SLEEP-DISORDERED BREATHING IN CHILDREN - OVERVIEW · 2016-03-07 · Sleep Disorders Parasomnia...
Transcript of SLEEP-DISORDERED BREATHING IN CHILDREN - OVERVIEW · 2016-03-07 · Sleep Disorders Parasomnia...
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SLEEP-DISORDERED BREATHING
IN CHILDREN - OVERVIEWיעקב סיון
לרפואת שינהנמרץ והמרכז טיפול , מכון ריאותאביב-הרפואי תלהמרכז , לילדים" דנה"ח "בי
“I have often imagined the monster of sleep as a heavy, giant
head with a tapering body held up by the crutches of reality.
When the crutches break we have the sensation of falling.”
Salvador Dali, 193727.3.2015מצפה הימים גלי כנרת פ"חיפ
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Talk outline
• SDB types
• pathogenesis and pathophysiology
• epidemiology & risk factors
• systemic involvement (inflammation, metabolic, CVS, brain)
• morbidity & sequalae (long & short term)
• co-morbidities (obesity, asthma)
• diagnosis (techniques)
• treatment and outcome results
(surgical, mechanical, medical)
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sleep disorders
Insomnia
Sleep Related
Breathing
DisordersHypersomnia
Circadian Rhythm
Sleep Disorders
Parasomnia Sleep Related
Movement Disorders
Insomnia due to Medical Cond.
Insomnia due to Drugs
Childhood Insomnia
Psychophysiologic Insomnia
Inadequate Sleep Hygiene
Snoring (8-10%)
OSAS (2-3%)
Idiopathic Hypersomnia
Narcolepsy (0.05%)
Kleine-Levine synd.
Rhythmic movement dis. (3-15%)
Periodic Limb Movement Syn.
Disorders of Arousal
Sleepwalking (5%)
Sleeptalking
Night Terrors (2-5%)
REM associated Delayed sleep phase syndrome (7% teens)
Jet lag, shift work
Free running
70%
7%
2%
8%
4%
9%
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• Sleep
• Sleep Medicine
• Sleep Medicine Reviews
• Sleep and Biological Rhythms
• Behavioral Sleep Medicine
• Journal of Sleep Research
• Sleep and Breathing
• Sleep Research
• Sleeping and Waking
• Open sleep Journal
• Sleep Medicine Clinics of North America
• Journal of Clinical Sleep Medicine
• Sleep Medicine Clinics of North America
• Sleep and Hypnosis
SDB in children recent 5 y. (En) = 1,352 papers - 22/m
14 SLEEP Journals - 2015
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Intermittent
hypoxia
Sleep
fragmentation
Alveolar
hypoventilation
Morbidity
Short term Long term
SDB & OSAS
PS - primary snoring: [7-10%]
OSA - obstructive sleep apnea: [2-5% at 3-8 y]
UARS – upper airway resistance syndrome: [?%]
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UARS – upper airway resistance syndrome
snoring, progressive increased neg. intrathoracic pressure to flow
limitation, arousals (RERAs), sleep disruption (abnormal physiology)
without gas exchange abnormalities (no A/H). Associated with
neurobehavioral changes similar to OSAS. Responds to similar treatments.
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patophysiology of UAOUA Narrowing
ATHCraniofacialObesity
Ventilatory driveUA reflexes
Arousals
Other factors
Genetics
Others
Abnormal UA Tone
Hormonal
patency of the upper airway is the
result of a fine balance between:
• UA resistance
• pharyngeal collapsibility
• tone of the pharyngeal dilators
• negative intraluminal pressure
generated by the inspiratory
muscles.
Effect of sleep:
No dis. during wake
Does (tonsils) size matter?
