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.     

Pericardial effusion and tamponade

Pericardial effusion may occur as a result of a variety of clinical conditions, including viral, bacterial, or fungal infections and inflammatory, postinflammatory, autoreactive, and neoplastic processes. More common causes of pericardial effusion and tamponade include malignancy, renal failure, viral and bacterial infectious processes, radiation, aortic dissection, and hypothyroidism. It can also occur after trauma or acute myocardial infarction (as in postpericardiotomy syndrome following cardiac or thoracic surgery) or as an idiopathic pericardial effusion. Although pericardial effusion is common in patients with connective tissue disease, cardiac tamponade is rare. Among medical patients, malignant disease is the most common cause of pericardial effusion with tamponade. Table 1 shows the causes of pericardial tamponade. The effusion fluid may be serous, suppurative, hemorrhagic, or serosanguineous. The pericardial fluid can be a transudate (typically occurring in patients with congestive heart failure) or an exudate. The latter type, which contains a high concentration of proteins and fibrin, can occur with any type of pericarditis, severe infections, or malignancy. Once the diagnosis of pericardial effusion has been made, it is important to determine whether the effusion is creating significant hemodynamic compromise. Asymptomatic patients without hemodynamic compromise, even with large pericardial effusions, do not need to be treated with pericardiocentesis unless there is a need for fluid analysis for diagnostic purposes (eg, in acute bacterial pericarditis, tuberculosis, and neoplasias). The diagnosis of pericardial effusion/tamponade relies on a strong clinical suspicion and is confirmed by echocardiography or other pericardial imaging modalities. Alternatively, when the diagnosis of cardiac tamponade is made, there is a need for emergency drainage of pericardial fluid by pericardiocentesis or surgery to relieve the hemodynamic compromise. Following pericardiocentesis, it is necessary to prevent recurrence of tamponade. Intrapericardial injection of sclerosing agents, surgical pericardiotomy, and percutaneous balloon pericardial window creation are techniques used to prevent reaccumulation of pericardial fluid and recurrence of cardiac tamponade.     

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.     

Should we try to determine the specific cause of cardiac tamponade?

INTRODUCTION: The causes of cardiac tamponade vary and it has been suggested that underlying causes should be sought in all cases. The purpose of this study was to determine the causes of cardiac tamponade in our environment, distinguishing between specific and idiopathic causes, and analyzing the proportion and causes in the subgroup of patients with relapsing tamponade. PATIENTS AND METHOD: We retrospectively studied all patients who underwent therapeutic pericardiocentesis between 1985 and 2001. The clinical and radiographic features and macroscopic characteristics of the pericardial fluid were analyzed. The final diagnosis in each patient was based on the clinical history, follow-up, pericardial fluid cytology, and pericardial biopsy, if available. RESULTS: Ninety-six patients were included (52 men/44 women), mean age 56.1 16.1 years. The cause of pericardial effusion was neoplasm in 50 patients (52.1%), 14 idiopathic pericarditis (14.6%), 12 renal failure (12.5%), 7 iatrogenic cases (7.3%), 4 mechanical tamponades (4.2%), 2 tuberculosis (2.1%), and 7 other causes (7.3%). Thirty-five patients had relapsing tamponade; only 2 of them had idiopathic pericarditis (5.7%). We found no significant differences in age, development time, extracted volume or fluid features between tamponade of specific or idiopathic origin. CONCLUSIONS: Most of the cardiac tamponades in our series had a specific cause. This made it necessary to identify a specific underlying cause in each case, especially in relapsing effusions. However, we did not find any variable suggestive of the cause of the disease.     

Pericardial involvement in end-stage renal disease

Pericardial involvement in end-stage renal disease (ESRD) is manifested most commonly as acute uremic or dialysis pericarditis and infrequently as chronic constrictive pericarditis. The causes of uremic and dialysis pericarditis remain uncertain. The clinical and laboratory manifestations of acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis in patients with chronic renal failure are similar to those observed in nonuremic patients with similar pericardial involvement, except that chest pain occurs less frequently in those with ESRD. Therapeutic interventions for acute uremic or dialysis pericarditis with or without pericardial effusion include intensive hemodialysis, pericardiocentesis (infrequently used), pericardiostomy with or without instillation of intrapericardial glucocorticoids, pericardial window, and pericardiectomy. Chronic constrictive pericarditis is treated with pericardiectomy.     

