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Article(id=1203033496089485757, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2023.05.0615, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1645977600000, receivedDateStr=2022-02-28, revisedDate=null, revisedDateStr=null, acceptedDate=1651593600000, acceptedDateStr=2022-05-04, onlineDate=1764755136748, onlineDateStr=2025-12-03, pubDate=1685203200000, pubDateStr=2023-05-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1764755136748, onlineIssueDateStr=2025-12-03, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1764755136748, creator=13701087609, updateTime=1764755136748, updator=13701087609, issue=Issue{id=1203033494428541350, tenantId=1146029695717560320, journalId=1189873630562394117, year='2023', volume='48', issue='5', pageStart='489', pageEnd='626', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1764755136353, creator=13701087609, updateTime=1764756085669, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1203037476202967229, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1203037476202967230, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=615, endPage=620, ext={EN=ArticleExt(id=1203033496458584516, articleId=1203033496089485757, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Phenotypes and individualized treatment of the acute respiratory distress syndrome, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Acute respiratory distress syndrome (ARDS) refers to acute diffuse lung injury and subsequent acute respiratory failure caused by various intrapulmonary and extrapulmonary pathogenic factors, with respiratory distress and refractory hypoxemia as clinical features. At present, the "standardized" mechanical ventilation for ARDS patients is a lung protective ventilation strategy with low tidal volume and high positive end-expiratory pressure. However, the results are often unsatisfactory, and most related clinical studies have ended up unsuccessfully. Because of the high heterogeneity of ARDS, accurate classification and individualized treatment are very important. In this paper, we reviewed the phenotypes of ARDS from the perspectives of etiology, onset time, disease severity, inflammation level, imaging characteristics pathology, etc., and preliminarily explained the ARDS phenotype associated with COVID-19, and summarized the individualized treatment strategies for ARDS with different phenotypes, hoping to provide evidence for the individualized and precise treatment of ARDS.

, correspAuthors=Zhi-Feng Liu, authorNote=null, correspAuthorsNote=
* E-mail:
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急性呼吸窘迫综合征（ARDS）是由各种肺内和肺外致病因素导致的急性弥漫性肺损伤，并可发展为急性呼吸衰竭，以呼吸窘迫和难治性低氧血症为临床特征。目前临床上ARDS患者的“标准化”机械通气多采用小潮气量、高呼气末正压的肺保护通气策略，然而其治疗效果往往不能令人满意，大多数临床研究以失败告终。由于ARDS的异质性很强，因此对其进行精准分型及个体化治疗非常重要。本文从病因学、发病时间、疾病严重程度、炎症水平、影像学特征及病理学等方面对ARDS的分型进行综述，并初步阐述新型冠状病毒感染相关ARDS的表型，总结不同表型ARDS的个体化治疗策略，以期为ARDS的个体化、精准化治疗提供依据。

, correspAuthors=刘志锋, authorNote=null, correspAuthorsNote=
刘志锋，E-mail：
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许呢妹，副主任医师，主要从事重症肺炎、急性呼吸窘迫综合征、慢性阻塞性肺疾病等的诊治以及肺部超声的临床应用等研究

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许呢妹，副主任医师，主要从事重症肺炎、急性呼吸窘迫综合征、慢性阻塞性肺疾病等的诊治以及肺部超声的临床应用等研究

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许呢妹，副主任医师，主要从事重症肺炎、急性呼吸窘迫综合征、慢性阻塞性肺疾病等的诊治以及肺部超声的临床应用等研究

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Clinical significance and corresponding treatment strategies of different types of ARDS

