Purpose of review: This review focuses on water shift and oedema in acute brain injury, with particular aspects on pathophysiology of water movements, the role of aquaporins and the potential of new therapies. This review reports on update of both significant experimental and clinical findings on factors implicated in oedema formation.
Recent findings: The main inputs came from the demonstrated role of aquaporins (especially AQP4) in brain oedema control. The absence of aquaporin agonist or antagonist does not help to clarify the net effect of aquaporins on brain oedema. The clinical practice of osmotherapy, especially with hypertonic saline failed to improve neurological outcome in a large randomized clinical trial. Colloid treatment was not proven efficient and potentially dangerous. Some hopes might come from targeting inflammatory cascade and neurogenic mediators to reduce lesion severity and to limit the blood-brain barrier dysrupture.
Summary: Water content control and partition can be better assessed in clinic with NMR helping to make decisions, but with limited proven therapies. The timing for such interventions might be crucial and future biomarkers might be very helpful.