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Obstructive sleep apnea: The sleeping giant of the childhood obesity epidemic

Mofid, Marcie PA-C

Journal of the American Academy of PAs: October 2014 - Volume 27 - Issue 10 - p 27–30
doi: 10.1097/01.JAA.0000453860.16582.9c
CME: Pediatrics
Free
CME

ABSTRACT Obstructive sleep apnea (OSA) is more common among obese children than in those of normal weight and can have serious consequences for neurocognitive function, behavior, and school performance. This article reviews OSA and steps for identifying the condition early and taking a multidisciplinary approach to long-term treatment.

Marcie Mofid practices otolaryngology and head and neck surgery at Ventura County (Calif.) Medical Center. The author has disclosed no potential conflicts of interest, financial or otherwise.

Earn Category I CME Credit by reading both CME articles in this issue, reviewing the post-test, then taking the online test at http://cme.aapa.org. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of October 2014.

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Since 1980, obesity prevalence among children and adolescents has almost tripled in the United States.1 Obese children are more likely to become obese adults and are at increased risk for other health conditions including diabetes, cardiovascular disease, hypertension, and obstructive sleep apnea (OSA).1 Between 25% and 45% of obese children have OSA, compared with 1% to 3% of their normal-weight counterparts.2

Untreated OSA has a marked social effect on children, being associated with behavioral problems, neurocognitive dysfunction, and poor school performance.3 Quality-of-life measures in children with OSA are similar to those in children with chronic conditions such as asthma and juvenile rheumatoid arthritis.4 The American Academy of Pediatrics recommends all children be screened for snoring as part of routine healthcare maintenance, especially children at high risk, including obese children.5 The recent epidemic of childhood obesity has prompted the healthcare community to be more aware of the increase in chronic diseases, healthcare costs, and the long-term effect of obesity on health and quality of life. In this growing subset of children, identification, early diagnosis, and proper long-term treatment are paramount to improving quality of life and avoiding long-term physical sequelae of disease.

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PATHOPHYSIOLOGY

Sleep-disordered breathing is characterized as recurrent upper airway obstruction causing snoring, mouth breathing, abnormal ventilation, and disruption of sleep patterns. Sleep-disordered breathing includes a spectrum of disease further classified into primary snoring, upper airway resistance syndrome, and OSA.

Primary snoring is defined as observed snoring without apnea, abnormalities in gas exchange, or excessive arousals.

Upper airway resistance syndrome is associated with fragmentation of sleep due to increased respiratory effort and related arousals, although oxygenation is not affected.

OSA is defined as obstructive events causing apnea, hypopnea, hypercarbia, hypoxemia, related arousals, and fragmentation of sleep.6 OSA is associated with a decrease in the cross-sectional area of the pharynx combined with dysfunctional neuromuscular tone and craniofacial anatomy.7 In most normal-weight children, tonsil and adenoid tissue is the main source of obstruction. Tonsillectomy and adenoidectomy alone is curative in most normal-weight children. According to a recent meta-analysis, 78% of normal-weight children achieved cure based on polysomnography parameters. Obese children were cured at a significantly lower rate, 38%.8 In obese children, the source of obstruction is multifactorial. In addition to the tonsil and adenoid tissue, the circumference of the pharynx is further narrowed from deposition of adipose tissue surrounding the pharyngeal airway and from external compression from the subcutaneous tissues of the neck. Adenoid and tonsillar hypertrophy is a risk factor for the presence of OSA; however, the size of the lymphoid tissue does not always correlate directly with polysomnogram-measured severity.9 These data suggest anatomy and neuromuscular tone are important factors in determining limitations in surgery alone for cure of disease. Children with craniofacial abnormalities, Down syndrome, and neuromuscular disorders also are considered high-risk groups.

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DIAGNOSIS

The most common and concerning complaint among parents and caregivers is loud snoring, witnessed apneas, or choking and gasping for air. Children may exhibit restless sleep, frequent position change, sweating, or enuresis. Nocturnal enuresis is thought to be caused by disruptions in sleep patterns affecting arousal. Daytime symptoms in children affected by OSA are different when compared with adults with OSA. Children are less likely to present with daytime hypersomnolence and falling asleep during tasks, which are common among adults with OSA. More commonly, children with OSA exhibit paradoxical behaviors such as inattention, aggression, or hyperactivity (externalizing behaviors) or anxiety, depression, somatic complaints, or withdrawal (internalizing behaviors). Inattention and hyperactivity have the potential to be misdiagnosed as attention-deficit disorder or attention-deficit hyperactivity disorder, delaying proper diagnosis and treatment.10

OSA impairs neurocognitive function, learning ability, and academic performance in children.3 The relationship between behavioral problems and neurocognitive dysfunction is not known; however, it is thought to be related to sleep fragmentation and chronic hypoxemia leading to neuronal cell damage.11 The severity of OSA does not make a clear correlation with severity of behavioral problems, neurocognitive impairment, or decrease in quality-of-life measures, suggesting that even mild disease can be significant enough to cause symptoms.10 However, multiple causes and factors may contribute to behavioral problems, poor school performance, and decrease in quality of life. Clinicians should be aware of the association of OSA and these signs and symptoms and be aware of other possible contributing factors.

