Summary

  1. There is level 5 evidence that individuals who sustain a severe ABI are more likely to develop SIADH than those with mild or moderate ABI.
     
  2. There is level 5 evidence that restricting fluid intake may assist in the resolution of SIADH symptoms post ABI.
     
  3. There is level 4 evidence that thyroid releasing hormone may be effective in treating post ABI hyponatremia by reducing circulating antidiuretic hormone.
     
  4. There is level 4 evidence that sodium supplementation therapy and hydrocortisone may be effective in treating post ABI hyponatremia.
     
  5. There is level 4 evidence that extensive fractures at the base of the skull may serve as a risk factor for the development of diabetes insipidus post ABI
     
  6. There is level 5 evidence that severe injury, brain edema, and/or intraventricular hemorrhage may serve as risk factors for the development of diabetes insipidus post ABI.
     
  7. There is level 5 evidence that anterior pituitary dysfunction may present within 24 hours of injury and persist up to 12 months post ABI.
     
  8. There is level 5 evidence that anterior pituitary dysfunction post ABI can occur in one or more axes in an unpredictable manner.
     
  9. There is level 5 evidence that the development of anterior pituitary dysfunction may produce unfavourable outcomes post ABI including poorer recovery, greater length of stay, and higher level of disability.
     
  10. There is level 5 evidence that the development of growth hormone deficiency may produce unfavourable outcomes post ABI including poorer cognitive functioning, lower Functional Independence Measure scores, and higher Disability Rating Scale scores.
     
  11. There is level 5 evidence that gonadotropic deficiency post ABI is associated with lower Glasgow Coma Scale Scores.
     
  12. There is level 5 evidence that hyperprolactinemia may not be associated with injury severity or recovery outcome post ABI.
     
  13. There is level 5 evidence that adrenocorticotropic hormone deficiency may produce unfavourable outcomes post ABI including mortality.
     
  14. There is level 5 evidence that thyroid-stimulating hormone deficiency is associated with greater injury severity.
     
  15. There is level 2 evidence that IGF-1 may improve clinical outcomes in patients with GHD post ABI
     
  16. There is level 4 evidence that GH replacement therapy may be effective in treating GHD post ABI by increasing IGF-1 levels.
     
  17. There is level 4 evidence that saline solution, enteral urea therapy, TRH stimulation, and hydrocortisone may be effective in treating hyponatremia post ABI by reducing ADH levels.