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BIO Magazine - Investigation and management of childhood sleep apnoea Δεκέμβριος 2015
Δεκέμβριος 2015 No38

BIO Health

Investigation and management of childhood sleep apnoea
Investigation and management of childhood sleep apnoea


Obstructive sleep apnoea syndrome (OSAS) is an increasingly-recognised clinical entity affecting up to 5.7% of children, which, if left untreated, is associated with adverse effects on growth and development including deleterious cognitive and behavioural outcomes. Evidence exists also that untreated OSAS impacts on cardiovascular risk. Close attention should be paid to assessment and investigation of this relatively common condition, instigating early and appropriate treatment to children with OSAS. First-line treatment in younger children is adenotonsillectomy, although other treatment options available include continuous positive airways pressure (CPAP), anti-inflammatory therapies (nasal corticosteroids and anti-leukotrienes), airway adjuncts and orthodontic appliances.


Corresponding author: Dr Don Urquhart MD, MRCPCH, Consultant in Paediatric Respiratory and Sleep Medicine,
Royal Hospital for Sick Children, 9 Sciennes Road, Edinburgh, EH9 1LF,
tel: +441315360634, fax: +441315360669,
e-mail: don.urquhart@nhslothian.scot.nhs.uk

Sleep-disordered breathing in children incorporates disorders of breathing that relate to airway patency (obstructive sleep apnoea syndrome) and also conditions which affect respiratory drive (central sleep disorders) or cause hypoventilation, either as a direct central effect or secondary to peripheral muscle weakness. This review aims to describe the aetiology, presentation and sequelae of OSAS, as well as reviewing the diagnostic tests available. Central apnoeas and central sleep-disordered breathing will be briefly reviewed.

Events during sleep are scored using the American Academy of Sleep Medicine (AASM) manual for the scoring of sleep and associated events1.

Figure 1: Obstructive events during sleep measured using limited-channel polysomnography (Source: Sleep Laboratory, Royal Hospital for Sick Children, Edinburgh).
SpO2: Arterial oxygen saturations measured by pulse oximetry, Flow Th: Airflow measured by thermistor, RIP Thorax: Thoracic respiratory effort measured by inductance plethysmography, RIP Abdomen: Abdominal respiratory effort measured by inductance plethysmography.

A central apnoea is an event associated with absent inspiratory effort and an absence (or >90% reduction) of airflow lasting for > 20 seconds duration, or lasting for >2 missed breaths and associated with a physiological consequence (arousal, awakening, a >3% fall in SpO2 or, in infants, bradycardia)1,2. A central hypopnoea is scored when a 30% reduction in airflow associated with concurrently reduced inspiratory effort lasting >2 missed breaths occurs in association with a physiological consequence1,2. An example of a sleep study demonstrating central events is shown in Figure 2.

Figure 2: Central events during sleep measured using limited-channel polysomnography (Source: Sleep Laboratory, Royal Hospital for Sick Children, Edinburgh).
SpO2 : Arterial oxygen saturations measured by pulse oximetry, Flow Th: Airflow measured by thermistor, RIP Thorax: Thoracic respiratory effort measured by inductance plethysmography, RIP Abdomen: Abdominal respiratory effort measured by inductance plethysmography.

Obstructive sleep apnoea syndrome (OSAS) is a phenomenon of repeated, episodic reduction or cessation of airflow (hypopnoea/apnoea) as a result of upper airways obstruction. Respiratory effort is preserved or increased at times of apnoea, as the subject attempts to overcome obstruction. OSAS may occur as a result of enlarged tonsils and adenoids3,be related to airway(s) anatomy for example in those with Pierre-Robin sequence4, airway(s) tone as in children with muscular weakness5, or exogenous tissue around the airways in those with obesity6.

Presentation of OSAS

Even with those caveats, history-taking is the cornerstone of diagnosis as in any medical condition. Questions on sleep pattern at night are important, including enquiring about snoring, work of breathing (restlessness, sweatiness, and faltering growth), and mouth breathing (whether child sleeps with mouth open, and whether thirsty in the mornings) and the presence of apnoea. The question of whether a child stops breathing is a poor discriminator of apnoea, and is better phrased by asking whether a child sounds ‘strangled’ during sleep, or whether a period is noted where the child’s breathing goes quiet that is then overcome by a gasp. Those with OSAS are more likely than primary snorers to have been witnessed to have an apnoea (p=0.01), to have been noticed to be struggling to breathe (p16.

