急性呼吸窘迫综合征(ARDS)的-影像学表现.ppt

急性呼吸窘迫综合征 (Acute Respiratory Distress Syndrome)影 像 学中国石油中心医院 影像科 杨景震 成人呼吸窘迫综合征 (Adult Respiratory Distress Syndrome，ARDS)lARDS，不是一个独立的呼吸系统疾病。l它是一种继发于机体严重损伤时出现的以急性、进行性、缺氧性呼吸窘迫（困难）及顽固性低氧血症为临床特征的综合征，是急性呼吸衰竭的一种类型。与 急性呼吸窘迫综合征 (Acute Respiratory Distress Syndrome，ARDS)l此综合征曾被称为成人透明膜肺、休克肺、创伤肺、肺毛细 血管渗透综合征等。l以上命名均有局限，不能反映该综合征本质及重要临床特征。lARDS不仅发生于成人，也见于儿童。ARDS的概念演变第一次世界大战 1914-1918 创伤相关性大片肺不张第二次世界大战 1939-1945 创伤性湿肺越南战争 1961-1975 休克肺1967 Ashbaugh首先报道 Acute Respiratory Distress Syndrome in adult1971 Petty正式称为 Adult Respiratory Distress Syndrome，ARDS1992 美国胸科协会提出将此征命名为 Acute Respiratory Distress Syndrome，ARDS1994 欧美ARDS会议 Acute Lung Injury（ALI.急性肺损伤）ARDS =严重的ALI Adult Acute（同时发生于小孩）2000年美国心肺与血液研究院（NHBLI）的ARDS net多中心系列研究2011年10月德国柏林欧洲重症医学年会Ranieri教授提出ARDS新的诊断标准-柏林标准 ARDS 病因、病理、发病机制严重肺部感染胃内容物吸入肺挫伤吸入有毒气体淹溺氧中毒严重感染严重的非胸部创伤急性重症胰腺炎大量输血体外循环弥漫性血管内凝血间接肺损伤因素直接肺损伤因素病 因 ARDS发病机制比较复杂，目前仍在研究之中l较统一的认识：为各种病因直接或通过炎症反应毛细血管内皮细胞和肺泡壁型上皮细胞。l毛细血管内皮细胞受损，血管通透性增高水及大分子蛋白漏出、转移到血管外高渗性间质及肺泡性肺水肿。发病机制及病理l肺泡型细胞受损肺泡表面活性物质合成障碍肺泡表面张力增高肺收缩、萎陷、顺应性减低、加重肺水肿。上述改变的后果：严重影响血氧交换血氧分压顽固性下降全身缺氧。l炎症反应是导致毛细血管内皮及肺泡壁型细胞损伤的主要原因。l而炎症反应是通过炎细胞（多核白细胞、单核细胞、巨噬细胞）及体液（细胞因子、脂类介质、氧自由基、蛋白酶补体、凝血和纤溶系统）发生作用。lARDS是因上述多种因素在多个环节发生作用的结果。肺泡表面张力（Surface tension)：在肺泡上皮内表面分布的极薄的液体层，与肺泡气体形成气-液界面。因界面液体分子密度大，导致液体分子间的吸引力大于液-气分子间的吸引力，犹如一拉紧的弹性膜，因而产生的肺泡表面张力。该表面张力使液体表面有收缩的倾向，因而使肺泡趋向回缩，是构成肺回缩力的主要成分。肺泡表面活性物质：主要为二棕榈酰卵磷脂，呈单分子层分布于肺泡表面，能降低肺泡液-气界面的表面张力。ARDS的病理改变 ARDS的基本病理改变：l肺重量增加,肺泡腔含气减少或不含气l镜下见:毛细血管床淤血、停滞、血栓形成、小灶性出血。l间质及肺泡水肿含水量增加。l肺透明膜形成：肺泡上皮被一层嗜酸性纤维蛋白膜覆盖。l治疗后遗留少许间质纤维化。ARDS呼吸膜弥漫性损伤正常肺ARDS肺 临床表现 l起病急而隐袭，多在原发病后1-3日内发生，常被原发病所掩 盖，常与肺部感染或心衰混淆。l多见于青状年，儿童亦可发生，无其它原发性心肺疾病的历史。l呼吸困难，进行性加重，紫绀，吸气时锁骨上窝及胸骨上窝 下陷。一般给氧治疗无改善。l主要体征为：呼吸急促，频率加速，一般在35次/min以上。l血痰或血水样痰；发热见于脓毒血症及脂肪栓塞引起的ARDS。重要的实验室检查重要的实验室检查l血氧分析：氧分压降低于8Kpa（60mmHg）并渐进性下降l氧合指数（PaO2FiO2）200mmHgl心导管检查肺毛细血管楔压（Pcwp）18mmHg（ARDS多并发感染，此时，可伴有感染性检验指标）ARDS的影像学 影像检查方法和时机选择l应首选普放胸部正侧位照片。l如为阴性（发病24h，特别是12h）而临床高度怀 疑ARDS时，可行CT检查。l一般发病2496h为渗出期平片及CT均有征象检出。影像学表现及诊断l24h以内无影像学表现，绝不能排除ARDS。其胸部X 线和CT异常征象多在发病后2448h出现。l按X线征象出现的顺序可分为4个阶段。1、双肺纹影增多、模糊，一般不出现Kery氏 A、B间隔线，亦无血流重分布X线征（上下肺静脉血管粗细、多少与正常相似），心脏一般正常。2、双肺弥漫分布淡薄、边界不清的腺泡结节及融合为小片、大片状斑片影。3、双侧叶段性实变，可见支气管气相，严重者出现“白肺”（氟中毒时常见）。4、上述阴影消散，代之以间质纤维化。上述X线征一般为双侧分布，亦有限于一侧或一叶者CT检查，以HRCT为优。l肺内弥漫性分布斑片状磨玻璃样密度增高影（GGO并非特异性 ，为炎性发生后肺泡残气量减少）多为初期（1周）表现。l肺叶、段实变影，可见支气管气相。l有时可见小叶中心密度增高影。l病变影可呈重力依赖区、非重力依赖区分布或密度特征。l小叶间隔线比心源性肺水肿少见。l牵拉性支气管扩张（纤维化信号；或为可逆性）。l后期（1周）CT影像多样化，典型是粗糙的网格结构及非重 力依赖区的磨玻璃影，提示有可能存在肺纤维化可能。