Obesity has a profound impact on the respiratory system. Excess adiposity alters structure, affects function, and may influence the metabolic status of the lung. Structurally, excess adipose tissue deposition in and around the pharynx has been implicated in increasing the likelihood of upper airway obstruction (UAO) (1). Abdominal fat deposition may compromise respiratory excursion (2), and infiltration of adipocytes into the diaphragmatic muscle may alter respiratory mechanics and function (3). The inflammatory state induced by the production of adipokines may exacerbate asthma (4).
Compromise of the respiratory system by obesity has implications for obesity progression and treatment.
The respiratory complications of obesity can also contribute to long-term morbidity. Severe obstructive sleep apnea syndrome (OSAS) can result in pulmonary hypertension, right ventricular enlargement, and heart failure. Left ventricular hypertrophy can occur and is linked to the severity of OSAS (9). Systemic hypertension has also been reported in children as well as adults (10). Some findings suggest that the severity of OSAS is related to that of neurocognitive impairment (5). Finally,
respiratory compromise from asthma can lead to inactivity, physical deconditioning, worsening obesity, and chronically impaired lung function.
Upper Airway Obstruction
State of the Problem
The effect of obesity on the incidence of UAO in childhood is superimposed on the traditional causes of UAO, such as enlarged tonsils and adenoids, craniofacial anomalies, and hypotonia. Therefore, the spectrum of symptomatology ranges from traditional childhood symptoms in younger aged patients, when tonsillar enlargement is prevalent, to a more adult presentation in the obese adolescent.
Obstructive sleep apnea is estimated to affect 0.7% to 3.4% of all children (11). In one series of obese children, polysomnographic abnormalities were found in 37% of patients studied (12). In obese children referred for snoring or abnormal breathing during sleep, 59% were diagnosed with OSAS (13). Symptoms of UAO may appear at any point in childhood as obesity worsens. Obese infants have been found to have an increased number of 3- to 10-second episodes of airway obstruction, more gross body movements, and more sleep stage shifts than nonobese infants (14).
UAO is a prominent respiratory manifestation of excess adipose tissue accumulation.
Other components of SDB include the following:
Appreciation of this continuum of SDB is important because sleep disruption, in addition to later hypoxemia and hypercarbia, is thought to account for significant compromise of prefrontal cortex function, which has direct implications for learning and behavior in childhood (8).
The following definitions are listed to help clarify the types of respiratory disturbances that are linked to obesity.
Although not all obese children have SDB, obesity increases the likelihood of SDB, and the more obese a child is, the more likely he or she will be to exhibit some symptoms of sleep disturbance and compromised daytime functioning (13).
It is easy to imagine that excess adipose tissue accumulation in the head, neck, and upper airway can cause narrowing and respiratory compromise (1). In addition, fatty infiltration of the muscles of the hypopharynx and diaphragm may affect muscle function (3). Obesity in adults has been shown to cause decreased chest wall compliance, reduced strength of inspiratory muscles, and a restrictive ventilatory pattern, which predicts hypercapnia (18), and reduced lung volumes have been thought to reflexly induce a reduction in the size of the upper airway (19). Evidence also suggests that the metabolic effects of obesity may contribute to disturbances of respiration during sleep. For example, leptin, an obesity-associated cytokine, has been found to correlate with OSAS, and it decreases when treatment with continuous positive airway pressure (CPAP) is administered (20). Tumor necrosis factor-α
(TNF-α) and interleukin-6 (IL-6) produce sleepiness and fatigue and are both elevated in sleep apnea and obesity (21). The presence of enlarged adenoids and tonsils will exacerbate hypercarbia and hypoxemia in obese children with SDB because the shape of the palate changes, nasal passages are narrowed, the face is flatter and broader, and the glabella is flattened (13).
Clinical manifestations of SDB can be divided into sleep-related nighttime symptoms, which involve disturbances of breathing and sleep, and daytime symptoms, which involve tiredness and reduced cognitive functioning (Table 6.1).
