细胞因子对渗出性胸腔积液的鉴别诊断价值

胸腔积液( pleural effusion,PE)是与多种良性和恶性疾病相关的临床常见并发症.根据 Light 标准[1] ,胸腔积液可分为渗出性和漏出性,由充血性心力衰竭、肝硬化、肾病综合征等病因引起的积液常为漏出性,而渗出性积液常见于恶性肿瘤以及感染如结核导致的胸膜炎症.胸腔积液的病因学诊断是临床实践的常见问题,...     

胸腔积液检查的临床意义

胸腔积液是一种常见的临床表现,由多种疾病引起.详细的胸水分析已成为确定胸腔积液病因诊断的重要揩施之一.一、漏出液与渗出液确诊有胸腔积液后,应作胸腔穿刺抽液,首先应分析胸水是漏出液或渗出液.过去把100ml胸水内蛋白质高于3g作为判断渗出液的标准.     

消化系统疾病引起的胸腔积液

胸腔积液（pleural effusion，简称胸液或胸水）是肺、胸膜或其他许多全身疾病的常见临床表现之一。胸腔积液的病因有100多种，除常见的肺、胸膜疾患外，还可有心脏、肾脏、结缔组织病和消化系统疾病等多系统疾病引起。消化系统疾病中有肝硬化、胰腺炎、消化道恶性肿瘤、食管穿孔、腹腔内脓肿和腹部手术后等，常可累及胸膜出现胸腔积液而产生呼吸困难、咳嗽、胸痛等相应的呼吸系统症状。认识这些疾病所致的胸腔积液并发症，有助于对疾病整体的判断，关系到明确胸腔积液的病因及拟定针对性的治疗措施。本文主要详细介绍肝硬化、胰腺炎、消化道恶性肿瘤所引起的胸腔积液的诊治。     

社区获得性肺炎并发胸腔积液的治疗进展

肺炎旁胸腔积液(Parapneumonic pleural effusion,PPE)是社区获得性肺炎(Community acquired pneumonia,CAP)的常见并发症之一[1],是指与肺炎、肺脓肿或支气管扩张相关的胸腔积液。由于炎症累及胸膜所致,并排除肿瘤、结核、气胸、心力衰竭、手术等其他原因,发生率约肺炎患者的14.5%~57%[2-3]。     

心源性胸腔积液的X线分析

胸腔积液在临床上较常见，可由多种疾病引起。而各种心血管疾病所致充血性心力衰竭引起的胸腔积液是漏出性胸腔积液最常见的原因［１］。临床上心源性胸腔积液易被误诊为结核性甚至恶性胸腔积液。因此认识心源性胸腔积液的Ｘ线特点对鉴别胸腔积液的病因减少误诊具有重要临...     

心力衰竭合并胸腔积液患者的临床分析

目的：探讨心力衰竭合并胸腔积液患的特点。方法：回顾性分析42例心力衰竭合并胸腔积液患的临床及实验室资料。结果：心力衰竭合并胸腔积液共42例，16例为渗出液，26例为漏出液。26例漏出液中19例经常规抗心力衰竭治疗，治愈或好转，3例未愈，4例反复胸腔穿刺抽液；其中2例变为渗出液，加用抗生素好转，另2例未愈。16例渗出液中14例无特殊病因，1例并发于肺癌，1例发生于外科手术后；经常规抗心力衰竭治疗11例治愈或好转，2例加用抗生素后好转，3例未愈。结论：心力衰竭引起的胸腔积液可表现为渗出液。     

机械通气相关胸腔积液25例临床分析

目的研究机械通气(MV)患者并发胸腔积液的临床特点。方法观察机械通气治疗后并发胸腔积液25例患者的临床资料,分析机械通气相关胸腔积液患者的病情特点及相关因素。结果 25例发生胸腔积液的患者中14例为渗出液,病因为肺炎旁积液和肺栓塞相关胸腔积液;11例为漏出液,病因为低蛋白血症和心力衰竭。结论 MV患者行床边超声指导下的胸腔穿刺是安全的,肺炎旁积液及低蛋白血症、心衰诱发的胸腔积液是最主要的病因。     

外泌体在恶性胸腔积液中的作用及临床意义

恶性胸腔积液(Malignant pleural effusion, MPE )是胸膜腔积聚大量的渗出液,并伴有恶性细胞或肿瘤组织的存在,是转移性疾病的常见并发症,可发生在15％的癌症患者中.据统计,在美国每年约有15 万例新发 MPE 病例,欧洲每年约有10 万例[1 ].MPE 的发病机制较复杂,除与血管生成、血管...     

血清CA125测定在胸腔积液患者中的临床意义

目的检测不同原因引起的胸腔积液的血清肿瘤标志物CA125(癌胚抗原125)在胸腔积液患者中的临床价值。方法选择130例胸腔积液患者,检测所有患者血清CA125的浓度,分别按照疾病的良恶性、胸水量的大小、渗出液与漏出液分组,比较各组间患者浓度水平的差别。结果 130例胸腔积液患者中有123例血清CA125升高,阳性率为94.62%;恶性胸腔积液组与良性胸腔积液组相比血清CA125浓度有显著性差异(P0.05);大量胸腔积液组与中小量胸腔积液组、渗出液与漏出液之间相比,血清CA125浓度无显著性差异(P0.05)。结论血清CA125可作为鉴别良恶性胸腔积液的重要辅助指标,但其对量的大小及渗出液、漏出液的鉴别无临床应用价值。     

