This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Pituitary function is rarely considered in the care of patients with traumatic brain injury. Yet, TBI poses significant risk to pituitary function given the gland's location at the base of the skull, its delicate connections to the brain and vulnerable vascular supply. Autopsy studies of fatal head injury victims confirm that up to one third of patients sustain acute pituitary necrosis. We and other investigators have documented chronic pituitary failure in long term follow up studies of TBI subjects. The purpose of this study is to define acute post-traumatic changes in the hypothalamic-pituitary adrenocortical axis given that this hormonal axis is essential for survival, particularly in times of critical illness such as head injury. The major hypotheses to be tested in this study are: i) a significant proportion of TBI victims suffer from unrecognized acute secondary adrenal insufficiency, ii) that ASAI results primarily from hypothalamic-pituitary hypoperfusion, iii) that the consequences of ASAI are systemic hypotension, increased vasopressor requirements to maintain the blood pressure and increased levels of potentially harmful substances (cytokines 0 and iv) that treatment of individuals with ASAI with acute stress doses of glucocorticoids will improve blood pressure control, decrease serum and CSF cytokine levels, shorten intensive care unit stay and improve neurological outcome.
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