72例心包积液病因及误诊分析

目的 分析72例心包积液病因及误诊原因。方法 回顾分析2000年1月-2006年3月诊断有心包积液的病例72例。结果 心包积液病因依次是肿瘤性（22．2％）；结核性（16．7％）；心力衰竭性（12．5％）；非特异性（11．1％）；甲状腺机能减退性（8．3％）；其他病因及诊断不明的占29．2％。结论 肿瘤性心包积液发病率最高，且肿瘤性心包积液误诊为结核性及非特异性最高。     

Prolonged persistence of a large pericardial effusion and hemodynamic evidence of cardiac tamponade during treatment of myxedema

We describe clinical, echocardiographic, and catheterization findings that were present initially and during therapy in a myxedematous patient with a large pericardial effusion and tamponade. Treatment with thyroxine resulted in a marked improvement of most of the clinical features of hypothyroidism and some improvement in cardiac function. However, the pericardial effusion as well as clinical and laboratory evidence of tamponade persisted for 2 months after full replacement doses of T4 had been achieved. The tamponade was finally relieved by fenestration of the parietal pericardium. These findings are consistent with evidence of an abnormality of pericardial drainage that persists for months after other thyroid hormone dependent functions are normalized by thyroxine replacement. Therefore prompt surgical drainage rather than dependence on medical therapy alone is indicated in myxedematous patients who have cardiac tamponade.     

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.     

Pericarditis caused by cholesterol. Apropos of a clinical case

A case of a 76 year-old woman with a large pericardial effusion is described. The microscopic examination of the scintillating, yellow-greenish fluid obtained by the first pericardiocentesis, showed numerous crystals of cholesterol. In search of the underlying diseases there were found values of T3, T4 and TSH diagnostic of hypothyroidism. Considering the rapid relapse of the effusion and after a second pericardiocentesis, it was decided to open a pleuro-pericardial window. The biopsy of the pericardium showed deposits of cholesterol on electronics microscopy. She was discharged from hospital two weeks after surgery, showing an evident clinical improvement. Six months later she was feeling well, keeping a normal activity for her age. The values of T3, T4 and TSH were normal, and there were no echocardiographic signs of pericardial effusion. It is presented a rare case of cholesterol pericarditis associated to sub-clinical hypothyroidism, showing the presence of cholesterol, as crystals in the pericardial effusion and, we think for the first time in this pathology, in vesicles of pinocytosis, in the pericardial biopsy. The six months period of follow-up showed a good clinical improvement with the selected therapeutic attitude.     

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.     

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.     

Percutaneous balloon pericardiotomy in patients with recurrent pericardial effusion]

BACKGROUND: Recurrent symptomatic pericardial effusion can complicate different cardiac and extracardiac diseases. When recurrent pericardial effusion after drainage with conventional catheter techniques occurred the creation of a pericardial window by open surgery used to be the unique treatment available until the recent development of percutaneous balloon pericardiotomy. OBJECTIVE: The aim of this paper is to review our initial experience with percutaneous balloon pericardiotomy for the treatment of patients with recurrent pericardial effusion. PATIENTS AND METHOD: Five patients with recurrent pericardial effusion have been treated with percutaneous pericardiotomy until now. Four patients had malignant pericardial effusion secondary to metastasis of extracardiac tumors, in one patient recurrent pericardial effusion was idiopathic. In all patients percutaneous balloon pericardiotomy was performed with a pediatric valvuloplasty balloon catheter, through a subxiphoid approach. RESULTS: Successful drainage and balloon pericardiotomy was achieved in all patients without severe complications. In all cases only one pericardial site was dilated. Minor complications were registered, which included mainly mild pleural effusion occurring in all patients with spontaneous resolution. During a mean follow-up period of 8.6 6.5 months (range 2 to 18 months) there were no recurrences of effusion or tamponade. Two patients died, 1 month and 9 months after the procedure, due to their malignant condition. CONCLUSIONS: Percutaneous balloon pericardiotomy is an easy and useful technique to manage patients with large recurrent pericardial effusion with a low r     

Pericardial tamponade in a patient with treated myxedema

Pericardial tamponade developed in a patient with hypothyroidism and a pericardial effusion after she had been successfully treated with levothyroxine sodium. Refractory pericardial effusion is an unusual complication of treated myxedema. A possible mechanism for its occurrence is presented.     

