Objective To systematically review the efficacy of steroids in the prevention of acute respiratory distress syndrome (ARDS) in critically ill adults, and treatment for established ARDS. Data sources Search of randomised controlled trials (1966( -April 2007 of PubMed, Cochrane central register of controlled trials, Cochrane database of systematic reviews, American College of Physicians Journal Club, health technology assessment database, and database of abstracts of reviews of effects. Data extraction Two investigators independently assessed trials for inclusion and extracted data into standardised forms; differences were resolved by consensus. Data synthesis Steroid efficacy was assessed through a Bayesian hierarchical model for comparing the odds of developing ARDS and mortality (both expressed as odds ratio with 95% credible interval) and duration of ventilator free days, assessed as mean difference. Bayesian outcome probabilities were calculated as the probability that the odds ratio would be ≥1 or the probability that the mean difference would be ≥0. Nine randomised trials using variable dose and duration of steroids were identified. Preventive steroids (four studies) were associated with a trend to increase both the odds of patients developing ARDS (odds ratio 1.55, 95% credible interval 0.58 to 4.05; P(odds ratio ≥1)=86.6%), and the risk of mortality in those who subsequently developed ARDS (three studies, odds ratio 1.52, 95% credible interval 0.30 to 5.94; P(odds ratio ≥1)=72.8%). Steroid administration after onset of ARDS (five studies) was associated with a trend towards reduction in mortality (odds ratio 0.62, 95% credible interval 0.23 to 1.26; P (odds ratio ≥1)=6.8%). Steroid therapy increased the number of ventilator free days compared with controls (three studies, mean difference 4.05 days, 95% credible interval 0.22 to 8.71; P(mean difference ≥0)=97.9%). Steroids were not associated with increase in risk of infection. Conclusions A definitive role of corticosteroids in the treatment of ARDS in adults is not established.

(65 ± 17.9, P < 0.001). These improvements continued up to the time of weaning (pH 7.38 ± 0.08, PaCO 2 54.7 ± 20) and maintained (within 12 h) postweaning from the ventilator (pH 7.39 ± 0.08, PaCO 2 51.9 ± 12.4). No significant change in the PaO 2 was observed during NIPPV; PaO 2 after 1 h, prior to weaning and after weaning was 90.53 ± 42.85, 84.80 ± 33.76, 78.71 ± 43.81

Inadvertent administration of enteral feed into an intravenous line is preventable usually by design of incompatible connectors, but these may not be available universally. We discuss a case report where this occurred and the subsequent management strategy.

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