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• Avoidin g late meals to prevent lying down with a full stomach can reduce the
chances of reflux.
• Sleep on the left side. Multiple research studies have found that lying on the left
side is the best sleeping position for people with GERD (Person et al.
2015)
• Improve sleep hygiene
• Elevate the head of the bed: Tilting the upper part of the bed by a minimum of six
inches can help reduce reflux symptoms while lying down.
16 Recent Advances on Sleep During Pregnancy and Postpartum 273
Medications are available for treating GERD and may be required if lifestyle
modifications alone do not consistently alleviate symptom
s. Over-the-counter med-
ications, such as antacids, can provide temporary relief but may have limited
effectiveness for many individuals. Additional medications, including proton
pump inhibitors (PPIs) and H2 blockers, are also utilized as treatment options, aim
to reduce the production of stomach acid. However, they can have side effects and
their use should be closely assessed.
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Chapter 17
Updates in Pediatric Sleep Apnea
Cláudio D’Elia, Chris Landon, and Miguel Meira e Cruz
Abstract Sleep-disordered breathing encompasses a group of highly impacting
conditions with a significant prevalence among the pediatric population. Although
manifested in a wide spectrum of clinical presentations, upper airway increased
resistance is often a common finding which therefore contributes to its deleterious
role on several systems and functions. Challenging diagnostic algorithms and novel
therapeutic options are relevant aspects that should be validated and established
under an evidence-based matrix applied to a real-world scenario to improve the
standards of care and reduce the negative consequences of a dangerous disturber of
sleep from infancy to adolescence. This chapter aims to clarify the factors subsiding
impaired respiratory function during sleep and provide an updated view of the
mechanisms, clinical manifestations, and treatment options available for this range
of pediatric ages.
Keywords Sleep-disordered breathing · Pediatric population · Upper airway
resistance · Diagnostic algorithms · Treatment options
17.1 Introduction
Obstructive sleep apnea is the most clinically impacting form of the sleep-disordered
breathing spectrum. During sleep, the disruption of normal respiratory patterns and
ventilation in children causes several health issues and significantly affects learning,
C. D’Elia
Department of Pediatrics, Lusíadas Hospital, Lisbon, Portugal
European Sleep Center, Lisbon, Portugal
C. Landon
Family Practice and Pediatrics, University of California, Los Angeles, CA, USA
M. Meira e Cruz (
✉)
European Sleep Center, Lisbon, Portugal
Cardiovascular Center, University of Lisbon, Lisbon School of Medicine, Lisbon, Portugal
e-mail: mcruz@medicina.ulisboa.pt
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. S. BaHammam, M. Hunasikatti (eds.), Sleep Apnea Frontiers, Progress in Sleep
Research,
https://doi.org/10.1007/978-981-99-7901-1_17
279
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academic performance, and quality of life. Recognition of the condition is impera-
tive and requires an adequate assessment with an active search for signs, symptoms,
and behaviors related to normal sleep deviation. Data on the appropriate sequence of
interventions is still scarce and standards of care are debatable. The ongoing medical
science is, however, looking to improve each of the algorithmic steps, from diag-
nosis to treatment pursuing successful approache
s allowing to reduce the burden of
OSA as well as its deleterious consequences. Knowledge of epidemiological aspects
will provide basics for improving screening strategies and performing accurate
diagnosis to achieve optimized results.
280 C. D’Elia et al.
17.2 Epidemiology
For the practicing clinician sleep problems are a common parental complaint,
occurring in up to 25% of children over the course of infancy, childhood, and
adolescence. Presentations of significance pointing toward obstructive sleep apnea
can include learning and behavioral problems, cardiovascular complications, and
impaired growth (including failure to thrive). Population estimates of obstructive
sleep apnea in children suggest it is most common between ages 2 and 6 years, with
incidence ranging between 1 and 5% of children (Marcus et al.
2012). The major risk
factors in otherwise healthy children are adenotonsillar hypertrophy and obesity
(BMI > 97th percentile for age and gender). Findings of obesity and adenotonsillar
hypertrophy can be mitigated by age and anatomic considerations.
The clinician must be aware of additional risk factors, keeping in mind medical,
neurological, skeletal, or dental conditions that reduce upper airway size, affect the
neural control of the upper airway, or impact the collapsibility of the upper airway. In
Cerebral Palsy the Pediatric Sleep Questionnaire was abnormal in 58% with
concomitant epilepsy increasing positivity to 67%, compared to population values
of 27%, while medical review for symptoms suggested only 8.2% (Garcia et al.
