Ann Thorac Surg 2003;75:1965-1967
© 2003 The Society of Thoracic Surgeons
Case report
Rupture of ascending aorta secondary to tuberculous aortitis
Jong Bum Choi, MDa*,
Hyun Woong Yang, MDa,
Seok Kyu Oh, MDa,
Ki Jung Yun, MDa
a Departments of Thoracic and Cardiovascular Surgery, Cardiology, and Pathology, Wonkwang University Hospital, Iksan, South Korea
Accepted for publication November 25, 2002.
* Address reprint requests to Dr Choi, Department of Thoracic and Cardiovascular Surgery, Wonkwang University School of Medicine, 344-2 Sinyong-dong, Iksan, Jeonbuk 570-711, South Korea
e-mail: jobchoi{at}wonkwang.ac.kr
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Abstract
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Tuberculous aortitis generally develops at the distal aortic arch and the descending aorta that are close to specific groups of mediastinal lymph nodes, but exceptionally it develops in the ascending aorta. We report a case of rupture of the ascending aorta after tuberculous aortitis in a 53-year-old man without a history of tuberculosis or evidence of a primary foci who underwent cardiopulmonary resuscitation due to severe hemoptysis with subsequent cardiac arrest. The tuberculous aortitis associated with rupture of the ascending aorta was treated with surgical resection and in situ graft placement.
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Introduction
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Aortic rupture secondary to tuberculous infection of the aorta is a rare entity and massive hemoptysis as a clinical manifestation of the aortic rupture is very exceptional with several cases having been described in the literature [1]. With the development of computed tomography and its widespread application recently, aortic rupture associated with massive hemoptysis can be readily diagnosed. In patients without certain history or evidence of primary foci of tuberculosis, however, it is difficult to suggest aortic rupture of tuberculous origin without postoperative pathologic diagnosis. In most of the reported cases tuberculous aortitis was localized in the descending thoracic aorta and the thoracoabdominal aorta but not in the ascending aorta [2]. We report a case of rupture of the ascending aorta after tuberculous aortitis.
A 53-year-old man was transferred to our hospital for massive and recurrent hemoptysis. His history included several episodes of mild hemoptysis for 2 weeks and three episodes of more than 500 mL of blood expectorated over a recent 36 hours. During the third episode of the massive hemoptysis, cardiac arrest had occurred as the result of blood aspiration and soon cardiopulmonary resuscitation was performed successfully. At admission to our hospital the patient was on ventilator support of FiO2 of 0.4, and his blood pressure was 100/60 mm Hg, pulse rate 110 beats per minute, and respiratory frequency 26 cycles per minute. Before admission, 3 U whole blood had been transfused and at that time the red blood cell count was 3.0 x 1003/µL and the hemoglobin 9.1 g/dL.
A chest roentgenogram on admission showed a confluent alveolar filling in the left upper lung field as the result of bleeding from the ruptured aorta and blood aspiration. No active bleeding or any intrinsic abnormality of the bronchial tree was seen at bronchoscopy. A chest computed tomographic (CT) scan revealed a markedly dilated ascending aorta and projecting aneurysm with its surrounding hematoma (Fig 1, A).
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Fig 1. Computed tomographic findings. (A) A preoperative axial computed tomography (CT) scan shows a markedly dilated ascending aorta and projecting aneurysm with surrounding hematoma. (B) The postoperative CT scan shows a patent aortic graft with exclusion of the aneurysm.
