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OBSTRUCTIVE SLEEP

APNEA
Definition
OSA or sleep disordered breathing (SDB)
is caused by complete (apnea) or partial
(hypopnea) collapse of one or more
muscles of the pharynx, which is most
evident during REM sleep.
Etiology
Adenotonsillar hypertrophy and obesity
are the major risk factors for OSA in
healthy children.
Also caused by medical, neurological, or
dental conditions:
reduce upper airway size
affect the neural control of the upper airway
impact the collapsibility of the upper airway
Epidemiology
2 to 5% of children have OSA and it can occur
at any age, but most common in children ages
2-6 yrs.
>2 million children today have some kind of
sleep disorder
30-40% of children do not get enough sleep
10 million Americans are undiagnosed
Sleep disorders have been linked to deaths in
adults as well as children and infants
Pathogenesis
Children with OSA tend to have:
smaller upper airways at all levels
pharyngeal AP dimension is larger than the lateral
dimension
substantial change in the size of the airway with
inspiration vs. expiration, which is most apparent in
the nasopharynx
This increase in upper airway resistance can be
extreme and leads to increased work of
breathing which is associated with snoring seen
in OSA.
Predisposing Factors
OSA has been linked to many other medical conditions in children
such as SIDS, ADD, ADHD, Autism, Narcolepsy, Insomnia,
Cardiovascular, etc.
Anatomic factors anywhere along the upper airway can decrease
airway size and stability, which may lead to the development of
OSA:
Enlarged tonsils and adenoids- MCC
Obesity- more common in adults
Mucopolysaccharidoses (ie. Sanfilippo or Hurler Syndrome)
Craniofacial abnormalities (ie. narrowed maxillary arch or midfacial
hypoplasia)
Neuromuscular factors (ie. hypotonia, cranial base anomalies)
Combined anatomic and neuromuscular factors (ie. trisomy 21)
Genetics (ie. obesity, craniofacial morphology)
Clinical Presentation
Clinical Presentation
History:
Habitual Snoring
Nighttime history of:
nocturnal enuresis
restless sleep
parasomnias
Apneas
Daytime history of:
morning headaches
difficult to awaken
falling asleep in school
inattention, learning and behavior problems (ie. ADD, ADHD)
Clinical Presentation
Exam
Growth:
Obesity
Failure to Thrive
Head and neck:
Anatomy
Mallampati score
Cardiopulmonary:
Check blood pressure
Auscultate for signs of pulmonary hypertension
Polysomnography
Overnight PSG is the GOLD standard for
diagnosing OSA.
Nasal and oral airflow as well as hypopnea,
ETCO2, SpO2, are the main variables of PSG
that are used to assess OSA.
From these variables, summary measures are
calculated such as:
Respiratory Effort Related Arousals (RERA)
Apnea Hypopnea Index (AHI)
Respiratory Disturbance Index (RDI)
Diagnostic Criteria
The following are diagnostic criteria for pediatric OSA defined by the
American Academy of Sleep Medicine. OSA is diagnosed if a child meets
EACH of the five criteria:
The care giver reports snoring, labored breathing, or obstructed breathing
during the child’s sleep.
The care giver has observed at least one or more of the following:
paradoxical inward rib cage motion during inspiration
movement arousals
diaphoresis
neck hyperextension during sleep
excessive daytime sleepiness
hyperactivity
aggressive behavior
slow growth
morning headaches
secondary enuresis
Diagnostic Criteria
Polysomnography reveals an apnea or hypopnea index >1 event per hour
Polysomnography reveals either of the following:
frequent arousals from sleep associated with:
increased respiratory effort,
oxyhemoglobin desaturation associated with apnea,
hypercapnia during sleep, or
markedly negative esophageal pressure swings
periods of hypercapnia, oxyhemoglobin desaturation, or both during sleep that
are associated with:
snoring,
paradoxical inward rib cage motion during inspiration, and either
frequent arousals from sleep or
markedly negative esophageal pressure swings.
The child’s findings can’t be explained by another sleep disorder, a
medical disorder, a neurological disorder, a medication, or substance
abuse.
Severity of OSA
Apnea Index SpO2 nadir ETCO2 peak ETCO2
(mmHg) (mmHg)

Mild OSA 1-4 86-91% > 53 > 50 for 10-


24% total
sleep time

Moderate 5-10 76-85% > 60 >50 for 25-


OSA 49% total
sleep time

Severe OSA >10 ≤ 75% > 65 ≥ 50 for >50%


total sleep
time
Management
First line recommendation is
adenotonsillectomy (T&A) for children with
adenotonsillar hypertrophy.
Children with risk factors for respiratory
compromise after T&A are recommended to
stay for postoperative inpatient observation.
Risk Factors include, not limited to:
< 3 yrs old
classified severe OSA
FTT
Management
CPAP or BiPAP
Avoid tobacco smoke, pollutants, and
allergens around OSA children
Weight loss is recommended for obese
children
Supplemental O2
It is not recommended to give
intranasal/systemic corticosteroids or
antibiotics as first line for OSA.
Prognosis
Majority of children with OSA and adenotonsillar
hypertrophy improve after a T&A
10% don’t improve after surgery, because a substantial
part of the OSA was caused by craniofacial or
neuromuscular factors or pharyngeal instability, not
simply enlarged tonsils and adenoids.
In other children, OSA initially improves, but later
recurs, secondary to adenoidal tissue regrowth, and will
resolve after a second surgery.
CPAP or BPAP improves symptoms, signs, and
polysomnographic outcomes in at least 85% of children.
Questions

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