2016). In Down Syndrome estimates of pediatric abnormality range from 50 to
100%, progressing to 100% in adulthood. In a group of unselected patients with
down syndrome, 66% were found to have OSA on full night polysomnogram (PSG),
and about half of these children presented with severe disease, even among those
children with no history of snoring or witnessed apneas, the majority (53%) were
found to have OSA on PSG and that traditional risk factors for OSA such as tonsil
size or body mass index (BMI) z-score were not associated with the risk of OSA
among a large cohort of children with Down Syndrome (Maris et al. 2016). Cra-
niofacial anomalies (e.g., retrognathia, micrognathia, midface hypoplasia) were
found in 15.5% of pediatric OSA patients in a population-based case control study
(Lam et al.
2010), while children with Apert, Crouzon, or Pfeiffer syndromes, which
all have significant maxillary hypoplasia as a key feature, reported an estimated
prevalence of OSA of 53% in this population based on symptom report on a mail-in
questionnaire (Pijpers et al. 2004). Children born preterm compared to term were
significantly more likely to be diagnosed with sleep apnea (<32 weeks versus term)
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hazard ratio 2.74 this remained even after adjustment for known confounding vari-
ables. Children born small for gestational age were not at increased risk of sleep
apnea compared to children born appropriate for gestational age, hazard ratio of 0.95
(Raynes-Greenow et al.
2012
). M
uscula
r dystrophy or other neuromuscular
disorders are frequently associated with sleep-disordered breathing (SDB) abnor-
malities, although the cumulative prevalence is not well known and probably
underestimated. Between 27–62% of children and 36–53% of adults with neuro-
muscular disorders have sleep-disordered breathing, depending on the type of
neuromuscular disorder involved, the definition of respiratory impairment, and the
tools used to measure it
(Arens and Muzumdar
2010)
. T
he prevalence of SDB in
myelomeningocele (MMC) has been reported between 62 and 81%; the prevalence
of moderate to severe OSA in this population has been reported to be as high as
20–31% (Wal ker Jr and Perez 2021
). Obstructive events are more likely to occur
during a rapid eye movement (REM) sleep state. Efforts to quantify the incidence of
central apneas are based on small series and case reports and likely represent under-
recognition/reporting. In children with myelomeningocele, risk factors for sleep-
related disordered breathing include higher spinal cord lesions, brain stem dysfunc-
tion resulting from decreased corticomedullary subarachnoid space, very abnormal
Chiari malformations, pulmonary function abnormalities (obstructive lung disease
and restrictive lung disease), and disorders of upper airway maintenance. Obesity is
an independent risk factor for SDB in all children with an estimated prevalence of
13–78% (Walker Jr and Perez 2021). The combination of higher obesity rates in
individuals with MMC and an abnormal brainstem respiratory brainstem control
center secondary to their Chiari malformation places this population at increased
risk. Obstructive sleep apnea (OSA) has been observed in individuals with achon-
droplasia and is associated with compression of the brain stem, although overnight
sleep studies showed a reduction in respiratory disturbance index (RDI) and move-
ments/arousals
after treatment to relieve upper airway obstruction. Improvement of
respiratory indices was associated with an increased proportion of slow-wave sleep
and a decrease in stage 1–2 sleep (Waters et al.
1995)
.
T
he prevalence of OSA across
studies in Prader–Willi syndrome (PWS) was 79.91% (Sedky et al. 2014). Among
youths with OSA, 53.07% had mild OSA, 22.35% moderate OSA, and 24.58%
severe OSA. Adenotonsillectomy was associated with improvement in OSA for
most children with PWS. However, residual OSA was present in most of the cases
post-surgery (Sedky et al. 2014). Forty patients out of 42 mucopolysaccharidoses
(MPS) (e.g., Hunter syndrome or Hurler syndrome) children tested with PSG had
OSA (95%) (Gönüldaş et al.
2014). Adenoid grade, Mallampati grade, restricted
mouth opening, and rate of dif ficult intubation were significantly different among
MPS subtypes. There was no significant difference between MPS subtypes
according to tonsil grade and OSA severity. Most MPS patients have airway
obstruction and OSA due to adenotonsillar hypertrophy and most benefit from
adenotonsillectomy, after which OSA significantly improves (Gönüldaş et al.
2014). Orthodontic problems (e.g., high narrow hard palate, overlapping incisors,
cross bite) are significantly associated with OSA (Galeotti et al.
2018)
. T
he preva-
lence of malocclusions in OSA children without genetic syndromes was 89.9%
17 Updates in Pediatric Sleep Apnea 281
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compared to 60.6% in the control group. Factors independently associated with OSA
compared to the control group were posterior crossbite, reduced overbite increased
overbite, and increased overjet (Galeotti et al. 2018). A high prevalence of OSA
among family members, suggested that a family history of OSA has a role apart
from the influence of obesity. Several small family-based studies have focused on
defining the genetic basis of OSA. In a case series, non-overweight relatives of
patients with OSA were found to have more daytime sleepiness, snoring, apneas, and
arousal compared with matched controls (Gharibeh and Mehra
2010). In the Cleve-
land Family Study, which is the largest, assembled familial aggregation study
investigating OSA, sleep apnea was identified to be more prevalent in relatives of
index probands of OSA (21%) compared with neighborhood control subjects (12%)
(Gharibeh and Mehra
2010
). Data from twin studies showed that the concordance of
snoring, a symptom of OSA, is higher among monozygotic twins than dizygotic.