, figureFileSmall=null, figureFileBig=null, tableContent=
表型分型依据临床意义治疗策略
肺内型/肺外型病因选择不同机械通气方式肺外型：高PEEP、肺复张或俯卧位通气
肺内型：与肺外型相反
早发型/晚发型发病时间ARDS的准确起始时间难以确定，早期识别与诊断存在困难有较大的局限性
轻度/中-重度病情严重程度中-重度ARDS同质性更高，其病理变化更倾向于DAD中-重度患者使用VV-ECMO和(或)俯卧位通气能进一步提高PaO2/FiO2，改善低氧血症
高炎症型/低炎症型血浆炎症程度两种亚型对机械通气和液体治疗的反应不同高炎症型患者使用高PEEP及开放性液体疗法，低炎症型则相反
局灶型/弥漫型影像学个体化机械通气策略局灶型：高潮气量(8 ml/kg)、低PEEP和俯卧位
弥漫型：小潮气量(6 ml/kg)、高PEEP和肺复张
有/无DAD病理学大多数的研究为来自尸检的回顾性分析，不具有代表性，对个体化治疗没有明确的指导意义临床适用性不强
新型冠状病毒感染
 L/H型肺顺应性指导机械通气方式的选择L型：低水平PEEP、稍高潮气量(7～8 ml/kg)
H型：低潮气量与俯卧位通气、相对高水平PEEP
 Ⅰ/Ⅱ/Ⅲ型胸部CT表现Ⅰ型：低水平PEEP、稍高潮气量(7～8 ml/kg)
Ⅱ型：中至高水平PEEP/肺复张/俯卧位通气
Ⅲ型：肺保护策略/激素/ECMO
), ArticleFig(id=1203033500111823452, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1203033496089485757, language=CN, label=表1, caption=

ARDS不同分型的临床意义及相应治疗策略

, figureFileSmall=null, figureFileBig=null, tableContent=
表型分型依据临床意义治疗策略
肺内型/肺外型病因选择不同机械通气方式肺外型：高PEEP、肺复张或俯卧位通气
肺内型：与肺外型相反
早发型/晚发型发病时间ARDS的准确起始时间难以确定，早期识别与诊断存在困难有较大的局限性
轻度/中-重度病情严重程度中-重度ARDS同质性更高，其病理变化更倾向于DAD中-重度患者使用VV-ECMO和(或)俯卧位通气能进一步提高PaO2/FiO2，改善低氧血症
高炎症型/低炎症型血浆炎症程度两种亚型对机械通气和液体治疗的反应不同高炎症型患者使用高PEEP及开放性液体疗法，低炎症型则相反
局灶型/弥漫型影像学个体化机械通气策略局灶型：高潮气量(8 ml/kg)、低PEEP和俯卧位
弥漫型：小潮气量(6 ml/kg)、高PEEP和肺复张
有/无DAD病理学大多数的研究为来自尸检的回顾性分析，不具有代表性，对个体化治疗没有明确的指导意义临床适用性不强
新型冠状病毒感染
 L/H型肺顺应性指导机械通气方式的选择L型：低水平PEEP、稍高潮气量(7～8 ml/kg)
H型：低潮气量与俯卧位通气、相对高水平PEEP
 Ⅰ/Ⅱ/Ⅲ型胸部CT表现Ⅰ型：低水平PEEP、稍高潮气量(7～8 ml/kg)
Ⅱ型：中至高水平PEEP/肺复张/俯卧位通气
Ⅲ型：肺保护策略/激素/ECMO
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急性呼吸窘迫综合征的分型及个体化治疗研究进展
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许呢妹 1, 2 , 张爽 1 , 刘志锋 2, *
解放军医学杂志 | 综述 2023,48(5): 615-620
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解放军医学杂志 | 综述 2023, 48(5): 615-620
急性呼吸窘迫综合征的分型及个体化治疗研究进展
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许呢妹1, 2, 张爽1, 刘志锋2, *
作者信息
  • 1江门市中心医院重症医学科，广东江门 529000
  • 2解放军南部战区总医院重症医学科，广东广州 510010

    • 许呢妹，副主任医师，主要从事重症肺炎、急性呼吸窘迫综合征、慢性阻塞性肺疾病等的诊治以及肺部超声的临床应用等研究

通讯作者:

