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61

Dysphagia Due to Mediastinal


Fibrosis in Advanced Pulmonary
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Tuberculosis

Ravi Ramakantan1 Dysphagia in patients with pulmonary tuberculosis may be due to tuberculous esoph-
Priti Shah agitis or compression of the esophagus by enlarged mediastinal lymph nodes or
mediastinal fibrosis. We studied the clinical and radiologic findings in nine patients with
advanced pulmonary tuberculosis who presented with dysphagia. In each patient,
dysphagia first occurred while the patient was on antituberculous therapy. Chest radio-
graphs in each case showed extensive tuberculous disease of the lung, affecting
especially the left upper lobe. In addition, dense mediastinal pleural fibrosis was seen
along the medial aspects of the upper thorax. Tomograms did not show mediastinal
lymph node enlargement. Barium esophagograms showed extrinsic compression and
various degrees of narrowing of the supracarinal part of the esophagus. No mucosal
abnormality was seen on esophagoscopy. On the basis of these findings, the compres-
sion of the esophagus in these patients was attributed solely to tuberculous mediastinal
fibrosis. The dysphagia remained constant in all patients except one, in whom worsening
dysphagia improved after balloon dilatation.
We conclude that mediastinal fibrosis is a significant cause of dysphagia in patients
with advanced pulmonary tuberculosis.

AJR 154:61-63, January 1990

Tuberculosis is an important cause of chronic mediastinitis. Although most


patients are asymptomatic, symptoms due to compression of the superior vena
cava, the esophagus, and the tracheobronchial tree have been reported [1]. In a
review of 1 03 cases of chronic granulomatous mediastinitis, Schowengerdt et al.
[1 ] found nine cases with esophageal compression. We studied nine patients with
advanced pulmonary tuberculosis who presented with dysphagia. In each patient,
dysphagia was due to compression of the esophagus caused by fibrosing medi-
astinitis due to tuberculosis.

Subjects and Methods


Nine patients (seven men, two women) between the ages of 30 and 60 years (mean age,
47 years) were included in the study. All patients had microbiologically proved pulmonary
tuberculosis; all developed dysphagia while undergoing treatment with antituberculous drugs
for 2-6 months (mean, 3.2 months). The duration of the dysphagia ranged from 1 5 days to
4 months (mean, 2.1 months).
All patients underwent upper gastrointesinal endoscopy, chest radiography, and barium

Received June 28, 1 989; accepted after revision esophagography.


August 8, 1989.
Both authors: Department of Radiology, King
Edward Memorial Hospital, 7/259, Seeta Sadan, Results
Sion (West), Bombay 400 022, India. Address re- . .
print requests to A. Ramakantan. Upper gastrointestinal endoscopy showed extrinsic compression of the esopha-
0361 -803X/90/1541-0061 gus without mucosal abnormality in all nine patients. The endoscope could not be
American Roentgen Ray Society passed beyond the narrowing in two patients.
62 RAMAKANTAN AND SHAH AJR:154, January 1990

Fig. 1.-42-year-old man with active


pulmonary tuberculosis and dysphagia.
A, Chest radiograph shows exten-
sive fibrocavitary tuberculosis in left
upper lobe. Note dense pleural thick-
ening and mediastinal fibrosis (arrow-
heads).
B, Barium esophagogram shows
esophageal compression (arrowhead).
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Chest radiographs in all patients showed extensive bilateral


cavitary disease of the lungs, mainly in the upper and mid
zones. A constant feature of all chest radiographs was mas-
sive thickening of the pleura, especially along the mediastinal
aspect and mainly on the left side (Fig. 1 A).
Barium esophagograms showed various degrees of
compression of the supracarinal portion of the esophagus
(Fig. 1 B). No mucosal abnormality was seen. The maximal
length of the compression was 7 cm (Fig. 2). The degree of
narrowing was never more than 60% (Fig. 3). Esophageal
peristalsis was poor in the affected segment. None of the
patients had significant dilatation of the esophagus proximal
to the narrowing.

Discussion
Dysphagia in tuberculosis can be due to several causes,
including intrinsic esophageal involvement with tuberculosis
or compression of the esophagus caused by tuberculous
mediastinal lymph nodes [2]. In addition, mediastinal fibrosis
resulting from tuberculosis can produce compression and
dysmotility in the esophagus, leading to dysphagia. That
mechanism has received only sparse attention in the literature
[2, 3]. On the basis of our experience, we believe that fibrosing
mediastinitis is the most common reason for dysphagia in
adult patients with advanced pulmonary tuberculosis. Fig. 2.-32-year-old man with pulmonary tuberculosis and dysphagia.
In our patients, the disease occurred more frequently in Barium esophagogram shows compression of esophagus (arrowheads).
men than in women (4:1 ); the patients were in their forties at Note adjacent pleural thickening (arrow).
the time of presentation. All patients had extensive pulmonary Fig. 3.-Barium esophagogram of a 38-year-old woman with pulmonary
tuberculosis. In each case, dysphagia appeared while the tuberculosis and dysphagia. Note long segment of narrowing in esophagus
(arrowheads).
patients were undergoing antituberculous treatment, sug-
gesting that fibrosis due to healing was causing esophageal
compression. None of the antituberculous drugs is known to lobes most severely and the left side was involved more than
produce esophagitis. the right side. In addition, the posterior segments of the upper
In all our patients, the pulmonary disease affected the upper lobes were involved most extensively. This predominant in-
AJR:154, January 1990 DYSPHAGIA AND MEDIASTINAL FIBROSIS 63

volvement of the posterior segment of the left upper lobe phagia. The radiologic appearances of the strictures could
explains the compression of the esophagus and the absence mimic benign strictures due to other causes (e.g., Barrett
of superior vena caval obstruction, although the latter is more esophagus and esophagitis caused by radiation, caustic
common in mediastinal fibrosis [1]. The limitation of pulmo- ingestion, oral medication, and opportunistic infection). How-
nary disease to the upper lobes explains the sparing of the ever, the exclusively supracarinal involvement, the presence
lower third of the esophagus in all of our patients. of normal mucosa, and the associated pleuropulmonary
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The pattern of compression produced on the barium eso- changes should allow a correct diagnosis in each case.
phagograms was constant and characteristic. The disease
was restricted to the supracarinal segment of the esophagus
REFERENCES
in each case. The compression involved a short segment with
smooth, tapering margins. Absence of mucosal abnormality 1. Schowengerdt CG, Suyemoto A, Main FB. Granulomatous and fibrous
and mass effect was characteristic. Most of the patients had mediastinitis. J Thorac Cardiovasc Surg 1969:57:365-378
2. Levine MS. Infectious esophagitis. In: Radiology of the esophagus. Phila-
modest strictures (<60%) with delay in passage only of a
delphia: Saunders, 1989:67-69
semisolid bolus of barium. Absence of peristalsis in the af- 3. Albrechtsen D, Nygaard K. Idiopathic mediastinal fibrosis. Acta Chir Scand
fected segment of the esophagus also contributed to dys- 1989;147:219-222

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