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Ann Thorac Surg 2002;74:1229-1231
© 2002 The Society of Thoracic Surgeons
a Department of Surgery, University of Virginia, Charlottesville, Virginia, USA
b Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Accepted for publication May 30, 2002.
* Address reprint requests to Dr Jones, Department of Surgery, University of Virginia, PO Box 800679, Charlottesville, VA 22908-0679 USA
e-mail: djones{at}virginia.edu
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A 15-year-old male native of Peru was noted to have mild dyspnea with exercise. He denied symptoms relating to congestive heart failure or recurrent respiratory infections. Five years prior to this presentation, the patient had had primary pulmonary tuberculosis of his right lower lobe that resulted in a right tuberculosis empyema necessitans. He was treated with multidrug chemotherapy for 1 year, had no subsequent problems, and moved to the United States shortly thereafter. On physical examination, the only significant findings were a continuous, loud bruit over his right hemithorax and a well-healed 2-cm scar in the right posterior axillary line in the seventh intercostal space.
Further evaluation included a chest roentgenogram that demonstrated mild cardiomegaly, a right lower lobe peripheral lung mass, and obvious ipsilateral rib notching. A transthoracic echocardiogram demonstrated no intracardiac anomalies but there was evidence of increased left atrial and ventricular volume overload. A spiral chest computed tomographic scan demonstrated a soft tissue density in the right lower lobe, prominent right-sided intercostal and internal mammary vessels, as well as numerous trans-diaphragmatic vessels apparently arising from the liver and coursing into the lung mass. Angiography demonstrated a pleural-based right lower lobe hypervascular mass fed by the ipsilateral intercostal, internal mammary, lateral thoracic, thoracodorsal, inferior phrenic arteries (Fig 1), as well as the right hepatic artery (Fig 2). Drainage of the AVM was via the right pulmonary artery and the right inferior pulmonary vein. The pulmonary artery pressure was 35/14 mm Hg, and flow in the pulmonary artery was retrograde distal to the truncus anterior (Fig 2). Bronchoscopy was performed and no endobronchial abnormalities were appreciated. Bronchoalveolar lavage of the right lower lobe revealed no mycobacterium species on subsequent culture analysis.
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We report an unusual sequelae of a patient with a history of a tuberculosis empyema necessitans who subsequently developed a pulmonary AVM with significant systemic-to-pulmonary collateral vessel formation. The majority of pulmonary AVMs are congenital and are associated with hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease) in 60% of patients [3]. Acquired pulmonary AVMs are the result of tuberculosis, trauma, schistosomiasis, long-standing hepatic cirrhosis, metastatic carcinoma, actinomycosis, and following the creation of a Glenn shunt [1, 3, 4]. In this patient, dyspnea was his initial complaint which corresponds with the 47% incidence observed in pulmonary AVMs in the Mayo Clinic series [5]. Similarly, like our patient, 29% of patients in that series had an audible thoracic bruit.
Once diagnosed, the primary indication to obliterate the shunt is related to an increase in neurologic events secondary to an incomplete pulmonary filter. These complications included transient ischemic attacks, hemiplegia, brain abscesses, and seizures. Other complications include hemoptysis, high-output congestive heart failure, and disseminated intravascular coagulation.
Our patient’s AVM with systemic collateralization was likely related to the inflammatory processes surrounding the tubercular nodule, associated empyema, and local structures (diaphragm, chest wall), all of which helped recruit local systemic arteries to feed the inflammatory mass. Another possible etiology for this AVM would be an acquired fistula between the intercostal artery and vein at the site where his empyema necessitated [6]. These systemic-to-systemic AVMs are typically associated with trauma and would be unlikely to invade the lung parenchyma or result in the massive collateralization seen in this case. Localized pulmonary tuberculosis inflammatory processes can result in the development of Rasmussen aneurysms (5%), pulmonary artery stenoses, tracheoesophageal fistulae, and pericardial erosion [2, 3].
Successful management of a pulmonary AVM may involve surgery, selective embolization, or a combination of the two [3]. Since its introduction for treatment of pulmonary AVMs in 1977, embolization of pulmonary AVMs using coils, detachable balloons, polyvinyl alcohol microparticles, Ferrosan or a combination of the above has gradually surpassed surgical resection for the majority of these lesions. Surgical resection is still indicated for larger pulmonary AVMs or in patients who fail embolization. In our patient, we chose to utilize both treatment strategies because of the significant systemic collateralization to the AVM, and concerns about identifying and controlling the multiple sub-diaphragmatic arterial vessels in a nearly obliterated postempyema pleural space. Surgery was performed within 24 hours of embolization to maximize the beneficial effects of preoperative embolization. Despite this, the dissection was tedious due to multiple systemic collaterals that were unaffected by the selective embolization.
In summary, we report the successful management of a patient with a large pulmonary AVM with massive systemic arterial collateralization associated with a prior history of a M. tuberculosis empyema necessitans. Combined preoperative intraarterial embolization, followed by thoracotomy and AVM resection, permitted a safe and complete removal of the pulmonary AVM.
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  R. Thomas, D. J. Christopher, J. Chacko, and J. Ponnaiya Pulmonary arteriovenous malformation in a patient with tuberculosis -- an association? Eur J Cardiothorac Surg, August 1, 2006; 30(2): 405 - 407. [Abstract] [Full Text] [PDF]
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