Obstructive sleep apnoea in children


Sleep-disordered breathing consists of a continuum from primary snoring, upper airway resistance syndrome, to obstructive sleep apnoea syndrome (OSAS). OSAS is characterized by episodic partial or complete upper airway obstruction during sleep, usually associated with desaturation of blood oxygen levels. It is increasingly recognized in children as a common and important health problem. Untreated, severe OSAS may lead to many significant sequelae, including growth retardation, behavioural and learning problems, and cardiopulmonary complications [1]. Many features of childhood OSAS are different from adult OSAS [2] (Table 1).

Table 1. Features of adult and childhood OSAS.
Adult Child
Snoring Alternating, with pauses Continuous
Excessive daytime sleepiness Main symptom Infrequent
Obesity Very common Infrequent
Failure to thrive / underweight Not reported Fairly common
Mouth breathing Less common Common
Male preponderance Yes (9:1) No (1:1 prepubertal)
Enlarged tonsils and adenoids Uncommon Most common
Most common obstructive pattern Apnoea Hypopnoea
Arousal on apnoea termination Very common Uncommon
Sleep pattern disruption Very common Uncommon
Complications Cardiopulmonary, EDS Cardiopulmonary, FTT, behaviour, perioperative
Surgery as treatment Selected cases, minority UP3 Most cases, T&A, UP3
CPAP as treatment Common treatment Selected cases, minority
Mortality CVS death during sleep Usually perioperative
CPAP = continuous positive airway pressure; CVS = cardiovascular; EDS = excessive daytime sleepiness; FTT = failure to thrive; T&A = tonsillectomy and adenoidectomy; UP3 = uvulopalatopharyngoplasty

Prevalence

The prevalence of OSAS was estimated to be 2.3% in a study of local children [3]. The prevalence of snoring among school children has been found to be greater than 15% [3,4]. The peak age of OSAS was reported in a local study to be between 4 and 8 years [3], coinciding with the developmental peak of adenotonsillar hyperplasia. The gender distribution is equal between males and females. There is a second peak of OSAS in adolescence and these patients usually present with symptoms of OSAS as adults, with a male preponderance [5]. Obese children are 10 times more likely to have OSAS than children of normal body weight [3]. Other risk factors for OSAS in children are allergic rhinitis, premature birth, craniofacial anomalies, neuromuscular diseases and Down syndrome [6,7].

Clinical presentation

Night-time symptoms include snoring and difficulty breathing, with paradoxical rib cage motion during inspiration. Parents often report unusual sleeping positions, with hyper-extended neck, restlessness and choking during sleep. Nocturnal enuresis has been associated with OSAS in children, which can be reversed by tonsillectomy and adenoidectomy in several reported studies [8].

Daytime symptoms include mouth breathing, nasal obstruction, morning headache, poor attention span, hyperactivity, tiredness and poor school performance. Excessive daytime sleepiness is less frequently seen in childhood OSAS than in adult OSAS [3].

Sequelae of OSAS in children

Growth impairment
Failure to thrive has previously been reported in children with OSAS. It is rarely seen now because of recognition of the disease at earlier stages. Nocturnal growth hormone
secretion is also found to be decreased in children with OSAS [9]. Treatment of childhood OSAS with adenotonsillectomy has been reported to be effective in improving growth and reducing energy expenditure during sleep [10].

Behaviour and learning problems
OSAS has been reported to be associated with behavioural and learning difficulties, poor attention span, hyperactivity, and poor school performance [11]. Studies have reported that a subset of children with behavioural and learning disabilities could have sleep-disordered breathing and were shown to have benefited from treatment of OSAS [12,13].

Cardiopulmonary complications
It is well known that severe, untreated OSAS can lead to pulmonary hypertension and cor pulmonale, especially in children with craniofacial and neurological disorders [14]. An association between sudden infant death and OSAS has also been suggested [15]. A study reported that adenotonsillectomy may improve the condition of left ventricular hypertrophy in children with severe OSAS [16].

