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.     

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.     

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.     

Cardiac tamponade of unknown aetiology in a dialyzed patient

A case of a 58 year-old male with renal failure and recurrent cardiac tamponade is presented. In spite of extensive work-up, aetiology of pericardial effusion remained unknown. Diagnostic difficulties in this setting are discussed.     

Pericardial effusion in renal disease: to tap or not to tap

The natural history of pericardial effusions attributable to renal disease is variable. Although aggressive hemodialysis may lead to the resolution of some effusions, some reports suggest that prompt drainage is optimal. We describe a case of a 49-year-old woman who presented with end-stage renal disease and a large pericardial effusion. Although she was hypertensive on presentation and had no pulsus paradoxus, transthoracic echocardiography revealed stigmata of cardiac tamponade, including right atrial and ventricular collapse, as well as a plethoric inferior vena cava. Because of the lack of certain clinical signs of tamponade and due to concern about excess bleeding risk in the setting of uremia, the effusion was initially managed with serial dialysis rather than pericardiocentesis. The effusion did not decrease in size despite 1 week of hemodialysis, and the patient developed acute dyspnea, relative tachycardia and hypotension after an increase in the blood flow rate during hemodialysis, all of which resolved with a decrease in the blood flow rate. The onset of dyspnea during a session of dialysis as a symptom of tamponade physiology has not been reported previously. We believe that this case supports early pericardiocentesis in patients with any degree of echocardiographic evidence of tamponade. We discuss this in the context of existing literature, which suggests that pericardiocentesis, rather than dialysis, is the preferred management strategy for large uremic pericardial effusions, even in the absence of evidence of clinical signs of pericardial tamponade.     

大量心包积液和心脏压塞的诊断和治疗

目的探讨大量心包积液和心脏压塞的诊断和治疗经验。方法回顾性分析1998年1月至2003年1月我科收治的36例心包积液致心脏压塞患者的临床资料，其中男性25例，女性11例，均由彩色超声心动图证实有心包积液及心脏压塞，15例采用剑突下心包开窗、放置引流管，21例采用经皮穿刺置管引流的方法。如病因不明，引流液尚需作进一步检查。结果经引流15min～2h后患者心脏压塞症状立即改善，早期34例生存，2例死亡病例分别因低心排出量和急性肝、肾功能衰竭于引流术后第2、7d死亡。结论早期准确诊断、彩色超声心动图指导下及时引流解除心脏压塞，可减轻症状并为进一步治疗提供保障。     

Percutaneous balloon pericardiotomy in a patient with end stage renal disease with recurrent pericardial effusion & pericardial tamponade

A case report of 37-year-old female with end stage renal disease presented with recurrent pericardial effusion and cardiac tamponade, who underwent percutaneous balloon pericardiotomy using an Inoue balloon dilating catheter, to create a non-surgical pericardial window. The procedure of non-surgical pericardial window is safe and effective alternative to conventional more invasive surgical pericardial window. It is concluded that percutaneous balloon pericardiotomy is helpful in the management of massive pericardial effusions particularly in patients with chronic renal failure and poor clinical condition.     

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.     

Pericarditis as a consequence and first symptom of microcellular lung carcinoma--case report

A case of a patient suffering from Streptococcal suppurative pericarditis with cardiac tamponade and acute renal failure as a first symptom of disseminated lung cancer is presented. The examination of pericardial fluid only confirmed Streptococcal infection as a cause of exudative pericarditis. The neoplasmatic cells were not found in the examined fluid. Next, chest CT and bronchoscopy were performed due to the lack of clinical improvement, recurrence of severe pericardial effusion and enlargement of the upper mediastinum found on chest radiogram. CT and bronchoscopy allowed to establish the final diagnosis - disseminated lung cancer.     

Delayed and recurrent cardiac tamponade following distal coronary perforation of hydrphilic guidewires during coronary intervention

Coronary artery perforation is a rare complication of percutaneous coronary intervention, but can result in cardiac tamponade and is thus potentially life-threatening. It is well recognized that the use of hydrophilic wires during interventional procedures increases the risk of coronary perforation. We report two cases in which a particular looping configuration was suspected of causing vessel laceration with subsequent development of pericardial effusion and tamponade. In one case, tamponade occurred several days after the index procedure, mimicking acute myocardial infarction. In the second case, tamponade was successfully treated with immediate pericardial drainage, but tamponade recurred several days later.     

