What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Patient Print
0 Find synonyms

Find synonyms Find exact match

Management of obstructive sleep apnea in children
UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
Management of obstructive sleep apnea in children
View in Chinese
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2017. | This topic last updated: Dec 09, 2016.

INTRODUCTION — Obstructive sleep apnea (OSA) is characterized by episodes of complete or partial upper airway obstruction during sleep, often resulting in gas exchange abnormalities and arousals causing disrupted sleep. The condition exists in 2 to 5 percent of children and can occur at any age [1,2]. Untreated OSA is associated with cardiovascular complications, impaired growth (including failure to thrive), learning problems, and behavioral problems. Early diagnosis and treatment may decrease morbidity [3].

An overview of surgical and medical management of children with confirmed OSA (defined as apnea hypopnea index [AHI] >1 on sleep study in the setting of clinically relevant symptoms) is reviewed here. The diagnostic evaluation of suspected OSA in children is described separately. (See "Evaluation of suspected obstructive sleep apnea in children".)

More detailed information about specific treatments for OSA in children is available from the following topic reviews:

(See "Adenotonsillectomy for obstructive sleep apnea in children".)

(See "CPAP for pediatric obstructive sleep apnea".)

CONSEQUENCES OF UNTREATED OSA — Potential consequences of untreated OSA in children include:

Inattention and behavioral problems (eg, hyperactivity, impulsivity, rebelliousness and aggression) (see "Cognitive and behavioral consequences of sleep disorders in children", section on 'Sleep-related breathing disorders')

Daytime sleepiness

Growth – Severe OSA can be associated with failure to thrive (FTT), and treatment can lead to weight gain and growth

Cardiopulmonary disease – Including systemic hypertension, right and left ventricular dysfunction, and cor pulmonale

Each of these conditions may benefit from treatment of OSA, though in some cases definitive proof at the level of randomized clinical trials does not yet exist. The evidence for these complications are discussed separately. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Clinical manifestations'.)

CHOICE OF THERAPY — The decision to initiate treatment is made on a case-by-case basis once OSA is confirmed. This requires carefully weighing the anticipated benefits and risks of treatment. Important considerations include the child's age, polysomnographic abnormalities, and any underlying medical issues or complications related to OSA [4]. (See "Evaluation of suspected obstructive sleep apnea in children".)

The following considerations are applicable to most children for whom it has been determined that treatment of OSA is warranted:

Adenotonsillectomy – Children with polysomnography-confirmed OSA should be offered a referral to otolaryngology for evaluation. Adenotonsillectomy is first-line therapy for otherwise healthy children who have OSA and adenotonsillar hypertrophy [4]. In the past, this approach was largely based upon clinical experience. In 2013, a randomized trial (Childhood Adenotonsillectomy Trial, CHAT) demonstrated an advantage of adenotonsillectomy over watchful waiting for children with uncomplicated OSA who were candidates for adenotonsillectomy (tonsil size ≥1) [5,6]. Specifically, adenotonsillectomy provided better improvement in daytime behavior, sleep apnea symptoms, subjective sleepiness, and quality of life. However, no differences emerged in cognitive measures of attention or executive function that were the primary outcomes of the study. Selected areas of cognitive functioning did show benefit from adenotonsillectomy; these areas included nonverbal reasoning, fine motor skills, and selective attention, though the extent of improvement was limited [7]. Outcomes of adenotonsillectomy are covered in more depth separately. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Success rates' and "Cognitive and behavioral consequences of sleep disorders in children", section on 'Sleep-related breathing disorders'.)

Adenotonsillectomy also may be initial therapy for children with multifactorial OSA if appreciable adenotonsillar tissue is present. The rationale is that adenotonsillectomy may improve upper airway patency enough to ameliorate or resolve the OSA, even if it does not correct all of the etiologies. Such patients should be managed by a clinician experienced with pediatric sleep-related respiratory abnormalities [4]. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Indications for surgery'.)

Positive airway pressure therapy – Positive airway pressure therapy (continuous positive airway pressure [CPAP] or bilevel positive airway pressure [BPAP]) is an alternate therapy to adenotonsillectomy. It can be employed when a patient with OSA has minimal adenotonsillar tissue, persistent OSA despite adenotonsillectomy, or a strong preference for a nonsurgical approach [4,8-11]. Positive airway pressure may also help to stabilize children with severe OSA prior to adenotonsillectomy or another surgical procedure [10]. (See 'Positive airway pressure' below and "CPAP for pediatric obstructive sleep apnea", section on 'Treatment decisions'.)

Watchful waiting – Several months of watchful waiting with supportive care may be considered in select cases of confirmed mild or moderate OSA (apnea-hypopnea index >1 and <30 on polysomnography), based on the acceptable outcomes for patients followed with watchful waiting in the CHAT trial described above. If this approach is chosen, the child should be reevaluated within six months for worsening of clinical symptoms, or reevaluated sooner if symptoms worsen.

