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，繼而淋巴細胞和單核細胞滲出。肺泡內(nèi)皮細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小網(wǎng)織陰影病變發(fā)展，不對稱性、彌漫性網(wǎng)狀、條索狀及結(jié)節(jié)狀陰影，可擴展至上肺野晚期，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，肺野透亮度增強囊腫破裂可發(fā)生自發(fā)性氣胸肺纖維化嚴重時可發(fā)生肺動脈高壓和肺心病5Idiopathicpulmonaryfibrosis磨玻璃樣影及實變影，內(nèi)見含氣支氣管影，支氣管血管數(shù)增粗Ground-glassattenuation與胸膜面垂直的細線形影，長1-2cm，寬約1mm，多見于兩肺下葉兩肺中內(nèi)帶小葉間隔增厚，分支狀細線形影，Reticularattenuationwithinterlobularseptalthickening胸膜下0.5cm內(nèi)與胸壁內(nèi)面弧度一致的弧線狀影，長5-10cm，邊緣較清或略模糊，見于兩下肺后外部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)展可漸見于肺中央部。胸膜下見1-2cm類圓形肺氣囊中小支氣管擴張，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，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。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，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、變短15CT縱隔、肺門淋巴結(jié)腫大，密度均勻，邊緣清楚，周圍脂肪界面存在。增強掃描呈均勻強化肺內(nèi)可見大小結(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；小葉間隔增厚和細小蜂窩影，見于胸膜下區(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?？v隔淋巴結(jié)腫大的程度常較肺門淋巴結(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)腫大亦不對稱。后縱隔多于前縱隔淋巴結(jié)腫大，晚期才有肺門淋巴結(jié)腫大。縱隔淋巴結(jié)多大于肺門淋巴結(jié)未分化型小細胞肺癌：多為單側(cè)縱隔或（和）肺門分葉狀淋巴結(jié)腫大，雙側(cè)縱隔淋巴結(jié)腫大較少見。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支氣管以上的肺癌Alveolartype：發(fā)生于細支氣管或肺泡上皮的肺癌34Histologicaltypesoflungcancer來自支氣管表面上皮的癌鱗狀上皮癌Squamouscellcarcinoma腺癌Adenocarcinoma腺鱗癌大細胞癌Largecellcarcinoma來自神經(jīng)內(nèi)分泌細胞的癌高分化：類癌carcinoid中分化：不典型類癌atypicalcarcinoid低分化：小細胞癌Smallcellcarcinoma來自細支氣管Clara細胞和Ⅱ型肺細胞的癌細支氣管肺泡癌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、肺門增大，為肺癌的淋巴結(jié)轉(zhuǎn)移40中心型肺癌：右肺門及右上縱隔不規(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，杯口狀截斷管外型：管壁環(huán)形增厚，腔外軟組織腫塊管腔狹窄或閉塞，繼發(fā)遠端肺炎癥、不張或氣腫肺門縱隔淋巴結(jié)轉(zhuǎn)移，呈軟組織樣等密度，單個或多個融合成分葉狀，增強掃描無強化肺內(nèi)，胸膜及遠處轉(zhuǎn)移43中心型肺癌44Centraltype--CTfindings45Centraltype--CTfindings46Centraltype47Squamouscellcarcinoma48Squamouscellcarcinoma49Squamouscellcarcinoma50Lungcancer--peripheraltype臨床表現(xiàn)：可無癥狀或胸痛、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，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，臍征肺門縱隔淋巴結(jié)轉(zhuǎn)移遠處轉(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)個轉(zhuǎn)移病灶82Lungmetastases83Lungmetastases,rectalcancer84Lungmetastases85食道癌肺轉(zhuǎn)移86Lungmetastases,coloncancer87錯構(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，見爆米花樣鈣化CT掃描：鈣化、鈣化、脂肪88錯構(gòu)瘤左肺門外上腫塊內(nèi)可見爆米花樣鈣化89Hamartoma90錯構(gòu)瘤91Hamartoma92肺栓塞(pulmonaryemboli)肺動脈分支被栓子堵塞引起的肺供血障礙常見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)于肺動脈的血栓進入血循環(huán)的脂肪、腫瘤栓子和氣體93PulmonaryembolismThethirdmostcommonacutecardiovasculardiseaseaftermyocardialinfarctionandstrokeResultsinthousandsofdeathseachyearbecauseitoftengoesundetectedCTAhassensitivitiesof53%–100%andspecificitiesof83%–100%Pulmonaryangiography,thediagnosticstandardofreferenceforconfirmingorrefutingdiagnosis94病理雙重供血，正常時兩組有豐富的吻合支當肺動脈的某一分支栓塞后，肺組織因支氣管動脈的側(cè)枝供血而不發(fā)生異常，栓子較小未能完全堵塞肺動脈分支時也不易發(fā)生供血障礙多數(shù)小栓子進入肺循環(huán)可引起肺動脈小分支多發(fā)性栓塞95臨床表現(xiàn)多無明顯癥狀，或有輕微不適可為突發(fā)的呼吸困難和胸痛肺動脈大分支或主干栓塞或廣泛的肺動脈小分支栓塞可出現(xiàn)嚴重的呼吸困難、發(fā)紺、休克或死亡較大的栓子堵塞肺動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，X線仍可正常肺缺血又稱Westermark征，當肺葉或肺段動脈栓塞時，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，但無肺體積膨脹現(xiàn)象97X線表現(xiàn)嵌塞在肺動脈內(nèi)的血栓使相應(yīng)部位血管陰影增寬，阻塞遠端致血流減少而變細多發(fā)于下葉且以右下葉多見，下葉體積縮小，膈肌升高，葉間裂下移。