Cerebral edema early stroke or hypoxia, cardiac arrest, and pseudotumor cerebri. During an ischemic stroke, a lack of oxygen and glucose leads to a breakdown of the sodium-calcium pumps on brain cell membranes, which in turn results in a massive buildup of sodium and calcium intracellularly. This causes a rapid uptake of water and subsequent swelling of the cells. It is this swelling of the individual cells of the brain that is seen as the main distinguishing characteristic of cytotoxic edema, as opposed to vasogenic edema, wherein the influx of fluid is typically seen in the interstitial space rather than within the
Cerebral edema and coma. Interstitial edema occurs in obstructive hydrocephalus due to a rupture of the CSF–brain barrier. This results in trans-ependymal flow of CSF, causing CSF to penetrate the brain and spread to the extracellular spaces and the white matter. Interstitial cerebral edema differs from vasogenic edema as CSF contains almost no protein. Treatment approaches can include osmotherapy using mannitol, diuretics to decrease fluid volume, corticosteroids to suppress the immune system, hypertonic saline, and surgical decompression to allow the brain tissue room to swell without compressive injury. Many studies of the mechanical properties of brain edema were conducted in the 2010s,