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中国防痨杂志, 2022, 44(9): 880-897 doi: 10.19982/j.issn.1000-6621.20220257

指南·规范·共识

结核性胸膜炎超声诊断、分型及介入治疗专家共识(2022年版)

中华医学会结核病学分会超声专业委员会, 中国医师协会介入医师分会超声介入专业委员会单位

Expert consensus on ultrasound diagnosis, classification and interventional therapy of tuberculous pleurisy (2022 Edition)

Ultrasound Professional Committee of Tuberculosis Branch of Chinese Medical Association, Interventional Ultrasound Professional Committee of Interventional Physician Branch of Chinese Medical Doctor Association Danwei

通信作者: 黄毅,Email: huang-yi-1980@163.com;左蕾,Email: zuolei0221@163.com;于铭,Email: yumingfmmu@126.com

责任编辑: 郭萌

收稿日期: 2022-07-12  

基金资助: 陕西省重点研发项目(2021SF-015)
陕西省两链融合重点专项(2021LL-JB-06)
西安市创新能力强基计划(21YXYJ0003)

Corresponding authors: Huang Yi, Email: huang-yi-1980@163.com;Zuo Lei, Email: zuolei0221@163.com;Yu Ming, Email: yumingfmmu@163.com

Received: 2022-07-12  

Fund supported: Key Research and Development Project of Shaanxi Province(2021SF-015)
Shaanxi Provincial Key Project of Two Chain Integration(2021LL-JB-06)
Innovation Capacity and Strengthening Basic Disciplines Plan of Xi’an(21YXYJ0003)

摘要

结核性胸膜炎是结核分枝杆菌侵犯胸膜腔发生高强度变态反应引起的胸膜炎症,属于肺结核的一种,临床现阶段认为是渗出性胸腔积液产生的最主要原因之一。结核性胸膜炎未经及时有效的诊断及治疗,可导致严重通气功能障碍及肺功能损害。胸部超声目前是结核性胸膜炎诊断及评估的首选影像学方法,超声引导下胸膜穿刺活检获得病原学和病理组织学阳性证据是结核性胸膜炎确诊的标准之一,依据超声不同征象对结核性胸膜炎进行分型及治疗,可有效提高治愈率,减少并发症,降低复发率。由于不同医院和检查者之间的检查方法、诊断结果及治疗方案存在一定差异,不利于结核性胸膜炎患者的综合管理。因此,本共识介绍了超声引导下胸膜穿刺活检、结核性胸膜炎超声分型及不同分型的临床介入治疗,旨在针对不同病程分期的结核性胸膜炎患者进行精准化、规范化、合理化的超声诊疗。

关键词: 结核,胸膜; 活组织检查; 超声检查,介入性; 指南

Abstract

Tuberculous pleurisy is pleural inflammation caused by delayed hypersensitivity response when Mycobacterium tuberculosis invades the pleural cavity. It is a kind of pulmonary tuberculosis, which is considered to be one of the main causes of exudative pleural effusion in clinic. Without timely and effective diagnosis or treatment, tuberculous pleurisy can lead to severe ventilatory dysfunction and pulmonary function damage. At present, chest ultrasound is the preferred imaging method for the diagnosis and evaluation of tuberculous pleurisy. One of the diagnostic criteria of tuberculous pleurisy is to obtain positive etiology or positive histopathology through ultrasound-guided pleural puncture biopsy. Classification and corresponding treatment of tuberculous pleurisy according to different ultrasound images can effectively improve the cure rate, reduce adverse complications and reduce the recurrence rate. Due to the differences in examination methods, diagnostic results and treatment between different hospitals and examiners, it is not conducive to the comprehensive management of patients with tuberculous pleurisy. Therefore, this consensus introduces ultrasound-guided pleural puncture biopsy, ultrasound classification of tuberculous pleurisy and clinical treatment of different types, aiming to provide precise, standardized and rational ultrasound diagnosis and treatment for tuberculous pleurisy patients at different stages.

Keywords: Tuberculosis,pleural; Biopsy; Ultrasonography,interventional; Guidebooks

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本文引用格式

中华医学会结核病学分会超声专业委员会, 中国医师协会介入医师分会超声介入专业委员会单位. 结核性胸膜炎超声诊断、分型及介入治疗专家共识(2022年版). 中国防痨杂志, 2022, 44(9): 880-897. Doi:10.19982/j.issn.1000-6621.20220257

Ultrasound Professional Committee of Tuberculosis Branch of Chinese Medical Association, Interventional Ultrasound Professional Committee of Interventional Physician Branch of Chinese Medical Doctor Association Danwei. Expert consensus on ultrasound diagnosis, classification and interventional therapy of tuberculous pleurisy (2022 Edition). Chinese Journal of Antituberculosis, 2022, 44(9): 880-897. Doi:10.19982/j.issn.1000-6621.20220257

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结核病是由结核分枝杆菌感染引起的慢性传染性疾病,结核性胸膜炎(tuberculous pleurisy)是由结核分枝杆菌直接感染和(或)胸膜对结核分枝杆菌菌体成分产生迟发型变态反应而发生的炎症,也是胸腔积液产生的主要原因之一[1-3]。我国结核性胸膜炎占所有结核病患者的6.5%~8.7%,其导致的积液含大量纤维蛋白和降解产物,未经及时和有效治疗可导致胸膜增厚、粘连,甚至包裹,最终导致严重通气功能障碍及肺功能损害[3-4]。结核性胸膜炎目前主要由影像学检查、实验室检查及组织病理学活检等多种方法进行临床诊断[5],治疗主要采用抗结核药物、胸腔置管引流、注射尿激酶及外科手术等方式[4,6],但因结核性胸膜炎起病隐匿、病程缓慢,虽然有多种诊断及治疗方式,但针对不同病程分期的结核性胸膜炎,目前仍缺乏简便、有效且规范和标准的诊断、分型及治疗方法[7-8]

胸部超声是临床最常用的结核性胸膜炎的影像学检查方法,能够准确评估胸腔积液及胸膜病变情况[9]。超声引导下胸膜穿刺活检对结核性胸膜炎具有较高的取材成功率和病理诊断率,且操作简单、并发症少[10]。依据胸部超声的不同表现对结核性胸膜炎进行的分型与病理分型存在较好的一致性[11],且基于此分型基础上采用相应的临床治疗方法,可快速、有效缓解患者临床症状,减少并发症,降低复发风险[3,12],为不同病程分期的结核性胸膜炎的规范化和标准化的诊断、分型及治疗提供有效依据。

本共识基于既往相关指南、共识及大量临床研究文献的总结,详细介绍了结核性胸膜炎超声检查、超声引导下胸膜穿刺活检、超声诊断分型及相应临床治疗的方法和建议,由中华医学会结核病学分会超声专业委员会和中国医师协会介入医师分会超声介入专业委员会结核病的相关专家讨论并制定,以促进结核性胸膜炎超声影像学专业诊疗技术的提高和规范化,进而有效推动全国结核性胸膜炎的超声诊断、分型及介入治疗工作的有序进行。

结核性胸膜炎概述

一、结核性胸膜炎定义

结核性胸膜炎是由于结核分枝杆菌直接感染和(或)胸膜对结核分枝杆菌菌体成分产生迟发型变态反应而发生的炎症[2-3],分为干性胸膜炎和渗出性胸膜炎。干性胸膜炎又称为纤维素性胸膜炎,病变多局限于脏层胸膜,胸膜表面粗糙而无光泽,一般无渗液或者很少有渗液,通常无明显的影像表现;渗出性胸膜炎主要表现为少量或中-大量的胸腔游离积液,或存在于胸腔任何部位的局限积液, 吸收缓慢者常合并胸膜增厚粘连,甚至演变为胸膜结核瘤及脓胸等[13]

二、结核性胸膜炎病因

1. 主要病因:(1)结核分枝杆菌感染:由结核分枝杆菌通过各种途径到达胸膜致病,可并发于原发性肺结核、继发性肺结核及肺外结核等(如肋骨、椎体结核及腹腔结核);(2)机体变态反应:迟发型高强度变态反应引起胸膜炎症[7]

2. 危险因素:(1)结核病患者密切接触史;(2)免疫功能低下[因劳累、紧张或合并糖尿病、人类免疫缺陷病毒(HIV)感染等][14]

三、结核性胸膜炎发病机制

结核性胸膜炎确切的发病机制尚不完全清楚,主要有两种学说[3,15]:

1. 结核分枝杆菌侵犯胸膜:结核分枝杆菌侵犯胸膜是引起结核性胸膜炎的主要发病机制。结核分枝杆菌通过直接蔓延、淋巴转移,以及血行播散3种途径侵犯胸膜。(1)邻近胸膜的结核病灶破溃,使结核分枝杆菌或结核感染的产物直接进入胸膜腔内;(2)肺门淋巴结结核的结核分枝杆菌经淋巴管逆流至胸膜;(3)急性或亚急性血行播散性结核导致胸膜炎。

2. 迟发型变态反应:胸膜对结核分枝杆菌分泌的毒素产生很强的炎性反应及渗出形成免疫损伤。(1)炎症反应导致毛细血管通透性增加,使得血浆蛋白进入胸膜腔,蛋白增加刺激胸膜产生更多胸腔积液;胸膜炎症引起胸膜壁层淋巴管水肿或阻塞,导致胸腔积液回流障碍;(2)炎症细胞反应期主要以大量中性粒细胞为主,随后胸腔积液中巨噬细胞和T淋巴细胞逐渐增多,并逐步发展为慢性炎症,细胞释放腺苷脱氨酶直至胸膜大量肉芽肿形成[2,7]

四、结核性胸膜炎临床表现

1. 结核性胸膜炎常见临床表现:结核性胸膜炎患者通常以急性或亚急性起病,主要表现为胸腔积液所致的局部症状及结核中毒的全身症状。局部症状主要表现为胸痛(75%)、干咳(70%~75%)和呼吸困难(50%)。全身症状主要表现为午后及夜间低热、畏寒、疲乏无力、饮食不佳、盗汗和体质量降低等[7,16 -17]

