Obstructive sleep apnoea in children

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 < 75, CO2 > 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