(Radiographics. 2001;21:839-858.)
© RSNA, 2001
Thoracic Sequelae and Complications of Tuberculosis1
Hyae Young Kim, MD,
Koun-Sik Song, MD,
Jin Mo Goo, MD,
Jin Seong Lee, MD,
Kyoung Soo Lee, MD and
Tae-Hwan Lim, MD
1 From the Department of Radiology, Ewha Women's University Mokdong Hospital, Seoul, Korea (H.Y.K.); the Department of Diagnostic Radiology, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Poongnap-Dong, Songpa-Ku, Seoul 138-040, Korea (K.S.S., J.S.L., T.H.L.); the Department of Radiology, Seoul National University Hospital, Seoul, Korea (J.M.G.); and the Department of Radiology, Samsung Medical Center, Seoul, Korea (K.S.L.). Presented as a scientific exhibit at the 1999 RSNA scientific assembly. Received July 24, 2000; revision requested August 18 and received October 2; accepted October 3. Address correspondence to K.S.S. (e-mail: kssong@www.amc.seoul.kr).
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Abstract
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Pulmonary tuberculosis is caused by Mycobacterium tuberculosis when droplet nuclei laden with bacilli are inhaled. In accordance with the virulence of the organism and the defenses of the host, tuberculosis can occur in the lungs and in extrapulmonary organs. A variety of sequelae and complications can occur in the pulmonary and extrapulmonary portions of the thorax in treated or untreated patients. These can be categorized as follows: (a) parenchymal lesions, which include tuberculoma, thin-walled cavity, cicatrization, end-stage lung destruction, aspergilloma, and bronchogenic carcinoma; (b) airway lesions, which include bronchiectasis, tracheobronchial stenosis, and broncholithiasis; (c) vascular lesions, which include pulmonary or bronchial arteritis and thrombosis, bronchial artery dilatation, and Rasmussen aneurysm; (d) mediastinal lesions, which include lymph node calcification and extranodal extension, esophagomediastinal or esophagobronchial fistula, constrictive pericarditis, and fibrosing mediastinitis; (e) pleural lesions, which include chronic empyema, fibrothorax, bronchopleural fistula, and pneumothorax; and (f) chest wall lesions, which include rib tuberculosis, tuberculous spondylitis, and malignancy associated with chronic empyema. These varieties of radiologic manifestations can mimic other disease entities. Therefore, recognition and understanding of the radiologic manifestations of the thoracic sequelae and complications of tuberculosis are important to facilitate diagnosis.
Index Terms: Tuberculosis, cardiovascular, 50.23 • Tuberculosis, musculoskeletal, 47.23 • Tuberculosis, pulmonary, 60.23 • Tuberculosis, soft tissues, 67.23
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LEARNING OBJECTIVES FOR TEST 3
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After reading this article and taking the test, the reader will be able to:
- List the thoracic sequelae and complications of pulmonary tuberculosis.
- Recognize the radiologic features of various forms of thoracic sequelae and complications of pulmonary tuberculosis.
- Describe the pathogenesis of thoracic sequelae and complications of pulmonary tuberculosis.
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Introduction
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Tuberculosis has been a disease of tremendous importance to the human race. Pulmonary tuberculosis is caused by Mycobacterium tuberculosis when droplet nuclei laden with bacilli are inhaled. The pathologic form of the pulmonary infection depends on the sensitivity of the infected host and is classified as primary or postprimary (1–4). Primary tuberculosis typically appears as air-space consolidation in the lower lobes, hilar and mediastinal lymphadenopathy, pleural effusion, and miliary disease. Postprimary tuberculosis appears most commonly as nodular and linear areas of increased opacity or increased attenuation at the lung apex. Pleural effusion and miliary disease are less common in postprimary tuberculosis (2–6).
At the microscopic level, the initial tissue reaction to a primary encounter with M tuberculosis is local mobilization of neutrophil polymorphs at the site of implantation. Caseation necrosis rapidly ensues, provoking a variable lymphocytic, histiocytic, and giant cell reaction, which is usually followed by mural fibrosis (4,6). In contrast to primary tuberculosis, in which fibrosis and healing are the rule, the postprimary form of the disease tends to progress, with foci of inflammation and necrosis enlarging to occupy greater portions of the lung parenchyma. During this process, communication with airways is common. In addition to erosion into an airway, the expanding infection may extend toward the periphery of the lung and rupture into the pleural space, resulting in development of tuberculous empyema (7,8).
The course of the disease depends on the interaction between the host response and the virulence of the organism. The major host defense against the tubercle bacillus is cell-mediated immunity, which is effected primarily by means of macrophages and T lymphocytes (9). When host factors prevail, there is gradual healing with formation of parenchymal scars. When the organism overpowers host defenses, the disease progresses, either locally or in other parts of the lung or body after spread of bacteria via the airways, lymphatic vessels, or bloodstream (5–9). There is a tendency toward more fulminant, disseminated, and even extrapulmonary disease in immunocompromised hosts (7). Therefore, various forms of sequelae and complications may result from both primary and postprimary pulmonary tuberculosis in pulmonary or extrapulmonary portions of the thorax (6,8–13).
In this article, we discuss and illustrate the imaging features of sequelae and complications of thoracic tuberculosis affecting the lung parenchyma, airways, vessels, mediastinum, pleura, and chest wall.
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Parenchymal Lesions
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Tuberculoma and Thin-walled Cavity
Tuberculoma may be a manifestation of either primary or postprimary tuberculosis. In postprimary tuberculosis, a tuberculoma is the main or only abnormality seen on chest radiographs in approximately 5% of patients (14). It is a round or oval granuloma caused by acid-fast bacilli with a wall lined by granulomatous inflammatory tissue or encapsulated by connective tissue (12–15). The central portion of the tuberculoma shows caseation necrosis. A healed, filled-in cavity and a rounded-off, contracted, healing tuberculous lesion are the reported possible mechanisms of tuberculoma formation (15).
