胸膜和胸膜腔的解剖和生理功能的研究

一、胸膜和胸膜腔的解剖胸膜 (ｐｌｅｕｒａ)分脏、壁两层 ,脏层胸膜被覆在肺的表面 ,壁层胸膜衬附胸壁内面、纵隔的外侧面和横膈的上面 ,两层胸膜在肺门根部移行汇合 ,包绕而成胸膜腔。左、右两侧胸膜腔是完全独立闭合而不是互相沟通的 ,籍此可避免一侧胸膜腔的病变迅速累及另一侧。正常成人胸膜表面积约有2 0 0 0ｃｍ2 ,胸膜腔的宽度大约为 18～ 2 0 μｍ ,基底部的宽度略增加。虽然曾有争论 ,但现已清楚 ,两层胸膜并不互相接触 ,因此Ｍｕｒｒａｙ等[1] 认为胸膜腔是一个真正的 ,而不是潜在的腔。无论是壁层或脏层胸膜均为平滑光亮的半透…     

老年人心源性胸腔积液的诊治进展

<正>慢性充血性心力衰竭是胸腔积液的常见原因,而且部分患者以胸腔积液为首发症状。随着人口老龄化,糖尿病、心血管疾病的增多,老年人心源性胸腔积液的发生呈增多趋势,且易被误诊、误治。若不能做出迅速、正确的诊断,患者将要面临不必要的检查及治疗,增加经济负担,延误最佳治疗时机。1发病机制胸膜腔是位于肺和胸壁之间一个潜在的腔隙,在正常情况下脏层胸膜和壁层胸膜表面上有一层很薄的液体,约3～15 ml,在呼吸运动中起润滑作用。正常情况下,胸膜腔内的     

胸膜疾病的病因和发病机制

在后天获得性胸膜疾病中胸腔积液是最常见的胸膜疾病 ,现仅就其病因和发病机制分述如下。一、渗出液病因及发病机制[1]1 感染性胸腔积液 :肺炎旁积液若符合下述条件即可诊断为脓胸 :(1)脓细胞存在 ;(2 )革蓝染色有细菌存在 ;(3)ｐＨ <7 0 ;(4 )糖 <2 2ｍｍｏｌ/Ｌ)。结核性胸膜炎 ,霉菌病、寄生虫病、非典型肺炎、膈下脓肿、肝脓肿、脾脓肿、自发性食道破裂及罕见的肝炎等均可为感染性胸腔积液的病因。感染性胸腔积液发病机制[2 ] :Ｂｒｏａｄｄｕｓ用麻醉的羊证实胸膜腔滴入无菌液 ,其淋巴管的清除能力比正常清除液体能力增加 2 8倍。但对…     

肺下积液

肺下积液乃指液体积聚于肺底与膈上之胸膜腔内,立位胸透或胸片显示类似膈肌升高之阴影。肺下积液的病因概括如下:①感染性:肺结核、肺炎、肺脓肿、膈下脓肿穿破所致之脓胸;②变态反应性:系统性红斑狼疮、类风湿性关节炎等;③肿瘤性:支气管癌胸膜转移、胸膜间皮瘤、淋巴瘤、纵隔肿瘤;④周身性疾病:急性风湿性心脏病、肝硬化、高血压及动脉硬化性心脏病并发心力衰竭、     

脓胸的外科治疗

脓胸处理的最佳方法一直存有争议。“成熟”脓胸的发病可分为几个阶段,每阶段均有其相应的治疗方法.肺部炎症引起的脏层胸膜及淋巴管郁滞阻塞,导致胸膜腔积液,此时也可因操作不当导致医源性脓胸,由肺进入胸膜腔的微生物是引起脓胸最多见的原因,对胸膜的持续刺激不仅可产生胸水,也可使胸膜水肿、增厚。胸水中的纤维蛋白可形成凝块,将脓液     

胸膜疾病的研究进展

近年来 ,胸膜疾病的研究已取得进展 ,例如美国胸科医师协会主办的网站上相关文献就增加了 4倍。尽管如此 ,有关胸膜疾病的诊断和治疗仍有许多问题没有解决 ,缺乏前瞻性对照研究。1　有关胸腔积液形成机制的新理论 [1]传统观点认为 :胸液是从壁层胸膜进入 ,脏层胸膜吸收的 ,胸液的形成是由于壁层与脏层胸膜之间的静水压、胶体渗透压和胸膜腔内负压的压力差改变。近年提出与传统观点不同的新理论认为 :胸液从体循环支配的壁层胸膜上的毛细血管滤过进入胸腔 ,然后经壁层胸膜上的淋巴管微孔重吸收 ,淋巴管泵的作用可产生静水负压 ,故胸腔的淋巴…     

