The Core Curriculum: Cardiopulmonary Imaging, 1st Edition (2004)

Chapter 16. The Central Airways

Computed Tomography Techniques

Imaging of the upper airways provides information that can lead to safer bronchoscopic evaluation, airway dilatation, or surgical repair for patients with airway compromise. Occasionally, imaging may preclude the need for bronchoscopy as a diagnostic tool. Although multidirectional tomography used to be the mainstay for imaging the upper airways, this equipment is rarely found now in most modern hospitals, and planar tomography is currently used (Fig. 16.1). This type of equipment is best suited for renal and musculoskeletal applications but is not optimal for evaluating the thorax. Moreover, because of its infrequent use in the thorax, there is a general lack of expertise on the part of the radiologic technologists obtaining the studies and the radiologists interpreting the examinations. High kilovoltage (150 kVp or greater) radiography with heavy filtration (using aluminum, brass, or copper) can provide high quality tracheal images, although in practice it is rarely used. Fluoroscopy is sometimes a useful dynamic method to evaluate for tracheomalacia, particularly in pediatric patients (1).

Ultrasound may be helpful in patients who are unable to breath-hold or lie flat for computed tomography (CT) evaluation. However, limitations of this technique include nonvisualization of the intrathoracic trachea, poor visualization of posterior wall lesions, and suboptimal evaluation of calcium. One report suggested that ultrasound may be useful as a follow-up investigation in some patients (2). Magnetic resonance imaging (MRI) produces excellent soft tissue contrast of structures and has the capability of imaging in multiple planes. Typically, T1-weighted images, before and after contrast, are most helpful (3). Unfortunately, limitations of MRI include potentially long imaging times, motion artifact, suboptimal evaluation of calcifications, and suboptimal spatial resolution as compared with CT (Fig. 16.1). Therefore, MRI currently has limited usefulness in this setting. For all intents and purposes, CT has virtually replaced all other modalities for imaging the tracheobronchial tree at the current time. In addition to its ability to image the airways, CT also enables visualization of extraluminal spread of disease.

CT is the modality of choice for evaluating the tracheobronchial tree.

Most published studies concerning CT evaluation of the central airways have used conventional CT scanners. On such equipment, a limited number of sections (typically three to six) can be obtained during a single breath-hold, necessitating pauses in scanning to allow the patient to breath. There may be significant misregistration between sections obtained on different breath-holds, leading to overlap and/or gaps between adjacent images. Unfortunately, such misregistration leads to highly suboptimal reconstruction of the CT data in other planes, and therefore the data are usually displayed only in the axial plane. In general, due to their orientation along the long axis of the body, the trachea and main bronchi are better suited to demonstration in the coronal or oblique planes rather than the axial plane. In addition, the necessity for frequent pauses for breathing leads to the use of relatively thick (5 to 10 mm) sections to cover the area of interest in a timely fashion. Despite these limitations, conventional CT is useful for evaluating focal and diffuse tracheal stenoses and masses and for assessing disease involvement of adjacent structures.

Figure 16.1 Wegener’s granulomatosis. A. Coronal tomogram of the trachea demonstrates marked subglottic luminal narrowing. B.Axial computed tomography through the subglottic trachea demonstrates submucosal thickening and luminal narrowing. C. Axial magnetic resonance imaging (TR 2,350, TE 90) shows mucosal thickening of high signal intensity within the tracheal lumen.

Recent technologic advances have led to the development of helical CT scanners (both single and multislice) that enable rapid aquisition of a large number of thin sections. Thus, an entire study can be performed during a single breath-hold, thereby eliminating misregistration artifacts from varying degrees of respiration. The technique can be particularly useful in patients with multiple stenoses, in whom a proximal stricture is not traversable by a bronchoscope. An entire set of images can be obtained in expiration and in inspiration to look for dynamic changes suggestive of tracheomalacia or bronchomalacia. Helically acquired CT data can be used to produce high quality multiplanar reconstructions (MPRs) (two-dimensional images) oriented along any desired axis and three-dimensional reconstructions and virtual reality bronchoscopic views of the airway lumen. MPRs occasionally provide information that is not evident on the axial images, although generally the addition of MPRs does not lead to significant increase in diagnostic accuracy when assessed by experienced radiologists. However, MPRs may be helpful in detecting mild stenoses, in more accurately depicting the length of tracheal lesions, and in detecting tracheal webs; MPRs are extremely useful in demonstrating findings to referring clinicians (Fig. 16.2). Three-dimensional images, including shaded surface displays, minimum intensity projections, volume rendering, and virtual bronchoscopy (endoluminal three-dimensional views) (Fig. 16.3), provide additional ways to display the helically acquired CT data.

Figure 16.2 Tracheal web. Multiplanar reformat in the coronal plane demonstrates a fine tracheal web that was not apparent on axial images.

All these techniques have potential pitfalls in interpretation, require accurate setting of thresholds to provide a true representation of the data, and may be time consuming to produce at a workstation (4,5,6,7). The virtual bronchoscope has the advantage of passing bronchial obstructions and stenoses, and both endobronchial and peribronchial anatomy can be studied. Unlike fiberoptic bronchoscopy, however, virtual bronchoscopy is unable to depict mucosal detail and true color. In general, three-dimensional postprocessing methods are time consuming to perform and are rarely required in routine clinical practice, although they may be complementary in some situations. The true incremental yield of such display techniques has yet to be established. Axial images with the addition of two-dimensional multiplanar reformats are generally sufficient and are quick to produce from the data set (8,9,10,11,12) (Fig. 16.4).

Figure 16.3 Virtual bronchoscopy. A. Axial computed tomography and (B) virtual bronchoscopic image demonstrate a small adenoid cystic carcinoma.

Figure 16.4 Postintubation tracheal stenosis. A. Axial contrast-enhanced computed tomography demonstrates irregular thickening of the subglottic tracheal wall with luminal narrowing. (B) Sagittal and (C) coronal multiplanar reformats help show the craniocaudal extent of the stenosis. D. Three-dimensional shaded surface display and (E) volume rendered reformats demonstrate the abnormality but do not add any further information.

One drawback of helical CT is the necessity for full patient cooperation, including the ability to breath-hold for at least 15 to 20 seconds (using a single slice scanner) and abstain from swallowing or other gross movement. Hyperventilation before scanning often aids the patient in accomplishing a sufficiently long breath-hold. The new, rapid, multislice helical scanners are useful in reducing the necessary breath-hold time. Examinations performed during free breathing are generally of limited diagnostic usefulness, and patients unable to suspend respiration during scanning are usually better imaged with conventional tomography. Cardiac motion causes some artifacts, although it usually does not compromise the diagnostic quality of the examination.

A suggested helical imaging protocol would include 1 to 3 mm sections from epiglottis to carina (tracheal study) or from mid-trachea to lower lobe bronchi (central bronchial study), depending on the area of interest. Overlapping images are reconstructed and used to create reformatted planar and three-dimensional images. The patient should be scanned with the neck hyperextended for a tracheal study. If the suspected region of interest is in the neck, the patient’s arms should be down; otherwise, the arms should be up. Initially, the patient is scanned in suspended inspiration, using a single breath-hold, if possible, after hyperventilation. The scan is then repeated during expiration. Intravenous contrast material may be given if a mass is suspected and/or if evaluation of the adjacent mediastinal and hilar structures is required (5). Increased pitch leads to increased stair step artifacts, especially in airways that course obliquely, such as the left main bronchus. Thin sections are essential to reduce partial volume averaging, and overlapping reconstructions help to reduce stair-step artifact (13).