Tuberculomas can be solitary or multiple and range in diameter from 0.5 to 4.0 cm or greater. Typically, they are smooth or sharply defined, although rarely the margin may be hazy or indistinct. Satellite lesions are seen in up to 80% of cases. Calcification is found in 20%–30% of tuberculomas and is usually nodular and diffuse (12) (Fig 1).
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Figure 1. Solitary tuberculoma in a 59-year-old man with postprimary tuberculosis. Computed tomographic (CT) scan shows a well-defined, round, 1.5-cm-diameter nodule with dense calcification (arrow) in the superior segment of the right lower lobe.
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Residual thin-walled cavities may be seen in both active and inactive disease. After antituberculous chemotherapy, the tuberculous cavity may disappear; occasionally, the wall becomes paper-thin and an air-filled cystic space remains (8). Serial imaging helps determine the stability or activity of pulmonary disease. The wall of a chronic cavity varies from 1 cm to less than 1 mm in thickness and may be smooth, sometimes simulating an emphysematous bulla (Fig 2). It can be difficult to distinguish true cavities from bullae, cysts, or pneumatoceles (10).
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Figure 2. Thin-walled cavity in a 38-year-old man with postprimary tuberculosis. High-resolution CT scan shows a relatively thin-walled cavity with even thickness (large arrows) in the superior segment of the right lower lobe; the cavity had been stable for 2 years. There are irregular fibrotic lesions with paracicatricial emphysema (arrowheads) in the right middle lobe. Bronchiectatic changes are also noted (small arrows).
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Cicatrization and Destruction of the Lung
Cicatrization atelectasis is a common finding after postprimary tuberculosis. Up to 40% of patients with postprimary tuberculosis have a marked fibrotic response, which manifests as atelectasis of the upper lobe, retraction of the hilum, compensatory lower lobe hyperinflation, and mediastinal shift toward the fibrotic lung. Tuberculosis is almost always present in the opposite upper lobe (8,16). A nonspecific radiologic pattern of fibrosis consisting of parenchymal bands, fibrotic nodules and cavities, or traction bronchiectasis is occasionally encountered (Fig 3). Apical pleural thickening associated with fibrosis may reveal proliferation of extrapleural fatty tissue and peripheral atelectasis at CT (17) (Fig 4).
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Figure 3. Fibrotic lungs in a 36-year-old man with postprimary tuberculosis. High-resolution CT scan shows parenchymal bands (arrows), traction bronchiectasis (arrowheads), and mild volume loss in both upper lobes. The large cystic lesions in the posterior aspects of both upper lobes represent cystic bronchiectasis. There is a spiculated, marginated, subpleural nodule (N) in the right upper lobe.
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Figure 4. Cicatrization atelectasis with apical pleural thickening in a 54-year-old man with postprimary tuberculosis. Contrast material-enhanced CT scan shows marked volume loss in the left upper lobe. There is associated proliferation of adjacent extrapleural fatty tissue (arrowheads).
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Complete destruction of a whole lung or a major part of a lung is not uncommon in the end stages of tuberculosis (Fig 5). Such damage results from a combination of parenchymal and airway involvement. It may result from a progressive primary infection or from postprimary tuberculosis with a prolonged process of cavitation, spread to new areas, and subsequent fibrosis (12). Secondary pyogenic or fungal infection may supervene. Once the lung is destroyed, the activity of tuberculosis is difficult to assess with radiologic studies (10).
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Figure 5a. Destruction of an entire lung in a 57-year-old man with postprimary tuberculosis who presented with fever and sputum. (a) Frontal radiograph shows marked volume loss in the left lung with several large cavities and multiple air-fluid levels (arrowheads). A small cavity is noted in the right upper lobe (arrow). (b) Contrast-enhanced CT scan shows marked shifting of the mediastinum toward the left side. The left lung is entirely destroyed and contains cavities with an air-fluid level (arrowheads), an appearance suggestive of superimposed bacterial infection.
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Figure 5b. Destruction of an entire lung in a 57-year-old man with postprimary tuberculosis who presented with fever and sputum. (a) Frontal radiograph shows marked volume loss in the left lung with several large cavities and multiple air-fluid levels (arrowheads). A small cavity is noted in the right upper lobe (arrow). (b) Contrast-enhanced CT scan shows marked shifting of the mediastinum toward the left side. The left lung is entirely destroyed and contains cavities with an air-fluid level (arrowheads), an appearance suggestive of superimposed bacterial infection.
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Aspergilloma
Approximately 25%–55% of patients with aspergilloma have a history of chronic cavitary tuberculosis. The prevalence of aspergilloma associated with chronic tuberculosis has been reported to be 11% (8). Although aspergilloma may exist for years without symptoms, hemoptysis is the most common clinical complication, with a prevalence of 50%–90% (18). Aspergilloma is usually located within a cavity or ectatic bronchus and consists of masses of fungal hyphae admixed with mucus and cellular debris (18–21).
At radiography, a mobile, rounded mass surrounded by a crescentic air shadow is noted inside a lung cavity (air-crescent sign) (Fig 6a). CT demonstrates a mobile fungus ball, usually with air interspersed between the masses of mycelia (Fig 6b). Calcification of the mycelial ball occurs in some cases (18–21). Thickening of the walls of tuberculous cavities or of the adjacent pleura is reported to be an early radiographic sign (8) (Fig 7).
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Figure 6a. Aspergilloma within a cavity in a 63-year-old man. (a) Frontal radiograph shows a mass of soft-tissue opacity with an air-crescent sign (arrowheads) in the left upper lobe. There are focal fibrotic and nodular areas of increased opacity (arrows) in the inferior aspect of the mass. (b) Contrast-enhanced CT scan shows a low-attenuation soft-tissue mass (M) within the cavity, along with the air-crescent sign (arrowheads).