胸腔穿刺别针胸腔引流并腔内注药治疗结核性胸腔积液的护理

1998～ 1999年 ,我院采用胸腔穿刺别针胸腔引流并腔内注药治疗 84例结核性胸膜炎 (均为渗出性 ) ,效果良好。临床资料 :本组男 6 4例 ,女 15例 ;年龄 5～ 76岁。胸膜腔大量积液 (>5 0 0 ml) 2 2例 ,中量积液 (2 0 0～ 5 0 0 ml) 19例 ,小量积液 (>2 0 0 ml) 19例。治疗方法 :以 B超确定穿刺位点 ,用 2 %碘酊局部皮肤消毒 ,75 %酒精脱碘 ,消毒范围直径为 10～ 15 cm,指示点处进针至胸膜腔 ,为避免损伤脏层胸膜引起气胸危险 ,顺肋间按压针尾 ,使针头斜面向胸膜腔 ,针体用无菌纱布包好贴近胸壁并用胶布固定抽出胸水。每次尽量抽净并根据患者情…     

胸膜X线改变在中心型肺癌诊断中的价值

目的探讨中心型肺癌伴胸膜改变的X线表现以及其在临床诊断中的应用价值。方法随机抽取我院1997～2006年间确诊中心型肺癌并伴有胸膜形态改变的住院患者50例,进行回顾性分析。结果中心型肺癌伴胸膜改变的X线表现以胸膜条状增厚,叶间裂弧形移位,胸膜局部丘状肥厚以及中大量胸膜腔积液为主。结论经手术后取近胸膜肺组织切片观察,X线下的胸膜增厚并非胸膜本身真正的增厚,而是由于段或叶的肺不张,使局部肺体积缩小,引起胸膜腔内负压增大,胸膜腔内液体增多,在虹吸作用下积存于不张的肺叶或肺段的周围,在X线表现下类似胸膜增厚。当有肺门肿块形成时,由于肺段或肺叶不完全性不张,叶间裂在移位过程中受肺门阻挡而表现为弧心性移位。而肺癌的胸膜转移灶则表现为胸膜的局部丘状突起和胸膜腔内的中大量积液,胸膜腔内的积液常常遮盖肺内改变与胸膜转移灶。并且此时患者因胸膜转移已失去手术机会。     

双侧胸腔积液的老年左心衰患者4例

双侧胸腔积液的老年左心衰患者４例王惠政１王竹芬２（１宁波市第一医院宁波３１５０１０２绍兴市第二医院绍兴３１２０００）关键词心力衰竭；胸膜腔积液；老年人左心功能不全时，心肌收缩力减弱，心输出量减少，左室舒张末压力增加，导致肺静脉压增高，胸液的正常回流受...     

双侧胸腔积液的老年左心衰患者4例

双侧胸腔积液的老年左心衰患者４例王惠政１王竹芬２（１宁波市第一医院宁波３１５０１０２绍兴市第二医院绍兴３１２０００）关键词心力衰竭；胸膜腔积液；老年人左心功能不全时，心肌收缩力减弱，心输出量减少，左室舒张末压力增加，导致肺静脉压增高，胸液的正常回流受...     

