The syndrome cerebral salt wasting is produced by excessive secretion of natriuretic peptides and causes hypo- natremia from excessive natriuresis, which may also provoke volume contraction.297 The diagnosis of cerebral salt wasting is more common in patients with poor clinical grade, ruptured anterior communicating artery aneurysms, and hydrocepha- lus, and it may be an independent risk factor for poor outcome.298 300 Uncontrolled studies using crystalloid or colloid agents suggest that aggressive volume resuscitation can ameliorate the effect of cerebral salt wasting on the risk of cerebral ischemia after aSAH.301,302 One retrospective study has suggested that 3% saline solution is effective in correcting hyponatremia in this setting.303 In addition, use of hypertonic saline solution appears to increase regional cere- bral blood flow, brain tissue oxygen, and pH in patients with Two randomized, controlled trials have been performed to evaluate fludrocortisones to correct hyponatremia and fluid balance. One trial found that it helped to correct the negative sodium balance, and the other reported a reduced need for fluids and improved sodium levels using this mineralocorti- coid.305,306 A similar randomized, placebo-controlled trial showed reduced natriuresis and a lower rate of hyponatremia in aSAH patients treated with hydrocortisone.307 The value of albumin as an efficient volume expander during the vasospasm phase in aSAH has been suggested in uncontrolled studies, but there is no clear evidence of its superiority over crystalloids in patients with aSAH.308 Fever is the most common medical complication in aSAH.309 The presence of fever of noninfectious (central) origin has been associated with severity of injury, amount of hemorrhage, and development of vasospasm, and it may represent a marker of a systemic inflammatory state triggered by blood and its byproducts.310 312 Analysis of data from a prospectively collected registry of aSAH indicated that fever was independently associated with worse cognitive outcome in survivors of aSAH.313,314 Improved functional outcome with effective control of fever has been reported.315 Both animal studies and human case series have demonstrated an association between elevated blood glucose concentration and poor outcome after ischemic brain injury.316 323 The mecha- nisms explaining such an association in human beings are unclear. 