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The next day an urgent operation was performed through a median sternotomy. The ascending aorta, aortic arch, and pulmonary artery were severely adhered to pericardium but the pericardial space on both atria and ventricles was intact except for a small amount of serous effusion. Cardiopulmonary bypass was instituted with arterial cannulation in the common femoral artery and venous cannulation in the right atrium. When the rectal temperature decreased to 18°C, femoral arterial perfusion was discontinued. The ascending aorta, which was markedly thickened by chronic inflammation, was opened by a transverse incision 1.0 cm above the sinotubular junction and then cold blood cardioplegia was retrograde infused into the coronary sinus. Retrograde cerebral perfusion of about 400 mL per minute was begun through a right-angled venous cannula in the superior vena cava. The ascending aorta was opened by a vertical incision, which was extended from the previous transverse aortic incision upward to the proximal aortic arch. The aortic rupture had occurred at the upper medial (inner) side of the ascending aorta. Aortic dissection beginning from the ruptured site was superiorly extended to the anterior and inferior wall of aortic arch. The uppermost space of the dissected aortic wall contained a conglomerate caseous material of 3.0 cm in diameter and the intima (inner wall) was calcified. The thick, hard ascending aorta was excised from 1 cm above the sinotubular junction to the proximal margin of origin of innominate artery and a half portion of the inferior wall of the aortic arch that had intimal calcification was also removed. A large volume of fresh hematoma was situated between the rupture site of the ascending aorta and the medial surface of the left upper lobe. The ascending aorta and the inferior half portion of the aortic arch were replaced with a synthetic graft (22-mm Vascutek; Sulzer Medica, Renfrewshire, Scotland). A round erosion of 2.0 cm diameter in the medial side of the left upper lobe was thought to be a communication site with the aortic exsanguination. There was no other palpable parenchymal lesion in the upper lobe. The eroded lung surface was sharply dissected from the mediastinal pleura and pericardium adhered around it and was readily closed with interrupted 4-0 absorbable sutures.
Preoperative and postoperative chest roentgenograms and CT scans showed no evidence of pulmonary tuberculosis (Fig 1, B). Histologic examination of aortic wall tissue showed caseous necrosis surrounded by epithelioid cells and multinucleated giant cell (Fig 2).
Acid-fast bacilli were negative by Ziehl-Neelsen staining but positive bands were shown in the polymerase chain reaction assay for detecting tuberculous DNA in the aortic tissue [3]. The postoperative course was uneventful and antituberculous medication was continued for 9 months. At the postoperative 19th month, the patient is doing well with no sign of recurrent tuberculosis on the follow-up chest films.
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Fig 2. Histopathologic findings of the diseased aortic tissue. Caseous necrosis surrounded by epithelioid cells and multinucleated giant cell is noted (hematoxylin & eosin, x100).
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Comment
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Tuberculous aortitis is expected to increase in incidence throughout world because tuberculosis has been increasing in developing areas and is reemerging steadily in advanced countries. Tuberculous infection into the aortic wall may occur by direct extension from contagious lesions such as infected lymph nodes, empyema, and pericarditis and by hematogenous or lymphangitic spread from primary lesions. Most reported cases of the tuberculous aortic disease had had other pulmonary or extrapulmonary tuberculous lesions [1, 2]. In the present case the tuberculous aortitis and aortic rupture occurred in the absence of any other significant lesion such as pulmonary or extrapulmonary tuberculosis and the adjacent calcified lymph node. Although the other various tuberculous lesions complicated the aortic diseases, the tuberculous aortitis in the previously reported cases was generated in either of two specific portions of the distal aortic arch and the descending aorta [1, 2, 4] that contain specific groups of mediastinal lymph nodes. In our case, however, the aortitis was localized in the ascending aorta and the inferior wall of the proximal aortic arch, which was an unusual lesion site. Moreover the aortic rupture occurred at the left side of ascending aorta that was away from both lungs. The ascending aorta above the sinotubular junction showed diffuse circumferential thickening and only the intima of the proximal aortic arch, which was the inner wall of the caseous cavity, was calcified. From the lesion of caseous necrosis and intimal calcification in the inferior wall of the proximal aortic arch, we infer that the tuberculosis began from the inferior wall of the proximal aortic arch and extended to the ascending aorta. Rupture of an aortic pseudoaneurysm may cause massive hemoptysis that results from an aortobronchial fistula [1, 5]. In the operative field we could see fresh hematoma between the ruptured site of the ascending aorta and the left upper lobe. The mediastinal surface of the upper lobe was eroded but there was no specific palpable lesion in lung parenchyme around the erosion. The tuberculous aortic aneurysm or pseudoaneurysm is treated with patch closure and primary repair of localized defects [1, 4] or resection and in situ graft placement [5–7]. For our patient we excised most of the diseased aortic wall and replaced the entire ascending aorta and the proximal part of aortic arch with a prosthetic vascular graft. For 19 months after the operation, laboratory studies and chest films showed no signs of recurrent tuberculosis. On the basis of this report we suggest that tuberculous aortitis may also develop in the ascending aorta and proximal aortic arch without a history of tuberculosis or evidence of the primary foci. The diffuse lesion of tuberculous aortitis can be satisfactorily managed with enough resection and implantation of a synthetic vascular graft.
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References
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