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Figure 6b. Aspergilloma within a cavity in a 63-year-old man. (a) Frontal radiograph shows a mass of soft-tissue opacity with an air-crescent sign (arrowheads) in the left upper lobe. There are focal fibrotic and nodular areas of increased opacity (arrows) in the inferior aspect of the mass. (b) Contrast-enhanced CT scan shows a low-attenuation soft-tissue mass (M) within the cavity, along with the air-crescent sign (arrowheads).
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Figure 7a. Formation of an aspergilloma within a cavity in a 46-year-old man with no symptoms and no changes in clinical condition. (a) Initial frontal radiograph shows a thin-walled cavity (arrows) in the right upper lobe. Multiple scattered calcified granulomas are also noted. (b) Frontal radiograph obtained 20 months after a shows mild thickening of the inferior wall of the cavity (arrowheads). A bandlike area of increased opacity (arrows) has also appeared. (c, d) Frontal radiographs obtained 24 months (c) and 42 months (d) after a show a well-defined, oval mass of soft-tissue opacity (arrows) within the cavity.
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Figure 7b. Formation of an aspergilloma within a cavity in a 46-year-old man with no symptoms and no changes in clinical condition. (a) Initial frontal radiograph shows a thin-walled cavity (arrows) in the right upper lobe. Multiple scattered calcified granulomas are also noted. (b) Frontal radiograph obtained 20 months after a shows mild thickening of the inferior wall of the cavity (arrowheads). A bandlike area of increased opacity (arrows) has also appeared. (c, d) Frontal radiographs obtained 24 months (c) and 42 months (d) after a show a well-defined, oval mass of soft-tissue opacity (arrows) within the cavity.
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Figure 7c. Formation of an aspergilloma within a cavity in a 46-year-old man with no symptoms and no changes in clinical condition. (a) Initial frontal radiograph shows a thin-walled cavity (arrows) in the right upper lobe. Multiple scattered calcified granulomas are also noted. (b) Frontal radiograph obtained 20 months after a shows mild thickening of the inferior wall of the cavity (arrowheads). A bandlike area of increased opacity (arrows) has also appeared. (c, d) Frontal radiographs obtained 24 months (c) and 42 months (d) after a show a well-defined, oval mass of soft-tissue opacity (arrows) within the cavity.
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Figure 7d. Formation of an aspergilloma within a cavity in a 46-year-old man with no symptoms and no changes in clinical condition. (a) Initial frontal radiograph shows a thin-walled cavity (arrows) in the right upper lobe. Multiple scattered calcified granulomas are also noted. (b) Frontal radiograph obtained 20 months after a shows mild thickening of the inferior wall of the cavity (arrowheads). A bandlike area of increased opacity (arrows) has also appeared. (c, d) Frontal radiographs obtained 24 months (c) and 42 months (d) after a show a well-defined, oval mass of soft-tissue opacity (arrows) within the cavity.
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Bronchogenic Carcinoma
Bronchogenic carcinoma and pulmonary tuberculosis often coexist, creating a difficult diagnostic problem. Manifestations of carcinoma may be obscured or misinterpreted as progression of tuberculosis. Tuberculosis may favor the development of bronchogenic carcinoma by local mechanisms (scar cancer), or tuberculosis and carcinoma may be coincidentally associated. In addition, carcinoma may lead to reactivation of tuberculosis, both by eroding into an encapsulated focus and by decreasing the patient’s resistance (22–25). Therefore, any predominant or growing nodule should be suspicious for coexisting lung cancer in patients with tuberculosis (Fig 8).
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Figure 8a. Bronchogenic carcinoma with postprimary tuberculosis in a 67-year-old man. (a) Contrast-enhanced CT scan shows a lobulated mass with eccentric calcifications (white arrows) in the right upper lobe. There is pleural (arrowheads) and extrapleural (black arrows) fat thickening adjacent to the mass. (b) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows mixed foci of caseation necrosis of tuberculosis (C) and tumor cells of adenocarcinoma (arrows).
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Figure 8b. Bronchogenic carcinoma with postprimary tuberculosis in a 67-year-old man. (a) Contrast-enhanced CT scan shows a lobulated mass with eccentric calcifications (white arrows) in the right upper lobe. There is pleural (arrowheads) and extrapleural (black arrows) fat thickening adjacent to the mass. (b) Photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows mixed foci of caseation necrosis of tuberculosis (C) and tumor cells of adenocarcinoma (arrows).
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Airway Lesions
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Bronchiectasis
Bronchiectasis may develop as a result of tuberculous involvement of the bronchial wall and subsequent fibrosis. Bronchiectasis is seen in 30%–60% of patients with active postprimary tuberculosis and in 71%–86% of patients with inactive disease at high-resolution CT (26,27). Although bronchiectasis in postprimary tuberculosis can be a result of cicatricial bronchostenosis after local infection (Fig 3), more commonly it occurs by destruction and fibrosis of the lung parenchyma with secondary bronchial dilatation (traction bronchiectasis) (Fig 9). Bronchiectasis located in the apical and posterior segments of the upper lobe is highly suggestive of a tuberculous origin (Figs 3, 10). When multiple apical cavities are encountered, the possibility that cystic bronchiectasis is present in addition to necrotic cavities must be considered (8,26–28).
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Figure 9. Traction bronchiectasis in a 52-year-old man. High-resolution CT scan shows dilatation of bronchi (black arrows) within the collapsed right upper lobe. There is a granuloma in the left upper lobe (white arrow).
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Figure 10. Bronchial dilatation with mucoid impaction in tuberculous bronchostenosis in a 42-year-old woman. Contrast-enhanced CT scan shows dilated bronchi with mucoid impaction (arrowheads) in the left upper lobe. A calcified granuloma (arrow) is noted in the posterior segment of the left upper lobe.
