Acute secondary adrenal insufficiency after traumatic brain injury: A prospective study*

Abstract

Approximately 50% of patients with moderate or severe TBI have at least transient AI. Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic suppressive agents are associated with AI. Because lower cortisol levels were associated with lower blood pressure and higher vasopressor use, consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol. A randomized trial of stress-dose hydrocortisone in TBI patients with AI is underway.

Etomidate increases susceptibility to pneumonia in trauma patients

“…Second, we used a more liberal CIRCI definition than the consensus statement, which was not available at the beginning of the study in 2006 (basal cortisolemia \10 vs. 15 lg/dL) [25]. Previous studies in trauma patients used a basal cortisolemia threshold of C15 lg/dL [12][13][14], and we chose a definition proposed by Annane et al [43]. Of the 149 patients, 23 (15 %) would not have had CIRCI if the current definition of the consensus statement had been used [25].…”

“…The duration of MV was 11 (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19) days in the nonetomidate group and 13 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22) days in the etomidate group (p = 0.275), and the ICU length of stay was 15 (9-28) days in the non-etomidate group and 16 (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27) days in the etomidate group (p = 0.422). Four (7.4 %) patients in the non-etomidate group and six (6 %) patients in the etomidate group died (p = 1).…”

“…It has been demonstrated that up to 70 % of trauma patients developed a critical illness-related corticosteroid insufficiency (CIRCI) [12][13][14] and that this could increase the risk of hospital-acquired pneumonia (HAP) [15,16]. We have recently demonstrated that lowdose hydrocortisone decreases the rate of HAP in multiple trauma patients with CIRCI [17].…”

American Association of Clinical Endocrinologists and American College of Endocrinology Disease State Clinical Review: A Neuroendocrine Approach to Patients With Traumatic Brain Injury

“…Central hypoadrenalism and diabetes insipidus (DI) may manifest in the acute phase after TBI, particularly in moderate and severe TBI, and should be considered early in the neuroendocrine evaluation of these patients (22,24). Up to 50% of hospitalized moderate or severe TBI patients may develop central hypoadrenalism, which can be associated with severe anemia, hypotension or hypoxia, as well as hyponatremia (24,25).…”

The Case of Hypopituitarism in Traumatic Brain Injury

“…A number of studies have assessed the acute neuroendocrine changes following TBI, in order to investigate their correlation to trauma severity, metabolic derangement and variables that may predict outcome (Cernak et al, 1999;Cohan et al, 2005;Della et al, 1998;Feibel et al, 1983;Hackl et al, 1991). The clinical implications of these findings remain unclear.…”