4呼吸病診斷課件

Respiratorydisease

放射學(xué)院劉林祥6222136lxliu@1特發(fā)性肺間質(zhì)纖維化原因不明的彌漫性纖維性肺泡炎又稱Hamman-Rich綜合征為肺泡壁損傷所引起的非感染性炎性反應(yīng)近認(rèn)為系免疫性疾病，可能與遺傳有關(guān)2病理急性期：肺泡內(nèi)皮細(xì)胞和基底膜受損，肺泡和間質(zhì)內(nèi)蛋白樣物質(zhì)滲出，伴透明膜形成，繼而淋巴細(xì)胞和單核細(xì)胞滲出。肺泡內(nèi)皮細(xì)胞再生覆蓋在滲出物表面并使其整合入肺間質(zhì)，肺泡壁增厚，膠原纖維扭曲、紊亂而機(jī)化。病變發(fā)展，間質(zhì)纖維化加重晚期：肺泡壁、小葉間隔及胸膜下廣泛纖維化，肺體積縮小變硬，毛細(xì)血管網(wǎng)和氣道的終末部分被破壞。在范圍較大的纖維化區(qū)域，可有終末氣道的代償性擴(kuò)張，形成直徑數(shù)mm至2cm的囊樣含氣腔隙3胸部X線平片早期兩肺中下野細(xì)小網(wǎng)織陰影病變發(fā)展，不對(duì)稱性、彌漫性網(wǎng)狀、條索狀及結(jié)節(jié)狀陰影，可擴(kuò)展至上肺野晚期，結(jié)節(jié)影增大，伴廣泛厚壁囊狀陰影，蜂窩肺并阻塞性肺氣腫時(shí)，肺野透亮度增強(qiáng)囊腫破裂可發(fā)生自發(fā)性氣胸肺纖維化嚴(yán)重時(shí)可發(fā)生肺動(dòng)脈高壓和肺心病5Idiopathicpulmonaryfibrosis磨玻璃樣影及實(shí)變影，內(nèi)見(jiàn)含氣支氣管影，支氣管血管數(shù)增粗Ground-glassattenuation與胸膜面垂直的細(xì)線形影，長(zhǎng)1-2cm，寬約1mm，多見(jiàn)于兩肺下葉兩肺中內(nèi)帶小葉間隔增厚，分支狀細(xì)線形影，Reticularattenuationwithinterlobularseptalthickening胸膜下0.5cm內(nèi)與胸壁內(nèi)面弧度一致的弧線狀影，長(zhǎng)5-10cm，邊緣較清或略模糊，見(jiàn)于兩下肺后外部6Idiopathicpulmonaryfibrosis蜂窩狀影，數(shù)mm至2cm不等的圓形或橢圓形含氣囊腔，壁薄而清楚，與正常肺交界面清楚。分布于兩肺基底部胸膜下區(qū).Ahoneycombpattern,predominantlybasalandperipheralindistribution小結(jié)節(jié)影，邊緣較清楚，纖維條索在橫斷面的表現(xiàn)，或相互交織而成小葉中心性肺氣腫：散在、2-4mm，肺外圍部，病變發(fā)展可漸見(jiàn)于肺中央部。胸膜下見(jiàn)1-2cm類圓形肺氣囊中小支氣管擴(kuò)張，柱狀，伴支氣管扭曲、并攏Architecturaldistortionwithassociatedtractionbronchiectasisandbronchiolectasis7IdiopathicpulmonaryfibrosisF47peripheralGGOInterlobularseptalthickeningIrregularityofthefissuresBronchiectasisEarlyinterstitialpneumonia22mlater,progressionofinterstitialpneumoniaDiffuseGGO,interlobularseptalthickeningAhoneycombpattern8結(jié)節(jié)?。⊿arcoidosis）AsystemicdisorderofunknowncauseNoncaseatinggranulomaswithproliferationofepithelioidcells,多系統(tǒng)肉芽腫性疾病，良性經(jīng)過(guò)，可累及淋巴結(jié)、肺、胸膜、皮膚、骨、眼、脾、肝、腮腺及扁桃體等病理特征為非干酪性肉芽腫淋巴結(jié)大，但不融合。肺門(mén)LN易受累，次為氣管旁和AA旁肺內(nèi)病變沿支氣管血管周圍結(jié)締組織鞘及小葉間隔發(fā)展蔓延，肺內(nèi)肉芽腫主要分布在間質(zhì)，小，直徑在0.4mm以下，胸膜下肺間質(zhì)內(nèi)肉芽腫更密集。小肉芽腫可融合成大結(jié)節(jié)急性發(fā)病者肉芽腫大多經(jīng)治療消退或自行消退。慢性發(fā)病者常導(dǎo)致進(jìn)行性肺纖維化10LaboratoryAngiotensinconvertingenzyme(ACE)levelelevatedandmaycorrelatewithactivityCD4:CD8ratioiscommonlydecreasedHypercalcemiaduetoincreasedintestinalabsorptionofcalcium,resultingfromactivationofvitaminDbymacrophagesinsarcoidgranulomas12Sarcoidosis肺部病變多發(fā)生在淋巴結(jié)病變之后兩肺彌漫性網(wǎng)狀結(jié)節(jié)影，但肺尖或肺底少或無(wú)。結(jié)節(jié)大小不一，多為1-3mm大小，輪廓尚清楚肺內(nèi)圓形病變，直徑約1.0-1.5cm，密度均勻，邊緣較清楚，單發(fā)者類似肺內(nèi)良性病變或周圍型肺癌，多發(fā)者酷似肺轉(zhuǎn)移瘤節(jié)段性或小葉性浸潤(rùn)，類似肺部炎性病變，一般伴或不伴胸腔內(nèi)淋巴結(jié)病變少數(shù)為單純粟粒狀，似急性粟粒型結(jié)核14Sarcoidosis以纖維性病變?yōu)橹髡?