The low-dose corticotropin stimulation test in acute traumatic and non-traumatic brain injury: incidence of hypo-responsiveness and relationship to outcome.

Abstract

To investigate adrenal responses to the low-dose corticotropin (ACTH) stimulation test in acute traumatic or non-traumatic brain injury (BI) and to assess its value in predicting outcome. Prospective study. SETTING. Intensive care unit (ICU) in a university hospital. Seventy-five patients with acute BI, with a median age of 45 years were investigated. BI was due to trauma ( n=51), ischemic stroke ( n=17), subarachnoid hemorrhage ( n=4) or intracerebral hemorrhage (n=3). Blood was taken on day 16 (median) after admission to the ICU to determine baseline cortisol and ACTH. Thereafter, a low-dose stimulation test (LDST) was performed: 1 microg of tetracosactrin was injected and 30 min later a second blood specimen was obtained to measure stimulated cortisol. Patients having a stimulated cortisol below 500 nmol/l were defined as non-responders to the LDST. Median baseline and stimulated cortisol were 491 nmol/l and 690 nmol/l, respectively. The median increment in cortisol was 154 nmol/l (range 5-579 nmol/l). Mean ACTH was 46+/-21 pg/ml. Ten (13%) patients were non-responders to the LDST; these had a higher mortality rate compared to patients with adequate cortisol production (70 vs 32%, p=0.034). Logistic regression analysis revealed that APACHE II ( p<0.001), Glasgow Coma Scale (GCS) ( p=0.04) and age ( p=0.02) were independent outcome predictors. In contrast, the increment in cortisol ( p=0.26) did not add to outcome prediction. Adrenal hypo-responsiveness in the setting of acute traumatic or non-traumatic BI is not an independent outcome predictor in the presence of high APACHE II, low GCS and older age.