SYMPOSIUM: RESPIRATORY
Sleep apnoea in children
Donald S Urquhart
Nicola Starritt
Abstract
Obstructive sleep apnoea (OSA) is an increasingly-recognized clinical
entity affecting 3e5% young children, which, if left untreated is associ-
ated with adverse effects on growth and development including adverse
cognitive and behavioural outcomes. Evidence also exists to suggest that
untreated OSA will impact on later cardiovascular risk. Close attention
should be paid to assessing and investigating this relatively common
condition. This review deals with the presentation, investigation,
management, and sequelae of OSA, as well as providing an overview of
the presentation, investigation, management of central apnoea in
children.
Keywords adenotonsillectomy; cognition; obstructive sleep apnoea
Introduction
OSA 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. OSA may
occur as a result of enlarged tonsils and adenoids, be related to
airway(s) anatomy for example in those with Pierre-Robin
sequence, airway(s) tone as in children with muscular weakness,
or exogenous tissue around the airways in those with obesity.
OSA is a common condition, which affects up to 3% of
preschool children, and one which carries significant morbidity
with regard to a deleterious effect on cognition and development,
growth, and possibly later cardiovascular risk.
This review aims to describe the aetiology, presentation and
sequelae of OSA, as well as reviewing the diagnostic tests
available. Central apnoeas and central sleep-disordered breathing
will be briefly reviewed.
Clinical implications of OSA
The sequelae of each obstructive event are such that a conse-
quence of the event, namely a desaturation, an arousal or an
awakening may occur. Repeated arousals and awakenings are
associated with sleep fragmentation which it is thought may be
a mechanism by which OSA is associated with delayed growth
and development.
Donald S Urquhart BScMedSci (Hons) MB ChB MSc MD MRCPCH is Consultant in
Paediatric Respiratory and Sleep Medicine at the Royal Hospital for Sick
Children, Edinburgh, Scotland, UK. Conflict of interest. none.
Nicola Starritt BScMedSci (Hons) MB ChB MD FRCS (ORL-HNS) is Consultant
Paediatric Otolaryngologist at the Royal Hospital for Sick Children,
Edinburgh, Scotland, UK. Conflict of interest. none.
PAEDIATRICS AND CHILD HEALTH 23:7
It is during REM sleep that memory consolidation is postu-
lated to occur, such that the sleep fragmentation may affect
cognition; whilst Growth Hormone is produced in slow wave
sleep 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.
It has been shown across a number of studies that childhood
OSA is associated with a negative effect on cognition and
behaviour, and that relief of obstruction is accompanied by
improvements in learning. A 1998 study by Gozal analysed the
lowest 10% of US schoolchildren with regard to academic
performance. He reported that abnormalities in overnight gas
exchange (presumed OSA) were found in 18% of the cohort, and
treatment (adenotonsillectomy) was suggested to the families of
these children. Less than half of those with presumed OSA
underwent adenotonsillectomy, but those that did showed
significant improvement in school grades a year later, whilst those
who had no surgery and those presumed not to have OSA showed
no change. There are several other studies highlighting the dele-
terious relationship of OSA and cognitive performance, with IQ
suggested to be up to 10 points lower than the healthy population
even in those with mild OSA. Furthermore, increased rates of
inattention and hyperactivity and difficulties with peer interaction
and emotional lability are also reported in children with OSA.
The effects of desaturations and arousals are known to stim-
ulate 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-recognized cause of adult hypertension.
Furthermore, OSA is pro-inflammatory with elevations in C
reactive protein (CRP) reported in both adults and children 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 production. CRP is
a factor used by the American Heart Association to stratify risk
for ischaemic heart disease, and has also been shown to correlate
with measures of radial artery stiffness and carotid artery intimal
thickness in children. It seems plausible therefore, that childhood
OSA may be a risk factor for later cardiovascular risk. In extreme
cases of OSA, right heart strain and development of cor pulmo-
nale are known to occur.
Presentation of OSA
Although it is estimated that up to 1 in 7 children snore, numbers
with OSA are estimated at only 3%. The role of history-taking as
a means of predicting those with OSA is limited at discriminating
those with OSA from those with primary snoring, with recent
work on the Paediatric Sleep Questionnaire concluding that the
questionnaire can predict sleep study results ‘to an extent that is
useful for research, but not reliable enough for most individual
patients.’ Even with those caveats, history-taking is the corner-
stone of diagnosis as in any medical condition and questions that
should be asked are detailed below (Table 1).
Some questions appear to be more discriminatory than
others; for example reports from parents of primary snorers and
those with OSA found no significant differences with regard to
307 Ó 2012 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: RESPIRATORY
History-taking in the child with suspected OSA
Symptom Comments on history-taking
Snoring
Increased work Restlessness
of breathing Exophoria (Sweatiness)
Faltering growth
Stertorous breathing by day in severe cases
Mouth ‘Does your child breathe through their mouth?’
breathing ‘Is your child thirsty in the mornings?’
Apnoea ‘Does your child’s breathing go quiet and
then he/she gasps?’
‘Does your child sound “strangled” during
sleep?’ (The question: ‘Does your child stop
breathing?’ is a poor discriminator of OSA
as respiratory effort is preserved during
an apnoea.)
Daytime Concentration difficulties
functioning Behaviour problems
(Somnolence)
Children with OSA often manifest with poor
concentration and behaviour problems
Adults with OSA fall asleep during the day
Any Respiratory, cardiac, neuromuscular disease
co-morbidities? Genetic/metabolic syndromes
Clinical obesity (BMI > 97th centile)
Co-morbidities matter
Table 1
excessive daytime sleepiness or snoring history. Whilst an adult
with OSA is likely to be sleepy during the day, children are more
likely to be hyperactive, exhibiting concentration and behaviour
problems. Those with OSA were, however, more likely than
primary snorers to have been witnessed to have an apnoea (74%
vs 46%, p ¼ 0.01), to have been noticed to be struggling to
