History of Presentation
A 70-year-old woman presented with positional, pleuritic chest pain, described as a heavy sensation exacerbated by sitting, deep inspiration, and exertion, accompanied by dyspnea. On admission she was in sinus tachycardia to 120 beats/min, but was normotensive and afebrile. Physical examination displayed reproducible left costal margin tenderness.
Take-Home Messages
MRSA pericarditis is rare, with sequalae including pericardial abscess, cardiac tamponade, and constrictive pericarditis, contributing to a high mortality rate.
Source control is challenging in patients with comorbidities as well as venous or intracardiac devices.
Past Medical History
Past medical history included multiple myeloma (treated with daratumumab administered via a right internal jugular vein port), atrial fibrillation, cirrhosis, and heart failure with reduced ejection fraction (left ventricular ejection fraction: 38%) due to nonischemic dilated cardiomyopathy after implantation of a biventricular implantable cardioverter-defibrillator (ICD) with an epicardial lead.
Differential Diagnosis
Differential diagnosis included skin and subcutaneous infection, costochondritis, pneumonia, pericarditis, pulmonary embolism, acute-on-chronic heart failure exacerbation, and acute coronary syndrome.
Investigations
Electrocardiography showed sinus tachycardia with no ischemic changes. Initial laboratory tests found high-sensitivity troponin of 29 mg/L (reference: <34 ng/L) and B-type natriuretic peptide of 370 pg/mL (reference: 0-100 pg/mL). Chest x-ray displayed no acute findings. Computed tomography (CT) pulmonary angiogram ruled out pulmonary embolism but identified a small left pleural effusion, cardiomegaly, and biatrial enlargement.
Initial transthoracic echocardiography (TTE) showed a thickened pericardium with small to moderate pericardial effusion adjacent to the right ventricle, without echocardiographic or clinical evidence of cardiac tamponade. Her hospitalization was complicated by community-acquired pneumonia requiring 7 days of amoxicillin-clavulanate and doxycycline, atrial fibrillation with rapid ventricular rate necessitating direct current cardioversion, and hypoxemic respiratory failure requiring 7 L of supplemental oxygen. On hospital day 7, chest CT demonstrated a moderate pericardial effusion with suggested proteinaceous or hemorrhagic components and an enlarged left pleural effusion ( Figures 1A to 1C ).
On hospital day 15, an episode of ventricular tachycardia, hypoxia, fever with rigors, and elevated lactate level (8.5 mmol/L; reference: 0.5-1.6 mmol/L) prompted treatment for presumed septic versus cardiogenic shock entailing intravenous metoprolol tartrate, intravenous fluid resuscitation, empiric antibiotics (vancomycin and ertapenem), and intermittent norepinephrine infusion. Cultures from the central venous port grew Enterobacter cloacae , while peripheral blood cultures grew E. cloacae along with methicillin-resistant Staphylococcus aureus (MRSA). The central venous port was removed on day 16, and blood cultures cleared E. cloacae by day 17. Chest CT on day 17 revealed multifocal pneumonia and an enlarged loculated anterior pericardial effusion with right ventricular compression ( Figures 1D to 1F ). Subsequent TTE demonstrated a large, anterior pericardial effusion with right ventricular free wall and outflow tract diastolic collapse and a plethoric inferior vena cava ( Figures 2A to 2D ). Physical examination was notable for hypotension (mean arterial pressure: 53 mm Hg), poor peripheral perfusion with cool extremities, jugular venous distension, and tachypnea (respiratory rate: 28 breaths/min), though the patient remained in a paced rhythm at 97 beats/min.
Management
Given clinical evidence of tamponade, emergent pericardiocentesis was performed. The anterior location of the effusion precluded standard subxiphoid or apical approaches, necessitating an ultrasound- and fluoroscopy-guided left parasternal approach. A phased-array probe was used to mark the access site at the left fourth intercostal space, with micropuncture needle entry superior to the rib. A 0.018-inch wire was advanced through the needle, and its placement within the pericardium was confirmed with fluoroscopy. Using the standard Seldinger technique, a pericardial drain was placed, yielding 400 mL of purulent, turbid, rust-colored fluid ( Figure 3 ). Fluid analysis was negative for malignant cells, but abundant neutrophils and necrotic debris were demonstrated ( Table 1 ). Fluid cultures grew MRSA, confirming purulent pericarditis. A pericardial drain was left in place, and antibiotics were switched to ceftaroline and daptomycin.
