Early recognition, accurate diagnosis, and appropriate treatment help to alleviate much of the childhood morbidity associated with obstructive sleep apnea.
by Ronald M. Perkin, MD, MA
Obstructive sleep apnea (OSA) is underdiagnosed in infants and children. In addition to causing physical ailments that range from failure to thrive to cor pulmonale, OSA is often an unrecognized cause of failure in school or of behavioral disorders.
Diagnosis of OSA requires a careful and detailed history and physical examination. Polysomnography is required to determine the nature of the problem, the magnitude of the physiologic disturbance, and (ultimately) the significance of the problem for the child. Earlier recognition, accurate diagnosis, and appropriate treatment all should alleviate much of the childhood morbidity associated with these conditions.
Conceptually, obstructed breathing during sleep lies on a continuum that ranges from benign primary snoring through upper-airway resistance syndrome (UARS) to severe OSA with clinical consequences that can lead to death.1 In a previous study,2 the authors were able to lend support to the concept of a sleep-disordered breathing (SDB) continuum. On polysomnograms, OSA patients had elevated arousal indices, more awakenings, longer apnea periods, lower oxygen saturation, and louder snoring (as reported by the sleep technician) than UARS patients and those without significant SDB. There was overlap between the conditions from patient to patient and within the variable measured.
The incidence of snoring in the general pediatric population ranges from 7% to 12%, and snoring is the most common presenting symptom of OSA.1,3-6 Not all snoring children, however, have OSA. Children who snore, but do not demonstrate apnea, hypoventilation, or excessive arousals from sleep during polysomnography have been termed primary snorers.5 Because snoring is so common in the pediatric population and may resolve itself over time, indications for medical or surgical treatment are controversial.5,7 In most children, primary snoring does not progress to OSA over the course of several years.5
UARS In Children
UARS patients not only snore, but have abnormal sleep histories and polysomnogram data.8 Guilleminault described UARS as early as 1982, yet it remains underrecognized and undertreated.1,9
Important overlap on key clinical variables exists among snoring, UARS, and OSA.8 In both UARS and OSA, there are increased negative esophageal-pressure swings (measured using esophageal manometry) associated with sleep arousals and sleep fragmentation.10 Moreover, there is usually a positive treatment response to continuous positive airway pressure (CPAP). The cardinal symptoms are also similar, with sleepiness being a hallmark symptom after childhood and restlessness, diaphoresis, irritability, and snoring also being prominent in both UARS and OSA.
Important differences exist between UARS and OSA. For example, UARS is not predicted well by the same clinical variables as OSA.1 Although the polysomnogram may be quite abnormal in OSA patients, UARS patients’ polysomnograms are generally quite normal, with the exception of an elevation in electroencephalographic arousals and certain characteristic breathing patterns.8
A polysomnogram can discriminate among primary snoring, UARS, and OSA, whereas questionnaires alone cannot.1 In a prospective study of 83 children, 25% were misclassified as either primary snorers of OSA patients when questionnaire classification was compared with polysomnogram-based diagnosis.6 The authors found overlap between the two conditions on various clinical measures, supporting the SDB continuum theory.
Observers are also inaccurate in discriminating between primary snoring and OSA. Loud snorers do attract parental attention, however. In one study, 94% of parents whose children had OSA watched them sleep and 71% of parents whose children had primary snoring watched them sleep. Observed apneas were reported by 74% of the parents of the OSA children and 39% of the parents of the primary-snoring children. Parental reports, however, were not predictive of true polysomnographic events.11
OSA In Children
OSA lies further along the severity continuum than UARS and has an incidence, among children, of 1% to 3%.12-16 More than 2 million children in the United States have OSA or other debilitating sleep disorders, yet only 20% of pediatricians screen for these problems.12 There is no consensus on what constitutes a clinically significant event in children, although it has been repeatedly demonstrated that adult criteria for the clinical significance of apnea fail in predicting clinically significant infant and childhood sleep apnea.17
OSA occurs when airflow is absent in the presence of chest-wall movement. In children, more than one obstructive apnea of any length per hour of sleep should be considered abnormal.13,16,18
The clinical consequences of OSA are the direct result of the disorder’s two fundamental abnormalities.1,19 First, the repeated arousals from sleep needed to reestablish the patency of the collapsed upper airway lead to sleep fragmentation and a loss of sleep’s restorative nature. Second, the apneic episodes represent periods of asphyxia that can result in hypoxemia, hypercapnia, acidemia, and profound hemodynamic alterations. The ill effects of these two abnormalities can be grouped into two broad categories: sleepiness (along with performance decrements) and cardiovascular dysfunction.