2. 结核性胸膜炎的并发症:结核性脓胸、胸膜增厚或纤维化、胸壁及肋骨结核性脓肿、乳糜胸及液气胸[7],大多数结核性脓胸会引起胸膜增厚、钙化及肺不张,最终导致严重限制性通气功能障碍。

五、结核性胸膜炎诊断标准

选择适宜的诊断技术对结核性胸膜炎的诊断及早期治疗至关重要[18]。目前,常用的诊断方法包括胸腔积液常规检查、病原学检查和生化指标检查,以及细胞免疫学诊断技术、分子诊断技术和超声引导下胸膜穿刺活检技术等。在临床诊疗过程中,需要将患者的临床症状和多种检查方法有效联合,以提高诊断效能。

结核性胸膜炎的诊断标准[13]:(1)确诊患者:胸腔积液或胸膜活检标本培养阳性,菌种鉴定为结核分枝杆菌,或胸膜活检组织符合结核改变;(2)临床诊断患者:影像学检查显示胸腔积液,积液为渗出液、腺苷脱氨酶升高,同时具备以下任意一项:①结核菌素纯蛋白衍生物(PPD)皮肤试验中度阳性或强阳性;②γ-干扰素释放试验阳性;③结核分枝杆菌抗体阳性。

六、结核性胸膜炎治疗方法

1. 化学治疗:抗结核药物化学治疗是结核性渗出性胸膜炎的主要治疗方法,需要遵循早期、联合、适量、规律、全程 5 项基本原则。结核性渗出性胸膜炎的治疗方案为2H-R-Z-E/7H-R-E(H:异烟肼;R:利福平;Z:吡嗪酰胺;E:乙胺丁醇)。对于重症患者,继续期适当延长3个月,治疗方案为2H-R-Z-E/10H-R-E;治疗期间一旦发现耐药,则按耐药方案进行治疗[4]。若持续治疗导致出现多种药物不良反应,需及时根据患者情况调整治疗剂量[19]

2. 胸腔介入治疗:胸腔穿刺抽液和/或置管引流,可促进患者胸腔积液消失,减少胸膜肥厚等并发症,降低复发风险[20-21]。同时,联合尿激酶或链激酶胸腔注入治疗,能够有效促进纤维蛋白溶解,降低积液中纤维蛋白含量,预防胸膜粘连[22-23]

3. 胸腔镜治疗:对于包裹性胸膜炎及结核性脓胸,胸腔镜胸膜剥脱术治疗具有创伤小、手术视野好及术后恢复快等优点[24],目前在临床手术中得到了较好的应用[25-26],能够有效改善患者肺功能。

4. 外科手术:对于机化期结核性脓胸、胸膜增厚严重的慢性包裹性胸膜炎,或合并其他并发症,如支气管胸膜瘘、慢性结核性脓胸等行外科手术治疗[27-28],可以有效改善患者临床症状,快速恢复肺功能。

胸部超声检查准备

一、超声仪器设备

1. 探头选择:基于对胸腔组织结构的观察与测量,需优化二维灰阶超声图像分辨率,尽量采用最小检测深度和尽可能高的超声波发射频率;建议采用凸阵探头(频率1~5MHz)与线阵高频探头(频率5~12MHz)相结合,清晰完整显示胸壁及肺内病变的特征[29-31]

2. 设备调节:(1)凸阵探头二维灰阶超声图像帧频为24~42帧/s,灰度为14~63,机械指数为0.8~1.3;彩色多普勒血流成像的帧频为14~30帧/s;焦点调至视野感兴趣区。选用适当的超声发射频率、增益、动态范围及灰阶彩色编码,清晰显示和识别胸腔组织结构。(2)高频线阵探头二维灰阶超声图像帧频为14~35帧/s,灰度为12~66,机械指数为0.5~1.3;彩色多普勒血流成像的帧频为14~30帧/s;焦点调至视野感兴趣区。

3. 超声测量参数单位:距离为cm或mm;面积为cm2;频谱及血流速度为cm/s;时间为ms;容积为ml;压力阶差为mm Hg。建议每一个参数应测量3次,取平均值。

4. 超声基本检查技术特征描述:(1)二维灰阶超声进行胸壁、胸腔、肺内组织及病灶的观察,结构径线的测量和相关解剖结构运动状态及功能的评估。(2)彩色多普勒血流成像是定性或半定量观测胸部组织和病变血流起始和终点、血流速度、血液流经路径和分布,以及血流状态的技术方法。(3)脉冲频谱多普勒超声是观察和测量胸部组织和病变内血流速度频谱、阻力指数等参数的技术方法。

二、患者检查准备

1. 体位:患者一般取坐位,检查背侧胸部时,患者背部转向操作者,检查时双臂交叉抱于胸前(将肩胛骨最大化向两侧移动,暴露最大扫查面积),躯干略向前倾斜(肋间隙距离最大化)时进行;检查侧胸部时,患者双臂举到头顶[32],侧胸部面向操作者,或取半仰卧位(左侧卧位扫查右侧,右侧卧位扫查左侧);检查前胸部时,患者双臂自然下垂,面向操作者。重症或患者体位受限时取平卧位、侧卧位或仰卧位检查[33]

患者采用不同体位(双臂下垂或交叉抱于胸前)会影响侧胸部及后背部肋间隙的位置。因此,对于超声定位后临床操作胸腔介入穿刺或置管引流的患者,请务必在同一体位下进行定位及穿刺,防止因体位不同引起定位点位置的偏差,造成临床穿刺失败或并发症的出现。

2. 呼吸:为排除呼吸对超声测量的影响,获取图像前应尽可能于平静呼气末进行观察及测量[34]。当胸腔积液为中-大量(坐位液体平面接近或超过第6后肋水平,液体量>500 ml)时,呼吸对超声检查及测量无明显影响。

结核性胸膜炎胸部声像图

结核性胸膜炎的进展存在动态演变过程,早期主要表现为无回声区的胸腔积液,会因发病时间的迁延和液体的吸收,致使积液黏滞度增加,出现纤维光带漂浮或纤维凝块,甚至形成胸膜粘连和包裹。采用超声动态观察及评估结核性胸膜炎的变化过程也尤为重要。其超声图像主要表现为:胸腔积液、胸膜增厚、胸膜粘连、肺不张及肺实变。

一、胸腔积液

正常胸腔内有(8.4±4.3)ml 的生理性液体,任何原因造成其渗出增加和(或)再吸收减少就会出现胸膜腔内液体积聚,形成病理性的胸腔积液[35]。胸腔超声可检测到低至 5~50ml 的胸腔积液,并且对积液的敏感度可接近100%,积液量>100ml时超声评估的敏感度可达到100%[36]。胸部超声可判断是否存在胸腔积液及积液位置,进行胸腔积液半定量评估,判定胸腔积液清晰度,判断周围肺组织活动度,确定胸腔穿刺或置管引流的适当位置。依据超声表现,胸腔积液分为游离性积液、分隔性积液及包裹性积液[35]

胸腔积液最基本、最重要的超声表现为胸腔内的无回声液性暗区,其范围大小随呼吸同步增加和减少,也可呈均质或低回声。复杂的胸腔积液内可有等回声或高回声成分,通常对应于纤维蛋白和血块等。

1. 游离性无分隔积液:超声表现为胸膜脏壁层分离,内可见无回声液性暗区,也可呈均质或低回声,取决于液体黏稠度。液区形态和范围随呼吸而变化,吸气时肺叶膨胀,液区变小,呼气时液区增大。研究表明,超声对于胸腔积液的定量评估是可行的[37],然而,超声评估胸腔积液的多种常用测量方法精准度不尽相同,仍无统一标准[38-39]。目前,针对非包裹性胸腔积液的定量评估,临床主要有以下方法:

患者取坐位,双手交叉抱于胸前,连续扫查后,将探头纵向放置于胸腔侧壁,于呼气末测量胸腔背外侧最大积液高度(H)以及肺底至中部膈肌顶的距离(LDD)(图1~3),使用 Goecke和Schwerk[40]提出的估算胸腔积液量的公式:胸腔积液量(EV;ml)=(H+LDD)(cm)×70(ml),或更为简单的公式:胸腔积液量(EV;ml)=H(cm)×90(ml)[38]

图1~3

图1~3   患者,男性, 38岁,临床诊断胸膜炎,采用坐位进行胸腔积液超声评估。图1显示,患者取坐位,双手交叉抱于胸前,连续扫查后,将探头纵向放置于胸腔侧壁;图2显示,在膈肌与肺底之间可见带样无回声区,其形态和宽度随体位和呼吸而变化;图3显示,患者于呼气末分别测量胸腔背外侧最大积液高度(白色长箭头),以及肺底至中部膈肌顶的距离(白色短箭头)


对于ICU内或其他不能坐起来的重症患者,一般采取平卧位估测[41]。可建议患者上身抬高15°,在胸壁后外侧,垂直于胸壁横向扫查,避免探头斜切,记录呼气末脏层和壁层胸膜的最大垂直距离(Sep)(图4~6),使用Balik等[42]提出的估算胸腔积液量的公式评估胸腔积液总量:EV(ml)=20×Sep(mm)。

图4~6

图4~6   患者,男性,47岁,临床诊断结核性胸膜炎,采用卧位进行胸腔积液超声评估。图4显示,患者取平卧位,上身抬高15°,在胸壁后外侧,垂直于胸壁横向扫查;图 5显示,胸腔内可见液性无回声,液区欠清晰,其形态和宽度随体位和呼吸而变化,压迫的肺组织呈实性中等回声(白色三角); 图 6显示,于呼气末测量脏层和壁层胸膜的最大垂直距离(白色箭头)