The watchful waiting approach is unlikely to be appropriate for children with severe OSA. Such patients were excluded from participation in the CHAT trial, which defined severe OSA by an apnea-hypopnea index >30; an apnea index >20; or >2 percent of total sleep time spent with oxygen saturations <90 percent [5]. The CHAT study also was not informative about outcomes of watchful waiting for other groups of excluded children, including those with recurrent tonsillitis, cardiovascular comorbidities, medication use for attention deficit hyperactivity disorder (ADHD) or psychiatric disorders, body mass index (BMI) Z-score ≥3, developmental delays requiring school accommodations, and known genetic, craniofacial, or neurological disorders likely to affect the airway, cognition, or behavior.

Other therapies – Selected children with OSA may derive benefit from adjunctive therapies. As examples, obese children with OSA may benefit from weight loss, and children with maxillary contraction may benefit from rapid maxillary expansion. In addition, nasal steroids, sinus rinses, positional therapy (eg, elevation of the head of the bed), or orthodontia can be considered. Several of these adjunctive therapies are described below. (See 'Other surgeries' below and 'Environmental controls' below and 'Weight loss' below and 'Orthodontics' below and 'Supplemental oxygen' below.)

SURGICAL THERAPY

Adenotonsillectomy — Adenotonsillectomy refers to surgical resection of the tonsils and adenoids. It is generally considered first-line therapy for otherwise healthy children who have OSA and adenotonsillar hypertrophy. This topic is covered in more depth separately, but an overview is provided here because most children with obstructive sleep apnea are offered adenotonsillectomy. (See "Adenotonsillectomy for obstructive sleep apnea in children".)

Adenotonsillectomy may also be initial therapy for children with multifactorial OSA, including contributions from obesity, if appreciable adenotonsillar tissue is present. OSA in obese children usually improves following adenotonsillectomy, although the outcome may be less satisfactory than in lean children. Finally, evaluation by an otolaryngologist should still be considered in a child with OSA who does not have obvious tonsillar hypertrophy because fiber-optic nasolaryngoscopy or other tests may reveal lymphoid tissue or other causes of airway obstruction that occupy a significant proportion of the potential upper airway.

Risk factors in children who are higher risk for perioperative complications following adenotonsillectomy include severe OSA on preoperative polysomnography, or the presence of complicating factors such as obesity (especially if severe), very young age (eg, <36 months), abnormal upper airway tone, or craniofacial anomalies (table 1). Patients with these characteristics warrant additional precautions during the evaluation and performance of adenotonsillectomy. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'High-risk populations'.)

All children who undergo surgical therapy should follow-up with their primary care clinician or sleep specialist six to eight weeks after surgery to ensure that the symptoms or signs of OSA have resolved [4]. Children who have persistent snoring or other symptoms or signs of increased upper airway resistance at this follow-up visit should also undergo polysomnography to ensure that their sleep-related breathing abnormalities have resolved [4,12]. Repeat polysomnography is also indicated for children who have had complications from OSA (eg, cor pulmonale), those with severe OSA on preoperative polysomnography, and those with craniofacial or neurologic abnormalities (including Down and Prader-Willi syndromes) [4,13-15]. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Indications for postoperative polysomnography'.)

Increased body weight, regrowth of adenotonsillar tissue, or changes in body shape due to puberty may lead to gradual reemergence of OSA months or years after adenotonsillectomy [16,17]. Thus, reevaluation with polysomnography is indicated later if symptoms or signs of OSA develop or worsen in a child who has a history of OSA, even if the OSA was thought to have resolved following initial therapy.

Adenoidectomy — Obstructive symptoms and signs frequently persist after adenoidectomy alone is performed for treatment of OSA [18-22]. In addition, many children who undergo adenoidectomy are not spared tonsillectomy, since children who undergo adenoidectomy for the treatment of OSA are twice as likely to need eventual tonsillectomy as compared with children who undergo adenoidectomy for other indications [20,23]. For these reasons, adenoidectomy alone is not recommended for treatment of OSA in children [4]. Conversely, some data also suggest that tonsillectomy without adenoidectomy is less effective than the combined procedure in treating pediatric OSA.

Other surgeries — Surgical procedures other than adenotonsillectomy are sometimes considered to treat OSA in children without significant tonsillar hypertrophy, or with residual disease after adenotonsillectomy. These adjuvant surgical procedures may also be beneficial in patients with a high probability that OSA is due to factors other than adenotonsillar hypertrophy alone, such as in children with obesity, Down syndrome, craniofacial syndromes, or neuromuscular disease. These alternative approaches include uvulopalatopharyngoplasty (UPPP), supraglottoplasty, tongue reduction, tongue base procedures, expansion sphincter pharyngoplasty, lateral pharyngoplasty, and mandibular distraction osteogenesis. Tracheotomy is reserved for children with severe OSA who have failed to respond to other treatment approaches. These techniques are discussed separately. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Adjuvant surgical procedures'.)