，不易與其他原因所致的肺纖維化區(qū)別，且可引起多種繼發(fā)性改變胸膜滲液可能為胸膜臟、壁層廣泛受累所致。肥厚的胸膜為非干酪性肉芽腫骨病變約占10%。損害一般限于手、足的短管狀骨，顯示小囊狀骨質(zhì)缺損并伴有末節(jié)指（趾）的骨質(zhì)吸收，變細(xì)、變短15CT縱隔、肺門(mén)淋巴結(jié)腫大，密度均勻，邊緣清楚，周圍脂肪界面存在。增強(qiáng)掃描呈均勻強(qiáng)化肺內(nèi)可見(jiàn)大小結(jié)節(jié)影或塊狀影晚期支氣管血管束扭曲、聚攏或變形，葉間裂、血管支氣管移位，支氣管擴(kuò)張和不同程度肺氣腫支氣管血管束增厚，邊緣不規(guī)則或結(jié)節(jié)狀，周圍可有大小不等的結(jié)節(jié)狀影；小葉間隔增厚和細(xì)小蜂窩影，見(jiàn)于胸膜下區(qū)胸膜初期為胸腔積液，可自然吸收，少數(shù)可發(fā)展為胸膜肥厚16鑒別診斷肺門(mén)結(jié)核：年輕，有輕度中毒癥狀。氣管旁、支氣管旁淋巴結(jié)腫大，可有鈣化。結(jié)素反應(yīng)陽(yáng)性，痰中找到結(jié)核桿菌霍奇金?。撼Ｏ扔蓄i部、鎖骨上淋巴結(jié)腫大，然后出現(xiàn)不對(duì)稱性雙側(cè)或單側(cè)縱隔淋巴結(jié)腫大，前縱隔較后縱隔多見(jiàn)?？v隔淋巴結(jié)腫大的程度常較肺門(mén)淋巴結(jié)腫大顯著非霍奇金淋巴瘤：多為單側(cè)縱隔淋巴結(jié)腫大，即使雙側(cè)縱隔淋巴結(jié)腫大亦不對(duì)稱。后縱隔多于前縱隔淋巴結(jié)腫大，晚期才有肺門(mén)淋巴結(jié)腫大?？v隔淋巴結(jié)多大于肺門(mén)淋巴結(jié)未分化型小細(xì)胞肺癌：多為單側(cè)縱隔或（和）肺門(mén)分葉狀淋巴結(jié)腫大，雙側(cè)縱隔淋巴結(jié)腫大較少見(jiàn)。部分伴有不同程度的阻塞性肺炎或肺不張。病程發(fā)展迅速間質(zhì)性病變：當(dāng)病變發(fā)展至纖維化期則需與癌性淋巴管炎、間質(zhì)性肺炎、嗜酸性肉芽腫等鑒別17SarcoidosisSymptomsandsignsarenonspecific,halfasymptomaticFatigue,weightloss,generalmalaise,feverBilateralhilarlymphadenopathyiscommonfindingOftenwithassociatedpulmonaryinfiltratesSkinandocularlesions,theliver,spleen,lymphnodes,parotidglands,CNS,genitourinarysystem,muscles,andbonesmaybeinvolved18HilaradenopathyM27ChestradiographTypicalbilateralhilaradenopathyAdenopathyintherightparatrachealandleftaortic-pulmonarywindownodesisalsoidentified20HilaradenopathyE+CTclearlydepictsthebilateralhilaradenopathy21MediastinaladenopathyM26SeverebackpainEnlargedrightparatrachealnodesLeftaortic-pulmonarywindownodeswithassociatedminimalhilarinvolvementarealsoseen23MediastinaladenopathyMediastinaladenopathy,60MCalcificationintheaffectedhilarnodes,hugesubcarinallymphnodesAnunusualfindinginothergranulomatousdiseasessuchastuberculosis24PulmonarysarcoidosisStageIVdiseasemaymanifestasconglomeratedmasseswithmarkedtractionbronchiectasisUsuallypredominantlyinthecentralandupperlung.thisdistributionistypicalofsarcoidosisbutcanalsobeseenintuberculosisandsilicosisExtensivecalcificationmaybeencounteredwithinfibroticgranulomasCavitationorcystformationmayalsobeseen26PulmonarysarcoidosisM37Smallnoduleswithaperivasculardistributionandirregularthickeningofbronchovascularbundlesandinterlobularsepta27PulmonarysarcoidosisM24HRCTMultiplemiliarynodulesanddiffusethickeningofthebronchialwallSimultaneouspresenceofsmallnoduleswithaperivasculardistributionandalongtheinterlobularpleura28PulmonarysarcoidosisHRCTWidespreadgroundglassattenuationReticulonodularMildbronchiectasisperipherally30PulmonarysarcoidosisF26