Pediatric Annals

CME Article 

Pediatric Obstructive Sleep Apnea: An Update

Darius A. Loghmanee, MD, FAAP; Stephen H. Sheldon, DO, FAAP, DABSM

Abstract

Pediatric obstructive sleep apnea (pediatric OSA) is a spectrum of obstructive sleep-disordered breathing ranging from snoring and mildly increased upper airway resistance to severe periodic occlusion of the upper airway. In 2002, the American Academy of Pediatrics (AAP) published a clinical practice guideline for practitioners outlining diagnosis and management of obstructive sleep apnea.1 Until that time, there was no clear evidence-based guidance for child health care practitioners regarding the approach to evaluation and treatment of the snoring child. This review focuses on key areas in which the understanding of pediatric OSA has advanced since those guidelines were published and how these advances have changed the approach to providing clinical care for the snoring child.

Abstract

Pediatric obstructive sleep apnea (pediatric OSA) is a spectrum of obstructive sleep-disordered breathing ranging from snoring and mildly increased upper airway resistance to severe periodic occlusion of the upper airway. In 2002, the American Academy of Pediatrics (AAP) published a clinical practice guideline for practitioners outlining diagnosis and management of obstructive sleep apnea.1 Until that time, there was no clear evidence-based guidance for child health care practitioners regarding the approach to evaluation and treatment of the snoring child. This review focuses on key areas in which the understanding of pediatric OSA has advanced since those guidelines were published and how these advances have changed the approach to providing clinical care for the snoring child.

Darius A. Loghmanee, MD, FAAP is assistant professor of Pediatrics, Northwestern University Feinberg School of Medicine. Stephen H. Sheldon, DO, FAAP, DABSM, is professor of Pediatrics, Northwestern University Feinberg School of Medicine.

Dr. Loghmanee and Dr. Sheldon have disclosed no relevant financial relationships.

Address correspondence to: Darius A. Loghmanee, MD, 2300 Children’s Plaza Mailbox #43, Chicago, IL 60614, 773.880.8230; fax: 773.880.6619; or e-mail: dloghmanee@childrensmemorial.org.

Pediatric obstructive sleep apnea (pediatric OSA) is a spectrum of obstructive sleep-disordered breathing ranging from snoring and mildly increased upper airway resistance to severe periodic occlusion of the upper airway. In 2002, the American Academy of Pediatrics (AAP) published a clinical practice guideline for practitioners outlining diagnosis and management of obstructive sleep apnea.1 Until that time, there was no clear evidence-based guidance for child health care practitioners regarding the approach to evaluation and treatment of the snoring child. This review focuses on key areas in which the understanding of pediatric OSA has advanced since those guidelines were published and how these advances have changed the approach to providing clinical care for the snoring child.

When a Snore Is Something More

Habitual snoring is currently defined as audible sonorous noises reported by an observer occurring more than three times a week without evidence of apnea, hypoventilation, or significant sleep fragmentation. Current estimates suggest that habitual snoring is present in about 7% of children.2 In 2002, much attention was paid to differentiating primary snoring, which was considered benign, from OSA, which had been shown to be associated with serious comorbidities. Since that time, however, the effect that snoring has on children has become better understood. Habitual snoring was associated with poor temper, hyperactivity, and poor school performance in recent survey data from parents of 6,349 children 5 to 14 years.2 This furthers earlier work demonstrating neurobehavioral deficits associated with snoring in children.3

Snoring has also been associated with enuresis4 and elevated blood pressure.5 Such evidence suggests that a history of habitual snoring alone warrants further evaluation and potential treatment and should not be considered simply benign.

OSA has been defined by the American Thoracic Society 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.

Affecting between 1% and 3% of all school-age children,6 pediatric OSA has been associated with failure to thrive,7 attention and behavior problems,8 cognitive impairment,9 hypertension,10 ventricular dysfunction,10 insulin resistance, 11 and lipid dysregulation.11 With recognition that the entire spectrum of pediatric OSA, including patients with snoring, obstructive hypoventilation, increased upper airway resistance, or OSA of any severity can be associated with comorbidities, it is clear that each habitually snoring child warrants careful evaluation and treatment.

Evaluation: By Whom, with What, and How Quickly?