Diagnosis

Early diagnosis and treatment of OSAS in children is helpful in decreasing OSAS-related morbidity. Studies showed that early diagnosis and intervention decreased the health utilization in the treatment of morbidities in children with OSAS [17,18].

History and physical examination
A thorough history of daytime and night-time symptoms and associated medical conditions is helpful in the diagnosis and planning of management. A local study showed that three criteria were found to be highly relevant for predicting the presence of OSAS in children: nocturnal mouth breathing, snoring, and daytime fatigue [1].

Physical examination should note the height and weight in a child growth chart to detect growth impairment. An adenoid face and mouth breathing may be the only positive findings in a general examination. Nasal examination should look for septal deformity, turbinate hypertrophy and obstructive intranasal mass, such as polyps. Oropharyngeal examination should document the size of tonsillar enlargement, palatal obstruction and tongue enlargement. Signs of predisposing factors for OSAS including obesity, neurological disorders and syndromic diseases are important for the planning of management. Cardiopulmonary complications of OSAS, including hypertension and cor pulmonale, may indicate treatment.

Overnight polysomnography
Overnight polysomnography (PSG) is the gold standard for the diagnosis of OSAS. Recommended measurements of a standard PSG are shown in Table 2. Marcus et al suggest an apnoea index of >1 episode per hour or an apnoeahypopnoea index of >1.5 episodes per hour as diagnostic for OSAS in children [19]. However, a full PSG in children may be difficult to obtain, and expensive. In current practice, PSG is not mandatory before surgical treatment of OSAS, such as adenotonsillectomy, in otherwise healthy children. PSG is recommended in high-risk children with severe OSAS with craniofacial anomalies or cardiopulmonary complications, to guide perioperative management [20].

Table 2. Polysomnography for obstructive sleep apnoea syndrome in children.
Sleep state
Electroencephalogram
Electrooculogram (right and left)
Electromyogram (submental)
Respiratory variables
Abdominal and chest wall movement (strain gauges, inductive plethysmography)
Oronasal airflow (thermistor)
End-tidal CO2
Arterial oxygen saturation with pulse oximetry
Nonrespiratory variables
Electrocardiogram
Electromyogram (tibial) to document movements and arousals
Recommended but not required
Audio-video recording
Oesophageal manometry


Other investigations
Lateral neck radiography
is useful to evaluate adenoid obstruction and should be obtained if the tonsils are non-obstructing.

Awake or sleep nasoendoscopy is not indicated in OSAS children with obvious adenotonsillar hypertrophy. It is recommended in patients with suspected hypopharyngeal or multiple level obstruction and craniofacial anomalies. It is useful in determining the site of the obstruction in upper airways [21].

Overnight pulse oximetry can be used as a screening test. It is simple, acceptable to children and is an inexpensive home-based test. It has been found to have a good positive predictive value, but less than desirable specificity and negative predictive values. When history and physical findings indicate OSAS, and oximetry findings are negative, PSG is recommended for further evaluation [22].

Treatment

A spectrum of treatment options are available for OSAS, including observation alone for mild grade OSAS, and a variety of medical, mechanical, and surgical interventions. The choice of treatment options is based on the severity of OSAS, site of upper airway obstruction, co-morbidities, and patient or family desires.

Medical therapy
A local study found that obese children are 10 times more likely to suffer from OSAS than normal weight control groups [3]. Weight loss has been shown to decrease upper airway obstruction and improve OSAS symptoms in children [23]. Weight reduction by aerobic exercise and diet control is recommended as an adjunct to treatment of OSAS in all overweight patients.

When adenotonsillar hypertrophy is due to recurrent bacterial infections, appropriate and prompt antibiotic treatment may reduce the size of the tonsillar enlargement. If adenotonsillar hypertrophy is secondary to acute viral infection, such as infectious mononucleosis, a short course of oral or intravenous steroid therapy has been shown to be effective in reduction of acute upper airway obstruction [24].

