Ann Thorac Surg 1996;61:1257-1259
© 1996 The Society of Thoracic Surgeons
Case Report
Pulmonary Artery Reconstruction for Tuberculosis
Andrew S. Cohen, FRCS,
Tina Beaconsfield, FRCR,
Aghiad Al-Kutoubi, FRCR,
Clive E. Handler, MRCP,
Brian E. Glenville, MS
Department of Cardiothoracic Surgery, St Mary's Hospital, London, England
Accepted for publication October 25, 1995.
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Abstract
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A 35-year-old woman underwent reconstruction of her right pulmonary artery for treatment of acquired right pulmonary artery stenosis. The stenosis was secondary to tuberculosis causing both an extrinsic and an intrinsic obstructive component. After her reconstruction, the patient made an uneventful recovery, and perfusion to the right lung was subsequently restored.
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Introduction
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Acquired pulmonary stenosis secondary to extrinsic compression of the pulmonary artery is rare [1]. Of the cases reported in the literature, the causes of the external compression include mediastinal teratoma [1], Hodgkin's disease [1], aneurysm of the ascending aorta [1, 2], bronchial carcinoma [1], sarcoidosis [3], hydatid cyst [4], bronchogenic cyst [5], cystic thymoma [6], and histoplasmosis [7]. Gough and associates [1], in their review of acquired pulmonary stenosis and pulmonary artery compression, described an additional case in which the probable diagnosis was thought to be tuberculosis. However, sputum cultures for tubercle bacilli were negative and, thus, the diagnosis of sarcoidosis is brought into question. We report a case of tuberculosis causing acquired right pulmonary artery stenosis secondary to both external compression and intrinsic obstruction.
A 35-year-old woman presented with a 4-week history of rapidly increasing shortness of breath on exertion and vague retrosternal chest pain. Examination revealed her to be in sinus tachycardia with normal heart sounds. She was hypoxic on room air with an oxygen tension of 72 mm Hg. Chest radiography revealed a generalized decrease in pulmonary vascular markings on the right. A perfusion-ventilation scan revealed normal ventilation to both lungs and no perfusion to the right lung with a presumptive diagnosis of pulmonary embolism. A pulmonary angiogram was performed, which revealed pulmonary artery stenosis on the right with no evidence of pulmonary embolism (Fig 1
). A right pulmonary angioplasty was attempted, but there was no significant radiologic improvement. A computed tomogram was performed, which showed a tight stenosis of the right pulmonary artery at the origin with abnormal tissue surrounding the point of stenosis and abnormal tissue in the region of the right hilum. A Mantoux test proved negative, and bronchoscopy was normal.
The patient was prepared for surgical reconstruction of her right pulmonary artery. Through a median sternotomy a stenosed right pulmonary artery was found with a fibrous reaction surrounding it and enlarged glands. The area of stenosis was from the origin of the right pulmonary artery distally over a length of 2.5 cm. Distal to this the right pulmonary artery was normal. The surrounding glands were debulked, and the patient was placed on cardiopulmonary bypass to facilitate the reconstruction of her pulmonary artery. A vascular clamp was placed distally on the normal right pulmonary artery, and another clamp was placed over the main pulmonary trunk. The stenosis was opened along its length. The vessel was fibrotic, with less than 15% of its circumference representing normal artery. Pericardial patch repair was, therefore, inappropriate. Formal reconstruction from the main pulmonary trunk to the normal distal right pulmonary artery was performed using a 12-mm reinforced polytetrafluoroethylene graft (Fig 2). Once distal and proximal anastomoses were performed, the patient was weaned from cardiopulmonary bypass with ease. Postoperatively the patient made an uneventful recovery and was given oral anticoagulants to achieve a target International Normalized Ratio of 2.5. Histologic examination of the excised pulmonary artery segment revealed intimal proliferation and granulomatous inflammation with granulomata showing central caseous necrosis and Langhan's multinucleate giant cells. Acid-fast bacilli were seen on Ziehl-Neelsen staining. The patient received standard anti-tuberculosis triple therapy.
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Fig 2. . Intraoperative photograph showing right pulmonary artery reconstruction with a polytetrafluoroethylene-reinforced graft, with the ascending aorta slung and retracted laterally.
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Postoperatively a perfusion-ventilation scan demonstrated perfusion to the right lung. The patient's symptoms of shortness of breath were abolished, and she was discharged on the tenth postoperative day.
At follow-up she remained in excellent condition at 2 months. A repeat pulmonary angiogram at 6 months postoperatively showed a patent graft with normal perfusion to the right lung (Fig 3).
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Fig 3. . Six months postoperative pulmonary angiogram showing a patent graft with normal perfusion to the right lung.
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Comment
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Pulmonary tuberculosis is known to cause acute respiratory distress resulting from major airway compression caused by enlarged tuberculosis mediastinal lymph nodes and dysphagia from compression of the esophagus. As Gough and associates [1] reported, external compression of the main pulmonary artery is rare; compression of the right or left branch, however, is more common. As in their cases in which the main pulmonary trunk was not involved, no clinical evidence of pulmonary stenosis or of pulmonary artery branch stenosis was present [1]. In our patient the heart sounds were normal and the electrocardiogram showed no evidence of right ventricular hypertrophy.
Gough and associates advocated the use of cardiac catheterization and selective angiography in patients who had evidence of right ventricular outflow obstruction to determine the site and severity of the obstruction and to differentiate extrinsic compression and intrinsic stenosis. In our case, before pulmonary angiography, the presumptive diagnosis was one of pulmonary embolism, ie, pathology within the lumen of the artery. Subsequent to pulmonary angiography, pulmonary embolism was excluded, and the combination of pulmonary angiography and computed tomography suggested that the stenosis was largely due to external compression. At operation external compression from tuberculosis lymph glands was certainly part of the problem, but it was intrinsic involvement of the right pulmonary artery itself, with only about 15% of normal artery circumference remaining, that was responsible for the stenosis.
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Footnotes
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Address reprint requests to Mr Cohen, Department of Cardiothoracic Surgery, St Mary's Hospital, London, W2 1NY, England.
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References
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- Gough JH, Gold RG, Gibson RV. Acquired pulmonary stenosis and pulmonary artery compression. Thorax 1967;22: 358–67.[Abstract/Free Full Text]
- Nasrallah A, Goussous Y, El-Said G, Garcia E, Hall RJ. Pulmonary artery compression due to acute dissecting aortic aneurysm: clinical and angiographic diagnosis. Chest 1975;67:228–30.[Medline]
- Faunce HF, Ramsay GC, Sy W. Protracted yet variable major pulmonary artery compression in sarcoidosis. Radiology 1976;119:313–4.[Abstract/Free Full Text]
- Mercante A, Colome JA, Diaz Fernandez AJ, Gallardo J, Saiz F. Acquired pulmonary stenosis. A case of pulmonary artery compression caused by hydatid cyst. Rev Clin Esp 1974;135:289–93.[Medline]
- Watts WJ, Rotman HH, Patten GA. Pulmonary artery compression by a bronchogenic cyst simulating congenital pulmonary artery stenosis. Am J Cardiol 1984;53:347–8.[Medline]
- Soorae AS, Stevenson HM. Cystic thymoma simulating pulmonary stenosis. B J Dis Chest 1988;74:193–7.
- Lloyd JE, Tillman BF, Atkinson JB, DesPrez RM. Mediastinal fibrosis complicating histoplasmosis. Medicine 1988;67:295–310.[Medline]
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Abstract
Introduction
