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Comorbid respiratory disorders in children
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studies assessing the benefits of interventions that aim to improve sleep duration and
sleep quality.
Interstitial lung disease
The term interstitial lung disease (ILD) covers a wide range of rare heterogeneous
disorders that involve the lung interstitium and the alveolar structure. Although they
share a common basis (abnormalities of the lung parenchyma), children’s interstitial
and diuse lung disease (chILD) diers from adult ILD. Several studies have shown
that adult patients with ILD complain of poor sleep quality and exhibit abnormal
sleep architecture, increased sleep fragmentation and SDB on PSG. OSA is particularly
common, especially in adults with idiopathic pulmonary fibrosis (IPF).
Data on sleep in chILD are scarce. A recent study analysing the PSG data of 20
children with dierent types of chILD showed that the median obstructive AHI (OAHI)
was normal at 0 events·h−1, with >4 events·h−1 being observed in two young adults
(Abdel-Latif Thomasson et al., 2021). The median total sleep time, sleep eciency,
% of wake aer sleep onset, and sleep stages were moderately disturbed. Thus, as
opposed to adults, OSA seems uncommon in children with chILD. However, children
with chILD may present nocturnal hypoxaemia, which can require O2 therapy; the
eects of nocturnal O2 therapy on sleep quality and daytime functioning are unclear.
Bronchopulmonary dysplasia
Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants and
represents the most common late morbidity of preterm birth. Studies evaluating sleep
in infants or children with BDP are scarce.
A recent study analysed the indications and results of respiratory polygraphy (PG) in
14 infants with BPD at a mean age of 26±19 months (De Pieri et al., 2022). Five
patients underwent PG to assess the need for long-term respiratory support; three
of these patients commenced CPAP, while two were weaned from their support. Four
patients underwent PG for suspicion of OSA; one commenced CPAP. Central apnoea
syndrome was confirmed in two patients; one commenced NIV. In two patients, PG
allowed safe tracheostomy decannulation.
A retrospective study used PSG in 140 children at a mean age of 1.3 years, with 58%
of patients still on supplemental O2 (Ortiz et al., 2017). The authors found an elevated
respiratory disturbance index of >2 in 82% of patients, with a median value of 7. An
improvement in the respiratory disturbance index, the central apnea index and the
S
nadir was observed with increasing age.
aO
2
Infants with BPD may thus present various sleep problems and indications for a sleep
study, possibly leading to important individualised therapeutic decisions.
Further reading
• Abdel-Latif Thomasson D, et al. (2021). Sleep in children and young adults with interstitial and
diuse lung disease. Sleep Med; 80: 23–29.
• Castro-Rodriguez JA, et al. (2017). Relation between asthma and sleep disordered breathing in
children: is the association causal? Paediatr Respir Rev; 22: 72–75.
• De Pieri C, et al. (2022). Respiratory polygraphy in subjects with bronchopulmonary dysplasia:
a retrospective study. Minerva Pediatr; 74: 1–6.
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ERS Handbook: Respiratory Sleep Medicine
Comorbid respiratory disorders in children
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• Fauroux B, et al. (2021). Sleep in children and young adults with cystic fibrosis. Paediatr Respir
Rev; in press [https://doi.org/10.1016/j.prrv.2021.09.006].
• Liu J, et al. (2020). The association between allergic rhinitis and sleep: a systematic review and
meta-analysis of observational studies. PLoS One; 15: e0228533.
• Ortiz LE, et al. (2017). Sleep disordered breathing in bronchopulmonary dysplasia. Pediatr
Pulmonol; 52: 1583–1591.
• Sánchez T, et al. (2016). Sleep-disordered breathing in children with asthma: a systematic
review on the impact of treatment. J Asthma Allergy; 9: 83–91.
• Wang R, et al. (2022). Asthma and obstructive sleep apnea in adults and children – an up-to-
date review. Sleep Med Rev; 61: 101564.