Systemic and pulmonary hemodynamics undergo acute and chronic changes as a consequences of OSA, most of which are reversed after successful treatment of the upper-airway obstruction.1,13,20 Significant increases in systemic arterial pressure occur cyclically with episodes of apnea, and maximal elevations follow the resumption of ventilation.19 If apneas occur in very close clusters throughout the night, especially in association with very severe oxygen desaturations, elevations may be extreme.
In general, systemic hypertension is less common in children than in adults, and it would, therefore, be less expected in children with OSA; however, a number of cases of children with hypertension related to OSA have been reported.20-22 In most such cases, the OSA was severe. One study measured blood pressure in consecutive children with primary snoring or OSA, and it found that children with OSA had increased blood pressure during sleep. The degree of hypertension correlated with the apnea index, as well as with the degree of obesity.22 This study raises the concern that children with undiagnosed OSA may develop long-standing elevations in blood pressure, which could result in an increased risk of cardiovascular complications later in life.
Moderate to severe increases in pulmonary arterial pressure occur with each apneic episode. Maximal pulmonary pressures are generated during rapid-eye-movement sleep. They coincide with maximal hypoxemic and hypercapnic values and probably reflect hypoxic pulmonary vasoconstriction.1,13 Elevation in pulmonary artery pressure can lead to cor pulmonale and right heart failure.
Despite the strong cerebral vasodilating effects of hypercapnia and hypoxemia, cerebral blood flow during sleep is decreased in apneic patients.23 Global and regional cerebral perfusion are decreased in apneic patients during wakefulness, and MRI spectroscopy studies show a metabolic pattern consistent with cerebral ischemia.24
The clinical consequences of disrupted sleep architecture and hypoxemia as a result of SDB in children are becoming defined in the pediatric population.1,13,25-28 Neurodevelopmental complications include developmental delay, poor school performance, hyperactivity, aggressive behavior, and social withdrawal.1,29 In rare instances, severe asphyxial brain damage, seizures, and coma have been reported. Apnea-induced hypoxemia combined with reduced cerebral perfusion may predispose to nocturnal cerebral ischemia in patients with OSA.23,24
Although excessive daytime sleepiness may interfere with school performance, there is increasing evidence that children often reveal cognitive, emotional, and behavioral manifestations of inadequate sleep without showing frank sleepiness.25 This appears to represent a bit of a paradox. That is, many toddlers and early school-age children respond to short-term sleep loss with what appears to be the opposite of sleepiness, including irritability, crankiness, low frustration tolerance, and short attention span. Numerous clinicians and clinical investigators have commented on how some sleep-deprived children can manifest cognitive and behavioral changes mimicking attention-deficit/hyperactivity disorder (ADHD).25,30 The association of snoring with inattention and hyperactivity suggests that SDB could be the cause of inattention and hyperactivity in some children. One study suggests that 81% of snoring children who have ADHD (25% of all children with ADHD) could have their ADHD eliminated if their SDB were effectively treated.30
Psychometric studies have shown that sleep disturbance can produce a range of cognitive impairments.26 Memory, attention, and visuospatial abilities can be affected, but sustained attention (vigilance) and, possibly, divergent intelligence (creativity) are particularly vulnerable.26
Although widely cited as major complications of OSA, developmental, cognitive, and behavioral disturbances in children with OSA have largely been inferred from case studies. In an initial attempt to establish a causal relationship between OSA and neurocognitive function, Rhodes et al28 reported inverse correlations between the apnea-hypopnea index and memory and learning performance in 14 morbidly obese children.
A recent report27 provides the first randomized prospective interventional study on the effects of OSA on learning. The study demonstrated unusually high prevalence of snoring and of nocturnal gas-exchange abnormalities in a cohort of children who were poor academic achievers. Following successful therapeutic intervention, their school grades improved significantly. Sleep-related symptoms should be actively sought in children with developmental or learning problems, and referral for evaluation of SDB should occur.27
Poor growth is a common complication of childhood OSA; early reports31,32 cited the prevalence of failure to thrive as being as much as 50%. Suggested causes of poor growth include anorexia or dysphagia as a result of adenotonsillar hypertrophy, abnormal nocturnal growth-hormone secretion, lack of end-organ responsiveness to growth factors, nocturnal hypoxemia, nocturnal respiratory acidosis, and increased work of breathing during sleep.13,32,33
Studies13,32,34 of children without underlying medical conditions have shown an increased weight-gain velocity in the majority of children after surgical correction of OSA. In addition, the improvement in growth after resolution of OSA in children is accompanied by a significant increase in serum levels of insulin-like growth factor.35 Since serum insulin-like growth-factor levels reflect daily mean growth-hormone levels, this indicates that the suppression of growth-hormone secretion in untreated patients with OSA is rapidly reversed by appropriate therapy.
