Positive for SAH

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In theory, higher pressures may increase the risk of rebleeding, whereas lower pressures may compromise cerebral perfusion pressure, leading to cerebral ischemia. A retrospective study of 134 patients with SAH, 80 of whom had systolic blood pressure reduced to <100 mm Hg, found that while rebleeding occurred in 15% of patients treated with antihypertensives, compared with 33% in the untreated group, the rates of cerebral infarction in the treatment group were nearly twice that of the nontreatment group (40 vs 22%).$^{191}$ Whether acute hypertension definitively increases rebleeding risk is still a controversial subject, based on the conflicting results of recent studies.$^{192,193}$

Although there are conflicting data on the causal relationship of the occurrence of hypertension in SAH patients, there may be some relationship between premorbid hypertension and both poor prognosis and higher severity of disease on presentation.$^{194}$ Acute management, however, has not been clearly demonstrated to alter clinical outcome. There are no conclusive data pointing to a target blood pressure or the ideal antihypertensive agent in the management of SAH, so these choices should follow the protocols of the consulting neurosurgical or neurointensive care team. The authors recommend the collaborative development and utilization of regional protocols to help guide management of these patients at every point in the system of care. The 2012 AHA/ASA guidelines recommended that from the time of symptom onset to obliteration of the aneurysm, blood pressure should be controlled with a titratable agent, with a goal systolic blood pressure of 160 mm Hg.$^{6}$ The guidelines note that an evidence-based goal has yet to be identified but that systolic blood pressure of 160 mm Hg is a reasonable target.$^{6}$ Titratable intravenous agents may include labetalol, nicardipine, clevidipine, and esmolol.$^{8,10}$ Clevidipine, an intravenous dihydropyridine with a pharmacokinetic profile similar to that of nicardipine, has not been studied extensively in SAH patients. Due to the addition of an ester linkage, it has a half-life of <1 minute and may therefore require less titration.$^{195,196}$ Nitroprusside should be avoided due to its tendency to increase intracranial pressure and the potential for toxicity with prolonged infusion.$^{8}$ If the patient is expected to remain in the ED for an extended period of time, an arterial catheter may be inserted to facilitate continuous blood pressure monitoring.$^{9}$

Cerebral vasospasm is a delayed complication that may develop several days up to 2 weeks post aSAH, with a peak incidence at 7 to 10 days after the event.$^{2,19}$ Vasospasm may be asymptomatic or may lead to delayed neurologic deterioration, which can cause significant morbidity related to aSAH.196 Nimodipine, a calcium-channel blocker, has been shown to reduce the occurrence of secondary ischemia with a favorable trend toward reducing case fatality. In a Cochrane review of 16 trials of calcium antagonists, nimodipine had a risk ratio of 0.67; 95% CI, 0.55-0.81.$^{197}$ The statistical significance of this review rests heavily on the largest randomized controlled trial of 554 patients, from which the standard dosing regimen is derived.$^{198}$ Nimodipine 60 mg can be administered orally every 4 hours, even starting in the ED.$^{8,9,197}$ If the patient is unable to swallow, nimodipine should be crushed and given via a nasogastric tube, as there is no evidence for the efficacy of intravenous nimodipine.$^{197}$ Nimodipine should be given to hemodynamically stable patients and in consultation with the specialist team. Note that nimodipine is part of the comprehensive stroke center measures and does not necessarily need to be administered in the ED. Nicardipine, another calcium-channel blocker, has also been shown to decrease vasospasm in a randomized trial but without any improvement in outcome.$^{199}$

Intravenous magnesium sulfate has not been shown to be effective in vasospasm prophylaxis.$^{197,200}$ Statins had shown some promise in early literature for preventing vasospasm,$^{201-203}$ and some trials showed decreases in vasospasm incidence with no improvement in delayed cerebral ischemia or mortality.$^{204-206}$ However, more recent studies on statin use in aSAH have shown no statistical difference in occurrence of cerebral vasospasm or delayed cerebral ischemia; therefore, statins are no longer recommended for prevention.$^{207-209}$

Up to 20% of patients have a seizure during or soon after aSAH.$^{210,211}$ Although there are no randomized controlled trials on the prophylactic use of antiepileptic drugs (AEDs), seizures can result in rebleeding from an unsecured aneurysm, so AEDs are commonly used in the acute period.$^{212,213}$

Phenytoin has been associated with worse outcomes, especially with prolonged use.$^{214,215}$ Data from 4 multicenter randomized controlled trials of aSAH were pooled to identify associations with AED use in aSAH. The analysis of 3552 patients admitted with aSAH found increased in-hospital complications and worse outcomes after antiepileptic therapy, based on GCS score, neurologic deterioration, and vasospasm.$^{214}$ Another prospective study of 527 patients with SAH found that higher serum phenytoin levels were associated with functional decline and cognitive disability at 2 weeks and 3 months.$^{215}$ A review of 7000 aSAH patients given AEDs found a 2.2% early seizure rate and a 5.5% late seizure rate, with no difference between the patients who received some course of AEDs and those who received no AEDs.$^{216}$

Common practice may include a short course (<3 days) of an AED versus using an AED until the aneurysm is secured, based on data showing that short courses have the same benefit of low in-hospital postoperative seizure rate (<2%) when compared with longer courses, without the cumulative adverse effects of the drugs.$^{212,217}$ In a patient who has not already seized, it is reasonable to defer AED initiation to the inpatient management service given limited data to support efficacy in the early phase. This is best done in accordance with protocol developed at local institutions. If used for prophylaxis, an AED with a better side-effect profile, such as levetiracetam 500 mg twice daily, can be used.