Glycemic management in critically ill patients

Figure 1 Response to metabolic stress. The metabolic homeostasis is affected once a stressor is identified. The response involves a series of neuroendocrine activations/inactivations and an inflammatory/immune component. The neuroendocrine response involves the activation of the hypothalamic-pituitary-adrenal axis resulting in an elevation of catecholamines and cortisol[73]. Other counter-regulatory hormones found also elevated during physiologic stress are CRH, GH and glucagon. These hormones inhibit hepatic glycogenesis and peripheral glycolysis while activating gluconeogenesis, hepatic and muscle glycogenolysis, and peripheral lipolysis[11]. The presence of glucagon activates the hepatic pathways of glycogenolysis and gluconeogenesis. Increased gluconeogenesis fueled by proteolytic, lipolytic, and glucolytic metabolites combined with hepatic insulin resistance are considered the main causes of stress-induced hyperglycemia, but more obvious factors such as exogenous dextrose, enteral or total parenteral nutrition, and simple bed rest can further aggravate this picture[11]. TNFα: Tumor necrosis factor α; IL: Interleukin; GH: Growth Hormone; CRH: Corticotrophin.