Skip Navigation LinksHome > November 2011 - Volume 26 - Issue 4 > Large Airway Diseases
Journal of Thoracic Imaging:
doi: 10.1097/RTI.0b013e31822428ef
Symposium

Large Airway Diseases

Kang, Eun-Young MD

Free Access
Article Outline
Collapse Box

Author Information

Department of Radiology, Korea University Guro Hospital, Korea University College of Medicine, Seoul, Korea

This review was exhibited in 2010 European Congress of Radiology and received cum lau de.

The author declares no conflicts of interest.

Reprints: Eun-Young Kang, MD, Department of Radiology, Korea University Guro Hospital, Korea University College of Medicine, 97 Guro-dong, Guro-gu, Seoul 152-703, Korea (e-mail: keyrad@korea.ac.kr).

Collapse Box

Abstract

Various neoplasms and nonneoplastic diseases affect the tracheobronchial tree and cause focal or diffuse airway luminal narrowing or dilatation. For the identification and characterization of various large airway diseases, imaging, particularly computed tomography, plays a key role. Advances in computed tomography technology and postprocessing techniques enable the rapid, noninvasive, comprehensive, and accurate evaluation of the tracheobronchial tree. This article provides a radiologic review of various large airway diseases, including congenital tracheobronchial abnormalities such as infection, inflammation, and infiltrative diseases causing large airway narrowing with wall thickening; tracheal stricture; tracheal neoplasm; bronchiectasis; broncholithiasis; and bronchial anthracofibrosis.

Radiography is traditionally the first step in the evaluation of large airway disease. However, large airway disease is usually overlooked initially at radiography. Computed tomography (CT) can improve the detection and characterization of large airway disease, and multidetector CT (MDCT) is the imaging modality of choice for the diagnosis of large airway disease. Advances in CT technology and postprocessing techniques allow a noninvasive, comprehensive, and accurate evaluation of the tracheobronchial tree in a rapid manner. Thin-section images of the large airways can be obtained in only a few seconds, creating an isotopic data set in which the resolution is the same in the axial, coronal, and sagittal planes. Therefore, MDCT provides higher spatial resolution, faster speed, greater anatomic coverage, and higher-quality multiplanar reformation and 3-dimensional reconstruction images.1,2 Axial CT images provide precise anatomical information about the airway lumen and wall, as well as about adjacent mediastinal and lung structures. Multiplanar 2-dimensional reformations and 3-dimensional reconstruction images can provide a more anatomically meaningful display of the airways and adjacent structures. These CT images have been shown to enhance the detection, localization, and determination of the extent of lesions; the evaluation of their relationship with adjacent structures; characterization of the airway disease; and clarification of complex congenital airway abnormalities.1–3 Furthermore, MDCT has proven to be an essential complementary tool for the bronchoscopist, facilitating planning and guidance for bronchoscopy and therapeutic interventions and allowing for postprocedural noninvasive assessment of the airways. Airway imaging is routinely performed at end inspiration during a single breath-hold. However, additional assessment of the airway during expiration plays an essential role in the diagnosis of airway malacia.2

Small airways are defined as airways <2 to 3 mm in diameter on the basis of the results of a physiological study of the lung4; airways smaller than 2 to 3 mm in diameter include the smallest cartilaginous bronchi, membranous bronchioles, and respiratory bronchioles. The smallest airways that can be normally seen on thin-section CT are 2 mm in outer diameter with 0.2 to 0.3 mm wall thickness.5 Therefore, we can conclude that large airways usually include the trachea and bronchi that are greater than 2 to 3 mm in diameter; large airways can be routinely identified on CT scans; and large airway diseases can also be detected on CT scans.

The spectrum of disorders involving the tracheobronchial tree is diverse. Diseases of the trachea and main bronchi are classified as either focal or diffuse, depending on the extent of involvement of the major airways. These diseases can also be classified as diseases causing airway luminal widening or diseases causing airway luminal narrowing.6–8 Focal diseases causing luminal narrowing include malignant or benign neoplasms and tracheal strictures caused by trauma or medical intervention. Diffuse luminal narrowing of the airway is caused by various infiltrative and infectious diseases. Diffuse luminal widening disease of the large airway is also called tracheobronchomegaly. Tracheobronchomalacia is another specific disease and is described in another study in this issue.

This article provides a radiologic review of various large airway diseases that may be seen in clinical practice, including the following: congenital tracheobronchial abnormalities; infectious, inflammatory, and infiltrative diseases causing large airway narrowing with wall thickening; postintubation tracheal stenosis; tracheal neoplasm; bronchiectasis; broncholithiasis; and bronchial anthracofibrosis.

Back to Top | Article Outline

CONGENITIAL TRACHEOBRONCHIAL ABNORMALITIES

Most congenital tracheobronchial abnormalities are rare; however, these abnormalities are being diagnosed with increasing frequency as a result of the increased use of MDCT. MDCT has improved our understanding of complex tracheobronchial abnormalities, even in infants and young children. Low-dose MDCT with virtual bronchoscopy has a high sensitivity and specificity for depiction of tracheobronchial narrowing and/or anomalies in the pediatric population.9 Although congenital tracheobronchial abnormalities usually manifest themselves in infancy and early childhood, some cases may remain asymptomatic until adulthood and are incidentally found on chest CT.10 The most common congenital tracheobronchial abnormalities that are incidentally found on chest CT scan in adults include tracheal bronchus and accessory cardiac bronchus.

Back to Top | Article Outline
Tracheal Bronchus

Tracheal bronchus refers to a congenitally abnormal bronchus originating from the trachea or main bronchi. Tracheal bronchus is found incidentally during bronchoscopy or CT scan and is well defined with chest CT. It often occurs more frequently in patients with congenital heart disease (3.74%) than in patients without congenital heart disease (0.29%).11 In a study of 9781 MDCT examinations, 30 cases of tracheal bronchus were observed, for an overall tracheal bronchus incidence of 0.31%.12 The anomalous origin is usually located in the right lateral wall of the trachea within 2 cm of the carina.1,11,12 Most commonly, this occurs as a displaced bronchus arising from the lower trachea and supplying the right upper lobe apical segment (Fig. 1). Less commonly, the entire right upper lobe bronchus may be displaced on the trachea, a condition known as pig bronchus (Fig. 1).13 Although this is usually an asymptomatic and incidentally detected finding, impaired drainage may result in recurrent infections in some cases.1

Figure 1
Figure 1
Image Tools
Back to Top | Article Outline
Accessory Cardiac Bronchus

An accessory cardiac bronchus is a rare congenital anomaly of the tracheobronchial tree. It is a supernumerary bronchus from the inner wall of the right main bronchus or an intermediate bronchus that advances toward the pericardium (Fig. 2).10,13–15 It presents with a blind distal end or shows a ventilated lobule.14,15 In a study of 11,159 spiral chest CT examinations, 9 cases of accessory cardiac bronchus were found, a frequency of 0.08%.14 Accessory cardiac bronchus is asymptomatic and incidentally discovered, but recognition of this anomaly is important because recurrent infection or hemoptysis can develop in a small percentage of patients.10,15

Figure 2
Figure 2
Image Tools
Back to Top | Article Outline
Mounier-Kuhn Syndrome

