Endocrine dysfunction following traumatic brain injury in acute stage

Abstract

Aim Only few studies of hormonal dysfunction in acute setting after traumatic brain injury (TBI) are available in literature with variable results. The aim of the present study was to determine the incidence of anterior pituitary hormone deficiencies, and correlate with in hospital mortality. Methods This study was carried out on 30 patients with moderate to severe TBI presenting within 24 h of injury. Chemiluminiscence immunoassay using an automated chemiluminiscence analyser was used to determine the basal hormone levels. Thyroid stimulating hormone (TSH), prolactin (PRL), cortisol, growth hormone (GH), and testosterone in males or luteinizing hormone (LH) and follicle stimulating hormone (FSH) in females were measured. Results Out of the 30 cases, 12 cases underwent surgery for various reasons. Six patients expired, and all of them had a poor GCS at presentation (mean 4.8 ? 0.9). In the acute setting high cortisol level showed a trend towards significance (p = 0.097) in terms of mortality. Other hormonal levels were also found to be abnormal, but no conclusion could be drawn due to small number. Conclusion Anterior pituitary hormone imbalance is common after TBI in acute setting. Elevated cortisol is associated with increased mortality.

Cortisol evaluation during the acute phase of traumatic brain injury—A prospective study

“…In the present study, the prevalence for the lowest cortisol cut‐off level of 83 nmol/L was 2.9%, almost identical with the prevalence reported in other studies …”

“…An association between acute post‐traumatic AI and mortality could not be shown in our study, in keeping with the work of Della Corte et al and Olivecrona et al and in contrast to Hannon et al . Nor could we confirm the work of Kakatti et al who showed a correlation between elevated cortisol levels of >23 μg/dL (634 nmol/L) and increased mortality . Nevertheless, the higher mortality seen in those of our patients with acute cortisol <276 nmol/L has influenced our recommendations for clinical care as shown below.…”

“…Serum cortisol is typically increased during the acute phase of TBI. Levels of >550 nmol/L (20 μg/dL) are usual and have been linked to increased mortality . Increased secretion due to activation of the corticotrophin axis, mediated by hypothalamic CRF secretion in response to stress, is one explanation for this finding.…”

“…This should be followed by hydrocortisone cover in those patients with cortisol <276 nmol/L given that mortality was higher in such patients. We also advise cortisol cover in patients with cortisol <414 nmol/L in whom AI risk factors persist given the Cohan recommendations and recognising that cortisol values of <500 nmol/L in stressed patients with TBI are relatively low . The rationale for choosing the <414 nmol/L in patients with no AI risk factors, a serum cortisol should be taken during the first week.…”

Comparison of Midazolam and Propofol Infusion to Suppress Stress Response in Patients With Severe Traumatic Brain Injury: A Prospective, Randomized Controlled Trial

“…Studies have shown that increased sympathetic responses found in the young male population during the early phase of TBI which associated with adverse outcomes. 5 8) In our study, we tried to assess the effect of sedation (propofol versus midazolam) on stress response by measuring serum cortisol as a biomarker for stress response. However, we found a statistically significant reduction in mean cortisol levels in both groups after 48 hours of infusion, but the difference among groups was statistically insignificant.…”