title: Adrenal axis function does not appear to be associated with hemodynamic improvement in septic shock patients systematically receiving glucocorticoid therapy.
abstract: OBJECTIVE
  There is mounting evidence showing the value of low-dose corticosteroids in patients with septic shock requiring vasopressor therapy. It remains unclear whether adrenal function tests should be carried out systematically to guide the decision on glucocorticoid therapy.
  
  
  METHODS
  The retrospective study was conducted in 52 patients in three university hospital ICUs. We included consecutive patients with catecholamine-dependent septic shock who had not received ketoconazole, glucocorticoids, or etomidate in the 24 h before the ACTH test, and who had survived to day 3 after the shock onset. All patients had a 250-microg ACTH test before systematic glucocorticoid therapy was started. Various definitions of relative adrenal insufficiency were used (based on cortisol basal level and/or change in cortisol level after ACTH stimulation). We defined hemodynamic improvement as a 50% reduction in the vasoactive agent dose in the 3 days following the initiation of glucocorticoid treatment. The relationship between the hemodynamic improvement and the results of the adrenal function tests was analyzed.
  
  
  RESULTS
  Hemodynamic improvement occurred in 29 patients (55.8%). Baseline characteristics, sites of infection, types of micro-organisms and antibiotic management did not differ between patients with and those without hemodynamic improvement. Relative adrenal insufficiency whatever the definition was not associated with hemodynamic improvement.
  
  
  CONCLUSIONS
  In catecholamine-dependent septic shock patients managed with systematic glucocorticoid therapy the results of ACTH stimulation do not predict hemodynamic improvement.
authors.affiliation: Polyvalent Intensive Care Unit, Hospital Bellevue, 42055 Saint Etienne Cedex 2, France.
authors.forename: Jerome
authors.initials: J
authors.lastname: Morel
authors.forename: Christophe
authors.initials: C
authors.lastname: Venet
authors.forename: Yannis
authors.initials: Y
authors.lastname: Donati
authors.forename: David
authors.initials: D
authors.lastname: Charier
authors.forename: Jerome
authors.initials: J
authors.lastname: Liotier
authors.forename: Delphine
authors.initials: D
authors.lastname: Frere-Meunier
authors.forename: Stephane
authors.initials: S
authors.lastname: Guyomarc'h
authors.forename: Eric
authors.initials: E
authors.lastname: Diconne
authors.forename: Jean Claude
authors.initials: JC
authors.lastname: Bertrand
authors.forename: Bertrand
authors.initials: B
authors.lastname: Souweine
authors.forename: Laurent
authors.initials: L
authors.lastname: Papazian
authors.forename: Fabrice
authors.initials: F
authors.lastname: Zeni
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects / Q000503:physiopathology*; D000368:Aged; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012772:Shock, Septic / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
chemical_list: D005938:Glucocorticoids; D014662:Vasoconstrictor Agents; D006854:Hydrocortisone