Management of Pediatric
OSA
Gerald D. Suh, MD
ENT and Allergy Associates
Board Certified in Otolaryngology and Sleep Medicine
Medical Director-Night and Day Sleep Centers
Queens Pediatric Symposium
January 16, 2013
Sleep Disordered Breathing
Sleep Disordered Breathing
(SDB)

Spectrum of abnormal breathing, affects 12% of children

Primary Snoring- Snoring without obstructive apnea, frequent arousals from
sleep, or gas exchange abnormalities

Upper Airway Resistance Syndrome (UARS) − Snoring, labored breathing
(increased negative intrathoracic pressure during inspiration), and disrupted
sleep (arousals and sleep fragmentation) without discrete obstructive apneas
or hypopneas.

Obstructive Hypoventilation Syndrome- Persistent partial upper airway
obstruction associated with gas exchange abnormalities, rather than discrete,
cyclic apneas.

Obstructive sleep apnea (OSA) − Recurrent partial or complete upper airway
obstruction/ absence of airflow despite respiratory effort

Central sleep apnea − No respiratory effort
Pediatric OSA-Epidemiology

Prevalence OSAS 1-4% Children
 Prevalence is higher among African Americans and
Asian children
 Most studies have shown 4% to 11% prevalence of
parent-reported apnea.
 Males=Females pre-puberty, M>F after puberty
 Peak incidence Preschoolers (2-8yo) (tonsils/adenoids
largest in relation to airway size overall)
 As obesity is increasing in pediatrics the age distribution
shifting
 25-30% snoring children have OSAS
EVALUATION

Medical History
 Developmental and School history
 Family History
 Behavioral assessment
 Physical Examination
 Growth
 HEENT
 Cardiac examination
 Radiologic Studies


Lateral Neck
Laryngoscopy
CLINICAL FEATURES
Nocturnal Symptoms

Symptoms vary by age-especially in
infants!
 Snoring-Volume does not correlate with the
degree of obstruction
 Observed apneic pauses
 Snorting / gasping / choking
 Restless sleep
 Diaphoresis
 Paradoxical chest wall movement
 Abnormal sleeping position
 Sweating
 Mouth Breathing
 Secondary enuresis
 Night terrors
CLINICAL FEATURES
Daytime Symptoms-Physical and Behavioral

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Morning headaches
Difficulty awakening in AM
Hyponasal Speech
Nasal congestion, Chronic Rhinorhea
Mouth breathing, Dry Mouth
Frequent infections
Difficulty swallowing
Poor appetite
Daytime somnolence-7-10%
Mood changes
Internalizing behaviors
Externalizing behaviors
ADHD like symptoms, School problems
Neurobehavioral Consequences

Deficits in learning, memory , vocabulary
 IQ loss of 5 points or more
 Apneic events inversely related to memory and
learning performance
 Treatment of OSA likely improves behavior,
attention, quality of life, neurocognitive
functioning.
Neurobehavioral Complications
(APRIL)
 Aggression
 Poor school performance
 Restless
 Irritable/ hyperactivity
 Lacks attention
ASSOCIATED FEATURES

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Increase in partial arousal parasomnias
Worsening GERD
Increase in seizure frequency in
predisposed children
Other CO-Morbid Sleep problems
-RLS,PLMS
-Circadian Rhythm Disorders
-Bedtime resistance , nightwakings
Metabolic Consequences
 Incidence:
type 2 Diabetes 30% OSA
patient vs. 18 % no OSA
 Increase
glucose intolerance and insulin
resistance
CAUSES/ RISK FACTORS
-Adenotonsillar Hypertrophy
-Upper airway congestion; allergies
-Upper airway obstruction , choanal stenosis, larnygomalacia, subglottic
stenosis
-GERD/LPR
-Cleft palate
-Craniofacial dsymorphism :
Mid -facial hypoplasia –Down’s syndrome
Micrognothia – Pierre-Robin syndrome
-Cranial base malformation- Achondroplasia
-Neuromuscular disorder:
Hypotonia-Down’s syndrome, Muscular dystrophy
Spasticity –Cerebral Palsy
-Overweight
-Mucopolysaccharidosis
-Sickle cell disease
-Cystic fibrosis (Nasal Polyps)
-Chronic lung disease/ BPD
-Scoliosis
-Brain and spinal disorders – Spin Bifida, ACM type II
High-Risk Groups
 Down
syndrome (54100% with OSA)
 Achondroplasia
 Metabolic
storage
diseases
 Craniofacial
syndromes
Anatomy
 Hard
to miss!
Waldeyer’s Ring
Septum
Adenoid
Adenoid
Lingual Tonsils
Adenoid Facies
 Elongated
face
 Gummy smile
 Open mouth posture
Dental Changes

