Table 1 Current knowledge concerning glucocorticoids in sepsis

What we know

   • Sepsis causes complex alterations of the hypothalamic-pituitary-adrenal axis and glucocorticoid signaling [1].

   • Etomidate causes suppression of cortisol synthesis for up to 24 hours [13].

   • High random cortisol levels are a marker of disease severity and a poor prognostic marker [14].

   • Short-course, high-dose glucocorticoids are not beneficial in the treatment of severe sepsis/septic shock [15–17].

   • Treatment of septic shock with moderate-dose glucocorticoids for 7 days significantly reduces vasopressor dependency (adrenocorticotropin responders and non-responders) and intensive care unit length of stay [15–17].

   • Glucocorticoids do not increase the risk of superinfections [15–17].

What we think we know

   • Glucocorticoids may reduce mortality in subgroups of patients with septic shock [15–17].

   • Glucocorticoids appear to be of no benefit in community-acquired pneumonia patients who are at a low risk of dying [7].

   • The addition of fludrocortisone does not appear to have additional benefits when treating patients with hydrocortisone [18].

   • Treatment with glucocorticoids may reduce the risk of post-traumatic stress disorder [19].

What we do not know

   • Which patients with severe sepsis/septic shock should be treated with glucocorticoids?

   • Should treatment with glucocorticoids be based on the results of a cosyntropin stimulation test?

   • What is the treatment window? Twenty-four hours?

   • How does one accurately diagnose adrenal insufficiency and inadequate cellular glucocorticoid activity?

   • What is the optimal dosing schedule of glucocorticoids?

   • Which glucocorticoid - methylprednisolone or hydrocortisone - should be used?

   • Do glucocorticoids cause long-term myopathy?

   • Do we need to treat a patient with glucocorticoids if he or she has received etomidate in the previous 24 hours?