Effusive-constrictive pericarditis

Effusive-constrictive pericarditis (ECP) is an increasingly recognized clinical syndrome. It has been best characterized in patients with tamponade who continue to have elevated intracardiac pressure after the removal of pericardial fluid. The disorder is due to pericardial inflammation causing constriction in conjunction with the presence of pericardial fluid under pressure. The etiology is diverse with similar causes to constrictive pericarditis and the condition is more prevalent with certain etiologies such as tuberculous pericarditis. The diagnosis is most accurately made using simultaneous intrapericardial and right atrial pressure measurements with pericardiocentesis, although non-invasive Doppler hemodynamic assessment can assess residual hemodynamic findings of constriction following pericardiocentesis. The clinical presentation has considerable overlap with other pericardial syndromes and as yet there are no biomarkers or non-invasive findings that can accurately predict the condition. Identifying patients with ECP therefore requires a certain index of clinical suspicion at the outset, and in practice, a proportion of patients may be identified once there is objective evidence for persistent atrial pressure elevation after pericardiocentesis. Although a significant number of patients will require pericardiectomy, a proportion of patients have a predominantly inflammatory and reversible pericardial reaction and may improve with the treatment of the underlying cause and the use of anti-inflammatory medications. Patients should therefore be observed for the improvement on these treatments for a period, whenever possible, before advocating pericardiectomy. Imaging modalities identifying ongoing pericardial inflammation such as contrast-enhanced magnetic resonance imaging or nuclear imaging may identify those subsets more likely to respond to medical therapies. Pericardiectomy, if necessary, requires removal of the visceral pericardium.     

A case of effusive constrictive pericarditis caused by Streptococcus milleri

A 55-year-old male presented with hypotension and marked elevation of jugular venous pressure suggesting impaired ventricular filling. Echocardiography demonstrated a moderate amount of pericardial effusion and dense and shaggy fibrinous strands attached to the pericardia. Pericardiocentesis was performed under the diagnosis of cardiac tamponade, but normal ventricular filling could not be restored even after pericardiocentesis. Hemodynamic evaluation after pericardiocentesis revealed persisting low cardiac output, elevation and equilibration of right atrial, right ventricular end-diastolic and pulmonary capillary wedge pressures, and deep y descent. Later, surgical removal of the thickened pericardium was required. This case appeared to be typical effusive-constrictive pericarditis. Regarding etiology, a rare organism, Streptococcus milleri, proved to be responsible, while the case history and clinical situation were suggestive of a tuberculous or tumorous origin.     

The normal and diseased pericardium: Current concepts of pericardial physiology,diagnosis and treatment

The past quarter century has seen remarkable contributions to understanding the role of the pericardium in health and disease and to diagnostic methods in the context of significant changes in the clinical spectrum of acute pericarditis, pericardial effusion and their sequelae. Anatomic studieshave demonstrated pericardial ultrastructure and its relation to function and delineated the pericardial lymphatics and their participation in inflammation and tamponade. Physiologic investigationshave revealed the pericardium's mechanical, membranous and ligamentous functions and its role in ventricular interaction, pericardial modification of cardiac responses during acute cardiocirculatory loading and effects on diastolic function (and, at high filling pressures, systolic function), including reduction by pericardial fluid of true filling pressure—the myocardial transmural pressure. The diastolic mean pressure plateau and phasic venoatrial pressure and flow during cardiac tamponade have been further characterized and the mechanisms producing pulsus paradoxus have been elucidated, including the importance of inspiratory increase in right ventricular filling. A far reaching compensatory response to tamponade has been revealed, particularly adrenergic stimulation, and, over time, blood volume expansion. Right heart tamponade and low pressure tamponade have been identified and the importance of the pericardium in the restrictive dynamics of right ventricular myocardial infarction has been demonstrated. Constrictive pericarditis,And the currently more common effusive-constrictive pericarditis,have been studied, in depth, clinically and hemodynamically.Cardiography in pericardial diseasenow includes M-mode and two-dimensional echographic studies, enabling rapid diagnosis and further physiologic study in cardiac tamponade and constriction. The four stages of typical electrocardiographic evolutionin acute pericarditis and atypical variants have been codified and characteristic PR segment deviations identified. The non-etiologic role of acute pericarditis in arrhythmiashas been clarified in prospective clinical and postmortem investigations. Electric alternation has been elucidated and its relation to cardiac "swinging" has been at least partly explained. Special roles now exist for contrast roentgenography, computed tomography(especially for cysts) and radionuclide imaging. Clinical advancesin pericardial disease include changes in the prevalence of established etiologies and identification of new etiologies, for example, immunopathic processes to explain recurrent pericarditis and the post-injury (including postoperative) pericardial syndromes. New forms of constriction—uremic, postoperative, radiation—have appeared in increasing numbers. The pericardial rubhas been characterized and codified, confirming a typical three-component structure (with frequent exceptions).     

