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The A to Z-z-z’s of Obstructive Sleep Apnea

The A to Z-z-z’s of Obstructive Sleep Apnea. Sherri Katz, MD, CM, FRCPC Pediatric Respirologist Assistant Professor Children’s Hospital of Eastern Ontario University of Ottawa. Outline. What is OSA? Why does it occur? How common is it and who is at risk? What are the signs/symptoms?

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The A to Z-z-z’s of Obstructive Sleep Apnea

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  1. The A to Z-z-z’s of Obstructive Sleep Apnea Sherri Katz, MD, CM, FRCPC Pediatric Respirologist Assistant Professor Children’s Hospital of Eastern Ontario University of Ottawa

  2. Outline • What is OSA? • Why does it occur? • How common is it and who is at risk? • What are the signs/symptoms? • What are the consequences of OSA? • How can the diagnosis be made? • What treatment options are available?

  3. What is OSA?Obstructive sleep apnea syndrome • Partial or complete upper airway obstruction during sleep associated with: • Sleep disruption • Hypoxemia • Hypercapnia • Daytime symptoms • Continued chest and abdominal motion in the absence of airflow during sleep

  4. What is OSA?The Spectrum of Disease Primary snoring – snoring, no obstruction, no gas exchange or sleep architecture abnormalities • Fuentes-Pradera, Arch Pediatr Adolesc Med, 2003 Upper airway resistance - increased WOB, no discrete obstructive apneas or gas-exchange abnormalities, but have snoring and daytime sleepiness • Guilleminault, Seminars in Ped Neurol, 2001 Obstructive sleep apnea syndrome

  5. What is OSA?Defining Disease • Obstructive Apnea: continued chest and abdominal motion in the absence of airflow during sleep • Obstructive Hypopnea: decreased airflow and alveolar ventilation in the presence of paradoxical motion of chest and abdomen • Apnea-Hypopnea Index: # of events/hour • Used to categorize severity of condition • AHI > 1 abnormal, but clinically significant? • Pathology in a snoring child not yet clearly defined

  6. Why does OSA occur? • We don’t breathe as deeply while sleeping as when awake • blunting of hypoxic / hypercapnic drive • 25% ¯ tidal volume • arterial pCO2­ 3-4 mmHg • arterial pO2¯ 5-10 mmHg

  7. Why does OSA occur? • Upper airway tone is decreased during sleep, especially in REM • Collapse/obstruction of the upper airway during sleep causes obstruction & apnea

  8. Why does OSA occur? • Adenotonsillar hypertrophy • Most common cause of OSA in children • Between 3-6 yrs, tonsils & adenoids are largest relative to size of airway  peak incidence of OSA

  9. Why does OSA occur? Large tonsils and adenoids (site of upper airway closure) BUT No direct correlation between airway or adenotonsillar size and OSAS THEREFORE Combination of structural abnormalities & neuromotor abnormalities must be present for OSA to occur

  10. Why does OSA Occur? • Neuromotor tone • Healthy children have narrower upper airway than adults, but maintain airway patency by increased neuromuscular activity • ?OSAS in children lacking these responses • Marcus, Respiration Physiology, 1999

  11. Why does OSA occur? • Structural factors: • Upper airway is narrower and more collapsible in children with OSA • Isono, AJRCCM, 1998 • Mild cephalometric abnormalities in children with habitual snoring/OSAS • Zucconi, Eur Respir J, 1999 • Craniofacial anomalies

  12. Pathophysiology Upper Airway Obstruction Progressive Asphyxia Stimulation Chemoreceptor / Laryngeal Pressure Sensors Arousal From Sleep Increasing Respiratory Effort Return Of Muscle Tone INEFFECTIVE Relief Of Obstruction Relief Of Asphyxia Progressive Hypoxemia Sleep Fragmentation

  13. Differences between Children & Adults

  14. How Common Is It? Prevalence • OSAS= 1-2% • 1-1.8% in 1207 Italian children screened with questionnaires & sleep studies • Brunetti, Chest, 2001 • Upper airway resistance syndrome = ? • Snoring “nightly” = 8-27% • > ½ who snore at 4-5yrs no longer snore by 7 yrs • Prevalence of snoring is higher in adolescents than preadolescents • Owen, Clin Otolaryngol, 1996 • Of 604 children, 265 snored  12% of snorers had “pathologic snoring” or oxygen desaturations • Castronovo, J Pediatr, 2003