The trachea is a midline structure. On the posteroanterior radiograph there is a slight deviation to the right and a smooth indentation on the left wall of the trachea due to indentation of the aortic arch. Location in the anteroposterior axis is variable but is usually midway between the sternum and spine (14). There is marked variation in cross-sectional shape. The most common shapes are round or oval; less commonly the trachea may be horseshoe shaped with a flat posterior wall, an inverted pear shape, or almost square. The length of the trachea as measured on CT is 6 to 9 cm (15). On chest radiography, the upper limits of normal coronal and sagittal diameter in men is 25 and 27 mm, respectively, and in women is 21 and 23 mm, respectively (16). The lower limit of normal is 13 mm for men and 10 mm for women.

The lower limit of normal tracheal diameter is 13 mm in men and 10 mm in women.

The trachea is made up of horseshoe-shaped bands of hyaline cartilage that support the anterior and lateral walls. Posteriorly is the trachealis muscle, which makes up the posterior tracheal membrane. The layers are the mucosa, submucosa, cartilage or muscle, and adventitia. The tracheal wall consists of 1 to 3 mm of soft tissue on CT. Cartilage may calcify; this is most common in older females. The posterior wall is thicker and may be flat, concave, or convex. The intrathoracic portion of the trachea starts at manubrium (17) and divides into the left and right main bronchi at the carina. The carinal angle, measured as the angle of divergence of the main bronchi along their inferior borders, can vary, with a range between 35 and 91 degrees (average, 55 to 60 degrees). In adults, the right main bronchus has a more vertical course than the left. In children up to age 15 years, the course is similar bilaterally. The right main bronchus is wider (15.3 mm on the right as compared with 13 mm on the left) (18) and shorter (2.2 cm on the right as compared with 5 cm on the left) than the left main bronchus (19,20). Although there are variations in the normal bronchial branching patterns that may be noted incidentally at bronchoscopy, these are mostly of no clinical significance. Generally, the locations of the bronchopulmonary segments are constant. Classification of the bronchial segments is presented in Table 16.1.

Table 16.1: Jackson and Huber Classification of Bronchial Segments

Right upper lobe


Right middle lobe


Right lower lobe

Medial basal
Anterior basal
Lateral basal
Posterior basal

Left upper lobe

   Upper division


   Lingular division


Left lower lobe

Lateral basal
Posterior basal

Congenital Anomalies

There may be either agenesis or aplasia of bronchi (i.e., with either absent or rudimentary lung tissue) with involvement of an entire lung, a lobe, or a single segment. This may be a primary phenomenon or secondary to factors such as a space-occupying lesion, thoracic cage abnormality, oligohydramnios, or reduced perfusion. In pulmonary agenesis, the carina is absent; in aplasia, there is a blind ending pouch. Congential bronchial anomalies are often associated with VACTERL (Vertebral dysgenesis, Anal atresia, Cardiac anomalies, Tracheo Esophageal fistula, Renal anomalies, Limb anomalies) abnormalities (21).

Focal mucoid impaction with a tubular soft tissue structure surrounded by hyperaerated lung should suggest bronchial atresia.

There are many variants of lobar and segmental agenesis, aplasia, and hypoplasia. Bronchial atresia is uncommon; it is possibly related to a vascular insult after 15 weeks’ gestation. There is focal obliteration of a segmental bronchus with normal distal structures. A distal mucoid impaction is generally present, showing an ovoid, round, or branching shape and sometimes containing an air–fluid level (Fig. 16.5). The distal lung, which is aerated via collateral air drift, may be hyperinflated. The most common site is the left upper lobe; 64% involve the left apicoposterior segmental bronchus, 14% the left lower lobe, and 8% the right middle and lower lobes (22). Bronchial atresias are often discovered incidentally, and bronchoscopy is used to exclude an endobronchial lesion (23).

The most congenital variant in tracheobronchial anatomy is the right tracheal (or “pig”) bronchus.

Other congential abnormalities include those of bronchial division. Right-sided isomerism is associated with asplenia, and left-sided isomerism is associated with polysplenia and cardiac abnormalities. The right tracheal bronchus is either a displaced right apical bronchus or a supernumerary bronchus; the incidence of this finding is approximately 0.1% to 2% (24). There may or may not be associated lung tissue; it may be a blind ending pouch. A left tracheal bronchus is rarer (0.3% to 1%) and is always an early origin of the left apicoposterior segmental bronchus. It is often associated with distal lung abnormality such as bronchiectasis, lymphangiectasia, and hyperinflation, possibly due to vascular compression by the left pulmonary artery (25). The bridging bronchus is an ectopic bronchus arising from the left main bronchus, crossing the midline and supplying the right lower lobe; the right main bronchus supplies the right upper and right middle lobes only. The accessory paracardiac bronchus has an incidence of 0.09% to 0.5% (26).

Although often asymptomatic, it may cause hemoptysis, infection, cough, or dyspnea. This is a true supernumerary anomalous bronchus and may or may not ventilate a rudimentary or accessory lobe, separated by a fissure. It arises from the medial wall of the bronchus intermedius (Fig. 16.6). Other minor bronchial branching variations are common (23).

Figure 16.5 Bronchial atresia. A. Posteroanterior chest radiograph demonstrates an ovoid mass in the left upper lobe. B. Axial computed tomography image demonstrates the mass with surrounding hyperinflation and a dilated tubular bronchus, representing mucoid impaction, extending anteriorly. C. Coronal T2-weighted magnetic resonance image demonstrates the high signal intensity of the mass and the tubular structure extending from it, representing mucus-filled bronchi.

Inflammatory Conditions

Postintubation Stenosis

Tracheal stricture or stenosis is most commonly a complication of tracheal intubation with a cuffed endotracheal tube; tracheostomy tube placement and trauma are less common etiologies. Postintubation stenosis may occur at the level of the tracheostomy stoma or at the level of the balloon for an endotracheal or tracheostomy tube. A stenosis is more likely with higher balloon cuff pressures, when the capillary pressure may be exceeded, leading to necrosis and fibrosis. Occasionally, stenosis is seen at level of the tube tip. The stricture generally results from pressure necrosis, causing ischemia and scarring. Stenosis can also be caused by inflammation with weakening of the tracheal wall (tracheomalacia) or by granulation tissue, especially at the level of the tube tip (27).

The most common cause of focal tracheal stenosis is prior intubation.

Figure 16.6 Accessory paracardiac bronchus. (A and B) Axial computed tomography and (C) coronal reformat shows accessory bronchus arising from the medial wall of the bronchus intermedius.

Acute stenoses are generally secondary to mucosal edema, granulation tissue, and necrotic pseudomembranes. Mucosal thickening is internal to the cartilage, and there is no change in the size of the tracheal lumen on expiration. Such stenoses may be single or multiple (28) and concentric, eccentric, web-like, or A-shaped, secondary to laterally impacted fractures of cartilage after tracheostomy. Chronic strictures may show cartilage and posterior membrane deformities and associated tracheomalacia (17,29,30).

CT using axial images alone is very accurate (approximately 90%) in detecting benign tracheal stenoses, although thin webs or short segment strictures may be missed. There is little gain to the addition of reformats. Reformats are useful, however, in more accurately depicting the longitudinal extent of the stenosis and may be helpful in detecting thin webs or short segment strictures (31) (Figs. 16.4 and16.7).

