CHAPTER 64 Care of Patients with Diabetes Mellitus

Benefits of Exercise

Appropriate exercise results in better blood glucose regulation and reduced insulin requirements for patients with type 1 DM. Exercise also increases insulin sensitivity, which enhances cell uptake of glucose and promotes weight loss. Regular exercise decreases risk for CVD. It decreases most blood lipid levels and increases high-density lipoproteins (HDLs). Exercise decreases blood pressure and improves cardiovascular function. Regular vigorous physical activity prevents or delays type 2 DM by reducing body weight, insulin resistance, and glucose intolerance.

Laboratory Assessment

Diabetes can be diagnosed by assessing blood glucose levels. The diagnosis of diabetes mellitus includes elevated glycosylated hemoglobin levels. Glycosylated hemoglobin (A1C) is a standardized test that measures how much glucose permanently attaches to the hemoglobin molecule. Because glucose binds to many proteins, including hemoglobin, through a process called glycosylation, the higher the blood glucose level is over time, the more glycosylated hemoglobin becomes. The ADA defines A1C levels greater than 6.5% as diagnostic of DM. Fasting plasma glucose (FPG) (fasting blood glucose [FBG]) is used to diagnose diabetes in nonpregnant adults. The patient should have no caloric intake for at least 8 hours (water is permitted). The blood sample needs to be obtained before insulin or oral antidiabetic agents have been taken. A diagnosis of diabetes is made with two separate test results greater than 126 mg/dL (7 mmol/L). Random or casual plasma (blood) glucose greater than 200 mg/dL (7.0 mmol/L) is used to diagnose diabetes in patients with severe classic hyperglycemia or hyperglycemic crisis. Oral glucose tolerance testing (OGTT) is the most sensitive test for the diagnosis of DM. It is often used to diagnose gestational diabetes mellitus (GDM) during pregnancy and is not routine. Type 1 DM results from autoimmune destruction of the beta cells of the pancreas. Markers of this destruction include islet cell autoantibodies (ICAs), autoantibodies to insulin, and autoantibodies to glutamic acid decarboxylase (GAD65). ICAs are present in 85% to 90% of people with new-onset type 1 DM. Measurement of C-peptide levels indicates beta secretory function of the pancreas. Low to absent C-peptide levels diagnose type 1 DM, as well as late-stage type 2 DM when the ability of the pancreas to secrete insulin is severely impaired.

Meal Planning Strategies 1

Carbohydrate (CHO) counting is a simple approach to nutrition and meal planning that uses label information of the nutrition content of packaged food items. CHO counting focuses on the nutrient that has the greatest impact on these levels. It uses total grams of carbohydrate, regardless of the food source. Patients using intensive insulin or pump therapies can use CHO counting to determine insulin coverage. After the amount of insulin needed to cover the usual meal is determined, insulin may be added or subtracted for changes in carbohydrate intake. An initial formula of 1 unit of rapid-acting insulin for each 15 g of carbohydrate provides flexibility to meal plans. People at high risk for type 2 diabetes are encouraged to achieve moderate weight loss (7% total body weight), participate in regular physical activity (150 minutes per week), and reduce caloric and dietary fat intake. These at-risk people are also encouraged to increase fiber intake to at least 14 g per 1000 calories consumed and to eat foods containing whole grains. Special considerations for type 1 diabetes include developing insulin regimens that conform to the patient's preferred meal routines, food preferences, and exercise patterns. Insulin-to-carbohydrate ratios are developed and are used to provide mealtime insulin doses. Blood glucose monitoring before and 2 hours after meals determines whether the insulin-to-carbohydrate ratio is correct. For patients who are on fixed insulin regimens and do not adjust premeal insulin dosages, consistency of timing of meals and the amount of CHO eaten at each meal is important to prevent hypoglycemia.

Chronic Complications of Diabetes

Diabetes mellitus (DM) can lead to health problems and early death because of changes in large blood vessels (macrovascular) and small blood vessels (microvascular) in tissues and organs. Macrovascular complications, including coronary heart disease, cerebrovascular disease, and peripheral vascular disease. Microvascular complications of blood vessel structure and function lead to nephropathy (kidney dysfunction), neuropathy (nerve dysfunction), and retinopathy (vision problems). Causes of these diabetic vascular complications include: • Chronic hyperglycemia thickens basement membranes, which causes organ damage. • Glucose toxicity directly or indirectly affects functional cell integrity. • Chronic ischemia in small blood vessels causes connective tissue hypoxia and microischemia. Chronic high blood glucose levels are the main cause of microvascular complications and allow premature development of macrovascular complications. Other include: smoking, physical inactivity, obesity, hypertension, and high blood fat and cholesterol levels. For every percentage point decrease in A1C (glycosylated hemoglobin A1C), a risk reduction of at least 25% to 30% for kidney and eye complications has been shown

Overview

Diabetes mellitus (DM) resulting in poor glucose regulation is a major public health problem, and its complications, especially hypertension and hyperlipidemia. DM is a leading cause of blindness, end-stage kidney disease, and foot or leg amputations. The complications of DM can be greatly reduced with glycemic (blood glucose) control along with management of hypertension and hyperlipidemia. For all types of diabetes mellitus (DM), the main feature is chronic hyperglycemia (high blood glucose level) resulting from problems with glucose regulation that include reduced insulin secretion or reduced insulin action.

Preventing Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is characterized by uncontrolled hyperglycemia, metabolic acidosis, and increased production of ketones. This condition results from the combination of insulin deficiency and an increase in hormone release that leads to increased liver and kidney glucose production and decreased glucose use in peripheral tissues. These changes increase ketoacid production with resultant ketonemia and metabolic acidosis. DKA occurs most often in patients with type 1 DM but also can occur in those with type 2 DM(e.g., trauma, surgery, infection). Some people with type 2 diabetes have a syndrome known as ketosis-prone diabetes or KPD. The most common precipitating factor for DKA is infection. Death occurs in up to 10% of these cases even with appropriate treatment. Hyperglycemia leads to osmotic diuresis with dehydration and electrolyte loss. Classic manifestations of DKA include polyuria, polydipsia, polyphagia, vomiting, abdominal pain, dehydration, weakness, confusion, shock, and coma. Mental status can vary from total alertness to profound coma. As ketone levels rise, the pH of the blood decreases. Kussmaul respirations (very deep and rapid respirations) cause respiratory alkalosis in an attempt to correct metabolic acidosis by exhaling carbon dioxide. Initial serum sodium levels may be low or normal. Initial potassium levels depend on how long DKA existed before treatment. After therapy starts, serum potassium levels drop quickly.

Diabetic Peripheral Neuropathy(MICRO) 1

Diabetic peripheral neuropathy (DPN) is a progressive deterioration of nerve function that results in loss of sensory perception. Damage to sensory nerve fibers results in either pain or loss of sensation. Damage to motor nerve fibers results in muscle weakness. Damage to nerve fibers in the autonomic nervous system can cause dysfunction in every part of the body. Risk factors: • Hyperglycemia, long duration of DM, hyperlipidemia, low insulin levels • Damaged blood vessels leading to reduced neuronal oxygen and other nutrients • Autoimmune neuronal inflammation • Increased genetic susceptibility to nerve damage • Smoking and alcohol use Hyperglycemia leads to DPN through blood vessel changes and reduced tissue perfusion. Both the axon and its myelin sheath are damaged by reduced blood flow(blocked nerve impulse transmission). Excessive glucose is converted to sorbitol, which collects in nerves and impairs motor nerve conduction. Autonomic nervous system neuropathy leads to problems in cardiovascular, GI, and urinary function.

NANDA-I nursing diagnoses

1. Risk for Injury related to hyperglycemia (NANDA-I) 2. Potential for impaired wound healing related to endocrine and vascular effects of diabetes 3. Risk for Injury related to diabetic neuropathy (NANDA-I) 4. Acute Pain and Chronic Pain related to diabetic neuropathy (NANDA-I) 5. Risk for Injury related to diabetic retinopathy-induced reduced vision (NANDA-I) 6. Potential for kidney disease related to impaired kidney circulation 7. Potential for hypoglycemia 8. Potential for diabetic ketoacidosis 9. Potential for hyperglycemic-hyperosmolar state and coma

Diabetic Peripheral Neuropathy(MICRO) 2

Cardiovascular autonomic neuropathy (CAN) affects sympathetic and parasympathetic nerves to the heart and blood vessels. This problem contributes to left ventricular dysfunction, painless myocardial infarction, and exercise intolerance. Most often, CAN leads to orthostatic hypotension (postural hypotension) and syncope (brief loss of consciousness on standing). These problems result from failure of the heart and arteries to adjust to position changes by increasing heart rate and vascular tone. As a result, blood flow to the brain is interrupted briefly. Increased fall risk!! Common GI problems from diabetic neuropathy include gastroesophageal reflex, delayed gastric emptying and gastric retention, early satiety, heartburn, nausea, vomiting, and anorexia. Sluggish movement of the small intestine can lead to bacterial overgrowth, which causes bloating, gas, and diarrhea. Diarrhea caused by diabetes is chronic, may be severe, and often occurs at night. Constipation, the most common GI problem with DM, is intermittent and may alternate with bouts of diarrhea. Gastroparesis (delay in gastric emptying) is a cause of hypoglycemia. Urinary problems from neuropathy result in incomplete bladder emptying and urine retention, which lead to urinary infection and kidney problems. Manifestations include frequency, urgency, and incontinence.

Psychosocial Preparation

Certain events surrounding diabetes are predictable. Taking an insulin injection and not eating for several hours causes hypoglycemia. Poorly controlled diabetes leads to complications and premature death. Tight control of blood glucose levels prevents complications. Mastery of blood glucose monitoring helps the patient feel that he or she has control over the disease. Knowing the effects of extra activities, extra food, or extra insulin is helpful in learning to adjust the regimen. Success in injecting insulin provides concrete evidence that he or she can master the disease. Teach by breaking a task into small, achievable units to ensure mastery. For example, a patient may begin learning how to inject insulin by first obtaining an accurate dose.

Incidence and Prevalence

>57 million American adults have prediabetes, defined as impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) or an A1C level between 5.5% and 6.0%. IFG (fasting blood glucose levels of 100 mg/dL [5.6 mmol/L] to 125 mg/dL [6.9 mmol/L]) and IGT (2-hr oral glucose tolerance values of 140 mg/dL [7.8 mmol/L] to 199 mg/dL [11.0 mmol/L]) are considered risk factors for diabetes and CVD. IFG and IGT are associated with obesity (especially abdominal or central obesity), dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension. Almost one third of the total U.S. population are affected by diabetes. About 90% of people with diabetes have type 2. It is more common among men. Prevalence of obesity rising in North America, diabetes will become even more common.

Type 2 Diabetes and Metabolic Syndrome

Combo of insulin resistance and decreased beta-cell secretion of insulin is type 2 DM. Insulin resistance (a reduced cell response to insulin) develops from obesity and physical inactivity. It occurs before the onset of type 2 DM and often is accompanied by the cardiovascular risk factors of hyperlipidemia, hypertension, and increased clot formation. Most patients with type 2 DM are obese. Metabolic syndrome is the simultaneous presence of metabolic factors known to increase risk for developing type 2 DM and cardiovascular disease. Features of the syndrome include: • Abdominal obesity: waist circumference of 40 inches (100 cm) or more for men and 35 inches (88 cm) or more for women • Hyperglycemia: fasting blood glucose level of 100 mg/dL or more or on drug treatment for elevated glucose • Abnormal A1C: between 5.5% and 6.0% • Hypertension: systolic BP of 130 mm Hg or more or diastolic BP of 85 mm Hg or more or on drug treatment for hypertension • Hyperlipidemia: triglyceride level of 150 mg/dL or more or on drug treatment for elevated triglycerides; high-density lipoprotein (HDL) cholesterol less than 40 mg/dL for men or less than 50 mg/dL for women

History

Age is important because type 2 diabetes mellitus (DM) is more common in older patients, especially among African Americans and Mexican Americans. Ask women how large their children were at birth, because many women who develop type 2 DM had gestational diabetes mellitus (GDM) or glucose intolerance during pregnancy. Assessing weight and weight change is important, because excess weight and obesity are risk factors for type 2 DM. With type 1 DM often has weight loss with increased appetite during the weeks before diagnosis. For both types of DM, patients usually have fatigue, polyuria, and polydipsia. Ask about recent major or minor infections. In particular, ask women about frequent vaginal yeast infections. Ask all patients whether they have noticed that small skin injuries become infected more easily or take longer to heal. Also ask whether they have noticed any changes in vision or touch.

Drug Alert

Albiglutide (Tanzeum) is only administered once per week, not daily like other incretin mimetics.

Drug Alert

All four DPP-4 inhibitors and the incretin mimetic liraglutide are associated with an increased risk for pancreatitis. Warn patients taking these drugs to immediately report these manifestations to the health care provider: jaundice; sudden onset of intense abdominal pain that radiates to the back, left flank, or left shoulder; or gray-blue discoloration of the abdomen or periumbilical area.

Preventing Injury from Hyperglycemia: Antidiabetic Drugs 2

Alpha-glucosidase inhibitors prevent after-meal hyperglycemia by delaying absorption of carbohydrate from the small intestine. These drugs inhibit enzymes in the intestinal tract. These drugs do not cause hypoglycemia unless given with sulfonylureas or insulin. Incretin mimetics work like the natural "gut" hormones - glucagon-like peptide-1(GLP-1) and glucose-dependent insulinotropic polypeptide(GIP)—that are released by the intestine in response to food intake and act with insulin to perform glucose regulation. Drugs in this class include the GLP-1 agonists exenatide (Byetta), exenatide extended-release (Bydureon), and the glucagon-like peptide-1(GLP-1) agonists liraglutide (Victoza) and albiglutide (Tanzeum). Used in addition to diet and exercise to improve glycemic control in adults with type 2 DM. Liraglutide carries a black box warning for thyroid tumors. The natural incretins GLP and GIP are rapidly metabolized and inactivated by the enzyme DPP-4 (dipeptidyl peptidase 4). DPP-4 inhibitors work by reducing the inactivation of the incretin hormones so that they remain available for blood glucose regulation. The four DPP-4 inhibitors approved for use in patients with type 2 DM are sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), and alogliptin (Nesina).

Preventing Injury from Hyperglycemia: Antidiabetic Drugs 3

Amylin analogs are drugs similar to amylin, a naturally occurring hormone produced by pancreatic beta cells that works with and is co-secreted with insulin in response to blood glucose elevation. Pramlintide (Symlin), an analog of amylin, is approved for patients with either type 1 or type 2 DM treated with insulin. It works by three mechanisms: delaying gastric emptying; reducing after-meal blood glucose levels; and triggering satiety (in the brain). Sodium-glucose co-transport inhibitors lower blood glucose levels by preventing kidney reabsorption of the glucose that was filtered from the blood into the urine. Filtered glucose is excreted in the urine rather than moved back into the blood. Drugs include canagliflozin (Invokana) and dapagliflozin (Farxiga). Combination agents combine drugs with different mechanisms of action. Glucovance, for example, combines glyburide with metformin. Combining drugs with different mechanisms of action may be highly effective in maintaining desired blood glucose control. Some patients may need a combination of oral agents and insulin.

Preventing Injury from Peripheral Neuropathy: Interventions 1

Foot injury is the most common complication of diabetes leading to hospitalization. Once a failure of tissue integrity has occurred and an ulcer has developed, there is an increased risk for wound progression that will eventually lead to amputation. Almost all lower extremity amputations are preceded by foot ulcers. The 5-year mortality rate after leg or foot amputation ranges from 39% to 67%. Neuropathy is the main factor for development of a diabetic ulcer, and an inadequate vascular supply is the main cause of poor healing. Motor neuropathy damages the nerves of foot muscles, resulting in foot deformities. These deformities create pressure points that gradually cause reduced tissue integrity with skin breakdown and ulceration. Thinning or shifting of the fat pad under the metatarsal heads decreases cushioning and increases areas of pressure. In claw toe deformity, toes are hyperextended and increase pressure on the metatarsal heads ("ball" of the foot). These changes predispose the patient to callus formation, ulceration, and infection. The Charcot foot is a type of diabetic foot deformity with many abnormalities, often including a hallux valgus (turning inward of the great toe) (Fig. 64-6). The foot is warm, swollen, and painful. Walking collapses the arch, shortens the foot, and gives the sole of the foot a "rocker bottom" shape.