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UA resistance increases
UA negative pressure increases
Airflow is possible
Reflex activation of the UA muscles and increasing
their tone, excessive respiratory effort
UA pressure receptors are activated
Sleep hypotonia, ATH, obesity
Airway collapse and hypopneic
or apneic events / hypercarbia / hypoxemia
EEG arousals
Further increased sympathetic tone, reactivation of the pharyngeal
dilator muscles restoration of the pharyngeal airway patency
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ASSESSMENT OF THE UPPER AIRWAY MECHANICAL PROPERTIES
P = F x RFlow limitation
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0
<-10
-7
0
-4
-7
sleep hypotonia +UAO
0+2
-30
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P-V relationshipמדידה שלMeasurement of the pressure-flow
relationships is an objective laboratory
tool for the evaluation of the UA function.
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Holding
pressure Holding
pressure
estimates mechanical and structural
properties of the airway (w. compensation)measure of airway collapsibility
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The pediatric airway is very resistant to collapse compared to
the adult airway; airway collapsibility increases with age during
adolescence and is not a function of pubertal development.
In children and adolescents with OSAS the critical closing pressure
is much higher than in non-OSAS children (1+3 cm H2O)
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Arousals
A normal phenomenon < 11/h. (respiratory vs. non-respiratory).
Arousals protect from OSAS (increased dilator muscle activity,
reduced upper airway resistance, restoration of normal ventilation).
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decreased vigilance, sleepiness
and neurocognitive impairments
disruption, fragmentation and interfere
with the restorative nature of sleep.
frequent arousals
Arousals
A normal phenomenon < 11/h. (respiratory vs. non-respiratory).
Arousals protect from OSAS (increased dilator muscle activity,
reduced upper airway resistance, restoration of normal ventilation).
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OSAS-age distribution
AGE DISTRIBUTION OF OSA IN CHILDREN
Age (years)
70%
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MORBIDITY
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DECREASED
QUALITY OF LIFE
INCREASED
HEALTHCARE UTILIZATION
morbidity
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Neurocognitive and neurobehavioral
adversely affect the
prefrontal cortex and hippocampus
intermittent hypoxia
and hypercarbia
respiratory-related EEG
arousals (RERAs)
insufficient
sleep duration
oxidative stress and systemic inflammation
CRP, IL-6, TNF
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Learning, memory, and visuospatial skills
Language, verbal fluency, and phonological skills
Concept formation, analytic thinking, and verbal and
nonverbal comprehension
School performance and mathematical abilities
(recently reported also in PS)
Executive functions
Cognitive deficits associated with pediatric SDB
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Neurobehavioral abnormalities in pediatric SDB
Behavior & attention
ADHD like symptoms and hyperactivity, ODD
Aggression / impulsiveness
Abnormal emotional, behaviors, mood, anxiety
Sleepiness
Daytime hypersomnolence
(less clinical, more lab – MSLT)
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Results of last 10 years studies of cognitive and behavior
Pre vs. Post surgical treatment
Most studies showed post treatment improvement of behavior,
quality of life, hyperactivity, ADHD, and impulsivity
AAP 2012: “In developing children, early diagnosis and
treatment of pediatric OSAS may improve a child’s
long-term cognitive and social potential and school
performance. The earlier a child is treated for OSAS,
the higher the trajectory for academic and, therefore,
economic success”.
Pediatrics 2012
TECHNICAL REPORT
Diagnosis and Management of Childhood Obstructive
Sleep Apnea Syndrome
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Obstructive Sleep Apnea Syndrome
“Chronic enlargement of the tonsillar
tissue is affection of great importance,
and may influence in extraordinary way
the mental and bodily development of
children…At night, the child’s sleep is
greatly disturbed, the respirations are
loud and snorting and there is
sometimes prolonged pauses…”
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The snoring child:“ The child responds slowly to questions...impossible to fix attention for long at a time...looks sullen....The influence upon mental development is striking”
William Osler: The Principles and Practice of Medicine, 1892
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cardiovascular
Hypertension
Myocardial function
Endothelial function
Autonomic regulation
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Hypertension in children with OSAS
Higher DBP during sleep and wake in children with AHI of 16
± 15. Differences in DBP correlated with respiratory events
suggesting a causal link (Marcus et al., 1998, Horne et al., 2011)
[SBP not or mildly increased]
Increased DBP - using ambulatory 24 h BP monitoring in a
dose dependent fashion in:
PS, “mild” OSAS (AHI = 1-5), “moderate” OSAS (AHI > 5).