目前,临床所使用的胸腔积液半定量的分级标准及超声表现为:(1)少量积液:因重力作用位于胸腔底部,于肺底与膈肌之间呈现长条新月状无回声区,位于后侧肋膈角的液性暗区呈三角形,液体量<500ml。(2)中等量积液:取坐位时液体平面不超过第6后肋水平,即肺门高度,液体压迫肺下叶,范围增大,呈上窄下宽分布,液体量在500~1000ml。(3)大量积液:取坐位时液体平面超过第6后肋水平,肺组织部分或全部向肺门方向萎缩,呈条状或三角形均匀等回声,液体量>1000ml(图7~9)。

图7

图7   患者,男性,45岁,临床诊断结核性胸膜炎,超声半定量评估为少量胸腔积液,于后肋膈角可见液性无回声区,呈三角形,吸气时无回声区变小或消失,呼气时无回声区增大


图8

图8   患者,女性,47岁,临床诊断结核性胸膜炎,超声半定量评估为中量胸腔积液(上界不超过第 6 后肋水平),液体无回声区范围及深度增大,呈上窄下宽分布,且受呼气及体位变化的影响


图9

图9   患者,男性,55岁,临床诊断胸膜炎,超声半定量评估为大量胸腔积液(上界超过第 6 后肋水平),胸腔大部分呈无回声液区,呼吸及体位的改变对积液范围影响不大,纵隔向健侧移位,肺组织因积液压迫萎缩呈均匀等回声


2. 分隔性积液:结核性胸膜炎由于大量纤维蛋白渗出[8],纤维蛋白充当炎性细胞的趋化物,并促进成纤维细胞黏附和增殖,从而使积液内产生胶原蛋白、黏多糖,进而形成纤维分隔,而纤维分隔数量的多少会影响胸腔积液引流效果。

分隔性胸腔积液超声表现为液区清晰或不清晰,内可见纤维分隔带,成网格状或蜂窝状分布,也可呈多个大小不等的腔。依据一个超声切面内显示的最多纤维分隔数目,可将胸腔积液分为4种类型:未发现纤维条索带为无分隔,0条<分隔数≤5条为少量分隔,5条<分隔数≤10条为中量分隔,分隔数>10条为大量分隔,以此来半定量评定结核性胸膜炎纤维蛋白渗出的严重程度(图10~12)。

图10

图10   患者,女性,29岁,临床诊断结核性胸膜炎,超声可见胸腔积液内少量分隔(<5条)


图11

图11   患者,女性,39岁,临床诊断结核性胸膜炎,超声可见胸腔积液内中量分隔(6~10条)


图12

图12   患者,男性,57岁,临床诊断结核性胸膜炎,超声可见胸腔积液内大量分隔(>10条)。白色箭头所指为纤维分隔带


3. 包裹性积液:胸腔积液未得到及时和彻底治疗时,胸膜表面可出现较多纤维素样及浆液性渗出,内含大量纤维蛋白原及纤维蛋白,其沉积于胸膜表面导致胸腔积液形成分隔包裹,引起胸膜增厚和粘连,从而形成包裹性积液[43]

包裹性胸腔积液超声表现为病变部位液性暗区欠清晰,内可见分隔光带成网格状分布,或液区内可见细小光点充填,部分患者随病变进展亦可见液区消失、实性低回声形成,积液周边可见脏壁层胸膜增厚,呈条带样低回声或中低回声包绕,部分患者周围肺组织受侵实变、活动受限。一般选取病灶显示最大切面进行超声评估,若一幅图显示不完全,可通过多幅图拼接,通常测量包裹性积液的最大上下径、左右径及前后径,判断不同时期病灶的变化情况,以便及时对患者病情及治疗效果进行评估(图13~15)。

图13

图13   患者,男性,28岁,临床诊断结核性胸膜炎,超声可见胸膜腔包裹性积液,内可见大量分隔(白色细箭头),肺实变区域呈低回声(白色三角),后方可见融合B线(白色粗箭头)


图14

图14   患者,男性,61岁,临床诊断结核性胸膜炎,超声可见胸膜腔内局部类圆形低回声区包裹性积液(白色三角),相邻肺组织活动度较差,后方可见融合B线(白色粗箭头)


图15

图15   患者,女性,37岁,临床诊断结核性胸膜炎,超声可见包裹性积液内大量分隔(白色箭头),以及增厚的壁层胸膜(白色三角)与脏层胸膜(灰色三角)


包裹性胸腔积液需与胸膜肿瘤进行鉴别,胸膜肿瘤多来源于转移性肿瘤,原发性多见于胸膜间皮瘤,是一种来源于胸膜脏层和壁层的原发性肿瘤,其声像图显示为与胸壁相连接的不规则中等或低等回声区,部分可侵犯胸壁肌肉及肋骨(图16)。

图16

图16   患者,男性,55岁,临床诊断胸膜间皮瘤,超声可见胸膜内局部低回声占位(白色三角),伴淋巴结转移(白色箭头)


二、胸膜增厚

结核性胸膜炎由于大量纤维蛋白沉着于胸膜,并有纤维化及肉芽组织增生形成,导致胸膜呈结节状突起或局限性/广泛性增厚,以壁层胸膜显著,广泛性的胸膜肥厚、粘连影响胸壁弹性,引起肺功能受限[2,44]

胸膜结节超声表现为单个或多个圆形或扁平形结节状突起,基底较宽;结节多呈不均匀的低回声、等回声或高回声,当存在胸腔积液或结节较大时较易显示。胸膜增厚超声表现为在胸壁与胸腔积液之间或胸壁与肺组织强回声之间的局限性或广泛性的条状低回声或稍高回声区,增厚的胸膜低回声内有时可见由纤维板形成的线状高回声的分层现象,超声测量其最厚处可判定胸膜厚度。彩色多普勒血流成像于增厚的胸膜内可探及点状、短棒样、迂曲条状血流信号,频谱多普勒检查可录得动脉或静脉血流频谱。在结核性胸膜炎后期,部分患者可见胸膜钙化现象,其超声表现为低回声的胸膜内可见弧形强回声,后方伴声影[44-46](图17~21)。

图17

图17   患者,男性,27岁,临床诊断结核性胸膜炎,超声可见局限性增厚的壁层胸膜(白色三角)


图18~19

图18~19   患者,女性,57岁,临床诊断结核性胸膜炎,图18 中超声可见广泛性增厚的壁层胸膜(白色三角);图19中超声可见广泛性增厚的壁层胸膜(白色三角)及脏层胸膜(灰色三角)


图20

图20   患者,男性,35岁,临床诊断结核性胸膜炎,超声可见胸壁与增厚的壁层胸膜内短棒样、迂曲条状血流信号(白色三角),脏层胸膜内可见细小、点状血流信号(白色箭头)


图21

图21   患者,男性,77岁,临床诊断结核性胸膜炎,增厚的低回声胸膜内可见长条状强回声(白色三角),后方伴声影(白色箭头)


对于局限性增厚的胸膜,需与胸膜间皮瘤等进行鉴别,对于病因不明的胸腔积液或胸膜增厚可行超声引导下胸膜穿刺活检协助诊断(图22)。

图22

图22   图20为同一例患者,增厚的胸膜穿刺活检后病理结果(HE染色,×400)可见增生的肉芽组织(白色虚线)


三、胸膜粘连

结核性胸膜炎胸腔积液液体逐渐黏稠化,形成纤维蛋白团块及粘连带,导致增厚的壁层胸膜与脏层胸膜以及相邻肺组织存在粘连,胸膜的相对滑动消失。于病灶顶部(近肺尖部方向)肺与胸壁交界处,以及肺底部肋膈角处相对运动受限最为显著。

胸膜相对运动消失超声表现为当嘱患者深呼吸时,脏、壁层增厚的胸膜在移行部位明显粘连,呼吸时肺与胸壁无相对运动。彩色多普勒血流成像于增厚的胸膜或实变肺组织内可探及点状、短棒样或迂曲条状血流信号相交通,频谱多普勒可录得动脉或静脉血流频谱(图23~25)。

图23

图23   患者,男性,37岁,临床诊断结核性胸膜炎,超声可见局限性增厚的壁层胸膜(白色三角)与脏层胸膜(灰色三角),于肺底部肋膈角处增厚、粘连(白色虚线)


图24

图24   患者,男性,41岁,临床诊断结核性胸膜炎,超声可见广泛性增厚的壁层胸膜(白色三角)与脏层胸膜(灰色三角)


图25

图25   患者,男性,43岁,临床诊断结核性胸膜炎,超声可见脏壁层胸膜广泛性增厚、粘连,彩色多普勒血流成像示壁层胸膜可见短棒样血流信号(白色箭头),脏层胸膜及脏层胸膜下实变肺组织内可见条状血流信号(灰色箭头)


四、肺不张及肺实变

部分原因引起的正常肺组织内肺泡不含气或含气量减少,导致肺组织萎缩塌陷,体积缩小,称为肺不张。结核性胸膜炎由于胸腔积液压迫肺组织,导致肺组织内肺泡气体含量减少,肺组织体积缩小,呈实质性改变,称为压迫性肺不张[47],因受积液影响,以肺下叶肋膈角处压迫性肺不张更多见。

超声主要表现为类似肝组织样结构的低回声及逐层分叉树枝样无回声,部分患者可见支气管充气征。彩色多普勒血流成像可见压迫性肺不张组织内多条树枝状血流,频谱多普勒可录得动脉或静脉血流频谱(图26,27)。

图26~27

图26~27   患者,男性,25岁,临床诊断胸膜炎,图26显示胸腔积液为无回声,不张的肺组织呈类似肝脏的低回声(白色三角);图27彩色多普勒血流成像示不张肺组织内存在多个点条状血流信号(白色箭头)


