what is asthma? - gp cme north/sat_sportsdrome_1430_yvas gp … · – wood 2000: [8-isopgf2 ]...
TRANSCRIPT
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AsthmaAetiology and Treatment
Julian VyasConsultant Respiratory Paediatrician
Starship Children’s Hospital, Auckland
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“A chronic inflammatory disorder of the airways … in susceptible
individuals, inflammatory symptoms are usually associated with
widespread but variable airflow obstruction and an increase in airway
response to a variety of stimuli. Obstruction is often reversible, either
spontaneously or with treatment.”
BTS/SIGN guidelines 2002
“The diagnosis of asthma is a clinical one; there is no
standardised definition of the type, severity or frequency of
symptoms, nor of the findings on investigation. The absence
of a gold standard definition means that it is not possible to
make clear evidence based recommendations on how to
make a diagnosis of asthma.”
BTS/SIGN guidelines 2012
Definition
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Childhood Asthma Definitions
• What is asthma?– Single disease
– Single final common pathway
• Asthma vs viral induced wheeze/ pre school wheeze
• Tendency to refer to “Asthma phenotype”– Suggests that a number of different processes result in
wheezing
• Ease/worth of differentiation complicated by absence of mechanisms to interrupt disease development
• Purpose of differentiation of pathophysiologies will become important when inflam modulation/ disease modifying Rx available.
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ASTHMA
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ASTHMA
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The Global Burden of Asthma, GINA, 2003
Oz 28.8%
NZ 26.8%
Highest =
Wales 29.8%
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• 15% of all New Zealanders
• Migrant > Indigenous
• Fatal 4.6 per 100,000
• Heavy burden on Maori
and Pacific Islanders
• Paed Hospitalisation rates
> adults by several times
Asthma in New Zealand
• 6-7 yr olds
– Maori 32%
– Euro 26%
– Pacific Islanders
21%
• Why such high
rates of asthma?
Asher et al. N Z Med J 2001;114:114-120
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Regional variation
•Prevalence
•Hospitalisation
rates
15-20%
20-30%
> 30%
Asthma in New Zealand
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Asthma aetiologyGenetic
Diet
Birth weight
Smoking
Allergy
Infection
GOR
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Identical twins > non-identical
FH of asthma/atopy
Risk of asthma = x3 for 1 parent; x6
for both
17 poss genes variety of asthma
related factors
receptors, ECP, TGF
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Antioxidant intake bronchial hyper-responsiveness
– Shaheen 2001: asthma severity negatively assoc with consumption of Selenium, red wine, apples
– Wood 2000: [8-isoPGF2] assoc with asthma severity;
• [Plasma antioxidant] (vit E, vit C, carotene, Zn, Se)
• Enzyme antioxidant activity (GSH peroxidase, SOD)
• Zn and Se assoc with severity asthma and [8-isoPGF2]
– Japan: decreased incidence ofasthma; increased fish oils
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
In utero exposure
abnormal lung growth, dilated bronchi, tortuous
bronchi, abnormal mucosa
increased neuroepithelial bodies (airway oxygen
sensors),
decreased fetal lung weight,
reduced number and size of fetal alveoli,
reduced peribronchial elastic tissue
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Smoking during childhood…
..increases airway hyper-responsiveness
..effect less striking with age
..early airway responsiveness to histamine
(1/12) predicts FEV1 at 6 years
..reduced parental smoking assoc with improved
asthma symptoms; mainly if no FH atopy
Smoking
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Increased wheezing in LBW infants
? Asthma
? viral induced wheezing
Barker hypothesis
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Many known ”allergic” precipitants:
Cats (saliva)
HDM (D. pteronyssius faeces)
Cockroach
Trees
Grasses
Rodents
? Salicylates in food (!)
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Good Bad
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
BadRSV “allergic type” residual effects
Anti-RSV IgE persists at least 12/12
[anti-RSV IgE] wheeze
(conc in wheezers > non-wheezers)
Anti-RSV IgE correlate with positive
allergen skin tests at 9 years
[histamine] at acute illness weak
correlation with severity of hypoxia - ?
