Pericarditis caused by beta-lactamase-producing Haemophilus influenzae: report of two cases in adults and review of the literature

Two adult patients with pericarditis caused by beta-lactamase producing Haemophilus influenzae are reported and their management reviewed. Both had pharyngitis, epiglottitis, pneumonia, empyema, or septicemia and were cured with antimicrobics and pericardial drainage (one by catheter and one by surgery). Eleven previously reported cases of pericarditis caused by Haemophilus influenzae are also reviewed. In reviewing this rare cause of bacteria pericarditis, it is important to recognize the antibiotic resistance profile, the incidence of pericardial tamponade, and the use of surgical drainage. Antibiotic selection for this organism is also discussed, as well as the importance of biotyping.     

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.     

Pericardial actinomycosis: case report and review

Pericardial actinomycosis is rare and frequently goes unrecognized during life, a circumstance due in part to a paucity of clinical manifestations and to a low rate of positivity in cultures. We present a case report of pericardial actinomycosis and a review of 18 other cases reported in the literature since 1950. Possible risk factors include aspiration pneumonia, alcohol abuse, and periodontal disease. Actinomyces may cause purulent pericarditis that evolves into cardiac tamponade or constrictive pericarditis. Clues to the identity of the causative organism (e.g., draining sinus tracts and the presence of sulfur granules) are frequently absent, and cultures often fail to yield the organism. Histologic examination of material obtained by biopsy is often necessary to make the diagnosis. Most cases originate from a thoracopulmonary site of actinomycosis and spread directly to the pericardium. Widespread dissemination to extrathoracic organs is uncommon. Treatment consists of high-dose, long-term antimicrobial therapy as well as drainage of the pericardial space.     

原发性心包间皮瘤七例临床病理分析

原发性心包间皮瘤临床罕见，本组分析７例原发性心包间皮瘤，其症状、体征无特异性．胸片、心电图、超声心动等检查不能确定诊断，常被误诊为结核性心包炎、缩窄性心包炎等病，明确诊断需借助心包积液及心包的活组织的病理学检查及Ｇａ￣（６７）血池扫描Ｂｅｖ－ＥＰ＿４，免疫组织化学标记等方法。     

Constrictive pericarditis in severe seronegative rheumatoid polyarthritis]

Constrictive pericarditis is a rare complication of rheumatoid arthritis, with 78 published cases. We report a new typical case where the pericardial disease was associated with a severe seronegative rheumatoid arthritis of 17 years duration. Constrictive pericarditis generally occurs in men (62.8% of all cases) aged 52.4 +/- 11.5 years. Its clinical features are identical with those of constrictive pericarditis due to other causes. Diagnosis rests on echocardiography and, chiefly, on right heart catheterization. The arthritis is seropositive in 85.7% of the cases, frequently nodular (75%) and advanced. There is no relation between its duration (mean: 9.6 +/- 7.4 years) and the occurrence of the pericardial pathology. The pericardial fluid has no specific abnormality. Histology shows fibrosis and a non-specific inflammatory cell infiltrate. Immunoglobulin and complement deposits in the walls of the pericardial vessels are detected by immunofluorescence. The only treatment is pericardiectomy; without it the disease is constantly lethal.     

Legionella pneumophila pericarditis proved by culture of pericardial fluid

Serogroup 1 Legionella pneumophila was isolated from the pericardial fluid of a nonimmunosuppressed patient with pulmonary infiltrates, cardiac tamponade, and histologic evidence of pericarditis. This is the first reported case in which the association of L. pneumophila infection and pericarditis has been proved by growth of the organism from pericardial fluid. Physicians caring for patients with pericarditis of unknown cause should consider L. pneumophila in their differential diagnosis because special diagnostic efforts and relatively specific therapy are required for its optimal management.     

Pericarditis

Pericarditis is a common disorder that has multiple causes and presents in various primary-care and secondary-care settings. New diagnostic techniques have improved the sampling and analysis of pericardial fluid and allow comprehensive characterisation of cause. Despite this advance, pericarditis is most commonly idiopathic, and radiation therapy, cardiac surgery, and percutaneous procedures have become important causes. Pericarditis is frequently self-limiting, and non-steroidal anti-inflammatory agents remain the first-line treatment for uncomplicated cases. Integrated use of new imaging methods facilitates accurate detection and management of complications such as pericardial effusion or constriction. Differentiation of constrictive pericarditis from restrictive cardiomyopathy remains a clinical challenge but is facilitated by tissue doppler and colour M-mode echocardiography. Most pericardial effusions can be safely managed with an echo-guided percutaneous approach. Pericardiectomy remains the definitive treatment for constrictive pericarditis and provides symptomatic relief in most cases. In the future, the pericardial space might become a conduit for treatments directed at the pericardium and myocardium.     

Effectiveness of Intrapericardial Administration of Streptokinase in Purulent Pericarditis

BACKGROUND AND PURPOSE: Purulent pericarditis is very rare. However, among patients suffering from this disease the mortality rate is very high. The aim of this study was to evaluate the effectiveness and side effects of intrapericardial streptokinase administration in patients with confirmed purulent pericarditis. PATIENTS AND METHODS: Three patients, one 50-year-old man and two women aged 64 and 40 years, who were admitted to the intensive care unit (ICU) due to purulent pericarditis, entered the study. In all three cases a subxiphoid pericardiotomy followed by insertion of a drainage line into the pericardial space was performed. Antibiotic therapy was started immediately on admission to the hospital. Despite continued antibiotic therapy in all three patients, daily drainage from the pericardium--during several days after surgery--staggered between 50-200 ml/day. Due to considerable purulent pericardial drainage loculations and/or fibrin deposits confirmed by echocardiography, streptokinase (500,000 IU dissolved in 50 ml of normal saline) was administered into the pericardial space over 10 min, using the previously inserted drainage catheter. This regimen was repeated after 12 and 24 h. The total dose of streptokinase was 1,500,000 IU. RESULTS: The clinical effect of intrapericardial streptokinase administration was excellent. Several days after intrapericardial administration of streptokinase, drainage of purulent pericardial fluid stopped. No complications associated with intrapericardial streptokinase administration were observed. In the follow-up echocardiography (in two patients repeated 6 and 9 months after delivery of streptokinase), pericardial fluid and echocardiographic signs of pericardial constriction were not observed. CONCLUSION: Intrapericardial administration of streptokinase in purulent pericarditis is effective and safe.     

PERICARDITIS (WITH PARTICULAR REFERENCE TO TUBERCULOUS PERICARDITIS)

In this study diseases of the pericardium which dominate the clinical picture have been analysed. In essence this means a discussion of infective pericarditis. Pericarditis is a common disorder in Cape Town, South Africa, particularly among the Bantu and Cape Coloured population. The high incidence in the non-White races is attributed to tuberculosis, mainly as a result of socio-economic conditions. Tuberculosis was found to be the cause in 40% of the patients; the diagnosis was established by the finding of pericardial fluid, which gave positive results on testing for tuberculosis, positive histological evidence or adequate evidence of associated organ tuberculosis. In another 40% of patients, tuberculosis appeared to be the most likely cause of the condition, on clinical grounds which are described. Twelve per centum of cases were due to causes unknown, a tuberculous or viral cause being the most likely. In 6% of cases the pericarditis was pyogenic. A few other uncommon conditions were also present. The clinical syndromes of dry pericarditis, pericarditis with effusion and constrictive pericarditis are described. The most important symptom is a distinctive type of chest pain due to inflammation of the pericardium. The important findings are a pericardial friction rub, systemic venous hypertension and pulsus paradoxus. Sudden splitting of the second sound in inspiration is more characteristic than the early third heart sound, and occurs far more frequently. The electrocardiogram is usually abnormal, drawing attention to the heart, but not very helpful in establishing the diagnosis. The findings on X-ray examination confirm the cardiomegaly in cases of effusion and in most cases of constrictive pericarditis. A cardiac shadow of normal size was uncommonly seen, and pericardial calcification occurred in a minor proportion of the cases in this series. Cardiac catheterization and angiocardiography was seldom required to establish the diagnosis. The pericardium should be aspirated whenever an effusion is suspected, and aspiration is a safe procedure with an electrode needle under electrocardiographic control. The course of pericardial effusion and constrictive pericarditis (in 195 and 220 patients respectively) is discussed, with particular reference to tuberculosis. With tuberculous pericardial effusions from which acid-fast bacilli were recovered there was an extremely high incidence of progression of the condition to constrictive pericarditis requiring surgery. Even when the fluid was sterile, most patients developed constriction and surgery was usually required, but the rate of ultimate cure was over 90%. Of 195 patients presenting with pericardial effusion, irrespective of the cause over half developed the signs of constrictive pericarditis, and 40% required surgery. A small but significant percentage of patients, however, can pass through the phase of constriction and ultimately recover without operation. There were 220 patients with constrictive pericarditis. In 38 the process was chronic, the only effective treatment being surgical. Seventy-eight presented with active pericarditis producing constriction without effusion. Most of these required surgical treatment, but a quarter recovered on conservative therapy alone. The remaining 104 developed pericardial constriction after their disease had passed through a phase of effusion, surgery being necessary for 75%. The overall surgical results were better than the results of medical therapy, which consisted of the use of antituberculous drugs, digitalis and diuretics. Surgery has a great deal to offer in the treatment of pericarditis, but the time to recommend this procedure must be carefully chosen.     

Candida albicans purulent pericarditis treated successfully without surgical drainage.

Cures of Candida pericarditis reported in the literature uniformly involved surgical drainage of the pericardial space. We report a patient with purulent pericarditis caused by Candida albicans who was treated successfully with antifungal chemotherapy combined with a single pericardiocentesis that did not completely evacuate the pericardial space. This case indicates that thoracotomy with surgical drainage of the pericardium is not mandatory for successful therapy of Candida pericarditis.     

A modern approach to tuberculous pericarditis

The human immunodeficiency virus (HIV) epidemic has been associated with an increase in all forms of extrapulmonary tuberculosis including tuberculous pericarditis. Tuberculosis is responsible for approximately 70% of cases of large pericardial effusion and most cases of constrictive pericarditis in developing countries, where most of the world's population live. However, in industrialized countries, tuberculosis accounts for only 4% of cases of pericardial effusion and an even smaller proportion of instances of constrictive pericarditis. Tuberculous pericarditis is a dangerous disease with a mortality of 17% to 40%; constriction occurs in a similar proportion of cases after tuberculous pericardial effusion. Early diagnosis and institution of appropriate therapy are critical to prevent mortality. A definite or proven diagnosis is based on demonstration of tubercle bacilli in pericardial fluid or on histologic section of the pericardium. A probable or presumed diagnosis is based on proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated biomarkers of tuberculous infection, and/or appropriate response to a trial of antituberculosis chemotherapy. Treatment consists of 4-drug therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months followed by 2 drugs (isoniazid and rifampicin) for 4 months regardless of HIV status. It is uncertain whether adjunctive corticosteroids are effective in reducing mortality or pericardial constriction, and their safety in HIV-infected patients has not been established conclusively. Surgical resection of the pericardium is indicated for those with calcific constrictive pericarditis or with persistent signs of constriction after a 6 to 8 week trial of antituberculosis treatment in patients with noncalcific constrictive pericarditis.     

Constrictive pericarditis: early and late complication of cardiac surgery.

Constrictive pericarditis is not considered a complication of cardiac surgery. However, three cases are presented in which equalization of diastolic pressures and the ventricular pressure pattern of early diastolic dip-late diastolic plateau, characteristic of restrictive disease, appeared after cardiac surgery. In one patients cardiac constriction developed less than 2 weeks after surgery, and loculated clotted and unclotted viscous blood was removed from the pericardial space. In the other two patients the pericardial space was obliterated by dense adhesions. Thus constrictive pericarditis should be considered in postoperative patients who either do not recuperate satisfactorily after surgery or whose condition deteriorates after initial recovery.     

Echocardiographic diagnosis of pericardial disease.

Echocardiograms were performed in 11 patients with constrictive pericarditis or effusive-constrictive pericarditis confirmed by cardiac catheterization and pericardiectomy. Three echocardiographic patterns of pericardial disease were noted and were related to three types of pericardial pathology. Parallel moving echoes separated by a clear space were reflected from chronically fibrosed and thickened pericardium without associated pericardial exudate. Effusive-constrictive pericarditis or subacute wet pericarditis was characterized on the echocardiogram by a posterior echo-free space representing the liquid pericardial effusion and multiple ultrasonic lines from the thickened visceral pericardium. Subacute dry pericarditis was associated with numerous ultrasonic signals filling the space between the visceral pericardium and the relatively flat parietal pericardium. These ultrasonic signals were reflected from coagulated pericardial exudate which was adherent both to the parietal pericardium and the visceral pericardium. Parallel moving echoes or dense bands of echoes were reflected from either or both thickened visceral and parietal pericardium.     

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.     

Wegener's granulomatosis and the heart.

Three cases of Wegener's granulomatosis with cardiac complications are described and the relevant published reports are reviewed. The first case of Wegener's granulomatosis was associated with aortic regurgitation and required aortic valve replacement. The second and third cases were associated with pericardial disease requiring pericardiectomy for constructive pericarditis in one case, and haemorrhagic pericarditis with pericardial effusion in the other. Aortic valve involvement in Wegener's granulomatosis is uncommon and valve replacement has been described on only one previous occasion. Pericardial involvement is relatively common pathologically, but pericardial surgery has been described in this condition only twice, once for tamponade and once for constrictive pericarditis after pericardiocentesis. Cardiac involvement is not uncommon in patients with Wegner's granulomatosis and may be clinically important. Diagnosis is aided by estimation of the anti-neutophil cytoplasmic antibody titre.     

Presentation pattern and management of effusive-constrictive pericarditis in Ibadan

Background: Effusive-constrictive pericarditis is a syndrome in which constriction by the visceral pericardium occurs in the presence of a dense effusion in a free pericardial space. Treatment of this disease is problematic because pericardiocentesis does not relieve the impaired filling of the heart and surgical removal of the visceral pericardium is challenging. We sought to provide further information by addressing the evolution and clinico-pathological pattern, and optimal surgical management of this disease. Methods: We conducted a prospective review of a consecutive series of five patients managed in the cardiothoracic surgery unit of University College Hospital, Ibadan, in the previous year, along with a general overview of other cases managed over a seven-year period. This was followed by an extensive literature review with a special focus on Africa. Results: The diagnosis of effusive-constrictive pericarditis was established on the basis of clinical findings of features of pericardial disease with evidence of pericardial effusion, and echocardiographic finding of constrictive physiology with or without radiological evidence of pericardial calcification. A review of our surgical records over the previous seven years revealed a prevalence of 13% among patients with pericardial disease of any type (11/86), 22% of patients presenting with effusive pericardial disease (11/50) and 35% who had had pericardiectomy for constrictive pericarditis (11/31). All five cases in this series were confirmed by a clinical scenario of non-resolving cardiac impairment despite adequate open pericardial drainage. They all improved following pericardiectomy. Conclusion: Effusive-constrictive pericarditis as a subset of pericardial disease deserves closer study and individualisation of treatment. Evaluating patients suspected of having the disease affords clinicians the opportunity to integrate clinical features and non-invasive investigations with or without findings at pericardiostomy, to derive a management plan tailored to each patient. The limited number of patients in this series called for caution in generalisation. Hence our aim was to increase the sensitivity of others to issues raised and help spur on further collaborative studies to lay down guidelines with an African perspective.     

Procainamide-induced lupus erythematosus pericarditis encountered during coronary bypass sugery

Procainamide is probably the most common offending drug responsible for the drug-induced lupus erythematosus syndrome today. Pericarditis has been reported to occur in from 14 to 18 per cent of the cases of procainamide-induced lupus erythematosus, and occasional reports of massive pericardial effusion, pericardial tamponade and constrictive pericarditis have appeared in the literature. We describe a patient who presented with features of procainamide-induced lupus erythematosus without any clinical evidence of pericarditis. He underwent coronary bypass surgery 12 days after administration of the drug was stopped and was found to have a significant pericardial effusion at the time of surgery; histologic examination of pericardial tissue and pericardial fluid confirmed that the pericardial effusion was related to the procainamide-induced lupus syndrome. The incidence of pericarditis in procainamide-induced lupus erythematosus may be higher than presently accepted figures would indicate. Symptoms and signs related to procainamide-induced lupus pericarditis may cause diagnostic confusion with common postoperative bypass complications; the full implications of this disease entity to the patient undergoing coronary bypass are unknown.     

