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, which disrupt sleep. The condition exists in 2 to 5 percent of children and can occur at any age [1,2]. Untreated pediatric OSA is associated with behavioral and learning problems; in more severe cases, it can be associated with impaired growth (including failure to thrive) and cardiovascular complications. Early diagnosis and treatment may decrease morbidity [3]. Treatment decisions are individualized and depend upon findings from a comprehensive evaluation, including nighttime sleep disruption, daytime dysfunction, physical examination findings, and sleep study findings.
An overview of surgical and medical management of children with confirmed OSA 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 "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea".)
CONSEQUENCES OF UNTREATED OBSTRUCTIVE SLEEP APNEA — 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, and treatment can lead to weight gain and growth
●Cardiovascular disease – Cardiovascular consequences may include systemic hypertension, right and left ventricular dysfunction, and cor pulmonale (see "Cardiovascular consequences of obstructive sleep apnea in children")
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 initial screening for OSA is typically done by the primary care clinician (algorithm 1). Children with suspected OSA should be referred to a specialist in sleep medicine or otolaryngology (ear, nose, and throat). Alternatively, the referring provider may be able to arrange for a polysomnogram (PSG) if a facility with experience in pediatric PSG is available. Children with abnormal results of PSG, or with other significant sleep problems, can then be referred to the appropriate specialist. OSA is typically defined by clinically relevant symptoms and an apnea hypopnea index (AHI) >1 or hypoventilation (carbon dioxide >50 mmHg for >25 percent total sleep time) as determined on PSG. (See "Evaluation of suspected obstructive sleep apnea in children".)
The decision to initiate treatment and choice of treatment depend upon the child's age, clinical symptoms (eg, nighttime sleep problems or daytime dysfunction), presence of comorbidities (especially underlying genetic, craniofacial, neuromuscular disorders), risk factors (eg, obesity, crowded oropharynx), and results of PSG if performed, as outlined below [4]:
●Adenotonsillectomy – Referral to a specialist for adenotonsillectomy evaluation is generally indicated for otherwise healthy children who have OSA and adenotonsillar hypertrophy (including ≥1+ tonsils) [4]. After the full evaluation, the decision about whether to proceed to surgery should be made collaboratively with the family, considering in particular the degree of clinical symptoms (nocturnal and daytime (table 1)) as well as the tonsil size and OSA severity. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Assessment of severity'.)
Adenotonsillectomy also may be initial therapy for children with other contributors to OSA such as obesity or other comorbidities, if appreciable adenotonsillar tissue is present, even if there is no clear hypertrophy. 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'.)
●Watchful waiting for up to six months – For otherwise healthy children with mild or moderate OSA confirmed by PSG (AHI >1 and <10), watchful waiting with supportive care is a reasonable alternative to adenotonsillectomy. Supportive care may include conservative medical management (with treatment or referral for treatment of comorbidities such as asthma and allergic rhinitis), education regarding sleep hygiene and healthy sleep behaviors, and the use of nasal saline spray as needed for nasal mucosal dryness or crusting. This approach is based on the acceptable outcomes for children five to nine years old who were followed with watchful waiting in the Childhood Adenotonsillectomy Trial (CHAT) [5] and a similar trial in younger children [6]. In both of these studies, adenotonsillectomy compared with watchful waiting led to improvement in daytime behavior, sleep apnea symptoms, subjective sleepiness, and quality of life. These observations underscore the importance of assessing the child's level of symptoms when making a decision between adenotonsillectomy and watchful waiting (see 'Adenotonsillectomy' below). If watchful waiting is chosen, the child should be reevaluated clinically within six months or reevaluated sooner if symptoms worsen.
We suggest against watchful waiting for children with severe OSA (eg, AHI >10 or other PSG measures suggesting severe OSA), particularly if multiple symptoms or risk factors are present. This suggestion is based upon observational studies and indirect evidence from the CHAT trial, as detailed below. (See 'Adenotonsillectomy' below.)
●Positive airway pressure therapy – For patients with minimal adenotonsillar tissue or a strong preference for a nonsurgical approach, positive airway pressure therapy is an alternative to adenotonsillectomy [4,7-10]. It also may be appropriate to stabilize children with severe OSA prior to adenotonsillectomy or another surgical procedure or for children with persistent OSA despite adenotonsillectomy [9]. Positive airway pressure may consist of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP). (See 'Positive airway pressure' below and "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'Treatment decisions'.)