  15. Who is at Risk? • Peak incidence 3-6 yrs • = • African-American • Family history of OSA • 20% of 1st degree relatives had Hx highly suggestive of OSA • Ovchinsky, Arch Otolaryngol Head Neck Surg, 2002 • Obesity • OR = 4.59 • Redline, AJRCCM, 1999 • 26-33% of obese children had SDB vs. 2.3-5% of controls • Wing, Arch Dis Child, 2003

  16. Who is at Risk? • Neurologic problems • CP • neuromuscular • Syndromes • Trisomy 21 • Prader-Willi • Achondroplasia • Arnold-Chiari • meningomyelocele • Respiratory disease

  17. What are the consequences? • Neurobehavioural • Cardiovascular • Growth

  18. Why should we treat?Neurobehavioral • Excessive daytime sleepiness is not very common • Gozal, Pediatrics, 2001 • Increase in nocturnal enuresis • Neurobehavioral & learning deficits common and reversible • Large cohort of 1st graders failing in school had 6-9 x  incidence of OSA • Overall school performance significantly improved 1 year later when children with OSA had T&A • Ali, Eur J Peds, 1996

  19. Why should we treat?Neurobehavioral • Young children who snore frequently & loudly are at risk of lower grades in school several years after SDB is resolved • 297 1st graders with school performance in lowest decile of class • Screened with questionnaires & overnight oximetry • OSA in 54  advised to seek medical attention • 24 had T&A  improved school performance • No improvement in school performance if OSA and not treated, or no OSA • Gozal, Pediatrics, 1998

  20. Why should we treat?Neurobehavioral • Young children who snore frequently & have abnormal sleep studies are more likely to have impaired cognitive performance • N= 114, 6-12 years with adenotonsillar hypertrophy and suspected sleep-disordered breathing • Presence of snoring and abnormal polysomnogram together best predicted impaired vocabulary and verbal memory • Related to sleep efficiency • Tonsil size did not predict cognitive or behavioral test scores • Suratt, Pediatrics, 2006, Kaemingk (tuCASA), J Int Neuropsychol Soc., 2003

  21. Why should we treat?Neurobehavioral • Magnitude of impairment in cognitive function, attributable to sleep-disordered breathing, is profound • Similar in magnitude to the effects of lead exposure in children • Reduction in vocabulary scores 1.3 SD below general population • Suratt, Pediatrics, 2006

  22. Why should we treat?Neurobehavioral • Children with suspected sleep-disordered breathing are more hyperactive, inattentive and sleepy pre-T&A compared to controls and get better post-op • Cohort of children 5-9 years old, about to undergo T&A for any indication (50% with OSA on sleep study) • Behavioral hyperactivity and cognitive-attention indices improved in all who had T&A, regardless of OSA or not. No improvement in controls. • Chervin, Pediatrics, 2006

  23. Why should we treat?Neurobehavioral • Relationship between parentally reported ADHD symptoms, sleep & neurobehavioral characteristics in 5-7 year-olds? • Questionnaire on ADHD & sleep habits sent to 5728 parents, response rate 46% • Snoring in 11.7% • ADHD symptoms in 7.3% (77% boys) • 83 children evaluated in sleep lab • OSA in 5% who had significant ADHD Sx, 26% with mild ADHD Sx, 5% with no Sx

  24. Why should we treat?Neurobehavioral • Unusually high prevalence of snoring in children with mild ADHD Sx in community sample • Sleep-disordered breathing is NOT more likely to occur in children with significant ADHD symptoms, but is significantly highly prevalent among children with mild hyperactive behaviors  SDB may induce a mild behavioral hyperactive/inattentive phenotype • O’Brien, Pediatrics, 2003

  25. Why should we treat?Cardiovascular • Diastolic BP can be elevated & persists after wakening due to increased sympathetic tone • Marcus, AJRCCM, 1998 • Left ventricular wall thickness changes indicative of high afterload • Amin, Sleep, 2000

