The pathophysiology of bronchiectasis

Abstract

Bronchiectasis is defined by permanent and abnormal widening of the bronchi. This process occurs in the context of chronic airway infection and inflammation. It is usually diagnosed using computed tomography scanning to visualize the larger bronchi. Bronchiectasis is also characterized by mild to moderate airflow obstruction. This review will describe the pathophysiology of noncystic fibrosis bronchiectasis. Studies have demonstrated that the small airways in bronchiectasis are obstructed from an inflammatory infiltrate in the wall. As most of the bronchial tree is composed of small airways, the net effect is obstruction. The bronchial wall is typically thickened by an inflammatory infiltrate of lymphocytes and macrophages which may form lymphoid follicles. It has recently been demonstrated that patients with bronchiectasis have a progressive decline in lung function. There are a large number of etiologic risk factors associated with bronchiectasis. As there is generally a long-term retrospective history, it may be difficult to determine the exact role of such factors in the pathogenesis. Extremes of age and smoking/chronic obstructive pulmonary disease may be important considerations. There are a variety of different pathogens involved in bronchiectasis, but a common finding despite the presence of purulent sputum is failure to identify any pathogenic microorganisms. The bacterial flora appears to change with progression of disease.

Keywords: bronchiectasis; inflammation; obstructive lung disease; pathology; pathophysiology.

Figure 1

HRCT examples of Reid’s three forms of bronchiectasis: A) tubular B), varicose, and C) cystic. Abbreviation: HRCT, high-resolution computed tomography.

Figure 2

Pathologic changes in follicular bronchiectasis as described by Whitwell. A) The first process involves infection of the small airways. B) This leads to the release of inflammatory mediators such as proteases which damage the large airways resulting in bronchial dilation and bronchiectasis. C) Infection drives progressive inflammation in the small airways which become thicker from a combination of cell-mediated inflammatory infiltrate and lymphoid follicles resulting in obstruction. D) The final process involves the spread of inflammation beyond the airways resulting in interstitial pneumonia.

Figure 3

Pathologic process in the right middle lobe with mycobacterial infection. A) Infection causes enlargement of peribronchial lymph nodes resulting in obstruction. B) The obstruction results in bronchiectasis that persists when the nodes return to normal size.

Figure 4

Change in severity of symptoms over time in those with childhood-onset bronchiectasis. A common finding in subjects whose symptoms began in childhood is improvement in late adolescence and then deterioration again from about the age of 50 years.