心源性胸腔积液 28 例临床分析

目的探讨心力衰竭(心衰)引起的胸腔积液的临床特点及诊治方法。方法对28例心力衰竭引起胸腔积液病人的临床资料进行回顾性分析。结果双侧胸腔积液17例占60.71%,右侧8例占28.57%,左侧3例占10.71%;小量积液16例占57.14%,中量积液10例占35.71%,大量积液2例占7.14%。胸水化验:12例抽取胸水进行化验,漏出液8例占66.67%,渗出液3例占25%,介于渗出液和漏出液间1例占8.33%。16例小量积液病人经抗心衰治疗后胸水1周内明显吸收,12例中、大量胸水则需配合胸腔引流。结论心衰引起的胸腔积液多为双侧,单侧则以右侧多见。胸水量以少量多见,多数呈漏出液,抗心衰治疗后可明显吸收。     

Rheumatoid pleural effusion

OBJECTIVES: To describe the clinical and laboratory features of rheumatoid pleural effusion (RPE) and the diagnostic and therapeutic approaches to this condition. METHODS: The review is based on a MEDLINE (PubMed) search of the English literature from 1964 to 2005, using the keywords "rheumatoid arthritis" (RA), "pulmonary complication", "pleural effusion", and "empyema". RESULTS: Pleural effusion is common in middle-aged men with RA and positive rheumatoid factor (RF). It has features of an exudate and a high RF titer. Underlying lung pathology is common. Generally RPE is small and resolves spontaneously but symptomatic RPE may require thoracocentesis. Rarely, RPE has features of a sterile empyematous exudate with high lipids and lactate dehydrogenase, and very low glucose and pH levels. This type of effusion eventually leads to fibrothorax and lung restriction. Superimposed infective empyema often complicates RPE. Oral, parenteral, and intrapleural corticosteroids, pleurodesis and decortication, have been used for the treatment of sterile RPE. Infected empyema is treated with drainage and antibiotics. CONCLUSIONS: RPE may evolve into a sterile empyematous exudate with the development of fibrothorax. Symptomatic effusions or suspicion of other causes of exudate (infection, malignancy) require thoracocentesis. The "rheumatoid" nature of the pleural exudate in patients without arthritis mandates a pleural biopsy to exclude tuberculosis or malignancy. The optimal therapy of RPE has yet to be established. The role of cytokines in the course of RPE and the possible usefulness of cytokine blockade in the treatment of this RA complication require further evaluation.     

Eosinophilic pleural effusion

Eosinophilic pleural effusion accounts for 5 to 10% of all clear liquid pleurisies. Its pathogenic significance is unclear and its relation to the causative diagnosis of pleural eosinophilia is diversely evaluated. In this study, 86 cases of eosinophilic pleural effusion observed at the Ariana Pneumophthisiology Hospital over a 5-year period are reviewed. At first aspiration, the proportion of pleural fluid eosinophils varied from 12% to 85% (54% on average). Blood eosinophilia was present in 60% of the patients. The main cause of effusion was tuberculosis (39.6%, but many other diseases were observed; despite numerous investigations, no cause could be found in 23.2% of the cases. The discovery of a pleural eosinophilia has an impact on the probable cause of the pleurisy, and this can be determined by applying Bayes' rule. The probability of tuberculous being the cause falls from 70.3% for clear liquid pleurisies generally to 44.6% for eosinophilic pleurisy. The probability of cancer as a cause falls from 4.5% to 0.66%; whereas that of "idiopathic" pleurisy rises from 13.5% to 59.56%. These findings are concordant with Adelman's conclusions. In other words, the finding of a pleural eosinophilia decreases the probability of tuberculous or malignant pleural effusion and increases the probability of benign or "idiopathic" effusion. Clinicians confronted with an eosinophilic pleural effusion should be particularly careful and accurate since this diagnosis may spare the patient an unnecessary exploratory thoracotomy and an unwarranted antituberculous treatment.     

Tuberculous pleural effusion

Tuberculous effusion is a common disease entity with a spectrum of presentations from a largely benign effusion, which resolves completely, to a complicated effusion with loculations, pleural thickening and even frank empyema, all of which may have a lasting effect on lung function. The pathogenesis is a combination of true pleural infection and an effusive hypersensitivity reaction, compartmentalized within the pleural space. Diagnostic thoracentesis with thorough pleural fluid analysis including biomarkers such as adenosine deaminase and gamma interferon achieves high accuracy in the correct clinical context. Definitive diagnosis may require invasive procedures to demonstrate histological evidence of caseating granulomas or microbiological evidence of the organism on smear or culture. Drug resistance is an emerging problem that requires vigilance and extra effort to acquire a complete drug sensitivity profile for each tuberculous effusion treated. Nucleic acid amplification tests such as Xpert MTB/RIF can be invaluable in this instance; however, the yield is low in pleural fluid. Treatment consists of standard anti‐tuberculous therapy or a guideline‐based individualized regimen in the case of drug resistance. There is low‐quality evidence that suggests possible benefit from corticosteroids; however, they are not currently recommended due to concomitant increased risk of adverse effects. Small studies report some short‐ and long‐term benefit from interventions such as therapeutic thoracentesis, intrapleural fibrinolytics and surgery but many questions remain to be answered.     

Myelomatous pleural effusion

Pleural effusion due to myelomatous involvement is rare. We are describing such a case who also had soft tissue extension from iliac bone with congestive heart failure.