A systematic diagnostic approach to primary acute pericardial disease. The Barcelona experience

Acute pericarditis and cardiac tamponade without a definite cause at the time of the initial hospital evaluation are defined as primary acute pericardial disease. In immunologically competent patients from the Western World, most cases (more than 80%) are idiopathic. However, severe specific diseases may be present in the remaining cases, the clinical features often providing insufficient clues to the etiologic diagnosis. A systematic approach to these patients is therefore needed. It is relevant to this approach that pericardiocentesis and pericardial biopsy have a much higher diagnostic yield when performed in patients with cardiac tamponade than when they are performed for purely diagnostic purposes. Strategies to increase this yield might be devised on the basis of noninvasive findings.     

Clinical management of acute pericardial disease: a review of results and outcomes.

Acute pericardial diseases are common disorders in several clinical settings. The presentation may include acute pericarditis and its recurrences, incidental pericardial effusion, cardiac tamponade, and occasionally constrictive pericarditis. New diagnostic techniques have improved the sampling and analysis of pericardial fluid and allow a comprehensive diagnostic approach. Deciding on the extent of diagnostic evaluation in the individual patient requires good clinical judgment based on careful evaluation of the risk-benefit ratio of the planned diagnostic and therapeutic options. Most cases of acute pericarditis are viral or idiopathic and self-limited; however, other etiologies should also be considered. The diagnostic yield of extensive laboratory evaluation and pericardiocentesis is low, and invasive procedures should be limited mainly to patients in whom therapeutic intervention is necessary. Treatment should focus on symptomatic relief, usually through the administration of non-steroidal anti-inflammatory drugs, and patients should be carefully evaluated and monitored for common complications of the disease.     

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.     

Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment

Thirteen patients with tuberculous pericarditis (12 men and 1 woman aged 13 to 70 years [mean 41]) were identified in a group of 294 patients consecutively admitted for primary acute pericardial disease. The diagnosis was made by the following studies: sputum culture (n = 4), culture of pericardial fluid obtained by pericardiocentesis (n = 3), histologic study and culture of pericardial biopsy (n = 3), lymph node biopsy (n = 2) and pleural biopsy (n = 1). Clinical presentation was remarkably variable: four patients had an acute, apparently self-limited course, one had relapsing tamponade, four had tamponade effectively treated with pericardiocentesis and four had toxic symptoms with persistent fever. The interval from hospital admission to diagnosis ranged from 1 to 14 weeks (mean 5.2). Constrictive pericarditis developed in six patients and effusive-constrictive pericarditis in one; all seven required pericardiectomy 2 to 3.5 months after admission. No patient died. It is concluded that 1) tuberculous pericarditis has a variable clinical presentation and therefore it should be considered in the evaluation of all instances of pericarditis without a rapidly self-limited course; 2) the diagnosis should be based only on objective data obtained with a systematic study protocol; 3) early definitive diagnosis is still difficult to achieve; and 4) development of subacute constrictive pericarditis requiring pericardiectomy is common.     

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.     