Examination findings are directed at examining the tonsils and grading their size (0-4) in accordance with the standardised tonsillar hypertrophy grading scale proposed by Brodsky18, as well as assessing the nose for mucosal inflammation, turbinate size, septal position, presence of polyps and nasal airflow. The nose may be directly auscultated with the stethoscope or a disposable mirror used to see whether it mists up in association with nasal exhalation19. Adenoid size may be assessed directly by either nasoendoscopy or by transoral mirror examination20. Mid-face hypoplasia or the “adenoidal facies” may be apparent in chronic OSAS. Pectus excavatum secondary to chronic sternal recession is rarely seen nowadays.

Investigation of OSAS in children


The undertaking of PSG requires resources in terms of time and also personnel to supervise the study. Attempts have been made to do snap-shot PSG studies during daytime sleeps, or so-called ‘nap studies’. Whilst these have an excellent positive predictive value (100%) in diagnosing OSAS, their negative predictive value is poor – 20%21. OSAS is likely to be worse during rapid-eye movement (REM) sleep, as airway tone falls in REM making obstruction manifest. REM sleep occurs later in the night – i.e. OSAS worsens as the night goes on, and may be missed in a short daytime nap.

Currently there are no universally accepted guidelines as to when children’s OSA is sufficiently severe as to warrant treatment. An AHI >1 is regarded as abnormal with treatment recommended for any child with an AHI >526. Severe childhood OSAS is defined as having an AHI >10 events per hour27. How to proceed is less clear in children with AHIs between 1 and 526. Table 1 illustrates the correlation of AHI and OSAS severity.

Many centres (our own included) undertake cardiorespiratory sleep studies with video camera, effort bands, airflow measures, heart rate and SpO2 +/- tcCO2 monitoring. This allows confident detection of apnoea, delineation between central and obstructive events, and quantification of the degree of ensuing hypoxia. An AHI can be generated from such studies, enabling one to embark on an appropriate treatment course.

Oximetry as a single-channel recording

Figure 3: Overnight oximetry findings in a child with OSAS (Source: Sleep Laboratory, Royal Hospital for Sick Children, Edinburgh).
SpO2 : Arterial oxygen saturations measured by pulse oximetry.

The utility of oximetry alone in the detection of OSA has been demonstrated to have limitations. Brouillette and colleagues showed that whilst oximetry is highly specific (98%), it has a sensitivity of only 43%29. The positive predictive value of an abnormal oximetry for diagnosing OSA was 97%, suggesting 3% cases where oximetry is abnormal are due to central apnoea. The negative predictive value (value of a negative oximetry in excluding OSA) was only 47%29, roughly the equivalent of tossing a coin.

Clinical implications of OSAS

It is during REM sleep that memory consolidation is postulated to occur31,such that the sleep fragmentation may affect cognition; whilst Growth Hormone is produced in slow wave sleep32 and its’ secretion may be interrupted by fragmented sleep. The increase in work of breathing to overcome obstruction and its’ consequent calorie demand are a further mechanism by which OSA impacts growth.

Known risk factors for cardiovascular disease in adulthood include hypertension and inflammation. The effects of desaturations and arousals are known to stimulate the sympathetic nervous system with an adrenaline surge and a transient rise in blood pressure. This is a frequent and oft-repeated insult in those with OSA and over time acts as a promoter of systemic hypertension, such that OSA has become an increasingly-recognised cause of adult hypertension35.Furthermore, OSA is pro-inflammatory with elevations in C reactive protein (CRP) reported in both adults36 and children37,with OSA, whilst an animal model of intermittent hypoxia and hypercapnia (mimicking OSA) resulted in increased levels of interleukin-6 (IL-6), a precursor of CRP production38. Levels of CRP are reported to fall with successful treatment of OSAS36,39. CRP is used by the American Heart Association to stratify risk for ischaemic heart disease40, and has also been shown to correlate with measures of radial artery stiffness and carotid artery intimal thickness in children41.In addition, endothelial dysfunction has been demonstrated to be present in a childhood OSAS population14,42 Thus, it seems plausible that childhood OSAS is a risk factor for later cardiovascular risk. In extreme cases of OSAS, right heart strain and development of cor pulmonale have been known to occur43.

