The escalating incidence of childhood and adolescent obesity continues to represent a significant public health crisis. Obesity is defined as a body mass index (BMI) ≥ 95th percentile for age. In the US, the percentage of obese children and adolescents increased dramatically in the 1980s but appears to have stabilized since 1999.1 In 2010, 18.4% of 12- to 19-year-olds were classified as obese. Thirteen percent of children in the same age range were found to more severely obese with a BMI of ≥ 97th percentile. The risk of obesity has been demonstrated as increased in those children and adolescents of non-Hispanic black and Mexican-American heritage as compared to their non-Hispanic, white counterparts. This difference is irrespective of gender.1
Obese children can be expected to experience serious health consequences; affected individuals are more likely to suffer from metabolic syndrome and type 2 diabetes and may further suffer from the effects of teasing and poor self-esteem.2 Obese children aged as young as 2 years have also been shown to be more than four times more likely to suffer with obesity as adults;3 they therefore possess an increased risk for continued obesity-related cardiovascular and metabolic disease.4 When followed to adulthood, obese adolescents have been found to have increased morbidity and mortality related to cardiovascular disease and diabetes. While many of these chronic medical complications were considered until recently to be adult in onset, 70% of obese 5- to 17-year-olds have been found to possess at least one risk factor for cardiovascular disease.4
The recognition and management of this preventable disease and its serious sequelae are of particular importance to the pediatrician, who is likely to have the most regular interaction with the pediatric patient and the greatest opportunity to advocate for optimal nutrition and intervene in the early stages of disease.
Genetic factors are known to predispose for obesity. The trends in obesity prevalence are not consistent with a single etiologic factor; indeed, recent increases are likely multifactorial with both inherited and environmental determinants. A genetic predisposition may be potentiated by social and familial determinants.
Multiple societal factors including an increase in portion sizes and the availability of processed foods and sweetened drinks are recognized as contributors to the obesity epidemic.5 A sedentary lifestyle has also been implicated. Scheduled physical activities at school have been increasingly curtailed and less than 25% of students currently meet recommendations for moderate physical activity (greater than or equal to 30 minutes on more than or equal to 5 of the past 7 days). An estimated 38% of children spend more than 3 hours per day in front of the television.5 This time is also an opportunity for excess caloric intake.
Other potentially modifiable factors have been studied. For example, several studies have supported the association between sleep deprivation and increased BMI in children and adolescents.6 In a 2007 study of approximately 1,400 children, Snell at al7 found that children who had fewer hours of sleep tended to have increased weight as compared with peers when studied 5 years later; when BMI was studied by age group, an extra hour of sleep decreased the likelihood of being overweight from 36% to 30% in 3- to 8-year olds and from 34% to 30% in children aged 8 to 13 years.8 This effect of sleep deprivation on BMI has been shown to be independent of physical activity and other confounding variables.
Obesity and Obstructive Sleep Apnea Syndrome
The spectrum of sleep-disordered breathing (SDB) consists of obstructive sleep apnea syndrome (OSA), upper airway resistance syndrome (UARS), and primary snoring. UARS is characterized by sleep fragmentation in the absence of apnea or gas exchange abnormalities. Primary snoring is a relatively common form of increased upper airway resistance.9 Although not all patients who snore will have evidence of SDB, a child or adolescent who snores ≥ 3 times per week must be carefully evaluated with a detailed history to ensure that evidence of OSA is absent. When additional history is suspicious, overnight attended polysomnography (PSG) is the gold standard test.10 PSG will also distinguish obstructive SDB from disorders of central apnea.
By definition, a patient with OSA experiences repeated and potentially prolonged occurrences of partial upper airway obstruction and/or recurrent episodes of complete upper airway obstruction; these derangements result in a disruption of normal ventilation and resulting gas exchange abnormalities during sleep. This can further result in a pathologic alteration of normal restorative sleep pattern and related difficulties with normal function during wakeful periods. In the pediatric patient, OSA is more commonly associated with partial rather than complete airway obstruction.
