A S T H M A

Posted 24 days ago in Education.

D E F I N I T I O N -Chronic inflammatory airways disease characterised by variable reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation.

A S T H M A

Chronic inflammatory airways disease characterised by variable reversible
airway obstruction, airway hyper-responsiveness and bronchial inflammation.


A E T I O L O G Y
Genetic factors: Positive family history of asthma or atopy.
Environmental triggers: Passive or active smoking, URTIs, exercise, cold weather, inhalant
allergies (house dust mite/pollens/moulds/pets) and food allergens.


A S S O C I A T I O N S / R E L A T E D

Eczema, allergic rhinitis, previous CLD of prematurity.
‘Hygiene’ hypothesis: Exposure to microbial products in infancy leads to switching off Th2
predispositionof T cells and increasingregulatory T cellsto prevent an allergic predisposition.
DD in <2 years: Aspiration, pneumonia, tracheomalacia, CF, tracheo-oesophageal fistula
(H-type), bronchiolitis.


E P I D E M I O L O G Y
Prevalence: 10–15%. Age: 80% of asthmatic children are symptomatic by the age of 5. M:
F, 2:1; equalises in adulthood. Distribution: Viral-associated wheeze/recurrent wheezy
bronchitis " in urban areas and in children of low socio-economic status families.

H I S T O R Y
Age-related symptoms:

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<1 year: Persistent or recurrent nocturnal cough, wheezing with URTIs.
2–3 years: Nocturnal cough, wheezing during exercise with URTIs.
<5 years: Non-productive cough may be the only symptom, often worse at night and in
the morning.

Assess severity: Frequency of attacks (mild: <1 attack in 2 months; moderate: >1 attack
in 2 months; severe: persistent symptoms, #exercise tolerance), effect on school
attendance, hospital attendances and admissions to PICU.

E X A M I N A T I O N
Respiratory: End-expiratory wheeze, recession, use of accessory muscles, tachypnoea,
hyper-resonant percussion note, diminished air entry, hyperexpansion, Harrison sulcus
(anterolateral depression of thorax at insertion of diaphragm).
Peak flow: Useful in >5 years of age; use as baseline (predicted best) and as determinant for
efficacy of treatment.
BTS guidelines for assessment of acute asthma attack

Severe asthma

Life-threatening asthma

Too breathless to speak or feed

Silent chest

Tachycardia:

Cyanosis

>120 bpm in 2–5 years

Poor respiratory effort

>130 bpm in <2 years

Hypotension

Tachypnoea:

Exhaustion

>30 breaths/min in 2–5 years

Confusion

>50 breaths/min in <2 years
Peak flow: <50% predicted >5 years

Coma
Peak flow: <33% predicted in >5 years

 

P A T H O P H Y S I O L O G Y
Acute phase (within minutes): Contact with exacerbating factor (cigarette smoke, inhalant
or food allergen or viral infection) leads to " airway receptor hyper-responsiveness !
narrowing of airways.
Late phase (onset after 2–4 hours, effect may last up to 3–6 months): Persistent
bronchoconstriction 2˚ to vicious cycle of inflammation, oedema and excess
mucous production.

I N V E S T I G A T I O N
CXR: In acute severe cases to exclude pneumothorax or first presentation to exclude
congenital anomaly.
Lung function (spirometry): Can be performed in >5 years. Obstructive airways disease:
FEV1 <80%, FVC normal or reduced, FEV1/FVC <70%. Assess reversibility after 400 mg
salbutamol inhalation.

M A N A G E M E N T
BTS guidelines 2008 for the management of acute asthma attack

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High-flow oxygen via reservoir bag.
Salbutamol and ipratropium bromide via volumatic spacer or nebulised.
Oral prednisolone 20 mg (2–5 years), 30–40 mg (>5 years) or IV hydrocortisone if unable
to retain oral medication.
Commence IV salbutamol (bolus then infusion) or aminophylline infusion.
Magnesium sulphate (40 mg/kg) IV.
If not responding (<92% O2 saturations) or any life-threatening features present, discuss
with PICU for ventilatory support.

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Discharge criteria: Patients can be discharged when stable on 3–4-hourly inhaled
bronchodilators. Peak flow 75% of predicted best, and O2 saturations >94%.
Education: On adherence to medication, recognition of acute attacks, emergency protocol,
maintaining normal activities.
BTS stepwise management of chronic asthma
Key principles:
1. Avoid obvious precipitants, e.g. passive smoking, allergen avoidance.
2. Ensure good inhaler technique þ / volumatic spacer.
3. Check compliance.
4. Review treatment every 3–6 months.
5. ‘Rescue’ prednisolone in acute deterioration.
6. If obese advise weight reduction.
When to start preventer inhaler:
1. Symptomatic/use b2-agonist inhalers 3 times/week.
2. Waking one night/week.
3. Frequent exacerbations.
Children <5 years
Step 1, mild intermittent asthma: Short-acting b2-agonist inhalers (e.g. salbutamol)
as necessary.
Step 2, regular preventer control: Add low-dose inhaled steroid (200–400 mg/day
budesonide equivalent) or leukotriene receptor antagonist if steroid cannot be used.
Step 3, add-on therapy: Trial of leukotriene receptor antagonist.
Step 4, persistent poor control: Refer to respiratory paediatrician.
Children 5–12 years
Step 1, mild intermittent asthma: Short-acting b2-agonist inhalers as necessary.
Step 2, regular preventer control: Add low-dose inhaled steroid (200–400 mg/day).
Step 3, add-on therapy: Add LABA, e.g. salmeterol.
1. Good response: continue LABA.
2. Benefit from LABA but control still inadequate: "dose of inhaled steroids to 400 mg/day.
3. No response to LABA: stop LABA, " dose of inhaled steroids to 400 mg/day, and add trial of
oral theophylline (monitor plasma levels) or leukotriene receptor antagonist.
Step 4, persistent poor control: " Dose of inhaled steroids to 800 mg/day.
Step 5, continuous or frequent use of oral steroids: Maintain " dose of inhaled steroids.
Add oral prednisolone at lowest dose to provide adequate control.
Refer to respiratory paediatrician.


C O M P L I C A T I O N S

Decreased linear growth rate due to poorly controlled asthma more
usual than from overprescription of inhaled steroids, chest wall deformity, recurrent infections,
status asthmaticus can be fatal. One-third of deaths occur under the age of 5 years.

P R O G N O S I S

Asthma often remits during puberty and many children are symptom free as
adults, especially those who have mild asthma and are asymptomatic between attacks, or
who develop asthma at >6 years. Rates of admission and mortality in asthma have # since the
early 1990s

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