The obesity-related obstruction of upper airway structure has led some authors to distinguish between two types of OSA in children: type I is associated with marked lymphadenoid hypertrophy without obesity and type II is first associated with obesity and with milder upper airway lymphadenoid hyperplasia. The two types of OSA in children can results in different morbidities and consequences. Studies have shown that weight loss in obese adolescents can reduce sleep apnea and thus the symptoms of OSA. Pathophysiology
The transition from wakefulness to sleep (either REM sleep or NREM sleep) is associated with a reduction in upper-airway muscle tone. During REM sleep, muscle tone of the throat and neck, as well as that of the vast majority of skeletal muscles, are almost completely relaxed. This allows the tongue and soft palate/oropharynx to relax, reducing airway patency and potentially impeding or completely obstructing the flow of air into the lungs during inspiration, resulting in reduced respiratory ventilation. If reductions in ventilation are associated with sufficiently low blood-oxygen levels or with sufficiently high breathing efforts against an obstructed airway, neurological mechanisms may trigger a sudden interruption of sleep, called a neurological arousal. This arousal can cause an individual to gasp for air and awaken. These arousals rarely result in complete awakening but can have a significant negative effect on the restorative quality of sleep. In significant cases of OSA, one consequence is sleep deprivation resulting from the repetitive disruption and recovery of sleep activity.
Poor growth occurs for two reasons: the work of breathing is intense enough that calories are burned at high rates even at rest, and the nose and throat are so obstructed that eating is both tasteless and physically uncomfortable. OSA in children, unlike adults, is often caused by obstructive tonsils and adenoids and may sometimes be cured with tonsillectomy and adenoidectomy.This problem can also be caused by excessive weight in children. In this case, the symptoms are more like the symptoms adults feel such as restlessness, exhaustion, etc. If adenotonsillar hypertrophy remains the most common cause of OSA in children, obesity can also play a role in the pathophysiology of upper airway obstruction during sleep which can lead to OSA, making obese children more likely to develop the condition. The recent epidemic increase of obesity prevalence has thus contributed to changes in the prevalence and in the characteristics of pediatric OSA, the severity of OSA being proportional to the degree of obesity. Obesity leads to the narrowing of upper airway structure due to fatty infiltration and fat deposits in the anterior neck region and cervical structures. Alongside with the additional weight loading on the respiratory system, it increases the risk of pharyngeal collapsibility while reducing the intrathoracic volume and diaphragm excursion. Moreover, excessive daytime sleepiness resulting from sleep fragmentation can decrease physical activity and thus lead to weight gain (by sedentary habits or increased food intake to overcome somnolence).