Topical intranasal steroids may be recommended as an alterative treatment for mild OSAS, secondary to severe allergic rhinitis or adenotonsillar hypertrophy. Brouillette et al conducted a prospective, randomized, double-blind control study on intranasal steroid treatment for children with mild OSAS [25]. It found a 50% improvement in the apnoeahypopnoea index after a 6-week course of nasal steroids compared with placebo. Demain and Goetz demonstrated that a 24-week course of nasal steroids reduced adenoid size and improved symptoms of nasal airway obstruction [26].

Surgical treatment
Adenoid and tonsillar hypertrophy appear to be key elements in upper airway obstruction during sleep in otherwise healthy children with OSAS [27]. Adenoidectomy and tonsillectomy are the most commonly indicated surgeries for removal of this upper airway obstructing tissue in children with OSAS. Most studies found that adenoidectomy and tonsillectomy are curative in 85% of children, including obese patients [28,29].

A small proportion of children with persistent problems after adenotonsillectomy tend to have smaller tonsils, narrower epipharyngeal airspace, and more poorly developed maxillary and mandibular skeletons than the responders [28]. A stepwise approach with further surgical treatment may be indicated for a specific site of airway obstruction. Alternative surgical procedures include uvulopalatopharyngoplasty, maxillary or mandibular surgery, or tracheostomy [30].

Mechanical treatment
Nasal continuous positive airway pressure (CPAP) or bi-level positive airway pressures (BiPAP)
are indicated as second-line treatment in children who fail to respond to, or are contraindicated for, adenotonsillectomy [31]. Positive airway pressure, delivered via a tight fitting nasal mask, is effective in relieving multiple level obstructions, but its long-term compliance is as low as 50% [32]. Mid-face hypoplasia has been reported to be associated with long-term use of a nasal mask [33].

Conclusion

OSAS in children is increasingly recognized as an important paediatric health problem. Early diagnosis and intervention are essential in preventing complications. Medical history taking and physical examinations are adequate to guide the decision of surgical intervention. PSG is recommended when the diagnosis of OSAS is in doubt or perioperative management is indicated in children with severe OSAS. Adenotonsillectomy is the mainstay of treatment in otherwise healthy children with OSAS, although children with OSAS and complicated medical conditions may require additional treatment.