Acknowledgement
This is an update of the ERS Handbook of Respiratory Sleep Medicine first edition chapter ‘Comorbid
respiratory disorders in children’, by Anita K. Simonds.
385ERS Handbook: Respiratory Sleep Medicine
Clinical assessment and
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diagnostic techniques
Maria Pia Villa and Stijn Verhulst
Clinical assessment
Sleep history and clinical assessment of an infant
Sleep diculties during infancy (1–12 months of age) are amongst the most
prevalent problems seen by paediatricians, and present as sleep initiation and sleep
maintenance disorders. Insomnia during infancy can be subdivided in two main
categories: behavioral insomnia and insomnia relating to disease.
Behavioural insomnia commonly occurs in 20–30% of infants. If le untreated, bedtime
problems and night awakenings can result in behavioural, emotional and learning
diculties, persisting into the preschool and school-aged years. Paediatric insomnia
represents a complex combination of biological, circadian, neurodevelopmental,
environmental and behavioural variables. History-taking should focus on the infant’s
sleeping environment, bedtime routines and parental expectations.
Insomnia due to a medical condition is mainly caused by SDB, infant colic, otitis and
gastrointestinal problems which may be a manifestation of gastro-oesophageal reflux
(GOR), an allergy to cow’s milk or lactose intolerance. Information about sleeping
arrangements – whether the baby sleeps in the parent’s room, in the parent’s bed
Key points
• Insomnia during infancy can be classified as: behavioural insomnia and
insomnia that is related to a specific medical condition.
• A BRUE is a frightening and unexpected change in an infant’s breathing
behaviour, requiring careful evaluation.
• PSG is indicated when OSAS or congenital central alveolar hypoventilation
syndrome are suspected.
• On physical examination, signs commonly associated with SDB, such as
‘adenoid facies’, may result from oral breathing due to enlarged adenoids.
• The gold standard for diagnosis of paediatric OSA is in-hospital PSG. There are
separate scoring rules and cut-os for children.
• Alternative diagnostic tools can be used but specific advantages and
disadvantages of these techniques should be taken into account.
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or in a crib in a separate room – the baby’s position while sleeping (on their back,
side or belly) and environmental tobacco smoke exposure are very important. The
bedtime routine should be investigated to understand whether good sleep hygiene
is present. Is it crucial to know the sleep–wake pattern of the baby; diculty falling
asleep, and frequent/prolonged nighttime awakenings should be reported by caregivers. Physical examination should include a general impression of the baby,
noting any dysmorphic features or obvious malformations. Height, weight and head
circumference measurements should be reported on appropriate growth charts. Signs
of respiratory, ear or urinary tract infection should be investigated.
If a suspected brief resolved unexplained event (BRUE), previously referred to as
apparent life-threatening event or ALTE, has occurred, history-taking should focus
on: skin colour at the time of the event; duration of the event; sleep position and type
of sleeping arrangement (chair, lounge, crib, car seat, bed); clothing; the presence of
abnormal movements, including abnormal eye movements; muscle tone; blood or
bloody fluid at the mouth or nose; vomiting; the relationship of the event to feeding; and
the degree of resuscitation required. Finally, relevant past medical history (especially
prematurity), immunisation status, family history of sudden unexplained death in
infancy or later, exposure to smoke and metabolic disease should be investigated.
Heart rate, respiratory rate and oxygen (O2) saturation, must be assessed. Careful
neurological examination and neurobehavioural assessment (e.g. head lag, posturing,
motor abilities, eye tracking, social smile) should also be performed.
Sleep history and clinical assessment of a child
Sleep disturbances such as bedtime struggles, delayed sleep onset and multiple night
awakenings in children and adolescents are common and are frequently associated
with both emotional and behavioural diculties (such as anxiety, mood disorders
and attention-deficit hyperactivity disorder (ADHD)). Sleep disruption aects daytime
functioning, with a significant impact on the family’s quality of life. The presence
of SDB needs to be ruled out as the daytime consequences and neurobehavioral
symptoms are the same as for paediatric insomnia (table 1).
