The pituitary–adrenal axis is activated more in non-survivors than in survivors of cardiac arrest, irrespective of therapeutic hypothermia

SummaryObjectiveTo investigate the effect of therapeutic hypothermia in the prognostic value of the pituitary–adrenal axis in comatose patients after cardiac arrest.DesignProspective observational study in intensive care units (ICU) of a university and an affiliated regional hospital.PatientsTwenty-nine consecutive patients, in coma after cardiac arrest, admitted to the ICU and treated by hypothermia.MeasurementsOn ICU-admission (T = 1), at reaching the target of 32–33 °C during therapeutic hypothermia (T = 2), at the end of hypothermia (T = 3) and 48 h later (T = 4), plasma adrenocorticotrophic hormone (ACTH), serum cortisol, albumin and corticosteroid-binding globulin (CBG) were measured. A short 250 μg ACTH test was performed at each time-point, except at T = 1. The free cortisol index (FCI) and free cortisol calculated by Coolens method were also evaluated.ResultsThe ICU mortality was 59%, including withdrawal of life-sustaining treatment in 45% because of negative somatosensory evoked potentials. ACTH and (free) cortisol levels (mean 13.1 pmol/L vs. 6.0 pmol/L and 1250 nmol/L vs. 596 nmol/L, respectively) were higher in non-survivors than in survivors. Levels decreased in time, but the relative difference between outcome groups was maintained until T = 4. The cortisol response to ACTH was lower in non-survivors at T = 3 (P = 0.047) only.ConclusionsIn comatose patients resuscitated from cardiac arrest, the pituitary–adrenal axis is activated particularly in those dying in the ICU, irrespective of therapeutic hypothermia. Hence, activation of the axis may be a marker of fatal cerebral damage. There is no firm evidence for relative adrenal insufficiency associated with death and a transiently blunted cortisol response to ACTH in non-survivors may be attributed to higher baseline values.