Transcript Obstructive Sleep Apnea and Hypopnea Syndrome (OSAHS) in

Anuj Chandra MD, D-ABSM
Medical Director- Advanced Center for Sleep Disorders
Adjunct Assistant Professor- University of Tennessee College
of Medicine Chattanooga, TN
Disclosures
 I have no financial relationships with
commercial entities
When is snoring concerning ?
 Habitual snoring: > 3 times/week without OSA
 “Benign”  poor concentration, school performances
 History alone cannot differentiate habitual snoring from
OSA
 When to treat snoring ?
Obstructive Sleep Apnea (OSA)
(American Thoracic Society)
Disorder of breathing during sleep characterized by
prolonged partial upper airway (Uaw) obstruction and/or
intermittent complete obstruction (obstructive apneas) that
disrupts normal ventilation during sleep and normal sleep
patterns
 Sleep fragmentation
 Intermittent hypoxemia
 Intermittent hypercarbia
OSA: Epidemiology

Prevalence of snoring: 7-12%
 Prevalence of OSA
 Infants: 1 - 2%
 Children: 2 - 4%
 Adults:
 Women 2 - 4%
 Men
3 - 7%
Snoring
OSA
OSA
Lean
8 – 10%
2 – 3%
Gender
Prepubertal: M=F
Post pubertal: M>F
Peak incidence
- 1.5 – 5 years (coincides with ATH)
- Adolescence
Obese
50%
36%
60% (metabolic syndrome)
Risk factors for OSA
 Obesity
 Sickle cell disease
 Male
 Down syndrome
 African-American
 Prader Willi syndrome
 Prematurity
 Cranio-facial disorders
 Cigarette smoke exposure
 Neuromuscular disorders
 Adenotonsillar hypertrophy
 Cerebral palsy
 Asthma
 Allergic rhinitis
Pediatric OSA: Overview
Pathophysiology
Anatomy
Craniofacial size
Soft tissues
Fat distribution
Ethnicity
Neuromuscular
Airway collapsibility
Arousal threshold
Ventilatory control
Fluid shift
Lung Volume
Sleep
OSA
Thoracic pressure changes
Sleep Fragmentation
Hypercarbia
Intermittent Hypoxia
Gene trait, susceptibility
Environment, diet, exercise
Consequences
Metabolic
Cardiovascular
Neurocognitive
Autonomic
Anatomical factors
Craniofacial Factors/Syndromes
Crouzon
Apert
Treacher Collins
Hemi-hypoplasia
Ziteli and Davis. Atlas of Pediatric Physical
Diagnosis. 1997
Abnormal Dental Alignment
Obesity & OSA: Partners in Crime !
 Fatty infiltrates of UAw
 Risk of OSA in obese:
 Decrease lung compliance
 Odds ratio of 4.5
 Increased resistive load
 ~ 36% - 55% have OSA
 Affect upper airway patency
 Post-T&A ~ 2/3rd have
residual OSA
OSA: Adverse Sequelae
Individual genetic and environmental susceptible factors influences the
ultimate expression of OSA sequelae….
OSA

Cardiovascular


 Intermittent Hypoxemia

 Hypercarbia
 Sleep fragmentation
Metabolic


  Respiratory Effort
Insulin resistance
Neuro-cognitive



Dyslipidemia
Endocrine


BP dysregulation
Endothelial Dysfunction
EDS, ADD, poor memory
Poor concentration
Nocturnal Enuresis
OSA:Neuro-behavioral consequences
 Hyperactivity/Inattentive
Chervin et al, 2002; 109:449-
 Poor school performance
Gozal et al, Pediatrics 1998: 102: 616-
 Aggressive behavior
Gottlieb et al, Pediatrics 2003; 112:870-
 Excessive daytime sleepiness uncommon with AHI <20/hr
Gozal et al, Pediatrics 2001; 108: 693-
 Cognitive deficits co-vary with endothelial dysfunction
Gozal et al, Pediatrics 2010; 126; e1161-
Diagnosis of OSA
 Evaluate symptoms and morbidity
 History, questionnaires
 Assessment for severity of obstruction
 Polysomnogram (Sleep Study)
 Assessment for site of obstruction:
 Clinical examination
 Radiological evaluation
 UA endoscopy
Clinical features of OSAS
Night time symptoms
 Snoring
Daytime symptoms
 Excessive daytime
 Apneas
 Mouth breathing