Tracheobronchomegaly is characterized by marked dilatation of the trachea and main bronchi. The congenital form of tracheobronchomegaly, also called Mounier-Kuhn syndrome, is extremely rare and is caused by severe atrophy of the longitudinal elastic fibers and thinning of the muscularis mucosa in the trachea and main bronchi.1,16 A weakened tracheobronchial wall allows diverticula formation, secretion retention, and marked dilatation on inspiration with expiratory collapse. Tracheomegaly is defined in women as a tracheal diameter greater than 21 mm in the coronal dimension and 23 mm in the sagittal dimension and is defined in men as a tracheal diameter greater than 25 mm in the coronal dimension and 27 mm in the sagittal dimension.1,16

On imaging, there is tracheobronchial luminal dilatation, often associated with a corrugated appearance of the tracheal wall and tracheal diverticulosis. Bronchiectasis and tracheobronchomalacia are also common.1,16

Back to Top | Article Outline

INFECTIOUS, INFLAMMATORY, AND INFILTRATIVE DISEASES CAUSING LARGE AIRWAY NARROWING

Tracheobronchial Tuberculosis

Tracheobronchial tuberculosis has been reported in 10% to 38.8% of patients with pulmonary parenchymal tuberculosis through bronchoscopic examination.17 Several mechanisms have been suggested for the development of tracheobronchial tuberculosis, including (1) direct contact of the mucosa with infected sputum from the lesions in the distal lung parenchyma; (2) submucosal spread of tubercle bacilli along the peribronchial lymphatic channels, supported by the fact that in many patients for whom the central airway biopsy is positive for tuberculosis the main tuberculous lesions are confined to the submucosa, with the mucosa either remaining intact or having only a shallow ulceration; and (3) direct extension from an adjacent parenchymal lesion or tuberculous lymphadenitis. The presence of lymphadenopathy contiguous to the tuberculous lesions in the trachea or main bronchi suggests that local extension is a probable mechanism.18–20

Endobronchial tuberculosis is more prevalent in young female patients.17 Involvement at multiple sites within the tracheobronchial tree is common; the long segment of the distal trachea and proximal bronchi are typically involved.21 Active disease involves both bronchi equally, but fibrotic disease more often involves the left main bronchus.20

Endobronchial tuberculosis undergoes several evolutional stages: early tubercle formation in the submucosal layer, infectious necrosis and ulceration of the bronchial wall, formation of granulation tissue, and finally residual fibrotic stenosis.19,20 Various stages of the disease may coexist in one patient.19 Despite appropriate antituberculous therapy, some degree of stenosis may develop in up to 90% of patients with endobronchial tuberculosis.7

Radiographic findings in postinfectious stenosis include focal narrowing of the trachea or bronchi. Calcification of the stenotic region is rare. Changes typical of tuberculous fibrocavitary parenchymal disease may be seen, and segmental or lobar atelectasis is a common feature. The CT manifestations of endobronchial tuberculosis differ according to disease evolution. In active disease, the CT scan shows irregular luminal narrowing with irregular, contrast-enhanced, and thick-walled airways, a pattern that is reversible (Fig. 3). However, patients with fibrotic disease generally have smooth narrowing of the tracheobronchial lumen and minimal uniform concentric wall thickening, a nonreversible pattern.7,19–21 CT may show lymphadenopathy and parenchymal inflammatory changes in addition to the airway lesion.

Figure 3
Figure 3
Image Tools

Endobronchial tuberculosis should be distinguished from bronchogenic carcinoma; however, CT findings of endobronchial tuberculosis are sometimes nonspecific, and patients with bronchogenic carcinoma have a high rate of reinfection with pulmonary tuberculosis.19 Therefore, the differential diagnosis from bronchogenic carcinoma is often difficult. CT findings of a longer segment of involvement, circumferential luminal narrowing, absence of an intraluminal mass, and younger age can lead to a diagnosis of endobronchial tuberculosis rather than to a diagnosis of bronchogenic carcinoma.20 However, to confirm the diagnosis, bronchoscopy and bronchial biopsy are often necessary.

Back to Top | Article Outline
Tracheobronchitis Caused by Aspergillus

The spectrum of airway and pulmonary involvement caused by aspergillus is variable according to the patient's immune status and preexisting lung disease. Large airway involvement of aspergillosis includes intrabronchial aspergilloma in nonimmunocompromised patients, allergic bronchopulmonary aspergillosis (ABPA) in asthma patients, chronic necrotizing bronchial aspergillosis as a form of semi-invasive aspergillosis, and acute tracheobronchitis as a form of invasive aspergillosis.22,23

Acute tracheobronchitis, also known as ulcerative and pseudomembranous tracheobronchitis, is a rare manifestation of invasive aspergillosis. It occurs in severely immunocompromised patients. Bronchoscopically, focal or diffuse ulcerative or plaque-like inflammatory lesion with pseudomembranes is characteristic. Nonspecific tracheobronchial wall thickening with smooth or nodular luminal narrowing is occasionally seen on CT scan.22

Back to Top | Article Outline
Tracheobronchopathia Osteochondroplastica

Tracheobronchopathia osteochondroplastica is an idiopathic benign disease of the trachea and large bronchi. It is characterized by multiple submucosal osteocartilaginous nodules protruding into the airway lumen. The nodules classically affect the lower two thirds of the trachea and proximal portions of the primary bronchi. At one center, over a period of 6 years, 10 of 8760 bronchoscopies were diagnosed as tracheobronchopathia osteochondroplastica; the median age was 51 years (16 to 68 y), and 6 cases were men.24 It is a rare disease but is increasingly being discovered during bronchoscopy and chest CT scan incidentally. Upon histopathologic examination, the nodules are identified as submucosal osteocartilaginous growths. The mucosal surface is intact, and a connection to the perichondrium of a tracheal ring is frequently seen. The posterior wall of the trachea is typically spared.

Chest radiography may reveal tracheal scalloping and nodular irregularity or irregular asymmetric stenosis in severe disease. CT can depict thickened tracheal cartilage with irregular calcification. The calcification is much more irregular than normal cartilage calcification. Multiple nodules, with or without calcification, may project into the airway lumen and typically do not involve the posterior membranous wall of the trachea (Fig. 4).6,7,24–26

Figure 4
Figure 4
Image Tools

Differential diagnosis based on CT images includes relapsing polychondritis and tracheobronchial amyloidosis. Sometimes, a normal tracheobronchial wall can show internal calcification, and normal cartilage calcifications of the airway wall are usually observed in old age, particularly in women.26 Normal tracheobronchial wall calcification can be differentiated from tracheobronchopathia osteochondroplastica due to the absence of airway wall thickening or nodularity. Relapsing polychondritis shows a smooth thickening and diffuse calcification of the cartilaginous parts of the tracheobronchial tree, sparing the posterior wall, but does not show any calcified nodules protruding into the airway lumen on CT scan. Tracheobronchial amyloidosis does not spare the posterior membranous wall.

Back to Top | Article Outline
Relapsing Polychondritis

Relapsing polychondritis is a rare autoimmune disease characterized by recurrent progressive episodes of cartilage inflammation of the ear, nose, peripheral joints, larynx, and tracheobronchial tree. Respiratory tract involvement is uncommon at presentation, but it will occur eventually in up to 50% of patients during the course of the disease.27–29 Respiratory tract involvement carries a poor prognosis. The disease affects men and women equally, but airway involvement is more common in women.30 The larynx and subglottic trachea are often the initial site of involvement. As the disease progresses, the distal trachea and bronchi are involved, and the distal bronchi may be involved to the level of the subsegmental bronchi.18 The airway is involved focally or diffusely. Pathologically, the disease is characterized by an acute inflammatory infiltrate in the cartilage and perichondrial tissue. Airway inflammation may result in luminal narrowing. Dissolution and fragmentation of the cartilage occur and may be followed by fibrosis.29 In the late stages of the disease, this fibrosis-induced contraction of the airway may lead to severe luminal narrowing. Loss of structural cartilaginous support may also result in tracheobronchomalacia.

