Asthma is an obstructive airways disorder characterised by chronic inflammation and hyperreactivity of the bronchial mucosa resulting in bronchoconstriction with reversibility.

It is the most common respiratory disorder in paediatrics, affecting up to 20% of children and causing around 40 childhood deaths in the UK each year.


Bronchial mucosa in children with asthma is hyperresponsive to aeroallergens. One current explanation for this is the ‘hygiene theory’: children who are exposed to lower concentrations of house-dust mites during infancy have an increased tendency towards IgE sensitivity and asthma by 5 years old. Irritants such as allergens, pollutants or cold air provoke a cytokine-mediated hypersensitive response in the smooth muscle layer resulting in bronchospasm and bronchoconstriction. The narrowed airway calibre is more resistant to airflow and gives rise to the classic wheeze.

Bronchial hyperesponsiveness causes decreased expiratory flow, and therefore asthma is an obstructive disorder with a decreased FEV1:FVC ratio. The lungs become hyperinflated as a result of decreased air expulsion, increasing intra-alveolar pressure causing vasoconstriction and hence hypoxia. Hyperventilation is driven by the hypoxic drive, accounting for the initial respiratory alkalosis that occurs early in acute exacerbations and the typical history of a child being unable to catch their breath. As the lungs continue to hyperinflate in severe exacerbations, tidal volume becomes insufficient to ventilate the alveoli and hypercapnia develops.


Acute Asthma

Clinical features

A wheezy child with an acute asthma exacerbation may present with respiratory distress (tachypnoea, tachycardia, recession, nasal flaring, cyanosis). The following signs are worrying:

    • Moderate: wheezy, talks in sentences with no altered consciousness, SpO2 >92%, mild tachycardia.
    • Severe: SpO2 <92%, PEFR <50% predicted, tachycardia & tachypnoea, agitation, unable to talk in full sentences (or too breathless to feed), use of accessory muscles (head bobbing and recession).
    • Life-threatening (pre-terminal signs): bradycardia, exhaustion, confusion, cyanosis, silent chest.



    Pulse oximetry and peak flow are valuable investigations and can be performed at the bedside.

    Chest x-rays and arterial blood gases are not routinely ordered and should not delay treatment. Their results are rarely useful, and in the worst scenario distressing a child could worsen respiratory compromise.



    Acute Management

    Response to treatment is variable in children younger than two years. Consider other differentials such as viral-induced wheeze. Management of acute asthma is by:

    • b2 agonist inhaled via spacer.
    • Early oral steroids: 10mg prednisolone.
    • Ipratropium bromide in severe cases.

    Chronic Asthma

    Clinical features

    Children typically present with a history of recurrent wheeze, cough, tight chest and difficulty breathing. With younger children in particular these symptoms should be clarified, as parents often label any respiratory noise as a ‘wheeze’ – ask about a musical whistling expiratory noise in order to differentiate from stridor or rattles.

    There will often be a family history of asthma or atopic allergic and the child themselves may have proven atopy such as eczema. Symptoms are often worse at night or early morning and there may be known triggers such as:

    • Exercise and cold air
    • House dust (inhaled dustmite faeces) and mould/fungal spores
    • Aeroallergens (pollutants, cleaning products, cigarette smoke, animal dander, pollen)
    • Infections (viral respiratory tract infections)


    Control of pre-existing asthma can be assessed by evaluation of:

    • Frequency of symptoms (“how often do you use your blue inhaler?”)
    • Nocturnal symptoms (“does your asthma wake you up at night?”)
    • Interval symptoms (SOB or chest tightness between attacks)
    • Impact on lifestyle (“has your asthma made you miss school?”)


    Examination of a symptomatic child will typically reveal a hyperinflated resonant chest with a prolonged expiratory phase and widespread, bilateral expiratory wheeze. Other clinical findings such as crackles or rashes may give clues towards triggers. Look for Harrison’s Sulcus (a horizontal groove at the subcostal margin, indicative of chronically increased work of breathing due to persistant poor control).



    Spirometry as a test for airflow obstruction and demonstration of reversibility of FEV1 deficit supports diagnosis; however, normal spirometry in asymptomatic children cannot exclude asthma. Children can be given a peak flow meter to use at home in order to prove diurnal variability, typically exhibiting poorer PEFR in the mornings. Peak flow readings and spirometry form a core part of exercise challenging, with measurements taken before and after a stress test.

    Atopic status is investigated using skin-prick tests or taking blood for radioallergosorbent tests (RAST), allowing specific allergens to be identified. Proven atopy increases the probability of asthma in a wheezy child.

    There is no need to x-ray children and the evidence is weak for sputum eosinophil counts.



    The mainstay of non-pharmacological treatment is avoidance of proven allergens. Education would include the use of high efficiency vacuum cleaners and barrier mattress covers to reduce exposure to house-dust mites. Parents should be encouraged to stop smoking.

    Pharmacological treatment of chronic asthma follows a stepwise approach. The SIGN guidelines are reproduced below. Patients should be started at the step appropriate to their initial severity and moved up or down the ‘ladder’ to the lowest controlling step. If asthma treatment produces no response, compliance should be confirmed and alternative diagnosis and specialist referral considered.


    Other pharmacological options include an anti-IgE monoclonal antibody, Omalizumab, which can be considered in severe allergic asthma. Immunotherapy exposes a child to increasing doses of allergen subcutaneously and may be appropriate when an allergen is unavoidable, although this option carries the risk of anaphylaxis. Asthmatic children should be immunised against influenza.

    Differential diagnoses

    In pre-school children there are 3 phenotypes of wheeze. There is significant overlap between ‘transient early wheeze’ and ‘non-atopic wheeze’, which account for the majority of some 50% of toddlers and infants who have episodes of wheeze associated with viral infections and in whom symptoms rarely persist beyond age 5. Here, a diagnosis of viral-induced wheeze or bronchiolitis may be more appropriate. Symptoms of the third phenotype, ‘IgE associated wheeze’, are more persistent and a diagnosis of asthma is appropriate. 

    Asthma is less likely in a child who has no interval symptoms or when symptomatic has absent wheeze and normal examination and spirometry. Disorders which are commonly mistaken for asthma include gastrooesophageal reflux, cystic fibrosis and croup. If on auscultation a wheeze is heard to be unilateral, a foreign body (aspiration) should be excluded.


    Children with well-controlled asthma can lead a normal life.

    Poorly controlled chronic asthma is associated with impaired quality of life due to interval symptoms and recurrent admissions; these children may miss a substantial amount of school. Some children with poorly controlled asthma may display only partially reversible airflow limitation due to airway remodelling, and prolonged increased work of breathing may have negative effects on growth. Severe exacerbations of asthma have the potential to be life-threatening.

    References and further reading

    Lung and Asthma Information Agency ( Epidemiology.

    BTS & SIGN. British Guideline on the Management of Asthma (Quick Reference Guide), 2011. Available at: Guidelines/AsthmaGuidelines/qrg101%202011.pdf.

    Russell, G. Wheeze in preschool children. BMJ 2008; 336:1387.



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