Diabetes mellitus is a common chronic disorder, affecting approximately 8 percent of the US population . Patients with diabetes have an increased incidence of cardiovascular disease and this, combined with the frequent microvascular complications of the disease, often translate into more surgical interventions.
Careful assessment of patients with diabetes prior to surgery is required because of their complexity and high risk of coronary heart disease, which may be relatively asymptomatic compared with the nondiabetic population. Diabetes mellitus is also associated with increased risk of perioperative infection and postoperative cardiovascular morbidity and mortality [2,3].
One key aspect of the perioperative management is glycemic control; complex interplay of the operative procedure, anesthesia, and additional postoperative factors such as sepsis, disrupted meal schedules and altered nutritional intake, hyperalimentation, and emesis can lead to labile blood glucose levels. A rational approach to diabetes mellitus management allows the clinician to anticipate alterations in glucose and improve glycemic control perioperatively .
This review will discuss the preoperative evaluation of patients with diabetes, general goals of glycemic control, and management of blood glucose in the perioperative phase. The special circumstances of glucocorticoid therapy and hyperalimentation are also reviewed. More details regarding glucose control in hospitalized patients in general are found separately. (See "Management of diabetes mellitus in hospitalized patients" and "Glycemic control and intensive insulin therapy in critical illness".)
EFFECT OF SURGERY ON GLUCOSE CONTROL
Surgery and general anesthesia cause a neuroendocrine stress response with release of counterregulatory hormones such as epinephrine, glucagon, cortisol, and growth hormone, and of inflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha. These neurohormonal changes result in metabolic abnormalities including insulin resistance, decreased peripheral glucose utilization, impaired insulin secretion, increased lipolysis and protein catabolism, leading to hyperglycemia and even ketosis in some cases [5-14].