A 5-year-old female was admitted to the department of pediatrics with a fever of 39.0 C, fatigue and chest pain. The symptoms appeared 3 days prior and were not preceded by an infection. The patient otherwise appeared healthy and did not require any specialist medical care. A SARS-CoV-2 infection was excluded by PCR test, that was negative for both the patient and her mother.
Because of tachycardia (150 bpm) and a silent murmur over the heart, echocardiography was ordered, which revealed a thin layer of fluid in the pericardial sac (3.8 mm thick). Additionally, there was a sinus tachycardia with diffuse ST elevations in precordial and limb leads (Figure 1). Laboratory evaluation revealed elevated C-reactive protein (CRP) level of 90 mg/ml (0-5 mg/ml normal range), while troponin (TnI), procalcitonin and complete blood count results within normal range. The tests for borreliosis, tuberculosis and HIV infection were negative as well as blood cultures for multiple organisms. The results of complex autoimmune diagnostics, including anti-nuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA) and anti-Scl-70 antibodies were unremarkable. Since the fever continued, with no satisfactory response to oral paracetamol and ibuprofen, empirical broad-spectrum antibiotic therapy was started. In the following days, as the changes on electrocardiogram disappeared and the layer of pericardial effusion appeared stable, the daily dose of ibuprofen was reduced. Despite that, the patient remained dysphoric and sleepy, with continuous low-grade fever. On her 15th day of admission to hospital, CRP increased to 115 mg/ml, TnI raised to 7 ng/L (0-2.5 ng/L normal range) and echocardiography revealed fibrinous adhesions between the pericardial laminae. High dose ibuprofen was re-administered and continued for another 9 days with the addition of colchicine. On the 24th day, the patient was discharged home with CRP reduced to 25 mg/mL and 2.2 mm thick layer of fluid in the pericardial sac. Ibuprofen (2 x 100 mg per os) and colchicine (1 x 0.5 mg per os) were prescribed until the next out-patient review.
The girl and her mother presented 10 days later at the Emergency Department in a different town with relapse of fever (38.6 C). Once again, the PCR test for SARS-CoV-2 RNA was found to be negative. Considering the patient's past medical history, current symptoms and elevated inflammatory markers, she was transferred to the Clinic of Pediatric Cardiology.
An echocardiogram was performed, which revealed a 4.5 mm thick layer of fluid between pericardial laminae. Moreover, a thickened parietal lamina was connected to the visceral lamina with hyper-echogenic fibrous adhesions (Figure 2A). At the time of examination, the girl did not complain of chest pain or dyspnea. On auscultation, there was a pericardial friction rub over Erb's point and inverted T-waves were recorded on the ECG (Figure 3A). The medical interview taken at that point revealed some additional information. Three days prior to the first episode of fever, the girl underwent a significant blunt force trauma to the chest while playing outside. Initially, she reported superficial pain of her ribs and thoracic spine. She attended the family doctor, who did not find any musculoskeletal lesions. Two days later, the fever appeared, and the location of the pain changed to deep inside the chest.
Considering all the above, the patient was diagnosed with incessant pericarditis and administered ibuprofen (3 x 200 mg daily). The girl was visited by specialists in pediatric rheumatology, hematology, and immunology, however the etiology of her pericarditis remained unknown. Chest CT showed no pathological features over the lungs or mediastinum, and no additional abnormalities in laboratory tests appeared.
After 4 days of treatment, the girls' overall condition improved considerably, however fibrinous pericardial effusion persisted, as did the elevated CRP. Steroid therapy with oral prednisone 1 mg/kg daily was initiated, which improved her condition considerably. On the 7th day of hospitalization (after four doses of prednisone), not only did the CRP level decrease, but the ECG improved (Figure 3B) and the effusion resolved completely (Figure 2B). The patient was discharged home and after 2 weeks of therapy (prednisone, high dose ibuprofen and colchicine) with a satisfactory echocardiographic and clinical effect, the dose of ibuprofen and prednisone were gradually reduced. After 4 weeks, the patient was only receiving colchicine, which was continued for another month. In a 5-month follow-up, she remained asymptomatic, with physiological amounts of pericardial fluid (Figure 2C) and a normal ECG for her age (Figure 3C).
Considering absence of other factors likely to cause pericarditis as well as an immediate response to steroids, we presume that a post-traumatic inflammatory reaction was the most probable etiological mechanism for patients' condition.