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。     

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。     

老年人缩窄性心包炎的特点

目的探讨老年人缩窄性心包炎的临床特点,并与非老年人比较。方法回顾性总结我院2000—2007年连续诊断的缩窄性心包炎患者门诊与住院资料,对60岁以上老年患者与非老年患者临床与病理情况进行比较分析。结果 150例中,48例为老年人,占32.0%,非老年人102例。结核分别占83.3%和76.5%(P>0.05)。老年人胸痛、呼吸困难的发生率和心包积液检出率均高于非老年人,分别是87.5%比59.8%(P=0.0006),79.2%比52.0%(P=0.0074),腹腔积液发生率老年人明显低于非老年,分别是32.2%比52.9%(P=0.0129),结核性腹膜炎发生率为6.3%比35.2%(P=0.0456);心律失常在两组各为6例,但老年组的心律失常均为持续不可逆的;老年组32例(66.7%)存在62种合并症,非老年组仅13例(12.8%)存在合并症(P<0.001);老年组心包剥脱手术率明显低于非老年组(56.3%比80.4%,P=0.002),70岁以上手术治疗率仅25.9%;病死率两组相似,分别为6.3%比9.8%(P>0.05)。结论老年人缩窄性心包炎发病率不低,结核也是老年人缩窄性心包炎的最常见病因;临床表现与非老年人比较有一定特殊性,合并症多,心包剥脱手术率随年龄增长下降;病死率、近期预后与非老年人相似。     

高龄老年心力衰竭患者的临床特点分析

目的:探讨高龄老年心力衰竭患者的临床特征。方法:收集304例,60岁以上心力衰竭患者的发病诱因、基础心脏疾病、症状体征、相关化验检查及并发临床情况。将304例心力衰竭患者按年龄分为两组,60~79岁为老年组,≥80岁为高龄组。对以上资料在两组间进行对比分析,了解高龄心力衰竭患者的临床体征。结果:1高龄组导致心力衰竭的首要病因是冠心病,但较老年组冠心病所占比例低(38.1%vs.62.8%,P=0.001);高血压、退行性心脏瓣膜病、无基础心脏疾病比例较老年组明显增加,(分别为29.5%vs.19.1%,P=0.013;37.1%vs.10.1%,P=0.000;7.6%vs.2.0%,P=0.016)。2心力衰竭发作诱因中,高龄组首位是呼吸道感染,较老年组增加(43.8%vs.23.6%,P=0.001),输液快、外科手术及无明显诱因较老年组比例明显增加,两组比较差异有统计学意义。3高龄组心力衰竭类型及临床特点与相应的基础疾病及诱因相关。4老年心力衰竭并发多种临床情况,低蛋白血症和贫血在高龄组中比例明显增高比例(分别是38.1%vs.14.1%,P=0.000;20.0%vs.11.6%,P=0.046)。结论:高龄心力衰竭患者诱因首位是呼吸道感染,另外诱因多样或诱因不明显;部分患者基础心脏病史不明确;舒张功能不全为主的心力衰竭比例偏高;症状不典型;合并有多种临床情况,尤其低蛋白血症、贫血、胸腔积液及栓塞比例增加;肺部X线检查、心脏彩超对早期诊断有帮助。     

胸腔镜在老年胸腔积液中的诊断价值及安全性分析

目的探讨胸腔镜在不同年龄人群中渗出性胸腔积液诊断中的价值。方法选择就诊于我院符合纳入标准的69例胸腔积液患者,根据胸水检验结果均为不明原因的渗出液,其中老年组30例,非老年组39例。结果老年组病理确诊率为93.3%(28/30),肿瘤和结核确诊率为66.7%(20/30),非老年组病理确诊率100%(39/39),肿瘤和结核确诊率为87.2%(34/39),肿瘤和结核确诊率两组有显著性差异。老年组术中及术后不良反应总的发生率为46.7%(14/30),非老年组不良反应总的发生率为28.2%(11/39),两组无显著性差异。结论内科胸腔镜检查对老年疑难性胸腔积液的诊断确诊率较高,对肿瘤及结核的诊断缺乏特异性,不良反应较非老年患者多,对不明原因的疑难性胸腔积液应在积极评估患者一般状况后值得推广。     

