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.     

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.     

Akute und chronisch-konstriktive Perikarditis

Acute pericarditis is an inflammatory disease of the pericardium of variable etiology. A viral infection may sometimes preceede symptoms but frequently the etiology remains unknown (idiopathic pericarditis). The disease is typically associated with left-sided chest pain and ECG abnormalities mimicking acute myocardial infarction. At physical examination the characteristic finding is a pericardial friction rub. A pericardial effusion of varying extent may be present or develop in the course of the disease. Pericardial tamponade, which may develop insidiously, represents a life-threatening complication. Pathophysiologically, filling of the cardiac chambers is impeded resulting in orthopnea, tachycardia, and eventually shock. Emergency pericardiocentesis is the treatment of choice. Constrictive pericarditis is the result of a chronic inflammation of the pericardium. Clinically it is characterized by dyspnea during exercise, symptoms of right heart failure and typical hemodynamic findings. Treatment primarily includes surgical removal of the thickened pericardium.     

Acute and chronic-constrictive pericarditis

Acute pericarditis is an inflammatory disease of the pericardium of variable etiology. A viral infection may sometimes precede symptoms but frequently the etiology re-mains unknown (idiopathic pericarditis). The disease is typically associated with left-sided chest pain and ECG abnormalities mimicking acute myocardial infarction. At physical examination the characteristic finding is a pericardial friction rub. A pericardial effusion of varying extent may be present or develop in the course of the disease. Pericardial tamponade, which may develop insidiously, represents a life-threatening complication. Pathophysiologically, filling of the cardiac chambers is impeded resulting in orthopnea, tachycardia, and eventually shock. Emergency pericardiocentesis is the treatment of choice. Constrictive pericarditis is the result of a chronic inflammation of the pericardium. Clinically it is characterized by dyspnea during exercise, symptoms of right heart failure and typical hemodynamic findings. Treatment primarily includes surgical removal of the thickened pericardium.     

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.     

Primary acute pericardial disease: a prospective series of 231 consecutive patients

A series of 231 patients with "primary" acute pericardial disease (acute pericarditis or tamponade presenting without an apparent cause) were studied according to the following protocol: general clinical and laboratory studies (stage I), pericardiocentesis (stage II), pericardial biopsy (stage III) and blind antituberculous therapy (stage IV). In 32 patients (14%) a specific etiologic diagnosis was obtained (13 with neoplasia, 9 with tuberculosis, 4 with collagen vascular disease, 2 with toxoplasmosis, 2 with purulent pericarditis and 2 with viral pericarditis). "Diagnostic" pericardiocentesis (32 patients) was performed when clinical activity and effusion persisted for longer than 1 week or when purulent pericarditis was suspected, whereas "therapeutic" pericardiocentesis (44 patients) was performed to treat tamponade; their diagnostic yield was 6% and 29%, respectively. "Diagnostic" biopsy (20 patients) was carried out when illness persisted for longer than 3 weeks, whereas "therapeutic" biopsy was performed whenever pericardiocentesis failed to relieve tamponade; their diagnostic yield was 5% and 54%, respectively. The diagnostic yield difference between "diagnostic" and "therapeutic" procedures was significant (p less than 0.001); in contrast, the global diagnostic yield of pericardiocentesis (19%) and biopsy (22%) was similar. At the end of follow-up (1 to 76 months, mean 31 +/- 20), no patient in whom a diagnosis of idiopathic pericarditis had been made showed signs of pericardial disease. It is concluded that a "diagnostic" procedure is not warranted as a routine method, a choice between "therapeutic" pericardiocentesis and biopsy is circumstantial and must be individualized, and only through a systematic approach can a substantial diagnostic yield be reached in primary acute pericardial disease.     

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.     

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.     

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 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.     

Cholesterol pericarditis--relapsing pericardial effusion in a patient with rheumatoid arthritis.

Cholesterol pericarditis is an uncommon form of pericardial disease, of unknown pathophysiology, that is characterized by chronic relapsing, usually large, pericardial effusions that are distinctive due to a high level of cholesterol. Usually it is idiopathic, but it can be associated with various systemic diseases such as hypothyroidism, rheumatoid arthritis and tuberculosis, among others. Its clinical course is usually indolent and complications such as cardiac tamponade and chronic constrictive pericarditis are relatively rare. However, the need for surgery for complete treatment has been reported in at least 10 % of cases. When rheumatoid arthritis is the underlying cause, this outcome is more frequent among those with an acute episode of pericarditis during the course of the disease. We report the case of a 61-year-old female rheumatoid arthritis patient, who presented with heart failure due to a large pericardial effusion and was successfully treated by a surgical approach.     

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.     

Use of colchicine in chronic pericardial effusion. Presentation of 2 clinical cases and review of the literature

Colchicine was introduced in 1987 for the treatment of recurrent pericarditis. Up to the present, papers have been published on a total of 117 patients treated with colchicine after the failure of treatment with FANS, corticosteroids and repeated pericardiocentesis. Here two cases of chronic pericardial effusion, one secondary to pericardiotomy, the second idiopathic, are reported. Both were recalcitrant to conventional therapy. Both patients were treated with 2 mg/die colchicine for 1 month followed by 1 mg/die for a further 5 months, without recurrence of the effusion after follow-up of 12 and 24 months respectively. No side-effects were observed. Colchicine is an anti-inflammatory drug which, by inhibiting various leukocyte functions, depresses the action of the leukocytes and of the fibroblasts at the site of the inflammation. We conclude that colchicine is effective in post-pericardiotomic and idiopathic chronic pericardial effusion as already reported in cases of recurrent pericarditis. Given the lack of side-effects, it could be considered as a drug of choice alternatively to FANS and corticosteroids.     

