Non-surgical treatment of purulent pericarditis, due to non-encapsulated Haemophilus influenzae, in an immunocompromised patient.

A 59-year-old woman suffering from rheumatoid arthritis was admitted with pleural empyema and pericarditis due to non-encapsulated H. influenzae, and developed signs of cardiac tamponade. Purulent pericarditis resolved after ultrasound-guided percutaneous aspiration and systemic antimicrobial therapy. Serial echocardiographic examinations showed a slowly vanishing effusion. Long term follow-up revealed no evidence of pericardial constriction. This case illustrates that life-threatening purulent pericarditis in an immunocompromised patient may respond well to non-surgical treatment.     

Gonococcal pericarditis with tamponade in a patient with systemic lupus erythematosus

Pericarditis is one of the most frequent manifestations of systemic lupus erythematosus; however, purulent pericarditis and tamponade are rare. We describe a patient with systemic lupus erythematosus and culture-proven gonococcal arthritis who developed purulent pericarditis with intracellular gram-negative diplococci. Evidence of tamponade was seen on echocardiography. There has not been a reported case of Neisseria gonorrhoeae in pericardial fluid or tissue since the introduction of antibiotics.     

A case of rheumatoid pericarditis with high concentrations of interleukin-6 in pericardial fluid

A case of rheumatoid pericarditis that developed into cardiac tamponade without deterioration of rheumatoid arthritis is described. The concentration of interleukin-6 (IL-6) in pericardial fluid was notably increased compared with serum. IL-6 may be associated with progression or maintenance of rheumatoid pericarditis.


Keywords: rheumatoid pericarditis; cardiac tamponade; interleukin-6     

44-j?hriger Patient mit kulturnegativer, purulenter Perikarditis

We report about a patient with purulent pericarditis due to Neisseria meningitidis pretreated with antibiotics. Clinical signs were suggestive of pericardial tamponade. Cultures from blood and pericardial aspirate remained negative. Broad-range polymerase chain reaction from pericardial fluid detected Neisseria sp.. Latex agglutination assay from pleural fluid showed positive reaction with meningococcal antigen serogroup C. Meningococcal pericarditis without meningitis is a rare manifestation. Non-culture based diagnostic methods in patients with such severe infections and negative cultures play an important role.     

Diagnosis and management of pericardial effusion

Pericardial effusion is a common finding in everyday clinical practice.The first challenge to the clinician is to try to establish an etiologic diagnosis.Sometimes,the pericardial effusion can be easily related to a known underlying disease,such as acute myocardial infarction, cardiac surgery,end-stage renal disease or widespread metastatic neoplasm.When no obvious cause is apparent,some clinical findings can be useful to establish a diagnosis of probability.The presence of acute inflammatory signs(chest pain,fever,pericardial friction rub) is predictive for acute idiopathic pericarditis irrespective of the size of the effusion or the presence or absence of tamponade.Severe effusion with absence of inflammatory signs and absence of tamponade is predictive for chronic idiopathic pericardial effusion,and tamponade without inflammatory signs for neoplastic pericardial effusion.Epidemiologic considerations are very important,as in developed countries acute idiopathic pericarditis and idiopathic pericardial effusion are the most common etiologies,but in some underdeveloped geographic areas tuberculous pericarditis is the leading cause of pericardial effusion.The second point is the evaluation of the hemodynamic compromise caused by pericardial fluid.Cardiac tamponade is not an"all or none"phenomenon,but a syndrome with a continuum of severity ranging from an asymptomatic elevationof intrapericardial pressure detectable only through hemodynamic methods to a clinical tamponade recognized by the presence of dyspnea,tachycardia,jugular venous distension,pulsus paradoxus and in the more severe cases arterial hypotension and shock.In the middle,echocardiographic tamponade is recognized by the presence of cardiac chamber collapses and characteristic alterations in respiratory variations of mitral and tricuspid flow.Medical treatment of pericardial effusion is mainly dictated by the presence of inflammatory signs and by the underlying disease if present.Pericardial drainage is mandatory when clinical tamponade is present.In the absence of clinical tamponade,examination of the pericardial fluid is indicated when there is a clinical suspicion of purulent pericarditis and in patients with underlying neoplasia.Patients with chronic massive idiopathic pericardial effusion should also be submitted to pericardial drainage because of the risk of developing unexpected tamponade.The selection of the pericardial drainage procedure depends on the etiology of the effusion.Simple pericardiocentesis is usually sufficient in patients with acute idiopathic or viral pericarditis.Purulent pericarditis should be drained surgically,usually through subxiphoid pericardiotomy. Neoplastic pericardial effusion constitutes a more difficult challenge because reaccumulation of pericardial fluid is a concern.The therapeutic possibilities include extended indwelling pericardial catheter,percutaneous pericardiostomy and intrapericardial instillation of antineoplastic and sclerosing agents.Massive chronic idiopathic pericardial effusions do not respond to medical treatment and tend to recur after pericardiocentesis, so wide anterior pericardiectomy is finally necessary in many cases.     