Open bite

Cross bite

Narrow maxillary arch
MALLAMPATI CLASSIFICATION
Adenoid Evaluation
Fiberoptic Laryngoscopy
MULLER MANEVEUR
LARNYGOMALACIA
SUBGLOTTIC STENOSIS
OSA Diagnosis
Home Sleep Testing
 Not validated below the age of
16
 Abbreviated (Nap) PSG
 High PPV but Low NPV.
Useful if results are positive.
 False positive results in patients
with coexistent medical
problems (obesity, asthma).
 Polysomnogram (PSG)
 “Gold Standard.”
 Can assess severity of SDB.
Includes EEG, EKG, EOG,
EMG, saturation monitor,
respiratory effort and airflow
monitor.

American Academy of Pediatrics
OSA Guidelines 2012
Evaluate
for snoring at all routine healthcare maintenance visits.
If children do snore or have signs or symptoms of OSAS, then a
more focused evaluation is warranted.
Children
who snore regularly and have any OSAS signs and
symptoms should undergo polysomnography or, alternatively, be
referred to a sleep specialist or to an otolaryngologist.

The gold standard is overnight, attended, in-laboratory
polysomnography.

Specific pediatric criteria should be used.

Polysomnography identifies the presence and severity of OSAS.

Specialists might be able to diagnose and determine the severity
of OSAS.
Only 55% of children with suspected OSA, based on clinical
evaluation, actually have OSA confirmed on sleep study
AAP OSA Guidelines


The first-line treatment of children with OSAS, adenotonsillar
hypertrophy, and no contraindication to surgery is
adenotonsillectomy.

Adenoidectomy or tonsillectomy alone may be insufficient.

The rate of serious complications is low.
High-risk patients undergoing adenotonsillectomy should be
monitored in the hospital postoperatively.

Risk factors for postoperative respiratory complications are age
younger than 3 years, severe OSAS by polysomnography,
cardiac complications of OSAS, failure to thrive, obesity,
craniofacial anomalies, neuromuscular disorders, and current
respiratory tract infection.
AAP OSA Guidelines 2012

High-risk patients, including those with significantly abnormal baseline
polysomnogram results, sequelae of OSAS, obesity, or symptoms of OSAS,
should be reassessed for persistent OSAS after adenotonsillectomy by
objective testing or by a sleep specialist.

A large proportion of high-risk children have persistent OSAS
postoperatively.
 Intranasal corticosteroids may relieve mild OSAS if adenotonsillectomy is
contraindicated or if mild postoperative OSAS is present.

Mild OSAS is defined as an apnea-hypopnea index of less than 5 per
hour.

Response should be measured objectively after approximately 6 weeks.

Patients should be observed for recurrence of OSAS and adverse
effects of corticosteroids.
AAO-HNS PSG Indications

Complex medical condition-should undergo PSG
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Obesity
Down Syndrome
Craniofacial Abnormalty
Neuromuscular Disorder
Sickle Cell Disease
Mucopolysaccaridoses
AAO-HNS PSG Indications

Advocate for PSG


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Differing opinions on need for surgery
Discordance between physical exam and reported
severity of symptoms
Other Recommendations


Recommend overnight admission for age <3 or
severe OSA (AHI>10, oxygen desaturations below
80%, or both
Laboratory-based PSG should be obtained
POLYSOMNOGRAPHY