There are many predisposing factors for OSA (Table 1). OSA may be caused by the same disproportionate anatomy found in adult OSA patients. In addition, it may also be due to impaired coordination of the muscles of the respiratory tract (and, especially, between the diaphragm and dilators of the respiratory tract) or congenital anomalies, whether anatomic and neurologic.
• Deviated nasal septum
• Nasal polyps
• Enlarged turbinates
• Choanal stenosis or atresia
• Hypertrophy of tonsils and adenoids
• Temporomandibular joint ankylosis
|• Prader-Willi syndrome
• Treacher Collins syndrome
• Cystic fibrosis
(Hunter and Hurler syndromes)
• Juvenile rheumatoid arthritis
• Cerebral palsy
• Chiari malformation
• Cranial basal malformations
• Craniofacial microsomia
• Pharyngeal encephalocele
• Sickle cell disease
|Table 1. Some of the causes of obstructive sleep-disordered breathing in infants and children.|
Enlarged tonsils and adenoids are the leading cause of OSA in children.15,36 Although symptoms usually appear early, diagnosis is often delayed owing to underestimation of clinical features and to the apparently normal daytime behavior of these children. The severity of OSA is not proportional to the size of the tonsils and adenoids; it results from an individual combination of adenotonsillar size, pharyngeal size, upper-airway motor tone, and central ventilatory drive.29,37
SDB is a consequence of childhood obesity for which aggressive evaluation and therapy are warranted. Obese children and adolescents have a high incidence of SDB, although, in many cases, it is mild. A third of children whose body weight was greater than 150% of ideal body weight and who had a history of breathing difficulties during sleep were found to have apnea.38 Another study found that 46% of obese patients (whose weight was greater than 120% of the ideal weight for height) had abnormal polysomnograms.39 Many studies39,40 have shown a positive correlation between the degree of obesity and the apnea index.
Obese patients may develop OSA for a number of reasons. In children, OSA is usually attributable to adenotonsillar hypertrophy.41 Not all obese children, however, have adenotonsillar hypertrophy. In obese subjects, upper-airway narrowing results from the deposition of adipose tissue within the muscles and soft tissues surrounding the airway, as well as from external compression exerted by the neck and jowls.39 Chest-wall compliance is decreased, and the obese abdomen causes cephalad displacement of the diaphragm (especially when the patient is supine), resulting in small lung volumes and creating ventilation-perfusion abnormalities.40 In addition, patients may have blunting of the central ventilatory drive.39,42
It is important that all health care professionals who treat children be familiar with the symptoms of OSA (Table 2). The most common nocturnal symptom of OSA in children is snoring.1,29 Snoring is, overall, less common in children than in adults. The disruptive snoring often described in OSA is usually a symptom noted by parents.43 Parents may report observing apnea or breathing pauses in children, although the absence of this symptom does not rule out the diagnosis of OSA. Parents may also describe snorting, gasping, or choking sounds at the conclusion of an apneic episode. Children with OSA often manifest very restless sleep, are diaphoretic during sleep, and may assume an abnormal sleeping position (such as sleeping with the neck hyperextended or sleeping in the upright position).44 Parents may report that the child uses several pillows to sleep comfortably. The incidence of cosleeping may be increased in younger children with OSA because of the high level of parental anxiety about the child’s SDB, and, in fact, parental anxiety has been shown to be one of the factors that correlates most strongly with polysomnographic confirmation of OSA.
|Developmental and behavioral problems
• Excessive daytime somnolence
• Behavioral disturbances
• Decreased school performance
• Developmental delay
• Failure to thrive
Abnormal sleep patterns
• Restless sleep
• Excessive sweating
• Unusual postures
|Table 2. Possible signs and symptoms of OSA.|
The daytime symptoms of OSA in children differ significantly from those of adults because of the much lower overall incidence of obvious daytime somnolence.1,13 The association of internalized behavior problems (such as a depressed affect, shyness, and social withdrawal) and externalized symptoms (such as hyperactivity and aggression) has been described clinically in several studies. Younger children with sleep fragmentation are more likely to manifest daytime symptoms of sleep deprivation behaviorally, through increased activity, aggression, acting-out behavior, and poor concentration and attention than to show direct symptoms of excessive daytime somnolence, such as falling asleep easily during the day.25 When complaints of excessive daytime sleepiness do occur, they may range from occasionally falling asleep during car rides or while watching television to more frequent naps and falling asleep during meals. Thus, the presence of these symptoms warrants aggressive investigation and intervention.
