- Chronic inflammatory airway disease characterized by variable reversiblemairway obstruction, airway hyper-responsiveness and bronchial inflammation.
- Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show some atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to allergens). Linkages to multiple chromosomal locations point to ‘genetic heterogeneity’.
- Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational allergens (isocyanates, epoxy resins).
- Early phase (up to 1 h): Exposure to inhaled allergens in a presensitized individual results in cross-linking of IgE antibodies on the mast cell surface and release of histamine, prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle contraction (bronchoconstriction), mucous hypersecretion, oedema and airway obstruction.
- Late phase (after 6–12 h): Recruitment of eosinophils, basophils, neutrophil and Th2 lymphocytes and their products results in perpetuation of the inflammation and bronchial hyper-responsiveness.
- Structural cells (bronchial epithelial cells, fibroblasts, smooth muscle and vascular endothelial cells), may also release cytokines, profibrogenic and proliferative growth factors, and contribute to the inflammation and altered function and proliferation of smooth muscle cells and fibroblasts (‘airway remodeling’).
- Affects 10% of children and 5% of adults. The prevalence of asthma appears to be increasing. ,¼<. Acute asthma is a very common medical emergency and still responsible for 1000–2000 deaths/year in the UK.
- Episodes of wheeze, breathlessness, cough; worse in the morning and at night.
- Ask about interference with exercise, sleeping, days off school and work.
- In an acute attack it is important to ask whether the patient has been admitted to hospital because of his/her asthma, or to ITU, as a gauge of potential severity.
- Precipitating factors: Cold, viral infection, drugs (b-blockers, NSAIDs), exercise, emotions.
- May have a history of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux and family history.
- Tachypnoea, use of accessory muscles, prolonged expiratory phase, polyphonic wheeze, hyperinflated chest.
- Severe attack: PEFR <50% predicted, pulse > 110/min, respiratory rate > 25/min, inability to complete sentences.
- Life-threatening attack: PEFR < 33%, silent chest, cyanosis, bradycardia, hypotension, confusion, coma.
- Acute : Peak flow, pulse oximetry, ABG, CXR (to exclude other diagnoses, e.g. pneumothorax, pneumonia), FBC (” WCC if infective exacerbation), CRP, U&Es, blood and sputum cultures.
- Chronic : PEFR monitoring: There is often a diurnal variation with a morning ‘dip’.
- Pulmonary function test: Obstructive defect, with improvement after a trial of a b2-agonist.
- Blood: Eosinophilia, IgE level, Aspergillus antibody titres (see allergic Aspergillus lung disease).
- Skin prick tests: May help in the identification of allergens.
- Resuscitate, monitor O2 sats, ABG and PEFR.
- High-flow oxygen.
- Nebulized b2-agonist bronchodilator salbutamol (5 mg, initially continuously, then 2–4hourly), ipratropium (0.5mg qds).
- Steroid therapy (100–200mg IV hydrocortisone, followed by 40mg oral prednisolone for 5–7 days).
- If no improvement : IV magnesium sulphate. Consider IV aminophylline infusion or IV salbutamol.
- Summon anaesthetic help if patient is getting exhausted (PCO2 increasing).
- Treat any underlying cause (e.g. infection, pneumothorax). Give antibiotics if there is evidence of chest infection (purulent sputum, abnormal CXR, ” WCC, fever). Monitor electrolytes closely (bronchodilators and aminophyline).
- May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.
- Discharge : When PEF >75% predicted or patients best, diurnal variation < 25%, inhaler technique checked, stable on discharge medication for 24 h, patient owns a PEF meter and has steroid and bronchodilator therapy. Arrange follow-up.
- Chronic ‘stepwise’ therapy: Start on the step appropriate to initial severity and step up or down to control symptoms. Treatment should be reviewed every 3–6 months.
- Growth retardation, chest wall deformity (e.g. pigeon chest), recurrent infections, pneumothorax, respiratory failure, death.