Hannon and co-investigators report that 78% of 100 patients with traumatic brain injury developed inappropriately low plasma cortisol levels following the injury; most of the low plasma cortisol levels were recorded during days 1–3 following hospital admission for the injury. Acute cortisol deficiency and cranial diabetes insipidus following traumatic brain injury was associated with subsequent mortality. Furthermore, acute hypocortisolaemia following injury was predictive of the development of chronic hypopituitarism.