How is bronchiectasis considered an obstructive lung disease when it involves dilation of the airways?

How Bronchiectasis Causes Airflow Obstruction Despite Airway Dilation

Bronchiectasis is classified as an obstructive lung disease because the pathological dilation of airways paradoxically leads to airflow obstruction through multiple mechanisms: mucus plugging, bronchial wall thickening, small airways disease, and dynamic airway collapse—not because the dilated airways themselves improve airflow. 1

The Paradox Explained: Structural Changes That Cause Obstruction

The confusion arises from thinking that wider airways should allow better airflow. However, the European Respiratory Society guidelines clarify that more than 50% of bronchiectasis patients have airflow obstruction despite the characteristic bronchial dilation. 1

Key Mechanisms of Obstruction

Mucus plugging is the primary obstructive mechanism:

• Impaired mucociliary clearance results from structural bronchiectasis, airway dehydration, and excess mucus volume and viscosity 1
• More than 70% of bronchiectasis patients expectorate sputum daily, indicating chronic mucus accumulation that physically blocks airflow 1
• Treatment specifically aims to prevent mucus stasis and the associated mucus plugging and airflow obstruction 1

Bronchial wall thickening compounds the problem:

• Chronic neutrophilic inflammation causes destruction of elastic and muscular components of bronchial walls 1
• The inflammatory process leads to bronchial wall thickening that narrows the effective airway lumen 1
• Excessive neutrophilic inflammation is linked to rapid lung function decline through degradation of airway elastin 1

Small airways disease and emphysema frequently coexist:

• Structural changes include not just bronchial dilation but also small airways disease and emphysema 1
• These distal airway changes contribute significantly to the obstructive physiology 1

Dynamic airway collapse occurs because:

• Destruction of elastic and muscular components weakens bronchial wall structural integrity 2, 3
• The dilated, weakened airways are prone to collapse during expiration, creating functional obstruction 4

Clinical Implications for Obstruction

Breathlessness results from multiple obstructive factors:

• Airflow obstruction is the primary cause of dyspnea 1
• Impaired gas transfer, exercise deconditioning, and comorbidities contribute additionally 1
• Breathlessness is one of the strongest predictors of mortality in bronchiectasis 1

The vicious cycle perpetuates obstruction:

• Chronic bronchial infection stimulates sustained lung inflammation 1, 2
• Inflammation causes progressive airway injury and structural damage 1, 2
• Impaired mucociliary clearance leads to further mucus stasis and bacterial colonization 1, 2
• This cycle results in progressive lung damage and worsening airflow obstruction 1

Physiologic Classification

Bronchiectasis demonstrates variable obstructive patterns:

• More than 50% of patients have airflow obstruction on pulmonary function testing 1
• Restrictive, mixed ventilatory patterns, and even preserved lung function are also observed 1
• The obstructive pattern predominates clinically, justifying its classification as an obstructive lung disease 4, 5

Management Targeting Obstruction

Treatment specifically addresses the obstructive components:

• Bronchodilators are used to treat airflow obstruction 2
• Airway clearance techniques prevent mucus plugging 1, 6
• Long-term mucoactive treatments reduce mucus viscosity and volume 1
• Pulmonary rehabilitation improves exercise capacity limited by obstruction 1, 2

Common Pitfall to Avoid

Do not assume that dilated airways in bronchiectasis mean improved airflow. The dilation represents pathological destruction of normal airway architecture, not functional improvement. The dilated airways are filled with mucus, have thickened walls, lack structural support, and are accompanied by small airways disease—all contributing to obstruction rather than relieving it. 1, 2