当病情进展,胸腔积液黏稠,脏层胸膜炎性反应进一步加重,胸膜增厚粘连,相邻肺组织肺泡内的空气或肺间质内被大量渗出物或细胞替代,肺组织呈实性改变,称为肺实变。超声主要表现为肝组织样征、碎片征(位于胸膜下的片状低回声)及支气管充气征[48]。部分脏层胸膜增厚引起周围肺组织实变的病灶内,采用彩色多普勒血流成像可见实变肺组织内多条树枝状血流信号或与脏层胸膜吻合支血流相交通,频谱多普勒可录得低速动脉或静脉血流频谱(图28,29)。对于胸膜增厚粘连且需要手术剥离治疗的患者,脏层胸膜与周边肺实变病灶的粘连程度、范围及吻合支血管情况是手术剥离难度及术中出血的主要影响因素。

图28~29

图28~29   患者,男性,43岁,临床诊断结核性胸膜炎,图28中超声可见肺实变区域呈低回声(白色三角),内可见树枝状支气管充气征(白色箭头);图29中彩色多普勒血流成像示实变肺组织内出现多条树枝状血流信号(白色箭头)


结核性胸膜炎超声分型

超声检查是评估疾病严重程度、判断预后和指导治疗的有效方法[49]。依据胸膜增厚程度、胸腔积液有无分隔及包裹、肺外周实变情况及活动度[11],以及胸腔镜下结核性胸膜炎病理分期表现,现将结核性胸膜炎超声表现分为以下3种类型。

一、结核性胸膜炎超声分型Ⅰ型

1. Ⅰ型病理改变:结核分枝杆菌通过各种途径到达胸膜并诱发炎症反应,早期病理改变以渗出性变态反应为主,胸膜局部毛细血管通透性增加,血浆成分渗出,胶体渗透压升高,导致胸腔内液体增加;同时胸膜下巨噬细胞及大量淋巴细胞浸润,淋巴管水肿阻塞,导致胸膜液回流受阻,最终导致胸腔积液形成[8]

2. Ⅰ型超声图像特征(图30,31):(1)胸腔内可见液性暗区,液区清晰,内无分隔光带;(2)脏、壁层胸膜光滑、无增厚或可见粟粒样低回声结节;(3)肺表面光滑,肺下极随呼吸活动度大。

3. Ⅰ型超声图像主要观察指标:(1)胸腔内液区是否清晰;(2)液区内有无分隔光带;(3)胸膜有无增厚;(4)肺下极活动度。

图30

图30   患者,女性,32岁,临床诊断结核性胸膜炎,超声显示大量胸腔积液,呈液性无回声暗区(灰色三角),液区清晰、无分隔光带,脏、壁层胸膜无增厚,超声分型为Ⅰ型结核性胸膜炎


图31

图31   患者,男性,45岁,临床诊断结核性胸膜炎,超声显示少量胸腔积液,呈液性无回声暗区(白色三角),液区清晰、无分隔光带,脏、壁层胸膜无增厚,超声分型为Ⅰ型结核性胸膜炎


图32

图32   患者,女性,42岁,临床诊断结核性胸膜炎,超声显示胸腔积液,呈液性无回声暗区,液区清晰,壁层胸膜可见局限性增厚(白色三角),超声分型为Ⅱa型结核性胸膜炎


图33

图33   患者,女性,29岁,临床诊断结核性胸膜炎,超声显示中量胸腔积液,呈液性无回声暗区,液区内可见3条分隔光带(白色箭头),脏、壁层胸膜无明显增厚,超声分型为Ⅱa型结核性胸膜炎


图34

图34   患者,男性,53岁,临床诊断结核性胸膜炎,超声显示胸腔积液,呈液性无回声暗区,液区清晰,壁层胸膜普遍性增厚(白色三角),胸膜表面可见纤维素附着(白色箭头),超声分型为Ⅱb型结核性胸膜炎


图35

图35   患者,男性,25岁,临床诊断结核性胸膜炎,超声显示中量胸腔积液,呈液性无回声暗区,液区内可见>5条分隔光带(白色箭头),超声分型为Ⅱb型结核性胸膜炎


二、结核性胸膜炎超声分型Ⅱ型

1.Ⅱ型结核性胸膜炎病理改变:结核特异性变态反应进一步进展,胸膜充血,毛细血管扩张,基膜通透性增加,蛋白等大分子物质滤入胸腔,使胸腔积液胶原蛋白、黏多糖纤维素产生,致使液体黏稠化,形成纤维蛋白团块及粘连带;纤维蛋白等物质引起胸膜淋巴管阻塞,并且胸膜淋巴孔受炎症破坏,引起蛋白吸收障碍,加重积液内纤维蛋白积聚,导致纤维分隔迅速增多[43,50];同时胸膜炎症反应逐渐由渗出性病变向增殖性病变进展,引起脏、壁层胸膜部分或整体水肿增厚,且厚度<1mm。

2. Ⅱ型结核性胸膜炎分型:超声图像依据胸腔积液内分隔粘连带的数量以及胸膜增厚的范围,将Ⅱ型结核性胸膜炎分为Ⅱa型及Ⅱb型[11]

3. Ⅱa型超声图像特征(图32,33):(1)胸腔内液区欠清晰,可见分隔光带,数目≤5条;(2)脏、壁层胸膜无或仅有局限性增厚,厚度<1mm;(3)脏、壁层胸膜可见中等条带状或中等偏强团絮状回声附着;(4)肺下极随呼吸活动度大;(5)彩色多普勒血流成像示脏、壁层增厚的胸膜内未见明显血流信号;(6)实时动态超声示,当嘱患者深呼吸时,脏、壁层增厚的胸膜在移行部位(肺尖方向)无粘连,呼吸时可见肺与胸壁的相对运动。

4. Ⅱa型超声图像主要观察指标:(1)液区是否清晰;(2)液区内有无分隔及分隔数目;(3)胸膜有无局限性增厚及增厚程度;(4)胸膜有无团絮状物附着;(5)肺与胸壁有无相对运动。

5. Ⅱb型超声图像特征(图34,35):(1)胸腔内液区欠清晰,内可见分隔光带,数目>5条或呈网格样分布;(2)脏、壁层胸膜局限性或普遍性增厚,厚度<1mm;(3)脏、壁层胸膜可见多处中等条带状或中等偏强团絮状回声附着;(4)肺下极随呼吸运动活动度大;(5)彩色多普勒血流成像示:脏、壁层胸膜内未见明显血流信号;(6)实时动态超声示:嘱患者深呼吸,脏、壁层增厚的胸膜在移行部位(肺尖方向)无粘连,呼吸时可见肺与胸壁的相对运动。

6. Ⅱb型超声图像主要观察指标:(1)液区是否清晰;(2)液区内分隔数目是否>5条,分隔是否呈网格样;(3)胸膜有无局限性或普遍性增厚及增厚程度;(4)胸膜有无团絮状物附着;(5)肺与胸壁有无相对运动。

图36

图36   患者,男性,29岁,临床诊断结核性胸膜炎,超声显示包裹性胸腔积液,胸腔内液区回声不清晰,脏、壁层胸膜弥漫增厚,可见肺周病灶(白色三角),壁层胸膜可见团状纤维附着物(白色箭头)


图37

图37   患者,男性,34岁,临床诊断结核性胸膜炎,超声显示包裹性胸腔积液,液区尚清晰,壁层胸膜(白色三角)、脏层胸膜增厚,可见絮状物附着(白色箭头)


图38

图38   患者,男性,65岁,临床诊断结核性胸膜炎,超声显示脏、壁层胸膜明显增厚(白色三角),液区内可见多条分隔光带(白色箭头)


图39

图39   患者,女性,63岁,临床诊断结核性胸膜炎,超声显示胸腔液区内可见分隔光带(白色箭头),脏、壁层胸膜增厚且相互粘连(白色三角),肺活动度受限


图40

图40   患者,男性,44岁,临床诊断结核性胸膜炎,超声显示液区内多条分隔光带(白色箭头),脏、壁层胸膜明显增厚,可见肺周实变及其后方融合B线(灰色粗箭头)


图41

图41   患者,女性,57岁,临床诊断结核性胸膜炎,超声显示液区内多条分隔光带(白色箭头),脏、壁层胸膜明显增厚,可见肺周实变(白色三角)


图42

图42   患者,男性,54岁,临床诊断结核性胸膜炎,超声显示胸腔内包裹性液区回声混杂,脏、壁层胸膜弥漫增厚,厚薄不均,彩色多普勒血流成像示壁层胸膜可见血流信号(白色粗箭头),肺周实变病灶可见粗大血流与脏层胸膜血流相连续(白色细箭头)


图43,44

图43,44   患者,男性,45岁,临床诊断结核性胸膜炎,图43中超声显示包裹性液区回声混杂,脏、壁层胸膜明显增厚、相互连续(白色三角),彩色多普勒血流成像示壁层胸膜可见点状血流信号(白色粗箭头),脏层胸膜可见丰富血流信号(白色细箭头);图44中超声显示壁层胸膜明显增厚,彩色多普勒血流成像可见点条状血流信号(白色粗箭头),脉冲频谱多普勒超声录得低速血流频谱。以上患者超声分型均为Ⅲ型结核性胸膜炎


三、结核性胸膜炎超声分型Ⅲ型

1. Ⅲ型结核性胸膜炎病理改变:结核性特异性变态反应后期渗出性病变逐渐转变为增殖性改变,覆盖于胸膜表层的间皮细胞受损、功能丧失,间皮细胞下胶原纤维和结缔组织明显增生,随后胸膜间皮细胞逐渐被胶原纤维、肉芽肿、结核结节所替代,引起胸膜广泛性增厚[51-53]

2. Ⅲ型超声图像特征(图36~44):(1)胸腔内液区不清晰,可见细小光点散在分布,或多条粗细不等强回声光带分布,可呈网格状改变;(2)脏、壁层胸膜广泛性增厚,且厚度≥1mm,可见胸膜钙化或团絮状中等偏强回声附着[54];(3)普遍增厚的脏、壁层胸膜及膈胸膜呈连续条带样暗淡回声,于移行处粘连;可见结节状回声附着于胸膜,呈中等、偏强或强弱不等的分层回声;部分可见周围肺组织实变病灶呈低或中等回声;(4)彩色多普勒血流成像示:增厚的脏、壁层胸膜与胸壁或实变肺组织间可见血流信号相交通;(5)实时动态超声示:嘱患者深呼吸,脏、壁层增厚的胸膜在移行部位(肺尖方向)明显粘连,呼吸时肺与胸壁无相对运动。