The following treatments can be considered in selected cases, either instead of or as an adjunct to the primary therapy:
●Rapid maxillary expansion (RME) – Prepubertal children with OSA and a narrow palate (crossbite) and little adenotonsillar tissue are candidates for treatment with RME. RME is an orthodontic technique that widens the palate and nasal passages, thereby increasing airway patency. Such patients should be managed by an orthodontist experienced with pediatric sleep-related respiratory abnormalities. (See 'Orthodontics' below.)
●Mandibular advancement device – A mandibular advancement device is a specific, common type of oral appliance that protrudes the mandible and helps to position the tongue anteriorly, thus increasing airway patency. Limited data are available from children about the relative efficacy and risks compared with other treatment methods. However, this approach may be reasonable to consider when other treatment methods have failed. Availability of a dentist experienced in oral appliance therapy for children may be a limiting reality in many areas. (See 'Mandibular advancement device' below.)
●Corticosteroids or antiinflammatory therapy – For children with mild or moderate OSA and nasal obstruction due to adenoidal hypertrophy/allergic rhinitis, a trial of intranasal corticosteroids or leukotriene modifier therapy may be performed for two to four weeks, prior to determining whether the therapy should be continued long-term as an adjunct or alternative to adenotonsillectomy or positive airway pressure. (See 'Intranasal corticosteroids or montelukast' below.)
●Other therapies – Selected children with OSA may derive benefit from adjunctive therapies. As examples, obese children with OSA may benefit from weight loss and all children may benefit from avoidance of environmental allergens or irritants such as tobacco smoke. In addition, positional therapy (eg, elevation of the head of the bed) can be considered. Several of these adjunctive therapies are described below. (See 'Adjunct therapies' below.)
SURGICAL THERAPY
Adenotonsillectomy — Adenotonsillectomy refers to surgical resection of the tonsils and adenoids. Key information relevant to the primary care clinician is summarized below, and details are discussed separately. (See "Adenotonsillectomy for obstructive sleep apnea in children".)
●Indications – Adenotonsillectomy is generally indicated for otherwise healthy children who have adenotonsillar hypertrophy and severe OSA (eg, apnea hypopnea index [AHI] >10, in the setting of relevant clinical symptoms). For patients with moderate OSA (eg, AHI 5 to 10), either adenotonsillectomy or watchful waiting for up to six months are reasonable approaches; the decision usually depends upon the degree of symptoms and the patient's and family's preferences. In obese children, OSA usually improves following adenotonsillectomy, although the outcome may be less satisfactory than in lean children. Considerations for children without apparent adenotonsillar hypertrophy, and for those with underlying conditions that are associated with multilevel OSA including Down syndrome and craniofacial anomalies, are discussed separately. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Indications for surgery'.)
●Outcomes – Children with OSA and adenotonsillar hypertrophy generally have improvements in clinical symptoms and polysomnogram (PSG) indices of OSA after adenotonsillectomy. In the past, this was largely based upon clinical experience and observational studies. In 2013, a randomized trial (Childhood Adenotonsillectomy Trial [CHAT]) demonstrated an advantage of adenotonsillectomy over watchful waiting for children five to nine years old with uncomplicated OSA (AHI 1 to 30) who were candidates for adenotonsillectomy (tonsil size ≥1) [5,11]. Specifically, adenotonsillectomy compared with watchful waiting led to 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, which were the primary outcomes of the study. Modest benefits of adenotonsillectomy were seen in selected areas of cognitive functioning, including nonverbal reasoning, fine motor skills, and selective attention [12]. Similar findings were reported in a randomized trial that involved 60 younger children (age 2 to <5 years) with mild to moderate OSA (AHI 2 to 10) [6]. Children who underwent adenotonsillectomy compared with watchful waiting for six months had significant improvements in a quality-of-life measure, and the subgroup with moderate OSA (AHI 5 to 10) had a potentially meaningful relative improvement in AHI (mean change in AHI -3.1, 95% CI -5.7 to -0.5).
