Diabetes Intraoperative Management

Earn CME/CE in your profession:

Continuing Education Activity

According to Center for Disease Control data, the incidence of diabetes mellitus in the United States in 2015 was 30.3 million and predicted to increase yearly with an already prediabetic population of 84 million. Prevalence of diabetes is highest in the Alaska Native and Native American populations, followed by African Americans, Hispanics, Asians, and Whites. This activity reviews the intraoperative management of diabetes and highlights the role of the interprofessional team in the management of patients with diabetes mellitus.


  • Identify the indications for intraoperative management of diabetes.
  • Describe the complications of unregulated hyperglycemia during surgery.
  • Review the clinical benefits of regulating blood glucose during surgery.
  • Discuss the role of the interprofessional team in improving care coordination to enhance the intraoperative management of diabetes and improve outcomes.


According to Center for Disease Control data, the incidence of diabetes mellitus in the United States in 2015 was 30.3 million and predicted to increase yearly with an already prediabetic population of 84 million.[1] Prevalence of diabetes is highest in the Alaska Native and Native American populations, followed by African Americans, Hispanics, Asians, and Whites.[1]  Diabetes classification is either being type 1, an autoimmune disorder, or type 2. Type 1 diabetes mellitus is due to the immune-mediated destruction of beta-pancreatic cells, insulin-producing cells. These patients have a deficiency of insulin; therefore, patients depend on lifelong exogenous administration of insulin to maintain euglycemia. Type 1 diabetes "aka juvenile diabetes" patients are younger and commonly diagnosed during their teens; frequently, at the time of diagnosis, patients are admitted because they are concomitantly in a diabetic ketoacidosis state, severe metabolic derangement. Type 2 diabetes, aka "adult-onset diabetes," was once a disease found in the older population, but now with an increasing rate of obesity, this is now a disease that afflicts anyone from children to geriatrics. Type 2 diabetes is due to peripheral insulin resistance or decreased amount of insulin secretion. Although there is no consensus on the mechanism, it is postulated that the intracellular concentration of fatty acid metabolites activates a serine kinase cascade, which leads to defects in insulin signaling downstream to the insulin receptor.[1] At the time of diagnosis, over 60% of pancreatic beta cells may have lost function.[2] Eventually, patients with diabetes mellitus type 2 can experience the complete destruction of pancreatic beta cells and become dependent on exogenous insulin. In most cases, patients diagnosed with type 2 diabetes will be managed with oral hypoglycemic agents but also encouraged to change their lifestyle. Studies have shown better glycemic control with caloric restriction and weight loss.[3]

Anatomy and Physiology

Surgery and acute illness are stressors that alter homeostasis and lead to hyperglycemia. Stress conditions raise counter-regulatory hormones such as glucagon, epinephrine, cortisol, and growth hormones. This process leads to insulin resistance, increased hepatic glucose production, impaired peripheral glucose utilization, and relative insulin deficiency.[4] Epinephrine stimulates glucagon secretion and inhibits insulin secretion by pancreatic beta cells.[5] Additionally, the increased level of stress hormones leads to enhanced lipolysis and high free fatty acid (FFA) concentrations. Increased FFA correlates with inhibiting insulin-stimulated glucose uptake and limit the intracellular signaling cascade in skeletal muscle responsible for glucose transport activity.[4] Hyperglycemia leads to the release of pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin 6, and interleukin 1B.[6] In addition, hyperglycemia has been shown to impair leukocyte function and to limit phagocytosis, chemotaxis, and bacterial destruction.[7] Hyperglycemia leads to increased reactive oxygen species that can result in direct cellular damage, vascular and immune dysfunction. Hyperglycemia leads to increased platelet aggregation and a prothrombotic state, partly attributable to oxidative stress.[8]


Diagnosis of diabetes is when a patient meets one of the following criteria:[9] 

  • A glucose level equal to or greater than 126 mg/dL after fasting for 8 hours
  • Random venous plasma glucose equal to or greater than 200 mg/dL in a patient with classic symptoms of hyperglycemia
  • Plasma glucose equal to or greater than 200 mg/dL measured two hours after a glucose load of 75 g in an oral glucose tolerance test
  • Hemoglobin A1C equal to or greater than 6.5 percent


