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烟雾吸入性肺损伤:最新进展

Smoke inhalation lung injury: an update.

作者信息

Demling Robert H

机构信息

Harvard Medical School, Burn and Trauma Center, Brigham and Women's Hospital, Boston, MA, USA.

出版信息

Eplasty. 2008 May 16;8:e27.

Abstract

OBJECTIVES

The purpose of this study is to present a multifaceted, definitive review of the past and current status of smoke inhalation injury. History along with current understanding of anatomical, physiology, and biologic components will be discussed.

METHODS

The literature has been reviewed from the early onset of the concept of smoke inhalation in the 1920s to our current understanding as of 2007.

RESULTS

The results indicate that the current pathophysiologic concept is of a disease process that leads to immediate and delayed pulmonary injury best managed by aggressive physiologic support. Management approaches for the biochemical changes have not kept up with current knowledge. The lung injury process is activated by toxins in the smoke's gas and particle components and perpetuated by a resulting lung inflammation. This inflammatory process becomes self-perpetuating through the activation of a large number of inflammatory cascades. In addition, smoke injury leads to significant systemic abnormalities injuring other organs and accentuating the burn injury process and subsequently leading to mediator-induced cellular injury leading potentially to multisystem organ failure.

CONCLUSIONS

Smoke inhalation injury results in the anatomic finding of denuded and sometimes sloughed airways mucosa. Physiologic findings include small airways containing fibrin casts of mucosa and neutrophils. Airway hyper-reactivity results as well, leading to further decreased collapse, causing obstruction.

摘要

目的

本研究旨在对烟雾吸入性损伤的过去和现状进行多方面的权威性综述。将讨论其历史以及目前对解剖学、生理学和生物学组成部分的理解。

方法

回顾了从20世纪20年代烟雾吸入概念出现之初到2007年我们目前理解的相关文献。

结果

结果表明,当前的病理生理概念是一种导致即刻和延迟性肺损伤的疾病过程,积极的生理支持是最佳的处理方式。针对生化变化的处理方法并未跟上当前的知识水平。肺损伤过程由烟雾的气体和颗粒成分中的毒素激活,并因由此产生的肺部炎症而持续存在。这种炎症过程通过激活大量炎症级联反应而自我延续。此外,烟雾损伤会导致显著的全身异常,损害其他器官,加重烧伤损伤过程,随后导致介质诱导的细胞损伤,可能导致多系统器官衰竭。

结论

烟雾吸入性损伤导致气道黏膜剥脱甚至有时脱落的解剖学表现。生理学表现包括小气道内有黏膜和中性粒细胞的纤维蛋白铸型。还会出现气道高反应性,导致进一步的肺萎陷减少,引起阻塞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2ae/2396464/0a7bd335a7b7/eplasty08e27_fig1.jpg

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