Using PET to Illuminate a Pericardial Puzzle

A 50-year-old man with no significant past medical history presents to the emergency department (ED) with 2 weeks of fevers, malaise, and intermittent chest pain. He was in his baseline state of health when he noted severe fatigue with his daily activities, such as getting dressed and shaving. He also noted decreased appetite, night sweats, fevers to 100°, splinter hemorrhages, and skin changes in his bilateral fingertips (Figure 1).

Figure 1

Figure 1

About 3 days prior to presentation, he developed chest pain that is non-exertional, diffuse, sharp in nature, and exacerbated when lying flat. He has no sick contacts, recent travel, occupational exposures, changes in weight, preceding viral illness, or prior history of cardiac disease or procedures. Given his continued symptoms, he called his primary care doctor, who recommended he present to his local ED.

In the ED, his vital signs are significant for a temperature of 102°F, heart rate of 114 bpm, and blood pressure of 117/76 mmHg. On cardiac exam, he is tachycardic with a regular rhythm, and no murmurs, rubs, or gallops are appreciated. Blood work is significant for a leukocytosis of 13k with neutrophilic predominance, troponin T of 0.011ng/mL, and elevated inflammatory markers (WSR 102 mm/hr, CRP 26 mg/dL, ferritin 800 ng/mL). An electrocardiogram (ECG) is obtained (Figure 2).

Figure 2

Figure 2

Based on typical chest pain and typical ECG findings of diffuse ST segment elevations with PR segment depression, a diagnosis of acute pericarditis is made. Transthoracic echocardiogram (TTE) and transesophageal echocardiogram (TEE) showed a small pericardial effusion with normal biventricular size and function, with no evidence of endocarditis. A serologic workup for rheumatologic disease is largely negative, including negative antinuclear antibody (ANA), antineutrophil cytoplasmic antibodies (ANCAs), cryoglobulins, antiphospholipid antibodies, and rheumatoid factor. Blood cultures reveal no culprit organism. An magnetic resonance imaging (MRI) is obtained, showing a small pericardial effusion with associated mild pericardial thickening and circumferential pericardial enhancement, supporting the diagnosis of acute pericarditis. Upper extremity vascular ultrasound revealed bilateral distal ulnar artery thrombosis. At this point, there was concern for a systemic inflammatory disease or occult malignancy as the underlying cause of his pericardial findings and ulnar thromboses. In this setting, a 18F-fluorodeoxyglucose-positron emission tomography (18F-FDG PET) scan is obtained, with representative images (Figure 3).

Figure 3

Figure 3
Figure 3: White arrows demonstrate areas of FDG-avidity throughout the pericardium.

Which of the following is a clinical use for 18F-FDG-PET in the evaluation of pericarditis?

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