To What Extent Is Adenotonsillar Hypertrophy the Greatest Risk Factor Associated with Paediatric Obstructive Sleep Apnoea?

DRAFT: To what extent is adenotonsillar hypertrophy the greatest risk factor associated with paediatric obstructive sleep apnoea?

Introduction

Paediatric obstructive sleep apnoea (POSA) is a condition which affects approximately 2% of children (Gulotta et al., 2019) and is characterised, according to Shen et al (2018), by the recurrent partial or complete upper airway obstruction during sleep. The disorder interrupts the normal respiratory ventilation leading to intermittent hypoxia and hypercapnia, frequent arousals and sleep fragmentation. This gives rise to symptoms such as habitual snoring, disturbed sleep patterns and daytime neurobehavioral problems to name a few. The development of this disorder in children is particularly problematic as it can lead to various pathophysiological changes such as stunted growth, behavioural abnormalities and cardiovascular disease (Gulotta et al., 2019).  

Unlike OSA in adults, there are still many aspects of the etiopathogenesis in children that are still disputed. Although the investigations studying the causes and risk factors of the disorder are limited, the majority conclude that the greatest risk factor and cause of paediatric obstructive sleep apnoea is adenotonsillar hypertrophy. Despite this, there are a handful of recent studies which have suggested that adenotonsillar hypertrophy actually has no significant correlation to the prevalence of OSA or that its impact is exacerbated by other more influential factors. Upon this revelation, the following literature review will explore the pathophysiology of adenotonsillar hypertrophy and obesity as well as evaluating the relative significance of the factors mentioned, weighing up which is the greatest risk factor associated with POSA. 
 

Adenotonsillar Hypertrophy

Adenotonsillar hypertrophy is a term used to describe the abnormal growth of the pharyngeal and palatine tonsils (Inoshita et al., 2018). The condition is regarded by many as the primary contributor towards the development of POSA (Alonso-Álvarez et al., 2017; Chang and Chae., 2010; Gulotta et al., 2019). 

The pathophysiology of POSA  with respect to adenotonsillar hypertrophy has been extensively studied in recent years. Sheldon et al (2014) found that POSA occurred only when the interaction between the anatomical restriction and the neuromuscular reflexes failed to preserve patency leading to airway collapse. He concluded that this was a state-dependent process as it did not occur during wakefulness. The study evidenced that as the upper airway developed, the rapid growth of the tonsils and adenoids was disproportionate to that of the skeletal boundaries and structures of the upper airway - this resulted  in a relatively narrow upper airway. Consequently, the upper airway muscles (genioglossus and tensor palatini) were activated to increase ventilatory drive preventing excessive upper airway collapsibility. However, changes to this innate mechanism (such as a conformational change in the dilator muscles) can lead to airway collapse resulting in symptoms such as snoring.

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It has been found that the magnitude of POSA is directly related to the  size of the adenotonsillar region – the larger the tonsils the narrower the airway and the greater the severity of symptoms suffered by the patient. Gulotta et al (2019) came to a similar conclusion, noting that the lymphoid tissue of the Waldeyer ring (pharyngeal, tubal, palatine and lingual tonsils) developed drastically  from the ages of three to six. It is interesting to note that the window of the growth period of the Waldeyer ring correlates to the peak incidence of POSA observed by Jennum, Ibsen and Kjellberg (2019) as well as Chang and Chae (2010). They found that this disease occurred in two peaks: the first occurring in children aged between two and eight years and  the second peak occurring during adolescence. Therefore, one may hypothesise that adenotonsillar hypertrophy would be the greatest contributor towards the cases of POSA occurring in the first peak as this correlates with the rapid growth in the upper respiratory tract anatomy. On the other hand, adenotonsillar hypertrophy cannot be the most prevalent risk factor in adolescents as the developmental changes in the anatomy has surpassed the greatest growth phase. Therefore, there must be another impacting factor which has an impact of a larger magnitude on the prevalence of adolescent OSA.