MEDICAL THERAPY

Positive airway pressure — Positive airway pressure is the most common nonsurgical therapy for obstructive sleep apnea (OSA) in children [8,9,24,25]. It involves administering airway pressure through a mask, which prevents upper airway obstruction and reduces both sleep disruption and the work of breathing [4]. Positive airway pressure is a long-term therapy that requires a motivated family. Adherence to therapy is challenging, but can be optimized with proper fitting, titration, and behavioral support.

Indications and contraindications – CPAP and BPAP are approved for home use in children who weigh 30 kg or more; however, not all equipment manufacturers recommend use in children. CPAP and BPAP have also been safely used and well-tolerated in some children who weigh less than 30 kg [8]. Positive airway pressure may not be feasible in all children, such as those with claustrophobia, although desensitization or cognitive behavioral therapy may increase successful use of CPAP or BPAP. Contraindications according to CPAP manufacturers include: "bullous lung disease, pneumothorax, pneumocephalus, cerebrospinal fluid leak, recent cranial surgery or trauma, abnormalities of the cribriform plate, pathologically low blood pressure or in patients whose upper airways have been bypassed." CPAP may not be effective in patients with clinically significant hypoventilation that is due to causes other than OSA. (See "CPAP for pediatric obstructive sleep apnea", section on 'Treatment decisions'.)

CPAP versus BPAP – Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) are the usual types of positive airway pressure (BiPAP is the name of a BPAP unit manufactured by Respironics Corporation; it is just one of several commercially available machines that can deliver BPAP). CPAP applies a constant level of positive airway pressure throughout the respiratory cycle, whereas BPAP applies a higher level of positive airway pressure during inspiration than during exhalation. (See "CPAP for pediatric obstructive sleep apnea", section on 'The CPAP prescription'.)

CPAP or BPAP titration – The pressure required to treat a child's OSA is initially determined by titration during polysomnography in the sleep laboratory [8,26]. It is important to discuss objective adherence markers obtained from the CPAP or BPAP device with caregivers and the child, to determine adherence and identify issues for intervention to improve use. The pressure level should be periodically rechecked with repeat polysomnography, especially if there are changes in the child's clinical status (eg, recurrence of snoring despite using CPAP, recurrent daytime symptoms) or body habitus such as substantial increases or decreases in the child's weight or body mass index (BMI) percentiles [27]. (See "CPAP for pediatric obstructive sleep apnea", section on 'Titration of CPAP in children'.)

Techniques for fitting, titrating, and monitoring positive airway pressure therapy in children are discussed in detail in a separate topic review. Proper technique and family support are essential to optimize adherence to therapy. (See "CPAP for pediatric obstructive sleep apnea".)

Efficacy — No randomized trials have compared positive airway pressure to placebo/sham CPAP therapy in children with OSA. However, observational studies suggest that positive airway pressure improves symptoms, signs, and polysomnographic outcomes in at least 85 percent of children [8-10,26,28,29]:

In a series of 80 children (≤15 years old) with OSA, nasal CPAP administered at a mean pressure level of 8 cmH2O for an average of 15 months eliminated the symptoms, signs, and polysomnographic abnormalities of OSA in 90 percent of the children. The apnea-hypopnea index diminished from a mean of 27.3 to 2.6 events per hour [9]. Approximately 80 percent of the children in the series had undergone previous adenotonsillectomy, and one-half had a congenital syndrome or malformation.

In a multicenter series of 94 children (<19 years old) with OSA, CPAP therapy administered at a median pressure level of 8 cm H2O was effective in 86 percent of children [8]. Effectiveness was defined as resolution of clinical symptoms, normal oxyhemoglobin saturation during sleep, and improvement of polysomnographic abnormalities. Among the children in whom CPAP was not effective, only one had adhered to the therapy, suggesting that poor adherence was the primary reason that most children failed therapy. Approximately 75 percent of the children in the series had undergone previous adenotonsillectomy.

Different modes of positive airway pressure have been directly compared. A multicenter trial randomly assigned 30 children (2 to 16 years old) with newly diagnosed OSA to receive either CPAP or BPAP [29]. Ten children dropped out of the trial. Among the 20 children who completed six months of therapy, the apnea-hypopnea index fell from a mean of 27 to 3 events per hour. There were no significant differences between the CPAP and BPAP groups. A slightly larger study, which randomized children to CPAP or BPAP with pressure release technology (Bi-Flex), also showed similar findings of efficacy and adherence between groups [30].

