Ann Thorac Surg 2005;80:e1-e2
© 2005 The Society of Thoracic Surgeons
Case report: e-only content
Reversible Tricuspid Valve Stenosis Due to a Metastatic Dissemination of a Noncardiac Sarcoma
Naia Uribe-Etxebarria, MDa,
Roberto Voces, MDb,
Miguel Angel Rodriguez, MDb,
Alberto Llorente, MDb,
Pedro Perez, MDc,
Jose I. Aramendi, MDb,*
a Division of Thoracic Surgery, Hospital de Cruces, Bilbao, Spain
b Division of Cardiac Surgery, Hospital de Cruces, Bilbao, Spain
c Division of Cardiology, Hospital de Cruces, Bilbao, Spain
Accepted for publication March 8, 2005.
* Address reprint requests to Dr Aramendi, Division of Cardiac Surgery, Hospital de Cruces, Plaza Cruces, Barakaldo, Vizcaya, 48903 Spain (Email: jiaramendi{at}hcru.osakidetza.net).
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Abstract
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Malignant disease is present in the pericardium of 1.5% to 20.6% of patients dying of malignant diseases as was examined postmortem. We present a case of a 57-year-old man with a history of Hodgkin’s disease and a sarcoma of gluteus who presented with tachypnea, generalized weakness, and anasarca for 7 days. The echocardiogram revealed the presence of a significant pericardial thickening and localized pericardial effusion resulting from a tricuspid stenosis. A right anterior thoracotomy was performed, and a pericardiectomy (4 x 4 cm) was done. The histologic examination of the pericardium revealed the presence of a metastatic dissemination from a sarcoma. The cause for the clinical presentation and the treatment of malignant pericardial disease are discussed.
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Introduction
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The most common tumors metastasizing to the pericardium in descending order of frequency are carcinoma of the lung, breast carcinoma, malignant melanoma, lymphomas, and leukemia [1]. Sarcomas very rarely metastasized to the pericardium. Clinical presentation is variable, with the vast majority of patients demonstrating gradual onset of symptoms rather than acute tamponade. Malignant pericardial disease almost always requires surgical drainage. The selection of the drainage procedure is controversial and may vary according to the particular needs and circumstances of the patients [2]. We present the rare case of a patient with a metastatic dissemination from a primary gluteus sarcoma that created a tricuspid stenosis.
A 57-year-old man with a history of Hodgkin’s disease was referred to our hospital because he presented with tachypnea, shortness of breath, generalized weakness, and anasarca for 7 days. In 1980, at the age of 32 he was diagnosed with Hodgkin’s lymphoma stage III 1 A. He received radiotherapy at a dosage of 40 Gy, plus a splenectomy, which resulted in a complete remission. In 1992, at the age of 44 a giant celiac adenopathy was found and was excised by laparotomy. Biopsy revealed Hodgkin’s disease with mixed cellularity. He was treated with four cycles of doxorubicin, bleomycin, vinblastine, and dacarbazine Adriamycin (total dose, 387 mg/m2) plus three cycles of mechlorethamine, vincristine, procarbazine, and prednisone. In April 2004 he was diagnosed with a fuso-cellular sarcoma of the gluteus. He was treated with four cycles of isofosfamide (dosage, 10 g/m2) plus lysosomal Adriamycin (compassionate treatment) in order to avoid cardiac toxicity.
On admission a chest roentgenogram of the cardiac silhouette was normal and a right pleural effusion was present. The transthoracic echocardiogram revealed the presence of a significant pericardial thickening and 2 cm of pericardial effusion that compressed into the lateral wall of the right atrium creating a tricuspid stenosis (maximum pressure gradient, 19 mm Hg and mean pressure gradient, 9 mm Hg; right ventricular diastolic diameter, 3.1 cm) (Fig 1). The computed tomographic scan of the chest showed an encapsulated pericardial effusion with a pericardial thickening in the lateral wall of the right atrium, a bilateral pleural effusion, and numerous lung nodes (Fig 2). He persisted with symptoms of right heart failure. A palliative pleuro-pericardial window operation was indicated.