刘志锋，E-mail：
Phenotypes and individualized treatment of the acute respiratory distress syndrome
Ni-Mei Xu1, 2, Shuang Zhang1, Zhi-Feng Liu2, *
Affiliations
  • 1Department of Critical Care Medicine, Jiangmen Central Hospital, Jiangmen, Guangdong 529000, China
  • 2Department of Critical Care Medicine, General Hospital of Southern Theatre Command of Chinese PLA, Guangzhou, Guangdong 510010, China
出版时间: 2023-05-28 doi: 10.11855/j.issn.0577-7402.2023.05.0615
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摘要
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急性呼吸窘迫综合征（ARDS）是由各种肺内和肺外致病因素导致的急性弥漫性肺损伤，并可发展为急性呼吸衰竭，以呼吸窘迫和难治性低氧血症为临床特征。目前临床上ARDS患者的“标准化”机械通气多采用小潮气量、高呼气末正压的肺保护通气策略，然而其治疗效果往往不能令人满意，大多数临床研究以失败告终。由于ARDS的异质性很强，因此对其进行精准分型及个体化治疗非常重要。本文从病因学、发病时间、疾病严重程度、炎症水平、影像学特征及病理学等方面对ARDS的分型进行综述，并初步阐述新型冠状病毒感染相关ARDS的表型，总结不同表型ARDS的个体化治疗策略，以期为ARDS的个体化、精准化治疗提供依据。

急性呼吸窘迫综合征  /  分型  /  个体化治疗  /  新型冠状病毒感染

Acute respiratory distress syndrome (ARDS) refers to acute diffuse lung injury and subsequent acute respiratory failure caused by various intrapulmonary and extrapulmonary pathogenic factors, with respiratory distress and refractory hypoxemia as clinical features. At present, the "standardized" mechanical ventilation for ARDS patients is a lung protective ventilation strategy with low tidal volume and high positive end-expiratory pressure. However, the results are often unsatisfactory, and most related clinical studies have ended up unsuccessfully. Because of the high heterogeneity of ARDS, accurate classification and individualized treatment are very important. In this paper, we reviewed the phenotypes of ARDS from the perspectives of etiology, onset time, disease severity, inflammation level, imaging characteristics pathology, etc., and preliminarily explained the ARDS phenotype associated with COVID-19, and summarized the individualized treatment strategies for ARDS with different phenotypes, hoping to provide evidence for the individualized and precise treatment of ARDS.