At radiography, diffuse or focal airway involvement may be seen. CT shows increased airway wall attenuation, increased airway wall thickness, and luminal narrowing of the trachea and bronchi. The degree of increased attenuation ranges from subtle to frank calcification.27 Airway wall thickening is smooth and diffuse and spares the posterior membranous wall. However, diffuse circumferential wall thickening is seen in advanced stages (Fig. 5). Destruction of cartilaginous rings associated with fibrotic stenosis may occur, and flaccidity of the airway wall may lead to considerable airway collapse on expiratory CT scan. Dynamic CT imaging during expiration may demonstrate airway wall collapse and air trapping.7,27

Figure 5
Figure 5
Image Tools
Back to Top | Article Outline
Wegener Granulomatosis

Wegener granulomatosis is characterized by necrotizing granulomatous inflammation and necrotizing vasculitis, which is capable of affecting all organs but has a predilection for the upper respiratory tract, lungs, and kidneys. Airway involvement is usually associated with disease affecting other organs but can be an isolated manifestation. Airway involvement is found in 15% to 55% of patients with Wegener granulomatosis.31 Patients younger than 30 years of age are more prone to developing airway involvement, and women are also more likely to develop airway disease compared with men.31

Lee et al32 reported that large airways were abnormal in 9 (30%) of 30 patients with Wegener granulomatosis, and bronchial wall thickening in the segmental and subsegmental bronchi was found in 22 (73%) patients. Airway involvement may be focal or diffuse. Airway involvement causes mucosal abnormalities, tracheal or bronchial mass mimicking malignancy, subglottic stenosis, stenosis at any level of the tracheobronchial tree, tracheomalacia, or bronchomalacia.31 Wegener granulomatosis may involve the trachea with resultant stenosis. Subglottic stenosis is the most frequent airway manifestation in Wegener granulomatosis, and 9 of 10 patients in a previous study had tracheal involvement in the subglottic region.33

CT scans show focal or diffuse airway stenosis, intraluminal and extraluminal soft tissue masses, and airway wall thickening, with or without lobar or segmental atelectasis.31 Tracheal involvement shows smooth or irregular circumferential wall thickening and luminal narrowing of approximately 2 to 4 cm in length on CT scan (Fig. 6).33 Other CT findings are mucosal irregularity and ulceration and involvement of the tracheal cartilage. Involvement of the cartilaginous rings is less common but may result in deformity and narrowing of the trachea.7,33

Figure 6
Figure 6
Image Tools
Back to Top | Article Outline
Sarcoidosis

Sarcoidosis is a systemic disease of unknown cause, and thoracic involvement is the most common manifestation of sarcoidosis. However, large airway involvement is unusual. Sarcoidosis will affect the larynx and upper trachea in 1% to 3% of patients. The distal part of the trachea and primary bronchi are affected infrequently.6,7 Bronchial involvement is more common, and bronchial abnormalities were seen in 39 (65%) of 60 patients with sarcoidosis on CT scan in a previous study.34 Narrowing of the airway may be secondary to extrinsic compression from enlarged lymph nodes or may be the result of granuloma formation within the airway mucosa and submucosa.6,7

The most common CT finding is regular or nodular bronchial wall thickening of the lobar, segmental, or subsegmental bronchi that reflects airway granuloma formation. Bronchial wall thickening may result in smooth or irregular bronchial luminal narrowing (Fig. 7).18 Other findings such as lymph node enlargement may also be present. The classic endobronchial finding is the raised “cobblestone” appearance of the mucosa. Whitish granulomatous material may also be seen in stenotic regions.7

Figure 7
Figure 7
Image Tools
Back to Top | Article Outline
Amyloidosis

Amyloidosis is characterized by abnormal extracellular deposition of amyloid, an autologous fibrillar proteinaceous material. This disease can be idiopathic or associated with various inflammatory, hereditary, or neoplastic diseases. The amyloid deposition may be generalized or may be localized to a single organ. Pulmonary amyloidosis may also be a part of a widespread process that involves many organs or may be localized to the airways and lung parenchyma. It can occur in 3 forms: diffuse interstitial deposits, single or multiple pulmonary nodules, and, most commonly, submucosal tracheobronchial deposits.35

Tracheobronchial amyloidosis is a rare disease, present in 1.1% of patients seen at the Boston University Amyloid Treatment and Research Center over the past 15 years.36 It manifests as localized or diffuse involvement of the tracheobronchial tree with submucosal deposition of amyloid. The radiographic appearance of tracheobronchial disease is nodular and irregular narrowing of the tracheal lumen. CT shows luminal surface nodules or circumferential airway wall thickening with luminal narrowing. Lobar or segmental collapse, recurrent pneumonia, bronchiectasis, and obstructive hyperinflation may be seen with endobronchial obstruction due to amyloid deposition.7,35,36 In certain cases of diffuse involvement, there is widespread dense mural calcification or ossification of the lesions. This finding may lead to a second diagnosis of tracheobronchopathia osteochondroplastica. In cases where calcification is present, differentiation can be made on the basis of the presence of posterior membrane involvement.7

Back to Top | Article Outline
Chronic Inflammatory Bowel Disease

Chronic inflammatory bowel disease, such as Crohn's disease and ulcerative colitis, rarely causes large airway disease. Tracheobronchial involvement of Crohn's disease is extremely rare and can present with airway obstruction.37,38 For example, diffuse luminal narrowing of the subglottic trachea to the proximal main bronchus was reported on a CT scan of a young woman with Crohn's disease, which corresponded to the histologic features of nonspecific acute and chronic tracheiitis.37 Large airway involvement is a rare extraintestinal manifestation of ulcerative colitis.39,40 It can cause diffuse sclerosing tracheobronchitis. Mucosal ulceration, diffuse and chronic submucosal inflammation, and fibrosis lead to irregular airway wall thickening with luminal narrowing. CT scan can show irregular narrowing of the trachea and main bronchi.39

Back to Top | Article Outline

TRAUMA

Postintubation Tracheal Stenosis

Endotracheal intubation is the most common cause of acquired tracheal stenosis, and it may occur following prolonged tracheal balloon inflation with high-pressure cuffs during endotracheal tube or tracheostomy tube placement. With the implementation of low-pressure cuffs, the incidence has been reduced to <1%.7 Postintubation tracheal stenosis typically occurs secondary to injury of the trachea from the high pressure of an endotracheal tube balloon against the wall of the trachea. This initially results in ischemic necrosis of the mucosa, followed by granulation formation, fibrosis, and subsequently stenosis.1 The site of stenosis caused by endotracheal intubation is the subglottic trachea at the level of the endotracheal balloon.

