Doctors Revision

Respiratory System

Chronic Obstructive Pulmonary Disease (COPD)

A progressive lung disease characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases (most commonly tobacco smoke). Airflow limitation is not fully reversible. Includes conditions previously known as chronic bronchitis and emphysema.

Also known as: COPD, Chronic Bronchitis, Emphysema

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Referral and warning signs

When to refer

Refer to specialist (Pulmonologist/Physician) for: Diagnostic uncertainty. Severe COPD (FEV1 <50%). Frequent exacerbations despite therapy. Need for Long-Term Oxygen Therapy assessment. Onset at young age (<40 yrs) or non-smoker (consider AAT deficiency). Co-morbidities complicating management. Consideration for pulmonary rehabilitation.

Red flags

  • Signs of acute respiratory failure (severe dyspnoea, cyanosis, confusion, drowsiness, inability to speak)
  • Worsening hypoxemia (SpO2 <88%) or hypercapnia
  • New signs of cor pulmonale (peripheral oedema, raised JVP)
  • Failure to respond to standard exacerbation treatment
  • Haemoptysis (consider malignancy, bronchiectasis, TB)

Signs and symptoms

  • Chronic cough (often productive of sputum, esp. morning)
  • Chronic sputum production
  • Progressive dyspnoea (worsens over time, typically worse with exertion)
  • Wheezing, chest tightness
  • History of exposure to risk factors (smoking, biomass fuel)
  • Often occurs in individuals >40 years old.
  • Examination findings (may be normal in mild disease): Barrel chest (increased AP diameter), reduced chest expansion, decreased breath sounds, prolonged expiration, wheezes/rhonchi.
  • Late signs: Use of accessory muscles, pursed-lip breathing, cyanosis, signs of right heart failure (cor pulmonale - peripheral oedema, raised JVP, hepatomegaly).

Risk factors

  • Tobacco smoking (primary cause)
  • Exposure to indoor air pollution (biomass fuel smoke - firewood, charcoal, dung)
  • Occupational exposure to dusts, chemicals, fumes
  • History of severe childhood respiratory infections
  • Tuberculosis (post-TB lung damage can lead to COPD features)
  • Alpha-1-antitrypsin deficiency (rare genetic cause)

Diagnosis

Clinical assessment

Consider in any patient >40 years with dyspnoea, chronic cough or sputum production, and/or history of exposure to risk factors. Clinical diagnosis supported by symptoms and exposure history. Differential diagnosis: Asthma (key features: earlier onset, variability, reversibility, allergy history), Heart Failure, Bronchiectasis, Tuberculosis, Lung Cancer, Obliterative Bronchiolitis.

Investigations

  • Spirometry: Gold standard for diagnosis. Required to demonstrate persistent airflow limitation (Post-bronchodilator FEV1/FVC ratio < 0.70 or below lower limit of normal). Also grades severity based on FEV1.
  • Chest X-ray: Used to exclude other diagnoses and assess for co-morbidities. May show signs of hyperinflation (flattened diaphragms, increased retrosternal air space), bullae, or pulmonary hypertension.
  • Peak Flowmetry: Limited diagnostic value, more for asthma monitoring.
  • Pulse Oximetry (SpO2): Assess oxygen saturation, especially during exacerbations.
  • Arterial Blood Gas (ABG): Assess for hypoxemia and hypercapnia in severe disease or acute exacerbations.
  • Echocardiogram: Assess for pulmonary hypertension and cor pulmonale.
  • Sputum Examination: Gram stain/culture during exacerbations if infection suspected.
  • Alpha-1-antitrypsin level (if young onset, non-smoker, family history).

Diagnostic criteria

Presence of persistent respiratory symptoms and/or risk factor exposure PLUS demonstration of persistent airflow limitation (post-bronchodilator FEV1/FVC <0.70) on spirometry.