breathe (89% vs 58%, p less than 0.01), to have been shaken by
parents in order to restart breathing (60% vs 31%, p ¼ 0.01) or
to have daytime mouth breathing (95% vs 61%, p less than
0.05).
Examination findings are directed at examining the tonsils
and grading their size (0e4) in accordance with the standardized
Brodsky tonsillar hypertrophy grading scale, as well as assessing
the nose for mucosal inflammation, turbinate size, septal posi-
tion, 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 exha-
lation. Adenoid size may be assessed directly by either nasen-
doscopy or by transoral mirror examination. Mid-face hypoplasia
or the “adenoidal facies” may be apparent in chronic OSA. Pectus
excavatum secondary to chronic sternal recession is rarely seen
nowadays.
Another important aspect of examination is to assess for co-
morbidities (obesity, Down syndrome, cleft palate, neuromus-
cular disease, etc.) and to formally plot growth. Growth is
important to measure as OSA may be a cause of faltering growth,
whilst obesity is a clear precipitant for OSA.
PAEDIATRICS AND CHILD HEALTH 23:7
Investigation of OSA in children
A variety of modalities exist that may help to make the diagnosis
of OSA.
Polysomnography
The internationally-recognized gold-standard investigation is pol-
ysomnography (PSG). A PSG utilizes electroencephalogram (EEG),
electrooculogram (EOG), and electromyogram (EMG) leads used to
distinguish sleep from wake, and to facilitate sleep staging. In
addition, arterial oxygen saturations measured by pulse oximetry
(SpO2) and heart rate are measured, along with airflow (via nasal
cannulae or thermistor) which allows detection of apnoea and/or
hypopnoea, and respiratory effort which is quantified by induc-
tance plethysmography measured via thoracic and abdominal
bands. Thus obstructive apnoea (effort maintained/increased) can
be distinguished from central apnoea (cessation of both effort and
airflow). An example of OSA detection on PSG is shown in Figure 1.
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 nap studies have an excellent positive predictive
value (100%) for OSA, their negative predictive value is poor e
20%. OSA 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 e i.e. OSA worsens as the night
goes on, and may be missed in a short daytime nap.
Paucisomnography (limited channel recordings)
Many centres (our own included) undertake cardiorespiratory
sleep studies with video camera, effort bands, airflow measures,
heart rate and SpO2 monitoring. This allows confident detection
of apnoea, delineation between central and obstructive events,
and quantification of the degree of ensuing hypoxia. Sleep stage
and the amount of sleep fragmentation can only be speculated
upon, unless a full PSG is performed. Cardiorespiratory studies
may be undertaken at home or in hospital. An example of OSA
detection on a cardiorespiratory study is illustrated in Figure 2.
Oximetry as a single-channel recording
As alluded to above, OSA is worst during REM sleep, as airway
tone is reduced in REM which promotes obstruction. Therefore,
there may be periods of sleep where airflow and gas exchange
are relatively stable, along with periods (REM) where obstruction
is at its’ worst. The SpO2 trace from the overnight hypnogram of
the study shown below (Figure 3) illustrates how an oximetry
may appear in a child with OSA.
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%. 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. Oximetry’s negative predictive
value (i.e. the value of a negative oximetry in excluding OSA) was
only 47%, roughly the equivalent of tossing a coin.
Pulse transit time
The pulse transit time (PTT) is quantified as the time taken for the R-
wave of the ECG to reach the photoplethysmographic pulse at the
finger. The PTT is inversely related to arterial wall stiffness, such
308 Ó 2012 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: RESPIRATORY
Figure 1 Detection of obstructive events during sleep using polysomnography.
that an increase in blood pressure (BP) results in a decrease in PTT.
Changes in PTT have been suggested as a measure of arousal e an
obstructive event will lead to an arousal, which causes sympathetic
nervous system activation, leading to an increase in blood pressure
and consequent reduction in PTT. The PTT arousal index (PTTAI)
has been shown to have good correlation with apnoea/hypopnea
index (AHI) measured by PSG, though the utility of PTTAI for
diagnosing those with mild OSA is limited and does not significantly
outperform pulse oximetry.
Summary
Clearly various diagnostic tests are available for the diagnosis of
obstructive sleep apnoea. In our centre, a cardiorespiratory
limited-channel study is used as it provides a measure of flow (to
allow detection of apnoea and hypopnoea), as well as a measure
of effort to allow discrimination of obstructive from central
events. Such a diagnostic modality cannot however quantify
sleep fragmentation or degree of sleep disturbance.
Treatment of childhood OSA
Adenotonsillectomy
Adenotonsillectomy (AT) remains the first line of treatment for OSA
in children. Since OSA results from the upper airway components’
PAEDIATRICS AND CHILD HEALTH 23:7
relative size and structure rather than the tonsils’ and adenoids’
absolute size, both tonsils and adenoids should be removed.
Studies have shown significant improvement in obstruction on
follow-up sleep studies, as well as improvements in school
performance, growth and behaviour following surgical interven-
tion. Success rates of surgery are commonly quoted at around 80%.
However, recent work suggests that this may be an overstatement
of benefit. A multicentre review of 578 children who underwent AT
for OSA reported that although undoubted improvement was noted
(apnoeic and hypopnoeic events falling from 18 per hour pre-
surgery to 4 per hour after AT), complete resolution of OSA (less
than1 event per hour) was achieved in only 27%.
The prevalence of OSA is higher, and outcomes of surgery are
poorer, in syndromic children and those with craniofacial and
neuromuscular disorders. For example, over 50% of children
with Down’s syndrome have OSA. This is a result of multiple-
level airway pathology including midfacial and mandibular
hypoplasia, glossoptosis, small upper airway, and generalized
hypotonia. Obstructive symptoms can be improved with surgery
but success rates are lower.
Children who undergo adenotonsillectomy for OSA have the
lowest risk of post-operative haemorrhage (0.6%). However,
they have an increased risk of significant respiratory compli
309 Ó 2012 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: RESPIRATORY

