Elsevier

The Lancet

Volume 369, Issue 9572, 5–11 May 2007, Pages 1553-1564
The Lancet

Review
Acute lung injury and the acute respiratory distress syndrome: a clinical review

https://doi.org/10.1016/S0140-6736(07)60604-7Get rights and content

Summary

Acute respiratory distress syndrome and acute lung injury are well defined and readily recognised clinical disorders caused by many clinical insults to the lung or because of predispositions to lung injury. That this process is common in intensive care is well established. The mainstay of treatment for this disorder is provision of excellent supportive care since these patients are critically ill and frequently have coexisting conditions including sepsis and multiple organ failure. Refinements in ventilator and fluid management supported by data from prospective randomised trials have increased the methods available to effectively manage this disorder.

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

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

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