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Tracheobronchial Stenosis
Tracheobronchial stenosis resulting from tuberculosis may be caused by granulomatous changes in the tracheobronchial wall or by extrinsic pressure from enlarged peribronchial lymph nodes. Endobronchial involvement occurs in approximately 2%–4% of patients with pulmonary tuberculosis (6). In tracheobronchial tuberculosis, the stenosis begins as simple erythema and edema with lymphocytic infiltration of the submucosa followed by tubercle formation. Extensive granulation tissue destroying and replacing the mucosa and submucosa and subsequent fibrosis may result in tracheobronchial narrowing. The left main bronchus is most frequently involved in fibrotic disease (29–32).
On CT scans, irregular luminal narrowing with wall thickening, enhancement, and enlarged adjacent mediastinal nodes are common findings in the active stage of stenosis. The CT findings include concentric narrowing of the lumen, uniform thickening of the wall, and involvement of a long bronchial segment in the fibrotic stage (Fig 11a). Multiplanar and three-dimensional images are helpful in understanding tracheobronchial status, particularly for evaluation of focal stenosis of the airways and the longitudinal extent of tracheobronchial lesions (32) (Fig 11b).
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Figure 11a. Tracheobronchial stenosis in a 40-year-old woman. (a) Contrast-enhanced CT scan shows narrowing of the left main bronchus (arrow) without significant wall thickening, enhancement, or calcification. (b) Coronal three-dimensional reconstruction image created with shaded-surface display shows mild narrowing of the distal trachea (arrowheads) and occlusion and irregular narrowing of the left main bronchus (arrows).
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Figure 11b. Tracheobronchial stenosis in a 40-year-old woman. (a) Contrast-enhanced CT scan shows narrowing of the left main bronchus (arrow) without significant wall thickening, enhancement, or calcification. (b) Coronal three-dimensional reconstruction image created with shaded-surface display shows mild narrowing of the distal trachea (arrowheads) and occlusion and irregular narrowing of the left main bronchus (arrows).
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Broncholithiasis
Broncholithiasis is an uncommon complication of pulmonary tuberculosis and is defined as the presence of calcified or ossified material within the lumen of the tracheobronchial tree. The calcific nidus in a tuberculous lymph node erodes into the bronchial wall and may occlude the bronchus (33). Presenting symptoms may include cough, hemoptysis, wheezing, or evidence of recurrent pneumonia (33–35).
Radiographic manifestations of broncholithiasis include a change in the position or disappearance of a calcific focus on serial radiographs or development of airway obstruction, resulting in lobar or segmental atelectasis, mucoid impaction, or expiratory air trapping. CT shows a calcified lymph node that is either endobronchial or peribronchial and is associated with findings of bronchial obstruction, such as atelectasis, obstructive pneumonitis, or bronchiectasis (34,35) (Fig 12).
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Figure 12. Broncholithiasis in a 58-year-old man who presented with a cough. Contrast-enhanced CT scan shows a broncholith (arrowhead) within the lateral segmental bronchus of the right middle lobe. There is distal obstructive atelectasis and calcified lymph nodes (arrows) adjacent to the bronchi. A right pleural effusion is noted.
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Vascular Complications
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Pulmonary arteries and veins in an area of active tuberculous infection may demonstrate vasculitis and thrombosis; thus, acid-fast staining should be performed in any case of necrotizing granulomatous pulmonary vasculitis to exclude a tuberculous cause (8). Bronchial arteries may be enlarged in bronchiectasis associated with tuberculosis or in parenchymal tuberculosis itself (36,37). High-resolution CT has been regarded as the imaging modality of choice in patients suspected of having bronchiectasis. In patients with bronchiectasis, nodular and tubular structures with an appearance unlike that of lymph nodes or normal vessels in the mediastinum and around the central airway on high-resolution CT scans are suggestive of hypertrophied bronchial arteries (Fig 13). Recognition of this finding is important so that the bronchoscopist will not biopsy the hypertrophied bronchial arteries protruding into the airway lumen (36).
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Figure 13a. Hypertrophied bronchial artery in a 53-year-old man who presented with hemoptysis. (a) Nonenhanced CT scan shows nodular structures in the subcarinal region (arrows). Atelectasis with traction bronchiectasis (arrowheads) is noted in the superior segment of the right lower lobe. (b) Bronchial arteriogram shows a dilated and tortuous right bronchial artery (arrows).
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Figure 13b. Hypertrophied bronchial artery in a 53-year-old man who presented with hemoptysis. (a) Nonenhanced CT scan shows nodular structures in the subcarinal region (arrows). Atelectasis with traction bronchiectasis (arrowheads) is noted in the superior segment of the right lower lobe. (b) Bronchial arteriogram shows a dilated and tortuous right bronchial artery (arrows).
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Rasmussen aneurysm is a rare phenomenon caused by weakening of the pulmonary artery wall from adjacent cavitary tuberculosis (Figs 14, 15). A review of autopsy findings in patients with a history of chronic cavitary tuberculosis showed a 5% prevalence of Rasmussen aneurysm (38). Hemoptysis is the usual presenting symptom and may be life-threatening when it is massive. Progressive weakening of the arterial wall occurs as granulation tissue replaces both the adventitia and the media. The granulation tissue in the vessel wall is then gradually replaced by fibrin, resulting in thinning of the arterial wall, pseudoaneurysm formation, and subsequent rupture (38,39).
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Figure 14a. Rasmussen aneurysm in a 62-year-old man who presented with a cough. (a) Contrast-enhanced CT scan shows a round, enhancing, 1.6 x 1.1-cm lesion (arrowhead) within the consolidated left upper lobe. (b) Left subclavian arteriogram shows contrast material filling the aneurysm (arrow), the origin of which was uncertain. Antituberculous medication was given. The consolidation and the aneurysm resolved.