Purulent Pericarditis in Sickle Cell Disease Due to Streptococcus agalactiae; a Unique Case Report and Literature Review

Purulent pericarditis is a localized infection with a thick, fibrinous hypercellular exudate and is historically associated with a high mortality. We describe a case of purulent pericarditis due to Streptococcus agalactiae (S. agalactiae) in a 30-year-old woman with sickle cell disease who presented with fever, dyspnea, and S. agalactiae septicemia. Despite timely initiation of antibiotics, she developed a large purulent pericardial effusion requiring surgical pericardiocentesis followed by a pericardial window. At 14?months follow-up, she has remained asymptomatic without sequelae. A review of the literature contained only four patients with purulent pericarditis in sickle cell patients. We discuss the unique aspects of this case in the context of purulent pericarditis in the age of modern antibiotics and hypothesize on the pathogenesis of delayed pericardial effusion after pericarditis.     

Cardiac tamponade, constrictive pericarditis and pericardial resection in rheumatoid arthritis.

Four patients with rheumatoid constrictive pericarditis and two patients with rheumatoid cardiac tamponade are presented, and 60 previously reported cases with these two complications are reviewed. Rheumatoid arthritis was moderate to severe in 84% of the patients with cardiac tamponade and in 74% of the patients with constrictive pericarditis. However, both these complications were also seen in patients who had only mild arthritis and in two previously reported cases constrictive pericarditis actually preceded the onset of rheumatoid arthritis. The duration of rheumatoid arthritis had no bearing on the development of these complications. In 75% of patients with cardiac tamponade, and in 66% of cases with constrictive pericarditis, subcutaneous nodules were present. In those cases where the rheumatoid factor was measured it was positive in 92% with cardiac tamponade and in 84% with constrictive pericarditis. In 63% of patients with cardiac tamponade and in 70% of cases with constrictive pericarditis a history of pericardial type of pain was obtained and/or a pericardial rub heard. The diagnosis of cardiac tamponade and constrictive pericarditis was made clinically and in doubtful cases confirmed by cardiac screening and intracardiac pressure recordings. The low sugar content in the pericardial fluid in the absence of infection or malignancy was an important clue to the rheumatoid etiology of the effusion. In the majority of the cases histological appearances of the pericardial tissue showed non-specific fibrous reaction and infiltration with plasma cells and lymphocytes. Only in five of the cases, including one from the present series, were typical rheumatoid granulomatous lesions demonstrated. Treatment with corticosteroids neither prevented the occurrence nor led to amelioration of either cardiac constriction or tamponade. Pericardial resection was life saving, producing both symptomatic and objective involvement of the cardiac function. In the present series of six cases two patients developed aortic incompetence. In one of these it was due to rheumatoid granulomatous valve disease and in the other due to non-specific aortic valvulitis. The combination of constrictive pericarditis and granulomatous aortic valve disease has not been previously recorded.     

The spectrum of pericardial tamponade in systemic lupus erythematosus: Report of ten patients

Objective. To describe the range of clinical manifestations and the outcome of pericardial tamponade in patients with systemic lupus erythematosus (SLE). Methods. Patients with pericarditis and with pericardial tamponade were identified from our computerized database of 395 SLE patients. Medical records were reviewed to establish activity of SLE at the time of tamponade, as well as clinical and laboratory features, treatment, and outcome of the tamponade. Results. Pericarditis occurred in 75 patients (19%), with 11 episodes of tamponade in 10 of them (13%; 2.5% of entire series). Tamponade was the initial manifestation of SLE in 4 patients. Seven episodes occurred during active lupus, with nephritis present in 6. Signs of venous congestion, including ascites and facial or peripheral edema, were the most common manifestation of tamponade. Pericardial fluid was exudative, and pericardial tissue demonstrated a range of findings including fibrinous and fibrotic changes, acute and chronic inflammatory infiltrates, and vascular proliferation. Tamponade was fatal in 1 patient, and 2 patients each had recurrent effusions and pericardial thickening. Conclusion. Pericardial tamponade may occur at any point in the course of SLE, and should be considered in patients with unexplained signs of venous congestion. The differential diagnosis includes active SLE, uremia, and infection. Treatment with high-dose steroids and either pericardiocentesis or placement of a pericardial window is indicated, but recurrent effusions or pericardial thickening may develop.     