Complications — Complications of positive airway pressure therapy are usually minor [8]. Many are related to a suboptimal mask fit and can be avoided by regular evaluation of the mask fit (eg, every four to six months). Examples include eye irritation, conjunctivitis, skin ulceration, skin discoloration (lightening or darkening) and discomfort or irritation at the site where the mask contacts the skin [25]. These problems can be minimized by proper fitting of the mask and refitting as the child grows. The mask should be fitted as loosely as possible while avoiding air leaks, to minimize the pressure on the face, because this pressure can alter facial or dental development during long-term use. Nasal complaints, such as congestion or rhinorrhea, are also common. Nasal corticosteroids or humidification of the delivered air can help relieve these symptoms. Aerophagia can occur if the child swallows air through the night resulting in bloating, burping, and passing gas in the mornings. (See "CPAP for pediatric obstructive sleep apnea", section on 'Choosing the right equipment' and "CPAP for pediatric obstructive sleep apnea", section on 'Barriers to effective CPAP therapy in children'.)

Hypoventilation or central apnea occasionally emerge during treatment with positive airway pressure therapy. Central sleep apnea that appears in this setting is termed "treatment-emergent central sleep apnea" [9]. To minimize the problem, the technologist in the sleep laboratory should try to avoid excessive CPAP pressure during the titration. If necessary, switching to a bilevel mode (BPAP) may be tried in cases where arousals become clinically significant. (See "CPAP for pediatric obstructive sleep apnea", section on 'Titration of CPAP in children'.)

Other adjunct therapies

Environmental controls — Tobacco smoke, other indoor pollutants, and indoor allergens should be avoided by all children with OSA because they may cause nasal congestion and increased upper airway resistance. Treatment of allergic rhinitis may be helpful but should not delay specific treatment. (See "Allergen avoidance in the treatment of asthma and allergic rhinitis" and "Pharmacotherapy of allergic rhinitis".)

Weight loss — Weight loss is recommended as an adjunctive therapy for obese children with OSA because obesity contributes to the increased upper airway resistance that characterizes OSA [4]. Nutritional counseling with close follow-up and reinforcement is usually necessary for such children. Weight loss surgery may be an option for adolescents with severe obesity and OSA and/or other obesity-associated morbidities. (See "Surgical management of severe obesity in adolescents", section on 'Comorbidity improvement'.)

The presumption that weight loss is beneficial to obese children who have OSA is based primarily upon evidence from adults. There are few studies of the effect of weight loss on OSA in children [31,32], but these do suggest that OSA is likely to improve if weight loss can be achieved. (See "Management of obstructive sleep apnea in adults", section on 'Weight loss and exercise'.)

Many children with OSA have normal or low body weight. Weight loss is potentially harmful in these children, probably does not improve their OSA, and should be avoided.

Orthodontics — Rapid maxillary expansion (RME) is an orthodontic treatment that widens the palate and nasal passages, thereby increasing airway patency and reducing nocturnal obstruction. The technique can only be used prior to midline fusion of the maxilla, which generally occurs shortly prior to puberty. RME can be used for children with OSA and narrow palate (crossbite) who have little adenotonsillar tissue, or for those with residual OSA after adenotonsillectomy.

RME involves the insertion of a metal dental appliance into the mouth (picture 1). The appliance contacts the roof of the mouth and is held in position by connections to the posterior teeth. The appliance is commonly referred to as a rapid palatal expander, rapid maxillary expansion appliance, palate expander, or orthodontic expander.

The value of RME in the treatment of OSA was investigated in 31 nonobese children who had OSA, maxillary contraction (high, arched palate and unilateral or bilateral crossbite), and either no adenotonsillar hypertrophy or a prior adenotonsillectomy [33]. After four months of RME, the mean apnea-hypopnea index had decreased from 12 to less than 1 event per hour. The same group demonstrated persistent improvement in this group of children after 3 years [34] and 12 years [35]. Other studies in similar patient populations reported similar results [36,37].

For patients with maxillary contraction and adenotonsillar hypertrophy, both RME and adenotonsillectomy might be needed to treat OSA. The efficacy of combination therapy with RME and adenotonsillectomy was explored in a pilot study of 31 children with these characteristics. In this study, only one of the 31 patients responded to one treatment alone, but OSA resolved in 94 percent of subjects after combination therapy, regardless of the sequence of treatments [38].

Supplemental oxygen — Nocturnal supplemental oxygen can be used to temporarily treat patients with severe hypoxemia associated with OSA until definitive therapy can be provided, as well as to support medically complicated patients who are poor candidates for surgical treatment and are unable to tolerate or use positive airway pressure [39,40]. When nocturnal oxygen supplementation is deemed necessary for children with OSA, it should be initiated by a specialist who has experience managing children with sleep disorders. All children receiving oxygen therapy should be assessed for daytime and nighttime hypercapnia.