Figure 16.7 Postintubation tracheal stenosis. A. Sagittal and (B) coronal reformats of a distal tracheal stricture after intubation.


Tracheobronchomalacia is a weakness of the tracheal and bronchial walls and cartilage. Wall collapse is present during forced expiration and may be focal or diffuse. The many causes include primary congenital or secondary to tracheal intubation, chronic obstructive pulmonary disease, trauma, infection, relapsing polychondritis, radiation, tumors, surgery, or tracheobronchial fistula. The incidence increases with age, and it is said to be the fifth most common cause of chronic cough (32). Other symptoms are wheeze or unexplained dyspnea. Complications, secondary to the reduced efficiency of the cough mechanism, are retained mucus, infection, and bronchiectasis (33).

Relapsing polychondritis is a rare disease (fewer than 500 cases have been reported) characterized by recurrent inflammation and destruction of cartilage of the ears, nose, larynx, trachea, and peripheral joints; cardiovascular manifestations (aortitis, vasculitis, valvular insufficiency, and aneurysms) occur in 30% of cases. Respiratory involvement, occurring in 50% to 70% of cases, imparts a poor prognosis and causes approximately 50% of deaths from this disease, generally from recurrent pneumonia (31,33,34,35). The cause of the disease is unknown but appears to be immune mediated. Histologically, the normal collagen is replaced by fibrous tissue. Airway obstruction can occur by three mechanisms. First, inflammatory swelling of the glottic or subglottic area is the most common cause of upper airway obstruction in this disorder. Second, encroachment of the glottic or tracheal lumen due to cicatricial contraction may occur late in the course of the disease. Finally, with dissolution of the cartilaginous supporting structure of the trachea, there is dynamic collapse of the airway, especially with forced inspiration and expiration. Granulation tissue and fibrosis may also lead narrowing of the tracheal lumen (17,34,35). Tracheal stenosis with relapsing polychondritis is usually a late manifestation of the disease and reflects diffuse tracheal involvement; however, localized stenosis occurring in the proximal, middle, or distal trachea may also occur. CT findings include thickening of the tracheal wall with or without calcifications; the posterior membranous wall of the trachea is spared (Fig. 16.8). There may be focal or diffuse tracheal narrowing, with or without expiratory airway collapse (28).

Figure 16.8 Relapsing polychondritis. Axial computed tomography demonstrates thickening of the tracheal wall with sparing of the posterior membrane.

Tracheobronchomalacia can be evaluated using bronchoscopy, fluoroscopy, and CT. Dynamic CT performed during inspiration and expiration may offer a useful alternative to bronchoscopy and fluoroscopy (Fig. 16.9). CT is performed either through the entire trachea with table movement or at a fixed point with the table stationary (note the trachea moves cranially on expiration; therefore, table position needs to compensate for this).

Images during full inspiration, followed by dynamic expiration (after patient coaching in the technique) are obtained (36,37,38). Aquino et al. (39) demonstrated that a reduction in tracheal cross-sectional area of greater than 18% in the upper trachea and 28% in the mid-trachea gave a high probability for malacia (89% to 100%).

A decrease in airway diameter from inspiration to expiration is a sign of tracheomalacia.

Figure 16.9 Tracheomalacia. Axial computed tomography during (A) inspiration and (B) expiration; multiplanar reformat during (C)inspiration and (D) expiration. Narrowing of the tracheal lumen during expiration, demonstrating tracheomalacia.

Wegener Granulomatosis

Wegener granulomatosis (WG) is a vasculitis involving the upper and lower respiratory tract. The kidneys and other organs are usually also involved. It involves the nasal sinuses and less commonly the nasal septum, uvula, subglottic larynx, trachea, and bronchi (Chapter 13) (33). Clinically, patients present with hoarseness, stridor, and upper airway obstruction. The tracheobronchial tree is affected by an ulcerating tracheobronchitis, subglottic stenoses, inflammatory pseudotumors, tracheal and bronchial stenoses without inflammation, bronchiectasis, and hemorrhage. Diffuse involvement is rare and late. Stenoses in the subglottic region may involve the adjacent vocal cords. Tracheal stenoses may extend into the main bronchi and are typically circumferential, either concentric or eccentric; there may be mucosal irregularity or ulceration (Figs. 16.10 and 13.9). Cartilage and paratracheal soft tissues are less commonly involved (40,41,42).

The classic triad of WG includes lung/airway, sinus, and renal involvement.

Figure 16.10 Wegener granulomatosis. A. Axial computed tomography at the level of the vocal cords demonstrates marked narrowing of the lumen and thickening of the vocal cords. B. Axial computed tomography and (C) coronal multiplanar reformat at the level of the right lower lobe bronchus demonstrates circumferential thickening of the bronchus wall (arrow), with narrowing of the lumen.

For reasons that are not clear, over 90% of cases of tracheal stenosis complicating WG have occurred in females, even though WG occurs equally in males and females. Tracheal symptoms typically develop months or years after WG has been documented in other sites. However, tracheal obstruction/stenosis may occasionally be the presenting feature of the disease or the first manifestation of relapse. Tracheobronchial WG is usually treated medically. Surgical treatments are sometimes done, although they may fail due to active inflammation, vasculitis, and necrosis, leading to complications such as poor healing at anastomotic sites.

Tracheal stenosis in WG is more common in women (more than 90%) than men.

CT findings include focal or diffuse airway narrowing anywhere from the hypopharynx to the lobar bronchi, with circumferential wall thickening (Fig. 16.11). Enlarged, abnormally calcified, tracheal cartilages have been described, and lobar collapse secondary to granulomatous obstruction of an airway may occur (33). Occasionally, there is concomitant mediastinal or hilar lymphadenopathy. These findings are often seen in association with pulmonary parenchymal manifestations of the disease, including multiple nodules or consolidation, often with cavitation. MRI findings have been described but are nonspecific, with T1-weighted imaging demonstrating thickening of the submucosal tissues, luminal narrowing, and marked gadolinium enhancement, and T2-weighted imaging demonstrating increased signal intensity (Fig. 16.1) (43).

Figure 16.11 Wegener granulomatosis. A. Axial computed tomography and (B) sagittal multiplanar reformat demonstrates circumferential wall thickening in a subglottic location. C and D. Axial computed tomography demonstrates circumferential thickening of the walls of the right and left main bronchi, with luminal narrowing.


Sarcoidosis is a systemic granulomatous disease of unknown etiology. The nonairway manifestations are described in Chapter 13. Histologically, noncaseating epithelioid granulomas are present. Tracheal or bronchial stenosis may complicate sarcoidosis in 1% to 10% of cases but is rarely severe. Rarely, the proximal airways may be affected without involvement of other body sites. There may be granulomatous lesions within the airways or there may be extrinsic compression due to adjacent enlarged lymph nodes. On occasion, chronic granulomatous infiltration of bronchial submucosa may lead to narrowing of lobar or segmental bronchi, resulting in suppurative complications or postobstructive pneumonitis.

On CT, the most common finding is thickening of the bronchial walls, which may be smooth or nodular. There may be bronchial compression secondary to extrinsic compression from enlarged lymph nodes (33).