For this reason, a detailed clinical history and assessment of a child referred for sleep
problems is relevant. It is important to collect a complete sleep diary, reporting daily
and sleep patterns (bed- and sleep-onset time, number of nocturnal awakenings)
on weekdays, on weekends and taking into account changes during summer.
Nocturnal symptoms suggestive of GOR, asthma or pain, the presence of snoring or
witnessed apnoeas need to be investigated. The frequency and pattern of snoring
is of interest – whether snoring is seasonal or related to any specific factor, such as
upper airway infection.
On physical examination, signs commonly associated with SDB need to be evaluated,
such as obesity or overweight (an elevated age-appropriate BMI) and structural features,
known as ‘adenoid facies’, which are characterised by a high-arched and narrow hard
palate, increased facial height, crossbite and oral breathing due to enlarged adenoids.
Nasal airflow should be assessed by holding a cold spatula or tongue depressor under
the nose and asking the child to breathe. Misting of the cold metal indicates airflow.
A lack of airflow may indicate the presence of nasopharyngeal obstruction resulting
from enlarged adenoids or nasal obstruction. The nasal cavity should be examined,
using an appropriate light, for the presence of rhinitis, obstructive polyps, enlarged
turbinates or a deviated septum. When examining the mouth, tonsillar size is usually
graded from 0 (small tonsils) to 4 (enlarged tonsils obstructing ≥75% of the lateral
airway dimension). The Mallampati score, based on visualisation of the airway when
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Table 1. Daytime and night-time symptoms suggestive of SDB
Night-time symptoms
Snoring
Apnoeas
Nocturnal sweating
Nightmares
Talking in sleep
Bruxism
Bedwetting
Sleepwalking
Restless sleep
Frequent arousals
Oral breathing
Daytime symptoms
Sleepiness
Hyperactivity
Inattention
Headache
Learning diculties
Oral breathing
Reproduced and modified from Simonds et al. (2012) with permission.
the mouth is open with the tongue protruded, is helpful in identifying a small airway,
such as the presence of macroglossia, and of a narrow and arched palate. A crossbite
or significant overjet or overbite are signs of maxillary or mandibular deficiency. The
patient’s profile may also reveal retrognathia or micrognathia. The presence of glue
ear might coexist with adenoid hypertrophy. The child’s BP should also be evaluated –
hypertension might be a consequence of SDB.
Several of these items are included in the Sleep Clinical Record, which consists of three
parts: physical examination, subjective symptoms and clinical history. The clinical
history section also analyses behavioural and cognitive problems. The Sleep Clinical
Record is useful for OSA screening in settings with limited resources, particularly
when it is used in combination with other diagnostic tools, such as oximetry, or as
part of follow-up aer treatment.
Indications for respiratory and non-respiratory investigation
Further investigation should be performed on the basis of history-taking and physical
examination.
Sleep questionnaires (which investigate sleep patterns and symptoms of several sleep
disorders) and sleep diaries are usually completed by parents. Objective assessment
of sleep may be obtained using actigraphy, where circadian disorders or sleep-related
movement disorders are suspected. An actigraph is an accelerometer that resembles
a wristwatch. It records motion and is generally worn on the non-dominant wrist. The
actigraph provides a noninvasive means of assessing patterns of activity that reflect
sleep–wake cycles across several consecutive days and nights.
PSG is indicated when clinical assessment suggests OSAS or congenital central
alveolar hypoventilation syndrome, BRUEs, sleep-related hypoventilation due to
neuromuscular disorders, or chest wall deformities. The most recent consensus
statement from the European Respiratory Society (ERS) on the management of
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paediatric OSA states that PSG or polygraphy (PG) is indicated in children with OSA
symptoms, prior to adenotonsillectomy, particularly when the need for treatment
is unclear or where the following are seen: obesity; craniofacial deformities;
neuromuscular disorders; complex abnormalities (e.g. Chiari malformation, Down
syndrome and Prader–Willi syndrome). Whilst alternative methods such as overnight
oximetry cannot be considered a complete substitute for PSG, they may be used in
low-resource settings.