The use of supplemental oxygen as a bridging therapy is rare in our practice and is reserved for children who cannot tolerate CPAP/BPAP. Although supplemental oxygen at night improves oxygenation during sleep, it does not always improve the episodic complete or partial upper airway obstruction that characterizes OSA, nor most of the consequences of OSA (eg, sleep fragmentation, hypercapnia). In some patients, it may suppress the ventilatory drive and worsen hypercapnia. This effect was seen in a crossover trial that randomly assigned 23 children with OSA to receive oxygen therapy or room air via nasal cannula for four hours [39]. Two children developed significant hypercapnia during treatment with supplemental oxygen.

Corticosteroids/Antiinflammatory therapy — Intranasal corticosteroids or leukotriene modifier therapy may be useful to treat mild OSA and can be considered when adenotonsillectomy or CPAP/BPAP are not options for the child [4]. No clear guidelines exist on duration of therapy necessary for sustained benefit. If nasal steroids are prescribed, patients should be advised to avoid spraying the septum, or "straight back", and instead aim for the sides of the nostril.

Intranasal corticosteroids – Several studies have shown beneficial effects of intranasal steroids for children with mild OSA:

In a randomized trial of 25 children treated with intranasal corticosteroids or placebo, the group receiving intranasal steroids for six weeks showed a modest improvement in OSA, with apnea hypopnea index (AHI) reduction from 11 to 6 events per hour [41].

Similar findings were noted in double-blind randomized crossover trial of 48 children with mild OSA treated with intranasal budesonide; one-half of the children had normalization of polysomnographic parameters during the budesonide treatment arm. In many of the children, the positive effects were sustained up to eight weeks after discontinuation of treatment [42].

A systematic review of seven studies (six randomized controlled trials and one cohort study) including 493 children showed significant efficacy of various intranasal corticosteroids in improving nasal obstruction symptoms, as measured by symptom scores (polysomnography was not performed) [43].

Leukotriene modifier therapy – Montelukast (Singulair) appears to modestly reduce AHI and adenotonsillar size [44,45].

Combination therapy – The combination of montelukast and intranasal corticosteroids also was effective in several studies. As an example, in a retrospective review of 752 children with mild OSA who were treated with combination of intranasal corticosteroids and montelukast, more than 80 percent experienced beneficial effects [46]. Among those who underwent follow-up polysomnography, 62 percent experienced normalization of findings. The combination was also effective in a group of children who had undergone adenotonsillectomy and had mild residual OSA [47]. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Medical therapy'.)

Systemic corticosteroids do not appear to be effective. In an open-label clinical trial, five days of treatment with oral prednisone did not reduce symptom severity or improve polysomnographic parameters of OSA [48].

Antibiotic therapy — Antibiotic therapy reduces the size of the tonsils and adenoids in some children. This may temporarily improve the OSA, but it does not provide persistent relief or obviate the need for surgery.

The effect of antibiotics on OSA was evaluated in a trial of 22 children (2 to 12 years old) with OSA [49]. The children were randomly assigned to receive azithromycin (12 mg/kg) or placebo on days 1 through 5, 11 through 15, and 21 through 25 during the 30-day trial. There were no significant differences in the groups according to polysomnography performed within the two weeks following the trial.

Given this and similar evidence, antibiotics are not indicated for the routine treatment of pediatric OSA.

Positional therapy — Positional therapy sometimes may be considered when a school-aged child, adolescent, or older teenager cannot be treated or treated completely by other means. If the AHI in supine sleep is much higher (eg, twice or more) than the AHI in other positions, the child may be able to significantly reduce OSA severity to the extent that he or she can avoid supine sleep. Several pillows and belts are commercially available, including but not limited to the Rematee belt (available in children's sizes) and the Sona Pillow. Additionally, the head of the bed can be raised to ease breathing. Positional therapy has not been well studied in children. The studies in adults have been small and lack randomization [50,51]. Positional therapy may be used in combination with several therapies listed above.

Nasal expiratory resistor device — This small nasal device (manufactured by "Provent", now owned by "Theravent, Inc") consists of a 0.25-inch diameter one-way valve attached externally to each nostril with adhesive tape at bedtime. The valve allows easy inhalation but on exhalation produces expiratory resistance. This approach has been studied in small adult trials [52] and one pediatric trial. The pediatric trial was a randomized, double-blind, placebo controlled, crossover study in which 14 teenage children were treated with nasal expiratory positive airway pressure devices [52]. The children showed a variable response; older children and children with less hypercapnia showed a better response to therapy. Thus, nasal expiratory resistor devices may be appropriate in older children with OSA who do not respond to or are unable to tolerate other treatment options [53].

