Diabetes occurs when the pancreas can't secrete insulin (type 1) or when the body's cells can't recognize insulin (type 2). Statistical spikes in type 2 diabetes incidence are directly linked to increased levels of obesity associated with unbalanced dietary patterns and decreased levels of physical activity. Inhalation of industrial air pollution and tobacco smoke has also been implicated as a cause of insulin resistance. In this article, I'll review the consequences of untreated and poorly-treated type 2 diabetes, lab values, medications and treatments, and critical patient teaching points.
Type 1 diabetes
Type 1 diabetes affects 5% of patients with diabetes. In this type, a genetic defect in the immune system causes the body to produce antibodies against its own insulin-producing pancreatic beta cells. Beta cell mass diminishes to the point where the patient must be supplied with exogenous insulin. The onset of this disease is usually between ages 10 and 12 in girls and between ages 12 and 14 in boys. In one-third of patients, type 1 diabetes appears before age 20, and most cases develop before age 30. There's also a delayed form in which pancreatic antibodies appear in adulthood.
Environmental factors associated with the onset of type 1 diabetes are rubella, coxsackie, and other viral infections. Type 1 diabetes may be accompanied by another autoimmune disorder, such as hypothyroidism, pernicious anemia, or alopecia. The type 1 patient is subject to rapid increases in blood glucose, with development of ketoacidosis.
Type 2 diabetes
Type 2 diabetes affects 95% of patients with diabetes and exists when insulin resistance causes extracellular glucose levels to rise above 126 mg/dL (after 8 hours of fasting). Patients at particular risk are those who exceed the recommended weight-for-height tables, eat poorly-balanced meals, and lead sedentary lifestyles. Pregnant women may also develop diabetes (see Warning! Gestational diabetes). Hypertension, tobacco smoking, and a family history of type 2 diabetes are considered risk factors as well.
Excess glucose in the circulation can cause oxidant damage to cell surfaces and metabolic derangements within the cell itself. This causes destruction of cells and, eventually, tissues. Even a slight upward trend in blood glucose is associated with an increased risk of damage to nerves and blood vessels throughout the body.
A healthy human body will keep its blood glucose level within a narrow range despite the level of food intake. In prediabetes, various cells within the body, such as in the liver, fat, and muscle, develop a resistance to the action of insulin. Glucose is less able to be metabolized into cells and accumulates in the extracellular circulation. The pancreatic beta cells, in an effort to compensate, secrete increased amounts of insulin, which increases insulin levels in the circulation. Over a period of approximately 7 years, the beta cells gradually burn out and the body's blood glucose levels rise. Development of insulin resistance is associated with obesity, lack of physical activity, and smoking. Forty-one million people in the United States have prediabetes; 25% of these individuals will develop type 2 diabetes within 10 years.
Immediate nursing interventions for the patient with prediabetes are to recommend healthier eating habits, cessation of smoking, and increased physical activity to reduce body weight by 1 to 2 lb/week. Skeletal muscle handles 80% of the body's glucose disposal. Exercise can thus intensify the action of insulin and lower blood glucose. Such lifestyle changes can significantly delay the onset of type 2 diabetes.
The damage done
Osmotic diuresis occurs in response to high blood glucose levels as the kidneys struggle to expel excess glucose. Here we see the classic symptoms of polyuria and polydipsia. If the body can't metabolize glucose into cells by conventional means, it will attempt to convert fat stores into glucose. However, this causes a release of fatty acids (ketones) into the bloodstream and the pH of the blood drops.
Acidic blood processing through the brain can put the patient into a coma-like state known as diabetic ketoacidosis (DKA). The symptoms of DKA may be mild early on, but can rapidly worsen. The patient may begin with nausea, vomiting, abdominal pain, and weakness. As dehydration worsens, the pulse rises and the BP drops. The lungs convert the ketones into acetone and exhale the classic fruity-odor breath. Respirations become deeper and labored as the body attempts to raise the pH. Some patients may still have enough insulin in reserve to avoid DKA, but will gradually develop hyperosmolar hyperglycemic nonketotic coma, with severe dehydration.
Sensory nerves are especially sensitive to the effects of surplus extracellular glucose because of their unique morphology. One of the earliest symptoms of diabetes is a subtle numbness and tingling of the distal extremities, which results from depletion of the myelin sheath that regulates sensory nerve conduction. This patient will be at an increased risk for falls and foot ulcers due to decreased reflexes and a decreased sense of pressure, temperature, and vibration. These symptoms are worse when blood glucose is poorly controlled.
An excess amount of insulin in the circulation (hyperinsulinemia) is associated with coronary and carotid artery disease and hypertension. Oxidation of low-density lipoprotein (LDL) cholesterol causes vascular plaque formation. Glucose binds with collagen, causing stiffening of the vascular walls. Cellular oxidation drops production of nitric oxide, a vasodilator, and hypertension results. Chronic hypertension intensifies vascular complications and places the patient at greater risk for renal failure.
