ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2013) 32 P26 | DOI: 10.1530/endoabs.32.P26

Longitudinal assessment of adrenocortical responses to low-dose ACTH in critically ill septic patients

Dimitra A Vassiliadi1, Ioanna Dimopoulou3, Maria Zervou2, Marinella Tzanela1, Hercules Tsagaris3, Callirrhoe Augustatou2, Evangelia Douka2, Olga Livaditi2, Stylianos Orfanos3, Anastasia Kotanidou2, Apostolos Armaganidis3 & Stylianos Tsagarakis1

1Department of Endocrinology, Diabetes and Metabolism, Evangelismos Hospital, Athens, Greece; 2Department of Critical Care Medicine, Medical School, Evangelismos Hospital, National and Kapodistrian University of Athens, Athens, Greece; 32nd Department of Critical Care Medicine, ‘Attiko’ University General Hospital, University of Athens, Greece, Athens, Greece.

Introduction: The hypothalamo-pituitary adrenal axis has been extensively investigated in sepsis. Most studies concentrated in the acute phase and in most the high-dose ACTH stimulation test has been applied. Studies extending in the post-acute phase by using the more physiological low-dose ACTH stimulation are scarce.

We aimed to investigate the time course of cortisol levels before and after stimulation with 1μg Synacthen in mechanically ventilated septic patients, over a 30-day period.

Methods/design: We studied 51 patients admitted to ICU with sepsis (n=16), severe sepsis (N=19), or septic shock (N=16). Total serum cortisol was measured before and 30-min after the i.v. administration of 1 μg Synacthen upon admission and every 3–4 days thereafter until administration of glucocorticoids (n=6), death (N=15), recovery (n=24) or completion of 30 days (n=6). Mixed-effect models were used to analyze the time progression of cortisol levels. Patients who received glucocorticoids were excluded from any analysis referring to survival.

Results: Administration of 1 μg Synacthen significantly increased cortisol levels at all time points (P<0.001). In the whole cohort, there was no significant variation in baseline and stimulated cortisol levels during the entire observation period. Throughout the study period patients admitted with septic shock had significantly higher baseline and stimulated cortisol levels compared to those admitted with sepsis or severe sepsis (P=0.01) and non-survivors had higher baseline cortisol levels compared to survivors (P<0.001). On admission, stimulated cortisol levels were similar between survivors and non-survivors but the difference between stimulated and baseline cortisol (ΔF) was lower in non-survivors. Subsequently, non-survivors had higher stimulated cortisol levels compared to survivors (P=0.001) with no difference in ΔF.

Conclusion: Baseline and stimulated cortisol levels remain relatively unchanged during the process of sepsis. Patients admitted with septic shock had higher baseline and stimulated cortisol levels, reflecting the severity of sepsis. Higher cortisol levels were associated with increased mortality.