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Fig 1. The preoperative echocardiogram (top panel images) revealing a significant pericardial thickening and pericardial effusion creating a tricuspid stenosis. The postoperative echocardiogram (bottom panel images) showing the disappearance of the pericardial effusion and the tricuspid stenosis.
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Fig 2. A computed tomographic scan of the chest showing an encapsulated pericardial effusion with a pericardial thickening and bilateral pleural effusion.
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The surgical technique was performed under general anesthesia with a 30° left lateral decubitus and a 5-cm right anterior small thoracotomy, similar to the left anterior small thoracotomy operation for off-pump surgery. Serous pleural effusion (1,500 mL) was aspirated. A good direct vision of the right-sided pericardium over the right atrium was obtained. The pericardium was open immediately above the right atrium and 50 mL of localized fibrinous effusion was evacuated. We observed an immediate relief of the tricuspid valve compression through an intraoperative transesophageal echocardiogram. There were multiple adhesions in the remaining pericardium caused by the previous radiotherapy that prevented the formation a diffuse pericardial effusion. A portion of 4 x 4 cm of pericardium was excised creating a pleuro-pericardial window. No gross tumor was observed in the pericardium. The pericardial fluid was bloody and contained no malignant cells. Stains and cultures of the fluid revealed no infectious source. The histologic examination of the pericardium revealed the presence of a metastatic dissemination of a sarcoma.
After the pericardiectomy, an echocardiogram showed the disappearance of the pericardial effusion and tricuspid stenosis without pressure gradient across the valve (Fig 1). No signs of pericardial constriction were evident. The patient recovered uneventfully and continued with palliative chemotherapy.
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Comment
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Malignant disease is present in the pericardium of 1.5% to 20.6% (average, 6%) of patients dying of neoplasia and examined postmortem [1]. They generally produce a diffuse infiltration of the pericardium associated with important pericardial effusion and cardiac tamponade [3]. Surgery, although palliative, is often indicated first to establish the definitive diagnosis and second to alleviate the tamponade. In stable patients a thoracoscopic approach is preferred. It is less aggressive, but it is time consuming. In this case, the patient was in critical condition and we preferred a small right thoracotomy because it is faster and more accurate. This is also a minimally invasive approach that permits performing a large pleuro-pericardial window, which prevents recurrent episodes of cardiac tamponade.
Our patient had a previous treatment with radiotherapy (14 years prior to treating the Hodgkin’s disease). It is possible that this treatment created the adhesions that encapsulated the pericardial effusion and caused the tricuspid stenosis. Survivors of Hodgkin’s disease are at high risk for radiation associated cardiovascular disease [4]. This includes coronary artery disease, valvular stenosis, and pericarditis that eventually produce constrictive pericarditis. Modern techniques of radiotherapy reduce volume and radiation exposure that diminish the incidence of cardiovascular disease [5]. Patients who were treated 20 years ago with total radiation dosages greater than 35 Gy (as in our case) are at greater risk of cardiac damage. There are some reports in the literature reporting localized pericardial effusion [6, 7]. In 1975, Wray and colleagues [6] described a case of traumatic pericardial hematoma producing tricuspid stenosis that was relieved by surgery. More frequently, localized hematoma or effusion is seen after heart surgery; it may compress the left heart chambers or the right atrium and is often responsible for hemodynamic deterioration in the postoperative period [8]. In fact, many authors believe that most instances of postoperative tamponade are due to localized compression of the atria rather than gross diffuse effusion.
Currently the most sensitive and the least invasive method for detecting pericardial effusion is echocardiography, which can detect effusions as small as 15 mL, characterize total volume, and demonstrate the presence of fibrin bands, pericardial masses, loculations, thickened pericardial membranes, and chamber compression. In our case, the echocardiogram revealed the presence of a significant thickening in pericardium and localized effusion producing the tricuspid stenosis.
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References
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- Wray TM, Prochaska J, Fisher RD, Shaker IJ. Traumatic pericardial hematoma simulating tricuspid valve obstruction Johns Hopkins Med J 1975;137(4):147-150.[Medline]
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Abstract
Introduction