MultiplenodulesbilaterallyMinimalhilaradenopathySimulatemetastates31PulmonarysarcoidosisAnodularconsolidationwithill-definedbordersAirbronchogramwithinthenodules32StageIVpulmonarysarcoidosisM60,ExtensivefibroticchangeandcavitarylesionswithacentraldistributiondistortinglungparenchymaIrregularthickeningofpleuraandoverinflationofperipherallungparenchyma33PrimaryBronchogenicCancerMacro-pathologyCentraltype：主支氣管、肺葉支氣管及肺段支氣管的肺癌Peripheraltype：肺段以下支氣管直到細(xì)支氣管以上的肺癌Alveolartype：發(fā)生于細(xì)支氣管或肺泡上皮的肺癌34Histologicaltypesoflungcancer來(lái)自支氣管表面上皮的癌鱗狀上皮癌Squamouscellcarcinoma腺癌Adenocarcinoma腺鱗癌大細(xì)胞癌Largecellcarcinoma來(lái)自神經(jīng)內(nèi)分泌細(xì)胞的癌高分化：類癌carcinoid中分化：不典型類癌atypicalcarcinoid低分化：小細(xì)胞癌Smallcellcarcinoma來(lái)自細(xì)支氣管Clara細(xì)胞和Ⅱ型肺細(xì)胞的癌細(xì)支氣管肺泡癌bronchialalveolarcarcinoma35中心型肺癌臨床表現(xiàn)：刺激性干咳、痰中帶血，胸痛、發(fā)熱直接征象：肺門(mén)腫塊，支氣管狹窄與阻塞間接征象：支氣管阻塞或狹窄后引起的阻塞性肺炎、肺不張、肺氣腫轉(zhuǎn)移征象36右肺上葉中心型肺癌37右肺上葉中心型肺癌38右肺上葉中心型肺癌39中心型

肺癌縱隔增寬、肺門(mén)增大，為肺癌的淋巴結(jié)轉(zhuǎn)移40中心型肺癌：右肺門(mén)及右上縱隔不規(guī)則腫塊，中上肺野片絮狀密度增高影。斷層示上葉支氣管鼠尾狀狹窄41中心型肺癌左肺肺癌，右肺代償性肺氣腫42Centraltype--CTfindings管壁型：管壁增厚，管腔不規(guī)則狹窄管內(nèi)型：腔內(nèi)軟組織腫塊，偏心性狹窄或閉塞，杯口狀截?cái)喙芡庑停汗鼙诃h(huán)形增厚，腔外軟組織腫塊管腔狹窄或閉塞，繼發(fā)遠(yuǎn)端肺炎癥、不張或氣腫肺門(mén)縱隔淋巴結(jié)轉(zhuǎn)移，呈軟組織樣等密度，單個(gè)或多個(gè)融合成分葉狀，增強(qiáng)掃描無(wú)強(qiáng)化肺內(nèi)，胸膜及遠(yuǎn)處轉(zhuǎn)移43中心型肺癌44Centraltype--CTfindings45Centraltype--CTfindings46Centraltype47Squamouscellcarcinoma48Squamouscellcarcinoma49Squamouscellcarcinoma50Lungcancer--peripheraltype臨床表現(xiàn)：可無(wú)癥狀或胸痛、咳嗽直接征象：肺內(nèi)結(jié)節(jié)和腫塊邊緣分葉，臍樣切跡，毛刺小于2cm的孤立結(jié)節(jié)，內(nèi)部密度不均勻。大于3cm時(shí)，密度較均勻厚壁空洞間接征象：小葉范圍的阻塞性肺炎、肺不張，彗尾征。胸膜凹陷轉(zhuǎn)移征象51右肺見(jiàn)結(jié)節(jié)性病灶，CT示分葉與毛刺52厚壁空洞，體層示空洞內(nèi)壁凹凸不平53周圍型肺癌--癌性空洞54Peripheraltype肺內(nèi)腫塊，下緣與胸膜間有牽拽，箭頭所指為慧尾征55Peripheraltype—CTfindings肺內(nèi)結(jié)節(jié)，腫塊軟組織密度，均勻或不均勻，空泡征，鈣化少肺窗：邊緣毛刺，胸膜凹陷征，血管集束征縱隔窗：深分葉，偏心空洞，小棘狀突起，臍征肺門(mén)縱隔淋巴結(jié)轉(zhuǎn)移遠(yuǎn)處轉(zhuǎn)移56周圍型肺癌57Peripheralcarcinoma58Peripheralcarcinomaground-glassopacity59PeripheralcarcinomaSofttissuemassSpicula60Peripheralcarcinoma61Peripheralcarcinoma62Peripheralcarcinoma--lobulation63Hilarmetastases64Peripheralcarcinoma65Peripheralcarcinoma66Peripheralcarcinoma67Peripheralcarcinoma68Peripheralcarcinoma-cavity69PancoasttumorsArisefromlungapexInvadecostovertebralgrooveinsuperiorsulcusInvadeparietalpleura,causingnonspecificshoulderpainradiatingdownmedialaspectofscapulaInvolveT1nerveroot,causingpainradiatingalongmedialaspectofarmandforearmasfaraswristInvadestellateganglion,causingHornersyndrome,includeptosis(narrowingofthepalpebralfissure),miosis(pupillaryconstriction),andanhidrosis(absenceofsweatingononesideoftheface)70PancoasttumorsInvadefirst,second,andthirdribsposteriorlySuperiorextensionencasingC8nerveroot,withresultantpaininmedialtwodigitsofhandandatrophyofintrinsicmusclesofhandAnteriorextensionintotracheoesophagealgrooveresultinvagalorrecurrentlaryngealnervepalsySuperomedialextensionmayresultininvolvementofvertebralartery,vertebralbodies,neurovertebralforamina,andspinalcanal,withaconsequentriskofparaplegia71右肺上溝癌右肺上野片狀陰影，第一、二肋骨溶骨性破壞72Pancoasttumor73M48，leftinterscapularchestwallpain

suggesteT1nerverootinvasion74SuperiorsulcustumorM48w/oneurologicsignsinleftupperextremitybutwithleftinterscapularchestwallpainsuggestiveofT1nerverootinvasionM48，leftinterscapularchestwallpain

suggesteT1nerverootinvasion75Alveolarcancinoma雙肺布滿結(jié)節(jié)性病灶病理證實(shí)為肺泡癌76肺泡癌77Alveolarcancinoma78Alveolarcancinoma79Alveolarcancinoma80Bronchioloalveolar

carcinoma

A

53-year-oldmanInitial(1mm)CTatthelevelofthebronchusintermediusasmallnodularareaofground-glassattenuationintherightupperlobeFollow-upCT(5mm)48monthslaterincreasednodulesize.81肺轉(zhuǎn)移瘤宮頸癌術(shù)后，肺內(nèi)數(shù)個(gè)轉(zhuǎn)移病灶82Lungmetastases83Lungmetastases,rectalcancer84Lungmetastases85食道癌肺轉(zhuǎn)移86Lungmetastases,coloncancer87錯(cuò)構(gòu)瘤(hamartoma)非真性腫瘤，內(nèi)胚層與間胚層發(fā)育異常形成根據(jù)部位，分為周圍型和中央型局限于某一肺葉或肺段的反復(fù)發(fā)作感染肺內(nèi)球形軟組織腫塊，見(jiàn)爆米花樣鈣化CT掃描：鈣化、鈣化、脂肪88錯(cuò)構(gòu)瘤左肺門(mén)外上腫塊內(nèi)可見(jiàn)爆米花樣鈣化89Hamartoma90錯(cuò)構(gòu)瘤91Hamartoma92肺栓塞(pulmonaryemboli)肺動(dòng)脈分支被栓子堵塞引起的肺供血障礙常見(jiàn)栓子是深靜脈脫落的血栓久病臥床、妊娠、大手術(shù)后和心功能不全可發(fā)生深靜脈血栓風(fēng)心病，原發(fā)于肺動(dòng)脈的血栓進(jìn)入血循環(huán)的脂肪、腫瘤栓子和氣體93PulmonaryembolismThethirdmostcommonacutecardiovasculardiseaseaftermyocardialinfarctionandstrokeResultsinthousandsofdeathseachyearbecauseitoftengoesundetectedCTAhassensitivitiesof53%–100%andspecificitiesof83%–100%Pulmonaryangiography,thediagnosticstandardofreferenceforconfirmingorrefutingdiagnosis94病理雙重供血，正常時(shí)兩組有豐富的吻合支當(dāng)肺動(dòng)脈的某一分支栓塞后，肺組織因支氣管動(dòng)脈的側(cè)枝供血而不發(fā)生異常，栓子較小未能完全堵塞肺動(dòng)脈分支時(shí)也不易發(fā)生供血障礙多數(shù)小栓子進(jìn)入肺循環(huán)可引起肺動(dòng)脈小分支多發(fā)性栓塞95臨床表現(xiàn)多無(wú)明顯癥狀，或有輕微不適可為突發(fā)的呼吸困難和胸痛肺動(dòng)脈大分支或主干栓塞或廣泛的肺動(dòng)脈小分支栓塞可出現(xiàn)嚴(yán)重的呼吸困難、發(fā)紺、休克或死亡較大的栓子堵塞肺動(dòng)脈大分支或主干可引起急性右心衰竭或心肌梗死而致死亡96X線表現(xiàn)肺動(dòng)脈較大分支栓塞或多發(fā)性小分支栓塞X線平片可出現(xiàn)異常陰影，較小分支栓塞即使出現(xiàn)癥狀并經(jīng)血管造影證實(shí)，X線仍可正常肺缺血又稱Westermark征，當(dāng)肺葉或肺段動(dòng)脈栓塞時(shí)，相應(yīng)區(qū)域內(nèi)肺血管紋理減少或消失，透亮度增加多發(fā)性肺小動(dòng)脈栓塞引起廣泛性肺缺血，顯示肺紋理普遍減少和肺野透亮度增加，但無(wú)肺體積膨脹現(xiàn)象97X線表現(xiàn)嵌塞在肺動(dòng)脈內(nèi)的血栓使相應(yīng)部位血管陰影增寬，阻塞遠(yuǎn)端致血流減少而變細(xì)多發(fā)于下葉且以右下葉多見(jiàn)，下葉體積縮小，膈肌升高，葉間裂下移。