2011年10月的柏林新标准指出：ARDSCT诊断的特异性明显高于胸片。在病情允许的情况下，尽可能做CT检查。ARDS肺部CT检查中涉及的重要概念病变的CT表现不均匀，因上侧、肺腹侧重量增加而导致下侧、肺背侧压缩性不张（该理论已被患者体位由仰卧位转到俯卧位后浓度梯度快速重新分配所证实）。ARDS早期（1周）典型肺部CT表现：仰卧位，肺部阴影自腹侧到背侧、从头侧到足侧的密度梯度，即从非重力依赖区（non-dependent）正常或过度膨胀的肺脏移行过渡为弥漫性磨玻璃影，直至重力依赖区（dependent）的致密实变影。Imaging of Acute Respiratory Distress Syndrome RESPIRATORY CARE APRIL 2012 V OL 57 N O 4 病变的非均一性重力依赖区域重力依赖区域 的肺不张的肺不张仰卧位和俯卧位通气的比较ARDS的诊断l诊断标准1、高危因素2、急性呼吸窘迫症状；3、低氧血症：氧合指数（PaO2FiO2）200mmHg 为 ARDS 300mmHg 为 ALI4、双肺浸润性改变，可与肺水肿共同存在5、肺毛细血管楔压（PAWP）18mmHg或无左心衰依据。l本症的诊断原则 临床表现+影像学资料二者紧密结合 心源性肺水肿l有心脏的原发病变，心影增大；而ARDS则多无。l最早表现肺血重分布；ARDS则多无。l间隔线多见，叶裂积液；而ARDS则少或无。l强心利尿有效、低氧血症相对易纠正。l端坐呼吸；而ARDS可平卧。l早期双下肺啰音；ARDS早期无啰音，后期广泛。鉴别诊断 肾性肺水肿l有慢性肾功不全的病史及体征l高血压l尿、肾功能检验有相应改变l影像学：血管束普遍增粗，血管蒂明显，可呈中 央蝶形影。肺感染性病变（支气管肺炎、金葡肺炎、霉菌性肺炎、病毒感染等）l首先出现的是肺部感染临床症状、检验学指标l感染性病变的影像学征象l无持续性低氧血症与其它肺损害或疾病鉴别。有时十分困难。l不具有ARDS的临床等特征l在CT上，ARDS可有重力依赖区与非重力依赖区的病变分布与密度特点，是认识和鉴别的影像学要点。这例？ARDSARDS病变分布不均匀性女，29岁，产后，突发憋气、咳血、体温不高、血象正常，血氧饱和度不吸氧80，吸氧后95，听诊右肺无明显湿性罗音，左肺可闻湿罗音，强心利尿3日后病变明显吸收 心源性肺水肿上例病人，治疗后再看这一例女，51岁。突发咳血，伴肾功能不全肺肾综合征Goodpasture syndrome(G P S)GPS 治疗后病变吸收女，59。高血压、糖尿病肾病胸片所见：心脏增大、肺水肿、奇静脉扩张、间隔线、支气管周袖口征女，24岁，产后心悸胸闷，超声诊断心肌病。治疗心衰一周后复查Imaging of Acute Respiratory Distress Syndrome RESPIRATORY CARE APRIL 2012 V OL 57 N O 4 Fig.A:Chest radiograph of patient with ARDS shows bilateral infiltrates.There is bilateral consolidation and a right pleural effusion.B:Chest radiograph of the same patient shows persistent bilateral infiltrates after 7 days.A）ARDS双侧肺侵润，右侧胸膜渗出B）7天后，持续性双侧肺侵润Fig.2.Computed tomogram of a patient with ARDS shows bilateral dense dependent consolidation,with areas of ground-glass opacification and normal lung in the non-dependent lung.Fig.3.Computed tomogram in ARDS shows bilateral reticulation and ground-glass opacification,containing areas of bronchial dilatation in the upper lobes.In the acute phase of ARDS,bronchial dilatation may indicate fibrosis or may be reversible.图2 ARDS病人，双侧重力依赖区显著实变；而磨玻璃密度区及正常肺在非重力依赖区。图3 ARD病人，双侧网格状及磨玻璃密度，其上叶病变内含支气管扩张。在ARDS的急性期出现支气管扩张，可提示纤维化，或为可逆性。Computed tomogram of the mid zones of a patient with ARDS shows bilateral ground-glass opacification.Note the presence of non-dependent consolidation in the right lower lobe，which raises the possibility of superadded infection.The esophageal stent is incidental.ARDS：显示双侧肺磨玻璃密度；注意，右下肺非重力依赖区的实变，可能为继发性感染。