Clinical clues to the causes of large pericardial effusions

PURPOSE: To examine whether the size of the effusion, the presence of tamponade, and inflammatory signs are useful in determining the causes of moderate or severe pericardial effusions.SUBJECTS AND METHODS: All echocardiograms performed at a general hospital between January 1990 and April 1996 were screened for pericardial effusion. Patients with moderate (echo-free space of 10 to 20 mm during diastole) or severe (echo-free space >20 mm) effusions were studied. RESULTS: We identified 322 patients (166 [52%] men, mean [+/- SD] age 56 +/- 17 years [range 15 to 88 years]), 132 (41%) with moderate and 190 (59%) with severe pericardial effusion. The most frequent etiologic diagnoses were acute idiopathic pericarditis (n = 66 [20%]), iatrogenic effusions (n = 50 [16%]), cancer (n = 43 [13%]), and chronic idiopathic pericardial effusion (n = 29 [9%]). In 192 (60%) of the patients, the cause of the effusion was a known medical condition. In the 130 other patients, inflammatory signs were associated with acute idiopathic pericarditis (likelihood ratio = 5. 4, P < 0.001), severe effusions without inflammatory signs or tamponade were associated with chronic idiopathic pericardial effusion (likelihood ratio = 20, P < 0.001), and tamponade without inflammatory signs was associated with malignant effusions (likelihood ratio = 2.9, P < 0.01).CONCLUSIONS: In many patients, pericardial effusions are due to a known underlying disease or condition. In patients without underlying diseases, inflammatory signs, the size of effusion, and the presence or absence of cardiac tamponade can be helpful in establishing cause.     

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.     

The syndrome of cardiac tamponade with "small" pericardial effusion

Cardiac tamponade is usually a consequence of increased pericardial pressure with accumulation of pericardial effusion. Pericardial effusion may be caused by acute pericarditis, tumor, uremia, hypothyroidism, trauma, cardiac surgery, or other inflammatory/noninflammatory conditions. In this article we describe four scenarios illustrated by case reports where a small or apparently small pericardial effusion may produce cardiac tamponade. The first scenario illustrates how a small pericardial effusion can cause clinically significant cardiac tamponade when it accumulates rapidly. The second scenario exhibits how an apparently small pericardial effusion on transthoracic echocardiogram (TTE) turned out to be a small amount of unclotted blood and an echogenic hematoma. The third scenario details how an apparently small pericardial effusion on TTE was actually a large loculated effusion in an unusual location seen only by transesophageal echocardiogram (TEE). The fourth scenario demonstrates how the combination of a large pleural effusion and a small pericardial effusion can result in cardiac tamponade. The role of echocardiography in the diagnosis and management of these scenarios is discussed here. Although many clinicians depend on the amount of pericardial effusion to suspect cardiac tamponade, it is important to suspect cardiac tamponade when patients have hemodynamic compromise regardless of the amount of pericardial effusion.     

Uremic pericarditis as a cause of cardiac tamponade.

Uremic pericarditis may complicate either acute or, more commonly, chronic renal failure. When dialysis is not employed, uremic pericarditis is usually a preterminal event and is characterized by a serofibrinous exudation of an amount inadequate to cause cardiac tamponade. Nevertheless, cardiac tamponade may uncommonly be observed in nondialyzed patients. Cardiac tamponade, which may be life-threatening, is more common in dialyzed than in nondialyzed patients with chronic renal failure. The primary causes of cardiac tamponade in uremic pericarditis in order of decreasing frequency are (1) pericardial effusion, usually of the serosanguineous type, (2) massive hemorrhage into the pericardial sac and (3) collagenization of pericardial exudate. From pathologic evidence, the following forms of therapy appear appropriate to manage uremic pericarditis that has reached the stage of causing cardiac tamponade. For effusion, pericardiocentesis or parietal pericardiectomy are logical procedures. Massive hemorrhage into the pericardial sac is usually attended by clotting and requires pericardiotomy and evacuation of clot. Collagenization of exudate yields an encasing, fibrous shell over the heart and requires decortication, as is practised in classical constrictive pericarditis.     