acute respiratory distress syndrome  /  phenotypes  /  individualized treatment  /  coronavirus disease 2019
许呢妹, 张爽, 刘志锋. 急性呼吸窘迫综合征的分型及个体化治疗研究进展. 解放军医学杂志, 2023 , 48 (5) : 615 -620 . DOI: 10.11855/j.issn.0577-7402.2023.05.0615
Ni-Mei Xu, Shuang Zhang, Zhi-Feng Liu. Phenotypes and individualized treatment of the acute respiratory distress syndrome[J]. Medical Journal of Chinese People’s Liberation Army, 2023 , 48 (5) : 615 -620 . DOI: 10.11855/j.issn.0577-7402.2023.05.0615
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Ashbaugh等[1]在1967年首次报道了急性呼吸窘迫综合征(acute respiratory distress syndrome，ARDS)，并提出使用呼气末正压可改善ARDS患者的氧合状况。欧美联席会议(American-European Consensus Definition，AECC)于1994年首次明确提出了ARDS的具体诊断标准[2]，并于2012年修订了柏林标准[3]。尽管关于ARDS的临床研究越来越多，但其死亡率仍居高不下[4]。本文针对ARDS的分型及个体化治疗策略综述如下。
1 ARDS分型
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1.1 按病因分型
1994年，AECC将ARDS分成两种类型，即肺内型和肺外型[2]。肺内型ARDS的病因主要有肺炎、机械通气损伤、肺挫伤、误吸、溺水、有毒气体及烟雾吸入等，是肺部病因对肺实质的内源性直接损伤；肺外型ARDS的病因主要有脓毒症、创伤、休克、药物中毒、输血、胰腺炎及弥散性血管内凝血(disseminated intravascular coagulation，DIC)等[5]，是肺外病变及炎症反应对肺组织的外源性损伤。研究表明，两种类型的ARDS在多个方面存在差异[6]：(1)生物学方面，肺内型ARDS与肺外型ARDS的生物标志物水平不一样。一项共纳入983例ARDS患者的多中心随机对照研究发现，相比肺外型ARDS，肺内型ARDS患者的特殊表现为发生肺泡上皮细胞损伤后，其生物标志物表面活性蛋白D水平明显升高，血管内皮细胞损伤标志物血管生成素2水平明显降低[7]。杨卿等[8]通过比较肺外型与肺内型ARDS患者血清相关生物标志物水平的变化得出了类似结论。上述研究显示，肺内型ARDS患者的肺泡上皮损伤比肺外型ARDS患者更严重，而肺外型ARDS患者的血管内皮损伤比肺内型ARDS患者更严重[9]。(2)在呼吸力学及治疗反应方面，肺内型ARDS比肺外型ARDS具有更高的肺弹性阻力及更差的呼气终末正压(PEEP)反应，肺外型ARDS对增加PEEP及肺复张有良好作用。为研究ARDS患者PEEP的个体化设置，意大利学者比较了电阻抗断层成像测量PEEP(PEEPEIT)与跨肺压测量PEEP(PEEPPL)的效果，结果显示，所有患者用两种方法设置的个体化PEEP完全不同：PEEPPL能降低动态应力，而PEEPEIT能使肺复张及通气更加均匀；肺外型ARDS患者的PEEPPL明显低于PEEPEIT，肺内型则相反[10]。在俯卧位通气开始后的各时间段，肺外型ARDS患者的氧合指数(PaO2/FiO2)及动脉血氧分压(partial arterial oxygen pressure，PaO2)改善程度明显高于肺内型ARDS患者，提示肺外型ARDS患者从俯卧位通气中获益更多。重症超声可用于评估ARDS患者俯卧位通气的效果，肺部超声评分联合PaO2/FiO2可对ARDS患者进行更全面的监测及评估[11]。
一项回顾性研究显示，肺内型ARDS患者的病死率高于肺外型ARDS[比值比(OR)=2.6][12]。但朱然[13]认为两种类型ARDS的病死率可能均受肺部病变及肺外病变的共同影响，与患者的基础状况及临床治疗有关，二者的重症监护室(ICU)停留时间及住院病死率无明显差异。
