Transcript Document

PEDIATRIC OBSTRUCTIVE
SLEEP APNEA
Leyla Akanli, M.D. F.A.A.P F.C.C.P
Pediatric Pulmonology and Sleep Medicine
DEFINITIONS
Sleep-disordered breathing (SDB) refers to the clinical
spectrum of repetitive episodes of complete or partial
obstruction of the airway during sleep.
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Primary Snoring (PS)
Snoring without obstructive apnea, frequent arousals from sleep,
or gas exchange abnormalities.
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Obstructive Hypoventilation Syndrome (OHS)
Persistent partial upper airway obstruction associated with gas
exchange abnormalities, rather than discrete, cyclic apneas.
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Upper Airway Resistance Syndrome (UARS)
Increasingly negative intrathoracic pressures during inspiration
that lead to arousals and sleep fragmentation.
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Obstructive sleep apnea (OSA)
Disorder of breathing during sleep characterized by prolonged
partial upper airway obstruction and/or intermittent complete obstruction.
PRIMARY SNORING
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Snoring is related to upper airway narrowing
Can not be diagnosed on clinical basis alone
PSG shows
No sleep fragmentation
No discrete events
No desaturation
No hypercapnia
PSG is essential to differentiate from PS from OSA
Clinical consequences of PSD is unknown
UPPER AIRWAY RESISTANCE
SYNDROME-UARS
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Snoring is due to upper airway narrowing or floppiness
Clinical history suggestive sleep fragmentation
PSG shows
Increased intra-thoracic pressure swings
Flow limitation of nasal pressure monitoring
Non –REM asynchronous breathing
Increased arousals
No gas exchange abnormalities
PSG is essential to differentiate UARS from OSA
OBSTRUCTIVE
HYPOVENTILATION
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Prolonged periods of partial airway obstruction
More common in children than adults
Clinical history similar to OSA
PSG demonstrates
Asynchronous breathing
Absence of discrete events
Sleep fragmentation
Abnormal gas exchange – maybe present only
during REM sleep –Hypoxia , Hypercarbia PetCO2 > 53
torr
MILESTONES
 1837 – Dickens – describes
overweight/hypersomnolent boy in the
Posthumous papers of the Pickwick Club
(term “pickwickian” used by Osler)
 1907- Osler
 1973-Guilleminault
 W. Hill described the obstructive sleep apnea sufferer
child as in 1889;
“ The stupid -lazy child who frequently suffers from
headaches at school, breathes through his mouth
instead of his nose, snores and restless at night and
wakes up with a dry mouth in the morning is well worthy
of the solicitous attention of the Scholl medical officer.”
ADULT VS PEDIATRIC OSA
Pediatric
OSA
Adult OSA
Age
Preschool
Elderly
Gender
M=F
M>F
Etiology
Adenoid/
Tonsil
hypertrophy
Obesity
Weight
FTT, normal,
or obese
Obese
Behavioral
Hyperactive
Somnolent
Sleep
architecture
Normal
Decreased
delta and
REM sleep
Surgical Rx
T&A
UPPP
Medical Rx
CPAP (rarely)
CPAP
EPIDEMIOLOGY
 Most studies showed 4% to 11% prevalence of parentreported apnea.
 Depending on threshold of AHI to diagnose, the
prevalence of pediatric OSA ranges from 1% to 4% in
most studies.
 Children with abnormal PSG that go untreated will
continue to have abnormal findings.
 Snoring and adverse neurocognitive, neurobehavioral
outcomes
 Overall prevalence of snoring in pediatric patient
population 8% and 5% in infants
 Always snoring in 1.5%-6%
EPIDEMIOLOGY
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Peaks ages two to 8 years
As obesity is increasing in pediatrics the age distributed shifted
Gender distribution: M>F after puberty, equal pre-puberty
Prevalence is higher among African Americans and Asian children
Family history
Prematurity
Other Co-Morbid conditions
PATHOPHYSIOLOGY
Structural factors
• Adenotonsillar hypertrophy
• Craniofacial abnormality
• Obesity
Neuromotor
tone
• Cerebral palsy
• Genetic diseases
OSA
Other factors
• Genetic
• Hormonal
• ? Diet,
Inflammation,
Passive smoking
Anatomic narrowing
Requires increased inspiratory pressures
Abnormal neuromuscular control
Reflex activation of dilators in response to airway obstruction often
fails
RISK FACTORS
Adenotonsillar Hypertrophy
Upper airway congestion; allergies
Upper airway obstruction , choanal stenosis, larnygomalacia,
subglottic stenosis
GER/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
Sickle cell disease
Cystic fibrosis
Chronic lung disease/ BPD
Scoliosis
Brain and spinal disorders – Spin Bifida, ACM type II
REDUCED MUSCLE TONE
 Trisomy 21
Small midface and cranium
Relatively narrow nasopharynx
Macroglossia
Hypotonia
Tendency for obesity
Relatively small larynx
 In addition, given their congenital
heart defects, they are already
predisposed to cor pulmonale.
 Because of these factors, the
incidence of OSA in patients with DS has
been estimated to be from 54% to 100%.
