Medications:
Lantus 20 units BID, HCTZ 25mg daily, Simvistatin 20 mg QHS, Lisinopril 20 mg daily.
Allergies:
Sulfa
Past Medical History:
Type 2 DM, hyperlipidemia, hypertension, obesity
Physical Exam
Height:
60 inches
Weight:
100 kg
VS:
BP 90/50
HR 110
Temp 38.5
RR 22
- 1.
How is diabetes mellitus characterized and what are the most common forms?
Hyperglycemia of DM is the consequence of relative or absolute deficiency of insulin and a relative or absolute excess of glucagon. In Type 1 DM, there is an absolute deficiency in insulin production and dependency on exogenous insulin to prevent lipolysis and eventually ketoacidosis. The onset of Type 1 diabetes usually occurs by adolescence, although it may occur at any age and is thought to result from to autoimmune destruction of the islets of Langerhans cells in the pancreas [1 ].
Type 2 DM is characterized by a relative deficiency of insulin, typically caused by insulin resistance. The onset is usually in adulthood and the specific etiology is unknown, however this form is strongly linked to obesity. Gestational diabetes is defined as any degree of glucose intolerance with the onset first recognized during pregnancy. These patients may have a predisposition to developing Type 2 DM later in life.
Hyperglycemia has been recognized as a major factor in the development of complications associated with diabetes. Chronic hyperglycemia leads to angiopathy and long-term complications involving the various organs. The cause of diabetic complications is multifactorial, including glycosylation of proteins and glucose reduction to sorbitol, which functions as a tissue toxin. This pathophysiologic process is associated with a decrease in myoinositol content, metabolism, and with a decrease in sodium-potassium-adenosine triphosphatase activity. Microangiopathy can cause: diabetic cardiomyopathy, nephropathy, neuropathy, retinopathy, and encephalopathy. Macroangiopathy leads to CAD, PVD, diabetic myonectosis, and stroke. Diabetes is a major risk factor for heart disease, stroke, kidney disease, blindness, and nontraumatic amputations.
- 2.
A medical student approaches you and asks if this patient could have Metabolic syndrome X. What is Syndrome X?
Metabolic syndrome is also known as insulin resistance syndrome, cardiometabolic syndrome, and Reaven’s syndrome. As the name implies, it is a syndrome rather than a specific disease state. The syndrome is caused by an underlying disorder of energy utilization and storage and the cause is still unknown. Diagnosis is made by co-occurrence of 3 out of 5 following medical conditions: central obesity, HTN, high fasting plasma glucose/impaired glucose tolerance, high serum triglycerides, and low HDL.
Prevalence in the USA is an estimated 34% of adult population and prevalence increases with age. The metabolic syndrome increases the risk of developing cardiovascular disease, particularly heart failure and diabetes. The hallmark of syndrome X is insulin resistance with hyperinsulinemia. The clinical significance of this condition stems from its association with multiple metabolic abnormalities, including low levels of high-density lipoprotein (HDL), increased blood pressure, and increased plasminogen activator inhibitor-1 levels. All these abnormalities have definite or possible association with coronary artery disease. Whether syndrome X and Type 2 DM are on a spectrum of disease with insulin resistance as a common denominator or are totally separate entities has yet to be clearly understood.
- 3.
What are some other less common causes of glucose intolerance?
There are several rare genetic diseases that result in defects in both Beta-cell production of insulin and insulin action [2 ]. Other causes result from destruction of the exocrine pancreas from inflammatory processes like pancreatitis, specific viral infections such as rubella, Coxsackie B, mumps, and cytomegalovirus, and immune mediated insulin autoantibodies or insulin receptor antibodies [2].
- 4.
What is the prevalence of diabetes?
Recent data suggest that the overall prevalence of diabetes in the United States is 9.3% [3]. Type 1 DM accounts for approximately 5–10% of diabetic population [1]. Type 2 DM accounts for the remaining 90–95% of patients. Gestational DM has an incidence of approximately 7% among pregnant women [1, 4]. Experts predict the overall prevalence of DM to increase by 200% in the next several decades as rates of obesity continue to climb worldwide [5, 6].
- 5.
What are the diagnostic criteria for diabetes mellitus?
Current diagnostic criteria from the American Diabetes Association include one of the following findings [7]:
- 1.
Hemoglobin A1c greater than or equal to 6.5%.
- 2.
Fasting plasma glucose level greater than or equal to 126 mg/dL
- 3.
Symptoms of diabetes and a random blood glucose level >200 mg/dL
- 4.
Oral glucose tolerance test with 2 h plasma glucose level greater than or equal to 200 mg/dL
- 6.
What are management strategies for the different types of DM?
Treatment of DM includes diet, oral hypoglycemic drugs, exogenous insulin, exercise, and weight reduction if warranted. Management of Type 1 DM requires administration of exogenous insulin analogues. Titration of rapid and long-acting analogues is often required to achieve euglycemia and to mimic the normal basal and postprandial insulin secretion responses. Different insulin preparations are encountered in diabetric patients being assessed for surgery, and understanding their time-action profiles and side effects is essential in clinical management.