分子生物学假阳性致肺癌性淋巴管炎误诊为肺结核的临床诊治过程分析

2019年4月17日,武汉市肺科医院呼吸科收治1例69岁男性因外院结核分子生物学阳性诊断为肺结核的肺癌性淋巴管炎患者。该患者因“发现肺部阴影3个月,间断咳嗽2个月”入院。既往有结肠癌病史。胸部CT扫描显示双肺弥漫性沿支气管血管束分布结节伴磨玻璃影,伴小叶间隔增厚,双肺门及纵隔淋巴结肿大,双侧胸腔积液,在外院行肺泡灌洗液(BALF)GeneXpert MTB/RIF(简称“ GeneXpert”)检出MTB(极低)及TB-PCR检出MTB,诊断为肺结核,转诊至武汉市肺科医院。入院后完善结核相关检查,PPD皮肤试验阴性,γ干扰素释放试验阴性,胸部CT影像学特征不符合肺结核改变,临床怀疑BALF结核病病原分子生物学检测假阳性,建议患者复查BALF、GeneXpert及经气管镜超声引导针吸活检术(EBUS-TBNA),患者拒绝。给予诊断性胸腔穿刺,抽出胸腔积液20ml,送检显示,癌胚抗原(118.4μg/L)明显升高,提示恶性胸腔积液;最后行内科胸腔镜胸膜活检,提示转移性低分化腺癌,结合胸部CT表现,诊断为肺癌性淋巴管炎。患者后因病情恶化死亡。笔者认为,影像学表现为沿支气管血管束分布结节伴小叶间隔增厚及纵隔淋巴结肿大时需鉴别肺癌性淋巴管炎。影像学表现与肺结核不相符时,分子生物学阳性诊断肺结核需谨慎,以避免误诊误治。     

A case of Mycobacterium avium pulmonary disease accompanied with pleural effusion

Nontuberculous mycobacterial infection is seldom complicated with pleural involvement. We report a very rare case of M. avium pulmonary disease accompanied with pleural effusion. A 76-year-old man was admitted to our hospital because of cough and low-grade fever. A chest radiograph and computed tomograph showed centrilobular nodules in the right middle lobe and left lingula, and right pleural effusion. The patient had had a right spontaneous pneumothorax 50 days before his admission. The sputum smear was negative for acid fast bacilli. The smear of pleural effusion was positive for acid fast bacilli, the level of adenosine deaminase in the effusion was markedly elevated, and pleural effusion was positive for M. avium as assessed by polymerase chain reaction (PCR). The pleural biopsy specimen showed fibrous change without granuloma, while the transbronchial biopsy specimen showed noncaseous epithelioid granulomas. We considered that the pneumothorax was caused by the spread of pulmonary M. avium infection to the visceral pleura with its perforation.     

肺淋巴管癌病

目的探讨肺淋巴管癌病（ＰＬＣ）的临床特征，分析相关诊断方法的特点，提高对ＰＬＣ的认识及其诊断水平。方法结合文献资料回顾分析４例临床病例。结果ＰＬＣ在临床上主要表现为咳嗽、气短；肺功能呈正常或限制性通气功能障碍；Ｘ线胸片常见双肺弥漫性网状、网状结节状或结节状等间质纤维样改变，并合并胸腔积液、高分辨ＣＴ可发现小叶间隔的不均匀增厚，不均一的支气管血管束结节状增厚，胸膜不规则增厚，纵隔淋巴结肿大等；胸膜肺组织病理可见胸膜下、肺内淋巴管内癌细胞生长。结论对双肺呈类间质纤维化改变，同时合并胸腔积液和纵隔淋巴结肿大的患者，应进一步行高分辨ＣＴ及胸膜肺组织病理活检，以期排除ＰＬＣ之诊断。     

A case of essential thrombocythemia with pulmonary hypertension and bilateral pleural effusions

A 79-year-old woman was admitted with general fatigue. Chest roentgenogram showed diffuse reticular shadows and bilateral pleural effusion. Peripheral blood studies revealed an elevation of platelet count (203.3 X 104/mm3). The case was diagnosed as essential thrombocythemia and treated with ACNU. The platelet count decreased. Bilateral pleural effusions increased gradually and their characteristics changed from bloody exudate to transudate. Biopsy of her pleura and thoracoscopy were carried out without significant results. Later, systemic edema, which suggested right heart failure, developed. The diagnosis of pulmonary hypertension and right heart failure was made by echocardiogram and right cardiac catheterization. Because perfusion scan of the lung revealed some perfusion defects, complication of pulmonary embolism was suspected. Bilateral pleural effusion and pulmonary artery pressure decreased with treatment by nifedipine, furosemide and isosorbide dinitrate. This is the first case report of essential thrombocythemia, pulmonary hypertension, right heart failure and bilateral pleural effusion.     

Physiology and pathophysiology of pleural fluid turnover.

