Review and Feature Article
Pediatric Sleep Apnea Syndrome: An Update

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Obstructive sleep apnea syndrome (OSAS) may be central neurologic (<5%) or obstructive (>95%) in origin and is a relatively prevalent condition in children. It affects 1%-5% of children aged 2-8 years and is caused by a variety of different pathophysiologic abnormalities. Cardiovascular, metabolic, and neurocognitive comorbidities can occur in both children and adults when left untreated. It also can cause severe behavioral problems in children. The American Academy of Pediatrics recommends that all children be screened with an appropriate history and physical examination for symptoms and signs suggestive of OSAS. The diagnosis is primarily made clinically and confirmed by polysomnographic findings. Treatment depends on the child's age, underlying medical problems, polysomnography findings, and whether or not there is upper airway obstruction usually secondary to enlarged adenoids and/or tonsils, allergic and nonallergic rhinitis, acute and chronic sinusitis, and other upper airway pathology. If enlarged adenoid or tonsils or both conditions exist, an adenoidectomy, tonsillectomy, or adenotonsillectomy remains the treatment of choice. Pharmacotherapy of OSAS has shown some effect in children with mild symptoms. This paper reviews the prevalence, pathophysiology, clinical presentation, diagnosis, and treatment of OSAS.

Section snippets

Case

A 5-year-old boy complains of sneezing, itchy nose, nose rubbing, clear rhinorrhea, postnasal drip, nasal stuffiness, and intermittent sore throat for 3 to 4 years. Perennial nasal symptoms are worse in Florida during late January through April. His grandmother, the historian, states that he has been diagnosed with attention deficit hyperactivity disorder. He has insomnia, night sweats, props himself up on several pillows to sleep, and is a chronic mouth breather. He snores so loudly that it

Epidemiology

Up to 50% of children may experience a sleep problem.1, 2 However, from that group only 1%-5% will end up been formally diagnosed with OSAS.3, 4, 5 OSAS has a peak incidence around 2-8 years of age, most likely due to the relative size of the adenoids and/or tonsils versus the diameter of the upper airway.6 Since the first case report of pediatric OSAS in 1976,7 much has been learned about this disease. First, the prevalence of OSAS in children varies from 1% to 5%3 and is more common in males

Pathophysiology

The pathophysiology of OSAS is not fully understood; however, factors that effectively decrease airway caliber or increase upper airway collapsibility can predispose to airway collapse that include anatomic, genetic, and neuromuscular factors as well as consciousness alterations during sleep stages and anesthesia (Table I). Systemic or upper airway inflammation, associated with allergic and nonallergic rhinitis and acute and chronic sinusitis, is also a risk factor for airway occlusion. The

Upper airway edema and narrowing

The most common anatomic cause of upper airway narrowing in children is adenoid and/or tonsil hypertrophy. The retropalatal area has the smallest cross-sectional area making it the most common site of obstruction. The adenotonsillar tissue is largest between ages 3 and 6, correlating with the peak incidence of OSAS.15, 16 However, the exact correlation between adenotonsillar size and OSAS severity is unclear.17 Hypertrophy and/or hyperplasia of the lymphoid tissue in the upper airway, allergic

Clinical Presentation

OSAS disrupts normal sleep patterns and normal ventilation and often results in gas exchange abnormalities and sleep fragmentation.52 Hill in BMJ described the symptoms of OSAS in the 19th century as follows: “The stupid-lazy child who frequently suffers from headaches at school, breathes through his mouth instead of his nose, snores and is restless at night, and wakes up with a dry mouth in the morning, is well-worthy of the solicitous attention of the school medical officer.”53

Cardiovascular system

Sustained hypoxia in severe untreated OSAS increases pulmonary vascular vasoconstriction and endothelial dysfunction thus promoting long-term susceptibility to pulmonary hypertension, cor pulmonale, and right heart failure.72 Increased brain natriuretic peptide was found in children with moderate to severe OSAS supporting the presence of left ventricular strain in these children population.73 Children with a high CRP level have an increased risk for cardiovascular complications74, 75 and

Diagnosis

Early diagnosis and treatment of pediatric OSAS are very important, yet challenging. Guidelines published in 2012 recommend screening every child and adolescent for snoring and sleep apnea-related signs and symptoms.95

Treatment

There are various therapeutic options for childhood OSAS, and treatments are based on the child's age, underlying medical conditions, and PSG findings.

Future Research

Nocturnal PSG remains the gold standard for diagnosis of OSAS. However, it is costly, time consuming and not always available. Other tests for OSAS diagnosis have variable sensitivity and specificity. Well-designed, large prospective studies are needed to determine the validity of these screening tools in the diagnosis of OSAS. In terms of noninvasive tests, systemic inflammation has shown association with OSAS. Further studies are required to determine whether biomarkers are potentially useful

Conclusion

OSAS is a very common and serious cause of cardiovascular, metabolic, neurocognitive, and behavioral functioning morbidity in children. The prevalence of OSAS in the pediatric population is increasing. This represents a major, yet poorly addressed public health burden, with many years of potential consequences for affected individuals, their families, and society. There has been extensive and meaningful research progress on the pathophysiology, morbidity, and treatment of pediatric OSAS since

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    No funding was received for this work.

    Conflicts of interest: Z. Li declares no relevant conflicts of interest. R. F. Lockey has received consultancy and lecture fees from Merck and AstraZeneca; is employed by the University of South Florida College of Medicine; receives royalties from Informa Publishing; and has received travel support from the National and International Congress for Presentations. J. Celestin has received lecture fees from the University of South Florida, Louisiana State University.

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