Bronchiectasis

Introduction bronchiectasis (bronchiectasis) is a common chronic purulent bronchial diseases, Most secondary to respiratory infections and bronchial obstruction, especially children and youth measles, Pertussis after bronchial pneumonia, bronchial wall broken ring, forming the lumen expansion and deformation. The clinical manifestations of chronic cough with a large number of SAP and repeated hemoptysis. With the improvement of people's lives, measles, pertussis vaccine inoculations, and the clinical application of antibiotics, This has led to the morbidity rate is greatly reduced. Pathology Disease etiology and pathogenesis of bronchiectasis the principal factors for bronchial-pulmonary infection and bronchial resistance Cypriots. Lumen mucosal infections caused by congestion and edema, so that the lumen narrow, easily blocked luminal secretions. led to poor drainage and increasing infection; Bronchial obstruction obstruction will cause a lung infection. They both influence each other, to promote the incidence of bronchiectasis and development. Congenital and developmental defects caused by genetic factors see less of bronchiectasis. A bronchial-pulmonary infection and obstruction of infant measles, whooping cough, pneumonia and other bronchial infection, yes bronchial-pulmonary infection and obstruction caused by bronchiectasis the most common reasons for infant bronchial wall weak, lumen smaller narrow, easily blocked, repeated infection damaged bronchial wall layers, or bronchioles surrounding tissue fibrosis, stretch wall, causing bronchial deformation expansion. Lesions are often tired bronchial pulmonary bottom and left more obvious. Tuberculosis fibrous tissue hyperplasia and contraction traction, or tuberculosis caused by bronchial stenosis and obstruction, with or without atelectasis may cause bronchiectasis, good hair is situated on the tip of the post of the superior or the next. Extension gas and aspergillus infection injury bronchial wall, showing the proximal bronchi expansion. Tumor, foreign body inhalation, or swelling of lymph nodes outside of oppression caused bronchial obstruction, can lead to the distal bronchial-pulmonary infection. Bronchial obstruction to atelectasis, the loss of alveolar elastic buffer, the direct negative pressure within the chest stretch bronchial wall, the result of bronchiectasis. Right middle lobe bronchus slender, cluster around a number of lymph nodes, often nonspecific or tuberculous lymphadenitis and swollen bronchial compression caused atelectasis. with bronchiectasis caused by the middle syndrome. Stimulate the corrosive gases and ammonia inhalation, direct injury trachea, bronchial wall and repeatedly secondary infection can lead to bronchiectasis. 2, bronchial congenital defects and genetic factors bronchial congenital developmental disorder, If huge tracheal - bronchial disease (trachobronchomegaly) Could congenital connective tissue abnormalities, due to weak wall expansion. For achondroplasia or lack of elastic fibers, leading to partial wall weak or poor flexibility. accompanied sinusitis and situs inversus (right-center), known as Kartagener syndrome. Right-heart with bronchiectasis were in the incidence of 15% -20%, much higher than the general population. Note the syndrome and congenital factors. And genetic factors related to the lungs of cystic fibrosis, as bronchial mucous glands sticky mucus secretion, serum may contain inhibitory effect of columnar epithelial cells cilia activities substances; induced secretion retention in bronchial, obstruction, pulmonary atelectasis and secondary infection, induced bronchiectasis. Gammaglobulin congenital deficiency and low in patients with Waldenstrom's immune function is low, repeated bronchitis disease can occur bronchiectasis. Pathological secondary to bronchial-pulmonary inflammatory diseases bronchiectasis was particularly prevalent in the lower lobe, and left lower lobe bronchus more slender, Also affected by the oppression of cardiovascular, affecting drainage, high incidence of infections, are more likely to become. Tongue bronchial close to opening under the superior support, due to lower lobe involvement and infection, it left lower lobe and tongue leaf branch expansion often also exist. Bronchiectasis mucosal surface often chronic ulcers, ciliated columnar epithelial cells of squamous metaplasia or shrink, stretch wall, muscle and cartilage injury, replaced by fibrous tissue, the cavity deformation expansion. Expansion patterns can be divided into two types of cystic and columnar, there are often mixed. Columnar expansion of the wall damage was slight, with the development of lesions, severe damage into cystic expansion. After treatment can make lesions stabilized or improved. Accompanied telangiectasia, or bronchial pulmonary artery and the terminal branches coincide with the expansion, the formation of hemangioma, there will be a large number of repeated hemoptysis. Bronchiectasis occurred repeatedly infected and the inflammation spread to the adjacent lung, caused varying degrees of pneumonia. and small abscess or lobular not strong, and chronic bronchitis associated with the pathological changes long it can be formed obstructive pulmonary fibrosis and emphysema, but also add bronchiectasis. Pathophysiological bronchiectasis early lesions light and limited, as reserves lung capacity, Respiratory function in the normal range; Lesions larger scope, there may be mild obstructive ventilation changes; When serious and widespread disease, peripheral bronchial pulmonary fibrosis, and pleural or pericardial involvement. Pulmonary function can be measured with obstruction of performance-oriented hybrid ventilation dysfunction, such as reduced lung capacity, Residual gas / total lung capacity ratio relative increase in FVC and FEV1 FVC occupation forces FVC ratio reduced, Ventilation largest volume decline. Gassing uneven, bronchiectasis drainage district lung alveolar ventilation decreased, and blood few limitations, so that ventilation / flow ratio less than the normal form of pulmonary arteriovenous shunt-like and diffuse dysfunction caused hypoxemia. Serious disease, alveolar capillary extensive damage, pulmonary vascular resistance, pulmonary hypoxemia caused artery vasospasm, pulmonary hypertension, right ventricular increased burden with pulmonary heart disease, and even the right heart failure.