Paediatric Snoring, Sleep Disordered Breathing & Obstructive Sleep Apnoea
Table of Contents
Definitions
Snoring: Audible vibrations of the upper airway during sleep. Affects 15-20% of children.
Sleep disordered breathing: Syndrome of upper airway dysfunction during sleep, characterised by snoring and/or increased respiratory effort due to upper airway resistance.
OSA: Repeated episodes of complete airway collapse or partial airway collapse with an associated decrease in oxygen saturation or arousal from sleep. It is the most common sleep-related breathing disorder, prevalent in up to 5% of children.
Aetiology
Sleep apnea is divided into two causes; central or obstructive.
Central
- Due to central nervous system pathology. Decreased airflow due to a neurologically mediated respiratory drive impairment without respiratory effort.
Obstructive (95% of paediatric OSA)
- Decreased airflow due to partial or complete collapse of the upper airway resulting from anatomical obstruction associated with respiratory effort.Snoring: Audible vibrations of the upper airway during sleep. Affects 15-20% of children.
Classification
OSA severity is determined by the Apnoea Hypopnea Index (AHI) and is classified differently compared to adults, with less events indicating higher severity.
- Mild: 1-2*- ≤4.99
- Moderate: 5 – 9.99
- Severe: ≥10
* The lowest value of the Apnoea-Hypopnea Index (AHI) varies across the literature and sleep laboratories.
Epidemiology
OSA affects over 10% of the adult population worldwide (primarily caused by obesity) and 5% of children (most commonly due to adenotonsillar hypertrophy). It is quite common in infants/newborns with a significant reduction over the first few months of life.(1)
The incidence of paediatric OSA peaks between 2 to 8 years of age due to the increased growth of tonsils and adenoids relative to the size of the upper airway in this age group. Risk factors for early-onset OSA include prematurity (up to 9.4% of school-aged children who were born prematurely were also eventually diagnosed with OSA), Down syndrome and African American race. Other causes of OSA at any age include:
- Obesity: up to 50% of overweight or obese children have OSA.
- For every kg/m2 increase in BMI above the 50th percentile, there is a 12% increase in the risk for OSA
- Medical conditions associated with weak muscles or low muscle tone, such as Down syndrome
- Narrow or restricted orthognathic structure (eg. very small jaws or flat faces)
- Chronic allergy
Diagnosis
Signs and Symptoms
Children with OSA have disrupted sleep, which can lead to behavioural issues, including hyperactivity, irritability, or even aggression. Sometimes a child with OSA may only show difficulties with attention, learning or behavioural problems.
Distinguishing between primary snoring and obstructive sleep apnoea can be difficult however proven features on history that increase the likelihood of OSA in a snoring child include;
- Snoring or noisy breathing during sleep present ≥3 nights/week
- Difficulty breathing whilst asleep (including increased effort of breathing, choking, gasping or snorting during sleep) observed by parents
- Parents who report being afraid for their child’s health because of the child’s breathing whilst asleep
- Frequent daytime mouth breathing
- Witnessed obstructive apnoea during sleep
Other symptoms may include restless or sweaty sleep, choking or gasping, nocturnal enuresis, having headaches and/or waking tired in the morning.
Examination
A comprehensive ear, nose, and throat examination includes evaluating height, weight, BMI, syndromic features, and skeletal structure, including the presence of retrognathia, maxillary retrusion, adenoid facies, a narrow high-arched palate, and the size of the tongue and tonsils. Nasal patency is confirmed bilaterally. Depending on the child’s age and tolerance, nasendoscopy may also be performed.
Investigations
The gold standard for diagnosis is nocturnal polysomnography (PSG). However, evaluation with a PSG can be expensive, time-consuming, and resource-limited. Overnight oximetry at home can be used as a tool to provide more information, but it does not replace a PSG in making a diagnosis of OSA. If there is a concern for an underlying cardiopulmonary process, a chest x-ray and ECG are also warranted as additional evaluation.
When to consider referral to paediatric sleep physician for PSG
- Paediatric patient ≤2 years old with clinical features of OSA
- Discordance between history and clinical examination (history suggestive of OSA however no cause for symptoms on examination, e.g. very small tonsils/adenoids without obesity or other risk factors present)
- Paediatric patient with a neurological disorder or genetic syndrome
- Persistent features of OSA despite adenotonsillectomy
Should we treat it?
Paediatric OSA is an independent risk factor for neurocognitive, cardiovascular, and metabolic sequelae and, when untreated, is associated with neurocognitive deficits, behavioural changes, low academic performance, and lower quality of life (QOL).