Outcomes of clinically significant idiopathic pericardial effusion requiring intervention

There is a paucity of outcome data on patients with idiopathic pericardial effusion requiring intervention. All patients who had clinically significant pericardial effusion confirmed by echocardiography and requiring interventions between 1979 and 2000 were identified through the Echo-guided Pericardiocentesis Registry and Echocardiography and Surgical Databases. Clinical data and outcomes were obtained by review of medical records and surveys. The study population consisted of 92 patients (mean age 59 +/- 15 years). Five patients were referred directly for pericardiectomy (3 had effusion in the context of chronic relapsing pericarditis, 2 had effusive constrictive disease), and 87 underwent echo-guided pericardiocentesis as their initial treatment. In 47 of these patients, primary management involved extended pericardial catheter drainage, which was associated with a trend to lower recurrence rates than in those without catheter drainage (p = 0.052). Three patients had transient right ventricular entry with no sequelae, and 7 patients (8%) later had surgical pericardiectomy because of the recurrence of effusion, 2 of whom were also found to have evidence of effusive constrictive disease during surgery. One patient had bleeding after pericardiectomy that required repeat thoracotomy. Mean follow-up of the cohort was 3.8 +/- 4.3 years. For most patients with clinically significant idiopathic pericardial effusion requiring intervention, echo-guided pericardiocentesis was the definitive treatment. Pericardiectomy was necessary for patients in whom effusion occurred in the context of effusive constrictive disease, chronic relapsing pericarditis, or recurrent effusion despite pericardiocentesis. The prognosis for the cohort was favorable, and survival did not appear to differ from that of the general population (p = 0.372).     

Etiology and prognostic implications of a large pericardial effusion in men

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

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.     

Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?

STUDY OBJECTIVES: The decrease in incidence of tuberculosis, along with the increase in invasive cardiovascular procedures, may have changed the frequency of causes of bloody pericardial effusion associated with cardiac tamponade, although this is not yet recognized by medical textbooks. We analyzed the causes of bloody pericardial effusion in the clinical setting of cardiac tamponade in the 1990s; patients' survival; the effect of laboratory results on discharge diagnosis; and how often bloody pericardial effusion is a presenting manifestation of a new malignancy or tuberculosis. DESIGN: Retrospective, observational, single-center study. SETTING: A community hospital. PATIENTS: The charts of all patients who underwent pericardiocentesis for cardiac tamponade and had bloody pericardial effusion were retrospectively reviewed. RESULTS: Of 150 patients who had pericardiocentesis for relieving cardiac tamponade, 96 patients (64%) had a bloody pericardial effusion. The most common cause of bloody pericardial effusion was iatrogenic disease (31%), namely, secondary to invasive cardiac procedures. The other common causes were malignancy (26%), complications of atherosclerotic heart disease (11%), and idiopathic disease (10%). Tuberculosis was detected as a cause of bloody pericardial effusion in one patient and presumed to be the cause in another patient. Bloody pericardial effusion was found to be a presenting manifestation of a newly diagnosed malignancy in two patients. The patients in the idiopathic and iatrogenic groups were all alive and had no recurrence of pericardial effusion at 24 +/- 27 and 33 +/- 21 months after hospital discharge, respectively, whereas 80% of patients with malignancy-related bloody effusions died within 8 +/- 6 months. CONCLUSIONS: In a patient population that is reasonably representative of that in most community hospitals in the United States, the most common cause of bloody pericardial effusion in patients with signs or symptoms of cardiac tamponade is now iatrogenic disease. Of the noniatrogenic causes, malignancy, complications of acute myocardial infarction, and idiopathic disease predominated. Hemorrhagic tuberculous pericardial effusions are uncommon and may likely reflect a low incidence of cardiac tuberculosis in community hospitals in the United States.     

持续性心包引流合并症的探讨

目的 持续性心包穿刺引流是治疗大量心包积液和心包填塞的常用方法,本文旨在探讨心包穿刺引流的合并症。方法 本文对5例发生了心包穿刺引流合并症的住院患者进行分析。结果 在5例合并症中,有2例因导管前端刺激发生神经介导性晕厥,1例发生急性右心室扩张并死亡,1例发生心包积液经导管管侧孔漏入左侧胸腔,1例出现急性肺水肿和心包积液经穿刺处漏入皮下组织。结论 应充分认识持续心包引流所引起的血流动力学改变,对危重患者应行床旁血流动力学监测。同时应注意引流导管本身对患者可能造成的损伤。     

Wegener's granulomatosis and the heart.

Three cases of Wegener's granulomatosis with cardiac complications are described and the relevant published reports are reviewed. The first case of Wegener's granulomatosis was associated with aortic regurgitation and required aortic valve replacement. The second and third cases were associated with pericardial disease requiring pericardiectomy for constructive pericarditis in one case, and haemorrhagic pericarditis with pericardial effusion in the other. Aortic valve involvement in Wegener's granulomatosis is uncommon and valve replacement has been described on only one previous occasion. Pericardial involvement is relatively common pathologically, but pericardial surgery has been described in this condition only twice, once for tamponade and once for constrictive pericarditis after pericardiocentesis. Cardiac involvement is not uncommon in patients with Wegner's granulomatosis and may be clinically important. Diagnosis is aided by estimation of the anti-neutophil cytoplasmic antibody titre.