Management Strategies in Pericardial Emergencies

BACKGROUND: The most frequent pericardial emergency is cardiac tamponade, but complications of an acute coronary syndrome and aortic dissection may also involve the pericardium. Acute pericarditis can also represent a medical emergency due to chest pain of upsetting intensity. Decompensations in chronic advanced constriction and in the clinical course of purulent pericarditis necessitate critical care as well. DIAGNOSIS AND MANAGEMENT: The diagnosis of cardiac tamponade is based on clinical presentation and physical findings, confirmed by echocardiography and cardiac catheterization. Tamponade is an absolute indication for urgent drainage, either by pericardiocentesis or surgical pericardiotomy. The approach for pericardiocentesis can be subxiphoid or intercostal using echocardiographic or fluoroscopic guidance. Urgent drainage, combined with intravenous antibiotics, is also mandatory in suspected purulent pericarditis. If confirmed, it should be combined with intrapericardial rinsing (best by a surgical drainage). Pericardiocentesis is contraindicated in cardiac tamponade complicating aortic dissection. This condition should immediately lead to cardiac surgery. Although pericardiectomy is the only treatment for permanent constriction, this procedure is contraindicated when extensive myocardial fibrosis and/or atrophy are demonstrated. CASE STUDY: Iatrogenic tamponade may occur during percutaneous mitral valvuloplasty, implantation of pacemakers, electrophysiology and radiofrequency ablation procedures, right ventricular endomyocardial biopsy, percutaneous coronary interventions, and rarely during Swan-Ganz catheterization. The authors report on a 79-year-old who suffered coronary perforation and cardiac tamponade during elective stent implantation. Tamponade was successfully treated with pericardiocentesis and implantation of a membrane-covered graft stent. Subsequent recurrent pericarditis/postpericardial injury syndrome with moderate pericardial effusion was initially treated with aspirin and then with aspirin and colchicine. At 6 months, the patient is in stable remission even after withdrawal of colchicine. CONCLUSION: Natural history of pericardial diseases can be complicated with pericardial emergencies requiring prompt diagnosis, intensive care with hemodynamic monitoring, and early aggressive management. Medical supportive measures, drainage of pericardial effusion, surgical pericardiotomy, and pericardiectomy should be applied when needed with no delay. This procedural approach also applies to iatrogenic interventions leading to tamponade.     

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.     

The clinical practice guidelines of the Sociedad Española de Cardiología on pericardial pathology

The pericardium is a serous membrane consisting of two layers (parietal and visceral), which may be involved by different infectious, physical, traumatic, or inflammatory agents as well as in metabolic or systemic diseases. The reactions of the pericardium to these insults result in rather nonspecific clinical features, such as the characteristic inflammatory findings in acute pericarditis, the development of pericardial effusion with the possible complication of cardiac tamponade, and a fibrous retractile reaction that may lead to constrictive pericarditis. These phenomena are not mutually exclusive and can be simultaneous or consecutive in the same patient; however, for the sake of clarity they are independently discussed.The aim of the present guidelines is to provide orientation about the management of patients with pericardial disease. Such management should basically rest on the knowledge of the clinical and epidemiological features (such as disease frequency) of the different types of pericardial disease that determine the diagnostic and therapeutic yield of the different invasive pericardial procedures (pericardiocentesis, pericardial biopsy and pericardiectomy), and, therefore, their respective indications. In addition, the indication of the different types of medical therapy are discussed. On the other hand, emphasis is made on the possible limitation of the validity of these guidelines for patients belonging to geographical areas or socioeconomic contexts with different etiologic spectra.     

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.     

Triage and management of acute pericarditis

The pericardium is involved in a large number of systemic disorders, and acute pericarditis may be due to several causes. The diagnosis is based on clinical criteria, and laboratory testing is not routinely recommended. Deciding on the extent of the diagnostic evaluation requires good clinical judgement based on a careful evaluation of the risk-benefit ratio, and knowledge of basic epidemiological data for the development of a rational management program. In clinical practice a probabilistic approach seems reasonable: in Western countries most cases are idiopathic or viral with a brief and benign course and an excellent response to non-steroidal anti-inflammatory drugs, thus an extensive diagnostic evaluation is not routinely necessary. On the contrary, in developing countries specific pericarditis such as tuberculous pericarditis is quite common and should be ruled out. A clinical triage is feasible on a clinical basis. Patients with pericarditis can be safely managed on an outpatient basis without a thorough diagnostic evaluation unless the patient has high risk features such as temperature >38 degrees C, a subacute onset, immunodepression, a history of recent trauma, oral anticoagulant therapy, myopericarditis, a large pericardial effusion, and cardiac tamponade. The reported diagnostic yield of extensive laboratory evaluation and pericardiocentesis is low in the absence of cardiac tamponade or suspected purulent, tuberculous, and neoplastic pericarditis. Invasive procedures should be limited mainly to patients in whom therapeutic intervention is necessary.     