1.2 按发病时间分型
2012年的柏林标准将ARDS的起病时间定义为：在1周之内危险因素明显表现出来，或在1周之内有新的呼吸系统症状出现或原有呼吸系统症状加重[3]。Croce等[14]率先将创伤后ARDS分为早发型、晚发型。其中早发型是指入院48 h内，疾病的发生与更严重的失血性休克存在相关性；而晚发型则为入院48 h后，疾病的发生与肺炎存在明显的相关性。Reilly等[15]发现，与晚发型ARDS相比，早发型ARDS的发生与失血性休克、胸部创伤的严重程度相关，患者的糖基化终产物受体、血管生成素2的水平较高，肺泡毛细血管屏障损伤的严重程度更高。Zhang等[16]对不同危险因素下的中、重度ARDS患者进行了研究，发现晚发型ARDS患者的28 d及60 d生存率相比早发型ARDS更低，而病死率更高。但由于许多病因(如脓毒症、休克)所致ARDS的准确起始时间难以确定，早期识别及诊断ARDS存在困难，这种分类方法有较大的局限性。因此，目前临床上尚难以根据发病时间分型对ARDS患者进行个体化、精准化治疗。
1.3 按疾病严重程度分型
2012年的柏林标准主要依据氧合状况的不同，将ARDS患者分成三类，即轻度、中度及重度ARDS[3]。中度与重度ARDS的同质性更高，其病理变化更倾向于弥漫性肺泡损伤(diffuse alveolar damage，DAD)[17]，即更符合典型ARDS的特征。有学者提出根据PaO2/FiO2重新划分ARDS等级。Maiolo等[18]尝试以PaO2/FiO2=150 mmHg(1 mmHg≈0.133 kPa)为阈值，将ARDS划分为轻-中度ARDS与中-重度ARDS两类，从相关数据来看，上述两种类型ARDS不论是在生理功能上还是解剖结构上差异都比较明显，中-重度ARDS的同质性更强。这些研究提示使用PaO2/FiO2这一新标准来进行严重程度分型，在试验人群纳入方式、治疗方案选择方面比以前的共识更具指导意义。ACURASYS研究纳入340例PaO2/FiO2<150 mmHg的ARDS患者，将其随机分成阿曲库铵组和安慰剂组，结果显示，早期使用阿曲库铵的患者机械通气时间更短，90 d生存率明显提高[19]。PROSEVA研究纳入PaO2/FiO2<150 mmHg的ARDS患者466例，将其分成俯卧位通气组和常规仰卧位组，结果显示，早期俯卧位通气可使患者的90 d病死率明显降低[20]。在接受静脉-静脉体外膜肺氧合(veno-venous extracorporeal membrane oxygenation，VV-ECMO)治疗的患者中，绝大多数为中-重度ARDS患者，应用VV-ECMO联合俯卧位通气能进一步提高患者的PaO2/FiO2，缓解低氧血症[21-23]。此外，一些严重程度评分如肺水肿放射学(RALE)评分[24]、人工神经网络模型(ANNs)[25]等有望成为ARDS临床分型的新工具。
1.4 按炎症程度分型
部分ARDS亚型无法通过某个简单变量进行识别，需要用到潜类别分析。Calfee等[26]对ARMA及ALVEOLI两项大型随机对照试验(RCT)研究的临床数据及生物标志物进行了潜类别分析，发现了以下两种不同的临床亚型：高炎症型ARDS与低炎症型ARDS。高炎症型ARDS的血浆炎性标志物水平高于低炎症型，且易发生休克及代谢性酸中毒，机械通气时间较长，脏器衰竭更严重，预后更差。两种亚型对机械通气的反应不同：高炎症型ARDS患者使用高PEEP后90 d的病死率低于使用低PEEP者，而预后好、炎症反应轻的低炎症型ARDS患者则相反，提示相对较高的PEEP可能更适合高炎症型患者。Famous等[27]对FACTT研究的数据进行二次分析发现，在高炎症型ARDS患者中，开放性液体疗法的90 d病死率低于保守性液体疗法(40% vs. 50%)，而在低炎症型ARDS患者中则有相反的效果(26% vs. 18%)，提示不同的ARDS亚型可能需要不同的液体治疗管理策略。上述研究均为回顾性分析，其结论尚未得到前瞻性研究的证实，因此不能用于临床实践，但可指导临床试验的设计。
1.5 按影像学分型
