Perioperative Glycemic

Surgery, anesthesia, pain, infection, and critical illness activate a stress response. Cortisol, catecholamines, glucagon, growth hormone, and inflammatory cytokines signal the liver to release more glucose while making muscle and adipose tissue less responsive to insulin. The result is increased glucose production paired with insulin resistance. This can occur in a patient with type 1 or type 2 diabetes, but it can also occur in a patient with no history of diabetes. A postoperative glucose of 240 mg/dL is not automatically “just stress.” Stress hyperglycemia is associated with surgical-site infection, delayed wound healing, longer hospitalization, and mortality. Risk may be at least as great in people without known diabetes because unrecognized diabetes, acute illness severity, or both may be present. Hyperglycemia impairs neutrophil function and promotes inflammation, which helps explain the higher infection risk. It also causes osmotic diuresis when severe, worsening dehydration and electrolyte loss at the very time that surgical patients may have limited intake, blood loss, or hemodynamic instability. The goal is not to force glucose into a normal outpatient range. Tight control can cause hypoglycemia, which...