Chronic Obstructive Pulmonary Disease — Risk Factors, Pathology, Clinical Features, Differentiation from Bronchial Asthma, Management and…

Chronic Obstructive Pulmonary Disease — Risk Factors, Pathology, Clinical Features, Differentiation from Bronchial Asthma, Management and Complications 15 marks High-Yield Points Definition and Epidemiology

Definition: COPD is airflow obstruction that is not fully reversible and shows little variability over time. It is usually progressive and is caused by small-airway disease plus emphysema.

Burden: COPD is the fifth-largest cause of disability worldwide and the fourth-leading cause of death in the US. World prevalence is 4–10%, but in the elderly it rises to 12–15%. Despite this it remains under-diagnosed and mis-diagnosed in older adults.

Tobacco smoke is the main risk factor. FEV1 normally falls by 25–30 mL/year after age 25; in a susceptible smoker it falls by more than 50 mL/year. Stopping smoking slows this decline back towards normal.

One in four to five COPD patients has never smoked. In India the important non-smoking causes are biomass fuel smoke (chulha smoke in poorly ventilated kitchens), outdoor air pollution, occupational dust, and post-tuberculous lung damage. Pathy's notes that kitchen ventilation, rural residence, low BMI and low education all alter prevalence.

Alpha-1 antitrypsin deficiency should be screened for in every COPD patient regardless of age (European Respiratory Society statement).

Inhaled irritants cause chronic neutrophilic airway inflammation, mucous gland hyperplasia and goblet cell metaplasia → chronic bronchitis; and protease–antiprotease imbalance destroying alveolar walls → emphysema.

Loss of elastic recoil and small-airway fibrosis cause expiratory flow limitation → dynamic hyperinflation and air trapping → breathlessness on exertion, flattened diaphragm and inefficient respiratory muscles.

Ventilation–perfusion mismatch causes hypoxaemia; later, alveolar hypoventilation causes hypercapnia. Chronic hypoxic pulmonary vasoconstriction → pulmonary hypertension → cor pulmonale.

Insidious onset of exertional breathlessness, chronic cough with sputum, wheeze and chest tightness; symptoms vary little from day to day. Older patients often attribute symptoms to old age, which delays diagnosis.

Signs: barrel chest, pursed-lip breathing, reduced cricosternal distance, hyperresonance, distant breath sounds, prolonged expiration. Signs of cor pulmonale — raised JVP, hepatomegaly, ankle oedema, loud P2.

Investigations: post-bronchodilator spirometry (FEV1/FVC <0.7, or better <lower limit of normal in the elderly); chest X-ray in all new cases to exclude cancer; 12-lead ECG (right heart strain carries poorer prognosis); echocardiography if heart failure suspected; TLCO and CT if symptoms are out of proportion. Good-quality spirometry is achievable in about 85% of older adults — cognitive impairment is the commonest reason for failure.

The key question is whether obstruction is fixed (COPD) or reversible (asthma). A >200 mL rise in FEV1 after a beta-2 agonist or after a two-week corticosteroid trial is strong evidence of asthma. PEF variability >20% also suggests asthma.

Where results are ambiguous, use more discriminating tests: a rise in total lung capacity is rare in asthma but typical of severe COPD, and a reduced TLCO indicates emphysema (loss of alveolar-capillary surface), not asthma. FeNO is a simple non-invasive marker of eosinophilic (asthmatic) inflammation and is valid in older people.

Non-pharmacological (do these first): smoking cessation using nicotine replacement, bupropion or varenicline — quit rates in older adults are as good as or better than in the young; e-cigarettes are not recommended. Add influenza and pneumococcal vaccination, pulmonary rehabilitation, nutritional support, self-management plans and early discussion of advance care planning.

Inhaled therapy (Pathy's Figure 42.1): avoid regular on-demand short-acting bronchodilators in the elderly (risk of overdosing and adverse drug reactions). Start a LAMA (tiotropium, umeclidinium, aclidinium — the latter two are safe in renal failure as they are liver-metabolised) or a LABA; step up to LABA+LAMA; add an ICS only for frequent exacerbators or asthma-like features. ICS raise the risk of non-fatal pneumonia, but this does not outweigh their benefit in the right patient.

Add-on options: slow-release theophylline in low dose (narrow therapeutic index, interacts with antibiotics); roflumilast (PDE-4 inhibitor) for frequent exacerbators with chronic bronchitis — watch weight loss, diarrhoea and mood change; high-dose acetylcysteine as a mucolytic/antioxidant; nebulised bronchodilators only when inhaler technique is irretrievably poor. Maintenance oral steroids: risks generally outweigh benefits.

LTOT if PaO2 <7.3 kPa, or 7.3–8.0 kPa with polycythaemia, pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia; used ≥15 hours/day improves survival (see Question 7).

Definition and burden: increased breathlessness, cough, sputum volume or purulence, wheeze and chest tightness. Exacerbations account for up to 10% of all medical admissions; about one-third are readmitted within 30 days and 15% die by three months. Commonest bacteria in the elderly are H. influenzae, S. pneumoniae and M. catarrhalis.

Treatment: nebulised bronchodilators; oral corticosteroids for 7–14 days (shorten stay, reduce treatment failure); antibiotics when sputum is purulent — these reduce mortality by 77% and treatment failure by 53%; avoid antibiotics if there is no purulence. Cover Pseudomonas (ciprofloxacin/anti-pseudomonal beta-lactam) if bronchiectasis coexists.

Oxygen and ventilation: target saturation 88–92% (Pathy's text prints "890–95%", a typographical error for 88– 92/90–95%) — excessive oxygen depresses hypoxic drive and worsens acidosis. Give NIV if pH <7.35 despite maximal therapy: it reduces mortality, intubation and length of stay. High-flow nasal oxygen is safe and effective in both normocapnic and hypercapnic exacerbation, and is useful where there is a do-not-intubate order. Consider hospital-at-home/early-discharge schemes for patients without acidosis and with good social support.

Respiratory: recurrent exacerbations, pneumonia, respiratory failure (type 2), pneumothorax, secondary polycythaemia, cor pulmonale, lung cancer, coexisting bronchiectasis (found on HRCT in up to 29% of primary-care COPD with chronic bronchitis).

Systemic: heart failure is present in 20% of COPD patients over 65; COPD is an independent cardiovascular risk factor. Also osteoporosis (screen routinely), sarcopenia and weight loss, chronic renal failure (masked by sarcopenia lowering creatinine), anxiety and depression, cognitive impairment, dysphagia and pulmonary embolism.