A video PSG recording with an extended EEG channel should be performed when:
nocturnal seizure is suspected; parasomnias and abnormal movements during sleep
are reported; and excessive daytime somnolence is not related to a sleep apnoea
syndrome. MSLT (which is used to measure the time elapsed from the start of a daytime
nap period to the first signs of sleep, also called sleep latency) should be performed in
all cases of daytime hypersomnolence, particularly where narcolepsy is suspected.
Diagnostic techniques
PSG
Sensors
For a complete overview of the appropriate sensors and techniques, we refer the
reader to the American Academdy of Sleep Medicine’s AASM Manual for the Scoring of
Sleep and Associated Events.
Full PSG includes the following sensors: EEG, EOG and chin EMG. Airflow should be
measured using a nasal air pressure transducer. A thermistor, an end-tidal carbon
dioxide tension (P
can also be used. Acceptable sensors for the detection of respiratory eort are
) monitor or summed calibrated inductance plethysmography
ETCO
2
oesophageal manometry or calibrated or uncalibrated inductance plethysmography.
Oesophageal manometry is rarely used in daily practice because it is too invasive for
use in children. Pulse oximetry should be used with a maximal signal averaging time
of 3 s. P
tcCO
or P
2
monitoring are used to assess alveolar hypoventilation.
ETCO
2
Scoring EEG in an infant/child
The following paediatric sleep scoring rules can be used to score sleep and wakefulness
in children aged ≥2 months post-term.
Sleep is divided into the following stages in children: W (wakefulness), N1, N2, N3 and
R. Stages N1, N2 and N3 are part of NREM sleep. Stage R is REM sleep. Sleep is scored
according to 30-s epochs commencing at the start of the study. A stage is assigned
to each epoch. If two or more stages coexist during a single epoch, the stage that
comprises the greatest part of the epoch should be assigned.
• Stage W. >50% of the epoch should have alpha rhythm or an age-appropriate
dominant posterior rhythm over the occipital region. Reactive EEG over the
occipital region is the dominant posterior rhythm in relaxed wakefulness with
eyes closed – this is slower in infants and children and attenuates with eye
opening or attention. The frequency is 3.5–4.5 Hz when first seen in infants of
3–4 months post-term, 5–6 Hz by 5–6 months and 7.5–9.5 Hz by 3 years of age
with an amplitude of >50 µV. In epochs without visually discernible alpha rhythm
or age-appropriate dominant posterior rhythm, stage W can be scored when there
are eye blinks at a frequency of 0.5–2 Hz, reading eye movements or irregular
conjugated eye movements associated with normal or high chin muscle tone.
• Stage N1 can be scored if the posterior rhythm is attenuated and replaced by low-
amplitude, mixed-frequency activity for >50% of the epoch. In subjects who do
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not generate a posterior rhythm, stage N1 is defined as the onset of EEG activity
at 4–7 Hz with background frequencies slowing by ≥1 Hz compared with those of
stage W, vertex sharp waves, slow eye movements, rhythmic anterior theta activity,
hypnagogic hypersynchrony or a diuse or occipiatal predominant high-amplitude
activity of 3–5 Hz. Hypnagogic hypersynchrony consists of paroxysmal bursts or
runs of diuse high-amplitude sinusoidal waves of 75–350 µV, 3–4.5 Hz, which
begin abruptly, are usually widely distributed but are oen maximally expressed
over the central, frontal or frontocentral scalp regions.
• Stage N2 starts if one or both of the following occur during the first half of the
epoch or the last half of the previous epoch: one or more K complex not associated
with arousals or one or more train of sleep spindles. Epochs can continue to be
scored with low-amplitude, mixed-frequency EEG activity without K complexes or
sleep spindles, as long as they are preceded by K complexes that are not associated
with arousals or sleep spindles.
• Stage N3 can be scored when ≥20% of an epoch consists of slow wave activity.