Critical Rescue

For patients being managed for hyperglycemic-hyperosmolar state, immediately report changes in the level of consciousness; changes in pupil size, shape, or reaction; or seizures.

Complications of Whole-Pancreas Transplantation 2

In acute rejection, decreased kidney function is indicated by increased serum creatinine, decreased urine output, hypertension, increased weight, graft tenderness, and fever. Proteinuria is often the first indicator of chronic graft rejection. Check for increased blood amylase, lipase, or glucose; decreased urine amylase; graft tenderness; hyperglycemia; and fever. It is especially important to assess for infection and start appropriate therapy. Fever can indicate both infection and rejection. Monitor for side effects of the anti-rejection drugs. Cyclosporine (Neoral) is toxic to the kidney. Indications of toxicity are elevated creatinine and decreased urine output. Monitor WBC counts daily, because azathioprine (Imuran) can suppress bone marrow function. Common side effects of tacrolimus (Prograf) are hypertension, kidney toxicity, neurotoxicity, GI toxicity, and glucose intolerance. Prednisone has many side effects, including elevated blood glucose levels.

Complications of Whole-Pancreas Transplantation 1

Early removal of IV and intra-arterial lines, use of sterile technique with dressing changes and catheter irrigations, strict handwashing by all health care personnel, and good pulmonary hygiene help prevent infection. Complications immediately after surgery include thrombosis, pancreatitis, anastomosis leak with infection, and rejection of the transplanted pancreas. Pancreatic blood vessel thrombosis occurs in about 30% of patients. Observe for and report any sudden drop in urine amylase levels, rapid increases in blood glucose, gross hematuria (bloody urine), and tenderness or pain in the graft area (iliac fossa). Pancreatitis in the transplanted organ occurs to some degree in all patients after surgery. Report elevations in serum amylase that persist after 48 to 96 hrs. The most serious complication of enteric-drained pancreas transplantation is leaking and infection with intra-abdominal abscess formation. Observe for and report elevation in temperature, abdominal discomfort, and elevation in WBCs. Bladder-drained pancreas transplantation has a lower rate of intra-abdominal abscess formation. However, drainage of bicarbonate-rich fluid with pancreatic enzymes into the urinary bladder can cause urinary tract infections, cystitis, urethritis, and balanitis. Metabolic acidosis occurs from the loss of large amounts of alkaline pancreatic secretions.

In-Depth Education 1

Educational sessions with patient and family are needed to "patientize" the diabetes regimen for their needs and abilities. He or she should be able to discuss the action of insulin in the body and the effects of insulin deficiency. He or she should also be able to explain the effects of diet, drugs, and activity on blood glucose. Provide education about the manifestations of hypoglycemia along with the prescribed treatment options if the patient takes any drugs that will lower blood glucose levels. Educate patients and their families about common causes of hypoglycemia such as changes in drug regimen, increase in physical activity, and delayed or missed meals. Review manifestations of hypoglycemia at each visit. Advise patients to check their blood glucose levels before driving and make sure they have easy-to-reach snacks or fast-acting sugars with them at all times. Encourage them to always wear a medical ID tag or bracelet and to contact their health care provider if they experience low blood glucose levels more than twice a week. If the patient takes an oral antidiabetic drug, ask him or her to identify the drugs and describe the prescribed schedule. Determine if the patient is able to administer insulin accurately by having him or her "teach back" injection techniques.

Preventing Injury from Hyperglycemia: Antidiabetic Drugs 1

Insulin secretagogues stimulate insulin release from pancreatic beta cells and are used for patients who are still able to produce insulin. Sulfonylurea agents lower fasting blood glucose levels by triggering the release of insulin from beta cells. Many drugs interact with sulfonylureas. Meglitinide analogs are classified as insulin secretagogues and have actions and adverse effects similar to those of sulfonylureas. They tend to increase meal-related insulin secretion. Metformin (Glucophage), a biguanide, does not increase insulin secretion. It decreases liver glucose production and decreases intestinal absorption of glucose. It also improves insulin sensitivity by increasing peripheral glucose uptake and utilization. Thiazolidinediones (TZDs), an insulin sensitizer, increase cellular utilization of glucose, which lowers blood glucose levels. Both of the TZDs—rosiglitazone (Avandia) and pioglitazone (Actos)—are associated with an increased risk for heart-related deaths, bone fracture, and macular edema. The Food and Drug Administration (FDA) has issued a black box warning for patient's with a CVD.

Preventing Injury from Peripheral Neuropathy: Footwear

It is best to be fitted by an experienced shoe fitter, such as a certified podiatrist. The shoe should be 1/2 to 5/8 inch longer than the longest toe. Heels should be less than 2 inches high. Shoes that are too tight damage tissue. Instruct the patient to change shoes by midday and again in the evening. Socks or stockings need to fit properly and be appropriate for the planned activity. Socks should feel soft and have no thick seams, creases, or holes. They should pad the foot and absorb excess moisture. Teach patients to avoid tight stockings or those that have constricting bands. Patients with toe deformities should buy custom shoes with high, wide toe boxes and extra depth. Those with severely deformed feet, such as Charcot feet, need specially molded shoes. All new shoes need a long break-in period with frequent inspection for irritation or blistering.

Assessing Physical, Cognitive, and Emotional Limitations

It is important to measure the patient's ability to read and understand written materials and conduct math calculations. It is important to match the literacy level of materials to the literacy level of the patient. Simplify the information you present by replacing technical terms with plain language (words people use in everyday conversation). Many with type 2 diabetes have age-related visual problems made worse by blurred vision caused by fluctuating blood glucose levels. Assess manual dexterity for any physical limitations that may alter the teaching plan. A hand injury, tremors, or severe arthritis often leads to dosing errors with a standard syringe and may require a change in insulin preparation. Visual learners think in terms of pictures and remember things best by seeing something written or by seeing visual aids. Auditory learners learn best through hearing. Kinesthetic or tactile learners learn best through touching, feeling, and experiencing what they are trying to learn. Tactile learners remember best by writing or physically manipulating the equipment. Successful diabetes self-management education uses all three learning styles.

Blood Glucose Control in Hospitalized Patients 1

In patients without a previous diagnosis of diabetes, elevated blood glucose is often "stress hyperglycemia." Hyperglycemia may result from decline in basic level of glucose regulation caused by illness, decreased physical activity, withholding of antidiabetic drugs, use of drugs that cause hyperglycemia such as corticosteroids, and initiation of tube feedings or parenteral nutrition. Hyperglycemia among medical-surgical patients is linked with higher infection rates, longer hospital stays, increased need for intensive care, and greater mortality. Admission glucose levels greater than 198 mg/dL (10.9 mmol/L) are associated with greater risk for mortality and complications. Hypoglycemia, defined as blood glucose values lower than 40 mg/dL (2.2 mmol/L), is an independent risk factor for mortality. Current American Association of Clinical Endocrinologists (AACE) and ADA Core Measures recommend treatment protocols that maintain blood glucose levels between 140 and 180 mg/dL (7.8 and 10.0 mmol/L) for critically the ill. Majority of non-critically ill patients, premeal glucose targets should be lower than 140 mg/dL (7.8 mmol/L) with random blood glucose values less than 180 mg/dL (10.0 mmol/L). To prevent hypoglycemia, insulin regimens should be reviewed if blood glucose levels fall below 100 mg/dL (5.6 mmol/L) and should be modified when blood glucose levels are less than 70 mg/dL (3.9 mmol/L).

Surgical Management

Include a pancreas transplantation. When successful, this procedure eliminates the need for insulin injections, blood glucose monitoring, and many dietary restrictions. It can eliminate the acute complications related to blood glucose control but is only partially successful in reversing long-term diabetes complications. Transplantation requires lifelong drug therapy to prevent graft rejection. Pancreas transplantation is considered in patients with diabetes and end-stage kidney disease who have had or plan to have a kidney transplant. Normal blood glucose levels after pancreas transplantation improve kidney graft survival. Pancreas graft survival is better when performed at the time of the kidney transplant.

Preventing Injury from Hyperglycemia: Drug Therapy

Indicated when a patient with type 2 DM does not achieve blood glucose control with lifestyle modifications. Patients with type 1 DM require insulin therapy. Drugs are started at the lowest effective dose and increased every 1 to 2 weeks. If the maximum dosage of one agent does not control blood glucose levels, a second agent with a different mechanism of action may be added. Insulin therapy is indicated for the patient with type 2 DM when blood glucose cannot be controlled with the use of two or three different antidiabetic agents. Antidiabetic drugs are not a substitute for dietary modification and exercise.

Factors Influencing Insulin Absorption

Injection site area affects the speed of insulin absorption. Absorption is fastest in the abdomen, and except for a 2-inch radius around the navel, it is the preferred injection site area. Rotating injection site areas prevents lipohypertrophy (increased fat deposits in the skin) and lipoatrophy (loss of fatty tissue, leaving an uneven appearance). Rotation within one anatomic site is preferred. Absorption rate is determined by insulin properties. The longer the duration of action, the more unpredictable is absorption. Larger doses of insulin also prolong the absorption. Factors that increase blood flow from the injection site, such as local application of heat, massage of the area, and exercise of the injected area, increase insulin absorption. Scarred sites often become favorite injection sites because they are less sensitive to pain, but these areas usually slow absorption. Injection depth changes insulin absorption. Usually, injections are made SubCu. IM injection has a faster absorption and is not used for routine. A 45-degree angle is advised for frail older adults and those who are cachexic. Aspiration for blood is not needed. With high body mass index (BMI) levels can use 4 mm or 5 mm needles to inject insulin at a 90-degree angle without pinching. Timing of injection affects blood glucose levels. The interval between premeal injections and eating, known as "lag time," affects blood glucose levels after meals. Insulin lispro, insulin aspart, and insulin glulisine have rapid onsets of action and should be given within 10 minutes before mealtime when blood glucose is in the target range. If hyperglycemia or hypoglycemia is not present, these insulins can be given at any time from 10 minutes before mealtime to just before eating or even immediately after eating. Regular insulin should be given at least 20 to 30 minutes before eating when glucose levels are within the target range. When blood glucose levels are above the target range, the lag time should be increased. Rapid-acting insulin analogs can be given 15 minutes before and regular insulin 30 to 60 minutes before eating a meal. When blood glucose levels are below the target range, injection of regular insulin should be delayed until immediately before eating and injection of rapid-acting insulin should be delayed until sometime after eating the meal. Mixing insulins can change the time of peak action. Mixtures of short- and intermediate-acting insulins produce a more normal blood glucose response in some patients than does a single dose.

Types of Insulin

Insulin is manufactured using DNA technology to produce pure human insulin. Insulin analogs are synthetic human insulins in which the structure of the insulin molecule is altered to change the rate of absorption and duration of action. An example is Lispro insulin, a rapid-acting insulin analog that is created by switching the positions of lysine and proline. Rapid-, short-, intermediate-, and long-acting forms of insulin can be injected separately, and some can be mixed. Insulin is available in concentrations of 100 units/mL (U-100) or 500 units/mL (U-500). U-500 is indicated only for patients with severe insulin resistance. Reinforce that changing insulins may affect blood glucose control and should be done only under supervision of the health care provider.

Exercise: Safety Assessment 1

Regular physical activity increases the risk for both musculoskeletal injury and life-threatening cardiovascular events. Patients with diabetes often take drugs to reduce blood pressure, to normalize blood lipid concentrations, and to inhibit platelet activity. These drugs may increase fall risk, change physiologic response to exercise and physical activity, alter muscle performance, and increase bleeding risk. The ADA recommends screening when any of these conditions exist: • Chest pain or discomfort • Abnormal electrocardiogram (ECG) suggestive of ischemia or infarction • Peripheral or carotid occlusive disease • Age older than 35 years with sedentary lifestyle in a patient who plans a vigorous exercise program • Two or more risk factors in addition to diabetes, such as dyslipidemia, hypertension, tobacco use • Family history for premature coronary artery disease, or microalbuminuria or macroalbuminuria of more than 10 years' duration • Age older than 25 years and type 1 diabetes of more than 15 years' duration • Severe autonomic neuropathy, severe diabetic peripheral neuropathy, history of foot lesions, and unstable proliferative retinopathy

Patient Education: Prescribed Nutrition Plan

Reinforce nutrition information provided by the RD. The patient with DM must understand how to adjust food intake during illness, planned exercise, and social occasions (e.g., restaurant meals) when the usual time of eating may be delayed. Share dietary information with the person who prepares the meals. Yearly adjustments or more frequent for weight-control programs done by RD.

Preventing Hypoglycemia

Once blood glucose levels fall below 70 mg/dL (3.88 mmol/L), a sequence of events begins with release of counterregulatory hormones, stimulation of the autonomic nervous system, and production of neurogenic and neuroglycopenic manifestations. Peripheral autonomic manifestations, including sweating, irritability, tremors, anxiety, tachycardia, and hunger, serve as an early warning system and occur before the manifestations of confusion, paralysis, seizure, and coma occur from brain glucose deprivation. Neuroglycopenic symptoms occur when brain glucose gradually declines to a low level. Neurogenic symptoms result from autonomic nervous activity triggered by a rapid decline in blood glucose. The first defense against falling blood glucose levels in the nondiabetic person is decreased insulin secretion, decreased glucose use, and increased glucose production. Normally, insulin secretion decreases when blood glucose levels drop to about 83 mg/dL (4.5 mmol/L). Counterregulatory hormones are activated at about 67 mg/dL (3.7 mmol/L), a level well above the threshold for manifestations of hypoglycemia. The main counterregulatory hormone is glucagon. Epinephrine also becomes important in patients with DM who are deficient in glucagon. Both glucagon and epinephrine raise blood glucose levels by stimulating liver glycogen breakdown and conversion of protein to glucose. Epinephrine also limits insulin secretion. Type 1 DM disrupts the body's response to hypoglycemia. Regulation of circulating insulin levels is lost because insulin comes from an injection rather than from the pancreas. As blood glucose levels fall, insulin levels do not decrease. Over time, the pancreas loses its ability to secrete glucagon in response to hypoglycemia. After a few more years of type 1 DM, the response of epinephrine to falling blood glucose levels does not occur until the blood glucose level is very low. These problems greatly increase the risk for severe hypoglycemia. With long-standing type 1 DM is hypoglycemic unawareness, in which patients no longer have the warning manifestations of impending hypoglycemia that should prompt them to take preventive action(30+ years). In mild hypoglycemia, the patient remains alert and able to self-manage symptoms. In severe hypoglycemia, neurologic function is so impaired that he or she needs another person's help to increase blood glucose levels.

Evaluation: Outcomes

Outcome success for diabetes education is the ability of the patient to maintain blood glucose levels within their established target range. Other outcomes: • Achieve blood glucose control • Avoid acute and chronic complications of diabetes • Avoid injury • Experience relief of pain • Maintain optimal visual sensory perception • Maintain a urine output in the expected range • Have an optimal level of mental status functioning • Have decreased episodes of hypoglycemia • Have decreased episodes of hyperglycemia

Rejection Management

Patients undergoing anti-rejection therapy first receive drugs to prevent viral, bacterial, and fungal infection because of the risk for opportunistic infections. Most patients receiving high-dose steroids, as well as those on chronic long-term steroid therapy, will require dosage adjustments in insulin to achieve desired levels of glucose control. In most episodes of rejections, kidney problems occur before pancreatic problems. An increase in serum creatinine indicates rejection of both the transplanted kidney and the pancreas. In patients with bladder drainage of pancreatic hormones, a decrease in the urine amylase level by 25% is an indication to treat rejection. High blood glucose levels are a later marker of rejection and usually indicate irreversible graft failure. Long-term anti-rejection therapy increases the risk for infection, cancer, and atherosclerosis. When insulin drains into systemic rather than portal (liver) circulation, blood insulin levels rise (hyperinsulinemia) and increase the risk for hypertension and macrovascular disease.

