心包积液住院患者的病因分析(附384例报告)

目的:分析近20年间384例心包积液患者的病因,探究其变化规律。方法:对我院1988～2007年收治的384例心包积液患者的临床资料进行回顾性分析。通过分析其病因构成,并按时间将其分组,了解病因构成是否发生改变。结果:肿瘤性、结核性、心力衰竭性和非特异性占心包积液病因的前4位,分别占24.5%、21.3%、14.6%、8.9%,其中结核性心包积液比例由10年前的26.8%降为18.2%(P<0.05),而肿瘤性心包积液则由10年前18.3%升为28.1%(P<0.05)。结论:不同时期病因构成不同,肿瘤已成为当前心包积液的首要病因。     

85例血性心包积液的病因及诊断方法分析

目的:总结分析血性心包积液的病因及其诊断方法,为诊断和鉴别诊断提供指导性资料。方法:对85例血性心包积液患者的临床表现、影像学检查、实验室检查结果进行回顾分析。结果:85例血性心包积液的病因中,肿瘤性41例(48.23%)、结核性27例(31.76%)、其他各种原因引起者17例(20.01%)。肿瘤性心包积液中癌胚抗原的平均值173μg/L,显著高于结核性心包积液的平均值0.62μg/L;结核性心包积液腺苷脱氢酶平均值44.5U/L,显著高于癌性心包积液平均值15U/L;结核性心包积液患者中心包积液和血液抗结核抗体(kjhkt)检测阳性率分别为62.5%和75%,显著高于肿瘤性心包积液患者(均为阴性)。结论:恶性肿瘤和结核是血性心包积液的主要病因。心包积液的脱落细胞学检查和腺苷脱氢酶、癌胚抗原、kjhkt等项实验室检查为血性心包积液病因诊断和鉴别诊断的主要手段,联合应用可提高诊断的准确性。     

689例心包积液病因及误诊分析

目的：分析心包积液病因变化及误诊原因。方法：病例回顾分析。结果：结核性、非特异性、肿瘤性、心力衰竭性及尿毒症性心包积液分别占６８９例心包积液的２５．５％、１２．６％、１２．２％、６．５％和６．１％，其他各种原因所致者合计占３７．１％。结核性心包积液由８０年代中期以前的２９．０％降至８０年代中期以后的２２．３％（Ｐ＜０．０５），而肿瘤性心包积液则由９．９％升至１４．１％（Ｐ＜０．０５）。结论：结核性心包积液比例明显下降，而肿瘤性心包积液所占比例则明显上升。心包积液病因误诊主要是将肿瘤性心包积液误诊为其他性质心包积液     

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。     

血性心包积液病因分析

目的探讨血性心包积液的病因分布特点。方法选自2002年1月至2012年7月北京军区总医院东区64例和2013年4月至2014年4月北京朝阳急诊抢救中心4例,行心包穿刺明确诊断为血性心包积液患者68例。其中男性28例,女性40例,年龄范围19~87岁。按年龄将患者分为2组,老年组33例(≥60岁)和中青年组35例(18~59岁)。按性别分男性组(28例)和女性组(40例)。收集所有患者临床资料,分析血性心包积液病因分布。结果患者常见病因为恶性肿瘤(55.9%)、结核(26.4%)及非特异性心包积液(7.4%)。其他病因分别为心力衰竭、主动脉夹层及先心病等。老年组与中青年组的常见病因分布比例比较,差异无统计学意义(P均0.05)。男性组和女性组血性心包积液的常见病因分别为肿瘤和结核,男性与女性病因分布比例比较,差异无统计学意义(P均0.05)。肿瘤致血性心包积液,肺肿瘤占60.5%,妇科肿瘤13.2%,消化道肿瘤10.5%,心包间皮瘤5.3%,肾及肾上腺肿瘤5.3%,皮肤及颈部淋巴瘤各2.6%。结论肿瘤和结核为血性心包积液的主要致病因素,与年龄和性别无明显相关。     

老年心包积液患者病因的调查分析

目的了解老年心包积液患者随年龄增大其病因构成的变化情况。方法450例确诊为心包积液的住院患者按年龄分为非老年(0~59岁)组,老年(60~79岁)组和高龄老年(80岁以上)组,建立心包积液住院患者临床资料数据库,对比分析各组的病因构成。结果随着年龄的增大,心包积液病因构成也发生着变化。所有患者前6位的基础病因为肿瘤(22.22%)、结核(19.11%)、心力衰竭(16.44%)、肾功能不全(8.22%)、非特异性心包炎(8%)和心脏术后并发症(7.78%),老年组是肿瘤(23.5%)、心力衰竭(19.13%)、结核(14.75%)、非特异性心包炎(11.48%)、肺部感染(8.74%)和肾功能不全(6.01%),高龄老年组心包积液病因构成相对集中,前4位的病因是心力衰竭(34.62%)、肺部感染(19.23%)、肿瘤(15.38%)、肾功能衰竭(15.38%)。结论心包积液的病因随患者年龄老化,肿瘤、心力衰竭、肺部感染比例呈逐步上升趋势,结核则呈下降走势。在高龄老人,心肺功能异常导致心包积液已经接近一半。     

