Radiography and main forms
On standard radiographs, bronchiectasis manifests as an enlargement of pulmonary structures and blurring of their contours due to concomitant peribronchial inflammation and fibrosis. Generalized forms of the lesion often present with a picture of lung hyperinflation, which is particularly typical for patients with cystic fibrosis. Localized forms, by contrast, are frequently accompanied by atelectasis, indirectly indicated by vascular crowding (vascular crowding), displacement of the interlobar fissure, or opacification of part of the diaphragmatic dome.
On computed tomography, the following pathological types are distinguished by morphology:
- Cylindrical: uniform dilation of the bronchial tube (often found as post-infectious).
- Varicose (varicose bronchiectasis): the lumen is unevenly dilated, and the walls acquire a beaded configuration.
- Cystic (cystic bronchiectasis): visualized as a cluster or chain of thin-walled cysts. When secretion is retained in the lower (dependent) parts of such cavities, characteristic air-fluid levels often form.
Specific CT symptoms
Computed tomography is the method of choice, with multidetector spiral scanning surpassing traditional step-by-step HRCT as it eliminates the risk of missing local foci between slices. The main marker of the pathology is the lack of tapering of the bronchial lumen as it extends toward the periphery (lack of tapering). Dilated bronchi may be visualized abnormally close to the pleura — within 1 cm of the ribs or adjacent to the mediastinum.
Characteristic visual patterns:
- Signet ring sign (signet ring sign): on an axial slice, the bronchial lumen becomes wider than the accompanying pulmonary artery.
- Finger-in-glove sign (glove-finger): V- or Y-shaped lobular opacities resulting from mucus accumulation in dilated lumens. If the slice passes perpendicularly to the bronchus, these plugs appear as dense nodular opacities.
- Tree-in-bud sign (tree-in-bud sign): small centrilobular nodules and branching lines. Found in approximately 70% of patients and indicates concomitant infectious bronchiolitis.
Small airways disease
The clinical severity of obstruction according to pulmonary function testing (PFT) correlates not with the collapse of large bronchi, but with small airways disease and their occlusion.
Severe bronchiectasis is frequently accompanied by obliterative bronchiolitis (obliterative bronchiolitis). On CT, this condition manifests as:
- Mosaic perfusion (mosaic perfusion).
- Expiratory air trapping (air trapping) during the expiration phase.
Areas of air trapping typically coincide with zones of decreased radiographic density on inspiration. This phenomenon is explained by local hypoperfusion, which occurs secondarily in response to hypoventilation due to bronchiolar obstruction. The most important structural factor determining further decline in lung function is bronchial wall thickening.
Features in cystic fibrosis
Cystic fibrosis (cystic fibrosis) is a classic cause of generalized bronchiectasis development. Due to an autosomal recessive genetic defect in the CFTR protein, mucus becomes viscous, and mucociliary clearance is reduced. Inflammation rapidly destroys the walls of the airways.
Radiological stages:
- Early stage: changes are minimal. Hyperinflation and thickening of the walls of upper lobe bronchi are noticeable (best seen in the lateral projection).
- Late stage: pronounced lung volume enlargement, cystic changes in the upper lobes (can simulate bullae or healed abscesses), prominent mucous plugs.
On CT, the pathology manifests in the upper lobes, with wall thickening appearing earlier than luminal dilation. To minimize radiation dose, low-dose CT with post-processing is used. Maximum intensity projection (MIP) images better demonstrate the tree-in-bud sign, while minimum intensity projection (MinIP) images show areas of mosaic perfusion. As a radiation-free alternative, lung MRI is increasingly used: it is slightly inferior in spatial resolution, but excellently shows perfusion defects and distinguishes reversible changes from irreversible ones.
Briefly: answers to topical questions
Which congenital diseases and syndromes, besides cystic fibrosis, are a frequent cause of bronchiectasis?
In addition to cystic fibrosis, frequent congenital causes of bronchiectasis development include genetic defects and airway malformations.
These include:
- Kartagener syndrome (Kartagener syndrome) / primary ciliary dyskinesia — manifests with a triad including bronchiectasis, sinusitis, and situs inversus (situs inversus).
- Dyskinetic Cilia Syndrome (Dyskinetic Cilia Syndrome) — an autosomal recessive disease leading to decreased mucociliary clearance.
- Alpha-1 antitrypsin deficiency — a genetic defect.
- Congenital structural anomalies — tracheomalacia, congenital bronchogenic cyst, and other malformations of the bronchopulmonary system.
What complications of bronchiectasis can be detected using diagnostic imaging methods?
Diagnostic imaging methods can detect the following complications and changes associated with bronchiectasis:
- Pulmonary hemorrhage / hemoptysis — a life-threatening condition. MDCT angiography identifies the source of bleeding and serves as a vascular roadmap; the most common source is the bronchial arteries.
- Pulmonary hypertension — enlargement of the pulmonary artery on CT reflects the presence of pulmonary hypertension and is an important prognostic sign.
To memorize the signet ring sign: imagine a signet ring, where the thin circular rim is the wall of the dilated bronchus, and the protruding stone is the adjacent pulmonary artery of smaller diameter.
Class and exam questions
Can CT precisely determine the cause of bronchiectasis?
In most cases, CT features alone are not enough. The cause is identified in less than 50% of patients, although distribution patterns (e.g., bilateral upper lobe involvement in cystic fibrosis) greatly narrow the search.
Why does pulmonary hypertension develop in bronchiectasis?
Chronic hypoxia and inflammation, as well as hypoventilation due to obliterative bronchiolitis, lead to local hypoperfusion and vascular spasm, which over time overloads the right heart chambers and dilates the pulmonary artery.
How is MRI useful in the diagnosis of cystic fibrosis?
MRI makes it possible to completely avoid ionizing radiation, which is critical for young patients requiring frequent monitoring. In addition, contrast enhancement on MRI correlates well with the degree of tissue destruction.
What else to study on this topic
- Distribution patterns of bronchiectasis as a key to differential diagnosis
- Obliterative bronchiolitis: pathophysiology and imaging findings
- Low-dose CT protocols in pulmonology
- Allergic bronchopulmonary aspergillosis (ABPA): similarities and differences from cystic fibrosis
- Image post-processing (MIP and MinIP) in the diagnosis of airway pathologies
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