Case Presentation: A 71 year old man with a past medical history of end-stage renal disease on hemodialysis, hyperlipidemia, and diabetes mellitus presented with 5 days of weakness, dry cough, and dyspnea after missing multiple dialysis sessions. His vitals were stable and his exam was notable only for trace lower extremity edema. Notable labs included troponin level of 3.21 ng/ml, BNP 23,600 pg/mL, creatinine level 15.6 mg/dL, BUN 118 mg/dL and potassium level was 6.8 mEq/L. He was found to have ST elevations in inferior-lateral leads and ST depressions in V1 and aVR leading to an emergent cardiac catheterization, which revealed no abnormalities. A subsequent echocardiogram showed a moderate sized pericardial effusion with no signs of tamponade or chamber collapse. It was determined that the etiology was likely uremic myopericarditis in the setting of missed dialysis. Despite urgent dialysis, his serial echocardiograms showed an increasing moderate to large pericardial effusion with a fibrous layer. Given evidence of hemodynamic compromise with hypotension and tachycardia, the patient underwent pericardiocentesis with aspiration of 510 mL of fluid. Analysis of the fluid revealed 46,060 white blood cells, 98% neutrophils and intracytoplasmic bacteria. Cultures grew pan-sensitive Staphylococcus aureus. The patient was started on Cefazolin with dialysis for four weeks and was discharged. His blood cultures both peripherally and from his AV fistula were negative. After treatment course and ongoing dialysis, his follow-up echocardiogram revealed no further effusion.
Discussion: Bacterial infections of the pericardial space are an uncommon cause of pericardial effusions. The reported incidence of this is < 1% of all cases of pericarditis. In healthy individuals, the pericardial cavity contains 15 to 50 mL of plasma. Infection can rapidly increase pericardial fluid volume and pressures leading to tamponade. Bacterial pericarditis usually occurs as a secondary infection by contiguous spread from a surrounding intrathoracic focus of infection or by hematogenous spread from a distant source. Dialysis, thoracic surgery, chemotherapy, immunocompromise, and AIDS are risk factors for purulent pericarditis. We present a rare presentation of purulent pericarditis in a patient with dialysis and uremia. This patient’s disease is unusual for several reasons, including his symptom presentation. Most notably, almost all reported patients with purulent pericarditis have fever, which this patient never developed. Only 50% of patients develop the classic signs of acute pericarditis (chest pain, friction rub, and pulsus paradoxus), with 25-37% having chest pain like this patient. No source of bacterial seeding was found in this patient, making it either a primary bacterial pericarditis or as a result of a transient bacteremia that was not captured on the blood cultures. Uremia can precipitate pericarditis due irritation of the toxins. Notably, this usually does not result in ST changes on EKG and rapidly improves with dialysis. Immune dysfunction also results from the uremic toxins, predisposing those patients to infection. Mortality in patients who are treated for purulent pericarditis is estimated to be 40%, while it is 100% for those who are untreated. This patients’ atypical symptoms and relatively indolent course was a rare presentation of a deadly disease.
Conclusions: It is important to consider infectious pericarditis in new pericardial effusions due to the rapid progression of the disease and high mortality rate.