Tight control of the volume and composition of the pleural liquid is necessary to ensure an efficient mechanical coupling between lung and chest wall. Liquid enters the pleural space through the parietal pleura down a net filtering pressure gradient. Liquid removal is provided by an absorptive pressure gradient through the visceral pleura, by lymphatic drainage through the stomas of the parietal pleura, and by cellular mechanisms. Indeed, contrary to what was believed in the past, pleural mesothelial cells are metabolically active, and possess the cellular features for active transport of solutes, including vesicular transport of protein. Furthermore, the mesothelium was shown, on the basis of recent experimental evidence, both in vivo and in vitro, to be a less permeable barrier than previously believed, being provided with permeability characteristics similar to those of the microvascular endothelium. Direct assessment of the relative contribution of the different mechanisms of pleural fluid removal is difficult, due to the difficulty in measuring the relevant parameters in the appropriate areas, and to the fragility of the mesothelium. The role of the visceral pleura in pleural fluid removal under physiological conditions is supported by a number of findings and considerations. Further evidence indicates that direct lymphatic drainage through the stomas of the parietal pleura is crucial in removing particles and cells, and important in removing protein from the pleural space, but should not be the main effector of fluid removal. Its importance, however, increases markedly in the presence of increased intrapleural liquid loads. Removal of protein and liquid by transcytosis, although likely on the basis of morphological findings and suggested by recent indirect experimental evidence, still needs to be directly proven to occur in the pleura. When pleural liquid volume increases, an imbalance occurs in the forces involved in turnover, which favours fluid removal. In case of a primary abnormality of one ore more of the mechanisms of pleural liquid turnover, a pleural effusion ensues. The factors responsible for pleural effusion may be subdivided into three main categories: those changing transpleural pressure balance, those impairing lymphatic drainage, and those producing increases in mesothelial and capillary endothelial permeability. Except in the first case, pleural fluid protein concentration increases above normal: this feature underlies the classification of pleural effusions into transudative and exudative.     

A histopathological study of 102 autopsy cases of primary lung cancer with respect to pleural carcinomatosis

Visceral pleural lesions in primary lung cancer were studied histopathologically in 102 autopsy cases. Pleural carcinomatosis was defined as the presence of cancer cells in the visceral pleura and/or pleural space. Ipsilateral and contralateral pleural carcinomatosis in the primary lung cancer were compared. They were found to be similar in that both were closely related with cancer cell infiltration of blood vessels in the lung parenchyma, lymphangiosis carcinomatosa in the lung parenchyma and multiple extrathoracic organ metastases. However, differences were observed. In the ipsilateral visceral pleura, cancer cells were thought to infiltrate the interstitium in the vascular layer of the visceral pleura from lymphatic vessels in the vascular layer of the visceral pleura with the following frequency; 3.6:8.52:6.52:1. In the contralateral visceral pleura, however, cancer cells were thought to infiltrate the interstitium in the vascular layer of the visceral pleura from lymphatic vessels in the vascular layer of the visceral pleura, the pleural space, the subpleural lung parenchyma and blood vessels in the vascular layer of the visceral pleura with the following frequency; 4:1.9:12.25:1. Disruption of the elastic layer of the visceral pleura was also studied. Twenty-eight of 66 pleural carcinomatosis cases showed no disruption of the elastic layer, and greater than 1-mm disruption was found in only 7 cases. The author thought that the disruption in these few cases was related to the manner of cancer-cell infiltration of the visceral pleura. When cancer cells spread to the visceral pleura from the lung parenchyma, they lost intercellular adhesiveness in four adenocarcinoma cases. Thus we suspected that cancer cells lost intercellular adhesiveness and became single cells or small cancer nests when infiltrating the visceral pleural from the lung parenchyma, and single cells or small cancer nests entered through the elastic layer of the visceral pleura. Therefore only small disruptions are found in the visceral pleura of pleural carcinomatosis cases.     

A case of pulmonary sarcoidosis with pneumothorax and pleural effusion after improvement of pulmonary impairment]

A 23-year-old man was admitted to our hospital for a complete medical evaluation of abnormal pulmonary shadows found on a chest radiograph during his annual check-up. Chest radiography and chest CT showed a diffuse spread of micronodules in both lung fields and mediastinal lymphadenopathy. A transbronchial lung biopsy demonstrated evidence of noncaseating epithelioid cell granuloma with multinucleated giant cells, and a diagnosis of sarcoidosis was made. The pulmonary shadows improved without therapy. Twenty months later, the patient was readmitted to the hospital because of chest pain and dyspnea. Pneumothorax appeared on the right in a chest radiograph, but subsided after drainage therapy, and two weeks later, a right side pleural effusion was seen. We determined that the pleura was involved in the sarcoidosis, and the patient was treated with oral prednisolone 20 mg daily. The pleural effusion gradually subsided. This is the first reported case in Japan of pulmonary sarcoidosis with pneumothorax and pleural effusion after improvement of pulmonary impairment.     