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。     

老年心力衰竭住院病人病因及诱因临床分析

目的分析老年心力衰竭病人的病因、诱因构成。方法选取125例确诊心力衰竭的住院病人,按年龄分为非老年组(19岁~59岁)和老年组(60岁~94岁),整理病历资料进行回顾性分析,通过对比分析各组的病因、诱因构成及多病因情况。结果扩张型心肌病、高血压是非老年组最常见的前两位病因,分别占42.5%、40.0%,冠心病、高血压是老年组最常见的前两位病因,所占比例均为55.3%;在老年组冠心病所占比例明显高于非老年组(55.3%vs 25.0%,P0.01),而扩张型心肌病在非老年组所占比例明显高于老年组(42.5%vs 18.82%,P0.05)。非老年组单病因多见,远高于老年组(P0.01);而老年组多病因多见,显著高于非老年组(P0.01)。老年组及非老年组病人的诱因均以感染最多见,差异无统计学意义(P0.05)。结论随着年龄的增长,心力衰竭基础病因中冠心病、高血压的比例逐渐增大;多病因心衰比例逐渐增大;感染成为心力衰竭病人发病及反复住院的最常见诱因。     

老年充血性心力衰竭住院患者病因状况调查

目的了解充血性心力衰竭患者随年龄增长其病因构成的变化及多重病因情况.方法704例确诊为心衰的住院患者按年龄分为老年前期(45～59岁)组,老年(60～79岁)组和高龄老年(80～95岁)组,通过计算机Foxpro软件建立的老年CHF住院患者临床资料数据库,对比分析各组的病因构成及多病因情况.结果前三位的基础病因在老年前期组是风湿性心脏病(47.1%)、冠心病(19.9%)和扩张性心肌病(12.7%),老年组是冠心病(62.2%)、高血压(14.6%)和风湿性心脏病(11.9%),高龄老年组是冠心病(92.0%)、高血压(30.0%)和贫血(22.0%);多病因心衰在老年前期组占25.7%,老年组占70.7%,高龄老年组82.0%;多病因组合中,双病因最多见的是冠心病、高血压,三种及以上病因中最多见的组合是冠心病、高血压和糖尿病.结论心衰患者随年龄老化,(1)风心病和心肌病的比率逐渐下降,而冠心病、高血压和贫血的比例逐渐增大;(2)多病因心衰比例逐渐增大;(3)冠心病、高血压和糖尿病成为最常见的多病因组合.上述特点在老年心衰的诊治和预防中应当引起注意.     

老年慢性心力衰竭患者肾功能损害的临床观察

目的观察老年慢性心力衰竭患者中肾功能不全的发生情况。方法选择老年慢性心力衰竭患者95例,根据年龄分为老年组44例(年龄<80岁),高龄组51例(年龄≥80岁)。测定血清尿素、肌酐、白蛋白等指标,通过慢性肾脏病流行病学协作组开发的公式计算肾小球滤过率,并依此判断慢性肾脏病的患病率。结果与老年组比较,高龄组慢性肾脏病患病率明显升高(60.8%vs 45.5%,P<0.05),肾小球滤过虑明显降低,差异有统计学意义[(52.69±2.95)ml/(min.1.73m2)vs(61.59±3.14)ml/(min.1.73m2),P<0.05]。结论老年慢性心力衰竭患者肾功能下降,应加以关注。     

169例胸腔积液病因分布和临床特点

目的探讨胸腔积液的病因分布和临床特征。方法分析我院所有收治并且资料完整的胸腔积液患的临床资料。结果 169例胸腔积液患者的病因依次为:结核性胸膜炎89例(52.66%)、恶性肿瘤35例(20.71%)、心功能不全18例(10.65%)、肺炎或肺部感染17例(10.06%),其他10例。结核性胸腔积液以40岁以下患者占48.3%,老年病人在增加,腺苷脱氨酶的敏感率为79.78%;恶性胸腔积液以60岁以上患者居多(65.7%),40岁以下极少(5.7%)。恶性胸腔积液查到肿瘤细胞者26例,阳性率为73%。结论胸腔积液主要病因是结核和肿瘤,结核患者以青年居多,恶性肿瘤以老年患者居多。临床综合分析是判断病因的关键。     