MDCT showed high sensitivity (92%) and specificity (100%) for the detection of tracheal stenosis as a complication of endotracheal and tracheostomy tubes.41 The most common CT finding is a focal area of proximal tracheal luminal narrowing with eccentric or concentric tracheal wall thickening measuring approximately 2 cm in length. Multiplanar reformatted images along the long axis of the trachea can help determine the location and extent of stenosis and show focal circumferential luminal narrowing with a characteristic hourglass configuration (Fig. 8).1,7,18

Figure 8
Figure 8
Image Tools
Back to Top | Article Outline
Foreign Body Aspiration

Foreign body aspiration into the tracheobronchial tree is a common and serious cause of respiratory problems in children,42 but it is rare in adults.43

Aspiration of a foreign body may cause chronic nonspecific respiratory symptoms and nonspecific findings on chest radiographs. Chest radiography is often inaccurate for the diagnosis of foreign body aspiration, particularly when the object is radiolucent. Thus, negative results on chest radiographs do not exclude the possibility of a foreign body. Chronic unexplained respiratory symptoms sometimes warrant further investigation by CT to exclude unsuspected foreign body aspiration. CT is a noninvasive technique that can detect the narrowing of the airway resulting from the presence of a foreign body.42 CT virtual bronchoscopy, particularly low-dose CT, can indicate the exact location of the aspirated foreign body, eliminating the need to submit patients to rigid bronchoscopy in the absence of a foreign body.44,45 Associated findings such as obstructive hyperinflation, atelectasis, and pneumonia can be seen due to secondary changes in the affected lobe.

Back to Top | Article Outline

TRACHEAL NEOPLASM

Primary tracheal neoplasm is rare; it has been estimated that a primary tracheal tumor is roughly 180 times less common than a primary lung cancer.1,46 Primary tumors of the trachea are usually malignant in adults and benign in children.47 The definitive diagnoses of these tumors are commonly delayed, and most patients present with advanced diseases, because symptoms of tracheal obstruction usually manifest only when the tracheal lumen is occluded more than 75%.

MDCT accurately defines tracheal neoplasm manifesting as an intraluminal nodule or mass and extraluminal extension of the tumor as well as postobstructive complications such as atelectasis, pneumonia, and mucous plugging. The majority of neoplasms show nonspecific findings, but some specific CT features can suggest a precise diagnosis. A fatty mass on CT scan indicates lipoma, hamartoma, and well-differentiated liposarcoma. Calcification within the mass indicates carcinoid, chondroma, and chondrosarcoma. Homogeneous strong enhancement suggests carcinoid.

Small intraluminal nodules are occasionally seen on routine chest CT scans. However, the most common intraluminal nodule is mucus. CT scans of mucoid pseudotumors show low attenuation and no enhancement; they may be seen to contain air bubbles, are located in the dependent portion, do not disrupt the cartilaginous rings, and are mobile after coughing. If an intraluminal nodule shows the above-mentioned findings, it can be differentiated from a true lesion. Sometimes, thick mucus may be mistaken for a true lesion. A repeated CT scan is necessary after vigorous cough or bronchoscopy to differentiate mucus from a true lesion.

Back to Top | Article Outline
Benign Neoplasm

Benign neoplasms of the trachea are quite rare. Many benign neoplasms are slow growing and often go unrecognized for months or even years. As a result, patients with such tumors often undergo prolonged treatment for obstructive lung disease or asthma.48 The clinical and radiologic features of benign neoplasms are often indistinguishable from those of malignant neoplasms. Although many of these lesions have similar radiologic features, a benign neoplasm is a polypoid, round, sessile, small intraluminal mass, usually less than 2 cm in diameter with well-defined, smooth borders, which is confined within the tracheal lumen, and does not invade the tracheal wall or adjacent mediastinum.1,48

Hamartoma is defined as a mass resulting from the abnormal growth and mixture of tissue elements or an abnormal proportion of a single element of tissue normally present in an organ. Most hamartomas are located in the lung parenchyma, and they occur rarely in the large airway. Endobronchial hamartoma originates from a large bronchus, grows into the lumen, and obstructs the bronchi before increasing in size.48 Endobronchial lesions tend to have relatively more fat compared with parenchymal lesions.48,49 On CT scan, if an endobronchial or endotracheal mass contains fat or calcification, hamartoma can be diagnosed.

Leiomyoma of the respiratory tract is located in the bronchi in two thirds of patients and in the trachea in one third. Tracheal leiomyoma arises from the smooth muscle in the tracheal wall, typically along the membranous portion of the lower third of the trachea because of the abundant smooth muscle fibers in this area.48 The tumor most commonly manifests on CT scans as a homogeneously enhancing airway tumor with intraluminal growth. In approximately 15% of patients, the tumor has an iceberg appearance.50

Neurogenic tumors arising from the trachea are rare. A search of the literature from 1950 to 2003 uncovered 26 primary tracheal neurogenic tumors including 23 neurilemmomas and 3 neurofibromas, of which none was associated with Von Recklinghausen disease.51 Neurilemmomas occur most frequently in the distal third of the trachea, followed in decreasing order by the proximal and middle thirds. Radiographic and CT findings include a round, ovoid, lobulated, well-defined, and intraluminal homogeneous soft tissue mass within the trachea. However, these features are not specific for neurilemmomas.48,51,52

Tracheobronchial papillomatosis is caused by human papillomavirus infection and is more frequently categorized as a nonneoplastic disease. This disease is most common in children but may also occur in adults. Infection occurs most frequently at the time of birth when the child passes through an infected birth canal.7 The larynx is almost invariably affected, but in a small minority of patients extension into the trachea and bronchi occurs. The trachea is almost always involved when distal spread occurs. Even more rarely, papillomas are present in the lung and are seen as multiple small, widely scattered, well-defined round pulmonary nodules, frequently with cavitation. Malignant degeneration of pulmonary lesions may occur, leading to squamous cell carcinoma. Radiographic findings include nodular narrowing of the airway, which may be either focal or diffuse. CT scan demonstrates nodules that arise from the mucosal surface and their intraluminal extent (Fig. 9). Airway obstruction may lead to atelectasis, air trapping, postobstructive infection, or bronchiectasis.7

Figure 9
Figure 9
Image Tools
Back to Top | Article Outline
Primary Malignant Neoplasm

Among primary tracheal neoplasms, malignant tumors are more common than benign tumors in adults, and squamous cell carcinoma and adenoid cystic carcinoma are most frequent. In a study comprising 37 patients with primary tracheal tumors for 18 years, 23 were malignant and 14 were benign, and most of the malignant tumors were squamous cell carcinomas (n=11) and adenoid cystic carcinomas (n=9).47 In a report from the University of Texas MD Anderson Cancer Center, 74 patients were diagnosed with primary tracheal cancers over a 60-year period. Among these, 34 (45.9%) cases were squamous cell carcinomas, 19 (25.7%) were adenoid cystic carcinomas, and 21 (28.4%) were of other histologic types.53

Squamous cell carcinoma is the most common primary malignant neoplasm of the trachea; it arises from the surface epithelium and is strongly associated with smoking. It more frequently affects men and individuals between the ages of 50 and 60 years. It is commonly infiltrative in nature, with exophytic or ulcerative lesions. Regional extension into adjacent structures and lymph nodes is common. Furthermore, metachronous or synchronous lesions are common in the oropharynx, larynx, and lungs. Chest radiographs are often considered unremarkable, but retrospective analysis usually shows a focal asymmetric intraluminal lesion. CT scans show a polypoid intraluminal mass with irregular, smooth, or lobulated contours. The relationship of the tumor with the tracheal wall varies from localized eccentric pedunculated lesions to circumferential invasion.

