Sleep Apnea in Children

The number of overweight and obese children is on the rise, and 17% of children ages 2 to 19 are now obese.[1] In children, a body mass index (BMI) equal to or greater than the 95th percentile based on age and sex-specific dimensions is considered obese.[1]
Childhood obesity, obstructive sleep apnea (OSA) and metabolic syndrome may be intertwined.[2,3] The comorbidities associated with OSA are the same as those associated with obesity. Coexistence of these disorders places a child at higher risk for developing coronary artery disease and type 2 diabetes in adolescence or young adulthood.[3]
Pathology of OSA in Children
OSA is defined as five or more episodes of apnea (nonbreathing) lasting 10 seconds or more per hour of sleep.[4] Supriyatno et al[5] suggest lowering the criteria to an apnea-hypoapnea index (AHI) of three or more episodes per night. This would allow at-risk children to be treated earlier and more aggressively. Children with OSA who are not treated experience a dose-dependent decline in cognitive function.[6]
Lack of breathing in the supine position during sleep is associated with narrowing and excessive collapsibility of the pharyngeal airway.[3] This upper airway obstruction causes the patient to stop breathing, snore excessively and awake frequently throughout the night.[3] Upper airway obstruction increases intrathoracic pressure, leading to increased systemic pressures both peripherally and centrally. Intermittent airway obstruction also produces periods of hypoxemia and hypercapnia.[3]
Upper airway collapsibility can result from increased neck circumference, craniofacial abnormalities or adenotonsillar hypertrophy.[3] Increased tissue size of the tonsils and adenoids decreases the patency of the airway. Excessive daytime sleepiness, behavioral problems and poor school performance may predominate the clinical picture of a child with sleep apnea.[3]
The comorbidities associated with OSA are numerous and mainly pertain to behavior disturbances, the cardiovascular system and metabolic alterations. Undertreated sleep apnea can lead to mood disorders, cognitive impairments, poor school performance and behavioral disturbances.[3] Untreated sleep apnea also has the potential to cause cardiovascular and metabolic disease.[3,6,7] Inflammatory mediators (cytokines, oxidative stressors) that occur in OSA and obesity predispose patients to cardiac comorbidities.[6]
OSA and Childhood Obesity
Clinical evidence of sleep apnea, insulin resistance and obesity in a child sets the stage for heart disease and endocrinopathies. Kheirandish-Gozal et al[7] have detailed the cardiac morbidities associated with pediatric OSA. Intermittent hypoxia and hypercapnia (elevated levels of carbon dioxide) alter the autonomic nervous system function, specifically the sympathetic nervous system.[7] Continuous activation of the sympathetic nervous system (fight-or-flight mode) has the potential to increase sympathetic vascular tone, ultimately elevating systemic blood pressures.
The long-term effects of chronically elevated blood pressures are well known. Hypertension can cause structural changes in the heart (left ventricular hypertrophy), which left untreated can cause heart failure. Bhattacharjee et al[6] blame inflammatory pathways for the atherosclerosis seen in OSA. Repeated oxidative stress from hypoxia releases inflammatory mediators such as C reactive protein (CRP) into the blood stream. CRP is a marker for atherosclerosis and atheroma formation.[7] Elevated CRP levels in children increase the likelihood of end-organ damage and neurocognitive deficits associated with endothelial dysfunction.[7]These inflammatory mediators potentiate CAD, stroke and type 2 diabetes.
The comorbidities associated with OSA are the same comorbidities associated with obesity. When sleep apnea and obesity occur together, the effects of both diseases are amplified.[6] These synergistic effects place our youngest generation at highest risk for long-term cardiac abnormalities including pulmonary hypertension, end-organ damage, left and right ventricular hypertrophy, insulin resistance, and decreased quality of life.[6]
Significance of Metabolic Syndrome
Insulin resistance, hypertension and dyslipidemia are common features of metabolic syndrome. It affects 30% to 50% of the obese adolescent population.[6] This "perfect storm" for cardiac disease and stroke is worsened by health consequences related to OSA.[6] Ievers-Landis and Redline[3] state that the risk of metabolic syndrome increases sixfold in obese children with sleep-disordered breathing.[3] NPs and PAs need to assess for this triad of syndromes (sleep apnea, obesity and metabolic syndrome) in order to identify the children at greatest risk for heart disease and diabetes.[6]
Diagnostic Strategies for OSA
The gold standard for diagnosing pediatric OSA is the same as for adults: overnight polysomnography (PSG).[5] This diagnostic tool is costly and impractical. Placing a child in a foreign environment is stressful for the patient and family. Subjective and objective screening tools are needed to identify patients at highest risk for OSA. BMI, neck circumference and tonsillar hypertrophy have been studied as reliable, objective indicators of OSA.[4]
Treatment options for childhood OSA include adenoid and tonsil removal, continuous positive airway pressure and weight loss.[8] The standard treatment remains adenoid and tonsil removal, but due to the body habitus of overweight and obese children, tonsillectomy is less effective and residual sleep apnea frequently exists post-surgery.[8]
Review of the Literature 
Increased adiposity predisposes older children and adolescents to obstructive sleep apnea. Supriyatno et al[5] found that OSA occurs in 38.2% of obese adolescents when using an AHI of three or more episodes per night. Other studies have demonstrated that OSA affects 36% to 60% of obese and overweight habitually snoring children and adolescents.[5] Infants and toddlers with OSA are more likely to have enlarged tonsils and adenoids, not increased fat accumulation around the neck like their older counterparts.[5] Enlarged tonsils and adenoids are successfully treated with tonsillectomy. However, OSA that is related to increased neck adiposity is harder to treat because of the anatomy of the neck. Obese patients with hypertrophy of these glands are somewhat resistant to surgical intervention.
Given the increased prevalence of childhood obesity and overweight, a surge in the diagnosis of pediatric OSA may occur. It is important to understand that the presentation of OSA in children differs from that in adults.[5] In the adult population, men are more affected than women.[5] This is due in part to the deposition of fat. Men deposit fat in the chest and neck areas, whereas women carry adipose tissue predominately in the waist and hips. Increased fat deposition in the neck creates an environment more susceptible to upper airway collapse and OSA.[5]

