Ann Thorac Surg 2004;77:1066-1068
© 2004 The Society of Thoracic Surgeons
Case report
Partial pericardial defect associated with ruptured aortic dissection of the ascending aorta: a rare feature presenting severe left hemothorax without cardiac tamponade
Masato Nakajima, MDa*,
Kouji Tsuchiya, MDa,
Yuji Naito, MDa,
Hidenori Inoue, MDa,
Kensuke Kobayashi, MDa,
Eiki Mizutani, MDa
a Department of Cardiovascular Surgery, Yamanashi Central Hospital, Kofu City, Yamanashi, Japan
Accepted for publication April 9, 2003.
* Address reprint requests to Dr Nakajima, Department of Cardiovascular Surgery, Yamanashi Central Hospital, 1-1-1 Fujimi, Kofu City, Yamanashi 400-0027, Japan
e-mail: m-nakajima2a{at}ych.pref.yamanashi.jp
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Abstract
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We report a very rare case of acute aortic dissection of the ascending aorta, which ruptured to the left pleural cavity through the left-side congenital pericardial defect. A preoperative computed tomographic scan and a roentgenogram showed localized dissection of the ascending aorta and severely deteriorating left hemothorax, which required emergency operation. Intraoperative findings revealed the ruptured aortic dissection of the ascending aorta and the defect at the left-side pericardium, and a graft replacement of the ascending aorta was performed. It was considered that congenital pericardial defect complicates the diagnosis in a case of catastrophic intrapericardial hemorrhage.
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Introduction
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Congenital pericardial defects are relatively rare anomalies that usually go undetected until fatal symptoms occur [1, 2]. Previous reports have described the difficulty of establishing a diagnosis and managing this anomaly, especially for patients with concomitant heart disease [3–6]. We present a very rare and complicated case of severe left hemothorax, which was caused by a rupture of the dissected ascending aorta to the left thoracic cavity through the pericardial defect.
An 84-year-old man diagnosed with acute aortic dissection was referred to our hospital for surgical treatment. The patient had syncope with chest discomfort and was transferred to another hospital before being transferred to ours. A computed tomographic scan performed at the hospital showed acute aortic dissection of the ascending aorta and a left-side pleural effusion that revealed hemothorax after direct puncture (Figs 1, 2). On being admitted to our hospital 27 hours after his first symptoms, the patient's hemodynamic status was maintained, with systolic blood pressure around 100 mm Hg, without the administration of an inotropic agent. However, his dyspnea deteriorated and his blood saturation decreased gradually. Laboratory findings at admission revealed deteriorated hematocrit and hemoglobin values of 25.8% and 8.8 g/dL, compared with those of 37.5% and 12.8 g/dL at the previous hospital. And another chest roentgenogram revealed increased pleural effusion (Fig 3). However, we could not identify the exact cause of severe hemothorax, because the dissected site was localized to the ascending aorta without dissection of the descending thoracic aorta. Furthermore, the absence of pericardial effusion complicated the situation. We finally initiated the emergency surgical repair of the dissected ascending aorta because the patient's hemodynamic and respiratory status deteriorated.
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Fig 1. Chest roentgenogram at previous hospital showing mild dilatation of the mediastinal shadow and mild left-side pleural effusion.
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Fig 2. (A, B) Computed tomography at previous hospital showing aortic dissection localized on ascending aorta and left pleural effusion. (C) Pericardial effusion was not present.
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After the induction of anesthesia, the patient's hemodynamics deteriorated even further. Therefore, after the prompt cannulation of the left femoral artery, a median sternotomy was performed. A massive hematoma was noticed around the ascending aorta, pulmonary trunk, and subepicardium on the right ventricle. A cardiopulmonary bypass was established, with right atrial drainage and left femoral arterial perfusion under monitoring of the right radial arterial pressure. During the removal of an intrapericardial hematoma on the pulmonary trunk, a 3 x 5 cm pericardial defect was noticed on the left upper border, and a large amount of old blood was evacuated from the left pleural cavity (Fig 4). At this point, we could finally recognize the cause of severe hemothorax, and the ruptured site of the dissected aorta, which required intervention. Graft replacement of the ascending aorta was performed with the patient placed under deep hypothermic circulatory arrest, and the patient could then be weaned from cardiopulmonary bypass without difficulty. The defect was left without closure or enlargement. Operation time, cardiopulmonary bypass time, aortic cross clamp time, and circulatory arrest time were 251, 129, 84, and 22 minutes, respectively. The patient survived the operation, but his condition was complicated with cerebral infarction, with right-side hemiplegia and respiratory failure, resulting in 2 months of respiratory support after a tracheotomy. The patient still requires hospitalization for rehabilitation 4 months after the operation.
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Fig 4. Operative findings showing a 3 x 5 cm pericardial defect on the upper border of the left side of the pericardium (black arrows).
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Comment
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Congenital pericardial defects are relatively rare anomalies, and they can be either complete or partial. These defects may result from the persistence of a pleuropericardial foramen owing to the arrested development of the pleuropericardial membrane. This in turn may be caused by compromised vascular circulation, and it has been hypothesized that the predominance of left-sided defects results from the premature atrophy of the left duct of Cuvier [3, 4].
Most patients who have pericardial defects are asymptomatic but are at risk for possibly symptomatic herniation of the atrial appendage or herniation of the left ventricle, which can lead to fatal myocardial strangulation [1, 2]. The most common symptom is chest pain, probably due to myocardial ischemia. This is caused by the impingement of the fibrous pericardial rim on the coronary arteries, torsion of the great artery, the lack of a cushioning effect of the pericardium, or tension on pleuropericardial adhesions. In such symptomatic patients, prompt diagnosis and proper treatment are essential [4, 5, 7].
The diagnosis of a congenital pericardial defect may be difficult to establish. In some cases, chest radiography can show a prominence in the hilar region, but it has been reported that magnetic resonance imaging and intraoperative direct findings are more reliable for an exact diagnosis [8]. Particularly for patients who have concomitant atherosclerotic coronary artery disease, establishing a proper diagnosis and management strategy, including surgical intervention, can be difficult [4–6].
In the present case, the existence of a left-side partial pericardial defect, which could not be detected preoperatively, complicated the situation and prolonged the time between diagnosis and surgical intervention. In other words, the causes of severe hemothorax could not be identified preoperatively. If the dissection involved the descending thoracic aorta, it was conceivably a case of severe hemothorax. However, preoperative echocardiographic and computed tomographic findings showed a localized dissection only in the ascending aorta and no pericardial effusion. The surgical strategy, including the approach to the diseased aorta and the establishment of a cardiopulmonary bypass, as well as the repair of the ascending aortic rupture, was different from what is appropriate in patients with descending thoracic aortic ruptures. Because of the deteriorating hemodynamic status of this patient, we performed an emergency operation by median sternotomy to repair the dissected ascending aorta. We thereby discovered a left-side partial pericardial defect. Had the dissection extended to both the ascending and descending thoracic aorta, the surgical strategy would have been more complicated because of the difficulty in identifying the ruptured site.
In conclusion, it should be noted that a pericardial defect occasionally makes clinical situations more complicated for patients with intrapericardial hemorrhage due to ruptured great vessels, postinfarct left ventricular ruptures, or a traumatic cardiac ruptures.
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References
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Abstract
Introduction
