Purulent pericarditis (PPc) is a rare but life-threatening condition characterized by the accumulation of pus in the pericardial sac, leading to significant morbidity and mortality. Although the incidence of PPc has declined in developed countries due to advances in antibiotic therapies, current literature quantifying the frequency, morbidity, and mortality of the condition remains limited. Even with prompt diagnosis and treatment, mortality is estimated at 20–40%, with nearly 100% mortality without intervention due to rapid progression to cardiac tamponade, sepsis, or constrictive pericarditis.1−3
PPc is of particular concern in immunocompromised patients or those with predisposing conditions such as pneumonia or septicemia.1 Common causative pathogens include Staphylococcus aureus, Streptococcus pneumoniae, and various anaerobic bacteria.3 Diagnosis may be difficult and sometimes delayed as patients typically present with nonspecific symptoms such as fever, chest pain, and dyspnea, which can rapidly deteriorate into cardiac tamponade and shock if untreated.2
The gold standard for diagnosing PPc involves echocardiography to detect pericardial effusion, followed by pericardiocentesis for microbiological analysis of the pericardial fluid.2,3 Immediate drainage and broad-spectrum antibiotic therapy are essential to prevent fatal outcomes.1 Despite aggressive management, the risk of complications, such as constrictive pericarditis or recurrent infections, contributes to a persistently high mortality rate.2,3
Case Presentation
A 56-year-old male with a history of non-alcoholic fatty liver disease, cirrhosis (complicated by previous esophageal varices, portal hypertension, and hypersplenism with chronic thrombocytopenia), type 2 diabetes, hypertension, and hyperlipidemia presented to our hospital with chest pain, cough, emesis, dyspnea, oliguria, jaundice, and subjective fevers for 2 days. The patient described his chest pain as a midsternal band of pressure across his chest which worsened when supine and with diaphragmatic breathing but improved when leaning forward. Physical exam was only remarkable for jaundice (head/neck, chest, and upper extremities) and tachycardia. The exam was negative for abnormal rhythm or murmur. Upper and lower extremity pulses were 2+ with no edema of the lower extremities. There were no rales. Abdomen was soft, nontender, and nondistended. Vitals included a temperature of 98.0°F (36.7°C), heart rate of 101 BPM, respiratory rate of 20 breaths/min, blood pressure of 139/88 mmHg, and O2 saturation of 96% on room air.
Initial laboratory workup showed the values detailed in Table 1. Of particular significance, the patient presented in diabetic ketoacidosis with multi-organ failure. Findings included a significant leukocytosis (with left shift), acute kidney injury (baseline creatinine 1.0–1.3 mg/dl), elevated liver function tests, hyperbilirubinemia, and additional elevations in lactate, β-hydroxybutyrate, erythrocyte sedimentation rate, C-reactive protein, NT-proBNP, and procalcitonin. Blood cultures grew methicillin-sensitive S aureus (2/2 cultures). HbA1c approximately 3 months prior to admission was 6.5%. Nasopharyngeal swab tested positive for COVID-19.
An EKG performed on arrival demonstrated diffuse ST elevation in leads I, II, aVF, and V2-V6, ST depression in aVR, and PR depression in leads I and II (Figure 1A). Chest X-ray was consistent with cardiomegaly and chest CT revealed a moderate pericardial effusion along with small bilateral pleural effusions (Figure 1B). Transthoracic echocardiogram (TTE) showed a large circumferential pericardial effusion without signs of tamponade and mild concentric left ventricular hypertrophy (Figure 1C). Of note, the patient presented to an outside hospital 48 hours prior for chest pain where his workup revealed grossly normal labs, EKG, and CT angiogram.
The patient was placed on broad-spectrum antimicrobial therapy (1,750 mg vancomycin, 2 g ceftriaxone, and 200 mg remdesivir) in addition to fluid resuscitation with 3 l of lactated Ringer’s solution for sepsis. An insulin drip was used to close the patient’s anion gap and lower serum glucose. The patient received 150 mEq of sodium bicarbonate and 2 mg of bumetanide. Thromboembolic prophylaxis was initiated with subcutaneous heparin. Colchicine therapy was deferred in the setting of acute kidney injury.