Table 1
Pericardial Fluid Analysis
| Parameter | Results |
| Appearance | Pink opaque gross appearance with hazy amber supernatant. |
| Total nucleated cells | 570,000 cells/μL |
| Red blood cells | 4,566 cells/μL |
| Cells counted | 100 |
| Neutrophils (%) | 98 |
| Lymphocytes (%) | 1 |
| Monocytes/Macrophages (%) | 1 |
| Eosinophils (%) | 0 |
| Basophils (%) | 0 |
| Bacterial culture | Moderate-growth methicillin-resistant Staphylococcus aureus (day 2 of 2) |
| Acid-fast culture | No growth (day 42 of 42) |
| Fungal culture | No growth (day 28 of 28) |
| Gram stain | Heavy neutrophils. Mononuclear cells, red blood cells, and Gram-positive cocci present. |
Outcome
Postprocedurally, the patient's ICD generator site appeared erythematous, with tenderness to palpation suggesting device infection. Chest CT on day 18 displayed decreased size of the pericardial effusion and decompression of the right ventricle ( Figures 1G to 1I ). Given the presence of an epicardial lead, electrophysiology and cardiac surgery were consulted for ICD removal but ultimately deferred procedural recourse given risks associated with her acute illness and comorbidities. TTE on day 20 showed trivial pericardial effusion, septal bounce, plethoric inferior vena cava, and >25% decrease in mitral inflow velocity during inspiration, suggesting pericardial constriction. At this point, the patient elected for inpatient hospice, where she was switched to oral linezolid for palliation and ultimately died.
Discussion
Purulent pericarditis comprises <1% of pericarditis cases. 1 Globally, Mycobacterium tuberculosis is the most common bacterial etiology, but in developed countries, Staphylococcus , Streptococcus , and Pneumococcus species predominate. Less commonly, anaerobic species are associated with oropharyngeal or mediastinal infections. 1 , 2 Spread of organisms into the pericardium can be hematogenous or via contiguous spread from cardiac tissue, subdiaphragmatic tissues, or the retropharyngeal space. 2 , 3 Common sources of contiguous spread include empyema and pneumonia. 2 Reported sources of MRSA pericarditis include endocarditis, musculoskeletal abscesses, osteomyelitis, thrombophlebitis, and skin infections. 1 , 3 , 4
The initial suspected source of infection was the central venous port, as evidenced by positive port cultures, though only blood cultures grew MRSA. Alternatively, purulent pericarditis may have stemmed from multifocal pneumonia, with MRSA reaching the pericardial space via hematogenous dissemination (given bacteremia) or contiguous spread from the pulmonary parenchyma or a likely parapneumonic pleural effusion. Thoracentesis was not performed to compare pleural and pericardial fluid cultures. The ICD was a less likely primary source, as no clinical signs of pocket infection were observed prior to pericardiocentesis.
Risk factors for purulent pericarditis include diabetes, chronic kidney disease (including end-stage renal disease), alcohol use, immunosuppression, malignancy, and prior thoracic surgery. 4 Our patient was likely susceptible to infection owing to advanced age, multiple myeloma, and daratumumab treatment. Untreated MRSA pericarditis carries a mortality rate approaching 100%, driven by sepsis and resultant multiorgan failure. Even with antibiotic therapy and invasive interventions, mortality remains high, ranging from 20.5% to 40%. 1 , 3 , 4 , 5 Although antibiotics are typically administered for 2 to 4 weeks, specific guidelines on treatment duration are lacking, and outcomes may be affected by concomitant infection(s) and effective source control. 1 , 4
In our case, the anterior location and complex nature of the pericardial effusion necessitated parasternal pericardiocentesis. To our knowledge, this is the first reported case of MRSA pericardial abscess drainage using this approach. Parasternal pericardiocentesis has been described for managing pericardial effusion of different etiologies, including non-MRSA infectious pericarditis, postoperative effusions, malignancy, post–myocardial infarction effusions, traumatic injuries, inflammatory diseases, and uremic pericarditis. 6 , 7 Both right and left parasternal approaches, typically performed with real-time ultrasound guidance using a linear probe for enhanced resolution, have been documented. 6 , 8 Needle entry is typically at a 45° angle to the skin in the fourth or fifth intercostal space, within 1 cm of the sternal border, to optimize visualization and access the pericardium at the cardiac notch of the left lung while avoiding injury to the internal mammary arteries and lungs. 7 , 9 The Seldinger technique facilitates drainage catheter placement after successful access. In our procedure, we used a phased-array probe for ultrasound-guided site marking, followed by fluoroscopy to confirm pericardial access upon guidewire advancement.
