Treatment of Obstructive Sleep Apnea in Children: An Opportunity for Cardiovascular Risk Modification

Statement of the Problem: In Canada, child and adolescent obesity, defined as a body mass index (BMI) of >95th percentile for age and gender1 represents one of the most common conditions effecting children in Canada with an obesity rate of 10% in 12-17 year old children, which currently equates to approximately half a million obese children in Canada. Obesity is not only complicated by cardiovascular and metabolic dysfunction, such as left ventricular modeling, hypertension, glucose intolerance and dyslipidaemia, it is also associated with obstructive sleep apnea syndrome (OSAS), occurring in up to 60% of obese children.

OSAS is characterized by snoring, recurrent partial (hypopneas) or complete obstruction (apneas) of the upper airway, frequently associated with intermittent oxyhaemoglobin desaturations, sleep disruption and fragmentation. The gold standard test for diagnosing obstructive sleep apnea is a polysomnogram (PSG). Specifically, OSAS affects 1-4% of healthy children who are typically 2-8 years of age6, coinciding with adenotonsillar hypertrophy, the commonest cause of OSAS in children. Usual treatment for OSAS in children with adenotonsillar hypertrophy is an adenotonsillectomy (AT). However, there is clear evidence that not only is there a high prevalence of obstructive sleep apnea in obese children, but further, the AT is not successful for resolution of OSAS. This is, in part due to the fact that adenotonsillar hypertrophy is not the single most significant risk factor for OSAS in the obese population.

The factors implicated in the pathophysiology of OSAS in obese children include soft tissues restricting the upper airway size such as fat pads in the soft palate, lateral pharyngeal wall and at the base of the tongue. However, despite the anatomic evidence predisposing obese children to OSAS there are also alterations in functional mechanisms that lead to increased airway collapsibility predisposing these children to OSAS. Specifically, obesity is associated with significant alterations in body composition that could affect chest wall mechanics by weighting the chest wall and reducing lung compliance. Functional residual capacity is diminished to abdominal visceral fat impinging on the chest cavity. Such a reduction in functional residual capacity and compliance increases the risk for sleep disordered breathing by mechanisms of hypoventilation, atelectasis and ventilation perfusion mismatch all increasing the work of breathing and fatigue. Moreover, hypoventilation in itself may reduce upper airway motor tone. Further, ventilator responses may be altered as studies focusing on obese adults have shown that morbidly obese subjects are more susceptible to decreased ventilatory responses to both hypoxia and hypercapnia.

Given this understanding that adenotonsillectomy is not curative in obese children with obstructive sleep apnea, weight loss would be considered the treatment of choice. However, obesity intervention programs have not been wholly successful in BMI reduction in children although in overweight adults, magnitude of weight loss was related to an improvement in OSAS. Thus, the delivery of positive airway pressure (PAP) either continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) is increasingly used as the first line of treatment for OSAS in obese children, although usually in conjunction with weight loss strategies.

Although the benefits of PAP are well established in adults, there is a paucity of available paediatric data.

As previously mentioned, obesity is a risk factor for cardiovascular and metabolic dysfunction; however, OSAS independent of obesity is further associated with cardiac remodeling and cardiovascular metabolic dysfunction. Specifically, if untreated, obstructive sleep apnea in children may lead to excessive daytime sleepiness, poor school performance, hypertension, changes in left ventricular mass and geometry, endothelial cell dysfunction, arterial stiffness, autonomic dysfunction inflammation, and the Metabolic Syndrome (MetS). Thus, OSAS in the context of obesity may independently or synergistically magnify the risk of an already compromised cardiometabolic regulation.

Several metrics will be utilized. Physical activity levels will be measured utilizing Habitual Activity Questionnaires. Insulin resistance will be measured using Fasting Glucose and Fasting Insulin Levels. Cardiovascular markers will include 24 hour blood pressure and cardiograms - left ventricular mass index. C Reactive Protein (CRP) will be utilized as the marker of inflammation.

The mechanisms linking both OSAS and obesity to cardiometabolic dysfunction is believed to be due to activity of the sympathetic nervous system (SNS) and effects of oxidative stress, exacerbating proinflammatory states. Chronic, awake sympathoactivation may promote vascular remodeling and can induce significant cardiovascular morbidity.