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      Endocrine Consequences of Adult Traumatic Brain Injury

      ,

      Hormone Research in Paediatrics

      S. Karger AG

      Traumatic brain injury, Hypopituitarism, Pituitary

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          Abstract

          Background: Traumatic brain injury (TBI) is the most common cause of death and disability in young adults living in industrialised countries. Over the last few years, there has been an increasing awareness that hypopituitarism can complicate TBI in a significant proportion of survivors: at least 25% of TBI survivors develop one or more pituitary hormone deficiencies. This remarkably high frequency has changed the traditional concept that hypopituitarism was a rare complication of TBI and suggests that most cases of posttraumatic hypopituitarism remain undiagnosed and untreated in clinical practice. It is therefore reasonable to infer that posttraumatic hypopituitarism may make an important contribution to the high rates of physical and neuropsychiatric morbidity in patients with head injury. Conclusions: There is clearly a need for identification as well as appropriate and timely management of hormone deficiencies in TBI patients to reduce morbidity, aid recovery and rehabilitation and avoid the long-term complications of pituitary failure.

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          Most cited references 11

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          Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study.

          To determine the prevalence, time course, clinical characteristics, and effect of adrenal insufficiency (AI) after traumatic brain injury (TBI). Prospective intensive care unit-based cohort study. Three level 1 trauma centers. A total of 80 patients with moderate or severe TBI (Glasgow Coma Scale score, 3-13) and 41 trauma patients without TBI (Injury Severity Score, >15) enrolled between June 2002 and November 2003. Serum cortisol and adrenocorticotropic hormone levels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols of < or =15 microg/dL (25th percentile for extracranial trauma patients) or one cortisol of < 5 microg/dL. Principal outcome measures included: injury characteristics, hemodynamic data, usage of vasopressors, metabolic suppressive agents (high-dose pentobarbital and propofol), etomidate, and AI status. AI occurred in 42 TBI patients (53%). Adrenocorticotropic hormone levels were lower at the time of AI (median, 18.9 vs. 36.1 pg/mL; p = .0001). Compared with patients without AI, those with AI were younger (p = .01), had higher injury severity (p = .02), had a higher frequency of early ischemic insults (hypotension, hypoxia, severe anemia) (p = .02), and were more likely to have received etomidate (p = .049). Over the acute postinjury period, patients with AI had lower trough mean arterial pressure (p = .001) and greater vasopressor use (p = .047). Mean arterial pressure was lower in the 8 hrs preceding a low (< or =15 microg/dL) cortisol level (p = .003). There was an inverse relationship between cortisol levels and vasopressor use (p = .0005) and between cortisol levels within 24 hrs of injury and etomidate use (p = .002). Use of high-dose propofol and pentobarbital was strongly associated with lower cortisol levels (p < .0001). Approximately 50% of patients with moderate or severe TBI have at least transient AI. Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic suppressive agents are associated with AI. Because lower cortisol levels were associated with lower blood pressure and higher vasopressor use, consideration should be given to monitoring cortisol levels in intubated TBI patients, particularly those receiving high-dose pentobarbital or propofol. A randomized trial of stress-dose hydrocortisone in TBI patients with AI is underway.
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            Prevalence of Neuroendocrine Dysfunction in Patients Recovering from Traumatic Brain Injury

             S. Lieberman (2001)
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              Anterior pituitary dysfunction following traumatic brain injury (TBI).

              Traumatic brain injury (TBI) is the commonest cause of death and disability in young adults living in industrialized countries. Several recent studies have convincingly shown that anterior hypopituitarism is a common complication of head trauma with a prevalence of at least 25% among long-term survivors. This is a much higher frequency than previously thought and suggests that most cases of post-traumatic hypopituitarism (PTHP) remain undiagnosed and untreated. These findings raise important questions about the potential contribution of PTHP to the high physical and neuropsychiatric morbidity seen in this group of patients. In this review, we examine the published reports on the neuroendocrine abnormalities in TBI patients and highlight new data that give novel insights into the natural history of this disorder. We discuss the potential contribution of PTHP to recovery and rehabilitation after injury and the need for the identification and the appropriate and timely management of hormone deficiencies to optimize patient recovery from head trauma, improve quality of life and avoid the long-term adverse consequences of untreated hypopituitarism.
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                Author and article information

                Journal
                HRE
                Horm Res Paediatr
                10.1159/issn.1663-2818
                Hormone Research in Paediatrics
                S. Karger AG
                978-3-8055-8475-3
                978-3-8055-8476-0
                1663-2818
                1663-2826
                2007
                December 2007
                10 December 2007
                : 68
                : Suppl 5
                : 18-21
                Affiliations
                Division of Endocrinology, Beaumont Hospital and the RCSI Medical School, Dublin, Ireland
                Article
                110466 Horm Res 2007;68:18–21
                10.1159/000110466
                18174698
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 1, References: 30, Pages: 4
                Categories
                Combined Plenary Session

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