Objective. To establish pathogenetic factors leading to the development of chronic nonspecific inflammation and bronchiectasis in the bronchi.

Materials and methods. Of the 125 patients who were diagnosed with bronchiectatic disease, 95 (76.0%) suffered from protracted pneumonia in childhood. Others did not remember this, but the pneumonia they had suffered in childhood could be confirmed by the identity of the radiologically detected changes in their lungs. Examinations were directed on revealing of reasons of the chronic indolent inflammatory process. A significant result for the diagnosis was obtained by studying the overview and lateral radiographs of the chest organs. All of them had the X-ray syndrome “lesion of bronchial patency”, which made it possible to assume the presence of pathology in the bronchi and served as an indication for bronchoscopy and bronchography (84 patients) or computed tomography (41 patients). These studies allowed us to establish a diagnosis.

Results. The connection of bronchiectatic disease with protracted pneumonia suffered in the past, clinical, X-ray, bronchological and morphological comparisons allow us to propose the following mechanism for the development of chronic inflammation and bronchiectasis in the bronchi of the affected lobe.

1. Severe lower lobe protracted pneumonia in a child leads to the development of carnification, obliteration of the bronchial branches of the 6—8 order and fibrous atelectasis of the lobe.
2. Fibrous atelectasis leads to a persistent embarrassment of ventilation in the affected lobe.
3. In case of embarrassment of ventilation, the bronchi lose their ability to self-clean.
4. In case of violation of self-purification, the secret of the bronchial glands constantly accumulates in the bronchi of the affected lobe of the lung, which serves as a breeding ground for bacteria.
5. The bronchi are colonized by a large number of conditionally pathogenic bacteria.
6. There is a latent chronic inflammation in the bronchial walls.
7. As a consequence of chronic local catarrhal, and then purulent endobronchitis, cicatricial degeneration of the bronchial walls occurs.
8. Cicatricial tissue in the bronchial walls is subjected to thinning, stretching, bronchiectasis is formed.

Conclusion. The pathogenesis of bronchiectatic disease is associated with fibrous atelectasis, which occurred after
a protracted lower lobe pneumonia suffered in childhood. Bronchiectases are formed through the sequential addition of
8 pathogenetic factors, but only 4 factors can be neutralized (accumulation of bronchial secretions in the bronchi). Removal of the accumulated bronchial secretions deprives the microflora of a nutrient medium, the microflora disappears, which leads to the elimination of the chronic inflammatory process in the affected bronchi and prevents the progression of bronchiectatic disease. This can be achieved by systematic therapeutic bronchoscopy in two-week courses (4—6 times
a year) in the course of dispensary observation (under the supervision of a doctor of the pulmonological office of the polyclinic) using one of three methods: 1). Intratracheal instillation with a larynx syringe of 15 ml of a warm 0.9% sodium chloride solution, daily; 2). Therapeutic bronchoscopy, 2 times a week, with the removal of bronchial secretion from the bronchi (do not inject anything into the bronchi); 3). Drip administration twice a week, through a nasotracheal catheter,
50 ml warm, 0.9% sodium chloride solution, 10—15 drops per minute, with frequent coughing.

Regular physical exercises in a gentle mode and slow running for 10—20 minutes (1—2 km) every other day or daily, in the evening, contribute to better sputum discharge and bronchial cleansing.

Surgical intervention is performed in 30—40% of cases. The reason for the rare use of surgical treatment is the spread of chronic inflammation and bronchiectasis to the bronchi of neighboring lobes of the lungs.