呼吸病診斷

1、1,Respiratory disease,放射學院 劉林祥6222136 lxliu@tsmc.edu.cn,2,特發(fā)性肺間質纖維化,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近認為系免疫性疾病，可能與遺傳有關,3,病 理,急性期：肺泡內皮細胞和基底膜受損，肺泡和間質內蛋白樣物質滲出，伴透明膜形成，繼而淋巴細胞和單核細胞滲出。肺泡內皮細胞再生覆蓋在滲出物表面并使其整

2、合入肺間質，肺泡壁增厚，膠原纖維扭曲、紊亂而機化。病變發(fā)展，間質纖維化加重晚期：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,4,Hamman-Rich Syndrome,多見于中年，男、女無差別多起病隱匿，初期無癥狀進行性呼吸困難和干咳進展速度因人而異：快者1～2年內出現(xiàn)發(fā)紺和杵狀指，并發(fā)肺心病慢

3、者可數(shù)年甚或十幾年不出現(xiàn)明顯缺氧癥狀，但最終出現(xiàn)缺氧及肺心病易合并肺部感染，反復感染可加快肺纖維化的發(fā)展肺功能檢查呈限制性通氣障礙及低氧血癥,5,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、條索狀及結節(jié)狀陰影，可擴展至上肺野晚期，結節(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,6,Idiopathic pulm

4、onary fibrosis,磨玻璃樣影及實變影，內見含氣支氣管影，支氣管血管數(shù)增粗 Ground-glass attenuation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帶小葉間隔增厚，分支狀細線形影，Reticular attenuation with interlobular septal thickening胸膜下0.5cm內與胸壁內面弧度一致的弧線狀影，長5-10cm，邊緣較清或略模糊，

5、見于兩下肺后外部,7,Idiopathic pulmonary fibrosis,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). A honeycomb pattern, predominantly basal and peripheral in distribution小結節(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

6、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 Architectural distortion with associated traction bronchiectasis and bronchiolectasis,8,Idiopathic pulmonary fibrosis,F47peripheral GGO Interlobular septal thickenin

7、gIrregularity of the fissuresBronchiectasisEarly interstitial pneumonia22m later, progression of interstitial pneumoniaDiffuse GGO, interlobular septal thickeningA honeycomb pattern,9,鑒別診斷,肺類風濕性病的廣泛性肺間質纖維化，最后發(fā)展為蜂窩

8、肺，與HRS相似。但前者有漸進性壞死結節(jié)即肉芽腫及胸腔積液表現(xiàn)，有別于HRS紅斑狼瘡的胸部表現(xiàn)以心肌炎所致的心臟增大、間質性肺炎、節(jié)段性盤狀肺不張和胸腔積液等所見為特征，與HRS不同硬皮病的肺間質纖維化發(fā)展至晚期可出現(xiàn)蜂窩肺，如有皮膚的改變以及在食管造影見其張力減低或狹窄等表現(xiàn)，則有助于硬皮病的診斷,10,結節(jié)病（Sarcoidosis）,A systemic disorder of unknown causeNoncaseati

9、ng granulomas with proliferation of epithelioid cells, 多系統(tǒng)肉芽腫性疾病，良性經(jīng)過，可累及淋巴結、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大，但不融合。肺門LN易受累，次為氣管旁和AA旁肺內病變沿支氣管血管周圍結締組織鞘及小葉間隔發(fā)展蔓延，肺內肉芽腫主要分布在間質，小，直徑在0.4mm以下，胸膜下肺間質內肉芽腫更密集。小肉芽腫可融合成大結節(jié)

10、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)病者常導致進行性肺纖維化,11,Sarcoidosis,見于任何年齡，20～40歲多見，女性多Young & middle-aged, slightly higher in womenDistinct geographic and racial predilections, commonly African-Americans, Swedes, & Danes病程緩

