Massive and fulminant cerebral edema is a serious and sometimes fatal complication of extensive cerebral infarction. Of patients sustaining large supratentorial ischemic infarctions, 20 to 25% manifest signs of brain stem compromise related to transtentorial herniation. Peak volume augmentation from cerebral edema occurs one and one-half to three days after infarction. Certainly, reduction of brain volume during the time of critical cerebral edema may be life saving in such settings. In the majority of ischemic infarctions, however, the quantity of edema is not sufficient to exhaust compensatory mechanisms, and brain herniations do not occur. Whether ischemic cerebral edema contributes to tissue injury is not clear in the more common, but less dire, circumstances of" submassive" infarction. However, local increases in tissue water may compromise survival of marginally viable, ischemic cells.

Progressive tissue edema may perpetuate and extend local ischemia by its effects on collateral microcirculation. It has been shown that clinical and electrical function of cerebral tissue or individual brain cells requires a minimum local cerebral blood flow in the range of 0.18 to 0.25 ml/g/min. For maintenance of viability of brain tissue, the lower limit of cerebral blood flow appears to be approximately 0.12 ml/g/min. After vascular occlusion the flow provided by collateral channels in areas of the ischemic distribution may be in these ranges. Edema may cause further reduction of local flow below the critical lower limits for tissue function and survival. The adverse local effects of evolving edema are