Surgical management of purulent pericarditis with diagnostic assistance from fluorodeoxyglucose positron emission tomography/computed tomography.

Purulent pericarditis is rarely the primary site of bacterial infection. It is usually a complication of an infection originating elsewhere in the body, arising by contiguous spread or haematogenous dissemination. This paper, however, describes a previously healthy young man, who developed a purulent streptococcal pericarditis with no localizable primary focus. Although many possibilities were investigated, the entry site of the pericarditis remains unknown.The incidence of purulent pericarditis has decreased considerably since the antibiotic era. It is typically an acute and potentially lethal disease, necessitating rapid diagnosis and adequate therapy to improve prognosis. Standard treatment combines appropriate antibiotic therapy with surgical drainage. However, the exact timing and type of surgery is still under discussion. Our patient was treated with antibiotics, subxiphoidal tube drainage of the pericardial fluid and intrapericardial thrombolysis. After three weeks, he developed tamponade, requiring partial pericardiectomy. He recovered completely and resumed his normal activities after a two-month hospitalisation

Purulent pericarditis is an acute and fulminant disease characterized by pus accumulation in the pericardial space. Its incidence has declined substantially and the common pathogen has changed since the beginning of the antibiotic era; however, it is still found in some patients with immunocompromised conditions. We report a rare case in which the onset of diabetes mellitus presented as extremely high HbA1c concentration, ketoacidosis, multi-site abscesses and purulent pericarditis. After antibiotic therapy and pericardiocentesis, the purulent pericarditis still did not resolve and further intrapericardial thrombolytic therapy also failed. Finally, this patient was treated successfully by surgical debridement and pericardiectomy. In the immunocompromised state of severe hyperglycaemia, purulent pericarditis is a possible complication of uncontrolled infection. If purulent pericarditis cannot be cured using non-surgical treatments, such as antibiotic therapy, pericardiocentesis and intrapericardial thrombolytic therapy, a surgical pericardiectomy should be considered to avoid morbidity and mortality.

PRIMARY PURULENT PERICARDITIS: A RARE CAUSE OF CARDIAC TAMPONADE AND CONSTRICTIVE PERICARDITIS

Bacterial pericarditis occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination. The frequent causes are Staphylococcus and Streptococcus (rheumatic pancarditis), Haemophilus, and M. tuberculosis. In AIDS pericarditis, the incidence of bacterial infection is much higher than in the general population, with a high proportion of Mycobacterium avium-intracellulare infection. Purulent pericarditis is the most serious manifestation of bacterial pericarditis, characterized by gross pus in the pericardium or microscopically purulent effusion. It is an acute, fulminant illness with fever in virtually all patients. Chest pain is uncommon. Purulent pericarditis is always fatal if untreated. The mortality rate in treated patients is 40%, and death is mostly due to cardiac tamponade, systemic toxicity, cardiac decompensation, and constriction. Tuberculous infection may present as acute pericarditis, cardiac tamponade, silent (often large) relapsing pericardial effusion, effusive-constrictive pericarditis, toxic symptoms with persistent fever, and acute, subacute, or chronic constriction. The mortality in untreated patients approaches 85%. Urgent pericardial drainage, combined with intravenous antibacterial therapy (e.g. vancomycin 1g twice daily, ceftriaxone 1-2g twice daily, and ciprofloxacin 400 mg/day) is mandatory in purulent pericarditis. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable. The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Pericardiectomy is reserved for recurrent effusions or continued elevation of central venous pressure after 4-6 weeks of antituberculous and corticosteroid therapy.

