New Insights into Sleep Disorders Gerald D. Suh, MD ENT and
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Transcript New Insights into Sleep Disorders Gerald D. Suh, MD ENT and
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
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
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
Obesity
Down Syndrome
Craniofacial Abnormalty
Neuromuscular Disorder
Sickle Cell Disease
Mucopolysaccaridoses
AAO-HNS PSG Indications
Advocate for PSG
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
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
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
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