Clinical meaning
Tracheomalacia is characterized by excessive dynamic collapsibility of the trachea due to weakness, softening, or malformation of the tracheal cartilage rings and the pars membranacea (posterior membranous wall), causing dynamic airway obstruction particularly during expiration when increased intrathoracic pressure collapses the weakened airway. Normal tracheal cartilage rings are C-shaped and maintain airway patency; in tracheomalacia, these rings are flattened, softened, or deficient, allowing the anterior and posterior walls to approximate during expiration, coughing, or crying. Primary (congenital) tracheomalacia results from intrinsic cartilage immaturity — cartilage matures over 12-24 months, and most cases resolve spontaneously by age 18-24 months. Secondary (acquired) tracheomalacia develops from extrinsic compression (vascular rings such as double aortic arch or pulmonary artery sling, mediastinal masses, esophageal atresia with tracheoesophageal fistula), prolonged endotracheal intubation (pressure necrosis of cartilage), chronic tracheostomy, relapsing polychondritis, or chronic obstructive lung disease (adult form). The hallmark symptom is expiratory stridor or wheeze that worsens with agitation, crying, feeding, or respiratory infections and improves with neck extension or prone positioning. The diagnosis is confirmed by flexible bronchoscopy during spontaneous breathing, which demonstrates >50% reduction in tracheal lumen diameter during expiration.