Clinical diagnosis characterised by acute and reversible obstruction of the airways caused by inflammation, most commonly secondary to an abnormal hypersensitivity of the bronchioles.


  • Most common respiratory disease and chronic disease of childhood: around 1 in 11 (1.1 million) children in the UK are receiving treatment (thought that 1 in 12 adults are being treated)
  • Acute attacks can be life-threatening
  • Note that many patients ‘grow-out’ their asthma symptoms and are not receiving active treatment but rather have a past history of the condition.

Risk Factors

  • Personal or family history of atopy (hayfever, asthma, eczema)
  • Inner city environment and socio-economic deprivation
  • Prematurity, low birth weight, viral infections in early childhood (particularly rhinovirus)
  • Maternal smoking, smoking environment or smoking personally


Consists of a triad of features:

  1. Airway Inflammation
    1. Inflammation is a feature consistent in all forms of asthma
    2. section2f2-3
      Inhaled antigens are recognised by IgE antibodies which activate mast cells and recruit T-helper (type 2) cells in the airway, which then produce inflammatory mediators such as histamine and leukotrienes) and cytokines (including IL-4 and IL-5). These cytokines cause the differentiation and production of eosinophils.
      Eosinophils migrate to the airway via binding of integrins to vascular cell-adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM). These produce more inflammatory mediators.

      It is possible that the inflammation also causes the over-production of IgE and further hyperresponsiveness of the airways in allergic/atopic cases

  2. Airflow Obstruction/Bronchoconstriction & Airway Oedema
    1. Early response (type I immediate): Smooth muscle contraction/spasm in response to allergen (IgE mediated- mast cell degranulation and histamine release)
      1. Occurs in all patients
    2. Late response (type IV delayed): recruitment of eosinophils, neutrophils, Th2 lymphocytes and macrophages which release lipid mediators and cytokines e.g PGE2, IL-4/5; to cause bronchoconstriction, vascular congestion, mucosal oedema, mucus production and reduce mucociliary transport.
  3. Bronchial Hyperresponsiveness
    1. Eosinophil granules such as major basic protein and cationic protein (MBP and ECP, respectively) affect smooth muscle tone by increasing intracellular calcium concentrations and inhibiting muscarinic (inhibitory) receptors, and thus increasing resting tone and hypersensitivity
    2. Hyperreactivity is thought to be as a result of hypertrophy of smooth muscle secondary to the inflammatory process (airway remodelling)
      1. NB Hypersensitivity is a ‘quicker’ reaction; hyperreactivity is a ‘bigger’ reaction.  Hyperresponsiveness is a mixture of both, as seen in asthma.

Presentation and Diagnosis

(According to SIGN/BTS guidelines)

  • Episodic respiratory symptoms (one or more of)
    • Wheeze (make sure to clarify what the patient/parent means by wheeze)
    • Cough
    • Difficulty breathing
    • Chest tightness
  • Particularly ask:
    • About things that will increase the likelihood of asthma:
      • Frequent/Recurrent attacks
      • Worse at night/early morning
      • Occur in response to a trigger e.g. exercise, pets, cold etc
      • Occur in response to taking aspirin or beta blockers
      • Occur separately/independently from colds/coughs (isolated coughs/colds are unlikely to be asthma-related)
        • Cough is usually non-productive.  A productive cough is unlikely to be asthmatic.  A chronic cough without wheeze is unlikely to be asthmatic
      • Personal/family history of atopy
      • Are there any triggers, e.g. temperature, exercise, allergy etc
  • If they are at school, ask whether they have to miss school/PE.
  • Other things that increase the likelihood of asthma
    • Widespread wheeze on auscultation
    • Improvement (in symptoms or lung function) with treatment (in children)
    • Otherwise unexplained low FEV1 or PEF or peripheral blood eosinophilia
  • Features that decrease the likelihood of asthma
    • Prominent dizziness, light headedness, peripheral tingling
    • Chronic productive cough in the absence of wheeze or breathlessness
    • Repeated normal chest examination during exacerbation
    • Voice disturbance
    • Symptoms with colds/URTIs only
    • Significant smoking history (>20 pack years)
    • Cardiac disease
    • Normal PEF or spirometry when symptomatic

On Examination

  • Widespread wheeze is the key feature of asthma patients.
    • Other signs may include increased work of breathing (intercostal recession, cyanosis, increased respiratory rate etc)
  • Stridor, focal signs, failure to thrive, productive cough etc- are NOT signs of asthma and thus should be assessed appropriatedly

Differential Diagnosis

Cystic Fibrosis; Bronchopulmonary dysplasia; Ciliary dyskinesia; Aspiration (consider if vomiting/swallowing difficulty)/inhaled foreign body; Panic attacks; Tracheo/laryngeal disorders; immunocomprimisation; chest infection 


  • In patients with a ‘high probability of asthma’ (based on above history/examination)- investigations are usually not required (straight to first-line management)
  • In patients with a ‘low probability’, consider a more detailed investigation, a different diagnosis or referral to a specialist
  • In patients with an ‘intermediate probability’, offer spirometry first line
    • FEV1 (Forced expiratory volume in 1 sec) may be reduced in asthma but is hugely dependent on build, fitness etc and is often unreliable in diagnosing asthma (serial FEV1 values are equally unhelpful)
    • Instead FEV1/FVC ratio may be more useful (decreased in obstructive disease)
    • Similarly, residual volume/total lung capacity ratios may be more useful
    • Reversibility testing (testing FEV1 after treatment)
      • Bronchodilator reversibility testing: before undertaking bronchodilator testing, the patient should stop short-acting beta2 agonists for 6 hours, long-acting bronchodilators for 12 hours and theophyllines for 24 hours. Administer bronchodilator (at least 400 micrograms salbutamol) and repeat spirometry after 15 minutes.
        • An increase of >400ml in FEV1 from baseline is suggestive of asthma
        • More commonly, a similar test can be done with steroid inhalers but over 2 weeks
      • NB If spirometry shows no evidence of obstruction/asthma, consider other tests e.g. allergy (skin prick) tests, tests for bronchial hyperresponsivity (using methacholine, exercise or mannitol)
  • Peak flow measurements may only be useful in demonstrating some obstruction but are otherwise not particularly reliable and so should be interpreted with caution


  • Non-pharmacological
    • Allergen avoidance is not practical and lacking in evidence
    • Smoking cessation (parent and patient)
  • Pharmacological
  • cdscds
  • 34844180
  • 34844180
    • NB Patients should start at step 2 if
      • they have had exacerbations in the last two years
      • using SABA 3 times a week or more
      • Symptomatic 3 or more times a week
      • waking one night a week
    • If there is a suggestion of occupational (or exposure) asthma (e.g. better during weekends/holidays) poorly responding to step 1-3, consider referral to specialist early (rather than later) for peak flow diary
      • Causes of occupational asthma include
        • Isocyanates (most common e.g. spray painting, foam moulding using adhesives)
        • Platinum salts
        • Soldering flux resin
        • Glutaraldehyde
        • Flour
        • Epoxy resins
        • Proteolytic enzymes

For Notes on Acute Asthma attacks see here

Leukotriene receptor antagonists e.g. Montelukast

  • have both anti-inflammatory and bronchodilatory properties
  • should be used when patients are poorly controlled on high-dose inhaled corticosteroids and a long acting beta-2 agonist
  • Particularly useful in Aspirin-induced asthma
  • Associated with the development of Churg-Strauss syndrome

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