86例ARDS患者机械通气治疗分析

急性呼吸窘迫综合征(ARDS)是在严重感染、休克、创伤及烧伤等非心源性疾病过程中,肺毛细血管内皮细胞和肺泡上皮细胞损伤造成弥漫性肺间质及肺泡水肿,导致的急性低氧性呼吸功能不全或衰竭。以肺气容积减少、肺顺应性降低和严重的通气/血流比例失调为病理生理特点,临床表现为不易缓     

血管内皮细胞分泌的炎性递质在急性肺损伤发病机制中的作用

肺血管内皮细胞损伤在急性肺损伤（ALI）／急性呼吸窘迫综合征（ARDS）的病理过程中起重要作用,各种血管源性炎症递质可导致血管内皮细胞损伤,提高肺泡-毛细血管通透性,肺血管间质和肺泡腔水肿,发生顽固性低氧血症、呼吸窘迫等临床表现。本文探讨了ALI时各种炎症递质的表达、对肺血管内皮的作用机制及对ALI的病理生理影响。这些可能成为ALI／ARDS新的治疗靶点和研究的方向。     

内毒素急性肺损伤相关标志物变化的研究

急性肺损伤(ALI)是直接或间接致伤因素导致肺泡上皮细胞及毛细血管内皮细胞损伤,造成弥漫性肺间质和/或肺泡水肿,导致的急性低氧性呼吸功能不全。以肺容积减小、顺应性减少、通气-灌注比例失调(死腔增加)为病理生理特征,临床上表现为进行性低氧血症和呼吸窘迫。X线表现为两肺渗出性病变,氧合指数(动脉氧分压Pa O2/吸入氧分数Fi O2)<300[1]。其发展至严重阶段(氧合指数<200)被称为急性呼吸窘迫综合征(ARDS)。ALI/ARDS的发病机制     

中性粒细胞活化与凝血纤溶系统异常的相互作用在急性肺损伤发病中的作用

急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)是临床中常见的危重症,发病率及死亡率均比较高.研究表明,凝血纤溶系统异常与炎症反应的相互促进、共同作用引起的肺微血管内皮损伤、肺微血栓形成、肺泡内纤维蛋白沉着和透明膜形成等组成了ALI/ARDS发生的病理基础.     

控制性肺膨胀复张通气策略9例临床观察

控制性肺膨胀(SI)是目前最常用的治疗急性呼吸窘迫综合征(ARDS)肺复张手法,是在吸气时,经气道对肺泡施加足够的压力,使塌陷的肺泡充分开放,并持续一定时间,使陷闭的肺组织重新充气。本研究回顾性总结兰州军区乌鲁木齐总医院综合ICU 9例基础疾病多,病情危重的ARDS患者应用SI复张法,旨在对ARDS患者在镇静、肌肉松弛状态下,采用控制性肺膨胀复张手法在压力控制通气     

防治震后伤者发生ARDS的“五早”原则

大地震后由于房屋坍塌等灾害因素，带来的多发伤和严重感染并由此引发急性肺损伤（Au）／急性呼吸窘迫综合征（ARDs）的比例大大增加，病死率高达34％～60％ALI／ARDS是在严重感染、休克、创伤及烧伤等非心源性疾病过程中，肺毛细血管内皮细胞和肺泡上皮细胞损伤造成弥漫性肺间质及肺泡水肿，导致的急性低氧性呼吸功能不全或衰竭。     

急性呼吸窘迫综合征的分型及个体化治疗研究进展

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。     

肺泡巨噬细胞在急性肺损伤中的作用

急性肺损伤（acute lung injury，ALI）及其重症形式，急性呼吸窘迫综合征（ARDS），是以肺泡及肺实质发生急性炎症过程为特征的临床综合征，表现为肺泡上皮与肺毛细血管内皮细胞屏障功能的丧失，重症病人可出现呼吸衰竭。肺泡巨噬细胞（alveolar macrophage，AM）是肺内主要的居留性吞噬细胞，构成机体防御呼吸道病原的第一道防线，在清除进入气道的感染性、有毒性或致敏性颗粒物中发挥着关键作用。越来越多的证据表明，AM激活后通过分泌炎性细胞因子、趋化因子、损伤介质和抗炎性细胞因子等，在ALI的发生、发展及转归中发挥重要作用。     

西宁地区急性呼吸窘迫综合征行肺保护性通气的临床研究

目的:观察西宁地区急性呼吸窘迫综合征(ARDS)应用肺保护性通气治疗的临床疗效.方法:将40例急性呼吸窘迫综合征患者随机分为两组,实验组20例,采用肺保护通气;对照组20例,采用传统通气,观察两组患者血气指标、呼吸动力学指标、呼吸机相关性肺损伤发生率及对预后的影响.结果:治疗第7天实验组动脉血氧分压( PaO2)较对照...     

高原慢性低氧暴露下的急性呼吸窘迫综合征:更应关注右心功能

急性呼吸窘迫综合征(ARDS)时肺血管收缩、肺血管阻力增加、肺动脉高压,导致患者右心后负荷过高,继而并发急性肺心病(ACP),加重右心功能损害,出现严重肺水肿及低氧血症.长期暴露在高原慢性低氧环境的健康人,极易出现生理性肺动脉高压及血液黏滞度改变等,这些因素会加重高原ARDS的严重程度.因此,高原ARDS与平原ARDS...     