Adenoid cystic carcinoma is a low-grade malignancy that is the second most common tracheal malignancy after squamous cell carcinoma. It occurs in younger patients than those afflicted with squamous cell carcinoma and peaks in patients in their 40s, demonstrating no sex predilection, and is unrelated to smoking.54 Adenoid cystic carcinomas usually arise in the lower trachea but are also found in the main bronchi, lobar bronchi, and, rarely, in the segmental bronchi and extrathoracic trachea.54 On CT, the tumor manifests as an intraluminal soft tissue mass with extension through the tracheal wall, diffuse or circumferential wall thickening of the trachea, a soft tissue mass filling the airway, or a homogeneous mass encircling the trachea with wall thickening in the transverse and longitudinal planes. The longitudinal extent of the tumor is greater than its transaxial extent. The tumors usually involve more than 180 degrees of the airway circumference and have a striking tendency toward submucosal extension. The tumor has a polypoid or broad-based, smooth, lobulated, or irregular margin. Calcification within the tumor is rare (Fig. 10).54 Adenoid cystic carcinomas, which are usually located in the intrathoracic distal trachea, tend to exhibit longitudinal extension and both intraluminal and extraluminal growth on CT. These findings correlate with histopathologic findings in most patients.54

Figure 10
Figure 10
Image Tools
Back to Top | Article Outline
Secondary Malignant Neoplasm

Secondary malignant involvement of the trachea is usually caused by local direct invasion, such as thyroid, laryngeal, esophageal, and lung cancers. CT demonstrates the primary malignant neoplasm and its direct extension into the trachea. Findings associated with direct extension into the trachea include intraluminal mass, destruction of the tracheal cartilage, and tracheoesophageal fistula.

Rarely is tracheal metastasis caused by hematogenous spread. Tracheal metastases from nonpulmonary malignancies such as breast cancer, colorectal carcinoma, renal carcinoma, and melanoma have been reported. Metastatic lesions are usually solitary, but multiple lesions have been observed. They can have imaging features simulating primary tracheal malignancies. Tracheal metastasis of primary lung cancer is extremely rare, although direct tracheal involvement by primary lung cancer is often seen and classified as T4 lung cancer. Tracheal metastasis of primary nonsmall cell lung cancer manifests as an endotracheal nodule or as an eccentric wall thickening of the trachea, showing contrast enhancement with a predilection for the upper trachea on CT.55

Back to Top | Article Outline

BRONCHIECTASIS

Bronchiectasis is defined as a permanent abnormal dilatation of the bronchi and is classified into 3 groups, cylindrical, varicose, and cystic, on the basis of the gross pattern of bronchial dilatation.56 Imaging plays a major role in the diagnosis of bronchiectasis, and high-resolution CT further improves the imaging diagnosis. High-resolution CT using 1- to 1.5-mm-collimation sections at 10-mm intervals has been regarded as the radiologic gold standard in diagnosis.57,58 Limitations of conventional thin-section CT studies in the detection of bronchiectasis are related to the gaps between noncontiguous slices and imaging degradation due to breathing and cardiac motion artifacts. The advent of MDCT enables narrower collimation and faster acquisitions during a single breath-hold with near isometric z-axis resolution. Volumetric MDCT using various reconstruction techniques results in significant improvements in the assessment of the presence, extent, and severity of bronchiectasis and in improvements in diagnostic accuracy and confidence for the diagnosis and exclusion of bronchiectasis compared with conventional high-resolution CT.59–61

Bronchiectasis can be diagnosed by the presence of a dilated, nontapered, thick-walled airway extending toward the lung periphery on CT. CT findings vary depending on the precise orientation of airways relative to the scan plane and whether the airway lumen is primarily distended with air or mucus (Figs. 11–13). These include signet-ring sign, tram tracts, a cluster of cysts, tubular or branching densities, and nodular or oval densities. One of the main CT findings is the presence of bronchial dilatation, which is considered to be present when the internal diameter of the bronchus is larger than that of the adjacent pulmonary artery. However, these criteria should be interpreted with caution because there are minor discrepancies in the bronchoarterial diameter ratio in normal individuals, and many factors can cause changes in the diameters of the pulmonary arteries. Bronchial wall thickening is seen in almost all cases but is an inconstant feature.57,62,63

Figure 11
Figure 11
Image Tools
Figure 12
Figure 12
Image Tools
Figure 13
Figure 13
Image Tools

Several other CT findings can be associated with bronchiectasis. Some reflect the associated bronchopulmonary lesions, whereas others express mechanical or infectious complications of bronchiectasis. Lobar or segmental collapse is due to cicatrizing atelectasis secondary to peribronchial fibrosis, associated with obstruction or destruction of distal airways. Consolidation usually signifies transbronchial spread of bronchial infection into the peribronchial airspace. The mosaic pattern of decreased attenuation is the result of associated bronchiolitis (Fig. 11).62–64

Accurate diagnosis of bronchiectasis requires detailed knowledge of several potential pitfalls, including artifacts resulting from respiratory and cardiac motions, as well as technical factors such as collimation and electronic windowing. Bronchiectasis is difficult to diagnose in patients with concurrent active parenchymal consolidation, as CT often discloses dilated peripheral airways that will revert to normal, an entity referred to as reversible bronchiectasis. Bronchiectasis may occur as a component of diffuse infiltrative lung disease. In patients with interstitial fibrosis, bronchial dilatation occurs due to tethering, the so-called traction bronchiectasis. Some nonbronchial cystic pulmonary lesions, such as Langerhans cell histiocytosis, Pneumocystis carinii pneumonia, cystic metastasis, and tracheobronchial papillomatosis, can simulate bronchiectasis. Bronchiectasis may also be misinterpreted as a mass lesion or cavitating lesion.57,62,63

Airflow obstruction is common in patients with bronchiectasis. Although the exact site and mechanism of airflow obstruction is uncertain and may be multifactorial, there is significant correlation between the extent of morphologic abnormality seen on high-resolution CT and the physiologic impairment seen on pulmonary function tests in patients with bronchiectasis. The extent and severity of bronchiectasis are positively related to the extent of decreased attenuation, the area of coexistent constrictive bronchiolitis. Furthermore, the extent of bronchiectasis and the area of decreased attenuation correlate well with the severity of functional impairment on pulmonary function tests.63,64 The major CT morphologic determinants of airflow obstruction in bronchiectasis are bronchial wall thickness and decreased attenuation on the expiratory CT scan.65

The most common cause of bronchiectasis is infection, and a wide variety of other disorders have been associated with bronchiectasis; therefore, identification of an underlying cause is important. The reliability of CT for determining the causes of bronchiectasis is somewhat controversial. The pattern and distribution of abnormalities revealed by high-resolution CT in patients with bronchiectasis are influenced by the underlying cause.66 The underlying causes of bronchiectasis are identified in less than half of patients; moreover, CT features alone do not usually allow for a confident distinction between idiopathic bronchiectasis and bronchiectasis with a specific cause, and CT remains of little value in diagnosing specific etiologies of bronchiectasis.67 Although no CT findings are diagnostic for the identification of the underlying cause, several CT findings may be characteristic of an identifiable cause in certain groups of patients.