Paradoxical hypertension with cardiac tamponade

Subacute (medical) tamponade develops over a period of days or even weeks. Previous studies have shown that subacute tamponade is uncommonly associated with hypotension. On the contrary, many of those patients are indeed hypertensive at initial presentation. We sought to determine the prevalence and predictors of hypertensive cardiac tamponade and hemodynamic response to pericardial effusion drainage. We conducted a retrospective study of patients who underwent pericardial effusion drainage for subacute pericardial tamponade. Diagnosis of pericardial tamponade was established by the treating physician based on clinical data and supportive echocardiographic findings. Patients were defined as hypertensive if initial systolic blood pressure (BP) was ≥140 mm Hg. Thirty patients with subacute tamponade who underwent pericardial effusion drainage were included in the analysis. Eight patients (27%) were hypertensive with a mean systolic BP of 167 compared to 116 mm Hg in 22 nonhypertensive patients. Hypertensive patients with tamponade were more likely to have advanced renal disease (63% vs 14%, p <0.05) and pre-existing hypertension (88% vs 46, p <0.05) and less likely to have systemic malignancy (0 vs 41%, p <0.05). Systolic BP decreased significantly in patients with hypertensive tamponade after pericardial effusion drainage. Those results are consistent with previous studies with an estimated prevalence of hypertensive tamponade from 27% to 43%. In conclusion, a hypertensive response was observed in approximately 1/3 of patients with subacute pericardial tamponade. Relief of cardiac tamponade commonly resulted in a decrease in BP.     

How do the clinical findings in patients with pericardial effusions influence the success of aspiration?

OBJECTIVE--To identify features associated with success or failure of aspiration of pericardial effusion. METHOD--A retrospective analysis of 36 drainage procedures in 30 patients with pericardial effusion was performed using patient records and echocardiograms. RESULTS--Unsuccessful aspiration was associated with pericardial loculation but not with the seniority of the operator or the size and position of the effusion. Pericardiocentesis relieved symptoms of breathlessness in 21 of 26 patients who had a pericardial effusion suspected of causing dyspnoea. These 21 patients had few clinical or echocardiographic signs of classic tamponade. CONCLUSION--The paucity of abnormal physical or echocardiographic signs of tamponade in breathless patients with pericardial effusion does not exclude symptomatic benefit being derived from pericardiocentesis. Pericardial aspiration is safe in appropriate hands, although aspiration of loculated effusions may not be as successful as aspiration of non-loculated effusions.     

Chylopericardium presenting as cardiac tamponade secondary to an anterior mediastinal cystic teratoma

Cardiac tamponade, the accumulation of fluid in the pericardial space, leads to impaired venous return, loss of left ventricular preload, and hemodynamic collapse. The many causes of tamponade include malignancy, infection, inflammation, connective tissue disorders, and uremia. Herein, we report the case of a young woman who presented with syncope. She was found to have cardiac tamponade secondary to a chylous pericardial effusion that was due to a mature and benign anterior mediastinal cystic teratoma. Numerous reports have described pericardial effusions secondary to an anterior mediastinal cystic teratoma; however, to our knowledge, this is the 1st case of a teratoma causing chylopericardium that presented as tamponade.     

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.     

Two-dimensional echocardiography in cardiac tamponade occurring after cardiac surgery

Cardiac tamponade is an important complication after cardiac surgery, yet little has been published on the echocardiographic diagnosis of this situation. The two-dimensional echocardiograms of 11 patients who required surgical relief of cardiac tamponade complicating cardiac surgery were therefore reviewed. Four had nonloculated pericardial effusions surrounding both ventricles. The other seven patients had a loculated posterior pericardial effusion; in three of these the effusion altered left ventricular posterior wall contour so that it was concave toward the effusion in the long-axis view; in two, a strikingly abnormal motion of the left ventricular posterior wall was noted, such that the width of the posterior pericardial space diminished in systole and widened abruptly in early diastole. The quantity of pericardial contents (fluid, blood or clot) evacuated surgically was smaller than usually encountered in patients with tamponade due to various "medical" conditions. Thus, unlike tamponade with other pericardial effusions, tamponade after cardiac surgery is due to a pericardial effusion that is smaller in volume, often loculated posteriorly and associated with certain unique two-dimensional echocardiographic features.     

