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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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          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.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                December 2007
                10 December 2007
                : 68
                : Suppl 5
                : 18-21
                Division of Endocrinology, Beaumont Hospital and the RCSI Medical School, Dublin, Ireland
                110466 Horm Res 2007;68:18–21
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 1, References: 30, Pages: 4
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