Assessing Learning Needs and Readiness to Learn

Patients want information that applies directly to them. Find out what concerns the patient most about having diabetes, and ask what he or she wants to learn. Start with what the patient already knows, and build on that base. Make sure that the patient's knowledge is current and applies to his or her type of diabetes. Your assessment may indicate that the patient is not ready to learn needed self-management behaviors. With the patient's permission, you would then teach a family member or someone close to the patient about diabetes management. You would also provide written materials on diabetes management as well as telephone numbers for the patient to call when he or she is ready to learn.

Exercise: Safety Assessment 2

Screening for coronary artery disease before an exercise program is started is recommended for patients with cardiovascular risk factors. Exercise treadmill testing (ETT) is used to determine if a person can exercise to 85% of his or her predicted heart rate without having ischemic changes. Failure to achieve 85% of the predicted heart rate is associated with increased incidence of death. Other studies to determine the risk for exercise-induced problems include medical stress tests with vasodilator therapy, stress echocardiography, presence of obstructive lesions in coronary arteries. Advise people with DM to perform at least 150 min/wk of moderate-intensive aerobic physical activity or 75 min/wk of vigorous aerobic physical activity or an equivalent combination of the two. In the absence of contraindications, patients with type 2 diabetes are urged to perform resistance exercise 3 times a week, targeting all major muscle groups. The ADA recommends that there be no more than 2 consecutive days without aerobic physical activity. A 5- to 10-minute warm-up period with stretching and low-intensity exercise before exercise required. After the activity session, a cool-down should be performed similarly to the warm-up. The cool-down should last 5 to 10 minutes and gradually bring the heart rate down to pre-exercise level. Recommend that the patient test blood glucose before exercise, at intervals during exercise, and after exercise to determine if it is safe to exercise and to evaluate the effects of exercise. The absence of urine ketones indicates that enough insulin is available for glucose transport and that exercise should be effective in lowering blood glucose levels. When urine ketones are present, the patient should NOT exercise. Ketones indicate that current insulin levels are not adequate and that exercise would elevate blood glucose levels. Carbohydrate foods should be ingested to raise blood glucose levels above 100 mg/dL (5.6 mmol/L) before engaging in exercise.

Patient Education: Blood Glucose Monitoring 1

Self-monitoring of blood glucose (SMBG) levels provides information to assess effectiveness of the management plan. Assessment of blood glucose levels is very important for these situations: • Manifestations of hypoglycemia/hyperglycemia • Hypoglycemic unawareness • Periods of illness • Before and after exercise • Gastroparesis • Adjustment of diabetes drugs • Evaluation of other drug therapies (e.g., steroids) • Preconception planning • Pregnancy Technique for SMBG follows principles that are the same for most self-monitoring systems. The finger is pricked, a drop of blood flows over or is drawn into a testing strip or disc impregnated with chemicals, and the glucose value is displayed in mg/dL or mmol/L. For vision-impaired patients, "talking-meters" are available. Data obtained from SMBG are evaluated along with other measures of blood glucose (e.g., A1C values). Results are affected by hematocrit values (anemia falsely elevates glucose values; polycythemia falsely depresses them). SMBG systems depends on accuracy of the specific blood glucose meter, operator proficiency, test strip quality, size and quality of the blood sample; the meter's calibration to the strip, altitude, temperature, moisture, hematocrit level, triglyceride level, high levels of substances such as ascorbic acid in blood, and the presence of hypotension or hypoxia.

In-Depth Education 3

Self-monitoring of blood glucose provides immediate information on a person's blood glucose level and provides feedback on the effects of recent activity, drugs, and meals. The nurse's role includes teaching skills of performing the test, educating how to interpret results, and problem solving to adjust behaviors and therapy based on the information. Teach patients how to recognize when blood glucose levels are out of range, how to adjust therapy and behaviors based on self-monitoring of blood glucose (SMBG) results, and how to verify the effects of these adjustments by performing subsequent glucose testing. Also, show patients who use insulin how to use SMBG to adjust dosages to achieve glucose control while avoiding episodes of hypoglycemia. Teach patients sick-day procedures when initially diagnosed with diabetes. Hyperglycemia often develops before infection manifestations and can serve as a warning that infection is developing. Provide guidelines for the frequency of glucose testing, for ketone testing, and for insulin adjustment for those patients able to self-adjust insulin doses.

Preventing Injury from Hyperglycemia: Drug Selection

Shorter-acting agents (e.g., glipizide) are preferable in older patients, those with irregular eating schedules, or those with liver, kidney, or cardiac dysfunction. Longer-acting agents (e.g., glyburide, glimepiride) with once-a-day dosing are better for adherence. Beta-cell function in type 2 DM often declines over time, reducing the effectiveness of some drugs. The treatment regimen for a patient with type 2 DM may eventually require insulin therapy either alone or with other antidiabetic drugs.

Chart 64-8 Patient and Family Education: Preparing for Self-Management Sick-Day Rules

Sick-Day Rules • Notify your health care provider that you are ill. • Monitor your blood glucose at least every 4 hours. • Test your urine for ketones when your blood glucose level is greater than 240 mg/dL (13.8 mmol/L). • Continue to take insulin or oral antidiabetic agents. • To prevent dehydration, drink 8 to 12 ounces of sugar-free liquids every hour that you are awake. If your blood glucose level is below your target range, drink fluids that contain sugar. • Continue to eat meals at regular times. • If unable to tolerate solid food because of nausea, consume more easily tolerated foods or liquids equal to the carbohydrate content of your usual meal. • Call your primary care provider for any of these danger signals: 1.Persistent nausea and vomiting 2.Moderate or large ketones 3.Blood glucose elevation after two supplemental doses of insulin 4.High (101.5° F [38.6° C]) temperature or increasing fever; fever for more than 24 hours • Treat symptoms (e.g., diarrhea, nausea, vomiting, fever) as directed by your primary care provider. • Get plenty of rest.

Cognitive Dysfunction

Significantly higher risk for developing all types of dementia. Chronic hyperglycemia with microvascular disease contributes to neuron damage, brain atrophy, and cognitive impairment. Depression is highly prevalent.

Patient Education: Drugs 2

Syringes are the most commonly used. The standard insulin syringes are marked in insulin units. They are available in 1 mL (100-U), 1/2 mL (50-U), and 3/10 mL (30-U) sizes. Insulin syringe needles are measured in 28-, 29-, 30-, and 31-gauge and in lengths of 6 mm, 8 mm, and 12.7 mm. To ensure accurate insulin measurement, instruct the patient to always buy the same type of syringe. Disposable needles should be used only once. A reason not to reuse smaller (30- and 31-gauge) needles is that even with one injection, the needle tip can become bent to form a hook, which can lacerate tissue or break off to leave needle fragments. Pen-type injectors hold small, lightweight, prefilled insulin cartridges. Discuss proper storage for prefilled insulin pens or cartridges. Ensure that the product is appropriate to the patient's unique needs. Pen-type injectors are not designed for independent use by visually impaired patients or by those with cognitive impairment. Patients using the FlexPen (Novo Nordisk) must be able to attach a needle and to perform an air shot of 2 units to ensure that a dose of insulin is administered. The Institute for Safe Medication Practices (ISMP) and The Joint Commission's National Patient Safety Goals identify insulin as a High-Alert drug. The ISMP cautions that digital displays on some of the newer insulin pens can be misread. If the pen is held upside down, as a left-handed person might do, a dose of 52 units actually appears to be a dose of 25

Preventing Diabetic Ketoacidosis: Fluid and Electrolyte Management 2

Tachycardia is a compensatory mechanism to increase cardiac output. Older adults may not exhibit tachycardia if they are taking beta blockers or calcium channel blockers. Dry mucous membranes may be caused by anticholinergic drugs, and postural hypotension may occur with antihypertensive drugs. Typically, initial infusion rates of 0.9% sodium chloride are 15 to 20 mL/kg/hr during the first hour. In general, hypotonic fluids, such as 0.45% sodium chloride, are infused at 4 to 14 mL/kg/hr after the initial fluid bolus. When blood glucose levels reach 250 mg/dL (13.8 mmol/L), 5% dextrose in 0.45% saline is usually prescribed. This solution prevents hypoglycemia and cerebral edema, which can occur when serum osmolarity declines too rapidly. Assess cardiac, kidney, and mental status to avoid fluid overload. Watch for manifestations of congestive heart failure and pulmonary edema. Central venous pressure may be monitored for older patients and those with myocardial disease. Assess the status of fluid replacement by monitoring blood pressure, intake and output, and changes in daily weight.

Reducing the Risk for Kidney Disease: Prevention 2

Teach patients about the roles of blood pressure and blood glucose levels in kidney disease. Help them maintain normal blood glucose levels and blood pressure levels below 140/80 mm Hg. Stress the need for yearly screening for microalbuminuria. Smoking cessation is important in halting the progression of diabetic kidney disease. Any urinary tract infection (UTI) can lead to kidney infection and further reduce kidney function. Explain the manifestations of UTI. Urge the patient to take antibiotics exactly as prescribed. Reinforce the need for follow-up urine cultures. Avoid indwelling catheters. Drugs can affect kidney function either through toxic effects on the kidney or by an acute but reversible reduction in function. The most common nephrotoxic drugs are antifungal agents and aminoglycoside antibiotics. Outside the hospital, the leading nephrotoxic agents are NSAIDs such as ibuprofen (Advil) or naproxen (Aleve), when used long-term. To prevent accidental ingestion of nephrotoxic drugs, teach the patient to check with HCP. Radiocontrast dyes can also affect kidney function, especially in patients with preexisting kidney problems. Monitor IV hydration before and after contrast is used to prevent contrast-induced nephropathy.

Preventing Injury from Peripheral Neuropathy: Peripheral Neuropathy Management

The feet should be evaluated closely at least annually. Complete a full foot assessment as outlined in Chart 64-5. Sensory examination with Semmes-Weinstein monofilaments is a practical measure of the risk for foot ulcers. The nylon monofilament is mounted on a holder standardized to exert a 10-g force. A person who cannot feel the 10-g pressure at any point is at increased risk for ulcers. To perform the examination: • Provide a quiet and relaxed setting. Ask the patient to close his or her eyes during the test. • Test the monofilament on the patient's cheek so he or she knows what to expect. • Test the sites noted in Fig. 64-7. • Apply the monofilament at a right angle to the skin surface. • Apply enough force to bend the filament using a smooth, not jabbing, motion • The approach, contact, and removal of the filament at each site should take 1 to 2 seconds. • Apply the filament along the perimeter and not on an ulcer site, callus, scar, or necrotic tissue. Do not slide the filament across the skin or make repeated contact at the test site. Randomize the sequence of applying the filament throughout the examination. Have the patient identify where the filament touched rather than asking "Do you feel this?"

Survival Skills Information

The initial phase of diabetes education involves teaching information necessary for the survival of anyone diagnosed with diabetes. Survival information includes: • Simple information on pathophysiology of diabetes • Learning how to prepare and administer insulin or how to take oral drugs for diabetes • Recognition, treatment, and prevention of hypoglycemia and hyperglycemia • Basic diet information • Monitoring of blood glucose and ketones • Sick-day management • Where to buy diabetes supplies and how to store them • When and how to notify the health care provider

Preventing Diabetic Ketoacidosis: Acidosis Management

The key feature of DKA is elevation in blood ketone concentration (serum β-hydroxybutyrate). A normal anion gap is between 7 and 9 mEq/L; an anion gap greater than 10 to12 mEq/L indicates metabolic acidosis. Mild to moderate hyperkalemia is common in patients with hyperglycemia. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. To prevent hypokalemia, potassium replacement is initiated after serum levels fall below the upper limit of normal (5.0 mEq/L). Assess for manifestations of hypokalemia, including fatigue, malaise, confusion, muscle weakness, shallow respirations, abdominal distention or paralytic ileus, hypotension, and weak pulse. An ECG shows conduction changes. Hypokalemia is a common cause of death in the treatment of DKA. Bicarbonate is used only for severe acidosis. Sodium bicarbonate, given by slow IV infusion over several hours, is indicated when the arterial pH is 7.0 or less or the serum bicarbonate level is less than 5 mEq/L (5 mmol/L).

Preventing Hyperglycemic-Hyperosmolar State: Fluid Therapy

Rhydrate the patient and restore normal blood glucose levels within 36 to 72 hours. Re-establishing fluid balance in brain cells is a difficult and slow process, and many patients do not recover baseline CNS function until hours after blood glucose levels have returned to normal. The first priority for fluid replacement in HHS is to increase blood volume. In shock or severe hypotension, normal saline is used. Otherwise, half-normal saline (0.45% sodium chloride). Infuse fluids at 1 L/hr until central venous pressure or pulmonary capillary wedge pressure begins to rise or until blood pressure and urine output are adequate. The rate is then reduced to 100 to 200 mL/hr. Half of the estimated fluid deficit is replaced in the first 12 hours, and the rest is given over the next 36. Body weight, urine output, kidney function, and the presence or absence of pulmonary congestion and jugular venous distention determine the ml/hr. With congestive heart failure, kidney disease, or acute kidney injury, monitor central venous pressure. Assess the patient hourly for signs of cerebral edema—abrupt changes in mental status, abnormal neurologic signs, and coma. Regression after initial improvement may indicate a too-rapid reduction in blood osmolarity. A slow but steady improvement in CNS function is the best evidence that fluid management is satisfactory.

Genetic/Genomic Considerations

Risk for type 1 diabetes is determined by inheritance of genes coding for the HLA-DR and HLA-DQA and DQB tissues types. However, inheritance of these genes only increases the risk and most people with these genes do not develop type 1 DM. Development of DM is an interactive effect of genetic predisposition and exposure to certain environmental factors. It is unclear why some genetically susceptible people develop diabetes and others do not. Ask patients newly diagnosed with type 1 diabetes whether any other relatives have diabetes or other autoimmune disease.

Urine Tests

Ketone bodies are a product of fat metabolism, and the presence of moderate to high urine ketones (hyperketonuria) indicates a severe lack of insulin. Hyperketonuria in the presence of hyperglycemia is a medical emergency. Urine testing for ketones should be performed during acute illness or stress, when blood glucose levels consistently exceed 300 mg/dL (16.7 mmol/L), during pregnancy, or when any manifestations of ketoacidosis are present. Ketone testing is recommended for patients with diabetes participating in a weight-loss program. Hyperketonuria without hyperglycemia suggests that weight loss is occurring without disrupting blood glucose control. Ketone bodies appear in urine and are affected by urine volume and concentration thus urine ketone bodies are not used to evaluate the effectiveness of treatment for ketoacidosis. Tests for kidney function are important for diabetics. Persistent albuminuria in the range of 30 to 299 mg/24 hr is an indicator of early-stage diabetic nephropathy in type 1 diabetes and a marker for development of nephropathy in type 2 diabetes. Persistent albuminuria is also a marker for increased cardiovascular risk. Screening for increased urinary albumin excretion can be performed by measurement of albumin-to-creatinine ratio. In patients with nephropathy, a rise in serum creatinine level is related to both poor blood glucose control and hypertension. Urine glucose testing is an indirect measurement of blood glucose and is not accurate.