A:Computed tomogram shows bilateral dependent consolidation in a patient with ARDS,as well as ground-glass opacities in the non-dependent lung.B:Follow-up computed tomogram after 1 year shows resolution of the consolidation and ground glass opacification with cyst formation in the anterior left lung.图A ARDS病人，CT显示双肺重力依赖区实变，以及在非重力依赖区肺野的磨玻璃影。图B 同一病人在1年后的随访显示实变和磨玻璃影消散，伴左肺前部囊肿形成。How large is the lung recruitability in early acute respiratory distress syndrome:a prospective case series of patients monitored by computed Tomography Critical Care 2012,16:R4positive end expiratory pressure,PEEP(呼气末正压通气)CT检测肺复张Acute pulmonary injury:high-resolution CT and histopathological spectrum Br J Radiol;86:20120614 A 54-year-old female with daptomycin-induced diffuse alveolar damage(DAD).high-resolution CT images at presentation show peripheral and basal predominant foci of consolidation with halos of ground-glassopacity(arrows).Over the course of a week,the patient developed acute respiratory distress syndrome.Early DAD can have an appearance similar to organising pneumonia,as in this case,but patients with DAD usually deteriorate rapidly.由达托霉素引发的弥漫性肺损伤（DAD）。HRCT：肺周围区域多灶性实变伴由磨玻璃密度形成的晕状边缘。经历一周后，病人发展成为ARDS。早期的DAD其表现可以类似于肺炎，如同本例，但DAD病人通常恶化迅速。A 71-year-old male with acute respiratory distress syndrome caused by sepsis.The high-resolution CT image shows bilateral consolidation predominantly affecting the dependent areas of the lungs and ground-glass opacity and septal thickening anteriorly.Small pleural effusions(arrow-heads)are present.男，71岁。由败血症引起的ARDS.HRCT：双侧肺重力依赖区显著实变；腹侧可见磨玻璃密度及小叶间隔增厚。箭头示少量胸膜渗出。An 80-year-old female with acute respiratory distress syndrome following surgery.(a)The high-resolution CT(HRCT)image shows patchy consolidation and ground-glass opacity in the lower lobes with mild septal thickening(arrow heads).Small pleural effusions are present.(b)The HRCT image taken 3 months later shows interstitial fibrosis characterised by reticulation,traction bronchiectasis(arrows)and ground-glass opacity.AB女，80岁。ARDS。双肺下叶小片状实变及磨玻璃影，伴轻度小叶间隔增厚（箭头）及少量胸膜渗出。同一病人3个月后，以网状结构、牵拉性支气管扩张（箭）以及磨玻璃密度为特征的肺间质纤维。Acute fibrinous and organising pneumonia.The photomicrograph shows predominantly intra-alveolar fibrin aggregates(“fibrin balls”).Associated mild interstitial mono-nuclear infiltrate is also present.急性纤维素性机化性肺炎（AFOP）：病理图显示肺泡内纤维聚合物（纤维球）伴轻度间质性单核细胞侵润A 57-year-old male with daptomycin-induced acute fibrinoid and organising pneumonia.