Aetiology
The aetiology of inpatient hyperglycaemia is multi-factorial and involves increases in circulating concentrations of stress hormones, along with possible deleterious effects on vascular, haemodynamic, and immune systems.[9] In some cases the hyperglycaemia may be due to concomitant therapy, such as corticosteroids, or to parenteral, and occasionally enteral, nutrition. Hyperglycaemia has been associated with an increased risk of complications and mortality in patients on parenteral nutrition.[10]
Hypoglycaemia - a fall in blood glucose to below 3.9 mmol/L (70 mg/dL) - is a known adverse effect of insulin and other antidiabetic drugs such as sulfonylureas. In addition, patients at increased risk of hypoglycaemia include those with reduced nutritional intake or interruption of parenteral or enteral nutrition, malnutrition, renal or hepatic impairment, heart failure, malignancy, infection, sepsis, older age, and cognitive impairment.[1][3][4][11]
Pathophysiology
Hyperglycaemia in patients admitted to hospital, with or without a previous history of diabetes, is a complex condition, usually associated with both insulin resistance and insulin deficiency. Insulin resistance is often related to inflammation induced by infections or stress hormones and cytokines. Some of these same factors affect pancreatic beta-cell function and induce insulin deficiency.
Concomitant treatments often exacerbate the problem. Corticosteroid therapy that induces insulin resistance is a good example.[12] In addition, parenteral nutrition with a high fat load leads to increased free fatty acids, which in turn affects glucose metabolism.
Hyperglycaemia has multiple consequences, which may affect clinical outcomes adversely. These include altered white blood cell function, blood flow and reactivity, and oxidative stress.
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