Rios Fernando, Iscar Teresa, Cardinal-Fernández Pablo
Departamento de Terapia Intensiva, Hospital Nacional Alejandro Posadas - Buenos Aires, Argentina.
Departamento de Patologia, Hospital Universitário HM Puerta del Sur - Madri, Espanha.
Rev Bras Ter Intensiva. 2017 Jul-Sep;29(3):354-363. doi: 10.5935/0103-507X.20170044. Epub 2017 Sep 28.
Acute respiratory distress syndrome is a challenging entity for the intensivist. The pathological hallmark of the acute phase is diffuse alveolar damage, which is present in approximately half of living patients with acute respiratory distress syndrome. It is clear that respiratory support for acute respiratory distress syndrome has gradually been improving over recent decades. However, it is also evident that these procedures are beneficial, as they reduce lung injury and keep the patient alive. This could be interpreted as a time-gaining strategy until the trigger or causal or risk factor improves, the inflammatory storm decreases and the lung heals. However, all except two pharmacological treatments (neuromuscular blockers and steroids) were unable to improve the acute respiratory distress syndrome outcome. The hypothesis that pharmacological negative results may be explained by the histological heterogeneity of acute respiratory distress syndrome has been supported by the recent demonstration that acute respiratory distress syndrome with diffuse alveolar damage constitutes a specific clinical-pathological entity. Given that diffuse alveolar damage is a pathological diagnosis and that open lung biopsy (the most common technique to obtain lung tissue) has several side effects, it is necessary to develop surrogate biomarkers for diffuse alveolar damage. The aim of this narrative review is to address the following three topics related to acute respiratory distress syndrome: (a) the relationship between acute respiratory distress syndrome and diffuse alveolar damage, (b) how diffuse alveolar damage could be surrogated in the clinical setting and
急性呼吸窘迫综合征对重症监护医生来说是一个具有挑战性的病症。急性期的病理特征是弥漫性肺泡损伤,约半数急性呼吸窘迫综合征的存活患者存在这种情况。显然,近几十年来,对急性呼吸窘迫综合征的呼吸支持在逐步改善。然而,同样明显的是,这些措施是有益的,因为它们能减少肺损伤并维持患者生命。这可以被解释为一种争取时间的策略,直到触发因素、病因或危险因素改善,炎症风暴减轻且肺部愈合。然而,除了两种药物治疗(神经肌肉阻滞剂和类固醇)外,所有其他治疗都未能改善急性呼吸窘迫综合征的预后。急性呼吸窘迫综合征的组织学异质性可能解释药物治疗阴性结果这一假说,已得到最近一项研究的支持,该研究表明伴有弥漫性肺泡损伤的急性呼吸窘迫综合征构成一种特定的临床病理实体。鉴于弥漫性肺泡损伤是一种病理诊断,且开胸肺活检(获取肺组织最常用的技术)有多种副作用,因此有必要开发弥漫性肺泡损伤的替代生物标志物。本叙述性综述的目的是探讨与急性呼吸窘迫综合征相关的以下三个主题:(a)急性呼吸窘迫综合征与弥漫性肺泡损伤之间的关系,(b)在临床环境中如何替代弥漫性肺泡损伤以及