Compared to laryngeal or bronchial cancers, primary malignant tumors are rare in the trachea. The most frequent histological types are squamous cell carcinoma and adenoid cystic carcinoma, accounting for nearly 80% of all tracheal neoplasms.

Direct invasion of the central airways by neoplasms of the thyroid, esophagus, lung, and larynx is much more common than hematogeneous metastases. CT demonstrates the primary neoplasm and its extension by contiguity within the main airways (endoluminal mass, destruction of cartilage, and tracheo-bronchial-esophageal fistula).

Many cancers have the potential to metastasize to the trachea and bronchi. Endotracheal or endobronchial metastases appear as endotracheal nodules or an eccentric thickening of the airway wall or as soft-tissue attenuation with contrast enhancement.

Benign tracheal neoplasms are rare, accounting for <2% of lung neoplasms. On CT, they present as endoluminal masses confined within the tracheobronchial lumen without evidence of involvement of surrounding structures. Benign neoplasms are typically sharply marginated, round and <2 cm in diameter. Because they originate in the mucosa or submucosa, the overlying epithelium is usually intact, resulting in a smooth appearance of the tumor surface in the airway lumen.

Histology includes mainly hamartomas, lipomas, leiomyomas, fibromas, chondromas, and schwannomas. Endobronchial harmartomas account for 30% of intrathoracic hamartomas. The presence of fat with or without calcification is diagnostic.

Respiratory papillomatosis (laryngotracheobronchial papillomatosis) is a neoplastic disease caused by human papillomavirus infection transmitted from mother to child at birth or acquired from orogenital contact. Papillomas arise in the larynx and involve the trachea and proximal bronchi in up to 50% of cases. Involvement of the lungs is rare, occurring in <1% of patients, and manifests on imaging studies as multiple lung nodules and cavitary and cystic lesions in the parenchyma. Malignant transformation into squamous cell carcinoma is a rare but serious complication of respiratory papillomatosis.

Post-traumatic strictures of the trachea are usually the result of ischemic injury from a cuffed endotracheal or tracheostomy tube or extrinsic neck trauma. These injuries initially heal by the formation of granulation tissue, with subsequent scarring characterized by dense mucosal and submucosal fibrosis associated with distortion of cartilage plates. The two principal sites of stenosis following intubation or tracheostomy tube are at the stoma or at the level of the endotracheal or tracheostomy tube balloon. CT with multiplanar reformations clearly depicts the severity and length of the stricture. Post-intubation stenosis extends for several centimeters and typically involves the trachea above the level of the thoracic inlet. Post-tracheostomy stenosis typically begins 1.0–1.5 cm distal to the inferior margin of the tracheostomy stoma and extends over 1.5–2.5 cm. These strictures typically have an hourglass configuration with a thickened tracheal wall. Less commonly, tracheal or bronchial stenosis may present as a thin membrane or granulation tissue protruding into the airway lumen. In select cases, the degree of stenosis may also be assessed by virtual bronchoscopy.

Involvement of the large airways is a common manifestation of granulomatosis with polyangiitis. Inflammatory lesions may be present with or without subglottic or bronchial stenosis, ulcerations, and pseudotumors. Radiologic manifestations include thickening of the subglottic and proximal trachea, with a smooth symmetric or asymmetric narrowing over variable length. Tracheal rings can become thickened and calcified. Cartilaginous erosions and ulcerations also may be seen. Stenosis may be present in any main, lobar, or segmental bronchus. Developing nodular or polypoid lesions can protrude into the airway lumen.

Relapsing polychondritis is a rare systemic autoimmune disease that affects cartilage at various sites, including the ears, nose, joints, and tracheobronchial tree. Histologically, the acute inflammatory infiltrate in both cartilage and perichondrial tissue induces progressive dissolution and fragmentation of the cartilage followed by fibrosis. Symmetric subglottic stenosis is the most frequent manifestation in the chest. As the disease progresses, the distal trachea and bronchi may be involved. CT scans show a smooth thickening of the airway wall associated with diffuse narrowing. In the early stages of the disease, the posterior wall of the trachea is spared but in advanced disease, circumferential wall thickening can occur. Tracheobronchomalacia can develop as a result of weakening of cartilage, resulting in considerable luminal collapse on expiration. Gross destruction of the cartilaginous rings with fibrosis may cause stenosis.

Amyloid deposition in the trachea and bronchi may occur in association with systemic amyloidosis or as an isolated process. The deposits can present as single, multifocal, or diffuse submucosal plaques or masses. The overlying mucosa is usually intact. Dystrophic calcification or ossification is frequently present. CT scans show focal or, more commonly, diffuse thickening of the airway wall and narrowing of the lumen. Calcification may be present. Narrowing of the proximal bronchi can lead to distal atelectasis, bronchiectasis, or both, with or without obstructive pneumonia.

This rare disorder is characterized by the presence of multiple cartilaginous nodules and bony submucosal nodules on the luminal surface of the trachea and proximal airways. Tracheobronchopathia osteochondroplastica involves males more frequently than females, and most patients are older than 50 years. Histologically, the nodules contain heterotopic bone, cartilage, and calcified acellular protein matrix. The overlying bronchial mucosa is normal, and, because it contains no cartilage, the posterior wall of the trachea is spared. On CT, tracheal cartilages are thickened and show irregular calcifications. The nodules may protrude from the anterior and lateral walls into the lumen; they usually show foci of calcification. The majority of patients are asymptomatic, with only a small number developing obstructive signs and symptoms.

Saber-sheath trachea is characterized by narrowing of the transverse diameter and an increase in the sagittal diameter of the intrathoracic trachea. It is almost always associated with COPD. The pathogenesis is unclear but is likely related to the altered mechanics resulting from the intrathoracic pressure changes associated with COPD. On radiographs and CT, the internal transverse diameter of the trachea is decreased to half or less than the corresponding sagittal diameter. The narrowing usually affects the whole intrathoracic trachea, with an abrupt return to normal caliber at the thoracic inlet. The trachea most often shows a smooth inner margin but occasionally has a nodular contour. Calcification of the tracheal cartilage is common.