Obstructive sleep apnoea in children

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Obstructive sleep apnoea in children

• Joanne Edwards
• Senior Paediatric Registrar TCH

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What is OSA

• Repeat episodes of partial or complete upper
  airway obstruction during sleep
• Result in a disruption of normal ventilation and
  sleep patterns

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Continuum of sleep disordered breathing
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Sleep in children

• After 6 months
• REM sleep and non-REM sleep

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REM sleep

• Muscle atonia
• Increased cerebral blood flow
• Variable HR RR BP
• Increased upper airway resistance
• During REM get bursts of phasic events causing
  rapid eye movements and myoclonic twitches

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Non REM sleep

• Reduced muscle tone
• Decreased cerebral blood flow
• Regular HR RR BP
• Increased upper airway resistance
• NREM sleep is divided into stages by EEG criteria
  which parallel depth of sleep

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Sleep cycles
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Respiration during sleep

• Increased upper airway resistance
• Relaxed pharyngeal muscles (dilator)
• Probably decreased central respiratory drive
• Decrease in lung volumes during REM

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Sleep disordered breathing

• Partial or complete collapse at the elvel of
  extrathoracic airway
• Caused by
• Small upper airway smaller in those with OSA
• Decreased tone of pharyngeal dilators during
  sleep
• SUbvstantial change in dimensions of airway
  between inspiration and expiration

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Predisposing factors

• Peak age 2-8 years old
• Coincides with peak age of lymphoid tissue ie
  tonsils and adenoids
• Enlarged tonsils and adenoids
• Obesity
• Mucopolysaccharidoses
• Children with airway or facial abnormalities
• Midface hypoplasia
• Retro or micrognathia Acutely angled skull base
• Narrow maxillary arch
• Nueromuscular factors hypotonia or hypertonia

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Predisposing factors

• Genetic factors
• Both obese and non-obese populations
• Drugs
• Alcohol
• Chloral hydrate
• Benzodiazepines
• GA
• Opioids

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Pathology

• Decreased upper airway patency
• Adenotonsillar hypertrophy
• Allergies causing rhinitis, nasal obstruction
• Reduced capacity to maintain airway
• Obesity
• Neuromuscular disorder
• Decreased drive to breathe
• Brain stem injury

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Patterns

• REM sleep
• Hypoventilation
• Significant oxygen desaturations
• NREM sleep
• Relatively protected

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What are the symptoms and signs?
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Symptoms night time

• Snoring
• 12 of children snore
• Most of children with OSA snore
• Pauses in snoring with apnoea
• Sleeping
• Mouth breathing or unusual positions
• Nighttime sweating
• Restless or agitated sleep
• Parasomnias sleep terror, sleep walking
• Nocturnal enuresis

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Symptoms day time

• Growth deviations
• Failure to thrive
• Obesity is predisposing factor
• Mouth breathing and hyponasal speech
• Sleepiness
• Daytime napping
• Inattention, learning problems, behavioural
  problems

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On examination head and neck

• Craniofacial anomalies midface hypoplasia,
  retrognathia
• Obstructive septal deformity
• Macroglossia
• Hyponasal speech
• Mouth breathing adenoidal hypertrophy
• Mucosal or turbinate swelling suggestive of
  chronic nasal congestion
• Suggestive of allergy if dark circles under eyes,
  swollen eyes, transverse nasal crease

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Examination

• Growth
• Neuromuscular tone
• Mallampati classification of oropharyngeal
  crowding
• BP (hypertension)

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How is OSA diagnosed

• Sleep study polysomnography
• What is measured
• Airflow apnoea and hypopnoea
• Abdominal and chest wall movements to indicate
  respiratory effort
• End tidal CO2 adequacy of ventilation
• Saturations
• EEG stage of sleep
• ECG cardiac rate and rhythm
• EMG arousals and leg movement
• Snore microphone

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Measurements made

• Apnoeas
• gt90 decrease in ariflow that lasts gt0 of the
  duration of 2 normal breaths
• Obstructive continued or increased respiratory
  effort during period
• Central no respriatory effort during period,
  event lasts gt 20 seconds
• Can be mixed
• Hypopnoea
• Respiratory effort related arousal

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What is measured

• Apnoea hyponoea index total number occurring
  during 1 hour
• Other measures
• End tidal CO2
• If CO2 exceeds 50 for gt 25 of ttoal sleep time
  hypoventilation
• Hypoexmia lt 92(lowest nadir in normal children)

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Diagnostic criteria

• History of snoring, laboured breathing or
  obstructed breathing during sleep
• History of arousals, sweating, neck
  hyperextension, excessive daytime sleepiness,
  aggressive or irritable behaviour, slow growth,
  morning headaches, secondary enuresis
• PSG AHIgt1 or frequent arousals with icnreased
  respriatory effrot, desaturations, hypercapnia
• Not explained otherwise

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Severity

• Mild
• AHI 1-4, sats nadir 86-91, CO2 peak gt 53
• Moderate
• AHI 5-10, sats nadir 76-85, CO2 gt 60
• Severe
• AHI gt 10, sats nadir lt 75, CO2 gt 65

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Management

• Adenotonsillectomy
• Based on clinical experience, difficult to
  randomize
• Known adenotonsillar hypertrophy
• CPAP or BiPAP
• If adenotonsillectomy too risky or already done
• Other
• Weight loss, maxillofacial surgery to correct
  anomalies, nasal steroids, oral appliances

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Adenotonsillectomy

• Meta-analysis of 355 children with OSA and
  adenotonsillar hypertophy
• Post adenotonsillectomy 83 had normalized PSG
  and reduced AHI
• If obese, less successful outcomes AHIgt2
  persisted in about 76 (compared to 28 lean
  children

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Positive airway pressure

• CPAP
• Constant level of positive airway pressure
  throughout cycle
• BiPAP
• Higher pressures during inspiration than
  expiration
• Pressures are determined by sleep study
• Very poor compliance

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Oxygen

• Supplemental oxygen useful in short term if
  severely hypoxemic until definitive therapy
  provided
• Rarely used
• For those who cannot tolerate PPV
• Does not improve episodic upper airway
  obstruction or hypercapnia or sleep fragmentation
  
• May suppress ventilatory drive and worsen
  hypercapnia

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