References
1. Li AM, Chan DFY, Fok TF, Wing YK. Childhood obstructive sleep apnoea: an update. Hong Kong Med J 2004;10(6):406-13.
2. Bower CM, Gungor A. Pediatric obstructive sleep apnea syndrome. Otol Clin North Am 2000;33(1):49-75.
3. Wing YK, Hui SH, Pak WM, et al. A controlled study of sleep related disordered breathing in obese children. Arch Dis Child 2003;88:1043-7.
4. Chau KW, Ng DK, Kwok CK, Chow PY, Ho JC. Clinical risk factors for obstructive sleep apnoea in children. Singapore Med J 2003;44:570-3.
5. Loughlin GM. Obstructive sleep apnea in children. Adv Pediatr 1992:39;307-36.
6. Schechter MS: Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Technical Report: Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109:E69.
7. Rosen CL, Larkin EK, Kirchner HL, et al. Prevalence and risk factors for sleep-disordered breathing in 8- to 11-year-old children: association with race and prematurity. J Pediatr 2003;142:383-9.
8. Cinar U, et al. Nocturnal enuresis and upper airway obstruction. Int J Pediatr Otorhinolaryngol 2001;59:115-8.
9. Nieminen P, et al. Growth and biochemical markers of growth in children with snoring and obstructive sleep apnea. Pediatrics 2002;109:55.
10. Marcus CL, et al. Determinants of growth in children with the obstructive sleep apnea syndrome. J Pediatr 1994;125:556-62.
11. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics 1998;102:616-20.
12. Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects of adenotonsillectomy on behaviour and psychological functioning. Eur J Pediatr 1996;155:56-62.
13. Goldstein NA, Post JC, Rosenfeid RM, Campbell TF. Impact of tonsillectomy and adenoidectomy on child behaviour. Arch Otolaryngol Head Neck Surg 2000;126:494-8.
14. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and Children. J Pediatr 1982;100:31-40.
15. Gulleminault C, Pelayo R, Leger D. Philip P, Ohayon M. Sleep-disordered breathing and upper-airway anomalies in first-degree relatives of ALTE children. Pediatr Res 2001;50:14-22.
16. Amin RS, Kimball TR. Bean JA, et al. Left ventricular hypertrophy and abnormal ventricular geometry in children and adolescents with obstructive sleep apnea. Am J Respir Crit Care Med 2002;165:1395-9.
17. Reuveni H, Simon T, Tal A, Elhayany A, Tarasiuk A. Health care services utilization in children with obstructive sleep apnea syndrome. Pediatrics 2002;110:68-72.
18. Tarasiuk A, Simon T, Tal A, Reuveni H. Adenotonsillectomy in children with obstructive sleep apnea syndrome reduces health care utilization. Pediatrics 2004;113:351-6.
19. Marcus CL, Omlin KJ, Basinki DJ, et al. Normal polysomnographic values for children and adolescents. Am Rev Respir Dis 1992;146:1235-9.
20. Kay DJ, Mehta V, Goldsmith AJ. Perioperative adenotonsillectomy management in children: current practices. Larynogoscope 2003;113:592-7.
21. Culturara A, et al. Preoperative sedation in pediatric patients with sleep disordered breathing. Int J Pediatr Otorhinolaryngol 2002:66:243-6.
22. Brouillette RT, et al. Nocturnal pulse oximetry as an abbreviated testing modality for pediatric obstructive sleep apnea. Pediatrics 2000;105:405-12.
23. Kudoh F, Sanai A. Effect of tonsillectomy and adenoidectomy on obese children with sleep-associated breathing disorders. Acta Otolaryngol Suppl (StockH) 1996;523:216-8.
24. Al-Ghamdi SA, et al. Do systemic corticosteroids effectively treat obstructive sleep apnea secondary to adenotonsillectomy hypertrophy. Laryngoscope 1997;107:1382-7.
25. Brouillette RT, Manoukian JJ, Ducharme FM, et al. Efficacy of fluticasone nasal spray for pediatric obstructive sleep apnea. J Pediatr 2001;138:838-44.
26. Demain JG, Goetz DW. Pediatric adenoidal hypertrophy and nasal airway obstruction: reduction with aqueous nasal beclomethasone. Pediatrics 1995;95:355-64.
27. Grundfast KM, Wittich DJ Jr. Adenotonsillar hypertrophy and upper airway obstruction in evolutionary perspective. Larynogoscope 1982;92:650-6.
28. Shintani T, Asakura K, Kataura A. The effect of adenotonsillectomy in children with OSA. Int J Pediatr Otorhinolaryngol 1998;44:51-8.
29. Stadling JR, et al. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet 1990;335:249-53.
30. Wiet GJ, et al. Surgical correction of obstructive sleep apnea in the complicated pediatric patient documented by polysomnography. Int J Pediatr Otorhinolaryngol 1997;41:133-43.
31. Gay PC, Herold DL, Olson EJ. A randomized, double-blind clinical trail comparing continuous positive airway pressure with a novel bilevel pressure system for treatment of obstructive sleep apnea syndrome. Sleep 2003;26:864-9.
32. Marcus CL, Ward SL, Mallory GB, et al. Use of nasal continuous positive airway pressure as treatment of childhood obstructive sleep apnea. J Pediatr 1995;127:88-94
33. Li KK, Riley RW, Guilleminault C. An unreported risk in the use of home nasal continuous positive airway pressure and home nasal ventilation in children: mid-face hypoplasia. Chest 2000;117:916-8.