Pericardial involvement in human immunodeficiency virus infection

STUDY OBJECTIVES: Previous studies have showed that the pericardium is frequently involved in HIV infection. However, the characteristics and etiology of the pericardial abnormalities that have been found remained poorly defined. We analyzed the features of pericardial involvement in these patients and investigated the clinical variables associated with moderate and severe effusions. DESIGN: Prospective, clinical, and echocardiographic study. SETTING: The service of infectious diseases of a university hospital. PATIENTS: 181 consecutive patients at all stages of HIV infection. RESULTS: Only one patient (0.55%) had acute pericarditis. Seventy-five patients (41%) had an asymptomatic pericardial effusion; in 23 patients (13% of all patients), the effusion was either moderate or severe. Ten cases (5.5% of all patients) of moderate or severe effusions resulted in right atrium diastolic compression, and three of these cases (1.6% of all patients) required pericardiocentesis for the management of tamponade. Six patients (3%) presented with echogenic pericardial masses of undetermined etiology. A moderate or severe effusion was present in a greater number of patients with symptomatic HIV infection than was present in asymptomatic HIV-infected patients, respectively: 17 vs 2% (p = 0.015). The following are variables independently associated with moderate or severe pericardial effusions: heart failure (odds ratio, 20.3; p = 0.0001); Kaposi's sarcoma (odds ratio, 8.6; p = 0.01), tuberculosis (TB; odds ratio, 47.2; p = 0.0006); and other pulmonary infections (odds ratio,15.0; p = 0.02). CONCLUSIONS: Most of these moderate or severe effusions are clinically unsuspected, but they can lead to life-threatening tamponade. This fact seems to justify echocardiographic surveillance in HIV-infected patients, especially in those with heart failure, Kaposi's sarcoma, TB, or other pulmonary infections.     

80岁以上老年男性患者103例胸腔积液临床分析

目的探讨80岁以上老年男性患者胸腔积液的病因、诊断、鉴别诊断及治疗特点。方法对我科收治的资料完整的103例胸腔积液患者的临床资料进行分析。结果103例患者中良性胸腔积液72例,其中主要因肺部感染引起的胸腔积液35例,由心功能衰竭引起的胸腔积液10例,肺部感染合并心衰或肾功能不全等原因导致的胸腔积液17例,肝硬化、慢性肾功能不全引起的胸腔积液6例,结核性胸腔积液4例;恶性胸腔积液的29例中,原发病为肺癌22例,其他肿瘤7例;此外,不能明确诊断者2例。结论在老年男性患者中,肺部感染、肺部肿瘤、心功能不全是导致胸腔积液的主要原因。     

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.     

Pericardial tamponade and large pericardial effusions: causal factors and efficacy of percutaneous catheter drainage in 50 patients

In 50 patients treated from January 1998 through March 2002 for pericardial effusion and tamponade, we retrospectively investigated the efficacy of percutaneous placement of an indwelling pericardial catheter guided by 2-dimensional echocardiography and fluoroscopy. We also investigated causation. In 80% of the patients, we were able to determine specific causes through clinical, serologic, and cytologic investigation: cancer in 15 patients, chronic renal failure in 11, systemic lupus erythematosus in 2 rheumatoid arthritis in 2, Dressler syndrome in 2, tuberculosis in 1, blunt chest trauma in 1, purulent pericarditis in 1, and probably viral pericarditis in 5. No specific cause could be determined in 10 patients (20%). We did not observe any complication due to the procedure. Two patients died during hospitalization. After hospitalization, 9 patients with metastatic cancer died within 3 months. A 2nd percutaneous drainage procedure was required in 2 cancer patients. Recurrence of pericardial effusion and tamponade and the requirement of pericardiectomy occurred in 2 patients with perfusion of unknown cause and in 1 patient with perfusion due to rheumatoid arthritis. Histologic examination of pericardial tissue in patients with idiopathic disease showed fibrinous pericarditis but no causal factor. In the group with idiopathic pericardial effusion, 2 patients with multiple mediastinal lymphadenopathy underwent mediastinal exploration; biopsy revealed nonspecific lymphadenitis and fibrinous pericarditis. In patients with large pericardial effusions and tamponade, the specific cause was in most cases already known or obtained by initial clinical and laboratory investigation. Sufficient cardiac decompression was achieved by percutaneous pigtail catheter drainage.     

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.     

Rheumatic valvulitis and constrictive pericarditis. Report of case.

