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Ann Thorac Surg 2002;74:241-243
© 2002 The Society of Thoracic Surgeons


Case report

Pyopneumopericardium caused by mediastinal granuloma

Lorne J. Gula, MD, FRCPC*a, Richard A. Malthaner, MD, FRCSCb, Mackenzie A. Quantz, MD, FRCSCc

a Division of Cardiology, London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada
b Division of Thoracic Surgery, London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada
c Division of Cardiac Surgery, London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada

Accepted for publication October 17, 2001.

* Address reprint requests to Dr Quantz, London Health Sciences Centre, University Campus, Room 4-TU32, 339 Windermere Rd, London, ON N6A 5A5, Canada
e-mail: maquantz{at}julian.uwo.ca


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We report the case of a previously healthy 32-year-old man who was seen with flulike symptoms, dyspnea, and chest pain. The diagnosis was pyopneumopericardium, and pericardial tap revealed 1.3 L of purulent material. Computed tomography of the chest demonstrated a calcified mass inferior to the carina. Urgent exploration through a right thoracotomy revealed that the mass was adherent to the esophagus and pericardium. The subcarinal mass was resected. Pathological study demonstrated granulomatous lymph nodes, which were likely due to histoplasmosis. This is among the first reports of granulomatous erosion into the pericardium causing pyopneumopericardium. The patient made a good recovery, and his case demonstrates the importance of early imaging and mediastinal exploration for pyopneumopericardium. cardiac tamponade, esophageal fistula, granuloma, histoplasmosis, pyopneumopericardium, pneumopericardium


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We report a case of pyopneumopericardium in a previously healthy 32-year-old man. Pathological study of a resected subcarinal mass demonstrated granulomatous lymph nodes, which was likely due to histoplasmosis. This is one of the first times that granulomatous erosion into the pericardium causing pyopneumopericardium has been reported.

A previously healthy 32-year-old man was admitted to the hospital with chest pain and dyspnea. He was employed as a chef and had no history of heart disease, lung disease, gastrointestinal symptoms, esophageal trauma, cancer, or hematologic disease and had no risk factors for human immunodeficiency virus. The patient was well until 2 weeks prior to admission when mild flulike symptoms developed. This progressed to dyspnea and sharp central chest pain radiating to the back. Ventilation/perfusion scan was negative, and no abnormalities other than possible right lower lobe consolidation were detected on chest radiograph and the symptoms progressively worsened. The patient was admitted to the hospital on December 2, 2000 with a provisional diagnosis of pleurisy, and treatment was initiated with methylprednisolone, ceftriaxone sodium, and azithromycin dihydrate. An echocardiogram intended to assess ventricular function revealed a moderate pericardial effusion, no evidence of tamponade, and normal ventricular function. Leukocyte count progressively increased, as did oxygen requirements, and the patient was transferred to our center on December 4.

On arrival, the patient was flushed and dyspneic. Heart rate was 88 beats per minute, respiratory rate was 30 breaths/min, and blood pressure was 100/80 mm Hg with no pulsus paradoxus. Oxygen saturation was 89% on 3 L/min of oxygen. Jugular venous pulsation was 10 cm above the sternal angle, and heart sounds were muffled with no extra sounds, murmurs, or rubs. Mild pedal edema was present. Laboratory abnormalities included leukocytosis (30.6 x 109/L with 28.1 neutrophils, 1.3 lymphocytes, 1.0 monocytes, 0.1 eosinophils, and 0.1 basophils) and a lactate dehydrogenase value of 1,238 U/L. Renal and liver function test results were normal. Human immunodeficiency virus and tuberculin test results were negative. Chest radiograph revealed cardiomegaly with a new air-fluid level (Fig 1). Electrocardiogram revealed sinus tachycardia, persistent ST segment elevation in all leads, and diffuse T-wave abnormalities. Repeat echocardiogram made 3 days after the initial study continued to show a large pericardial effusion with no evidence of diastolic right atrial collapse.



