Chronic Obstructive Pulmonary Disease typically occurs in smokers, manifesting as as hyperinflated lungs with bronchial wall thickening and emphysematous changes due to bronchitis and alveolar destruction.
Description
COPD is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. It is characterised by a combination of small airway disease (bronchiolitis) and parenchymal destruction (emphysema), leading to decreased lung function.
Pathogenesis
The primary pathogenetic mechanism is chronic inflammation in response to inhaled irritants, especially cigarette smoke, leading to structural changes in the airways and lung parenchyma. Other factors include genetic predisposition (such as alpha-1 antitrypsin deficiency) and environmental exposures.
Emphysema involves the destruction of alveolar septa and pulmonary capillaries, leading to decreased elastic recoil and resultant air trapping.
Subtypes
- Emphysema: Destruction of alveolar walls leading to large, abnormal air spaces.
- Chronic Bronchitis: Persistent cough with sputum production for at least 3 months in two consecutive years.
Epidemiology, Risk Factors & Associations
- Strongly associated with cigarette smoking and long-term exposure to other lung irritants (consider occupational history, e.g. miners)
- Cystic fibrosis
- Alpha-1 antitrypsin deficiency
- More common in individuals over 40 years of age.
- Worldwide, a leading cause of morbidity and mortality.
Clinical Features
- Progressive and persistent dyspnoea, especially on exertion.
- Chronic cough and sputum production.
- Frequent respiratory infections and exacerbations.
Complications
- Acute infective or non-infective exacerbations leading to increased breathlessness, cough, and sputum production.
- Pulmonary hypertension and right heart failure (cor pulmonale).
- Increased risk of lung infections and pneumothorax.
- Chronic respiratory failure.
Pathological Features
Histopathology
- Macroscopic: Overdistended lungs, decreased lung elasticity.
- Microscopic: Mucous gland hyperplasia, inflammation, fibrosis of small airways; destruction of alveolar walls in emphysema.
Radiological Features
General Features
- Hyperinflation with flattened diaphragms, increased retrosternal air space, bronchial wall thickening, and emphysematous changes.
XR
- Hyperinflated lungs, a flattened diaphragm
- Barrel chest on lateral radiograph – Widened AP diameter
- Increased bronchovascular markings
- Saber-sheath trachea – Coronal narrowing of the intrathoracic trachea less than or equal to two-thirds of the sagittal dimension. There is concomitant sagittal widening. The extrathoracic trachea is normal
- Bullae may be seen in emphysema.
CT
- Chronic bronchitis – Bronchial wall thickening. Bronchovascular irregularity and fibrosis.
- Emphysema –
- Centrilobular (centriacinar): associated with smoking and spreads peripherally from bronchioles
- Panacinar: homozygous AAT1 deficiency and uniformly destroys alveoli
- Paraseptal (distal acinar): involves the distal airways
MRI
- Limited role in COPD but can be useful in assessing comorbidities and complications.
Grading and Staging
- Based on the severity of airflow limitation using spirometry (GOLD criteria: Stages I to IV).
Diagnosis
- Clinical diagnosis based on history, physical examination, and confirmation with spirometry.
- Chest X-ray and HRCT for assessment of lung structure and comorbidities.
Differential Diagnosis
- Asthma: Reversible airway obstruction and different clinical history.
- Congestive heart failure: Presents with cardiac symptoms and signs.
- Bronchiectasis: Persistent productive cough with dilated airways on imaging.
- Lung cancer: Focal lung lesions with or without associated COPD changes.
Management
- Smoking cessation as the most critical intervention.
- Bronchodilators (beta-agonists and anticholinergics) and inhaled corticosteroids.
- Pulmonary rehabilitation and physical activity.
- Management of exacerbations with antibiotics and systemic corticosteroids.
- Supplemental oxygen therapy in advanced stages.