obstructive sleep apnoea in children joanne edwards senior paediatric registrar tch
TRANSCRIPT
Obstructive sleep apnoea in children
Joanne Edwards
Senior Paediatric Registrar TCH
What is OSA
• Repeat episodes of partial or complete upper airway obstruction during sleep
• Result in a disruption of normal ventilation and sleep patterns
Continuum of sleep disordered breathing
Sleep in children
• After 6 months
• REM sleep and non-REM sleep
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
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
Sleep cycles
Respiration during sleep
• Increased upper airway resistance – Relaxed pharyngeal muscles (dilator)
• Probably decreased central respiratory drive
• Decrease in lung volumes during REM
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
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
Predisposing factors
• Genetic factors – Both obese and non-obese populations
• Drugs – Alcohol– Chloral hydrate – Benzodiazepines – GA – Opioids
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
Patterns
• REM sleep – Hypoventilation – Significant oxygen desaturations
• NREM sleep – Relatively protected
What are the symptoms and signs?
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
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
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
Examination
• Growth
• Neuromuscular tone
• Mallampati classification of oropharyngeal crowding
• BP (hypertension)
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
Measurements made
• Apnoeas– >90% decrease in ariflow that lasts >0% of the
duration of 2 normal breaths – Obstructive – continued or increased respiratory effort
during period– Central – no respriatory effort during period, event
lasts > 20 seconds– Can be mixed
• Hypopnoea • Respiratory effort related arousal
What is measured
• Apnoea hyponoea index – total number occurring during 1 hour
• Other measures – End tidal CO2
• If CO2 exceeds 50 for > 25% of ttoal sleep time – hypoventilation
– Hypoexmia < 92%(lowest nadir in normal children)
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 – AHI>1 or frequent arousals with icnreased respriatory effrot, desaturations, hypercapnia
• Not explained otherwise
Severity
• Mild – AHI – 1-4, sats nadir 86-91%, CO2 peak > 53
• Moderate – AHI 5-10, sats nadir 76-85, CO2 > 60
• Severe – AHI > 10, sats nadir < 75, CO2 > 65
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
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 – AHI>2 persisted in about 76% (compared to 28% lean children
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
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