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1952年 Holinger 等报道3例伴有严重喘鸣、发绀和明显呼吸道阻塞的气管软化症婴儿,支气管镜检查发现气管壁异常软弱。Baxter 等(1963)认为本症是由于气管壁支持软骨软化和肌弹性成份张力减弱,致使气管前后壁靠近而管腔变小。Weiloo 等(1979)证实气管软化症常伴发气管食管瘘,这与气管壁软化的畸形和缺失以及气管横肌宽度增加有关。本文作者按组织病理学和支气管镜所见将气管软化症分为原发性和继发性二类:原发性气管软化症见于早产儿、其他方面正常的婴儿和软骨发育不良者;继发性气管软化症见于伴有气管食管瘘、无名动脉“压迫”和外部有压迫,如血管环、先天性囊肿或肿瘤的患者。
In 1952, Holinger et al. Reported three cases of infantile bronchodilators with severe wheezing, cyanosis and significant airway obstruction. Bronchoscopy revealed abnormal weakness of the tracheal wall. Baxter et al (1963) that this disease is due to the tracheal wall to support the cartilage softening and muscle tension elastic components weakened, leading to the trachea anterior and posterior wall and the smaller the lumen. Weiloo et al. (1979) demonstrated that tracheobronchitis is often associated with tracheal esophageal fistulas, which is associated with deformity and absence of tracheal wall softening and increased tracheal transverse muscle width. The authors classify tracheal inflammation by primary histopathology and bronchoscopy into two primary and secondary categories: primary tracheal astrocytosis seen in preterm infants, other infants with normal infants and achondroplasia; secondary Mild tracheomania is found in patients with tracheoesophageal fistula, anonymous artery “oppression” and external oppression, such as vascular rings, congenital cysts or tumors.