Background: Purulent pericarditis is a rare, often life-threatening infection of the pericardial space, characterized by the accumulation of pus. Seeding of the pericardium may occur through hematogenous or contiguous spread from an intrathoracic, myocardial, or subdiaphragmatic focus. Streptococcus pneumoniae is the most common intrathoracic bacterial source, although infection has become exceedingly rare in the modern era of pneumococcal vaccination and antibiotics. Constrictive physiology (CP) is a known complication of purulent pericarditis although the exact incidence is unknown. Case Summary: A middle-aged woman presented with chest pain. Initial imaging showed no evidence of pneumonia or pericardial effusion. A repeat echocardiogram after approximately 16 hours demonstrated the development of cardiac tamponade and obstructive shock. Emergent pericardiocentesis yielded purulent fluid, which grew Streptococcus pneumoniae . Despite hemodynamic improvement, she subsequently developed CP, which was diagnosed with cardiac catheterization and cardiac magnetic resonance (CMR). Discussion: This case illustrates an uncommon and critical presentation of purulent pericarditis in a previously healthy adult without initial evidence of pneumonia or an identifiable infectious source. The patient’s rapid progression to cardiac tamponade and obstructive shock highlights the importance of early recognition, timely pericardial drainage, and targeted antimicrobial therapy. Additionally, the classic signs of CP were seen just days after the development of pericardial disease. Cardiac catheterization is the gold standard diagnostic tool because enhanced ventricular interdependence by analysis of the left ventricular and right ventricular pressure contours during the respiratory cycle is highly sensitive and specific. However, CMR offers a non-invasive diagnostic adjunct by revealing pericardial thickness, pericardial contrast enhancement, and ventricular coupling during real-time cine imaging. This complementary information can help guide treatment decisions on medical therapy versus surgical intervention. Take Home Messages: Purulent pericarditis is a rare condition that may present without a clear infectious source. It may be complicated by the development of CP and both cardiac catheterization and CMR are important diagnostic tools.

Introduction: Austrian Syndrome is a rare, life-threatening triad of pneumonia, meningitis, and endocarditis caused by Streptococcus pneumoniae, typically in immunocompromised or alcoholic patients. Though it accounts for ~14% of S. pneumoniae endocarditis cases, purulent pericarditis is exceptionally rare. We present a case complicated by purulent pericarditis with tamponade, highlighting the need for early recognition and multidisciplinary care. Case Description: A 63-year-old unhoused woman with tobacco and fentanyl use was found unresponsive by her son and brought to the emergency department by EMS. She presented with acute hypoxic respiratory failure, altered mental status, and abdominal pain. Vitals: BP 172/96 mmHg, HR 132 bpm, and hypoxia on 3 L oxygen via nasal cannula. Exam showed Kussmaul respirations, jugular venous distention, and cool extremities. Labs showed leukocytosis, lactic acidosis, acute kidney injury, and elevated troponin suggesting demand ischemia. ECG demonstrated electrical alternans; chest CT revealed a moderate-to-large pericardial effusion. Point-of-care ultrasound confirmed tamponade with right ventricular diastolic and right atrial systolic collapse; pulsus paradoxus was 27 mmHg. Emergent pericardiocentesis drained 465 mL of turbid fluid; cultures of pericardial fluid and blood grew S. pneumoniae, confirming purulent pericarditis. Transthoracic echocardiogram showed fibrinous strands along the right ventricular septum, suggesting endocarditis. Bronchoscopy confirmed pneumonia, completing Austrian Syndrome. Follow-up chest CT showed loculated pericardial fluid with mediastinal abscess, requiring urgent surgical washout, window creation, and drain placement. Despite intensive antibiotics and multidisciplinary care, she developed septic shock, respiratory failure requiring intubation, and renal failure managed with CRRT, the patient died from multiorgan failure. Discussion: Purulent pneumococcal pericarditis with tamponade is a rare, often fatal complication of Austrian Syndrome. Early recognition via bedside imaging and clinical signs like pulsus paradoxus and electrical alternans is critical. Due to the purulent loculated effusion, surgical washout, pericardial window, and mediastinal drains are typically required, as medical therapy alone is inadequate. Mortality remains high, particularly with shock and multiorgan failure. Rapid diagnosis and coordinated care are essential in invasive pneumococcal infections.