Children with severe OSA (eg, AHI >10) are probably particularly likely to benefit from adenotonsillectomy rather than watchful waiting, based upon clinical experience and indirect evidence from the CHAT trial. The CHAT trial did not specifically analyze this subgroup of patients, but it did find that for those with AHI above the median (>4.7 events/hour), adenotonsillectomy compared with watchful waiting led to greater improvement in AHI [5]. The CHAT trial was not informative about patients with very severe OSA, because it excluded such patients (those with an AHI >30, an apnea index >20, or >2 percent of total sleep time spent with oxygen saturations <90 percent). 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 or psychiatric disorders; severe obesity (body mass index Z-score ≥3); developmental delays requiring school accommodations; and known genetic, craniofacial, or neurologic disorders likely to affect the airway, cognition, or behavior.
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'.)
●Risk factors for complicated OSA – Risk factors in children that predict increased risk for perioperative complications following adenotonsillectomy include severe OSA on preoperative PSG or the presence of complicating factors such as obesity (especially if severe), very young age (<36 months), abnormal upper airway tone, congenital syndromes, or craniofacial anomalies (table 2). Patients with these characteristics warrant additional precautions during the evaluation and performance of adenotonsillectomy and may require adjuvant surgical procedures. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'High-risk populations' and 'Adjuvant surgical procedures' below.)
●Follow-up after adenotonsillectomy – 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 PSG to ensure that their sleep-related breathing abnormalities have resolved [4,13]. Repeat PSG is also indicated for children who have had complications from OSA (eg, cor pulmonale), those with severe OSA on preoperative PSG, and those with craniofacial or neurologic abnormalities (including Down and Prader-Willi syndromes) [4,14-17]. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'Indications for postoperative polysomnography'.)
Some patients will have gradual reemergence of OSA months or years after adenotonsillectomy due to increases in body weight, regrowth of adenotonsillar tissue, or changes in body shape due to puberty [18,19]. Thus, reevaluation with PSG 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 — Adenoidectomy alone (without tonsillectomy) is not recommended for treatment of OSA in children [4]. Obstructive symptoms and signs frequently persist after adenoidectomy alone is performed [20-24]. 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 [22,25]. Conversely, some data also suggest that tonsillectomy without adenoidectomy is less effective than the combined procedure in treating pediatric OSA.
Adjuvant surgical procedures — Children with congenital syndromes, craniofacial abnormalities, mucopolysaccharidosis, or neuromuscular disorders are likely to have multifactorial OSA, in which the obstruction is due to factors other than adenotonsillar hypertrophy alone and may occur at multiple sites within the airway. In addition to adenotonsillectomy, these children may need adjuvant surgical procedures, including uvulopalatopharyngoplasty, supraglottoplasty, tongue reduction, tongue base procedures, hypoglossal nerve stimulation, 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. Management is discussed separately. (See "Adenotonsillectomy for obstructive sleep apnea in children", section on 'High-risk populations' and "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 OSA in children [7,8,26,27]. 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 mask fitting, positive pressure titration, and behavioral support. For example, desensitization or programs to enhance motivation, administered by a child psychologist or behavioral developmental pediatrician, may be helpful when adherence is suboptimal.
●Indications and contraindications – Positive airway pressure is indicated for children with OSA (apnea hypopnea index [AHI] >1 and clinically relevant symptoms) and minimal adenotonsillar tissue. It also may be useful for children with a strong preference for a nonsurgical approach or for persistent OSA despite adenotonsillectomy. 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. Contraindications and other considerations are discussed separately. (See "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'Treatment decisions'.)
●Continuous positive airway pressure (CPAP) versus bilevel positive airway pressure (BPAP) – CPAP and BPAP are the usual types of positive airway pressure. 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. 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. (See "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'The CPAP prescription'.)
●Implementation – The fitting of equipment, titration of pressure settings, and monitoring of positive airway pressure therapy should be performed in a sleep laboratory with expertise in managing pediatric patients [7,28]. Proper technique and family support are essential to optimize adherence to therapy. The pressure level should be periodically rechecked with repeat polysomnography (PSG), especially if there are changes in the child's clinical status (eg, recurrence of snoring despite using CPAP, recurrent daytime symptoms) or substantial changes in the child's weight or body mass index percentiles [29]. (See "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'Titration of CPAP in children'.)
