Purulent pericarditis caused by methicillin-sensitive Staphylococcus aureus bacteriuria

An 81-year-old male presented to our Emergency Department with severe, sharp, non-radiating, epigastric pain that worsened with inspiration. Past medical history included open-angle glaucoma, sciatica, urinary retention due to benign prostatic hyperplasia for which he self-catheterized twice daily, and urinary tract infections and asymptomatic bacteriuria due to MSSA resistant to trimethoprim-sulfamethoxazole. Two years prior to admission he presented for dysuria and received antibiotic treatment for a urinary tract infection due to this specific isolate of MSSA. The episode of asymptomatic bacteriuria occurred a few months prior to presentation when he underwent pre-operative workup for a cystolithotripsy for two bladder stones. Immediately prior to that procedure he received vancomycin as a pre-operative antibiotic. He tolerated the procedure well and did not experience any urinary tract infections after that.

He lived an active lifestyle with frequent exercise and denied worsening chest pain or dyspnea with exertion. Review of systems was negative for orthopnea, paroxysmal nocturnal dyspnea, and lower extremity edema. Notably, in the preceding two weeks of admission, he had several Emergency Department visits for left hip pain. A hip x-ray was negative for fracture, joint dislocation, and significant degenerative disease. There were no signs of joint erythema or effusion to warrant workup for septic arthritis. He was prescribed diclofenac gel, lidocaine patches, acetaminophen and, notably, a course of prednisone for presumed inflammatory hip pain. For 5 days prior to admission, he had been taking 60 milligrams of prednisone daily, with plans for a 12-day taper.

On presentation the patient was afebrile and hypertensive with a blood pressure of 168/81 mmHg. Labs were notable for a white blood cell count of 22.95 × 109/L (4.0–11.0 × 109/L), absolute neutrophil count of 21.55 × 109/L ​​(2.0-7.7 × 109/L), troponin of 0.174 ng/mL (≤ 0.028 ng/mL), with a repeat value at 0.165 ng/mL, and a C-reactive protein of 64.28 mg/L (≤ 5.0 mg/L). Urinalysis was notable for turbid urine with 2 + blood, 19 red blood cells per high power field, 49 white blood cells per high power field, and a leukocyte esterase of 250 leukocytes/µL. ECG revealed normal sinus rhythm without ST segment or T wave abnormalities. Chest x-ray demonstrated mild cardiomegaly, but was otherwise unremarkable, and an echocardiogram revealed normal biventricular function, an ejection fraction of 60–65%, and no evidence of regional wall motion abnormalities, valvular vegetations, or significant pericardial effusion (Fig. 1A).

Fig. 1figure 1

Echocardiographic Images

Transthoracic echocardiogram on hospital day #1 showing no significant pericardial effusion on parasternal long axis (A). Repeat echocardiogram on hospital day #3 showing a large pericardial effusion on parasternal long axis (B) and apical (C) views. Mitral inflow variability on pulsed wave Doppler was present (D) along with right atrial wall collapse (E), concerning for a hemodynamically significant effusion

The patient was admitted, and the next day underwent a nuclear stress test which did not expose any fixed or reversible perfusion defects. Later in the day, the patient developed severe back pain and tachycardia of 110 beats per minute. Computed tomography scan displayed a large pericardial effusion measuring 18 millimeters in thickness and bibasilar pulmonary atelectasis. Over the course of the day, the patient became febrile to 101.5º F, persistently tachycardic, and required 3 L per minute of oxygen via nasal cannula to maintain an oxygen saturation over 90%. The patient was started empirically on intravenous vancomycin and piperacillin-tazobactam after cultures of the blood, urine, and sputum were obtained. Inflammatory markers such as white blood cell count, C-reactive protein, erythrocyte sedimentation rate, and procalcitonin progressively increased. Repeat imaging was obtained and a chest x-ray demonstrated interval enlargement of the cardiac silhouette and worsening bibasilar opacifications. A second echocardiogram was performed and demonstrated a circumferential pericardial effusion measuring 2.5 centimeters to 3.0 centimeters with findings suggestive of evolving cardiac tamponade based on the mitral and tricuspid valve inflow variabilities, dilated inferior vena cava with reduced collapse on inspiration, subtle right atrial collapse, and sinus tachycardia (Fig. 1B-E).

The patient underwent pericardiocentesis during which 360 milliliters of red-brown, turbid pericardial fluid was removed. A pericardial drain was placed, and fluid was sent for analysis. Blood, urine, and pericardial fluid cultures grew MSSA resistant to trimethoprim-sulfamethoxazole, and > 100,000 colony forming units of this isolate of MSSA were present in the urine (Table 1).

Table 1 Antibiotic susceptibilities

For 24 h while cultures finalized the patient was treated with intravenous vancomycin and cefazolin because of a positive nasopharyngeal polymerase chain reaction test for methicillin-resistant Staphylococcus aureus and clinical decompensation. Treatment was subsequently narrowed to intravenous cefazolin thereafter. Unfortunately, the patient became increasingly encephalopathic and pulled out the pericardial drain, after which he became progressively dyspneic and went into cardiac arrest with pulseless electrical activity. Cardiopulmonary resuscitation was initiated immediately and return of spontaneous circulation was achieved within 10 min. Repeat echocardiography revealed a recurrent moderate-sized effusion measuring 1.5 centimeters to 2.0 centimeters and signs of hemodynamic effect. The patient underwent a subxiphoid pericardiotomy with a pericardial ‘window’. Although there was no discrete source of bleeding, the patient was noted to have oozing and diffuse inflammation of the pericardial surface. A total of 200 milliliters of thin sanguineous fluid were removed during the procedure, and 2 chest tubes were placed. The patient was initiated on the post-arrest therapeutic hypothermia protocol (targeted body temperature of 33º Celsius) after which he was noted to have large amounts of sanguineous chest tube output. After discussion with the family, the patient was transitioned to comfort care measures and expired.

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