|As evident in this article and the others featured in this issue of Pediatric Directions, there is an emerging epidemic of obesity within children worldwide. Lifestyle changes over the last few decades, such as excessive television, video games, cell phones and computers have resulted in sedentary activities with children sleeping for fewer hours. Obesity is a recognized risk factor for the development of many adverse health outcomes, and sleep related disorders are no exception. Evidence suggests that obesity is modestly associated with Obstructive sleep apnea syndrome (OSAS) in young children but strongly associated with OSAS in older children. It is therefore believed that the|
|increased prevalence of childhood obesity will be accompanied by an increase in the incidence of OSAS and other sleep disorders. Sleep disordered breathing (SDB) is a continuum of events ranging from benign snoring to most severe OSAS.|
Obstructive sleep apnea (apnea OSA) is characterized by temporary but intermittent episodes of upper airway obstruction resulting in cessation of breathing or reduction in tidal volume in sleep. OSA is associated with snoring, hypoventilation, hypoxemia, leading to sleep fragmentation, poor sleep, excessive daytime sleepiness, poor school performance in children, inattention, hyperactivity, mood problems, and poor quality of life. Excessive daytime sleepiness due to OSA can result in morbid obesity. It has been shown that OSA is present in more than 50 percent of a population of adult obese patients with a mean BMI higher than 40. This percentage is much higher than that commonly reported in previous studies, particularly in women. Nocturnal hypoventilation seems to be present in more than 29 percent of severe obese population. Moreover, this study indicated that morbid obesity can be associated with excessive daytime sleepiness even in the absence of sleep apnea. Neck circumference in men and BMI in women seem to be the strongest predictors of the severity of OSA in obese patients. Such studies have not yet been reported in children.
The exact role obesity plays in the incidence of pediatric OSA has been debated among researchers. However, one proposed mechanism is weight gain increases fat deposition around the pharynx leading to upper airway narrowing and collapse during sleep contributing to the development of OSA. Evidence from multiple studies in children links obesity to OSA. In a recent study of 90 children from China, aged 7 to 11 years, OSAS was identified in 32.6 percent of children who were overweight, compared with 4.5 percent of normal weight children. The Cleveland Family study of 4 to 18 year olds found that obese children are at 4.6 fold increased risk for sleep apnea than normal weight children. A one percent change in body mass index (BMI) is estimated to increase apnea hypopneic index (AHI) by three percent and a 10 percent increase in BMI increases AHI six fold. Not inversely, weight loss does not result in a comparative decrease in AHI. In general there is no gender difference in the prevalence of pediatric OSA in contrast to what is seen in adult OSA. Pediatric OSA affects roughly 13 percent of 3 to 6 year olds and two to three percent of middle-school typical children, largely due to enlarged tonsils, allergies, asthma and craniofacial abnormalities. The prevalence is reported to be two to four times higher in blacks, Hispanics, prematurely born children, and children from poor neighborhoods.
OSA is also a contributing cause of the obesity hypoventilation syndrome (OHS) which is well recognized in obese children. Not all patients who have OHS have OSA. OHS is characterized by obesity, hypercapnia, hypoxemia, and excessive daytime sleepiness without intrinsic pulmonary disease. It is thought that repeated episodes of nocturnal hypercapnia and hypoxemia results in attenuation of hypercapneic and hypoxic drives during wakefulness, ventilatory drive during sleep and poor chest wall compliance. Individual predisposition depending on carbon dioxide response and amount of stress may be responsible because not every obese person develops OHS.
OSA and OHS are serious consequences of obesity and may mediate components of the association between obesity and metabolic and cardiovascular morbidities. Intermittent hypoxemia may amplify the adverse effects of adiposity, most likely by potentiation of inflammatory cascades that activate systemic inflammation and activate metabolic states associated with vascular disease and diabetes.
There is a complex relationship between obesity and sleep duration. Sleep duration may be an important regulator of body weight and metabolism. In western societies, where chronic sleep restriction is common and food is widely available, changes in appetite regulatory hormones as a result of sleep reduction may contribute to obesity, leading to other sleep disorders. In a recent study, participants with short sleep had reduced leptin, which reduces appetite, and elevated ghrelin, which increases appetite. The changes in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration. Clinical support of this observation comes from large studies in adults where an association was found between habitual short sleep time and increased BMI and obesity. A similar observation in children was found in a recent study that noted that a decline in sleep duration paralleled a dramatic increase in the prevalence of obesity and diabetes. This association suggests a link between decreased sleep duration and increased insulin resistance in obese children.
