PATHOLOGY OF SLEEP-DISORDERED BREATHING IN CHILDREN
Carole L. Marcus, M.B.B.Ch.
University of Pennsylvania, Philadelphia, PA, USA
The obstructive sleep apnea syndrome (OSAS) is thought to result from a combination of anatomic and neuromotor factors. The upper airway is collapsible in order to accommodate such diverse functions as swallowing and speech. During wakefulness, there is activation of the upper airway muscles; thus, the airway remains patent. During sleep, there is a decrease in upper airway muscle tone. If this decrease in tone is severe, or if it is compounded by anatomic factors resulting in a narrow upper airway, then upper airway obstruction will ensue.
The commonest cause of anatomic obstruction in young children is adenotonsillar hypertrophy. Most children with OSAS have large tonsils and adenoid, and will improve following adenotonsillectomy. The tonsils and adenoid grow progressively during childhood, with a peak at approximately 12 years of age. In normal children, the airway caliber increases proportionally. Although children with OSAS tend to have bigger tonsils and adenoid than age-matched controls, this relationship accounts for only a small part of the relationship between adenotonsillar hypertrophy and the apnea hypopnea index. The geometric configuration of the lymphoid tissue around the airway, including the degree to which the tonsils and adenoid overlap, may explain part of this discrepancy. However, the persistence of some degree of OSAS following adenotonsillectomy in as many as 25% of otherwise normal children supports the contention that neuromotor abnormalities need to be present in addition to adenotonsillar hypertrophy. Current research shows that normal children have active upper airway reflexes during sleep in response to stimuli such as subatmospheric pressure and CO2; these reflexes decrease during adolescence. Children with OSAS have blunted upper airway reflexes. In addition, they have deficits in upper airway sensation that may contribute to the pathophysiology.
Craniofacial anomalies, particularly those associated with either midfacial hypoplasia or retro/micrognathia, are associated with OSAS. Recently, data have shown that orthodontic abnormalities such as maxillary restriction may also be associated with OSAS.
Obesity has become a common cause of OSAS in children and adolescents, as it is in adults. In obese adolescents, new data suggest that both structure and neuromotor function play a role. Significant amounts of adenotonsillar tissue tend to be present even in adolescents, but a key factor in the pathogenesis of OSAS in this population may be the diminution of upper airway reflexes.