Two cases of primary cardiac lymphoma presenting with pericardial effusion and cardiac tamponade

The heart as the primary site of lesion in malignant lymphoma is extremely rare. We experienced 2 cases of malignant lymphoma whose initial presentation was massive pericardial effusion with cardiac tamponade. The first case was a 75-year-old man who had shortness of breath for 1 week. Chest X-ray showed cardiomegaly (CTR 65%), and his condition was diagnosed as congestive heart failure at first and thereafter echocardiogram revealed pericardial effusion. The second case was a 76-year-old man who complained of exertional dyspnea which worsened over 2 weeks. His condition was diagnosed as congestive heart failure at first and echocardiogram revealed pericardial effusion. Pericardial drainage tapped bloody fluid and cytological examination revealed malignant lymphoma. After treatment, the first case lived for eleven months with no recurrence of pericardial effusion. The second case has lived for 4 years. We present these 2 cases can be defined as primary cardiac lymphoma according to McALLISTER and FENOGLIO, i.e., a lymphoma that involves only the heart and pericardium. More cases of primary cardiac lymphoma will be found in the future because of the ease with which the echocardiogram can detect pericardial effusion.     

Cardiac tamponade from acute pericarditis associated with a cystic fibrosis (CF) lung infection

Cystic fibrosis (CF) is a genetically inherited autosomal recessive disease characterized by dehydration of the airway surface liquid and impaired mucociliary clearance leading to chronic respiratory infections, bronchiectasis and ultimately death from respiratory causes. Common pulmonary related complications resulting from bronchiectasis include pneumothorax and hemoptysis. A rare, seldom reported complication is acute pericarditis complicating cystic fibrosis. Our review of the literature identified only a single case of culture-proven purulent pericarditis attributed to Pseudomonas aeruginosa in a patient receiving systemic corticosteroids. A second reported case of acute pericarditis in a CF patient was attributed to Mycoplasma pneumoniae which is a known cause of infectious-related pericarditis independent of CF. Both cases required open pericardial drainage with 1 fatality. Here we present a case of cardiac tamponade from a fibrinous pericardial effusion in a 21-year-old female as a complication of CF related parenchymal lung disease. To our knowledge, this is the first reported case of a non-infectious parapneumonic pericardial effusion causing near fatal cardiac tamponade as a complication of CF lung disease.     

Pericardial effusion diagnosed by echocardiography. Clinical and electrocardiographic findings in 171 patients

Clinical and electrocardiographic findings in 171 patients with pericardial effusion diagnosed by echocardiographic studies were reviewed. In 70 patients the effusion was unsuspected. There were 87 small, 50 moderate, and 31 large effusions. Cardiac tamponade was present in three patients. Congestive heart failure was the most common cause of pericardial effusion and occurred in 37 patients. Other frequently noted conditions included cardiac disease without congestive heart failure, neoplasms, acute nonspecific pericarditis, renal failure, and acute myocardial infarction. A pericardial friction rub was present in 23 patients, two-thirds of whom had moderate or large effusions. Atrial arrhythmias were common. Low voltage occurred in 31 of 136 patients and was more common with large effusions. The ability to distinguish between a small effusion and the quantity of pericardial fluid present normally is a problem requiring further clarification.     

Echocardiographic manifestations of tense pericardial effusion

Echocardiography has emerged as a sensitive study in the evaluation of pericardial effusion. The specificity of echocardiographic signs in cardiac tamponade remains undefined, however. Two such signs, early diastolic collapse of the right ventricular free wall and late diastolic collapse of the right atrial wall, were observed in two patients without clinical evidence of cardiac tamponade. Increased intrapericardial pressure was documented in each patient. Accumulation of pericardial fluid under high pressure results in a reversal of the instantaneous transmural pressure gradients in early and late diastole, causing collapse of the right ventricular and the right atrial wall, respectively; however, such a tense pericardial effusion may not cause hemodynamic embarrassment severe enough to yield clinical signs of cardiac tamponade.     

Systemic lupus erythematosus: an unusual cause of cardiac tamponade in a young man.

Although pericarditis and pericardial effusion are common cardiac complications of systemic lupus erythematosus (SLE), cardiac tamponade is a very rare initial manifestation of this disease. We describe a case of a young male patient in whom cardiac tamponade secondary to a loculated pericardial effusion was the presenting symptom of SLE.