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