Bronchiectasis
A condition marked by chronic abnormal dilation of bronchi and destruction of bronchial walls, bronchiectasis can occur throughout the tracheobronchial tree or can be confined to one segment or lobe. However, it’s usually bilateral and involves the basilar segments of the lower lobes. This disease has three forms: cylindrical (fusiform), varicose, and saccular (cystic).
It affects people of both sexes and all ages. Because of the availability of antibiotics to treat acute respiratory tract infections, the incidence of bronchiectasis has dramatically decreased in the past 20 years. Its incidence is highest among the Inuit of the Arctic and the Maoris of New Zealand. Bronchiectasis is irreversible once established.
Causes
The different forms of bronchiectasis may occur separately or simultaneously. In cylindrical bronchiectasis, the bronchi expand unevenly, with little change in diameter, and end suddenly in a squared-off fashion. In varicose bronchiectasis, abnormal, irregular dilation and narrowing of the bronchi give the appearance of varicose veins. In saccular bronchiectasis, many large dilations end in sacs.
This disease results from conditions associated with repeated damage to
bronchial walls and abnormal mucociliary clearance, which cause a breakdown of supporting tissue adjacent to airways. Such conditions include:
bronchial walls and abnormal mucociliary clearance, which cause a breakdown of supporting tissue adjacent to airways. Such conditions include:
mucoviscidosis (cystic fibrosis)
immunologic disorders (agammaglobulinemia, for example)
recurrent, inadequately treated bacterial respiratory tract infections, such as tuberculosis, and complications of measles, pneumonia, pertussis, or influenza
obstruction (by a foreign body, tumor, or stenosis) in association with recurrent infection
inhalation of corrosive gas or repeated aspiration of gastric juices into the lungs
congenital anomalies (uncommon), such as bronchomalacia, congenital bronchiectasis, immotile cilia syndrome, and Kartagener’s syndrome, a variant of immotile cilia syndrome characterized by situs inversus viscerum, bronchiectasis, and either nasal polyps or sinusitis.
With bronchiectasis, hyperplastic squamous epithelium denuded of cilia replaces ulcerated columnar epithelium. Abscess formation involving all layers of the bronchial wall produces inflammatory cells and fibrous tissue, resulting in dilation and narrowing of the airways. Mucus or fibrous tissue obliterates smaller bronchioles, and peribronchial lymphoid tissue becomes hyperplastic. Extensive vascular proliferation of bronchial circulation occurs and produces frequent hemoptysis.
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