Diabetes isn't without its effects on the gastrointestinal (GI) tract. High blood glucose levels trigger the release of pancreatic amylase, which slows gastric emptying. Neuropathy of the nerves supplying the stomach can also contribute to this process. The patient may experience nausea, vomiting, bloating, or a feeling of early satiety when eating. Neuropathy can affect bladder functioning, with a decreased sensation of bladder filling. And glucose in the urine puts the patient at higher risk for urinary tract infections.
High blood glucose delays the function of white blood cells, making the patient more prone to infection. For example, patients with diabetes are at nearly twice the risk for developing periodontal disease. High glucose levels in saliva combine with plaque to form an acidic environment conducive to dental caries.
Neurovascular disease in the retina can occur as a result of high blood glucose levels. The patient may at first experience blurred vision. In response to chronic vascular damage, the retina produces new vessels. However, the new vessels are fragile and cause bleeding, scarring, and retinal detachment. Diabetes is the most common cause of adult blindness.
Nephropathy develops insidiously over a period of years. The increased glomerular filtration rate from chronic purging of glucose brings on renal cell hypertrophy and kidney enlargement. Damage to the renal filtration system begins with microalbuminuria, moving to frank proteinuria and then end-stage renal disease.
A randomly drawn plasma glucose level of greater than 200 mg/dL suggests the presence of diabetes. More specifically, diabetes is present if an individual's blood glucose level is greater than 126 mg/dL after 8 hours of fasting. Prediabetes is present if an individual's fasting blood glucose level is between 100 and 125 mg/dL. The American Diabetes Association recommends an HbA1C value of less than 6.5%; a value of greater than 6.5% indicates diabetes (see What's HbAlC?).
Diabetes is also associated with high triglyceride levels (greater than 250 mg/dL); triglycerides should be reduced to less than 150 mg/dL. Patients with diabetes often have high-density lipoprotein cholesterol levels below 35 mg/dL; target levels for men should be greater than 45 mg/dL and for women, greater than 55 mg/dL. The target level for LDL cholesterol in patients with diabetes is less than 70 mg/dL. High urine albumin (greater than 20 mcg/minute) can be a marker of early renal disease in patients with diabetes.
The march of the treatments
There are treatments that address all manifestations of diabetes. First and foremost is control of blood glucose levels, which can delay the onset of severe complications. Maintaining good finger-stick and food intake records helps keep glucose levels under control. Balanced nutrition must be practiced to lower triglycerides, LDL, HbA1C levels, and body weight. An HbA1C blood draw should be performed at least twice a year. BP must be kept under control, smoking should be discontinued, and exercise should be encouraged (see “Exercise and diabetes—Small Steps to Success”). Remember that exercise increases caloric needs and has a 24-hour residual effect on blood glucose levels. Blood glucose must be checked before and after exercise to avoid severe drops in glucose levels. Exercise shouldn't be done if the patient's blood glucose level is less than 80 mg/dL or greater than 240 mg/dL.
Feet should be inspected daily for any break in the skin using a mirror and/or another person's assistance. Shoes and socks should be worn regularly to avoid lacerations. Feet should be washed with mild soap in lukewarm water and dried well, especially between the toes. Toenails should be trimmed straight across. Any foot ulcer should be treated aggressively to avoid infection and the possibility of amputation. Special shoes, casts, splints, and thick dressings have been developed to promote healing and reduce friction on the foot. Antibiotic treatment of infection is done cautiously; topical antibiotics are preferred. Any pain from neuropathy in the distal extremities can be treated with tricyclic antidepressants, antiepileptic drugs, or capsaicin cream.
Regular inspection of the oral cavity for edema, redness, bleeding, loose teeth, and thrush should be done to prevent periodontal infection. An active infection causes the release of cytokines and stress hormones, which can increase insulin resistance. Antimicrobial rinses can be used, as well as nystatin to treat oral thrush.
Earlier treatment with insulin has been recommended for tighter blood glucose control to delay the onset of renal failure. Hypertension should also be addressed with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers. Antihypertensive medications should be tried early in the course of renal failure because these aren't tolerated as well when renal failure is more advanced. The patient will need to restrict protein intake to less than 0.8 g/kg/day at the onset of renal failure and to less than 0.6 g/kg/day if renal failure is advanced.
During insulin resistance, a false signal is sent to the liver that the body needs more glucose. The liver then mobilizes its glycogen supply and spills more glucose into a circulation already saturated with extracellular glucose. The biguanides, such as metformin, are given to reduce the liver's glucose production. The dosage of metformin is increased cautiously due to GI adverse reactions such as diarrhea. Contraindications include renal dysfunction, congestive heart failure (CHF), DKA, and hypoxemia.