并盤(pán)狀肺不張較大肺動(dòng)脈栓塞或多發(fā)性小動(dòng)脈栓塞可引起心影增大，主要是右心室增大，同時(shí)有肺動(dòng)脈高壓右心功能不全時(shí)心影增大更為顯著，奇靜脈和上腔靜脈增粗98X線血管造影肺動(dòng)脈分支內(nèi)充盈缺損或截?cái)嗑窒扌匝軠p少或無(wú)血管區(qū)，血灌流緩慢小分支多發(fā)性栓塞引起肺動(dòng)脈外圍分支迂曲，突然變細(xì)，呈剪枝樣細(xì)小分支的栓塞血管造影不能顯示血栓24hs后開(kāi)始溶解，故48hs后造影可正常繼發(fā)肺動(dòng)脈高壓和肺心病時(shí)，肺動(dòng)脈干和大分支擴(kuò)張，周圍分支變細(xì)99CT平掃：較大肺動(dòng)脈栓塞見(jiàn)血管內(nèi)高密度或低密度病灶。高密度為新鮮血栓，低密度為陳舊性血栓增強(qiáng)：血栓為長(zhǎng)條狀及不規(guī)則形充盈缺損栓塞的肺動(dòng)脈可有不同程度的擴(kuò)張較大肺血管栓塞可見(jiàn)相應(yīng)區(qū)域肺血管分布減少100Acute

pulmonaryembolismArterialocclusionwithfailuretoenhancetheentirelumenduetoalargefillingdefectArterymayenlargedvs.adjacentpatentvesselsApartialfillingdefectsurroundedbycontrastmaterial,"polomint"sign,"railwaytrack"signPeripheralwedgeshapedareasofhyperattenuationrepresentinfarcts,alongwithlinearbandsaresignificantancillaryfindings101AcuteocclusivepulmonaryembolismF32ChestpainApulmonaryemboluswithinposterobasalsegmentofrightlowerlobearteryArteryenlargevs.adjacentpatentvessels102AcutepulmonaryembolismF45chestpainApulmonaryembolusaffectsthesegmentalarteryofthelaterobasalsegmentofrightlowerlobePartialfillingdefectsurroundedbycontrastmaterialproducesthepolomintsign103AcutepulmonaryembolismM66ChestpainanddyspneaAcutepulmonaryemboluscausesapartialfillingdefectsurroundedbycontrastmaterialAnotheracutepulmonaryembolusaffectstheleftmainpulmonaryartery104AcutepulmonaryembolismF58ChestpainanddyspneaApulmonaryembolusresultsinaneccentricallypositionedpartialfillingdefectSurroundedbycontrastmaterialandformsacuteangleswiththearterialwall105AcutepulmonaryembolismF58chestpainanddyspneaAncillaryfindingsofaperipheralwedge-shapedareaofhyperattenuation106AcutepulmonaryembolismMorphologicabnormalitiessuggestrightventricularfailurecanbequantifiedwithCTpulmonaryangiographyRVdilatation(RVcavityiswiderthanLVcavityintheshortaxis),w/ocontrastmaterialrefluxintohepaticveinsDeviationofinterventricularseptumtowardLVApulmonaryembolismindexgreaterthan60%107AcutepulmonaryembolismM42chestpainandseveredyspneashortaxisofRViswiderthanthatofLV,causedbyacutepulmonaryembolismandcreatedRVstrain108AcutecentralpulmonaryembolismF87asymptomaticSubtleregionsofhyperattenuationCTA:acutepulmonaryembolismwithintherightmainandleftinterlobarpulmonaryarteries109ChronicPulmonaryEmbolism