Polymicrobial bacterial pericarditis after transbronchial needle aspiration. Case report with an investigation on the risk of bacterial contamination during fiberoptic bronchoscopy.

A 63-yr-old man developed pericardial effusion with tamponade after transbronchial needle aspiration (TBNA) of a subcarinal mass. A diagnosis of polymicrobial bacterial pericarditis was made when pericardiocentesis revealed purulent fluid that grew a mixed culture of anaerobes and aerobes, organisms that constitute part of the normal upper respiratory tract flora. To examine the possibility that contamination of the transbronchial needle (TBN) could lead to purulent pericarditis by inoculation of bacteria into the mediastinum, quantitative cultures of the TBN content were performed in seven consecutive patients. Abundant growth of multiple anaerobic and aerobic organisms was demonstrated in all seven cultures. We conclude that subcarinal TBNA is another potential cause of purulent pericarditis. This results from upper respiratory tract contamination of the open distal end of the TBN as it passes through the suction channel of the bronchoscope.     

Pericardial tamponade and large pericardial effusions: causal factors and efficacy of percutaneous catheter drainage in 50 patients

In 50 patients treated from January 1998 through March 2002 for pericardial effusion and tamponade, we retrospectively investigated the efficacy of percutaneous placement of an indwelling pericardial catheter guided by 2-dimensional echocardiography and fluoroscopy. We also investigated causation. In 80% of the patients, we were able to determine specific causes through clinical, serologic, and cytologic investigation: cancer in 15 patients, chronic renal failure in 11, systemic lupus erythematosus in 2 rheumatoid arthritis in 2, Dressler syndrome in 2, tuberculosis in 1, blunt chest trauma in 1, purulent pericarditis in 1, and probably viral pericarditis in 5. No specific cause could be determined in 10 patients (20%). We did not observe any complication due to the procedure. Two patients died during hospitalization. After hospitalization, 9 patients with metastatic cancer died within 3 months. A 2nd percutaneous drainage procedure was required in 2 cancer patients. Recurrence of pericardial effusion and tamponade and the requirement of pericardiectomy occurred in 2 patients with perfusion of unknown cause and in 1 patient with perfusion due to rheumatoid arthritis. Histologic examination of pericardial tissue in patients with idiopathic disease showed fibrinous pericarditis but no causal factor. In the group with idiopathic pericardial effusion, 2 patients with multiple mediastinal lymphadenopathy underwent mediastinal exploration; biopsy revealed nonspecific lymphadenitis and fibrinous pericarditis. In patients with large pericardial effusions and tamponade, the specific cause was in most cases already known or obtained by initial clinical and laboratory investigation. Sufficient cardiac decompression was achieved by percutaneous pigtail catheter drainage.     

Purulent Pericarditis Caused by Haemophilus parainfluenzae

Bacterial pericarditis is a rare disease in the era of antibiotics. Purulent pericarditis is most often caused by Staphylococcus aureus, Streptococcus pneumoniae, or Haemophilus influenzae. The number of H. parainfluenzae infections has been increasing; in rare cases, it has caused endocarditis. We report a case of purulent pericarditis caused by H. parainfluenzae in a 62-year-old woman who reported a recent upper respiratory tract infection. The patient presented with signs and symptoms of pericardial tamponade. Urgent pericardiocentesis restored her hemodynamic stability. However, within 24 hours, fluid reaccumulation led to recurrent pericardial tamponade and necessitated the creation of a pericardial window. Cultures of the first pericardial fluid grew H. parainfluenzae. Levofloxacin therapy was started, and the patient recovered. Haemophilus parainfluenzae should be considered in a patient who has signs and symptoms of purulent pericarditis. Prompt diagnosis, treatment, and antibiotic therapy are necessary for the patient''s survival. To our knowledge, this is the first report of purulent pericarditis caused by H. parainfluenzae.Key words: Endocarditis, bacterial/diagnosis/microbiology/pathology; haemophilus/isolation & purification; haemophilus infections/diagnosis/drug therapy; haemophilus parainfluenzae; pericarditis/complications/diagnosis/etiology/microbiology/therapy; suppuration/diagnosis; treatment outcomePurulent pericarditis is a disease process that is usually described as a secondary infection from a primary site in the respiratory tract. The condition has been associated with respiratory disease processes such as pneumonia or empyema, but it can be a sequela of endocarditis, chest trauma, chest surgery, or the hematogenous spread of infection from elsewhere in the body.¹ Haemophilus influenzae has been suspected as a cause of purulent pericarditis; however, H. parainfluenzae has not previously been reported as a cause. Haemophilus parainfluenzae organisms are considered to be normal respiratory flora with low pathogenicity. However, H. parainfluenzae is being more frequently implicated in a variety of infections.^2,3 We present what we think is the first report of purulent pericarditis caused by H. parainfluenzae.     

