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  1. Severe sepsis and septic shock are major public health problems globally and are associated with substantial morbidity and mortality.1 No specific therapy exists apart from antibiotics and supportive care with intravenous (IV) fluids and vasopressors.(1) Recent large-scale clinical trials have failed to demonstrate improved outcomes with various treatment strategies for septic shock despite promising preliminary studies.(2-5) One of the first treatments studied in patients with septic shock was corticosteroids, based on the recognition of the role of excessive inflammation in the pathophysiology of multisystem organ dysfunction.(1,6) Studies published before 1995 demonstrated increased rates of adverse outcomes and complications with short courses of high-dose glucocorticoids in septic shock, so this practice was abandoned.(6-8) Critical illness is characterized by complex abnormalities in hypothalamic-pituitary-adrenal axis (HPA) function, including reduced total serum cortisol levels (often with increased free cortisol levels due to reduced protein binding), reduced cortisol secretion in response to adrenocorticotropic hormone (ACTH), reduced metabolism of cortisol, and impaired tissue response to cortisol.(6,9-12) More than 50% of patients with septic shock have an impaired cortisol response to exogenous ACTH consistent with relative adrenal insufficiency, which is associated with adverse outcomes.(9,11,13-15) The definition and diagnosis of relative adrenal insufficiency in critically ill patients and its treatment are surrounded by controversy.