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Figure 14b. Rasmussen aneurysm in a 62-year-old man who presented with a cough. (a) Contrast-enhanced CT scan shows a round, enhancing, 1.6 x 1.1-cm lesion (arrowhead) within the consolidated left upper lobe. (b) Left subclavian arteriogram shows contrast material filling the aneurysm (arrow), the origin of which was uncertain. Antituberculous medication was given. The consolidation and the aneurysm resolved.
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Figure 15a. Rasmussen aneurysm in a 43-year-old man who presented with a mild fever and a cough. (a) Contrast-enhanced CT scan shows an enhancing, ovoid, 3.0 x 2.2-cm nodular lesion (arrow) arising from a branch of the pulmonary artery (arrowhead). A left pleural effusion is noted. There is a large cavity with an air-fluid level in the right middle lobe. (b) Contrast-enhanced CT scan obtained after 9 months of treatment with antituberculous medication shows that the aneurysm has disappeared. The extent of the left pleural effusion is slightly increased.
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Figure 15b. Rasmussen aneurysm in a 43-year-old man who presented with a mild fever and a cough. (a) Contrast-enhanced CT scan shows an enhancing, ovoid, 3.0 x 2.2-cm nodular lesion (arrow) arising from a branch of the pulmonary artery (arrowhead). A left pleural effusion is noted. There is a large cavity with an air-fluid level in the right middle lobe. (b) Contrast-enhanced CT scan obtained after 9 months of treatment with antituberculous medication shows that the aneurysm has disappeared. The extent of the left pleural effusion is slightly increased.
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Mediastinal Lesions
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Lymph Node Calcification and Extranodal Extension
Tuberculous mediastinal lymphadenitis is a frequent manifestation of primary pulmonary tuberculosis. Although enlarged nodes occur in 83%–96% of pediatric cases, the prevalence of lymphadenopathy decreases with increasing age (40–42). Pubertal and young adult women, the elderly, and patients with acquired immunodeficiency syndrome are the most commonly affected among adult patients (43). Tuberculous mediastinal lymphadenitis is caused by the formation of tuberculous caseating granulomas in lymph nodes, which more commonly involves the right side. In the active stage, the nodes have central low attenuation and peripheral rim enhancement at CT, which correspond to caseation or liquefaction necrosis and granulation tissue with inflammatory hypervascularity, respectively, at pathologic analysis. With treatment, the nodes change in appearance, first becoming homogeneous and finally disappearing or resulting in a residual mass composed of fibrotic tissue and calcifications without low-attenuation areas (44,45) (Fig 16). Extranodal extension may occur into adjacent structures such as the bronchus, pericardium, and esophagus (Figs 17–21).
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Figure 16a. Lymph node calcification in a 29-year-old woman with primary tuberculosis. (a) Contrast-enhanced CT scan shows an enlarged lymph node with areas of low attenuation and calcification in the right paratracheal region. (b) CT scan obtained after treatment with antituberculous medication shows that the lymph node (arrow) is smaller and the calcification is denser.
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Figure 16b. Lymph node calcification in a 29-year-old woman with primary tuberculosis. (a) Contrast-enhanced CT scan shows an enlarged lymph node with areas of low attenuation and calcification in the right paratracheal region. (b) CT scan obtained after treatment with antituberculous medication shows that the lymph node (arrow) is smaller and the calcification is denser.
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Figure 17. Extranodal extension into the bronchus in a 74-year-old woman. Nonenhanced CT scan shows calcified lymph nodes in the pretracheal area (arrows) and an irregular area of air attenuation (arrowheads) communicating with the carina.
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Figure 18a. Extranodal extension into adjacent lung parenchyma in a 19-year-old man who presented with acute chest pain. (a) Frontal chest radiograph shows right-sided paratracheal bulging (arrows), which is suggestive of lymph node enlargement. (b) Frontal chest radiograph obtained 2 months after a shows consolidation in the right upper lobe (arrows). (c) Contrast-enhanced CT scan shows a poorly marginated, enlarged right paratracheal lymph node with foci of low attenuation (arrowheads).
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Figure 18b. Extranodal extension into adjacent lung parenchyma in a 19-year-old man who presented with acute chest pain. (a) Frontal chest radiograph shows right-sided paratracheal bulging (arrows), which is suggestive of lymph node enlargement. (b) Frontal chest radiograph obtained 2 months after a shows consolidation in the right upper lobe (arrows). (c) Contrast-enhanced CT scan shows a poorly marginated, enlarged right paratracheal lymph node with foci of low attenuation (arrowheads).
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Figure 18c. Extranodal extension into adjacent lung parenchyma in a 19-year-old man who presented with acute chest pain. (a) Frontal chest radiograph shows right-sided paratracheal bulging (arrows), which is suggestive of lymph node enlargement. (b) Frontal chest radiograph obtained 2 months after a shows consolidation in the right upper lobe (arrows). (c) Contrast-enhanced CT scan shows a poorly marginated, enlarged right paratracheal lymph node with foci of low attenuation (arrowheads).
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Figure 19a. Esophagomediastinal fistula in a 59-year-old man who presented with chest pain. (a) Contrast-enhanced CT scan shows linear or small oval gas collections (arrows) in an enlarged right paratracheal lymph node. There is a communication (arrowhead) between the esophagus and a mediastinal area of air attenuation. (b) Esophagogram shows irregular barium leakage outlining the fistula (arrows).
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Figure 19b. Esophagomediastinal fistula in a 59-year-old man who presented with chest pain. (a) Contrast-enhanced CT scan shows linear or small oval gas collections (arrows) in an enlarged right paratracheal lymph node. There is a communication (arrowhead) between the esophagus and a mediastinal area of air attenuation. (b) Esophagogram shows irregular barium leakage outlining the fistula (arrows).