Eye and Vision Complications(MICRO)

Legal blindness (a corrected visual acuity of 20/200 or less) is 25 times more common in diabetics. Diabetic retinopathy (DR) is strongly related to the duration of diabetes. After 20 years of DM, nearly all patients with type 1 disease and most with type 2 disease have some degree of retinopathy. DR is related to problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia, poor retinal circulation, edema, hard fatty deposits in the eye, and retinal hemorrhages. Other retinal problems include optic nerve atrophy from hypoxia and venous beading. Venous beading is the abnormal appearance of retinal veins in which areas of swelling and constriction along a segment of vein resemble links of sausage. It occurs in areas of retinal ischemia. Proliferative diabetic retinopathy is the growth of new retinal blood vessels, also known as "neovascularization." Non-proliferative diabetic retinopathy is without the formation of abnormal blood vessels. When retinal blood flow is poor and hypoxia develops, retinal cells secrete growth factors that stimulate formation of new blood vessels. New vessels are thin, fragile, and bleed easily, leading to eye hemorrhage and vision loss. Central vision may be impaired by macular edema, characterized by increased blood vessel permeability and deposits of hard exudates at the center of the retina. This problem is the main cause of vision loss. Monthly injections of ranibizumab (Lucentis) into the vitreous can improve vision for some people with macular edema. Vision loss also occurs from macular degeneration, corneal scarring, and changes in lens. Hyperglycemia may cause blurred vision, even with eyeglasses. Hypoglycemia may cause double vision. Cataracts occur at a younger age and progress faster. Open-angle glaucoma also is more common. Patients with DM should have routine ophthalmic evaluations to detect vision problems early. The ADA recommends eye care examinations with an ophthalmologist every year after a person has been diagnosed with type 2 diabetes and yearly for a person who has had type 1 diabetes for more than 5 years

Complications of Insulin Therapy

Lipoatrophy is a loss of fat tissue in areas of repeated injection that results from an immune reaction to impurities in insulin. Treatment consists of injection of insulin at the edge of the atrophied area. Lipohypertrophy is an increased swelling of fat that occurs at the site of repeated insulin injections. The overlying skin has decreased sensitivity, and the area can become large and unsightly. Treatment consists of rotating the injection site. Dawn phenomenon results from a nighttime release of growth hormone that causes release of liver glucose resulting in blood glucose elevations at about 5 to 6 am. It is managed by providing more insulin for the overnight period (e.g., giving the evening dose of intermediate-acting insulin at 10 pm). Somogyi phenomenon is morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia resulting in release of liver glucose. It is managed by ensuring adequate dietary intake at bedtime and evaluating the insulin dose and exercise programs to prevent conditions that lead to hypoglycemia. Both problems are diagnosed by blood glucose monitoring during the night. Hypoglycemia from insulin excess has many causes. Its effects and treatment are discussed later(PG1330 IGGY).

Managing Pain: Interventions 1

Many patients with diabetes suffer from the painful neuropathy. Manifestations of diabetic neuropathy include: • Burning • Muscle cramps • Piercing, stabbing, or darting pain • Metatarsalgia (feeling as if you are walking on marbles) • Hyperalgesia (exaggerated pain response) • Allodynia (pain in response to normally nonpainful stimuli) • Tingling, numbness, and loss of proprioception in lower extremities Maintaining normal blood glucose levels and avoiding extreme fluctuations prevent neuropathy and relieve manifestations. Rapid improvement in blood glucose control may actually trigger acute peripheral neuropathy.

Screening for Diabetes

Measurement of islet cell antibodies may identify people who are at risk for developing type 1 DM. Testing to detect prediabetes and type 2 DM should be considered in patients older than 45 years and those defined as overweight (body mass index [BMI] greater than 25 kg/m2). Testing is considered for patients who are younger than 45 years and are overweight if they have additional risk factors for diabetes or have other health problems associated with diabetes. Screening for diabetes usually is done with either hemoglobin A1C levels or fasting plasma glucose levels (ADA, 2014d). The use of portable glucose meters for the diagnosis of diabetes is not recommended because of imprecise results and variance.

Drug Alert

Metformin can cause lactic acidosis in patients with renal insufficiency and should not be used by anyone with kidney disease. To prevent kidney damage, the drug should be withheld after using contrast material or any surgical procedure requiring anesthesia until adequate kidney function is established.

Preventing Hypoglycemia: Blood Glucose Management

Monitor blood glucose levels before giving antidiabetic drugs, before meals, before bedtime, and when the patient is symptomatic. All patients who take insulin, those taking long-acting insulin secretagogues (glyburide [glibenclamide]), and those taking metformin in combination with glyburide (Glucovance) are at risk for hypoglycemia. This risk is increased if they are older, have liver or kidney impairment, or are taking drugs that enhance the effects of antidiabetic. Hypoglycemia may be difficult to recognize in those who take beta-blocking drugs. Manifestations are less intense and less obvious. Manifestations of hypoglycemia in older patients may be mistaken for other conditions. The most common causes of hypoglycemia are: • Too much insulin compared with food intake and physical activity • Insulin injected at the wrong time relative to food intake and physical activity • The wrong type of insulin injected at the wrong time • Decreased food intake resulting from missed or delayed meals • Delayed gastric emptying from gastroparesis • Decrease liver glucose production after alcohol ingestion • Increased insulin sensitivity as a result of regular exercise and weight loss • Decreased insulin clearance from progressive kidney failure

Enhancing Surgical Recovery: Monitoring

Patients with autonomic neuropathy or vascular disease need close monitoring to avoid hypotension or respiratory arrest. Those who take beta blockers for hypertension need close monitoring for hypoglycemia because these drugs mask manifestations of hypoglycemia. Patients with increased protein or nitrogen waste products in the blood may have problems with fluid management. Glucose levels are a sensitive marker of counterregulatory hormones, which are often activated before patients become febrile. Hyperglycemia comes before a fever. Hyperkalemia (high blood potassium level) is common in patients with mild to moderate kidney failure and can lead to cardiac dysrhythmia. In other patients, hypokalemia (low blood potassium level) may occur and be made worse by insulin and glucose given during surgery. Monitor the cardiac rhythm and serum potassium. Cardiovascular monitoring by continuous electrocardiograms (ECGs) is recommended for older patients with diabetes, those with long-standing type 1 DM, and those with heart disease. Changes in ECG or in potassium level may indicate a silent MI. Kidney monitoring, especially observing fluid balance, helps detect acute kidney injury (AKI). Diagnosis of kidney impairment may require the use of x-ray studies using dyes. Management of infection may require the use of nephrotoxic antibiotics. Ensure adequate hydration when these drugs are used. Check for impending kidney failure by assessing fluid and electrolyte status.

Reducing the Risk for Kidney Disease: Nutrition Therapy

Patients with nephropathy should restrict protein intake to 0.8 g/kg of body weight per day. Once the 1330glomerular filtration rate (GFR) starts falling, further reducing protein may slow the decline in kidney function.

Home Care Management

Older adults who live alone need to have daily telephone contact with a friend or neighbor. The patient may also need help shopping and preparing meals. He or she may have limited access to transportation and may not have sufficient supplies of food, particularly in bad weather. Because of the likelihood of visual problems in older patients, they may need assistance in preparing insulin syringes for injection or in monitoring blood glucose. Make referrals to home care or public health agencies as needed.

Considerations for Older Adults

Older patients are at increased risk for poor nutrition, hypoglycemia, and especially dehydration, a factor in the development of hyperglycemic-hyperosmolar state (HHS). Many factors contribute to malnutrition. Nutrition needs of the older adult change as the person's taste, smell, and appetite diminish and his or her ability to obtain and prepare food decreases. Older patients who prepare their own food or have tooth loss or poorly fitting dentures may not eat enough food. Neuropathy with gastric retention or diarrhea compounds poor food intake. Impaired cognition and depression may disrupt self-care. Older patients may have a marginal food supply because of inadequate income, may have poor understanding of meal-planning needs, or may live alone and have reduced incentive to prepare or eat proper meals. They may eat in restaurants or live in situations in which they have little control over meal preparation. Regular visits by home health nurses can assist older patients in following a diabetic meal plan. A realistic approach to nutrition therapy is essential for the older patient with diabetes. Changing the eating habits of 60 to 70 years is very difficult. The nurse, dietitian, and patient assess the patient's usual eating patterns. Teach the older patient taking antidiabetic drugs about the importance of eating meals and snacks at the same time every day, eating the same amount of food from day to day, and eating all food allowed on the diet.

Absence of Insulin

The lack of insulin in diabetes, from either a lack of production or a problem with insulin use at its cell receptor, prevents some cells from using glucose for energy. The body then breaks down fat and protein in an attempt to provide energy and increases levels of counterregulatory hormones to make glucose from other sources. Hyperglycemia causes fluid and electrolyte imbalances, leading to the classic manifestations of diabetes: polyuria, polydipsia, and polyphagia. Polyuria is frequent and excessive urination and results from an osmotic diuresis caused by excess glucose in the blood and urine. With diuresis, electrolytes are excreted in the urine and water loss is severe. Dehydration results, and polydipsia (excessive thirst) occurs. Because the cells receive no glucose, cell starvation triggers polyphagia (excessive eating). Despite eating, the person remains in cellular starvation until insulin is available to move glucose into the cells. Conversion of fatty acids to ketone bodies (small acids) provides a backup energy source. Ketone bodies or "ketones" are abnormal breakdown products that collect in the blood when insulin is not available, leading to a type of metabolic acidosis known as ketoacidosis. Dehydration with diabetes leads to hemoconcentration (increased blood concentration); hypovolemia (decreased blood volume); thick, concentrated blood; poor tissue perfusion; and hypoxia (poor tissue oxygenation). The Krebs' cycle is blocked, and lactic acid increases, causing more acidosis. Absence of insulin increase hydrogen ion (H+) and carbon dioxide (CO2) levels in the blood, causing anion-gap metabolic acidosis. These products trigger the brain to increase the rate and depth of respiration. This type of breathing is known as Kussmaul respiration. Acetone is exhaled, giving the breath a "rotting fruit" odor. Arterial blood gas studies show a metabolic acidosis (decreased pH with decreased arterial bicarbonate [HCO3−] levels) and compensatory respiratory alkalosis (decreased partial pressure of arterial carbon dioxide [Paco2]). Insulin lack initially causes potassium depletion. With the increased fluid loss from hyperglycemia, excessive potassium is excreted in the urine, leading to low serum potassium levels. High serum potassium levels may occur in acidosis because of the shift of potassium from inside the cells to the blood.

TABLE 64-9 Desired Outcomes of Nutrition Therapy for the Patient With Diabetes

• Achieving and maintaining blood glucose levels in the normal range or as close to normal as is safely possible • Achieving and maintaining a blood lipid profile that reduces the risk for vascular disease • Achieving blood pressure levels in the normal range or as close to normal as is safely possible • Preventing or slowing the rate of development of the chronic complications of diabetes by modifying nutrient intake and lifestyle • Addressing patient nutrition needs taking into account personal and cultural preferences and willingness to change • Maintaining the pleasure of eating by limiting food choices only when indicated by scientific evidence • Meeting the nutrition needs of unique times of the life cycle, particularly for pregnant and lactating women and for older adults with diabetes • Providing self-management training for patients treated with insulin or insulin secretagogues for exercising safely, including the prevention and treatment of hypoglycemia, and managing diabetes during acute illness

Chart 64-9 Focused Assessment The Insulin-Dependent Patient with Diabetes During a Home or Clinic Visit

• Assess overall mental status, wakefulness, ability to converse. • Take vital signs and weight: 1. Fever could indicate infection. 2. Are blood pressure and weight within target range? If not, why? • Question patient regarding any change in visual acuity; check current visual acuity. • Inspect oral mucous membranes, gums, and teeth. • Question patient about injection areas used; inspect areas being used; assess whether patient is using areas and sites appropriately. • Inspect skin for intactness, wounds that have not healed, new sores, ulcers, bruises, or burns; assess any previously known wounds for infection, progression of healing. • Question patient regarding foot care. • Assess lower extremities and feet for peripheral pulses, lack of or decreased sensation, abnormal sensations, breaks in skin integrity, condition of toes and nails. • Question patient regarding color and consistency of stools and frequency of bowel movements; assess abdomen for bowel sounds. • Review patient's home health diary: 1. Is blood glucose within targeted range? If not, why? 2. Is glucose monitoring being recorded often enough? 3. Is the patient's food intake adequate and appropriate? If not, why? image Is exercise occurring regularly? If not, why? • Assess patient's ability to perform self-monitoring of blood glucose. • Assess patient's procedures for obtaining and storing insulin and syringes, cleaning equipment, disposing of syringes and needles. • Assess patient's insulin preparation and injection technique.

Acute Complications of Diabetes

• Diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis • Hyperglycemic-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration • Hypoglycemia from too much insulin or too little glucose All three problems require emergency treatment and can be fatal if treatment is delayed or incorrect.

Key Points: Health Promotion and Maintenance

• Encourage all patients to maintain weight within an appropriate range. • Encourage all patients, including patients with diabetes, to participate regularly in exercise or physical activity appropriate to their health status. • Teach the patient and family about the manifestations of infection and when to seek medical advice. • Instruct patients with diabetes to wear a medical alert bracelet. • Instruct patients to not share blood glucose monitoring equipment. • Reinforce to all patients with diabetes that tight control over blood glucose levels reduces the risk for the vascular complications of diabetes. • Remind patients with diabetes to have yearly eye examinations by an ophthalmologist. • Teach patients with peripheral neuropathy to use a bath thermometer to test water for bathing, to avoid walking barefoot, and to inspect their feet daily. • Assess patients' visual acuity and peripheral tactile sensation to determine needed adjustments in teaching self-medication and self-monitoring of blood glucose levels. • Instruct all patients with diabetes to avoid becoming dehydrated and to drink at least 2 L of water each day unless another medical condition requires fluid restriction. • Instruct patients who are taking sulfonylurea drugs about an increased risk for hypoglycemic reactions. • Teach patients who are taking metformin the clinical manifestations of lactic acidosis (fatigue, dizziness, difficulty breathing, stomach discomfort, irregular heartbeat). • Warn patients to not take over-the-counter drugs with their oral antidiabetic drugs without consulting their primary care provider. • Teach patients to rotate insulin injection sites within one area rather than to other areas, to prevent changes in absorption. • Use return demonstration and "teach-back" strategies when teaching the patient about drug regimen, insulin injection, blood glucose monitoring, and foot assessment. • Teach patients to administer an accurate dose of insulin using a prefilled or disposable insulin pen. • Teach patients who experience Somogyi phenomenon (early morning hyperglycemia) to ensure an adequate dietary intake at bedtime. • Instruct patients to always carry a glucose source. • Teach patients who exercise to test urine for ketone bodies if blood glucose levels are greater than 250 mg/dL before engaging in strenuous exercise. • Instruct patients in foot care as outlined in Chart 64-6.

Key Points: Psychosocial Integrity

• Explore with the patient what the diagnosis of diabetes means to him or her. • Allow the patient the opportunity to express concerns about the diagnosis of diabetes or the treatment regimen. • Explain all procedures, restrictions, drugs, and follow-up care to the patient and family. • Instruct the patient and family on the manifestations of complications and when to seek assistance. • Pace your education sessions to match the learning needs and style of the patient.

TABLE 64-14 Assessment of Learning Needs for the Patient with Diabetes

• Health and medical history • Nutrition history and practices • Physical activity and exercise behaviors • Prescription and over-the-counter medications and complementary and alternative therapies and practices • Factors that influence learning such as education and literacy levels, perceived learning needs, motivation to learn, and health beliefs • Diabetes self-management behaviors, including experience with self-adjusting the treatment plan • Previous diabetes self-management training, actual knowledge, and skills • Physical factors including age, mobility, visual acuity, hearing, manual dexterity, alertness, attention span, and ability to concentrate or special needs or limitations requiring adaptive support and use of alternative skills • Psychosocial concerns, factors, or issues including family and social support • Current mental health status • History of substance use including alcohol, tobacco, and recreational drugs • Occupation, vocation, education level, financial status, and social, cultural, and religious practices • Access to and use of health care resources

Chart 64-6 Patient and Family Education: Preparing for Self-Management Foot Care Instructions

• Inspect your feet daily, especially the area between the toes. • Wash your feet daily with lukewarm water and soap. Dry thoroughly. • Apply moisturizing cream to your feet after bathing. Do not apply to the area between your toes. • Change into clean cotton socks every day. • Do not wear the same pair of shoes 2 days in a row, and wear only shoes made of breathable materials, such as leather or cloth. • Check your shoes for foreign objects (nails, pebbles) before putting them on. Check inside the shoes for cracks or tears in the lining. • Purchase shoes that have plenty of room for your toes. Buy shoes later in the day, when feet are normally larger. Break in new shoes gradually. • Wear socks to keep your feet warm. • Trim your nails straight across with a nail clipper. Smooth the nails with an emery board. • See your physician or nurse immediately if you have blisters, sores, or infections. Protect the area with a dry, sterile dressing. Do not use adhesive tape to secure dressing to the skin. • Do not treat blisters, sores, or infections with home remedies. • Do not smoke. • Do not step into the bathtub without checking the temperature of the water with your wrist or thermometer. Optimal temperature is 95° F (35° C). Maximum temperature is 110° F (43° C). • Do not use very hot or cold water. Never use hot water bottles, heating pads, or portable heaters to warm your feet. • Do not treat corns, blisters, bunions, calluses, or ingrown toenails yourself. • Do not go barefooted. • Do not wear sandals with open toes or straps between the toes. • Do not cross your legs or wear garters or tight stockings that constrict blood flow. • Do not soak your feet.