Bacteroides pericardial effusion and cardiac tamponade in a patient with chronic renal failure

A 31-year-old woman with chronic renal insufficiency and recurrent pericarditis developed and enlarging cardiac silhouette and physical signs of cardiac tamponade. Cardiac catheterization demonstrated pericardial effusion with hemodynamic evidence of cardiac compression. At pericardial exploration, 1.5 L. of foul-smelling purulent material was removed from a distended pericardial sac. Cultures of both the exudate and pericardium revealed pure growth of Bacteroides fragiles. The patient was subsequently treated with intravenous chloramphenicol and has had an uncomplicated clinical course since that time.This represents the first reported case of cardiac tamponade secondary to culturally proved Bacteroides pericarditis in the setting of chronic renal insufficiency.     

A case of rheumatoid pericarditis associated with a high IL-6 titer in the pericardial fluid and tocilizumab treatment

We report a 60-year-old woman with rheumatoid arthritis complicated by pericarditis. Treatment with tocilizumab improved her polyarthritis, but the pericardial effusion increased so rapidly as to cause cardiac tamponade before the treatment could prove its efficacy. Pericardial effusion disappeared after pericardiocentesis. The pericardial fluid contained a remarkably high concentration of interleukin-6 (IL-6; 351,000 pg/mL), which tocilizumab appeared to have made yet higher compared to the reported IL-6 levels in rheumatoid pericarditis. No further exacerbation of pericarditis was observed after retreatment with tocilizumab. This case has important implications in that it suggests that the prominently elevated IL-6 level in pericardial fluid during tocilizumab treatment may be an indicator of its efficacy for pericarditis.     

Successful treatment of refractory cardiac tamponade due to rheumatoid arthritis using pericardial drainage

Rheumatoid pericarditis occurs in patients with rheumatoid arthritis (RA). However, cardiac tamponade due to rheumatoid pericarditis is rare; we describe a case of a 72-year-old man with a 6-year history of rheumatoid arthritis who developed rheumatoid pericarditis with recurrent cardiac tamponade. The patient experienced relapse of the cardiac tamponade despite treatment with pericardiocentesis. Therefore, the patient underwent surgical pericardial drainage. The patient was also subsequently treated with increasing doses of corticosteroid, methotrexate and leukocytapheresis. These treatments resulted in a successful outcome without any complication. This case suggests that in addition to immunosuppressive therapy, pericardial drainage should be considered in the treatment of life-threatening refractory cardiac tamponade caused by rheumatoid arthritis.     

Diagnosis and management of acute pericardial syndromes

Essentially, acute pericardial syndromes include acute pericarditis and cardiac tamponade. This article focuses on the diagnosis and management of acute pericarditis. In Spain, most cases of acute pericarditis whose etiology is not apparent at initial clinical presentation are either idiopathic or viral pericarditis, which follow a benign or self-limiting clinical course (although tamponade may develop in some patients). Knowledge of this basic epidemiologic fact is essential for the development of a rational management protocol that, on the one hand, avoids the unnecessary use of invasive pericardial diagnostic procedures in patients with idiopathic pericarditis and that, on the other hand, correctly identifies most cases of specific pericarditis, which mainly comprise purulent, tuberculous or neoplastic pericarditis. In accordance with this rationale and on the basis of our own experience, we have proposed a protocol for the management of acute pericardial disease that differs markedly from the "Guidelines on the Diagnosis and Management of Pericardial Disease" recently produced by the European Society of Cardiology. In addition, we have made some comments on the cardiac tamponade and the acute and subacute constrictive pericarditis that can occur during the resolution of acute pericarditis.     

Possible contribution of pericardial tamponade to coronary artery bypass graft occlusion

We report an association between pericardial tamponade and early post-surgical occlusion of a coronary bypass graft. The presented patient developed pericarditis following myocardial infarction and bypass surgery. He was readmitted with myocardial reinfarction and cardiogenic shock 1 week after surgery. Coronary angiography revealed occlusion of a saphenous-vein graft to the right coronary artery. Concomitantly, pericardial tamponade was diagnosed on the basis of typical hemodynamics and echocardiographic findings. The patient recovered following pericardiocentesis and coronary angioplasty. We suggest a possible link between the 2 pathologies, whereby post-surgical pericarditis led to tamponade which decreased cardiac preload and resulted in systemic hypotension. Decreased coronary perfusion pressure and extrinsic compression by fluid in the pericardial space may have contributed to graft occlusion. Pericarditis and pericardial tamponade may therefore be risk factors for coronary bypass graft occlusion.     

