Sleep and Its Disorders in Children

Timothy F. Hoban, MD

Disclosures

Semin Neurol. 2004;24(3) 

In This Article

Sleep-Related Breathing Disorders in Children

The first modern description of obstructive sleep apnea hypoventilation syndrome (OSAHS) in children dates from 1976, in a report of eight children presenting with snoring and variable daytime symptoms including headache and somnolence.[68] Like obstructive sleep apnea (OSA) in adults, childhood OSAHS is characterized by recurrent episodes of partial or complete airway obstruction during sleep, often accompanied by oxyhemoglobin desaturation or hypercarbia. Unlike adults, however, children are more likely to exhibit periods of prolonged partial airway obstruction rather than discrete events such as apneas and hypopneas.[69,70,71] Prolonged partial airway obstruction sometimes takes the form of obstructive hypoventilation, in which pulmonary ventilation falls below the level necessary to maintain normocapnea, even when normal oxygen saturation is maintained. Upper airway resistance syndrome (UARS), in which abnormally high upper airway resistance leads to increased respiratory effort and disrupted sleep even in the absence of gas exchange abnormalities, has also been described in children.[72]

It is estimated that between 10 and 12% of children snore habitually and that between 1 and 3% of children suffer from OSAHS.[73,74,75,76,77] The prevalence of UARS in children remains unknown. Obstructive sleep apnea hypoventilation syndrome may present at any age during childhood, with peak incidence between 2 and 5 years of age, when adenotonsillar hyperplasia is most common.[78] Prevalence of OSAHS is equal in boys and girls until adolescence, when a male preponderance becomes strikingly evident.[73,76,79] Obesity is less strongly associated with OSAHS in children than in adults. Craniofacial abnormalities (e.g., cleft palate, choanal atresia, macroglossia) may be associated with increased risk of OSAHS. Other genetic and neurological conditions may also be associated with increased risk, most notably Down syndrome, in which at least one-third of children are affected.[80,81]

The clinical features of OSAHS in children overlap only partially with those exhibited by adults ( Table 2 ). Snoring is almost universal in affected children. Other common nighttime symptoms include prominent mouth breathing, unusual sleeping positions, excessive perspiration, and refractory enuresis.[82] Symptoms upon waking often include transient grogginess, headache, or sore throat. In contrast to adults, however, daytime somnolence is seldom a prominent complaint.[83] When present, somnolence is often intermittent or tends to occur during sedentary activities such as reading or riding in an automobile. Many recent reports support the premise that even childhood sleep-related breathing disorders (SRBDs) of mild severity may be associated with attentional, behavioral, and learning problems. Habitual snoring has been reported to be three times as frequent in children with ADHD compared with control groups drawn from child psychiatry and general pediatrics clinics.[84] In a study of 297 first-grade children with poor academic achievement, 54 (18.1%) exhibited either significant hypoxemia or hypercapnia during limited overnight monitoring.[85] Of these, the 24 children treated with adenotonsillectomy exhibited significant academic improvement (P < 0.01) compared with the untreated children.

Physical examination of children with SRBDs is often normal. Tonsillar hypertrophy, although common, is neither necessary nor sufficient for the diagnosis of SRBDs. Adenoid facies (long face syndrome), daytime mouth breathing, or micrognathia may be apparent. Elevated blood pressure may be occasionally evident in affected children.[86]

Because full polysomnography in children is both costly and time-consuming, inexpensive and easily administered screening measures have long been sought. Screening tests such as home audiotapes[87] and overnight oximetry[88] have demonstrated only limited sensitivity for detection of SRBDs in children. A recently developed Pediatric Sleep Questionnaire has demonstrated sensitivity of 0.81 to 0.85 and specificity of 0.87 for the prediction of SRBDs in a clinical research environment but has not been validated for use outside this setting.[89] Polysomnography in children monitors at minimum the same respiratory, cardiac, and neurophysiological data measured in adult PSGs. End-tidal or transcutaneous CO2 monitoring is sometimes added to augment the sensitivity of the study when hypoventilation is suspected (Fig. 2). Esophageal pressure monitoring may be used selectively when increased upper airway resistance or prolonged partial airway obstruction is suspected.[90] Interpretation of the pediatric polysomnogram differs from that of adults. Although scoring of sleep stages and arousals is performed in the manner used for adult studies,[91] there exist no universally accepted pediatric standards for the scoring and interpretation of respiratory disturbances. Some centers score apnea according to adult criteria, which typically require a minimum duration of 10 seconds. Other centers score apneas that exceed the length of two respiratory cycles, which is often less than 10 seconds due to the high respiratory rates seen normally in young children. In addition, there is no consensus on the definition of hypopnea in children.

Figure 2.

Thirty-second epoch from the polysomnogram of a 10-year-old girl with mitochondrial myopathy documenting hypoventilation. Elevated end-tidal carbon dioxide (ETCO2) levels of 66 to 68 Hg and low oxyhemoglobin saturations of 79 to 81% are demonstrated on adjacent channels, indicated by arrows. Channels are as follows: electrooculogram (left, right), chin EMG, EEG (left central, right central, left occipital, right occipital), electrocardiogram, limb EMG (left leg, right leg), snoring, nasal-oral airflow, respiratory effort (thoracic, abdominal), nasal pressure, capnogram, average ETCO2, oxygen saturation.

Despite the present lack of uniformity regarding how respiratory events are defined and scored for children, it has been convincingly argued that adult criteria for the diagnosis of OSA frequently fail to identify children with clinically significant obstruction.[92] Alternative polysomnographic norms for children have been proposed, based on data from 50 normal children, suggesting that more than one obstructive apnea per hour of sleep is statistically abnormal for healthy children.[93] Norms defining a threshold rate or severity of respiratory disturbance associated with clinically significant sleep disruption, however, have not been established for children.

Treatment of SRBDs in children has received remarkably little formal study. This is in large part due to the fact that the most common treatment, adenotonsillectomy, is usually recommended solely on the basis of clinical symptoms without preoperative polysomnography to document whether sleep-disordered breathing is unequivocally present. Available data suggest that adenotonsillectomy results in an improved respiratory index for most children with OSAHS, with improvement apparent as soon as the first postoperative night.[94] In one study of 26 children having a preoperative respiratory disturbance index (RDI) of at least five apneas per hour, all exhibited a lower RDI upon follow-up polysomnography at least 6 weeks after adenotonsillectomy.[95] Despite this improvement, four children (15%) continued to have RDIs exceeding five events per hour, suggesting that a substantial minority of treated patients may still experience residual obstruction. Continuous positive airway pressure (CPAP) is used to treat SRBDs in children without significant adenotonsillar obstruction and those children having residual upper airway obstruction despite surgery. Effectiveness of CPAP has been documented for children of all ages,[96,97,98] although maintaining compliance can be challenging for parents and medical providers. Uvululopalatopharyngoplasty is performed only occasionally for children[99,100] and tracheostomy is used as a last resort for the treatment of severe, refractory OSAHS.[101]

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