DiagnosticcriteriaCompleteoccludedvesselissmallerthanadjacentpatentvesselsAperipheral,crescentshapedintraluminaldefectformsobtuseangleswithvesselwallContrastmaterialflowingthroughthickened,oftensmallerarteriesduetorecanalizationAweborflapwithinacontrastfilledarterySecondarysignsExtensivebronchialcollateralvesselsAnaccompanyingmosaicperfusionpatternCalcificationwithineccentricvesselthickening110Chronicpulmonaryembolism27MdyspneaCompleteoccludedvesselsinleftlungaresmallerthanadjacentpatentvesselsCollateralbloodsupplyfromabranchofrighthemidiaphragmaticartery111ChronicpulmonaryembolismM62DyspneaAneccentricallylocatedthrombusformsobtuseangleswithvesselwallDilatedcollateralbronchialartery112ChronicpulmonaryembolismAsmall,recanalizedpulmonaryarterywithcontrastmaterialinthecentrallumen113ChronicpulmonaryembolismM56dyspneaAflapwithinasmallrightinterlobarpulmonaryarteryCollateralbronchialarterydilatationisalsonoted114ChronicpulmonaryembolismAlargechronicpulmonaryembolusinthemainandleftmainpulmonaryarteriesArrowsindicatecollateralbronchialarteries115ChronicpulmonaryembolismF60,dyspnea.Amosaicperfusionpattern:Darkregionsofunderperfusedlungcontainvesselsthataresmallerthanadjacentpatentvesselsinnormallyperfusedlung116ChronicpulmonaryembolismM62DyspneaPulmonaryarterialwallcalcificationAsecondarysignofchronicpulmonaryembolism117PulmonaryarterialhypertensionsecondarytochronicpulmonaryembolismAncillaryfindingspulmonaryarterydiameter＞33mmpericardialfluidPulmonaryarterymeasures41mmindiameterindicateshypertension118ChronicpulmonaryembolismPericardialfluidassociatedwithpulmonaryarterialhypertensionSecondarytochronicpulmonaryembolism119塵肺Pneumocomosis肺通過(guò)氣道與外界相通，吸入在空氣中懸浮的無(wú)機(jī)和有機(jī)塵粒，這些塵粒部分可致病正常肺有很強(qiáng)的能力來(lái)清除這些塵粒但過(guò)多的生產(chǎn)性粉塵則可引起氣道和肺泡的損傷，導(dǎo)致肺部彌漫性纖維化，稱為塵肺120國(guó)家現(xiàn)行規(guī)定的12種塵肺矽肺silicosis煤工塵肺coalworkerpneumoconiosis石墨塵肺graphitepneumoconiosis炭黑塵肺anthracosis石棉肺abestosis滑石塵肺talcpneumoconiosis水泥塵肺cementpneumoconiosis云母塵肺micapneumoconiosis陶工塵肺kaolinpneumoconiosis鋁塵肺aluminumpneumoconiosis電焊工塵肺electricandwelderpneumoconiosis鑄工塵肺foundryworkerpneumoconiosis121塵肺的診斷原則①根據(jù)目前我國(guó)現(xiàn)行政策的規(guī)定：塵肺的診斷必須是由國(guó)家衛(wèi)生行政部門(mén)指定的塵肺診斷小組來(lái)進(jìn)行，任何個(gè)人作出的診斷都是無(wú)效的②許多疾病可形成類似塵肺的肺部彌漫性改變，因此作為影像專業(yè)醫(yī)師，應(yīng)對(duì)引起塵肺的病因?qū)W、生產(chǎn)現(xiàn)場(chǎng)的流行病學(xué)調(diào)查及其臨床病理資料有所了解③塵肺診斷的前提是病人必須有明確的生產(chǎn)性粉塵接觸史，并且有同行業(yè)人發(fā)病年齡作為參考資料122基本影像學(xué)表現(xiàn)類圓形小陰影：最常見(jiàn)和最重要表現(xiàn)，見(jiàn)于矽肺不規(guī)則形小陰影：網(wǎng)狀，有時(shí)呈蜂窩狀大陰影：指直徑超過(guò)10mm的陰影，邊界清楚，周圍有明顯的肺氣腫；多出現(xiàn)于兩肺上、中區(qū)，常對(duì)稱出現(xiàn)；大陰影的長(zhǎng)軸常與后肋垂直，不受葉間裂的限制?！鞍俗中巍被蜷L(zhǎng)條形大陰影常見(jiàn)于典型矽肺胸膜斑：不同程度的胸膜肥厚、粘連及鈣化等改變，局限性胸膜斑則是石棉肺的主要表現(xiàn)之一。