Primary malignant pericardial mesothelioma presenting as effusive-constrictive pericarditis

Effusive-constrictive pericarditis is a clinical hemodynamic syndrome characterized by constriction of the heart by the visceral pericardium in the presence of a tense pericardial effusion. The hallmark of effusive-constrictive pericarditis is the persistence of elevated right atrial pressures and ventricular interdependence after relief of the elevated intrapericardial pressures. The present report discusses the unique case of a 46-year-old white female who presented with dyspnea on exertion and chest tightness in the setting of an effusive-constrictive pericarditis. The patient was subsequently diagnosed with primary malignant pericardial mesothelioma, an extremely rare neoplasm with a very poor prognosis.     

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.     

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.     

Predictors of constrictive pericarditis after tuberculous pericarditis.

OBJECTIVE--To identify features which predict the subsequent development of constrictive pericarditis from acute or subacute tuberculous (TB) pericarditis. SETTING--Tertiary referral centre, chest hospital. PATIENTS--The records of 16 consecutive patients in whom acute or subacute TB pericarditis was diagnosed between 1988 and 1990 at a chest hospital were reviewed. These records included a follow up of at least 12 months. RESULTS--During a follow up of 14.2 (12-30) months, 8 patients had constrictive pericarditis diagnosed by cardiac catheterisation or by inspection at the time of operation (group A). There was no evidence of constriction in the other eight patients (group B). There was no significant difference between the two groups in the type or duration of symptoms of TB pericarditis before admission or the volume and characteristics of pericardial fluid obtained at hospital admission. Clinical features of cardiac tamponade on admission correlated closely with the subsequent development of constrictive pericarditis requiring pericardectomy (7/8 v 2/8; P = 0.01), despite the fact that the signs of tamponade resolved completely after pericardiocentesis. CONCLUSION--The findings suggest that cardiac tamponade in the early clinical stage of TB pericarditis is the most predictive factor of subsequent constrictive pericarditis. The degree of fibrosis of pericardium when treatment starts may be the most important determinant of whether or not constriction develops.     

Echocardiographic diagnosis of pericardial disease.

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

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.     

A case of subacute effusive-constrictive pericarditis]

A 30-year-old female with effusive-constrictive pericarditis was admitted to our hospital because of dyspnea, ascites and edema. On examination, her blood pressure was 118/94 mmHg and her pulse rate was 90 bpm. Physical examination revealed pulsus paradoxus, markedly raised venous pressure and pericardial knock sound. Chest X-ray showed marked cardiomegaly and bilateral pleural effusion. After cardiac catheterization there was elevation of mean right atrial pressure, right ventricular end-diastolic pressure, pulmonary-capillary-wedge pressure, and their pressures during diastole were approximately 30 mmHg. After successful pericardiocentesis, their diastolic pressures still remained at 15 mmHg. Additionally, pressure wave of the right ventricle showed distinct diastolic dip and plateau pattern, and that of the right atrium showed deep x and y descents. The pressure pattern suggested that not only pericardial effusion but also decreased compliance of the pericardium was the main factor contributing to the cardiac diastolic dysfunction. Histological examination of the pericardium showed diffuse lymphocyte infiltration and fibrosis. These findings strongly suggested that there might have been viral infection.     

Cardiac constriction syndromes

This article focuses on syndromes associated with cardiac constriction (i.e., constrictive pericarditis). These include classic chronic constrictive pericarditis, subacute constriction including effusive-constrictive pericarditis, transient cardiac constriction, and occult constrictive pericarditis, all of which have their own clinical and developmental peculiarities. Establishing clinical suspicion is the basic first step in making a diagnosis, which can subsequently be confirmed by careful interpretation of imaging studies. With pericardial calcification, a simple chest radiograph may be sufficient; in other cases, Doppler echocardiography or chest computed tomography are necessary. The diagnosis of effusive-constrictive pericarditis requires cardiac catheterization combined with pericardiocentesis and the recording of intracavitary and intrapericardial pressures both before and after pericardiocentesis. It should be remembered that spontaneous regression is possible in some forms of constrictive pericarditis, particularly those that appear during the resolution of acute idiopathic pericarditis with effusion or that develop after cardiac surgery. Finally, there are only a few reports in the literature about occult constrictive pericarditis and its diagnosis is problematic.     

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.     

A case of effusive-constrictive epicarditis found by electrocardiogram at a school health examination

An effusive-constrictive pericarditis confined to the epicardium is extremely rare in childhood. We report case of a 7-year-old boy with such a condition. During an annual school health examination, he was found to have low voltage activities on electrocardiogram. On admission, physical examination showed markedly distended abdomen due to ascites and hepatomegaly. Two-dimensional echocardiography revealed small ventricular cavities, extremely dilated inferior vena-cava, and a moderate amount of pericardial fluids. Pericardial and epicardial thickening were also suspected. Retrospectively, epicardial thickening was suspected on computed tomogram as well. Cardiac catheterization showed a typical diastolic dip and plateau pattern on the right ventricular pressure tracing, and deep x and y descents on that of the right atrium, suggesting that not pericardial effusion, but pericardial thickening mainly contributed to the cardiac dysfunction. Pericardiocentesis did not improve the clinical symptoms and high central venous pressure. On thoracotomy, we unexpectedly found intact pericardium and fibrotic epicardium covering the whole heart, so epicardiectomy was performed. Despite the fact that most of the fibrotic epicardium was removed, there were no immediate responses such as decrease in central venous pressure within the first 5 days after the surgery. Furthermore, it was not until two months later that all symptoms and hemodynamic parameters returned to normal levels. There have been several case reports of isolated epicardial constriction associated with pericardial effusion in English literature. However, we are unaware of such a report n Japanese. We concluded that it is important to evaluate the hemodynamics before and after pericardiocentesis, and to detect peri-and/or epicardial thickening by serial echocardiography and CT scan.(ABSTRACT TRUNCATED AT 250 WORDS)     