Children and adolescents do not carry adipose tissue in quite the same fashion; therefore, providers need to have a higher level of suspicion regardless of body composition.[5] OSA is more prevalent in Hispanic and black people, preterm infants and children residing in low-income homes.[3] OSA affects 2% to 3 % of middle school children and 13% of 3- to 6-year-olds.[3] Children tend to exhibit various signs and symptoms of OSA, such as attention deficit disorder, poor concentration, behavior disturbances and poor school performance related to poor sleep and repeated episodes of nocturnal hypoxia.[3]
A correlation analysis of 62 children (37 of whom were obese) previously diagnosed with OSA via PSG found that treatment of OSA identified substantial decreases in LDL cholesterol, as well as decreases in liver enzymes, and increases in HDL cholesterol and insulin sensitivity.[6] These laboratory changes were identified in both obese and non-obese children. This study suggests that treatment of sleep apnea, regardless of BMI, has the ability to enhance metabolic and cardiac profiles.[6]
Supriyatno et al[5] developed a scoring system for diagnosing pediatric sleep apnea without overnight testing. The scoring system is based on tonsillar and adenoid hypertrophy and neck circumference. The scoring system has a sensitivity and specificity of 62% and 100%, respectively.[5] Additional screening tools
incorporating this scoring system are needed to correctly identify children with OSA. The addition of BMI to the scoring system may increase the sensitivity of the scoring model.

A study by Keene et al[4] demonstrated a strong predictive power for BMI to identify children and adolescents with OSA. The researchers took a convenience sample of 200 children ages 2 to 13. These children had completed an overnight polysomnography test. The independent variable was diagnosis of OSA and the dependent variable was BMI. According to the retrospective chart review, BMI greater than the 95th percentile had a 90% predictive power of an abnormal polysomnography test.[4]
Proposed Screening Tool
Table 1 shows an example of a questionnaire for parents and guardians to fill out during well-child visits. Table 2 is a screening tool for use by healthcare providers. I developed the screening tool and questionnaire based on scientific markers, risk factors, signs and symptoms and objective markers for OSA.[5] The objective markers add to the validity of the proposed tools and are not the basis for their formation. Enhanced diagnosis of OSA in children will allow healthcare providers to treat early, curtailing the comorbidities associated with the condition.
If healthcare providers continue to misdiagnose and undertreat children with OSA, the costs to health and resources can be devastating. Further research into the proper treatment of OSA and prevention of OSA is needed. The proposed screening tool could be incorporated into a pilot study conducted in an urban primary care setting where a high volume of Hispanic, white and black children are treated.[3]                                                                                                                                       
1. Centers for Disease Control and Prevention. Childhood Overweight and Obesity.
2. Jessup A, Harrell JS. The metabolic syndrome: look for it in children and adolescents, too! Clin Diabetes. 2005;23(1):26-32.
3. Ievers-Landis CE, Redline S. Pediatric sleep apnea: implications of the epidemic of childhood overweight. Am J Resp Crit Care Med. 2007;175(5):436-441.
4. Keene S, et al. BMI percentile a potential tool for predicting pediatric obstructive sleep apnea. Canad J Respir Ther.2010;46.2:33-37.
5. Supriyatno B, et al. Risk factors of obstructive sleep apnea syndrome in obese early adolescents: a prediction model using scoring system. Acta Med Indones. 2010;42(3):152-157.
6. Bhattacharjee R, et al. Obesity and obstructive sleep apnea syndrome in children: a tale of inflammatory cascades. Pediatr Pulmonol. 2011;46(4):313-323.
7. Kheirandish-Gozal L, et al. Autonomic alterations and endothelial dysfunction in pediatric obstructive sleep apnea. Sleep Med. 2010;11(7):714-720.
8. Brietzke SE, Gallagher D. The effectiveness of tonsillectomy and adenoidectomy in the treatment of pediatric obstructive sleep apnea/hypopnea syndrome: a meta-analysis. Otolaryngol Head Neck Surg. 2006;134(6):979-984.
Brooke Elizabeth Holman is a family nurse practitioner at Oncology Hematology Care in Cincinnati.