Pericarditis: differential diagnostic considerations.

A retrospective analysis of 133 patients was performed to define the factors identifying those individuals at risk for the more serious causes of pericardial disease. In 90% of the cases, the initial assessment from data obtained without pericardiocentesis or pericardiectomy proved correct. Underlying tuberculous or maligant pericarditis were the most common sources of error on initial assessment. Hemodynamic compromise exclusive of anticoagulants, roentgenographic cardiomegaly, pleural effusion, low voltage on ECG, and large pericardial effusion by echocardiography were more common (P less than .05) in tuberculous pericarditis than in acute idiopathic pericarditis. We discuss similar risk factors in patients with chronic idiopathic, rheumatologic, and uremic pericarditis. Anterior pericardiectomy is favored as the diagnostic procedure of choice in patients at risk for the more serious causes of pericarditis because of greater safety, diagnostic sensitivity, and potential therapeutic benefit.     

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.     

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.     

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

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

Pericardial 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.     

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.     

Pericardial tamponade in systemic sclerosis (scleroderma).

The frequency of pericardial disease in scleroderma found at necropsy in high. The clinical recognition of pericarditis with or without effusion is rare and tamponade with haemodynamic impairment is exceptional. Three patients with scleroderma presented with an acute syndrome of dyspnoea, chest pain, and cardiomegaly requiring pericardiocentesis for relief of pericardial tamponade. One patient died. The mechanism of the pericardial effusion remains unknown. The haemodynamic data recorded from one patient suggested that pericardial fibrosis in scleroderma may predispose to pericardial tamponade.     

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.     

Streptococcus pneumoniae-associated pneumonia complicated by purulent pericarditis: case series

Objective:

In the antibiotic era, purulent pericarditis is a rare entity. However, there are still reports of cases of the disease, which is associated with high mortality, and most such cases are attributed to delayed diagnosis. Approximately 40-50% of all cases of purulent pericarditis are caused by Gram-positive bacteria, Streptococcus pneumoniae in particular.

Methods:

We report four cases of pneumococcal pneumonia complicated by pericarditis, with different clinical features and levels of severity.

Results:

In three of the four cases, the main complication was cardiac tamponade. Microbiological screening (urinary antigen testing and pleural fluid culture) confirmed the diagnosis of severe pneumococcal pneumonia complicated by purulent pericarditis.

Conclusions:

In cases of pneumococcal pneumonia complicated by pericarditis, early diagnosis is of paramount importance to avoid severe hemodynamic compromise. The complications of acute pericarditis appear early in the clinical course of the infection. The most serious complications are cardiac tamponade and its consequences. Antibiotic therapy combined with pericardiocentesis drastically reduces the mortality associated with purulent pericarditis.     

Pericardial diseases

Opinion statement Pericardial diseases have multiple clinical presentations with acute and chronic complications. Early diagnosis and prompt treatment markedly enhance the chance of complete resolution of the hemodynamic complications of pericardial disease. The treatment of patients with acute idiopathic pericarditis is mainly to alleviate symtoms of chest pain. A nonsteroidal anti-inflammatory agent such as indomethacin is our first drug of choice. Therapy is effective and symptoms resolve within 24 to 48 hours. In patients with chronic recurrent idiopathic pericarditis, we advise the use of colchicine at 1 mg/d. Constrictive pericarditis is a progressive disease and surgical pericardiectomy is the only definite treatment. It should be performed early in the disease process before myocardial fibrosis occurs. Cardiac tamponade is a cardiac emergency and patients should be treated promptly. We often start with volume expansion with intravenous fluid in preparation for transcutaneous pericardiocentesis. Echocardiographically guided, transcutaneous pericardiocentesis is the procedure of choice. Patients with asymptomatic pericardial effusion are followed with serial echocardiography, and reserve drainage for enlarging effusions if there are signs of cardiac compression.