Rapid acting insulin (lispro/Humalog® and aspart / NovoLog ®) analogues have quick onset of action (between 5 and 15 min), peak activity at 2 h after injection and their duration of action does not exceed 5 h [1].
Long-acting insulin analogues include NPH and glargine (Lantus®) which have a prolonged effect secondary to lower solubility. Lower solubility is achieved by amino acid substitution and addition of zinc to human insulin [8, 9]. This time-action profile allows for once-daily dosing and duration of action of 18–24 h.
Regular insulin is short-acting insulin best utilized intravenously for glucose control during intraoperative period.
In the past decade, newer therapies for newly diagnosed Type 1 DM have been introduced, including immunosuppression with varied successes. It is important to realize that 15% of patients with Type 1 DM have other autoimmune processes and that the elevated glucose levels are probably caused by destruction of pancreatic beta cells in these instances.
Management of Type 2 DM entails a wide array of anti-diabetic medications and lifestyle modifications that can also be supplemented by insulin analogues if needed. An overview of the various anti-diabetic pharmacological agents currently available is described below:
Sulfonylureas (glyburide, glipizide, glimepiride): These medications act by both stimulating insulin secretion by beta cells and improving peripheral sensitivity to insulin.
Biguanides (metformin): This class of medications acts by improving skeletal muscle insulin sensitivity, decreasing hepatic gluconeogenesis, and decreasing glycogenolysis. These should be stopped 48–72 h prior to surgery to prevent an increased risk of lactic acidosis.
Thiazolidinediones (pioglitazone and rosiglitazone): These act as insulin sensitizers by increasing the efficiency of glucose transporters via altering gene transcription. Side effects include potential hepatic injury, fluid retention, and increased incidence of myocardial ischemia.
Alpha-glucosidase inhibitors (acarbose and miglitol): Glucosidase is an enzyme that is present in the brush border of the small intestine. Enzyme inhibition results in reduction of carbohydrate breakdown and subsequent delayed glucose absorption. This helps to attenuate postprandial glucose surges.
Meglitinides (repaglinide and nateglinide): These work by increasing beta-cell insulin secretion. Of note, they have a faster onset and shorter duration of action relative to Sulfonylureas.
Amylin analogues: Amylin is a pancreatic hormone that is released in conjunction with insulin. Its release induces a decrease in glucagon secretion, slower gastric emptying, and satiety. Pramlintide is an example and is administered subcutaneously.
Incretin mimetics (exenatide and liraglutide): Incretins are intestinal peptides that are secreted in response to food intake. These peptides work by decreasing glucagon secretion, hepatic glucose production, and gastric emptying subsequently resulting in appetite suppression. Their use is limited by rapid enzymatic breakdown by DPP-4.
Dipeptidyl peptidase-IV(DPP-4) inhibitors (sitagliptin and saxagliptin): DPP-4 is responsible for the rapid degradation of incretins. Thus inhibition prolongs the beneficial effects of endogenous incretins. Examples include sitagliptin and saxagliptin.
- 7.
Preoperatively, how would you determine patient’s degree of glycemic control?
Close monitoring of glucose levels by both the patient and physician are imperative to prevent or prolong the onset of systemic consequences. Active involvement by a motivated patient is essential to effectively manage the disease. Fingerstick blood sampling should be done one to three times daily depending on the degree of insulin deficiency. Patients should also keep a log of eating habits and daily blood glucose levels to assess the need for lifestyle and or medication modifications. Regularly scheduled checkups for onset of hypertension and hyperlipidemia are important as these can significantly increase the risk of vascular disease.
Hemoglobin A1c (HgbA1c) is a measure of glycosylated hemoglobin and is considered a marker of long-term glycemic control. HgbA1c correlates with the average blood glucose over a 3-month span, or the life span of a red blood cell. An HgbA1c of 6% indicates average blood glucose less than 120 mg/dl. An HgbA1c of 8% correlates with an average blood glucose of 180 mg/dl. An HgbA1c of 10% corresponds to average blood glucose of 240 mg/dl [5].
- 8.
What are complications associated with DM?
DM is a complex disease that involves all organ systems with numerous wide-ranging complications. A summary of these are below.
Cardiovascular Disease
Chronic DM can lead to significant complications in both the micro- and macrovasculature. Diabetics are at a significantly increased risk of developing hypertension, coronary artery disease, peripheral artery disease, systolic and diastolic dysfunction, and congestive heart failure [5]. Cardiovascular pathology has been shown to be the cause of death in 80% of diabetic patients [5]. Numerous studies have shown that diabetics have a two- to threefold increase of perioperative cardiovascular morbidity and mortality compared to nondiabetics [10]. The American College of Cardiology and the American Heart Association guidelines for preoperative cardiac assessment classify diabetics as a minimum of intermediate risk if undergoing noncardiac surgery [5, 11]. Autonomic neuropathy in patients with DM can greatly impair the sensation of ischemic cardiac pain and can result in an unrecognized cardiac event or silent myocardial infarction. The Framingham study found that 39% of diabetic patients had an unrecognized myocardial infarction compared to 22% in nondiabetics [5, 12].
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