Nutrition Therapy

A registered dietitian (RD) should be a member of the treatment team. The nurse, RD, patient, and family work together on all aspects of the meal plan, which must be realistic and as flexible as possible.

Focal neuropathies

Affect a single nerve or nerve group and usually are caused by an acute ischemic event that leads to nerve damage or nerve death. Ischemic neuropathies occur when the blood supply to a nerve or nerve group is disrupted. Manifestations begin suddenly, affect only one side of the body area, and are self-limiting. The most common neuropathies affect the nerves that control the eye muscles. Manifestations begin with pain on one side of the face near the affected eye. The eye muscles become paralyzed, resulting in double vision. The problem usually resolves in 2 to 3 months.

Considerations for Older Adults

HHS occurs most often in older patients with type 2 diabetes mellitus, many of whom did not know that they had diabetes. Mortality rates in older patients are as high as 40% to 70%. The onset of HHS is slow and may not be recognized. The older patient often seeks medical attention later and is sicker than the younger patient. HHS does not occur in adequately hydrated patients. Older patients are at greater risk for dehydration and HHS because of age-related changes in thirst perception, poor urine-concentrating abilities, and use of diuretics. Stress to all older adults, especially those who have diabetes, the importance of maintaining hydration.

Enhancing Surgical Recovery: Nutrition

Patients requiring clear or full liquid diets should receive about 200 g of carbohydrate daily in equally divided amounts at meals and snack times. Initial liquids should not be sugar-free. Most patients require 25 to 35 calories per kg of body weight every 24 hours. After surgery, food intake is initiated as quickly as possible with progression from clear liquids to solid foods occurring as rapidly as tolerated. Returning to a normal meal plan as soon as possible after surgery promotes healing and metabolic balance. When oral foods are tolerated, make sure the patient takes at least 150 to 200 g of carbohydrate daily to prevent hypoglycemia. If total parenteral nutrition (TPN) is used after surgery, severe hyperglycemia may occur. Monitor blood glucose often.

Type 1 Diabetes

Type 1 diabetes mellitus (DM) is an autoimmune disorder in which beta cells are destroyed. Immune system cells and antibodies take destructive actions against the insulin-secreting cells in the islets. Viral infections, such as mumps and coxsackievirus infection, may trigger autoimmune destruction.

Reducing the Risk for Kidney Disease: Drug Therapy

Use of angiotensin-converting enzyme (ACE) inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) is recommended for all patients with microalbuminuria or advanced stages of nephropathy. ACE inhibitors reduce the level of albuminuria and the rate of progression of kidney disease, although they do not appear to prevent microalbuminuria. Monitor serum potassium levels for development of hyperkalemia.

Preventing Hypoglycemia: Prevention Strategies

(1) excess insulin, (2) deficient intake or absorption of food, (3) exercise, and (4) alcohol intake. Insulin excess from variable absorption of insulin can cause hypoglycemia even when insulin is injected correctly. Increased insulin sensitivity can occur with weight loss, exercise programs, and resolution of an infection. Differences in insulin formulation can result in hypoglycemia. Teach the patient to not change insulin brands without medical supervision. Deficient food intake from inadequate or incorrectly timed meals can result in hypoglycemia. Changes in gastric absorption may cause hypoglycemia in patients with delayed gastric emptying, which is more severe with solid meals, and is made worse by illness or poor glucose control. Teach the patient the importance of scheduled routine. Exercise often causes blood glucose levels to fall in a patient with type 1 DM. Prolonged exercise increases cellular glucose uptake for several hours after exercise. Teach the patient about blood glucose monitoring and carbohydrate consumption before and during. Alcohol inhibits liver glucose production and leads to hypoglycemia. It interferes with the counterregulatory response to hypoglycemia and impairs glycogen breakdown, making exercise-induced hypoglycemia more severe. Teach the patient to ingest alcohol only with or shortly after eating a meal with enough carbohydrate to prevent hypoglycemia. Warn patients to avoid excess alcohol at bedtime to prevent nighttime hypoglycemia.

Patient Education: Blood Glucose Monitoring 2

Accuracy of the blood glucose monitor is ensured when the manufacturer's directions are followed. Help the patient select a meter based on cost, ease of use, and availability of repair and servicing. Provide training, explain and demonstrate procedures, assess visual acuity, and check the patient's ability to perform the procedure using "teach-back" strategies. Teach patients to properly calibrate ("code") the machine. Instruct them to re-check the calibration and re-test if they obtain a test result that is unusual. Retraining of patients performing SMBG helps ensure accurate results because performance accuracy deteriorates. Frequency of testing varies. The ADA recommends that patients taking multiple insulin injections or using insulin pump therapy monitor glucose levels 3 or more times daily. For patients taking less-frequent injections of insulin, non-insulin therapy, or diet therapy alone, SMBG is useful for evaluation of therapy. Blood glucose therapy target goals are set individually. The ADA recommends that patients with type 1 diabetes aim for A1C values less than 6.5%, premeal glucose levels of 70 to 130 mg/dL (3.9 to 7.2 mmol/L), and postmeal glucose levels less than 180 mg/dL (10.0 mmol/L). Infection control measures are needed for SMBG. The chance of becoming infected from blood glucose monitoring processes is reduced by handwashing. Instruct patients to not share their blood glucose monitoring equipment. Hepatitis B virus can survive in a dried state for at least 1 week. Infection can be spread by the lancet holder. Regular cleaning of the meter is critical. With testing wear gloves(family/staff). Post-meal glucose monitoring provides information about the effects of the size and content of their meals. SMBG allows the patient to assess effects of exercise on glucose control and provides critical information to help patients who take insulin to exercise safely. When results are consistently out of range for a 3-day period when no change in meal plan, medications, or activity has occurred, patient must adjust therapy.

Preventing Injury from Reduced Vision: Environmental Management

Adjustments in lighting, contrast, color, distance, type size of printed materials, and eye movement often improve visual abilities. Coding objects such as vials of insulin with bright colors or with felt-tipped markers helps identify the correct bottle. Bringing the blood glucose lancet or insulin syringe close to the eye makes it easier to see. Prefilled insulin pens are not approved for use by people with severe visual impairment unless they are assisted. Some syringes may have a magnifier attached to the syringe. Other devices include preset dose gauges (which measure the space between the end of the syringe barrel and the plunger) to help the patient draw up the correct amount of insulin by feeling this distance. The blind patient can accurately measure insulin by using products such as the Count-A-Dose Insulin Measuring Device. This device is designed to be used with the BD Lo-Dose syringe. It holds two insulin vials and has a slot to direct the syringe needle into the vials' rubber stoppers. The patient draws insulin into the syringe by turning a thumb-wheel, which clicks for each unit. When teaching the patient to use an adaptive device, stress: • Differentiating between bottles of fast-acting and slower-acting insulin by wrapping a rubber band around the fast-acting insulin bottle • Ensuring proper placement of the device on the syringe • Holding the insulin bottle upright when measuring insulin • Avoiding air bubbles in the syringe by pulling a small amount of insulin into the syringe, moving the plunger in and out 3 times, and measuring insulin on the fourth draw Design a system to determine how many doses can be drawn from a bottle so the patient does not inject air from an empty bottle. Assist the patient to select a blood glucose monitoring device best suited to his or her level of visual impairment. Some monitors have large display screens and easy-to-use features. Fully audio systems are available for patients who are visually impaired. The monitor uses no coding, has automatic turn-on with test strip insertion, and has a button for repeating the last message.

Enhancing Surgical Recovery: Preoperative Care

Admitted to the hospital 2 to 3 days before surgery to optimize blood glucose control. Sulfonylureas are discontinued 1 day before surgery. Metformin (Glucophage) is stopped at least 24 hours before surgery and restarted only after kidney function is normal. All other oral drugs are stopped the day of surgery. Patients taking long-acting insulin may need to be switched to intermediate-acting insulin forms 1 to 2 days before. Preoperative blood glucose levels should be less than 200 mg/dL (11.1 mmol/L). Higher levels are associated with increased infection rates and impaired wound healing. Pain, a stressor, triggers the release of counterregulatory hormones, increasing blood glucose levels and insulin needs. Opioid analgesics slow GI motility and alter blood glucose levels. The older patient who receives opioids is more at risk for confusion, paralytic ileus, hypoventilation, hypotension, and urinary retention. Patient-controlled analgesia (PCA) systems reduce respiratory complications and confusion.

Enhancing Surgical Recovery: Interventions

Anesthesia and surgery cause a stress response with release of counterregulatory hormones that elevate blood glucose. Stress hormones suppress insulin action, increasing the risk for ketoacidosis. Hyperglycemic-hyperosmolar state (HHS) is a common complication after major surgery and is associated with increased mortality. Diuresis from hyperglycemia can cause dehydration and increases the risk for kidney failure. Patients with DM are at higher risk for hypertension, ischemic heart disease, cerebrovascular disease, MI, and cardiomyopathy. Heart failure is a serious risk factor and must be improved before surgery. Autonomic neuropathy may result in sudden tachycardia, bradycardia, or postural hypotension. The patient with DM is at risk for acute kidney injury and urinary retention after surgery, especially if he or she has albumin in the urine (indicator of kidney damage). Nerves to the intestinal wall and sphincters can be impaired, leading to delayed gastric emptying and reflux of gastric acid, which increases the risk for aspiration with anesthesia. Autonomic neuropathy may cause paralytic ileus.

Preventing Diabetic Ketoacidosis: Fluid and Electrolyte Management 1

Assess for acute weight loss, thirst, decreased skin turgor, dry mucous membranes, and oliguria with a high specific gravity. Also assess for weak and rapid pulse, flattened neck veins, increased temperature, decreased central venous pressure, muscle weakness, postural hypotension, and cool, clammy, and pale skin to determine if the patient is at risk for dehydration and shock. Fuid volume excess include acute weight gain, full and bounding pulses, distended neck veins, pulmonary crackles, peripheral edema, and elevated central venous pressure. Acute pulmonary edema can develop quickly. Hypertension is common, especially in patients with kidney failure. Age-related skin changes, such as loss of elasticity and dryness, make 1334skin turgor an unreliable indicator of dehydration. With severe hyperglycemia, the kidneys are less able to respond to changes in pH or fluid and electrolyte balance, to concentrate urine, or to regulate blood osmolarity. The risk for kidney failure rises with age, and acidosis occurs more quickly. Cardiovascular disease can cause fluid retention. In patients with poor kidney function and excess fluid volume, assess for edema around the eyes and in the limbs, increasing blood pressure, jugular venous distention, and orthostatic hypotension. Edema occurs with excess interstitial fluid and often is not apparent until interstitial volume increases by 2 to 3 L. Jugular venous pressure increases with volume overload. In severe volume depletion, the jugular venous pulsation may not be visible even with the patient lying flat.

Preventing Hypoglycemia: Patient and Family Education

At the onset of menses, a fall in hormone levels decreases insulin needs and contributes to hypoglycemia. When patients switch to a new bottle of insulin, hypoglycemia may occur bc of potency. Some have hypoglycemia when they change injection sites. Beta-blocking drugs mask manifestations that are warning signs and thus predispose patients to severe hypoglycemia. Using the estimate that each 5 g of carbohydrate raises blood glucose about 20 mg/dL is a good starting plan. For example, the patient may be directed to take: • 20 to 30 g of carbohydrate if the blood glucose level is 50 mg/dL (2.8 mmol/L) or less • 10 to 15 g of carbohydrate if the blood glucose level is 51 to 70 mg/dL (2.9 to 3.9 mmol/L) Use blood glucose monitoring results to revise. Encourage the patient to wear a medical alert bracelet. Emphasize that delaying a meal for more than 30 minutes raises the risk for hypoglycemia when using insulin. Instruct him or her to keep a carbohydrate source nearby at all times. Teach the patient and family how to administer glucagon. Explain that nightmares or headaches on days after prolonged or severe exercise may indicate hypoglycemia.

Preventing Injury from Peripheral Neuropathy: Interventions 2

Autonomic neuropathy causes loss of normal sweating and skin temperature regulation, resulting in dry, thinning skin. Skin cracks and fissures increase the risk for infection. Sensory neuropathy may cause pain, tingling, or burning (Funnell, 2014). More often it produces numbness and reduced sensory perception. Without sensation, the patient does not notice injuries and loss of tissue integrity in the foot and does not treat them. Foot injuries can be caused by walking barefoot, wearing ill-fitting shoes, sustaining thermal injuries from heat (e.g., hot water bottles, heating pads, baths), or chemical burns from over-the-counter corn treatments. These injuries can lead to loss of tissue integrity and to amputation. Ulcers result from continued pressure. Plantar ulcers (on the sole, usually the ball) are from standing or walking. Those on the top or sides of the foot usually are from shoes. The increased pressure causes calluses. Ulcers usually form over or around the great toe, under the metatarsal heads, and on the tops of claw toes. Infection impairs glucose regulation, leading to higher blood glucose levels and reduced immune defenses, which further increases the risk for infection.

Reducing the Risk for Kidney Disease: Fluid and Electrolyte Management

Avoiding dehydration is important for kidney perfusion and function. The most common cause of dehydration in patients with diabetes is overuse of diuretics. Teach patients to report edema or symptoms of orthostatic hypotension, and provide ongoing education to promote nutrition therapy. Dialysis for patients with DM and kidney failure is the same as for patients without diabetes. The dosage of insulin needs to be adjusted when dialysis starts.

Action Alert

Because of the potential for alcohol-induced hypoglycemia, instruct the patient with diabetes to ingest alcohol only with or shortly after meals.

Critical Rescue

Before giving IV potassium-containing solutions, make sure the urine output is at least 30 mL/hr.

Blood Glucose Control in Hospitalized Patients 2

Continuous IV insulin solutions are the most effective method for achieving glycemic targets in the critically ill. Scheduled subcutaneous injection with basal, meal, and correction elements is the preferred method for achieving and maintaining glucose control in non-critically ill. Using correction dose or "supplemental insulin" to correct premeal hyperglycemia in addition to scheduled prandial and basal insulin is recommended. Causes of inpatient hypoglycemia include an inappropriate insulin type, mismatch between insulin type and/or timing of food intake, and altered eating plan without insulin dosage adjustment. The Joint Commission (TJC), together with the ADA, has established Core Measures for preventing hypoglycemia, these involve protocols for hypoglycemia treatment that direct staff to provide carbohydrate replacement if the patient is alert and able to swallow or to administer 50% dextrose intravenously or glucagon by subcutaneous injection if the patient cannot swallow. Administration of rapid-acting or short-acting insulin, as well as amylin and incretin mimetics, will cause hypoglycemia if a patient is NPO. Basal insulin should be administered when the patient is NPO because it controls baseline glucose levels. Insulin mixtures are not administered because they contain some short-acting or rapid-acting insulin and will cause hypoglycemia.

Alternative Methods of Insulin Administration

Continuous subcutaneous infusion of a basal dose of insulin (CSII) with increases in insulin at mealtimes is more effective in controlling blood glucose levels than other schedules. It allows flexibility in meal timing, because if a meal is skipped, the additional mealtime dose of insulin is not given. CSII is given by an externally worn pump containing a syringe and reservoir with rapid-acting insulin and is connected to the patient by an infusion set. Rapid-acting insulin analogs are used with insulin infusion pumps. Problems with CSII include skin infections that can occur when the infusion site is not cleaned or the needle is not changed every 2 to 3 days. Stress the importance of testing for ketones when blood glucose levels are greater than 300 mg/dL (16.7 mmol/L). Patients using CSII need intensive education. Because of the risk for hypoglycemia or hyperglycemia, he or she must be able to operate the pump, adjust the settings, and respond appropriately to alarms. Provide supplemental insulin schedules for times when the pump is not operational. Injection devices include a needleless system and a pen-type injector in addition to traditional insulin syringes. With a needleless device, the needle is replaced by an ultrathin liquid stream of insulin forced through the skin under high pressure known as "jet injection." Insulin given by jet injection is absorbed at a faster rate and has a shorter duration of action.