It should be performed without
sedation and sleep deprivation
 In a child- friendly environment
 By personnel with training in
recording and scoring pediatric
PSG’s
 Should be interpreted by physicians
with expertise in pediatric sleep
medicine
Pediatric PSG Parameters
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Apnea:
Any pause in respiration (>90% decreased airflow) lasting
longer than two breaths.
 Versus at least 10 s in adults.
Hypopnea:
Reduction of airflow by >30% for two respiratory cycles
accompanied by reduction of saturation by 3% or arousal from
sleep.
AHI:
Sum of Apneas and Hypopneas per hour of sleep.
RDI:
Sum of Apneas, Hypopneas, and respiratory event-related
arousals per hour of sleep.
RERAs:
Arousals associated with increased respiratory effort,
decreased airflow, snoring, or increased end-tidal PCO2
PEDIATRIC OSA -SEVERITY
OSA
SEVERITY
LEVEL
AHI
SpO2 NADIR
%
PEAK
ETCO2
TORR
PEAK ETCO2 > 5O T0rr
%TST
MILD
1-4
86-91
>53
10-24
MODERATE
5-10
76-85
>60
25-49
SEVERE
>10
<75
>65
>50
MANAGEMENT



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Any child with AHI> 5 intervention is necessary.
Less of a consensus regarding AHI 1-5.
Surgical

Adenotonsillectomy – First Line of therapy

Turbinate reduction

Craniofacial surgeryMandibular advancement/ Maxillary distraction.

Lingual Tonsillectomy/ Epiglottopexy

Hyoid Suspension

Tracheostomy
Medical

Weight loss

Continuous positive airway pressure

Intranasal steroids (modest effect)-Mild patients

Leukotriene antagonist- Mild patients

Oral appliances

Positional therapy
Tonsillectomy and OSA
 Tonsillectomy
“effective” 60-70% of
children with significant tonsillar
hypertrophy (if use AI<1 as measure of
success)
 82% of children had resolution of OSA (if
use AHI <5 as measure).
 Tonsillectomy produces resolution of OSA
in only 10-25% of obese children
Adenotonsillectomy

Efficacy

AHI

Quality of life

Cognition
 Pediatric Sleep Questionnaire
 IQ Test

Cardiovascular Parameters
 Cerebral blood flow
 Hemoglobin Saturation
 Pulse Rate
 Pulse variability

School performance
 Significant improvement in grades from 1st to 2nd
grade in cohort that underwent adenotonsillectomy.
 No significant change in control group and group that
chose not to have adenotonsillectomy..

Enuresis/Incontinence
 Children with OSA have increased risk for enuresis.
 Possibly related to increased levels of BNP?
 Significant decrease in nocturnal enuresis and
voids/day after adenotonsillectomy.
HIGH RISK PATIENTS
Risk Factors for Postoperative Respiratory Complications in Children
with OSAS undergoing Adenotonsillectomy
– Age Younger than 3 years
– Severe OSAS on PSG, AHI>10
– Pulmonary hypertension
– Congenital heart disease
– Failure to Thrive
– Prematurity, CLD.
– Recent URI
– Morbid Obesity
– Trisomy 21
– Craniofacial abnormalities
– Neuromuscular disorders, Cerebral Palsy
– Asthma
– Seizures
CPAP
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Almost always an
alternative to surgery
Surgical failure
Morbid Obesity
Complex OSA
Non-Surgical candidates
FDA approved for
children > 30 kg
Role of Sleep Endoscopy
 Performed
with IV Propofol infusion
 Highest reliability for evaluation of
hypopharyngeal structures
 Consider for patients who have failed
previous sleep apnea surgery or initially as
part of staged surgery
Sleep Endoscopy

BOT Collapse
Conclusion

Loudness of snoring does not correlate with degree
of OSA
 In-lab PSG is gold-standard to confirm OSA
 Only 55% of children with suspected OSA, based on
clinical evaluation, actually have OSA confirmed on
sleep study
 Adenotonsillectomy is first line treatment
 T&A 60+% effective if use AI<1 as measure of
success and over 80% effective if use AHI<5 as
measure
 Need to think of multi-disciplinary approach
 ENT, sleep medicine physician, nutritionist, oral
surgeon, bariatric surgeon