We identified 25 trials, of which 20 (17 randomized and three quasi-randomized trials) could be pooled in a meta-analysis.
Corticosteroids did not change 28-day mortality (20 trials, n = 2138, relative risk (RR) 0.87, 95% confidence interval (CI) 0.74 to 1.01; random-effects model). There was significant heterogeneity that was partly related to the dosing strategy. Treatment with a long course of low dose corticosteroids significantly reduced 28-day mortality (RR 0.84, 95% CI 0.72 to 0.97; P = 0.02), increased the proportion of shock reversal by day seven (six trials, n = 965, RR 1.35, 95% CI 1.16 to 1.57; random-effects model) and day 28 (six trials, n = 952, RR 1.12, 95% CI 1.02 to 1.23), reduced the sepsis-related organ failure assessment (SOFA) score by day seven (five trials, n = 916, RR -1.47, (95% CI -2.01 to -0.92), and survivors' length of stay in the intensive care unit (eight trials, n= 622, RR -4.49, 95% CI -7.04 to -1.94), without inducing gastroduodenal bleeding (13 trials, n = 1594, RR 11.12, 95% CI 0.81 to 1.53), superinfection (14 trials, n = 1917, RR 1.01, 95% CI 0.82 to 1.25), or neuromuscular weakness (three trials, n = 811, RR 0.63, 95% CI 0.12 to 3.35). Corticosteroid increased the risk of hyperglycaemia (nine trials, n = 1434, RR 1.16, 95% 1.07 to 1.25) and hypernatraemia (three trials, n= 805, RR 1.61, 95% CI 1.26 to 2.06).