A review of the roles of allergic rhinitis in childhood obstructive sleep apnea syndrome

Daniel K. Ng, F.R.C.P., Chung-hong Chan, B.Sc., Gloria Yu-yan Hwang, M.B., B.S., Pok-yu Chow, M.R.C.P., and Ka-li Kwok, F.R.C.P. (China)
ABSTRACT The aim of this study was to review the literature to evaluate the association between allergic rhinitis (AR) and obstructive sleep apnea syndrome (OSAS) in childhood. A PubMed literature search (January 1970 to February 2005) was conducted using the following key words: obstructive sleep apnea, allergic rhinitis, and mouth breathing. The retrieved articles were reviewed and the levels of evidence were assessed. AR affected 40% of children and OSAS occurred in 2% of children. AR is a risk factor for OSAS because AR is associated with nasal obstruction, enlargement of tonsils and adenoids, and an elongated face, which, taken together, constitute a smaller upper airway size. Adequate treatment of AR is helpful to decrease the severity of OSAS and prevent emergence of an elongated face, which predispose for OSAS. There is convincing evidence that AR increases the risk of OSAS in children. Appropriate treatment of AR regularly could prevent the occurrence of OSAS and reduce the severity of existing OSAS. (Allergy Asthma Proc 27:240 242, 2006; doi: 10.2500/aap.2006.27.2855) llergic rhinitis (AR) is a common disease in childhood and adolescence. Globally, AR is the most common allergic disease and one of the leading chronic conditions in children 18 years of age.1 In one study, 52% of adolescents aged between 13 and 14 years in Hong Kong had AR.2 For the 6- to 7-year-old group, the prevalence of current AR was 37%.3 The prevalence of AR in children appeared to be rising as shown in a study conducted in Finland that reported a threefold increase in prevalence of AR in children from 1977 to 1991.1 A similar increase was reported from Hong Kong.3 Childhood AR was associated with a number of comorbid disorders, including asthma, eczema, conjunctivitis, speech impairment, and failure to thrive.4 The quality of life in children with AR was reported to be significantly impaired.5 The underlying mechanism of daytime symptoms in children with AR was suggested to be mediated by sleep-disordered breathing (SDB).6 SDB is a spectrum of breathing problems ranging from primary snoring to upper airway resistance syndrome to obstructive sleep apnea syndrome (OSAS).7 Primary snoring referred to snoring without any of the following abnormalities, including apnea, hypoventilation, hypoxemia, hypercapnia, sleep disturbance, and daytime symptoms. It is considered to be a benign

condition. Upper airway resistance syndrome is a more severe form of SDB. There is sleep-related increase in airway resistance leading to arousals and excessive daytime sleepiness without desaturation or apnea. The most severe form of SDB is OSAS. There is obstructive apnea with hypoxemia leading to complications such as hypertension, left ventricular hypertrophy, arrhythmia, pulmonary hypertension, cor pulmonale, and failure to thrive. Some OSAS children were reported to have excessive daytime sleepiness and impaired cognition.8 The most common symptom of SDB is habitual snoring that was reported to occur in 312% of children.9 The estimated prevalence of OSAS in children was reported to be 2%.10 Polysomnography is the gold standard for the diagnosis of SDB. AR has long been recognized to be a risk factor of childhood OSAS in various epidemiologic studies11,12 (Table 1). Children with AR were three times more likely to have disturbed sleep.13 In one study comparing OSAS patients and nonapnoeic habitual snorers, positive radioallergosorbent test was more likely to be found in the OSAS group (57% versus 40%).13 In polysomnography done among patients with AR and normal controls, more microarousals were observed in the AR group.14 These studies provided the evidence of an association between AR and OSAS. PATHOPHYSIOLOGY Nasal airway resistance is a major determinant of total airway resistance. It accounts for two-thirds of the total airway resistance.15 Nasal patency is predominantly controlled by the capacitance vessels of the middle and inferior turbinates. AR leads to markedly in-

From the Department of Paediatrics, Kwong Wah Hospital, Hong Kong, SAR, China This work was not supported by any external grant Address correspondence and reprint requests to Daniel K. Ng, F.R.C.P., Department of Paediatrics, Kwong Wah Hospital, Waterloo Road, Kowloon, Hong Kong SAR, China E-mail address: dkkng@ha.org.hk Copyright 2006, OceanSide Publications, Inc., U.S.A.

