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Acute Glucocorticoid Deficiency and Diabetes Insipidus Are Common After Acute Traumatic Brain Injury and Predict Mortality

JCEM, The Journal of Clinical Endocrinology and Metabolism

M. J. Hannon, R. K. Crowley, L. A. Behan, E. P. O'Sullivan, M. M. C. O'Brien, M. Sherlock, D. Rawluk, R. O'Dwyer, W. Tormey and C. J. Thompson

Author Affiliations

Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Neurosurgery (D.R.), Critical Care (R.O'D.), and Chemical Pathology (W.T.), Beaumont Hospital/Royal College of Surgeons in Ireland Medical School, Dublin 9, Ireland


Context: Published data demonstrates that hypopituitarism is common after traumatic brain injury (TBI). Hormone deficiencies are transient in many, but the natural history of the acute changes after TBI has not been documented. In addition, it is not clear whether there are any early parameters that accurately predict the development of permanent hypopituitarism.

Objectives: There were 3 main objectives of this study: 1) to describe the natural history of plasma cortisol (PC) changes and sodium balance after TBI; 2) to identify whether acute hypocortisolemia or cranial diabetes insipidus (CDI) predict mortality; and 3) to identify whether the acute pituitary dysfunction predicts the development of chronic anterior hypopituitarism.

Design: Each TBI patient underwent sequential measurement of PC, plasma sodium, urine osmolality, and fluid balance after TBI. All other anterior pituitary hormones were measured on day 10 after TBI. The results from 15 surgical comparisons defined a PC less than 300 nmol/L as inappropriately low for an acutely ill patient. CDI was diagnosed according to standard criteria. Surviving TBI patients underwent dynamic anterior pituitary testing at least 6 months after TBI.

Setting: The patients were recruited from the Irish National Neurosurgery Centre.

Patients: One hundred sequential TBI patients were recruited. Fifteen patients admitted to Intensive Therapy Unit (ITU) after major surgery were recruited as comparison patients.

Main Outcome Measures: PC in TBI patients was compared with that of comparison patients. The mortality rate was compared between TBI patients with and without acute hypocortisolemia. Results of follow-up dynamic pituitary testing were compared between those with and without acute hypocortisolemia.

Results: Most of the TBI patients (78%) developed inappropriately low PC after TBI. Low PC and CDI were predictive of mortality. Thirty-nine percent of the patients who had follow-up testing had at least 1 pituitary hormone deficit, all of whom had had previous acute hypocortisolemia or CDI.

Conclusions: Acute hypocortisolemia and CDI are predictive of mortality and long-term pituitary deficits in TBI.


CBG: cortisol binding globulin
CDI: cranial diabetes insipidus
CV: coefficient of variation
FT4: free T4
GCS: Glasgow Coma Scale
LOS: length of stay
PC: plasma cortisol
SIADH: syndrome of inappropriate antidiuretic hormone
TBI: traumatic brain injury.

Received March 3, 2013.
Accepted May 10, 2013.

Copyright © 2013 by The Endocrine Society



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