We searched the Cochrane Library and MEDLINE (for entries up to October, 2005). We used the search terms “acute lung injury”, “ALI”, “acute respiratory distress syndrome”, and “ARDS”. Animal and human studies were reviewed. We mainly selected publications in the past 5 years, but did not exclude commonly referenced and highly regarded older publications. We also searched the reference lists of articles identified by this search and selected those we judged relevant. Generally, preference was
ReviewAcute lung injury and the acute respiratory distress syndrome: a clinical review
Section snippets
Definition and diagnosis
Acute respiratory distress syndrome and acute lung injury were first described in 1967, and are characterised by the abrupt onset of clinically significant hypoxaemia with presence of diffuse pulmonary infiltrates. These infiltrates show on radiograph (figure) as pulmonary oedema resulting from increased pulmonary vascular permeability.1 These disorders affect patients of all ages and usually happen soon after an easily identified triggering event (panel 1). The likelihood of developing acute
Histopathology
Early acute lung injury is characterised histologically by a diffuse neutrophilic alveolar infiltrate, with haemorrhage, and the accumulation of a protein-rich pulmonary oedema. During this acute, so-called exudative phase, a panoply of cytokines (eg, tumour necrosis factor, interleukin 1, interleukin 8) incites and perpetuates inflammation. By increasing oxidant stress and protease activity, the inflammatory mixture in the alveoli and interstitium reduces surfactant production, and inactivates
Pathophysiology
In the early phase of acute lung injury, leakage of oedema fluid into the lung and inflammatory cellular infiltrates cause diffusion abnormalities and ventilation-perfusion mismatch, which clinically manifest as hypoxaemia. Concurrently, cellular infiltration, diffuse atelectasis, and oedema fluid reduce thoracic compliance. The combination of regional alveolar over-distention and small-vessel thrombosis increases dead space. Hypoxaemic vasoconstriction and capillary obliteration raise
Treatment
Acute lung injury has no specific treatment, although some doctors would argue that ventilation with a normal tidal volume, which results in reduced airway pressure, is a specific treatment. The mainstay of treatment is supportive care, mainly to avoid iatrogenic complications and treat the underlying cause, while maintaining adequate oxygenation. Almost all patients with acute lung injury need positive-pressure ventilation with supplemental oxygen and PEEP. Physical support is usually provided
Conclusion
Acute lung injury and acute respiratory distress syndrome are common, costly, and potentially lethal diseases, for which treatment of the underlying cause is the first step to recovery. Prevention of nosocomial complications has an important role to achieve the optimum outcome. With respect to lung support, the only ventilatory practice proven to be beneficial in a large randomised trial is reduction of tidal volume to 6 mL/kg predicted bodyweight (or lower if needed), to achieve a plateau
Search strategy and selection criteria
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