ArticleCureus2025
Hemorrhagic Pericardial Effusion Secondary to Coxsackie B Pericarditis.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Acute pericarditis is caused by inflammation of the pericardial sac. Among the vast number of potential causes, viruses tend to trigger pericarditis most frequently. Some of the more common viral causes are Coxsackie A/B, echovirus, adenovirus, cytomegalovirus, herpes simplex virus, and human immunodeficiency virus. Pericardial effusion is a common complication and can be visualized on echocardiogram. In some cases, the pericardial effusion can be hemorrhagic in nature, which is extremely rare in the setting of viral pericarditis. The most common causes of hemorrhagic effusion are myocardial infarction, trauma, aortic dissection, or coronary artery bypass graft surgery. Pericardial effusion can sometimes result in serious complications such as cardiac tamponade. In cases of significant pericardial effusion, pericardiocentesis may be required. We present an interesting case of pericarditis caused by the Coxsackie B virus, causing significant hemorrhagic pericardial effusion requiring pericardiocentesis in a young patient. A 37-year-old female with no relevant past medical history presented with substernal chest pain radiating to the left arm and shoulder that improved with leaning forward and dyspnea for two weeks. She had a two-week history of a cough, dysphagia, fever, and chills that started two days prior to the presentation. EKG showed widespread ST elevations and PR interval depressions, which is consistent with a diagnosis of pericarditis. A large pericardial effusion was present on echocardiogram, further suggesting possible pericarditis. Around 350 mL of fluid was removed by pericardiocentesis. Cell count showed 201,000 red blood cells (RBCs)/mcL and 9,350 nucleated cells/mcL. Cytology was negative for malignancy. Cultures were negative for bacteria and fungi. Serum serology showed elevated inflammatory markers (C-reactive protein of 140 mg/L and erythrocyte sedimentation rate of 112 mm/hr) and increased Coxsackie B antibody titers (1:160 for type 2 and 1:320 for type 3). She was started on non-steroidal anti-inflammatory drugs and colchicine. This is a unique case showing that while small exudative pericardial effusions may occur with viral pericarditis, viral infections can also cause a significant hemorrhagic pericardial effusion. Most Coxsackie virus infections are benign. However, there are a few documented case reports of hemorrhagic pericardial effusion from Coxsackie B causing tamponade and death. The importance of this case is that it highlights the consideration of viral infections such as Coxsackie B as a potential cause of hemorrhagic tamponade, especially during autumn and winter months, seasons with the highest risk.
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