Myofascial reeducation (nasal breathing retraining) — Myofunctional reeducation consists of exercises designed to strengthen the tongue and orofacial muscles, repositioning muscles to the appropriate position. In a retrospective review of 24 children with residual OSA after adenotonsillectomy who were referred for myofascial reeducation services, those who completed myofascial reeducation experienced improved AHI and minimum oxygen saturation on follow-up polysomnography compared with those who did not complete the myofascial reeducation [54].

An example of myofascial reeducation exercises can be found here:

Passive myofunctional therapy consists of an oral device used to induce tongue muscle activity during sleep. In a study of 29 children, 3 to 15 years in age, children were fitted with an adjustable mandibular advancement device with a bead mounted to the lower part of the frame for the tip of the tongue to roll. Children were instructed to wear the device to bed and use their tongue to roll the bead during sleep nightly. After six months, most children experienced improved AHI on follow-up polysomnography [55].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders including obstructive sleep apnea in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Tonsillectomy and adenoidectomy in children (The Basics)")

SUMMARY AND RECOMMENDATIONS

Obstructive sleep apnea (OSA) is characterized by episodes of complete or partial upper airway obstruction during sleep, often resulting in gas exchange abnormalities and arousals that cause disrupted sleep. (See 'Introduction' above.)

The decision about whether to initiate therapy is made on a case-by-case basis once the diagnosis of OSA is confirmed on a sleep study. (See 'Choice of therapy' above.)

For most otherwise healthy children who have OSA and adenotonsillar hypertrophy, we suggest evaluation for adenotonsillectomy (Grade 2C). Adenotonsillectomy is also an option for children with multifactorial OSA if appreciable adenotonsillar tissue is present. Despite adenotonsillectomy, children may have residual OSA or redevelop OSA in the future. Careful clinical follow-up for signs and symptoms of OSA is advisable. (See 'Choice of therapy' above and 'Adenotonsillectomy' above.)

Up to six months of watchful waiting with supportive care may be considered in select cases of polysomnography-confirmed mild or moderate OSA, based on the acceptable outcomes for patients followed with watchful waiting in the Childhood Adenotonsillectomy Trial (CHAT). If this approach is chosen, the child should be reevaluated within six months for worsening of clinical symptoms, or reevaluated sooner if symptoms worsen. (See 'Choice of therapy' above.)

For children in whom adenotonsillectomy is contraindicated, those who have OSA with minimal adenotonsillar tissue, those who have persistent OSA despite adenotonsillectomy, or those for whom there is a strong preference for a nonsurgical approach, we suggest positive airway pressure therapy (Grade 2C). Positive airway pressure can be delivered as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP). (See 'Choice of therapy' above and 'Positive airway pressure' above.)

Tobacco smoke, other indoor pollutants, and indoor allergens should be avoided by all children with OSA. (See 'Environmental controls' above.)

For obese children with OSA, we recommend weight loss as adjunctive therapy (Grade 1B). (See 'Weight loss' above.)

Supplemental oxygen that is administered at night until definitive therapy can be provided may improve oxygenation in children who have severe OSA-related hypoxemia. When nocturnal supplemental oxygen therapy is necessary, we recommend that it be initiated under monitored conditions with frequent assessment of the arterial carbon dioxide tension (PaCO2) (Grade 1B). (See 'Supplemental oxygen' above.)

Positional therapy using specially designed belts or pillows to avoid supine sleep, or elevation of the head of the bed, may be considered for patients in whom the severity of sleep disordered breathing varies substantially with the sleep position and other OSA treatments are not adequately effective. (See 'Positional therapy' above.)

For most children with OSA, we suggest that intranasal corticosteroids, systemic corticosteroids, or antibiotics NOT be administered as first-line therapy for OSA (Grade 2B). (See 'Corticosteroids/Antiinflammatory therapy' above and 'Antibiotic therapy' above.)

Use of UpToDate is subject to the  Subscription and License Agreement.