The physical examination should include height, weight, and age- and sex-specific percentile for BMI. Perform a full head and neck examination to identify the areas of upper airway obstruction. Nasal patency can be compromised by nasal polyps, turbinate hypertrophy, septal deviation, or adenoid hypertrophy. Adenoid tissue is difficult to examine routinely; however, signs of hypertrophy include nasal obstruction, hyponasal speech, and chronic mouth breathing. A lateral neck radiograph may be a helpful objective test to identify obstructive adenoid tissue. Examine the oropharynx to identify tonsil size, redundancy of the palate and uvula, tongue base hypertrophy, retrognathia, and oropharyngeal dimensions. Tonsil size is graded using the established Brodsky classification (Figure 1). As discussed above, tonsil size is an important factor in oropharyngeal obstruction; however, the total cross-sectional area of the airway is affected by multiple other factors, especially in the obese patients. Mallampati or Friedman tongue classifications are more descriptive grading systems assessing oropharyngeal patency, and take into account tongue position and palate redundancy (Figure 2).

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Clinical history and physical examination are the most common initial methods for identifying children at risk for sleep-disordered breathing; however, history and examination alone are known to be poor predictors of presence and severity of disease.12 Polysomnography testing, more commonly known as a “sleep study,” is the gold standard for objectively assessing sleep disorders. However, not all sleep centers perform polysomnography on children, and centers may have a minimum age requirement. Only about 10% of children undergo polysomnography testing before tonsillectomy, likely due to issues with the availability of pediatric sleep centers, insurance reimbursement, healthcare cost, and the time required to perform the test. Diagnosis of sleep-disordered breathing can be made based on combination of history, physical examination findings, portable monitoring devices, video recording devices, pulse oximetry, or formal polysomnography testing. Portable and at-home monitoring may ease access to diagnostic testing, be less costly, and better tolerated, but its accuracy has not been well studied. Polysomnography testing is not necessary for all children if OSA is suspected. Tonsillectomy and adenoidectomy is curative for most normal-weight children; therefore, most experts feel that polysomnography is not needed routinely if the pretest probability is high for OSA.13 On the contrary, children in high-risk groups, such as obese children and those with craniofacial abnormalities, Down syndrome, or neuromuscular disorders, should undergo polysomnography.13 Obese children have a statistically significant increase in mean apneas, hypopneas, and arousals, and spend less time in REM stage sleep. Also, they are more likely to have severe OSA, fragmented sleep, and lower mean oxygen nadir.14

Clinical guidelines published by the American Academy of Otolaryngology (AAO) recommend polysomnography testing for obese children to improve quality of care of medical treatment, risk assessment, and perioperative planning.13 In adults, untreated severe OSA can lead to structural changes in the myocardium, pulmonary and systemic hypertension, and cor pulmonale. Additional testing for children with severe hypoxia or evidence of cardiopulmonary disease includes chest radiograph, echocardiogram, or full cardiopulmonary evaluation by a pediatric cardiologist.

A polysomnogram is an objective test that provides quantitative data for diagnosis of primary snoring, upper airway resistance syndrome, and OSA. This test also can predict which children may be at risk of perioperative complication following upper airway surgery. The test is performed and interpreted by a physician specializing in sleep medicine. Parameters measured include respiratory effort, airflow, pulse oximetry, snoring, body position, and limb movement. An ECG assesses cardiac rate and rhythm, and electromyogram and electroencephalogram are used to determine length of time spent in each stage of sleep. Obstructive apnea is defined as near-complete cessation of airflow despite ongoing respiratory effort. Obstructive hypopnea is diagnosed when partial upper airway obstruction results in a greater than 50% reduction in airflow associated with either an arousal or a desaturation of 3 percentage points or greater from baseline. These events are calculated together to provide the apnea-hypopnea index (AHI), describing the number of obstructive events per hour. Although well-established criteria exist for diagnosing OSA in adults based on AHI, few data are available to determine valid severity scales for children. Growing evidence indicates that adult criteria are not sufficient in diagnosing children with OSA and will miss the majority of clinically significant disease.15

Despite the lack of evidence-based parameters, most experts accept a normal polysomnography with an AHI less than or equal to 1 and oxygen nadir above 92%.13 Severe disease is commonly accepted as an AHI of 10 or more and oxygen nadir below 85%.13

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TREATMENT

Tonsillectomy and adenoidectomy is the treatment of choice for OSA. Removing the obstructive hyperplastic lymphoid tissue increases the patency of the oral airway, improving OSA in most children.8 Numerous studies have shown that tonsillectomy and adenoidectomy significantly improve many patient quality-of-life parameters, including hyperactivity, inattention, behavioral problems, school performance, and somatization.3 Objectively, AHI and oxygen levels significantly improve after tonsillectomy and adenoidectomy.