BACKGROUND: Purulent pericarditis is a rare occurrence in the era of modern antibiotics. It is most often caused by organisms such as Staphylococcus aureus, Streptococcus pneumoniae, viridans streptococci, Haemophilus influenzae, and anaerobic bacteria with Streptococcus pyogenes (S. pyogenes) being a possible, though very uncommon etiology. It is usually associated with an underlying infection or compromised immune system. Purulent bacterial pericarditis is a high mortality entity and represents only 1% of the causes of pericarditis, among these only a few cases have been reported of Streptococcus pyogenes pericarditis. This is an extremely rare case of acute purulent bacterial pericarditis caused by S. pyogenes in an immunocompetent adult patient with no underlying chronic medical conditions. CASE PRESENTATION: A 37-year-old healthy female with no known comorbidities came in for chills, dyspnea, chest pain radiating to the upper back aggravated by deep breathing and relieved with leaning forward. She initially presented with unstable vital signs (hypotension and tachycardia). Electrocardiography demonstrated diffuse ST-segment elevation and PR segment depression, while chest Xray and CT scan showed lobar pneumonia. Blood tests showed leukocytosis with neutrophilic predominance indication infection and workup for autoimmune disease was done which was negative. 2D echo showed large pericardial effusion with tamponade physiology. An urgent pericardiocentesis was done with drainage of 350cc nonclotting purulent serous fluid. Cultures grew Streptococcus pyogenes (S. pyogenes) confirming the diagnosis of acute purulent bacterial pericarditis. Management for pericarditis including daily drainage of pericardial effusion, colchicine, ibuprofen was initiated together with antibiotics for the pneumonia and the patient had resolution of the pericardial effusion as documented by repeat 2DED upon follow up.

Introduction: Purulent pericarditis is a rare, potentially fatal infection characterized by pus in the pericardial space. The most common culprit is streptococcus pneumoniae, and it typically occurs in immunocompromised patients. This case highlights pneumococcal purulent pericarditis in an immunocompetent patient who presented with pneumonia and recent chest trauma. Case Description: A 45-year-old male with hypertension presented with chest pain, cough, and malaise. Chest computerized tomography (CT) revealed right upper lobe pneumonia and several acute and chronic rib fractures. He was tachycardic, febrile (102.9°F), and hypoxic. Labs showed leukocytosis (19.8) and elevated lactate (2.5). Electrocardiogram demonstrated low voltage (Figure A). Bedside trans thoracic echocardiogram (TTE) showed large pericardial effusion with right ventricular collapse (Figure B). Thus, a drain was placed, releasing 850 mL of purulent fluid. Post drainage, formal TTE revealed small residual effusion (Figure C). Vancomycin, cefepime, and metronidazole were started. Fluid studies showed 32,000 cells (91% neutrophils). Fluid cultures grew streptococcus pneumoniae. By day seven, the drain produced less than 50 mL over the previous twenty four hours. Bedside echocardiogram was confirmatory, so the drain was removed. The patient was discharged on six weeks of cefuroxime and a three month course of colchicine. Discussion: Although our patient endorsed chest pain, he did not demonstrate classic pericarditis signs. Unlike non infectious acute pericarditis, purulent pericarditis typically manifests as fever, tachycardia, and workup that parallels sepsis, highlighting the importance of comprehensive workup. In his case, purulent pericarditis likely resulted from contiguous spread of bacterial pneumonia, the most common route by which streptococcus pneumoniae enters the pericardium. While purulent pericarditis typically affects immunocompromised patients, our immunocompetent patient had recent chest trauma, which likely increased susceptibility by creating a pro inflammatory state. Prompt drainage and antibiotics were essential, as untreated purulent pericarditis mortality is near 100%. Even with correct treatment, mortality can reach up to 30%. Conclusion: Even in immunocompetent states, providers should consider purulent pericarditis especially when patients present with sepsis and concerns for pericardial effusion. Early recognition, drainage, and antibiotics are critical to survival.