原发性甲状腺功能减退性心包积液与甲状腺功能、心肌酶、胆固醇的关系

目的探讨原发性甲状腺功能减退性心包积液与甲状腺功能、心肌酶、总胆固醇的关系。方法回顾性分析90例原发性甲状腺功能减退症合并心包积液患者,进行甲状腺功能、心肌酶、总胆固醇的调查,并按有无心包积液分为2组进行比较。结果 (1)两组患者在年龄、性别构成、病程、病因上差异无统计学意义。(2)甲状腺功能减退伴心包积液组患者TT3、TT4、FT3、FT4均较无心包积液组低[(0.66±0.48)nmol/L比(1.20±0.57)nmol/L,(14.64±24.46)nmol/L比(62.22±50.67)nmol/L,(2.11±0.74)pmol/L比(3.66±2.02)pmol/L,(3.12±4.49)pmol/L比(6.37±4.78)pmol/L],而TSH较无心包积液组高[(68.85±32.05)mU/L比(46.47±39.44)mU/L,均为P<0.05]。(3)心包积液组心肌酶谱、胆固醇均较无心包积液组高(P<0.05)。(4)偏相关分析提示心包积液与TT3、TT4、FT3、FT4、TSH相关(r=-0.400,-0.467,-0.368,-0.340,0.284;均为P<0.05)。结论原发性甲状腺功能减退性心包积液与甲状腺功能严重程度有关,与年龄、病程、病因无关,同时多伴有胆固醇及心肌酶谱升高。     

PERICARDIAL EFFUSION IN HYPOTHYROIDISM

Thirty-nine patients with untreated hypothyroidism have been examined using echocardiography for the presence of a pericardial effusion. Effusions were present in twelve patients who tended to be more severely hypothyroid. Plasma creatine phosphokinase and lactate dehydrogenase levels were higher in the presence of an effusion. Nine were reinvestigated during thyroxine replacement therapy and the effusions did not disappear until thyroid function tests had returned to normal. There were no specific electrocardiographic changes associated with the presence of an effusion which could be associated with a normal cardiac silhouette on a standard P.A. chest X-ray.     

Transient elevation of serum tumor markers in a patient with hypothyroidism

We report a case of a 66-year-old woman admitted to our hospital for examination and treatment of uterine and rectal prolapse, pleural and pericardial effusion, and ascites. On further examination, she was diagnosed with hypothyroidism. Test results showed markedly elevated concentrations of serum carcinoembryonic antigen (CEA) and carbohydrate antigen 125 (CA 125). We consequently performed multiple imaging studies, none of which detected a malignancy. Hormonal replacement therapy with levothyroxine was started, and the pleural and pericardial effusion and ascites gradually abated. Concentrations of serum CEA and CA125 also decreased gradually after therapy with levothyroxine. These findings indicate that in patients with hypothyroidism, elevated CEA and CA125 levels do not necessarily indicate malignancy. Conversely, in any patient with elevated serum CEA and/or CA125, hypothyroidism should be considered in the differential diagnosis.     

甲状腺功能减退症与心血管病

目的全面了解甲状腺功能减退症(甲减)患者心血管系统表现和心血管并发症、合并症,为诊断甲减提供参考。方法回顾性分析心血管内科收入的甲减患者心血管系统表现和心血管并发症、合并症及其构成比、内在的相互关系。结果本研究甲减患者男性少于女性(男女人数1∶3),半数以上有相关病史;可合并(并发)贫血、心房纤颤、高血压病、冠心病、心包积液、高脂血症等心血管病;可存在多种非特异性的心电图异常,可有血清肌酶升高;贫血、血脂升高、心包积液、肌酶升高可同时存在或两种以上情况并存,如一个患者同时无这四种(或后三种)情况可排除甲减。结论甲减与心血管病有密切、广泛的联系,血脂升高、心包积液、肌酶升高、贫血至少存在一项异常。     

大量心包积液病因影响因素的回顾性分析

目的 收集并分析41例大量心包积液患者病因的影响因素，为诊治大量心包积液提供更为清晰诊疗思路。方法 根据2015年欧洲心血管病学会《心包疾病的诊断和治疗指南》诊断大量心包积液的标准，收集2017.1.1-2019.10.1期间入住福建省立医院及福建省立金山医院的大量心包积液患者41例，根据其病因诊断将所有入组对象分为4组：结核性心包积液组（TB组）、恶性肿瘤性心包积液组（MT组）、非TB感染性心包积液组（NTB组）及其他病因心包积液组（OE组）。采用SPSS统计软件分析所有入组患者心包积液患者病因的影响因素。结果 41例大量心包积液患者中男性24人，女性17人，平均年龄为60.3±14.9岁。TB组、MT组、NTB组及OE组患者分别占24.4%，24.4%，29.3%，21.9%。按照Light标准的定义，大量心包积病例中97.6%为渗出液。结核性心包积液的腺苷脱氨酶水平最高，达57.0±37.3U/L，远高于其他病因所致的心包积液（P<0.01）。腺苷脱氨酶诊断结核性心包积液的ROC曲线下面积0.961，最佳诊断切点为20.5U/L，此时敏感性达100%，特异性达80.6%。多元Logistics回归分析显示大量心包积液病因的主要影响因素有血红蛋白、心包积液腺苷脱氨酶水平和心包积液癌胚抗原水平。结论 本研究发现大量心包积液最常见病因是结核和恶性肿瘤，腺苷脱氨酶是诊断结核性心包积液的敏感指标，Light标准无法鉴别大量心包积液的病因，血红蛋白、心包积液腺苷脱氨酶和心包积液癌胚抗原是影响大量心包积液病因判定的重要指标，具有一定临床指导意义。     

Endoscopic pericardial fenestration for a patient with sustained lupus pericarditis.