Amyloidosis is the extracellular deposition of an insoluble protein that stains with Congo red. Amyloidosis has localized and diffuse forms and may involve many organ systems (Chapter 13). Tracheobronchial amyloidosis is the most common form of localized pulmonary amyloid (44). Males are affected twice as frequently as females (45). Symptoms include cough, dyspnea, hemoptysis, stridor, and wheeze. Laryngeal involvement may present early with hoarseness. Airway involvement is usually diffuse but may be focal. In diffuse disease the larynx, trachea, and main and segmental bronchi can be involved contiguously or with skip lesions. Submucosal amyloid deposits protrude into the airway lumen, and eccentric or concentric stenoses can occur. The chest radiograph can be normal; however, segmental or lobar collapse is seen in 50%. CT will demonstrate areas of collapse or hyperinflation secondary to an endobronchial deposit, creating a check-valve effect. Strictures and submucosal nodular deposits will also be shown. Contrast enhancement and stippled calcifications of the nodular deposits have been identified (33,43). Occasionally, these amyloid deposits develop calcification and even ossification (17), and some investigators believe this is the etiology for tracheobronchopathia osteochondroplastica (see below).

Airway wall thickening with enhancement or calcification should suggest amyloidosis.

Tracheobronchopathia Osteochondroplastica

Tracheobronchopathia osteochondroplastica is a rare disorder of unknown etiology. Patients are often asymptomatic, although they may exhibit hemoptysis, cough, hoarseness, stridor, or recurrent lower respiratory tract infections. The disease typically occurs in middle-aged men and is of uncertain etiology (see Amyloidosis, above). Typically, a long segment of trachea, extending to involve the main bronchi, is involved. Multiple submucosal osteocartilaginous nodules involve the anterior and lateral walls; these may occlude the airway lumen, causing distal collapse (33). CT will demonstrate thickened cartilage with 3 to 8 mm irregular nodules and calcifications protruding into the airway lumen, leading to irregular narrowing of the distal trachea and main bronchi. There is characteristic sparing of the posterior membrane (17,31).

Ulcerative Colitis

A tracheobronchitis is occasionally associated with ulcerative colitis. CT demonstrates thickened tracheal or bronchial walls, with luminal narrowing. Bronchiectasis and bronchiolitis obliterans are also seen, affecting the more distal airways. There is concentric fibrosis of the submucosa, with ulceration and inflammation of the mucosa on pathologic analysis (31).

Infectious Conditions

Fibrosing Mediastinitis

Fibrosing mediastinitis (also termed granulomatous, collagenous, or sclerosing mediastinitis) is a rare disorder in which exuberant proliferation of fibrous and connective tissue compresses and encases vital structures within the mediastinum. Mediastinal lymphadenopathy is invariably present, but clinical manifestations of fibrosing mediastinitis are a result of an exaggerated granulomatous and fibrotic response beyond the confines of lymph nodes. This fibrotic process may continue to accrue over several years, invading, encasing, and obliterating mediastinal vessels (superior vena cava, pulmonary arteries, and veins) (Fig. 21.31); esophagus; trachea; and major bronchi. Most patients present between ages 20 and 40; the process is usually indolent and progresses slowly over months or years. Histoplasma capsulatum has been implicated in 50% to 70% of cases, but occasional cases attributable to Mycobacteria tuberculosisCoccidioides immitis, Aspergillus flavus, and other fungi have been described. Narrowing or compression of the trachea occurs in 15% to 30% of cases, usually in association with other regional manifestations; tracheal obstruction may rarely occur as an isolated feature. Tracheoesophageal fistulas have also been described. Bronchial stenosis appears to be among the more common manifestations of fibrosing mediastinitis, although the actual prevalence is not clear. Obstruction of lobar or main bronchi may result in recurrent atelectasis or pneumonitis associated with purulent sputum, cough, wheezing, and fever. Broncholiths may also occur when granulomas erode through the bronchial wall and may result in bronchial obstruction or severe hemoptysis. CT findings include soft tissue masses in the mediastinum that encase and narrow vessels and central airways. Focal calcifications are often, although not always, present (Fig. 16.12).

Fibrosing mediastinitis classically appears as infiltrative mediastinal soft tissue with calcification. If not calcified, infiltrating malignancy must be considered.

Up to half of the cases of fibrosing mediastinitis are considered idiopathic, because no infectious organism is recovered.

Figure 16.12 Fibrosing mediastinitis A and B. Axial computed tomography shows extensive abnormal soft tissue within the mediastinum with calcifications. There is narrowing of the right main bronchus (arrows). Note stenting of the superior vena cava (S). C. Coronal reformat after stenting of right bronchus intermedius again demonstrates extensive mediastinal lymph node enlargement (N) and subcarinal calcifications.

Unfortunately, the prognosis of fibrosing mediastinitis is poor. Spontaneous resolution does not occur, and no pharmacologic treatment has been shown to be effective. The course is usually chronic, with gradual worsening over 3 to 7 years. Mortality exceeds 30%, with most deaths resulting from cor pulmonale, progressive respiratory failure, or complications of surgery. When a specific infectious agent (such asH. capsulatum or M. tuberculosis) has been identified, antifungal or antituberculous therapy is recommended, but it is unlikely that these antimicrobial therapies will reverse the fibrotic lesion, once established.

Tuberculosis and Other Infections

The incidence of tuberculous bronchial stenosis has dropped to 10% after the introduction of antibiotics. Airway disease is caused by granulomatous disease within the tracheal or bronchial wall or by extrinsic pressure or extension from involved peribronchial lymph nodes (33,46,47). There are three stages:

1. Hyperplastic—tubercles present within the submucosal layer;

2. Ulceration and necrosis of the airway wall;

3. Fibrosis and stenosis.

Tuberculosis usually involves the distal trachea and proximal main bronchi. Active tuberculosis leads to irregular (or rarely smooth) circumferential thickening of the airway wall with narrowing or occlusion of the airway (Fig. 16.13). The thickened wall may enhance with contrast material. There may be increased density of adjacent mediastinal fat at CT due to inflammatory infiltration and/or there may be enlarged mediastinal lymph nodes. Lesions in the airway may ulcerate and form fistulas with adjacent structures. In contrast, inactive fibrotic disease leads to smooth narrowing with minimal or no wall thickening or adjacent inflammatory disease. Often, the left main bronchus is involved. Generally, the findings of active disease are reversible with medical therapy.

Bacterial, viral, and fungal infections affecting the airway typically cause subglottic and laryngeal narrowing (31). Rhinosclerosis (scleroma) is a chronic granulomatous disorder of the upper respiratory tract associated with the bacterium Klebsiella rhinoscleromatis.

It affects the nose, paranasal sinuses, pharynx, and occasionally the trachea (2% to 9%). Diffuse symmetric narrowing or nodular masses may develop. The course is slowly progressive with healing by fibrosis (33,48,49).

Figure 16.13 Tuberculosis of the trachea. A. Axial computed tomography demonstrates irregular narrowing of the mid-trachea with adjacent fibrocalcific lung changes. B. Multiplanar reformat showing craniocaudal extension.

Traumatic Rupture

Bronchial rupture is rare; the usual mechanism of injury is rapid deceleration with associated shearing forces. Mortality is high (30%). Rupture usually occurs within 2.5 cm of the carina, more commonly on the right (33). The imaging findings depend on the site of rupture. Tracheal or proximal left main bronchus ruptures do not communicate with the pleural space; therefore, pneumomediastinum but not pneumothorax will be present (Fig. 12.21). Right main bronchus or distal left main bronchus ruptures do communicate with the pleural space, and pneumothorax will be present (50). Other signs include air around the bronchus, subcutaneous emphysema, and lung collapse. There may be associated thoracic bone fractures (33).