As cultural and societal norms do not always identify snoring as a problem, parents often do not report this symptom to the child health care practitioner as a complaint. Therefore, it is important for primary care providers to screen regularly for snoring during routine health maintenance visits. Sleep disorders in children are easy to miss,12 which has led to the development of screening tools that increase the identification of such disorders, including snoring.13 Once snoring is identified, however, a series of decisions must be made. Habitual snoring during sleep cannot be differentiated from OSA by history alone14 or by clinical history and physical examination.15

Citing the difficulty in identifying pediatric OSA by means of history and physical, AAP guidelines, along with guidelines from other professional organizations, consider polysomnography (PSG) as the gold standard for diagnosing and quantifying OSA.1 Unfortunately, the limited number of pediatric sleep medicine centers and child health care specialists specifically trained in interpretation of polysomnograms and treatment of sleep disorders may lead to delays in comprehensive pediatric sleep medicine evaluations.

Polysomnographic criteria for scoring respiratory events for children were revised in 2007 in the American Academy of Sleep Medicine (AASM) Manual for the Scoring of Sleep and Associated Events. According to these guidelines, obstructive apnea lasts for at least two respiratory efforts with a greater than 90% fall in nasal pressure signal amplitude for greater than or equal to 90% of the entire respiratory event compared with pre-event baseline amplitude. Hypopneas must last the duration of two baseline breaths with a fall in the amplitude of the nasal pressure or alternative signal that is greater than or equal to 50% of baseline airflow and is associated with an arousal, an awakening, or at least 3% desaturation.

Respiratory-effort-related arousals (RERAs) are respiratory events associated with an abrupt shift of EEG frequency that do not meet criteria of apneas or hypopneas but indicate the presence of increased upper airway resistance. RERAs are scored when there is a fall in nasal pressure signal that is accompanied by snoring, noisy breathing, elevation of carbon dioxide levels, or visual evidence of increased work of breathing. Obstructive hypoventilation, another condition demonstrating increased upper airway resistance but not meeting criteria to be considered apnea or hypopnea, is diagnosed when the carbon dioxide level measured by either end tidal CO2 or transcutaneous CO2 monitoring is greater than 50 mm Hg for more than 25% of the total sleep time.

The apnea plus hypopnea index (AHI) is calculated by dividing the total number of apneas and hypopneas by the total sleep time in hours. In the 2005 edition of the International Classification of Sleep Disorders, the AASM defines an AHI greater than 1/hr as abnormal in children, but no studies have clearly demonstrated that specific AHI values correlate closely with morbidity.

Therefore, the AHI and other polysomnographic data require clinical correlation by a physician who understands what information is provided by the PSG and how to apply it to patient care. With this in mind, once habitual snoring has been identified, a child should be referred to a physician who is board certified in sleep medicine or an accredited sleep medicine center. If such resources are not available, a pulmonologist, neurologist, otolaryngologist, pediatrician or other practitioner who has obtained additional training or experience in the evaluation and treatment of children with sleep disorders can provide guidance as to the next step in evaluation and treatment of habitually snoring children.

Limited access to PSG and controversy about the relationship between polysomnographic data and morbidity have contributed to the drive to develop new diagnostic approaches that could enhance our ability to detect pediatric OSA more definitively. Acute phase reactants, such as C-reactive protein levels, have been shown to be elevated in children with OSA, and the decrease in these levels after treatment of OSA has been correlated with the change in AHI.16

Urinary biomarkers have also gained attention since specific patterns of protein concentrations were noted to be associated with pediatric OSA.17 Although neither of these methods has been validated as an alternative to polysomnography for the diagnosis of pediatric OSA, such biomarkers may be of future value in the diagnosis of pediatric OSA.

Once concern about pediatric OSA has been raised, thought must be given to how expeditiously further evaluation and treatment should be sought. Complex, high-risk patients should be referred to a sleep specialist for evaluation, and patients with cardiorespiratory compromise should be evaluated as soon as possible.1 “High-risk” patients include: infants; patients with craniofacial disorders; Down syndrome; cerebral palsy; neuromuscular disorders; chronic lung disease; sickle cell disease; central hypoventilation syndromes; and genetic metabolic or storage diseases.

