Adrenocortical function during prolonged critical illness and beyond: a prospective observational study.

Area of Science:

• Endocrinology
• Critical Care Medicine

Background:

• Prolonged critical illness can cause alterations in the hypothalamus-pituitary-adrenal (HPA) axis.
• The recovery patterns and clinical significance of these HPA axis changes remain unclear.

Purpose of the Study:

• To investigate the recovery of HPA axis function in patients with prolonged critical illness.
• To determine the relationship between adrenocortical function, sepsis/septic shock, glucocorticoid treatment needs, and survival.

Main Methods:

• Included 392 ICU patients on day 7 and 20 healthy controls.
• Collected daily blood and urine samples; performed weekly cosyntropin tests.
• Repeated tests one week after ICU discharge.

Main Results:

• In patients not receiving glucocorticoids until day 28, plasma ACTH was low/normal, while free cortisol was high due to reduced binding proteins and suppressed breakdown.
• Beyond day 28, cortisol levels normalized. One week post-ICU discharge, ACTH and cortisol rose to supra-normal levels.
• Low cortisol binding proteins invalidated cosyntropin tests in long-stayers, despite normal free cortisol responses.

Conclusions:

• Reduced cortisol binding proteins and suppressed breakdown, not HPA axis suppression, explain high cortisol in prolonged critical illness up to day 28.
• A uniform rise in ACTH and cortisol post-ICU discharge suggests recovery from central adrenocortical suppression.
• Low cortisol binding invalidates the cosyntropin stimulation test in this context.