  26. Why should we treat?Cardiovascular • Pulmonary hypertension can result from vasomotor recruitment of pulmonary circulation with hypoxemia & hypercapnia • 37% of children with OSAS had evidence of right ventricular dysfunction suggestive of increased pulmonary artery pressures • Tal, Ped Pulmonol, 1988 • ECG evidence of right heart strain in 3% of 92 children scheduled for T&A • Wilkinson, Br Med J, 1981 • Cor pulmonale rarely seen – ?earlier detection & Tx

  27. Why should we treat?Cardiovascular • Echocardiographic changes in children with OSA • 47 children with OSA or primary snoring • LV mass index and relative wall thickness were greater in OSA than primary snorers • AHI > 10 significantly associated with RV dimension > 95 %ile (OR=6.7) & LV mass > 95 %ile (OR=11.2)  OSA in children is associated with cardiac remodeling and hypertrophy, related to the severity of OSA • Amin, AJRCCM, 2002

  28. Why Should we Treat?Growth • Children with OSAS are at higher risk for FTT • >50 % of OSA had FTT in early studies • Now < 25% - ? earlier Dx and Tx • Mechanisms proposed: • Dysphagia due to large tonsils/adenoids (minority) •  appetite from  olfactory acuity •  respiratory effort during sleep   work of breathing   energy expenditure (disproved) • Bland, Eur Resp J, 2001 •  insulin growth factor-1 levels and growth hormone release

  29. Why Should we Treat?Growth •  insulin growth factor-1 levels and growth hormone release • 70 children – 30 OSAS, 40 primary snorers, 35 controls • No differences in height, weight, IGF-1 • Both OSAS and primary snorers had decreased IGF-binding protein 3 • IGF-binding protein 3 & IGF-1 increased after T&A in children with OSAS  GH secretion is impaired in children with OSAS & primary snoring, improves after T&A and  weight gain

  30. Diagnosis • History & physical • Questionnaires • Audiotape, videotape, nap studies • Overnight oximetry • Polysomnography • “Home” studies

  31. DiagnosisHistory • Sleeping environment • Snoring, Witnessed apneas • Sleep history – bedtime behavior/routine, parasomnias, nocturnal awakenings/movement, time/difficulty awakening in AM, naps, enuresis • Daytime symptoms –behavioral/functional, school performance, morning headaches, irritability • PMHx – associated cardiopulmonary or genetic syndromes • Family Hx

  32. DiagnosisPhysical exam • Vital signs – Ht, Wt, BP • ENT: adenotonsillar hypertrophy, mouth breathing, nasal obstruction, hyponasal speech • Cardiac: cor pulmonale • Digital clubbing (rare)  usually normal, may see large tonsils Clinical diagnosis is confirmed in only 30-56% • Messner, Arch Otolaryngol Head Neck Surg, 1999

  33. Clinical Symptoms • Hx of snoring and difficulty breathing during sleep • Retractions, paradoxical breathing, episodes of increased respiratory effort associated with lack of airflow (pauses in snoring) • gasping, choking, movement, arousal

  34. DiagnosisQuestionnaires • Brouillette’s OSA questionnaire initially appeared accurate in small sample, but on subsequent studies was indeterminate in 47% • Brouillette, J Pediatr, 1984 • Parents cannot predict severity of OSA based on their observations • Preutthipan, Acta Paediatr, 2000

  35. Diagnosis • Audiotapes – lack specificity to distinguish OSAS from primary snoring. • Lamm, Ped Pulm 1999 • Videotapes – sensitivity 94%, specificity 68% • Sivan, Eur Respir J, 1996 • Nap studies – spontaneous daytime sleep in unfamiliar environment unrealistic & unlikely to contain REM  low sensitivity & underestimates severity • Saeed, Chest, 2000

  36. DiagnosisOvernight Oximetry • Repetitive airway obstruction in REM can give appearance of clusters of desaturation on oximetry BUT • Obstructive events not associated with desaturation will be missed on oximetry alone • Movement artifact can lead to false desaturation events • Oximeters have a built-in averaging time – can underestimate or miss short desaturations

