Endocrine alterations that occur soon after severe brain injury are an indication of prolonged stress, rather than brain damage, and are important in predicting the 1-year functional outcome of the injury. The routine use of pituitary assessment soon after traumatic brain injury (TBI) is not recommended, and instead it should be reserved for patients suspected of hypopituitarism. Djordje Marina, MD, Rigshospitalet–Copenhagen University Hospital, Copenhagen, Denmark, presented a poster with the conclusions from a study conducted by Danish researchers to assess pituitary hormone alterations after TBI.

The study involved 163 patients aged ≥ 15 years who had suffered TBI (n = 111) or nontraumatic brain injury (non-TBI; n = 52) and who were receiving neurorehabilitation. Pituitary assessment at baseline and a median of 3.3 months (range, 2.1 to 4.9 months) post injury included gonadal and thyroid hormones, stress-related hormones (cortisol, prolactin, and insulin-like growth factor 1), and adrenal function. The primary outcomes at the time of referral, discharge, and the 1-year follow-up were daily functioning as assessed by the Functional Independence Measure (FIM), which covers 18 items of activities of daily living, with score-related outcomes ranging from total assistance to full independence, and ability measured by the Extended Glasgow Outcome Scale (GOS-E), a ranking of independence at and outside the home, and social and work capability. The characteristics of the TBI and non-TBI groups at the time of admission to rehabilitation are summarized in Table 1.

FIM scores were similar in the TBI and non-TBI groups at admission, discharge, and follow-up concerning complete dependency (TBI: 90%, 40%, and 25% of patients, respectively; non-TBI: 90%, 50%, and 25% of patients, respectively), moderate dependency (TBI: 3%, 5%, and 4% of patients, respectively; non-TBI: not applicable, 4%, and 5% of patients, respectively), and low-to-absent dependency (TBI: 3%, 50%, and 70% of patients, respectively; non-TBI: 10%, 50%, and 70% of patients, respectively). The data indicated improvements in activities of daily living during follow-up. At discharge, low GOS-E scores indicated a low degree of independent activities. The improvements in the capability of independent activity at the 1-year follow-up were not as marked in these patients, compared with patients who were more capable of independent activities at discharge (Table 2).

Thirty-two percent of all patients had suppressed gonadal or thyroidal function. The majority (68%) of all patients had elevated stress hormones. One-quarter of all patients displayed both features.

Secondary hypogonadism and elevated stress-related hormones were related to worse 1-year FIM scores in univariate analyses (p = .001 and p = .01, respectively). These associations remained following multivariate analysis (p = .01). Reduced gonadal or thyroid hormones and elevated stress-related hormones were related to a worse 1-year GOS-E score in univariate analyses (p = .04 and p = .006, respectively). Elevated stress-related hormones remained independently associated with a worse 1-year GOS-E score in multivariate analysis (p = .01).

The results indicate that endocrine changes occurring in brain injury may not necessarily be a consequence of brain damage. Rather, the endocrine alterations may represent physiological stress adaptations to the acute illness, and a subsequent prolonged stress response. The data do not support the routine use of pituitary assessment soon after TBI. This assessment should be reserved for patients with clinical features indicative of hypopituitarism.