11、慢，輕者無癥狀；癥狀與影像表現(xiàn)不相稱咳嗽，少量粘痰、乏力、低熱、盜汗、納差及胸悶肝脾腫大、皮膚結節(jié)、關節(jié)疼痛、腮腺腫大、外周淋巴結腫大及眼部病變癥狀,12,Laboratory,Angiotensin converting enzyme (ACE) level elevated and may correlate with activityCD4:CD8 ratio is commonly decreasedHypercalce

12、mia due to increased intestinal absorption of calcium, resulting from activation of vitamin D by macrophages in sarcoid granulomas,13,胸部X線平片,縱隔、肺門淋巴結腫大，半數(shù)為唯一異常多組淋巴結腫大，兩肺門對稱性淋巴結腫大，狀如土豆，為典型表現(xiàn)肺門淋巴結腫大的程度比其他部位更加顯著少有縱隔淋巴結而無

13、肺門淋巴結者淋巴結腫大一般在6-12個月期間可自行消退，恢復正常；或在肺部出現(xiàn)病變過程中，開始縮小或消退；或不繼續(xù)增大，為結節(jié)病的發(fā)展規(guī)律,14,Sarcoidosis,肺部病變多發(fā)生在淋巴結病變之后兩肺彌漫性網(wǎng)狀結節(jié)影，但肺尖或肺底少或無。結節(jié)大小不一，多為1-3mm大小，輪廓尚清楚肺內圓形病變，直徑約1.0-1.5cm，密度均勻，邊緣較清楚，單發(fā)者類似肺內良性病變或周圍型肺癌，多發(fā)者酷似肺轉移瘤節(jié)段性或小葉性浸潤，類似肺部炎

14、性病變，一般伴或不伴胸腔內淋巴結病變少數(shù)為單純粟粒狀，似急性粟粒型結核,15,Sarcoidosis,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，顯示小囊狀骨質缺損并伴有末節(jié)指（趾）的骨質吸收，變細、變短,16,CT,縱隔、肺門淋巴結腫大，密度均勻，邊緣清楚，周圍脂肪界面存在。增強掃描呈

15、均勻強化肺內可見大小結節(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)則或結節(jié)狀，周圍可有大小不等的結節(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,17,鑒別診斷,肺門結核：年輕，有輕度中毒癥狀。氣管旁、支氣管旁淋巴結腫大，可有鈣化。結素反應陽性，痰中找到結核桿菌霍奇金?。撼Ｏ扔蓄i部、鎖骨上淋巴結腫大

16、，然后出現(xiàn)不對稱性雙側或單側縱隔淋巴結腫大，前縱隔較后縱隔多見?？v隔淋巴結腫大的程度常較肺門淋巴結腫大顯著非霍奇金淋巴瘤：多為單側縱隔淋巴結腫大，即使雙側縱隔淋巴結腫大亦不對稱。后縱隔多于前縱隔淋巴結腫大，晚期才有肺門淋巴結腫大?？v隔淋巴結多大于肺門淋巴結未分化型小細胞肺癌：多為單側縱隔或（和）肺門分葉狀淋巴結腫大，雙側縱隔淋巴結腫大較少見。部分伴有不同程度的阻塞性肺炎或肺不張。病程發(fā)展迅速間質性病變：當病變發(fā)展至纖維化期則需與癌

17、性淋巴管炎、間質性肺炎、嗜酸性肉芽腫等鑒別,18,Sarcoidosis,Symptoms and signs are nonspecific, half asymptomaticFatigue, weight loss, general malaise, feverBilateral hilar lymphadenopathy is common findingOften with associated pulmonary in

18、filtratesSkin and ocular lesions, the liver, spleen, lymph nodes, parotid glands, CNS, genitourinary system, muscles, and bones may be involved,19,Radiologic stages,Stage 0: normal chest radiographstage 1: lymphadenopa

19、thy only (1/2)stage 2: lymphadenopathy with parenchymal infiltrationstage 3: parenchymal disease onlystage 4: pulmonary fibrosis,20,Hilar adenopathy,M27Chest radiograph Typical bilateral hilar adenopathyAdenopathy