  37. DiagnosisOvernight Oximetry • Cross-sectional study of 349 children referred for sleep study for ? OSA • 60% had sleep study proven OSA (AHI > 1) • Oximetry had PPV of 97% (doesn’t tell severity) • 47% of those with negative oximetry had OSA on PSG • Brouillette, Pediatrics, 2000  Positive oximetry is helpful, but doesn’t tell severity or distinguish OSA from central apneas  Negative pulse oximetry does not rule out OSA

  38. DiagnosisPSG • Polysomnography = sleep study • “Gold standard” • Only technique that allows comprehensive monitoring of both cardiorespiratory function and sleep noninvasively

  39. Diagnosis PSG EEG & EMG Chest & Abdominal movement Airflow Oxygen saturation Carbon dioxide Video • Can also detect seizures, PLM’s, night terrors, etc. • Under constant observation by sleep technologist • No significant night-to night variability in respiratory parameters • Katz E, J Pediatr, 2002 ; Scholle, Clin Neurophys, 2003

  40. DiagnosisPSG

  41. DiagnosisPSGdrawbacks • $$$ • Labor-intensive • Not readily available – 5 Canadian pediatric centres • Long waiting lists • Disruptive for families • Monitoring may interfere with normal sleep  On survey of ENT surgeons < 12% of children who had T&A for OSA had prior PSG • Weatherly, Sleep Medicine, 2003

  42. DiagnosisHome Testing • 21 children 2-12 y.o., highly selected • Compared lab and home PSG (saturation, respiratory impedence, ECG & video) • For OSAS (AHI > 1): sensitivity 100%, specificity 62% • Used sophisticated system for ambulatory assessments, not commercially available • Jacob, Pediatr Pulmonol, 1995 • Other studies using less detailed techniques have not had good results

  43. Treatment • Surgery • Adenotonsillectomy • Nasal / facial surgery • Tracheostomy • UPPP • CPAP • Adjunctive Therapies • Observation with follow-up

  44. Treatment T&A • Adenotonsillectomy is the most common treatment for childhood OSA • Cure rate = 75-100% • Suen, Arch Otolaryngol Head and Neck Surg, 1995 • Complications • anesthetic • post-op pain, poor oral intake and bleeding • airway edema • pulmonary edema

  45. Treatment T&A • Increased risk of post-op complications if: • Age < 2 y.o. (OR = 4.3) • Associated medical condition (OR=3) • Pre-op AHI > 5 (OR=7.2) • Pre-op oxygen saturation nadir < 80% (OR=3.1) • Wilson, Anaesthesiology, 2002 • Obesity is also a risk factor for post-op complications • If at increased risk should be monitored in hospital 24 hours post-op • If symptoms resolve likely cured  If ongoing snoring or underlying condition  repeat sleep study at 6-8 weeks post-op

  46. Treatment T&A BENEFITS OF TREATMENT • High cure rate • Improved sleep: respiratory distress index & arousals • Tal, Chest, 2003 •  energy expenditure & weight gain • Marcus, J Peds, 1994 • Improved GH secretion –  circulating IGF-1 • Selimoglu, J Int Med Research, 2003 • Improved QOL • De Serres, Arch Otolaryngol Head Neck Surg, 2002; Flanary, Laryngoscope, 2003, Goldstein, Arch Otolaryngol Head Neck Surg, 2002

  47. Treatment CPAP

  48. Treatment CPAP • Used if surgical contraindication or failure • Long-term therapy that requires ongoing titration & compliance • 86% success rate in improving OSA with CPAP • Marcus, J Pediatr, 1995 • In 10 children using CPAP/BIPAP AHI decreased from 19.7 to 1.01 and lowest oxygen saturation increased from 76% to 90% • Padman, Clin Pediatr, 2002

  49. TreatmentAdjunctive Therapies • Avoidance of smoke, pollutants, allergens • Weight loss/maintenance crucial if obese • Nasal steroids can modestly improve OSA over 6 week period vs.placebo • Brouillette, J Pediatr, 2001 • Oral appliances may help • Villa, AJRCCM, 2002

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