Traumatic airway rupture usually occurs within 2.5 cm of the carina.

Postoperative Stenosis and Dehiscence

Postoperative bronchial stenosis may be seen after a partial lung resection with bronchial anastomosis or after lung transplantation. Bronchial stenosis is due to granulation tissue, fibrous stricture, or bronchomalacia. CT accuracy for diagnosis of anastomotic stenosis is very high (approximately 90%) using axial images alone, and there is very slightly higher accuracy when MPR or virtual bronchoscopy images are added (Fig. 16.14).

The most sensitive and specific indicator of a bronchial dehiscence at CT is the demonstration of a bronchial defect, followed by the presence of extraluminal air (this can be seen in the immediate postoperative period without the presence of a defect). An endoluminal flap or spherical air collections can also be a normal feature of a telescoping anastomosis; however, irregular air collections and posterior wall defects suggest dehiscence (51,52). It has been reported that a small dehiscence (less than 4 mm) or a small amount of extraluminal air generally indicates that the anastomosis will heal without adverse sequelae. However, when the CT shows a large dehiscence (greater than 4 mm) or a large amount of extraluminal air, CT is not useful in predicting which patients will require intervention for optimal anastomotic healing. An incomplete dehiscence will heal by fibrosis, typically causing an hourglass stenosis (33).

Figure 16.14 Post–lung transplant bronchial stenosis. Axial computed tomography shows focal narrowing (arrow) at the anastomosis.

Figure 16.15 Tracheal stent. Sagittal multiplanar reformat through the trachea demonstrates stent position across a benign stricture caused by tuberculosis (same case as Fig. 16.13).


Stents are occasionally used in the management of benign tracheal or bronchial stenoses or obstruction. Conditions in which they are used include post–lung transplant anastomotic stricture, tracheomalacia, external compression, and inflammatory conditions such as relapsing polychondritis. They can be located as far as second-order bronchial branches and can be placed via a flexible bronchoscope. The stents eventually become epithelialized, which helps to prevent migration. CT is used to evaluate the prestent airway, including airway anatomy, diameter, malacia, and distal collapse or air trapping. Poststent CT can assess complications including inflammation, stent migration, airway erosion, stent fracture, and distal lung collapse (Fig. 16.15) (53).

Diffuse Airway Enlargement

Diffuse enlargement of the trachea and main bronchi may be associated with tracheobronchomegaly (see below) or Ehlers-Danlos syndrome. Upper lobe fibrosis secondary to conditions such as sarcoidosis and cystic fibrosis may also enlarge the tracheal lumen due to traction. Allergic bronchopulmonary aspergillosis sometimes causes central bronchiectasis, affecting the main and segmental bronchi (28).


Tracheobronchomegaly or Mounier-Kuhn syndrome is a rare condition of unknown etiology that presents with marked dilatation of the trachea and main bronchi. The more distal bronchi are of normal caliber; however, repeated infections may lead to bronchiectasis. Histologically, there is atrophy of the tracheobronchial elastic and muscle fibers (54). A congenital defect has been suggested, and associations have been made with the Ehlers-Danlos and cutis laxa syndromes (55). Males are more commonly affected, mostly in the third and fourth decades. Subjects present with a history of repeated chest infection. Chest radiographs characteristically demonstrate a dilated trachea, which has a corrugated appearance secondary to prolapse of atrophied muscle fibers and mucosa through the tracheal rings. This is best appreciated on a lateral chest radiograph. CT also demonstrates dilatation of the trachea and mucosal prolapse and shows the abrupt transition between dilated central bronchi and normal caliber distal bronchi (Fig. 16.16) (56,57). The diagnosis is confirmed by any tracheal or bronchial diameter exceeding the mean plus 3 standard deviations on standard chest radiograph (trachea greater than 3 cm, right main bronchus greater than 2.4 cm, or left main bronchus greater than 2.3 cm) (54,56).

Tracheobronchomegaly is often associated with bronchiectasis.

A tracheal diameter of more than 3 cm indicates tracheomegaly.

Figure 16.16 Tracheobronchomegaly. A. Lateral chest radiograph demonstrates dilatation of the trachea, which has a corrugated appearance due to atrophied muscle fibers and mucosa prolapsing through tracheal rings. B and C. Axial computed tomography shows marked dilatation of the trachea and central bronchi. The distal bronchi are of normal caliber.

Saber Sheath Trachea

Saber sheath trachea is a condition associated with chronic obstructive pulmonary disease and is most commonly seen in males (58). It is a sign of lung hyperinflation (59). Characterized by a reduced transverse diameter of the intrathoracic portion of the trachea, the diagnosis is made if the ratio of the anteroposterior to transverse tracheal diameters is greater than 2:1 (28). On CT the trachea has a smooth inner margin and a normal wall thickness. There is frequent calcification of the cartilage rings (15,31). Inward bowing of the cartilage rings may occur, and weakening of the cartilage may lead to tracheomalacia (17).

Focal Foreign Body

Foreign body aspiration is most common in children under the age of 10 years. Alcohol, sedation, increased age, and poor dentition increase the risk of foreign body aspiration in adults. Aspirated material is most likely to enter the lower lobes, more often on the right because the right main bronchus is of larger caliber and has a more direct line from the trachea. Most aspirated material is of vegetable origin, which can calcify over time (33). Chest radiographs may show acute air trapping, accentuated on an expiratory view, or atelectasis. Unless very radiopaque, the foreign body is rarely seen on conventional radiographs; fluoroscopy may demonstrate air trapping. CT can show the site of bronchial obstruction and associated air trapping or atelectasis. Radiolucent foreign bodies such as denture base material may be identified (60). In chronic obstruction, bronchial stenoses, bronchiectasis, and an endobronchial mass or granulation tissue may be identified. MRI has been used specifically to identify peanut aspiration; fat within the nut will produce a high signal on T1-weighted imaging (61,62). Mucus is usually of low attenuation on CT, has a bubbly appearance, and occupies the dependent portion of the airway. If there is diagnostic doubt, CT can be repeated after vigorous coughing (63).

Aspirated foreign bodies are an often overlooked cause of chronic or recurrent pneumonia in otherwise healthy adults.


Broncholithiasis is calcified material within a bronchus. It is secondary to calcified lymph nodes compressing the adjacent airway or eroding into it, leading to bronchial obstruction. Lymph node calcification is usually secondary to histoplasmosis, tuberculosis or fungal infection, sarcoidosis or silicosis. It is more common on the right. Endobronchial calcific material may be seen at bronchoscopy. CT is often useful for evaluation of peribronchial disease (33,64). Patients may develop broncholithoptysis (coughing up of broncholiths).

Right middle lobe syndrome is the occlusion or narrowing of the bronchus by a usually calcified lymph node adjacent to or within (broncholith) the airway.

Tracheal Diverticula

Tracheal diverticula are often associated with chronic obstructive pulmonary disease (65). They are mostly located on the posterolateral tracheal wall, near the thoracic inlet, and are usually right sided. The diverticulum protrudes between the cartilage and the muscular portion of the tracheal wall. On CT, they may appear as isolated air cysts or may demonstrate a connection with the trachea (17).

Tracheobronchial Neoplasms

Tracheal masses often remain undiagnosed and only produce symptoms when more than three-fourths of the tracheal lumen is occluded (66). Standard frontal and lateral chest radiographs diagnose only 23% to 45% of tracheal intraluminal masses (67,68,69). CT generally demonstrates the mass but cannot differentiate between mucosal or submucosal neoplasm or assess the presence of submucosal spread.

