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OBSTRUCTIVE SLEEP DISORDERS IN BREATHING IN CHILDHOOD Adenotonsillar Hypertrophy A. Kaditis, MD Pediatric Pulmonology Unit, Sleep Disorders Laboratory.

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Presentation on theme: "OBSTRUCTIVE SLEEP DISORDERS IN BREATHING IN CHILDHOOD Adenotonsillar Hypertrophy A. Kaditis, MD Pediatric Pulmonology Unit, Sleep Disorders Laboratory."— Presentation transcript:

1 OBSTRUCTIVE SLEEP DISORDERS IN BREATHING IN CHILDHOOD Adenotonsillar Hypertrophy A. Kaditis, MD Pediatric Pulmonology Unit, Sleep Disorders Laboratory First Department of Pediatrics University of Athens School of Medicine and Aghia Sophia Children’s Hospital Athens, Greece

2 Obstructive Sleep-Disordered Breathing (SDB) Spectrum of abnormal respiratory patterns during sleep characterized by snoring and increased respiratory effort Primary snoring Upper airway resistance syndrome Obstructive hypoventilation Obstructive sleep apnea (OSA)

3 Adenotonsillar Hypertrophy Pathophysiology of Obstructive SDB

4 A Mechanical Model for Obstructive Sleep- Disordered Breathing (SDB) Upper Airway Resistance

5 Arens et al. Changes in Upper Airway Size during Tidal Breathing in Children with OSAS. AJRCCM 2005;171:1298 HealthyOSA Inspiration Expiration

6 Symptoms of Obstructive SDB directly associated with intermittent upper airway obstruction Snoring Reported apneas during sleep Difficulty breathing during sleep Mouth breathing Restless sleep Frequent arousals

7 Conditions affecting Upper Airway Resistance and/or Pharyngeal Collapsibility Adenotonsillar hypertrophy, allergic rhinitis, nasal septum deviation, nasal polyps Obesity Craniofacial abnormalities Neuromuscular disorders

8 Upper Airway Dysfunction and Adenotonsillar Hypertrophy

9 Adenotonsillar Hypertrophy Pathogenesis of Adenotonsillar Tissue Hypertrophy

10 Risk factorsDependent variable: tonsillar hypertrophy OR (95% CI) p value Age0.97 (0.90-1.04) 0.321 Gender1.03 (0.64-1.65) 0.906 Obesity0.69 (0.38-1.25) 0.219 Passive Smoking 0.96 (0.60-1.53) 0.851 History of wheezing2.23 (1.37-3.63) 0.001 Kaditis et al. Associations of Tonsillar Hypertrophy and Snoring with History of Wheezing in Childhood. Pediatr Pulmonol 2010;45:275

11 Dayyat et al. Leukotriene pathways and in vitro adenotonsillar cell proliferation in children with obstructive sleep apnea. Chest 2009;135:1142

12 Goldbart et al. Leukotriene Modifier Therapy for Mild SDB. AJRCCM 2005; 172: 364 OSARecurrent tonsillitis

13 Kaditis et al. CysLT-Rs in Tonsillar Tissue of Children with OSA. Chest 2008;134:324-31 OSARecurrent tonsillitis

14 Adenotonsillar Hypertrophy Does Adenotonsillectomy Cure OSA?

15 Brietzke et al. The Effectiveness of AT in the Treatment of Pediatric OSA. Otolaryngol Head Neck Surg 2006;134:979

16 Garetz et al. Behavior, Cognition and Quality of Life after AT for Pediatric SDB: Summary of the Literature. Otolaryngol Head Neck Surg 2008;138: s19-26

17 Pediatrics 2006;117:e61-6 Nasal budesonide + po montelukast vs. Placebo for 12 weeks in children with residual SDB pAT

18 Bhattarjee et al. AT outcomes in Treatment of OSA in Children. AJRCCM 2010; 182:676-683

19 Amin et al. Growth Velocity Predicts Recurrence of SDB 1 Year After AT. AJRCCM 2008;177:654-9 70 children (mean age: ≈ 10 y.o.)

20 Guilleminault et al. AT and OSA in Children: A Prospective Study. Otolaryngol Head Neck Surg 2007;136:169-75

21 Villa et al. Randomized controlled study of an oral jaw- positioning device for treatment of OSA in children with malocclusion. AJRCCM 2002;165:123-7 BeforeAfter

22 Conclusions Adenotonsillar hypertrophy is a major risk factor for obstructive sleep-disordered breathing in childhood  Cysteinyl leukotrienes promote adenotonsillar hypertrophy Residual sleep-disordered breathing post AT may be the result of co-existing nasal inflammation, obesity or craniofacial abnormalities.


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