Traumatic brain injuries (TBI) represent a leading cause of morbidity and mortality globally. Whilst clinical care has significantly improved in recent years, there is still significant scope to improve patient outcomes, particularly in relation to quality of life. However, there is a window of opportunity for clinical intervention, since most of the mortality and morbidity is associated with secondary injury processes that arise after the initial trauma. In the brain, as with any tissue, inflammation plays an important role in the response to injury. However, particularly with severe injuries, an excessive inflammatory response can have detrimental effects. Following TBI, inflammation can lead to the development of cerebral oedema and a rise in intracranial pressure. Without effective control, these processes can rapidly lead to patient deterioration. This narrative review focusses on the role of inflammation in TBI in order to examine the strategies that may help improve patient outcomes. Whilst there is clearly a relationship between the development of cerebral oedema, rising intracranial pressure (ICP), and poor patient prognosis, there are also discrepancies in terms of their impact on patient outcomes. In addition to causing a rise in ICP, this review examines in what other ways inflammation and the development of cerebral oedema may contribute to the injury process. The potential for these factors to impact upon microvascular function and reduce cerebral tissue perfusion and oxygenation is explored. In addition, the impact of TBI on glymphatic function is discussed. Following an evaluation of the potential injury processes, the scope for intervention and the development of novel therapeutic approaches is explored.