Figure 2 Detection of obstructive events during sleep using a limited channel cardiorespiratory recording.

Figure 3 Oximetry findings in a child with OSA.

Figure 4 Detection of a central apnoeic event on a cardiorespiratory sleep study.

PAEDIATRICS AND CHILD HEALTH 23:7 310 Ó 2012 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: RESPIRATORY

cations; 1e2% in otherwise well children, rising to 20e25% in
those with high levels of co-morbidities. Recent guidelines
recommend that those children with severe OSA or significant
medical conditions should be managed in a children’s hospital
with access to PICU facilities.
As at least 20% of children will have residual sleep-disordered
breathing following surgery, follow-up is recommended. In these
children 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.
Other surgical options
Tracheostomy is an effective treatment for life-threatening
airway obstruction but is associated with significant morbidity.
Complex craniofacial procedures such as midfacial distraction
are rarely used in the treatment of OSA. Endoscopic nasal

Figure 5 (a) Response of repeated central apnoeas to oxygen treatment. (b) In air. (c) In oxygen at 0.25 litre/minute.

PAEDIATRICS AND CHILD HEALTH 23:7 311 Ó 2012 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: RESPIRATORY

polypectomy and septoplasty can improve nasal airflow.
However, nasal polyps are rare in children and septal surgery is
usually deferred until over the age of sixteen as it can have
a detrimental effect on nasal growth. Tongue reduction surgery
may improve upper airways obstruction associated with macro-
glossia e.g. BeckwitheWiedemann syndrome.
Continuous positive airways pressure (CPAP)
CPAP avoids the need for a tracheostomy in those children who
have ongoing upper airways obstruction after adenotonsillec-
tomy. Continuous positive airways pressure (CPAP) is applied
via a face-mask or nasal mask during sleep, pushing upper
airway tissues apart and ‘splinting’ the airways open to allow
relief of obstruction with maintenance of normal gas exchange
and preservation of sleep quality.
Anti-inflammatory medication
Topical nasal steroids and the leukotriene-receptor antagonist,
Montelukast, may be useful for the treatment of mild OSA or
residual sleep-disordered breathing following adenotonsillec-
tomy. Montelukast has been demonstrated to significantly reduce
the size of adenoids and both treatments have resulted in
improved breathing in children with OSA. Systemic steroids are
not effective in the treatment of paediatric OSA.

