Physiological trajectories after traumatic brain injury: markers or makers of disease?

The variability in outcomes after traumatic brain injury (TBI) cannot be fully accounted for by the heterogeneous characteristics of the primary injury and demographics, suggesting that a patient's physiological reaction to the initial insult could play a part in secondary injuries, like cerebral oedema or seizures.1 Particularly in patients with TBI who are admitted to intensive care units (ICUs), the physiological reaction is complex—it spans intracranial and extracranial processes, continuously evolves, and is iteratively affected by second insults (eg, hypoxia or hypotension) and therapies.