On day 2, blood cultures returned consistent with methicillin-sensitive S aureus (MSSA)-bacteremia and initial broad-spectrum antibiotics were subsequently deescalated to cefazolin monotherapy (1 g every 12 hours). The patient’s oxygen requirement increased overnight, with a peak requirement of 6 l by nasal cannula. Soon thereafter, the patient developed AF with rapid ventricular response resulting in symptomatic hypotension. Amiodarone bolus (150 mg) was administered followed by emergent direct current cardioversion, with successful conversion to normal sinus rhythm. Amiodarone maintenance drip at 1 mg/min in addition to 200 mg orally every 12 hours was started. Repeat TTE demonstrated large circumferential pericardial effusion with right ventricular diastolic collapse, suggesting cardiac tamponade requiring pericardiocentesis. 630 ml of turbid yellow-brown fluid was aspirated from the pericardial space (Figure 1D) with a WBC count of 160.2×103/µl, lactate dehydrogenase at 7,450 U/l, glucose <20 mg/dl, and protein at 6.2 g/dl (Table 2). Cultures of the pericardial aspirate grew MSSA. The patient’s rhythm returned to AF with rapid ventricular response immediately after pericardiocentesis, and he underwent repeat direct current cardioversion to restore normal sinus rhythm. The patient was transferred to the intensive care unit, where he intermittently went in and out of AF and was started on diltiazem 60 mg every 6 hours for AF rate control. Heparin prophylaxis was transitioned to therapeutic heparin given the patient’s CHA2DS2-VASc score of 3 (hypertension, diabetes, vascular disease).
On day 3, the patient was started on sustained low-efficiency dialysis due to worsening creatinine (>5 mg/dl), hyponatremia, hyperkalemia, and persistent oliguria despite resuscitation with IV fluids followed by diuretic challenge with bumetanide. He was advanced to conventional dialysis (Monday, Wednesday and Friday) over the ensuing days. The patient’s scheduled amiodarone was increased to 400 mg every 12 hours for intermittent AF.
On day 5, a repeat TTE was performed, demonstrating reaccumulation of pericardial fluid with a large circumferential effusion and signs of tamponade. Repeat pericardiocentesis yielded 520 ml of fluid. A pericardial drain was placed and remained in position for 4 days prior to inadvertent removal, with a total output of 2,725 ml. The patient went on to reaccumulate a moderate effusion on day 16 of his hospital stay, which was monitored clinically as the cardiovascular-thoracic surgery team deemed the patient to not be a surgical candidate secondary to newly onset thrombocytopenia (platelet count 39×103/µl) and a positive heparin-induced platelet factor 4 antibody result. Cefazolin and heparin were replaced with daptomycin (8 mg/kg body weight every 48 hours) and argatroban, respectively, due to thrombocytopenia. Repeat TTE was completed at 48- to 72-hour intervals to monitor effusion status. No further cardiac intervention was necessary.
Further complications developed during the remainder of his hospital stay, including the onset of ascites with abdominal pain and discomfort on day 9, for which he underwent 1 l paracentesis (Table 2). Abdominal and pelvic CT were negative for acute infectious pathology, but revealed moderate ascites, splenomegaly, and varices in addition to recurrent moderate pericardial effusion and small bilateral pleural effusions. Following a 33-day admission, the patient was discharged in stable condition on a regimen of amiodarone (200 mg daily), apixaban (5 mg twice daily for 1 month), daptomycin (8 mg/kg body weight daily for 6 weeks), and basal/bolus insulin.
One year post-discharge, the patient is doing well, with no signs of recurrent pericarditis or significant cardiac sequelae. Amiodarone was replaced with dronedarone (400 mg twice daily).
Discussion
This case report details the presentation and management of a 56-year-old male with concurrent MSSA bacteremia and SARS-CoV-2 infection, who developed recurrent PPc with significant pericardial effusion. To our knowledge, this is the first reported instance of MSSA-induced PPc in the setting of SARS-CoV-2 with persistent fluid reaccumulation despite comprehensive management with antimicrobial therapy (14 days daptomycin, 5 days remdesivir) and pericardial drainage. The combination of SARS-CoV-2 and MSSA as contributing factors in the development of PPc, along with ongoing purulent fluid reaccumulation despite aggressive interventions, underscores the complexity of this clinical scenario. Throughout his hospitalization, a total of 3,875 ml of pericardial fluid was drained: 1,150 ml via serial pericardiocentesis and 2,725 ml through pericardial drain placement. This case highlights challenges in managing recurrent PPc, particularly in the context of dual infections and significant comorbidities.
