A 16 year old Liberian male presented with acute chest pain, abdominal pain, nausea, and hypotension. He had intermittent pleuritic chest pain for several weeks, but not this severe. He was previously hospitalized for chest pain at another institution and was found to have calcified mediastinal adenopathy. Work up during that admission was not diagnostic, and since symptoms improved, he was discharged and scheduled to have an outpatient bronchoscopy. He immigrated to the United States 4 years ago from Liberia and lived in Ghana as a child. He received the Bacillus Calmette-Guerin (BCG) vaccine and did not have any exposure to tuberculosis. Blood pressure on presentation was 84/44, pulse 101, respiratory rate 16, temperature 98.4, with 99% oxygen saturation on room air. Pulsus paradoxus was present with 10-12 mmHg respiratory variation. He was somnolent, but arousable to voice. When awake, he was alert and answering questions. He had mild tachycardia with distant heart sounds; no murmur or rub was heard. Lungs were clear. Transthoracic echocardiogram showed a large circumferential pericardial effusion, right atrial diastolic collapse, and significant tricuspid valve inflow variation with respiration. Emergent pericardiocentesis withdrew 900 ml of serosanguinous fluid. Blood pressure improved to normal levels after the procedure. Pericardial fluid testing was undiagnostic. Testing from his previous hospitalization later revealed serum detection of Histoplasma antibody immunodiffusion M band and Histoplasma antibody complement fixation titer of 1:128. He was placed on amphotericin B for 7 days and then transitioned to oral itraconazole. He was also prescribed colchicine and ibuprofen. Chest pain slowly resolved. Pericardial effusion did not reaccumulate, and an echocardiogram two months later had no signs of granulomatous pericardium.
Discussion:
This case illustrates pulmonary histoplasmosis causing pericarditis with a large inflammatory pericardial effusion resulting in cardiac tamponade. Pericarditis is caused by an inflammatory response to Histoplasma capsulatum since pericardial fluid is usually culture negative. Patients can recover with anti-inflammatory medications alone such as nonsteroidal anti-inflammatory agents or steroids. Pericardial fluid must be drained if it is causing hemodynamic instability.
Conclusions:
Pulmonary histoplasmosis should be considered in those who present with mediastinal lymphadenopathy and pericarditis. An inflammatory reaction by the fungus can result in a large, culture negative pericardial effusion.