Despite having a different (and, sometimes, more subtle) clinical presentation than that seen in adults, children often have unexpected degrees of airway obstruction, impairment of gas exchange, and sleep disturbance that are difficult to predict on the basis of clinical history and physical examination alone.1 OSA syndrome cannot be reliably distinguished from simple snoring through clinical assessment.6 The clinical history does not have sufficient diagnostic sensitivity on which to base a recommendation for surgery, such as adenotonsillectomy or adenoidectomy.1,6,37 Additional data beyond clinical history should be obtained to establish the diagnosis.
Polysomnography has been the gold standard for the diagnosis of OSA in adults and is equally useful in determining its presence and severity (as well as the efficacy of treatment for it) in children.1,17,29 The recently published American Thoracic Society36 consensus statement concerning the appropriate standards and indications for pediatric cardiopulmonary sleep studies recommends polysomnography in children:
- to detect the presence and severity of OSA;
- to differentiate between benign snoring and snoring associated with partial or complete airway obstruction, hypoxemia, and sleep disruption;
- to evaluate disturbed sleep, daytime hypersomnolence, cor pulmonale, failure to thrive, or polycythemia that is unexplained by other medical conditions;
- to assess relevant symptoms in children with major risk factors for OSA;
- to assess the child with OSA who is at increased risk for perioperative and postoperative complications; and
- to titrate CPAP therapy in pediatric OSA.
Supplemental oxygen has been used with mixed results in selected patients with OSA. Some patients have less SDB and improved oxygen saturation when using supplemental oxygen.45 Oxygen must be used with caution, however, because it may depress ventilatory drive and aggravate apnea in a few patients.45,46 Supplemental oxygen should not be considered a definitive therapy for OSA because it does not address the fundamental problem of upper-airway collapse. It should not be used to delay needed, effective, and safe surgical treatment. If supplemental oxygen is used for children with OSA, oxygen and carbon dioxide levels, heart rate, and respiratory rate should be carefully monitored before it is prescribed for home use.46,47
The most common treatment for young children with symptomatic OSA who have evidence of adenotonsillar hypertrophy is removal of the tonsils or adenoids, or both.1,13,29 The number of adenotonsillectomies performed in the United States has increased substantially since the 1970s, and SDB has become the primary indication for adenotonsillectomy in some pediatric centers.43,48 Although adenotonsillectomy is helpful in relieving OSA in patients with adenotonsillar hypertrophy, children with severe disease or other contributing factors for OSA (Down syndrome, obesity, cerebral palsy, or craniofacial abnormalities) may not be completely cured by surgery.1,13,48
Nasal CPAP works by creating a pneumatic splint in the upper airway.49,50 During apnea, there is a decrease in upper-airway dilator-muscle activity. Through constant air pressure, CPAP creates a pneumatic splint by pushing the soft palate against the tongue.51 CPAP levels must be set at various pressures to eliminate apneas, sleep arousals, and hypoxemia.50 The child should be brought into the sleep laboratory for an exact pressure titration.1,50,52 Because pressure requirements change with patient growth, CPAP requirements should be regularly reevaluated. Some children may also outgrow their need for CPAP therapy.
The CPAP level needed to maintain airway patency in pediatric patients is approximately equal to the median generally found in adults.53,54 CPAP has been used in clinical practice for more than a decade in children of various ages.55 It is considered the primary therapeutic choice for OSA in adults, but CPAP has not yet achieved consensus as the first-line therapeutic choice in the general pediatric population (adenotonsillectomy has).56
Nearly 10% of children who snore have significant sleep and breathing disorders.29 OSA results in nocturnal hypoxemia and sleep fragmentation that can lead to poor school performance, behavior problems, hypertension, cor pulmonale, and failure to thrive.