3. Ⅲ型超声图像主要观察指标:(1)液区是否清晰,有无细小光点分布;(2)液区内有无分隔,分隔是否成网格样;(3)胸膜有无普遍性增厚及增厚程度;(4)胸膜有无团絮状物附着;(5)脏层胸膜下肺组织是否有实变;(6)增厚的脏、壁层胸膜是否与胸壁或实变肺组织存在血流信号相交通;(7)增厚的脏、壁层胸膜移行部位是否有粘连,呼吸时是否有相对运动。

超声引导下胸膜穿刺活检

胸膜穿刺活检获得病原学和组织病理学检查结果是结核性胸膜炎确诊标准之一,是弥补其他临床常规检查不足的有效诊断方法。超声引导下的胸膜穿刺活检能精准穿刺局限增厚性病变胸膜,避免损伤正常胸膜组织和血管,减少相关并发症,具有微创、安全、经济、准确率高、灵活性高以及检查过程无辐射等优势[55],易被患者接受。

一、适应证

(1)影像学提示胸膜病变;(2)其他无创检查不能明确病因的胸膜病变。

二、禁忌证[56]

(1)凝血功能异常;(2)无法配合呼吸、严重肺气肿、严重肺动脉高压、呼吸衰竭或存在意识和精神障碍;(3)缺乏超声可视化的安全活检路径;(4)近期心肌梗死或不稳定型心绞痛。

三、超声引导下胸膜穿刺活检操作步骤

1. 术前准备:(1)核对超声检查申请单,排查患者适应证,讲解患者相关注意事项;(2)完善患者术前相关检查(包括血常规、凝血时间、心电图、血压、肝肾功能及术前感染四项),避免造成手术不良风险;(3)患者术前均进行胸部超声检查,明确胸腔积液的程度,测量并记录胸膜有无增厚、增厚位置和粘连情况,评估病变血管和周围结构,以及最佳进针深度和进针路径;(4)告知患者穿刺活检相关风险,请患者签署知情同意书。

2. 操作流程(图45~47):(1)患者采取坐位、半卧位、侧卧位或俯卧位;(2)采用徒手或带有穿刺架的低频(2~5MHz)或高频(5~10MHz)探头;低频探头置于患者肋间隙,观察患侧胸腔积液、胸膜厚度情况;选取胸膜较厚处或有结节的部位进行活检,选择穿刺路径无遮挡的部位作为拟穿刺切面;穿刺点一般紧贴下个肋骨上缘,避开肋间神经及肋间动脉;(3)高频探头对拟穿刺部位胸壁进行扫查,确定肋间血管位置及走行,避免穿刺损伤肋间血管;(4)穿刺部位行常规消毒、戴无菌手套、铺洞巾;(5)超声引导下2%利多卡因逐层浸润麻醉直至胸膜腔,局部麻醉和胸腔穿刺点为同一部位,且为同一角度和路径,动作宜缓慢;(6)安装探头无菌保护套,采用探头穿刺引导架及镶嵌件者,需调节穿刺引导架进针角度,确保穿刺架角度和超声屏幕引导线所选角度一致;(7)于超声实时引导下或通过引导架插入穿刺针,穿刺针沿超声引导方向刺入胸壁,确保预活检胸膜病灶位于活检针射程内,行穿刺活检;(8)一般穿刺3针,确保获取足够病变组织,现场评估标本满意情况(胸膜组织为灰白色,呈完整的实心条带),标本不满意时可取5针;(9)将组织标本放置在福尔马林固定液送检;(10)活检结束后,需即刻应用超声探查穿刺针道是否存在出血征象,向患者及家属讲解术后注意事项,观察15~30min 无异常可护送患者返回。

图45~48

图45~48   患者,男性,52岁,临床诊断结核性胸膜炎 图45中超声可见壁层胸膜广泛性增厚,呈条状低回声(白色三角);图46为超声引导下增厚胸膜穿刺活检术(白色箭头示活检针针尖);图47显示穿刺活检取出标本呈灰白色组织条;图48为病理结果(HE染色,×400),提示为慢性肉芽肿


四、超声引导下胸膜穿刺活检操作注意事项

(1)术前嘱患者尽量放松,避免紧张引起的不良反应(常见胸膜反应),应告知可能发生的并发症(出血、气胸及疼痛等);(2)结合低频及高频探头进行定位,以确定肋间血管走行位置;(3)逐层注入局部麻醉药,并进行回抽,注意回抽物性质;(4)穿刺过程中实时观察患者生命体征变化(建议行心电监护、血压及血氧饱和度监测);血管迷走神经反应较常见,表现为头晕、低血压、恶心和/或短暂的心动过缓;若患者出现不适应,及时停止操作或进行抢救;(5)术后24h密切观察患者的生命体征和症状、血红蛋白和影像学变化,如有必要,采取进一步的影像学检查或相应治疗。

五、胸膜活检组织送检

所有组织标本置于10%福尔马林溶液内,常规石蜡切片,行HE染色后镜检。结核性胸膜炎诊断标准[13]:胸膜组织检出结核分枝杆菌或结核分枝杆菌脱氧核糖核酸阳性、胸膜组织病理符合典型的干酪样肉芽肿(图48)。

六、胸膜活检并发症处理

1. 出血:少量出血患者无需特殊处理,可自行吸收;出血明显或加重时可给予注射用血凝酶治疗;胸腔内出血量大且药物治疗无效或出血继续加重的患者需立即采用介入方法或外科手术止血。

2. 气胸:少量气胸患者无需特殊处理。中量气胸(肺萎缩>30%)或者大量气胸(肺萎缩>50%)或患者出现胸闷、气急等低氧血症表现,应行超声引导下置管抽吸或胸腔闭式引流。

3. 疼痛:轻度疼痛无需特殊处理,若患者疼痛无法忍受,可适当给予镇痛药物。

4. 胸膜反应:应立即停止操作,嘱患者卧床休息,注意保暖,监测患者生命体征(心率、血压、血氧饱和度等)。症状轻者可自行缓解;如有低血压休克的征象,可给予吸氧或对症输液处理,必要时给予肾上腺素治疗,预防休克。

结核性胸膜炎超声介入治疗

结核性胸膜炎引起的胸腔渗出性积液采用胸腔穿刺抽液和/或置管引流,已获得临床满意疗效,具有操作方便、 费用低且安全性高等优势,可减轻胸膜肥厚,降低复发风险[20-21]。同时联合尿激酶或链激酶胸腔注入治疗,能够有效促进纤维蛋白溶解,预防胸膜粘连[22-23]

适应证:(1)原因未明的胸腔积液,可做诊断性穿刺置管,以明确病因;(2)胸腔内液体或气体对肺组织存在压迫,引流出胸腔内积液或积气,促使肺组织复张,缓解呼吸困难等症状;(3)需引流胸腔脓液或进行胸腔冲洗的脓胸患者;(4)需胸腔注药治疗的患者。

禁忌证:(1)存在严重或危急的基础疾病对手术无法耐受者;(2)因其他原因无法配合者;(3)血小板计数低于50g/L,应先输血小板;(4)出血时间延长、凝血机制异常及服用抗凝药物者;(5)穿刺处或附近皮肤感染;(6)无超声可视下的安全穿刺路径。

一、Ⅰ型结核性胸膜炎治疗方法

Ⅰ型结核性胸膜炎患者胸腔内的液体多清晰,多数呈游离性,无明显分隔光带,脏、壁层胸膜无或仅有局限性增厚。治疗主要原则为安全、有效、彻底的清除积液。推荐在抗结核药物治疗的基础上采用超声引导下经皮穿刺抽液或置管引流治疗。此方法可确保胸腔积液充分排尽,并减轻反复穿刺导致的胸膜损伤,减少胸膜肥厚的发生[20,57 -59]

(一)超声引导下胸腔穿刺抽液或置管引流操作步骤[58,60]

1. 术前准备:(1)核对超声检查申请单,排查患者适应证,讲解患者相关注意事项及物品准备;(2)完善患者术前相关检查(包括血常规、凝血时间、心电图、血压、肝肾功能及术前感染四项),避免造成手术不良风险;(3)告知患者穿刺或置管相关风险,请患者签署知情同意书。

2. 操作流程:(1)嘱患者取坐位,面向椅背;病重或体弱者采用半坐卧位,上肢上举;(2)首先将低频探头置于患者肋间隙,沿肋间隙横向和纵向移动扫查,观察患侧胸腔积液分布情况,选择积液量最大且穿刺路径无遮挡的部位作为拟穿刺切面;穿刺点一般紧贴下个肋骨上缘,避开肋间神经及肋间动脉;(3)采用高频探头对拟穿刺部位胸壁进行扫查,确定肋间血管位置及走行,避免穿刺损伤肋间血管;(4)穿刺部位行常规消毒、戴无菌手套、铺巾及2%利多卡因逐层浸润麻醉;(5)安装探头无菌保护套,于超声实时引导下进行穿刺抽液,或置入导管穿刺针后,依次按照插入导丝、拔出穿刺针、扩皮器扩张皮肤并顺导丝置入引流导管(导管规格6-16Fr,多采用8Fr)、抽出导丝的步骤进行操作,导管一般置入深度15cm,宁深勿浅,对于疼痛敏感患者,可酌情采用较细、较软导管,同时注意导管深度;(6)确认积液引流通畅的情况下,连接抗反流引流袋并计算液体总引流量,建议横向固定引流管;(7)若积液呈血性,则对患者进行跟踪随访;(8)穿刺或置管结束后,向患者及家属讲解术后注意事项,护送患者安全返回病房,送检标本。