ARDS形态学差异的最直接证据是胸部CT，通过CT影像学的不同可将ARDS分为两种类型，即局灶型和弥漫型。典型的肺内型ARDS的胸部CT表现通常为磨玻璃影与实变影同时存在，实变不对称且“不均一”；而肺外型ARDS的磨玻璃影多对称分布，实变影少见[28]。对于ARDS患者而言，不同影像学分型使用相同机械通气策略的效果可能是截然不同的。一项多中心随机对照研究(LIVE研究)[29]将400例ARDS患者分为个体化组与对照组(标准治疗)，个体化组患者接受基于局灶型及弥漫型的个体化机械通气：局灶型给予高容量(8 ml/kg)、低PEEP及俯卧位治疗，弥漫型给予小潮气量(6 ml/kg)、高PEEP及肺复张治疗。结果显示，个体化组与对照组的90 d病死率差异无统计学意义(P=0.980)。然而，排除个体化组误分患者(约21%)后，个体化机械通气提高了患者生存率(P=0.045)。这些发现为ARDS的临床研究提供了新思路：准确而快速有效的分型是临床个体化治疗的前提，个体化机械通气策略可能更有益于临床治疗。
由于ARDS患者的病情危重，CT检查转运风险高，且有辐射危害，不适宜反复检查。近年来，重症超声因具有床旁实施、连续观察病情演变等独特优势，在ARDS患者中的应用越来越成熟。肺部超声可有效评估肺实变、肺渗出、气胸、胸腔积液等病理改变[30]。ARDS患者肺部病理改变可表现为局灶性(主要位于重力依赖区)或弥漫性(均匀分布)，还可累及双侧不同区域，有渗出、实变、不张、胸腔积液或气胸等不同病变表现形式，床旁肺部超声可反复多次、多角度检查肺部情况[31]，多种特殊的肺部征象对ARDS的诊断、鉴别诊断、分型均有重要价值，而且可用于评估ARDS患者俯卧位通气的效果[32]，具有广阔的应用前景。
1.6 按病理学分型
ARDS的组织学特征主要是DAD[12]，透明膜的存在是诊断DAD的关键[33]。肺内型ARDS主要由肺泡上皮损伤导致，伴有厚而不连续的透明膜沉积；肺外型ARDS主要由血管内皮损伤引起，透明膜薄且分布均匀[6]。然而，在临床确诊的ARDS患者中，只有不到一半的患者病理变化与DAD一致。DAD并不是ARDS特有的病理改变，急性间质性肺炎或特发性肺纤维化急性加重也可表现为DAD[12]。一项对ARDS患者的尸检研究发现，与无DAD的患者相比，有DAD的患者有更高的病死率、更差的PaO2/FiO2及肺顺应性，且序贯器官衰竭(SOFA)评分更高[34]。考虑到ARDS患者肺活检的高风险、高难度及肺病变的异质性，不同的采样部位及疾病分期可能导致不同的病理结果，因此DAD并不是诊断ARDS的必备条件。ARDS患者有无DAD所造成的临床表现的差异，对判断预后有一定意义，然而，大多数研究为来自尸检的回顾性分析，不具有代表性，对个体化治疗没有明确指导意义。因此，ARDS患者病理学分型的临床适用性不强。
2 新型冠状病毒感染(coronavirus disease 2019，COVID-19)相关ARDS表型
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COVID-19相关ARDS的临床表现存在异质性，至今已有多项研究对其进行分型[35]。主要有以下几种分型方法：(1)根据肺顺应性分为L型及H型[5,36]。COVID-19患者在早期基本上都表现为L型，此类患者的肺弹性阻力低，含气量高，重量较轻，弹性差，呼吸顺应性好，之所以会出现严重缺氧的问题，主要是由于在缺氧的影响下，肺血管收缩反应下降，再加上肺血流调节出现障碍，因此极易造成肺的肺泡通气量/肺血流量(Va/Q)失衡。L型患者的可复张区域一般不明显，因此较高的PEEP及俯卧位通气并不能明显改善氧合，但俯卧通气可重新分配肺血流，改善Va/Q。L型患者宜采用低水平PEEP，稍高潮气量(7～8 ml/kg)可使呼吸困难症状明显减轻，从而避免低通气造成的二氧化碳潴留及再吸收性肺不张。H型ARDS患者具有较高的肺弹性阻力，同时水肿症状较明显，具有较好的可复张性，重量较大，呼吸系统顺应性差，其治疗方案与“经典”重度ARDS患者相似，具体包括低潮气量、俯卧位通气及相对高水平的PEEP等。目前还未确定H型是否由L型进展而来，其病因也未确定。(2)以CT表现为依据分型。COVID-19患者胸部CT主要表现为双肺浸润影，呈磨玻璃样改变，以外周分布为主。Robba等[37]根据COVID-19患者的肺部CT表现将其分成3种类型。Ⅰ型：磨玻璃影主要分布于胸膜下区域，多发，局灶，可能与相对高灌注有关。Ⅱ型：肺不张、支气管旁斑片状阴影分布不均匀，在中、高水平PEEP或实施俯卧位通气的情况下，可使患者未充气的肺达到复张效果，如果依旧无法纠正低氧状态，可进行肺复张、俯卧位通气等处理。Ⅲ型：分布不均的ARDS样改变。可以用“经典”ARDS治疗方案对肺顺应差的患者实施治疗，如果依旧不能改善其低氧状态，可使用激素治疗，或应用体外膜肺氧合。Zhao等[38]报道，电阻抗成像(electrical impedance tomograph，EIT)、超声等床旁工具可能在识别COVID-19不同表型方面发挥重要作用。此外，这些功能性工具可以监测患者对各种治疗措施的反应，并因此有助于指导治疗。
