Asthma
D E FI N I T ION
Chronic inflammatory airway disease characterized by variable reversible
airway obstruction, airway hyper-responsiveness and bronchial inflammation.
AE T IOLOGY
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).
PATHOLOGY/PATHOGENESI S
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’).
E P IDEMIOLOGY
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.
H ISTORY
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.
EXAMINA T I ON
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.
INVE S T I G A T IONS
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
Asthma (continued)
MANAGEMENT
Acute:
. Resuscitate, monitor O2 sats, ABG and PEFR.
. High-flow oxygen.
. Nebulized b2-agonist bronchodilator salbutamol (5 mg, initially continuously, then 2–4
hourly), 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 # K
þ
).
. May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.
Discharge: When PEF >75% predicted or patient’s 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.
Step 1: Inhaled short-acting b2-agonist as needed. If used >1/day, move to Step 2.
Step 2: As Step 1 plus regular inhaled low-dose steroids (400 mcg/day).
Step 3: As Step 2 plus inhaled long-acting b2-agonist (LABA). If inadequate control with LABA,
" steroid dose (800 mcg/day). If no response to LABA, stop and " steroid dose (800 mcg/
day).
Step 4: " Inhaled steroid dose (2000 mcg/day), add a fourth drug, e.g. leukotriene receptor
antagonist, SR theophylline or b2-agonist tablet.
Step 5: Addition of regular oral steroids. Maintain high-dose inhaled steroid. Consider other
treatments to minimize the use of oral steroids. Refer for specialist care.
Advice: Educate on proper inhaler technique and routine monitoring of peak flow. Develop
an individualized management plan, with emphasis on avoidance of provoking factors.
COMPL I C A T IONS
Growth retardation, chest wall deformity (e.g. pigeon chest), recurrent
infections, pneumothorax, respiratory failure, death.
P ROGNOS I S
Many children improve as they grow older. Adult-onset asthma is usually
chronic.
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