急性呼吸窘迫综合征(ARDS)的-影像学表现

单击此处编辑母版标题样式,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,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峻损伤时消失的以急性、进展性、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亮膜肺、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的概念演化,第一次世界大战 1914-1918 创伤相关性大片肺不张,其次次世界大战 1939-1945 创伤性湿肺,越南战斗 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 = 严峻的ALI,Adult Acute同时发生于小孩,2022年美国心肺与血液争论院NHBLI的ARDS net多中心系列争论,2022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,严峻肺部感染,胃内容物吸入,肺挫伤,吸入有毒气体,淹溺,氧中毒,严峻感染,严峻的非胸部创伤,急性重症胰腺炎,大量输血,体外循环,布满性血管内凝血,间接肺损伤因素,直接肺损伤因素,病 因,ARDS发病机制比较简单，目前仍在争论之中l较统一的生疏：为各种病因直接或通过炎症反响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外表活性物质合成障碍肺泡外表张力增高肺收缩、萎陷、顺应性减低、加重肺水肿。,上述转变的后果：严峻影响血氧交换血氧分压顽固性下降全身缺氧。,l炎症反响是导致毛细血管内皮及肺泡壁型细胞损伤的主要缘由。l而炎症反响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。,肺泡外表张力Surface tension)：在肺泡上皮内外表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，因而产生的肺泡外表张力。,该外表张力使液体外表有收缩的倾向，因而使肺泡趋向回缩，是构成肺回缩力的主要成分。,肺泡外表活性物质：主要为二棕榈酰卵磷脂，呈单分子层分布于肺泡外表，能降低肺泡液-气界面的外表张力。,ARDS的病理转变,ARDS的根本病理转变：l肺重量增加,肺泡腔含气削减或不含气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肺透亮膜形成：肺泡上皮被一层嗜酸性纤维蛋白膜掩盖。l治疗后遗留少许间质纤维化。,ARDS呼吸膜布满性损伤,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，进展性加重，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。,重要的试验室检查l血氧分析：氧分压降低于8Kpa60mmHg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Pcwp18mmHgARDS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，特殊是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，绝不能排解ARDS。其胸部X 线和CT特别征象多在发病后2448h消失。l按X线征象消失的挨次可分为4个阶段。,1、双肺纹影增多、模糊，一般不消失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、多少与正常相像，心脏一般正常。2、双肺布总分值布淡薄、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，严峻者消失“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肺内布满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削减多为初期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病变影可呈重力依靠区、非重力依靠区分布或密度特征。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，典型是粗糙的网格构造及非重 力依靠区的磨玻璃影，提示有可能存在肺纤维化可能。,2022年10月的柏林新标准指出：ARDSCT诊断的特异性明显高于胸片。在病情允许的状况下，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安排所证明。,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，即从非重力依靠区 non-dependent 正常或过度膨胀的肺脏移行过渡为布满性磨玻璃影，直至重力依靠区dependent的致密实变影。,Imaging of Acute Respiratory Distress Syndrome RESPIRATORY CARE APRIL 2022 V OL 57 N O 4,病变的非均一性,重力依靠区域,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、急性呼吸窘迫病症；,3、低氧血症：氧合指数PaO2FiO2, 200mmHg 为 ARDS, 300mmHg 为 ALI,4、双肺浸润性转变，可与肺水肿共同存在,5、肺毛细血管楔压PAWP18mmHg或无左心衰依据。,l本症的诊断原则 临床表现+影像学资料二者严密结合,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、低氧血症相对易订正。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、肾功能检验有相应转变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首先消失的是肺部感染临床病症、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。有时特别困难。l不具有ARDS的临床等特征l在CT上，ARDS可有重力依靠区与非重力依靠区的病变分布与密度特点，是生疏和鉴别的影像学要点。,这例？,ARDS,ARDS,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日后病变明显吸取,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 治疗后病变吸取,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 2022 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.,AARDS双侧肺侵润，右侧胸膜渗出,B7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，双侧重力依靠区显著实变；而磨玻璃密度区及正常肺在非重力依靠区。,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的急性期消失支气管扩张，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；留意，右下肺非重力依靠区的实变，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显示双肺重力依靠区实变，以及在非重力依靠区肺野的磨玻璃影。,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 2022, 16:R4,positive 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;86:20220614,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.,由达托霉素引发的布满性肺损伤DAD。HRCT：肺四周区域多灶性实变伴由磨玻璃密度形成的晕状边缘。经受一周后，病人进展成为ARDS。早期的DAD其表现可以类似于肺炎，犹如本例，但DAD病人通常恶化快速。,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：双侧肺重力依靠区显著实变；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.,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，以网状构造、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双侧中心性及支气管四周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、支气管四周、胸膜下以及小叶四周实变和磨玻璃影箭。,C10周后，HRCT：小叶旁实变的剩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：不规章分布的片状实变、磨玻璃影。,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：布满性间隔增厚和四周多发性局灶性肺实变箭,Ichikado K, Muranaka H, Gushima Y, et al. BMJ Open 2022;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,E N D,