与其他病因引起的ARDS相比，COVID-19相关ARDS存在较多特殊性。COVID-19患者具有高度活化的凝血功能[39]，有研究认为，COVID-19本质上是血管病变[40]。Ackermann等[41]发现，与死于流感相关呼吸衰竭的患者相比，死于COVID-19相关呼吸衰竭的患者肺组织除了表现为弥漫性肺泡损伤及血管周围T细胞浸润外，还显示出独特的血管特征，包括与细胞内病毒存在相关的严重内皮损伤及细胞膜破裂，肺血管的组织学分析显示广泛的血栓形成及微血管病变。COVID-19患者肺泡毛细血管微血栓的发生率是流感患者的9倍(P<0.001)，肺部新血管生长量是流感患者的2.7倍(P<0.001)。
目前，有关COVID-19相关ARDS的认识刚刚起步，在病理生理特点、生物标志物及呼吸力学等方面依然存在着大量不明确的地方[42]，且目前表型界定依据的研究样本量非常小，属于观察性研究，可能存在较大偏倚，未来还需要扩大样本量，并通过临床RCT研究进一步证实。
3 ARDS的个体化治疗策略
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ARDS不同分型的临床意义及相应治疗策略见表1，可为ARDS的个体化、精准化治疗提供依据。
4 总结与展望
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综上所述，ARDS是一组异质性很强的临床综合征，精准分型有利于其个体化治疗。目前ARDS分型还处于初步阶段，无论是基于临床资料的病因分型、发病时间分型、严重程度分型、影像学分型和病理学分型，还是基于复杂的临床数据二次统计学分析的炎症程度分型，均为回顾性研究，缺乏前瞻性大型随机对照研究验证。因此需要收集更多可靠的数据，才能准确识别不同亚型，从而进行个体化精准治疗。近年来，ARDS相关基因组学研究取得了一定进展，例如，Fang等[43]的研究表明，血管紧张素转换酶2(angiotensin converting enzyme 2，ACE2)是miRNA的靶基因，miRNA通过对ACE2的抑制来介导脂多糖(lipopolysaccharide，LPS)引起的肺内皮细胞凋亡及急性肺损伤。未来，易感基因可作为对ARDS进行精准分型的依据之一。
基金
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  • 国家自然科学基金(82072143)
  • 广东省自然科学基金(2021A1515010170)
文献
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doi: 10.11855/j.issn.0577-7402.2023.05.0615
  • 接收时间：2022-02-28
  • 首发时间：2025-12-03
  • 出版时间：2023-05-28
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  • 收稿日期：2022-02-28
  • 录用日期：2022-05-04
基金
National Natural Science Foundation of China(82072143)
国家自然科学基金(82072143)
Natural Science Foundation of Guangdong Province(2021A1515010170)
广东省自然科学基金(2021A1515010170)
作者信息
    1江门市中心医院重症医学科，广东江门 529000
    2解放军南部战区总医院重症医学科，广东广州 510010

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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
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