Pediatric obstructive sleep apnea syndrome (OSAS) is a common health problem diagnosed and managed by various medical specialists, including family practice physicians, pediatricians, pulmonologists, and general and pediatric otolaryngologists. If left untreated, the sequelae can be severe. Over the last decade, significant advancements have been made in the evidence-based management of pediatric OSAS. This article focuses on the current understanding of this disease, its management, and related clinical practice guidelines.
Key points
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Pediatric obstructive sleep apnea syndrome (OSAS) is a common health problem, which if left untreated, may have a deleterious impact on neurocognitive and behavioral outcomes, physical development, and cardiovascular health.
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Nocturnal polysomnography (PSG) is the gold standard method for diagnosing pediatric OSAS, however its performance and interpretation in the pediatric population has not been well standardized.
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The first-line treatment for pediatric OSAS is adenotonsillectomy. Reduced efficacy rates are seen in obese children. Persistent OSAS postoperatively must be investigated, and other levels of airway obstruction should be addressed.
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Patients at high risk for respiratory complications after adenotonsillectomy should undergo preoperative PSG, and those less than 3 years of age and those with severe OSAS should be considered for postoperative admission.
Introduction
Pediatric obstructive sleep apnea syndrome (OSAS) is a common health problem diagnosed and managed by various medical specialists, including family practice physicians, pediatricians, pulmonologists, and general and pediatric otolaryngologists. If left untreated, the sequelae can be severe. In the last decade, significant advancements have been made in the evidence-based management of pediatric OSAS. This article focuses on the current understanding of this disease and its management, and related clinical practice guidelines.
Introduction
Pediatric obstructive sleep apnea syndrome (OSAS) is a common health problem diagnosed and managed by various medical specialists, including family practice physicians, pediatricians, pulmonologists, and general and pediatric otolaryngologists. If left untreated, the sequelae can be severe. In the last decade, significant advancements have been made in the evidence-based management of pediatric OSAS. This article focuses on the current understanding of this disease and its management, and related clinical practice guidelines.
Terminology
Sleep-disordered breathing (SDB) is characterized by an abnormal respiratory pattern during sleep and includes snoring, mouth breathing, and pauses in breathing. SDB is the most common indication for tonsillectomy with or without adenoidectomy; 530,000 such procedures are performed annually in the United States on children younger than 15 years of age. SDB is a clinical diagnosis and encompasses the spectrum of disorders ranging in severity from primary snoring (PS) to upper airway resistance syndrome (UARS) to OSAS. It is estimated that 3% to 12% of children have PS, which is characterized by snoring without associated apneas, gas exchange abnormalities, or arousals on polysomnography (PSG). UARS is characterized by snoring associated with repetitive occurrences of respiratory effort-related arousals (RERAs) without oxygen desaturations. It is hypothesized that UARS can lead to daytime symptoms resembling OSAS. The diagnosis of UARS requires the use of an esophageal pressure monitor during overnight PSG. This is not routine in most centers, thus its prevalence is not well known in the pediatric population. There is some variability in the exact definition of the term OSAS. The American Academy of Pediatrics (AAP) clinical practice guideline on the diagnosis and management of childhood OSAS defines OSAS in children as a disorder of breathing during sleep characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction that disrupts normal ventilation during sleep and normal sleep patterns accompanied by associated signs and symptoms characteristic of the disorder. The American Academy of Otolaryngology Head and Neck Surgery (AAOHNS) clinical practice guideline on PSG for SDB before tonsillectomy in children states that OSAS is diagnosed when SDB (clinically) is accompanied by an abnormal PSG with obstructive events. The prevalence of OSAS in children is believed to range from 1% to 10%.
Morbidity
Signs/Symptoms
The signs and symptoms of pediatric OSAS are variable and are often dependent on age. Some daytime symptoms are more apparent in the older child. Nocturnal symptoms are often the most obvious to the parents of the child, and these often prompt the initial evaluation. Snoring is the most common associated symptom seen in children with SDB and OSAS. Some of the additional signs and symptoms are listed in Table 1 . Excessive daytime sleepiness is seen more frequently in adolescents and/or obese children, but hyperactivity and inattention are more characteristic of pediatric OSAS. One way to measure sleepiness is by applying the Epworth Sleepiness Scale (ESS). Melendres and colleagues compared 108 children with suspected SDB with 72 controls using a modified ESS and the Conners Abbreviated Symptom Questionnaire. They demonstrated that the children with suspected SDB were both sleepier and more hyperactive than the control patients. They found only weak correlation with the ESS and the PSG data obtained on the children with suspected SDB. Attempts to correlate physical examination findings to sleep apnea severity have also been made. The tonsils are typically graded on a clinically subjective scale from 0 to 4+, describing the amount of space occupied between the tonsillar pillars in the oropharynx (0, tonsils within fossa; 1+, <25%; 2+, >50%; 3+, >75%; 4+, >75%), Nolan and Brietzke recently demonstrated in a systematic literature review that the association between subjective tonsil size and objective OSAS severity is weak at best.
