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.