Effects of Hyperglycemia on Neurologic Outcome in Stroke Patients

Alison S. Paolino; Krista M. Garner

Disclosures

J Neurosci Nurs. 2005;37(3):130-135. 

In This Article

Hyperglycemia Pathophysiology

Overview of Postprandial Glucose Metabolism

In healthy individuals without DM, the regulation of blood glucose concentration is maintained through hormonal, neural, and hepatic autoregulatory mechanisms (Robinson & van Soeren, 2004). Under normal circumstances, a postprandial increase in blood glucose concentration stimulates the release of insulin from the pancreas, specifically the b-cells. Insulin mediates peripheral glucose disposal and suppresses glucogenesis in the liver. This process maintains blood glucose homeostasis. After uptake into the skeletal muscle, glucose either is directed to glucagon formation (pathway for carbohydrate storage) or glycolysis (used in the Kreb's cycle, resulting in energy production). Excess glucose also can be stored in the liver or converted to fatty acids for storage in adipose tissue.

Altered Glucose Metabolism in Critical Illness

Critical illness induces a number of adaptive changes in human physiology; the most prominent are changes in the neuroendocrine function (Ferrando, 1999). An increase in counterregulatory hormones, such as glucagons, epinephrine, norepinephrine, and growth hormone, results in increased hepatic glucose production and decreased peripheral glucose uptake, subsequently inducing a hyperglycemic state (Montori, Bistrian, & McMahon, 2002). In addition, critical illness exacerbates the circulation of abnormal levels of cytokines—particularly tumor necrosis factor, alpha, and interleukin—further elevating serum glucose (McCowen, Malhotra, & Bistrian, 2001). Patients with DM exhibit a greater response to counterregulatory hormones, and may not increase insulin secretion as a compensatory response to needed levels, resulting in even higher glucose levels (Montori et al., 2002).

Effects of Exogenous Insulin

Hyperglycemic treatment with exogenous insulin alters the metabolic abnormalities seen in hyperglycemia (American Association of Clinical Endocrinologists [AACE], 2003). Improved outcomes from insulin administration in critically ill people may be due to favorable alterations in myocardial and skeletal muscle metabolism, oxidative glycolisis, and increased nitric oxide production that results in arterial vasodilatation. Insulin inhibits both lipolysis and inflammatory growth factors that have been associated with poor outcomes in patients with cardiac arrhythmias and acute myocardial infarction (AACE, 2003).

In global ischemia (e.g., anoxic brain injury and encephalopathy), insulin acts directly on brain parenchyma to reduce neuronal necrosis in the brain cortex, striatum, and hippocampus (Auer, 1998). Animal data indicate that the direct mechanism is mediated by insulin-like growth factor-1 receptors. The direct effect appears to predominate in global ischemia. In focal ischemia, unlike global ischemia, the effect of insulin is predominantly via peripheral hypoglycemia because neuroprotection largely is annulled by coadministration of glucose (Auer, 1998). Insulin also has been shown to improve cell membrane stability, assisting with cerebral edema resolution (American Association of Clinical Endocrinologists, 2003).

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