(a)High-resolution CT(HRCT)image at presentation shows bilateral central peribronchial ground-glass opacity(arrows)with mild septal thickening.(b)The HRCT image 17 days later shows extensive peribronchial,subpleural(arrows)and perilobular consolidation and ground-glass opacity,similar to but more extensive than organising pneumonia.(c)The HRCT image 10 weeks after presentation shows residual bands of perilobular consolidation(arrows)and mild bronchial dilation(arrowheads).因达托霉素引发的急性纤维性机化性肺炎：A）双侧中央性及支气管周围磨玻璃灶伴轻度间隔增厚（箭）。B）这是17天后的HRCT显示广泛性、支气管周围、胸膜下以及小叶周围实变和磨玻璃影（箭）。C）10周后，HRCT：小叶旁实变的残余条索及轻度支气管扩张（箭头）。A 58-year-old female with rheumatoid arthritis and acute fibrinoid and organising pneumonia:The high-resolution CT images show patchy consolidation and ground-glass opacity in a random distribution.女，58岁。类风湿性关节炎并急性纤维性机化性肺炎。HRCT：不规则分布的片状实变、磨玻璃影。Figure 9.Acute eosinophilic pneumonia.The photomicrographshows interstitial widening accompanied by mixed infiltratesof lymphocytes,macrophages and eosinophils.Focal alveolarfibroblastic proliferation is also present(arrow).Figure 10.An 18-year-old female with acute eosinophilicpneumonia resulting from new-onset cigarette smoking.The high-resolution CT image shows diffuse septal thickening(arrowheads)and multiple peripheral foci of lung consolidation(arrows).图9 急性过敏性肺炎：间质增厚伴淋巴细胞、巨噬细胞、嗜酸细胞混合侵润，并肺泡成纤维细胞增生（箭）。图10 女，18岁。急性过敏性肺炎。HRCT：弥漫性间隔增厚和周围多发性局灶性肺实变（箭）Ichikado K,Muranaka H,Gushima Y,et al.BMJ Open 2012;2Fibroproliferative changes on high-resolution CT in the acute respiratory distress syndrome predict mortality andventilator dependency:a prospective observational cohort study(A)M 68-y with ARDS due to Streptococcus pneumonia.HRCT findings corresponding to exudative phase of ARDS.At the level of right middle lobe shows dependent airspace consolidation without traction bronchiectasis and non-dependent areas of sparing.(B)F,84-y with ARDS due to sepsis.HRCT findings corresponding to fibroproliferative phase of ARDS.Right lower lobe shows extensive airspace consolidation and ground-glass attenuation associated with traction bronchiectasis(arrows).(C)F,65-y with ARDS due to viral pneumonia.HRCT findings corresponding to fibrotic phase of ARDS.Right inferior pulmonary vein shows extensive ground-glass attenuation associated with traction bronchiectasis(arrows),coarse reticulation and cystic changes(arrowheads).ARDS渗出期：右中叶没有牵拉性支扩。ARDS纤维增殖期：实变、GGO区伴牵拉性支扩。ARDS纤维化期：牵拉性支扩、网格、囊样变 E N D