Case Description
A 56-year-old white male with a previous medical history of stroke, hyperlipidemia, hypertension, sacral decubitus ulcer and a long-term indwelling Foley catheter presented with severe dyspnea. His vital status was remarkable for a heart rate of 108 beats per minute, respiratory rate of 22, blood pressure of 106/81mmHg and temperature of 37oC. Physical exam was negative for murmurs, rub or gallop. Initial workup was significant for elevated white blood cells at 36.6(10x3/uL), elevated troponin level at 0.45ng/L and positive urine and blood cultures for methicillin-resistant staphylococcus aureus (MRSA). The ECG showed sinus tachycardia and diffuse ST-elevations in leads I, II, III and V2-V6 with PR-elevation in lead aVR suggestive of pericarditis. To rule out myocardial infarction, coronary angiography was done and showed no significant coronary stenosis. 2DTTE demonstrated a large circumferential pericardial effusion measuring 23mm in maximum depth with echogenic material consistent with fibrin overlying the cardiac walls.[9,10] Signs of cardiac tamponade including pulsus paradoxus, plethoric inferior vena cava, RV diastolic collapse and right atrial inversion were present. Both left and right ventricular size and function were normal with no valve abnormalities. Subcostal pericardiocentesis was performed and 490mL of cloudy purulent fluid was drained with relief of dyspnea. The culture of pericardial fluid came back positive for MRSA. The patient was begun on daptomycin and piperacillin/tazobactam. A repeat 2DTTE 2 days post pericardiocentesis showed only a small amount of residual effusion, but continued presence of the fibrinous material over the RV wall. Because of this and in an effort to prevent possible progression to constrictive pericarditis, 2mg of fibrinolytic agent (tissue plasminogen activator, alteplase) diluted in 10 ml of normal saline was administered intrapericardially followed by 10ml normal saline flush. The pericardial drain was clamped for 24 hours. The next day, the patient drained 450mL of pericardial fluid. A repeat 2DTTE 2 days later revealed trivial pericardial effusion (Figures 1A, 1B and 2A, 2B, Movies 1A, 1B and 2A, 2B). In the parasternal long axis view, the area of the RV wall together with fibrin deposition measured by planimetry decreased from 261.9mm2 to 155.48mm2, a substantial reduction of 40.6%. In the apical four chamber view, the RV wall plus fibrin area decreased from 270.82mm2 to 139.4mm2, also a substantial reduction of 48.5%. Fibrin deposition on the RV wall could be recognized using 2DTTE by its uneven irregular contour/localized bulging on the outer pericardial aspect of the RV wall. However, the inner boundary of fibrin deposit could not be distinguished from the contiguous RV wall and hence planimetry included both the fibrin deposit and RV wall. These declines in RV wall areas in our patient are indicative of marked decrease in the amount of fibrinous material by dissolution following IFA.
Our patient did not suffer from any side effects following IFA such as hemorrhage or cardiac tamponade which have been reported previously.[3, 6, 9] Subsequently, intravenous vancomycin was substituted for daptomycin, and the patient was transferred to an acute care rehabilitation for further treatment and care. After 30 days of inpatient rehabilitation, the patient was discharged in stable condition with no clinical evidence of pericardial constriction.