Chapter 51 Assessment and Management of Patients With Diabetes

Diabetes A group of diseases characterized by hyperglycemia caused by defects in insulin secretion, insulin action, or both Affects nearly 25.8 million people in the United States; one third of cases are undiagnosed Prevalence is increasing Minority populations and older adults are disproportionately affected

Functions of Insulin Transports and metabolizes glucose for energy Stimulates storage of glucose in the liver and muscle as glycogen Signals the liver to stop the release of glucose Enhances storage of fat in adipose tissue Accelerates transport of amino acids into cells Inhibits the breakdown of stored glucose, protein, and fat

Type 1 Diabetes Insulin-producing beta cells in the pancreas are destroyed by an autoimmune process Requires insulin because little or no insulin is produced Onset is acute and usually before 30 years of age 5% to 10% of persons with diabetes

Type 2 Diabetes Decreased sensitivity to insulin (insulin resistance) and impaired beta cell function result in decreased insulin production 90% to 95% of person with diabetes, onset over age 30 years, increasing in children, obesity Slow, progressive glucose intolerance Treated initially with diet and exercise Oral hypoglycemic agents initially may need to convert to insulin or use both

Risk Factors Type 1: early onset, familial, genetic predisposition, possible immunologic or environmental (viral or toxins) factors Refer to Chart 51-1 Type 2: obesity, age, previous identified impaired fasting glucose or impaired glucose tolerance, hypertension ≥140/90 mm Hg, HDL ≤35 mg/dL or triglycerides ≥250 mg/dL, history of gestational diabetes or babies over 9 pounds

Clinical Manifestations “Three Ps” Polyuria Polydipsia Polyphagia Fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections Type 1 may have sudden weight loss

Diagnostic Findings Fasting blood glucose 126 mg/dL or more Random glucose exceeding 200 mg/dL Gerontologic considerations: age-related elevation of blood glucose A1-C

Treatment Goal: Maintain Normal Blood Glucose Levels (Hgb A1c <7%) Intensive control, defined as three or four insulin injections per day or continuous subcutaneous insulin infusion, insulin pump therapy plus frequent blood glucose monitoring, and weekly contacts with diabetic educators, dramatically decreases development and progression of complications such as retinopathy, nephropathy, and neuropathy.

Dietary Management Goals Maintain the pleasure of eating; include personal and cultural preferences Promote exercise and activity Achieve and maintain BMI <25 Prevent wide fluctuations of blood glucose levels Decrease serum lipids, if elevated

Role of the Nurse Be knowledgeable about dietary management Communicate important information to the dietician or other management specialists Reinforce patient understanding Support dietary and lifestyle changes

Glycemic Index Combining starchy foods with protein and fat slows absorption and glycemic response. Raw or whole foods tend to have lower responses than cooked, chopped, or pureed foods. Eat whole fruits rather than juices; this decreases glycemic response because of fiber (slowing absorption).

Other Dietary Concerns Alcohol Nutritive and nonnutritive sweeteners Reading labels

Exercise Lowers blood sugar Aids in weight loss Lowers cardiovascular risk

Educating Patients in Insulin Self-Management Use and action of insulin Symptoms of hypoglycemia and hyperglycemia Required actions Blood glucose monitoring Self-injection of insulin Insulin pump use

Oral Antidiabetic Agents Used for patients with type 2 diabetes who require more than diet and exercise alone Combinations of oral drugs may be used Major side effect: hypoglycemia Nursing interventions: monitor blood glucose for hypoglycemia and other potential side effects Patient education

Acute Complications of Diabetes Hypoglycemia DKA Hyperglycemic hyperosmolar syndrome (HHS) Comparison of DKA and HHS: refer to Table 51-7

Hypoglycemia Abnormally low blood glucose level (below 50–60 mg/dL); too much insulin or oral hypoglycemic agents, excessive physical activity, and not enough food Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, hunger Central nervous system symptoms: inability to concentrate, headache, confusion, memory lapses, slurred speech, drowsiness Severe hypoglycemia: disorientation, seizures, loss of consciousness, death

Management of Hypoglycemia Give 15 g of fast-acting, concentrated carbohydrate Three or four glucose tablets 4 to 6 oz of juice or regular soda (not diet soda) Retest blood glucose in 15 minutes; retreat if >70 mg/dL or if symptoms persist more than 10 to 15 minutes and testing is not possible Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within 30 to 60 minutes

Emergency Measures If the patient cannot swallow or is unconscious: Subcutaneous or intramuscular glucagon (1 mg) 25 to 50 mL of 50% dextrose solution IV

Diabetic Ketoacidosis (DKA) Absence or inadequate amount of insulin resulting in abnormal metabolism of carbohydrate, protein, and fat Clinical features Hyperglycemia Dehydration Acidosis Refer to Figure 51-7 “Sick day rules”: refer to Chart 51-9

Assessment of DKA Blood glucose levels >300 to 1,000 Severity of DKA not only due to blood glucose level Ketoacidosis is reflected in low serum bicarbonate, low pH; low PCO2 reflects respiratory compensation (Kussmaul’s respirations) Ketone bodies in blood and urine Electrolytes vary according to degree of dehydration; increase in creatinine, Hct, BUN

Treatment of DKA Rehydration with IV fluid IV continuous infusion of regular insulin Reverse acidosis and restore electrolyte balance Note: rehydration leads to increased plasma volume and decreased K; insulin enhances the movement of K+ from extracellular fluid into the cells Monitor blood glucose, renal function and urinary output, ECG, electrolyte levels, VS, lung assessments for signs of fluid overload

Hyperglycemic Hyperosmolar Syndrome Hyperosmolar hyperglycemia is caused by a lack of sufficient insulin; ketosis is minimal or absent Hyperglycemia causes osmotic diuresis, loss of water and electrolytes, hypernatremia, and increased osmolality Manifestations include hypotension, profound dehydration, tachycardia, and variable neurologic signs caused by cerebral dehydration High mortality rate

Treatment of HHS Rehydration Insulin administration Monitor fluid volume and electrolyte status Prevention BGSM Diagnosis and management of diabetes Assess and promote self-care management skills

Long-Term Complications of Diabetes Macrovascular: accelerated atherosclerotic changes, coronary artery disease, cerebrovascular disease, and peripheral vascular disease Microvascular: diabetic retinopathy (refer to Figure 51- 8), and nephropathy Neuropathic: peripheral neuropathy, autonomic neuropathies, hypoglycemic unawareness, neuropathy, sexual dysfunction