Despite improvements in quality of life and severity of disease, most obese children do not have complete resolution of OSA after tonsillectomy and adenoidectomy.8 A recent meta-analysis found that 88% of obese children had evidence of persistent OSA following this surgery.16 Mitchell studied normal-weight and obese children after tonsillectomy and adenoidectomy, documenting via polysomnography. Obese children were found to have more severe preoperative and postoperative AHI and were significantly less likely to have complete resolution of OSA after surgery. Thirty-four percent of obese children had resolution of OSA based on polysomnography, compared with 72% of normal-weight children.15 Severe disease, indicated by a higher AHI, is a risk factor for persistent disease independent of obesity.2 Obesity is likely an independent risk factor due to the multilevel areas of obstruction, causing tonsillectomy and adenoidectomy alone to be less effective.

In select patients, uvulopalatopharyngoplasty is performed to address redundant soft tissues of the palate and uvula causing obstruction. This procedure has not been well-studied in children and is beyond the scope of this article.8

Perioperative management is imperative as postoperative complication in obese children occurs significantly more often as compared with their normal-weight counterparts after tonsillectomy and adenoidectomy. Respiratory compromise is the most common and significant risk encountered, resulting in intraoperative desaturations, difficulty with mask ventilation, and multiple attempts at laryngoscopy. Obese children are more likely to receive medical intervention for upper airway obstruction and require prolonged stays in the postanesthesia care unit or require overnight hospitalization.17

Risk assessment is evaluated by severity of OSA based on polysomnography and comorbidities seen more often in obese children, such as diabetes, asthma, and hypertension. The AAO clinical practice guidelines recommend overnight inpatient observation with continuous oxygenation monitoring for children with severe OSA, defined as an AHI of 10 or oxygen saturation nadir of 80%, or both. Other high-risk groups requiring overnight observation include children under age 3 years and those with Down syndrome, neuromuscular disorders, or sickle cell disease.13 Proper precautions and risk assessment are imperative in perioperative planning to avoid complications.

Repeat polysomnography after surgical intervention may be indicated in children with persistent symptoms, severe baseline OSA, cardiopulmonary disease, or obesity to effectively identify residual disease and manage long-term treatment.5 A split night study is preferred, as continuous positive airway pressure (CPAP) ventilation titration may be performed at the same study. CPAP or bilevel positive airway pressure (BiPAP) ventilation can be used in patients who are not candidates for surgical treatment or fail treatment, or until more definitive treatment can be performed. Compliance ranges from 50% to 100% and tends to be caregiver-dependent. Adolescents tend to be less compliant. Weight loss cannot be overemphasized and is an important component for OSA cure.13 In addition, healthful eating habits and daily exercise are important for prevention of other chronic diseases and creating healthful habits and lifestyle into adulthood. Weight loss techniques should be started as soon as possible, but should not delay surgery significantly, especially if the patient has an obvious upper airway obstruction amenable to surgery.

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CONCLUSION

OSA is a serious disease causing significant disruption of social, emotional, and educational development. The lack of complete resolution of OSA by surgery alone reflects the multifactorial nature of the disease; therefore, comprehensive therapy is key, including primary care providers, otolaryngologists, anesthesiologists, sleep medicine specialists, nutritionists, and caregivers. Awareness, early identification, and appropriate long-term treatment of obese children with OSA are paramount to eliminating physical morbidity and improving quality of life for the children, family, and caregivers.

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REFERENCES

1. Centers for Disease Control and Prevention. Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 Through 2007-2008. http://www.cdc.gov/nchs/data/hestat/obesity_child_07_08/obesity_child_07_08.htm. Accessed July 1, 2014.
2. Xu Z, Jiaqing A, Yuchuan L, Shen K. A case-control study of obstructive sleep apnea-hypopnea syndrome in obese and nonobese Chinese children. Chest. 2008;133(3):684–689.
3. Mitchell RB, Kelly J. Behavior, neurocognition and quality-of-life in children with sleep-disordered breathing. Int J Pediatr Otorhinolaryngol. 2006;70(3):395–406.
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13. Roland PS, Rosenfeld RM, Brooks LJ, et al. Clinical practice guideline: polysomnography for sleep-disordered breathing prior to tonsillectomy in children. Otolaryngol Head Neck Surg. 2011;145(suppl 1):S1–S15.
14. Mitchell RB, Kelly J. Outcome of adenotonsillectomy for obstructive sleep apnea in obese and normal-weight children. Otolaryngol Head Neck Surg. 2007;137(1):43–48.
15. Rosen CL, D'Andrea L, Haddad GG. Adult criteria for obstructive sleep apnea do not identify children with serious obstruction. Am Rev Respir Dis. 1992;146(5 Pt 1):1231–1234.
16. Costa DJ, Mitchell R. Adenotonsillectomy for obstructive sleep apnea in obese children: a meta-analysis. Otolaryngol Head Neck Surg. 2009;140(4):455–460.
17. Fung E, Cave D, Witmans M, et al. Postoperative respiratory complications and recovery in obese children following adenotonsillectomy for sleep-disordered breathing: a case-control study. Otolaryngol Head Neck Surg. 2010;142(6):898–905.
Keywords:

obstructive sleep apnea; childhood obesity; sleep-disordered breathing; polysomnography; tonsillectomy; adenoidectomy

© 2014 American Academy of Physician Assistants.