Treatment should be considered only when the syndrome’s severity has been established by objective testing. Overnight polysomnography in a sleep laboratory experienced in the evaluation of children remains the gold standard for differentiating primary snoring from OSA. A polysomnogram can also guide the choice of treatment, intensity of monitoring, and need for follow-up care. In otherwise normal children with OSA and adenotonsillar hypertrophy, adenotonsillectomy usually cures mild-to-moderate OSA. In children with more severe OSA, nasal CPAP may be required. Nasal CPAP is also helpful for children with neurologic problems or craniofacial problems in whom surgery is not yet appropriate.
Ronald M. Perkin, MD, MA, is professor and associate chairman in the Department of Pediatrics, director of Critical Care Medicine, Inpatient Respiratory Care, and Chronic Ventilation Program, and medical director of the Sleep Disorders Center; Ralph Downey III, PhD, is associate professor of medicine and pediatrics and director of the Adult and Pediatric Sleep Disorders Center; and Joanne MacQuarrie, RRT, RPSGT, is clinical supervisor of the Adult and Pediatric Sleep Disorders Center, all at Loma Linda University Children’s Hospital, Loma Linda, Calif.
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- Downey R, Ascuito TJ, Perkin RM, Gold PM. Sleep disordered breathing in children. RT. 1997;10:53-58.
- Rosen CL. Clinical features of obstructive sleep apnea hypoventilation syndrome in otherwise healthy children. Pediatr Pulmonol. 1999;27:403-404.
- Smedje H, Broman JE, Hetta J. Parents’ reports of disturbed sleep in 5-7 year old Swedish children. Acta Paediatr. 1999;88:858-865.
- Marcus CL, Hamer A, Longhlin GM. Natural history of primary snoring in children. Pediatr Pulmonol. 1998;26:6-11.
- Carroll JL, McColley SA, Marcus CL, et al. Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children. Chest. 1995;108:610-615.
- Ali NJ, Pitson DJ, Stradling JR. Natural history of snoring and related behavior problems between the ages of 4 and 7 years. Arch Dis Child. 1994;71:74-76.
- Guilleminault C, Pelayo R, Leger D, et al. Recognition of sleep-disordered breathing in children. Pediatrics. 1996;98:871-882.
- Downey R III, Perkin RM, MacQuarrie J. Upper airway resistance syndrome: sick, symptomatic but under recognized. Sleep. 1993;16:620-623.
- Guilleminault C, Stools R, Clerk A, et al. A cause of excessive sleepiness: the upper airway resistance syndrome. Chest. 1993;104:781-787.
- Carroll JL, Longhlin GM. Obstructive sleep apnea syndrome in infants and children: clinical features and pathophysiology. In: Ferber R, Kryger M, eds. Principles and Practice of Sleep Medicine in the Child. Philadelphia: WB Saunders; 1995:163-191.
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- American Thoracic Society Workshop. Cardiorespiratory sleep studies in children: establishment of normative data and polysomnographic predictors of morbidity. Am J Respir Crit Care Med. 1999;160:1381-1387.
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- Rosen CL, D’Andrea L, Haddad GG. Adult criteria for obstructive sleep apnea do not identify children with serious obstruction. Am Rev Respir Dis. 1992;146:1231-1234.
- Marcus CL, Omlin KJ, Businski DJ, et al. Normal polysomnographic values for children and adolescents. Am Rev Respir Dis. 1992;146:1235-1239.
- Epstein LJ, Weiss JW. Clinical consequences of obstructive sleep apnea. Seminars in Respiratory and Critical Care Medicine. 1998;14:123-132.
- Ross RD, Daniels SR, Loggie JMH, et al. Sleep apnea associated hypertension and reversible left ventricular hypertrophy. J Pediatr. 1987;111:253-255.
- Guilleminault C, Suzuki M. Sleep related hemodynamics and hypertension with partial or complete upper airway obstruction during sleep. Sleep. 1992;15:S20-S24.
- Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med. 1998;157:1098-1103.
- Balfors EM, Franklin KA. Impairment of cerebral perfusion during obstructive sleep apneas. Am J Respir Crit Care Med. 1994;150:1598-1591.
- Kamba M, Suto Y, Ohtu Y, et al. Cerebral metabolism in sleep apnea: evaluation by magnetic resonance spectroscopy. Am J Respir Crit Care Med. 1997;156:296-298.
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- Rhodes SK, Shimoda KL, Weid LR, et al. Neurocognitive deficits in morbidly obese children with obstructive sleep apnea. J Pediatr. 1995;127:741-744.
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- Marcus CL, Carroll JL, Koerner CB, et al. Determinants of growth in children with the obstructive sleep apnea syndrome. J Pediatr. 1994;125:556-562.
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