Normally, sympathetic stimulation of pancreatic β-cells promotes the synthesis of insulin, which facilitates the uptake of glucose into liver, muscle, and adipose tissues and its conversion to glycogen. In association with surgical stress, insulin secretion is suppressed. Failure to secrete adequate levels of insulin during surgery, at least partially, is thought to be caused by α2-adrenergic inhibitory effects of epinephrine on pancreatic β-cells.
Cortisol affects carbohydrate, protein and fat metabolism. It promotes protein (skeletal muscle) breakdown to amino acids and gluconeogenesis. Cortisol also promotes lipolysis, which increases the production of gluconeogenic precursors from triglycerides, i.e., glycerol and fatty acids. While increasing glucose levels, cortisol also has an anti-insulin effect, which impairs cellular glucose uptake and contributes to perioperative hyperglycemia.
Consequently, the perioperative period is characterized by hyperglycemia due to three factors; relative lack of insulin, increased glucose production, and peripheral insulin resistance. Glucagon secretion increases briefly, but it is not thought to be a major factor. The excess glucose associated with surgical stress is a ready source of energy for obligate tissues such as the brain, wound cells, and red blood cells, which do not require insulin for glucose transport.2
Persistent perioperative hyperglycemia is a recognized sequela of surgical stress.1-3 Yet, two prospective surveys over a 10-year period, involving 4,309 dentists, documenting a total of 30,602 medical emergencies, identified hypo- and not hyperglycemia as the major problem with glucose homeostasis in dental settings.10 This provides further evidence that dental procedure-related stress is low and the causes of perioperative hypoglycemia are not procedure-related.