Back to Top | Article Outline
Bronchiectasis With Specific Causes

ABPA is a hypersensitivity reaction to aspergillus fumigates that occurs in patients with asthma. Although asthma is common, ABPA is infrequently diagnosed. Essential diagnostic criteria include asthma, skin prick test positivity to Aspergillus fumigates, elevated levels of serum total immunoglobulin E, elevated levels of serum Aspergillus-specific immunoglobulin E, and either a history of pulmonary infiltrates on chest radiography or central bronchiectasis. Central bronchiectasis is viewed as being pathognomonic of ABPA. Radiographs demonstrate homogeneous, tubular, finger-in-glove-shaped opacity in a bronchial distribution, usually predominant in the upper lobes. These opacities are related to the plugging of airways by hyphal masses with distal mucoid impaction and can migrate from one region to another. Isolated lobar or segmental atelectasis may occur. CT findings consist primarily of mucoid impaction and bronchiectasis involving predominantly the segmental and subsegmental bronchi of the upper lobes. In approximately 30% of patients, the impacted mucus shows high density or demonstrates frank calcification on CT.68 The presence of randomly distributed, predominantly central, moderate-to-severe bronchiectasis affecting 3 or more lobes, bronchial wall thickening, and centrilobular nodules in an asthmatic patient is highly suggestive of ABPA.69

Cystic fibrosis is the most common lethal autosomal recessive childhood disorder in Caucasians. The disease inevitably leads to periodic exacerbations, with worsening of pulmonary symptoms attributed to inflammation of large and small airways. Chest radiography still remains the primary imaging tool in the follow-up of patients with cystic fibrosis. CT is valuable in the follow-up of cystic fibrosis patients because it has advantages over pulmonary function tests and clinical scoring in the depiction of sequential morphologic changes over time.70 CT can identify highly relevant structural lung changes, such as bronchiectasis and air trapping. Bronchiectasis, which is progressive and irreversible, is probably the most relevant structural change on CT scans.

Ciliary dyskinesia syndrome, previously known as immotile cilia syndrome, results from an autosomal recessive genetic abnormality and is characterized by abnormal ciliary structure and function, leading to a reduced mucociliary clearance and chronic airway infection. Bronchiectasis and sinusitis are common manifestations. About half of the patients also have situs inversus. The combination of bronchiectasis, sinusitis, and situs inversis is termed Kartagener syndrome (Fig. 12). Men and women are equally affected; however, in men the syndrome may be associated with immotile spermatozoa and infertility. Bronchiectasis develops in childhood and adolescence and is associated with recurrent pneumonia. Radiologic findings include bronchial wall thickening, hyperinflation, segmental atelectasis, consolidation, and bronchiectasis. Bronchiectasis has a predilection for the anatomic middle lobe. Although it has a similar radiological appearance and clinical state to cystic fibrosis, ciliary dyskinesia syndrome is less severe and less progressive.71

Nontuberculous mycobacterium (NTM) is a ubiquitous organism in the environment. The isolation of NTM from respiratory samples is not sufficient for the diagnosis of NTM pulmonary disease. Therefore, NTM pulmonary disease is diagnosed on the basis of clinical, radiologic, histologic, and bacteriologic criteria. The radiologic manifestation is variable, depending on preexisting disease and the NTM species. NTM pulmonary disease has 2 distinct subtypes: cavitary disease of the upper lobe and nodular bronchiectatic disease.72 Nodular bronchiectatic disease is most frequently caused by a Mycobacterium avium intracellulare complex and is predominantly reported in middle-aged or elderly women. CT findings of multifocal, small, centrilobular nodules and branching densities and bronchiectasis in both lungs with predominent right middle lobe and lingular segment involvement can suggest nodular bronchiectatic disease caused by NTM (Fig. 13).72

Back to Top | Article Outline

BRONCHOLITHIASIS

Broncholithiasis is a condition in which a peribronchial calcified lymph node erodes into and distorts an adjacent bronchus. The underlying abnormality is usually granulomatous lymphadenopathies caused by Mycobacterium tuberculosis or Histoplasma capsulatum. Calcified material in a bronchial lumen or bronchial distortion by peribronchial disease results in airway obstruction, which leads to collapse, obstructive pneumonitis, mucoid impaction, or bronchictasis. Broncholithiasis is more common in the right lung, and obstructive changes particularly affect the right middle lobe.

Radiographic findings include the disappearance of a previously identified calcific nidus or change in position of a calcified nidus on serial chest radiographs, as well as a calcific nodule with evidence of airway obstruction including segmental or lobar atelectais, mucoid impaction, obstructive pneumonitis, or obstructive oligemia with air trapping.73 Broncholithiasis is recognized on CT by the presence of a calcified endobronchial or peribronchial lymph node, associated with bronchopulmonary complications caused by obstruction including atelectasis, pneumonia, bronchiectasis, and air trapping, and by the absence of an associated soft tissue mass (Fig. 14).73,74

Figure 14
Figure 14
Image Tools

Endobronchial actinomycosis has been reported to be associated with broncholithiasis and presents with proximal broncholiths associated with distal postobstructive pneumonitis of the involved lobe or segment on CT scan (Fig. 14).75,76 The preexisting broncholith is secondarily infected by actinomyces, and the subsequent inflammatory process enlarges the endobronchial lesion and progressively obstructs the airway, resulting in distal obstructive pneumonia. Progressive shedding of actinomyces colonies from the nidus further aggravates the distal pneumonia.75

Back to Top | Article Outline

BRONCHIAL ANTHRACOFIBROSIS

Bronchial anthracofibrosis has been defined only recently. Bronchoscopic findings of dark anthracotic pigmentation with bronchial narrowing or obliteration that is not associated with environmental exposure to coal dust or smoking are called anthracofibrosis.77 Bronchial anthracofibrosis is a benign condition, and it may progress very slowly and lead to progressive bronchial stenosis. The etiologic factors of bronchial anthracofibrosis are still unclear. In a study by Chung et al,77 17 of 28 patients with anthracofibrosis had confirmed active tuberculous infection, suggesting a strong correlation between anthracofibrosis and active pulmonary tuberculosis. Occupational exposure has been considered an etiological cause of anthracofibrosis.78,79 In a study by Wynn et al,79 of the 7 patients reported, only 1 patient had a history of tuberculosis, whereas 6 had a history of occupational dust exposure, including 1 patient with pneumoconiosis. However, many patients encountered in daily practice have neither exposure to mining nor a history of smoking.

The mechanism of anthracofibrosis is obscure. It has been hypothesized that the black pigments in the bronchial walls are derived from anthracotic material in the adjacent lymph nodes. The involved lymph nodes may perforate into the adjacent bronchi, and carbon particles in the lymph nodes may penetrate the bronchial wall to as deep as the mucosa, resulting in coloring of the bronchial mucosa. Subsequently, healing with fibrotic response may occur and result in bronchial narrowing or obstruction with anthracotic pigmentation.18,77,80 Most patients are elderly women, and the right middle lobe is the most commonly involved site, with multiple site involvements being common.80

The main CT findings are bronchial narrowing with peribronchial soft tissue thickening, surrounding calcified or noncalcified lymph nodes, and lobar or segmental atelectasis distal to the involved bronchus (Fig. 15).77,80 Findings of bronchial narrowing, distal atelectasis, and hilar and mediastinal lymphadenopathies are similar to those of endobronchial malignancy or endobronchial tuberculosis. Calcified lymph nodes around the involved bronchi, multifocal involvement of bronchial narrowing, and absence of definite endobronchial nodular lesions can differentiate bronchial anthracofibrosis from endobronchial bronchogenic carcinoma. Bronchoscopy and bronchoscopic biopsy are often necessary to differentiate between tuberculosis and malignancy (Fig. 15).

