Medicine – Chronic Asthma

Asthma is a chronic inflammatory disorder of the airways characterised by variable respiratory symptoms and variable expiratory airflow limitation. The airways become hyperresponsive to different stimuli, resulting in episodes of bronchoconstriction that are usually reversible either spontaneously or with treatment.

The characteristic symptoms are wheeze, breathlessness, chest tightness, and cough, which typically vary in intensity over time. Unlike the persistent airflow obstruction of COPD, airflow limitation in asthma is often substantially reversible.

1. Prevalence

Asthma is extremely common and can occur at any age, although it frequently begins during childhood.

Older teaching quotes figures of approximately 20% in children and 15% in adults, but prevalence varies substantially according to country, age group, diagnostic criteria, and population studied. It is therefore better to regard these as approximate historical figures rather than universal incidence rates.

2. Chronic Airway Inflammation

Asthma is fundamentally a chronic inflammatory airway disease.

The bronchial mucosa contains increased numbers of inflammatory cells, including eosinophils, mast cells, and T lymphocytes in many asthma phenotypes.

Inflammation causes airway hyperresponsiveness, mucosal oedema, increased mucus production, and increased sensitivity of bronchial smooth muscle to various stimuli.

3. Variable Airflow Obstruction

A defining characteristic of asthma is that airflow obstruction is variable.

Bronchial smooth-muscle contraction, airway inflammation, mucosal oedema, and mucus production narrow the airways during symptomatic periods.

When the trigger disappears or bronchodilator treatment is administered, airway calibre may improve considerably.

Genetic and Environmental Factors

4. Genetic Predisposition

Asthma has an important genetic component, although it is not inherited through a simple single-gene pattern.

A family history of asthma or other allergic disorders increases the likelihood of developing the condition.

5. Atopy

Atopy describes a genetic tendency to develop exaggerated IgE-mediated responses to common environmental allergens.

Atopic individuals are more likely to develop conditions such as asthma, allergic rhinitis, and atopic eczema.

However, not every patient with asthma is atopic, and several distinct inflammatory asthma phenotypes are now recognised.

6. Environmental Factors

Environmental exposures interact with genetic susceptibility to influence the development and expression of asthma.

Important factors include allergens, respiratory infections, tobacco smoke, occupational exposures, and air pollution.

Pulmonary Function Tests

Objective evidence of variable expiratory airflow limitation is important when establishing the diagnosis of asthma.

7. Peak Expiratory Flow Variability

Serial peak expiratory flow (PEF) measurements may demonstrate significant variation over time.

Older teaching often uses >20–25% variability as evidence supporting asthma. Modern diagnostic thresholds and calculation methods vary between guidelines, so the exact percentage should be interpreted within the appropriate diagnostic protocol.

The important principle is that substantial variability in expiratory airflow supports asthma.

8. FEV₁

During periods of airflow obstruction, the forced expiratory volume in one second (FEV₁) may be reduced.

Between attacks, however, spirometry may return completely to normal, particularly in patients with mild asthma.

9. FEV₁/FVC Ratio

Airflow obstruction causes the FEV₁/FVC ratio to decrease because FEV₁ falls disproportionately compared with forced vital capacity.

Again, the ratio may normalise when asthma is well controlled.

10. Bronchodilator Reversibility

A characteristic feature is an improvement in airflow following administration of a bronchodilator.

Both FEV₁ and peak expiratory flow may increase significantly after inhaled salbutamol or another rapidly acting bronchodilator.

Demonstrating significant bronchodilator reversibility provides objective evidence supporting the diagnosis of asthma.

11. Lung Volumes

During significant airway obstruction, air trapping and hyperinflation may increase residual volume and sometimes total lung capacity.

However, increased lung volumes are not required for the diagnosis, and patients with well-controlled or mild asthma may have completely normal lung volumes.

Triggers of Asthma

Asthma symptoms and acute exacerbations can be triggered by numerous environmental, physiological, and pharmacological factors.

12. Allergens

Exposure to allergens is an important trigger in patients with allergic asthma.

Common allergens include grass and tree pollens, house-dust mites, moulds, and animal dander, particularly from cats and dogs.

Exposure triggers airway inflammation and bronchoconstriction in susceptible individuals.

13. Exercise

Exercise can provoke transient bronchoconstriction, particularly when breathing large volumes of cold or dry air.

