急性呼吸窘迫综合征ARDS的影像学表现课件

,单击此处编辑母版标题样式,*,精选ppt,*,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,急性呼吸窘迫综合征,(Acute Respiratory Distress Syndrome),影 像 学,1,精选ppt,急性呼吸窘迫综合征 1精选ppt,成人呼吸窘迫综合征,(Adult Respiratory Distress Syndrome,，,ARDS),l,ARDS,，,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),2,精选ppt,成人呼吸窘迫综合征,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。,l,ARDS,不仅发生于成人，也见于儿童。,3,精选ppt,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,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 adult,1971,Petty,正式称为,Adult Respiratory Distress Syndrome,，,ARDS,1992,美国胸科协会提出将此征命名为,Acute Respiratory Distress Syndrome,，,ARDS,1994,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,4,精选ppt,ARDS的概念演变第一次世界大战 1914-1918,ARDS,病因、病理、发病机制,5,精选ppt,ARDS 病因、病理、发病机制5精选ppt,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,6,精选ppt,严重肺部感染严重感染间接肺损伤因素直接肺损伤因素病 因6精选,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。,7,精选ppt,ARDS发病机制比较复杂，目前仍在研究之中l较统一的认,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。,l,ARDS,是因上述,多种因素在多个环节发生作用的结果。,8,精选ppt,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。,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。,9,精选ppt,肺泡表面张力（Surface tension)：在肺泡上皮内,ARDS,的病理改变,10,精选ppt,ARDS的病理改变10精选ppt,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。,11,精选ppt,ARDS的基本病理改变：l肺重量增加,肺泡腔含气减少或,ARDS,呼吸膜弥漫性损伤,12,精选ppt,ARDS呼吸膜弥漫性损伤12精选ppt,13,精选ppt,13精选ppt,正常肺,ARDS,肺,14,精选ppt,正常肺ARDS肺14精选ppt,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,。,15,精选ppt,临床表现 l起,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（,PaO,2,FiO,2,）,200mmHg,l,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）,16,精选ppt,重要的实验室检查l血氧分析：氧分压降低于8Kpa,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,24,96h,为渗出期平片及,CT,均有征象检出。,17,精选ppt,ARDS的影像学,影像学表现及诊断,l,24,h,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,24,48h,出现。,l,按,X,线征象出现的顺序可分为,4,个阶段。,18,精选ppt,影像学表现及诊断l24h以内无影像学表现，绝不能排,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。,19,精选ppt,1、双肺纹影增多、模糊，一般不出现Kery氏 A、B间隔线，,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,20,精选ppt,3、双侧叶段性实变，可见支气管气相，严重者出现“白肺”（氟中,21,精选ppt,21精选ppt,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。,22,精选ppt,CT检查，以HRCT为优。l肺内弥漫性分布斑片状磨玻璃样密,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 4,23,精选ppt,ARDS肺部CT检查中涉及的重要概念病变的CT表现不均匀，因,病变的非均一性,重力依赖区域,的肺不张,24,精选ppt,病变的非均一性重力依赖区域24精选ppt,仰卧位和俯卧位通气的比较,25,精选ppt,仰卧位和俯卧位通气的比较25精选ppt,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（,PaO,2,FiO,2,）,200mmHg,为,ARDS, 300mmHg,为,ALI,4,、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,26,精选ppt,ARDS的诊断l诊断标准1、高危因素l本症的诊断原则,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,27,精选ppt,心源性肺水肿l有心脏的原发病变，心影增大；而ARD,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。,28,精选ppt,肾性肺水肿l有慢性肾功不全的病史及体征l高,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,29,精选ppt,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）,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。,30,精选ppt,与其它肺损害或疾病鉴别。有时十分困难。l不具有ARDS的,这例？,ARDS,31,精选ppt,这例？ARDS31精选ppt,ARDS,病变分布不均匀性,32,精选ppt,ARDS病变分布不均匀性32精选ppt,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,33,精选ppt,女，29岁，产后，突发憋气、咳血、体温不高、血象正常，血氧饱,心源性肺水肿,上例病人，治疗后,34,精选ppt,心源性肺水肿上例病人，治疗后34精选ppt,再看这一例,35,精选ppt,再看这一例35精选ppt,女，,51,岁。突发咳血，伴肾功能不全,肺肾综合征,Goodpasture syndrome(G P S),36,精选ppt,女，51岁。突发咳血，伴肾功能不全肺肾综合征Goodpast,GPS,治疗后病变吸收,37,精选ppt,GPS 治疗后病变吸收37精选ppt,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,38,精选ppt,女，59。高血压、糖尿病肾病38精选ppt,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,39,精选ppt,女，24岁，产后心悸胸闷，治疗心衰一周后复查39精选ppt,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,40,精选ppt,Imaging of Acute Respiratory D,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。,41,精选ppt,Fig. 2. Computed tomogram of a,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。,42,精选ppt,Computed tomogram of the mid,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。,43,精选ppt,A: Computed tomogram shows bi,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:R4,positive end expiratory pressure,PEEP,(,呼气末正压通气,),CT,检测肺复张,44,精选ppt,How large is the lung recruita,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-glass,opacity (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。,45,精选ppt,Acute pulmonary injury: high-r,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。,46,精选ppt,A 71-year-old male with acute,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.,A,B,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。,47,精选ppt,An 80-year-old female with acu,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,48,精选ppt,Acute fibrinous and organising,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）。,49,精选ppt,A 57-year-old male with daptom,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。,50,精选ppt,A 58-year-old female with rhe,Figure 9. Acute eosinophilic pneumonia. The photomicrograph,shows interstitial widening accompanied by mixed infiltrates,of lymphocytes, macrophages and eosinophils. Focal alveolar,fibroblastic proliferation is also present (arrow).,Figure 10. An 18-year-old female with acute eosinophilic,pneumonia 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）,51,精选ppt,Figure 9. Acute eosinophilic p,Ichikado K, Muranaka H, Gushima Y, et al. BMJ Open 2012;2,Fibroproliferative changes on high-resolution CT in the acute respiratory distress syndrome predict mortality and,ventilator 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,52,精选ppt,Ichikado K, Muranaka H, Gushim,E N D,53,精选ppt,E N D53精选ppt,