Obesity

According to Katz and D’Ambrosio (2008) the prevalence of childhood obesity has tripled since the early 1980s with this figure ever increasing due to genetic and environmental factors. It is therefore unsurprising that obesity has changed the clinical landscape of paediatric obstructive sleep apnoea, particularly in adolescents (Chang and Chae, 2010).

Gulotta et al (2019) analysed the major risk factors associated with POSA noting that the disease affects the condition by: 

1. Reducing the width of the lumen and increasing the collapse of the structures themselves as a result of the presence of fat at the level of the pharyngeal soft tissue. 
2. Reducing respiratory function as a result of the increased presence of fat in the thoracic and abdominal walls.

These findings can be supported by research conducted by Wang et al (2019) which concluded that in children of abnormal weight, obesity played a role in the paediatric obstructive sleep apnoea  development. Obese children exhibited a higher apnoea-hypopnoea index (AHI) than underweight, normal weight and overweight meaning that obese patients suffered from a greater sum of apnoeas and hypopneas than patients in any other category. From the data set, one can therefore infer that obesity at the very least exacerbates paediatric obstructive sleep apnoea and to an extent worsens it as the children suffering from both adenotonsillar hypertrophy and obesity experienced more severe adenotonsillar hypertrophy accompanied by more prominent symptoms. This supports the findings made by Gulotta et al (2019).From the conclusions drawn from these papers, one could therefore argue that obesity is a greater risk factor of paediatric obstructive sleep apnoea as it induces more severe symptoms, worsening the severity of the condition.
 

However, it should be noted that the research conducted by Wang et al (2019) was limited.  The number of children in the underweight, overweight and obese groups were relatively small; this is problematic as it can lead to skewed results lowering the power of the study and increasing the margin of error which makes the conclusion drawn from the data set unreliable. In this case, adjustments to the data had been made in order to accommodate for the small sample size and minimise accompanying issues. Other limitations to the data include the fact that a normal control group is lacking in the study as almost all the children subject to polysomnography and lateral cephalometric radiography had sleep disordered breathing. Although having a control group is preferable, in this particular study it would have been unethical to examine children in such a manner  as they did not suffer from the condition and would therefore be less likely to comply in the trial and thus possibly skewing the results. This limits the research conducted as the data set lacks a benchmark measure to assess the true impact between paediatric obstructive sleep apnoea and obesity. Nevertheless, the study still has merit and the results do provide significant data points to show the impact obesity has on paediatric obstructive sleep apnoea. Clearly, further evaluation of upper airway structure and neuromuscular function in the context of the pathophysiological mechanisms at play in POSA of various weight statuses are needed for more conclusive results to be obtained and patterns to be seen.

Conclusion

It can be said that adenotonsillar hypertrophy is the primary contributor towards paediatric obstructive sleep apnoea in prepubertal children as many extensive research projects and studies have reached the same conclusion. However, it would be foolish to assume that this factor remains the primary contributor, particularly through adolescence (the second peak of paediatric obstructive sleep apnoea cases) due to the need for more research in this new area of medicine With the increasing prevalence of obesity studies suggesting that the impact of adenotonsillar hypertrophy becomes lessened as the phase of rapid upper airway growth is nearing the end and therefore reducing the likelihood of hypertrophy causing obstructive sleep apnoea which shows that obesity surpasses adenotonsillar hypertrophy as the primary cause of obstructive sleep apnoea in adolescent children. Therefore it can be concluded that adenotonsillar hypertrophy is the greatest risk factor of paediatric obstructive sleep apnoea as more children suffer from this condition after developing enlarged tonsils and adenoids but it is imperative to note that this changes once children have surpassed prepubescence. The relationships between adenotonsillar hypertrophy size ad obstructive sleep apnoea in detailed age groups and the respective effect of adenoid and tonsil size on obstructive sleep apnoea in obese and non-obese children need to be investigated more in order to ascertain a more definitive answer to the proposed question. This literature review provides some insight into the current landscape and has hypothesised ideas based on relevant research available.

