Acute Hypothalamic-pituitary-adrenal response in traumatic brain injury with and without extracerebral trauma.
OBJECTIVE
Endocrine disturbances are common after traumatic brain injury (TBI). Hypothalamic-pituitary-adrenal (HPA) axis response in TBI patients may be related with hemodynamic status. However, its relationship with outcome is unclear. Our objective was to evaluate HPA axis response in the acute phase after TBI in patients with or without extracerebral trauma (ECT), and to investigate the impact of systemic injury and the mechanisms underlying HPA response.


METHODS
We prospectively studied 165 patients with moderate to severe TBI. Between 24 and 48 h after TBI, blood samples were taken for plasma adrenocorticotrophin hormone (ACTH) and baseline cortisol measurements. Afterwards, a short corticotrophin hormone test (250 mug Synacthen) was performed and samples were obtained at 30 and 60 min. We compared HPA response in TBI patients presenting with and without ECT and investigate potential mechanisms underlying this response.


RESULTS
One hundred and eight patients presented with isolated TBI, whereas 57 patients presented associated ECT. Both groups were comparable. Overall, 23.6% of patients fulfilled adrenal insufficiency (AI) criteria. Patients with plasma ACTH <9 pg/ml and patients presenting with hemorrhagic shock were more likely to present adrenal impairment. Variables associated with mortality were Injury Severity Score, Glasgow Coma Scale, Traumatic Coma Data Bank classification different than type II, need of second level measures to control intracranial pressure and plasma ACTH >9 pg/ml.


CONCLUSIONS
Patients with TBI presenting with or without associated ECT present similar acute HPA response. AI is present in 23.6% of patients. Risk is increased in patients with low plasma ACTH levels and in patients with hemorrhagic shock. Both primary and secondary mechanisms of HPA failure were found. However, AI did not affect outcome.
Servicio de Medicina Intensiva, Hospital Universitario Son Dureta, Andrea Doria n 55. 07014, Palma de Mallorca, Illes Balears, Spain. jallompart@hsd.es
Juan A
JA
Llompart-Pou
Joan M
JM
Raurich
Jon
J
Pérez-Bárcena
Antonia
A
Barceló
Jordi
J
Ibáñez
José I
JI
Ayestarán
D018806:APACHE; D000208:Acute Disease; D000309:Adrenal Insufficiency / Q000453:epidemiology / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001930:Brain Injuries / Q000453:epidemiology / Q000503:physiopathology*; D003422:Critical Care / Q000706:statistics & numerical data; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000453:epidemiology / Q000503:physiopathology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011446:Prospective Studies; D012307:Risk Factors; D012771:Shock, Hemorrhagic / Q000453:epidemiology / Q000503:physiopathology; D015599:Trauma Severity Indices; D055815:Young Adult
D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone