Comparison of effectiveness and safety of operations on the pericardium

A ten-year experience with operations on the pericardium in 71 consecutive patients was reviewed. The patients ranged in age from nine months to 75 years old. Fifty-three patients were operated upon for pericardial effusion and 14 for pericardial constriction. Sixty-seven patients had pericarditis: 21 of them underwent subxiphoid tube drainage; ten, limited pericardiectomy; and the remaining 36, extensive pericardiectomy. There were two trauma victims who underwent diagnostic pericardiotomy. Two patients underwent excision of pericardial cysts. There was one operative death during extensive pericardiectomy for constrictive tuberculous pericarditis. Thirty-day mortality was three of 21 patients after subxiphoid tube drainage, three of ten after limited pericardiectomy and five of 36 after extensive pericardiectomy. Postoperative complications consisted of pulmonary problems in four patients (two after pericardiectomy and two after extensive pericardiectomy), cardiac arrhythmia in one patient after tube drainage and postpericardiotomy syndrome in one patient after extensive pericardiectomy. Mean follow-up was 3.2 years. Recurrent pericardial effusion occurred in two patients; one had limited pericardiectomy but did not require reoperation and one had diagnostic pericardiotomy without drainage. Six patients with persistent postirradiation pericardial effusion were treated effectively with extensive pericardiotomy. Our experience indicates that subxiphoid tube drainage is effective for the treatment of pericardial effusion and safer than limited pericardiectomy, while extensive pericardiectomy is the operation of choice for pericardial constriction and radiation-related pericardial effusion.     

MASSIVE PERICARDIAL EFFUSION IN SCLERODERMA: A REVIEW OF FIVE CASES

Medical records of five patients with sclerodenna (SSc), eachof whom had pericardial effusion with an estimated volume ofmore than 200 ml, were reviewed to study the clinical and immunologicalsignificance of massive pericardial effusion in SSc. DiffuseSSc (4/5), with a wide area of pigmentation (4/5), flexion contracture(4/5), oesophageal hypomotility (5/5), pulmonary fibrosis (4/5)and autoantibodies to topoisomerase I (3/5) were the commonfeatures in this group. High protein, lactate dehydrogenaseand low white blood cell count were the characteristics of pericardialfluid. None of the patients had signs of acute pericarditis.Four of the five cases died within 9 months of the diagnosisof pericarditis; two with renal failure, one with cardiac tamponadeand another with sudden death. The pericarditis in diffuse SSc,especially in cases with anti-topoisomerase I, may be characterizedby a chronic form of pericarditis with poor prognosis, oftencomplicated by ,renal failure. KEY WORDS: Scleroderma, Pericardial effusion, Antitopoisomerase I antibodies, Antinuclear antibodies, Renal failure     

Constrictive pericarditis after myocardial revascularization: report of three cases.

Although postoperative constrictive pericarditis is rare, the diagnosis should be considered when unexplained right-sided heart failure develops after cardiac surgery. Within a 6 week interval, evidence of constrictive pericarditis developed in three patients who had recently undergone myocardial revascularization. One patient presented with biventricular failure, pericardial effusion and suspected tamponade. Severe constrictive pericarditis was demonstrated at subsequent operation. An apparent postpericardiotomy syndrome preceded evidence of right heart failure in the other two patients. Etiologic considerations include the possibility that pericardial irrigation with povidone-iodine (Betadine) solution may have contributed to subsequent fibrosis.     

Evaluation of children with a large pericardial effusion and cardiac tamponade

OBJECTIVES: Large pericardial effusions and cardiac tamponade are rare in childhood.The aim of this study was to evaluate the aetiological factors and clinical findings of large pericardial effusion and cardiac tamponade in children. METHODS: We reviewed retrospectively the records of 10 (6 male, 4 female) patients (mean age: 8.05 +/- 4.4 y) with the diagnosis of large pericardial effusion and cardiac tamponade requiring pericardiocentesis and pericardial drainage between 2002 and 2004. RESULTS: After extensive diagnostic investigation we detected that three patients had tuberculosis, one patient had uraemic pericarditis; one patient had bacterial pericarditis; one patient had post-pericardiotomy syndrome; two patients had malignancy and two patients had no identifiable aetiology. Echocardiography-guided percutaneous pericardial puncture and pigtail catheter placement is safe and effective for initial treatment of patients with large pericardial effusion and cardiac tamponade and in most cases, initial assessment with clinical, serologic, and radiologic investigation and careful follow-up can reveal the aetiology. CONCLUSIONS: Although tuberculosis is rare in industrialized countries, in developing countries it remains one of the most important causes of large pericardial effusion and should be investigated and excluded in each patient.     

Malignant pericardial effusions: usefulness of pericardioscopy.

In cases of malignant pericardial effusion, surgical subxiphoid biopsy sometimes fails to prove malignancy. To assess the usefulness of pericardioscopy, which allows an endoscopic investigation of the pericardial cavity, this technique was systematically performed during surgical drainage procedures that were performed on 40 patients who had pericardial effusions of suspected malignant origin. Twenty-six patients had a history of neoplasm, 10 had a history of hematologic malignancy, and four had recent tumors or lymphadenopathies that were suspected to be of malignant origin. Classical tests that are usually performed during a conventional surgical drainage procedure (fluid studies and subxiphoid biopsy) were combined with direct visualization of the pericardial surfaces and guided biopsies of suspicious areas. The follow-up period after pericardioscopy was at least 12 months. Two early deaths occurred after pericardioscopy, but no death was directly related to the endoscopy. According to all of the tests that were performed, diagnoses were malignant pericardial effusion in 15 of 40 patients (group I, 37%) and nonmalignant pericardial effusion in 25 of 40 patients (group II, 73%). In 3 of 13 patients (23%) in group I, the diagnosis was obtained only by pericardioscopy (results of cytologic studies and subxiphoid biopsy were negative). In two patients in group I, pericardioscopy could not be completed, but the diagnosis of malignant pericardial effusion was obtained by pericardiocentesis. In group II, effusion was considered to be postradiation pericarditis in five cases, infectious pericarditis in three cases (bacterial in one and tuberculous in two), hemopericardium induced by coagulation disturbances in three cases, and idiopathic pericarditis in 14 cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Large pericardial effusions of inflammatory origin in childhood

OBJECTIVES: Our aim was to review the clinical records from children with large pericardial effusions of inflammatory origin presenting to a tertiary referral centre over the last 21 years, with emphasis on their clinical presentation, management and outcome. BACKGROUND: The common identifiable causes of pericardial effusion in children include prior cardiac surgery, bacterial pericarditis, malignancy, and connective tissue disorders. In a significant number of children, however, despite extensive investigation, it is not possible to identify a clear aetiology. A viral cause is often considered, though rarely confirmed. The clinical course of such large idiopathic pericardial effusions in children has not been extensively reported. METHODS AND RESULTS: We reviewed retrospectively the records of all patients seen between 1981 and 2001 with large pericardial effusions of inflammatory origin requiring drainage, excluding the effusions related to cardiac surgery or malignancy. We found 31 patients fulfilling our criterions for study. They could be divided into three groups, with 15 patients having no specific identifiable aetiology despite extensive investigation, 12 patients having evidence of bacterial pericarditis, and four with a probable immunologic disorder. Fever was present in only eight patients (53%) in the idiopathic group. All patients in the other groups had fever. Except for fever and the resultant tachycardia, it was not possible to distinguish on clinical grounds, nor on the presence or otherwise of cardiac tamponade, between those with idiopathic aetiology and those with bacterial infection. Of the patients with presumed bacterial pericarditis, five (42%) had both positive blood and pericardial fluid cultures, three (25%) had positive blood cultures, while a further three patients (25%) had only positive pericardial fluid cultures. All patients required drainage of the pericardial effusion, either under echocardiographic guidance or surgically. None of the patients died. The hospital stay was significantly shorter for those with idiopathic as opposed to bacterial pericarditis. Of those with an idiopathic aetiology, six required readmission due to recurrence of the pericardial effusion, with four patients requiring further surgical drainage. No patients required readmission with a bacterial or immunologic aetiology. No patient developed constrictive pericarditis after a median follow-up of 22 months. CONCLUSION: Patients with large idiopathic pericardial effusion had relatively few constitutional symptoms as compared with their gross echocardiographic findings. Those with bacterial pericarditis had more urgent need for treatment. Patients with pericardial effusion of inflammatory origin, when treated appropriately, had an excellent outcome with no mortality or development of constrictive pericarditis.     

To anticoagulate or not: implications for the management of patients with acute myocardial infarction complicated by both left ventricular thrombus and pericardial effusion

We reviewed the clinical and echocardiographic characteristics of seven patients with left ventricular thrombus and pericardial effusion. Each patient had a recent anterior wall myocardial infarction with an apical left ventricular thrombus. Two patients had clinical evidence of pericarditis. On two-dimensional echocardiography, the effusion was judged to be small in five cases and moderate in two. All patients received parenteral heparin therapy; six of the seven patients subsequently received long-term oral anticoagulation therapy. None of the patients had any clinical or two-dimensional echocardiographic evidence of increasing pericardial effusion or tamponade. Documented systemic embolization was seen in only one patient, whose anticoagulant therapy was stopped 2 weeks after myocardial infarction. In five patients, repeat two-dimensional echocardiography was performed from 2 to 4 months after infarction; in four patients, neither pericardial effusion nor left ventricular thrombus was found. In this group of patients, both short- and long-term anticoagulants were safely administered despite pericardial effusion.     

Cardiac tamponade due to low-volume effusive constrictive pericarditis in a patient with uncontrolled type II autoimmune polyglandular syndrome

Abstract

Type II autoimmune polyglandular syndrome (APS), a relatively common endocrine disorder, includes primary adrenal insufficiency coupled with type 1 diabetes mellitus and/or autoimmune primary hypothyroidism. Autoimmune serositis, an associated disease, may present as symptomatic pericardial effusion. We present a case of a 54-year old male with APS who developed pericarditis leading to cardiac tamponade with a subacute loculated effusion. After urgent pericardiocentesis intrapericardial pressure dropped to 0, while central venous pressures remain elevated, consistent with acute effusive constrictive pericarditis. Contrast computerized tomography confirmed increased pericardial contrast enhancement. The patient recovered after prolonged inotropic support and glucocorticoid administration. He re-accumulated the effusion 16 days later, requiring repeat pericardiocentesis. Effusive–constrictive pericarditis, an uncommon pericardial syndrome, is characterized by simultaneous pericardial inflammation and tamponade. Prior cases of APS associated with cardiac tamponade despite low volumes of effusion have been reported, albeit without good demonstration of hemodynamic findings. We report a case of APS with recurrent pericardial effusion due to pericarditis and marked hypotension with comprehensive clinical and hemodynamic assessment. These patients may require aggressive support with pericardiocentesis, inotropes, and hormone replacement therapy. They should be followed closely for recurrent tamponade.     

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.     

Etiology and prognostic implications of a large pericardial effusion in men

To assess the etiology and prognosis of a large pericardial effusion, we reviewed 25 consecutive patients who presented with a large pericardial effusion and underwent a drainage procedure. Large pericardial effusion was defined as: (1) an echo-free space greater than or equal to 10 mm anteriorly and posteriorly by M-mode echocardiography and (2) removal of greater than or equal to 350 ml of fluid at pericardial drainage. The etiologies of large pericardial effusion were: neoplastic (36%), idiopathic (32%), uremic (20%), postmyocardial infarction (8%), and acute rheumatic fever (4%). Of our patients, 44% presented with cardiac tamponade, while 25% of patients with idiopathic pericarditis had hemorrhage effusion and cardiac tamponade. At follow-up, 37 +/- 17 months after pericardial drainage, 68% had died from complications of their underlying disease. There were no deaths attributed to pericardial disease. While 88% of patients with idiopathic large pericardial effusion were alive at follow-up, none of the neoplastic large pericardial effusion patients survived longer than 5 months after initial pericardial drainage (p less than 0.001). Additionally, the survival of patients with uremic large pericardial effusion was better than patients with neoplastic large pericardial effusion (p less than 0.05). We conclude: (1) neoplastic, idiopathic, and uremic pericarditis are the most common causes of large pericardial effusion in men, (2) idiopathic pericarditis can be hemorrhagic and cause cardiac tamponade, and (3) the prognosis of large pericardial effusion is related to patients' underlying disease.     

T wave changes consistent with epicardial involvement in acute myocardial infarction: Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis

Objectives. This study was designed to evaluate the presence or absence of atypical T wave evolution in patients with a postinfarclion pericardial effusion but without clinically recognized postinfarction pericarditis. A second purpose was to evaluate the frequency of atypical T wave evolution in a previous study of postinfarction pericarditis.Background. Electrocardiographic (ECG) criteria involving the evolution of the T wave after an acute myocardial infarction were recently described in patients with regional postinfarction pericarditis. Atypical T wave evolution was found to have a sensitivity of 100% and a specificity of 77% for clinically recognized regional postinfarction pericarditis with or without a pericardial effusion.Methods. The hospital records and serial ECGs of 20 patients with clinically recognized postinfarction pericarditis (Group I) were reviewed. The records and serial ECGs of 20 additional patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis (Group II) were also examined. The type of postinfarction T wave pattern, typical or atypical, was recorded in both groups.Results. All 20 patients in Group I had atypical T wave evolution. Among the 20 patients in Group II, every patient also had atypical T wave evolution. Fifteen percent of all 40 patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred postinfarction pericarditis.Conclusions. The high sensitivity of atypical T wave evolution in diagnosing regional postinfarction pericarditis was confirmed. However, similar T wave alterations were also observed when a postinfarction pericardial effusion existed in the absence of clinically recognized pericarditis. Fifteen percent of patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred pericardial involvement. Thus, the presence of atypical T wave evolution may be a more sensitive indicator of a transmural infarction than the development of a Q wave.     

Effusive-constrictive hemodynamic pattern due to neoplastic involvement of the pericardium

Eight patients with metastatic malignancy of the pericardium who demonstrated the hemodynamics of subacute effusive-constrictive pericarditis were studied. All patients had clinical evidence of cardiac tamponade due to malignant pericardial effusion and were referred for therapeutic pericardiocentesis. In six in whom pericardiocentesis was successfully performed, right atrial pressure remained elevated after pericardiocentesis and return of the intrapericardial pressure to zero; in these patients, hemodynamic data were initially compatible with tamponade but suggested constriction after removal of the pericardial fluid. In the remaining two patients, echocardiography revealed pericardial fluid, but attempted pericardiocentesis was unsuccessful. In these two patients, the hemodynamic data suggested pericardial constriction; subsequent pathologic examination revealed neoplastic involvement of the visceral pericardium. Thus, subacute effusive-constrictive pericarditis, previously recognized as a complication of tuberculosis or mediastinal radiation, may also be due to metastatic malignancy. The syndrome can readily be demonstrated when right heart catheterization is performed in conjunction with pericardiocentesis.     

Coronavirus Disease 2019 (COVID-19) and Severe Pericardial Effusion: From Pathogenesis to Management: A Case Report Based Systematic Review

The Severe acute respiratory syndrome coronavirus-2 (SARS-COV-2) created a global pandemic that continues to this day. In addition to pulmonary symptoms, the virus can have destructive effects on other organs, especially the heart. For example, large pericardial effusion has been observed as a critical and life-threatening finding in Coronavirus disease of 2019 (COVID-19) patients. In this case report based systematic review, we review the reports of moderate to severe pericardial effusion associated with tamponade physiology. Direct cardiomyocyte and pericardium invasion, inflammation and cytokine storms and oxidative stress due to acute respiratory distress syndrome, are the pathogenesis of this phenomenon. The results showed that the manifestations of this finding are variable. Pericardial effusion can be seen as a delayed complication, accompanied by myocarditis or pericarditis, isolated, or with acute respiratory distress syndrome. In most patients, emergency percutaneous pericardiocentesis was performed, and fluid analysis was often exudative in 3 pattern of hemorrhagic, serous, and serosanguinous. Medical treatment and follow-up are recommended, especially in cases of pericarditis.     