SDB is associated with insulin resistance and dyslipidemia in adults and in obese children. Among children with suspected SDB, insulin resistance and dyslipidemia seem to be determined primarily by the degree of body adiposity rather than by the severity of SDB Children with short sleep duration have greater insulin resistance than children with normal sleep duration. In addition, they spend proportionally less time in REM sleep. In normal subjects glucose utilization during REM sleep is higher than during non- REM sleep, so that short sleep duration may place children at risk of decreased glucose utilization (e.g., increased insulin resistance). The severity of overweight may also be worsened by the effects of sleep apnea, such as excessive daytime sleepiness (EDS) which may lead to reduced physical activity, low energy and mood problems. In the Wisconsin Sleep Cohort Study increased BMI were observed in people who usually slept for less than six hours. Levels of total cholesterol, HDL-cholesterol, triglycerides and blood pressure were inversely associated with sleep duration in adults.
The interplay between obesity and respiratory function has implications on lung functions, sleep disordered breathing and asthma. Obesity may lead to OSA which complicates asthma and its management. Obesity-associated GERD can also lead to airway inflammation and asthma. Severe obesity can restrict lung functions in childhood, although the extent of obstructive airway disease due to obesity in childhood is not clear. OSA leads to poor quality sleep which is in fact sleep deprivation. Sleep deprivation, upper airway edema and systemic inflammation associated with OSA could complicate asthma. Obese children with asthma tend to have more symptoms of asthma; particularly obese girls, have a greater likelihood of developing asthma later in life.
Prevention and Treatment
Management of sleep disorders that are associated with obesity requires a multidisciplinary approach involving pediatricians, endocrinologists, sleep physicians, parents, the media and industry as well to curtail the development of obesity.
Once obesity is diagnosed a continuing effort should be undertaken for its management to reduce weight gain. To be more effective, the prevention of obesity in childhood should be focused on the population at risk. Obesity in childhood increases the risk of obesity in adulthood. Obesity in adulthood is a risk factor for chronic diseases such as hypertension and atherosclerosis. Therefore, it is important to eliminate factors influencing the development of obesity in children from the viewpoint of preventive medicine.
This requires a multidisciplinary medical subspecialty approach involving endocrinologists, nutritionists and the primary care physician. If all fail and obesity related sleep problems develop, then some treatment modalities may be considered. Weight loss should be the ultimate goal for the treatment of OSA resulting from obesity but since this is difficult to achieve fast enough and to maintain to treat OSA, immediate treatment modalities include adenotonsillectomy for those who have large tonsils, continuous positive airway pressure and bariatric surgery for patients who qualify for such procedures.
Obstructive Sleep Apnea Syndrome
Not every obese child has obesity as the cause of OSA. In some, the cause is adenotonsillar hypertrophy. Even though adenotonsillectomy (T&A) may cure OSA, the outcome in obese children is often less satisfactory. In a recent study, a T&A resolved SDB in 77.5 percent of non-obese, but only in 45 percent of obese children, implying that obesity at the time of diagnosis has a higher risk for persistent OSA after T&A.
Continuous positive airway pressure and bi-level positive airway pressure is effective treatment in obese children who do not respond to or are not candidates for T&A. It is also effective in stabilizing obese children with severe OSA who are awaiting T&A or other upper airway surgery.
In a 2006 pediatric prospective multi center study, both CPAP and BIPAP were highly effective in reducing the apnea hypopnea index from 27 ± 32 to 3 ± 5/hour, and an improvement in arterial oxygen saturation nadir from 77 ± 17% to 89 ± 6% after six months of usage. The problem with assisted ventilation is compliance.
If all medical therapies fail, surgical interventions for obesity management is available. In general 2 types of bariatric surgical approaches are used which include Roux-en Y gastric bypass (RYGB) and Laparoscopic adjustable Band (LapBand®) which are currently employed in our institution. Current evidence suggests that after bariatric surgery, adolescents lose significant weight resulting in improvement of serious obesity-related medical conditions. Permanent weight loss of 50 to 65 percent has been reported in some series. Some advocate that bariatric surgery be performed as soon as possible in the obese child with OSA who has failed other medical therapies. (See page 24 for additional information on bariatric surgery.)
Obesity Hypoventilation Syndrome
Evidence suggests that OHS is under-recognized, under-treated, and associated with a significant increase in morbidity and mortality if untreated.
The optimal treatment for OHS is weight loss, but for most patients, it is hard to achieve. Weight loss improves most of the physiologic derangements believed to be involved in the pathogenesis of OHS. Although the exact amount of weight loss required is not known, about 10 percent loss may lead to normalization of daytime PaCO2, improvement in vital capacity, central ventilatory drive and voluntary ventilation. For those who have concomitant OSA, weight loss also reduces the degree of sleep disordered breathing and improves oxygen saturation.
Both CPAP and BIPAP are effective treatment for OHS. When daytime hypoxia is present supplemental oxygen is added to the CPAP.
Progesterone has been used in treatment of OHS or as an adjunctive to those who do not fully respond to CPAP or BIPAP. It increases the chemical drive (which may be blunted in OHS) to breathe. However, side effects include hyperglycemia and alopecia. Adverse effects of long-term use are not known.
source : Nationwide Children’s Sleep Center
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