A 57-year-old woman was diagnosed in January 1982 with SLE based on ANA 1:640, positive LE cell preparation, proteinuria (3+), and pericarditis. In 1984, 1994, and 1997, the pericardial effusion was noted to have increased without signs of disease exacerbation or cardiac tamponade, and pericardial drainage was repeated to control the effusion. A massive pericardial effusion developed in August 1997. After tuberculosis, hypothyroidism, neoplasm, and progression of SLE were ruled out, we decided to perform pericardial fenestration. A safe and minimally invasive pericardial fenestration was successfully completed endoscopically. Pathologic study of the specimen revealed chronic pericarditis. We consider endoscopic pericardial fenestration to be useful for at risk patients with pericarditis to control the effusion and establish a differential diagnosis.     

A case of diminished pericardial effusion after treatment of a giant hepatic cyst

A 75-year-old woman was discovered to have a pericardial effusion when she was admitted to our hospital because of a giant hepatic cyst. We could not detect the cause of the effusion and diagnosed idiopathic pericardial effusion. The patient underwent transcutaneous drainage of the hepatic cyst and an injection of antibiotics. There was no communication between the pericardial effusion and the hepatic cyst. Although the hepatic cyst was reduced in size, the pericardial effusion showed no remarkable change immediately after treatment; however, 5 months later, the pericardial effusion was found to be diminished. The pericardial effusion might have been caused by the physical pressure of the giant hepatic cyst and disturbance in the balance between the production and reabsorption of the pericardial fluid. When we experience a huge hepatic cyst, we should take into account its influence against the surrounding organs, including the intrapleural space.     

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.     

Tuberculosis on regular hemodialysis--a case of pericardial tamponade

The patient presented in this paper had been stable for 3 months after the induction of hemodialysis, when nausea, vomiting and hepatomegaly suddenly developed. A chest film revealed rush cardiomegaly, and massive pericardial effusion was demonstrated by echocardiography. One liter of hemorrhagic fluid was removed by pericardiocentesis and subsequent pericardial drainage under echocardiography. The patient received chemotherapy against pulmonary tuberculosis 30 years ago and calcification on chest film was apparent. Although sputum smear and pericardial effusion was negative for acid-fast organisms, combination therapy was initiated for suspected tuberculosis. The patient recovered completely and 2 months later it was demonstrated that cultures of sputum grew mycobacterium tuberculosis. Tuberculin skin test (PPD), which was negative 2 months previously, converted to positive. Tuberculosis must be considered as a potential cause of pericardial tamponade in patients on regular hemodialysis, and prompt therapy for both cardiac tamponade and the occult infection is warranted.     

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.     

Recurrent pericardial effusion with a common clinical disorder

We present a case of recurrent pericardial effusion in a patient with Down's syndrome in whom the underlying cause was not considered because of unfamiliarity with the care of people with Down's syndrome. The diagnosis hypothyroidism only became apparent by means of a routine panel of biochemical tests.     

系统性硬化症合并甲状腺功能减退患者的临床分析

目的了解系统性硬化症(SSc)合并甲状腺功能减退患者的发病率及其临床特点,指导临床早期诊断、治疗。方法回顾性分析2002年1月至2010年9月在北京协和医院住院治疗的SSc患者的临床及实验室资料,并与中国EUSTAR(EULAR Scleroderma Trial and Research group)数据库中2009年2月至2009年11月入组的未合并甲状腺功能减退的92例SSc患者的临床资料进行对比。结果 8年间在北京协和医院住院治疗的SSc患者共344例,合并甲状腺疾病20例(6.1%),其中甲状腺功能减退14例(70%)。14例患者均为女性,与未合并甲状腺功能减退患者相比,合并甲状腺功能减退的患者更易出现心包积液(50%vs.16.3%,P=0.012)及红细胞沉降率(ESR)升高(64.3%vs.27.2%,P=0.011),抗Scl-70抗体阳性者少见(21.4%vs.46.7%,P=0.018)。结论 SSc患者合并甲状腺疾病以甲状腺功能减退(含亚临床甲状腺功能减退)最为常见,当SSc患者同时存在心包积液、ESR升高及抗Scl-70抗体阴性时应警惕甲状腺受累的可能。