Diabetes Intraoperative Management


Article Author:
Kimpreet Kaur


Article Editor:
Robert Joyner


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
2/9/2019 11:17:51 PM

Introduction

According to CDC data, the incidence of diabetes in the United States in the year 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 population, followed by African Americans, Hispanics, Asians, and Caucasians, respectively.[1]  Diabetes classification is as 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 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, type 2 diabetic patients 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 lifestyle. Studies have shown better glycemic control with caloric restriction and weight loss.[3]

Anatomy

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 in 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]

Indications

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

Equipment

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

Technique

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, 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 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. 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 20mg), and usual insulin (all others).[4]

Complications

Control of hyperglycemia intraoperatively is of great importance because there is a 50% increase in morbidity and mortality in diabetic compared to nondiabetic counterparts.[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 40mg/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; 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), tight glucose control (111 to 150), and liberal blood glucose control (BG less than 220).[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 the post-anesthesia care unit to ensure perioperative glucose control. Communication amongst a multidisciplinary group is necessary as surgeons, anesthesiologists, intensivists, internal medicine providers, pharmacists, and nurses are all closely involved in patient care. Most patients will be coming either from the main floor or ICU so there should be a good handoff. 


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    Contributed by Kimpreet Kaur, DO
Attributed To: Contributed by Kimpreet Kaur, DO

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Diabetes Intraoperative Management - Questions

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Intraoperatively, a patient with diabetes on an insulin drip and D5NS experiences an increase in glucose level. What is the most appropriate next step?



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Diabetes Intraoperative Management - References

References

Saini V, Molecular mechanisms of insulin resistance in type 2 diabetes mellitus. World journal of diabetes. 2010 Jul 15;     [PubMed]
Cerf ME, Beta cell dysfunction and insulin resistance. Frontiers in endocrinology. 2013;     [PubMed]
Henry RR,Scheaffer L,Olefsky JM, Glycemic effects of intensive caloric restriction and isocaloric refeeding in noninsulin-dependent diabetes mellitus. The Journal of clinical endocrinology and metabolism. 1985 Nov;     [PubMed]
Duggan EW,Carlson K,Umpierrez GE, Perioperative Hyperglycemia Management: An Update. Anesthesiology. 2017 Mar;     [PubMed]
McDonnell ME,Umpierrez GE, Insulin therapy for the management of hyperglycemia in hospitalized patients. Endocrinology and metabolism clinics of North America. 2012 Mar;     [PubMed]
Hotamisligil GS,Murray DL,Choy LN,Spiegelman BM, Tumor necrosis factor alpha inhibits signaling from the insulin receptor. Proceedings of the National Academy of Sciences of the United States of America. 1994 May 24;     [PubMed]
Delamaire M,Maugendre D,Moreno M,Le Goff MC,Allannic H,Genetet B, Impaired leucocyte functions in diabetic patients. Diabetic medicine : a journal of the British Diabetic Association. 1997 Jan;     [PubMed]
Yamagishi SI,Edelstein D,Du XL,Brownlee M, Hyperglycemia potentiates collagen-induced platelet activation through mitochondrial superoxide overproduction. Diabetes. 2001 Jun;     [PubMed]
2. Classification and Diagnosis of Diabetes: {i}Standards of Medical Care in Diabetes-2018{/i}. Diabetes care. 2018 Jan;     [PubMed]
Duggan EW,Klopman MA,Berry AJ,Umpierrez G, The Emory University Perioperative Algorithm for the Management of Hyperglycemia and Diabetes in Non-cardiac Surgery Patients. Current diabetes reports. 2016 Mar;     [PubMed]
Frisch A,Chandra P,Smiley D,Peng L,Rizzo M,Gatcliffe C,Hudson M,Mendoza J,Johnson R,Lin E,Umpierrez GE, Prevalence and clinical outcome of hyperglycemia in the perioperative period in noncardiac surgery. Diabetes care. 2010 Aug;     [PubMed]
Johansen NJ,Christensen MB, A Systematic Review on Insulin Overdose Cases: Clinical Course, Complications and Treatment Options. Basic     [PubMed]
Kang ZQ,Huo JL,Zhai XJ, Effects of perioperative tight glycemic control on postoperative outcomes: a meta-analysis. Endocrine connections. 2018 Dec 1;     [PubMed]
Misal US,Joshi SA,Shaikh MM, Delayed recovery from anesthesia: A postgraduate educational review. Anesthesia, essays and researches. 2016 May-Aug;     [PubMed]
Joshi GP,Chung F,Vann MA,Ahmad S,Gan TJ,Goulson DT,Merrill DG,Twersky R, Society for Ambulatory Anesthesia consensus statement on perioperative blood glucose management in diabetic patients undergoing ambulatory surgery. Anesthesia and analgesia. 2010 Dec;     [PubMed]

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