Patients may develop cough, wheeze, chest tightness, or breathlessness during or shortly after exercise.

Well-controlled asthma should generally allow patients to remain physically active.

14. Aspirin and NSAIDs

Aspirin and other NSAIDs can provoke severe bronchospasm in susceptible patients.

This is particularly important in aspirin/NSAID-exacerbated respiratory disease, which is associated with asthma and chronic rhinosinusitis with nasal polyps.

Not every patient with asthma needs to avoid NSAIDs; the problem occurs in susceptible individuals.

15. β-Blockers

β-blockers can cause bronchoconstriction by blocking β₂ receptors in bronchial smooth muscle.

Non-selective β-blockers present the greatest concern, although even β₁-selective drugs require appropriate consideration in patients with asthma.

β-blocking ophthalmic preparations can also occasionally cause systemic bronchospasm.

16. Respiratory Infection

Respiratory viral infections are among the most common triggers of asthma exacerbations.

Inflammation produced by infection increases airway hyperresponsiveness and can substantially worsen pre-existing asthma.

17. Gastro-Oesophageal Reflux

Gastro-oesophageal reflux disease (GORD/GERD) frequently coexists with asthma and may worsen respiratory symptoms in some patients.

However, reflux is not necessarily the cause of poor asthma control in every patient who has both conditions.

18. Smoke and Air Pollution

Cigarette smoke, vaping aerosols, environmental pollution, fumes, and other respiratory irritants can aggravate airway inflammation and trigger asthma symptoms.

Smoking can also reduce responsiveness to inhaled corticosteroids and contributes to poorer asthma control.

19. Poor Adherence

Poor adherence to regular controller medication, particularly inhaled corticosteroid-containing treatment, is an important cause of poorly controlled asthma and exacerbations.

Before escalating treatment, clinicians should therefore assess adherence, inhaler technique, ongoing triggers, and whether the diagnosis is correct.

Treatment of Chronic Asthma

Modern asthma treatment differs considerably from the older stepwise regimen in the supplied notes.

The major change is that treatment now emphasises inhaled corticosteroid (ICS)-containing therapy from an early stage, because airway inflammation is present even in patients with apparently mild asthma.

Reliance on a short-acting β₂-agonist such as salbutamol alone is generally no longer preferred in modern adult and adolescent asthma management.

20. Reliever Treatment

Historically, patients with mild asthma were treated with a short-acting β₂-agonist (SABA) such as salbutamol whenever symptoms occurred.

Modern approaches increasingly favour an ICS-containing reliever strategy, commonly using a low-dose inhaled corticosteroid combined with the rapid-onset LABA formoterol, where appropriate and available.

This provides both rapid bronchodilation and anti-inflammatory treatment when symptoms occur.

21. Inhaled Corticosteroids

Inhaled corticosteroids are the foundation of long-term asthma control.

They suppress airway inflammation, reduce symptoms, improve lung function, decrease airway hyperresponsiveness, and importantly reduce the risk of severe exacerbations and asthma-related death.

Examples include budesonide, beclometasone, and fluticasone.

22. Leukotriene Receptor Antagonists

A leukotriene receptor antagonist, such as montelukast, may be useful as additional controller therapy in selected patients.

It may be particularly helpful when asthma coexists with allergic rhinitis or in some patients with exercise- or aspirin/NSAID-associated symptoms.

It is generally less effective than inhaled corticosteroids as the main anti-inflammatory controller treatment.

23. Long-Acting β₂-Agonists

A long-acting β₂-agonist (LABA) may be added when asthma remains inadequately controlled with inhaled corticosteroid therapy.

Examples include formoterol and salmeterol.

Importantly, a LABA should not normally be used without an inhaled corticosteroid in asthma, because LABA monotherapy does not treat the underlying airway inflammation and is associated with safety concerns.

24. ICS–Formoterol Maintenance and Reliever Therapy

An important modern strategy is maintenance-and-reliever therapy (MART) using an ICS–formoterol inhaler.

The same inhaler provides regular maintenance anti-inflammatory treatment and additional doses when symptoms occur.

Because formoterol has a rapid onset of bronchodilation, it can function as both a long-acting controller and a reliever when combined appropriately with an ICS.

Escalation of Treatment

25. Persistent Symptoms

If asthma remains uncontrolled, treatment should be increased gradually while repeatedly checking adherence, inhaler technique, environmental exposures, comorbidities, and diagnostic accuracy.