局限胸膜增厚的厚度大于3mm時(shí)稱為胸膜斑，多見(jiàn)于側(cè)胸壁，亦見(jiàn)于部分心緣和膈面，可發(fā)生鈣化123基本影像學(xué)表現(xiàn)肺門(mén)改變：早期肺門(mén)陰影增大增濃，有時(shí)見(jiàn)腫大淋巴結(jié)影。淋巴結(jié)蛋殼樣鈣化多于兩側(cè)肺門(mén)對(duì)稱出現(xiàn)，也可見(jiàn)于一側(cè)，呈圓形、橢圓形或不整形，常數(shù)個(gè)同時(shí)出現(xiàn)；殼壁可呈斷續(xù)的殘缺狀肺紋理改變：早期有肺紋理增強(qiáng)、變粗等改變。肺間質(zhì)纖維化的進(jìn)一步發(fā)展，使肺紋理變形。隨著小陰影出現(xiàn)和逐漸增多，特別是不規(guī)則小陰影的增多，肺紋理則逐漸變成模糊、減少或消失124矽肺Silicosis

二氧化硅粉塵引起的肺部彌漫性纖維化塵肺中最多見(jiàn)且危害最大的一種，多見(jiàn)于采礦、玻璃、陶瓷、耐火材料、石英制粉、機(jī)械制造業(yè)工人基本改變是慢性進(jìn)行性肺間質(zhì)纖維化及矽結(jié)節(jié)形成多個(gè)小結(jié)節(jié)可相互融合形成大結(jié)節(jié)或融合團(tuán)塊，周圍有肺氣腫，是矽肺晚期常見(jiàn)改變125Silicosis粉塵中游離二氧化硅含量越高，肺內(nèi)改變?cè)揭越Y(jié)節(jié)為主，矽結(jié)節(jié)越致密清楚。游離二氧化硅含量越低，間質(zhì)性纖維改變?cè)矫黠@，矽結(jié)節(jié)淡而輪廓模糊早期可無(wú)癥狀晚期則可有呼吸困難，甚至發(fā)紺、咯血合并結(jié)核及慢性炎癥者癥狀更為嚴(yán)重最后因肺源性心臟病而致心肺功能衰竭126X線表現(xiàn)肺紋理增強(qiáng)并伸展至肺外帶，細(xì)網(wǎng)狀紋理，在網(wǎng)格交叉處見(jiàn)有極小顆粒，肺野透亮度減低呈磨玻璃樣矽結(jié)節(jié)：診斷矽肺和混合性矽肺的主要依據(jù)。多在兩側(cè)中、下肺野內(nèi)中帶區(qū)域開(kāi)始出現(xiàn)典型表現(xiàn)為直徑約3mm左右，輪廓清楚，致密孤立的結(jié)節(jié)陰影，多與肺紋理分離病變發(fā)展，矽結(jié)節(jié)漸增大增多，融合成致密而均勻的團(tuán)塊，即大結(jié)節(jié)影，常見(jiàn)于兩上肺野外帶，輪廓清楚。典型大結(jié)節(jié)陰影在兩肺分布對(duì)稱，呈翼狀127X線表現(xiàn)肺門(mén)影增大，密度增高。晚期可見(jiàn)肺門(mén)上提或外移。肺門(mén)呈殘根樣。肺門(mén)淋巴結(jié)蛋殼樣鈣化肺紋理增多增粗，延長(zhǎng)到肺野外帶。病程進(jìn)展，肺紋理發(fā)生扭曲變形、紊亂及中斷現(xiàn)象。晚期由于矽結(jié)節(jié)增多，肺氣腫加劇，肺紋理減少肺氣腫可為彌漫性或局限性或灶性肺氣腫胸膜改變：早期以肋膈角變鈍或消失最多見(jiàn)，隨病變進(jìn)展，肺底胸膜肥厚，表現(xiàn)膈面毛糙，或膈胸膜粘連所形成幕頂樣改變，縱隔胸膜增厚粘連表現(xiàn)為縱隔陰影增寬，邊緣平直或呈不規(guī)則狀。128矽肺合并結(jié)核早期矽肺或混合矽肺并發(fā)的結(jié)核病灶大都趨向于一側(cè)或兩側(cè)肺尖或鎖骨上下區(qū)晚期，各肺野包括肺尖區(qū)都已散布有明顯矽結(jié)節(jié)時(shí)，并發(fā)一側(cè)或兩側(cè)結(jié)核病灶與矽結(jié)節(jié)早期融合鑒別較為困難，伴有空洞者支持結(jié)核的診斷129Simplesilicosis59M,workedinhard-rockminingfor10yearsdiffusenodularopacities,relativesparingofbasallungzones130Simplesilicosisnumerousmicronodulesinbothupperlungswithposteriorzonalpredominance.multiplesubpleuralnodulesandpseudoplaques131塵肺的胸部X線片表現(xiàn)分期無(wú)塵肺（0）0：X線胸片無(wú)塵肺表現(xiàn)0＋

：胸片表現(xiàn)尚不夠診斷為Ⅰ者一期塵肺（Ⅰ）Ⅰ：有總體密集度1級(jí)的小陰影，分布范圍至少達(dá)到兩個(gè)肺區(qū)Ⅰ＋：有總體密集度1級(jí)的小陰影，分布范圍超過(guò)4個(gè)肺區(qū)或有總體密集度2級(jí)的小陰影，分布范圍達(dá)到4個(gè)肺區(qū)二期塵肺（Ⅱ）Ⅱ：有總體密集度2級(jí)的小陰影，分布范圍超過(guò)4個(gè)肺區(qū)；或有總體密集度3級(jí)的小陰影，分布范圍達(dá)到4個(gè)肺區(qū)Ⅱ＋：有總體密集度3級(jí)的小陰影，分布范圍超過(guò)4個(gè)肺區(qū)；或有小陰影聚集；或有大陰影，但尚不夠診斷為Ⅲ者Ⅲ：有大陰影出現(xiàn)，其長(zhǎng)徑不小于20mm，短徑不小于10mmⅢ＋：?jiǎn)蝹€(gè)大陰影的面積或多個(gè)大陰影面積的總和超過(guò)右上肺區(qū)面積者132矽肺0-I期雙肺門(mén)擴(kuò)大增濃，肺門(mén)角隆起雙肺紋理增多，隱約可見(jiàn)小粟狀結(jié)節(jié)133矽肺Ⅱ期兩肺門(mén)散在大小不等，互相重疊的圓形、卵圓形鈣化影，上縱隔增寬，中上野有片狀影134矽肺Ⅱ-Ⅲ期兩肺野散在大小不等致密影，兩肺門(mén)區(qū)有大小不等的蛋殼樣淋巴結(jié)鈣化135煤工塵肺Coalworkerpneumoconiosis煤礦工人長(zhǎng)期吸入生產(chǎn)環(huán)境中的粉塵引起的塵肺巖石掘進(jìn)工作面工人接觸游離二氧化硅含量較高的硅塵，所患?jí)m肺有典型矽結(jié)節(jié)，為矽肺。