Effects of Hyperglycemia on Neurologic Outcome in Stroke Patients

Alison S. Paolino; Krista M. Garner


J Neurosci Nurs. 2005;37(3):130-135. 

In This Article

Hyperglycemic Effects on the Injured Brain

The effects of hyperglycemia on the injured brain have been studied in both animals and humans. Hyperglycemia has been associated with increased cerebral lactate resulting in local brain tissue acidosis (Kagansky, Levy, & Knobler, 2001). Brain tissue acidosis worsens mitochondrial function in the penumbra, the moderately ischemic tissue of the brain surrounding the injured core, and increases cerebral infarct size (Alvarez-Sabín et al., 2003). In a study of 63 patients with sudden-onset focal neurological deficit consistent with hemispherical ischemic stroke who received serial MRI, hyperglycemia was shown to reduce penumbral salvage, resulting in greater final infarct size (Parsons et al., 2002).

Hyperglycemia also adversely affects the ischemic brain by disrupting the blood-brain barrier and promoting cerebral edema. In their study of rats with hemorrhagic stroke and hyperglycemia, Song et al. (2003) found that hyperglycemia-induced brain injury resulted in increased free radical formation. In turn, the increased amount of free radical formation increased blood-brain barrier permeability and brain edema. The authors hypothesized that elevated glucose levels aggravated brain edema, which culminated in cell death surrounding hemorrhagic stroke tissue.

Hyperglycemia also is thought to play a role in negative outcomes in stroke patients treated with early reperfusion therapy. Research indicates that elevated glucose levels impair cerebrovascular reactivity in the microvasculature (Alvarez-Sabín et al., 2003). As a result, there is decreased reperfusion after tissue plasmogin activator (tPA)-induced recanalization, contributing to a worsened neurologic outcome (Kawai, Keep, & Benz, 1997). It has also been suggested that hyperglycemia may be an important risk factor for hemorrhagic conversion of stroke after tPA. Alvarez-Sabín et al. (2003) found that elevated blood glucose before reperfusion partly offsets the benefit of early restoration of blood flow, translating into decreased neurologic improvement, greater infarct size, and worsened outcomes in hyperglycemic patients. The PROACT II stroke thrombolysis trial (Kase et al., 2001) also found conclusive evidence that hyperglycemia is a significant risk factor for symptomatic hemorrhagic conversion of an ischemic stroke. When serum glucose was stratified into categories of increasing levels of hyperglycemia, subjects with values higher than 200 mg/dL had a 36% risk of symptomatic intracerebral hemorrhage (ICH).


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