The pathogenesis of pediatric OSA Stijn Verhulst, MD, PhD Pediatric - - PowerPoint PPT Presentation

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The pathogenesis of pediatric OSA Stijn Verhulst, MD, PhD Pediatric - - PowerPoint PPT Presentation

Feb 27, 2024 249 likes •842 views

The pathogenesis of pediatric OSA Stijn Verhulst, MD, PhD Pediatric Pulmonology and Pediatric Sleep Medicine Pediatric Pulmonology and Pediatric Sleep Medicine Antwerp University Hospital Belgium stijn.verhulst@uantwerp.be Introduction

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The pathogenesis of pediatric OSA

Stijn Verhulst, MD, PhD Pediatric Pulmonology and Pediatric Sleep Medicine Pediatric Pulmonology and Pediatric Sleep Medicine Antwerp University Hospital Belgium stijn.verhulst@uantwerp.be

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Introduction

  • Combinatie kritische anatomie en additionele

risicofactoren

1

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Introduction

  • This presentation will focus on 3 parts of the

pathogenesis that are becoming increasingly clinically relevant:

, The role of obesity as an anatomical risk factor

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, The role of obesity as an anatomical risk factor , The role of upper airway inflammation , Natural history

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3

OBESITY

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Prevalence

  • Childhood obesity is associated with an

increased prevalence of obstructive sleep apnea.

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increased prevalence of obstructive sleep apnea.

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5

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Prevalence

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Prevalence

  • Both childhood obesity and OSAS are associated

with a number of complications.

  • Second, obesity and OSAS can interact in

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  • Second, obesity and OSAS can interact in

causing these complications, i.e. cardiovascular and metabolic complications.

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KEY MESSAGE: An optimal treatment should therefore target

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both conditions. This requires a good knowledge of the (individual) contributing anatomical factors.

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Anatomical correlates

  • The exact contributions of both adenotonsillar

hypertrophy and obesity to the pathogenesis

  • f OSAS are still controversial.

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  • f OSAS are still controversial.
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The scope of the problem

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Anatomical correlates

  • However, the relation between obesity and

sleep apnea in children is complex…

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sleep apnea in children is complex…

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Anatomical correlates

  • AHI is not a unique marker of OSAS: BMI often

correlates better with other markers of the severity

  • f sleep apnea, i.e. oxygen desaturation.

12

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Anatomical correlates

  • AHI < 2

2 < oAHI < 5

  • AHI ≥ 5

P VC (%pred)

106 ± 13 103 ± 13 95 ± 15 0.01

FEV1 (%pred)

104 ± 13 101 ± 14 95 ± 17 0.05 13 !"#

FEV1/VC (%pred)

99 ± 8 98 ± 7 101 ± 7 0.4

RVHe (%pred)

89 ± 36 86 ± 35 85 ± 26 0.6

TLCHe (%pred)

101 ± 21 101 ± 11 91 ± 20 0.03

FRCHe (%pred)

82 ± 21 76 ± 31 65 ± 21 0.008

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Anatomical correlates

  • Second, BMI is not the only marker of obesity.

However, there is limited data on the association between OSAS and markers of

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association between OSAS and markers of visceral adiposity in children.

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15 $% &&

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16 '( %) *+&&

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Anatomical correlates

  • Furthermore, the association seems to be age,

dependent:

, Obese children: Adenotonsillar hypertophy > Obesity

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, Obese teenagers: Obesity > Adenotonsillar hypertrophy

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Anatomical correlates

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Anatomical correlates

19 "" ,

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Anatomical correlates

20 "",

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Anatomical correlates

  • The magnitude of adenotonsillar hypertrophy

is more likely to be smaller in obese children compared to nonobese children with comparable AHI.

21 "",

  • Increased Mallampati scores in obese children

suggest that soft,tissue changes and potentially fat deposition in the upper airway may play a significant role in obese children with OSA.

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Anatomical correlates

22 %&&

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Anatomical correlates

23 %&&

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Anatomical correlates: treatment data

24 *"--".'/#-",

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Anatomical correlates: treatment data

25 *"--".'/#-",

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Anatomical correlates: treatment data

  • Multi,center retrospective study investigated the
  • utcome of adenotonsillectomy for OSAS in 578

children (50% obese):

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, AHI significantly dropped from 18.2±21.4 to 4.1±6.4 (p<0.001). , Only 157 (27.2%) had complete resolution of OSAS (AHI<1).

012%"&

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Anatomical correlates: treatment data

27 012%"&

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Anatomical correlates: treatment data

30 *+"3

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Anatomical correlates: treatment data

  • 61 obese teenagers.
  • 50% with OSAS.
  • After 6 months, these subjects lost an average
  • f 24 kg which corresponded to a relative

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  • f 24 kg which corresponded to a relative

decrease in BMI of approximately 30%.

*+",

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Anatomical correlates: treatment data

Definition of success Success rate (%) Apnea hypopnea index ≤ 2 62 Oxygen desaturation index ≤ 2 81

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Apnea hypopnea index ≤ 5 91

*+"

*+",

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Anatomical correlates: treatment data

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*+"

'+# )&4

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Functional imaging

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Obesity , conclusion

  • The pathogenesis of OSA in obese children is

complex illustrated by suboptimal response to adenotonsillectomy.

  • In view of the established link with metabolic

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  • In view of the established link with metabolic

and cardiovascular morbidity, there is a clear need to validate tools that identify the anatomical contributors in the individual child.

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Obese child with OSA Obese child with OSA Weight management Weight management Work up site

  • f

Work up site

  • f

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  • f
  • bstruction
  • f
  • bstruction

T&A T&A Non,invasive ventilation Non,invasive ventilation

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Obesity , conclusion

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UPPER AIRWAY INFLAMMATION

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Introduction

  • The size of tonsils and adenoids increases

from birth to approximately 12 years of age.

  • There is gradual concomitant growth in the

size of the skeletal boundaries of the upper airway.

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airway.

  • Between 2 and 8 years of age, the tonsils and

adenoids are the largest in relation to upper airway size, resulting in a relatively narrower upper airway.

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Introduction

  • However, despite this relative physiological

narrowing, young children exhibit less collapsible upper airways when compared with adults:

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adults:

, Increased tonic activation UA muscles , Increased central ventilatory drive

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Introduction

  • Classical stimuli for proliferation:

, Environmental irritants

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, Recurrent infections

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43 Kheirandish,Gozal et al, Expert Opin Investig Drugs, 2013

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44

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  • Cysteinyl leukotriene receptors are expressed

by small,size B,lymphocytes in the tonsillar

  • mantle zones and by T,lymphocytes in the

tonsillar extrafollicular areas.

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tonsillar extrafollicular areas.

  • Since these are immunologically active areas

participating in the generation of mature germinal centers, it is proposed that cysteinyl

  • leukotriene receptors are involved in the

pathogenesis of lymphoid tissue hyperplasia.

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UA inflammation , conclusion

  • Increased UA inflammation – leukotrien

modified.

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  • Pharmacological treatment is an alternative to

adentonsillectomy.

  • More data needed.
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NATURAL HISTORY

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