الفهرس 
Pathophysiology of HyperglycemiaOnly 14 pages are availabe for public view
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Abstract
Stress hyperglycemia is defined as a transient plasma glucose level above 200 mg/dL and it is thought to be caused by the increased levels of cortisol, glucagon, and epinephrine. These hormones increase gluconeogenesis and decrease peripheral uptake of glucose to ensure substrate availability
Causes of hyperglycemia in critical ill patients include diabetes mellitus stimulation of stress hormones (epinephrine, cortisol), glucocorticoid therapy, continuous enteral nutrition and decreased activity.
In healthy individuals without DM, the regulation of blood glucose concentration is maintained through hormonal, neural, and hepatic autoregulatory mechanisms 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, esulting in energy production), excess glucose also can be stored in the liver or converted to fatty acids for storage in adipose tissue.
Hyperglycemia after acute stroke may be attributable to several underlying mechanisms. These include: a non-specific reaction to acute stress; autonomic, hormonal, and metabolic alterations as a result of tissue injury; uncovering of underlying latent diabetes by the acute stroke; activation of the hypothalamo-hypophyseal-adrenal axis attributable to a direct effect of brain ischemia on the pituitary; and irritation of the glucose regulatory centers in the brain by a stroke.
Anyone experiencing symptoms of a stroke requires immediate medical help. Even if the ultimate diagnosis is not stroke, many diseases that can mimic a stroke are also medical emergencies, if a physician cannot be contacted by telephone , the person should be taken to the nearest hospital emergency department at once. Many types of stroke require immediate treatment, and most of the promising new therapies for stroke are effective only if started within a few hours of the onset of symptoms.
A variety of diagnostic tools are available to the physician, from history-taking and trained observation to sophisticated radiologic imaging studies, the tests performed will vary with the type of stroke, its severity, and the planned therapies. Regardless of the tests used, the goals are the same: to exclude nonvascular reasons for the neurological symptoms and to pinpoint the cause, location, and extent of the stroke.
Continuous intravenous insulin infusion is the most rational and physiologic method of management of hyperglycemia in ICU. Various studies have demonstrated that this method is safe, effective and flexible , It is imperative however to monitor blood glucose hourly and titrate the rate, this would necessitate adequate staffing of the ICU .
A continuous insulin infusion is considered superior to a sliding-scale regimen because it allows for an immediate response to a specific blood glucose level, with potential for frequent adjustments. Serum glucose levels are required every 1–2 hours when using a continuous insulin infusion, promoting tighter control of glycemic levels. In contrast, the sliding-scale method allows only for a retrospective assessment of glucose requirements and the arbitrary scale cutoff points may not be relevant to patients, consequently, a sliding scale may result in overall higher glycemic levels
The typical chronic complications of diabetes take several years to develop; therefore, the explanation for a rise in harm that is related to stress hyperglycemia needs further consideration, Stress hyperglycemia is mediated by much greater inflammatory and neuroendocrine derangements than are expected in chronic hyperglycemia associated with diabetes. Possibly, these derangements heighten susceptibility to benefits of interventions, for example, multiorgan failure is associated with widespread micro vascular endothelial dysfunction, and improved outcomes associated with intensive insulin therapy have been attributed in part to endothelial protection.