Treatment
The American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) and American Academy of Paediatrics (AAP) recommend adenotonsillectomy as first-line treatment for OSA in healthy children over two years of age with moderate-severe OSA and adenotonsillar hypertrophy.
Observation
Two large international randomised trials demonstrated that a portion of paediatric patients will normalise their AHI with time and conservative treatment including nasal steroid sprays and leukotriene antagonist therapy. However, there are several issues to consider. In order to validate resolution of AHI multiple PSGs should be performed at each time point, which is impractical and both studies demonstrated that there is poor correlation between quality of life and PSG parameters in children. Untreated paediatric patients with OSA have the potential to remain symptomatic despite a normal AHI with persistent snoring and obstructive symptoms, despite improvements in PSG parameters. Furthermore, children who are obese or have more severe OSA are much more likely to benefit from early intervention with adenotonsillectomy.
Tonsillectomy versus intracapsular tonsillotomy
Traditionally tonsillectomy has been used which completely removes all palatine tonsil tissue whilst intracapsular tonsillotomy (most commonly with Coblation) leaves the lateral aspect of the tonsil capsule intact so that the pharyngeal muscle is not damaged or exposed. There is some evidence in the literature that supports slightly less pain and bleeding with tonsillotomy however there is a higher rate of tonsillar regrowth with a small (approximately 3%) chance of revision surgery required in future. Procedure selection is surgeon dependent.
Persistent OSA following adenotonsillectomy
Persistent sleep disordered breathing and OSA post adenotonsillectomy is seen in up to 20% of children. It is particularly high in those with baseline severe OSA (≥10/h), obesity (50%), underlying medical complexities (chronic cardiopulmonary and neuromuscular disorders) and genetic disorders (50% in Down syndrome). Current international guidelines support a personalised treatment paradigm based on symptoms, relative benefit versus risks and medical comorbidities. All patients treated with adenotonsillectomy should be post operatively evaluated to ensure resolution of symptoms and consider formal PSG if symptoms persist. Typically, patients with persistent features should be referred to sleep trained paediatric ENT surgeons for further evaluation and management, which may include awake flexible nasendoscopy or drug induced sleep endoscopy (DISE).
Lingual Tonsillectomy
Tongue-base obstruction caused by lingual tonsillar hypertrophy (LTH) is a common cause of persistent OSA. LTH is defined as>50% airway obstruction (typically diagnosed with awake flexible nasendoscopy or DISE) and may cause the posterior tongue to prolapse and lead to persistent OSA in up to 85% of affected children. The lingual tonsil is a component of the Waldeyer ring of lymphoid tissue located at the base of the tongue. Hypertrophy can result from lymphoid hyperplasia from prior AT, obesity, and/or laryngopharyngeal reflux.
Supraglottoplasty
Sleep-dependent laryngomalacia is an increasingly recognised cause of persistent OSA and is preferentially diagnosed by DISE demonstrating inspiratory collapse of redundant supra-arytenoidal mucosa. It is treated with supraglottoplasty, performed under general anaesthesia and includes division of shortened aryepiglottic folds and trimming of redundant supra-arytenoidal mucosa
Non-Surgical treatments
International censuses guidelines suggest that children with persistent OSA who are overweight or obese undergo weight loss intervention. Children with specific craniofacial features may be considered candidates for orthodontic treatment, most commonly maxillary expansion. Patients who do not qualify for site-specific upper airway treatment due to neurological conditions or lack of anatomical obstruction, can be considered for treatment with continuous positive airway pressure (CPAP).
Who & when to refer to a paediatric sleep trained ENT surgeon
- All patients with persistent snoring, sleep disordered breathing or witnessed apnoea’s
- Nasal obstruction (ideally after failing trial of medical treatment, eg. intranasal corticosteroid sprays)
- Persistent symptoms post adenotonsillectomy
Who & when to refer to a paediatric sleep trained ENT surgeon
- Snoring is common in childhood but should not be regarded as normal as it is the key symptom of OSA
- OSA has an adverse impact on sleep quality, daytime functioning and cardiovascular health
- Symptoms of OSA should be inquired in any child with enlarged tonsils and/or disturbed sleep
- Adenotonsillectomy should be considered in children ≥2 years with clinical features supporting a diagnosis of OSA and appropriate examination findings
- Coblation tonsillotomy is a new surgical technique with evidence to support slightly decreased bleeding and pain that can be considered in certain cases, but is associated with higher tonsillar regrowth rates
- Persistent OSA post adenotonsillectomy is seen in up to 20% of children with higher rates in obese children or children with severe preoperative OSA
- International paediatric guidelines support formal polysomnogram, DISE and flexible nasendscopy in the evaluation of persistent OSA when required
- In experienced hands lingual tonsillectomy and supraglottoplasty can be highly effective in treatment of persistent OSA post adenotonsillectomy
- Conservative treatments including weight loss, orthodontic procedures and CPAP can be considered in the appropriately selected patients
Can OSA in childhood retard growth
Yes OSA can cause decreased height in paediatric patients. In a 2018 a retrospective study on 745 healthy paediatric patients <18 years with OSA symptoms (and no medical conditions, syndromes or medication that could affect growth) underwent PSG and BMI were evaluated. Obstruction related results, such as AHI, RDI, OA, and hypopnea plus frequent low oxygen saturation had a statistically significant negative relationship with z- score for height. Park DY, Choi JH, Kang SY, Han J, Park HY, Hwang JS, Cho JH, Cho MH, Kim HJ. Correlations between pediatric obstructive sleep apnea and longitudinal growth. Int J Pediatr Otorhinolaryngol. 2018 Mar;106:41-45.
