A large body of evidence has accumulated to indicate that between 2030% of survivors of acute traumatic brain injury (TBI) develop permanent pituitary dysfunction. Growth hormone (GH) deficiency is the commonest abnormality documented in most studies followed by ACTH and gonadotrophin deficiency and hyperprolactinaemia, with TSH deficiency least common. In contrast to other forms of pituitary disease, the classical hierarchy of pituitary hormone failure is not always seen and there is a higher proportion of single hormone defects. Many of the symptoms of chronic TBI are similar to those of untreated hypopituitarism, which suggests that identification and appropriate treatment of hypopituitarism offers a valuable service to survivors of TBI. Who should be tested? Most studies have been confined to survivors of moderate to severe TBI and the rationale for investigation is currently confined to this subgroup. There is little relationship between severity of TBI, neuro-imaging studies or operative intervention and the likelihood of hypopituitarism so until better guidance is available from prospective studies, all survivors should be tested. The choice of dynamic stimuli for ACTH and GH are centre-dependent. The timing of testing is important.
In the acute phase of TBI the key deficiency to identify is ACTH; patients who develop hypotension, hypoglycaemia or hyponatraemia should be systematically screened for ACTH deficiency. Studies of the natural history of pituitary dysfunction after TBI suggest a dynamic process, with many acute abnormalities recovering within 36 months of TBI, while new deficiencies may manifest in this period. New deficiencies are rare after 6 months. Most authorities therefore recommend formal dynamic testing at 36 months following TBI. Clinicians should be aware of occasional late recovery of function. Prospective studies are needed to better identify those at greatest risk of hypopituitarism, in order to improve the logistics of post-TBI pituitary hormone assessment.