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Figure 20. Esophagobronchopleural fistula in a 63-year-old woman who presented with dysphagia and fever. Contrast-enhanced CT scan shows pleural thickening with calcification and extrapleural fat proliferation and foci of air (arrowheads) within the pleural cavity. There is a communication (short arrows) between the area of parenchymal consolidation and the pleural cavity. Esophageal air is noted (long arrow).
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Figure 21a. Tuberculous pericarditis in a 53-year-old man. (a) Contrast-enhanced CT scan shows enlarged lymph nodes (arrows) in the right lower paratracheal and aorticopulmonary window areas. Bilateral pleural effusions are noted. (b) Contrast-enhanced CT scan shows marked thickening of the pericardium (arrows) with a small amount of fluid in the pericardial cavity.
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Figure 21b. Tuberculous pericarditis in a 53-year-old man. (a) Contrast-enhanced CT scan shows enlarged lymph nodes (arrows) in the right lower paratracheal and aorticopulmonary window areas. Bilateral pleural effusions are noted. (b) Contrast-enhanced CT scan shows marked thickening of the pericardium (arrows) with a small amount of fluid in the pericardial cavity.
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Esophagomediastinal Fistula
Esophageal involvement by tuberculosis is rare. The most common cause of esophageal tuberculosis is secondary involvement from adjacent tuberculous lymphadenitis. Esophageal involvement results in strictures due to granulomatous inflammatory tissue in active disease and scar tissue after healing, tracheobronchial or mediastinal fistulas, and traction diverticula (8,46). Presenting symptoms may include fever, cough, weight loss, dysphagia, chest discomfort, or back pain. The preferential involvement of the subcarinal region occurs mainly because of the anatomic proximity of the esophagus to diseased lymph nodes (47). When tuberculous lymph nodes erode the adjacent esophageal or bronchial wall, an esophagonodal or esophagobronchial fistula may be formed, which manifests as a localized gaseous collection within the mediastinum (46,47) (Figs 19, 20).
Pericardial Tuberculosis
Tuberculous pericarditis is reported to complicate up to 1% of cases of tuberculosis (48). Pericardial involvement is commonly caused by extranodal extension of tuberculous lymphadenitis into the pericardium because of the close anatomic relationship between the lymph nodes and the posterior pericardial sac. The pericardium can also be involved in miliary spread of the disease (12). At CT, lymphadenopathy and pericardial thickening with or without effusion may be seen (Fig 21).
Constrictive pericarditis occurs in about 10% of patients with tuberculous pericarditis. It is characterized by fibrous or calcific constrictive thickening of the pericardium, which prevents normal diastolic filling of the heart (49). CT shows pericardial thickening of more than 3 mm with or without pericardial effusion. Secondary CT findings are dilatation of the inferior vena cava secondary to right-sided heart failure and acute angulation or sinus configuration of the interventricular septum, which may be related to redundancy of the septum secondary to the restriction of expansion of the pericardium (49). Visceral pericardial calcification may occur at the atrioventricular grooves, the interventricular grooves, or especially the crux of the heart (49) (Fig 22).
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Figure 22a. Constrictive pericarditis in a 48-year-old woman. (a) Lateral chest radiograph shows dense calcification in the anterior and inferior portions of the pericardium (arrows). (b) Contrast-enhanced CT scan shows a densely calcified mass in the anterior portion of the pericardium (arrow). Note the acute angulation of the interventricular septum (arrowheads) and the dilatation of the atria (A).
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Figure 22b. Constrictive pericarditis in a 48-year-old woman. (a) Lateral chest radiograph shows dense calcification in the anterior and inferior portions of the pericardium (arrows). (b) Contrast-enhanced CT scan shows a densely calcified mass in the anterior portion of the pericardium (arrow). Note the acute angulation of the interventricular septum (arrowheads) and the dilatation of the atria (A).
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Fibrosing Mediastinitis
Fibrosing mediastinitis is uncommon and involves the presence of excessive fibrosis in the mediastinum (50). Although tuberculosis is an important cause of chronic mediastinitis, tuberculous mediastinitis is rare; the most common cause of mediastinitis is histoplasmosis (51). Tuberculous mediastinitis progresses insidiously without significant clinical symptoms and may result in mild symptoms, including cough and low-grade fever, and symptoms due to compression of the superior vena cava, esophagus, and tracheobronchial tree (52). The mediastinal granulomatous lymph nodes coalesce, and the development of multiple tuberculous granulomas creates both reactive fibrous changes and acute inflammatory changes in the mediastinum. The granulomas evolve into fibrosing mediastinitis when reactive changes predominate (50).
The radiographic findings include mediastinal widening or a localized mass. CT findings include a mediastinal or hilar mass, calcification in the mass, tracheobronchial narrowing, pulmonary vessel encasement, superior vena cava obstruction, and pulmonary infiltrates (Fig 23). Pulmonary lesions in fibrosing mediastinitis may be caused by bronchial obstruction with subsequent obstructive pneumonia or atelectasis or by obstruction of major pulmonary veins with resultant pulmonary infarction (50,52).
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Figure 23. Fibrosing mediastinitis in a 41-year-old woman. Contrast-enhanced CT scan shows a soft-tissue lesion adjacent to the bronchi of the right middle lobe and left lower lobe, resulting in smooth narrowing of the airway (arrows). The linear lesions with high attenuation in the left parahilar regions (arrowheads) represent vascular enhancement within the collapsed superior segment of the left lower lobe.
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Pleural Lesions
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Chronic Tuberculous Empyema and Fibrothorax
Pleural infection is usually caused by rupture of a subpleural caseous focus into the pleural space; less commonly, it is caused by hematogenous dissemination and contamination by adjacent infected lymph nodes. Tuberculous pleurisy progresses to become chronic tuberculous empyema, which may be defined as persistent, grossly purulent pleural fluid containing tubercle bacilli (53–57). However, it may be difficult to culture the bacilli in chronic empyema.