  • Alaris pump and tubing 
  • 100 cc bag of normal saline
  • Insulin 
  • POC glucose testing strips (alternative arterial line or venous blood gas analysis) 
  • 50% dextrose 


There are no strict guidelines to canceling a surgical case due to hyperglycemia. The Society for Ambulatory Anesthesia (SAMBA) recommends canceling a case if a patient is experiencing diabetic ketoacidosis, hyperosmolar non-ketotic state, or severe dehydration.[10] On the day of surgery, if a patient has a blood sugar over 140 mg/dL, blood glucose should be monitored every 2 hours intraoperatively with a point of care glucose via arterial line or venous blood from a peripheral intravenous line. If a patient has a blood glucose level greater than or equal to 180 mg/dL and is critically ill, an IV insulin drip should be initiated.[11] Starting dose of insulin drip (units/hour) can be calculated with blood glucose/100 and titrated according to table 1.[4] The half-life of insulin is 35 minutes, so it titrates easily, and blood sugar should monitoring should occur hourly. For those who are not critically ill and having a short procedure (less than 4 hours) that does not anticipate large fluid shifts, it is preferable to use rapid-acting subcutaneous (SC) insulin. Table 2 below gives guidance as to how to dose SC insulin the day of surgery for those who are insulin sensitive (no history of diabetes), insulin resistant (those with a total daily dose (TDD) insulin exceeding 80 units, BMI greater than 35, prednisone greater than 20 mg), and usual insulin (all others).[4]


Control of hyperglycemia intraoperatively is of great importance because there is a 50% increase in morbidity and mortality in patients with diabetes mellitus compared to patients without diabetes mellitus.[12] Research correlates perioperative hyperglycemia with increased hospital and intensive care unit length of stay and higher numbers of postoperative cases of pneumonia, systemic blood infection, urinary tract infection, acute renal failure, and acute myocardial infarction.[12] Hypokalemia is an associated complication of hyperglycemia treatment with insulin, especially with coinciding diabetic ketoacidosis. Insulin drives potassium extracellular and hydrogen ions intracellular.  Excess potassium is lost in urine due to osmotic diuresis. Other derangements include hypocalcemia, hypomagnesemia, and QT prolongation.[13] Other life-threatening complications of insulin use include hypoglycemia. Those treated with tight glycemic control were five times as likely to experience severe hypoglycemia (blood glucose less than 40 mg/dL) postoperatively in comparison to liberal glucose treatment.[14] Symptoms of hypoglycemia include tremors, sweating, dizziness, light-headedness, seizures, and loss of consciousness. Intraoperatively hypoglycemia can cause a delay in emergence from anesthesia until exogenous glucose is administered to normalize blood sugar.[15]

Clinical Significance

There is no agreement among the anesthesiology community exactly what the standard of care for blood glucose levels should be, but there is consensus to aim for blood glucose levels below 180 mg/dL; more aggressive goals may cause hypoglycemia. Recent metanalysis revealed there is no difference in mortality in patients treated with very tight glucose control (BG less than 110 mg/dL), tight glucose control (111 to 150 mg/dL), and liberal blood glucose control (BG less than 220 mg/dL).[14] There was a decrease in adverse events in the tight glucose control group for surgical site infection, acute kidney injury, sepsis, and atrial fibrillation.

Enhancing Healthcare Team Outcomes

Each institution should develop its own standardized protocol for hyperglycemia for use in the pre-op area, intraoperative, and post-anesthesia care unit to ensure perioperative glucose control. Communication amongst an interprofessional group is necessary as surgeons, anesthesiologists, intensivists, internal medicine providers, pharmacists, and nurses are closely involved in patient care. Most patients will be coming either from the main floor or ICU, so there should be a good handoff. 

(Click Image to Enlarge)
Intraoperative Diabetes Management Tables
Intraoperative Diabetes Management Tables
Contributed by Kimpreet Kaur, DO
Article Details

Article Author

Kimpreet Kaur

Article Editor:

Robert W. Joyner


6/5/2022 12:36:12 PM



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