Benign Neoplasms

Benign neoplasms account for less than 10% of trachea and main bronchus tumors. Stridor is the most common presenting symptom. CT appearances are nonspecific, but generally the mass is smooth, well circumscribed, of soft tissue attenuation, and measures less than 2 cm (31,63). The neoplasm may be polypoid or sessile and does not breach the tracheal wall (70).

Squamous cell papilloma is the most common benign tracheal tumor. It consists of a proliferation of stratified squamous cell epithelium and grows in a papillary or sessile fashion around a fibrovascular core. More often found in the larynx than the trachea, it is more common in males and probably associated with smoking. Squamous cell papilloma has a wide age of presentation but generally occurs in adulthood (70) (Fig. 16.17).

The most common benign tracheal tumor is a squamous cell papilloma.

Tracheobronchial papillomatosis is caused by the human papilloma virus and is usually acquired at birth from an infected mother. Children aged between 2 and 5 years are most commonly affected. Papillomas tend to be multiple and usually spontaneously resolve; however, they can recur and have the potential to undergo malignant transformation into squamous cell carcinoma (63,71). Rarely, tracheobronchial dissemination can occur (less than 5%); less than 1% disseminate to the lung parenchyma. Pathology consists of small sessile or pedunculated masses with flattened squamous epithelium and a fibrovascular core. CT demonstrates the intraluminal masses that may carpet the airways. Lung lesions consist of nodules, air-filled cysts or thick-walled cavities, predominantly in the caudal aspects of the chest (70).

Figure 16.17 Squamous cell papillomas. A. Axial computed tomography shows multifocal small masses within the tracheal lumen. B.Coronal multiplanar reformat shows narrowing of the tracheal lumen by the multifocal papillomas.

Although there are many other benign tumors affecting the tracheobronchial tree, all are rare and often do not possess specific imaging characteristics. Hamartomas are the most common benign lung tumor; however, just 3% occur within bronchi. They are slow growing and are seen in large bronchi. Endobronchial hamartomas contain the same cartilage, fat, fibrous, and epithelial components as pulmonary hamartomas (33). Pleomorphic adenomas are rare, there is a wide age range, and they are more common in males. They arise in the upper and middle thirds of the trachea (70).

Hemangiomas are seen in adults as a cavernous hemangioma of the larynx. Children present with capillary hemangiomas involving the subglottic trachea. They are a submucosal lesion, covered with respiratory epithelium, and appear as a rounded soft tissue mass on CT. Over 90% of infants will develop symptoms in the first 6 months of life and present with stridor (70). Granular cell tumors are of neurogenic origin and are more common in the bronchi than the trachea. They are most common in the fourth decade and in black females. They may be multiple and can be aggressive with local invasion. Most are seen at the level of the cervical trachea (70).

Chondromas are benign cartilaginous tumors rarely found in the trachea. They contain either hyaline or elastic cartilage and arise from the tracheal rings; therefore, growth may be intra- or extraluminal. Foci of calcification are seen in 75% of these tumors on CT. They have the potential to undergo malignant transformation (70). Leiomyomas are benign tumors of smooth muscle. They arise from the membranous portion of the trachea, usually in the lower third (Fig. 8.12). There is a wide age range and males and females are equally affected. They have a tendency to bleed, so biopsy is a relative risk (70). Schwannomas and neurofibromas are very rare and usually present in the fourth decade. They affect the lower third of the trachea (70).

Primary Malignant Neoplasms

Primary malignant neoplasms account for over 90% of tracheobronchial tumors. The most common is squamous cell carcinoma, followed by adenoid cystic carcinoma, bronchial carcinoid, mucoepidermoid tumor, and rare tumors such as chondrosarcoma (Fig. 16.18) and leiomyosarcoma (63). Squamous cell carcinoma accounts for 55% of tracheobronchial tumors. These tumors are seen generally seen in middle-aged male smokers, often with a history of alcohol abuse. About one-third of patients have other malignancies of the respiratory tract. About 10% are multifocal, often in the bronchi. The lesion may extend into the esophagus, leading to a fistula. Usually these cancers manifest as a large irregular mass on CT (Fig. 16.19) (63), although they can rarely grow circumferentially in the tracheal wall. If the entire tumor can be resected, surgical resected is usually advised, often followed by postoperative therapy. Generally, up to 6 cm of tracheal length can be resected successfully. One study reported median survival after surgery of 34 months.

The most common primary malignant tracheal tumor is squamous cell carcinoma.

Adenoid cystic carcinomas can arise from mucous glands in the trachea and bronchi. There is no smoking relationship, although males appear to be more often affected, usually in the third to fifth decades. They are slow-growing polypoidal masses that thicken the mucosa and can spread submucosally. Typically they arise in the middle or lower trachea on the posterolateral wall, and extraluminal growth is common (Fig. 16.20) (33,63,72). Adenoid cystic tumors used to be called cylindromas and classified with bronchial adenomas; however, this name and classification were discarded due to their misleading nature, erroneously suggesting a benign process. The best treatment is generally surgical resection with tracheal anastomosis, whenever possible. Postoperative radiation is often given. Patient survival is excellent (10-year median survival after surgery in one study), although late recurrences or metastases (e.g., 15 to 30 years after diagnosis) have been reported. Metastases tend to occur in lung, liver, bone, and brain.

Adenoid cystic carcinomas arise from the posterolateral tracheal wall, which is the location of the mucous glands from which they arise.

Eighty percent to 90% of carcinoid tumors are endobronchial; the remainder are pulmonary nodules.

Carcinoid tumors are of neuroendocrine origin (73), originating from Kulchitsky cells, which can secrete serotonin, corticotropin, and bradykinin. They are divided into two types. The first type, typical carcinoids, accounts for 75% to 90% (63). They present in the fifth and sixth decades, often with hemoptysis or obstructive atelectasis. They mostly arise in central bronchi; however, 10% may be peripheral. They are typically well defined and smooth and may be lobular, round, or ovoid (Fig. 16.21). They are slow growing and rarely metastasize (33). Stromal ossification or calcification may be demonstrated on CT and there is marked contrast enhancement with iodinated contrast (74,75,76). MRI characteristics include high signal intensity on T2-weighted images and marked enhancement with gadolinium (63). The second type, atypical carcinoids, are less common, accounting for 10% to 25% of cases (63). They arise in a slightly older population (55 to 60 years). They may be central or peripheral, tend to be larger, and are more aggressive with an increased incidence of nodal metastases (33).

A markedly enhancing endobronchial mass should suggest carcinoid tumor.

Figure 16.18 Tracheal chondrosarcoma. Axial computed tomography shows an exophytic mass arising from the wall of the trachea, deviating and narrowing the lumen.

Figure 16.19 Squamous cell carcinoma of the trachea. A and B. Axial contrast-enhanced computed tomography demonstrates a focal irregular mass (arrows) arising from the tracheal wall. There is ill definition of the fat plane between the tracheal wall and the esophagus (arrowheads), suggesting local invasion.

Figure 16.20 Adenoid cystic carcinoma. A. Axial computed tomography demonstrates a polypoid mass (arrows) arising from the posterolateral wall of the trachea. No extraluminal growth demonstrated. B. Multiplanar reformats help assess the craniocaudal extent of the mass.

