Pituitary Function in the Acute Phase of Traumatic Brain Injury and Subarachnoid Hemorrhage — Oak Academic Publishing
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Pituitary Function in the Acute Phase of Traumatic Brain Injury and Subarachnoid Hemorrhage
Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden
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Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden
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Department of Clinical Neuroscience, Section for Neurosurgery, Karolinska Institutet, Stockholm, Sweden
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Department of Molecular Medicine and Surgery, Karolinska Institutet and Department of Endocrinology, Metabolism and Diabetology, Karolinska University Hospital, Stockholm, Sweden
1 Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden
2 Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden
3 Department of Clinical Neuroscience, Section for Neurosurgery, Karolinska Institutet, Stockholm, Sweden
4 Department of Molecular Medicine and Surgery, Karolinska Institutet and Department of Endocrinology, Metabolism and Diabetology, Karolinska University Hospital, Stockholm, Sweden
Background: Pituitary insufficiencies after traumatic brain injury (TBI) and subarachnoid haem-orrhage (SAH) have been reported with very varying frequencies. The aim of this study was to describe the pituitary function in the acute phase after TBI and SAH in a cohort of adults and relate the results to injury variables. Methods: Adults admitted to the neurointensive care unit in our hospital after moderate and severe TBI or SAH were included prospectively. Demographic, clinical, laboratory, including ACTH stimulation test, and radiological data were collected. Results: A total of 130 adults, 84 (19 women/65 men) with TBI and 46 (38 women/8 men) with SAH were included. Nine patients with TBI and six patients with SAH responded insufficiently to ACTH stimulation; 14 patients with TBI and 9 patients with SAH had low fT4 and low-normal TSH levels. No relations were seen between hormonal levels and injury variables. Conclusions: Pituitary deficiencies occur after TBI and SAH, and a continuous endocrine evaluation of these patients is important. Our study could not define a marker for increased risk for pituitary deficiency. The long-term clinical outcome of the pathological hormone levels in the early phase after TBI and SAH is not known in detail and further studies to elucidate this are needed.
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