ENO2 and delirium: The most widely accepted theory of delirium pathophysiology involves systemic injury and inflammation, leading to the blood-brain barrier (BBB) disruption, glial and neuronal activation, increased inflammation, and subsequent cell death.6 Similarly, sepsis can cause endothelial and BBB damage, resulting in the release of neuronal proteins into the bloodstream.7 Neuron-specific enolase (NSE) is a recognized biomarker of neuronal death and has prognostic value in patients who are neurocritical.