Figure 16.21 Carcinoid. A and B. Axial computed tomography demonstrates a polypoid endoluminal mass (asterisks) within the superior segmental bronchus of the left lower lobe, protruding into the left lower lobe bronchus lumen.

Mucoepidermoid tumors account for 1% to 5% of bronchial neoplasms. Males and females are equally affected, and there is a wide age range, with an average of 37 years (77). There is no association with smoking. They usually present with a focal endobronchial mass within a large central airway (33).


Metastatic tracheobronchial tumors arise either by local invasion or hematogenous spread. Common locally invading tumors include thyroid, esophageal, laryngeal, and lung carcinoma (Fig. 16.22). Hematogenous spread of tumor has been described with melanoma, breast, colon, genitourinary, and renal tumors. They produce an endoluminal, polypoidal, soft tissue mass (31,78). CT can demonstrate local invasion and endobronchial masses and complications such as distal atelectasis.

Figure 16.22 Thyroid carcinoma. A. Axial computed tomography demonstrates carcinoma of the thyroid invading the adjacent mediastinal structures, including the left posterolateral wall of the trachea (arrows). B. Esophageal carcinoma. Axial computed tomography demonstrates direct invasion of the adjacent trachea (arrow).


1. Holbert JM, Strollo DC. Imaging of the normal trachea. J Thorac Imaging 1995;10:171–179.

2. Shih JY, Lee LN, Wu HD, et al. Sonographic imaging of the trachea. J Ultrasound Med 1997;16:783–790.

3. Callanan V, Gillmore K, Field S, Beaumont A, et al. The use of magnetic resonance imaging to assess tracheal stenosis following percutaneous dilatational tracheostomy. J Laryngol Otol 1997;111:953–957.

4. Salvolini L, Bichi Secchi E, Costarelli L, DeNicola M. Clinical applications of 2D and 3D CT imaging of the airways—a review. Eur J Radiol 2000;34:9–25.

5. Remy-Jardin M, Remy J, Artaud D, et al. Volume rendering of the tracheobronchial tree: clinical evaluation of bronchographic images.Radiology 1998;208:761–770.

6. Remy-Jardin M, Remy J, Artaud D, et al. Tracheobronchial tree: assessment with volume rendering—technical aspects. Radiology1998;208:393–398.

7. Ferretti GR, Thony F, Bosson JL, et al. Benign abnormalities and carcinoid tumors of the central airways: diagnostic impact of CT bronchography. AJR Am J Roentgenol 2000;174:1307–1313.

8. Remy-Jardin M, Remy J, Deschildre F, et al. Obstructive lesions of the central airways: evaluation by using spiral CT with multiplanar and three-dimensional reformations. Eur Radiol 1996;6:807–816.

9. Quint LE, Whyte RI, Kazerooni EA, et al. Stenosis of the central airways: evaluation by using helical CT with multiplanar reconstructions. Radiology 1995;194:871–877.

10. Naidich DP, Lee JJ, Garay SM, et al. Comparison of CT and fiberoptic bronchoscopy in the evaluation of bronchial disease. AJR Am J Roentgenol 1987;148:1–7.

11. Mayr B, Ingrisch H, Haussinger K, et al. Tumors of the bronchi: role of evaluation with CT. Radiology 1989;172:647–652.

12. Henschke CI, Davis SD, Auh Y, et al. Detection of bronchial abnormalities: comparison of CT and bronchoscopy. J Comput Assist Tomogr 1987;11:432–435.

13. Perhomaa M, Lahde S, Rossi O, Suramo I. Helical CT in evaluation of the bronchial tree. Acta Radiol 1997;38:83–91.

14. Kittredge RD. Computed tomography of the trachea: a review. J Comput Tomogr 1981;5:44–50.

15. Gamsu G, Webb WR. Computed tomography of the trachea: normal and abnormal. AJR Am J Roentgenol 1982;139:321–326.

16. Breatnach E, Abbott GC, Fraser RG. Dimensions of the normal human trachea. AJR Am J Roentgenol 1984;142:903–906.

17. Webb EM, Elicker BM, Webb WR. Using CT to diagnose nonneoplastic tracheal abnormalities: appearance of the tracheal wall. AJR Am J Roentgenol 2000;174:1315–1321.

18. Fraser RG. Measurements of the calibre of human bronchi in three phases of respiration by cinebronchography. J Can Assoc Radiol1961;12:102.

19. Jesseph JE, Merendino KA. The dimensional interrelationships of the major components of the human tracheobronchial tree. Surg Gynecol Obstet 1957;105:210.

20. Merendino KA, Kiriluk LB. Human measurements involved in tracheobronchial resection and reconstruction procedures: report of case of bronchial adenoma. Surgery 1954;35:590.

21. Alper H, Sener RN. Pulmonary aplasia: MR angiography findings. Eur Radiol 1996;6:89–91.

22. Kinsella D, Sissons G, Williams MP. The radiological imaging of bronchial atresia. Br J Radiol 1992;65:681–685.

23. Beigelman C, Howarth NR, Chartrand-Lefebrier, Grenier P. Congenital anomalies of tracheobronchial branching patterns: spiral CT aspects in adults. Eur Radiol 1998;8:79–85.

24. Rappaport DC, Herman SJ, Weisbrod GL. Congenital bronchopulmonary diseases in adults: CT findings. AJR Am J Roentgenol1994;162:1295–1299.

25. Remy J, Smith M, Marache P, Nuyts JP. La bronche “tracheale” gauche pathogene. Revue de la litterature a propos de 4 observations.J Radiol Electrol 1977;58:621–630.

26. McGuinness, G, Naidich DP, Garay SM, et al. Accessory cardiac bronchus: CT features and clinical significance. Radiology1993;189:563–566.

27. Stark P. Imaging of tracheobronchial injuries. J Thorac Imaging 1995;10:206–219.

28. Marom EM, Goodman PC, McAdams HP. Diffuse abnormalities of the trachea and main bronchi. AJR Am J Roentgenol 2001;176:713–717.

29. Ferretti GR, Bricault I, Coulomb M. Helical CT with multiplanar and three-dimensional reconstruction of nonneoplastic abnormalities of the trachea. J Comput Assist Tomogr 2001;25:400–406.

30. Brichet A, Verkindre C, Dupont J, et al. Multidisciplinary approach to management of postintubation tracheal stenoses. Eur Respir J1999;13:888–893.

31. Kwong JS, Muller NL, Miller RR. Diseases of the trachea and main-stem bronchi: correlation of CT with pathologic findings.Radiographics 1992;12:645–657.

32. Palombini BC, Villanova CA, Araujo E, et al. A pathogenic triad in chronic cough: asthma, postnasal drip syndrome, and gastroesophageal reflux disease. Chest 1999;116:279–284.

33. Shepard JA. The bronchi: an imaging perspective. J Thorac Imaging 1995;10:236–254.

34. McAdam LP, O’Hanlan MA, Bluestone R, Pearson CM. Relapsing polychondritis: prospective study of 23 patients and a review of the literature. Medicine (Baltimore) 1976;55:193–215.

35. Dolan DL, Lemmon GB Jr, Teitelbaum SL. Relapsing polychondritis. Analytical literature review and studies on pathogenesis. Am J Med 1966;41:285–299.

36. Stern EJ, Graham CM, Webb WR, Gamsu G. Normal trachea during forced expiration: dynamic CT measurements. Radiology1993;187:27–31.