●Efficacy – No randomized trials have compared positive airway pressure with placebo/sham CPAP therapy in children with OSA. However, observational studies suggest that positive airway pressure improves symptoms, signs, and PSG indices of OSA in at least 85 percent of children [7-9,28,30,31].
•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 PSG abnormalities of OSA in 90 percent of the children. The AHI diminished from a mean of 27.3 to 2.6 events per hour [8]. 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 cmH2O was effective in 86 percent of children [7]. Effectiveness was defined as resolution of clinical symptoms, normal oxyhemoglobin saturation during sleep, and improvement of PSG 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.
●Complications – Complications of positive airway pressure therapy are usually minor [7]. 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 [27]. 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. With positive airway pressure, central sleep apnea occasionally emerges; this is known as "treatment-emergent central sleep apnea." (See "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'Choosing the right equipment' and "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'Barriers to effective CPAP therapy in children'.)
Orthodontics
Rapid maxillary expansion — Rapid maxillary expansion (RME), also known as rapid palate expansion (RPE), 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, RME 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 [32]. After four months of RME, the mean AHI had decreased from 12 to less than 1 event per hour. The same group demonstrated persistent improvement after 3 years [33] and 12 years [34]. Other studies in similar patient populations reported similar results [35,36].
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 1 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 [37].
Mandibular advancement device — A mandibular advancement device is an oral appliance, typically consisting of a top tray and bottom tray that can be used to advance the mandible and keep the tongue in an anterior position, thus increasing airway diameter. Accumulating evidence supports the use of this type of device for selected children with OSA (and without craniofacial abnormalities). The indications, relative efficacy compared with other treatment methods, and potential adverse effects have not been established.
●Indications – Due to the limited evidence for efficacy of mandibular advancement devices in children and lack of long-term outcomes on the growth of the mandible and teeth, it is the author's clinical practice to recommend oral appliance evaluation if other therapies fail or are inappropriate or for children with OSA who are transitioning to college and do not want to continue on CPAP.
●Efficacy – A meta-analysis of mandibular advancement devices in children with OSA (without craniofacial syndromes) showed modest beneficial effects for this intervention. The mean difference in AHI change for the mandibular advancement group compared with the control group was -1.75 events/hour (95% CI -2.07 to -1.44) [38].
One of the included studies was a randomized crossover trial in 18 children (8 to 12 years) with OSA. Participants were treated with three weeks of either active mandibular advancement device (upper and lower acrylic plates titrated to 75 percent of the maximum jaw protrusion) or a sham oral appliance, followed by a two-week washout period, then an additional three weeks of the other oral appliance [39]. Compared with sham therapy, the mandibular advancement device modestly reduced the overall AHI (-0.6 events/hour, 95% CI 0.5-0.8) and supine AHI (-4.1 events/hour, 95% CI -6.4 to -1.8) and improved minimum oxygen saturation (+3.4 percentage points, 95% CI 0.9-5.9). Some children experienced hypersalivation, feelings of pressure, tightness, or dental discomfort, which improved over the first week.
●Implementation – If the clinician and patient choose to pursue this therapy, the first step is an evaluation by a trained sleep dentist with certification in dental sleep medicine to evaluate the child's oral cavity and potential tolerance to the device. This specialized expertise is important and may not be available in many areas. Evaluation may include Mallampati score, intraoral and extraoral photographs, lateral cephalograms in maximum intercuspal position, and dental impressions. Contraindications to oral appliance therapy may include temporomandibular joint disease, instability of the jaw, limited range of motion of the jaw, missing teeth, or young age (because young children will require multiple oral appliances to accommodate growth). Only a few devices have been tested in children with published data. Once a child is fit with a mandibular advancement device, a new PSG should be performed to confirm improvement in AHI and oxygen desaturation, in addition to clinical improvements.
Guidelines for titrating mandibular advancement devices are available for adults with OSA; however, no separate guidelines exist for children. Children should be monitored closely for unexpected shift in teeth, changes to expected growth of the jaw and teeth, or side effects such as discomfort or pain.
