Potential factors affecting lung inhomogeneity in acute respiratory distress syndrome.
Potential factors affecting lung inhomogeneity in acute respiratory distress syndrome.
复制标题
影响急性呼吸窘迫综合征肺不均匀性的潜在因素。
DOI：
10.1007/s00134-017-4897-7
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Shime N
中科院分区：
文献类型：
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作者：
Tanabe Y;Ohshimo S;Shime N
亲爱的编辑，我们怀着极大的兴趣阅读了Cressoni等人最近发表的《重症监护医学》文章。[1]他使用计算机断层扫描，前瞻性研究了33例急性呼吸窘迫综合征（ARDS）患者传统开放肺通气策略的效果。他们表明，平台压高达30 cmH 2 O和呼气末正压高达15 cmH 2 O的肺开放策略不足以打开肺并保持肺开放。由于这些是关于当前开放肺策略的潜在有害影响的重要发现，我们感谢这项研究提供临床有用的信息。然而，应讨论可能影响其结果的几个因素。首先，本研究中肺不均匀性的定义似乎存在争议。他们将肺不均匀性阈值定义为根据同一组的先前研究，呈现大于1.61的充气比的肺体积百分比[2];然而，后一个队列没有ARDS。肺不均匀性的程度随着ARDS的严重程度而增加，与生理死腔相关，并与总体死亡率相关[3]。因此，最佳阈值应在与当前队列相似的ARDS人群中计算。第二，患者的背景存在显著差异。轻、中度组ARDS的发病机制主要与脓毒症和创伤有关，而重度组ARDS的发病机制主要为肺炎。Morisawa等人证明，与肺外ARDS患者相比，肺ARDS患者的肺血管通透性受损更严重，与序贯器官衰竭评估评分无关[4]，尽管两组之间的28天死亡率、机械通气天数和住院时间无显著差异。这些结果表明，在ARDS的发病机制的差异，而不仅仅是疾病的严重程度所确定的氧合能力，可能已与不同的临床表现，以及观察到的效果的开放肺strategy.Third，疾病发作和研究招募之间的间隔，以及治疗策略，应考虑。治疗开始延迟1-5天、不同的呼吸机设置和液体管理[5]可能会影响ARDS患者的结局和开放肺策略的观察效果。
Dear Editor, We read with great interest the recent Intensive Care Medicine article by Cressoni et al.[1], who, using computed tomography scans, prospectively studied the effect of the traditional open lung strategy for ventilation in 33 patients with acute respiratory distress syndrome (ARDS). They showed that the open lung strategy with a plateau pressure of up to 30 cmH2O and positive endexpiratory pressure up to 15 cmH2O were not sufficient to open up the lung and keep it open. Since these are important findings in terms of the potentially harmful effects of the current open lung strategy, we appreciate this research for providing clinically useful information. However, several factors potentially affecting their results should be discussed. First, the definition of lung inhomogeneity in this study seems to be controversial. They defined the lung inhomogeneity threshold as the percentage of lung volume presenting an inflation ratio of greater than 1.61 in accordance with a previous study by the same group [2]; however, the latter cohort did not have ARDS. The extent of lung inhomogeneities increased with the severity of ARDS, correlated with the physiological dead space, and was associated with overall mortality [3]. Therefore, the optimal threshold should have been calculated in an ARDS population similar to the current cohort. Second, there was a significant difference in the background of patients. The pathogenesis of ARDS in the mild and moderate groups was predominantly related to sepsis and trauma, while the pathogenesis of ARDS in the severe group was predominantly pneumonia. Morisawa et al. demonstrated that pulmonary vascular permeability was more severely compromised in patients with pulmonary ARDS than those with extrapulmonary ARDS, independent of the Sequential Organ Failure Assessment score [4], although no significant differences were observed in 28-day mortality, mechanical ventilation days, and duration of hospitalization between the two groups. These results suggest that the differences in the pathogenesis of ARDS, and not just the severity of the disease as determined by oxygenation capacity, might have been associated with the different clinical manifestations as well as the observed effect of the open lung strategy.Third, the interval between disease onset and study enrollment, as well as the treatment strategy, should be taken into account. The delay of 1–5 days in commencement of treatment, different ventilator settings, and fluid management [5] could have affected both the outcome in ARDS patients and the observed effect of the open lung strategy.