Pulmonary tumor embolism from primary cardiac B-cell lymphoma

We report the case of a 54-year-old man with pulmonary embolism during convalescence from "idiopathic" pericarditis. A transthoracic echocardiographic examination indicated a large mass within the right atrium. Subsequently, he died from refractory hypotension. On autopsy, two large whitish nodules were found in the right atrium; there was also nodular epicardial infiltration. Both lungs showed multiple, grossly visible tumor emboli with pulmonary infarction and no evidence of conventional thromboembolism. This is the first report of pulmonary tumor embolism due to large cell B-cell primary cardiac lymphoma. Refractory unexplained pericardial effusion, pulmonary embolism without risk factors for venous thrombosis, and/or the existence of a mass in the right heart should arouse clinical suspicion for this rare malignancy.     

Dressler's syndrome following pulmonary vein isolation for atrial fibrillation

Dressler's syndrome, characterized by features of fever, pericarditis and pericardial effusion typically occurs in the weeks to months following a myocardial infarction. The syndrome has also been described following several other myocardial and pericardial pathologies, including two reports of Dressler's syndrome following radio-frequency ablation. We describe a case of Dressler's syndrome following a pulmonary vein isolation procedure, which is being performed with increasing frequency as a treatment strategy for atrial fibrillation.     

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.     

Dressler's syndrome following pulmonary vein isolation for atrial fibrillation

Dressler's syndrome, characterized by features of fever, pericarditis and pericardial effusion typically occurs in the weeks to months following a myocardial infarction. The syndrome has also been described following several other myocardial and pericardial pathologies, including two reports of Dressler's syndrome following radio-frequency ablation. We describe a case of Dressler's syndrome following a pulmonary vein isolation procedure, which is being performed with increasing frequency as a treatment strategy for atrial fibrillation.     

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.     

Pericarditis caused by Histoplasma capsulatum.

Sixteen patients with pericarditis caused by Histoplasma capsulatum were studied. Fourteen were less than 30 years old, and no patient had an underlying illness or was receiving immunosuppressive therapy. All patients experienced a flu-like prodromal illness lasting from 2 weeks to 4 months. Pneumonitis or hilar adenopathy, or both, was found in 12; pleural effusion, uncommon in primary pulmonary histoplasmosis, was found in seven patients. Pericardial fluid, pleural fluid and bone marrow cultures yielded no growth. All patients demonstrated a fourfold or greater change in complement-fixing antibody titers. No patient had disseminated disease, and only one required treatment with ampholericin B. The illness ran a protracted course, and in six patients symptomatic pericarditis recurred. Ultimately all recovered. Ten patients were restudied 6 months to 12 years after recover. Only one patient had pericardial calcification, and none had constrictive pericarditis. This form of granulomatous pericarditis, unlike that caused by Mycobacterium tuberculosis, appears to carry a good prognosis.     

Clinically silent pericardial effusions in patients on long-term hemodialysis. Pericardial effusions in hemodialysis.

The danger of cardiac tamponade occurring when pericarditis is accompanied by pericardial effusion, as opposed merely to the presence of a friction rub without effusion, has been unclear. Forty patients on hemodialysis were studied by physical examination, chest x-ray film, and echocardiography for evidence of pericarditis and pericardial effusion. Only two patients developed a friction rub during the study and were placed on regional heparin. Ten of 11 patients who were positive on echocardiogram for pericardial effusion had unremarkable physical examinations. These 11 patients had cardiomegaly as noted on chest x-ray examination. Eighteen of 25 patients without effusion also had cardiomegaly on chest x-ray film. No patient remaining on systemic heparin and having a pericardial effusion developed cardiovascular complications during hemodialysis. This study suggests that while many patients on longterm hemodialysis have pericardial effusion undiagnosed on the basis of physical examination, but noted on echocardiogram, special precautions to prevent tamponade during hemodialysis are not necessary. Also, posterior-anterior chest x-ray film showing a normal-sized heart will usually exclude significant pericardial effusion.