PURULENT PERICARDITIS AND PURULENT PERICARDIAL EFFUSION DUE TO METHICILLIN-SENSITIVE STAPHYLOCOCCUS AUREUS (MSSA) IN A PATIENT TAKING SARILUMAB AND STEROIDS

Purulent pericarditis is an infrequent but fulminant and frequently lethal disease. Purulent pericarditis tends to occur as direct extension of bacterial pneumonia or empyema in past. In recently, purulent pericarditis tends to occur in adult via contiguous spread from an early postoperative infection after thoracic surgery or trauma, infection related to infective endocarditis, extension from a subdiaphragmatic suppurative source, and hematogenous spread during bacteremia. Endogenous causes of purulent pericarditis are frequently characterized as esophageal perforations. Common causes of esophageal perforations related to purulent pericaditis which usually develop in association with mediastinitis, pneumonia and empyema include corrosive esophagitis, complication after esophageal and tracheal instrumentation and Boerhaave’s syndrome. There is very little reference to the development of pericarditis in associated with esophageal perforation which does not directly communicate with the pericardium. while, although most uncommon, it is well documented that the esophagus can perforate directly into the pericardium and produce pericarditis. We experienced a case of acute purulent pericarditis after esophageal and pericardial perforation by a small fish bone in a previously healthy man. The patient was treated successfully with systemic antibiotics and pericardiotomy.

RARE PRESENTATION OF ACUTE PURULENT PERICARDITIS AFTER MYOCARDIAL INFARCTION

Fungal Purulent Constrictive Pericarditis in a Heart Transplant Patient

To The Editors: Superficial skin and soft tissue infections are common bacterial complications after varicella; less frequently deep-seated infections occur. Cardiac complications of chickenpox are rare and occur as a result of virus-induced injury or secondary bacterial infections of the heart and great vessels. We report an infant at the Hospital Nacional de Niños de Costa Rica, who developed chickenpox complicated by acute purulent pericarditis. An 11-month-old girl was admitted to a rural hospital with a 2-day history of fever and respiratory distress 12 days after the onset of uncomplicated varicella. A discrete right sided pneumonia with secondary reactive airway disease prompted treatment with nebulized albuterol and beclomethasone and intravenous ampicillin and oxacillin. Blood culture was negative, and a complete blood count revealed only moderate anemia. Two days after admission worsening in her respiratory condition prompted endotracheal intubation and mechanical ventilation. A repeat chest roentgenograph revealed cardiomegaly and air trapping, and she was transferred to the Hospital Nacional de Niños de Costa Rica for specialized care. On admission temperature was 38.8°C, heart rate 193/min, respiratory rate 76/min and blood pressure 108/66 mm Hg. Nasal flaring, costal retractions, bilateral wheezes and crackles, cyanosis, heart gallop, a pericardial rub and hepatomegaly were found. A diagnosis of bilateral pneumonia and congestive heart failure secondary to dilated myocardiopathy was made, and intravenous furosemide, dopamine, oxacillin and cefotaxime were started. She was transferred to the intensive care unit. Hemoglobin was 7.8 g/dl, platelets 89 000/mm3 and leukocytes 6760/mm3 (64% neutrophils, 32% lymphocytes, 3% band forms). A repeat chest roentgenograph showed increased cardiomegaly and bilateral pulmonary congestion. An echocardiogram showed no vegetations, a mild left pleural effusion and a severe pericardial effusion compatible with purulent pericarditis. Dilated myocardiopathy was ruled out, and on pericardiocentesis 30 ml of fluid were extracted. She went to the operating room and a pericardial window was done. Abundant fluid and fibrin were removed from the pericardial cavity, visceral pericardium and myocardial wall, and a pericardial drainage tube was left for 5 days. Pericardial fluid revealed an exudate, no organisms were seen on Gram stain and pericardial biopsy was consistent with acute infectious pericarditis. Cerebrospinal fluid was negative. Within 24 h Staphylococcus aureus was grown from the pericardial culture (susceptible to oxacillin, gentamicin, clindamycin, trimethoprim-sulfamethoxazole, erythromycin, ciprofloxacin and vancomycin). Cefotaxime was stopped on Day 3, and gentamicin was added as possible synergistic therapy for 7 days. Further blood cultures were sterile. After 16 days of intravenous oxacillin therapy and a repeat normal echocardiogram, she was discharged home. Follow-up at 1 month revealed a healthy child with no cardiac findings or sequelae. Cardiac complications during or after varicella are uncommon, but can be life-threatening. The most common of these is varicella-zoster virus (VZV) myocarditis, but other VZV-induced cardiac injuries include pericarditis, tamponade, heart failure, arrhythmias and pericardial effusion. 1, 2 Cardiac bacterial complications are extremely rare and include endocarditis, 3 aortic and ventricular aneurysms, 3, 4 purulent pericarditis with effusion 5–8 and cardiac tamponade. 7, 8 The presumed route in the majority of these episodes is hematogenous dissemination after skin barrier breakdown, although contiguous extension from other sites may occur. Bacterial pericarditis after chickenpox is uncommon, with few reports published thus far. 1,4–8 Its clinical picture and the presence of cardiomegaly may initially confuse the clinician with the possibility of VZV myocarditis. Rolando Ulloa-Gutierrez, M.D. Maria L. Avila-Aguero, M.D.