Other mediators of wheeze
RSV+ LRTI assoc with LTC4 by ? IgE
dependent mechanism (83% IgE pos vs
29% IgE neg)
LTB4 (neut and eo chemoattractant) +
LTD 4 in 30% RSV-LRTI
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
BadRSV Infection; cellular response
Viral clearance in 7/7 (N cell med
immunity)
N response to viral inf = T lymps bind to
target cell receptors; ICAM-1 ligands.
Other viral infections release IFN-,
TNF-.
These cytokines amplify inflam
response to infection
RSV infection appears to block some of
these early cellular responses. ?
significance
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
GoodSome evidence that infection with
non-pathogenic mycobacterium can reduce
eczema in genetically modified mice
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Asthma
CD4+
TH2
TH1
IFN-
IL-12IL-4
-
-
IL-2
IL-3
IFN-
TNF-
IL-4
IL-5
IL-6
IL-10
IL-13
Anderson. Trends Pharmacol Sci 1994; 15
ALLERGIC RESPONSE
INFLAMMATORY RESPONSE
IFN-
IL-12
IL-4
RSV
+
TB
+
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
Increased prevalence of GOR in children
with asthma
? GOR causes wheeze / ? Asthma causes GOR
Not the same as possetting
Can be clinically unexpected
Not just with aspiration – acid in lower oesophagus
can cause bronchspasm
pH probe needs to be related to symptoms
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Asthma
Aetiology
– Genetic
– Diet
– Smoking
– Birth weight
– Allergy
– Infection
– GOR
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Pathophysiology
www.azmacort.com
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Stepwise management ofasthma in children aged 5-12 years
SIGN 2012
Step 1: Mild intermittent asthma
Step 5: Continuous or frequent use of oral steroids
Step 4: Persistent poor control
Step 3: Add-on therapy
Step 2: Regular preventer therapy
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Stepwise management ofasthma in children aged 5-12 years
SIGN 2012
Step 1: Mild intermittent asthma
Inhaled short acting ß2 agonist as required
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Stepwise management ofasthma in children aged 5-12 years
SIGN 2012
Step 2: Regular preventer therapy
Add inhaled steroid 200-400mcg/day *
(other preventer drug if inhaled steroid cannot be used)
200mcg is an appropriate starting dose for many patients
Step 1: Mild intermittent asthma
Start at dose of inhaled
steroid appropriate to
severity of disease.
* BDP or equivalent
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Stepwise management ofasthma in children aged 5-12 years
SIGN 2012
Step 3: Add-on therapy
1. Add inhaled long-acting ß2 agonist (LABA)
2. Assess control of asthma:
• good response to LABA – continue LABA.
• benefit from LABA but control still inadequate – continue LABA and increase
inhaled steroid dose to 400mcg/day * (if not already on this dose).
• no response to LABA – stop LABA and increase inhaled steroid to
400mcg/day *. If control still inadequate, institute trial of other therapies (e.g.
leukotriene receptor antagonist or SR theophylline).
Step 1: Mild intermittent asthma
Step 2: Regular preventer therapyStart at dose of inhaled
steroid appropriate to
severity of disease.
* BDP or equivalent
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Stepwise management ofasthma in children aged 5-12 years
SIGN 2012
Step 4: Persistent poor control
Increase inhaled steroid up to 800mcg/day *
Step 1: Mild intermittent asthma
Step 3: Add-on therapy
Step 2: Regular preventer therapyStart at dose of inhaled
steroid appropriate to
severity of disease.
* BDP or equivalent
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Stepwise management ofasthma in children aged 5-12 years
SIGN 2012
Step 5: Continuous or frequent use of oral steroids
Use daily steroid tablet in lowest dose providing adequate control
Maintain high dose inhaled steroid at 800mcg/day *
Refer patient to respiratory paediatrician
Step 1: Mild intermittent asthma
Step 3: Add-on therapy
Step 2: Regular preventer therapyStart at dose of inhaled
steroid appropriate to
severity of disease.
