Abstract

PurposeReports on long-term variations in pituitary function after traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH) diverge. The aim of the current study was to evaluate the prevalence and changes in pituitary function during the first year after moderate and severe TBI and SAH and to explore the relation between pituitary function and injury variables.MethodsAdults with moderate and severe TBI or SAH were evaluated at 10 days, 3, 6 and 12 months post-injury/illness. Demographic, clinical, radiological, laboratory, including hormonal data were collected.ResultsA total of 91 adults, 56 (15 women/41 men) with TBI and 35 (27 women/8 men) with SAH were included. Perturbations in pituitary function were frequent early after the event but declined during the first year of follow-up. The most frequent deficiency was hypogonadotrope hypogonadism which was seen in approximately 25 % of the patients. Most of the variations were transient and without clinical significance. At 12 months, two patients were on replacement with hydrocortisone, four men on testosterone and one man on replacement with growth hormone. No relations were seen between hormonal levels and injury variables.ConclusionsPerturbations in pituitary function continue to occur during the first year after TBI and SAH, but only a few patients need replacement therapy. Our study could not identify a marker of increased risk of pituitary dysfunction that could guide routine screening. However, data demonstrate the need for systematic follow-up of pituitary function after moderate or severe TBI or SAH.

Highlights

  • Traumatic brain injury and subarachnoid haemorrhage may cause permanent physical, cognitive, behavioural and psychosocial disabilities limiting daily activities [1,2,3,4]

  • Perturbations in pituitary function continue to occur during the first year after traumatic brain injury (TBI) and subarachnoid haemorrhage (SAH), but only a few patients need replacement therapy

  • We explore the relation between pituitary function and injury variables such the GCS score, pupil size or light reaction, peak of S100B (12–36 h), and hospitalisation length on the Neurointensive care unit for both TBI and SAH patients, and Fisher grade, Hunter and Hess grade for SAH patients, and Computed tomography (CT) scan pathology for TBI patients

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Summary

Introduction

Traumatic brain injury and subarachnoid haemorrhage may cause permanent physical, cognitive, behavioural and psychosocial disabilities limiting daily activities [1,2,3,4]. There is accumulating evidence that specialised neurorehabilitation may enhance recovery and long-term outcome after acquired brain injury [9,10,11,12] and that this should start in parallel with the acute care [13] in order to prevent secondary complications and enhance functional improvement. Several medical complications, such as infection, hydrocephalus, respiration problems (tracheostomy), nutrition problems and heterotopic ossification may interfere with the post-acute rehabilitation process [14], while this. Until now, there is no consensus about either the prevalence, type or the clinical impact of pituitary disturbances after TBI and SAH and current recommendations for screening of pituitary function and replacement therapy are debated [24]

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