 Choking or snorting arousals

 Paradoxical breathing

 Restless sleep

 Hyper-extended neck

 Frequent awakening

 Recent onset parasomnias

sleepiness
Morning headaches
Mid-afternoon dip
Hyperactivity
Attention deficits
Poor school performance
Aggressive behaviors
Chronic cough
Physical Examination
 Weight
 Nose:
 BMI
 Deviated septum
 Neck circumference
 Turbinates
 Mouth
 Bite
 Tonsils
 Malampatti/Friedman
 Airway crowding
 Macroglossia
 Polyp
 Adenoids
 Face
 Mid-face hypoplasia
 Retro/micrognathia
 Allergic shiners
 Respiratory
 Cardiac: S2 and murmurr
Staging of airways
Friedman Classification
Tonsils size
Polysomnography (Sleep Study)
 EEG - For sleep stages
 EMG – for chin tone and leg movements
 EOG – eye movements
 Nasal pressure
Airflow
 Oro-nasal thermister
 Chest and abdominal belts/summary – respiratory effort
 Oximetry with waveform
Gas exchange
 ETCO2 with waveform
 Snoring microphone
 EKG - heart rate and rhythm
 Body position
 Video
Grigg-Damberger et al, JCSM 2007: 3: 201
Indications for Sleep Studies
Indications
 Respiratory

Sleep related breathing disorders





OSA
Central sleep apnea
Sleep Hypoventilation
Periodic breathing
Sleep hypoxemia
 Non-Respiratory



Periodic limb movement of sleep (PLMS)
Narcolepsy
Nocturnal events


seizures vs. parasomnia
REM behavior disorders
Not indicated
 Typical Parasomnias
 Insomnia
 Circadian rhythm sleep
disorders
 Restless legs syndrome
Obstructive apnea
Severity of OSA
Children
 Mild OSA
 AHI 1 – 5/hour
 Moderate OSA
 5-10/hour
 Severe OSA
 > 10/hour
Adults
 AHI > 5/hour with Symptoms
 AHI > 15/hour (without Sx)
 Mild: 5-15/hour
 Moderate: 15-30/hour
 Severe: > 30/hour
Classification of OSA severity on PSG
Principles and Practice of Pediatric Sleep Medicine 2nd Edn. 2014
Biomarkers of Pediatric OSA
 Helps with screening (urine, saliva, blood, exhaled breath)
 Early detection, cheap
 Bedside and can be done in clinic
 Follow up of response to medical or surgical intervention
 Potential biomarkers:
 Pediatrics: Combination of kallikrein-1, uromodulin, urocortin-3 and orosomucoid-1
appears to provide sufficient accuracy to be considered a potential OSA diagnostic test in
children.
 Adults: IL- 6 and IL-10 appear to exhibit a favorable profile as biomarkers aiming to
discriminate patients with and without OSA.
Treatment of OSA in children
 Life style changes
 Weight loss: Diet, exercise
 Positional
 Alcohol avoidance
 Pharmacological treatment
 Inhaled steroids
 Leukotriene antagonist
 High flow nasal cannula
 Oxygen
 Surgical treatment
 Adenoidectomy
 Tonsillectomy
 Supraglottoplasty
 Positive airway pressure therapy
 CPAP
 Bi-PAP
Pharmacological Treatment
Effect of Intranasal Budesonide on OSA
OAHI (/hr TST)
Randomized double blind placebo controlled trial with the cross over
design on children with mild OSA
13
PRE
POST
13
12
12
11
11
10
10
9
9
8
8
7
7
6
6
5
5
4
4
3
3
2
2
1
1
0
0
0 5 10 15 20 25 30 35 40 45 50
Tx Group
0
62 recruited, 48 completed
Budesonide or Placebo
6 weeks on treatment
2 week washout
6 weeks other treatment
5
10 15 20 25 30
Control
Kheirandish-Gozal et al, Pediatrics 2008
Anti-inflammatory therapy outcomes for
mild OSA
 Retrospective analysis 2-14 years old
 2007 – 2012
 Mild OSA
 Combination ICS and oral montelukast x 12 weeks
 N = 3027, 836 fulfilled criteria, 752 received Rx
 Overall beneficial effect > 80%
 Normalization of PSG 62% (17% no change)
 Non responders: age > 7 years and obesity
Kheirandish-Gozal Chest 2014
Adeno-tonsillectomy
 First line of therapy
 Recent data: 25-60% have residual OSA
 Discrepancy between tonsillar size & OSA severity
 No consensus AHI cut-off to perform T&A
 Adenoidectomy alone: 30% likely for 2nd surgery within 3 yr2
 Complications: pain, bleeding and death
1. Guilleminault et al. J Pedriatr 1989
2. Brietzke, Katz and Roberson et al: Int J Ped Otorhinol 2006
 Washtenaw County Adenotonsillectomy Cohort
Giordani et al, J Int Neuropsych Soc 2012; 18: 212-
Follow-up at 1 year:
Sleep Variables
Apnea
Index
Subjective
Sleepiness
MSLT
OSA
(n=40)
5.6
0.1
49%
rare
15.6
17.5
Snoring
(n=38)
0.2
0.1
27%
rare
15.9
17.3
17.4
17.3
Surgical
Controls
(n=27)
0.1
Rare
Improvement over time. No Differences at Follow-up vs. Controls
High Risk Groups for Residual
OSA after T&A
 Older children: > 7 years
 Obese children
 Severe baseline OSA
 Syndromic patients:
 Down syndrome, Prader Willi,
 Craniofacial syndromes (Treacher Collins, Pierre Robin)
 Neuromuscular disorders: hypotonia, cerebral palsy
 Significant Allergies and Asthma
 Orthodontic disorders
 12 obese children
 BMI ~ 35
 Age: 10 years
 Range of AHI: 2-36/hour
 High flow nasal cannula (20 L/min) room air
 2 PSGs: on and off Nasal cannula
 High flow NC group:
 AHI reduction: 11+3 to 5+2 per hour) P<0.001