Dose dependent BP dysregulation:
Increased BP variability
Reduction of the physiologic nocturnal dipping
Both phenomena are precursors of systemic HT.
(Amin et al., 2004)
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Cardiac function
Subtle LV dysfunction and increased mass – OSAS
severity (AHI) dependent (Amin 2005)
RV dysfunction (Tal, 1988)
Pulm. Ht (Amin, 2005)
left and right ventricular hypertrophy is significantly
associated with postoperative respiratory complications
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Autonomic Nervous System
HRVLF/HF band power
extracted from ECG
by fast Fourier
transformation.
3 techniques
(Baharav et al.)
(parasympathetic
activity)
frequency
frequency
po
wer
po
wer
(parasympathethic +
sympathethic activity)
LF
LF/HF is dependent on the
balance of sympathetic to
parasympathetic activity.
LF
HF
normal
OSA
During sleep and awake
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• Measures the arterial volume changes in the fingertip
• A continuous monitoring of the vascular-tone
• Reflection of the sympathetic nervous system
Systole
Diastole
PAT Amplitude = Pulse Volume ChangePulse arterial tonometry
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PAT Signal
Attenuation
PAT Amplitude
Sympathetic activation
Digital artery
vasoconstriction
- receptors
PAT probe
Respiratory event (OSA)
Reperfusion normalized after T&A
in 20/26 children (Gozal et al. 2007)
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normaldys
systemic inflammation
OSAS
endothelial function
(Lavie and Lavie, 2009)
vasodilationinhibition of
platelet
aggregation
Inhibition of
leukocyte adhesion
Inhibition of
smooth muscle
cell proliferation
end organ injury
Obesity
systemic inflammation
endothelial dysfunction
end organ injury
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Inflammation
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ילדים נורמלים ערים
DIAGNOSIS
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Polysomnography – gold standard
Sleep Laboratory, DANA Children’s Hospital
sleep
Amount REM latency architecture (stages) arousalsEfficiency awakeningsLatency fragmentation
breathing
AHI sPO2
RDI pCO2
RR
CardiacHR. HRVarrythmias
Skeletal: movements, PLMS
Sleep quality is summarized by: arousal index respiratory arousal index (RERAs) sleep efficiency (sleep time/sleep opportunity).
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Sleep Laboratory, DANA Children’s Hospital
Obstructive apnea
SDB: oAHI (>1), O2 desats (>3%)
duration of O2 <90%, O2 nadir
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Measurement of flow limitation by nasal pressure
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PSG-OSA-GER
pH = 3.2pH = 5.3
Sleep Laboratory, DANA Children’s Hospital
Apnea associated with GER
EtCO2
SpO2
Esoph
Flow
RC
EFF
ABD
EFF
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Limitations of PSGstressful to children and parents
requires hospitalization
not child’s natural environment
not widely available, long waiting
expensive
not correlated with outcome
Is it really a gold standard???
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SDB and asthma are inflammatory diseases
potentially have a cumulative effect on morbidity
OSAS and Wheezing / ASTHMA
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*
* Objective data using PSG
Total n > 2,500 children. Most studies are based mainly on questionnaires
Increase rate of snoring and elevated AHI in children with history of
wheezing and asthma (‘‘dose-dependent’’)
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Airway inflammation related to leukotrienes and airway oxidative stress are
possibly implicated in the pathogenesis of both disorders.
PATHOGENETIC LINKS BETWEEN OBSTRUCTIVE
SDB AND RECURRENT WHEEZING/ASTHMA
Goldbart A, Chest 2006
(Kaditis 2011)
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Increased expression of cysteinyl leukotrienes and their receptors within the
pharyngeal lymphoid tissues contributes to adenotonsillar hypertrophy and
severity of SDB.
Goldbart A, 2004 LKG, Ped Pulm 2011
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LKG, Ped Pulm 2011
92 children with poorly-controlled asthma (3-10 y.)
