A 22-year-old woman with Coxsackie B pericarditis presented atypically with a large unilateral pleural effusion, leading to cardiac tamponade requiring drainage of 360 mL of serous fluid.
Case Report (n=1)
A large unilateral pleural effusion can be a rare, atypical initial manifestation of viral pericarditis, and delayed recognition can result in life-threatening cardiac tamponade.
Abstract Pericarditis is characterized by inflammation of the pericardial sac, most commonly due to viral infection, with Coxsackie B virus among the leading etiologies. Although pericardial effusion frequently complicates pericarditis, pleural involvement is rare, and previously documented cases note bilateral involvement. Unilateral pleural effusions, particularly when large, may obscure diagnosis and misdirect clinicians toward pulmonary pathology. This case describes Coxsackie B pericarditis presenting with a large unilateral pleural effusion, an exceedingly uncommon manifestation that led to delayed diagnosis and eventual hemodynamic compromise. A 22-year-old woman with no past medical history presented with one week of fever, pleuritic chest pain, dyspnea, and dry cough. She denied recent travel, oral contraceptive use, or thromboembolic history. On admission, she was tachycardic and tachypneic but with normal blood pressure and oxygen saturation. Point-of-care ultrasound demonstrated a small pericardial effusion with mild right ventricular dilation. C-reactive protein and erythrocyte sedimentation rate were elevated, while troponin was normal. CT chest revealed a large, left-sided pleural effusion. Empiric therapy for community-acquired pneumonia was initiated. Thoracostomy drained 160 mL of orange, exudative (cell count 369) fluid with neutrophilic predominance (43%) and elevated red blood cells (2,850). Total chest tube output was 1.2 liters over four days. Cytologic analysis, bacterial and fungal cultures, mycobacterial smear, and autoimmune studies (including anti-nuclear, anti-DsDNA/smith antibodies, and rheumatoid factor) were negative. On hospital day six, the patient developed recurrent fever, leukocytosis, and tachycardia. Repeat imaging showed interval enlargement of the pericardial effusion. On echocardiography, no tamponade was initially noted, but progressive hypotension prompted transfer to the cardiac ICU and repeat echocardiography, which demonstrated right ventricular diastolic collapse and pulsus paradoxus. Urgent pericardiocentesis yielded 360 mL of serous fluid, with rapid hemodynamic improvement. Serum and pericardial fluid studies showed elevated Coxsackie B antibody titers, confirming viral pericarditis. Follow-up echocardiography revealed mild constrictive physiology, and she was discharged on colchicine and ibuprofen. At rheumatology follow-up, rilonacept and a prednisone taper were initiated, resulting in full clinical recovery. Cardiac MRI confirmed pericarditis without myocarditis. Coxsackie B infection is a common cause of pericarditis, and can rarely cause pleural effusions, which are often small and bilateral. This case demonstrates that a large unilateral pleural effusion can represent an atypical manifestation of viral pericarditis. Recognition of this presentation is essential, as in this case, diagnostic delay may allow for progression to tamponade physiology. Viral pleural effusion, although rare, should be considered in an otherwise healthy patient presenting with polyserositis. This abstract is funded by: None
Reichard et al. (Fri,) conducted a case report in Coxsackie B Pericarditis (n=1). Pericardiocentesis and medical therapy was evaluated. A 22-year-old woman with Coxsackie B pericarditis presented atypically with a large unilateral pleural effusion, leading to cardiac tamponade requiring drainage of 360 mL of serous fluid.