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Original Report |
1
Department of Radiology and the Institute of Radiation Medicine MRC, Seoul
National University, College of Medicine, #28, Yongon-dong, Chongno-gu, Seoul,
110-744, Korea.
2
Department of Internal Medicine, Seoul National University, College of
Medicine, Seoul, 110-744, Korea.
Received March 15, 1999;
accepted after revision July 9, 1999.
Address correspondence to J.-G. Im.
Abstract
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CONCLUSION. Atelectasis caused by smooth bronchial narrowing, surrounded by calcified or noncalcified lymph nodes, in elderly and nonsmoking women is a typical finding of anthracofibrosis. Calcified lymph nodes adjacent to the involved bronchi and multifocal involvement of bronchial narrowing may be helpful in differentiating this condition from lung cancer.
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This group of 54 patients was composed of 16 men and 38 women who ranged in age from 33 to 78 years old (mean, 67 years). The patients were all Korean. Forty-six patients (85%) were non-smokers. No patients had an occupational history of exposure to mining or industry, except for two patients who were exposed to coal dust for 3 and 5 years. The severity and extent of dark pigmentation on bronchoscopy did not differ between the patients with and those without a history of occupational coal dust exposure. Thirty-three patients lived in urban areas, and the rest in rural areas. Thirty-two patients (59%), including two patients with pneumoconiosis, had a history of tuberculosis, and the diagnosis was confirmed pathologically (n = 10), bacteriologically (n = 12), and clinically through improvement of clinical symptoms and on chest radiographs after antituberculous medication (n = 10). Presenting clinical symptoms were cough, sputum, dyspnea, hemoptysis, chest pain, fever, and general weakness, in order of frequency.
CT was performed before bronchoscopy to evaluate lung lesions such as consolidation or masslike opacities seen on chest radiographs. CT scans were obtained using either a 9800 or a HiSpeed scanner (General Electric Medical Systems, Milwaukee, WI). Thick-section CT scans with 10-mm collimation at 10-mm intervals were obtained on the 9800 scanner (n = 24) and 7-mm collimation at 7-mm intervals (1:1 pitch) were obtained on the HiSpeed scanner (n = 21). Scanning was performed in 45 patients with (n = 39) or without (n = 6) the administration of IV contrast medium. High-resolution CT was performed in nine patients at 10-mm intervals with 1-mm collimation.
CT scans were retrospectively reviewed by two chest radiologists and a consensus was reached. These radiologists were aware of the diagnosis of bronchial anthracofibrosis but were unaware of the sites of the lesions and the findings on bronchoscopy. The CT analysis included the location of the lesion, bronchial narrowing, lymph nodes adjacent to the bronchi (presence or absence, size, and calcification), and associated lung parenchyma lesions.
Bronchial narrowing was designated as the presence of focal or diffuse narrowing of the lumen as compared with its proximal and distal bronchi for vertically oriented bronchi, or with the adjacent same-order bronchus for horizontally or obliquely oriented bronchi. When the imaged planes were not centered on the bronchus, it was not considered to be narrowed. Mediastinal and hilar lymph nodes, either with or without calcification, were considered to be enlarged when larger than 1 cm and 0.5 cm, respectively, in the short diameter.
The original radiology reports were reviewed, and the radiologic diagnosis included tuberculosis (n = 30); lung cancer (n = 7); atelectasis (n = 7); and inflammatory lesions including pneumonia (n = 6), bronchiectasis (n = 2), and pneumoconiosis (n = 2).
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On CT, bronchial narrowing or atelectasis was observed in 94% of patients (n = 51) with abnormalities seen on bronchoscopy. The most common CT finding was atelectasis distal to the smoothly narrowed bronchus (Table 1). Bronchial narrowing with distal atelectasis was noted in 39 patients. In eight patients, despite the evidence of lung parenchyma abnormalities, the bronchial abnormality was not identified on CT. Bronchial narrowing without distal atelelectasis was noted in four patients.
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Smooth narrowing of the bronchi was noted in 43 patients (80%) (Figs. 1A, 1B and 2A, 2B, 2C). Of the 28 patients with bronchoscopic findings of multiple site involvement, 16 (57%) showed CT findings of bronchial narrowing. Bronchial wall thickening was noted in 16 patients (Fig. 3A, 3B); 13 patients showed these findings in more than one bronchus. No demonstrable endobronchial nodular lesion was seen in the involved bronchi except in one patient who had a focal obstructive lesion containing calcification in the right middle lobe bronchus (Fig. 4).
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The mediastinal lymph nodes were 0.5-4 cm (mean, 1.4 cm) in diameter, and the hilar lymph nodes were 0.3-2 cm (mean, 0.9 cm). Enlarged lymph nodes were noted in the mediastinal (n = 31, 57.4%), both mediastinal and the hilar (n = 17, 31.5%), and the hilar (n = 3, 5.6%) areas. Of the 51 patients (94%) who had enlarged mediastinal or hilar lymph nodes, 29 (57%) had calcification within the nodes (Figs. 2A, 2B, 2C and 3A, 3B).
Other associated findings in the lung included fibrotic bands (46%), nodules (41%), and bronchiectasis (30%), all of which were suggestive of old pulmonary tuberculous lesions. These findings were seen in 41 patients (76%) and were located in areas distal to either the involved (n = 24, 59%) or the uninvolved (n = 17, 41%) bronchi.
