Adenoid size is related to severity but not the number of episodes of obstructive apnea in children

Brooks, Lee J.; Stephens, Bryan M.; Bacevice, Ann

doi:10.1016/s0022-3476(98)70360-9

Cited by 154 publications

(74 citation statements)

References 19 publications

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“…Literature review a) Low quality studies (class III-IV) suggest that increased adenotonsillar tissue size as detected by lateral neck radiography overdiagnoses OSAS in children [59][60][61]. b) Flexible nasopharyngoscopy has been used in otherwise healthy children with SDB and in young children with Pierre Robin sequence (class IV) [26,62].…”

Section: Literature Reviewmentioning

confidence: 99%

Obstructive sleep disordered breathing in 2- to 18-year-old children: diagnosis and management

et al. 2015

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This document summarises the conclusions of a European Respiratory Society Task Force on the diagnosis and management of obstructive sleep disordered breathing (SDB) in childhood and refers to children aged 2-18 years. Prospective cohort studies describing the natural history of SDB or randomised, double-blind, placebo-controlled trials regarding its management are scarce. Selected evidence (362 articles) can be consolidated into seven management steps. SDB is suspected when symptoms or abnormalities related to upper airway obstruction are present (step 1). Central nervous or cardiovascular system morbidity, growth failure or enuresis and predictors of SDB persistence in the long-term are recognised (steps 2 and 3), and SDB severity is determined objectively preferably using polysomnography (step 4). Children with an apnoea-hypopnoea index (AHI) >5 episodes·h, those with an AHI of 1-5 episodes·h −1 and the presence of morbidity or factors predicting SDB persistence, and children with complex conditions (e.g. Down syndrome and Prader-Willi syndrome) all appear to benefit from treatment (step 5). Treatment interventions are usually implemented in a stepwise fashion addressing all abnormalities that predispose to SDB (step 6) with re-evaluation after each intervention to detect residual disease and to determine the need for additional treatment (step 7). @ERSpublications Management of obstructive sleep disordered breathing in childhood should follow a stepwise approach

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Section: Literature Reviewmentioning

confidence: 99%

Obstructive sleep disordered breathing in 2- to 18-year-old children: diagnosis and management

et al. 2015

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“…Furthermore, we now show that LT concentrations in such tissues are also increased, indicating that an active inflammatory process is present in the upper airway of these children, and that the coordinated increase in LT production and receptor expression may underlie signaling pathways leading to proliferation and hyperplasia of the lymphoid tissue in these children. Thus, if these biological processes are indeed pathophysiologically relevant to the increased size of adenotonsillar tissue, treatment with LT receptor blockers should abrogate the proliferative signals, and thereby lead to progressive reductions in overall lymphoid tissue volume within the upper airway, thus ameliorating the respiratory disturbances during sleep (42).…”

Section: Definition Of Abbreviationsmentioning

confidence: 99%

Leukotriene Modifier Therapy for Mild Sleep-disordered Breathing in Children

Goldbart

Goldman

Veling

et al. 2005

Am J Respir Crit Care Med

284

157

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Background: Children with mild sleep-disordered breathing (SDB), who may not be recommended for adenotonsillectomy, frequently exhibit neurocognitive and behavioral morbidity, and may benefit from alternative therapeutic interventions, such as leukotriene modifier therapy. Methods: Twenty-four children with SDB completed an open-label intervention study for 16 weeks with daily montelukast therapy. Sleep studies and adenoid size estimates from lateral X-ray films of the neck were obtained before and after treatment. In a parallel study, adenoid and tonsillar tissues from children with obstructive sleep apnea or recurrent throat infections were subjected to quantitative polymerase chain reaction, immunohistochemistry, and Western blotting for gene and protein expression of leukotriene receptors LT1-R and LT2-R, and for concentrations of LTB4 and LTC4/D4/E4. Results: Montelukast treatment induced significant reductions in adenoid size and respiratory-related sleep disturbances, which were absent in 16 children with SDB who did not receive treatment. LT1-R and LT2-R mRNA was similarly abundant in adenoid tissues, but increased LT1-R and LT2-R protein expression and higher levels of LTB4 and LTC4/D4/E4 emerged in children with obstructive sleep apnea. Conclusions: Oral therapy with a leukotriene modifier appears to be associated with improved breathing during sleep. Double-blind, placebo-controlled trials will be needed to corroborate current findings and solidly establish antiinflammatory strategies, such as leukotriene modifiers, as therapeutic alternatives in children with SDB too mild to justify referral for adenotonsillectomy.

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“…[1][2][3][4][5][6] Although it is accepted overall that the primary pathophysiologic mechanism involved in pediatric OSA consists of hypertrophy of adenoid and tonsillar tissues in the upper airway, [7][8][9][10][11] several studies [12][13][14][15][16] have thus far failed to demonstrate the anticipated corollary to such findings, namely, a very strong association correlation between upper airway adenotonsillar size and OSA severity. These findings suggest that OSA represents the end point of the interactions between multiple factors contributing to upper airway collapsibility during sleep, which also include neuromotor responses as well as other important anatomic factors such as retrognathia and upper airway length.…”

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confidence: 99%