REFERENCES

  1. Rosen CL, Storfer-Isser A, Taylor HG, et al. Increased behavioral morbidity in school-aged children with sleep-disordered breathing. Pediatrics 2004; 114:1640.
  2. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed, American Academy of Sleep Medicine, Darien, IL 2014.
  3. Cardiorespiratory sleep studies in children. Establishment of normative data and polysomnographic predictors of morbidity. American Thoracic Society. Am J Respir Crit Care Med 1999; 160:1381.
  4. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012; 130:576.
  5. Marcus CL, Moore RH, Rosen CL, et al. A randomized trial of adenotonsillectomy for childhood sleep apnea. N Engl J Med 2013; 368:2366.
  6. Redline S, Amin R, Beebe D, et al. The Childhood Adenotonsillectomy Trial (CHAT): rationale, design, and challenges of a randomized controlled trial evaluating a standard surgical procedure in a pediatric population. Sleep 2011; 34:1509.
  7. Taylor HG, Bowen SR, Beebe DW, et al. Cognitive Effects of Adenotonsillectomy for Obstructive Sleep Apnea. Pediatrics 2016; 138.
  8. Marcus CL, Ward SL, Mallory GB, et al. Use of nasal continuous positive airway pressure as treatment of childhood obstructive sleep apnea. J Pediatr 1995; 127:88.
  9. Waters KA, Everett FM, Bruderer JW, Sullivan CE. Obstructive sleep apnea: the use of nasal CPAP in 80 children. Am J Respir Crit Care Med 1995; 152:780.
  10. Guilleminault C, Pelayo R, Clerk A, et al. Home nasal continuous positive airway pressure in infants with sleep-disordered breathing. J Pediatr 1995; 127:905.
  11. Padman R, Hyde C, Foster P, Borkowski W Jr. The pediatric use of bilevel positive airway pressure therapy for obstructive sleep apnea syndrome: a retrospective review with analysis of respiratory parameters. Clin Pediatr (Phila) 2002; 41:163.
  12. Standards and indications for cardiopulmonary sleep studies in children. American Thoracic Society. Am J Respir Crit Care Med 1996; 153:866.
  13. McColley SA, April MM, Carroll JL, et al. Respiratory compromise after adenotonsillectomy in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992; 118:940.
  14. Marcus CL. Sleep-disordered breathing in children. Am J Respir Crit Care Med 2001; 164:16.
  15. Aurora RN, Zak RS, Karippot A, et al. Practice parameters for the respiratory indications for polysomnography in children. Sleep 2011; 34:379.
  16. Guilleminault C, Partinen M, Praud JP, et al. Morphometric facial changes and obstructive sleep apnea in adolescents. J Pediatr 1989; 114:997.
  17. Huang YS, Guilleminault C, Lee LA, et al. Treatment outcomes of adenotonsillectomy for children with obstructive sleep apnea: a prospective longitudinal study. Sleep 2014; 37:71.
  18. Nieminen P, Tolonen U, Löppönen H. Snoring and obstructive sleep apnea in children: a 6-month follow-up study. Arch Otolaryngol Head Neck Surg 2000; 126:481.
  19. Nieminen P, Tolonen U, Löppönen H, et al. Snoring children: factors predicting sleep apnea. Acta Otolaryngol Suppl 1997; 529:190.
  20. Kay DJ, Bryson PC, Casselbrant M. Rates and risk factors for subsequent tonsillectomy after prior adenoidectomy: a regression analysis. Arch Otolaryngol Head Neck Surg 2005; 131:252.
  21. Guilleminault C, Li KK, Khramtsov A, et al. Sleep disordered breathing: surgical outcomes in prepubertal children. Laryngoscope 2004; 114:132.
  22. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012; 130:e714.
  23. Gov-Ari E, Mills JC, Basler KJ. Predictors of tonsillectomy after previous adenoidectomy for upper airway obstruction. Otolaryngol Head Neck Surg 2012; 146:647.
  24. Indications and standards for use of nasal continuous positive airway pressure (CPAP) in sleep apnea syndromes. American Thoracic Society. Official statement adopted March 1944. Am J Respir Crit Care Med 1994; 150:1738.
  25. Guilleminault C, Nino-Murcia G, Heldt G, et al. Alternative treatment to tracheostomy in obstructive sleep apnea syndrome: nasal continuous positive airway pressure in young children. Pediatrics 1986; 78:797.
  26. McNamara F, Sullivan CE. Obstructive sleep apnea in infants and its management with nasal continuous positive airway pressure. Chest 1999; 116:10.
  27. Epstein LJ, Kristo D, Strollo PJ Jr, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009; 5:263.
  28. Downey R 3rd, Perkin RM, MacQuarrie J. Nasal continuous positive airway pressure use in children with obstructive sleep apnea younger than 2 years of age. Chest 2000; 117:1608.
  29. Marcus CL, Rosen G, Ward SL, et al. Adherence to and effectiveness of positive airway pressure therapy in children with obstructive sleep apnea. Pediatrics 2006; 117:e442.