| Nocturnal Symptoms | Daytime Symptoms | Signs/Findings |
|---|---|---|
| Snoring | Difficulty waking | Tonsil hypertrophy |
| Gasping | Unrefreshed on waking | High/large tongue position |
| Noisy breathing (typically inspiratory) | Excessive sleepiness | Growth disturbance |
| Paradoxic breathing | Hyperactivity | Obesity |
| Retractions (cervical or costal) | Aggression/moodiness | Failure to thrive |
| Witnessed apneas | Mouth breathing | Pulmonary hypertension |
| Restless sleep | Poor appetite | Systemic hypertension |
| Neck hyperextension | Dysphagia | Craniofacial abnormalities |
| Mouth breathing | Difficulty in school | Laryngomalacia |
| Nocturnal sweating | Nasal airway obstruction | |
| Enuresis (after 6 mo continence) | Hypotonia | |
| Parasomnia (walking, talking, terrors) | Gastroesophageal reflux | |
| Bruxism | ||
| Mouth breathing |
Academic/Behavioral
The association of SDB and OSAS with impaired neurocognitive and behavioral development has been well studied in the past decade. Untreated OSAS has been associated with poor learning, lower achievement, and attention deficit/hyperactivity disorder. Recent studies further delineate the association. For example, Gottlieb and colleagues found significantly lower performance on measures of memory, executive function, and general intelligence in 5-year-old children with symptoms of SDB than in asymptomatic children. In addition, Gozal and colleagues demonstrated that children with lower academic performance in middle school (lower 25% of their class) were more likely to have snored during early childhood and to have required adenotonsillectomy (T&A) for snoring compared with their schoolmates in the top 25% of the class. Other studies have shown improved attention, executive functioning, analytical thinking, verbal functioning, memory, and academic progress at 6 to 12 months after T&A, suggesting a reversible effect of the neurocognitive morbidity incurred from SDB and obstructive sleep apnea (OSA). Gozal was the first to suggest that “learning debt” created by a delay in treatment or untreated SDB may only be partially reversible. Early sleep fragmentation may adversely affect future academic performance. These studies also suggest that snoring may not be as benign as once believed.
Behavioral problems such as social withdrawal and aggression have also been described in children with OSAS. The prevalence of attention deficit/hyperactivity (ADHD) in the school-age population is 8% to 10%, whereas 20% to 30% of children with snoring and/or OSAS have significant problems with inattention and hyperactivity. This connection is theorized to be secondary to the effect of fragmented, nonrestorative sleep with intermittent hypoxia on the development of the prefrontal cortex, which is believed to be responsible for working memory, behavioral control, analysis, organization, and self-regulation of motivation.
Medical
Failure to thrive and growth failure are believed to be slightly more common in children with OSAS. This may be a result of increased energy consumption from increased work of breathing, decreased oral intake, and alterations of nocturnal growth hormone secretion patterns. Growth spurt or some associated weight gain after T&A is often reported. A recent study by Smith and colleagues demonstrated that aged 6 years or younger at the time of T&A was significantly predictive of having postoperative weight gain.
Cardiovascular morbidity in children with OSAS includes systemic hypertension, pulmonary hypertension, and cor pulmonale with heart failure. Intermittent airway obstruction may lead to alterations in intrathoracic pressure, sustained changes in systemic blood pressure and endothelial function, associated oxidative stress, and increased sympathetic tone. Several studies have shown significant improvement of ambulatory blood pressure measurements, both systolic and diastolic, after treatment of OSAS with T&A. Tezer and colleagues conducted a prospective noncontrolled study on 21 children with OSA diagnosed clinically and with lateral neck radiography and no reported cardiovascular disease. Using transthoracic echocardiography, they demonstrated abnormal ventricular diastolic functions, and subsequent normalization 3 months after T&A. Tal and colleagues used radionucleotide vetriculography in 27 children clinically diagnosed with OSA, with no known preoperative cardiovascular disease. They demonstrated that 35% had a reduced right ventricular ejection fraction, and 67% had a wall motion abnormality preoperatively; both of these variables were markedly improved in 11 of the 27 children after T&A.
Systemic inflammation, as assessed by C-reactive protein (CRP) is notably higher in children with OSAS, which may place them at risk for substantial end-organ damage. Recent studies have shown that T&A significantly reduced the CRP levels in these children.
Diagnosis
The AAP published clinical practice guidelines for the diagnosis and management of childhood OSAS in 2002, and updated the guidelines in 2012. PSG is the gold standard method for diagnosing OSAS. However, because of a shortage of sleep laboratories with pediatric expertise, alternative diagnostic tests, such as videotaping, nocturnal pulse oximetry, and daytime nap PSG, may be helpful adjuncts to the clinical history and physical examination. The drawback is that these alternative tests have weaker positive and negative predictive values than PSG. The action statements from the AAP are listed in Box 1 , and those patients considered to be at high risk (and therefore require postoperative observation) are listed in Box 2 .
As part of routine health maintenance, the clinician should inquire if the child snores. If yes, or if the child presents with signs/symptoms of OSAS, the clinician should perform a more focused examination.
