asthma

Written by Sarah Lee

Last Reviewed: April 2019

Review Due: April 2020

DEFINITION

‘a chronic inflammatory disease of the airways that is characterised by bronchial hyperresponsiveness and reversible airflow obstruction resulting in recurrent episodes of breathlessness, cough, chest tightness and wheeze that is often made worse by specific triggers’

AETIOLOGY

Complex interactions between genetic and environmental factors are thought to contribute to the development of asthma:

Genetic

Many genes are associated with the condition

A strong family history is very significant

Environmental

Hygiene Hypothesis

Smoking during pregnancy/secondary exposure

Air pollution

Infections

Viral - Rhinovirus, Influenza Virus, Respiratory Syncytial Virus etc

Bacterial - Mycoplasma Pneumoniae, Chlamydia Pneumoniae etc

Allergen Exposure

RISK FACTORS

Family History

Triad of Atopy

History of eczema, atopic dermatitis, allergic rhinitis

Exposure to Allergens

Common Allergens: animal fur, dust mites, pollen, moulds

Occupational Allergens: flour, dusts, chemicals

SIGNS AND SYMPTOMS

Symptoms

Intermittent Dyspnoea

Cough (often nocturnal)

Wheeze

Sputum Production (yellow)

Chest Tightness

Exercise Intolerance

Signs

Tachypnoea

Widespread wheeze on auscultation

Hyper-resonant percussion

PRECIPITANTS

Cold

Exercise

Stress

Allergens

Respiratory Tract Infections

Drugs (e.g. NSAIDs, Beta Blockers)

Smoking/Passive Smoking

PATTERN OF CLINICAL PRESENTATION

Diurnal Variation - symptoms worse at night/early morning

Worsens in the presence of precipitants, improves when removed

Nocturnal cough

Patients may complain of disturbed sleep and days off school/work

PATHOPHYSIOLOGY

1. Airway Inflammation

Exposure to allergen triggers an IgE-mediated Type 1 hypersensitivity reaction within the lungs.

Mast cell degranulation and production of inflammatory mediators (eg histamine, leukotrines) and cytokines (eg Il-4, IL-5) occurs.

Inflammatory cells including eosinophils migrate to airways produce more mediators, propagating the inflammatory response.

2. Airway Obstruction

Inflammation causes bronchospasm, mucosal oedema and increased mucus secretion within airways.

Chronic inflammation may cause bronchial smooth muscle hypertrophy and airway remodelling over time which may cause airflow limitations to be only partially reversible.

3. Bronchial Hyperresponsiveness

Eosinophil products increase resting tone of bronchial smooth muscle.

Bronchi become hyperresponsive and produce a larger response, more quickly to the allergen on the next exposure.

Investigations

Spirometry

Gold standard diagnostic test for asthma

Should show an obstructive pattern (i.e. FEV1:FVC <0.7)

Must also show reversibility (at least 15% improvement) after bronchodilator

Peak Expiratory Flow (PEF)

PEF in asthmatic patients is typically lower than expected for the patient's height, age and gender

Monitoring and recording PEF can help establish variability, triggers and efficacy of medicine

FBC

Normal or Eosinophilia

CXR

May show hyperinflation in chronic asthma

TREATMENT

NON-PHARMACOLOGICAL

Identify and avoid precipitants

Reduce exposure to cigarette smoke

Breathing exercises (physiotherapist-taught)

pharmacological

Guidelines from the British Thoracic Society and Scottish Intercollegiate Guidelines Network suggest the best approach to the long-term management of asthma. They recommend a five-step approach, that can be escalated or de-escalated as guided by the patient's symptoms. Guidelines for the management of asthma in children follow a similar approach.

Common classes of drugs used in the management of asthma include:

Short Acting Beta2 Agonists/SABA (e.g. Salbutamol)

Long Acting Beta2 Agonists/LABA (e.g. Salmeterol)

Inhaled Corticosteroids (e.g. Beclometasone)

Leukotriene Receptor Antagonists (e.g. Montelukast)