Chronic Pericardial Effusion: Causes and Management

Chronic pericardial effusion is a common pericardial syndrome whose approach has been well standardised in recent years. The main challenge associated with this condition is the progression (sometimes unheralded) to cardiac tamponade. Pericardial effusions may present either as an isolated finding or in the context of a specific etiology including autoimmune, neoplastic, or metabolic disease. Among investigations used during diagnostic work-up, echocardiography is of paramount importance for the diagnosis, sizing, and serial evaluation of the hemodynamic impact of effusions on heart diastolic function. In an individualised manner, advanced imaging including computed tomography and cardiac magnetic resonance imaging should be performed, especially if baseline tests are inconclusive. Triage of these patients according to the most recent 2015 European Society of Cardiology Guidelines for the diagnosis and management of pericardial diseases should take into account the presence of hemodynamic compromise as well as suspicion of malignant or purulent pericarditis as first step, C-reactive protein serum level measurement as second step, investigations for a specific condition known to be associated with pericardial effusion as third step, and finally the size and the duration of the effusion. Treatment depends on the evaluation of the above-mentioned parameters and should ideally be tailored to the individual patient. Prognosis of chronic pericardial effusions depends largely on the underlying etiology. According to novel data, the prognosis of individuals with idiopathic, chronic (> 3 months), large (> 2 cm), asymptomatic pericardial effusions is usually benign and a watchful waiting strategy seems more reasonable and cost-effective than routine drainage as previously recommended.     

Diagnosis and management (by subxiphoid pericardiotomy) of large pericardial effusions causing cardiac tamponade.

To determine the clinical features, course and outcome of patients with cardiac tamponade, 57 consecutive patients with new, large pericardial effusions were prospectively studied. Twenty-five patients (44%) developed cardiac tamponade with venous hypertension and a pulsus paradoxus greater than 10 mm Hg. Electrocardiography, radiographic studies and echocardiography did not differentiate patients with and without tamponade. All 57 patients underwent thorough diagnostic evaluation followed by subxiphoid pericardial biopsy and drainage. A diagnosis was obtained in 53 patients (93%). Collagen vascular disease was significantly more frequent in the 25 patients with than in the 32 without cardiac tamponade (24 vs 3%; p less than 0.05). The frequency of malignant and uremic effusions was equal in both groups, whereas radiation-induced effusions seldom produced tamponade. At 1-year follow-up, 3 patients (12%) with tamponade had recurrent effusions, and 1 needed reoperation. This was not significantly different from the 32 patients without tamponade. Twelve-month mortality was also similar in both groups (36 vs 44%). This prospective series disclosed several unexpected findings: (1) Cardiac tamponade occurred in almost 50% of patients with new large pericardial effusions; (2) both malignancy and collagen vascular disease occurred with equal frequency as etiologies, whereas radiation-induced tamponade was unusual; (3) thorough clinical evaluation resulted in few idiopathic etiologies; and (4) subxiphoid pericardiotomy was effective for both diagnosis and therapy of tamponade.     

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.     

Uremic pericarditis complicating cardiac tamponade: a case report

A 29-year-old man developed diabetes mellitus in 1983 and diabetic nephropathy which gradually worsened from 1998. He was admitted to our hospital for initiation of peritoneal dialysis in May 2002. However, the efficiency of dialysis was not sufficient to improve elevated levels of blood urea nitrogen and serum creatinine. His body weight and cardiothoracic index by chest roentgenography gradually increased starting 9 days after admission. To improve the efficiency of dialysis, we tried to increase the dialysis fluid. Nevertheless, the efficiency of peritoneal dialysis remained low, and the patient complained of nausea 14 days after admission. Hypotension suddenly occurred 16 days after admission. Echocardiography showed massive pericardial effusion and collapse of the right ventricle. The diagnosis was cardiac tamponade. We performed cardiac centesis and pericardial drainage which revealed bloody pericardial effusion. Urgent hemodialysis was performed. The differential diagnosis of cardiac tamponade was established. After hemodialysis, the amount of pericardial effusion decreased, the gastro-intestinal symptoms disappeared, and the blood urea nitrogen and serum creatinine levels decreased. We speculated that the cause of cardiac tamponade was uremic pericarditis after ruling out infectious disease, collagen disease, malignant disease, and aortic dissection. Cardiac tamponade due to uremic pericarditis has become very rare since hemodialysis was developed.     