In chronic tuberculous empyema, CT scans show a focal fluid collection with pleural thickening and calcification and with or without extrapleural fat proliferation (Fig 24). Fibrothorax with diffuse pleural thickening but without effusion on CT scans suggests inactivity (Fig 24) (55–57). Chyliform or pseudochylous pleural effusion is a high-lipid nonchylous effusion and is most commonly caused by tuberculous empyema. The diseased pleura may result in an abnormally slow transfer of cholesterol and other lipids, originating from degenerated red and white blood cells, out of the pleural space and lead to accumulation of cholesterol in the pleural fluid (58,59). CT shows a fat-fluid or fat-calcium level (Fig 25).
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Figure 24. Chronic empyema and fibrothorax in a 44-year-old man. Contrast-enhanced CT scan shows pleural thickening with parietal pleural calcification (arrowheads) and a fluid collection in the right hemithorax. Extrapleural fat thickening is noted, which is suggestive of chronicity. There is pleural thickening with interrupted calcification in the left hemithorax (arrows).
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Figure 25a. Chronic empyema with pseudochyle and milk of calcium in a 71-year-old man. (a) Contrast-enhanced CT scan shows a fluid collection in the right hemithorax with visceral and parietal pleural calcification. A small area of fat attenuation (arrow) is noted in the nondependent portion of the fluid collection (so-called pseudochyle). (b, c) Contrast-enhanced CT scans obtained with the patient supine (b) and prone (c) show shifting of the fluid-calcification level (arrowheads) according to the patient’s position.
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Figure 25b. Chronic empyema with pseudochyle and milk of calcium in a 71-year-old man. (a) Contrast-enhanced CT scan shows a fluid collection in the right hemithorax with visceral and parietal pleural calcification. A small area of fat attenuation (arrow) is noted in the nondependent portion of the fluid collection (so-called pseudochyle). (b, c) Contrast-enhanced CT scans obtained with the patient supine (b) and prone (c) show shifting of the fluid-calcification level (arrowheads) according to the patient’s position.
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Figure 25c. Chronic empyema with pseudochyle and milk of calcium in a 71-year-old man. (a) Contrast-enhanced CT scan shows a fluid collection in the right hemithorax with visceral and parietal pleural calcification. A small area of fat attenuation (arrow) is noted in the nondependent portion of the fluid collection (so-called pseudochyle). (b, c) Contrast-enhanced CT scans obtained with the patient supine (b) and prone (c) show shifting of the fluid-calcification level (arrowheads) according to the patient’s position.
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Bronchopleural Fistula
Bronchopleural fistula associated with tuberculosis usually follows trauma or a surgical procedure but can also occur spontaneously, presumably due to an open pathway between bronchus and pleura established by tuberculosis. High mortality can result from both the acute and chronic phases. The former occurs because of toxicity, spread of disease, and tension pneumothorax; the latter progresses to repeat small seedings and massive aspiration of empyema fluid (60). The diagnosis is based on an increasing amount of sputum production, air in the pleural space, a changing air-fluid level, and contralateral spread of pneumonic infiltration. CT can demonstrate the sites of communication between the pleural space and either one or more airways or the lung parenchyma in patients with bronchopleural fistula (61) (Fig 26).
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Figure 26a. Bronchopleural fistula in a 49-year-old man. (a) Frontal chest radiograph shows consolidation with a cavity in the right upper lobe (arrow). There are patchy and nodular areas of increased opacity in the left middle lung zone (arrowheads). (b) Frontal radiograph obtained 2 months after a shows multiple air-fluid levels in the right hemithorax (arrowheads). (c) Contrast-enhanced CT scan shows consolidation in the anterior segment of the right upper lobe with peripheral bronchiectasis that communicates directly (arrow) with the pleural space (P).
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Figure 26b. Bronchopleural fistula in a 49-year-old man. (a) Frontal chest radiograph shows consolidation with a cavity in the right upper lobe (arrow). There are patchy and nodular areas of increased opacity in the left middle lung zone (arrowheads). (b) Frontal radiograph obtained 2 months after a shows multiple air-fluid levels in the right hemithorax (arrowheads). (c) Contrast-enhanced CT scan shows consolidation in the anterior segment of the right upper lobe with peripheral bronchiectasis that communicates directly (arrow) with the pleural space (P).
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Figure 26c. Bronchopleural fistula in a 49-year-old man. (a) Frontal chest radiograph shows consolidation with a cavity in the right upper lobe (arrow). There are patchy and nodular areas of increased opacity in the left middle lung zone (arrowheads). (b) Frontal radiograph obtained 2 months after a shows multiple air-fluid levels in the right hemithorax (arrowheads). (c) Contrast-enhanced CT scan shows consolidation in the anterior segment of the right upper lobe with peripheral bronchiectasis that communicates directly (arrow) with the pleural space (P).
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Pneumothorax
Pneumothorax secondary to tuberculosis often heralds severe and extensive pulmonary involvement by the infectious process and the onset of bronchopleural fistula and empyema. It occurs in approximately 5% of patients with postprimary tuberculosis, usually in severe cavitary disease (Fig 27) but rarely in miliary tuberculosis (Fig 28). The pathogenesis involves pleural caseous infiltrates that undergo liquefaction, resulting in pleural necrosis and rupture. If any apical abnormality is seen after reexpansion of a spontaneous pneumothorax, active tuberculosis should be considered. In some cases, the lung will seal and reexpand over a long period in response to chemotherapy. However, tube drainage is the treatment of choice (62,63).
