A 71-year-old man with a history of chronic obstructive pulmonary disease (COPD), pulmonary hypertension, and TB status posttreatment in 1985, presented for evaluation of chronic, progressive dyspnea. The patient had previously been seen at our institution for dyspnea and had been diagnosed with and treated for numerous COPD exacerbations. He had been treated with bronchodilators, corticosteroids, and occasional antibiotics without improvement. He had no history of tobacco use, significant alcohol consumption, or any illicit drug use.
On examination, the patient was in no significant distress and was able to speak in full sentences. His vital signs were normal except for a respiratory rate of 20 breaths/min and oxygen saturation of 90% on room air at rest. Cardiovascular examination was notable for jugular venous distension to the angle of the mandible. A parasternal heave, an accentuated P2, and an S3 were appreciated. Lung auscultation was notable for decreased breath sounds. The remainder of the examination was unremarkable.
Transthoracic echocardiography revealed right ventricular dilatation with flattening of the interventricular septum and an estimated pulmonary artery systolic pressure of 85 mmHg. Pulmonary function testing (PFT) demonstrated severe obstructive ventilatory defect with diffusion impairment.
Chest radiograph demonstrated bilateral perihilar soft tissue densities with right apical scarring, pleural thickening and volume loss [Figure 1]. Contrast-enhanced chest CT revealed ill-defined, infiltrative bilateral hilar soft tissue densities with calcifications, enlargement of the main and right pulmonary artery, and irregular narrowing of the right mainstem and upper lobe bronchi [Figure 2]. Positron emission tomography (PET) showed mild fluorodeoxyglucose uptake in the bilateral perihilar regions, right more prominent than left. Of note, the patient had undergone a non contrast-enhanced thoracic CT three years prior, which documented relative stability all the abnormal findings, including the bronchial narrowing and pulmonary artery dilation [Figure 3].
The patient had previously undergone a bronchoscopy with bronchoalveolar lavage, brushings, and biopsies which were negative for fungal organisms and acid-fast bacilli.
The patient's known history of TB and findings of old granulomatous disease on imaging along and with negative bronchoscopy results established fibrosing mediastinitis as the likely cause of his mediastinal infiltrates. Although the PET scan showed mild uptake in the perihilar regions consistent with an active inflammatory process, the stability noted on imaging over a prolonged course was reassuring that the mediastinal and hilar infiltrates did not represent malignancy. The patient had compression of his pulmonary artery due to fibrosing mediastinitis and findings of pulmonary hypertension on the examination and by echocardiography. He also had tracheobronchial narrowing as a result of this entity as seen on chest imaging which likely manifested as obstruction on spirometry. The patient's respiratory symptoms stabilized on supportive medications, and no further interventions were required.
A 71-year-old man with a history of chronic obstructive pulmonary disease, pulmonary hypertension, and prior pulmonary tuberculosis infection presenting with progressive dyspnea, diagnosed with tuberculosis-associated fibrosing mediastinitis. Contrast-enhanced chest computed tomography, soft tissue window. (a-d) Demonstrates ill-defined, infiltrative bilateral hilar soft tissue densities with calcifications (white arrows); enlargement of the main and right pulmonary artery (black arrow heads); and irregular narrowing of the right mainstem and upper lobe bronchi (black arrow).