Increasing the dose of inhaled corticosteroid or adding another controller may be appropriate depending on the treatment pathway being followed.

26. Long-Acting Muscarinic Antagonists

A long-acting muscarinic antagonist (LAMA), such as tiotropium, may be added in selected patients whose asthma remains inadequately controlled despite appropriate ICS/LABA treatment.

This has largely replaced the older concept of routinely adding short-acting ipratropium for long-term asthma control.

27. Theophylline

Theophylline was historically used more frequently as additional therapy for chronic asthma.

Its role is now limited because it has a narrow therapeutic index, important drug interactions, and significant adverse effects, while more effective and safer treatment options are available.

28. Nebulised Bronchodilators

Regular nebulised bronchodilators are not standard routine maintenance therapy for most patients with chronic asthma.

Nebulised therapy is much more commonly used during significant acute exacerbations.

Severe Asthma

29. Specialist Assessment

Patients whose asthma remains uncontrolled despite appropriately prescribed high-level inhaled therapy should undergo specialist assessment.

Before diagnosing severe treatment-resistant asthma, clinicians should confirm the diagnosis and carefully evaluate adherence, inhaler technique, smoking, allergen exposure, occupational factors, obesity, rhinosinusitis, reflux, and other comorbidities.

30. Biological Therapies

Modern treatment of severe asthma includes biological therapies directed at specific inflammatory pathways.

Depending on the asthma phenotype and biomarkers, treatment may target IgE, interleukin-5 or its receptor, interleukin-4/13 signalling, or other inflammatory pathways.

These therapies can substantially reduce exacerbations and the need for systemic corticosteroids in appropriately selected patients.

31. Oral Corticosteroids

Maintenance oral corticosteroids should generally be avoided whenever possible because prolonged systemic steroid exposure can cause major adverse effects.

These include osteoporosis, diabetes, hypertension, weight gain, cataracts, adrenal suppression, infection, and muscle weakness.

They may still be necessary in selected patients with severe refractory asthma, but modern biologic therapies can often reduce the requirement for long-term oral steroids.

32. Treatment Escalation – Note Form

Initial/Mild Asthma

Preferred principle: use an ICS-containing treatment strategy, rather than relying solely on salbutamol.

Reliever: low-dose ICS–formoterol is commonly preferred in appropriate adult/adolescent treatment pathways.

Alternative approaches: regular or symptom-linked low-dose ICS with an appropriate reliever may be used according to the treatment guideline and patient circumstances.

Persistent Asthma

Controller treatment: regular low-dose inhaled corticosteroid-containing therapy.

If symptoms persist: increase anti-inflammatory treatment and/or add a LABA.

Important: LABA therapy in asthma should be combined with an ICS, rather than used alone.

Moderate Asthma

Treatment: combination ICS + LABA therapy.

Option: ICS–formoterol may be used as maintenance-and-reliever therapy (MART) when appropriate.

Before escalation: always reassess inhaler technique, adherence, triggers, and comorbidities.

More Difficult-to-Control Asthma

Treatment: increase ICS-containing therapy according to the appropriate treatment pathway.

Additional options: consider a LAMA or other add-on controller treatment.

Theophylline: now has a limited role because of adverse effects and drug interactions.

Regular nebulisers: not routinely required for chronic stable asthma.

Severe Asthma

Management: specialist respiratory assessment.

Treatment options: phenotype-directed biological therapies may be appropriate.

Oral corticosteroids: intermittent courses may be required for exacerbations, while long-term maintenance therapy should be minimised whenever possible because of significant systemic toxicity.

Key Clinical Pattern

Think of asthma as:

Chronic airway inflammation + bronchial hyperresponsiveness + variable symptoms + variable expiratory airflow obstruction.

Typical symptoms are wheeze, breathlessness, chest tightness, and cough, with objective evidence such as variable peak flow, reduced FEV₁/FVC during obstruction, and improvement following bronchodilator treatment.

Important triggers include allergens, exercise, respiratory infections, smoke, NSAIDs/aspirin in susceptible patients, β-blockers, and poor adherence to controller treatment.

For modern treatment, the key principle is early ICS-containing therapy, followed when necessary by ICS/LABA treatment, MART where appropriate, additional controller therapy, and phenotype-directed biologics for severe asthma, while avoiding unnecessary dependence on SABA-only therapy or long-term oral corticosteroids.