102例心包积液患者临床病因分析

目的回顾性总结分析心包积液患者的病因分布特点及临床类型,探究其变化规律,提高病因诊断。方法对我院2001年01月至2008年12月因心包积液住院的102名患者的临床资料进行分析。结果心包积液常见病因依次为肿瘤（25．5％）,结核（22．6％）,心力衰竭（19．4％）,非特异性（13．8％）,尿毒症（9．9％）和结缔组织疾病（6．3％）,其他原因引起者占（2．5％）。结论引起心包积液的首要病因为肿瘤,其次为结核;随着诊疗水平的提高,心包积液的病因分布更趋广泛。原因不明的心包积液在排除恶性肿瘤、甲状腺功能减退等常见病因的前提下,试验性抗结核治疗有助于明确诊断。     

心包积液101例病因分析

心包积液病因分析已有众多报道 ,但结果不尽相同。作者对本所 1996～ 1999年收治的 10 1例心包积液患者做病因分析。1　临床资料　全组 10 1(男 5 0 ,女 5 1)例 ,年龄 1～ 78(平均33.8)岁。其中 30例大量积液行心包穿刺术 ,占 2 9.7%。有 3例未行心包积液实验室检查。病因诊断是根据病史、症状、体征、心电图、超声心动图、胸片、血液、心包积液的实验室检查综合判定。2　结果　心包积液常见病因前 4位依次为 :心力衰竭 2 8例(占 2 7.7% ) ,心包切开综合征 2 1例 (占 2 0 .8% ) ,肿瘤 14例(占 13.9% ) ,风湿热 14例 (占 13.9% ) ,其中肺癌为…     

多因素心包积液患者的临床特点分析

目的探讨心包积液住院患者的临床特点。方法选择合并心包积液的463例住院患者,男211例,女252例,分为青少年组92例(5~39岁)、中年龄组138例(40~59岁)和老年组233例(60~92岁)。收集临床资料,并回顾性分析。结果所有患者居前3位的病因为肿瘤(22.7%)、免疫系统疾病(15.8%)和不明原因(14.7%)。女性免疫系统疾病、甲状腺功能减退比例高于男性,慢性肾病和结核比例低于男性(P0.05,P0.01)。青年少组、中年组和老年组免疫系统疾病、不明原因和血液病比例有显著差异(33.7%vs 18.8%vs 6.9%、9.8%vs 8.0%vs20.6%、18.5%vs 13.8%vs 3.0%,P0.01)。多病因构成主要为心力衰竭、感染、低蛋白血症和肾功能不全,感染为最常见(61.6%)的合并因素。结论多数心包积液患者合并≥1种诱发或加重心包积液发生的病因。     

以心包积液为主多浆膜腔积液患者的病因学分布和临床特征分析

目的:明确以心包积液为主多浆膜腔积液患者的病因学分布以及恶性积液和非恶性积液患者临床特征的差异。方法:回顾性分析2010年1月至2017年12月于北京大学人民医院住院治疗的326例以心包积液为主多浆膜腔积液患者的临床资料,明确病因分布情况;并根据多浆膜腔积液是否为恶性肿瘤所致,分为恶性积液组和非恶性积液组,分析两组患者临床特征差异。结果:(1)病因学分布:326例患者中78例(23.9%)病因不明;在病因明确患者中,常见原因依次为自身免疫性疾病(n=50,15.3%)、恶性肿瘤(n=47,14.4%)、心功能不全(n=37,11.3%)、结核(n=26,8.0%)和低白蛋白血症(n=17,5.2%)。在恶性肿瘤所致患者中,97.9%(46/47)为其他部位恶性肿瘤(肺癌、乳腺癌和淋巴瘤)转移所致。(2)临床特征差异:与非恶性积液组患者(n=279)相比,恶性积液组患者(n=47)主要以急性起病、大量心包积液和易发生心包填塞为主;血液实验室检查阳性率低,CT或正电子发射型计算机断层扫描显像(PET-CT)检查阳性率高;心包积液以血性为主,细胞总数、乳酸脱氢酶和多个肿瘤标志物水平明显升高,但Light标准在鉴别恶性和非恶性积液中无明显作用;此外,细胞病理检查作为诊断恶性积液的“金标准”,阳性率低。结论:自身免疫性疾病、恶性肿瘤和心功能不全是以心包积液为主多浆膜腔积液患者的主要病因。恶性积液患者起病急、病情重且易恶化,CT或PET-CT以及心包积液实验室检查在恶性与非恶性积液的鉴别中具有重要作用。     

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。     

心包积液100例临床分析

目的探讨心包积液病因之间所占比重变化。方法从症状、体征、实验室检查、心脏超声、心包穿刺抽液及手术病理活检等来确立其病因，其后分析各类病因所占比重。结果100例心包积液病因前四位是心衰、心包切开综合征、肿瘤与结核。结论心衰是引起心包积液最常见原因。     

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.     

