Obstructive sleep apnea syndrome (OSA), which affects 2% to 3% of young children with peak prevalence at 2 to 8 years, is caused by complete or partial upper airway obstruction during sleep. It presents as episodes of respiratory pauses, gasping, and restless sleep that can result in hypoxia and hypercarbia. Children may have difficulty awakening in the morning, daytime somnolence, behavioral changes, poor school performance, and poor somatic growth as a result of poor sleep quality. Nighttime hypoxia or hypercarbia can lead to morning headaches and, in severe cases, to pulmonary hypertension and cor pulmonale. Adenotonsillar hypertrophy is the most common cause of OSA in young children, but other risk factors for OSA include obesity, craniofacial malformations (Pierre Robin sequence, trisomy 21), glossoptosis, and neuromuscular diseases. Not all children who snore have OSA, and not all children who have OSA snore. Many young children with OSA do not have the classic findings of daytime somnolence and gasping respirations; restless sleep, behavioral problems, and inattention/hyperactivity are much more common. Thus, when the diagnosis is in question, it should be confirmed with a polysomnogram.
Polysomnogram (PSG) is the only definitive test for evaluation of obstructive and central sleep apnea. It involves continuous recording of EEG and electro-oculogram for sleep staging, oronasal airflow and pressure, audible snore, chest and abdominal wall excursion, leg and chin electromyogram, electrocardiogram, pulse oximetry, and capnography. The measured score from a PSG is the apnea-hypopnea index(AHI) or number of times in an hour of sleep that the child has cessation or reduction of airflow of a significant magnitude to negatively affect ventilation or sleep stage. An AHI less than 1 is the generally accepted norm for pediatric patients, although the decision to treat often hinges on the severity of daytime impairment. Measured AHI is typically worse in rapid eye movement (REM) sleep and when the child is supine, so an ideal study captures all sleep stages and positions.
Treatment of OSA starts with determining whether the child will benefit from an adenoidectomy, with or without a tonsillectomy. If surgical intervention is not indicated or fails
Table 134-2 Categories of Apnea DISEASE EXAMPLE(S) MECHANISM SIGNS TREATMENT Apnea of prematurity Premature (<36 wk) Central control, upper airway obstruction Apnea, bradycardia Caffeine, HFNC, CPAP, intubation
Central apnea/ CCHS, Arnold-Chiari Abnormal central control Apnea Mechanical ventilation hypoventilation malformation
BiPAP, Bi-level positive airway pressure; CCHS, congenital central hypoventilation syndrome; CPAP, continuous positive airway pressure; HFNC, high flow nasal cannula.
to alleviate the problem, then the use of continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) via nasal interfaces can be used to distend the upper airway during sleep. This requires a tight-fitting nasal mask, which may not be well tolerated in young children. Supplemental oxygen can blunt hypoxemia in milder cases of OSA but does not alter obstruction and sleep fragmentation. In extreme cases, especially those associated with craniofacial abnormalities or hypotonia, tracheostomy may be indicated.