20、in the right paratracheal and left aortic-pulmonary window nodes is also identified,21,Hilar adenopathy,E+ CT clearly depicts the bilateral hilar adenopathy,22,Mediastinal Lymph Nodes,Bilateral hilar adenopathyRight pa

21、ratracheal adenopathyLeft paratracheal and aortic-pulmonary window nodes are also commonly enlargedCalcification occurs in affected nodes，It can be amorphous, punctate, or eggshell-like; it is closely related to the du

22、ration of the disease and suggests a chronic condition,23,Mediastinal adenopathy,M26Severe back painEnlarged right paratracheal nodesLeft aortic-pulmonary window nodes with associated minimal hilar involvement are als

23、o seen,24,Mediastinal adenopathy,Mediastinal adenopathy, 60MCalcification in the affected hilar nodes, huge subcarinal lymph nodesAn unusual finding in other granulomatous diseases such as tuberculosis,25,Pulmonary sar

24、coidosis,Lung involvement in 20% of patientsStrong predilection for the upper lungDyspnea and dry cough are commonSarcoid granulomas in lung are distributed along lymphatic vessels in interstitial tissues of bronchova

25、scular bundles and subpleural and perilobular spacesMultiple miliary nodules, bronchial wall thickening, and ground-glass attenuationPerivascular or subpleural distribution Coalescing granulomas can form multiple mass

26、like nodulesNodules have irregular margins and may contain an air bronchogram,26,Pulmonary sarcoidosis,Stage IV disease may manifest as conglomerated masses with marked traction bronchiectasisUsually predominantly in t

27、he central and upper lung. this distribution is typical of sarcoidosis but can also be seen in tuberculosis and silicosisExtensive calcification may be encountered within fibrotic granulomasCavitation or cyst formation

28、 may also be seen,27,Pulmonary sarcoidosis,M37Small nodules with a perivascular distribution and irregular thickening of bronchovascular bundles and interlobular septa,28,Pulmonary sarcoidosis,M24HRCTMultiple miliary

29、nodules and diffuse thickening of the bronchial wallSimultaneous presence of small nodules with a perivascular distribution and along the interlobular pleura,29,Pulmonary sarcoidosis,F31Hazy ground-glass opacity with a

30、 lower lung predominance, both of which are unusual findings.,30,Pulmonary sarcoidosis,HRCTWidespread ground glass attenuationReticulonodular Mild bronchiectasis peripherally,31,Pulmonary sarcoidosis,F26Multiple nod

31、ules bilaterallyMinimal hilar adenopathySimulate metastates,32,Pulmonary sarcoidosis,A nodular consolidation with ill-defined bordersAir bronchogram within the nodules,33,Stage IV pulmonary sarcoidosis,M60, Extensi

32、ve fibrotic change and cavitary lesions with a central distribution distorting lung parenchymaIrregular thickening of pleura and overinflation of peripheral lung parenchyma,34,Primary Bronchogenic Cancer,Macro-pathology

33、Central type：主支氣管、肺葉支氣管及肺段支氣管的肺癌Peripheral type：肺段以下支氣管直到細支氣管以上的肺癌Alveolar type：發(fā)生于細支氣管或肺泡上皮的肺癌,35,Histological types of lung cancer,來自支氣管表面上皮的癌鱗狀上皮癌 Squamous cell carcinoma腺癌 Adenocarcinoma腺鱗癌大細胞癌 Large cell car

34、cinoma來自神經(jīng)內分泌細胞的癌高分化：類癌 carcinoid中分化：不典型類癌 atypical carcinoid低分化：小細胞癌 Small cell carcinoma來自細支氣管Clara細胞和Ⅱ型肺細胞的癌細支氣管肺泡癌 bronchial alveolar carcinoma,36,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

35、的阻塞性肺炎、肺不張、肺氣腫轉移征象,37,右肺上葉中心型肺癌,38,右肺上葉中心型肺癌,39,右肺上葉中心型肺癌,40,中心型肺癌,縱隔增寬、肺門增大，為肺癌的淋巴結轉移,41,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,42,中心型肺癌,左肺肺癌，右肺代償性肺氣腫,43,Central type--CT findings,管壁型：管壁增厚，管腔不規(guī)則狹窄管內型：腔內軟組織腫塊，