Diagnostik und Therapie der Perikarditis und des Perikardergusses

This article describes the diagnostics, differential diagnostics, multimodal imaging, medicinal and invasive diagnostic therapy of acute and chronic pericarditis, constrictive pericarditis, pericardial effusion and cardiac tamponade under etiological aspects and on the basis of the guidelines of the European Society of Cardiology (ESC). The starting point of the decision tree is the symptomatic patient with echocardiographic evidence of pericardial effusion. The principle feature of the diagnostics is the etiopathogenetic allocation of the pericardial disease which influences the clinical picture, course therapy and prognosis. Infectious pericarditis (e.g. viral, bacterial and tuberculous) is differentiated from sterile autoreactive pericarditis and from neoplastic pericardial effusion by the cytology of the effusion and immunohistological and molecular investigations of the pericardial and epicardial biopsies. Pericardioscopy plays an important role in the recognition of suspicious areas. In many cases intrapericardial administration of cisplatin for neoplastic pericardial effusion and instillation of triamcinolone for autoreactive pericarditis prevent recurrence just as a treatment of several months with colchicine.     

尿毒症心包炎的临床研究

本文40例维持性血透尿毒症患者中,心包炎的发生率约为35％.除心包摩擦音外,来见其它特殊临床症状.约50％的患者无任何症状.诊断依靠超声心动图检查.查明患者有无心包积液、心包填塞、心包积液量以及心包炎及范围具有一定价值。该病需加强透析治疗,包括延长透析时间、缩短透析间隔,使用高效、高通透膜,加用血滤及血液灌流,减少肝素用量或改为腹透。本文也讨论了该病的病因.     

Neoplastic pericardial disease

The spread of metastatic cancer to the pericardium is the most common cause of cardiac tamponade in medical inpatient settings. Lung cancer, breast cancer, and the hematologic malignancies account for some three quarters of the cases. Occasionally, usually in lung cancer, the pericardial involvement is the first clinical presentation of the neoplastic disease. Differential diagnosis includes radiation pericarditis and cardiac toxicity from chemotherapeutic drugs, as well as any of the causes of pericardial disease in patients without neoplasm. Idiopathic nonneoplastic, noninflammatory pericardial effusion is surprisingly common in cancer patients. The initial cardiac tamponade may be managed with either needle tap or subxiphoid pericardiostomy. Pericardiocentesis, performed with echocardiographic guidance and followed by percutaneous catheter drainage for several days, is safe and effective in neoplastic pericardial effusion. It may be the only local therapy that is needed. Further local treatment, for those patients who develop recurrent cardiac tamponade after an initial drainage procedure, may include tetracycline sclerosis of the pericardial space, instillation of cancer chemotherapeutic agents, radiation therapy, and pericardiectomy. No controlled clinical trials of these methods of treatment are available. The choice of therapy is based on various considerations in individual patients, particularly the patient's general condition and the likelihood of a long-term response to treatment of the systemic neoplastic disease.     

Neoplastic pericarditis--the role of different diagnostic procedures

The aim of the study was to assess the role of different diagnostic procedures in the recognition of malignant pericarditis. Consecutive medical records of the patients with pericardial effusion treated with pericardiocentesis or pericardioscopy in the period of 1982-2002 were analyzed retrospectively. Criteria of neoplastic pericarditis were: positive result of pericardial fluid cytology and/or neoplastic infiltration found in pericardial biopsy specimen. Criteria of non-neoplastic pericarditis were: negative result of pericardial fluid cytology and pericardial biopsy specimen, no neoplastic disease diagnosed at presentation and during 3-years of follow up. Malignant pericarditis was diagnosed in 47 patients (pts), nonmalignant in 51. Echocardiographic signs of cardiac tamponade were found in 80% of pts with neoplastic pericarditis and 40% of pts with non-malignant disease (p = 0.0001). Chest CT scan revealed the presence of enlarged mediastinal lymph nodes in 94% of pts with malignant pericarditis and only 11% of pts with non-malignant disease (p = 0.00001). Pericardial thickness on CT scan exceeded 8 mm in 75% of the pts with malignant pericarditis and 8% of pts with nonmalignant disease (p = 0.0003). Pericardial fluid (pf) CEA concentration was significantly higher in the patients with neoplastic pericarditis than in the pts with non-malignant process. CEA > 5 ng/ml and Cyfra 21-1>50 ng/ml were found in 43% of the pts with malignant pericarditis and none of the pts with benign pericarditis. Thus we recommend chest CT scan and pericardial fluid tumor markers (CEA and Cyfra 21-1) assessment as the procedures helpful in the recognition of malignant pericarditis.     

