Obesity as a Risk Factor for Pediatric OSAS
Concomitant with the increased awareness of childhood OSAS, our society is facing a dramatic increase in the prevalence of obesity worldwide. The epidemic increase in obesity seems to be leading to substantial changes in the anthropometric and demographic characteristics of children being referred for evaluation of OSAS. The classic presentation of children with OSAS as underweight children with adenotonsillar hypertrophy is being substantially replaced by an increasing proportion of young patients who are either overweight or obese.
Obese children are at increased risk for developing SDB and the degree of OSAS is proportional to the degree of obesity. In a case–control study design, Redline et al. examined risk factors for SDB in children aged 2–18 years, and found that the risk among obese children was increased four- to five-fold. In fact, for every increment in BMI of 1 kg/m beyond the mean BMI for age and gender, the risk of OSAS increased by 12%. Similarly to nonobese children, several investigators have emphasized the role of adenotonsillar hypertrophy in obese children with OSAS.
However, the requirement for adenotonsillar hyperplasia/hypertrophy is not always as prominent in the development of OSAS in obese children. In other words, intrinsic loading factors to the upper airway that are contributed by the presence of obesity appear to reduce the dependency on adenotonsillar hypertrophy in obese children with OSAS. The interaction(s) between obesity and OSAS can be therefore explained by, for example upper airway narrowing resulting from fatty infiltration of upper airway structures promoting pharyngeal collapsibility. Indeed, the magnitude of adenotonsillar hypertrophy required for any given magnitude of OSAS severity was found to be smaller and Mallampati scores were found increased in obese children compared with nonobese children, suggesting that soft-tissue changes and potentially fat deposition in the upper airway may play a significant role in the global differences in tonsillar and adenoidal size among obese and nonobese children with OSAS. In addition, adiposity and central obesity reduce the intrathoracic volume and diaphragmatic descent during inspiration, particularly in the supine position, resulting in lower oxygen reserves and increased work of breathing during sleep. Reduced lung volumes decrease airway stiffness by reducing the tracheal tethering effect and may further increase the risk of airway collapse and OSAS. Obesity could also result in blunted ventilatory responses to hypoxia and hypercapnia. Leptin, an adipocyte-derived hormone regulating energy expenditure and food intake is readily found in the circulation, and its level appears to be determined by the degree of obesity. In addition, leptin appears to affect overall ventilatory drive, as well as influence peripheral chemoreceptor activity. Animal studies have demonstrated that hypoxia induces an increase in both leptin gene expression and plasma leptin levels. Obesity is associated with peripheral and central leptin resistance, which in turn leads to relatively ineffective elevation of circulating leptin levels. Thus, reduced bioavailability of leptin resulting in altered ventilatory responses may also play a role in the interaction between obesity and OSAS.
In snoring children, both obesity and OSAS severity were found to contribute to the elevation in plasma leptin levels. Plasma leptin levels were found to be elevated in children with OSAS independent of obesity, and were significantly lower in those children with OSAS, but with minimal hypoxemia, when compared with children with OSAS and more pronounced hypoxemia. Thus, another possible explanation of the elevated plasma leptin levels observed in obesity and in OSAS is that leptin release provides an adaptive mechanism aiming to enhance ventilation in patients with respiratory depression subsequent to obesity, as well as in those with respiratory impairment due to OSAS. More research in children and adolescents is required to clarify these relationships.