In otherwise healthy children, the decision to monitor snoring over time without further evaluation must be made cautiously. One study based on PSG evaluation of patients with snoring but without evidence of OSA showed that 1 to 3 years after their initial PSG, snoring continued in most subjects and progression to mild OSA occurred in 10% of patients.18

Recently, a study of Chinese children with mild OSA who were not treated showed that 29% had more severe OSA on a second PSG 2 years after initial diagnosis. Risk factors for worsening of OSA included large tonsils at baseline, male gender, and younger age.19 Although these studies were relatively small, evidence suggests that OSA does not consistently improve over time and may worsen in some cases. Careful evaluation of any snoring patient as soon as possible and treatment based on the underlying etiology should be provided to avoid the comorbidities associated with the spectrum of pediatric OSA.

Adenotonsillectomy

With upper airway obstruction as the most common indication for adenotonsillectomy20 and the recognition that this treatment can have significant complications, 21 attention has naturally turned to evaluating the efficacy of this approach to the treatment of the spectrum of pediatric OSA. Adenotonsillectomy leads to resolution of pediatric OSA in up to 71% of children,22 improves sleep and behavior,23 and improves quality of life.6 However, residual OSA after adenotonsillectomy may be more common than previously believed. Tauman et al. demonstrated that only 25% of children had AHI values less than 1/hr after adenotonsillectomy and 46% had AHI values between 1 and 5/hr.24

Meta-analysis of studies that included 110 obese children demonstrated that only 25% of children had AHI values less than 2/hr after tonsillectomy, and only 12% had AHI values less than 1/hr.25 A recent multicenter retrospective review analyzed data from 578 children and demonstrated that although the AHI values were reduced significantly after surgery, only 27.2% had complete resolution of the OSA as defined as AHI value of less than 1/hr.26 There is also an indication that adenotonsillectomy is associated with overweight later in childhood,27 thereby putting children at risk for developing OSA when they are older.

Therefore, although adenotonsillectomy is still often the best initial treatment for nonobese children with obstructive sleep apnea and adenotonsillar hypertrophy, rather than viewing adenotonsillectomy as a definitive treatment, it is more appropriate to see it as part of a management plan that includes careful follow-up to evaluate for signs and symptoms of residual OSA. Careful evaluation before and after adenotonsillectomy, in some cases with postoperative PSG, is essential to ensure that children with pediatric OSA receive appropriate care.

Inflammation and OSA: Implications for Medical Management

As multiple markers of inflammation have been shown to be elevated in children with OSA and appear to normalize after treatment of the subjects’ OSA, the connection between systemic inflammation and OSA has become increasingly clear.28 The advances made in understanding this area have helped explain some of the comorbidities associated with OSA, demonstrated the importance and efficacy of treatment of pediatric OSA, and have also directed attention to alternative means of therapy.

As the correlation between inflammation and OSA has been more clearly established, attention has been drawn to the use of anti-inflammatory medications in treating OSA. One double-blind crossover study revealed considerable improvement with intranasal budesonide even 8 weeks after treatment ended.29 Explanation for the efficacy of nasal steroids when systemic steroids failed to achieve improvement was proposed by a study that demonstrated that the number of glucocorticoid alpha receptors were noted in abundance in the tonsils and adenoids of subjects with OSA.30

The topical application of steroids over these receptors appears to have a local therapeutic effect. Treatment with the leukotriene modifier montelukast was also evaluated and shown to result in decreased apnea plus hypopnea index (AHI) and improved adenoidal/nasopharyngeal ratios.31 These studies suggest that nasal steroids and leukotriene antagonists might be considered either as an adjunct to or in lieu of adenotonsillectomy in the treatment of OSA.

Nonsurgical Airway Expansion

Besides the medical approaches mentioned above, there are other nonsurgical approaches available to those children in whom surgery is either ineffective or contraindicated. The most well known in adults is continuous or bilevel positive airway pressure (PAP). This treatment can serve as an effective means of treating pediatric OSA.32 However, it is difficult for children to tolerate mask and airflow. Adherence to noninvasive PAP is likely to improve with desensitization protocols, further developments in the comfort of PAP masks, as well as advances in the sophistication of the PAP flow generators.

Aside from adherence, another concern about PAP in the very young patient is the risk of midface malformation due to the pressure from a tight-fitting mask that is applied to the developing maxilla and nasal bridge. PAP by means of a high-flow nasal cannula (HFNC) presents an attractive alternative because it does not require a firmly fitting face mask and could be more comfortable. A study comparing CPAP with HFNC showed that HFNC was well tolerated and reduced AHI to 2/hr +/− 1, while CPAP improved it to 1/hr +/− 1.33 Although it is as yet unclear how this treatment modality achieves its results and it has yet to be fully evaluated, the advantages it offers with reference to likelihood of adherence and decreased risk of craniofacial malformation make it appealing.

