Abstract
Pediatric obstructive sleep apnea syndrome (OSAS) is a disorder characterized by repetitive episodes of upper airway obstruction, intermittent hypoxemia and hypercapnia, and snoring. Increasing data indicate the disorder is common, particularly among vulnerable subgroups, and associated with a wide range of co-morbidities. Limited epidemiological data suggest that the disorder affects 1–4% of children. Childhood OSAS appears to vary among age, gender, and ethnic subgroups. Childhood OSASprevalence tends to peak at two ages. The first peak occurs in children 2–6 years of age and coincides with the peak age of lymphoid hypertrophy. A second peak occurs during adolescence and appears related to an increase in prevalence of overweight.Gender differences are less than what has been observed in adult populations, with approximately equal distributionofOSASamongpre-adolescent boys and girls. However, a greater prevalence of OSAS has been observed among adolescent boys compared to adolescent girls. Associations between overweight and childhood OSAS also seem stronger among adolescents than among younger children. Themost commonly recognized risk factor for childhood OSAS is adeno-tonsillar lymphoid hypertrophy. Several studies, however, suggest that OSASmay persist in 9–30% of children post-tonsillectomy/adenoidectomy. Paradoxically, a history of tonsillectomy is associated with a twoto threefold increased risk of snoring, suggesting that symptoms of OSAS may trigger surgery, but addressing lymphoid tissue may not always resolve intermittent upper airway obstruction. Susceptibility to childhood OSAS may also relate to other factors that influence airway patency, including genetic factors, craniofacial morphology, abnormalities in ventilatory control, as well as overweight, suggesting the complexity of the phenotype. The importance of genetic factors is suggested by ethnic differences in OSAS prevalence, which is twoto fourfold higher in Black children [1,2]; symptoms of OSAS also appear increased inHispanic children [3]. In addition, recent data suggest that OSAS is also more common in children from poor neighborhoods [4], suggesting that environmental influences associated with chronic irritant/allergen exposures or physical environment stresseswhich influence airway inflammation or breathing and sleep properties may be of importance. Influences of developmental factors on airway and/or respiratory function are also suggested by increased risk of childhood OSAS among former preterm children. The chronic co-morbidities associated with untreated pediatric OSAS include cognitive deficits, behavioral problems (inattention, hyperactivity, aggression, conduct problems, Attention-Deficit/Hyperactivity Disorder), mood impairments, excessive daytime sleepiness, impaired school performance, and poor quality of life [5–8]. Untreated pediatric OSAS also has been associated with adverse cardiovascular and metabolic outcomes. Children with OSAS have higher levels of blood pressure, C-reactive protein (an inflammatory risk factor associated with cardiovascular disease) and increased insulin resistance, as well as left ventricular hypertrophy [9–12] [13], suggesting that childhood OSAS also may increase the risk of developing severe chronic cardiovascular and metabolic conditions. Despite the frequency and severity of OSAS during childhood, there are large knowledge gaps, including scant data that address causal pathways and population vulnerability to the disorder, responses to therapy, and long term influences on health.
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