© 2004 Foundation for Promotion of Cancer Research
Case Report |
Direct Pericardial Involvement of Non-small Cell Lung Cancer Rapidly Developing Pericardial Constriction
1 The First Department of Medicine, Shinshu University School of Medicine, Matsumoto and 2 The Fujimi-Kogen Hospital, Suwa-gun, Nagano, Japan
For reprints and all correspondence: Tomonobu Koizumi, The First Department of Medicine, Shinshu University School of Medicine, Asahi, Matsumoto 390-8621, Japan. E-mail: tomonobu{at}hsp.md.shinshu-u.ac.jp
Received March 10, 2004; accepted July 6, 2004
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Abstract |
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A 71-year-old male, who had been followed up after being treated with chemo-radiotherapy for non-small cell lung cancer (adenocarcinoma), rapidly developed dyspnea and mild fever. Radiographs showed left pleural effusion and cardiomegaly, and echocardiographic examination revealed echo-free space, suggesting a pericardial effusion. The patient was treated conservatively without any surgical procedures such as pericardiocentesis. Disappearance of the echo-free space was followed by development of pericardial constriction within two months. At post-mortem examination, a direct extension to the pericardium from the primary lesion of the right upper lobe through the mediastinum was observed. The rapid development of pericardial constriction is extremely rare in patients with malignant pericarditis.
Key Words: constrictive pericarditis • cardiac tamponade • lung cancer • cardiac failure
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INTRODUCTION |
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Metastatic tumor progression to the pericardium is generally characterized by effusional pericarditis (1,2). Malignant neoplastic pericarditis occasionally causes cardiac tamponade, which results in acute cardiac failure (1–3). On the other hand, direct extension of the tumor to the pericardium without intrapericardial effusion causes constriction of the heart, especially in patients with lung cancer (4,5) or mesothelioma (5,6), although this situation is rarely encountered (1–5,7). This report concerns a case with rapidly developing pericardial effusion due to the direct extension of non-small cell lung cancer. This led to pericardial constriction accompanying disappearance of pericardial effusion within 2 months. This clinical manifestation appears to be extremely rare.
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CASE REPORT |
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A 71-year-old male was admitted to our hospital in May 2001 because of detection of an abnormal mass in the right upper lung field. A diagnosis of primary lung cancer (adenocarcinoma) with clinical stage IV (T4N2M1) was made, and a distant metastasis was observed in the right kidney. The patient was treated with systemic chemotherapy (CDDP plus Docetaxel), followed by radiotherapy (60 Gy) for the primary lesions, resulting in minor response. In December 2002, the thoracic mass in the right upper lobe showed a slight increase in spite of subsequent chemotherapy; however, the patient had no clinical symptoms and abnormal finding in the pericardium on chest computed tomography (CT). Chemotherapy with CPT-11 (60 mg/m2) was initiated on January 20, 2003. The patient presented with dyspnea and low-grade fever on January 28, 2003, and was admitted to a local hospital, where chest radiography showed left pleural effusion and cardiomegaly. Echocardiography indicated an echo-free space around the heart with normal systolic function (Fig. 1). Laboratory findings included a white blood cell count of 7500/µl, CRP of 11.5 mg/dl and an erythrocyte sedimentation rate of 34 mm/h. While the patient was being treated with diuretics and antibiotics, his physical condition gradually worsened. He was referred to Shinshu University Hospital on March 27, 2003. Physical examination revealed peripheral edema and hepatomegaly. Blood pressure was 116/72 mmHg with a regular pulse rate of 120 beats per minute. In the sitting position, the neck veins were distended, precluding assessment of respiratory changes. Hematological and biochemical analyses were as follows: white blood cell count, 12870/µl; hemoglobin, 12.2 g/dl; platelets, 12.2 x 104/µl; total protein, 7.4 g/dl; albumin, 2.8 g/dl; BUN, 95 mg/dl; creatinine, 2.2 mg/dl; LDH, 1232 U/l; AST, 84 U/l; ALT, 58 U/l;
GTP, 120 U/l and CRP, 10.0 mg/dl. Arterial blood gas analysis during 10 l oxygen inhalation showed PaO2 of 62.7 Torr, PaCO2 of 28.7 Torr and pH of 7.536. Repeated two-dimensional echocardiograms did not indicate any pericardial effusion or cardiac mass, and showed a narrow space between the epicardium and the pericardium, suggesting possible adhesion of the epicardium and pericardium. In addition to the mass in the right upper lobe, the chest CT scan visualized a thickened pericardium (Fig. 2). Cardiac catheterization showed a high mean pulmonary artery pressure (29 mmHg), right atrial pressure (19 mmHg), pulmonary wedge pressure (19 mmHg) and low cardiac index (1.29 l min–1 m–2), although the pressure curve of the right ventricle did not show a typical dip-and-plateau pattern.
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The patient's hemodynamics deteriorated rapidly and he died of heart failure 6 days after admission. Post-mortem examination found that the pericardium was thickened and diffusely infiltrated with fibrous tissues and tumor cells (Fig. 3a). The tumor tissue extended from the primary lesion in the right upper lobe to the pericardium through the mediastinum. The histological finding was metastasis from adenocarcinoma of the lung that invaded slightly into the myocardial tissue (Fig. 3b).
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DISCUSSION |
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TOPAbstractINTRODUCTIONCASE REPORTDISCUSSIONReferences |
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The initial manifestation in the present case was acute onset characterized by fever, dyspnea, mild pericardial effusion and positivity for C-reactive protein, which closely resembled the clinical presentation of acute pericarditis. Subsequently, the patient rapidly developed pericardial constriction within 2 months and died of cardiac compression. The pericardium had thickened in association with the disappearance of the pericardial fluid. Neoplastic pericardial diseases generally cause major pericardial effusions, and cardiac tamponade is their most common complication (1–3). Some case reports, however, have indicated that neoplastic encasement of the heart caused constriction without pericardial effusion, especially in patients with lung cancer (4–6). Histological analysis of these cases showed that the tumor was located in adjacent tissues and not in the pericardium. However, the occurrence of pericardial effusion prior to the development of pericardial constriction is rare (1–4,6–8). Post-mortem findings suggest that the clinical aspects of the onset of pericardial involvement represented direct metastasis.
Initially, we speculated that the accumulation of hemorrhagic effusion in the pericardial space could explain the development of the constrictive condition in this case. Indeed, mediastinal hematoma can lead to the development of constrictive pericarditis within weeks or months after a cardiac operation (7–9). However, post mortem examination showed no pathological findings suggesting bleeding around the pericardium or the presence of other diseases.
The hemodynamic conditions in the present case appeared to be difficult to differentiate from restrictive cardiomyopathy. However, the pathological findings could not explain the restriction to ventricular filling, because of a few myocardial infiltrations of malignant cells. In addition, patients with underlying malignancies may have pericardial effusion and/or constriction due to non-neoplastic causes. Radiation therapy for the mediastinum, in particular, can produce acute or delayed abnormalities in the pericardium (1–3,7,10), although the symptoms of pericardial disease occur in only a minority of the irradiated patients. The clinical aspects of our patient included pericardial effusion and subsequent development of thickening of the pericardium. Although he had been treated with thoracic radiation, the irradiated area was the right upper thoracic area (primary tumor area), not the mediastinum. We therefore speculated that the clinical manifestation of the case presented here was not related to the previous thoracic-radiation therapy.
In summary, the case presented here demonstrated that severe pericardial constriction develops within a short time after the effusive phase in patients with malignancies. The possibility of severe pericardial constriction should thus be included in the diagnosis and management of patients with lung cancer.
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References |
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