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CLINICAL STUDY |
1 Academic Department of Endocrinology, 2 Department of Neurosurgery and 3 Department of Clinical Chemistry, Beaumont Hospital, Dublin, Ireland
(Correspondence should be addressed to C J Thompson; Email: christhompson{at}beaumont.ie)
Background and objectives: Posterior pituitary function remains poorly investigated after traumatic brain injury (TBI). We report the results of a study designed to prospectively define the natural history of post-traumatic diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone secretion (SIADH) using standard reliable methodology.
Design and methods: 50 consecutive patients with severe or moderate TBI (initial Glasgow Coma Scale (GCS) score 3/15–13/15) were prospectively studied on three occasions: at the acute phase and at 6 months and at 12 months following TBI. In the acute phase, DI was diagnosed either by the presence of hypernatraemia in association with hypotonic polyuria or by the water-deprivation test (WDT) and, at 6 and 12 months by the WDT in all patients. Normative data on response to the WDT were obtained from healthy matched volunteers. Functional outcome was assessed using the Glasgow Outcome Scale (GOS).
Results: 13 patients (26%) had DI in the acute post-TBI phase, of whom nine patients recovered by 6 months and one additional patient recovered by 12 months. Of the remaining three patients with permanent DI, two had partial vasopressin deficiency. Acute-phase peak plasma osmolality correlated negatively with the initial GCS scores (r = –0.39, P = 0.005) and with the GOS scores (r = –0.45, P = 0.001). Seven patients had SIADH in the acute phase of TBI but none did at 6 or 12 months. No new cases of DI or SIADH were noted after the acute phase.
Conclusion: This prospective study shows that posterior pituitary dysfunction is common following TBI. Most cases recover completely but there is an appreciable frequency of long-term DI which can be subtle and should be recognized and managed appropriately.
This article has been cited by other articles:
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  L A Behan, J Phillips, C J Thompson, and A Agha Neuroendocrine disorders after traumatic brain injury J. Neurol. Neurosurg. Psychiatry, July 1, 2008; 79(7): 753 - 759. [Abstract] [Full Text] [PDF]
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 C. L Acerini Head-injury-induced pituitary dysfunction. An old curiosity rediscovered Arch. Dis. Child., May 1, 2008; 93(5): 364 - 365. [Full Text] [PDF]
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 H. J. Schneider, I. Kreitschmann-Andermahr, E. Ghigo, G. K. Stalla, and A. Agha Hypothalamopituitary Dysfunction Following Traumatic Brain Injury and Aneurysmal Subarachnoid Hemorrhage: A Systematic Review JAMA, September 26, 2007; 298(12): 1429 - 1438. [Abstract] [Full Text] [PDF]
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 A. Helmy, M. Vizcaychipi, and A. K. Gupta Traumatic brain injury: intensive care management Br. J. Anaesth., July 1, 2007; 99(1): 32 - 42. [Abstract] [Full Text] [PDF]
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 C. L Acerini, R. C Tasker, S. Bellone, G. Bona, C. J Thompson, and M. O Savage Hypopituitarism in childhood and adolescence following traumatic brain injury: the case for prospective endocrine investigation. Eur. J. Endocrinol., November 1, 2006; 155(5): 663 - 669. [Abstract] [Full Text] [PDF]
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N Karavitaki, J Wass, J D Henderson Slater, and D Wade A case of post-traumatic isolated ACTH deficiency with spontaneous recovery 9 months after the event J. Neurol. Neurosurg. Psychiatry, February 1, 2006; 77(2): 276 - 277. [Full Text] [PDF]
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