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Obstructive sleep apnoea in children Joanne Edwards Senior Paediatric Registrar TCH.

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Presentation on theme: "Obstructive sleep apnoea in children Joanne Edwards Senior Paediatric Registrar TCH."— Presentation transcript:

1 Obstructive sleep apnoea in children Joanne Edwards Senior Paediatric Registrar TCH


3 What is OSA Repeat episodes of partial or complete upper airway obstruction during sleep Result in a disruption of normal ventilation and sleep patterns

4 Continuum of sleep disordered breathing

5 Sleep in children After 6 months REM sleep and non-REM sleep

6 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

7 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

8 Sleep cycles

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


11 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

12 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


14 Predisposing factors Genetic factors –Both obese and non-obese populations Drugs –Alcohol –Chloral hydrate –Benzodiazepines –GA –Opioids

15 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

16 Patterns REM sleep –Hypoventilation –Significant oxygen desaturations NREM sleep –Relatively protected

17 What are the symptoms and signs?

18 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

19 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


21 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

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

23 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

24 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

25 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)



28 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

29 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 65


31 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

32 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

33 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

34 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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