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Figure 27. Spontaneous pneumothorax in a 47-year-old man with extensive pulmonary tuberculosis. High-resolution CT scan shows extensive areas of consolidation and cavities in both upper lobes. Pneumothorax is noted in the left hemithorax and was treated with insertion of a thoracostomy tube (arrow).
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Figure 28. Spontaneous pneumothorax in a 23-year-old woman with miliary tuberculosis. High-resolution CT scan shows tiny nodules scattered throughout both lungs. Pneumothorax is noted in the right hemithorax.
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Chest Wall Lesions
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Chest Wall Tuberculosis
Tuberculosis occasionally involves the sternum, the sternoclavicular joint, or a rib, leading to osseous destruction and localized abscess formation. Such involvement may occur by direct extension from a pleuropulmonary tuberculous lesion or by hematogenous spread from a distant focus (64,65). When spontaneous discharge of empyema through the parietal pleura into the chest wall forms a subcutaneous abscess, it is termed empyema necessitatis (66).
Tuberculosis of the chest wall is characterized by bone or costal cartilage destruction and soft-tissue masses that may demonstrate calcification or rim enhancement with or without evidence of underlying lung or pleural disease at CT (64,65) (Fig 29). Bone or cartilage may be intact in chest wall tuberculosis (64). Rarely, it is associated with development of retromammary or intramammary tuberculous abscesses (Fig 30).
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Figure 29a. Chest wall tuberculosis in a 38-year-old woman. (a) Contrast-enhanced CT scan shows a multiloculated mass with low attenuation and peripheral rim enhancement (arrows) in both the intracostal and extracostal portions of the right side of the back. There is an extrapleural nodule adjacent to the ribs in a more anterior portion (arrowhead). (b) Contrast-enhanced CT scan obtained 1 year after a after radical excision and débridement and treatment with antituberculous medication shows a chest wall abscess (arrowheads) at the site of the extrapleural nodule. Sclerotic change of the adjacent rib is noted (arrow). Note the soft-tissue defect in the right lateral thoracic wall due to surgery.
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Figure 29b. Chest wall tuberculosis in a 38-year-old woman. (a) Contrast-enhanced CT scan shows a multiloculated mass with low attenuation and peripheral rim enhancement (arrows) in both the intracostal and extracostal portions of the right side of the back. There is an extrapleural nodule adjacent to the ribs in a more anterior portion (arrowhead). (b) Contrast-enhanced CT scan obtained 1 year after a after radical excision and débridement and treatment with antituberculous medication shows a chest wall abscess (arrowheads) at the site of the extrapleural nodule. Sclerotic change of the adjacent rib is noted (arrow). Note the soft-tissue defect in the right lateral thoracic wall due to surgery.
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Figure 30. Chest wall abscess in the retromammary area in a 42-year-old woman. Contrast-enhanced CT scan shows a mass with low attenuation and peripheral enhancement (M) in the pectoralis muscle under the right breast. The abscess has an intracostal portion with calcifications (arrows). Excision of the mass was performed.
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Tuberculous Spondylitis
Tuberculous spondylitis (Pott disease) is caused primarily by hematogenous spread of pulmonary infection and most commonly affects the lower thoracic and upper lumbar spine. The early radiographic manifestations of spinal involvement consist of irregularity of the vertebral end plates, decreased height of the intervertebral disk space, and sclerosis of the adjacent bone. With progression of disease, there is a tendency toward anterior wedging of the vertebral body, leading to kyphosis and development of a paravertebral abscess. CT demonstrates paravertebral abscesses with peripheral rim enhancement and low-attenuation centers after enhancement (Fig 31) (67–69).
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Figure 31. Tuberculous spondylitis in a 37-year-old man who presented with back pain. Contrast-enhanced CT scan shows a paravertebral abscess (arrows) with destruction of the lower thoracic spine. There is an associated left pleural effusion with pleural enhancement.
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Malignancy Associated with Chronic Empyema
Malignancy associated with chronic empyema, especially tuberculous empyema, is rare (70–72). The mean duration of chronic empyema before diagnosis of malignancy is reported to be about 25 years. The histopathologic diagnoses in reported cases have been malignant lymphoma, squamous cell carcinoma, mesothelioma, malignant fibrous histiocytoma, liposarcoma, rhabdo-myosarcoma, angiosarcoma, and hemangioendothelioma, in order of frequency (72). The pathogenesis of malignancy developing in chronic empyema may be a long-standing severe inflammatory process of a nonautoimmune nature in malignant lymphoma or chronic stimulation of mesothelial cells or the action of oncogenic substances contained in the pleura in other malignancy, including mesothelioma (70,71,73).
Radiographic findings that suggest the occurrence of malignancy include increased opacity in the thoracic cavity, soft-tissue bulging and blurring of fat planes in the chest walls, destruction of bone near the empyema, and extensive medial deviation of the calcified pleurae (72). CT can demonstrate an abnormal mass with soft-tissue attenuation around the empyema and usually shows enhancement of the mass (Fig 32). Biopsy is necessary because differentiation between malignancy and infection is rather difficult.
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Figure 32. Malignant lymphoma associated with chronic tuberculous empyema in a 77-year-old man with a 35-year history of chronic tuberculous empyema. Contrast-enhanced CT scan shows a lobulated mass with low attenuation and peripheral irregular enhancement (L) in the posterior portion of the right chest wall. Calcified thickened parietal pleura (arrows) and extrapleural fatty tissue are seen.
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Conclusions
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Various forms of thoracic sequelae and complications may result from tuberculosis and may involve the lungs, airways, vessels, mediastinum, pleura, chest wall, or any combination of these structures. Knowledge of the full spectrum of radiologic features of the sequelae and complications of tuberculosis in pulmonary and extrapulmonary portions of the thorax is important to facilitate diagnosis.
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Footnotes
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See the commentary by Katz
following this article.
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LEARNING OBJECTIVES FOR TEST...