37. Gilkeson RC, Ciancibello LM, Hejal RB, Montenegna H, Lange P. Tracheobronchomalacia: dynamic airway evaluation with multidetector CT. AJR Am J Roentgenol 2001;176:205–210.

38. Webb WR, Stern EJ, Kanth N, Gamsu G. Dynamic pulmonary CT: findings in healthy adult men. Radiology 1993;186:117–124.

39. Aquino SL, Shepard JA, Ginns LC, et al. Acquired tracheomalacia: detection by expiratory CT scan. J Comput Assist Tomogr2001;25:394–399.

40. Daum TE, Specks U, Colby TV, et al. Tracheobronchial involvement in Wegener’s granulomatosis. Am J Respir Crit Care Med1995;151(2 Pt 1):522–526.

41. Maskell GF, Lockwood CM, Flower CD. Computed tomography of the lung in Wegener’s granulomatosis. Clin Radiol 1993;48:377–380.

42. Screaton NJ, Sivasothy P, Flower CD, Lockwood CM. Tracheal involvement in Wegener’s granulomatosis: evaluation using spiral CT.Clin Radiol 1998;53:809–815.

43. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 1-1995. An elderly man with a questionable bronchial carcinoid tumor of long duration and recently increasing tracheal obstructions. N Engl J Med 1995;332:110–115.

44. Urban BA, Fishman EK, Goldman SM, et al. CT evaluation of amyloidosis: spectrum of disease. Radiographics 1993;13:1295–1308.

45. Armstrong P, Wilson AG, DeeP, Hansell DM, et al. Imaging diseases of the chest, 3rd ed. St. Louis: Mosby, 2000.

46. Choe KO, Jeong HJ, Sohn HY. Tuberculous bronchial stenosis: CT findings in 28 cases. AJR Am J Roentgenol 1990;155:971–976.

47. Jokinen K, Palva T, Nuutinen J. Bronchial findings in pulmonary tuberculosis. Clin Otolaryngol 1977;2:139–148.

48. Feldman F, Seaman WB, Baker DC Jr. The roentgen manifestations of scleroma. Am J Roentgenol Radium Ther Nucl Med1967;101:807–813.

49. Miller RH, Shulman JB, Canalis RF, Ward PH. Klebsiella rhinoscleromatis: a clinical and pathogenic enigma. Otolaryngol Head Neck Surg 1979;87:212–221.

50. Harvey-Smith W, Bush W, Northrop C. Traumatic bronchial rupture. AJR Am J Roentgenol 1980;134:1189–1193.

51. Semenkovich JW, Glazer HS, Anderson DC, et al. Bronchial dehiscence in lung transplantation: CT evaluation. Radiology1995;194:205–208.

52. McAdams HP, Murray JG, Erasmus JJ, et al. Telescoping bronchial anastomoses for unilateral or bilateral sequential lung transplantation: CT appearance. Radiology 1997;203:202–206.

53. Lehman JD, Gordon RL, Kerlan RK Jr, et al. Expandable metallic stents in benign tracheobronchial obstruction. J Thorac Imaging1998;13:105–115.

54. Katz L, Levine M, Herman P. Tracheobronchomegaly: the Mounier-Kuhn syndrome. AJR Am J Roentgenol 1962;88:1084–1094.

55. Aaby G. Tracheobronchomegaly. Ann Thorac Surg 1966;2:64–70.

56. Shin MS, Jackson RM, Ho KJ. Tracheobronchomegaly (Mounier-Kuhn syndrome): CT diagnosis. AJR Am J Roentgenol 1988;150:777–779.

57. Doyle AJ. Demonstration on computed tomography of tracheomalacia in tracheobronchomegaly (Mounier-Kuhn syndrome). Br J Radiol1989;62:176–177.

58. Greene R.“Saber-sheath” trachea: relation to chronic obstructive pulmonary disease. AJR Am J Roentgenol 1978;130:441–445.

59. Trigaux JP, Hermes G, Dubois P, et al. CT of saber-sheath trachea. Correlation with clinical, chest radiographic and functional findings. Acta Radiol 1994;35:247–250.

60. Newton JP, Abel RW, Lloyd CH, Yemm R. The use of computed tomography in the detection of radiolucent denture base material in the chest. J Oral Rehabil 1987;14:193–202.

61. Imaizumi H, Kaneko M, Nara S, Saito H, Asakura K, Akiba H. Definitive diagnosis and location of peanuts in the airways using magnetic resonance imaging techniques. Ann Emerg Med 1994;23:1379–1382.

62. O’Uchi T, Tokumaru A, Mikami I, Yamasoba T, Kikuchi S. Value of MR imaging in detecting a peanut causing bronchial obstruction.AJR Am J Roentgenol 1992;159:481–482.

63. Marom EM, Goodman PC, McAdams HP. Focal abnormalities of the trachea and main bronchi. AJR Am J Roentgenol 2001;176:707–711.

64. Conces DJ Jr, Tarver RD, Vix VA. Broncholithiasis: CT features in 15 patients. AJR Am J Roentgenol 1991;157:249–253.

65. Goo JM, Im JG, Ahn JM, et al. Right paratracheal air cysts in the thoracic inlet: clinical and radiologic significance. AJR Am J Roentgenol 1999;173:65–70.

66. Weber AL, Grillo HC. Tracheal tumors. A radiological, clinical, and pathological evaluation of 84 cases. Radiol Clin North Am1978;16:227–246.

67. Hajdu SI, Huvos AG, Goodner JT, Foote FW Jr, Beattie EJ Jr. Carcinoma of the trachea. Clinicopathologic study of 41 cases. Cancer1970;25:1448–1456.

68. Houston HE, Payne WS, Harrison EG Jr, Olsen AM. Primary cancers of the trachea. Arch Surg 1969;99:132–140.

69. Manninen MP, Paakkala TA, Pukander JS, Karma PH. Diagnosis of tracheal carcinoma at chest radiography. Acta Radiol 1992;33:546–547.

70. McCarthy MJ, Rosado-de-Christenson ML. Tumors of the trachea. J Thorac Imaging 1995;10:180–198.

71. Gruden JF, Webb WR, Sides DM. Adult-onset disseminated tracheobronchial papillomatosis: CT features. J Comput Assist Tomogr1994;18:640–642.

72. Spizarny DL, Shepard JA, McLoud TC, Grillo HC, Dedrick CG. CT of adenoid cystic carcinoma of the trachea. AJR Am J Roentgenol1986;146:1129–1132.

73. Müller NL, Miller RR. Neuroendocrine carcinomas of the lung. Semin Roentgenol 1990;25:96–104.

74. Rosado de Christenson ML, Abbott GF, Kirejczyk WM, Galvin JR, Travis WD. Thoracic carcinoids: radiologic-pathologic correlation.Radiographics 1999;19:707–736.

75. Zwiebel BR, Austin JH, Grimes MM. Bronchial carcinoid tumors: assessment with CT of location and intratumoral calcification in 31 patients. Radiology 1991;179:483–486.

76. Shin MS, Berland LL, Myers JL, Clary G, Zorn GL. CT demonstration of an ossifying bronchial carcinoid simulating broncholithiasis.AJR Am J Roentgenol 1989;153:51–52.

77. Heitmiller RF, et al. Mucoepidermoid lung tumors. Ann Thorac Surg 1989;47:394–399.

78. Aberle DR, Brown K, Young DA, Batra P, Steckel RJ. Imaging techniques in the evaluation of tracheobronchial neoplasms. Chest1991;99:211–215.