Obese children with OSAS have shown deficits in memory and learning on standardized tests when compared with obese children without OSAS (5). Even normal weight children with simple snoring showed deficits in attention and lower memory and intelligence scores than nonsnorers, along with reduced performance and verbal and global intelligence quotient (IQ) scores (22). Symptoms of UAO can be confused with those of attention deficit disorder (ADD), and children with UAO may be thought to have ADD or unfortunately may be labeled “lazy” or “unmotivated.” In one study of a cross-section of school children, early childhood snoring was associated with poor academic performance in middle school (23). Serious complications of UAO can occur in childhood, such as the following:
TABLE 6.1. Clinical manifestations of sleep-disordered breathing
Obesity hypoventilation syndrome is at one end of the spectrum of respiratory disturbances caused by excess adiposity. It results from the interactions of small lung volume due to relatively mobile chest wall and restriction of diaphragmatic movement due to abdominal fat, which increase the work of breathing (16). This sets up a breathing pattern that is shallow and rapid and reduces the proportion of each breath available for gas exchange (16). The Pickwickian syndrome is marked by an impaired ventilatory response to hypercarbia, which occurs centrally. The exact mechanism of obesity-related hypoventilation is unknown. In leptin-deficient ob/ob mice, a diminished central response to hypercapnia is reversed by administration of leptin (24). This finding may be pertinent to obese patients who, although having high levels of leptin, are leptin resistant (20).
Clinical manifestations of the obesity hypoventilation syndrome (18) are as follows:
Total lung capacity, functional residual capacity, and expiratory reserve volume are decreased, resulting in alveolar hypoventilation, arterial hypoxemia, and hypercarbia (18). Ventilation-perfusion mismatches may also occur, and patients so affected may be more susceptible to respiratory compromise when pulmonary infections occur (16). These patients have a complex course and significant morbidity and should be under the care of a specialist.
Every obese child should be asked about the quality of his or her sleep, and attention paid to any problems in school performance or behavior, as they may be symptoms of SDB.
The physical examination reveals an obese child who may or may not also show evidence of adenotonsillar hypertrophy, such as mouth breathing, nasal obstruction during wakefulness, adenoidal facies, and hypernasal speech. Complications such as systemic hypertension or increased component of the second heart sound, indicative of pulmonary hypertension, may be detected (15).
The “gold standard” of diagnosis of SDB is nighttime polysomnography (7). Although some symptom checklists have proved useful in predicting SDB in the research setting, there has been no large-scale clinical evaluation of these scales (25).
Parental observation, video taping, and audio taping are suggestive but not necessarily predictive of a positive or negative sleep study (7).
Standards of measurement on polysomnography are the following (6):
If cardiac disease is suspected, a chest radiograph, echocardiogram, and electrocardiogram should be obtained (9).
The definitive treatment for obesity-associated SDB is weight loss (26). When indicated, tonsilloadenoidectomy (T & A) is performed. If T & A is not indicated, or if the sleep study is positive after a T & A, CPAP, bilevel airway pressure (BiPAP), or oxygen therapy is used.
Postsurgical complications have been reported in children with obstructive sleep apnea after T & A, which have included (28):
These complications were associated with younger age, more severe apnea, decreased oxygen saturation, and associated medical problems, including hypotonia, morbid obesity, craniofacial abnormalities and upper airway burn, young age, cor pulmonale, respiratory distress index (RDI) greater than 40, or oxygen saturation nadir lower than 70% (28). In a small series of obese patients (14 patients) ages 4 to 15, two patients required overnight BiPAP, one required prolonged intubation, and three required supplemental oxygen after T&A (32).
In obese Prader-Willi syndrome (PWS) patients, hypercapnic ventilatory responses were blunted compared with those in nonobese PWS patients or obese control subjects. Isocapnic hypoxic ventilatory responses were absent or severely reduced in both obese and nonobese PWS patients (33). There have been case reports of PWS patients treated with growth hormone who experienced obstructive apnea, respiratory infection, and sudden death (34). Such reports would militate against the use of growth hormone in these patients.
State of the Problem
The rise in childhood obesity since the 1980s has been paralleled by a rise in asthma rates. Asthma and obesity also often occur together (35), and increases in body mass index (BMI) have been associated with a greater incidence of asthma (36).
Weight reduction in obese individuals has been shown to alleviate asthma symptoms (35).
In a longitudinal population-based cohort study adjusted for risk factors, being overweight or obese at age 11 years was associated with a threefold increased risk for persistence of infrequent wheezing after adolescence and with a twofold increased risk for persistence of asthma (37). A study of 5- to 6-year-old children showed that the prevalence of doctor-diagnosed asthma rose with increased BMI; interestingly, this effect was confined to girls (38). In a meta-analysis of overweight and asthma, high body weight in infancy or childhood was linked with a higher incidence of asthma (39). In a study of urban minority children, those with asthma were more likely to be obese than those without, and 30% of the children with asthma had a BMI greater than the 95th percentile, whereas only 12% of the children without asthma were obese (40).
