EDITORIAL
Manipulation of inflammation in ARDS
Manipulation of inflammation in ARDS: achievable goal or distant target?
Correspondence to:
Correspondence to:
Dr S V Baudouin
Senior Lecturer in Critical Care Medicine, Royal Victoria Infirmary, Newcastle upon Tyne, UK;s.v.baudouin@ncl.ac.uk
A possible role for thioredoxin
Keywords: acute lung injury; acute respiratory distress syndrome; inflammation; thioredoxin
| The first 150 words of the full text of this article appear below. |
The acute respiratory distress syndrome (ARDS) was only recognised as a distinct clinical entity less than 50 years ago.1 It arose as a consequence of the success of modern resuscitation and organ support and was first described in severely injured military personnel. It is defined by the development of rapidly progressing respiratory failure, usually within 24–48 hours of the initiating insult. Plain chest radiographs show widespread airspace shadowing with a pattern similar to cardiogenic pulmonary oedema. However, when measured, left sided cardiac pressures are normal and the pulmonary oedema fluid has a high protein content.
This picture of normal cardiac filling pressures and high air space protein content suggested that the central pathophysiology was a result of increased pulmonary epithelial/endothelial permeability. Histological examination of biopsy and autopsy specimens showed widespread epithelial and endothelial damage and radioisotope studies confirmed that lung permeability was abnormal.
Histological studies
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Thorax 2006 61: 459.[Extract] [Full Text] [PDF]
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