  30. Marcus CL, Beck SE, Traylor J, et al. Randomized, double-blind clinical trial of two different modes of positive airway pressure therapy on adherence and efficacy in children. J Clin Sleep Med 2012; 8:37.
  31. Verhulst SL, Franckx H, Van Gaal L, et al. The effect of weight loss on sleep-disordered breathing in obese teenagers. Obesity (Silver Spring) 2009; 17:1178.
  32. Kalra M, Inge T, Garcia V, et al. Obstructive sleep apnea in extremely overweight adolescents undergoing bariatric surgery. Obes Res 2005; 13:1175.
  33. Pirelli P, Saponara M, Guilleminault C. Rapid maxillary expansion in children with obstructive sleep apnea syndrome. Sleep 2004; 27:761.
  34. Villa MP, Rizzoli A, Miano S, Malagola C. Efficacy of rapid maxillary expansion in children with obstructive sleep apnea syndrome: 36 months of follow-up. Sleep Breath 2011; 15:179.
  35. Pirelli P, Saponara M, Guilleminault C. Rapid maxillary expansion (RME) for pediatric obstructive sleep apnea: a 12-year follow-up. Sleep Med 2015; 16:933.
  36. Villa MP, Malagola C, Pagani J, et al. Rapid maxillary expansion in children with obstructive sleep apnea syndrome: 12-month follow-up. Sleep Med 2007; 8:128.
  37. Pirelli P, Saponara M, De Rosa C, Fanucci E. Orthodontics and obstructive sleep apnea in children. Med Clin North Am 2010; 94:517.
  38. Guilleminault C, Monteyrol PJ, Huynh NT, et al. Adeno-tonsillectomy and rapid maxillary distraction in pre-pubertal children, a pilot study. Sleep Breath 2011; 15:173.
  39. Marcus CL, Carroll JL, Bamford O, et al. Supplemental oxygen during sleep in children with sleep-disordered breathing. Am J Respir Crit Care Med 1995; 152:1297.
  40. Aljadeff G, Gozal D, Bailey-Wahl SL, et al. Effects of overnight supplemental oxygen in obstructive sleep apnea in children. Am J Respir Crit Care Med 1996; 153:51.
  41. Brouillette RT, Manoukian JJ, Ducharme FM, et al. Efficacy of fluticasone nasal spray for pediatric obstructive sleep apnea. J Pediatr 2001; 138:838.
  42. Kheirandish-Gozal L, Gozal D. Intranasal budesonide treatment for children with mild obstructive sleep apnea syndrome. Pediatrics 2008; 122:e149.
  43. Chadha NK, Zhang L, Mendoza-Sassi RA, César JA. Using nasal steroids to treat nasal obstruction caused by adenoid hypertrophy: does it work? Otolaryngol Head Neck Surg 2009; 140:139.
  44. Goldbart AD, Goldman JL, Veling MC, Gozal D. Leukotriene modifier therapy for mild sleep-disordered breathing in children. Am J Respir Crit Care Med 2005; 172:364.
  45. Goldbart AD, Greenberg-Dotan S, Tal A. Montelukast for children with obstructive sleep apnea: a double-blind, placebo-controlled study. Pediatrics 2012; 130:e575.
  46. Kheirandish-Gozal L, Bhattacharjee R, Bandla HP, Gozal D. Antiinflammatory therapy outcomes for mild OSA in children. Chest 2014; 146:88.
  47. Kheirandish L, Goldbart AD, Gozal D. Intranasal steroids and oral leukotriene modifier therapy in residual sleep-disordered breathing after tonsillectomy and adenoidectomy in children. Pediatrics 2006; 117:e61.
  48. Al-Ghamdi SA, Manoukian JJ, Morielli A, et al. Do systemic corticosteroids effectively treat obstructive sleep apnea secondary to adenotonsillar hypertrophy? Laryngoscope 1997; 107:1382.
  49. Don DM, Goldstein NA, Crockett DM, Ward SD. Antimicrobial therapy for children with adenotonsillar hypertrophy and obstructive sleep apnea: a prospective randomized trial comparing azithromycin vs placebo. Otolaryngol Head Neck Surg 2005; 133:562.
  50. Chan AS, Lee RW, Cistulli PA. Non-positive airway pressure modalities: mandibular advancement devices/positional therapy. Proc Am Thorac Soc 2008; 5:179.
  51. Zuberi NA, Rekab K, Nguyen HV. Sleep apnea avoidance pillow effects on obstructive sleep apnea syndrome and snoring. Sleep Breath 2004; 8:201.
  52. Patel AV, Hwang D, Masdeu MJ, et al. Predictors of response to a nasal expiratory resistor device and its potential mechanisms of action for treatment of obstructive sleep apnea. J Clin Sleep Med 2011; 7:13.
  53. Kureshi SA, Gallagher PR, McDonough JM, et al. Pilot study of nasal expiratory positive airway pressure devices for the treatment of childhood obstructive sleep apnea syndrome. J Clin Sleep Med 2014; 10:663.
  54. Guilleminault C, Huang YS, Monteyrol PJ, et al. Critical role of myofascial reeducation in pediatric sleep-disordered breathing. Sleep Med 2013; 14:518.
  55. Chuang LC, Lian YC, Hervy-Auboiron M, et al. Passive myofunctional therapy applied on children with obstructive sleep apnea: A 6-month follow-up. J Formos Med Assoc 2016.
Topic 6373 Version 33.0

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.