Artikel
Prospective evaluation of neuroendocrine function following traumatic brain injury and subsequent intensive care treatment
Prospektive Untersuchung der neuroendokrinen Funktion nach Schädel-Hirn-Trauma und intensivmedizinischer Behandlung
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Autoren
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A. Kleindienst
- Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
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G. Brabant
- Christie Hospital, Department of Endocrinology, Manchester, United Kingdom
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M. Buchfelder
- Klinik für Neurochirurgie, Universität Erlangen-Nürnberg
| Veröffentlicht: | 30. Mai 2008 |
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Gliederung
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Objective: Neuroendocrine dysfunction following traumatic brain injury (TBI) has extensively been described. The present study was designed to prospectively assess endocrine function early after TBI and to identify predictors of a late endocrine insufficiency.
Methods: In 71 consecutive patients, TBI was documented by a computed tomography (CT). The Glasgow Coma Score (GCS), duration of analgosedation, and pituitary function (cortisol, GH, IGF-1, TSH, free T4, total T3, LH, FSH, testosterone, estradiol) were routinely examined during the first week. An additional dynamic endocrine testing with an ACTH- and GHRH-Arginine test was performed 24 to 36 months post-injury. The Mann-Whitney rank sum test was used for statistical analysis.
Results: Age ranged from 18 to 87 years and trauma severity was mild to severe (mean GCS 9.6±4.6). There was no association of skull fracture (n=34) or skullbase fracture (n=16), open TBI (n=19), epidural (n=8) or subdural hematoma (n=14), intracerebral (n= 20) or subarachnoid hemorrhage (n=17). In moderate TBI, cortisol levels were highest on day 0 (p<0.05), while in severe TBI cortisol levels were significantly decreased on day 7 (p<0.05) as well as in patients analgo-sedated for more than 24hr on day 3 and 7 (p<0.05). In severe TBI, TSH was decreased on day 3 (p<0.05), while T3 and T4 were low on day 7 (p<0.05). Sedated patients had a thyrotropic insufficiency on day 3 (p<0.001), and low T3 and T4 on day 7 (p<0.01). Similarly, in severe TBI and in sedated patients, hormone levels were suggestive of a gonadotropic insufficiency on day 3 and 7 (p<0.05). However, injury severity was not correlated with GH or IGF-1 levels during the acute phase after injury. Interestingly, moderately injured patients were more likely to develop a late somatotropic insufficiency (p<0.05) and patients with an axonal injury (p=0.091).
Conclusions: We could not identify any CT findings predicting alterations in the neuroendocrine function following TBI. Both, severe TBI and the subsequent intensive care treatment result in central and peripheral hormonal dysfunction early after injury. Moderately injured patients are in danger of developing a late somatotropic deficiency.