并盤狀肺不張較大肺動脈栓塞或多發(fā)性小動脈栓塞可引起心影增大，主要是右心室增大，同時有肺動脈高壓右心功能不全時心影增大更為顯著，奇靜脈和上腔靜脈增粗98X線血管造影肺動脈分支內(nèi)充盈缺損或截斷局限性血管減少或無血管區(qū)，血灌流緩慢小分支多發(fā)性栓塞引起肺動脈外圍分支迂曲，突然變細，呈剪枝樣細小分支的栓塞血管造影不能顯示血栓24hs后開始溶解，故48hs后造影可正常繼發(fā)肺動脈高壓和肺心病時，肺動脈干和大分支擴張，周圍分支變細99CT平掃：較大肺動脈栓塞見血管內(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：血栓為長條狀及不規(guī)則形充盈缺損栓塞的肺動脈可有不同程度的擴張較大肺血管栓塞可見相應(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肺通過氣道與外界相通，吸入在空氣中懸浮的無機和有機塵粒，這些塵粒部分可致病正常肺有很強的能力來清除這些塵粒但過多的生產(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)目前我國現(xiàn)行政策的規(guī)定：塵肺的診斷必須是由國家衛(wèi)生行政部門指定的塵肺診斷小組來進行，任何個人作出的診斷都是無效的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)對引起塵肺的病因?qū)W、生產(chǎn)現(xiàn)場的流行病學(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：最常見和最重要表現(xiàn)，見于矽肺不規(guī)則形小陰影：網(wǎng)狀，有時呈蜂窩狀大陰影：指直徑超過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)，常對稱出現(xiàn)；大陰影的長軸常與后肋垂直，不受葉間裂的限制?！鞍俗中巍被蜷L條形大陰影常見于典型矽肺胸膜斑：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時稱為胸膜斑，多見于側(cè)胸壁，亦見于部分心緣和膈面，可發(fā)生鈣化123基本影像學(xué)表現(xiàn)肺門改變：早期肺門陰影增大增濃，有時見腫大淋巴結(jié)影。淋巴結(jié)蛋殼樣鈣化多于兩側(cè)肺門對稱出現(xiàn)，也可見于一側(cè)，呈圓形、橢圓形或不整形，常數(shù)個同時出現(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、變粗等改變。肺間質(zhì)纖維化的進一步發(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且危害最大的一種，多見于采礦、玻璃、陶瓷、耐火材料、石英制粉、機械制造業(yè)工人基本改變是慢性進行性肺間質(zhì)纖維化及矽結(jié)節(jié)形成多個小結(jié)節(jié)可相互融合形成大結(jié)節(jié)或融合團塊，周圍有肺氣腫，是矽肺晚期常見改變125Silicosis粉塵中游離二氧化硅含量越高，肺內(nèi)改變越以結(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)性纖維改變越明顯，矽結(jié)節(jié)淡而輪廓模糊早期可無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)肺紋理增強并伸展至肺外帶，細網(wǎng)狀紋理，在網(wǎng)格交叉處見有極小顆粒，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塊，即大結(jié)節(jié)影，常見于兩上肺野外帶，輪廓清楚。典型大結(jié)節(jié)陰影在兩肺分布對稱，呈翼狀127X線表現(xiàn)肺門影增大，密度增高。晚期可見肺門上提或外移。肺門呈殘根樣。肺門淋巴結(jié)蛋殼樣鈣化肺紋理增多增粗，延長到肺野外帶。病程進展，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，隨病變進展，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，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)分期無塵肺（0）0：X線胸片無塵肺表現(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級的小陰影，分布范圍至少達到兩個肺區(qū)Ⅰ＋：有總體密集度1級的小陰影，分布范圍超過4個肺區(qū)或有總體密集度2級的小陰影，分布范圍達到4個肺區(qū)二期塵肺（Ⅱ）Ⅱ：有總體密集度2級的小陰影，分布范圍超過4個肺區(qū)；或有總體密集度3級的小陰影，分布范圍達到4個肺區(qū)Ⅱ＋：有總體密集度3級的小陰影，分布范圍超過4個肺區(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)，其長徑不小于20mm，短徑不小于10mmⅢ＋：單個大陰影的面積或多個大陰影面積的總和超過右上肺區(qū)面積者132矽肺0-I期雙肺門擴大增濃，肺門角隆起雙肺紋理增多，隱約可見小粟狀結(jié)節(jié)133矽肺Ⅱ期兩肺門散在大小不等，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煤礦工人長期吸入生產(chǎn)環(huán)境中的粉塵引起的塵肺巖石掘進工作面工人接觸游離二氧化硅含量較高的硅塵，所患塵肺有典型矽結(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%，所患塵肺有典型的煤塵灶，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)核則可見進行性大塊纖維改變136Coalworkerpneumoconiosis早期無癥狀。勞動時氣急、吐痰、咳嗽和胸痛是最常見的主訴。無陽性體征胸片可見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?？梢娋窒扌苑螝饽[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