Discuss the aetiopathogenesis, clinical features, investigations and management of bronchial asthma, including acute severe asthma.

Definition

Asthma is a heterogeneous disease characterised by CHRONIC AIRWAY INFLAMMATION, defined by variable respiratory symptoms — wheeze, breathlessness, chest tightness and cough — that vary over time and in intensity, with VARIABLE EXPIRATORY AIRFLOW LIMITATION. VARIABILITY and REVERSIBILITY are what distinguish it from COPD.

Triggers

Also DRUGS — aspirin and NSAIDs (Samter's triad: asthma, nasal polyps, aspirin sensitivity), and BETA-BLOCKERS including ophthalmic timolol drops; reflux; occupational sensitisers; obesity.

Pathogenesis — Three Phases

1. Sensitisation: allergen → dendritic cells → Th2 differentiation → IL-4 and IL-13 → IgE binding mast cells

2. Early phase (minutes): allergen cross-links IgE → mast cell degranulation releasing histamine, leukotrienes, prostaglandin D2, PAF → bronchoconstriction, oedema and mucus

3. Late phase (3–12 hours): IL-5-driven EOSINOPHIL recruitment → major basic protein → epithelial damage and airway hyperresponsiveness

4. Remodelling (chronic uncontrolled disease): basement membrane thickening, smooth muscle hypertrophy, goblet cell hyperplasia → partially FIXED obstruction — which is why early control matters

Pathological findings: Curschmann's spirals, Charcot–Leyden crystals, Creola bodies.

Clinical Features

• Episodic wheeze, breathlessness, chest tightness and cough, characteristically worse at night and early morning, and after trigger exposure
• Diurnal variation — a hallmark ("morning dipping")
• Cough-variant asthma — chronic dry cough as the sole symptom; commonly missed
• Between attacks the examination may be entirely normal — a normal examination never excludes asthma
• During an attack: tachypnoea, prolonged expiration with widespread polyphonic wheeze, hyperinflation, accessory muscle use, pulsus paradoxus in severe attacks

Investigations

• SPIROMETRY WITH REVERSIBILITY — the key test: obstructive pattern with FEV1 increase of ≥ 12% AND ≥ 200 mL after bronchodilator
• PEAK FLOW monitoring — diurnal variability > 10% supports the diagnosis; valuable for self-management
• Bronchial provocation testing (methacholine, exercise, mannitol) where spirometry is normal
• FeNO — marker of type 2 airway inflammation; predicts corticosteroid response
• Allergy assessment — skin prick tests, specific IgE, blood eosinophil count
• Chest X-ray — usually normal; excludes alternatives and complications
• Consider ABPA in poorly controlled asthma with fleeting infiltrates and high total IgE

Management — Chronic Asthma

The fundamental principle, and a major change from older teaching: NO ADULT OR ADOLESCENT SHOULD BE TREATED WITH A SHORT-ACTING BETA-AGONIST ALONE. SABA-only treatment relieves symptoms while leaving inflammation untreated, and is associated with increased exacerbations and asthma death. Every patient should receive inhaled corticosteroid-containing therapy.

• Preferred reliever throughout: low-dose ICS–formoterol
• Steps 1–2: as-needed low-dose ICS–formoterol, or daily low-dose ICS
• Step 3: low-dose ICS–LABA maintenance
• Step 4: medium-dose ICS–LABA; add LAMA (tiotropium) or a leukotriene antagonist
• Step 5: high-dose ICS–LABA plus phenotype-specific BIOLOGIC — anti-IgE (omalizumab), anti-IL-5 (mepolizumab, benralizumab), anti-IL-4R (dupilumab), anti-TSLP (tezepelumab); oral steroids as a last resort

Before stepping up, always check: (1) INHALER TECHNIQUE — wrong in a large majority and the commonest cause of apparent failure; (2) ADHERENCE; (3) triggers and comorbidity — rhinitis, reflux, obesity, smoking; (4) whether the diagnosis is right.

Non-pharmacological: trigger avoidance, smoking cessation, weight reduction, treatment of rhinitis, a written personalised action plan with peak flow monitoring, vaccination, and education.

Acute Severe Asthma

Management — immediate and simultaneous:

1. High-flow OXYGEN, target SpO2 94–98%

2. Nebulised SALBUTAMOL driven by OXYGEN (not air), back-to-back or continuous in severe attacks

3. Nebulised IPRATROPIUM in severe and life-threatening attacks

4. SYSTEMIC CORTICOSTEROIDS in ALL patients — give early; the effect takes 4–6 hours

5. INTRAVENOUS MAGNESIUM SULPHATE — single dose in severe or life-threatening attacks not responding

6. Intravenous aminophylline — limited benefit, significant toxicity; specialist use only

7. ITU referral for exhaustion, deteriorating gases, altered consciousness or arrest

Blood gas interpretation is critical:

• Early attack: respiratory ALKALOSIS with low PaCO2 — expected
• A "NORMAL" PaCO2 in an acutely breathless asthmatic is an OMINOUS sign of exhaustion
• A RAISED PaCO2 indicates NEAR-FATAL asthma requiring immediate intensive care

Discharge planning — the phase most often neglected: do not discharge until PEF > 75% of best; give oral steroids to complete the course, a written action plan, an inhaler technique check, and follow-up within 48 hours.