In addition paediatric patients with OSA typically show a growth spurt after adenotonsillectomy as demonstrated in two smaller non randomised studies.
Bar, A. Tarasiuk, Y. Segev, M. Phillip, A. Tal, J. Pediatr. 1999 (135) (1999) 76–80. X.M.Zhang,J.Shi,G.Z.Meng,H.S.Chen,L.N.Zhang,Z.Y.Wang,H.Wu,J.Pediatr. 2015 (166) (2015) e641646–650.
Opinion on vagus nerve stimulator for OSA management
Currently there are various nerve targets for stimulation in the treatment of obstructive sleep apnoea. Currently hypoglossal nerve stimulation is the most common type, most extensive studied and available in the US, Europe and many other parts of the world with different commercial manufactures. Since its approval in 2014 by the US FDA over 50,000 patients in the US have been implanted. The most well known device is Inspire. It works by selectively stimulating branches of the hypoglossal nerve such as the genioglossus which when activated (whilst the patient is asleep) protrude the tongue forward to alleviated retro lingual (base of tongue obstruction). In numerous studies including randomised control trials and long term (5 year follow up) it has been shown to normalise Epworth Sleepiness Scale scores in 80% and significantly reduce AHI by >68% with improvements in oxygen saturation and other sleep parameters. Woodson BT, Strohl KP, Soose RJ, Gillespie MB, Maurer JT, de Vries N, Padhya TA, Badr MS, Lin HS, Vanderveken OM, Mickelson S, Strollo PJ Jr. Upper Airway Stimulation for Obstructive Sleep Apnea: 5-Year Outcomes. Otolaryngol Head Neck Surg. 2018 Jul;159(1):194-202.
It is currently approved by the TGA in Australia but not by Medicare which limits its application to clinical trials – which I have been involved in last year and will be involved in a new hypoglossal nerve stimulation device later this year with a US company. Hypoglossal nerve stimulation has been recently approved by paediatric patients with down syndrome with less than 100 paediatric patients implanted worldwide in the literature. All studies have been retrospective thus far but with evidence of improving QOL, reduction in AHI, improvement in oxygen saturation and parent/care giver satisfaction.
Ansa cervicalis stimulation is the second most commonly studied target for treatment of OSA however it is still in clinical trial stage and not been approved or commercialised for use. It acts to “tension and stiffen” the airway making it less collapsable which improves airway flow. Kent DT, Zealear D, Schwartz AR. Ansa Cervicalis Stimulation: A New Direction in Neurostimulation for OSA. Chest. 2021 Mar;159(3):1212-1221. doi: 10.1016/j.chest.2020.10.010.
Vagal nerve stimulation is currently used for treatment of certain neurological, anti seizure treatment and psychological conditions however has been associated in case reports and meta-analaysis of causing OSA in up to 27%.
Marzec M, Edwards J, Sagher O, Fromes G, Malow BA. Effects of vagus nerve stimulation on sleep-related breathing in epilepsy patients. Epilepsia. 2003;44:930-5.
Oh DM, Johnson J, Shah B, Bhat S, Nuoman R, Ming X. Treatment of vagus nerve stimulator-induced sleep-disordered breathing: a case series. Epilepsy & Behav. 2019;12:100325. doi:10.1016/j.ebr.2019.100325
Is surgery recommended for persistent tonsil stones
Tonsillectomy can be performed in patients with chronic infection/recurrent tonsillitis and persistent tonsil stones. In patients that have persistent tonsil stones surgery can be considered after a trial of observation and lifestyle changes if it is significantly affecting their quality of life or associated with chronic infection. It is important to have a very open conversation with the patients about the risks of surgery balanced against the potential benefit which is less than the indication for OSA and recurrent tonsillitis.
Is GLP-1a useful in OSA in children?
