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J Thorac Cardiovasc Surg 1997;114:295-297
© 1997 Mosby, Inc.
BRIEF COMMUNICATIONS |
San Diego, Calif.
Received for publication Dec. 2, 1996. Accepted for publication Jan. 23, 1997. Address for reprints: Stuart W. Jamieson, FRCS, Department of Cardiothoracic Surgery, UCSD Medical Center, 200 West Arbor Dr., No. 8892, San Diego, CA 92103-8892.
Chronic pulmonary embolism with pulmonary hypertension is optimally treated by bilateral pulmonary thromboendarterectomy with the use of cardiopulmonary bypass and profound hypothermic circulatory arrest.
1 With very few exceptions, chronic pulmonary embolism is a bilateral disease. However, we recently performed a unilateral pulmonary thromboendarterectomy with exploration of the contralateral side for a patient with a chronic pulmonary embolus after a right nephrectomy for renal cell carcinoma.
Clinical summary
The patient is a previously healthy 40-year-old man who was referred for the evaluation and treatment of pulmonary hypertension. Three months earlier he had had chest pain and severe dyspnea on exertion. A ventilation/perfusion scan revealed the absence of perfusion to the entire left lung, with a few areas of subsegmental defects in the right lower lobe. He was initially treated with intravenous streptokinase, but this was discontinued because of a toxic reaction. After systemic anticoagulation, a computed tomographic scan of the abdomen and pelvis revealed a large renal tumor impinging on the inferior vena cava. A cardiac echocardiogram demonstrated normal left ventricular wall function with no evidence of a right atrial or ventricular mass, a lower extremity duplex scan showed no deep venous thrombosis, magnetic resonance imaging of the head showed no abnormalities, and results of a bone scan were negative.
A right nephrectomy was performed. Pathologic examination showed a renal cell carcinoma with invasion into the renal vein. Lymph nodes were not diseased. The patient was transferred to our medical center for further diagnostic workup. He still had severe dyspnea on exertion. A second ventilation/perfusion scan confirmed the lack of perfusion to the left lung. Results of pulmonary function tests were consistent with a mild restrictive defect (diffusing capacity for carbon monoxide of 21.5 or 65%, total lung capacity of 5.59 L or 79%, and normal flow rates). Blood gases with the patient breathing room air were 7.38/83/39 with no desaturation during exercise.
Preoperative catheterization of the right side of the heart demonstrated normal right-sided pressures at rest and a marginally elevated pulmonary vascular resistance (162 dynes · sec · cm5). With exercise, the pulmonary artery pressure increased to 50/15 mm Hg (mean 30 mm Hg). A pulmonary arteriogram demonstrated complete occlusion of the left main pulmonary artery with normal flow to the right lung (Fig. 1). Pulmonary angioscopy revealed a reddish-gray intraluminal lesion occluding the left main pulmonary artery.
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1 On the left side a large clot with fibrous margins incorporating the intima and media was identified, which occluded the entire left main pulmonary artery. This was removed. The appearances were of a yellow-white fibrinous mass measuring 6 cm x 3 cm x 1.5 cm (Fig. 2). No occluding material was found on the right side. The final pathologic examination of the specimen revealed only organized thrombus and embolus with no evidence of tumor.
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Discussion
In a small percentage of cases of acute pulmonary embolism the clot persists in the pulmonary artery and eventually becomes organized into a fibrotic mass resulting in chronic pulmonary hypertension. 1 In our series of 800 patients operated on for thromboembolic pulmonary hypertension, almost all have had bilateral disease with severe pulmonary hypertension. A few patients had a pulmonary vascular resistance of less than 300 dynes · sec · cm5 and had unilateral pulmonary artery occlusion with a large dead space resulting in unacceptable dyspnea on exertion, as in this case.
This patient was also unusual in that the embolus derived from a renal tumor. Large-tumor embolization from renal cell carcinoma resulting in vascular compromise occurs infrequently, accounting for only seven of 1248 deaths (0.6%) in one series. 2 The pathologic finding of clot without evidence of tumor is consistent with previous findings that most of the pulmonary emboli in patients with renal cell carcinoma contain benign fibrinous clot with no gross or microscopic evidence of tumor. 3 This would suggest that the embolized tumor fragments are either destroyed in the pulmonary artery or remain latent within the vessel wall without parenchymal invasion. Tumor pulmonary embolism therefore does not necessarily imply metastatic disease. 4,5
In this patient the embolic material on the right side was resolved, but not on the left, probably because of total occlusion. The operation restored the circulation to normal, but an embolectomy did not suffice—a true endarterectomy was required because of the fibrotic, chronic nature of the lesion, with distal thrombosis. Operation in this patient resulted in the complete resolution of symptoms and was likely curative. To our knowledge, this is the first known case of removal of renal cell carcinoma embolus by pulmonary thromboendarterectomy.
References
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