Key Points

 

  • Individuals with severe ABI are more likely to develop SIADH.
  • Reducing the fluid intake of patients has been shown to be effective in treating SIADH post ABI.
  • Individuals with severe ABI are more likely to develop hyponatremia.
  • Thyroid releasing hormone therapy may be an effective treatment for hyponatremia post ABI.
  • Sodium supplementation therapy and hydrocortisone may be an effective treatment for hyponatremia post ABI.
  • Prevalence of diabetes insipidus post ABI ranges from approximately 2% to 51%.
  • Severe injury, brain edema, intraventricular hemorrhage, and extensive skull fractures may serve as risk factors for the development of diabetes insipidus post ABI.
  • The incidence of anterior pituitary dysfunction post ABI ranges from 15% to 76%.
  • Anterior pituitary dysfunction may present within 24 hours of injury and persist up to 12 months post ABI.
  • Anterior pituitary dysfunction post ABI can occur in one or more axes in an unpredictable manner.
  • Several risk factors have been reported to be associated with the development of anterior pituitary dysfunction post ABI; however further research is required.
  • Compared to individuals with normal function, the development of anterior pituitary dysfunction may produce unfavourable outcomes post ABI including poorer recovery, greater lengths of stay, and higher levels of disability.
  • Prevalence of growth hormone deficiency post ABI ranges considerably from 2.8% to 63.6%.
  • Several risk factors have been reported to be associated with the development of post-ABI growth hormone deficiency; however further research is required.
  • Compared to individuals with normal functioning, the development of growth hormone deficiency may produce unfavourable outcomes post ABI including poorer cognitive functioning, lower levels of functional independence, and higher levels of disability.
  • Prevalence of gonadotropic deficiency post ABI ranges from 13% to 80% and can persist up to 12 months, and in some cases longer.
  • Gonadotropic deficiency post ABI is associated with greater injury severity.
  • Compared to individuals with normal functioning, the development of gonadotropic deficiency may produce unfavourable outcomes post ABI including poorer cognitive functioning, lower levels of functional independence, and higher levels of disability.
  • Prevalence of hyperprolactinemia post ABI ranges considerably from 5% to 50%; however prevalence rates may be impacted by hyperprolactinemia-inducing drugs.
  • Prevalence of adrenocorticotropic hormone deficiency post ABI is variable ranging from 8.8% to 78% and persisting up to 12 months and beyond.
  • Several risk factors have been reported to be associated with the development of post-ABI adrenocorticotropic dysfunction; however further research is required.
  • Compared to individuals with normal functioning, the development of adrenocorticotropic hormone deficiency may produce unfavourable outcomes post ABI.
  • Thyrotropic deficiency is uncommon post ABI.
  • Post-ABI thyrotrophic deficiency may be associated with injury severity.
  • Growth hormone deficiency can be effectively treated with hormone replacement therapy and insulin growth like factor-1 therapy.
  • Syndrome of inappropriate antidiuretic hormone can be effectively treated with a variety of interventions that regulate levels of ADH.