD may have underlying sleep-disordered breathing, and treatment of the sleep disorder can substantially improve symptoms.

Cognitive deficits documented in children with untreated OSA include impairments in attention, executive function, memory, and overall intellectual ability. These deficits likely result from sleep fragmentation, intermittent hypoxia, or both. Academic performance and school achievement may suffer, with children performing below their potential.

Treatment of OSA generally results in behavioral and cognitive improvement, though the degree and speed of improvement varies. Some studies suggest that certain cognitive deficits may not fully normalize, particularly in children with long-standing severe disease treated later, supporting the importance of early intervention.

Cardiovascular Complications

While less common in children than adults, cardiovascular complications of severe, untreated pediatric OSA include pulmonary hypertension, right heart strain (cor pulmonale), systemic hypertension, and alterations in cardiovascular autonomic regulation. The intermittent hypoxia and hypercapnia associated with obstructive events, combined with swings in intrathoracic pressure and sympathetic activation, stress the cardiovascular system.

Pulmonary hypertension develops when chronic hypoxemia causes pulmonary vasoconstriction and, over time, pulmonary vascular remodeling. The right heart must work harder to pump blood through the lungs, eventually leading to right ventricular hypertrophy and failure if uncorrected. While uncommon in otherwise healthy children with OSA, pulmonary hypertension risk is higher in children with severe disease, chronic lung disease, or other predisposing factors.

These cardiovascular changes typically reverse with treatment, though children with established pulmonary hypertension require careful perioperative management and may need additional cardiac evaluation before and after surgery.