Discuss the aetiology, pathogenesis, clinical features, investigations and management of chronic obstructive pulmonary disease.

Definition

COPD is a common, preventable and treatable condition characterised by persistent respiratory symptoms and PERSISTENT, PROGRESSIVE AIRFLOW OBSTRUCTION due to airway and/or alveolar abnormalities. Diagnosis requires spirometry: a post-bronchodilator FEV1/FVC < 0.70. Unlike asthma, the obstruction is largely irreversible.

• Chronic bronchitis — a clinical definition: productive cough for ≥ 3 months in ≥ 2 consecutive years
• Emphysema — a pathological definition: permanent enlargement of airspaces distal to the terminal bronchiole with alveolar wall destruction

Aetiology

• CIGARETTE SMOKING — the single most important cause (85–90% in developed settings)
• BIOMASS FUEL SMOKE — of enormous importance in India: wood, dung and crop residue burnt indoors is the leading cause of COPD in rural non-smoking Indian women
• Occupational dusts — coal, silica, cadmium, grain dust; outdoor air pollution (PM2.5)
• Post-tuberculous obstructive airway disease — a major and distinctly Indian contributor
• ALPHA-1 ANTITRYPSIN DEFICIENCY — suspect with emphysema before 45, in a non-smoker, basal (panlobular) distribution, or associated liver disease
• Childhood respiratory infection; abnormal lung development; low birth weight

Pathogenesis

Noxious particles activate macrophages and epithelial cells, releasing IL-8, LTB4 and TNF-alpha, recruiting neutrophils and CD8+ lymphocytes. Two mechanisms follow:

1. PROTEASE–ANTIPROTEASE IMBALANCE — neutrophil elastase destroys elastin, normally opposed by alpha-1 antitrypsin → emphysema

2. OXIDATIVE STRESS — inactivates antiproteases and amplifies inflammation

Structural results: mucus gland hypertrophy (chronic bronchitis); alveolar destruction with loss of elastic recoil and expiratory airway collapse (emphysema, reduced DLCO); and small airway fibrosis producing fixed obstruction.

Clinical Features

• Chronic cough, often the first symptom; sputum (mucoid when stable, purulent in exacerbation)
• PROGRESSIVE EXERTIONAL DYSPNOEA — the main determinant of disability
• Wheeze, chest tightness, fatigue, weight loss in advanced disease

Signs: barrel chest, hyperresonance with loss of cardiac and liver dullness, reduced breath sounds, prolonged expiration, accessory muscle use, pursed-lip breathing, Hoover's sign, and in advanced disease cyanosis, raised JVP and oedema (cor pulmonale).

Investigations

• SPIROMETRY — post-bronchodilator FEV1/FVC < 0.70 is diagnostic; severity graded by FEV1 % predicted (GOLD 1 ≥ 80%, 2 = 50–79%, 3 = 30–49%, 4 < 30%)
• Chest X-ray — hyperinflation (> 6 anterior ribs), flattened diaphragms, increased retrosternal air space, narrow heart, bullae; also excludes alternatives
• HRCT — quantifies emphysema, identifies bullae and bronchiectasis
• Arterial blood gas — type I or II respiratory failure, especially when SpO2 < 92%
• CBC — secondary polycythaemia; blood EOSINOPHIL COUNT, which now guides inhaled corticosteroid use
• ECG and echocardiography — P pulmonale, right ventricular hypertrophy, pulmonary hypertension
• Alpha-1 antitrypsin level in the young, non-smokers, or basal emphysema
• Sputum for AFB and CBNAAT where TB is a consideration — essential in India

Assessment combines symptoms (mMRC or CAT score) with exacerbation history, giving groups A, B and E; exacerbation history is the strongest predictor of future exacerbations.

Management

1. Non-pharmacological — where the greatest gains lie

• SMOKING CESSATION — the ONLY intervention proven to slow the accelerated decline in FEV1; beneficial at any age and stage
• Reduce biomass and indoor air pollution exposure — as important as smoking cessation for many Indian patients
• PULMONARY REHABILITATION — improves exercise capacity, dyspnoea and quality of life more than any drug; markedly under-used
• Vaccination — influenza, pneumococcal, COVID-19, RSV
• Nutritional support; treat comorbidity — cardiovascular disease, osteoporosis, depression

2. Pharmacological

• Group A: a bronchodilator. Group B: LABA + LAMA — dual bronchodilation is superior to either alone
• Group E: LABA + LAMA, adding inhaled corticosteroid if the blood eosinophil count is raised (≥ 300 cells/µL) or there is asthma overlap; triple therapy for continued exacerbations
• Inhaled corticosteroids are NOT for everyone — they increase pneumonia and, importantly in India, tuberculosis reactivation
• Roflumilast for chronic bronchitis with FEV1 < 50% and frequent exacerbations; azithromycin prophylaxis in selected frequent exacerbators
• CHECK INHALER TECHNIQUE AND ADHERENCE AT EVERY VISIT — poor technique is very common and the commonest reason for apparent treatment failure

3. LONG-TERM OXYGEN THERAPY — for PaO2 ≤ 55 mmHg (SpO2 ≤ 88%) at rest, or PaO2 56–60 with cor pulmonale, oedema or polycythaemia. Must be used ≥ 15 hours/day. With smoking cessation, one of only two interventions proven to improve SURVIVAL.

4. Surgical — lung volume reduction surgery or endobronchial valves for selected upper-lobe emphysema; bullectomy; transplantation.

Acute Exacerbation

Precipitants: viral and bacterial infection, pollution, non-adherence, pulmonary embolism (actively consider).

• CONTROLLED OXYGEN — target SpO2 88–92% via Venturi mask
• Nebulised salbutamol with ipratropium
• Systemic corticosteroids — short course; prolonged courses add toxicity without benefit
• Antibiotics for purulent or increased-volume sputum, or if ventilation is needed
• NON-INVASIVE VENTILATION (BiPAP) for respiratory acidosis (pH < 7.35 with PaCO2 > 45) — reduces intubation, complications and mortality
• Assess for LTOT and rehabilitation after recovery