Obstructive sleep apnoea in children Joanne Edwards Senior Paediatric Registrar TCH

4 month old with book over face to assist learning

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 Drugs 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 NREM sleep Hypoventilation Significant oxygen desaturations NREM sleep Relatively protected

What are the symptoms and signs?

Symptoms – night time Snoring Pauses in snoring with apnoea Sleeping 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 Hypopnoea Respiratory effort related arousal >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)

4 year old girl Bold bars are REM sleep – most desats durign REM sleep, preserved sleep architecture CA – central apnoea, CAP – capnography MA mixed apnoea OA obstructive apnoea

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 Moderate Severe 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 CPAP or BiPAP Other 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