Acute renal failure as the presenting symptom of pericardial effusion

Pericardial effusion from any cause may lead to decreased cardiac output and blood pressure, causing heart failure and reduced renal blood flow. Although pericardial effusion is not uncommon, it is usually not associated with hemodynamic compromise unless the effusion causes cardiac tamponade. Acute renal failure resulting from pericardial effusion is surprisingly rare, with only six cases described to date. We describe the first case known to us of pericardial effusion without tamponade causing acute anuric renal failure. The case was characterized initially by non-specific symptoms and signs; anuria dominated the clinical picture, and was completely reversed after pericardiocentesis.     

Human immunodeficiency virus-associated pericardial effusion: report of 40 cases and review of the literature

BACKGROUND: Human immunodeficiency virus (HIV)-associated pericardial effusion is common. We present its clinical features, cause, and prognosis on the basis of a review of 40 cases at a single public hospital. METHODS: A retrospective study was conducted of 122 patients with pericardial effusion (of which 40 were HIV associated) admitted to Queens Hospital Center from January 1988 to April 1997. A review of the literature is also presented. RESULTS: Forty patients with HIV-associated pericardial effusion represent 33% of the 122 patients with pericardial effusion admitted during that period. The most common symptom of the 40 patients was dyspnea (75%). Echocardiogram detected small effusions in 18 (45%), moderate effusions in 10 (25%), and large effusions in 12 (30%). Sixteen (40%) patients had cardiac tamponade, in 15 of whom pericardiocentesis or pericardiostomy was performed. Causes of cardiac tamponade were Mycobacterium species in 3 (19%), Streptococcus pneumoniae in 1 (6%), Staphylococcus aureus in 1 (6%), Kaposi's sarcoma in 1 (6%), and unknown in 10 (63%). In comparison, causes of cardiac tamponade in 74 cases of acquired immunodeficiency syndrome in the literature were 45% idiopathic, 20% mycobacteria, 19% bacteria, 7% lymphoma, 5% Kaposi's sarcoma, 3% viruses, and 1% fungus. Thirteen of the 40 patients were lost to follow-up. Among the other 27, 11 (41%) were alive at 3 months and 5 (19%) at 1 year. Ten of the 27 patients had cardiac tamponade, of whom 5 (50%) were alive at 3 months and 3 (30%) at 1 year. CONCLUSIONS: HIV-associated pericardial effusion is the most common type of pericardial effusion in our inner city hospital. Causes are diverse. The development of pericardial effusion predicts a poor prognosis in HIV infection.     

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.     

Evaluation and Management of Pericardial Effusion in Patients with Neoplastic Disease

The incidence and extent of pericardial involvement in neoplastic disease varies. In a considerable number of patients with breast or lung cancer or with mediastinal lymphoma, in addition to direct involvement by the tumor, radiation therapy as well as systemic tumor treatment can also lead to pericardial effusion. In addition, in immunosuppressed tumor patients, pericardial effusion can also arise from viral, bacterial, and autoimmune causes. To distinguish between these 3 different conditions leading to pericardial effusion, the diagnosis should be based on pericardiocentesis followed by fluid analysis for cytology and biomarkers, on epicardial and pericardial biopsy facilitated by flexible pericardioscopy with analysis of specimens by conventional histology and molecular biology techniques for viral and microbial aetiology. We collected prospectively but analyzed retrospectively 357 patients undergoing pericardiocentesis from 1988 to 2008 and identified 68 patients who had cancer-related pericardial effusion. With these methods, 42 patients demonstrated malignant effusion, 15 patients had radiation-induced pericardial, effusion, and in 11 patients without radiation therapy, the effusion could be attributed to either viral infection in 5 cases or to an autoimmune process in the remaining 6 patients. Consequently, intrapericardial treatment could be tailored for each cohort: neoplastic effusion was treated with intrapericardial cisplatin (single instillation of 30 mg/m² per 24 hours); in addition to the tumor-specific systemic chemotherapy, intrapericardial triamcinolone acetate (Volon A) was given in a dose of 500 mg/m² in the patients with autoimmune and radiation-induced effusion. Saline rinsing and intrapericardial sclerosing treatment were the treatment of choice in viral pericardial effusion. Oral colchicine treatment (2-3 × 0.5 mg) was given in all patients for at least 3 months. Recurrence of pericardial effusion was prevented for at least 3 months in more than 85% of patients. This differential diagnostic approach and the results of treatment were compared with published series.