Figure 15
Figure 15
Image Tools
Back to Top | Article Outline

REFERENCES

1. Boiselle PM. Imaging of the large airways. Clin Chest Med. 2008;29:181–193 vii.

2. Boiselle PM, Lee KS, Ernst A. Multidetector CT of the central airways. J Thorac Imaging. 2005;20:186–195

3. Chen Q, Goo JM, Seo JB, et al. Evaluation of tracheobronchial diseases: comparison of different imaging techniques. Korean J Radiol. 2000;1:135–141

4. Hogg JC, Macklem PT, Thurlbeck WM. Site and nature of airway obstruction in chronic obstructive lung disease. N Engl J Med. 1968;278:1355–1360

5. Murata K, Itoh H, Todo G, et al. Centrilobular lesions of the lung: demonstration by high-resolution CT and pathologic correlation. Radiology. 1986;161:641–645

6. 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

7. Prince JS, Duhamel DR, Levin DL, et al. Nonneoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. Radiographics. 2002;22:S215–S230

8. Javidan-Nejad C. MDCT of trachea and main bronchi. Radiol Clin North Am. 2010;48:157–176

9. Heyer CM, Nuesslein TG, Jung D, et al. Tracheobronchial anomalies and stenoses: detection with low-dose multidetector CT with virtual tracheobronchoscopy—comparison with flexible tracheobronchoscopy. Radiology. 2007;242:542–549

10. Yildiz H, Ugurel S, Soylu K, et al. Accessory cardiac bronchus and tracheal bronchus anomalies: CT-bronchoscopy and CT-bronchography findings. Surg Radiol Anat. 2006;28:646–649

11. Ming Z, Lin Z. Evaluation of tracheal bronchus in Chinese children using multidetector CT. Pediatr Radiol. 2007;37:1230–1234

12. Suzuki M, Matsui O, Kawashima H, et al. Radioanatomical study of a true tracheal bronchus using multidetector computed tomography. Jpn J Radiol. 2010;28:188–192

13. Ghaye B, Szapiro D, Fanchamps JM, et al. Congenital bronchial abnormalities revisited. Radiographics. 2001;21:105–119

14. Ghaye B, Kos X, Dondelinger RF. Accessory cardiac bronchus: 3D CT demonstration in nine cases. Eur Radiol. 1999;9:45–48

15. McGuinness G, Naidich DP, Garay SM, et al. Accessory cardiac bronchus: CT features and clinical significance. Radiology. 1993;189:563–566

16. Woodring JH, Howard RS II, Rehm SR. Congenital tracheobronchomegaly (Mounier-Kuhn syndrome): a report of 10 cases and review of the literature. J Thorac Imaging. 1991;6:1–10

17. Lee JH, Park SS, Lee DH, et al. Endobronchial tuberculosis. Clinical and bronchoscopic features in 121 cases. Chest. 1992;102:990–994

18. Grenier PA, Beigelman-Aubry C, Brillet PY. Nonneoplastic tracheal and bronchial stenoses. Radiol Clin North Am. 2009;47:243–260

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

20. Moon WK, Im JG, Yeon KM, et al. Tuberculosis of the central airways: CT findings of active and fibrotic disease. AJR Am J Roentgenol. 1997;169:649–653

21. Kim Y, Lee KS, Yoon JH, et al. Tuberculosis of the trachea and main bronchi: CT findings in 17 patients. AJR Am J Roentgenol. 1997;168:1051–1056

22. Franquet T, Muller NL, Oikonomou A, et al. Aspergillus infection of the airways: computed tomography and pathologic findings. J Comput Assist Tomogr. 2004;28:10–16

23. Franquet T, Serrano F, Gimenez A, et al. Necrotizing Aspergillosis of large airways: CT findings in eight patients. J Comput Assist Tomogr. 2002;26:342–345

24. Jabbardarjani HR, Radpey B, Kharabian S, et al. Tracheobronchopathia osteochondroplastica: presentation of ten cases and review of the literature. Lung. 2008;186:293–297

25. Leske V, Lazor R, Coetmeur D, et al. Tracheobronchopathia osteochondroplastica: a study of 41 patients. Medicine (Baltimore). 2001;80:378–390

26. 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

27. Behar JV, Choi YW, Hartman TA, et al. Relapsing polychondritis affecting the lower respiratory tract. AJR Am J Roentgenol. 2002;178:173–177

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

29. Tillie-Leblond I, Wallaert B, Leblond D, et al. Respiratory involvement in relapsing polychondritis. Clinical, functional, endoscopic, and radiographic evaluations. Medicine (Baltimore). 1998;77:168–176

30. Ernst A, Rafeq S, Boiselle P, et al. Relapsing polychondritis and airway involvement. Chest. 2009;135:1024–1030

31. Polychronopoulos VS, Prakash UB, Golbin JM, et al. Airway involvement in Wegener's granulomatosis. Rheum Dis Clin North Am. 2007;33:755–775 vi.

32. Lee KS, Kim TS, Fujimoto K, et al. Thoracic manifestation of Wegener's granulomatosis: CT findings in 30 patients. Eur Radiol. 2003;13:43–51

33. Screaton NJ, Sivasothy P, Flower CD, et al. Tracheal involvement in Wegener's granulomatosis: evaluation using spiral CT. Clin Radiol. 1998;53:809–815

34. Lenique F, Brauner MW, Grenier P, et al. CT assessment of bronchi in sarcoidosis: endoscopic and pathologic correlations. Radiology. 1995;194:419–423

35. Kim HY, Im JG, Song KS, et al. Localized amyloidosis of the respiratory system: CT features. J Comput Assist Tomogr. 1999;23:627–631

36. O'Regan A, Fenlon HM, Beamis JF Jr, et al. Tracheobronchial amyloidosis. The Boston University experience from 1984 to 1999. Medicine (Baltimore). 2000;79:69–79

37. Henry MT, Davidson LA, Cooke NJ. Tracheobronchial involvement with Crohn's disease. Eur J Gastroenterol Hepatol. 2001;13:1495–1497

38. Ahmed KA, Thompson JW, Joyner RE, et al. Airway obstruction secondary to tracheobronchial involvement of asymptomatic undiagnosed Crohn's disease in a pediatric patient. Int J Pediatr Otorhinolaryngol. 2005;69:1003–1005

39. Wilcox P, Miller R, Miller G, et al. Airway involvement in ulcerative colitis. Chest. 1987;92:18–22

40. Cross DL, Scudder DD. Airway obstruction in ulcerative colitis. South Med J. 1997;90:249–250

41. Sun M, Ernst A, Boiselle PM. MDCT of the central airways: comparison with bronchoscopy in the evaluation of complications of endotracheal and tracheostomy tubes. J Thorac Imaging. 2007;22:136–142

42. Huang HJ, Fang HY, Chen HC, et al. Three-dimensional computed tomography for detection of tracheobronchial foreign body aspiration in children. Pediatr Surg Int. 2008;24:157–160

43. Zissin R, Shapiro-Feinberg M, Rozenman J, et al. CT findings of the chest in adults with aspirated foreign bodies. Eur Radiol. 2001;11:606–611

44. Adaletli I, Kurugoglu S, Ulus S, et al. Utilization of low-dose multidetector CT and virtual bronchoscopy in children with suspected foreign body aspiration. Pediatr Radiol. 2007;37:33–40

