ADRENOCORTICAL FUNCTION DURING SEPTIC SHOCK

Citation
G. Bouachour et al., ADRENOCORTICAL FUNCTION DURING SEPTIC SHOCK, Intensive care medicine, 21(1), 1995, pp. 57-62
Citations number
35
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
03424642
Volume
21
Issue
1
Year of publication
1995
Pages
57 - 62
Database
ISI
SICI code
0342-4642(1995)21:1<57:AFDSS>2.0.ZU;2-Q
Abstract
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.