Enhancing Surgical Recovery: Postoperative Care

Current AACE and ADA Core Measures recommend insulin protocols that maintain blood glucose between 140 and 180 mg/dL (7.8 and 10.0 mmol/L) for critically ill patients. Continue glucose and insulin infusions as prescribed until the patient is stable and can tolerate oral feedings. Short-term insulin therapy may be needed after surgery for the patient who usually uses oral agents. For those receiving insulin therapy, dosage adjustments may be required until the stress of surgery subsides.

Principles of Nutrition in Diabetes 2

Dietary fat and cholesterol intake for people with diabetes is the same as the Institute of Medicine's (IOM) recommendations for the general population to reduce the risk for cardiovascular disease. These recommendations are based on the issue that fat quality is more important in lipid control than is fat quantity. Recommendations are: • Limiting total fat intake to 20% to 35% of daily calorie intake • Choosing monounsaturated and polyunsaturated fats over saturated fats and trans fats • Limiting dietary cholesterol to less than 200 mg/day • Having two or more servings of fatty fish per week (with the exception of commercially fried fish) to provide n-3 polyunsaturated fatty acids Trans fatty acids increase the risk for CVD. Teach the patient to limit the amount of commercially fried foods and bakery goods eaten. Adults with diabetes should be tested annually for abnormalities of fasting serum cholesterol, triglyceride, HDL cholesterol, and calculated LDL cholesterol levels. Protein intake of 15% to 20% of total daily calories is appropriate for patients with diabetes and normal kidney function. Diets higher in protein have demonstrated improvement in insulin response but do not prevent hypoglycemia. In patients with progressive kidney disease, reducing protein intake is needed and the level of protein reduction individual. Fiber improves carbohydrate metabolism and lowers cholesterol levels. Include foods containing a minimum of 25 g of fiber daily for women and 38 g daily for men. Teach the patient to select a variety of fiber-containing foods such as legumes, fiber-rich cereals (more than 5 g fiber/serving), fruits, vegetables, and whole-grain products because they provide vitamins, minerals, and other substances important for good health.

Drug Alert

Do not mix any other insulin type with insulin glargine, with insulin detemir, or with any of the premixed insulin formulations, such as Humalog Mix 75/25.

Drug Alert

Do not mix pramlintide and insulin in the same syringe because the pH of the two drugs is not compatible.

Mnemonic

Dry and hot need a shot; cold and clammy need a candy.

Male Erectile Dysfunction

ED occurs at a higher rate and 10 to 15 years earlier among men with DM as compared with the general population. It is related to poor blood glucose regulation, obesity, hypertension, heavy cigarette smoking, and the presence of other chronic vascular complications.

Meal Planning Strategies 2

Exercise can cause hypoglycemia if insulin is not decreased before activity. For planned exercise, reduction in insulin dosage is used for hypoglycemia prevention. For unplanned exercise/intense activity, additional CHO is usually needed. Moderate exercise increases glucose utilization by 2 to 3 mg/kg/min. A 70-kg (154-lb) person would need about 10 to 15 g additional CHO per hour of moderate-intensity activity. Important for patients with type 1 diabetes to avoid gaining weight. Chronic high insulin levels (hyperinsulinemia) can occur with intensive management schedules and may result in weight gain. These patients may need to manage hyperglycemia by restricting calories rather than increasing insulin. Weight gain can be minimized by following the prescribed meal plan, getting regular exercise, and avoiding overtreatment of hypoglycemia. Special considerations for type 2 diabetes focus on lifestyle changes. Nutrition therapy stresses lifestyle changes that reduce calories eaten and increase calories expended through physical activity. Many patients also have abnormal blood fat levels and hypertension (metabolic syndrome), making reductions of saturated fat, cholesterol, and sodium desirable. A moderate caloric restriction (250 to 500 calories less than average daily intake) and an increase in physical activity improve diabetes control and weight control. Decreases of more than 10% of body weight can result in significant improvement in A1C. Decreasing intake of cholesterol-raising fatty acids helps reduce the risk for CVD.

Preventing Diabetic Ketoacidosis: Blood Glucose Management

First assess the airway, level of consciousness, hydration status, electrolytes, and blood glucose level. Check the patient's blood pressure, pulse, and respirations every 15 minutes until stable. Record urine output, temperature, and mental status every hour. When a central venous catheter is present, assess central venous pressure every 30 minutes or as prescribed. After treatment starts and these values are stable, monitor and record vital signs every 4 hours. Use blood glucose values to assess therapy and determine when to switch from saline to dextrose solutions.

Preventing Hypoglycemia: Drug Therapy

Glucagon given subcutaneously or IM and 50% dextrose given IV are used for patients who cannot swallow. Glucagon is the main counterregulatory hormone to insulin and is used as first-line therapy for severe hypoglycemia in DM. It converts liver glycogen to glucose but is not effective in severely starved patients. Take care to prevent aspiration in patients receiving glucagon, because it often causes vomiting. Give 50% dextrose carefully to avoid extravasation(diapedesis). After the patient responds and is no longer nauseated, give a simple sugar followed by a small snack or meal. IV glucose is used to maintain mild hyperglycemia. Diazoxide (Proglycem) or octreotide (Sandostatin) may be required to treat sulfonylurea-induced hypoglycemia. Evaluate response by monitoring blood glucose levels. A target blood glucose level is 70 to 110 mg/dL (3.9 to 6.2 mmol/L).

Glucose Regulation and Homeostasis

Glucose is the main fuel for central nervous system (CNS) cells. Because the brain cannot produce or store much glucose, it needs a continuous supply from circulation to prevent neuron dysfunction and cell death. During fasting, when the stomach is empty, blood glucose is maintained between 60 and 150 mg/dL (3.3 and 8.3 mmol/L) by a balance between glucose uptake by cells and glucose production by the liver. Insulin plays a pivotal role in this process. Insulin is like a "key" that opens "locked" membranes to glucose, allowing blood glucose to move into cells to generate energy. Insulin starts this action by binding to insulin receptors on the cell membranes, which changes membrane permeability to glucose. In the liver, insulin promotes the production and storage of glycogen (glycogenesis) at the same time that it inhibits glycogen breakdown into glucose (glycogenolysis). It increases protein and lipid (fat) synthesis and inhibits ketogenesis (conversion of fats to acids) and gluconeogenesis (conversion of proteins to glucose). In muscle, insulin promotes protein and glycogen synthesis. In fat cells, it promotes triglyceride storage. In the fasting state (not eating for 8 hours), insulin secretion is suppressed, which leads to increased gluconeogenesis in the liver and kidneys, along with increased glucose generation by the breakdown of liver glycogen. Insulin enhances glucose uptake and use by cells and reduces both fat breakdown (lipolysis) and protein breakdown (proteolysis). When more glucose is present in liver cells than can be used for energy or stored as glycogen, insulin causes the excess glucose to be converted to free fatty acids (FFAs). These extra FFAs are deposited in fat cells. Incretin hormones (e.g., GLP-1), secreted in response to food in the stomach, increase insulin secretion, inhibit glucagon secretion, and slow the rate of gastric emptying. Glucagon is the main counterregulatory hormone. Other hormones that increase blood glucose levels are epinephrine, norepinephrine, growth hormone, and cortisol.

Ongoing Assessment

Glycosylated hemoglobin assays are useful because blood glucose permanently attaches to hemoglobin. The higher the blood glucose level is over time, the more glycosylated hemoglobin becomes. Glycosylated hemoglobin A1C (A1C) is a good indicator of the average blood glucose levels because it shows the average blood glucose level during the previous 120 days—the life span of RBCs. Unlike the fasting blood glucose test, A1C test results are not altered by eating habits the day before the test. A1C testing is recommended at least twice yearly in patients who are meeting expected treatment outcomes and have stable blood glucose control. Quarterly assessment is recommended for patients whose therapy has changed or who are not meeting prescribed glycemic levels. When glucose binds to amino groups on serum proteins, especially albumin, the glycosylated protein product is called fructosamine. This product increases with elevated blood glucose levels in the same way as hemoglobin does but can indicate blood glucose control over a shorter period. These measures are useful for short-term follow-up of treatment changes or in patients with hemoglobin abnormalities in which A1C is not an accurate reflection of glucose control. Available tests are called glycosylated serum albumin (GSA), glycosylated serum protein (GSP), and fructosamine.

Preventing Hyperglycemic-Hyperosmolar State

Hyperglycemic-hyperosmolar state (HHS) is a hyperosmolar (increased blood osmolarity) state caused by hyperglycemia. Both HHS and diabetic ketoacidosis (DKA) are caused by hyperglycemia and dehydration. HHS differs from DKA in that ketone levels are absent or low and blood glucose levels are much higher. Blood glucose levels may exceed 600 mg/dL (33.3 mmol/L), and blood osmolarity may exceed 320 mOsm/L. HHS results from a sustained osmotic diuresis. Kidney impairment in HHS allows for extremely high blood glucose levels. As blood concentrations of glucose exceed the renal threshold, the kidney's capacity to reabsorb glucose is exceeded. Decreased blood volume, caused by osmotic diuresis, or underlying kidney disease, common in many older patients with diabetes, results in further deterioration of kidney function. The decreased volume further reduces glomerular filtration rate, causing the glucose level to increase. Myocardial infarction, sepsis, pancreatitis, stroke, and some drugs (glucocorticoids, diuretics, phenytoin [Dilantin], beta blockers, and calcium channel blockers) also may cause HHS. Central nervous system (CNS) changes range from confusion to complete coma. Patients with HHS may have seizures and reversible paralysis. The degree of neurologic impairment is related to serum osmolarity, with coma occurring once serum osmolarity is greater than 350 mOsm/L. The development of HHS is related to residual insulin secretion. In HHS, the patient secretes just enough insulin to prevent ketosis but not enough to prevent hyperglycemia. The hyperglycemia of HHS is more severe than that of DKA, greatly increasing blood osmolarity, leading to extreme diuresis with severe dehydration and electrolyte loss.

Enhancing Surgical Recovery: Intraoperative Care

IV infusion of insulin, glucose, and potassium is standard therapy for perioperative management of diabetes. In accordance with The Joint Commission's NPSGs, the objective is to keep the blood glucose level between 140 and 180 mg/dL (7.8 and 10.0 mmol/L) during surgery to prevent hypoglycemia and reduce risks from hyperglycemia. Higher insulin doses may be needed because stress releases glucagon and epinephrine. Patients with DM usually receive about 5 g of glucose per hour during surgery to prevent hypoglycemia, ketosis, and protein breakdown. Monitor the patient's temperature. Hypothermia decreases metabolic needs, depresses heart rate and contractility, causes vasoconstriction, and impairs insulin release, resulting in high blood glucose levels. Monitor arterial blood gas values for acidosis.

Preventing Hyperglycemic-Hyperosmolar State: Continuing Therapy

IV insulin is administered after adequate fluids have been replaced. The typical intervention is an initial bolus dose of 0.15 unit per kg IV followed by an infusion of 0.1 unit per kg per hour until blood glucose levels fall to 250 mg/dL (13.9 mmol/L). A reduction of blood glucose of 50 to 70 mg/dL per hour is expected. Monitor for hypokalemia. ody potassium depletion is often unrecognized because the blood potassium level may be normal or high as a result of dehydration. The potassium level may drop quickly when insulin therapy is started. Potassium replacement is initiated once urine output is adequate. Serum electrolytes are checked every 1 to 2 hours. The cardiac rhythm is monitored continuously for signs of hypokalemia or hyperkalemia.

Preventing Injury from Peripheral Neuropathy: Foot Care

Identify patients with high-risk foot conditions. Explain problems caused by loss of protective sensory perception, the importance of monitoring the feet daily, proper care of the feet (including nail and skin care), and how to select appropriate footwear. Assess the patient's ability to inspect all areas of the foot and to perform foot care. Teach family members how to inspect and care for the patient's feet

Patient Education: Drugs 1

Insulin storage varies by use. Teach patients to refrigerate insulin that is not in use to maintain potency, prevent exposure to sunlight, and inhibit bacterial growth. Insulin in use may be kept at room temperature for up to 28 days to reduce irritation(cold). To prevent loss of drug potency, teach the patient to avoid exposing insulin to temperatures below 36° F (2.2° C) or above 86° F (30° C), to avoid excessive shaking, and to protect insulin from direct heat and light. Insulin should not be allowed to freeze. Insulin glargine (Lantus) should be stored in a refrigerator (36° to 46° F [2.2° to 7.8° C]) even when in use. Teach patients to discard any unused insulin after 28 days. Teach patients to always have a spare bottle of each type used. A slight loss in potency may occur for bottles in use for more than 30 days, even when not expired. Prefilled syringes are stable up to 30 days when refrigerated. Store prefilled syringes in the upright position, with the needle pointing upward, so that insulin particles do not clog. Teach patients to roll, not shake, prefilled syringes between the hands. Dose preparation is critical. Teach patients that the person giving the insulin needs to inspect the insulin before each use(e.g., clumping, frosting, precipitation, or change in clarity or color). Rapid-acting, short-acting, and glargine insulins should be clear. Preparations containing NPH insulin should be uniformly cloudy after gently rolling the vial between the hands.

Preventing Injury from Hyperglycemia: Insulin Therapy

Insulin therapy is needed for type 1 DM and also may be used for type 2. Many types of insulin and regimens to achieve normal blood glucose levels. Because insulin is a small protein that is quickly digested and inactivated in the GI tract, it must be administered as an injection.

Preventing Diabetic Ketoacidosis: Drug Therapy

Insulin therapy is used to lower serum glucose by about 50 to 75 mg/dL/hr. Unless the episode of DKA is mild, regular insulin by continuous IV infusion is the usual. Blood insulin levels are reached quickly when an IV bolus dose is given at the start of the infusion. An initial IV bolus dose of 0.1 unit/kg is followed by an IV infusion of 0.1 unit/kg/hr. Continuous insulin infusion is used because insulin half-life is short. Subcutaneous insulin is started when the patient can take oral fluids and ketosis has stopped. DKA is considered resolved when blood glucose is less than 200 mg/mL along with a serum bicarbonate level higher than 18 mEq/L, venous pH higher than 7.3, and a calculated ion gap less than 12 mEq/L.

Diffuse neuropathies

Involve widespread nerve function loss and sensory perception loss. The onset is slow, affects both sides of the body, involves motor and sensory nerves, progresses slowly, is permanent, and includes autonomic nerve dysfunction. Late complications include foot ulcers and deformities.

Islet Cell Transplantation.

Islet cell transplantation eliminates the need for insulin and protects against the complications of diabetes. Islet cells from tissue-typed (HLA-matched) cadaver pancreas glands are injected into the portal vein. The new cells lodge in the liver and begin to function, secreting insulin and maintaining near-perfect blood glucose control. Islet cell transplantation may successfully restore long-term endogenous insulin production and glycemic control in patients with type 1 diabetes and unstable baseline control. Most patients undergoing this procedure eventually have a progressive loss of islet cell function. Very few islet cell transplant recipients have remained insulin-free for more than 4 years. The reasons for this gradual loss of function are not known and make this procedure a long-term but temporary intervention.

Exercise Therapy

It has beneficial effects on carbohydrate metabolism and insulin sensitivity. Programs of increased physical activity and weight loss reduce the incidence of type 2 diabetes. The patient with type 1 DM cannot make the hormonal changes needed to maintain stable blood glucose levels during exercise. Without an adequate insulin supply, cells cannot use glucose. Low insulin levels trigger release of glucagon and epinephrine (counterregulatory hormones) to increase liver glucose production, further raising blood glucose levels. In the absence of insulin, free fatty acids become the source of energy. Exercise in the patient with uncontrolled diabetes results in further hyperglycemia and the formation of ketone bodies. He or she may have prolonged elevated blood glucose levels after vigorous exercise. Exercise in the person with diabetes also can cause hypoglycemia because of increased muscle glucose uptake and inhibited glucose release from the liver. It can occur during exercise and for up to 24 hours after exercise. Replacement of muscle and liver glycogen stores, along with increased insulin sensitivity after exercise, causes insulin requirements to drop.