F-18 FDG PET/CT in acute respiratory distress syndrome: a case report

F-18 FDG PET/CT has become a useful technique in the evaluation of pulmonary lesions. We present a case of markedly increased and diffuse pulmonary F-18 FDG activity in a patient with acute respiratory distress syndrome (ARDS). High rates of glucose utilization by the inflammatory cells involved in the pathogenesis of ARDS might explain the increased pulmonary F-18 FDG uptake we observed. In the proper clinical setting, ARDS should be considered in the differential diagnosis of patients with diffusely increased F-18 FDG activity in the lungs.     

Determinants of early adult respiratory distress syndrome with special reference to chest radiography. A retrospective analysis of 220 patients with major skeletal injuries

The medical records of 220 consecutive patients with traumatic injuries admitted to the intensive care unit in the years 1974-1982 were scrutinised in an attempt to find radiographic signs and clinical determinants of early adult respiratory distress syndrome (ARDS). All patients included in this study were considered to run a risk of developing ARDS and had 'pure' major fractures in the sense that there were no accompanying severe brain, chest or abdominal injuries. There were no deaths in this series of patients. ARDS developed in 27 patients (12.3%), on an average on the second day of trauma. Chest radiographs of 21 of these patients showed features indicative of ARDS, whereas those of the other 6 patients were normal despite hypoxaemia. In most of the 27 patients the only radiographic manifestation of ARDS was interstitial oedema; only a minority presented with alveolar oedema in addition. In 6 patients no radiographic changes ever occurred. Ventilator treatment with positive end expiratory pressure may have prevented the pulmonary insufficiency from becoming radiographically manifest. The clinical determinants of post-traumatic ARDS were a high fracture index, based on the number and severity of fractures, implying severe trauma, and shock on admission. Fluid overload was not found to be the cause of ARDS.     

Value of chest radiography in adult respiratory distress syndrome

In a prospective investigation of 19 patients with traumatic (n = 11) and septic (n = 8) shock at risk of developing the adult respiratory distress syndrome (ARDS), serial chest films were monitored. Eight patients developed ARDS, 2 following traumatic shock and 6 following septic shock. Only 2 of these 8 patients exhibited radiographic abnormalities consisting in bilateral widespread infiltrates of the alveolar type. In the 2 patients ARDS had already developed before artificial ventilation with positive end expiratory pressure (PEEP) was instituted. In the other 6 patients, in whom ventilator treatment with PEEP was initiated prophylactically or early in the disease, the chest films remained virtually normal despite development of a marked pulmonary insufficiency. It is concluded that early ventilator treatment with PEEP counteracts the classical radiographic abnormalities of ARDS, probably by reducing alveolar oedema and atelectasis. Thus, presently, with use of early or prophylactic ventilator treatment with PEEP as a therapeutic measure against ARDS chest radiography may be of limited value in the diagnosis. However, it should be essential for early recognition of therapy requiring complications.     

Acute respiratory distress syndrome: imaging of the injured lung.

In patients with the acute respiratory distress syndrome (ARDS), there is non-specific but widespread exudation of oedema and inflammatory fluid into the lungs. The clinical corollary (dyspnoea, refractory hypoxia, reduced pulmonary compliance and diffuse pulmonary infiltrates) is catastrophic and generally associated with a poor outcome. Imaging is integral to the care of these critically ill patients on the intensive care unit. In the present review, the radiological changes on plain radiography and computed tomography (CT) in patients with ARDS are discussed. Particular attention is directed at the appearances on CT: the relationships between CT features, histopathological changes and the inevitable alterations in pulmonary physiology are explored.     

内皮祖细胞治疗急性肺损伤的研究进展

急性肺损伤(ALI)是临床上常见的危重疾病,目前尚无特效疗法。保护内皮细胞受损并逆转已形成的损伤成为ALI治疗发展的新趋势,受到广泛关注。一系列研究提示从骨髓动员至外周血的内皮祖细胞(EPCs)在受损的肺组织处可以直接分化为血管内皮细胞,并能调节失控的炎症反应、增强受损肺组织的抗氧化能力,对血管内皮细胞的修复和维持肺泡毛细血管屏障的完整性起着重要作用,因此内皮祖细胞的移植治疗将成为降低ALI/急性呼吸窘迫综合征(ARDS)死亡率的治疗新靶向。     

Immunohistochemistry of pulmonary surfactant-associated protein A in acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a fatal complication in severe traumas and diseases. Although the contribution of pulmonary surfactant abnormality to the pathogenesis of ARDS has been clinically fairly well investigated, the histopathological evidence has not been established. The aim of this study was to clarify the immunohistochemical distribution of surfactant-associated protein A (SP-A) for early diagnosis of ARDS with special regard to hyaline membrane (HM) formation. Two-hundred-and-ten autopsy cases of prolonged death from various traumas and diseases were investigated. ARDS were observed in 23 cases, showing speckled SP-A immunostaining. During the early, exudative phase of ARDS, characteristic SP-A distribution showed intense staining in the intra-alveolar massive aggregates and thick 'peeling'-like substances accompanied with a lot of granular staining. During the proliferative phase, localized accumulation of granular SP-A and macrophages containing dense granular SP-A became predominant. During the final fibrotic phase, SP-A staining in HMs became weak, and disseminated granular staining was observed in the alveolar spaces. These findings provide morphological evidence of the increase of SP-A during the early phase of ARDS, including some molecular alteration and its decrease during the late phase. Characteristic SP-A distribution in the exudative phase appeared to be especially useful for early histopathological diagnosis of respiratory distress, even prior to the appearance of typical HMs.     