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On CT, a segmental collapse distal to the involved bronchi was the most common finding. The right middle lobe was the most frequently involved lobe (51%), followed by the right upper, left upper, lingular division, right lower, and left lower lobe bronchi, in order of frequency. Bronchial narrowing, commonly accompanied by thickening of the wall, was noted in 80% of patients. Enlarged mediastinal or hilar lymph nodes adjacent to the involved bronchi were noted in nearly all patients (94%), and calcified nodes adjacent to the bronchi supplying the atelectatic lung were seen in 56% of patients. The bronchial abnormalities on CT images, such as thickening of the wall or narrowing of the lumen, were noted in 80% of the patients. In our study, CT scans with thin sections through the central bronchi were not obtained specifically for evaluating bronchial obstruction. We suggested proximal bronchial abnormalities caused by atelectasis on the basis of CT scans in eight patients. Though we did not examine the patients with contiguous thin-section CT with two-dimensional reformation or three-dimensional reconstruction, two-dimensional or three-dimensional images might have shown the bronchial narrowing more comprehensively.
Establishing the origin of anthracotic pigments and the cause for bronchial stenosis in each patient is difficult. Nevertheless, several findings indicate that bronchial tuberculosis is one of the most likely causes for the development of bronchial anthracofibrosis. Those findings are the association of either active (41-61%) or old stable pulmonary tuberculosis (12%) with anthracofibrosis [1, 5], the reported evidence of development of the anthracotic pigmentation during the course of antituberculous chemotherapy [5], and similar CT findings between bronchial tuberculosis and anthracofibrosis [6, 7]. CT findings of bronchial tuberculosis and anthracofibrosis include bronchial narrowing or obstruction, thickening of the wall or peribronchial cuffing, endobronchial low-attenuation nodule, and lymphadenitis compressing the bronchi. In cases of the fibrotic stage of bronchial tuberculosis, the involved bronchi become smooth and thin-walled [6], which also resembles bronchial anthracofibsosis.
The reason our patients are mostly elderly women may be explained by the fact that tuberculous lymphadenitis and endobronchial tuberculosis are common in young women [8], whereas a fibrotic response is more prevalent in elderly patients [1]. Perforation of a tuberculous lymph node into the bronchus may develop insidiously, and the healing process may appear without apparent clinical symptoms in the aged population [1].
The black pigments in the bronchial wall might be derived from anthracotic material in the adjacent lymph nodes, which might subsequently be incorporated into the scarred area of the bronchus. The involved lymph nodes, however, may perforate into the adjacent bronchi, and carbon particles in the lymph nodes may penetrate through the bronchial wall as deep as the mucosa, resulting in coloring of the bronchial mucosa. Subsequently, healing with fibrotic response may occur in the bronchi, resulting in bronchial narrowing or obstruction with anthracotic pigmentation [1]. Stradling [4] and Abraham [9] described the appearance of anthracotic deposits in the bronchial mucosa after intrabronchial perforation of tuberculous lymph nodes. In our patients, lymph nodes were located adjacent to the involved bronchi, with or without calcification, vicariously supporting these facts.
Inhaled anthracotic particles alone did not induce focal bronchial abnormality in our patients because carbon is inert, elicits little or no fibrosis, and the patients lack a history of exposure. Nevertheless, in patients without a history of tuberculosis, previously injured bronchial mucosa with an accumulation of anthracotic pigment from air pollutants or smoke might subsequently undergo healing and fibrosis resulting in anthracofibrosis. Two of our patients had a history of pneumoconiosis. Thirty-nine percent of the elderly women in our study had a history of working in a closed smoky cooking area, where coal or firewood was used as the major heat source. Most anthracotic pigmentation is removed by normal pulmonary dust-ridding mechanisms, including ciliary action and bronchial mucus, but some is retained as macrophages in dust sumps located at branching sites of the terminal and respiratory bronchioles [10] and possibly in injured bronchial mucosa.
The etiology of mediastinal lymph node enlargement and bronchial stenosis in our patients without tuberculosis is not known. Granulomatous lymphadenitis with bronchial stenosis from histoplasmosis, nongranulomatous inflammatory bronchostenosis, or bronchiectasis might show similar radiologic findings similar to those seen in anthracofibrosis. In histoplasmosis, bronchostenosis is caused by extrinsic compression by enlarged calcified lymph nodes associated with mediastinal fibrosis and intrinsic mucosal thickening [11], a finding similar to findings in our patients. However, histoplasmosis has never been reported in Korea. Bronchostenosis in patients with Wegener's granulomatosis usually involves mainstem or lobar bronchi, causing distal lobe collapse or consolidation of the lung [12]. However, calcified mediastinal lymph nodes and anthracotic pigmentation in the bronchial mucosa on bronchoscopy have not been documented in these patients [12].
Because bronchial narrowing with distal atelectasis and mediastinal lymphadenopathy suggest the possibility of malignancy, the recognition of anthracofibrosis as one of the disease entities is important to avoid invasive thoracotomy [1]. In our patients with anthracofibrosis, calcified lymph nodes around the involved bronchi and multifocal involvement of bronchial narrowing were common. Moreover, no definite endobronchial nodular lesions were seen on CT, whereas endobronchial nodular protrusion is commonly observed in central bronchogenic carcinoma. These findings help in the radiologic diagnosis of anthracofibrosis and are especially useful with patients in whom tuberculosis was not seen.
In conclusion, atelectasis caused by smooth bronchial narrowing, surrounded by either calcified or noncalcified lymph nodes, in elderly nonsmoking women is a typical CT finding of bronchial anthracofibrosis. Endobronchial tuberculosis or tuberculous lymphadenitis may be closely related to the development of bronchial anthracofibrosis.
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