Overview
Why Surgery Changes Glucose Control
Surgery, anaesthesia, pain, inflammation, and critical illness activate cortisol, catecholamines, glucagon, growth hormone, and inflammatory cytokines.
Surgery, anaesthesia, pain, inflammation, and critical illness activate cortisol, catecholamines, glucagon, growth hormone, and inflammatory cytokines. These signals tell the liver to release glucose and make muscle and adipose tissue less responsive to insulin. The result is stress hyperglycemia. This response occurs in people with diabetes and in people without a known diagnosis. A postoperative glucose elevation is therefore not automatically “just the diabetes.” It may reflect previously unrecognized diabetes, an inadequate insulin plan, infection, worsening illness, or the expected stress response. Hyperglycemia is not benign in the surgical setting. Elevated glucose impairs leukocyte function, promotes infection, and interferes with wound healing. It is associated with surgical-site infection, longer length of stay, and increased mortality. Stress hyperglycemia in a person without known diabetes deserves the same attention as hyperglycemia in a person with established diabetes. The goal is controlled glucose, not normal glucose at any cost. Aggressively chasing a normal value can create hypoglycemia in a fasting, sedated, or haemodynamically unstable patient whose warning symptoms are hidden.