采煤工作面工人，主要接觸煤塵，游離二氧化硅含量不足5%，所患?jí)m肺有典型的煤塵灶，為煤塵肺煤塵肺在肺內(nèi)只引起彌漫的間質(zhì)性纖維改變，可見(jiàn)到數(shù)量不等，直徑大小不一的煤斑，并伴有散在的局限性肺氣腫改變，即單純煤塵肺，通常不形成矽結(jié)節(jié)病變或大塊纖維病灶。合并結(jié)核則可見(jiàn)進(jìn)行性大塊纖維改變136Coalworkerpneumoconiosis早期無(wú)癥狀。勞動(dòng)時(shí)氣急、吐痰、咳嗽和胸痛是最常見(jiàn)的主訴。無(wú)陽(yáng)性體征胸片可見(jiàn)兩肺有廣泛的肺紋理改變和纖維條紋以及網(wǎng)織陰影，肺野透亮度減低呈磨玻璃樣混合矽結(jié)節(jié)的直徑比較小，形態(tài)不規(guī)則，密度較低，邊緣不如典型矽結(jié)節(jié)那樣銳利肺內(nèi)有散在局灶性肺氣腫透亮區(qū)域存在大陰影僅見(jiàn)煤矽肺137CoalworkerpneumoconiosisHRCT以間質(zhì)性肺纖維化為主，小結(jié)節(jié)影不如矽肺明顯兩肺廣泛不規(guī)則線條狀陰影或網(wǎng)狀影，肺血管紋理扭曲、紊亂晚期隨肺氣腫的發(fā)展，肺紋理減少小結(jié)節(jié)影以兩肺中、下野分布為主?；旌衔Y(jié)節(jié)的直徑較小，形態(tài)不規(guī)則，密度低，邊緣不如矽結(jié)節(jié)銳利，一般不融合?？梢?jiàn)局限性肺氣腫胸膜改變不如矽肺明顯138CWP,48M,HRCT,numeroussmallnodulesthatarelesswelldefinedthanthoseseeninsilicosis139ComplicatedCWP:57MAconglomerationofsmallnoduleswithsparingofthebibasilarareaandegg-shellcalcificationsinbothhila140ComplicatedCWPHRCTConglomeratemasses(progressivemassivefibrosis)andadjacentsmallnodulesAthoracostomytubewasplacedinthelefthemithoraxforapneumothorax.141CalcifiedprogressivemassivefibrosisM60,retiredcoalworkerAdenselycalcifiedrightparahilarmass142Complicatedsilicosis,58MAcavitaryconglomeratemassintheleftupperlobetheparacicatricialemphysemaAlthoughtuberculosismaycomplicatesilicosisorCWP,progressivemassivefibrosissometimesdemonstratescavitationduetoischemicnecrosis143SilicoproteinosisM52,quarryworkerHRCTPatchyareasofground-glassattenuationwithfineintralobularreticulationBiopsyconfirmedthealveolarproteinosisandsilicaparticles144ArcwelderpneumoconiosisM46,nonsmokerwitha15yearsofashipyardwelderNumeroussmallnodulesandbranchingareasofhyperattenuationarepoorlydefinedandcentrilobularSiderosiswasprovedattransbronchiallungbiopsy145ArcwelderpneumoconiosisM57,formersmoker13yearsworkinshipyardsasymptomatic,pulmonaryfunctiontestswerenormalGGOisdiffuseandmainlycentrilobularFollow-upHRCT1yearlatershowednochangeintheparenchymaldisease146Carbonpneumoconiosis49man10-yearhistoryofacarbonblackfactoryAfinereticulonodularpatternwithlowerzonalpredominance147CarbonpneumoconiosisDiffuseareasofGGoandnumeroussmallcentrilobularnodules148Giantcellinterstitialpneumonia52mpatchyareasofGGOandfinereticulationinbothlowerlungzones149GiantcellinterstitialpneumoniaBilateralareasofsmallcysts,GGO,finereticularhyperattenuation,andtractionbronchiectasis,sugestfibrosis150Giantcellinterstitialpneumonia45ySawmanufacturingplantpatchyareasof