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© 2000 American Society for Clinical Oncology
Nonmalignant Diagnoses in PatientsArthur Skarin, MDConsultant Editor
Departments of Medicine and Pathology; Dana-Farber Cancer Institute, Massachusetts General Hospital, and Harvard Medical School; Boston, MA CASE 1. MEDIASTINAL LYMPHADENOPATHY ASSOCIATED WITH CONGESTIVE HEART FAILURE A 66-year-old man with dilated cardiomyopathy secondary to coronary artery disease was noted to have diffuse mediastinal lymphadenopathy on computed tomography (CT) scan during evaluation for an orthotopic heart transplant. The patient had pulmonary congestion, recurrent ventricular tachycardia that required automatic internal cardioverter-defibrillator, atrial fibrillation, and a history of non–insulin-dependent diabetes. He reported a 75 pack-year smoking history but had ceased smoking more than 20 years earlier. Cardiac catheterization revealed a 15% left ventricular ejection fraction and reversible pulmonary hypertension. The chest CT showed enlargement of multiple mediastinal nodes in the precarinal, subcarinal, pericardial, anterior-posterior window, and hilar lung regions. Nodes measured 1 to 1.5 cm and included a 2 to 3-cm subcarinal lymph node (Fig 1, arrow). The chest CT also demonstrated cardiomegaly and a "ground glass" appearance in the lung fields consistent with pulmonary edema. After receiving medical therapy for congestive heart failure, a repeat CT scan showed improved pulmonary edema but no change in mediastinal lymphadenopathy. A third chest CT showed persistent mediastinal lymphadenopathy. Because of the persistent adenopathy and the potential for heart transplantation, a mediastinoscopy with biopsies of both the subcarinal and paratracheal nodes was performed. Histopathology revealed no evidence of malignancy and was only significant for anthracosis with numerous histiocytes containing carbon particles, consistent with his smoking history (Fig 2). A follow-up chest CT 8 months later showed increased bulky lymphadenopathy in the mediastinum. A subcarinal lymph node was estimated to be 4 x 2 cm. Abdominal, pelvic, and head CTs revealed no evidence of further lymphadenopathy or malignancy. A bone marrow biopsy showed normal morphology and iron stores. Cultures of the marrow for fungi and mycobacteria were negative. Because repeat cardiac evaluation showed fixed pulmonary hypertension, the patient was withdrawn from the organ transplant list. The patient has remained stable with advanced congestive heart failure.
The demonstration of mediastinal lymphadenopathy on chest CT as a result of congestive heart failure is not widely recognized. Slanetz et al1 reported one series of 46 patients who underwent chest CT during periods of symptomatic congestive failure. Some degree of mediastinal node enlargement was observed in 55% of cases. In a subset of 17 patients who had documented elevated pulmonary capillary wedge pressures within 24 hours of the CT scan, some degree of lymphadenopathy was observed in 82%. No patient was known to develop lymphoma or other malignancy during clinical follow-up of 2 years. Storto et al,2 however, failed to draw the association between congestive heart failure and mediastinal lymphadenopathy in a report of seven patients studied with high-resolution CT imaging. The pathogenesis of mediastinal lymphadenopathy in congestive heart failure is not known. In an experimental study, Drake et al3 used rapid ventricular pacing to induce heart failure in sheep. They demonstrated that efferent lymph flow was impeded when venous pressures exceeded 15 cm of water. A chronic impairment of lymph efferent flow might presumably lead to passive congestion of the node, resulting in lymphadenopathy in addition to the other more well-known findings of congestive heart failure on CT. Other than congestive failure, we found little evidence for another cause of bulky adenopathy in our patient. Although captopril, one of the patient’s chronic medications, has been associated with adenopathy, we would not expect that to be restricted to the mediastinal and hilar nodes.4 The differential diagnosis of mediastinal lymphadenopathy includes infectious, inflammatory, or neoplastic processes. It should be emphasized that patients with advanced congestive heart failure may demonstrate significant mediastinal lymphadenopathy on chest CT. Traditionally, 1.0 cm has been used as the upper limit of normal for the short axis of a mediastinal node in the transverse plane as detected on CT scan.5 Slanetz et al1 suggest that cases such as the one reported here in which the lymph nodes are larger than 2 cm or fail to decrease after resolution of pulmonary edema may warrant further investigation by biopsy. Ultimately, the decision to biopsy enlarged mediastinal nodes must be individualized for each patient, and further noninvasive studies, including gallium or positron-emission tomography scan, might help guide the clinician and avert unnecessary or further invasive procedures. REFERENCES
1.
Slanetz PJ, Truong M, Shepard JOA, et al: Mediastinal lymphadenopathy and hazy mediastinal fat: New CT findings of congestive heart failure. AJR Am J Roentgenol 171:1307-1309, 1998
2.
Storto ML, Kee ST, Golden JA, et al: Hydrostatic pulmonary edema: High-resolution CT findings. AJR Am J Roentgenol 165:817-820, 1995
3.
Drake RE, Dhother S, Teague RA, et al: Lymph flow in sheep with rapid cardiac ventricular pacing. Am J Physiol 272:R1595–1598, 1997 4. Aberg H, Morlin C, Frithz G: Captopril-associated lymphadenopathy. Br Med J (Clin Res Ed) 283:1297-1298, 1981
5.
Glazer GM, Gross BH, Quint LE, et al: Normal mediastinal lymph nodes: Number and size according to American Thoracic Society mapping. AJR Am J Roentgenol 144:261-265, 1985
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Copyright © 2000 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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