Causes Bronchiectasis can be classified as congenital or secondary. Congenital is less common and is due to congenital bronchial dysplasia, the presence of congenital defects or genetic disorders that prevent further development of the periphery of the lung, resulting in dilated developed bronchi, such as bronchial chondrodysplasia. In some patients bronchiectasis occurs after birth, but there are also congenital anomalies present, such as, Kartagener’s syndrome, where patients may have visceral ectopic and pancreatic cystic fibrosis lesions in addition to bronchiectasis, which actually belongs to a subtype of ciliac akinesia syndrome. Bronchiectasis is also seen in Young syndrome, which is characterized by obstructive sperm deficiency, chronic sinusitis, recurrent pulmonary infections and bronchiectasis. Some patients with bronchiectasis show immunoglobulin deficiency. IgG deficiency predisposes to recurrent bacterial infections, with IgG2 and IgG4 deficiency being more important. The main factors in the pathogenesis of secondary bronchiectasis are recurrent infections of the bronchi and lungs, bronchial obstruction, and bronchial involvement, all three interacting with each other. Measles, pertussis, influenza or severe pulmonary infections such as Klebsiella pneumoniae, Staphylococcus, influenza virus, fungi, Mycobacterium and mycoplasma infections in childhood damage the bronchial layers, especially smooth muscle fibers and elastic fibers, reduce mucus cilia clearance, weaken the support of the tube wall, increase the pressure in the lumen during inspiration and coughing, expand the lumen, and during expiration Bronchial tumors, granulomas caused by bronchial endothelial tuberculosis, scar stenosis, foreign body inhalation, mucus embedding or extra-tubular causes can cause different degrees of stenosis or obstruction in the bronchial lumen, resulting in poor distal drainage and infection and bronchial dilatation; as the disease progresses, peribronchial fiber hyperplasia, extensive pleural thickening and As the disease progresses, peribronchial fibroplasia, extensive pleural thickening, and pulmonary atelectasis, the traction of negative pressure in the thoracic cavity on the diseased lung produce a pull on the bronchus, while the local defense mechanism and clearance function are reduced, and repeated infections cause atrophy of the bronchial wall muscle layer, destruction of cartilage, and decrease in tension, resulting in a lasting dilatation under the action of pulling force outside the wall.