Figure 6 Illustration of central hypoventilation in association with an intracerebral tumour. (a) Prior to commencing ventilatory support. (b) On ventilation.

PAEDIATRICS AND CHILD HEALTH 23:7 312 Ó 2012 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: RESPIRATORY
Airway adjuncts
Nasopharyngeal airways can be effective in infants with Pierre-Robin
sequence and those children with hypotonia. Orthodontic appli-
ances, such as mandibular repositioning devices, are commonly
used in the treatment of OSA in adults, but less so in children.
However, some centres advocate them as a means of countering the
effects of skeletal dysmorphology on airway anatomy.
Central apnoea in children
Central apnoeas represent absences of airflow that are accompa-
nied an absence of respiratory effort. Infrequent central apnoeas are
found in normal children, in particular following a sigh. 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 asso-
ciated with prematurity as well as certain medical conditions such
as PradereWilli syndrome. Finally, some children will have central
apnoeas as part of a central hypoventilation disorder, causes for
which may be inherited (Congenital Central hypoventilation
Syndrome) or acquired (for example as a consequence of an Arnold
eChiari malformation, brain tumour, or spinal injury).
Investigation of central apnoeas in children
A sleep study including measures of flow, effort and SpO2 allows
one to quantify the number and the effect of central apnoeas in
children (Figure 4). In addition, simultaneous monitoring of CO2
(either via a transcutaneous or an end-tidal CO2 monitor) should
be undertaken to assess for the presence of hypoventilation in
those with central sleep-disordered breathing.
Treatment of central apnoeas in children
A variety of treatments including pharmacological therapies
(methylxanthines, acetazolamide), oxygen and ventilator
support may be used in the treatment of childhood central
apnoea. These are each briefly discussed.
Methylxanthines
Methylxanthines (Caffeine and Theophyllines) have been used
mainly for treatment of central apnoeas in premature infants. A
recent meta-analysis spanning five trials and a total of 192 babies
reported a reduction in apnoeas as well as a reduced need for
ventilation in the first week of life. The use of these agents has
been extrapolated to older children with central apnoeas, though
little evidence other than a small number of reported cases exists
to support this strategy.
Acetazolamide
There is some evidence for the use of Acetazolamide as a treat-
ment for central apnoea. Acetazolamide is a carbonic anhydrase
inhibitor which blocks reabsorption of bicarbonate in the prox-
imal tubule. It causes a metabolic acidosis, and it is this change
in pH which stimulates ventilation. Thus it is reported that the
hypercapnic ventilatory response to CO2 is left-shifted i.e.
ventilation is stimulated at a lower CO2 level.
Oxygen
It is known that periodic breathing can be induced under hypoxic
conditions in babies and also in adults whilst oxygen therapy in
PAEDIATRICS AND CHILD HEALTH 23:7
babies has been shown to lead to abolition of periodic breathing
and central apnoea numbers. Figure 5 shows a split night sleep
study of a child with idiopathic central sleep-disordered breathing
in whom a good response to oxygen treatment was observed.
Ventilation
In some cases of central sleep-disordered breathing, apnoea is
accompanied by hypoventilation. Such cases require the insti-
tution of bi-level ventilatory support with a back-up rate in order
to restore normal gas exchange during sleep. Figure 6 illustrates
a sleep study undertaken on a boy who had undergone cranial
irradiation following resection of a posterior fossa tumour. Gas
exchange was normalized following the institution of non-
invasive bi-level ventilation.
Conclusion
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 cardio-
vascular 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 minimize the
disease burden of this important group of conditions. A
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Practice points
C Untreated obstructive sleep apnoea (OSA) is associated with
cognitive deficit
C Untreated OSA may be related to later cardiovascular risk
C OSA is more common in those with co-morbities including
Down Syndrome and craniofacial disorders
C A sleep study is needed to confidently rule in/rule out OSA
C The mainstay of treatment for OSA is adenotonsillectomy and
this leads to improvement in the majority of cases
314 Ó 2012 Elsevier Ltd. All rights reserved.