Obesity has been shown to be a major causal factor in the development of OSA across the lifespan. The prevalence of OSA has been approximated as 1% to 4% in the general pediatric population.11 Notably, obese children and adolescents have been shown to be at markedly higher risk for the development of OSA; the incidence in this population has been reported to be as high as 20% to 30%.12,13 In the Cleveland Family study of 4- to 18-year-olds, obese children were found to be at a 4.6-fold increased risk for OSA compared with their normal body weight counterparts.14 Risk factors for OSA in obese children and adolescents include comorbidities such as craniofacial anomalies and muscular weakness as well as adenotonsillar hypertrophy, ethnicity, and age. Adenotonsillar hypertrophy is the most common etiology for obstructive hypoventilation in the pediatric patient and appears to potentiate the severity of upper airway obstruction and OSA when occurring in combination with obesity. Additionally, the efficacy of adenotonsillectomy (AT) appears to be diminished in obese patients. African-American descent appears to be an independent risk factor for OSA. Finally, the effect of obesity on the patency of the upper airway during sleep appears to be a greater risk for OSA in older children and adolescents compared with younger children.15–17
Distribution of adiposity has also been shown to have an adverse correlation with OSA in adults and adolescents and may be more impactful than BMI alone. The severity of SDB has been positively associated with a visceral distribution of adipose tissue. A similar association has been found with other variations in body composition.18 A BMI in the obese range also may not be required for a patient to exhibit signs of SDB; overweight children (BMI >75th percentile) have also demonstrated SDB and hypoxemia of variable severity during sleep.19
Obesity may result in decreased lung volume, loss of functional residual capacity, and a decreased patency of the upper airway. All of these factors can be expected to exacerbate a tendency toward SDB. Obesity has also been associated with abnormal central nervous system ventilatory responses. Obese adolescents with OSA have been shown to have a blunted ventilatory response to hypercapnia.20,21 Therefore, abnormalities of central respiratory control may play an important pathophysiologic role in obese adolescents with OSA.
Obesity Hypoventilation Syndrome
Obesity hypoventilation syndrome (OHS, previously Pickwickian syndrome) is defined as the association of obesity, SDB, and arterial hypercapnia while awake (PaCO2 > 45 mm Hg). Patients affected with OHS are more likely to be morbidly obese and may present with impaired memory, difficulty with concentration, headaches, and hypersomnolent behavior.9 Importantly, affected patients are at significantly increased risk for pulmonary hypertension and cardiopulmonary failure. The diagnosis of OHS requires the exclusion of other etiologies of hypoventilation such as chronic pulmonary disease, severe hypothyroidism, neuromuscular weakness, and chest wall derangements. Additionally, congenital central hypoventilation syndrome, Chiari malformation, and ROHHAD (Rapid-onset Obesity with Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation) syndrome must be considered.
Neuropsychiatric Complications of Obesity and SDB
Neuropsychiatric symptoms and complications of OSA include neurocognitive deficits and a variety of behavioral disorders. Affected children may have profound sleepiness and impaired daytime functioning, although young children are far less likely than older children and adolescents to exhibit somnolence as a primary symptom of SDB. The likelihood of excessive daytime somnolence has been found to be greater in obese children compared with non-obese children regardless of the degree of OSA.22 Both fragmentation of normal sleep architecture and impaired sleep quality have been shown to have an adverse effect on neurocognitive function in obese adolescents with OSA. In severely obese adolescents, sleep fragmentation has been associated with decreased psychomotor efficiency and lower scores on standardized vocabulary testing. Poor sleep efficiency has further been associated with poor memory recall.23 Hyperactivity and attention-deficit/hyperactivity disorder are common sequelae of OSA, particularly in younger children. Social withdrawal is also more frequently encountered in these children. Other psychological correlates may include depression, somatization, and aggressive or oppositional behaviors.24
In a recent randomized trial of early AT compared with “watchful waiting” for childhood OSA, school-aged children who had surgical intervention (AT) showed improvements in quality of life and polysomnographic findings as well as a reduction in symptoms and improvements in secondary behaviors. Significant changes in the study’s primary outcome measures of attention and executive function were not shown during the study period.25
In the last 10 years, research has concentrated on the impact of OSA in the systemic inflammatory response. It has been suggested that OSA and its associated intermittent hypoxemia results in the production of reactive oxygen species. The hypoxemic response and sleep disruptions further result in increased sympathetic tone and result in an inflammatory response. Serum levels of C-reactive protein (CRP) have been shown to be increased in both non-obese and obese children with OSA. Furthermore, elevated levels of CRP have been shown to decrease in a degree proportional to improvements in OSA after AT.26
BMI has been recognized as a determinant of elevated systolic and diastolic blood pressure (BP). In a study by Amin, obese patients with SDB had a higher waking systolic BP and sleeping systolic BP compared with the non-obese SDB group. SDB was found to be a greater contributor to sleeping diastolic BP than obesity.27 A number of similar publications have established that obesity and SDB are associated with elevations of daytime and nocturnal BP in the pediatric population. Increases in BP variability and loss of the normal circadian rhythm of BP have also been reported.28 Hypoxemia-related increases in sympathetic tone are proposed as the etiology for these changes in BP; supportive evidence for this hypothesis has been provided by the finding of increased levels of urinary catecholamines (norepinephrine and normetanephrine) in correlation with worsening OSA parameters.29 In the Bogalusa Heart Study, cardiovascular disease was most strongly correlated with BMI and insulin resistance.30
Obesity is a known risk factor for impairments in glucose tolerance, dyslipidemia, and non-alcoholic fatty liver disease. The metabolic syndrome consists of hyperinsulinemia, dyslipidemia, and abdominal obesity. Patients with metabolic syndrome exhibit three of five of the following abnormalities: 1) waist circumference >75% of normal for age and gender, 2) mean BP or diastolic BP > 90% of normal or current treatment with anti-hypertensive medication, 3) elevation of triglycerides, 4) low levels of high-density lipoprotein (HDL), or 5) abnormal oral glucose tolerance or elevated fasting glucose.
