Objective: To investigate, in patients with severe septic shock, the a
drenocortical function assessed by daily plasma cortisol determination
s during the first 72 h and by the short synthetic ACTH stimulation te
st performed within 24 h of the onset of shock. Design: Prospective cl
inical investigation. Setting: Medical intensive care unit in a univer
sity teaching hospital. Patients: 40 consecutive patients with documen
ted septic shock requiring at least hemodynamic resuscitation and resp
iratory support. Interventions: There were no interventions. Measureme
nts and results: Basal cortisol concentrations were increased with a m
ean value of 36.8 mug/dl (range 7.9 - 113). Of the overall cortisol de
terminations 92% were above 15 mug/dl. No statistically significant di
fferences in basal cortisol concentrations were found when survival, t
ype of infection, and positive blood cultures were considered. Patient
s with hepatic disease had significantly higher cortisol (50.1(+/- 6.2
) mug/dl versus 35.9(+/- 3.3) mug/dl, p = 0.035) levels compared to ot
her patients. No correlations were found between basal plasma cortisol
concentrations and factors such as SAPS, OSF, hemodynamic measurement
s, duration of shock, and amount of vasopressor and/or inotropic agent
s. Cortisol concentrations and significant but weak correlation with A
CTH levels in survivors (r = 0.4; p = 0.03; n = 28) but not in non-sur
vivors (r = 0.03; p = 0.85; n = 52). Cortisol levels in non-survivors
increased significantly from enrollment time to the 72nd hour of the s
urvey (day 1: 38.9(+/-3.8)mug/dl versus day 3: 66.7(+/-17.1) mug/dl; p
= 0.046) and were significantly higher than those recorded in survivo
rs. Responses to the short ACTH stimulation test were not significantl
y different between survivors and non-survivors. According to the diff
erent criteria used to interpret the response to the ACTH stimulation
test, incidence of adrenocortical insufficiency was highly variable ra
nging from 6.25 - 75% in patients with septic shock. Only one patient
had absolute adrenocortical insufficiency (basal cortisol level below
10 mug/dl; response to the ACTH stimulation test below 18 mug/dl). Con
clusion: Our data suggest that in a selected population of patients wi
th severe septic shock single plasma cortisol determination has no pre
dictive value. The short ACTH stimulation test performed within the fi
rst 24 h of onset shock can neither predict outcome nor estimate impai
rment in adrenocortical function in patients with high basal cortisol
level. Adrenal insufficiency is rare in septic shock and should be sus
pected when cortisol level is below 15 mug/dl and then confirmed by a
peak cortisol level lower than 18 mug/dl during the short ACTH stimula
tion test.