Routine Echocardiographic Views Miss Significant Pleural Effusions

Objectives: To determine the benefit of adding chest scanning to the routine echocardiographic examination to diagnose pleural effusions. Background: Pleural effusions are common in several cardiac disorders, yet routine echocardiography is insensitive in delineating pleural fluid. Methods: Bilateral chest scanning was performed in addition to the routine echo examination in 100 consecutive inpatients referred for echocardiography with recent chest X rays (CXRs). Detection and quantification of pleural effusion by sonographic chest scanning was compared blindly with CXRs. Identification of pleural fluid was analyzed for correlation with clinical diagnosis of congestive heart failure (CHF) and elevated pulmonary artery pressures if found by echo-Doppler examination. Results: Agreement on presence or absence of pleural effusion occurred in 88 of 100 patients—in 5 patients bilateral chest scanning detected pleural effusion with negative CXRs; in 7 patients CXRs suggested pleural effusion with negative bilateral chest scanning (all 7 patients had minor blunting of the costophrenic angle). Routine echo views only detected 22 of 51 patients (43%) with pleural effusion detected by bilateral chest scanning. In 45 patients with CHF, 29 (64%) had pleural effusion by bilateral chest scanning (25 bilateral, 1 left, 3 right) vs 12 (27%) by routine echo (only left pleural effusion seen). Ejection fraction and estimated pulmonary artery pressure did not differ between CHF patients with and without pleural effusion. Conclusions: Routine echocardiographic views underestimate the presence of pleural effusion in patients referred for study. Bilateral chest scanning is equal to CXRs for pleural effusion detection and provides clinically useful information which may be of particular benefit to patients with CHF.     

Unilateral pulmonary edema after talc pleurodesis

Talc is commonly given after drainage of the pleural space to create pleural symphysis. Recognized complications of pleural drainage followed by talc pleurodesis include reexpansion pulmonary edema, pneumonia, and adult respiratory distress syndrome. This report describes a complication of talc pleurodesis that appears not to have been appreciated previously. Chest radiographs obtained before and after talc pleurodesis were evaluated in a total of 108 patients in three groups; 89 of these patients were receiving palliative therapy for malignant pleural effusion. Approximately 16% of the 108 patients developed a transient interstitial process in the lung ipsilateral to the treated pleural space. The recognized complications are inadequate to account for these radiographic findings. Other interstitial diseases such as hydrostatic pulmonary edema and lymphangitic carcinomatosis also are not adequate explanations. The observed complication is most likely the result of endothelial damage leading to a capillary leak type of pulmonary edema.     

Primary malignant mesothelioma of the pericardium masquerading as malignant pleural mesothelioma: report of an autopsy case and review of the reported cases in Japan as to its invasion to neighboring organs

The Patient was a 72-year-old man who presented with dyspnea and general fatigue. Chest X-ray and CT-scan at the admission showed bilateral pleural effusion with collapse of the left lung and pericardial effusion. Cytology from the left pleural effusion suggested malignant mesothelioma. For this reason, malignant mesothelioma of the left pleura was diagnosed clinically and it was supposed to have spread subsequently to the pericardium. At autopsy, entire surface of the heart was found to be encroached in a diffuse fashion by a thick layer of mesothelioma tissues, which formed a small mass around the left pulmonary vein over the left atrium and invaded deep into the myocardium of all cardiac chambers. The endocardium and the intima of the left pulmonary vein were free of the invasion. The parietal pericardium adhered in places to the cardiac lesion, but no direct invasion to the adjacent pleurae through the pericardial wall was present. The left pleura over the lung and chest cavity disclosed only a superficial invasion by similar mesothelioma which was identifiable only on microscopic study. No distant metastasis was present in any thoracic and other organs as well as lymph nodes including the hilar ones of the lung. It seemed most likely from this anatomical finding that the primary site of the present mesothelioma was in the pericardium (visceral) and the tumor spread to the left pleura by a continuous extension along the outside of the left pulmonary vein. Primary malignant mesothelioma of the pericardium is of very rare occurrence and we found only 51 cases of it in the Japanese literature since 1915.(ABSTRACT TRUNCATED AT 250 WORDS)