J Thorac Cardiovasc Surg 1996;111:1283-1286
© 1996 Mosby, Inc.
MEDIASTINAL HISTOPLASMOSIS CAUSING MASSIVE HEMATEMESIS
Margarita T. Camacho, MDa,
Morris Edelman, MB, BChb,
Alla Rozenblit, MDc,
John C. McKitrick, PhDb,
Kenneth Pinsker, MDd,
Stanley C. Fell, MDa
Bronx, N.Y.
Received for publication Sept. 12, 1995 Accepted for publication Sept. 19, 1995.
The granulomatous lymphadenitis that occasionally follows pulmonary infection with Histoplasma capsulatum (HC) may lead to the development of mediastinal granuloma or may progress to diffuse mediastinal fibrosis. In some cases, the superior vena cava, tracheobronchial tree, pulmonary vasculature, or the esophagus is compressed or entrapped, with resultant compromise in function.
1 Recurrent massive hematemesis from an esophageal ulcer caused by HC mediastinal granuloma has not previously been reported.
A 27-year-old, previously healthy Ecuadorian man was admitted after an episode of hematemesis. Ten days before admission, he reported pleuritic chest pain, cough, and fever, for which antibiotics were prescribed. Physical examination revealed a hemodynamically stable man with a hematocrit of 40%. Results of chest radiography and routine laboratory studies were within normal limits, tuberculin test results were positive, and results of human immunodeficiency virus testing were subsequently reported as negative. Esophagogastroduodenoscopy revealed a 5 mm ulcer on the right anterolateral wall of the esophagus 30 cm from the incisors. The biopsy sample from the ulcer was described as granulation tissue with no growth on culture. The esophageal lumen was not narrowed, and the stomach and duodenum appeared unremarkable. Computed tomography of the chest demonstrated a 3 x 4 cm subcarinal mass inseparable from the midthoracic esophagus and deformity of the medial wall of the bronchus intermedius (Fig. 1). During the ensuing 10 days during which further diagnostic studies were performed, the patient had four episodes of hematemesis, necessitating transfusions of 8 units of blood; on one occasion, the patient's hematocrit fell to 20%. A barium esophogram was unremarkable. Flexible bronchoscopy revealed elevation and edema of the floor of the right main bronchus. Bronchial brushings were nondiagnostic. Wang needle aspiration of the subcarinal mass yielded budding yeast forms characteristic of HC (Fig. 2). Treatment with 200 mg itraconazole twice daily was commenced. In an effort to occlude the upper esophageal arteries, bronchial arteriography was performed (Fig. 3). Two right bronchial arteries were demonstrated, one of which was successfully embolized. The other bronchial artery perfused a zone of hypervascularity corresponding with the mass noted on the computed tomographic scan. Hematemesis recurred after the incomplete bronchial artery embolization, and right thoracotomy was performed. A ligneous mass was noted posterior to the right main stem bronchus, extending inferiorly to the level of the lower lobe bronchus. The mass was densely adherent to the bronchus and the esophagus. Half the circumference of the esophagus was decompressed by partial excision of the nodal mass. Histopathologic study of this tissue showed acute and chronic inflammation as well as focal nonnecrotizing granulomata. Silver staining demonstrated rare budding yeast forms approximately 2 µm in diameter with the morphologic appearance of HC. Bacterial and fungal cultures remained sterile. Urine was tested twice for HC antigen, with negative results. Massive hematemesis recurred on the fifth postoperative day; 5 L blood was transfused before reoperation, at which time the esophagus was further separated from the nodal remnant, creating a mural defect at the site of ulceration. Brisk arterial bleeding from the node was controlled by suture ligatures, and the esophageal defect was repaired. The postoperative course was uneventful, and bleeding has not recurred in the year since discharge. Itraconizol therapy was continued for that year, with radiologic evidence of resolution of the mediastinal granuloma.
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Fig. 1. Contrast-enhanced computed tomography demonstrates a 3 x 4 cm subcarinal mass, marked narrowing of esophageal lumen, and deformity of medial wall of bronchus intermedius.
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Fig. 3. Right bronchial arteriogram demonstrates a zone of hypervascularity corresponding to the subcarinal mass.
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HC is a ubiquitous fungus present in soil and endemic in several areas of the United States, where as many as 80% of inhabitants demonstrate positive skin test reactions. 1 Infection with HC is usually acquired by inhalation and may produce no significant symptoms. The few thoracic complications that may develop usually follow asymptomatic infection in an immunocompetent host or opportunistic infection in an immunocompromised host. Accordingly, the disease course may vary from a relatively insignificant respiratory infection to a lethal, disseminated illness. It is often difficult to establish the diagnosis of thoracic infection with HC. Culture results may be negative; sensitivity of the urine antigen test is 25% to 39% in limited disease and 10% to 21% in chronic pulmonary disease. 2 Complement fixation test results are positive in only 39% of cases. 3 Right paratracheal, subcarinal, and tracheobronchial adenopathy, best demonstrated by computed tomographic scan, are commonly noted mediastinal manifestations. The development of HC mediastinal granuloma has been reported in 5% to 15% of cases, with symptoms developing in 60% of these patients. 1 Esophageal involvement by mediastinal HC is uncommon and has been reported in 5% to 13% of cases. 4 Esophageal involvement has been reported in cases of disseminated HC, in which oral or intestinal ulcerations also occur, however, and esophageal bleeding has been reported in acquired immunodeficiency syndrome and disseminated HC. 5 Mediastinal fibrosis does develop in 34% of patients who have had mediastinal granuloma. On occasion, the diagnosis has been established by mediastinoscopy when paratracheal adenopathy is present. 4
The previously reported cases of esophageal involvement describe obstruction, bronchoesophageal fistula, traction diverticulum, and esophageal erosion and ulceration. 3,4 Esophageal bleeding caused by an eroding mediastinal granuloma has not been previously described. The cause of the bleeding was a hypervascularized nodal mass that eroded into the esophagus. Transbronchial Wang needle aspiration demonstrated HC in this case. This technique may obviate the need for thoracotomy to establish the diagnosis when mediastinal granuloma caused by HC is suspected. Had the bronchial artery embolization been successful in occluding the bleeding source, it is quite likely that treatment with antifungal agents might have obviated the need for operation. A case of tracheal esophageal fistula caused by mediastinal HC granuloma and diagnosed by mediastinoscopy was successfully treated in this fashion. 4
Footnotes
From the Departments of Cardiothoracic Surgery,a Pathology,b Radiology,c and Medicine,d Montefiore Medical Center, Bronx, N.Y. 
J THORAC CARDIOVASC SURG 1996;111:1283-6
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