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 Whites, 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, 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 lifestyle. Studies have shown better glycemic control with caloric restriction and weight loss.[3]

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]

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