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In more recent times, the advent of semiquantitative methodologies such as subarachnoid hemorrhage early brain edema score, a score system based on early changes in clinically obtained computed tomography, and quantitative methodologies (selective sulcal volume, automated or not), have yielded heightened EBI identification rates (37 to 61% of patients with aSAH) ( The imperative nature of identification lies in its robust association with an escalated risk of unfavorable outcomes post-aSAH ( The initial pathological consequences of aneurysmal rupture, namely, the extravasation of haem-laden blood and its toxic substrates, the abrupt elevation of ICP, impaired cerebral perfusion, and dysregulation of cerebral autoregulation culminating in cerebral edema, serve as triggers for a cascade of secondary pathophysiological mechanisms that underlie the development of EBI

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