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hypotension should be sought; among the potential causes are aortic dissection, volume depletion, blood loss, and decreased cardiac output secondary to myocardial ischemia or cardiac arrhythmias. Patients with stroke may have depleted blood volume. Correction of hypovolemia and optimization of cardiac output are important priorities during the first hours after stroke. Treatment includes volume replacement with normal saline and correction of cardiac arrhythmias, such as slowing a ventricular response to rapid atrial fibrillation. If these measures are ineffective, vasopressor agents such as dopamine may be used. Trials have tested the utility of volume expansion and drug-induced hypertension for treatment of acute ischemic stroke. These measures are described later in the present guideline. F. Hypoglycemia Because hypoglycemia may produce neurological signs that mimic ischemic stroke and because hypoglycemia itself may lead to brain injury, prompt measurement of the serum glucose concentration and rapid correction of a low serum glucose level are important. G. Hyperglycemia Hyperglycemia will be detected on admission in approximately one third of patients with stroke.271–273 Most patients have moderate elevations of glucose levels.274 Clinical studies demonstrate that the presence of hyperglycemia is associated with poor outcomes after ischemic stroke, including among patients treated with thrombolytic agents.275–279 A history of diabetes mellitus also is associated with a poorer outcome after stroke.280,281 The detrimental effects of hyperglycemia are not clearly understood but include increasing tissue acidosis secondary to anaerobic glycolysis, lactic acidosis, and free radical production.281,282 Hyperglycemia also may affect the blood–brain barrier and the development of brain edema281 and may be associated with an increased risk of hemorrhagic transformation of the infarction.283 Unfortunately, the contribution of hyperglycemia to poor outcomes may be affected by other factors.284 Elevations of blood glucose concentration may be secondary to the stress of the acute cerebrovascular event.285 In particular, hyperglycemia after stroke in nondiabetic patients may be a stress response.285 Candelise et al286 found that hyperglycemia is a marker of a more severe stroke. Thus, the poor outcomes among patients with hyperglycemia may in part reflect the seriousness of the vascular event itself. Recent clinical and imaging studies have highlighted the importance of hyperglycemia as a negative prognostic factor.271,278–280,282 Baird et al280 found that persistent hyperglycemia (blood glucose level >200 mg/dL) during the first 24 hours after stroke independently predicted expansion of the volume of ischemic stroke and poor neurological outcomes. These reports provide reasonable evidence that persistent elevations of blood glucose levels are associated with neurological worsening.281,287 These data suggest that management of hyperglycemia is an important part of acute management of patients with ischemic stroke. The outstanding issues relate to the effectiveness of management of stroke-associated hyperglycemia in improving outcomes after stroke and the level of glucose concentration that should be sought during the first 24 hours. On the basis of the aforementioned data, the panel concluded that the level of hyperglycemia that previously mandated emergency treatment in the setting of stroke was too high. The exact level of blood glucose that should prompt interventions is not known. A reasonable approach would be to initiate treatment among patients with a blood glucose level >200 mg/dL. The management of hyperglycemia among patients with stroke likely will be influenced by the approach to treating
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