* BDP or equivalent
Step 4: Persistent poor control
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Stepwise management ofasthma in children under 5 years
SIGN 2012
Step 1: Mild intermittent asthma
Step 4: Persistent poor control
Step 3: Add-on therapy
Step 2: Regular preventer therapy
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Stepwise management ofasthma in children under 5 years
SIGN 2012
Step 1: Mild intermittent asthma
Inhaled short acting ß2 agonist as required
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Stepwise management ofasthma in children under 5 years
SIGN 2012
Step 2: Regular preventer therapy
Add inhaled steroid 200-400mcg/day * †
(leukotriene receptor antagonist if inhaled steroid cannot be used)
Step 1: Mild intermittent asthma
Start at dose of inhaled steroid
appropriate to severity of disease.
* BDP or equivalent† Higher nominal doses may be
required if drug delivery is difficult
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Stepwise management ofasthma in children under 5 years
SIGN 2012
Step 3: Add-on therapy
In children aged 2-5 years consider addition of leukotriene
receptor antagonist
In children under 2 years consider proceeding to step 4
Step 1: Mild intermittent asthma
Step 2: Regular preventer therapy
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Step 3: Add-on therapy
Step 2: Regular preventer therapy
Stepwise management ofasthma in children under 5 years
SIGN 2012
Step 4: Persistent poor control
Refer to respiratory paediatrician
Step 1: Mild intermittent asthma
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Treatment Administration
Inhaled vs oral vs other
• Inhaled : large vol spacers, aerochambers, dry
powder, nebs
• Oral: monteleukast, theophyllines, salbutamol
• Other: sub cutaneous
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Asthma
• Chronic inflammatory disorder
• “There’s a lot of it about”
• Rx stepwise
• Monitor symptom control
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Diagnosis
DDx (other causes of wheezing and dyspnoea)
Infection: viral inf, mycoplasma, TB
Congenital: CF, PCD, immunodeficiency
Anatomical abnormality: TOF, airway malacia, airway stenosis, vasc ring
GOR
Foreign body
Laryngeal dysfunction
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Diagnosis
Can be difficult
2 key questions:
“Are the symptoms significant”
“Is this something else, other than asthma”
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Diagnosis
“Are the symptoms significant”
Symptoms / History:
– Episodic wheeze ± cough, increased with intercurrent RTI’s,
– Recognisable/predictable precipitants (e.g. cats etc, cold air,
exercise)
– Dry cough in wee small hours
– Periods when completely well
– Periods when admitted to hospital with breathing difficulties
– Response to inhalers and/or steroids
– Family history of atopy or asthma
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Diagnosis
“Are the symptoms significant”
Signs:
– Polyphonic wheeze heard now/in the past
– Hyperinflation observed now/in the past
– Harrison’s sulcus (?)
Investigations:
– Normal CXR when well
– Obstructive lung function tests (spirometry), with bronchodilator
responsiveness - ??? Peak flow
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Diagnosis
“Is this something else, other than asthma”
History/symptoms:
– Persistent symptoms even on best day
– Moist cough
– No response to bronchodilators and/or steroids
– Better with antibiotics
– FH of other lung disease e.g. CF, TB; or of early death in childhood
from “pneumonia”
– PMH:
• recurrent pneumonia/bronchitis;
• Infections elsewhere – purulent ear infections, abscesses, boils, chronic
diarrhoea
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Diagnosis
“Is this something else, other than asthma”
Signs:
– Clubbing
– Chronic purulent ear infections, skin scars from infection
– smokers cough
– Focal chest signs, esp crackles >> wheeze
Investigations:
– Sputum culture +ve
– CXR abnormal when “well”
– Spirometry shows restrictive pattern, or no improvement with
bronchodilators, or steroids
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What to remember
Asthma is:
• Multifactorial
• Common in NZ
• If no response to treatment (assuming proper Rx
use/techniques etc) or if picture not typical consider
other Dx – even if only to return to original Dx of
asthma