OSA = 63% (AHI >5 by PSG), OR = 40.1
T&A in 35
No T&A in 24 (controls)
Follow-up – 1 year
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AJRCCM 2010
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A multicenter, retrospective review of children who underwent
polysomnography before and after T&A. The presence of asthma was
a significant predictor of residual SDB in non-obese subjects.
Bhattacharjee R, AJRCCM 2010
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Outcome of T&A for OSAS
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Residual OSAS = up to 27% (Tauman et al. J Pediatr 2006)
Residual OSAS (by PSQ): = 15% (Sivan et al. ATS 2014)
Bhattacharjee et al.
2010
T&A resulted in a reduction in AHI in 91% of children
Only 27.2% normalized their AHI (<1)
50% were obese
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Childhood Adenotonsillectomy Trial (CHAT)
2013
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The primary outcome was a neurobehavioral measure of
attention and executive function, a domain that has been
shown to be sensitive to intermittent hypoxemia related to the
OSAS.
Aim: to evaluate the efficacy of early T&A versus watchful
waiting with respect to cognitive, behavioral, quality-of-life,
and sleep factors.
Selection criteria:
In Out
Age: 5-9 years AHI>30 or OAI>20
AHI > 2 or OAHI > 1 spO2 < 90% for >2% TST
BMI z score > 3
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Outcome assessment at
baseline and 7 m. post randomization
PSG
cognitive and behavioral testing
NEPSY (Developmental Neuropsychological Assessment - scores range
50 to 150 [100 representing the population mean])
Conners’ (caregiver and teacher ratings of behavior)
BRIEF (summary measures of behavioral regulation and metacognition)
PSQ-SRBD (pediatric sleep questionnaire for SDB)
Epworth sleepiness score
PedsQL (Pediatric Quality of Life Inventory)
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1.2008-9.2011
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NEPSY-Developmental Neuropsychological Assessment
Conners’ - caregiver and teacher ratings of behavior (
BRIEF - summary measures of behavioral regulation and metacognition
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Figure 2. Normalization of Polysomnographic Findings.
Median AHI
WW = 4.5
T&A = 4.8
obese - BMI > 95th percentile
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CHAT study limitations
Age – 5-9 years
Mild-moderate cases (median AHI<5), therefore,
baseline functions were within normal range, hence
improvement was mild.
No A group
surgery resulted in greater improvement in:
Symptoms
Behavior
Quality of life
Polysomnographic findings
no greater improvement in attention and executive functions
CHAT study summary
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The effects of treatment on the cardiovascular
consequences of OSA in children
studies that show improvement in the cardiovascular outcome with treatment
? Conflicting results
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TREATMENT OPTIONS
Surgical
Mechanical
Medications
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19.2.2015
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AHI - no sig. change (p = 0.07)
OAI – did not normalize (no “cure”)
Destauration index - no sig. change (p = 0.09)
Mild OSA, minor change
OAI N = 23 N = 23
12 weeks
Goldbart & Tal, Pediatrics 2012
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Goldbart & Tal, Pediatrics 2012
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LKG, Chest 2014
Retrospective review – LTA + intranasal CS in mild OSA (AHI <5)
*
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non-invasive positive pressure ventilation
Main problem – adherence and compliance (4/4)
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CPAP - Continuous Positive Airway Pressure (CPAP)
BIPAP – Bi-level positive airway pressure ventilation
APAP - Automatically titrated positive airway pressure
AVAPS - Average volume assured pressure support
PAV - Proportional assisted ventilation
ASV - Adaptive servo-ventilation
C-Flex®, Bi-Flex® - Expiratory pressure relief and flexible bi-level
positive airway pressure
non-invasive positive pressure ventilation
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HFHHNC in children McGinley et al. Pediatrics 2009
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McGinley et al. Pediatrics 2009
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0
5
10
15
20
25
30
35
40
45
50
Without treatment With HFNC treatment
Ap
ne
a h
yp
op
ne
a i
nd
ex
Apnea hypopnea index with and without HFNC treatment for each of the five cases.
p=0.034
Goldberg et Al. 2014
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תודה