Sulfonylureas, such as glipizide and glyburide, stimulate the pancreatic beta cells to secrete insulin.
Thiazolidinediones, such as rosiglitazone and pioglitazone, represent an attempt to reverse insulin resistance. These drugs mobilize a protein to the surface of muscle and fat cells that allows recognition of insulin and influx of glucose. However, they're idiopathically associated with fluid retention and peripheral edema. Thiazolidinediones aren't recommended for CHF patients. This is especially true when they're given in combination. Recent warnings have been issued that link rosiglitazone with an increased risk of myocardial infarction.
According to the CDC, 16% of patients with diabetes are prescribed insulin therapy and 12% are prescribed combination therapy. If the patient's fasting blood glucose level exceeds 350 mg/dL or the HbA1C exceeds 6.5%, exogenous insulin must be initiated. Insulin combined with a sulfonylurea gives the patient a better chance of getting the HbA1C below 6.5%. Most patients with type 2 diabetes will eventually need both basal and bolus insulins.
Bolus insulins are short- and rapid-acting analogs given to control postmeal spikes in blood glucose. Subcutaneous short-acting regular insulin takes effect in 30 minutes and peaks in 2 to 5 hours. The patient's finger stick will read most accurately 4 hours after the dosage. Regular insulin is best suited to treat a more slowly absorbed fat/protein meal. The beta chain of the human insulin molecule has been reengineered to yield the rapid-acting aspart analog, which takes effect in 15 minutes, peaks in 45 minutes, and tapers off after 90 minutes. Subcutaneous insulin aspart provides better control of a quickly absorbed, high-carbohydrate meal. The finger stick will read most accurately 2 hours after the dosage.
Basal insulins are the intermediate- and long-acting analogs that provide 50% of the daily insulin requirement. They're usually administered at bedtime, or twice a day (at breakfast and bedtime). Subcutaneous intermediate-acting insulin peaks in 3 to 6 hours and tapers off in less than 16 hours. The alpha and beta chains of the human insulin molecule have been reengineered to create the less-soluble, long-acting glargine analog, which provides 24-hour coverage. The abdominal route provides the most rapid and consistent dosage. Beta-blocking medications potentiate the action of insulin. Steroids, lithium, nifedipine, and oral contraceptives antagonize insulin.
Covering the bases
Basic diabetes teaching leads to better patient compliance. Because so much of diabetes care is dependent on self-care, assess the patient's ability to access and prepare medications, correctly administer insulin, and correctly respond to episodes of hypo- or hyperglycemia. Give the patient printed material, including a written follow-up plan and available education classes and community services. Tell the patient about the availability of assistive devices such as drug organizers and voice-prompting glucometers. Patients with diabetes should be aware that they're at increased risk for cardiovascular complications and that tight glycemic control lessens the rate of microvascular symptoms and improves LDL and triglyceride levels.
Balanced nutrition and weight control play a major role in diabetes teaching (see Warning! Older patients and diabetes). A patient trying to lose weight should reduce caloric intake by 500 to 1,000 kcal/day. Nonpregnant women need at least 1,000 to 1,200 kcals/day; men need 1,200 to 1,600 kcals/day. Help patients fashion a flexible diet based on their lifestyle, motivation level, foods they usually consume, and medication schedule. A sensible diet for patients with diabetes is low in fat, low in sugar, sufficient in fiber, and smaller in food portions. Remember that carbohydrates are the primary nutrient that raises blood glucose levels (see “The Great Carbohydrate Debate”).
Meals must be timed with subcutaneous insulin doses. Snacks are added to prevent hypoglycemia. The patient should estimate total caloric need and then divide this evenly over the day. Meals should be spaced at least 3 hours apart. Having meals at set times reduces fluctuation in glucose levels.
Finger sticks are a key to diabetes treatment, although capillary blood specimens aren't as accurate as plasma draws. The forearm and thigh are possible alternative sites for testing, but rapid changes in glucose levels are best detected in a fingertip sample. Glucometer user error accounts for most of the variation in readings. Artificially low readings are often caused by an insufficient amount of blood on the test strip or drying out of strips from exposure to air. Patients using insulin should check their blood glucose level at least four times a day (see Do the math). Patients using multiple insulins should perform finger sticks before and after meals.
Controlling the future
With type 2 diabetes, an ounce of prevention is worth a pound of cure. Coach patients who are still in the prediabetes phase that exercise and proper diet can prevent or significantly delay the onset of this disease. And help patients with type 2 diabetes envision a future of tight glycemic control to avoid cardiovascular, vision, and neuropathic complications.