36、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轉移，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，胸膜及遠處轉移,44,中心型肺癌,45,Central type--CT findings,46,Central type--CT findings,47,Central type,48,Squamous cell carcinoma,49,S

37、quamous cell carcinoma,50,Squamous cell carcinoma,51,Lung cancer--peripheral type,臨床表現(xiàn)：可無癥狀或胸痛、咳嗽直接征象：肺內結節(jié)和腫塊邊緣分葉，臍樣切跡，毛刺小于2cm的孤立結節(jié)，內部密度不均勻。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。胸膜凹陷轉移征象,52,右肺見結節(jié)性病灶，CT示分葉與毛刺,53,厚

38、壁空洞，體層示空洞內壁凹凸不平,54,周圍型肺癌--癌性空洞,55,Peripheral type,肺內腫塊，下緣與胸膜間有牽拽，箭頭所指為慧尾征,56,Peripheral type—CT findings,肺內結節(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轉移遠處轉移,57,周圍型肺癌,58,Peripheral carcin

39、oma,59,Peripheral carcinoma,ground-glass opacity,60,Peripheral carcinoma,Soft tissue massSpicula,61,Peripheral carcinoma,62,Peripheral carcinoma,63,Peripheral carcinoma--lobulation,64,Hilar metastases,65,Peripheral car

40、cinoma,66,Peripheral carcinoma,67,Peripheral carcinoma,68,Peripheral carcinoma,69,Peripheral carcinoma-cavity,70,Pancoast tumors,Arise from lung apexInvade costovertebral groove in superior sulcus Invade parietal pleur

41、a, causing nonspecific shoulder pain radiating down medial aspect of scapulaInvolve T1 nerve root, causing pain radiating along medial aspect of arm and forearm as far as wristInvade stellate ganglion, causing Horner

42、syndrome, include ptosis (narrowing of the palpebral fissure), miosis (pupillary constriction), and anhidrosis (absence of sweating on one side of the face),71,Pancoast tumors,Invade first, second, and third ribs posteri

43、orlySuperior extension encasing C8 nerve root, with resultant pain in medial two digits of hand and atrophy of intrinsic muscles of handAnterior extension into tracheoesophageal groove result in vagal or recurrent lar

44、yngeal nerve palsySuperomedial extension may result in involvement of vertebral artery, vertebral bodies, neurovertebral foramina, and spinal canal, with a consequent risk of paraplegia,72,右肺上溝癌,右肺上野片狀陰影，第一、二肋骨溶骨性破壞,73,

45、Pancoast tumor,74,M48，left interscapular chest wall pain suggeste T1 nerve root invasion,75,Superior sulcus tumor,M48 w/o neurologic signs in left upper extremity but with left interscapular chest wall pain suggestive o

46、f T1 nerve root invasion,M48，left interscapular chest wall pain suggeste T1 nerve root invasion,76,Alveolar cancinoma,雙肺布滿結節(jié)性病灶病理證實為肺泡癌,77,肺泡癌,78,Alveolar cancinoma,79,Alveolar cancinoma,80,Alveolar cancinoma,81,Br

47、onchioloalveolar carcinomaA　53-year-old man,Initial (1mm) CT at the level of the bronchus intermedius a small nodular area of ground-glass attenuation in the right upper lobeFollow-up CT (5mm) 48 months later incre

48、ased nodule size.,82,肺轉移瘤,宮頸癌術后，肺內數(shù)個轉移病灶,83,Lung metastases,,84,Lung metastases, rectal cancer,85,Lung metastases,86,食道癌肺轉移,87,Lung metastases, colon cancer,88,錯構瘤(hamartoma),非真性腫瘤，內胚層與間胚層發(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

