Chronic Obstructive Pulmonary Disease (COPD)

RADIOLOGY READING ASSIGNMENT

Group Members

  • Nahom Tadele ---------------- MMR/904/15
  • Nahom Aschenaki -------------- MMR/814/15
  • Amanuel Agegnhu -------------- MMR/671/15
  • Yonas Tadesse --------------- MMR/869/15
  • Biniam Mekonnen -------------- MMR/563/15
  • Submitted to: Dr. Walid Ali
  • Date of submission: 19/12/25

Chronic Obstructive Pulmonary Disease (COPD)

Definition

  • Chronic Obstructive Pulmonary Disease (COPD) is defined as a common, preventable, and treatable chronic lung disease characterized by:
    • Persistent respiratory symptoms.
    • Airflow limitation that is due to airway and/or alveolar abnormalities.
    • Commonly caused by significant exposure to noxious particles or gases.
  • Notably, the airflow limitation is not fully reversible and tends to progress over time.
  • COPD encompasses two main phenotypic conditions:
    • Chronic Bronchitis: Inflammation and mucus hypersecretion in the airways.
    • Emphysema: Destruction of the lung's alveolar air sacs.
    • Most often, both conditions coexist in patients with COPD.

Pathogenesis

  • The primary cause of COPD is chronic inhalation of toxic particles.
    • Most commonly from cigarette smoke, but also from biomass fuels, occupational dusts, and air pollution.
  • This exposure triggers a chronic inflammatory response in the lungs, involving:
    • Neutrophils
    • Macrophages
    • T-Lymphocytes
Consequences of Inflammation
  • The chronic inflammation leads to several significant alterations:
    • Structural Changes (Remodeling):
    • Damage to the lung parenchyma (emphysema) arises from an imbalance between proteases (which break down elastin) and anti-proteases. This results in:
      • Destruction of alveolar walls.
      • Reduction in elastic recoil, leading to air trapping.
    • Airway Disease:
    • Characterized by chronic inflammation, fibrosis, and excessive mucus production (chronic bronchitis), which narrows the small airways (obstructive bronchiolitis).
    • Systemic Effects:
    • Inflammation can extend into the bloodstream, leading to:
      • Weight loss
      • Muscle wasting
      • Increased risk of cardiovascular disease
    • A critical pathophysiological concept is identified:
      • Loss of elastic recoil (from emphysema) + Increased airway resistance (from bronchitis) = Expiratory airflow limitation, hyperinflation of the lungs, and impaired gas exchange.

Clinical Presentation

  • Key Symptoms include:
    • Chronic and Progressive Dyspnea (Shortness of Breath):
    • Initially occurs during exertion; progresses to resting state.
    • Often described using terms like "increased effort to breathe," "air hunger," or "heaviness."
    • Chronic Productive Cough:
    • Often the first symptom to emerge; sputum production is typically mucoid but can become purulent during exacerbations.
    • Wheezing and Chest Tightness.
    • Frequent Respiratory Infections.
Relevant Physical Examination Findings
  • Early Disease:
    • May present as normal or with only a prolonged expiratory phase and wheezes on forced exhalation.
  • Moderate to Severe Disease:
    • Increased Anteroposterior Chest Diameter ("Barrel Chest"):
    • Observed due to hyperinflation.
    • Use of Accessory Muscles:
    • Involvement of sternocleidomastoid and scalene muscles, as well as pursed-lip breathing to generate positive pressure and maintain patency of small airways.
    • Decreased Breath Sounds:
    • Due to poor airflow.
    • Hyperresonance on Percussion:
    • Due to trapped air.
    • Distant Heart Sounds.
    • Digital Clubbing:
    • Is NOT typical for COPD alone; its presence should prompt investigation for lung cancer or bronchiectasis.
    • Signs of Right Heart Failure ("Cor Pulmonale") in Advanced Disease:
    • Peripheral edema, jugular venous distension, hepatomegaly.

Radiographic Features

Chest X-ray (Primary Initial Imaging)
  • Initial findings may be normal in early disease.
  • Signs indicative of hyperinflation include:
    • Flattened hemidiaphragms (best visualized on lateral view).
    • Increased retrosternal air space.
    • Barrel-shaped thoracic cage.
  • Lung Parenchyma Changes:
    • Decreased lung markings (vascular attenuation) in peripheral lungs due to emphysematous destruction.
    • Bullae (large air-filled spaces >1cm) may also be visible.
  • Chronic Bronchitis Signs:
    • Typically non-specific; may demonstrate "dirty lungs" with increased bronchovascular markings.
  • Exclusion of Other Conditions:
    • Essential for ruling out pneumothorax, pneumonia, or heart failure as potential causes for exacerbation.
High-Resolution Computed Tomography (HRCT) – More Sensitive and Specific
  • Assists in precise classification and localization of emphysema:
    • Centrilobular Emphysema:
    • Most common and associated with smoking.
    • Shows small, round low-attenuation areas (resembling black holes) without walls, primarily in upper lobes.
    • Panlobular (Panacinar) Emphysema:
    • Associated with Alpha-1 Antitrypsin Deficiency.
    • Involves destruction of the entire acinus, resulting in widespread vascular attenuation, most severe in the lower lobes.
  • Airway Wall Thickening:
    • Characteristic of chronic bronchitis.
  • Bullae and Blebs:
    • Clearly defined and identifiable through imaging.
  • Pulmonary Hypertension:
    • Noted through enlarged pulmonary artery diameter (>29mm).

Examples

  • Lateral Chest X-ray:
    • Presented from a different patient (normal but well-inflated).
  • Measurements:
    • Thickness of the space between the ascending aorta and the sternum should not exceed 2.5cm under normal conditions.
    • The normal dome of each hemidiaphragm should rise at least 1.5cm above a line connecting the costophrenic angle posteriorly and the sternophrenic angle anteriorly.

References

  1. Harrison's Principles of Internal Medicine
  2. https://radiopaedia.org/cases/chronic-obstructive-pulmonary-disease-marked-hyperinflation
  3. Robbins Basic Pathology