Osman et al 7 reported a 100% complication-free success rate in a retrospective analysis of 11 patients who underwent parasternal pericardiocentesis for cardiac tamponade in an emergency department setting, performed by emergency medicine physicians without fluoroscopy. A parasternal approach is particularly valuable when subxiphoid or apical approaches are not feasible, such as in patients with obesity or anteriorly located effusions. Ultrasound confirmation of needle access is crucial but may be challenging in mechanically ventilated patients or those with emphysematous lung architecture. 6 , 8 , 10 Deep effusions may necessitate a phased-array probe, as linear probes may inadequately visualize surrounding structures. However, a parasternal approach may be impractical during tamponade-induced cardiac arrest, as it can impede active resuscitation efforts. 8 , 10
Conclusions
MRSA pericarditis is rare, with significant sequalae including pericardial abscess and constrictive pericarditis, and a high mortality rate despite optimal management. A high index of suspicion and prompt recognition of this uncommon entity is crucial in potentially reducing morbidity and mortality. In our case, an anterior pericardial abscess necessitated nontraditional parasternal pericardiocentesis. Source control is challenging in patients with comorbidities as well as venous or intracardiac devices. Future studies should compare the efficacy and complication rates of various pericardiocentesis approaches for purulent pericarditis and their impact on sequelae development.
Visual Summary
A Timeline of the Case
CAP = community-acquired pneumonia; CT = computed tomography; DCCV = direct current cardioversion; ICD = implantable cardioverter-defibrillator; IV = intravenous; MRSA = methicillin-resistant Staphylococcus aureus ; RVR = rapid ventricular rate; TTE = transthoracic echocardiography.
| Time | Events |
| Day 1 | A 70-year-old woman presents with positional and pleuritic chest pain and dyspnea requiring admission; begins treatment for costochondritis. CT pulmonary angiogram shows small left pleural effusion, cardiomegaly, and biatrial enlargement. TTE shows a thickened pericardium with a small to moderate pericardial effusion without signs of tamponade. |
| Day 5 | Patient develops acute encephalopathy and begins treatment for CAP with augmentin/doxycycline. |
| Day 6 | Patient develops atrial fibrillation with RVR. |
| Day 7 | Noncontrast chest CT shows moderate pericardial effusion with proteinaceous or hemorrhagic components but no evidence of tamponade. |
| Day 9 | Patient develops hemodynamic instability with ongoing atrial fibrillation and undergoes bedside DCCV. |
| Day 12 | Patient exhibits worsening hypoxemia necessitating supplemental oxygen. |
| Day 15 | Worsening lactic acidosis prompts treatment for presumed septic shock via IV fluid resuscitation, broad-spectrum antibiotics (vancomycin and ertapenem), and vasopressors. Port blood cultures grow Enterobacter cloacae ; peripheral blood cultures grow Enterobacter and MRSA. |
| Day 16 | Port removed |
| Day 17 | Noncontrast chest CT demonstrates multifocal pneumonia and enlarged anterior loculated pericardial effusion with right ventricular compression; TTE findings support imaging and clinical diagnosis of tamponade. Patient exhibits worsening shock, prompting emergent pericardiocentesis and pericardial drain placement. Antibiotics targeting MRSA broadened to ceftaroline and daptomycin. ICD generator site demonstrates signs concerning for device infection. |
| Day 18 | Pericardial fluid grows MRSA. Noncontrast chest CT shows decreased size of pericardial effusion and decompression of the right ventricle. Cardiac surgery recommends against ICD extraction given risks associated with patient's acute illness and comorbidities. |
| Day 20 | TTE shows features of pericardial constriction. Patient elects for inpatient hospice and is discharged on palliative linezolid. |
| Day 30 | Patient dies peacefully. |
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
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References
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