If the child snores on a regular basis and has signs/symptoms of OSAS, the clinician should either (1) obtain PSG or (2) refer the patient to a sleep specialist or otolaryngologist for more extensive evaluation.
If PSG is not available, the clinician may order alternative diagnostic tests, such as nocturnal video recording, nocturnal pulse oximetry, daytime nap PSG, or ambulatory PSG.
If the child has OSAS with adenotonsillar hypertrophy, adenotonsillectomy is recommended as first-line treatment. If the child has OSAS without adenotonsillar hypertrophy, other treatments should be considered.
Clinicians should monitor high-risk (see Box 2 ) patients undergoing adenotonsillectomy as inpatients postoperatively.
Clinicians should clinically reassess all patients with OSAS for persisting signs/symptoms after therapy to determine if further therapy is required.
Clinicians should reevaluate high-risk patients for persistent OSAS after adenotonsillectomy, including those who had a significantly abnormal baseline PSG, have sequelae of OSAS, are obese or remain symptomatic after treatment, with an objective test or referral to a sleep specialist.
Clinicians should refer patients for continuous positive airway pressure management if symptoms/signs or objective evidence of OSAS persists after adenotonsillectomy or if adenotonsillectomy is not performed.
Clinicians should recommend weight loss in addition to other therapy if a child with OSAS is overweight or obese.
Clinicians may prescribe topical intranasal corticosteroids for children with mild OSAS in whom adenotonsillectomy is contraindicated or for children with mild postoperative OSAS (apnea-hypopnea index <5/h).
Younger than 3 years of age
Severe OSAS on PSG (apnea-hypopnea index ≥10 and/or oxygen saturation nadir ≤80%)
Cardiac complications of OSAS
Failure to thrive
Obesity
Craniofacial anomalies
Neuromuscular disorders
Current respiratory infection
The designation of PSG as the gold standard method for diagnosing OSAS in children highlights that the subjective clinical history and physical examination have poor sensitivity in distinguishing OSAS from PS. Goldstein and colleagues prospectively evaluated 30 children with obstructive symptoms by standard history, physical examination, and tape-recorded breathing during sleep. Only 55% of patients predicted clinically to have definite OSAS had a positive nocturnal PSG. Sixteen percent of the patients thought to be unlikely to have OSAS had a positive nocturnal PSG.
The diagnostic PSG parameters for pediatric OSAS are different from those for adult OSAS. OSAS in adults is defined as a respiratory pause lasting more than 10 seconds; the higher respiratory rate in children portends that shorter intervals of apnea are likely to be clinically significant. The parameters that are primarily used in evaluating OSAS are the apnea-hypopnea index (AHI), RERAs, respiratory disturbance index (RDI), lowest oxygen saturation, and percentage of time with an end tidal CO 2 level greater than 50 mm Hg. In children, apnea is defined as a complete interruption of air flow lasting at least 2 breath periods, whereas hypopnea is defined as a reduction in air flow of 50% or more with associated arousal, awakening, or desaturation of 3% or more for the same duration using a nasal cannula pressure transducer. RERAs are defined as a sequence of at least 2 breath periods that does not meet the requirements for apnea or hypopnea but results in increased respiratory effort and subsequent arousal from sleep. The AHI and RERAs may be combined to give the RDI.
The performance and interpretation of pediatric nocturnal PSG have not been well standardized. There is controversy as to what constitutes an abnormal threshold in pediatric PSG. The American Academy of Sleep Medicine (AASM) published guidelines for the diagnosis of pediatric OSAS in 2007. The AASM guidelines incorporate caregiver reporting as well as PSG data. AHI of 1 or more per hour, frequent arousals from sleep associated with increased respiratory effort, arterial oxygen desaturation in association with apneic episodes, hypercapnea during sleep, and markedly negative esophageal pressure swings are all considered abnormal. Several other studies associate AHI of 1 or more as the threshold diagnostic for OSAS. In addition, most sleep specialists consider a pulse oximetry level less than 92% to be abnormal (in adults, an oximetry level <85 is abnormal). However, some consider an AHI greater than 5 to be more representative of the abnormal threshold and more diagnostic of pediatric OSAS. Many would consider that an AHI greater than 5 warrants T&A; however, because there is no evidence-based cutoff value, some children with AHI less than 5 may still be symptomatic and require intervention. Although there is no general consensus on defining the level of severity of SDB in children based on AHI, the American Society of Anesthesiologists guideline defines severe OSA as AHI of 10 or more.
Every child with SDB and suspected OSAS does not need overnight PSG before treatment (T&A). AAOHNS published clinical practice guidelines advocating the use of PSG before tonsillectomy in children with SDB if they exhibit any of the following: obesity, Down syndrome, craniofacial abnormalities, neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses. In addition, it was recommended that the clinician advocate for PSG before tonsillectomy for SDB in children without any of these comorbidities for whom the need for surgery is uncertain or when there is discordance between tonsillar size on physical examination and the reported severity of SDB.
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