(二)超声引导下胸腔穿刺抽液或置管引流操作注意事项

(1)术前嘱患者尽量放松,避免紧张引起的不良反应,对于存在肺大泡的患者,应告知可能发生的并发症(气胸及疼痛);(2)术中定位时,低频及高频探头可结合使用,以确定肋间血管走行位置;(3)逐层注入局部麻醉药,并进行回抽,注意回抽物性质;若麻醉过程中抽到回血,说明损伤肋间血管,立即停止进针,进行按压后重新换定位点;(4)穿刺过程中实时观察患者生命体征变化,可向患者讲解过程,缓解患者紧张情绪;若患者出现不适应,及时停止操作或进行抢救;(5)单侧胸腔积液的初次引流量建议不超过800ml[61],合理控制积液引流速度及引流量,密切监测患者引流过程中的临床反应及生命体征,以最大程度降低气胸、复张性肺水肿等不良反应发生率;(6)引流导管拔管之前,建议采用超声进行复查,确保胸腔积液引流完全后,可拔除留置的引流导管。

二、Ⅱa型结核性胸膜炎治疗方法

Ⅱa型结核性胸膜炎胸腔内液区多数清晰,可见少量分隔光带且数目≤5条,脏、壁层胸膜无或仅有局限性增厚,肺组织活动度正常。因此,治疗主要原则为胸腔积液清除和(或)纤维分隔溶解。推荐在抗结核药物治疗的基础上可采用超声引导下胸腔穿刺抽液或置管引流清除胸腔积液,而针对因少量分隔导致胸腔积液不能彻底引流的患者,可行超声引导下胸腔置管并注入尿激酶进行引流。此治疗方法能够有效促进纤维蛋白溶解,达到充分引流的目的。

1. 超声引导下胸腔穿刺抽液或置管引流操作步骤:超声引导下胸腔穿刺抽液或置管引流操作步骤见上一章节所述。

2. 超声引导下胸腔尿激酶注入引流步骤:置管后即可进行胸腔积液引流,观察10~20min,如引流通畅则无需尿激酶注射,直至将积液彻底引流;如引流受阻或不畅进入以下步骤:(1)进行胸腔内药物注射,注入尿激酶10万单位(以0.9%氯化钠溶液10ml稀释);(2)嘱患者每10min不同体位翻身一次,使药物在胸腔积液内尽可能充分混合,均匀分布;(3)注药后0.5~1h,根据超声评估积液内分隔溶解情况,建议分隔光带充分溶解后进行积液引流(图49,50)。

图49,50

图49,50   患者,女性,29岁,临床诊断结核性胸膜炎,超声分型为Ⅱa型结核性胸膜炎 图49中超声显示胸腔积液呈液性无回声暗区,液区清晰,其内可见3条分隔光带(白色箭头),并可见不张的肺组织(白色三角);图50显示,注入尿激酶10万单位,充分溶解分隔后行胸腔积液引流,胸腔内可见极少量液性暗区(白色三角),肺组织充气良好(白色箭头)


3. 超声引导下胸腔尿激酶注入禁忌证:有过敏史的患者禁用;有出血倾向的患者禁用。

4. 超声引导下胸腔尿激酶注入引流操作注意事项:对于有尿激酶过敏史、有出血倾向,以及无尿激酶治疗条件等无法行超声引导下胸腔置管及尿激酶注入治疗的患者,可行超声引导下穿刺分隔抽液治疗,建议先穿刺较深处分隔腔进行抽液,然后依次后退至较浅处分隔腔,分别进行穿刺抽液,直至积液清除。但此治疗方法对操作者的技术要求较高,建议在有丰富介入穿刺治疗经验的单位开展,以便将治疗危险降到最低,避免造成不必要的医源性损伤。胸腔注入尿激酶后鼓励患者多翻身活动,在超声评估分隔光带充分溶解后,建议在防反流引流袋作用下进行引流。

三、Ⅱb型结核性胸膜炎治疗方法

Ⅱb型结核性胸膜炎患者胸腔内液体逐渐黏稠化,液区欠清晰,并可见>5条的纤维分隔光带,部分可呈网状,同时脏、壁层胸膜呈局限性或普通性增厚,但肺组织活动度尚正常。因此类患者较多的纤维分隔影响积液的引流效果,治疗主要原则为纤维分隔溶解+胸腔积液清除。推荐在抗结核药物治疗的基础上采用超声引导下胸腔置管并注入尿激酶引流治疗。此治疗方法能够有效促进纤维蛋白溶解,清除淋巴孔,从而改善引流[62-63],促进积液吸收,减轻胸膜肥厚及胸膜粘连,且安全性较高,不良反应发生率低[22-23,64]

图51~56

图51~56   患者,男性,33岁,临床诊断结核性胸膜炎 图51显示,治疗前超声图像存在大量胸腔积液,并可见大量分隔,呈网格样改变,超声分型为Ⅱb型结核性胸膜炎;图52为注射尿激酶超声图像,胸腔积液内可见大量分隔,呈网格样;图53为注射尿激酶0.5h超声图像,显示胸腔积液内分隔明显减少,为中-大量,呈网格样;图54为注射尿激酶1h超声图像,显示胸腔内仅见少量分隔;图55为注射尿激酶1.5h超声图像,显示胸腔内无明显分隔,液区尚清晰;图56为胸腔积液引流后超声图像,显示胸腔无明显积液暗区,肺组织充气良好


有研究提出,对于儿童包裹性胸膜炎患者,采用胸腔内注射尿激酶与电视胸腔镜胸膜剥脱术治疗的临床疗效及住院时间差异无统计学意义[62],尿激酶治疗是一种更经济的选择,也是Ⅱb型结核性胸膜炎首选的治疗方法。

1. 超声引导下胸腔置管+胸腔尿激酶注入治疗操作步骤:超声引导下胸腔置管操作步骤见前章节所述。引流管尽量置于较大分隔腔内进行引流,观察10~20min,如引流通畅则无需注射尿激酶,直至积液完全引出;如引流受阻或不畅进入以下步骤:(1)行胸腔内尿激酶注射,注入尿激酶20万单位(以0.9%氯化钠溶液20ml稀释);(2)嘱患者每10min不同体位翻身一次,使药物在胸腔积液内尽可能充分混合,均匀分布;(3)注药后1~2h,采用超声评估分隔溶解情况,确保分隔光带充分溶解后进行引流(图 51~56);(4)儿童可根据情况注射尿激酶5~10万单位,胸腔内留置1~1.5h。

2. 超声引导下胸腔置管+尿激酶注入引流操作注意事项:尿激酶治疗结核性胸膜炎已在多项研究中证明是安全的,且在包裹性胸膜炎的治疗中也发挥重要作用,在规定浓度下可以安全使用,但对于有过敏史及出血倾向的患者禁用;尿激酶的用量及浓度应根据分隔数目、分隔厚度及胸膜粘连的程度在安全范围内进行适当调整,过少的尿激酶达不到充分溶解分隔的效果,而过量使用尿激酶会增加患者的出血风险;尿激酶注入后鼓励患者活动,确保分隔光带有效溶解;患者的初次引流量不应超过800ml,合理控制液体引流速度、引流量,密切监测患者引流过程中的生命体征及不良反应等;采用超声定期随访复查,确保胸腔积液引流完全后,则可拔除留置导管。

目前,对于大多数Ⅱb型结核性胸膜炎患者,采用超声引导下胸腔置管+尿激酶注入引流可获得满意疗效,少数效果不明显者,可选择电视胸腔镜胸膜剥脱术或开胸手术[65]。个别研究依据结核性脓胸的实验室指标进行分期,指出使用尿激酶可能会导致胸腔粘连,增加电视胸腔镜胸膜剥脱术的难度[49,66],但该分期方法与超声分型诊断的标准不同。因此,建议Ⅱb型患者在胸腔置管+尿激酶治疗后,需进行动态随访观察,以确保治疗效果,必要时采取下一步治疗方案,避免延误病情。

四、Ⅲ型结核性胸膜炎治疗方法

Ⅲ型结核性胸膜炎患者胸腔积液黏稠并形成包裹腔,同时胸膜肉芽肿和纤维组织增生,导致胸膜广泛增厚、粘连,可引起周围肺组织实变,且肺周实变病灶与增厚胸膜之间存在血管交通。临床治疗主要原则为清除脓腔+胸膜纤维板分离。多采用在抗结核药物治疗的基础上通过电视胸腔镜胸膜剥脱术或外科开胸胸膜剥脱术治疗。电视胸腔镜胸膜剥脱术创伤小,术后恢复快,患者耐受性好[67],能有效解除分隔及胸膜粘连,减少胸膜增厚[68-69]。而外科开胸胸膜剥脱术更适合于具有胸廓塌陷、肋间隙狭窄或者机化性脓胸的患者[70-71]

五、术后随访

(一)随访时间

行超声介入治疗的患者于术后1周、1个月、2个月、3个月分别进行随访,行电视胸腔镜胸膜剥脱术或外科开胸手术的患者术后每个月进行随访[31,59,72]

(二)随访评估内容[73-74]

1. 临床症状评估:发热、咳嗽、胸闷、气短、乏力、盗汗、纳差、胸痛等临床症状是否改善,肺功能是否提升。

2. 影像学评估:胸腔积液以及分隔情况;胸膜厚度、粘连情况;术后有无并发症,包括残腔、肺不张、气胸等。

(三) 随访资料保存归档

整理所有患者完整的随访资料,同时进行纸质版和电子版双重备份并进行归档。

结核性胸膜炎超声诊断、分型及介入治疗流程

超声引导下的诊断及介入治疗已成为结核性胸膜炎临床诊疗的关键技术方法。本共识主要由结核性胸膜炎的超声检查、超声分型、超声引导下胸膜穿刺活检及超声介入治疗等部分组成,并形成合理化和规范化的诊治流程,具体见图57