Purulent pericarditis with tamponade in a postpartum patient due to group F streptococcus.

Bacterial pericarditis with cardiac tamponade is a life-threatening disorder that has been associated with a variety of organisms. There is usually an associated underlying condition or a seeding of the pericardium from an infection elsewhere. We report the development of cardiac tamponade and a subsequent pericardial constriction due to group F streptococcus purulent pericarditis. We believe this to be the first report of a postpartum patient with purulent pericarditis.     

Primary acute pericardial disease: a prospective series of 231 consecutive patients

A series of 231 patients with "primary" acute pericardial disease (acute pericarditis or tamponade presenting without an apparent cause) were studied according to the following protocol: general clinical and laboratory studies (stage I), pericardiocentesis (stage II), pericardial biopsy (stage III) and blind antituberculous therapy (stage IV). In 32 patients (14%) a specific etiologic diagnosis was obtained (13 with neoplasia, 9 with tuberculosis, 4 with collagen vascular disease, 2 with toxoplasmosis, 2 with purulent pericarditis and 2 with viral pericarditis). "Diagnostic" pericardiocentesis (32 patients) was performed when clinical activity and effusion persisted for longer than 1 week or when purulent pericarditis was suspected, whereas "therapeutic" pericardiocentesis (44 patients) was performed to treat tamponade; their diagnostic yield was 6% and 29%, respectively. "Diagnostic" biopsy (20 patients) was carried out when illness persisted for longer than 3 weeks, whereas "therapeutic" biopsy was performed whenever pericardiocentesis failed to relieve tamponade; their diagnostic yield was 5% and 54%, respectively. The diagnostic yield difference between "diagnostic" and "therapeutic" procedures was significant (p less than 0.001); in contrast, the global diagnostic yield of pericardiocentesis (19%) and biopsy (22%) was similar. At the end of follow-up (1 to 76 months, mean 31 +/- 20), no patient in whom a diagnosis of idiopathic pericarditis had been made showed signs of pericardial disease. It is concluded that a "diagnostic" procedure is not warranted as a routine method, a choice between "therapeutic" pericardiocentesis and biopsy is circumstantial and must be individualized, and only through a systematic approach can a substantial diagnostic yield be reached in primary acute pericardial disease.     

Value of pericardioscopy in pericardial effusion. Apropos of 20 patients

The value of pericardioscopy in pericardial effusion of uncertain origin was evaluated in 20 patients, aged from 18 to 77 years, whose pericardial effusion had been diagnosed by ultrasonography; 2 patients presented with clinical signs of tamponade. The cause of the pericarditis was unknown, but the clinical context suggested a malignant disease in 13 patients, tuberculosis in 5 patients and another cause in 2 patients. The pericardium was explored by means of a direct vision, cold-light endoscope, usually a mediastinoscope, introduced by the retroxiphoidal route under general of local anaesthesia. This method made it possible to study the pericardial fluid, examine the pericardial serous membrane, perform biopsies at a distance from the orifice of entry and cleanse the pericardium thoroughly in cases with blood or pus collection. Apart from 2 cases where the examination could not be completed because of an anterior mediastinal mass and a pericardial symphysis, valuable information could be obtained in purulent pericarditis (n = 1), chronic radiation induced lesions (n = 2), metastases (n = 2), haemopericardium (n = 2), and biopsies could be performed in tumoral or suspicious areas. These guided biopsies revealed a metastasis in 3 cases where the pericardial window was negative. No sign of tuberculosis was found in the 5 cases where the disease was suspected. The final diagnoses were: neoplastic pericarditis in 4 cases, radiation-induced pericarditis in 2 cases, purulent pericarditis in 2 cases, haemopericardium in 3 cases and idiopathic or reactive pericarditis in 9 cases. The post-operative period was uneventful, with no major complication ascribable to the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Purulent pericarditis and cardiac tamponade caused by Nocardia asteroides in mixed connective tissue disease

Pericardial nocardiosis is extremely rare, but may affect especially immunocompromised hosts. We describe the first reported case of purulent pericarditis with cardiac tamponade as the initial presentation of systemic nocardiosis in a patient with mixed connective tissue disease. Our case emphasizes the importance of identifying infectious causes of pericarditis in patients with connective tissue diseases. Longterm survival was achieved with a combined medical and surgical approach.