49、的反復發(fā)作感染肺內球形軟組織腫塊，見爆米花樣鈣化CT掃描：鈣化、鈣化、脂肪,89,錯構瘤,左肺門外上腫塊內可見爆米花樣鈣化,90,Hamartoma,91,錯構瘤,92,Hamartoma,93,肺栓塞(pulmonary emboli),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、大手術后和心功能不全可發(fā)生深靜脈血栓風心病，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,94,Pulm

50、onary embolism,The third most common acute cardiovascular disease after myocardial infarction and strokeResults in thousands of deaths each year because it often goes undetectedCTA has sensitivities of 53%–100% and spe

51、cificities of 83%–100%Pulmonary angiography, the diagnostic standard of reference for confirming or refuting diagnosis,95,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

52、小分支多發(fā)性栓塞,96,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,97,X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，相應區(qū)

53、域內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,98,X線表現(xiàn),嵌塞在肺動脈內的血栓使相應部位血管陰影增寬，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,99,X線

54、血管造影,肺動脈分支內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,100,CT,平掃：較大肺動脈栓塞見血管內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

55、的擴張較大肺血管栓塞可見相應區(qū)域肺血管分布減少,101,Acute pulmonary embolism,Arterial occlusion with failure to enhance the entire lumen due to a large filling defectArtery may enlarged vs. adjacent patent vessels A partial filling defect su

56、rrounded by contrast material, "polo mint" sign, "railway track" signPeripheral wedge shaped areas of hyperattenuation represent infarcts, along with linear bands are significant ancillary findings,1

57、02,Acute occlusive pulmonary embolism,F32Chest painA pulmonary embolus within posterobasal segment of right lower lobe arteryArtery enlarge vs. adjacent patent vessels,103,Acute pulmonary embolism,F45chest painA pul

58、monary embolus affects the segmental artery of the laterobasal segment of right lower lobePartial filling defect surrounded by contrast material produces the polo mint sign,104,Acute pulmonary embolism,M66Chest pain an

59、d dyspneaAcute pulmonary embolus causes a partial filling defect surrounded by contrast material Another acute pulmonary embolus affects the left main pulmonary artery,105,Acute pulmonary embolism,F58Chest pain and d

60、yspneaA pulmonary embolus results in an eccentrically positioned partial filling defectSurrounded by contrast material and forms acute angles with the arterial wall,106,Acute pulmonary embolism,F58chest pain and dys

61、pneaAncillary findings of a peripheral wedge-shaped area of hyperattenuation,107,Acute pulmonary embolism,Morphologic abnormalities suggest right ventricular failure can be quantified with CT pulmonary angiographyRV di

62、latation (RV cavity is wider than LV cavity in the short axis), w/o contrast material reflux into hepatic veinsDeviation of interventricular septum toward LVA pulmonary embolism index greater than 60%,108,Acute pulmona

63、ry embolism,M42chest pain and severe dyspnea,short axis of RV is wider than that of LV, caused by acute pulmonary embolism and created RV strain,109,Acute central pulmonary embolism,F87 asymptomatic Subtle regions of h

64、yperattenuation CTA: acute pulmonary embolism within the right main and left interlobar pulmonary arteries,110,Chronic Pulmonary EmbolismDiagnostic criteria,Complete occluded vessel is smaller than adjacent patent vess

65、elsA peripheral, crescent shaped intraluminal defect forms obtuse angles with vessel wallContrast material flowing through thickened, often smaller arteries due to recanalizationA web or flap within a contrast filled

66、artery Secondary signsExtensive bronchial collateral vesselsAn accompanying mosaic perfusion patternCalcification within eccentric vessel thickening,111,Chronic pulmonary embolism,27MdyspneaComplete occluded vessel

67、s in left lung are smaller than adjacent patent vesselsCollateral blood supply from a branch of right hemidiaphragmatic artery,112,Chronic pulmonary embolism,M62DyspneaAn eccentrically located thrombus forms obtuse a

68、ngles with vessel wallDilated collateral bronchial artery,113,Chronic pulmonary embolism,A small, recanalized pulmonary artery with contrast material in the central lumen,114,Chronic pulmonary embolism,M56dyspneaA fl