Sleep spindles may persist in this stage.
• Stage R can be scored in epochs with all of the following: a low-amplitude, mixed-
frequency EEG, a low chin EMG tone and REMs. Epochs can continue to be scored
if the EEG continues to show low-amplitude, mixed-frequency activity without K
complexes or sleep spindles and if the chin EMG remains low.
• A major body movement is defined as movement and muscle artifact that obscures
the EEG for more than half of the epoch to the extent that the sleep stage cannot
be determined. An epoch with a major body movement should be scored as stage
W if alpha rhythm is present or if no alpha rhythm is discernible but an epoch
scorable as stage W either precedes or follows the epoch. Otherwise, the epoch
should be scored as the same stage as the epoch that follows it.
• An arousal is defined as an abrupt shi of EEG frequency, including alpha, theta
and/or frequencies of >16 Hz (but not spindles) of ≥3 s, with ≥10 s of stable sleep
preceding the change. Scoring of an arousal during REM requires a concurrent
increase in submental EMG lasting ≥1 s.
The terms quiet sleep (QS) and active sleep (AS) are also used when scoring sleep in
infants 0–2 months of age. QS is characterised by tracé alternant or high-voltage slow
wave activity. Tracé alternant is an EEG pattern in which 3–8-s bursts of moderate-tohigh voltage slow waves intermixed with sharply contoured waveforms, alternate with
4–8-s intervals of attenuated mixed-frequency EEG activity. It commonly disappears
aer the first month of life. High-voltage slow wave activity consists of continuous
moderately rhythmic 50–150 µV, 0.5–4 Hz slow activity without the bursting activity
of tracé alternant.
AS consists of either low-voltage 5–6 Hz EEG activity called ‘activité moyenne’ or a
mixture of high- and low-voltage activity including delta activity called ‘mixed’. The
AASM task force recommends that sleep in infants ≥2 months post-term should be
scored as NREM and REM, because all of the EEG and PSG features of REM sleep are
present at this age and QS, if not NREM sleep by this age, is at least not REM sleep.
This is also generally true most full-term infants.
Sleep is undierentiated before 32 weeks conceptional age (CA). At ∼32 weeks
CA, REMs and phasic muscle twitches identify AS, while QS is associated with
the presence of far fewer movements. Recognisable EEG patterns of AS and QS
appear at ∼34 weeks CA. By 36 weeks CA, all the EEG and behavioural correlates
of wakefulness, AS and QS are clearly recognisable, although a large proportion of
sleep is scored as indeterminate sleep. This is defined when mixtures of at least
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sleep/wake states are seen within an epoch. The percentage of indeterminate
sleep declines rapidly aer 36 weeks CA. Non-EEG correlates are oen required
to distinguish between QS and AS in young infants. AS is typically associated with
irregular respiration, chin EMG atonia, transient muscle activity and REMs. Regular
respiration, no eye movement or vertical eye movement, and preserved chin EMG
are all associated with QS.
The various factors comprising NREM sleep need to develop over time in infants. Sleep
spindles are present in infants of aged ≥2–3 months post-term, while K complexes
are usually present in infants aged ≥4–6 months. Slow wave activity usually develops
by 4–5 months post-term. On average, NREM sleep can be scored as stage N1, N2
and N3 by ≥5–6 months post-term.
In view of the variability of sleep in infants, four possible scenarios are described:
• If all epochs of NREM sleep contain no recognisable sleep spindles, K complexes or
slow wave activity, score all epochs of NREM sleep as stage N.
• If some epochs of NREM sleep contain sleep spindles or K complexes, score these
epochs as stage N2. If there is no recognisable slow wave activity in the other
epochs, score as stage N.
• If some epochs of NREM sleep contain >20% of slow wave activity, score these
epochs as stage N3. If there are no recognisable K complexes or sleep spindles in
the other epochs, score as stage N.
• If NREM is suciently developed that some epochs contain sleep spindles or K
complexes and other epochs contain sucient slow wave activity, then score
NREM sleep according to the paediatric rules.