In a 2023 review of clinical trials GLP-1 drugs such as exenatide, semaglutide, and liraglutide were used as the pharmacotherapy option for childhood obesity. However, there is limited evidence as only eight clinical trials were conducted with a pharmacotherapy treatment for childhood obesity. Alorfi NM, Alshehri FS. Usage of Glucagon-Like Peptide-1 for Obesity in Children; Updated Review of Clinicaltrials.gov. J Multidiscip Healthc. 2023 Jul 31;16:2179-2187. doi: 10.2147/JMDH.S419245
Whilst treating obesity can reduce the severity and incidence of OSA in children to my knowledge there has been no studies specifically evaluating if treating obese children that have OSA with a GLP-1a reduces OSA however this may be a future therapy for recalcitrant cases of obesity not responding to diet and exercise.
Currently tirzepatide (Mounjaro) is a combined incretin GLP-1 plus glucose dependent insulinotropic polypeptide (GIP) agonist and has shown the largest degree of weight loss that has been sustained amongst GLP-1a drugs. The TGA has approved tirzepatide for the treatment of overweight and obesity for those with comorbidities, via private prescription. It is currently FDA approved for treatment of OSA in the United States and may be incorporated into international guidelines in future. SURMOUNT OSA was a phase 3 double blinded randomised controlled trial involving 469 non diabetic adults with obesity and OSA separated into those with and without CPAP comparing Mounjaro (tirzepatide) against placebo. It demonstrated amongst adults with moderate-to-severe obstructive sleep apnea and obesity, tirzepatide reduced the AHI by 27.4/hr compared to 4.8/hr placebo (Non CPAP group) and 29.3/hr versus 5.5/hr (CPAP group). Body weight was reduced by 17.7 and 19.6% for Non CPAP and CPAP groups respectively. Reduction in Hypoxic burden, hsCRP concentration, and systolic blood pressure and improved sleep-related patient-reported outcomes was also demonstrated. Malhotra A, Grunstein RR, Fietze I, Weaver TE, Redline S, Azarbarzin A, et al. Tirzepatide for the Treatment of Obstructive Sleep Apnea and Obesity. New England Journal of Medicine. 2024 Oct
Is a mandibular splint useful in OSA in children or adults?
Oral appliance therapy most commonly a Mandibular Advancement Splint/Device (MAS or MAD) helps treat obstructive sleep apnoea (OSA) by repositioning the lower jaw (mandible) forward and downward. This action increases the size of the airway by pulling the tongue forward (genioglossus) and to a lesser extent, the soft palate (palatoglossus and pharyngeal constructor muscles). The increase in the airway size occurs in both the front-to-back (antero-posterior and side-to-side (lateral) directions, with the greatest expansion observed in the lateral dimension in the velopharynx in one study.
The American Academy of Sleep Medicine and the American Academy of Dental Sleep Medicine 2015Click or tap here to enter text.and 2021 NICE guideline recommend that OAT should be offered to ADULT patients with OSA who are unable to tolerate or declined CPAP. OAT should be custom made by a dentist qualified and experienced in dental sleep medicine and who preferably holds a Fellowship of Dental Sleep Medicine postgraduate qualification.
In children due to the nature of deciduous teeth, changing orthodontics with time and long term benefits of rapid maxillary expansion MAS is not typically used in clinical practice. A literature review in 2024 found that the limited number and quality of existing studies require caution when concluding the effectiveness of mandibular advancement and maxillary expansion for OSA. In the future, larger and well-designed randomized controlled trials (RCTs) are needed to provide more robust evidence. Sun, Y., Jia, Y., Wang, S. et al. Effectiveness of mandibular advancement orthodontic appliances with maxillary expansion device in children with obstructive sleep apnea: a systematic review. BMC Oral Health 24, 1303 (2024).
Mandibular distraction osteogenesis and mandibular advancement have been used to treat children with mandibular insufficiency and obstructive sleep apnea (OSA. In a 2018 meta-analysis Meta-analysis demonstrated a reduction in the apnea-hypopnea index (AHI), from a mean ± SD of 41.1 ± 35.8 to 4.5 ± 6.0 events per hour (89.1% decrease). The lowest oxygen saturation (LSAT) in 211 patients increased from a mean ± SD of 76.8 ± 13.0 to 91.1 ± 8.6 (14.3 oxygen saturation point increase) Noller MW, Guilleminault C, Gouveia CJ, Mack D, Neighbors CL, Zaghi S, Camacho M. Mandibular advancement for pediatric obstructive sleep apnea: A systematic review and meta-analysis. J Craniomaxillofac Surg. 2018 Aug;46(8):1296-1302.
