We have located links that may give you full text access.
JOURNAL ARTICLE
REVIEW
Adrenal insufficiency following traumatic brain injury in adults.
Current Opinion in Critical Care 2008 April
PURPOSE OF REVIEW: Hypoadrenalism occurs in approximately 25% of patients soon after traumatic brain injury. Neurosurgeons or critical care physicians should be prepared to diagnose and treat this and other related hormonal deficiencies.
RECENT FINDINGS: The severity of traumatic brain injury, location of basilar skull fractures and edema or hemorrhage within the hypothalamic-pituitary axis appear correlated with secondary adrenal failure. Primary hypoadrenalism also may occur due to injury-related systemic inflammation. Hypotension requiring vasoactive drug support, hyponatremia and hypoglycemia may be corresponding clinical signs. Evaluation of either primary or secondary hypoadrenalism should include measurement of basal and post-adrenocorticotropin stimulation cortisol blood concentrations. If the basal cortisol is under 15 microg/dl or increases by over 9 microg/dl after stimulation treatment should be considered. Intravenous hydrocortisone at 50-100 mg every 8 h or by continuous infusion is usually sufficient but may be supplemented with a mineralocorticoid if hyponatremia persists. All patients sustaining severe traumatic brain injury should be tested for endocrine failure (adrenal, thyroid and growth hormone) 3 months after injury.
SUMMARY: Adrenal gland failure or the inability to produce adrenocorticotropin and other pituitary hormones may occur early after traumatic brain injury. Acute treatment of either cause of hypoadrenalism may correct associated hypotension, hypoglycemia, or hyponatremia.
RECENT FINDINGS: The severity of traumatic brain injury, location of basilar skull fractures and edema or hemorrhage within the hypothalamic-pituitary axis appear correlated with secondary adrenal failure. Primary hypoadrenalism also may occur due to injury-related systemic inflammation. Hypotension requiring vasoactive drug support, hyponatremia and hypoglycemia may be corresponding clinical signs. Evaluation of either primary or secondary hypoadrenalism should include measurement of basal and post-adrenocorticotropin stimulation cortisol blood concentrations. If the basal cortisol is under 15 microg/dl or increases by over 9 microg/dl after stimulation treatment should be considered. Intravenous hydrocortisone at 50-100 mg every 8 h or by continuous infusion is usually sufficient but may be supplemented with a mineralocorticoid if hyponatremia persists. All patients sustaining severe traumatic brain injury should be tested for endocrine failure (adrenal, thyroid and growth hormone) 3 months after injury.
SUMMARY: Adrenal gland failure or the inability to produce adrenocorticotropin and other pituitary hormones may occur early after traumatic brain injury. Acute treatment of either cause of hypoadrenalism may correct associated hypotension, hypoglycemia, or hyponatremia.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app