Chronic obstructive pulmonary disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD) is a progressive, long-term respiratory condition characterized by airflow limitation that is not fully reversible. It encompasses two main pathological entities: chronic bronchitis (persistent inflammation of the bronchi leading to excess mucus production and cough) and emphysema (destruction of alveoli resulting in reduced gas exchange). COPD is primarily caused by prolonged exposure to harmful substances, most notably cigarette smoke, but also occupational dust, air pollution, and biomass fuel exposure. It remains a major cause of morbidity and mortality worldwide, significantly impairing quality of life and imposing a heavy burden on healthcare systems.

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Pathophysiology

• Airway inflammation: Chronic exposure to irritants activates neutrophils, macrophages, and CD8+ T-lymphocytes, leading to persistent inflammation and release of proteases.

• Mucus hypersecretion: Hypertrophy of goblet cells results in thick mucus, contributing to airway obstruction.

• Airflow limitation: Small airway remodeling and loss of elastic recoil reduce expiratory flow.

• Gas exchange impairment: Alveolar wall destruction (emphysema) decreases surface area for oxygen-carbon dioxide exchange, causing hypoxemia and hypercapnia.

• Pulmonary hypertension: Chronic hypoxia leads to vasoconstriction, potentially progressing to cor pulmonale (right heart failure).

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Risk Factors

• Smoking: The leading risk factor; accounts for 80–90% of COPD cases.

• Occupational exposures: Dust, fumes, and chemical irritants.

• Air pollution: Both indoor (biomass fuel use) and outdoor pollutants.

• Genetics: Alpha-1 antitrypsin deficiency (rare inherited condition).

• Age and sex: More common in older adults; prevalence historically higher in men but now increasing in women.

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Clinical Features

• Chronic cough: Usually productive, often termed "smoker’s cough."

• Sputum production: Particularly in chronic bronchitis.

• Breathlessness (dyspnea): Initially exertional, later at rest.

• Wheezing and chest tightness.

• Frequent respiratory infections.

• Fatigue and weight loss in advanced stages.
  Patients are often described as:

• “Blue bloaters” (chronic bronchitis type): Cyanosis, edema, hypoxemia.

• “Pink puffers” (emphysema type): Dyspnea, pursed-lip breathing, cachexia, relatively preserved oxygenation until late disease.

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Complications

• Acute exacerbations (often triggered by infections).

• Pneumonia.

• Respiratory failure.

• Cor pulmonale (right-sided heart failure).

• Pneumothorax (in emphysema).

• Reduced quality of life and increased mortality.

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Diagnosis

Diagnosis requires a combination of clinical assessment and objective testing:

• History and examination: Chronic cough, smoking history, dyspnea.

• Spirometry (gold standard):

  • FEV1/FVC ratio < 0.70 post-bronchodilator confirms airflow limitation.

  • FEV1 determines severity (mild >80%, moderate 50–79%, severe 30–49%, very severe <30% predicted).

• Chest X-ray or CT scan: Shows hyperinflated lungs, flattened diaphragm, bullae.

• Arterial blood gases (ABG): To assess hypoxemia and hypercapnia in advanced disease.

• Alpha-1 antitrypsin testing: In younger patients or non-smokers.

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Management

COPD management focuses on symptom relief, slowing progression, reducing exacerbations, and improving quality of life. Treatment involves non-pharmacological and pharmacological strategies.

Non-Pharmacological Management

• Smoking cessation: Most effective intervention to slow disease progression. Nicotine replacement therapy (patches, gum) or medications such as varenicline 1 mg twice daily or bupropion SR 150 mg once daily for 3 days then twice daily can be used.

• Pulmonary rehabilitation: Exercise training, nutrition counseling, education.

• Vaccinations: Annual influenza and pneumococcal vaccination to prevent infections.

• Oxygen therapy: Long-term oxygen therapy for chronic hypoxemia (PaO₂ ≤ 55 mmHg or ≤ 60 mmHg with cor pulmonale).

• Nutritional support: Address cachexia or obesity.

• Patient education: Inhaler technique, self-management strategies.

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Pharmacological Treatment

Treatment is guided by symptom severity and risk of exacerbations (GOLD guidelines).

1. Bronchodilators (first-line)

   • Short-acting beta-2 agonists (SABA):

     • Salbutamol 100–200 mcg inhaled as needed.

     • Terbutaline 250–500 mcg inhaled as needed.

   • Short-acting muscarinic antagonists (SAMA):

     • Ipratropium bromide 20–40 mcg inhaled every 6–8 hours.

   • Long-acting beta-2 agonists (LABA):

     • Formoterol 12 mcg twice daily.

     • Salmeterol 50 mcg twice daily.

   • Long-acting muscarinic antagonists (LAMA):

     • Tiotropium 18 mcg once daily.

     • Aclidinium 400 mcg twice daily.

2. Inhaled Corticosteroids (ICS)

   • Indicated in patients with frequent exacerbations and high eosinophil counts.

   • Examples:

     • Budesonide 200–400 mcg twice daily.

     • Fluticasone propionate 100–500 mcg twice daily.

   • Usually given in combination with LABA (e.g., budesonide/formoterol, fluticasone/salmeterol).

3. Phosphodiesterase-4 inhibitors

   • For severe COPD with chronic bronchitis and frequent exacerbations.

   • Roflumilast 500 mcg orally once daily.

4. Methylxanthines (less commonly used due to side effects)

   • Theophylline 200–400 mg daily in divided doses (requires serum level monitoring).

5. Systemic corticosteroids

   • Reserved for acute exacerbations.

   • Prednisolone 30–40 mg orally once daily for 5–7 days.

6. Antibiotics

   • Used for acute exacerbations with purulent sputum or signs of infection.

   • Amoxicillin 500 mg three times daily for 5–7 days.

   • Doxycycline 100 mg once daily for 5 days.

   • Azithromycin 500 mg once daily for 3 days (or 250 mg once daily for 5 days).

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Exacerbation Management

• Increase bronchodilator frequency.

• Short course of oral corticosteroids.

• Antibiotics if bacterial infection suspected.

• Oxygen therapy if hypoxemic (target saturation 88–92%).

• Hospital admission if severe (respiratory distress, confusion, hypoxemia).

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Prognosis

COPD is progressive and incurable, but appropriate treatment can slow its progression and improve quality of life. Prognosis depends on:

• Severity of airflow obstruction (FEV1 level).

• Frequency of exacerbations.

• Smoking status (continued smoking worsens outcomes).

• Presence of comorbidities (cardiovascular disease, lung cancer, osteoporosis).