Warning! Gestational diabetes
The stress of pregnancy in an otherwise healthy woman can induce insulin resistance known as gestational diabetes. A woman is at higher risk for gestational diabetes if she's older than age 25, has a family history of diabetes, has a history of poor obstetric outcomes, or has delivered a baby weighing more than 9 lb. Treatment with insulin may be required.
Pregnant patients with diabetes need to check their blood glucose levels before meals and 1 hour postmeal. If the result is high, the urine should also be dipstick tested for ketones. However, the first morning urine specimen can yield a false-positive result. Tight blood glucose control reduces the possibility of birth defects.
Glucose binds irreversibly to the hemoglobin portion of red blood cells to form glycohemoblogin. HbA1C makes up 80% of this complex. The HbA1C value measures the patient's average postmeal plasma glucose over the previous 2- to 3-month period. Glucose, however, can bind to either the alpha or beta chain of the Hgb molecule, which can cause a measurement artifact depending on the lab method used. Altered protein levels secondary to liver disease can also make the test less accurate. Every percentage point decrease in HbA1C equals a 40% reduced risk of microvascular complications. It's advisable to keep the HbA1C under 6.5%.
Do the math
In adult patients with diabetes:
1,500 ÷ total daily insulin dosage = expected mg/dL blood glucose decrease/unit of insulin
Warning! Older patients and diabetes
Blood glucose control should be less aggressive for the older patient with diabetes. Any drop in blood glucose from overtreatment can bring on catecholamine secretion, which can task a weak cardiovascular system. Glucose levels should be moderately controlled to prevent the development of immediate symptoms (such as blurred vision). Any development of a hyperglycemic, hyperosmolar state in an older patient with diabetes can be serious.
Carbohydrate intake should be consistent to avoid abrupt changes in insulin dosages. However, because of limited resources and reduced mobility, many older patients don't have access to a variety of foods and tend to consume lower levels of calories, iron, calcium, and vitamins A and C. Weight gain, not loss, may be the goal for some.
Physical exercise goals should be more moderate if the patient has active arthritis or a history of cardiovascular disease. Well-fitting shoes are necessary with exercise. Patients must check their feet after exercise for calluses and ulcers and may need help doing so. Despite a blunted sense of thirst, adequate hydration is needed with exercise to prevent episodes of orthostatic hypotension. Distal sensory neuropathy may place older patients with diabetes at higher risk for falls.
Learn more about it
Acharya D, Falik R. Cardiovascular effects of thiazolidinediones: a review of the literature. South Med J. 2009;102(1):51-56.
Albright A. The public health approach to diabetes. Am J Nurs. 2007;107(6 suppl):39-42.
Anselmino M, Malmberg K, Ohrvik J, Rydén L, Euro Heart Survey Investigators. Evidence-based medication and revascularization: powerful tools in the management of patients with diabetes and coronary artery disease: a report from the Euro Heart Survey on diabetes and the heart. Eur J Cardiovasc Prev Rehabil. 2008;15(2):216-223.
Buyken AE, von Eckardstein A, Schulte H, Cullen P, Assmann G. Type 2 diabetes mellitus and risk of coronary heart disease: results of the 10-year follow-up of the PROCAM study. Eur J Cardiovasc Prev Rehabil. 2007;14(2):230-236.
Chiverton P, Lindley P, Tortoretti DM, Plum KC. Well-balanced: 8 steps to wellness for adults with mental illness and diabetes. J Psychosoc Nurs Ment Health Surv. 2007;45(11):46-55.
Colberg S. Enhancing insulin action with physical activity to prevent and control diabetes. Health Fitness J. 2008;12(2):16-21.
Gattullo B, Kumar C. Get a leg up on diabetic peripheral neuropathy. Nursing made Incredibly Easy! 2009;7(4):24-30.
Haas L. Functional decline in older adults with diabetes. Am J Nurs. 2007;107(6 suppl):50-54.
Hur NW, Kim HC, Nam CM, Jee SH, Lee HC, Suh I. Smoking cessation and risk of type 2 diabetes mellitus: Korea Medical Insurance Corporation Study. Eur J Cardiovasc Prev Rehabil. 2007;14(2):244-249.
McCarron K, Riebel T. Spotlight on type 2 diabetes. Nursing made Incredibly Easy! 2008;6(5):44-53.
Peeples M, Seley JJ. Diabetes care: the need for change. Am J Nurs. 2007;107(6 suppl):13-19.
Raef H, Khairi S. Self-monitoring of blood glucose in the management of diabetes mellitus. Point of Care. 2008;7(4):258-260.
Susla GM. Implementing glucose control protocols in critically ill patients. AACN Adv Crit Care. 2007;18(1):5-9.
Wattana C, Srisophan W, Pothiban L, Upchurch S. Effects of a diabetes self-management program on glycemic control, coronary heart disease risk, and quality of life among Thai patients with type 2 diabetes. Nurs Health Sci. 2007;9(2):135-141.