BACKGROUNDPericarditis is the inflammation of the pericardial sac due to a variety of stimuli that ultimately trigger a stereotyped immune response. This condition accounts for up to 5% of emergency department visits for nonischemic chest pain in Western Europe and North America. The most common symptoms of clinical presentation are chest pain and shortness of breath with associated unique electrocardiographic changes. Acute pericarditis is generally self-limited. However, some cases may be complicated by either tamponade or a large pericardial effusion, which carries a significant risk of recurrence. Risk factors for acute pericarditis include viral infections, cardiac surgery, and autoimmune disorders. A rarer cause of pericardial inflammation includes pneumonia, which can induce purulent pericarditis that has been increasingly rare since the advent of antibiotics. Purulent pericarditis carries a high fatality rate, especially in the setting of tamponade, and is invariably deadly without the administration of antibiotics. Bedside transthoracic echocardiogram is a quick and helpful method that can aid in the diagnosis and management.CASE SUMMARYWe present the case of a 62-year-old woman who sought medical attention at the emergency department (ED) due to a 5-day history of chest pain, shortness of breath, and subjective fevers. Laboratory findings in the ED were significant for leukocytosis and elevated erythrocyte sedimentation rate and C-reactive protein. A chest X-ray revealed a new focal density within the left lower lung base, and a bedside point-of-care ultrasound showed a pericardial fluid collection. The patient was subsequently admitted, where she underwent pericardiocentesis. Fluid cultures from drainage grew streptococcus pneumoniae. She was started on broad-spectrum antibiotics immediately after the procedure. The patient was ultimately discharged in stable condition with cardiology and infectious disease follow-up.CONCLUSIONThis case report emphasizes a unique complication of community-acquired pneumonia. Purulent pericarditis due to streptococcus pneumonia occurs via intrathoracic spread of the organism to the pericardium. This condition is virtually fatal without the administration of antibiotics. Therefore, in the context of suspected pneumonia and a new pericardial fluid collection on imaging, clinicians should suspect purulent pericarditis until proven otherwise, which requires emergent intervention.

Septic shock is common, with approximately 200,000 cases recognized annually. This syndrome is so well characterized that when a patient is febrile and in shock, septic shock may be diagnosed without regard to alternative possibilities. Purulent pericarditis is a relatively rare disorder in which fever and hypotension are common. Classic signs and symptoms, such as chest pain, pericardial friction rub, pulsus paradoxus, and elevation of jugular venous pressure, are seen in only 50%. In this report, we describe four patients in whom purulent pericarditis and pericardial tamponade was initially misdiagnosed as septic shock. During a 3-month period, three men and one woman (mean age, 44.5 years) came to Kern Medical Center with purulent pericarditis and pericardial tamponade. These cases represented 13% of patients admitted with a diagnosis of septic shock. All patients were bacteremic, and the classic findings of pericardial tamponade were absent or relatively subtle. Hemodynamic findings of elevated systemic vascular resistance, low cardiac output, and normal pulmonary artery occlusion pressure were critical to the diagnosis. Consideration of purulent pericarditis is important in cases diagnosed as septic shock. Clinicians should be aware that patients with purulent pericarditis may not exhibit classic signs and symptoms, and a high index of suspicion is necessary for appropriate management.