The link between obesity and asthma is not entirely clear, although both are associated with chronic inflammatory states. Asthma is a chronic inflammatory disease of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough. This inflammation also produces an increase in existing bronchial hyperresponsiveness (41). Obese children may have gastroesophageal reflux as well, which can precipitate wheezing and asthma. Obesity has also been characterized as an inflammatory state (42), and overweight nonasthmatic children have been shown to have a higher susceptibility to exercise-induced bronchospasm (43). In addition, leptin, a proinflammatory cytokine present in higher levels in obese children (42), has also been found in increased levels in normal weight boys with asthma when compared with nonasthmatic controls (44).
Mechanical factors may also contribute to asthmatic symptoms. Lung volumes and thoracic wall distensibility were found to be decreased in obese girls (45), and obesity is associated with a breathing pattern of higher frequencies and lower tidal volumes (35). As a result of this shallower breathing pattern, there is less bronchial smooth muscle stretch and greater muscle stiffness, resulting in more difficulty stretching, muscle fiber shortening, and increased bronchial hyperresponsiveness (35).
Overweight may contribute to increased severity of asthma and, in a study of inner city black and Hispanic children, was associated with a lower than predicted peak expiratory flow rate. In addition, these obese asthmatic children were reported to miss more school days and receive more medications than nonobese asthmatic children (46). Obese children with and without asthma report more coughing, wheezing, and dyspnea than nonobese children (47). Increased bronchial responsiveness may lead to avoidance of exercise, which can lead to or exacerbate obesity (48).
Evaluation and Treatment
Obese children are at higher risk for asthma and may present with a diagnosis already in place. However, obese children may have a very low level of activity and may not voluntarily report symptoms, so a careful history for asthma, particularly exercise-induced asthma, should be obtained. Care must be taken to identify altered activity patterns, such as dropping out of sports or activities, “slowing down,” and losing interest, which might be the result of increased respiratory symptoms such as shortness of breath, chest tightness, and wheezing. Attention to changes in exercise symptoms needs to be maintained over time. As increased physical activity becomes part of a weight management strategy, previously unrecognized respiratory symptoms may emerge.
Asthma treatment should be optimized in all children and is especially critical in obese children. Those who may have decreased physical activity because of asthma symptoms need to feel confident that exercise is safe and possible, and optimal asthma care can provide this support.
Impact on Weight Management
OSAS may contribute to worsening of the metabolic and cardiovascular picture associated with obesity. Nocturnal sleep and respiratory disturbances in obese patients with sleep apnea are independent risk factors for hyperinsulinemia (49). SDB may increase the risk of developing the metabolic syndrome (50). Repeated episodes of apnea and hypopnea are known to cause transient elevations in blood pressure during sleep, and daytime blood pressure increases linearly with an increasing
apnea/hypopnea index (51). Moreover, OSAS is associated with stroke and heart disease in adults (52).
In adults, SDB has also been associated with increased sympathetic nervous system activity (53), decreased baroreceptor sensitivity (54), accentuated vascular responsiveness (55), and abnormal salt and water metabolism (56), all of which could contribute to hypertension.
An inverse correlation between memory and learning performance and the apnea/hypopnea index was found in morbidly obese children with OSAS (5). Beebe and Gozal (8) have proposed that the effect of OSAS in children, causing sleep disruption and intermittent hypoxemia and hypercarbia, alters cellular and chemical homeostasis that leads to deficits in prefrontal cortex function. Deficits in behavioral inhibition, set shifting, self-regulation of affect and arousal, working memory, analysis/synthesis, and contextual memory, all of which play an important role in executive functioning, can occur (8). Executive functioning has been referred to as the ability to develop and sustain an organized future-oriented and flexible approach to problem situations (8). These are all skills important for participating in therapies to create behavior and lifestyle change involved in obesity treatment.
Asthma is a consideration in any weight management plan. Poorly controlled asthma may preclude the increased activity necessary to achieve improved energy balance. In addition, asthma and exercise asthma may become apparent in an obese child who initiates exercise as part of a weight management plan. Exercise is also important in asthma treatment, and a prescription for exercise has been endorsed for all asthmatic subjects by the American College of Sports Medicine and the American Thoracic Society (57).