The patient was evaluated by hepatology 3 weeks prior to hospitalization for decompensated cirrhosis. Significant portal hypertension with hypersplenism and varices was documented, although his liver disease remained grossly compensated. During the same visit, chronic thrombocytopenia was noted. Interestingly, the patient’s normal platelet count on admission may represent reactive thrombocytosis in the setting of chronic thrombocytopenia. Additionally, the patient was evaluated by cardiology 5 years prior due to shortness of breath, during which a stress echocardiogram was found to be within normal limits. At that time, hyperlipidemia (LDL cholesterol of 122 mg/dl) was identified but remained inadequately controlled due to statin intolerance.
Although initial blood cultures confirmed MSSA bacteremia, the primary source of infection remains unclear. Potential etiologies for PPc include direct spread from an intrathoracic infection, hematogenous dissemination from a distant focus, or extension from a subdiaphragmatic suppurative site. Given the patient’s medical history of decompensated cirrhosis with portal hypertension, hypersplenism, and esophageal varices, a subdiaphragmatic focus appears plausible. However, the patient did not display overt signs of decompensation upon arrival, such as variceal hemorrhage or abdominal distension, and reported no recent bleeding.
Although the patient’s HbA1c was 6.5% 3 months prior to presentation, his HbA1c levels ranged between 5.7% and 6.4% over the previous 4 years, indicating good glycemic control. Therefore, uncontrolled diabetes is less likely to be the primary cause of the PPc.
Furthermore, the role of COVID-19 or COVID-related myocarditis as a potential contributing factor cannot be disregarded. Although the exact mechanism remains unknown, SARS-CoV-2 infection or its sequelae, such as myocarditis, might have played a role in exacerbating the patient’s susceptibility to PPc. This case highlights the diagnostic and therapeutic challenges of managing recurrent PPc amidst complex infections and underlying conditions, underscoring the need for further investigation into potential interactions between COVID-19 and PPc pathogenesis. The etiology of jaundice at presentation remains unclear, although it improved during the initial 15–16 days of hospitalization.
Following a literature review conducted via PubMed and Google Scholar, we systematically evaluated 10 peer-reviewed studies documenting clinical manifestations of PPc attributed to MSSA and methicillin-resistant S aureus (MRSA; Table 3).4−13 The analysis revealed estimated mortality rates of 12.5% for MSSA-specific PPc and 9.09% for PPc cases involving both MSSA and MRSA. The average length of hospital stay was determined to be 26.0 days for MSSA PPc and 23.2 days for MSSA/MRSA PPc. Fluid volume drained during treatment averaged 882 ml. The cohort had a mean age of 63 years and was predominantly male. Notably, fewer than 50% of the patients initially presented with chest pain as their primary symptom.
Given our findings and the case presented, we recommend a comprehensive surveillance protocol for similar patients. This should include post-discharge monitoring with echocardiography within 1–2 weeks, followed by imaging at 1–3-month intervals during the first year to evaluate for recurrent pericardial effusion, constrictive pericarditis, or other sequelae. Regular assessments of liver function, metabolic panels, and glycemic control should commence monthly and transition to quarterly evaluations as stability is achieved. Emphasis should also be placed on patient education regarding early recognition of pericarditis recurrence, infection, and therapy-related complications. Long-term surveillance for constrictive pericarditis over a 12–24-month period, combined with reinforcement of lifestyle interventions targeting diabetes, hepatic disease, and hyperlipidemia, remains essential to comprehensive management.
Limitations to consider in this presentation include possible extenuating social factors contributing to the patient’s illness that were not disclosed despite a thorough history taken during the initial encounter. A urine drug screen was not completed during the encounter, so intravenous drug use cannot be ruled out as a source of MSSA bacteremia.
Conclusion
This is the case of a 56-year-old male with a significant medical history including hypertension, type 2 diabetes, and cirrhosis, who exhibited recurrent MSSA PPc. Although the exact impact of SARS-CoV-2 on the development of PPc remains unresolved, our findings propose a potential association suggesting that SARS-CoV-2 may have increased the patient’s susceptibility to PPc. This observation emphasizes the need for further research into the possible interaction between COVID-19 and the pathogenesis of PPc.