Intranasal corticosteroids or montelukast — Children with mild or moderate OSA and nasal obstruction due to adenoidal hypertrophy, especially those with seasonal allergies, may be candidates for treatment with intranasal corticosteroids or leukotriene modifier therapy. These therapies are typically considered as an alternative or adjunct to adenotonsillectomy or as a temporizing measure during the watchful waiting period prior to other interventions. If this approach is selected, a two- to four-week trial of the medication should be performed to decide if it would be useful for long-term therapy [4]. If nasal steroids are prescribed, patients should be advised to aim for the lateral sides inside of the nostril rather than "straight back" to avoid spraying the septum. No clear guidelines exist on duration of therapy necessary for sustained benefit.
●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 AHI reduction from 11 to 6 events per hour [40].
•Similar findings were noted in a double-blind randomized crossover trial of 48 children with mild OSA treated with intranasal budesonide; one-half of the children had normalization of PSG parameters during the budesonide treatment arm. In many of the children, the positive effects were sustained up to eight weeks after discontinuation of treatment [41].
•A systematic review concluded that intranasal corticosteroids may improve nasal obstruction symptoms [42], but their effect on PSG measures was uncertain [43].
●Leukotriene modifier therapy – Montelukast (Singulair) appears to modestly reduce AHI and, possibly, adenotonsillar size [43-45]. However, use is limited by the possible increased risk of neuropsychiatric events associated with this class of drugs. Patients/caregivers should be counseled about these risks. (See "Antileukotriene agents in the management of asthma".)
●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 a combination of intranasal corticosteroids and montelukast, more than 80 percent experienced beneficial effects [46]. Among those who underwent follow-up PSG, 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 PSG parameters of OSA [48].
Adjunct therapies — The following interventions may be helpful in selected patients as adjuncts to primary surgical or medical therapy.
●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, which may include nasal saline irrigation, 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", section on 'Nasal saline'.)
●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 "Prevention and management of childhood obesity in the primary care setting" and "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 [49,50], 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.
●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 [51,52]. 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 wake and sleep hypercapnia by measuring end-tidal carbon dioxide or transcutaneous carbon dioxide during the overnight sleep study when the supplemental oxygen is titrated.
The use of supplemental oxygen as a bridging therapy is rare in our practice and is reserved for children who cannot tolerate CPAP or 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 [51]. Two children developed significant hypercapnia during treatment with supplemental oxygen.
●Antibiotics – Antibiotics are not indicated for the routine treatment of pediatric OSA. Although antibiotic therapy reduces the size of the tonsils and adenoids in some children, this may temporarily improve the OSA but does not provide persistent relief or avoid the need for surgery. An occasional course of antibiotics may be appropriate for children with recurrent throat infections; for these children, the decision about when to proceed to adenotonsillectomy depends on the frequency and severity of the infections. (See "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications", section on 'Recurrent throat infection'.)
The effect of antibiotics on OSA was evaluated in a trial of 22 children (2 to 12 years old) with OSA [53]. 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 PSG performed within the two weeks following the trial.
●Positional therapy – OSA is positional if the AHI in supine sleep is substantially higher (eg, twofold or more) than the AHI in other positions, and this pattern may be more common in children with obesity [54]. Paradoxically, the prone position may exacerbate OSA in some patients, so the optimal position varies [55,56]. In patients whose AHI varies markedly with position and whose OSA cannot be treated or treated completely by other means, positional therapy (avoidance of the position that appears on PSG to exacerbate sleep apnea) may be a consideration. Tools to maintain a nonsupine position include several commercially available belts and pillows, including the Rematee belt (available in children's sizes) and the Sona Pillow. However, positional therapy has not been well studied in children. Studies in adults have been small and lack randomization [57,58]. Another alternative in some cases may be to raise the head of the bed. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Polysomnography'.)
●Myofascial reeducation – Myofunctional reeducation (nasal breathing retraining) is a form of physical therapy consisting of exercises designed to strengthen the tongue and orofacial muscles, with a goal of repositioning muscles to the appropriate position. This approach can be offered to patients who have failed adenotonsillectomy surgery or CPAP therapy, but data on efficacy are limited. An example of myofascial reeducation exercise can be found here.
A meta-analysis (nine studies, 230 patients) evaluating effects of myofunctional therapy on children with mild to moderate obstructive sleep apnea concluded that myofunctional therapy reduced AHI from 4.32 (5.2) to 2.48 (4.0) events per hour, increased mean oxygen saturation, and decreased persistent mouth breathing in children with mild to moderate OSA [59].