Bibliography 
 

1. Alonso-Álvarez, M., Terán-Santos, J., Gonzalez Martinez, M., Cordero-Guevara, J., Jurado-Luque, M., Corral-Peñafiel, J., Duran-Cantolla, J., Ordax Carbajo, E., MasaJimenez, F., Kheirandish-Gozal, L. and Gozal, D. (2017). Metabolic biomarkers in community obese children: effect of obstructive sleep apnea and its treatment. Sleep Medicine, 37, pp.1-9.
2. Bhattacharjee, R., Kim, J., Kheirandish-Gozal, L. and Gozal, D. (2010). Obesity and obstructive sleep apnea syndrome in children: A tale of inflammatory cascades. Pediatric Pulmonology, 46(4), pp.313-323.
   (Bhattacharjee et al., 2010)
3. Chang, S. and Chae, K. (2010). Obstructive sleep apnea syndrome in children: Epidemiology, pathophysiology, diagnosis and sequelae. Korean Journal of Pediatrics, 53(10), p.863.
4. Deegan, P. and McNicholas, W. (1995). Pathophysiology of obstructive sleep apnoea. European Respiratory Journal, 8(7), pp.1161-1178.
5. Garg, R., Afifi, A., Garland, C., Sanchez, R. and Mount, D. (2017). Pediatric Obstructive Sleep Apnea. Plastic and Reconstructive Surgery, 140(5), pp.987-997.
6. Gulotta, G., Iannella, G., Vicini, C., Polimeni, A., Greco, A., de Vincentiis, M., Visconti, I., Meccariello, G., Cammaroto, G., De Vito, A., Gobbi, R., Bellini, C., Firinu, E., Pace, A., Colizza, A., Pelucchi, S. and Magliulo, G. (2019). Risk Factors for Obstructive Sleep Apnea Syndrome in Children: State of the Art. International Journal of Environmental Research and Public Health, 16(18), p.3235.
7. Inoshita, A., Kasai, T., Matsuoka, R., Sata, N., Shiroshita, N., Kawana, F., Kato, M. and Ikeda, K. (2018). Age-stratified sex differences in polysomnographic findings and pharyngeal morphology among children with obstructive sleep apnea. Journal of Thoracic Disease, 10(12), pp.6702-6710.
8. Jennum, P., Ibsen, R. and Kjellberg, J. (2019). Morbidity and mortality in children with obstructive sleep apnoea: a controlled national study.
9. Katz, E. and D'Ambrosio, C. (2008). Pathophysiology of Pediatric Obstructive Sleep Apnea. Proceedings of the American Thoracic Society, 5(2), pp.253-262.
10. Kim, A., Keenan, B., Jackson, N., Chan, E., Staley, B., Poptani, H., Torigian, D., Pack, A. and Schwab, R. (2014). Tongue Fat and its Relationship to Obstructive Sleep Apnea. Sleep, 37(10), pp.1639-1648.
11. Kim, S. and Taranto-Montemurro, L. (2019). When do gender differences begin in obstructive sleep apnea patients?. Journal of Thoracic Disease, 11(S9), pp.S1147-S1149.
12. Sheldon, S., Kryger, M., Ferber, R. and Gozal, D. (2014). Principles and Practice of Pediatric Sleep Medicine. 2nd ed. London: Elsevier Health Sciences, pp.411-425.
13. Shen, L., Lin, Z., Lin, X. and Yang, Z. (2018). Risk factors associated with obstructive sleep apnea-hypopnea syndrome in Chinese children: A single center retrospective case-control study. PLOS ONE, 13(9), p.e0203695.
14. Tan, H., Gozal, D. and Kheirandish-Gozal, L. (2016). The Status of Pediatric Obstructive Sleep Apnea in 2015: Progress?. Current Sleep Medicine Reports, 2(1), pp.20-30.
15. Wang, J., Zhao, Y., Yang, W., Shen, T., Xue, P., Yan, X., Chen, D., Qiao, Y., Chen, M., Ren, R., Ren, J., Xu, Y., Zheng, Y., Zou, J. and Tang, X. (2019). Correlations between obstructive sleep apnea and adenotonsillar hypertrophy in children of different weight status. Scientific Reports,  9(1).