Cardiovascular Disease(MACRO)

Most patients with DM die as a result of a thrombotic event, usually myocardial infarction (MI). Systolic and diastolic heart failure are associated with DM. Patients with DM are more likely to develop left ventricular dysfunction with heart failure and fatal cardiac dysrhythmias after MI. Risk affects women to a greater degree than men and is influenced by ethnicity. Patients with diabetes often have the traditional CVD risk factors of obesity, smoking, family history, high blood lipid levels, hypertension, and sedentary lifestyle. Kidney disease, indicated by albuminuria (presence of albumin in the urine), increases the risk. Patients with DM often have higher levels of C-reactive protein (CRP), an inflammatory marker. The presence of diabetic retinopathy is associated with an increased risk for mortality and cardiovascular events. The American Diabetes Association (ADA) recommends that blood pressure be maintained below 140/80 mm Hg and that low-density lipoprotein (LDL) cholesterol remains below 100 mg/dL (2.60 mmol/L) for patients without manifestations of CVD and below 70 mg/dL (1.8 mmol/L) for patients with manifestations of CVD. Lifestyle modifications that focus on reducing saturated fat, trans fat, and cholesterol intake; increasing intake of omega-3 fatty acids, fiber, and plant sterols; weight loss (if indicated); and increasing physical activity are recommended to improve the lipid profile. Priority nursing actions focus on interventions to reduce modifiable risk factors associated with CVD, such as smoking cessation, diet, exercise, blood pressure control, maintaining prescribed aspirin use, and maintaining prescribed lipid-lowering drug therapy. Manifestations of MI in diabetics are more subtle. These include dyspnea with or without cough, extreme fatigue, and sudden onset of nausea and vomiting. Teach patients to report any of these subtle manifestations of MI.

Diabetic Nephropathy

Nephropathy is a pathologic change in the kidney that reduces kidney function and leads to kidney failure. Diabetes is the leading cause of chronic kidney disease (CKD) and end-stage kidney disease (ESKD). Risk factors include a 10- to 15-year history of DM, poor blood glucose control, uncontrolled hypertension, and genetic predisposition. Patients who have a genetic predisposition appear to have higher serum uric acid levels and higher levels of tumor necrosis factor receptors. Drugs that protect the kidneys are the angiotensin-converting enzyme (ACE) inhibitors and the angiotensin receptor blockers (ABRs). Early manifestations of nephropathy are microalbuminuria (small amounts of albumin in the urine) and elevated serum uric acid levels. Annual testing for microalbuminuria is recommended for patients who have had type 1 DM for at least 5 years and in everyone with type 2 DM. Increased pressure damages the kidney in many ways. The blood vessels become leakier, especially in the glomerulus. This leakiness allows filtration of albumin and other proteins, which then form deposits in the kidney tissue and blood vessels. Blood vessels narrow, decreasing kidney oxygenation and leading to kidney cell hypoxia and cell death. These processes worsen over time.

Health Promotion and Maintenance

No interventions are successful in preventing type 1 DM, but health promotion activities focus on controlling hyperglycemia to reduce its long-term complications. Adopting a low calorie diet that results in weight loss and increasing physical activity improve metabolic and cardiac risk factors. These improvements include reducing hypertension, increasing heart rate variability between resting rate and exercise rate, lowering triglyceride levels, increasing high-density lipoprotein cholesterol (the "good" cholesterol) levels, and reducing low-density lipoprotein cholesterol (the "bad" cholesterol) levels. Teach all patients with DM that tight control of blood glucose levels can prevent many complications. Urge all patients with DM to regularly follow up with their health care provider or endocrinologist, to have their eyes and vision tested yearly. Have urine microalbumin levels assessed yearly. Encourage all people to maintain weight within an appropriate range for height and body build and to engage in physical activity at least 3 times per week.

Principles of Nutrition in Diabetes 1

No one meal plan is right for all patients with diabetes. Day-to-day consistency in the timing and amount of food eaten helps control blood glucose. Teach patients using intense insulin therapy to adjust premeal insulin to allow for timing and quantity changes in their meal plan. Carbohydrate intake and available insulin are responsible for postmeal glucose levels, and managing carbohydrate intake is the main strategy for achieving glucose regulation. The recommendation for the patient with diabetes is a diet containing 45% of calories from carbohydrate, with a minimum intake of 130 g carbohydrate/day. However, the upper limit on daily carbohydrate intake is now considered somewhat flexible. Carbohydrate from fruit, vegetables, whole grains, legumes, and low-fat milk products. The total amount of carbohydrate consumed each day rather than the source of the carbohydrate is still important.

Preventing Injury from Hyperglycemia: Nonsurgical Management.

Nonsurgical management of diabetes mellitus (DM) involves nutrition interventions, blood glucose monitoring, a planned exercise program, and often, drugs to lower blood glucose levels. The American Diabetes Association (ADA) has proposed these treatment outcomes for glycosylated hemoglobin (A1C) and blood glucose levels: • A1C levels are maintained at 6.5% or below. • The majority of premeal blood glucose levels are 70 to 130 mg/dL (3.9 to 7.2 mmol/L). • Peak after-meal blood glucose levels are less than 180 mg/dL (<10.0 mmol/L).

TABLE 64-1 Classification of Diabetes Mellitus

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TABLE 64-2 Physiologic Response to Insufficient Insulin

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TABLE 64-3 Features of Diabetic Neuropathy

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TABLE 64-4 Differentiation of Type 1 and Type 2 Diabetes

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Cultural Considerations and TABLE 64-5 Indications for Testing People for Type 2 Diabetes

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TABLE 64-6 Criteria for the Diagnosis of Diabetes

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Chart 64-1 Laboratory Profile Blood Glucose Values

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TABLE 64-7 Correlation Between A1C Level and Mean Blood Glucose Levels

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Chart 64-2 Common Examples of Drug Therapy Diabetes Mellitus

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TABLE 64-8 Time Activity of Pharmaceutical Insulin

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Chart 64-5 Focused Assessment The Diabetic Foot

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TABLE 64-10 Foot Risk Categories

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TABLE 64-11 Manifestations of Hypoglycemia

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TABLE 64-12 Differentiation of Hypoglycemia and Hyperglycemia

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Chart 64-7 Patient and Family Education: Preparing for Self-Management Management of Hypoglycemia at Home

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TABLE 64-13 Differences Between Diabetic Ketoacidosis and Hyperglycemic-Hyperosmolar State

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Considerations for Older Adults

Patients in the older age-groups are especially vulnerable to hypoglycemia. Age-related declines in kidney function and liver enzyme activity may interfere with the metabolism of sulfonylureas and insulin, thereby potentiating their hypoglycemic effects. Older patients with diabetes have impaired epinephrine release and a diminished glucagon response to falling blood glucose levels. They often have a reduced awareness of hypoglycemic manifestations. Confusion and any impairment in psychomotor performance when blood sugars are low prevent the older adult from taking appropriate steps to return the blood sugar to normal. Instruct the older patient and family to check blood glucose values when symptoms such as unsteadiness, light-headedness, poor concentration, trembling, or sweating occur. Assess eating patterns to make sure sufficient foods are eaten at appropriate times. Encourage a patient with a poor appetite to eat a small snack at bedtime to prevent hypoglycemia during the night. The highest rates of severe and fatal episodes of hypoglycemia are associated with the use of glyburide in patients older than 70 years. Drug regimens that require that meals be eaten on time increase the potential for hypoglycemic reactions. Complex regimens that require multiple decision points should be simplified, especially for patients with decreased functional status.

Preventing Injury from Peripheral Neuropathy: Prevention of High-Risk Conditions

Poor blood glucose control increases the risk for neuropathy and amputation. Urge smoking cessation to reduce the risk for vascular complications. The risk for ulcers or amputation increases with duration of diabetes. Other associated factors are male gender; poor glucose control; and cardiovascular, retinal, or kidney complications. Foot-related risks include poor gait and stepping mechanics, peripheral neuropathy, increased pressure (callus, erythema, hemorrhage under a callus, limited joint mobility, foot deformities, or severe nail pathology), peripheral vascular disease, and a history of ulcers or amputation

Preventing Injury from Reduced Vision: Blood Glucose Control

Poor blood glucose regulation (control), proteinuria, diastolic hypertension, and long duration of diabetes are risk factors for vision loss among diabetics. Surgical intervention for retinal hemorrhage or new retinal blood vessel growth can reduce vision loss. Besides regular eye examinations to evaluate retinopathy, urge the patient with impaired vision to have an optometrist or ophthalmologist assess the remaining vision and prescribe appropriate vision support. A functional vision assessment, performed by a low-vision technician, rehabilitation teacher, or diabetes educator, determines the patient's use of lighting, contrast, non-optical and low-vision devices, large-print options, and use of central or peripheral vision. Many low-vision reading aids are available

Action Alert

Prevent hypoglycemia by ensuring that appropriate blood glucose testing products are used for patients receiving parenteral maltose, parenteral galactose, and oral xylose products.

Reducing the Risk for Kidney Disease: Prevention 1

Progression to end-stage kidney disease (ESKD) can be delayed or prevented by normalizing blood pressure, correcting hyperlipidemia, and restricting dietary protein. Control of hypertension is essential for the reduction of diabetic nephropathy. Stress the need for evaluation of kidney function according to the ADA Standards of Care. Serum creatinine should be measured at least annually for an estimation of GFR in all patients with diabetes. An annual test for microalbuminuria is performed for patients who have had type 1 DM for over 5 years and in all those with type 2 DM starting at diagnosis and during pregnancy. Persistent albuminuria in the range of 30 to 299 mg/24 hr (formerly called microalbuminuria) is the earliest stage of nephropathy in type 1 DM and a marker for the development of nephropathy in type 2 DM. Patients with albumin levels greater than 300 mg/24 hr (formerly called macroalbuminuria) are likely to progress to end-stage kidney disease (ESKD). Screening for increased urinary albumin excretion is performed by measurement of the albumin-creatinine ratio in a spot collection. Aggressive control of blood glucose and hypertension in patients without microalbuminuria can avoid nephropathy. Once microalbuminuria develops, management focuses on controlling blood pressure and blood glucose, restricting dietary protein, avoiding nephrotoxic agents, promptly treating urinary tract infections, and preventing dehydration.

Preventing Hypoglycemia: Nutrition Therapy

Start carbohydrate replacement per physician prescription or standing protocols—usually ingestion of 15 to 20 g of glucose. If the patient can swallow, give a liquid form of carbohydrate, although any carbohydrate source can be used. Ingestion of 15 to 20 g of glucose is the preferred management for blood glucose levels less than 70 mg/dL (3.9 mmol/L), repeated in about 15 minutes if manifestations have not improved or if blood glucose levels are still less than 70. The amount of carbohydrate should be increased to 30 g for glucose levels less than 50 mg/dL (2.8 mmol/L). Ten grams (g) of oral glucose raises blood glucose levels by about 40 mg/dL over 30 minutes, and 20 g of oral glucose raises blood glucose levels by about 60 mg/dL over 45 minutes. Test blood glucose again in about 60 minutes because additional management may be needed. Fluid is absorbed much more quickly from the GI tract than are solids. Concentrated sweet fluids, such as juice with sugar added or a soft drink, may slow absorption. Management of hypoglycemia requires ingestion of glucose or glucose-containing foods. The blood glucose response correlates better with the glucose content rather than the carbohydrate content of the food. Adding protein to carbohydrate does NOT improve blood glucose response and does NOT prevent subsequent hypoglycemia. Adding fat may retard and then prolong the blood glucose response, resulting in post-treatment hyperglycemia. Commercial products available.

In-Depth Education 2

Teach patients receiving diet therapy alone, glucose-lowering drugs, or fixed insulin doses to eat consistent amounts of carbohydrate at meals and snacks. Patients who adjust mealtime doses of insulin or those on insulin pump therapy can be taught to match their insulin dose to the carbohydrate content of their diet. The patient needs to understand what to eat, how much to eat, and when to eat. Stress the importance of eating on time, the dangers of skipping meals, and how to maintain food intake during illness. Ask the patient to describe the meal plan and explain the adjustments needed to meet diabetic diet requirements. Include the family member usually responsible for buying groceries and preparing meals in this teaching. Regular physical activity is important for physical fitness, weight management, and blood glucose control. Assist all patients to identify activities they can do to achieve the goal of moderate-intensity activity 3 or more days a week. For patients taking insulin and/or insulin secretagogues, physical activity can cause hypoglycemia if drug dosage or carbohydrate intake is not increased. Review how to perform physical activities safely. Instruct the patient on blood glucose levels that are safe for exercise, the frequency of glucose monitoring during exercise, drug adjustments before exercise, food required before exercise, and what food to have available during exercise. He or she should be aware of the risk for injury during exercise and be able to explain the importance of protective footwear.

Critical Rescue

Teach patients with a history of hypoglycemic unawareness not to test at alternative sites.

Critical Rescue

Teach patients with type 1 diabetes to perform vigorous exercise only when blood glucose levels are 100 to 250 mg/dL (5.6 to 13.8 mmol/L) and no ketones are present in the urine.

Preventing Diabetic Ketoacidosis: Patient and Family Education

Teach the patient and family to check blood glucose levels every 4 to 6 hours as long as manifestations such as anorexia, nausea, and vomiting are present and as long as glucose levels exceed 250 mg/dL (13.8 mmol/L). Teach them to check urine ketone levels when blood glucose levels exceed 300 mg/dL (16.7 mmol/L). Teach the patient to prevent dehydration by maintaining food and fluid intake. Suggest that he or she drink at least 2 L of fluid daily and increase this amount when infection is present. When nausea is present, instruct the patient to take liquids containing both glucose and electrolytes (e.g., soda pop, diluted fruit juice, and sports drinks [Gatorade]). Small amounts of fluid may be tolerated even when vomiting. When the blood glucose level is normal or elevated, the patient should take 8 to 12 ounces (240 to 360 mL) of calorie-free and caffeine-free liquids every hour while awake to prevent dehydration. Liquids containing carbohydrate can be taken if the diabetic patient cannot eat solid food. Ingesting at least 150 g of carbohydrate daily reduces the risk for starvation ketosis. After consulting a primary care provider, urge the patient to take additional rapid-acting (lispro) or short-acting (regular) insulin based on blood glucose levels. Instruct the patient and family to consult the health care provider when these problems occur: • Blood glucose exceeds 250 mg/dL (13.8 mmol/L). • Ketonuria lasts for more than 24 hours. • The patient cannot take food or fluids. • Illness lasts more than 1 to 2 days. Detect hyperglycemia by monitoring blood glucose whenever the patient is ill. Illness can result in dehydration with DKA, hyperglycemic-hyperosmolar state, or both. The sooner the patient seeks treatment, the less severe the metabolic alteration. He or she should not omit insulin therapy during illness.

Principles of Nutrition in Diabetes 3

Teach the patient that adding high-fiber foods to the diet gradually can reduce abdominal cramping, loose stools, and flatulence. An increase in fluid intake should accompany increased fiber intake. Teach the patient to pay careful attention to blood glucose levels because hypoglycemia can result when dietary fiber intake increases significantly. Sucrose, fructose, and nonnutritive sweeteners (NNSs) are present in a variety of foods. Dietary sucrose does not increase blood glucose more than equal amounts of other starches. Intake of sucrose and sucrose-containing foods by patients with diabetes does not need to be restricted out of a concern for causing hyperglycemia. Sucrose can be included in the meal plan as long as it is adequately covered with insulin or other glucose-lowering agents; however, all people with diabetes are encouraged to avoid sugar sweetened beverages. The use of nonnutritive sweeteners to enhance the taste of food while not disturbing blood glucose control is desirable. Foods sweetened with high-fructose corn syrup should be avoided by people with diabetes because this substance has been found to increase the levels of triglycerides and other lipids. Free fructose, such as that found in fruit, does not appear to alter lipid metabolism. Alcohol consumption can affect blood glucose levels. Levels are not affected by moderate use of alcohol when diabetes is well controlled. Teach patients with diabetes that two alcoholic beverages for men and one for women daily can be ingested with, and in addition to, the usual meal plan. (One alcoholic beverage equals 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of distilled spirits.) Because alcohol raises blood triglycerides, reducing or abstaining from alcohol is important for patients with high blood lipid levels.