45. Haliloglu M, Ciftci AO, Oto A, et al. CT virtual bronchoscopy in the evaluation of children with suspected foreign body aspiration. Eur J Radiol. 2003;48:188–192

46. Yang KY, Chen YM, Huang MH, et al. Revisit of primary malignant neoplasms of the trachea: clinical characteristics and survival analysis. Jpn J Clin Oncol. 1997;27:305–309

47. Ahn Y, Chang H, Lim YS, et al. Primary tracheal tumors: review of 37 cases. J Thorac Oncol. 2009;4:635–638

48. Ko JM, Jung JI, Park SH, et al. Benign tumors of the tracheobronchial tree: CT-pathologic correlation. AJR Am J Roentgenol. 2006;186:1304–1313

49. Ahn JM, Im JG, Seo JW, et al. Endobronchial hamartoma: CT findings in three patients. AJR Am J Roentgenol. 1994;163:49–50

50. Kim YK, Kim H, Lee KS, et al. Airway leiomyoma: imaging findings and histopathologic comparisons in 13 patients. AJR Am J Roentgenol. 2007;189:393–399

51. Righini CA, Lequeux T, Laverierre MH, et al. Primary tracheal schwannoma: one case report and a literature review. Eur Arch Otorhinolaryngol. 2005;262:157–160

52. Woo OH, Yong HS, Shin BK, et al. Wide spectrum of thoracic neurogenic tumours: a pictorial review of CT and pathological findings. Br J Radiol. 2008;81:668–676

53. Webb BD, Walsh GL, Roberts DB, et al. Primary tracheal malignant neoplasms: the University of Texas MD Anderson Cancer Center experience. J Am Coll Surg. 2006;202:237–246

54. Kwak SH, Lee KS, Chung MJ, et al. Adenoid cystic carcinoma of the airways: helical CT and histopathologic correlation. AJR Am J Roentgenol. 2004;183:277–281

55. Chong S, Kim TS, Han J. Tracheal metastasis of lung cancer: CT findings in six patients. AJR Am J Roentgenol. 2006;186:220–224

56. Reid LM. Reduction in bronchial subdivision in bronchiectasis. Thorax. 1950;5:233–247

57. McGuinness G, Naidich DP, Leitman BS, et al. Bronchiectasis: CT evaluation. AJR Am J Roentgenol. 1993;160:253–259

58. Grenier P, Maurice F, Musset D, et al. Bronchiectasis: assessment by thin-section CT. Radiology. 1986;161:95–99

59. Dodd JD, Souza CA, Muller NL. Conventional high-resolution CT versus helical high-resolution MDCT in the detection of bronchiectasis. AJR Am J Roentgenol. 2006;187:414–420

60. Hill LE, Ritchie G, Wightman AJ, et al. Comparison between conventional interrupted high-resolution CT and volume multidetector CT acquisition in the assessment of bronchiectasis. Br J Radiol. 2010;83:67–70

61. Jung KJ, Lee KS, Kim SY, et al. Low-dose, volumetric helical CT: image quality, radiation dose, and usefulness for evaluation of bronchiectasis. Invest Radiol. 2000;35:557–563

62. Kang EY, Miller RR, Muller NL. Bronchiectasis: comparison of preoperative thin-section CT and pathologic findings in resected specimens. Radiology. 1995;195:649–654

63. Hansell DM. Bronchiectasis. Radiol Clin North Am. 1998;36:107–128

64. Hansell DM, Wells AU, Rubens MB, et al. Bronchiectasis: functional significance of areas of decreased attenuation at expiratory CT. Radiology. 1994;193:369–374

65. Roberts HR, Wells AU, Milne DG, et al. Airflow obstruction in bronchiectasis: correlation between computed tomography features and pulmonary function tests. Thorax. 2000;55:198–204

66. Cartier Y, Kavanagh PV, Johkoh T, et al. Bronchiectasis: accuracy of high-resolution CT in the differentiation of specific diseases. AJR Am J Roentgenol. 1999;173:47–52

67. Reiff DB, Wells AU, Carr DH, et al. CT findings in bronchiectasis: limited value in distinguishing between idiopathic and specific types. AJR Am J Roentgenol. 1995;165:261–267

68. Franquet T, Muller NL, Gimenez A, et al. Spectrum of pulmonary aspergillosis: histologic, clinical, and radiologic findings. Radiographics. 2001;21:825–837

69. Ward S, Heyneman L, Lee MJ, et al. Accuracy of CT in the diagnosis of allergic bronchopulmonary aspergillosis in asthmatic patients. AJR Am J Roentgenol. 1999;173:937–942

70. Helbich TH, Heinz-Peer G, Fleischmann D, et al. Evolution of CT findings in patients with cystic fibrosis. AJR Am J Roentgenol. 1999;173:81–88

71. Nadel HR, Stringer DA, Levison H, et al. The immotile cilia syndrome: radiological manifestations. Radiology. 1985;154:651–655

72. Koh WJ, Lee KS, Kwon OJ, et al. Bilateral bronchiectasis and bronchiolitis at thin-section CT: diagnostic implications in nontuberculous mycobacterial pulmonary infection. Radiology. 2005;235:282–288

73. Seo JB, Song KS, Lee JS, et al. Broncholithiasis: review of the causes with radiologic-pathologic correlation. Radiographics. 2002;22:S199–S213

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

75. Kim TS, Han J, Koh WJ, et al. Endobronchial actinomycosis associated with broncholithiasis: CT findings for nine patients. AJR Am J Roentgenol. 2005;185:347–353

76. Seo JB, Lee JW, Ha SY, et al. Primary endobronchial actinomycosis associated with broncholithiasis. Respiration. 2003;70:110–113

77. Chung MP, Lee KS, Han J, et al. Bronchial stenosis due to anthracofibrosis. Chest. 1998;113:344–350

78. Naccache JM, Monnet I, Nunes H, et al. Anthracofibrosis attributed to mixed mineral dust exposure: report of three cases. Thorax. 2008;63:655–657

79. Wynn GJ, Turkington PM, O'Driscoll BR. Anthracofibrosis, bronchial stenosis with overlying anthracotic mucosa: possibly a new occupational lung disorder: a series of seven cases from one UK hospital. Chest. 2008;134:1069–1073

80. Kim HY, Im JG, Goo JM, et al. Bronchial anthracofibrosis (inflammatory bronchial stenosis with anthracotic pigmentation): CT findings. AJR Am J Roentgenol. 2000;174:523–527

Cited By:

This article has been cited 2 time(s).

Chest
A 30-Year-Old Woman With Recurrent Lower Respiratory Tract Infections
Khasawneh, FA; Jou-Tindo, AJ
Chest, 143(5): 1500-1503.
10.1378/ehest.12-2279
CrossRef
American Journal of Roentgenology
Tumors and Tumorlike Conditions of the Large Airways
Ngo, AVH; Walker, CM; Chung, JH; Takasugi, JE; Stern, EJ; Kanne, JP; Reddy, GP; Godwin, JD
American Journal of Roentgenology, 201(2): 301-313.
10.2214/AJR.12.9043
CrossRef
Back to Top | Article Outline
Keywords:

large airway disease; tracheal disease; tracheal neoplasm; tracheobronchial tuberculosis; bronchiectasis; bronchial anthracofibrosis

© 2011 Lippincott Williams & Wilkins, Inc.

Login

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.