Toxoplasma pericarditis without immunosuppressant disorder detected by polymerase chain reaction of pericardial fluid: a case report

There have been several case reports, a total of 22 up to the present, of toxoplasma pericarditis. Out of them, in only a few cases the diagnosis was properly made with a proof of the microscopic presence of Toxoplasma gondii. This is the first report of toxoplasma pericarditis in which the presence of Toxoplasma gondii was detected by polymerase chain reaction of pericardial effusion. In addition, the previous reports will be reviewed, and compared to this present case. A 29-year-old woman, without immunosuppressant disorder, suffering from fever and orthopnea was admitted to our hospital. Blood chemistry findings indicated mild liver dysfunction and inflammation. Chest radiography showed cardiac enlargement. Electrocardiography showed sinus tachycardia and ST elevation. Echocardiography revealed a massive pericardial effusion. Pericardiocentesis demonstrated 638 ml of bloody fluid. Cytologic study of the fluid was class II for malignancy, and polymerase chain reaction to tuberculosis was negative. However, a high titer of the anti-toxoplasma antibody of 1: 20,480 (passive hemagglutination) indicated pericarditis caused by Toxoplasma gondii. Subsequently, Toxoplasma gondii was identified in the pericardial effusion by polymerase chain reaction. Clinical symptoms improved after pericardiocentesis, but 2 months later pericarditis recurred. Treatment was started with 800 mg acetylspiramycin daily but failed to improve the symptoms. Because of the development of pleuritis, treatment was changed to sulfadoxine 1,000 mg/pyrimethamine 50 mg. After the treatment with them, her symptoms improved. Only 22 cases of toxoplasma pericarditis have been reported worldwide and 15 of those cases were without immunosuppressant disorder. The usual symptoms at the onset of pericarditis without immunosuppressant disorder are fever, dyspnea and chest pain. Seven patients developed cardiac tamponade. Pericardiocentesis was performed in 8 cases and the pericardial fluid was hemorrhagic in 6. Pericardial thickening was detected in 5 cases. The diagnosis of toxoplasma infection is very difficult, because asymptomatic infection of Toxoplasma gondii is very common. Pericarditis is a disease difficult to confirm the etiology. Detection of Toxoplasma gondii in pericardial effusion by the polymerase chain reaction is very useful for its diagnosis.     

Purulent pericarditis caused by Candida: report of three cases and identification of high-risk populations as an aid to early diagnosis

Purulent pericarditis due to fungal organisms is rare and often unrecognized because of the subtle clinical clues and insidious onset. The records of 11 cases of purulent pericarditis were selected from records of 11,000 cases of pericarditis at Duke University Medical Center and reviewed, and experience with three cases of candida purulent pericarditis (CPP) was evaluated. One case occurred in a patient recovering from complicated cardiac surgery, one in a patient with hematologic malignancy, and one in an alcoholic patient requiring intubation for a severe respiratory infection. Each case is representative of a group at increased risk for the development of CPP. Given the poor prognosis for CPP, treatment should include both medical and surgical interventions. Although amphotericin B achieves good penetration into the inflamed pericardial space, the only survivors of CPP have received both amphotericin B and pericardiectomy. Careful attention to clinical indications of pericardial inflammation and systemic infection in the three groups of patients may lead to earlier recognition of CPP, implementation of appropriate therapy, and perhaps a higher rate of cure.     

慢性缩窄性心包炎的外科治疗

目的 :总结 1978年 7月至 2 0 0 2年 7月手术治疗缩窄性心包炎的经验。方法 :2 0 3例病人在全麻下行心包剥脱术 ,左四肋间切口 6 9例 ,左四肋间加横断胸骨切口 4例 ,局部 4肋间加肋软骨切除 1例 ,正中切口 14 9例。结果 :术后病人死亡 3例 ,复发 5例 ,再次行心包剥脱术。其余病人术后心功能恢复至Ⅰ～Ⅱ级。结论 :手术治疗缩窄性心包炎是最有效的手段 ,如病人确诊为该疾病应尽早手术治疗。