Traumatic brain injury (TBI) remains one of the most challenging pathologies in clinical neuroscience and has been described as the most complex disease in the most complex organ in the body [1]. All current treatments rely on attempting to mitigate secondary brain injury by providing critical care support, or by surgical management.

Initial assessment follows the principles of Advanced Trauma Life Support (ATLS), ensuring airway protection, adequate ventilation, and haemodynamic stability. Imaging, typically with a non contrast CT scan, is crucial for identifying haematomas, cerebral oedema, and midline shift. Surgical interventions, such as craniotomy for evacuation of an intracranial haematoma (eg. subdural, extradural, or intracerebral), and placement of intracranial pressure (ICP) monitors can be considered based on the patient’s neurological condition and radiological findings. ICP management is further supported through medical management including osmotherapy (mannitol or hypertonic saline), sedation, and optimisation of ventilation to maintain normocapnia. Decompressive craniectomies involve the removal of a large bone flap measuring at least 12 cm in diameter. In some patients in whom the ICP remains elevated, a trial of cerebrospinal fluid (CSF) diversion by placing an external ventricular drain (EVD) or lumbar drain (LD) can be considered and can prove effective in managing high ICPs.

It is recognised that brain injury results in activation of a neuroinflammatory cascade [2] and all attempts to mitigate this using disease modifying drugs over the past three decades have failed to reach their primary outcome measures *[3], [4] and this is likely at least in part due to the extreme heterogeneity of TBI. Some trials involving symptoms control such as headaches [5] or epilepsy control [6] have reached their primary endpoints but this is likely because patients suffering TBI and presenting with a specific symptom have all self selected themselves in to a particular subset of patients. It is recognised that up to 50% of mild TBI patients will not have returned to their baseline after 6 months [7] and it is likely that at least a proportion of this is related to endocrine dysfunction [3].

Intensive Care (ICU) management of severe TBI involves assuming control of the much of the patient’s physiology, especially the cardiovascular system meaning that disruption of neuroendocrine homeostasis, particularly within the hypothalamic-pituitary axis (HPA) will not be apparent acutely. Given its central regulatory role and anatomical vulnerability, the HPA is disproportionately susceptible to both primary and secondary brain injury. Hypopituitarism following TBI may be partial or complete, transient or permanent, and is often missed entirely without targeted investigation.