The use of prophylactic anticonvulsants may be considered in the immediate posthemorrhagic pe- riod (Class IIb; Level of Evidence B). 2. The routine long-term use of anticonvulsants is not recommended (Class III; Level of Evidence B) but may be considered for patients with known risk factors for delayed seizure disorder, such as prior seizure, intracerebral hematoma, intractable hyper- tension, infarction, or aneurysm at the middle cere- bral artery (Class IIb; Level of Evidence B). Management of Medical Complications Associated With aSAH Both hypernatremia and hyponatremia are frequently ob- served in the acute phase after aSAH.293,294 The reported incidence of hyponatremia in this disease ranges from 10% to 30%. Hyponatremia has been chronologically associated with the onset of sonographic and clinical vasospasm.295,296 Hy- ponatremia can develop from different mechanisms after aSAH. 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. 