Active myofunctional reeducation may reduce oral breathing, reduce lip hypotonia, restore normal tongue resting position, and increase mean tongue strength and endurance [60-62].
An alternate approach is passive myofunctional therapy, which consists of an oral device used to induce tongue muscle activity during sleep. In a study of 29 children ages 3 to 15 years, 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 PSG [63].
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".)
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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: Sleep apnea in children (The Basics)" and "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.)
●Children with suspected or confirmed OSA should be referred to a specialist (eg, otolaryngology or sleep medicine) for further evaluation and planning (algorithm 1). The decision about whether and when to initiate therapy should be made collaboratively with the caregivers once the diagnosis of OSA is confirmed by the clinical evaluation, which may include a polysomnogram (PSG) in a sleep laboratory. Important considerations include the amount of nighttime sleep disruption and daytime dysfunction, child's age, presence of adenotonsillar hypertrophy, and PSG abnormalities. Other factors influencing treatment decisions are underlying medical issues or risk factors for complicated OSA, such as a congenital syndrome, craniofacial abnormalities, neuromuscular disorders, or mucopolysaccharidosis (table 2). (See 'Choice of therapy' above.)
●Adenotonsillectomy evaluation is generally indicated for otherwise healthy children who have adenotonsillar hypertrophy (≥1+ tonsils) and OSA (eg, apnea hypopnea index [AHI] >1 in the setting of relevant clinical symptoms). (See 'Choice of therapy' above and 'Adenotonsillectomy' above.)
•After the full evaluation, the decision about whether to proceed to surgery should be made collaboratively with the family, considering in particular the degree of clinical symptoms (nocturnal and daytime (table 1)), as well as the tonsil size and OSA severity.
•Risk factors in children that predict increased risk for perioperative complications following adenotonsillectomy include severe OSA on preoperative PSG or the presence of complicating factors such as obesity (especially if severe), age <3 years, abnormal upper airway tone, congenital syndrome, or craniofacial anomalies (table 2).
•Despite adenotonsillectomy, OSA may persist or recur, especially in children with obesity. Careful clinical follow-up for signs and symptoms of OSA is advisable.
●For children with OSA and minimal adenotonsillar tissue, a strong preference for a nonsurgical approach, or contraindications to adenotonsillectomy, we suggest positive airway pressure therapy (Grade 2C). This is also an option for patients who have undergone adenotonsillectomy but have residual OSA. Positive airway pressure can be delivered as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP). (See 'Positive airway pressure' above and "Continuous positive airway pressure (CPAP) for pediatric obstructive sleep apnea", section on 'Indications'.)
●For patients with nonsevere OSA that has been confirmed by PSG (eg, AHI 1 to 10), watchful waiting with supportive care (continued treatment for seasonal allergies and asthma) for up to six months can be a reasonable consideration as an alternative to adenotonsillectomy. This is based on the acceptable outcomes for patients followed with watchful waiting in a randomized trial. 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 and 'Adenotonsillectomy' above.)
●For all children with OSA, efforts should be made to minimize exposure to environmental allergens or irritants such as tobacco smoke. Children who are overweight or obese should be offered support for weight loss, with the intensity depending on the child's age and degree of obesity. (See 'Adjunct therapies' above.)
●Prepubertal children with OSA and a narrow palate (crossbite) and little adenotonsillar tissue are candidates for treatment with rapid maxillary expansion (RME). RME is an orthodontic technique that widens the palate and nasal passages, thereby increasing airway patency. Mandibular advancement devices (oral appliances) typically consist of a top tray and bottom tray and are used to advance the mandible and keep the tongue in an anterior position, thus increasing airway diameter. (See 'Orthodontics' above.)
●Children who have severe OSA-related hypoxemia may benefit from supplemental oxygen that is administered at night until definitive therapy can be provided. When nocturnal supplemental oxygen therapy is necessary, it should be initiated during a PSG with assessment for hypercapnia. (See 'Adjunct therapies' above.)
●Positional therapy 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. Positional therapy consists of positioning to avoid supine sleep by using specially designed belts or pillows or elevation of the head of the bed. (See 'Adjunct therapies' above.)