图57

图57   结核性胸膜炎超声诊断、分型及介入治疗流程图


注:共识内所有患者图片均来自西安市胸科医院

执笔者 黄毅 左蕾 崔文琦(西安市胸科医院)

指导专家 党丽云(西安市胸科医院);杨高怡(浙江大学医学院附属杭州市胸科医院);徐栋(中国科学院大学附属肿瘤医院);初乃惠(首都医科大学附属北京胸科医院);郭佑民(西安交通大学第一附属医院);严昆(北京大学肿瘤医院);董刚(郑州大学第一附属医院)

核心专家组成员(排名不分先后) 李向前、许优(西安市胸科医院);雷志锴(浙江大学医学院附属杭州市第一人民医院);于铭(空军军医大学第一附属医院西京医院);袁丽君(空军军医大学第二附属医院唐都医院);曹兵生(中国人民解放军总医院第八医学中心);高磊(中国医学科学院病原生物学研究所);夏宇(北京协和医院);阮骊韬(西安交通大学第一附属医院);王茵(同济大学附属上海市肺科医院);王雷(上海交通大学附属胸科医院);赵齐羽(浙江大学医学院附属第一医院);郑瑜(西安市中心医院);岳瑾琢(西安市大兴医院);农恒荣(广西医科大学附属南宁市传染病医院);赵萍(商洛市中心医院);常建东(北京中医药大学厦门医院);张建蕾(延安市人民医院);郭倩茹(新疆维吾尔自治区胸科医院);徐静(天津市海河医院);李宏明(黑龙江省传染病防治院);黎秋(广西传染病医院)

专家组成员(排名不分先后) 周晓东(西安国际医学中心);段云友、杨勇(空军军医大学第二附属医院唐都医院);张军(空军军医大学第一附属医院西京医院);李小鹏、周琦、姜珏(西安交通大学第二附属医院);管湘平(陕西省人民医院);王黎霞、李敬文、范永德、郭萌(《中国防痨杂志》期刊社);王建宏(西安市人民医院);杨青(首都医科大学附属北京胸科医院);张朝阳(商洛市中心医院);贾明(杨凌示范区医院);王胜利(延安大学附属医院);申健(西安医科大学附属辅仁医院);程润生(商洛市商州区医院);李逢生(西安高新医院);边莉莉(延安市传染病医院);毛晓辉、庞健健、赵坚、丁超、韦林、薛莲、王思翰、郭晓茹、郑楚云、赵楠、赵敏、剧猛(西安市胸科医院)

利益冲突 所有作者均声明不存在利益冲突

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PMID      [本文引用: 1]

Different pleural fluid biomarkers have been found useful in the discrimination between tuberculous pleural effusion (TPE) and non-TPE, with interferon gamma (IFN-γ) showing the highest single marker diagnostic accuracy. The aim of the present study was to develop predictive models based on clinical data and pleural fluid biomarkers, other than IFN-γ, which could be applied in differentiating TPE and non-TPE. Two hundred and forty two patients with newly diagnosed pleural effusion were prospectively enrolled. Upon completion of the diagnostic procedures, the underlying disease was identified in 203 patients (117 men and 86 women, median age 65 years; 44 patients with TPE and 159 with non-TPE) who formed the proper study group. Pleural fluid level of ADA, IFN-γ, IL-2, IL-2sRα, IL-12p40, IL-18, IL-23, IP-10, Fas-ligand, MDC, and TNF-α was measured and then ROC analysis and multivariate logistic regression were used to construct the predictive models. Two predictive models with very high diagnostic accuracy (AUC > 0.95) were developed. The first model included body temperature, white blood cell count, pleural fluid ADA and IP-10. The second model was based on age, sex, body temperature, white blood cell count, pleural fluid lymphocyte percentage, and IP-10 level. We conclude that two new predictive models based on clinical and laboratory data demonstrate very high diagnostic performance and can be potentially used in clinical practice to differentiate between TPE and non-TPE.

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PMID      [本文引用: 1]

Multidisciplinary management of thoracic infection, including experts in thoracic surgery, pulmonology, infectious disease, and radiology, is ideal for optimal outcomes. Initial assessment of parapneumonic effusion and empyema requires computed tomographic evaluation and consideration for fluid sampling or drainage. Goals for the treatment of parapneumonic effusion and empyema include drainage of the pleural space and complete lung reexpansion. Pulmonary abscess is often successfully treated with antibiotics and observation. Surgical intervention for the treatment of fungal or tuberculous lung disease should be undertaken by experienced surgeons following multidisciplinary assessment. Sternoclavicular joint infection often requires joint resection. Copyright © 2014 Elsevier Inc. All rights reserved.

Coote N, Kay E.

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PMID      [本文引用: 1]

The scope of lung ultrasound (LUS) in emergency and critical care settings has been studied extensively. LUS is easily available at bedside, free of radiation hazard and real time. All these features make it useful in reducing need of bedside X-rays and CT scan of chest. LUS has been proven to be superior to the bedside chest X-ray and equal to chest CT in diagnosing many pleural and lung pathologies. The first International Consensus Conference on Lung Ultrasound (ICC-LUS) has given recommendations for unified approach and language in major six areas of LUS. The LUS diagnosis is to be given after integration of findings of both lungs. The BLUE protocol is first LUS-based systematic approach in diagnosing pleural and lung pathologies. The protocol suggested in this article includes history and conventional clinical assessment along with LUS features.

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PMID      [本文引用: 1]

Interest in transthoracic ultrasound (US) procedures increased after the availability of portable US equipment suitable for use at the patient's bedside. It is possible to detect space-occupying lesions of the pleura, pleural effusion, focal or diffuse pleural thickening and subpleural lesions of the lung, even in emergency settings. Transthoracic US is useful as a guidance system for thoracentesis and peripheral lesion biopsy, where it minimises the occurrence of pneumothorax and haemorrhage. Transthoracic US imaging is strongly influenced by physical interaction of the ultrasonic beam at the tissue/air interface, which gives rise to reverberations classified as simple (A-line), "comet tail" and "ring down"(B-line) artifacts. Although these artifacts can be suggestive of a disease condition, they are essentially imaging errors present even in normal subjects and in empty-pleura post-pneumonectomy patients. In order to clarify some confusion and to report on the state of the art, we present a review of the literature on transthoracic US in diseases of the pleura and peripheral lung regions and our own clinical experience over 3 decades. The review focuses on quality assurance procedures and their value in diagnostic imaging and patient monitoring and warns against possible inappropriate indications and misleading information. Thoracic US is much more than "fishing for the moon in the well".

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PMID      [本文引用: 1]

To compare the results of gray scale ultrasound with those of color Doppler ultrasound in order to evaluate the minimal pleural effusion and to differentiate the minimal pleural effusion from pleural thickening.We prospectively analyzed 86 patients who, according to their chest radiographs, were suspected of having minimal pleural effusion. All patients were examined by ultrasonography on gray scale and color Doppler and the presence or absence of pleural effusion was confirmed by thorax CT. Using the color Doppler examination we analyzed the fluid color sign of pleural effusion.In our study, the ultrasonography on gray scale in real time detected pleural effusion with 60% specificity, 100% sensitivity and 88.37% accuracy. By applying the color Doppler the specificity of the method is higher (specificity 100%, sensitivity 96.72% and accuracy 97.57%).The evidence of pleural effusion on grayscale ultrasound has a greater sensitivity than that of color Doppler ultrasound, but has a smaller specificity. Therefore, color Doppler ultrasound proved to be a useful diagnostic aid in gray-scale ultrasound for the assessment of minimal effusion, having the highest accuracy.

Teichgräber UK, Hackbarth J.

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PMID      [本文引用: 2]

To validate the accuracy of previously published equations that estimate pleural effusion volume using ultrasonography.Only equations using simple measurements were tested. Three measurements were taken at the posterior axillary line for each case with effusion: lateral height of effusion (), distance between collapsed lung and chest wall () and distance between lung and diaphragm (). Cases whose effusion was aspirated to dryness were included and drained volume was recorded. Intra-class correlation coefficient (ICC) was used to determine the predictive accuracy of five equations against the actual volume of aspirated effusion.46 cases with effusion were included. The most accurate equation in predicting effusion volume was ( + ) × 70 (ICC 0.83). The simplest and yet accurate equation was × 100 (ICC 0.79).Pleural effusion height measured by ultrasonography gives a reasonable estimate of effusion volume. Incorporating distance between lung base and diaphragm into estimation improves accuracy from 79% with the first method to 83% with the latter.

Scarlata S, Venditti I, Fulco G, et al.

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PMID      [本文引用: 1]

Computed tomography (CT) scanning is the gold standard when estimating pleural effusion volume; however, the procedure exposes patients to ionizing radiation. Our study was aimed at developing ultrasound-based calculation models that can quantify the volume of pleural effusion in seated patients and validating each model using volumetric chest CT analyses as reference. Our study enrolled 36 hospitalized patients who underwent a chest CT scan and ultrasound, in the seated position, with the aid of a convex probe. To estimate the volume of pleural effusions, we applied one linear and two multiplanar ultrasound-based equations using a CT reconstruction as reference. Testing these models in our validation set (n = 16), we determined that 0.42 was the R coefficient for the linear equation, and 0.97 and 0.98, respectively, were the R coefficients for the cylindrical-sector models, and observed that the latter had the lowest dispersion of data and an optimal intraclass correlation coefficient. We then concluded that multiplanar ultrasound-based equations are accurate and reliable in estimating pleural effusions and outperform previously developed equations.Copyright © 2020 World Federation for Ultrasound in Medicine & Biology. Published by Elsevier Inc. All rights reserved.