Whole-Pancreas Transplantation

The 1-year survival rate for patients is above 95%, with more than 83% of patients remaining free of insulin injection and diet restrictions after 1 year. Pancreatic transplantation is performed in one of three ways: pancreas transplant alone (PTA), pancreas after kidney (PAK) transplant, and simultaneous pancreas and kidney (SPK) transplant. SPK transplant is the ideal procedure for patients with DM and uremia(BUN). The recipient's pancreas is left in place, and the donated pancreas is placed in the pelvis. The insulin released by the pancreas graft is secreted into the bloodstream. The new pancreas also produces about 800 to 1000 mL of fluid daily, which is diverted to either the bladder or the bowel. Excretion of pancreatic fluids can cause dehydration and electrolyte imbalance, and drainage of these fluids into the urinary bladder causes irritation.

Patient Education: Blood Glucose Monitoring 3

The U.S. Food and Drug Administration issued an Important Safety Information Notice about blood glucose measurement following use of parenteral maltose, parenteral galactose, oral xylose-containing products, and the peritoneal dialysis solution icodextrin (EXTRANEAL). Galactose and xylose are found in some foods, herbs, and dietary supplements; they are also used in diagnostic tests. Some meters and test strips read these substances as glucose and falsely report the blood glucose as elevated. There have been insulin overdoses with severe hypoglycemia, coma, and death when patients have used this falsely elevated glucose reading. The Core Measures of The Joint Commission and other agencies recommend meters and test strips that use a technology in which only glucose in the blood is recognized. It is safest to monitor blood glucose patterns by laboratory methods. Blood glucose monitoring needs to be performed with a system in which the test strips use a different enzyme technology. The best resource for guidance in selecting a glucose monitoring system that is not reactive to maltose interference is the manufacturer of the test strip. Alternate site testing allows patients to obtain blood from sites other than the fingertip and is available on many meters. However, use caution when interpreting results obtained from alternate sites. Comparison studies have shown wide variation. Rely on fingertip. Continuous glucose monitoring (CGM) systems monitor glucose levels in interstitial fluid to provide real-time glucose information to the user. The system consists of three parts: a disposable sensor that measures glucose levels, a transmitter that is attached to the sensor, and a receiver that displays and stores glucose information. After an initiation or warm-up period, the sensor gives glucose values every 1 to 5 minutes. Sensors may be used for 3 to 7 days, depending. Provides information about the current blood glucose level, provides short-term feedback about results of treatment, and provides warnings when glucose readings become dangerous. Require at least two capillary glucose readings per day for calibration of the sensor. Sensor accuracy depends on these calibrations. Continuous glucose monitoring is meant to supplement, not replace, finger stick tests. Insulin should be given only after confirming the results of any of the continuous glucose monitoring systems!

Managing Pain: Interventions 2

The anticonvulsants gabapentin (Neurontin) and pregabalin (Lyrica) and the serotonin-norepinephrine reuptake inhibitor (SNRI) duloxetine (Cymbalta) are used in management of neuropathic pain. Tricyclic antidepressants such as amitriptyline hydrochloride (Elavil, Levate image) and nortriptyline (Pamelor) are widely used for pain but are not approved for this purpose. Their use is contraindicated for older adults and those with cardiovascular disease. The burning of neuropathy may respond to capsaicin cream 0.075% (Axsain image, Zostrix-HP). Teach the patient to apply it 4 times daily for several weeks. The pain may worsen for several days after therapy is started before improving. Unpleasant symptoms are noted with abrupt discontinuation of many of these drugs. A gradual reduction in the dose is recommended. Having a bed cradle to lift bed clothes off hypersensitive skin can be beneficial. Assist the patient to maintain stable glucose control. All patients with neuropathy are at increased risk for foot ulcers and require more frequent assessment and education in routine foot management.

Self-Management Education

The concept of diabetes self-management refers to the patient's daily responsibility for almost all tasks involved in diabetes care. Physicians, nurses, registered dietitians, pharmacists, social workers, and psychologists all participate in the education. People with diabetes are best able to learn through educational efforts that are tailored to their individual needs.

The Endocrine Pancreas

The endocrine portion, the islets of Langerhans, consists of the alpha cells, which secrete glucagon, and the beta cells, which produce insulin and amylin. Glucagon is a "counterregulatory" hormone that has actions opposite those of insulin. It prevents hypoglycemia (low blood glucose levels) by triggering the release of glucose from cell storage sites. Insulin prevents hyperglycemia by allowing body cells to take up, use, and store carbohydrate, fat, and protein. Proinsulin is converted into active insulin by removal of the C-peptide. It is secreted at low levels during fasting (basal insulin secretion) and at increased levels after eating (prandial). An early burst of insulin secretion occurs within 10 minutes of eating. This is followed by an increasing release

Drug Alert

To avoid adverse drug interactions, teach the patient who is taking an antidiabetic drug to consult with his or her primary care provider or pharmacist before using any over-the-counter drugs.

Considerations for Older Adults

The older patient with diabetic retinopathy also has visual changes from aging, and his or her ability to perform self-care may be seriously affected. The patient with retinopathy may have blurred vision, distorted central vision, fluctuating vision, loss of color perception, and mobility problems resulting from loss of depth perception. It is especially important to assess the patient's ability to measure and inject insulin and to monitor blood glucose levels to determine if adaptive devices are needed to assist in self-management activities.

Insulin Regimens

The pancreas produces a constant (basal) amount of insulin that balances liver glucose production with glucose use and maintains normal blood glucose levels between meals. The pancreas also produces additional (prandial) insulin to prevent blood glucose elevation after meals. A usual starting dose is between 0.5 and 1 unit/kg of body weight per day. For multiple-dose regimens or continuous subcutaneous insulin infusion (CSII), basal insulin makes up about 40% to 50% of the total daily dosage, with the remainder divided into premeal doses of rapid-acting insulin analogs or regular insulin. Basal insulin coverage is provided by intermediate-acting insulin such as NPH insulin or by long-acting insulin analogs, such as insulin glargine (Lantus) or insulin detemir (Levemir). Single daily injection protocols require insulin injection only once daily. This protocol may include one injection of intermediate- or long-acting insulin or a combination of short- and intermediate-acting insulin. Many patients with type 2 diabetes combine once-daily insulin injection with oral agent. Multiple-component insulin therapy combines short- and intermediate-acting insulin injected twice daily. Two thirds of the daily dose is given before breakfast and one third before the evening meal. Intensified regimens include a basal dose of intermediate- or long-acting insulin and a bolus dose of short- or rapid-acting insulin designed to bring the next blood glucose value into the target range. Blood glucose elevations above the target range are treated with "correction" doses of short- or rapid-acting insulin. Blood glucose testing 1 to 2 hours after meals and within 10 minutes before the next meal helps determine the adequacy of the bolus dose. The patient determines the effects of basal insulin by monitoring blood glucose levels before breakfast (fasting) and before the evening meal. Patients on intensified insulin regimens need extensive education. They need to know how to adjust insulin doses and understand nutrition therapy. Must also be able to accurately monitor blood glucose levels. Adherence to insulin injection schedules is critical in achieving glycemic control and maintaining A1C levels below the 6.5% needed to reduce long-term complications.

Cerebrovascular Disease(MACRO)

The risk for stroke is 2 to 4 times higher in people with DM. Diabetes also increases the likelihood of severe carotid atherosclerosis. Hypertension, hyperlipidemia, nephropathy, peripheral vascular disease, and alcohol and tobacco use further increase the risk for stroke. Patients with DM are likely to suffer irreversible brain damage with carotid emboli. Elevated blood glucose levels at the time of the stroke may lead to greater brain injury and higher mortality.

Preventing Injury from Peripheral Neuropathy: Wound Care

The standards of care for diabetic ulcers are a moist wound environment, débridement of necrotic tissue, and elimination of pressure (offloading). Eliminating pressure on an infected area is essential to wound healing. Teach patients with foot ulcers to not wear a shoe on the affected foot. Pressure necrosis from sensory loss delays healing and increases ulcer size. Pressure is reduced by specialized orthotic devices, custom-molded shoe inserts, or shoe adjustments that redistribute weight. Available products include total-contact casting, half shoes, removable cast walkers, wheelchairs, and crutches. Total-contact casts redistribute pressure over the bottom of the foot. Casting material is molded to the foot and leg to spread pressure along the entire surface of contact, reducing vertical force. The almost complete elimination of motion of the total-contact cast reduces plantar shear forces. The cast is removed 24 to 48 hours after application to inspect the foot and cast fit. The cast is replaced and then removed and reapplied weekly until the ulcer is healed. Teach the patient that foot ulcers will recur unless weight is permanently redistributed.

Exercise: Adjustments for Diabetes Complications

Vigorous aerobic or resistance exercise should be avoided in the presence of proliferative diabetic retinopathy or severe nonproliferative diabetic retinopathy. Teach the patient with retinopathy to avoid the Valsalva maneuver (breath holding while bearing down) and activities that increase blood pressure. Heavy lifting, rapid head motion, or jarring activities can cause vitreous hemorrhage or retinal detachment. Decreased pain sensation in the extremities increases the risk for skin breakdown and infection and for joint destruction. Teach patients with diabetic peripheral neuropathy (DPN) to wear proper footwear and to examine their feet daily. Teach anyone with a foot injury or open sore to engage in non-weight-bearing activities such as swimming, bicycling, seated yoga, or arm exercises. Those with autonomic neuropathy are at increased risk for exercise-induced injury from impaired temperature control, postural hypotension, and impaired thirst with risk for dehydration. Physical activity also can increase urine protein excretion. Encourage high-risk patients to start with short periods of low-intensity exercise.

What might you NOTICE in a patient with diabetes mellitus who demonstrates adequate glucose regulation?

Vital signs: • Blood pressure less than 140/80 • Heart rate and rhythm within the normal range • Temperature within the normal range Physical assessment: • Skin intact, especially on the feet, no open wounds or sores that have failed to heal • Weight proportionate to height; does not appear overweight or underweight • Vision adequate for safety and participation in ADLs • No report of pain, tingling, numbness, or burning in extremities Psychological assessment: • Oriented and not confused • Willing to learn and participate in self-care • Energy level good; can engage in desired work, recreational, and personal activities Laboratory assessment: • A1C levels are maintained at 6.5% or below. • The majority of premeal blood glucose levels are 70 to 130 mg/dL (3.9 to 7.2 mmol/L). • Peak after-meal blood glucose levels are less than 180 mg/dL (<10.0 mmol/L). • Urine is free from ketone bodies and albumin. • 24-hour intake and output balance. • Blood urea nitrogen (BUN) and serum creatinine are within the normal ranges. • Serum electrolytes are within the normal ranges.

Critical Rescue

When a patient who has had reasonably controlled blood glucose levels in the hospital develops an unexpected rise in blood glucose values, check for wound infection.

Considerations for Older Adults

With age, the ability of the heart and lungs to deliver oxygen to tissues and organs declines. Muscle strength and power decline gradually. Connective tissue becomes less elastic, affecting range of motion and flexibility. Limited range of motion can alter gait, increasing risk for falls. Older adults who remain active can limit losses in muscle mass and function. The emphasis for any activity program is on changing sedentary behavior to active behavior at any level. Encourage sedentary older adults to begin with low-intensity physical activity. Start low-intensity activities in short sessions (less than 10 minutes); include warm-up and cool-down components with active stretching. Changes in activity levels should be gradual. Formal evaluation by a physical therapist or occupational therapist may be needed. Examples of specific exercise can be found at www.geri.com.

Key Points: Physiological Integrity

• Never dilute or mix insulin glargine with any other insulin or solution. • Avoid injecting insulin within a 2-inch radius of the umbilicus. • Avoid IM insulin injection. • Assist patients who have pain from peripheral neuropathy to determine what pain-relieving drugs and techniques work best for them. • Assess the patient's A1C level for indications of adherence to prescribed regimens and their effectiveness. • Start carbohydrate replacement per physician prescription or standing protocols immediately on identifying a patient with hypoglycemia. • Give glucagon subcutaneously or IM and 50% dextrose IV to patients identified with hypoglycemia who cannot swallow. • First assess the airway, level of consciousness, hydration status, electrolytes, and blood glucose level of any patient with diabetic ketoacidosis. • Use blood glucose values to assess therapy effectiveness and determine when to switch from saline to dextrose-containing solutions in a patient with diabetic ketoacidosis. • Continually assess fluid status and level of consciousness in a patient with hyperglycemic-hyperosmolar state (HHS) during the resuscitation period. • Immediately report manifestations of cerebral edema (abrupt changes in mental status; changes in level of consciousness; changes in pupil size, shape, or reaction; seizures) in a patient with HHS to the health care provider. • Collaborate with the health care provider, diabetes nurse educator, registered dietitian, pharmacist, social worker, and case manager to individualize patient care for the person with diabetes in any care setting.

Chart 64-4 Patient and Family Education: Preparing for Self-Management Exercise

• Teach the patient about the relationship between regularly scheduled exercise and blood glucose levels, blood lipid levels, and complications of diabetes. • Reinforce the level of exercise recommended for the patient based on his or her physical health. • Instruct the patient to wear appropriate footwear designed for exercise. • Remind the patient to examine his or her feet daily and after exercising. • Remind the patient to stay hydrated and not to exercise in extreme heat or cold. • Warn the patient not to exercise within 1 hour of insulin injection or near the time of peak insulin action. • Teach patients how to prevent hypoglycemia during exercise: 1 Do not exercise unless blood glucose level is at least 80 and less than 250 mg/dL. 2 Have a carbohydrate snack before exercising if 1 hour has passed since the last meal or if the planned exercise is high intensity. 3 Carry a simple sugar to eat during exercise if symptoms of hypoglycemia occur. 4 Ensure that identification information about diabetes is carried during exercise. • Remind the patient to check blood glucose levels more frequently on days in which exercise is performed and that extra carbohydrate and less insulin may be needed during the 24-hour period after extensive exercise.

Before being discharged to home, the patient with diabetes or the significant other should be able to:

• Tell why insulin or an oral hypoglycemic agent is being prescribed • Name which insulin or oral hypoglycemic agent is being prescribed, and name the dosage and frequency of administration • Discuss the relationship between mealtime and the action of insulin or the oral hypoglycemic agent • Discuss plans to follow diabetic diet instructions • Prepare and administer insulin accurately • Test blood for glucose, or state plans for having blood glucose levels monitored • Test urine for ketones, and state when this test should be done • Verbalize how to store insulin • List manifestations that indicate a hypoglycemic reaction • Tell what carbohydrate sources are used to treat hypoglycemic reactions • Tell what manifestations indicate hyperglycemia • Tell what dietary changes are needed during illness • Verbalize when to call the physician or the nurse (frequent episodes of hypoglycemia, manifestations of hyperglycemia) • Verbalize the procedures for proper foot care

Key Points: Safe and Effective Care Environment

• Use aseptic technique during any invasive procedure when caring for a patient with diabetes. • Administer antidiabetic drugs and insulin in a safe manner. • Ensure that meals are available immediately after the patient receives an antidiabetic drug or insulin. • Use good handwashing techniques before providing any care to a patient who has diabetes.

Chart 64-3 Patient and Family Education: Preparing for Self-Management Subcutaneous Insulin Administration

• Wash your hands. • Inspect the bottle for the type of insulin and the expiration date. • Gently roll the bottle of intermediate-acting insulin in the palms of your hands to mix the insulin. • Clean the rubber stopper with an alcohol swab. • Remove the needle cover, and pull back the plunger to draw air into the syringe. The amount of air should be equal to the insulin dose. Push the needle through the rubber stopper, and inject the air into the insulin bottle. • Turn the bottle upside down, and draw the insulin dose into the syringe. • Remove air bubbles in the syringe by tapping on the syringe or injecting air back into the bottle. Redraw the correct amount. • Make certain the tip of the plunger is on the line for your dose of insulin. Magnifiers are available to assist in measuring accurate doses of insulin. • Remove the needle from the bottle. Recap the needle if the insulin is not to be given immediately. • Select a site within your injection area that has not been used in the past month. • Clean your skin with an alcohol swab. Lightly grasp an area of skin, and insert the needle at a 90-degree angle. • Push the plunger all the way down. This will push the insulin into your body. Release the pinched skin. • Pull the needle straight out quickly. Do not rub the place where you gave the shot. • Dispose of the syringe and needle without recapping in a puncture-proof container.