EEG arousal, RR, desaturation were also noted
Pediatrics 2009
Positive airway pressure therapy
 First described use in OSA in 1981
 Considered the "gold standard" of therapy
 Treatment, not cure
 Stents UAw open, preventing dynamic collapse
 Increases FRC, pulmonary reserve
 Indications
 Residual OSA
 Surgery contraindicated
 Hypoventilation
Pediatric CPAP mask
Resmed Infant Bubble Mask
Pixie nasal mask
Respironics Petit Gel Full Face Mask
Mini Me 2
Pixie nasal mask
Other upper airway surgeres
 NASAL CAVITY
 Septoplasty, Turbinate reduction
 NASOPHARYNX
 Revision adenoidectomy
 PALATE and OROPHARYNX
 Uvulopalatopharyngoplasty (UPPP)/ Expansion pharyngoplasty
 ORAL CAVITY
 Tongue reduction
 HYPOPHARYNX
 Lingual tonsillectomy, Tongue base reduction / Glossoptosis
procedures
 LARYNX
 Supraglottoplasty, dilatation of subglottic stenosis
Rapid maxillary expanders:
 Increase in the width of the palate,
 nasal cavity, corrects deviated septum
 Age 5-13 years
Mandibular repositioning devices
Role of Bariatric Surgery in Adolescence
 Failed clinical treatment with multidisciplinary and
adequate therapy
 Body Mass Index:
 BMI > 40 kg/m2 with comorbidities (DM2, HTN,
dyslipidemia)
 BMI > 50 kg/m2 without comorbidities
 Good comprehension and cognition to follow all
necessary procedures before and after surgery
 Not pregnant in year before surgery
 Good family support.
Bariatric surgery
 Most centers: Age >16 years
 Roux-en-Y gastric bypass & adjustable gastric ban
 Sleeve gastrostomy
 Kalra et al 2005
 34 obese adolescents
 19 patients had AHI > 5/hour
 10 had repeat sleep study
 After significant weight loss (mean, 58 kg), OSA severity
markedly decreased in all patients
 Baseline median AHI vs. after weight loss = 9.1 vs. 0.65 per hr
Take home messages
 OSA is very common in children, but under recognized &
under treated
 Carries many short & long term health risks, some of which
are unique to children and may be irreversible
 Consider medical management for mild OSA
 Although A&T is effective, recent data shows increasing
number of children with residual OSA despite surgery
 Consider referral to pediatric sleep specialist when indicated
41
American Academy of Pediatrics: Guidelines
for Pediatric OSA
 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
Pediatrics 2002;109:704
Childhood Parasomnias
Undesirable events or experiences occurring:
 At entry into sleep
 Within sleep
 During arousal from sleep
Parasomnia Classification
 Disorders of Arousal (from NREM sleep)
 Parasomnias Associated with REM Sleep
 Other Parasomnias
Sleep Terrors
•
•
•
•
Peak age: 5-7 years
Prevalence rate of 2.0 - 6.5%
Most will later sleepwalk
Usual duration in children:- 4 years
– 50% end by age 8
– 36% continue into adolescence
Sleep Terrors
•
•
•
•
Begin abruptly from NREM sleep
Episodes of agitation and apparent terror
Heralded by a blood-curdling scream or cry
Followed by confusion, agitation and autonomic
disturbances
• Patient difficult to arouse
• If patient can be awakened, may describe:
– Vague sense of terror
– Isolated or fragmented dream imagery
Parasomnias Associated with REM Sleep
• Nightmares
• Sleep paralysis
• REM Sleep Behavior Disorder
Nightmares
 75% of children experience nightmares
 10 - 50% of children have nightmares severe
enough to disturb their parents
 Proportion of children reporting nightmares
reaches a peak around ages 6-10 years and
decreases thereafter
Nightmares: Clinical Characteristics
• Usually during last half of night
• Complex dream mentation: - “Good dream gone bad”
• Emotional reaction more significant than autonomic
response
• Fully alert upon awakening
• Responsive to comforting