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PMID      [本文引用: 1]

To develop a practical method of estimating the volume of pleural effusions with sonography.Fifty-one patients underwent sonography of the pleural space while supine. Sonographic results and results of lateral decubitus radiography were compared with actual effusion volumes. The maximum thickness of the pleural fluid layer was measured with both modalities, while actual effusion volume was determined by means of complete drainage.Sonographic measurements correlated statistically significantly better with actual effusion volume (r =.80) than did radiographic measurements (r =.58) (P < or =.05). With sonographic measurement, an effusion width of 20 mm had a mean volume of 380 mL +/- 130 (standard deviation), while one of 40 mm had a mean volume of 1,000 mL +/- 330. Prediction error with sonographic measurement (mean, 224 mL) was statistically significantly less (P < or =.002) than that with radiographic measurement (mean, 465 mL).In quantification of pleural effusions, the sonographic measurement method presented is preferable to radiographic measurement.

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Tuberculous empyema represents a chronic, active infection of the pleural space that contains a large number of tubercle bacilli. It is rare compared with tuberculous pleural effusions that result from an exaggerated inflammatory response to a localized paucibacillary pleural infection with tuberculosis. The inflammatory process may be present for years with a paucity of clinical symptoms. Patients often come to clinical attention at the time of a routine chest radiograph or after the development of bronchopleural fistula or empyema necessitatis. The diagnosis of tuberculous empyema is suspected on computed tomography imaging by finding a thick, calcific pleural rind and rib thickening surrounding loculated pleural fluid. The pleural fluid is grossly purulent and smear positive for acid-fast bacilli. Treatment consists of pleural space drainage and antituberculous chemotherapy. Problematic treatment issues include the inability to re-expand the trapped lung and difficulty in achieving therapeutic drug levels in pleural fluid, which can lead to drug resistance. Surgery, which is often challenging, should be undertaken by experienced thoracic surgeons.

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The aim of this study was to assess the safety and efficacy of image-guided percutaneous catheter drainage (IGPCD) of thoracic empyemas, and to correlate the outcome of IGPCD with the pre-procedural sonographic appearance. One hundred three patients (74 males and 29 females) with thoracic empyema (age range 1 month to 70 years, median age 28 years) underwent IGPCD. In 63 (61.17%) patients, IGPCD was the primary treatment modality; in 40 (38.84%) patients it was used after unsuccessful intercostal chest tube drainage (ICTD). Ultrasound was the main modality used for guidance; CT guidance was used in only 7 patients (6.8%). Eight- to 12-F pigtail catheters or 10- to 14-F Malecot catheters were used. The outcome was correlated with the pre-procedural US appearance (anechoic, complex non-septated or complex septated) of the empyema. The IGPCD technique was successful in 80 of 102 patients. Based on the US appearance, IGPCD was successful in 12 of 13 (92.3%) patients with anechoic empyemas; 53 of 65 (81.54%) patients with complex non-septated empyemas, and in 15 of 24 (62.5%) patients with complex septated empyemas. A statistically significant difference (p < 0.01) was seen in the outcome of IGPCD in the three categories. Twenty-two patients required further treatment: ICTD (n = 9; 2 of them later also underwent surgery); and surgery (n = 15). The duration of catheter drainage ranged from 2-60 days. No major complications were encountered. Percutaneous catheter drainage of thoracic empyemas with imaging guidance ensures accurate catheter placement with a high success and a low complication rate. Pre-procedural US can predict the likelihood of success of IGPCD.

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胡连锋.

胸腔置管联合尿激酶治疗结核性胸膜炎的疗效及安全性评价

中国现代药物应用, 2021, 15(13):127-129. doi: 10.14164/j.cnki.cn11-5581/r.2021.13.046.

[本文引用: 1]

Petrakis IE, Kogerakis NE, Drositis IE, et al.

Video-assisted thoracoscopic surgery for thoracic empyema: primarily, or after fibrinolytic therapy failure?

Am J Surg, 2004, 187(4):471-474. doi: 10.1016/j.amjsurg.2003.12.048.

PMID      [本文引用: 1]

Traditional and modern treatments are proposed for thoracic empyema. The efficacy of video-assisted thocoscopic surgery (VATS) has been studied when the method is applied either as primary treatment for thoracic empyema or after the failure of fibrinolytic therapy.Thirty-eight patients treated with VATS for thoracic empyema have been reviewed. Of those, 20 patients (group 1) with empyema thoracis were referred to VATS after failure of the fibrinolytic treatment. Another 18 patients (group 2) with primary empyema thoracis were treated thoracoscopically immediately when empyema was diagnosed. Both groups were staged 5, 6, or 7 according to Light's criteria.The group 2 patients showed a higher empyema resolving rate (95% versus 85%), shorter hospital stay (4.5 versus 7.5 days), and significantly shorter duration of the procedure (70 +/- 14 versus 62 +/- 10 minutes) in comparison with the patients of group 1.The VATS technique for thoracic empyema is a well-tolerated, minimally invasive technique, with excellent therapeutic results, mild postoperative complications, and reduced hospitalization. VATS should be considered as the treatment of choice for thoracic empyema, in the fibrinopurulent stage, as it is more effective when applied primarily than when applied after fibrinolytic therapy.

Kearney SE, Davies CW, Davies RJ, et al.

Computed tomography and ultrasound in parapneumonic effusions and empyema

Clin Radiol, 2000, 55(7): 542-547. doi: 10.1053/crad.1999.0480.

PMID      [本文引用: 1]

Imaging of pleural empyema by ultrasound (US) or computed tomography (CT) is used to confirm the diagnosis and facilitate drainage. However, the information gained from US and CT may also have prognostic significance. The aim of the present study was to determine if CT and US appearances correlated with the severity of infection as determined by established microbiological and biochemical indicators, and to establish whether either technique could predict those patients who will fail drainage and require surgery.Fifty patients with parapneumonic effusions were assessed. All had thoracic CT and the results of thoracic US were available in 36 patients. Imaging features were compared to the stage of the effusion and clinical outcome.At US, 7/36 (19%) pleural collections were anechoic, 5/36 (14%) were hyperechoic without septae and 24/36 (67%) were hyperechoic with septae. There was no relationship between US appearances and the presence of pus, the effusion stage or the need for surgical treatment. On CT pleural enhancement was seen in all patients. There was evidence of pleural thickening in 46/50 (92%) and thickening of extrapleural fat in 38/50 (76%). There was a trend for mean pleural thickness to increase with an increasing stage of pleural infection. However, a wide range of appearances were seen and overall the thickness of pleural/extrapleural tissues was not significantly related to the stage of effusion or to the requirement for surgery.Although US and CT have established roles in the investigation of parapneumonic effusions, neither technique reliably identifies the stage of pleural infection or predicts those patients who subsequently require surgical intervention after failed management by chest tube drainage and intrapleural fibrinolytics. Kearney, S. E. (2000). Clinical Radiology 55, 542-547.Copyright 2000 The Royal College of Radiologists.

熊洁, 任小平, 魏声泓, .

内科胸腔镜对老年患者渗出性胸腔积液的诊断价值及安全性

临床肺科杂志, 2017, 22(1):11-14. doi: 10.3969/j.issn.1009-6663.2017.01.004.

[本文引用: 1]

唐晓媛, 左慧敏, 陈国峰, .

内科胸腔镜治疗结核性胸膜炎的意义

中国内镜杂志, 2018, 24(7): 1-4. doi: 10.3969/j.issn.1007-1989.2018.07.001.

[本文引用: 1]

Terashita S, Kawachi H, Tajiri T, et al.

Intrapleural urokinase directly under medical thoracoscopy for the diagnosis of tuberculous pleurisy

Respirol Case Rep, 2019, 8(1): e00498. doi: 10.1002/rcr2.498.

[本文引用: 1]

Wurnig PN, Wittmer V, Pridun NS, et al.

Video-assisted thoracic surgery for pleural empyema

Ann Thorac Surg, 2006, 81(1):309-313. doi: 10.1016/j.athoracsur.2005.06.065.

PMID      [本文引用: 1]

After we gained considerable experience with video-assisted thoracic surgery (VATS) and became familiar with its advantages, we started to use it for the treatment of thoracic empyema.We treated 130 patients with pleural empyema in whom chest tube drainage and antibiotic therapy had failed to produce a satisfactory result. Six months after surgery they had clinical and radiologic assessment and spirometry.Video-assisted surgery was performed in all patients. Mean operative time was 93 minutes (range, from 55 to 180 minutes), mean duration of postoperative chest tube drainage was 10 days (range, from 5 to 32 days), and mean hospital stay was 16 days (range, from 3 to 56 days). The rate of conversion to open thoracotomy was 3.1%. Complications for which reoperation was necessary occurred in 9% of patients. At follow-up after six months, the mean forced expiratory volume in 1 second was 87.7% (range, from 69.5% to 105.9%), the mean postoperative vital capacity was 84.4%, (range, from 59.9% to 97.9%). There were no postoperative or procedure-related deaths.Video-assisted thoracic surgery is a safe and effective treatment option for fibropurulent empyema with low morbidity and mortality. Conversion to thoracotomy should be used if necessary to remove all of the fibropurulent material and achieve complete expansion of the lung to insure a good outcome.

Davies CW, Gleeson FV, Davies RJ, et al.

BTS guidelines for the management of pleural infection

Thorax, 2003, 58 Suppl 2(Suppl 2): ii18-28. doi: 10.1136/thorax.58.suppl_2.ii18.

[本文引用: 1]

钟红红, 赵丽青, 孙丽娟.

中心静脉导管胸腔置管治疗结核性包裹性胸腔积液疗效观察

中华保健医学杂志, 2020, 22(2): 207-208. doi: 10.3969/j.issn.1674-3245.2020.02.030.

[本文引用: 1]

唐先梅, 赵英仁, 江自成, .

新方法初治结核性胸膜炎的疗效观察

中国感染控制杂志, 2018, 17(1): 52-55. doi: 10.3969/j.issn.1671-9638.2018.01.011.

[本文引用: 1]

张雪元.

胸膜腔微创置管引流联合尿激酶注入治疗结核性胸膜炎的效果分析

中国现代药物应用, 2021, 15(2):179-181. doi: 10.14164/j.cnki.cn11-5581/r.2021.02.079.

[本文引用: 1]

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