• M Clodi.
• Klinische Abteilung für Endokrinologie und Stoffwechsel, Universitätsklinik für Innere Medizin III, Währinger Gürtel 18-20, A-1090 Wien. martin.clodi@univie.ac.at
• Wien Med Wochenschr. 2002 Jan 1;152(21-22):555-8.

AbstractAdequate adrenocortical function is essential to survive critical illness. Most critically ill patients display an elevated plasma Cortisol level, reflecting activation of the pituitary-adrenal axis, which is considered to be a homeostatic adaptation. In the setting of critical illness, the failure of an appropriate neuroendocrine response can lead to the picture of vasopressor-dependent refractory hypotension. In randomised trials with patients in septic shock, a more rapid haemodynamic recovery was obtained with physiological doses of hydrocortisone than with placebo. The observed haemodynamic response following hydrocortisone administration supports the concept of relative adrenal insufficiency. Causes of this relative adrenal insufficiency are a dysfunction of the hypothalamic-pituitary-adrenal axis and/or Cortisol resistance. There is increasing evidence that Cortisol physiology and regulation are substantially altered in the course of septic shock. Several controlled studies have shown that stress doses of hydrocortisone given in patients with septic shock reduce the time to shock reversal and decrease mortality. A multicenter large-scale trial (CORTICUS) is on the way investigating the benefit of stress doses of hydrocortisone on the mortality of septic shock. In this review glucocorticoid physiology and regulation during septic shock and the effects of hydrocortison administration in the course of septic shock are being discussed.

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