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Table 1 Studies supporting the role of AR in the pathogenesis of childhood OSAS Key Clinical Recommendation AR is suggested to be a risk factor of childhood OSAS Treatment of AR as part of the treatment of childhood OSAS Strength of Recommendation B B References 11, 12, and 13 29, 31, and 32 Comment and References Observational studies and epidemiological studies Two case series and one randomized control trial with a limited sample size

Strength of recommendation: A, recommendation based on consistent and good-quality patient-oriented evidence; B, recommendation based on inconsistent or limited-quality patient-oriented evidence; C, recommendation based on consensus, usual practice, opinion, disease-oriented evidence, or case series for studies of diagnosis, treatment, prevention, or screening. creased nasal resistance with dilatation of these capacitance vessels, leading to mucosal edema and excessive mucous secretions. Although objective measures of nasal resistance were not shown to be predictive of SDB,16 several studies showed that nasal congestion was a strong independent risk factor for snoring as well as an increased likelihood for moderate or severe SDB.7 Any anatomic narrowing of the upper airway, e.g., hypertrophy of nasal turbinate, retrognathia, adenoid enlargement, or tonsillar enlargement, would predispose for snoring and OSAS. Increased nasal resistance secondary to AR results in mouth breathing. Hence, mouth breathing results in secondary tonsillar enlargement and dysfunction of genioglossus muscle and geniohyoid muscle. Enlarged tonsils and adenoids in children play a significant role in upper airway obstruction. Significant improvement in SDB was observed in 80% of children after tonsillectomy and adenoidectomy.17 Arens et al.18 conducted a case control study of the upper airway structure of children with OSAS by magnetic resonance imaging. Among the 18 pairs of children studied, OSAS children had larger tonsils, adenoids, and soft palate. The prolonged oral breathing also imposes a passive tension on the soft tissue of the face and neck, unloading the posterior and anterior force on the facial skeleton. This results in a typical long face as the mandible grows more caudally than anteriorly.19,20 This abnormal facial growth will lead to an increased likelihood of SDB. For the untreated AR child, they will have hyponasal speech, retrognathia, lip-apart posture and gummy smile, disuse atrophy of lateral alar cartilage of the nose, slit-like nostrils, and OSAS. Hence, the role of tonsils, adenoids, enlarged nasal turbinates, mouth breathing, and tongue position on orthodontic changes and abnormal craniofacial growth should be appreciated by all medical practitioners dealing with children.21 In addition, recent studies suggested that receptors in the nasopharynx controlled the muscle tone in the oropharynx.22 Upper airway muscle tone is higher with nasal breathing. Lignocaine spray blocking these receptors increases the risk of SDB events four times. Moreover, minute ventilation is greater with nasal breathing compared with mouth breathing, suggesting that nasal breathing has a stimulatory effect on respiration.23 AR-induced mouth breathing compromises the upper airway muscle tone and the respiratory drive during sleep. TREATMENT OF AR AS A TREATMENT OF OSAS Treatment of AR is an important component in the management of childhood OSAS. In addition, a growing number of evidence showed that local and systematic inflammation were closely linked to the pathogenesis of OSAS.24,25 Treatment of AR as a possible treatment of coexisting OSAS is an attractive alternative to surgical treatment and continuous positive airway pressure treatment in the pediatric population. Topical nasal steroid is currently the treatment of choice in pediatric AR.26 Previous studies showed that treatment for AR also was useful to reduce the severity of OSAS in adults. 27,28 Four pediatric studies were done to evaluate the efficacy of corticosteroids as a treatment of OSAS (Table 1). Brouillette et al.29 indicated that a 6-week course of intranasal fluticasone was effective in reducing severity of OSAS. However, the same group showed no improvement in OSAS after a short course of systemic steroid.30 In another study conducted by Mansfield et al.,31 14 children with AR and SDB were treated with a short course of intranasal budesonide. The mean respiratory disturbance index (RDI) was significantly reduced from 8.4 to 1.2. The reduction of the RDI in studied children was contributed mainly by resolution of hypopneas. Quality of life in studied children was significantly improved in the treated group. Twenty-two children with mild-to-moderate OSAS (apnea-hypophea index [AHI] 15) were treated with intranasal steroid.32 They were followed

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for 1 year in our department. Sixteen of them were found to have a significant improvement in their clinical symptoms. Even though the beneficial effect of treatment of AR in children with OSAS was established in three studies, the sample size in three pediatric studies generally was limited. In addition, the reduction of RDI or clinical symptoms by intranasal steroid therapy in children with OSAS may not be adequate because 43% of children with OSAS who showed improvement after intranasal steroid therapy ultimately required tonsillectomy and adenoidectomy.29 Additional studies with a larger sample size and a longer follow-up period are warranted. CONCLUSIONS There is convincing evidence that AR increases the risk of OSAS in children. It is important to recognize this association because AR is a very common pediatric problem. It is likely that a substantial group of AR children have unrecognized SDB. Appropriate treatment of AR regularly could prevent the occurrence of OSAS and reduce the severity of existing OSAS.
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