In an adolescent cohort, children with metabolic syndrome and OSA show more severe sleep-related hypoxemia. As the apnea-hypopnea index (AHI) increased, the number of patients with metabolic syndrome increased in parallel. Adolescents who experience SDB were seven times more likely to suffer from metabolic syndrome. The prevalence of metabolic syndrome in the general adolescent population has been reported to be 4%. In overweight children, the prevalence is markedly increased and approximated at 30% to 50%. Furthermore Weiss et al31 reported that even small incremental increases in BMI were associated with a significantly increased risk of metabolic syndrome in overweight children and adolescents.32
OSA is recognized as having a potentiating effect on these metabolic derangements. The characteristic gas exchange abnormalities and sleep arousals in OSA have a proatherogenic effect on serum lipid concentrations; low-density lipoprotein (LDL) is increased, whereas cardioprotective HDL is decreased. The severity of SDB has been found to independently correlate with impairments in glucose homeostasis and the severity of dyslipidemia. Mean oxygen saturation (SpO2) and the nadir of oxygen saturation with sleep are significant predictors of the metabolic syndrome. In a study of adolescents, an apnea hypopnea index of greater than or equal to 5 was associated with a 6.5-fold increase in the odds of developing metabolic syndrome.33
In addition, adiposity and OSA interact to potentiate the level of insulin resistance found in association with obesity alone. Fasting insulin levels may be used as a marker of insulin resistance and have repeatedly been found to be increased in obese patients with OSA. The severity of OSA correlates with fasting insulin levels in obese children, and this correlation has been found to be independent of age and BMI. When adjusted for BMI, SBD has been found to be independently associated with increases in fasting insulin levels, LDL and BP.33
Recently, levels of a hunger-inducing hormone (ghrelin) have been found to be increased in obese children with OSA; this hormonal imbalance is likely to have an adverse impact on behavioral and nutritional weight management interventions.34 Adiponectin has also been implicated for its significant role in obesity, OSA, and metabolic syndrome. Adiponectin is a protein hormone that is secreted from adipose tissue and is involved in glucose regulation and fatty acid oxidation. Low serum adiponectin levels have been associated with hypertension, obesity, and type 2 diabetes. Catecholamines have been shown to suppress both the production and secretion of adiponectin in vitro. Therefore, it is postulated that the increased sympathetic tone and the associated catecholamine release previously described in OSA may contribute to insulin resistance and metabolic syndrome.29
Management of OSA in the Setting of Obesity
Although adenotonsillar hypertrophy is recognized as a common etiology of SDB in non-obese children, the contributions of excess adenoidal and tonsillar tissue should not be overlooked in the population of obese children with OSA.35 In 2012, a clinical practice guideline from the American Academy of Pediatrics suggested that careful clinical judgment be used in consideration of AT for obese children with OSA.10 In this population of patients, the risks of surgery must be compared against the potential benefits and preoperative risk; quantification of the severity of disease and the attendant risk with a polysomnographic examination should be advocated.36 Individual tolerance for a trial of noninvasive positive-pressure ventilation (NIPPV) may also be considered during a period of observed dietary management. A relative contraindication to AT in this group of patients is morbid obesity with small tonsillar/adenoidal tissue. In this population, the outcome of AT alone is likely to be suboptimal.10
Studies of the response to AT in obese children with OSA have indicated that patients show marked improvements in respiratory disturbance index (RDI) and quality of life after surgical intervention; these effects are independent of a change in BMI. Although the severity of OSA is likely to be decreased after AT, multiple studies have shown that OSA does not resolve after this surgical intervention.37 In fact, obesity has been found to be associated with an increased risk of persistent OSA after treatment.16 A meta-analysis by Costa and Mitchell38 reported that 60% to 88% of obese children had findings of persistent SDB following surgical intervention.