Scoring breathing in an infant/child
The paediatric rules can be used in children up to 18 years of age. However, a sleep
specialist can decide to use the adult rules in a child of ≥13 years, depending on the
clinical context. The following definitions are used:
• Obstructive apnoea. The event lasts for at least two missed breaths or the duration
of two breaths, as determined by the baseline breathing pattern. The event is
associated with a fall of ≥90% in the signal amplitude for ≥90% of the entire
respiratory event compared with the pre-event baseline amplitude. The event is
associated with continued or increased respiratory eort for the entire period.
• Mixed apnoea. Apnoea (as defined previously) is initially associated with absent
respiratory eort followed by resumption of inspiratory eort before the end of the
apnoea.
• Central apnoea. Absent inspiratory eort throughout the entire event with a
duration of ≥20 s or of at least two missed breaths, associated with arousal,
awakening or ≥3% desaturation. For infants <1 year of age, bradycardia is also
included in the definition. Central apnoeas occurring aer a snore, sigh, respiratory
event or arousal are normal phenomena in children and are not scored unless
associated with arousal, awakening or ≥3% desaturation.
• Hypopnoea. A fall in amplitude of ≥30% of nasal pressure or an alternative signal,
with a duration of at least two missed breaths (or the duration of two breaths,
as determined by the baseline breathing pattern). The fall in amplitude must last
at least two missed breaths and the event should be associated with an arousal,
awakening or ≥3% desaturation.
• Respiratory eort-related arousal (RERA). A sequence of breaths lasting for at
least two breaths that do not meet apnoea/hypopnoea criteria and lead to an
arousal from sleep. The breathing sequence can be characterised when at least
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one of the following is present: increasing respiratory eort, flattening of the
inspiratory portion of the nasal pressure, snoring or an elevation in the P
ETCO
above pre-event baseline.
• Sleep-related hypoventilation. CO2 is >6.7 kPa (>50 mmHg) as measured by P
or P
• Periodic breathing. More than three episodes of central apnoea lasting >3 s
sensors for >25% of the total sleep time.
ETCO
2
tcCO
separated by no more than 20 s of normal breathing.
Normative data in an infant/child
Neonates express a high percentage of REM sleep, accounting for 50–60% of total
sleep time. This percentage is even higher in premature infants. Infants can also enter
sleep in REM. Total sleep time for neonates ranges 16–20 h per day and they express
no day–night dierentiation. A sleep cycle typically lasts 40 min.
In the first year of life, total sleep time decreases to 14 h per day and day–night
dierentiation appears from 1 month onward. Most infants show a longer undisrupted
sleep time of 3–4 h at 3 months and sleep ‘through the night’ at around 9 months
of age. They also have two naps lasting 2–4 h. During the first months of life, the
various sleep stages develop and sleep can be completely scored at an average age of
6 months. The percentage of REM sleep reaches 30% around the age of 1 year.
In the preschool period, total sleep time further diminishes, until it reaches 12 h per
day. Preschool children usually have one nap per day, which disappears at 3–5 years
of age. The percentage of REM sleep decreases (to 20–25%) and stage N3 increases.
The sleep cycle length slowly increases towards adult levels.
School-aged children have an average total sleep time of 11 h and adolescents
should typically get 9–10 h of sleep. REM latency increases. The percentage of stage
N3 increases until adolescence, aer which it steadily decreases until reaching
adult levels.
In healthy infants, central apnoeas frequently occur but are of short duration and are
not followed by bradycardia or O2 desaturation. REM sleep is associated with a higher
incidence of central apnoeas. Obstructive and mixed apnoeas are less frequently
seen. Obstructive apnoea or mixed apnoea appear to be more common in premature
infants and decrease in frequency over the first year of life. Studies have shown that
in general, the obstructive apnoea index is below 1 in the first year of life in both term
and preterm infants. Obstructive events are associated with a much greater decline in
oxygenation and heart rate compared with central apnoeas of equal lengths. During
the first year of life, the number of central apnoeas decreases. Periodic breathing
normally disappears in the first 6 months of life. The median baseline O2 saturation
during sleep in a term infant at birth is ∼98% and the median low is 83%. Short
desaturations can be observed in infants during periodic breathing, following normal
respiratory pauses and during REM sleep.
