INTRODUCTION: Bacterial pericarditis accounts for less than 1% of cases of pericarditis and carries a 40% risk of mortality. Enterococcus faecalis pericarditis has been very rarely described as a cause of pericardial effusion sufficient to cause cardiac tamponade.
CASE PRESENTATION:A 73-year-old male with history of transfusion dependent primary myelofibrosis, on ruxolitinib, presented with one week of progressive fatigue, dyspnea, and generalized weakness. On admission, blood pressure was 113/65, heart rate 97, and he was afebrile. Hemoglobin was 8.0g/dl and platelet 41,000/mm3. Symptoms improved after transfusion with two units of red blood cells. Two days after admission, he was found obtunded by staff. His vitals were initially normal. CT angiography of the head and neck was normal other than presence of a large pericardial effusion. He rapidly became hypotensive (82/52) but heart rate remained 70. Norepinephrine was started. Bedside ultrasound demonstrated a large, circumferential pericardial effusion with right atrial diastolic collapse. He was intubated and placed on mechanical ventilation due to severe hypercapnic respiratory failure (pH 6.99, PaCO2 >165). His blood platelet count was 21,000/mm3. An emergent bedside pericardiocentesis with catheter drainage was performed, and 250ml of grossly bloody fluid was removed. Immediately following drainage, his blood pressure improved and his vasopressor requirements decreased by 50%. He developed fever and was started on broad-spectrum antibiotics with vancomycin and cefepime. The fluid was hemorrhagic and exudative(Table 1). CT chest the following day showed reaccumulation of the pericardial effusion and a right lower lobe consolidation. 90ml was drained on repeat pericardiocentesis. Culture of the initial pericardial fluid grew pan-sensitive Enterococcus faecalis. Over the next several days his multiorgan failure progressed until he ultimately passed away.DISCUSSION: This patient was transfusion-dependent, and his symptomatic improvement after transfusion provided false reassurance. In hindsight, volume expansion from transfusion may have inadvertently temporized his obstructive shock. He developed mixed obstructive and septic shock. Ultrasound was critical in identifying cardiac tamponade. The source of E. faecalis in the pericardial fluid remains obscure. Possibilities include direct spread from right lower lobe pneumonia. Alternatively, hemorrhage from thrombocytopenia may have caused metastatic infection from bacteremia. Potential sources for this are contaminated blood products or bacterial translocation from the GI tract into the bloodstream. However, blood, urine and sputum cultures did not grow any bacteria.CONCLUSIONS: Primary myelofibrosis causes chronic immunodeficiency and thrombocytopenia. Hemorrhagic bacterial pericarditis should be considered in the differential when evaluating the etiology of dyspnea in these patients.
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