Case Report

A Forgotten Cause of Cardiac Tamponade

Although purulent pericarditis is rare, it is essential to recognize its clinical features due to the high mortality rate in patients with a missed diagnosis.

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References

Purulent pericarditis is an infection within the pericardial space rarely seen in the modern antibiotic era. Most cases are secondary to another infectious process of bacterial, viral, fungal, or parasitic origin.1,2 Predisposing factors include malignancy, chronic kidney disease, immunosuppression, diabetes mellitus, and alcohol misuse disorder.1 Although purulent pericarditis has been described extensively in the literature, it is a challenging diagnosis if it is not initially considered within the differential diagnosis repertoire.1-4 Most authors agree that this may be because it has become an infrequent diagnosis.1,2 In addition, purulent pericarditis may have an atypical presentation when compared with a classic case of pericarditis.2,3 The authors believe that this forgotten entity will be revisited through this case.

Case Presentation

A 66-year-old-man was transferred to Veterans Affairs Caribbean Healthcare System (VACHS) from a community hospital with a diagnosis of community-acquired pneumonia (CAP) and bilateral pleural effusions. Four days prior to arrival at the community hospital, the patient had developed diffuse, watery diarrhea, which resolved in 3 days. After resolution of diarrhea, he began experiencing shortness of breath on exertion that progressed to onset at rest. The patient reported no fever, chills, nausea, vomiting, cough, or contact with others who were not healthy. He had a history of alcohol misuse without liver cirrhosis and reported no chronic diseases or use of medications. The patient had no history of tuberculosis exposure or pneumococcal vaccination, and had a negative interferon gamma release assay.

On admission to the community hospital, the patient was treated for CAP with ceftriaxone and azithromycin. On hospital day 3, the patient developed hypoxemia and an altered mental status. He was started on supplemental oxygen and transferred to the intensive care unit (ICU). Antibiotic therapy consequently was changed to levofloxacin and meropenem. However, no clinical improvement was noted on the following days.

On hospital day 7, the patient developed acute respiratory failure that required mechanical ventilation while being transferred to VACHS via air ambulance. His vital signs on arrival were the following: temperature, 97° F; heart rate, 86 beats/min; blood pressure, 103/61 mm Hg; respiratory rate, 14 breaths/min and SaO2 of 97%, measured while he breathed supplemental oxygen at an FiO2 of 0.4.

Laboratory results revealed a white blood cell count (WBC) of 11.2 × 103/µL, with 92% neutrophils, 4% bands, 1% lymphocytes; lactic acid, 1.3 mmol/L; and high sensitivity C-reactive protein, 43.1 mg/L. A chest radiograph demonstrated bibasilar pulmonary opacities, bilateral pleural effusions, and cardiomegaly (Figure 1).

Hours after arrival, the patient developed sinus tachycardia and hypotension. A bedside 2D echocardiogram demonstrated a large pericardial effusion with diastolic collapse of the right atrium (Figure 2).

Aggressive fluid resuscitation with normal saline and inotropic support with dopamine were started as an immediate percutaneous pericardiocentesis was performed with drainage of 400 mL of frank purulent fluid (Figure 3).
After percutaneous pericardiocentesis was completed, a temporary catheter was placed into the pericardial space using the Seldinger technique in order to aspirate fluid as needed.

The patient’s clinical condition improved following drainage of pericardial fluid, with no further need for inotropic support. Antibiotic therapy was changed to vancomycin and meropenem. Initial microbiologic samples from pericardial fluid demonstrated Gram-positive diplococci, suggestive of Streptococcus pneumoniae (S pneumoniae) (Figure 4). Other diagnostic pericardial fluid test results included: WBC count 25,330 cmm, with 99% neutrophils and 1% lymphocytes; total protein, 3.8 mg/dL; glucose, < 2.0 mg/dL,LDH, > 2,500 U/L, potassium hydroxide preparation. The tests found no fungus, and the acid fast bacilli smear revealed no Bacillus. However, the pericardial fluid culture failed to demonstrate growth of any organism. Blood cultures also were negative.

The patient underwent anterior thoracotomy with partial pericardiectomy, and a pericardial tube was left in place connected to drainage. During the procedure, an abundant amount of fibrinous tissue was evacuated from the pericardial space (Figure 5).

The patient’s status improved the following day, and inotropic support once again was stopped. Bilateral pleural tubes were placed for evacuation of loculated effusions. Laboratory results from left-sided fluid were suggestive of complicated parapneumonic effusion with a WBC count of 6,683 cmm and glucose, 12 mg/dL. Right-sided pleural fluid was consistent with exudate with a WBC count of 2,006 cmm; pH 7.49; LDH, 1450 U/L; and glucose, 66 mg/dL. Gram stain and cultures of pleural fluid were negative.

The patient was extubated, pericardial and pleural tubes were removed, and he was transferred to the internal medicine ward 24 days after admission to the ICU. He received in-patient physical rehabilitation while completing a 6-week course of IV antibiotics (vancomycin and meropenem). After completion of therapy, the patient received the pneumococcal polysaccharide vaccination, and an echocardiography was repeated. No significant re-accumulation of pericardial effusion or constrictive pattern was evidenced. The patient was discharged to his out-of-state home, and follow-up was consequently lost.

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