Alternatives to CPAP and adenotonsillectomy have been evaluated that also aim to alter the airway mechanically so as to decrease obstruction. These include functional dental appliances for mandibular advancement, rapid maxillary expansion, and redirecting maxillomandibular growth. A study of a jaw positioning appliance designed to advance the growth of the mandible evaluated subjects with malocclusion and showed that all of those treated with the appliance had improvement or resolution of their OSA.34 An evaluation of treatment with rapid maxillary expansion demonstrated that the device lowered AHI values and decreased symptoms.35

Although sleep parameters were not measured, an evaluation of an appliance designed to guiding maxillomandibular growth horizontally led to a relative 31% increase in nasopharyngeal airway area; 23% increase in oropharyngeal airway area; and 9% increase in hypopharyngeal area; suggesting that this treatment modality could decrease the likelihood of obstruction.36 Because these devices work best in specific patient populations, it is important that practitioners know what features from the physical exam suggest that the patient would demonstrate a beneficial response to such treatments. More studies will be required before use of these devices is fully understood.

OSA in the Obese and Nonobese Patient

OSA is seen in obese and nonobese children, but its effects manifest in divergent ways. Obese children are at increased risk for developing OSA.37 When they show symptoms, they are more likely to demonstrate excessive daytime sleepiness38 or insulin resistance11 than nonobese children. Treatment of obese children must be approached carefully. When used to treat obese children with OSA, adenotonsillectomy has been associated with increased body mass index (BMI) and high rates of recurrence 1 year after adenotonsillectomy.39

This highlights the importance of continued follow-up and attention to weight loss in addition to adenotonsillectomy in the treatment of obese children with OSA.

Although treatment with CPAP for obese children with residual OSA after adenotonsillectomy is an option, alternative and adjunct treatment options have also been studied. Exercise, even without weight loss, can improve snoring,40 and weight loss by means of bariatric surgery is effective in decreasing AHI.41

The differences in complication rates and treatment response in obese children compared with those who have normal weight makes their evaluation and treatment more difficult, adding yet another layer of complexity to the approach to patients with OSA.

Looking Ahead

As awareness of the serious sequelae of pediatric OSA grows, the need for a systematic approach to its diagnosis and treatment has become increasingly clear. As suggested by the 2002 AAP guidelines,1 every child who snores regularly should be screened expeditiously. Those for whom further evaluation is warranted should be tested for OSA by validated means, and if OSA is diagnosed, a child should undergo a definitive treatment.

What we have learned since that time about approaches to diagnosis and treatment, however, brings us to a new stage in the evolution of our understanding and the approach to the spectrum of pediatric OSA. Developing definitive diagnostic and therapeutic means to care for children with OSA remains an important goal, and there is every indication that these means will become available. However, further research is needed to assure that every child has effective, efficient, and efficacious therapy.

As regular screening for snoring is incorporated as part of health maintenance visits, fewer children with OSA will go undetected. As education about sequelae of pediatric OSA improves, physicians in training will be less likely to treat its myriad manifestations without identifying their common cause.

As more child health care practitioners seek out additional training in sleep medicine, more resources will be available to serve children afflicted with this common disorder. In these ways, child health care practitioners will improve the snoring child’s chances of avoiding serious health issues and meeting their full neurocognitive potential.

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CME Educational Objectives

  1. Define obstructive sleep apnea (OSA).

  2. Identify two sequelae of snoring without the presence of obstructive sleep apnea.

  3. Describe three alternatives to adenotonsillectomy for treatment of OSA.

Authors

Darius A. Loghmanee, MD, FAAP is assistant professor of Pediatrics, Northwestern University Feinberg School of Medicine. Stephen H. Sheldon, DO, FAAP, DABSM, is professor of Pediatrics, Northwestern University Feinberg School of Medicine.

Dr. Loghmanee and Dr. Sheldon have disclosed no relevant financial relationships.

Address correspondence to: Darius A. Loghmanee, MD, 2300 Children’s Plaza Mailbox #43, Chicago, IL 60614, 773.880.8230; fax: 773.880.6619; or e-mail: .dloghmanee@childrensmemorial.org

10.3928/00904481-20101116-09

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