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

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

Catheter drainage of the pericardium. Practical method to maintain long-term patency

Pericardiocentesis with catheter insertion and drainage is widely used in management of large pericardial effusions and cardiac tamponade. Two potential problems with an indwelling pericardial catheter system are catheter blockage and infection. We have utilized slow infusion of heparinized saline solution (3 ml/hr) via a continuous flush device to maintain catheter patency for up to seven days (mean 3.6) in 16 patients. Pericardial effusions were secondary to malignancy, uremia, and cardiac surgery. This article describes practical aspects of the technique. Most pericardial effusions can be successfully treated with pericardiocentesis and catheter drainage, provided the drainage is continued reliably and safely for several days. Surgical treatment such as subxiphoid pericardiostomy or partial pericardiectomy should be reserved for loculated effusions, clotted blood, subacute effusive-constrictive pericarditis, or significant recurrences after initial drainage.     

Primary malignant pericardial mesothelioma—a rare cause of superior vena cava thrombosis and constrictive pericarditis

Primary malignant pericardial mesothelioma (PMPM) is an extremely rare, highly lethal and often misdiagnosed tumor. We report a 60-year-old woman complaining of dry cough, shortness of breath and exertional dyspnea due to a large pericardial effusion. The pericardial fluid volume declined after pericardiocentesis; analysis of the fluid revealed malignant cells and was negative for tuberculosis. Subsequently, the patient developed a compression of the superior vena cava and pericardial constriction. The patient’s symptoms marginally improved after partial pericardiectomy, and a diagnosis of pericardial mesothelioma was made on pathology. However, her symptoms continued to aggravate, and she died 8 months after presentation. Pericardial mesothelioma should be discovered earlier to treat patients who develop repeatedly pericardial effusion after pericardiocentesis and pericardial tamponade or those develop constrictive pericarditis.     

Cardiac tamponade: hemodynamic observations in man

Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreases significantly, from 16 +/- 4 mm Hg (mean +/- SD) to 7 +/- 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 +/- 1.77 to 7 +/- 2.2 l/min) and inspiratory systemic arterial pulse pressure (45 +/- 29 to 81 +/- 23 mm Hg). The remaining five patients did not demonstrate cardiac tamponade, as evidenced by lack of significant change in these hemodynamic parameters. In all patients with tamponade, right ventricular end-diastolic pressure (RVEDP) was elevated and equal to pericardial pressure; equilibration was uniformly absent in patients without tamponade. During gradual fluid withdrawal in the tamponade group, significant hemodynamic improvement was largely confined to the period when right ventricular filling pressure remained equilibrated with pericardial pressure. In 10 patients with tamponade and pulsus paradoxus, pulmonary arterial wedge pressure (PAW) was equal to pericardial pressure except during early inspiration and expiration when it was transiently less and greater, respectively; however, inspiratory right atrial pressure never fell below pericardial pressure. In these 10 patients, PAW decreased significantly following pericardiocentesis (P less than 0.001). In the remaining four patients with tamponade but without pulsus paradoxus, all of whom had chronic renal failure, PAW was consistently higher than pericardial pressure or RVEDP and did not decrease after pericardiocentesis. These data tend to confirm the hypothesis that in patients with tamponade, the venous pressure required to maintain any given cardiac volume is determined by pericardial rather than ventricular compliance. When pericardial compliance determines diastolic pressure in both ventricles, relative filling of the ventricles will be competitive and determined by their respective venous pressures (pulmonary vs systemic), which vary with respiration and alternately favor right and left ventricular filling. This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent.     

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.     

Primary operation of pericardiectomy and decortication of the right lung for tuberculous pericarditis with empyema

A 28-year old man who complained of ortho-apnea and fever was diagnosed to have cardiac tamponade. Pericardiocentesis was immediately carried out and peri-cardiac window was created on the 11th day. Typical caseating granulomas with acid-fast bacilli were detected in sections of the pericardium. A positive culture of Mycobacterium tuberculosis was observed in the sputum and the pericardial fluid. Though 3-month anti-tuberculosis treatment with streptomycin, isoniazid, and rifampicin was continued with 6-week steroid therapy, progressive thickness of the pericardium was suggested subsequent constriction. Pericardiectomy for pericarditis and decortication for empyema in the right thorax was performed at the same time. After 10 x 12 cm pericardium was resected through median sternotomy, decortication of the right lung was performed through right posterolateral thoracotomy. In the case with thickened pericardium, early pericardiectomy is recommended.