A 13-year-old girl was admitted with congestive heart failure, edema, ascites, and jaundice. There was an apical pansystolic murmur of mitral insufficiency and marked cardiomegaly. Her venous pressure was elevated. Despite medical treatment her condition deteriorated, hepatic and renal failure as well as disseminated intravascular coagulation ensued, leading to her death. At post mortem she was found to have rheumatic mitral valvulitis and constrictive pericarditis. The pathologic picture of pericarditis was nonspecific, but in presence of a positive skin test for tuberculosis the latter is considered to be the most likely cause of the pericarditis, nevertheless, rheumatic etiology of pericarditis in this case cannot be excluded. The presence of rheumatic heart disease and cardiomegaly may have led to the exacerbation of symptoms and signs of constrictive pericarditis and severe right heart failure.     

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.     

Pericardial windows or pericardiocentesis for pericardial effusions

The hospital records of 20 patients admitted to Parkland Memorial Hospital in Dallas with pericardial effusion during the four-year period of 1966 to 1969, and who underwent pericardiocentesis and percutaneous open pericardial windows, were reviewed. The etiologies of the effusions were as follows: purulent pericarditis (5), hypertensive and ischemic heart disease with congestive heart failure (4), and chronic idiopathic effusion (4). Specific etiologic diagnoses were made from the pericardial biopsy in only two cases (10 per cent), while 13 (65 per cent) had at least one serious complication in the postoperative period with eight (40 per cent) developing secondary infection. Twenty-one patients underwent pericardiocenteses without complications and four etiologic diagnoses (20 per cent) were made. Suggestions for indications for these procedures are presented.     

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。     

PERICARDITIS (WITH PARTICULAR REFERENCE TO TUBERCULOUS PERICARDITIS)

In this study diseases of the pericardium which dominate the clinical picture have been analysed. In essence this means a discussion of infective pericarditis. Pericarditis is a common disorder in Cape Town, South Africa, particularly among the Bantu and Cape Coloured population. The high incidence in the non-White races is attributed to tuberculosis, mainly as a result of socio-economic conditions. Tuberculosis was found to be the cause in 40% of the patients; the diagnosis was established by the finding of pericardial fluid, which gave positive results on testing for tuberculosis, positive histological evidence or adequate evidence of associated organ tuberculosis. In another 40% of patients, tuberculosis appeared to be the most likely cause of the condition, on clinical grounds which are described. Twelve per centum of cases were due to causes unknown, a tuberculous or viral cause being the most likely. In 6% of cases the pericarditis was pyogenic. A few other uncommon conditions were also present. The clinical syndromes of dry pericarditis, pericarditis with effusion and constrictive pericarditis are described. The most important symptom is a distinctive type of chest pain due to inflammation of the pericardium. The important findings are a pericardial friction rub, systemic venous hypertension and pulsus paradoxus. Sudden splitting of the second sound in inspiration is more characteristic than the early third heart sound, and occurs far more frequently. The electrocardiogram is usually abnormal, drawing attention to the heart, but not very helpful in establishing the diagnosis. The findings on X-ray examination confirm the cardiomegaly in cases of effusion and in most cases of constrictive pericarditis. A cardiac shadow of normal size was uncommonly seen, and pericardial calcification occurred in a minor proportion of the cases in this series. Cardiac catheterization and angiocardiography was seldom required to establish the diagnosis. The pericardium should be aspirated whenever an effusion is suspected, and aspiration is a safe procedure with an electrode needle under electrocardiographic control. The course of pericardial effusion and constrictive pericarditis (in 195 and 220 patients respectively) is discussed, with particular reference to tuberculosis. With tuberculous pericardial effusions from which acid-fast bacilli were recovered there was an extremely high incidence of progression of the condition to constrictive pericarditis requiring surgery. Even when the fluid was sterile, most patients developed constriction and surgery was usually required, but the rate of ultimate cure was over 90%. Of 195 patients presenting with pericardial effusion, irrespective of the cause over half developed the signs of constrictive pericarditis, and 40% required surgery. A small but significant percentage of patients, however, can pass through the phase of constriction and ultimately recover without operation. There were 220 patients with constrictive pericarditis. In 38 the process was chronic, the only effective treatment being surgical. Seventy-eight presented with active pericarditis producing constriction without effusion. Most of these required surgical treatment, but a quarter recovered on conservative therapy alone. The remaining 104 developed pericardial constriction after their disease had passed through a phase of effusion, surgery being necessary for 75%. The overall surgical results were better than the results of medical therapy, which consisted of the use of antituberculous drugs, digitalis and diuretics. Surgery has a great deal to offer in the treatment of pericarditis, but the time to recommend this procedure must be carefully chosen.