沐舒坦预防和治疗ARDS研究进展

沐舒坦（Ambroxol)是一种较新的粘液溶解剂，近年来其对呼吸系统的保护作用倍受关注，已较多学者将其应用于ARDS的预防和治疗，取得了较好的临床效果，并对其机制进行了深入的研究。其预防和治疗ARDS的机制可能是：（1）减少TNFα和IL－1及相关炎性介质的释放，减轻SIRS在肺部的表现；（2）抗氧化作用，阻止氧自由基对肺组织的损伤；（3）刺激肺泡Ⅱ型上皮细胞合成、分泌内源性肺表面活性物质，同时抑制磷脂酶A对肺表面活性物质的降解，增加肺的顺应性；（4）减轻ARDS时气管壁离子转运和电位差的破坏。临床应用大剂量沐舒坦对ARDS的预防、治疗和转归可能具有一定疗效。     

肺挫伤致急性呼吸窘迫综合征临床分析

目的　探讨肺挫伤致ARDS相关危险因素。方法　总结 1 2 6例肺挫伤的临床资料 ,并将住院时间 >2 4小时的 1 1 0例分为ARDS组和非ARDS组 ,对其致伤原因、伤情及治疗结果进行对比分析。结果　本组ARDS发生率 30 .2 % ,肺挫伤并严重多发伤ARDS发生率较单纯肺挫伤高 (P <0 .0 1 )。交通伤为肺挫伤最主要原因 ,ARDS组挤压伤多 ,坠落伤较少 (P <0 .0 1 ) ;ARDS组损伤严重 (ISS >2 5 ) ,ISS评分明显高于非ARDS组 (P <0 .0 1 ) ,其浮动胸壁、休克、多发伤发生率明显高于非ARDS组 (P <0 .0 1 )。结论　合并严重多发伤 (ISS >2 5 )、浮动胸壁、休克等是肺挫伤致ARDS重要危险因素 ,应针对其进行早期有效治疗     

Air transportation of patients with acute respiratory failure: theory

Adult respiratory distress syndrome (ARDS) that results from severe trauma often occurs in remote places, making it necessary to transport the patients to tertiary medical facilities by air. Since these severely hypoxic patients are exposed to additional risk of reduced inspired oxygen tension due to decreased barometric pressure, the feasibility of transportation of these patients was investigated by computer analysis. Mathematical models of pulmonary gas exchange in patients with ARDS were developed to calculate arterial and mixed venous blood tensions while breathing room air and oxygen at sea level, 8,000 ft, and 40,000 ft. Under each condition the following parameters were varied: alveolar ventilation (VA), cardiac output (Q), metabolic rate (VO2), hematocrit (Hcrit), and membrane diffusing capacity for oxygen (DmO2). Most of the gas exchange problems at altitude could be overcome by breathing oxygen as long as cardiac output and hematocrit were adequate. Hypoxemia in ARDS patients will not be greatly affected by the reduced inspired oxygen tensions at altitude in much the same way that hypoxemia in ARDS is poorly responsive to increased inspired oxygen tensions at sea level.     

肺复张策略治疗内源性和外源性急性呼吸窘迫综合征效果的比较研究

目的对比研究肺复张策略对肺内/外源性急性呼吸窘迫综合征治疗效果。方法18例急性呼吸窘迫综合征机械通气的患者,分肺内源性组和肺外源性组,其中肺内源性急性呼吸窘迫综合征10例,肺外源性急性呼吸窘迫8例。在肺保护性通气策略基础上行肺复张,在镇静、非肌松状态下,采用高水平持续正压通气,呼吸末正压为40 cm H2O,持续时间40 s。结果与肺复张前比较,两组复张后10 min3、0 min1、h2、h动脉血气分析氧饱和度、动脉氧分压均有提高（P〈0.05）,两组比较肺外源性组升高较为明显（P〈0.05）;复张前后两组二氧化碳分压均无明显变化（P〉0.05）,呼吸系统顺应性在复张后明显提高（P〈0.05）;气道峰压、平台压、中心静脉压、平均动脉压在复张过程中时提高（P〈0.05）,但复张后5 min与治疗前比较没有明显变化（P〉0.05）;复张前后心率没有明显变化（P〉0.05）。结论肺复张措施对急性呼吸窘迫综合征患者能改善氧合、对血流动力学影响短暂、安全有效,对于肺外源性急性呼吸窘迫综合征治疗效果更明显。