Management

Non-pharmacological management

  • Smoking Cessation: Single most effective intervention. Offer counseling and support.
  • Reduce Exposure to Indoor/Occupational Pollutants: Improve kitchen ventilation, use cleaner fuels/stoves, use respiratory protection at work.
  • Pulmonary Rehabilitation: Supervised program including exercise training, education, psychosocial support. Improves exercise tolerance and quality of life.
  • Physical Activity: Encourage regular exercise as tolerated.
  • Vaccinations: Influenza (annual) and Pneumococcal vaccinations recommended.
  • Nutritional Support: Address malnutrition or obesity.
  • Oxygen Therapy (Long-term - LTOT): For chronic severe hypoxemia (PaO2 ≤55 mmHg or SpO2 ≤88% at rest). Requires specialist assessment. Target SpO2 88-92% (avoid over-oxygenation).

Pharmacological treatment

  • Bronchodilators (Mainstay for symptom relief):
  • - Short-acting beta2-agonists (SABA) e.g., Salbutamol PRN or scheduled.
  • - Short-acting muscarinic antagonists (SAMA) e.g., Ipratropium Bromide PRN or scheduled.
  • - Long-acting beta2-agonists (LABA) e.g., Salmeterol, Formoterol.
  • - Long-acting muscarinic antagonists (LAMA) e.g., Tiotropium, Glycopyrronium.
  • - Combination LABA/LAMA inhalers often used for moderate/severe disease.
  • Inhaled Corticosteroids (ICS):
  • - Typically used in combination with LABA (ICS/LABA inhalers) for patients with moderate/severe COPD AND frequent exacerbations (≥2 moderate exacerbations/year or ≥1 hospitalization).
  • - Examples: Beclomethasone, Budesonide, Fluticasone.
  • - Not recommended as monotherapy.
  • Oral Theophylline (e.g., Aminophylline): Limited role due to narrow therapeutic index and side effects. May be considered by specialists in severe disease.
  • Management of COPD Exacerbations:
  • - Increase dose/frequency of short-acting bronchodilators (Salbutamol +/- Ipratropium) via nebulizer or MDI+spacer.
  • - Systemic Corticosteroids: Oral Prednisolone 30-40 mg daily for 5 days.
  • - Antibiotics: If signs of bacterial infection (increased sputum purulence AND increased sputum volume OR increased dyspnoea). E.g., Amoxicillin 500mg TID OR Doxycycline 100mg BID for 5-7 days.
  • - Controlled Oxygen Therapy: Target SpO2 88-92% (beware CO2 retention).
  • - Consider Non-Invasive Ventilation (NIV) for acute respiratory failure (hypercapnia, acidosis) - specialist setting.
  • - Admit to hospital if severe exacerbation, respiratory failure, inadequate response, significant co-morbidities.

Monitoring

  • Monitor symptoms (dyspnoea, cough, sputum).
  • Assess exacerbation frequency.
  • Monitor spirometry periodically (e.g., annually).
  • Assess inhaler technique and adherence.
  • Monitor SpO2.
  • Assess need for LTOT.

Complications

  • Acute exacerbations
  • Respiratory failure (acute or chronic; hypoxemic or hypercapnic)
  • Pneumonia
  • Pulmonary hypertension
  • Cor pulmonale (right heart failure)
  • Chronic bronchitis
  • Emphysema
  • Weight loss, muscle wasting
  • Osteoporosis
  • Depression, anxiety
  • Increased risk of cardiovascular disease
  • Lung cancer

Prevention

  • Smoking cessation
  • Reduce exposure to biomass fuel smoke and occupational dusts/chemicals.
  • Vaccinations (influenza, pneumococcal).

Patient education

  • Explain COPD as chronic, progressive lung damage (often from smoking/smoke exposure).
  • Emphasize smoking cessation as critical.
  • Explain purpose and correct use of inhalers (bronchodilators, ICS).
  • Recognizing and managing exacerbations early (action plan).
  • Importance of vaccinations.
  • Benefits of pulmonary rehabilitation and regular activity.
  • Oxygen therapy use and safety (if prescribed).
  • Nutritional advice.

Uganda-specific notes

Biomass fuel exposure is a major cause alongside smoking. Post-TB lung disease is common and can mimic/overlap with COPD. Spirometry is often unavailable; diagnosis relies heavily on clinical assessment and risk factor history. Access to inhaled therapies (especially LABA/LAMA/ICS combinations) and oxygen therapy is limited.

References

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 5, Section 5.1.2

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