Treatment of childhood OSAS


The benefit of AT on ameliorating obstruction is clear with consequential benefits on growth, behaviour and school performance7,33. For a some children however, obstruction may persist or recur and careful counselling of parents or carers is required pre-operatively as in some patients other means to alleviate airway obstruction may need to be considered. Such treatments include continuous positive airways pressure (CPAP) therapy, anti-inflammatory therapies, as well as airway adjuncts such as nasopharyngeal airways or orthodontic appliances.

The rationale for CPAP is that one applies a continuous positive airways pressure (CPAP) via a face-mask or nasal mask during sleep47, pushing upper airway tissues apart to splint the airway open, allowing relief of obstruction, whilst maintaining normal gas exchange and preserving sleep quality. CPAP is instituted in hospital with a team of nurses, play therapists, medical staff and of course parents involved; and sleep studies are undertaken to titrate CPAP pressures to the patients’ needs.

Anti-inflammatory treatments

Airway adjuncts

Orthodontic appliances, such as mandibular advancement splints, have also been advocated in some centres as a means of countering the effects of skeletal dysmorphology on airway anatomy.54

There is some evidence supporting rapid maxillary advancement surgery on having benefit on both signs and symptoms of OSASand also AHI55-57 in childhood populations. Tracheostomy, whilst effective, is considered a last resort because of its associated significant morbidity.

Central apnoeas represent absences of airflow that are accompanied by an absence of respiratory effort. Infrequent central apnoeas are found in normal children23,24,58-60, in particular following a sigh58.There are some cases where the number of central apnoeas and/or the gravity of associated desaturations are felt to be pathological. Such patterns may be related to immaturity of respiratory control and are associated with prematurity61 as well as certain medical conditions, such as Prader-Willi syndrome62. Finally, some children will have central apnoeas as part of a central hypoventilation disorder, causes for which may be inherited (Congenital Central hypoventilation Syndrome)63 or acquired (for example as a consequence of an Arnold-Chiari malformation64,65, brain tumour66, or spinal injury67).

In cases of central apnoea, polsomnography with capnometry is recommended68. Measures of flow, effort and SpO2 allow the number and the effect of central apnoeas to be quantified. In addition, simultaneous monitoring of CO2 (via transcutaneous or end-tidal methods) allows for assessment of hypoventilation in those with central sleep-disordered breathing.

A variety of treatments including pharmacological therapies (methylxanthines, acetazolamide), oxygen and ventilator support may be used in the treatment of childhood central apnoea. Each of these, is briefly discussed.




Figure 4: a) Response of repeated central apnoeas to oxygen treatment, b) In air, c) In oxygen at 0.25 L/minute (Source: Sleep
Laboratory, Royal Hospital for Sick Children, Edinburgh). ECG: Electrocardiogram, SpO2: Arterial oxygen saturations measured by pulse oximetry, Flow Th: Airflow measured by thermistor, RIP Thorax: Thoracic respiratory effort measured by inductance plethysmography, RIP Abdomen: Abdominal respiratory effort measured by inductance plethysmography.

In some cases of central sleep-disordered breathing, apnoea is accompanied by hypoventilation. Such cases require the institution of bi-level ventilatory support with a back-up rate in order to restore normal gas exchange during sleep. As discussed above, causes may be congenital or acquired. Figure 5 (a,b) illustrates a sleep study undertaken on a boy who had undergone cranial irradiation following resection of a posterior fossa tumour. Gas exchange was normalised following the institution of non-invasive bi-level ventilation.

Figure 5: Illustration of central hypoventilation in association with an intracerebral tumour a) Prior to commencing ventilatory support, b) On ventilation (Source: Sleep Laboratory, Royal Hospital for Sick Children, Edinburgh). ECG: Electrocardiogram,
SpO2: Arterial oxygen saturations measured by pulse oximetry, Flow Th: Airflow measured by thermistor, RIP Thorax: Thoracic respiratory effort measured by inductance plethysmography, RIP Abdomen: Abdominal respiratory effort measured by inductance plethysmography.

The short-term effects of undetected sleep-disordered breathing in children include detrimental effects on school performance, behaviour, and cognition. Effects in later life affecting cardiovascular risk are also suggested. The stakes are high, as it is the future health and behaviour of our children that we are dealing with. Successful treatments are readily available. Being mindful of sleep apnoea, taking an appropriate history, and undertaking to investigate and treat appropriately, will all serve to minimise the disease burden of this important group of conditions.

There are no conflicts of interest to declare.

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