Nightmares: Precipitating Factors
• Anxiety / Stress
• Personality – association with creativity
• Post-traumatic stress disorder
Nightmares: Treatment
• Explanation and reassurance
• Sleep hygiene
• Behavioral therapies
Nightmares vs Sleep Terrors
Nightmares
•
•
•
•
•
•
•
•
REM sleep
Most common
parasomnia
Second half of night
Delayed return to sleep
Easily comforted
Detailed narrative
description of episode
Mild autonomic activity
Alert upon awakening
Sleep Terrors
•
•
•
•
•
•
•
•
NREM sleep
2.0 - 6.5% prevalence
First half of night
Rapid return to sleep
Resists comforting
Fragmented recall /
amnesia
Intense autonomic
activity
Confusion on waking
Enuresis: Definition
 Persistent bedwetting more than twice a month
past the age of five years
 Primary enuresis:
Patient has never been dry on a regular basis
 Secondary enuresis:
Patient becomes enuretic after being dry for at
least six months
Enuresis: Declines with Age
Enuresis: Theories
Plasma Vasopressin
(pg/ml)
4
3
2
1
0
8:00 AM 12 Noon 4:00 PM 8:00 PM
Normals
12 Mid
4:00 AM 8:00 AM
Enuretics
Enuresis: Other Theories
 Functionally small bladder capacity
 Dysfunctional detrusor activity
 Higher arousal threshold
Percentage of Children with Frequent Enuresis
Enuresis and Pediatric OSA
60
 Obstructive sleep apnea
should be considered in
the differential diagnosis
of enuresis in children
50
40
 Frequent enuresis is
30
more common in
children with a higher
apnea hypopnea index
(AHI)
20
10
0
AHI < 1
AHI > 1
Enuresis: Evaluation
 History
 Developmental milestones
 Family history
 Physical / neurological exam
 Urinalysis
 Evaluation of urinary stream and bladder
capacity
Enuresis: Behavioral Treatment
 Limit fluids / caffeine near bedtime
 Positive reinforcement
 Hypnosis and imagery
 Bladder stretching
 Sphincter training
 Scheduled wakings
 Urine alarms
Enuresis: Pharmacologic Rx
 DDAVP (Desmopressin)
 Effective in most patients
 Tablets and nasal spray
 Low frequency of side effects: Concern for diabetes insipidus
 Hyponatremia
 Imipramine
 ECG abnormalities
 Possible behavior problems
Disorders of Arousal
 Arousals from NREM sleep
 First half of night, typically short duration
 Prolonged or multiple episodes may occur
 Confusion / automatic behavior
 Difficult to awaken during event
 Fragmented imagery
 Rapid return to sleep after event
 Amnesia of events
Disorders of Arousal
Abrupt Arousal
Partial or complete arousal from sleep
Confusional Arousals: Clinical
Characteristics
•
•
•
•
Occur on arousal from NREM sleep
May not recognize parents
May cry, yell, or moan
Speech often unintelligible,
sounds like words
• Most common words: “No, No!”
Sleepwalking: Clinical Characteristics
• Quiet wandering (injury unlikely)
• Agitated wandering (injury more likely)
• Behaviors of variable complexity
• Inappropriate behaviors
• Most sleepwalkers have few daytime effects
Disorders of Arousal: Familial Basis
– 60% of children have positive family history
– 10-fold increased prevalence in first-degree
relatives of an affected individual
Disorders of Arousal: Evaluation
Video-PSG needed if:
– Spells have atypical features
– Spells are stereotyped
– Patients describe potentially injurious behavior or
have injured themselves or others
PSG needed if OSA is suspected
Disorders of Arousal: Treatment
 Allow episodes to run their course:
 Interfere only to prevent injury
 May try to lead the patient calmly to bed
 Emphasize sleep hygiene
 Secure the bedroom to prevent injury:
 Consider ground floor bedrooms
 Window and door locks, pad bedrails
 Remove sharp objects or toys on bedroom floor
 Alarms or barriers at door/stairs
 Medications may be necessary in severe cases
Pediatric RLS