The heritability of OSA is partially explained by intermediate, genetically deter-
mined risk factors. Obesity, which is a known risk factor for OSA, is partially under
genetic control. Other risk factors which predispose to OSA that are genetically
determined include craniofacial morphologic characteristics and ventilatory control
mecha
nisms (Gharibeh and Mehra
2010)
.
282 C. D’Elia et al.
17.3 Pathophysiology
OSA is caused by complete or partial collapse during sleeping, of one or multiple
segments of the extrathoracic airway, including the nasal vault, oral cavity, pharynx,
larynx, and trachea. Although interactively related, the pathophysiological factors
involved in OSA can be broadly and arbitrarily divided into anatomical factors that
effectively reduce airway caliber and those that promote increased upper airway
collapsibility (Tan et al.
2013). A clear anatomic factor cannot always be identified
and several contributing factors may coexist to a greater or lesser degree (Arens and
Marcus 2004; Gozal et al. 2020).
Key pathophysiologic possible causes include (1) an anatomically compromised
or collapsible upper airway (high passive critical closing pressure of the upper
airway [Pcrit]); (2) inadequate responsiveness of the upper airway dilator muscles
during sleep (minimal increase in EMG activity to negative pharyngeal pressure);
(3) waking up prematurely to airway narrowing (a low respiratory arousal thresh-
old); and (4) having an oversensitive ventilatory control system (high loop gain)
(Eckert et al.
2013).
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17 Updates in Pediatric Sleep Apnea 283
17.3.1 Dysregulation of the Upper Airway Neuromotor
System During Sleep
The upper airway h as important physiologic functions such as respiration,
swallowing, speech and vibration, and local immunity. The pharynx is a collapsible
segment that performs these functions under the balanced control of dilator and
constrictor muscles (Chang and Chae
2010). Neuromuscular factors for upper
airway patency are affected by central ventilatory drive, arousal responses to respi-
ratory occlusion (arousal threshold), and upper airway reflexes (Chang and Chae
2010).
The respiratory cycle is controlled by an extensive network of neurons within the
brainstem, which is dependent upon unspecific and specific drives like hypoxia or
hypercapnia. The typical changes in this network and its drives during the trans ition
from wakefulness to sleep and within the various sleep states favor destabilization of
breathing during sleep (Schäfer
2006). During sleep in a normal child there is a
modest increase in upper airway resistance and alterations in central respiratory
drive, both resulting in a decrease in nocturnal ventilation, a slight drop in oxygen
saturation, and a rise in end-tidal PCO
2
. Brief central pauses are common in children,
but obstructive apneas are never normal in children (Marcus et al. 1992).
The upper airway is a complex, multifunctional, dynamic neuromechanical
system. Maintaining the openness of the airway during breathing necessitates con-
stant coordination between neural and mechanical factors, and this can vary
depending on the individua l’s posture. Failure to continuously recruit and coordinate
dilator muscles to counterbalance the forces that act to close the airway results in
hypopneas or apneas (Bilston and Gandevia 2014).
During wakefulness and sleep, the pharyngeal dilators help to maintain pharyn-
geal patency by tonic contraction and/or phasic contractions, thereby helping to
stiffen the upper airway prior to and during inspiration. At sleep onset, airway
muscle activity is reduced, and ventilatory variability increases. Airway collapse is
offset by pharyngeal dilator activity in response to hypercapnia and negative luminal
pressure (Katz and D’Ambrosio
2008). In children with sleep-related breathing
disorders, this response does not completely relieve the upper airway obstruction
although, in many children with OSA, this is usually sufficient to maintain a partially
open pharyngeal airway for lengthy periods of sleep without experiencing discrete
obstructive apneic events.
The upper airway is more collapsib le in lighter sleep and REM sleep compared to
deeper SWS (Carberry et al.
2016). During REM sleep, paroxysmal reductions in
pharyngeal dilator activity related to central REM sleep processes likely account for
the predisposition toward an increase in resistance and obstructive events (Katz and
D’Ambrosio 2008; Ayappa and Rapoport 2003). The withdrawal of excitatory
noradrenergic and serotonergic inputs to upper airway motor neurons during REM
sleep further reduces pharyngeal muscle activity and substantially increases the
propensity for upper airway collapse (Mokhlesi and Punjabi
2012). Obstructive
sleep events in children with OSA have an inverse pattern concerning the sleep
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