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Bronchiectasis

Morbus bronchiectaticus

For medical students2 min readUpdated 2026-10-10

Bronchiectasis is a condition characterized by a complex of pulmonary and extrapulmonary, as well as obstructive and restrictive changes. The underlying pathology is permanent abnormal bronchial dilation accompanied by chronic respiratory failure, signs of tissue hypoxia, and the development of cor pulmonale.

Common localizationBronchi of the right lower lobe

Morphological basisDestruction of the muscular and elastic layers of the bronchial wall

Cardiac complicationRight ventricular hypertrophy and development of cor pulmonale

Extrapulmonary signsDigital clubbing, nail changes, and cyanosis

Classification of Bronchiectasis

A bronchiectasis is an irreversible dilation of one or more bronchi containing cartilage plates and mucous glands. Based on origin, there are two groups:

Congenital: accounting for about 2–3% of all diffuse lung diseases.
Acquired: developing in bronchiectasis disease and chronic bronchitis. Differential diagnosis between these conditions is based on assessing the degree of bronchial dilation and the presence of a characteristic extrapulmonary symptom complex.

According to macroscopic features (shape), bronchiectasis is divided into:

Saccular (cystic): localized predominantly in proximal bronchi (up to the 4th generation) and shaped like a sac.
Cylindrical (fusiform): affects the 6th–10th generation bronchi, visually appearing as sequentially connected cylindrical hollow "beads".
Varicose: externally resembles varicose veins.

Pathogenesis and Causes

Pathogenesis and morphogenesis differ depending on the form of the disease.

Congenital bronchiectasis forms in children with prenatal and postnatal developmental defects of the tracheobronchial tree. A favorable background includes cystic fibrosis (due to abnormal secretion quality) and Kartagener syndrome (due to ciliary functional impairment). Pathogenesis includes bronchial secretion stasis and subsequent infection. Bacterial infection triggers the destruction of the elastic framework and muscular layer, leading to wall sclerosis and luminal dilation. The lesion is diffuse in nature.

Acquired bronchiectasis is local in character (restricted to one or several bronchi). The leading mechanism is bronchial obstruction combined with secondary bacterial infection. The main risk group includes patients with diffuse bronchial obstruction. Often, the pathology develops secondary to bronchopneumonia with marked tissue destruction (in measles, diphtheria, adenovirus infection, influenza). Obstructive and compression causes include foreign body aspiration, caseous mass blockage in tuberculosis, and bronchial compression by a tumor.

Pathological Anatomy and Histology

Bronchiectasis represents a combination of marked bronchiectasis and an extrapulmonary symptom complex. The lesion is predominantly acquired, local in character, and most commonly localized in the bronchi of the right lower lobe.

Microscopic examination demonstrates profound changes across all layers:

Luminal contents: purulent exudate, microbial bodies, and desquamated epithelium.
Epithelium and membrane: the surface layer is represented by basal cells, with foci of polyposis and squamous cell metaplasia. The basement membrane is hyalinized and corrugated.
Bronchial wall: dystrophy and destruction of cartilage plates, as well as atrophy and destruction of muscular and elastic layers, are observed.
Inflammation and sclerosis: diffuse histiolymphocytic infiltration of all layers with an admixture of polymorphonuclear leukocytes (neutrophils) is present, along with wall sclerosis.
Adjacent parenchyma: fields of fibrosis and foci of obstructive pulmonary emphysema are formed.

Extrapulmonary Manifestations and Complications

The extrapulmonary symptom complex is caused by marked respiratory hypoxia and pulmonary hypertension. Clinically, this manifests as cyanosis, digital clubbing (thickening of the distal phalanges of the fingers), and nail curvature changes. Cardiac changes develop sequentially: pulmonary hypertension leads to right ventricular hypertrophy, culminating in the formation of cor pulmonale.

Each of the complications of bronchiectasis can be fatal. Major life-threatening conditions include pulmonary hemorrhage, lung abscess, pleural empyema, and chronic cor pulmonale. Rare complications, such as secondary amyloidosis (AA amyloid) and brain abscesses, are also encountered today.

Mnemonic

To memorize the triad of extrapulmonary symptoms in hypoxia, use the visual association: "Drumsticks" (clubbed fingers), "Watch glass" nails (curved nails), and a bluish skin tint (cyanosis).

Frequently asked questions

Which microorganisms are the most common causative agents of secondary infection in bronchiectasis?

The most common causative agents of secondary infection in bronchiectasis are Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis.

Depending on the clinical situation, the following pathogens are identified:

Haemophilus influenzae — typical microflora during exacerbations.
Streptococcus pneumoniae — a frequent infectious agent.
Moraxella catarrhalis — one of the main causative agents.
Pseudomonas aeruginosa — causes chronic airway colonization, especially in the setting of cystic fibrosis.

In which lung segments are acquired bronchiectases most frequently localized?

Acquired bronchiectases are most frequently localized in the bronchi of the right lower lobe.

Depending on the shape of the dilation, different levels of the bronchial tree are affected:

Saccular (cystic) — predominantly proximal bronchi, including 4th-generation bronchi.
Cylindrical (fusiform) — the level of 6th–10th generation bronchi.

What is the pathogenetic mechanism of digital clubbing in chronic hypoxia?

Digital clubbing in bronchiectasis is caused by marked respiratory hypoxia and pulmonary hypertension. Clinically, it manifests as thickening of the distal phalanges of the fingers. Hypertrophic osteoarthropathy is also described in cyanotic congenital heart defects.

How do congenital and acquired bronchiectasis differ?

Congenital forms are diffuse and associated with developmental defects or genetic syndromes (cystic fibrosis, Kartagener syndrome). Acquired forms are localized and arise due to bronchial obstruction and secondary infection.

Where are acquired bronchiectases most commonly localized?

The most typical localization is the bronchi of the right lower lobe.

What is the morphological basis of bronchial dilation?

Destruction of the elastic framework and muscular layer of the bronchial wall under the influence of bacterial infection and chronic inflammation.

How does cor pulmonale form in this disease?

Chronic hypoxia causes pulmonary hypertension, leading to compensatory right ventricular hypertrophy and the development of cor pulmonale.

Go deeper

Differential diagnosis of bronchiectasis and chronic bronchitis.
The role of cystic fibrosis and Kartagener syndrome in the pathogenesis of congenital bronchiectasis.
Histological features of squamous cell metaplasia of the respiratory epithelium.
Pathogenesis of secondary AA amyloidosis in chronic purulent inflammation.
Mechanisms of obstructive emphysema development in the pulmonary parenchyma adjacent to bronchiectasis.