Asthma is characterised by episodes of breathlessness, wheeze, and cough. It affects 5-8% of the population and is on the increase. It is the most common chronic disease in children. Asthma is defined as episodes of reversible increase in airway resistance in response to irritant stimuli. Increased airway resistance is caused by (1) bronchial smooth muscle contraction, (2) mucosal inflammation, and (3) increased mucus production.
Acute asthma exacerbations can be fatal – see our guide on how to recognise and manage them.
Bronchial calibre is controlled by a balance between:
The sympathetic nervous system which causes bronchodilation and decreases mucous secretion via β2-adrenoceptors
The parasympathetic nervous system which causes bronchoconstriction and increases mucus secretion via M3-receptors
Mucosal inflammation involves T-helper cell activation and cytokine production. Attracted granulocytes (especially eosinophils) produce the spasmogens histamine, prostaglandin D2, and leukotrienes.
There is no one symptom, sign or test that is diagnostic of asthma. There are a number of useful investigations outlined below which help to diagnose asthma. They are used to demonstrate variable airway obstruction and airway inflammation to support a clinical assessment. If investigations are inconclusive, an asthma diagnosis may be ‘suspected’ – in this case, treatment should be initiated and monitored carefully by regular reviews. A good response to treatment supports an asthma diagnosis.
Inadults with suspected asthma:
Measure spirometry and FeNO test.
Carry out a bronchodilator reversibility (BDR) test if spirometry is positive.
If the diagnosis is still uncertain, monitor peak expiratory flow (PEF) variability for 2-4 weeks.
If the diagnosis is still uncertain, consider direct bronchial challenge test.
Inchildren ages 5-16 with suspected asthma:
Carry out a BDR test if spirometry is positive.
If the diagnosis is still uncertain, consider FeNO test.
If the diagnosis is still uncertain, monitor PEF variability for 2-4 weeks.
What is it?
Measures exhaled nitric oxide, which is a marker of eosinophilic inflammation.
Measures maximum speed of expiration. Monitor twice daily for 2-4 weeks.
Variability ≥ 20%
Direct bronchial challenge test
Measures change in spirometry after methacholine/histamine inhalation.
8mg/mL or less causing a ≥ 20% drop in FEV1
Diagnose asthma in:
Adults with symptoms and positive investigation results.
Children aged 5-16 with symptoms and positive investigation results.
Children under 5 on signs and symptoms alone. Review them on a regular basis and carry out investigations if they are still symptomatic when they reach 5 years.
Airway obstruction (foreign body, tumour)
Managing chronic asthma
Non-pharmacological management includes advice on smoking cessation and weight loss in overweight/obese patients. Advise patients to avoid asthma triggers where possible.
There is clear guidance on the stepwise pharmacological management of asthma. Management is based on (1) bronchodilator ‘relievers’ and (2) anti-inflammatory ‘preventers’.
Short-acting β2-agonist (SABA)
e.g. Salbutamol, as required
Mechanism of action: β2-agonism causes bronchial smooth muscle relaxation which dilates bronchi to improve airflow in obstructed airways.
Adverse effects: Tremor is the most common unwanted effect. Others include tachycardia, palpitations, and cardiac dysrhythmia.
Low dose inhaled corticosteroid (ICS)
e.g. Beclometasone, twice daily
Mechanism of action: Corticosteroids reduce leukocyte proliferation and downregulate pro-inflammatory cytokine, leukotriene, and chemokine production. This reduces mucosal inflammation, dilates airways, and reduces mucous secretion.
Adverse effects: Oral candidiasis is the main unwanted effect. They can also cause a hoarse voice. Regular high dose steroid use can cause adrenal suppression, especially in children – monitor their growth annually.
β2-agonists and inhaled corticosteroids form the basis of chronic asthma management. They should be offered as first-line treatments to all adults and children over the age of 5.
If symptoms remain uncontrolled, add-on therapies can be considered. Before initiating an add-on therapy, recheck adherence, inhaler technique, and elimination of trigger factors.
Leukotriene receptor antagonist (LTRA) – oral therapy taken at night to downregulate inflammatory leukotrienes
Long-acting β2-agonist (LABA) – must always be given in combination with ICS
Medium dose inhaled corticosteroids
Trial of additional drugs – theophylline or a long-acting muscarinic antagonist (LAMA)
High dose inhaled corticosteroids
For all inhalers: Proper inhaler technique is very important, and poor technique is the most common reason for uncontrolled asthma.
For SABA: Ensure the patient knows how and when to take the inhaler (e.g. for acute symptoms, preemptively before exercise). They should understand that this treats symptoms, not the disease.
For ICS: A spacer should be used with ICS therapy to improve deposition and reduce the risk of oral candidiasis. Also, advise the patient to rinse their mouth and gargle after use. Reassure the patient that little steroid is absorbed into the blood so systemic effects are minimal.
Interactions: NSAIDs may provoke asthma (by inhibiting the COX pathway they promote arachidonic acid conversion to leukotrienes). Beta-blockers are contraindicated in asthma as they reduce the effectiveness of β2-agonists.