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Fig 1. Posteroanterior chest radiograph showing cardiomegaly and air-fluid level in pericardium (arrow).

 
On December 7, the patient’s respiratory status deteriorated with signs of tamponade. Pericardiocentesis revealed a pyopneumopericardium yielding 1,300 mL of foul-smelling purulent material. Fluid cell count was 69.2 x 109/L with 69% lymphocytes, 28% monocytes, and 3% polymorphonuclear cells. Protein value was 11 g/L and glucose level, 0.4 mmol/L. Cultures revealed 3+ {alpha}-hemolytic streptococci, 2+ nonhemolytic streptococci, 2+ nonsporulating gram-positive rods, and 3+ anaerobic organisms (Peptostreptococcus, Fusobacterium, and gram-negative rods). Acid-fast bacilli culture was negative, as were blood cultures. There was a temporary and modest improvement in hemodynamic status.

Later the same day, thoracic computed tomogram demonstrated a calcified mass inferior to the carina (Fig 2). There was substantial soft-tissue attenuation surrounding the mass, which stretched from the esophagus to the posterior pericardium. Pneumomediastinum was present and extended to the level of the arch vessels. There was no evidence of oral contrast medium in the mediastinum.



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Fig 2. Computed tomographic scan of thorax showing calcified mass (arrow) adherent to pericardium and esophagus, and air in mediastinum (arrowheads). (L = left; R = right.)

 
Urgent exploration was performed through a right thoracotomy. A subcarinal mass measuring 2.5 x 1.5 x 1 cm was found adherent to the esophagus and the pericardium. The mass was resected, the esophagus was repaired primarily, and a pericardial window was created. Pathological study revealed a lymph node containing necrotizing granuloma, with hyalinization and calcification. There was no evidence of malignancy, and stains for fungus and acid-fast bacilli were negative. Samples of pericardial tissue revealed fibrinous pericarditis. Postoperatively, rapid atrial fibrillation developed but responded to diltiazem hydrochloride. The condition of the patient gradually improved, and he was discharged home on postoperative day 21.


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Pyopneumopericardium is an ominous diagnosis with a mortality rate near 100% [1]. The presence of pneumopericardium necessitates consideration of esophagopericardial fistula. Such a fistula is most often caused by erosion of esophageal ulcers, ingestion of a foreign body, or an iatrogenic source [2], and 20% are missed by barium studies [3].

Mediastinal granulomas result from the fusion of caseous mediastinal lymph nodes. The most common cause is histoplasmosis, although special stains and cultures are often negative. Granulomas have been known to erode into the esophagus and airway [4] and to cause pericarditis and pericardial effusion [5]. This is one of the first reports of granuloma eroding into the pericardium. In our patient, a mediastinal granuloma, presumed due to histoplasmosis, eroded into the esophagus and the pericardium resulting in pyopneumopericardium and cardiac tamponade. The good outcome demonstrates the importance of early imaging and mediastinal exploration when pyopneumopericardium is diagnosed.


    References
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 References
 

  1. Cummings R.G., Wesly R.L.R., Adams D.H., Lowe J.E. Pneumopericardium resulting in cardiac tamponade. Ann Thorac Surg 1984;37:511-518.[Abstract]
  2. Miller W.I., Osborn M.J., Sinak L.J., Westbrook B.M. Pyopneumopericardium attributed to an esophagopericardial fistula: report of a survivor and review of the literature. Mayo Clin Proc 1991;66:1041-1045.[Medline]
  3. Gyrlak D., Cohen A.J., Dana E.R. Esophagopericardial fistula: causes and radiographic features. AJR 1983;141:177-179.[Free Full Text]
  4. Garrett H.E., Jr, Roper C.L. Surgical intervention in histoplasmosis. Ann Thorac Surg 1986;42:711-722.[Abstract]
  5. Wheat L.J., Stein L., Corya B.C., et al. Pericarditis as a manifestation of histoplasmosis during two large urban outbreaks. Medicine 1983;62:110-119.[Medline]



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This Article
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