Classification of bronchiectasis
Bronchiectasis represents irreversible dilation of one or more bronchi containing cartilaginous plates and mucous glands. According to their origin, two groups are distinguished:
- Congenital: account for about 2–3% of all diffuse lung diseases.
- Acquired: develop in bronchiectasis 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 the proximal bronchi (up to the 4th order) and have a sac-like appearance.
- Cylindrical (fusiform): affect the 6th–10th order bronchi, visually appearing as sequentially connected hollow cylindrical "beads".
- Varicose: outwardly resemble varicose veins.
Pathogenesis and causes
Patho- and morphogenesis vary depending on the form of the disease.
Congenital bronchiectasis develops in children with prenatal and postnatal developmental defects of the tracheobronchial tree. Favorable backgrounds include cystic fibrosis (due to altered secretion quality) and Kartagener syndrome (due to impaired ciliary motility). Pathogenesis includes bronchial secretion stasis and subsequent infection. The addition of a bacterial infection causes destruction of the elastic framework and muscular layer, leading to wall sclerosis and lumen dilation. The lesion is diffuse in nature.
Acquired bronchiectasis has a focal nature (limited 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 against the background of bronchopneumonia with marked tissue destruction (in measles, diphtheria, adenovirus infection, influenza). Obstructive and compression causes include foreign body aspiration, occlusion by caseous masses in tuberculosis, and bronchial compression by a tumor.
Pathological anatomy and histology
Bronchiectasis is a combination of pronounced bronchiectasis and an extrapulmonary symptom complex. The lesion is predominantly acquired, focal in nature, and most frequently localized in the bronchi of the lower lobe of the right lung.
Microscopic examination demonstrates profound changes in all layers:
- Lumen content: purulent exudate, microbial bodies, and desquamated epithelium.
- Epithelium and membrane: the lining 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 the cartilaginous plate are observed, along with atrophy and destruction of the muscular and elastic layers.
- Inflammation and sclerosis: there is diffuse histiolymphocytic infiltration of all layers admixed with polymorphonuclear leukocytes (neutrophils), with developing 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 severe respiratory hypoxia and pulmonary hypertension. Clinically, this manifests as cyanosis, digital clubbing (thickening of the terminal phalanges), and watch-glass nails (deformation of the nail plates). Cardiac changes develop sequentially: pulmonary hypertension leads to right ventricular hypertrophy, culminating in the formation of cor pulmonale (cor pulmonale).
Each complication of bronchiectasis can be fatal. Major life-threatening conditions include pulmonary hemorrhage, lung abscess, pleural empyema, and chronic cor pulmonale. Currently, rare complications such as secondary amyloidosis (AA amyloid) and brain abscesses are also encountered.
Briefly: answers to topical questions
Which microorganisms are most frequently the causative agents of secondary infection in bronchiectasis?
The most frequent causative agents of secondary infection in bronchiectasis are Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella.
Depending on the clinical situation, the following pathogens are distinguished:
- Haemophilus influenzae (Haemophilus influenzae) — typical microflora during exacerbations.
- Pneumococcus (Streptococcus pneumoniae) — a frequent infectious agent.
- Moraxella (Moraxella catarrhalis) — one of the main pathogens.
- Pseudomonas aeruginosa (Pseudomonas aeruginosa) — causes chronic colonization of the airways, especially in cystic fibrosis.
In which lung segments is acquired bronchiectasis most frequently localized?
Acquired bronchiectasis is most frequently localized in the bronchi of the lower lobe of the right lung.
Depending on the shape of the dilation, different levels of the bronchial tree are affected:
- Saccular (cystic) — predominantly proximal bronchi, including 4th-order bronchi.
- Cylindrical (fusiform) — level of 6th–10th order bronchi.
What is the pathogenetic mechanism of digital clubbing in chronic hypoxia?
Digital clubbing in bronchiectasis is caused by severe respiratory hypoxia and pulmonary hypertension. Clinically, it manifests as thickening of the terminal phalanges of the fingers. Hypertrophic osteoarthropathy is also described in cyanotic congenital heart defects.
To memorize the triad of extrapulmonary symptoms in hypoxia, use the visual association: "Drumsticks" (thickened fingers), "Watch glasses" (convex nails), and a bluish skin tint (cyanosis).
Class and exam questions
How do congenital bronchiectasis and acquired bronchiectasis differ?
Congenital ones are diffuse and associated with developmental defects or genetic syndromes (cystic fibrosis, Kartagener syndrome). Acquired ones are focal and arise due to bronchial obstruction and secondary infection.
Where is acquired bronchiectasis most frequently localized?
The most typical localization is the bronchi of the lower lobe of the right lung.
What is the morphological basis of bronchial dilation?
Destruction of the elastic framework and muscular coat of the bronchial wall under the influence of bacterial infection and chronic inflammation.
How does cor pulmonale develop in this disease?
Chronic hypoxia causes pulmonary hypertension, leading to compensatory hypertrophy of the right ventricle and the development of cor pulmonale (cor pulmonale).
What else to study on this topic
- 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 formation in the lung parenchyma adjacent to bronchiectasis.
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