REDUCED MUSCLE TONE
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Neuromuscular disease
Hypothyroidism
Cerebral Palsy
Moebius, MG
Reduced Central Ventilatory Drive
ACM type I/II
Myelomeningocele
Brainstem injury or masses
MEDICAL CONDITIONS
Craniofacial syndromes
Apert
Crouzon
Pierre-robin
Treacher-Collins
Pfeiffer
Miscellaneous
Achondroplasia
Beckwith-Wiedeman
Goldenhar
Marfan
Mucopolysaccoridoses
Prader Willi
Sickle Cell Disease
Prematurity /CLD
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
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
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
EVALUATION
 Medical History
Developmental and School history
Family History
Behavioral assessment
 Physical Examination
Growth
HEENT
Cardiac examination
 Diagnostic Tests
For the most part are unnecessary
 Radiologic Studies
Lateral Neck
Laryngoscopy
EKG/ECHO
Cine-MRI
MALLAMPATI CLASSIFICATION
MULLER MANEVEUR
LARNYGOMALACIA
SUBGLOTTIC STENOSIS
GERD
MRI
Excellent soft tissue anatomy
Multiple planes
No ionizing radiation
Disadvantages
Cost
Weight limitations
Noisy
claustrophobia
HOME OXIMETRY TESTING
 Readily available and relatively inexpensive
 Subject to presence of significant artifact
 Artifact reduction maybe accomplished with
simultaneous –heart rate measurement and
Pletsymography waveform
 Excellent positive predictive value-97%*
 Poor negative predictive value-47%*
 Disorders with predominant sleep disruption and
hypercapnia will be missed.
*Brouillette RT et al. Pediatrics 2000
NAP STUDY
 Child may not achieve natural sleep – REM sleep may
not be captured
 Severity may be underestimated- Events usually
worsens as the sleep progress
 Excellent positive predictive value-77-100%*
 Poor negative predictive value-17-49%*
Keens TG, et al.Pediatric Pulmonol 1992, &Chest
2000
POLYSOMNOGRAPHY
 PSG IS THE GOLD STANDARD
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Meet diagnostic criteria of pediatric OSAS according to ICSD 2
Differentiate OSA from other SDB
Define severity of OSAS
Screen high risk children
Evaluate success of treatment
Titrate PAP therapy
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 POLYSOMNOGRPAHY
EEG
EOG
Nasal EtCO2
Nasal Oral Airflow
Chin EMG (2)
Microphone
Sao2
EKG
Tech Observer
Video Camera
Respiratory Effort
Documents arousals,
parasomnias, abnormal
sleeping position, and attends
to any technical problem
Leg EMG (2)
Record behavior
Courtesy of Dr. Carol Rosen
PSG PARAMETERS
 Apnea
Any pause in respiration lasting longer than two breaths.
 Versus at least 10 s in adults.
 Hypopnea
Reduction of airflow by 50% 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.
 No universally accepted PSG normal reference values
 AHI >1.5 or AI >1 per hour is most often used to identify
children- up to 12 years with OSA.
 Oxygen saturation<91%
 Change in nadir 02 from baseline>9%
 Maximal ETCO2>54
PEDIATRIC POLYSOMNOGRAPHY
In contrast to adults, children have:
Obstructive hypoventilation
Fewer obstructive apneas
Desaturation with shorter events
– Higher respiratory rate
– Lower functional residual capacity
– Smaller oxygen store
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
PARADOXICAL RIB-CAGE MOTION
HYPERCAPNIA
OBSTRUCTIVE APNEA
This tracing depicts cyclic obstructive apneas
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
Lefort osteotomies and maxillary distraction.
– Uvulopalatopharyngoplasty- Not a good idea !
– Tracheostomy
 Medical
– Weight loss
– Continuous positive airway pressure
– Intranasal steroids (modest effect)-Mild patients
– Leukotriene antagonist- Mild patients
– Oral appliances
– Positional therapy
– Snore aids
ADENOTONSILLECTOMY
 First-line of treatment
 Presence of additional risk factors not a contraindication to
adenotonsillectomy
 25 % residual OSA
 Re-assessment of high risk groups with post-operative
polysomnography is recommended
 CHAT study –RCT 5-9 years old
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
– FTT
– Prematurity, CLD.
– Recent URI
– Morbid Obesity
– Trisomy 21
– Craniofacial abnormalities
– Neuromuscular disorders, CP
– Asthma
SEVERE OSA
 Children with severe OSA show a
significant improvement in RDI and
quality of life.
 OSA does not resolve in the
majority of these patients.
 Postoperative PSG is recommended
for all children with severe OSA.
 To identify those who may
require further therapy.
SEVERE OSA
CPAP
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Almost always an alternative to surgery
Surgical failure;
Morbid Obesity
Complex OSA
Non-Surgical candidates
Local and systemic anti-inflammatory effect
Act as a pneumatic splint
Stimulates ventilation
Reduces activity of inspiratory, upper airway muscles
and diaphragm
Restores sleep, promotes weight loss
Improves cardiac function, Suppresses GERD
Decrease AHR
FDA approved for children > 30 kg
CPAP
CPAP-AIRWAY
Management Algorithm
COMPLICATIONS OF OSA
 Effects on growth
 Neurocognitive morbidity
 Cardiovascular consequences
 Metabolic
IMPROVEMENT IN WEIGHT
Girls
Boys
Marcus et al. J Pediatr 1994
NEUROCOGNITIVE MORBIDITY
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Hyperactivity, inattention, aggression
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Impaired school performance
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Daytime sleepiness
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Depression
CARDIOOVASCULAR MORBIDITY
 Pulmonary Hypertension
 Cor Pulmonale
 Systemic Hypertension
HYPERTENSION
HYPERTENSION
Marcus et al. Am J Respir Crit Care Med 1998
AAP GUIDELINES
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Screening of all children for snoring
Specialty referral of complex high-risk patients
Urgent evaluation of cardio-respiratory failure
PSG as Gold Standard for diagnosis
Adenotonsillectomy as first-line treatment
Inpatient monitoring of high-risk patients
Post-operative reevaluation to determine if additional
treatment is required