During childhood and adolescence, central apnoeas can still occur, although at a
lower frequency which decreases with age. Obstructive and mixed events are rarely
seen. Mean saturation during sleep is ∼97% with a mean nadir ≥90%.
Interpretation and reporting of PSG in an infant/child
Studies have shown that a single night of PSG is sucient to diagnose sleep apnoea in
children. However, when sleep architecture is the primary outcome, 2 nights are oen
necessary to overcome the first-night eect.
A PSG report should indicate the equipment and sensors used, and whether the child is
using any medication. It should start at the child’s regular bedtime. The time of waking
2
2
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up in the morning should be indicated so that the total time in bed can be calculated.
The following sleep parameters should be reported: time in bed, total sleep time, sleep
eciency, sleep onset latency, wake aer sleep onset, REM latency, time and percentage
of total sleep time spent in stage N1, N2, N3 and REM, movement time, periodic limb
movements and arousal index. Abnormal EEG features should also be reported.
Respiratory variables include the number of central, obstructive and mixed apnoeas,
hypopnoeas, RERAs and the presence of snoring. Sleep-stage distribution and
position-related distribution of these respiratory events should be noted.
The number of desaturations with the S
average saturation during sleep and a saturation histogram. The same applies to P
or P
also be calculated.
. The average, minimum and maximum heart rate and respiratory rate should
ETCO
2
nadir should be recorded, as well as the
aO
2
tcCO
2
The 2016 ERS consensus statement provides two definitions for paediatric OSA
using PSG:
• OSA definition 1. If OSA is defined as an obstructive AHI of ≥2 events·h−1 or an
obstructive apnoea index of ≥1 in the presence of symptoms, adenotonsillar
hypertrophy with or without obesity and no other abnormalities, it is likely that
the AHI will become normal aer adenotonsillectomy. This likelihood is lower with
mild OSA (obstructive AHI of 2–5 events·h−1) than with moderate-to-severe OSA
(obstructive AHI of >5 events·h−1).
• OSA definition 2 (used in most studies). When OSA is defined as SDB symptoms in
combination with an AHI of ≥1 events·h−1, there is improvement in the symptoms
of inattention and hyperactivity following adenotonsillectomy. Children with
moderate-to-severe OSA (AHI >5 events·h−1) have significant elevations in average
wake SBP, and wake and sleep DBP compared with controls (AHI ≤1 events·h−1).
Similar cut-os are used to diagnose OSA in infants using PSG.
In children without craniofacial or neuromuscular disorders, an AHI of >1 event·h−1 on PG
predicts AHI >1 event·h−1 on PSG, with moderate sensitivity (88%) and specificity (71%).
Home studies in children
Home-based and portable monitoring studies oer a potentially very interesting
approach to studying sleep and breathing in children in their home environment. The
2016 ERS consensus statement states that PG is a suitable tool for the diagnosis of
paediatric OSA, as an alternative to PSG. Limited studies have shown that the rate of
technically acceptable recordings exceeds 95%. PG with limited montage (airflow,
respiratory eort, oximetry and electrocardiography) has also been used, with a
sensitivity of ∼90% for OSA diagnosis.
Oximetry
Oximetry is used to detect sleep-related desaturations and hypoxaemia. It is a very
easy technique suitable for home monitoring.
In children with adenotonsillar hypertrophy, abnormal oximetry according to the
McGill criteria corresponds with OSA of at least moderate severity, but a negative
result does not exclude OSA with certainty. For this subset of patients, PSG is still
required. Abnormal oximetry is frequently seen in children with Down syndrome
where there is clinical suspicion of obstructive SDB; however, this might not just
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