Pericarditis in end-stage renal disease

Our approach to the clinical management of uremic and dialysis-associated pericarditis has been presented previously and is outlined in Figure 1. In hemodynamically stable patients with no effusion and in those with small to medium effusions, we recommend initial therapy with intensified dialysis. Close monitoring, perhaps every third day, with echocardiography should be carried out. If pericardial effusion progressively increases or if a large pericardial effusion fails to resolve after 7 to 10 days of intensive dialysis, the pericardial effusion may be drained by subxiphoid pericardiotomy or by pericardiectomy. Similarly, if hemodynamic evidence of cardiac pretamponade or tamponade appears, surgical drainage also should be carried out. If the echocardiogram is inadequate for interpretation but tamponade physiology is present, we recommend confirmation by cardiac catheterization before surgical drainage is attempted, recognizing that there may be circumstances such as left ventricular failure and pulmonary hypertension that may complicate the interpretation of the catheterization data. The type of invasive pericardial procedure chosen is determined by local experience. As stated, we prefer not to perform pericardiocentesis before surgery unless tamponade-induced hypotension is so severe that an adequate blood pressure cannot be maintained by means of plasma volume expansion. Under these circumstances, we prefer that pericardiocentesis be performed in the operating room immediately before the induction of anesthesia for the definitive surgical procedure. Although pericardiectomy is a definitive procedure for pericarditis with effusion in the uremic patient, the procedure has substantial morbidity. The results of subxiphoid pericardiotomy are encouraging, and it is clear that it can be carried out safely in patients who are debilitated or who are at increased risk from general anesthesia and major surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pericardial effusion in the elderly: A different disease?

INTRODUCTION AND OBJECTIVES: The aim of the present study was to assess possible differences in etiologic spectrum and clinical course of pericardial effusion in elderly patients, as has been previously suggested, and therefore determine whether clinical, management should be based on patient age. METHODS: All echocardiograms performed in our hospital from 1990 to 1996 were screened for pericardial effusion, and those with moderate or large effusions were selected. Patients under 66 years of age were included in group I, and those above 65 years were assigned to group II. RESULTS: We selected 322 patients with moderate (122) or with large (200) effusions. 221 patients being included in group I (aged 15-65, mean 47) and 101 in group II (aged 66-88, mean 72.5). Effusion was large in 60% of group I and in 66% of group II (p = NS), and tamponade occurred in 36% and 38.6%, respectively (p = NS). Specific pericardial infections (tuberculous and purulent pericarditis) were more frequent in group I (5.9 versus 0.9%; p < 0.05). No significant differences were found in incidence of idiopathic (33 vs 38%) or neoplastic (14.4 vs 10.8%) etiologies. During follow-up (96% of the patients, median time of 11 months, range 1-58 months) the mortality (24 vs 30%) and evolution to cardiac constriction (4 vs 2%) were similar in the two groups, but persistence of effusion was more common in group II (6.3 vs 14%; p < 0.05). CONCLUSIONS: Our study suggests that etiology, clinical course and prognosis of moderate and large pericardial effusion are, in general, similar in elderly and younger patients. Thus, management should be similar in the different age groups, and no etiologic form of pericardial disease should be ruled out because of patient's age when considering the differential diagnosis.     

Adult-Onset Still's Disease and Cardiac Tamponade: A Rare Association

Adult-onset Still''s disease is a rare disorder with potentially severe clinical features, including cardiac involvement. This systemic inflammatory disease of unknown origin should be considered in the differential diagnosis of pericarditis, with or without pericardial effusion. Cardiac tamponade is a very rare sequela that requires an invasive approach, such as percutaneous or surgical pericardial drainage, in addition to the usual conservative therapy.The authors describe a case of adult-onset Still''s disease rendered more difficult by pericarditis and cardiac tamponade, and they briefly review the literature on this entity.