An urge to move legs, caused by discomfort as
described in child’s own words





Begins or worsens during periods of inactivity
Partially or totally relieved by movement
Worse in the evening or night
Biological parent / sibling with definite RLS
Periodic limb movements of five or more per
hour of sleep on PSG
Pediatric RLS: Clinical Features
 Attention sought for “growing pains”
 These present as:
 Sleep onset problems
 Sleep maintenance problems
 Daytime irritability and attention problems may
occur, likely due to sleep deprivation
 Family history is positive for RLS
 Iron deficiency may play a role as in adults
Pediatric RLS: Prevalence
“Night-Walkers” Survey
 138 adults with RLS (mean age 60 years)
 18% reported symptoms began before age 10 years
 25% reported symptoms began before age 20 years
 Childhood RLS case reports
Walters AS. Neurology 1996;46:92
Pediatric RLS: Treatment
 Strict sleep hygiene is necessary to avoid sleep
deprivation
 Limiting setting often required (day and at
bedtime)
 Treatment of iron deficiency
 Medications:
 Clonazepam 0.25 to 1.0 mg qHS
Insomnia
Complaint of:


Difficulty initiating sleep (bedtime resistance)
Maintaining sleep (inability to sleep
independently)
Daytime impairment:



Inattention, mood disturbance
Problems with memory and concentration
Impaired performance (at school in children)
Behavioral Insomnia of Childhood

Symptoms meet criteria of insomnia

Pattern consistent with either:


Sleep-onset association type
Limit-setting type
Behavioral Insomnia of Childhood
Evaluation
 History
 Precise description of the problem
 Parent response and interaction with child
 Typical night, not extremes
 Careful description of bedtime routines,
including naps
 Evaluate the 24-hour schedule
(weekday, weekend, vacation)
Behavioral Insomnia of Childhood:
Sleep-onset Association Type
•
•
Child begins to associate
sleep onset with
circumstances that are
problematic and demanding
of the caregiver.
Child is unable to fall asleep
without these associations
either at initial sleep onset or
during nocturnal
awakenings.
Treatments for
Sleep-onset Association Type
Education
 Awakenings during the
night are normal
 Sleep onset
associations are
learned
 Sleep onset
associations are
present at all ages
 New sleep onset
associations can be
taught
Behavioral treatment
•
•
•
•
•
•
Place child in crib/bed awake
and leave room
If child is upset, return to
comfort
Do not pick up the child;
comfort verbally
Stay in room briefly, leave
before child sleeps
Increase time between
responses
Same routine for awakenings
and naps
Treatments for
Sleep-onset Association Type
• Usual response between
three to five nights
• If symptoms persist,
consider:
–
–
–
–
–
Instructions not followed
Co-existing problems
Error in diagnosis
More time needed
Modifying the technique
• Modified techniques:
– Eliminate associations in
stages
– Parents present longer
– Limit physical contact
– Gradually withdraw
Behavioral Insomnia of Childhood:
Limit-setting Type
•
•
Refusal to go to bed
at an appropriate
time or following a
nighttime awakening
Insufficient or
inappropriate limit
setting
demonstrated by the
caregiver
Behavioral Insomnia of Childhood
Limit-setting Type: Favorite Delay Tactics
“Mommy …”
“Daddy, I need…”











I’m hot.
I’m cold.
I’m scared.
I’m not sleepy.
I’m thirsty.
My tummy hurts.
I hear something.
I have to go to the bathroom.
Fix my blanket.
I need to be tucked in again.











A drink.
One more kiss.
One more hug.
The light on.
The light off.
To tell you something
A band-aid.
My mommy.
You to cover me up.
You to rub my back.
A tissue.
Some medicine
Behavioral Insomnia of Childhood:
Limit-setting Type
•
•
•
Bedtime refusals,
stalling and repeated
demands
May also occur at
naptime and nighttime
awakenings
May be straightforward
or complex
Treatment of Limit-setting Type
 Emphasize the importance
of limit-setting
 Teach general limit-setting
guidelines (day as well as
night)
 Specific and individualized
techniques (gate, progressive
door closure)
 Positive reinforcement (star
chart)
Thank you
85