The Case of Hypopituitarism in Traumatic Brain Injury

Traumatic brain injury (TBI) has until recently been considered a rare cause of loss of pituitary function, accounting for less than one percent of all new cases of hypopituitarism. Newer studies have, however, indicated otherwise, and overlooking the condition in case of the life-threatening adrenal insufficiency after brain trauma may be fatal (Schneider et al., 2007a). Thus, chronic anterior pituitary hormone deficits have been described with a higher frequency than previously anticipated and have caused expert panels to propose recommendations for routine assessment of pituitary function after TBI with appropriate replacement of insufficient axes (Ghigo et al., 2005; Ho, 2007; Tanriverdi et al., 2011). Most populations have a high incidence of TBI of more than 100 in 100,000 inhabitants. On the one hand it is of clinical importance to identify all patients that would benefit from relevant substitution therapy, but on the other hand it is also of major socio-oeconomic interest to ensure a cost-effective strategy. To perform pituitary testing of all TBI patients would be an impossible task both logistically and financially. It is therefore unfortunate that the area despite numerous studies still lacks identification of valid predictors for development of hypopituitarism, and it has also not yet been clarified, which part of the TBI population that should be tested. Additionally, no larger treatment intervention studies have been performed, and it therefore remains quite unclear whether or not patients would benefit from treatment of hypopituitarism at an early or later stage to facilitate neurorehabilitation and improve survival, morbidity and quality of life. In this chapter, the published clinical studies of posttraumatic hypopituitarism are scrutinized, and current recommendations are discussed in the lines of currently available evidence, with reference to socio-oeconomic aspects.