It should also be noted that children with severe OSA and obesity are at increased risk for perioperative and post-operative complication and should be observed as inpatients as they may require NIPPV such as continuous positive airway pressure (CPAP) for improvement of functional residual capacity and optimal ventilatory support. The ready availability of an anesthesia team capable of managing the child’s airway should be confirmed, and the anesthesiologist should be made aware of a clinical history of OSA during any procedure requiring sedation as affected children are at greater risk for hypoventilation with sedative and opioid medications as well as with anesthetics.
In those patients with obesity and/or severe OSA who proceed to surgical management, clinical reassessments for residual signs and symptoms and objective testing (PSG) should be performed. This evaluation should occur 6 to 8 weeks after the surgical intervention to allow adequate healing and resolution of post-operative edema. Alternatively, referral to a sleep specialist may be considered. In this manner, any persistent disease may be recognized and treated in a timely manner.
In a follow-up study of metabolic markers after treatment with AT, those children with resolution of OSA showed a small but significant decrease in total cholesterol.39 In adults with OSA, treatment with CPAP has been found to reverse cardiovascular derangements. Short-term follow-up studies in children after AT have shown a decrease in diastolic BP.35 However, children with residual degrees of OSA were found to have increases in systolic and diastolic BP at a later follow-up.17
Non-surgical interventions in the pediatric population have included structured exercise programs. Weight loss and physical exercise appear to provide benefit for patients with OSA and should be recommended as a component of treatment. However, weight loss and other behavioral therapies may be slow and variable in their results. Therefore, definitive therapy aimed at maintaining adequate gas exchange and moderating symptoms should be implemented while patients are participating in behavioral modification and weight loss programs.
In severely obese adolescents, additional surgical management may be considered in the form of bariatric surgery. Current guidelines include BMI >35 kg/m2 with major comorbid conditions or BMI >40 kg/m2. In the subset of morbidly obese adolescents, bariatric surgery has been found to have a superior treatment effect compared with lifestyle modifications.40
The adverse impact of obesity, OSA, and metabolic syndrome on cardiovascular health and other health outcomes has been extensively documented. When these diagnoses coexist in the same patient, disease-related morbidity and mortality are expected to be potentiated. Recommendations for healthier eating habits and increased levels of physical activity have been universally promoted by health care professionals. The practitioner must be aware of the early signs of disease and modification strategies. However, significant social and biological barriers may exist and should not be overlooked in the approach to the patient. Routine screening of obese children and adolescents for symptoms of OSA and markers of metabolic syndrome should be strongly considered.
- Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity and trends in body mass index among US children and adolescents, 1999–2010. JAMA. 2012;307(5):483–490. doi:10.1001/jama.2012.40 [CrossRef]
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- Freedman DS, Kettel L, Serdula MK, Dietz WH, et al. The relation of childhood BMI to adult adiposity: the Bogalusa Heart Study. Pediatrics. 2005;115:22.
- Freedman DS, Zuguo M, Srinivasan SR, Berenson GS, Dietz WH. Cardiovascular risk factors and excess adioposity among overweight children and adolescents: the Bogalusa Heart Study. J Pediatr2007;150(1):12–17. doi:10.1016/j.jpeds.2006.08.042 [CrossRef]
- Krebs NF, Himes JH, Jacobson D, et al. Assessment of child and adolescent overweight and obesity. Pediatrics2007;120:S193 doi:10.1542/peds.2007-2329D [CrossRef]
- Beebe DW, Lewin D, Zeller M, et al. Sleep in overweight adolescents: shorter sleep, poorer sleep quality, sleepiness and sleep disordered breathing. J Pedia Psychol 207;32(1):69–79
- Snell EK, Adam EK, Duncan GJ. Sleep and the body mass index and overweight status of children and adolescents. Child Dev. 2007;78(1):309. doi:10.1111/j.1467-8624.2007.00999.x [CrossRef]
- Carter PJ, Taylor BJ, Williams SM, Taylor RW. Longitudinal analysis of sleep in relation to BMI and body fat in children: the FLAME study. BMJ. 2011;342:d2712. doi:10.1136/bmj.d2712 [CrossRef]
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- Marcus CL, Brooks LJ, Draper KA, Gozal D, et al. AAP Clinical Practice Guideline: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3):576. doi:10.1542/peds.2012-1671 [CrossRef]
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- Verhuist SL, Schrauwen N, Haentjens D, et al. Sleep disordered breathing in overweight and obese children and adolescents: prevalence, characteristics and the role of fat distribution. Arch Dis Child. 2007;92:205–208. doi:10.1136/adc.2006.101089 [CrossRef]
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