Jonathan E. Rhoads Lecture 2011

This lecture reviews the current understanding of how insulin resistance, as a marker of the metabolic stress, is involved in recovery after major surgery. Insulin resistance develops as a graded response related to the magnitude of the operation. It lasts for weeks after medium-size surgery and affects all parts of body metabolism. Although hyperglycemia develops, muscle and fat uptake is reduced and other non-insulin-sensitive cells have an increase in glucose uptake as a result of the elevated glucose levels. Reduced glucose uptake and storage in muscle along with loss of lean body mass help explain reduced muscle function that will impair mobilization. The increased uptake of glucose in non-insulin-sensitive cells is involved in the development of several of the most common postoperative complications, including infections and cardiovascular problems. Many of the perioperative treatments in use are outdated, and modern care involves a multimodal approach with several treatments, such as preoperative carbohydrate treatment instead of overnight fasting, continuous epidural anesthesia for postoperative pain care, early feeding, and mobilization, all of which affect insulin by reducing the stress and enhancing recovery. Most of the previous mandatory catabolic responses to surgery can be avoided, resulting in substantially faster recovery and fewer complications. Methods to implement these modern treatments have been developed and used in Europe, resulting in improved care and shorter length of stay.